Atlas Hematologie Crop

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INTERNATIONAL
STUDEI\lT ED!TIOJ.V
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INTRODUCTION
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The book contains a short descriptive text of the development of the blood cells followed by a
table of normal haematological va lues and thereafter the illustrations are placed in seven main
sections . The first section covers the red cell series which includes both normoblastic and
megaloblastic erythropoiesis; the next section covers illustrations of all white cell series in the
order of granular lcucocytcs, which arc sub-divided into neutrophil, eosinophil, and basophil
polymorphonuclear lcucocytcs, followed by lymphocytes, monocytcs and plasma cells . This is
followed by a section on the megakaryocyte series and platelet formation. Following this there
is a section on phase contrast microscopy. A short section of illustrations of parasitic conditions
of the blood follows. The following section, tu mours of the lymphoid tissue and other
neoplasms, includes a table of compara tive terminology with particular reference to tumours of
the lymphoid tissue . Finally a section on artefacts and other abnorma li ties follows. For ease of
comparison a separate section has not been devoted to the leukaemias, the several types being
included under the appropriate white cell sub-division.
An attempt has been made to maintain the same sequence for each cell series, i.e. normal
marrow, normal blood, non-neoplastic conditions of marrow and blood, neoplastic conditions
and then cell abnormalities and anoma lies, as these are common to both non-neoplastic and
neoplastic cells. This has not always been possible however, and on occasion the marrow and/or
blood pictures have been placed immediately preceding the illust rations of tissue changes in the
same condition.
At first glance it might appear that some illustrations of a cell series have been duplicated
but, if the captions are read carefully , it will be seen that various cell types, e.g. early
megaloblasts and promyclocytcs, may figure in one illustration, thereby allowing the reader to
compare cell types within the one field. It would be as impossible to give an accurate diagnosis
from one high-power photomicrograph as it would be to do so from one microscopic field;
t his is the reason for showing more than one illustration in several of the more common
conditions. Wherever great variation in size and nuclear configuration of any cell type is a
common feature, many small illustrations have been built up to a composite thus giving the
trainee in haematology a ready means of comparison.
Throughout the book low- and high-power illustrations of the principal and common
histological appearances of the visceral tissues in the various blood conditions have been
included in their proper context and illustrations of normal tissues have been included in close
proximity for comparison of overall pattern and cell type. No attempt has been made to
demonstrate a comprehensive series of the lesions in such conditions as lupus erythematosus
and no attempt has been made to cover the enormous range of mixed patterns seen in tumours
of the lymphoid tissue .
A separate maturation scheme is provided for easy comparison when studying the
illustrations.
I NTRODUCTION
The book contains a short descriptive text of the development of the blood cells followed by a
table of normal haematological values and thereafter the illustrations are placed in seven main
sections. The first section covers the red cell series which includes both normoblastic and
megaloblastic eryt hropoiesis; the next section covers ill ustrations of all white cell series in the
order of granular leucocytes, which are sub-divided into neutrophil, eosinophil, and basophil
polymorphonuclear leucocytes, followed by lymphocytes, monocytes and plasma cells. This is
followed by a section on the megakaryocyte series and platelet formation. Following this there
is a section on phase contrast microscopy. A short section of illustrations of parasitic conditions
of the blood follows. The following section, tumours of the lymphoid tissue and other
neoplasms, includes a table of comparative terminology with particular reference to tumours of
the lymphoid tissue. Finally a section on artefacts and other abnormalities follows. For ease of
comparison a separate section has not been devoted to the leukaem ias, the several types being
included under the appropriate white cell sub-division.
An attempt has been made to maintain the same sequence for each cell series, i.e. normal
marrow, norma l blood, non-neoplastic conditions of marrow and blood, neoplastic conditions
and then cell abnormalities and anomalies, as these are common to both non-neoplastic and
neoplastic cells. This has not always been possible however, and on occasion the marrow and/or
blood pictures have been placed immediately preceding the illustrations of tissue changes in the
same condition.
At first glance it might appear that some illust rations of a cell series have been duplicated
but, if the captions are read carefully, it will be seen that various cell types, e .g. early
megaloblasts and promyelocy tes, may figure in one ill ustration, thereby allowing the reader to
compare cell types within the one field. It wou ld be as impossible to give an acc urate diagnosis
from one high-power photomicrograph as it would be to do so from one microscopic field;
this is the reason for showing more than one ill ustration in several of t he more common
conditions. Wherever grea t va riation in size and nuclea r configuration of any cell type is a
common feature, many small ill ustrations have been built up to a composite thus giving the
trainee in haematology a ready means of comparison.
T hroughout the book low- and high-power illustrations of the principal and common
histological appearances of the visceral tissues in the various blood conditions have been
included in their proper context and illustrations of normal tissues have been included in close
proximity fo r comparison of overall pattern and cell type. No attempt has been made to
demonstrate a comprehensive series of the lesions in such conditions as lupus erythematosus
and no attempt has been made to cover the enormous range of m ixed patterns seen in tumours
of the lymphoid tissue .
A separate maturation scheme is provided for easy comparison when studying t he
illustrations .
DEVELOPMENT OF THE BLOOD CELLS
All blood cells are derived from the undifferentiated mesenchymal cell of the reticuloendothelial system (haemohistioblast). Normally these primitive blood cells are present in small
numbers and are difficult to identify in marrow smears but in pathological states with marrow
hyperplasia they may be more numerous.
In haemopoietic tissue the haemohistioblast gives rise to the haemocytoblast which has a
potentiality of progression to the eryth roid, myelo id or mega karyocyte series . Thus, the
haemocytoblast may develop to a pronormoblast, a myeloblast or a megakaryoblast. The cells of
the monocytic, lymphocytic and plasmocytic series also develop from the haemocytoblast but
their main source of origin is the lymphoid tissue outwith the bone marrow.
Stem cell ( haemohistioblast). This cell varies in size from 20 to 40 !J.m, its cytoplasm is
abundant and spreading with indefinite limits in many instances; it is commonly ru ptured
during the 'prepa ration of t he film. The cytoplasm is faintl y basophilic and on occasion contains
a few azurophilic granules. Usually the nucleus is oval, small in comparison to the volume of
the cytoplasm and invariably fou nd to be lying in relation to the long axis of the cell. The
nucleus shows a finely reticular chromatin pattern and generally stains a pale rose colour. One
or more nucleoli are usually discernible.
Haemocytoblast. In this cell, which is approximately 2~ !J.m in diameter, the volume of the
cytoplasm is small in comparison to the size of the nucleus. The cell is usually irregular in
outline, moderately basophilic and non-granular. The nucleus, which is large, round or oval
shows a fine reticular chromatin network , the stainingreact ion being heavier than that seen in
the haemohistioblast. It contains several definite blue stained nucleoli which may show
considerable variation in shape.
It should be borne in mi nd thin the process of maturations is progressive and con ti nuous and
that transitional forms between t he various stages will be seen.
H istioblast. This cell, which is the precursor of the monocyte, the plasma cell, the m ast cell
and possibly the lymphocyte, develops directly from the haemohistioblast. It is usually oval in
shape and approximately 20 1-l-m in diameter, w ith a high nucleo-cytoplasmic ratio. The
nucleus, which is usually positioned to the long ax is of the cell , stains a rose colour and contains
one or two pa.Je bl~e nucleoli which are bounded by a well-marked rim of deeply stained
chromatin. The cytoplasm shows a blue-grey staining reaction similar, but deeper in shade, to
t hat of t he monocyte.
ERYTHROPOIESIS
NORMOB LASTIC ERYTHROPOIESIS
Pronormoblast. This is the first cell which is recognisable as defi nitely belonging to the
erythroid series. It is approximately 12 to 20 IJ.m in diameter and is distinguishable from the
myeloblast by its deep blue cytoplasm, which is usually only a narrow rim arou nd the relativel y
large n ucleus; it often stains unevenly and may show a perinuclear halo. The nucleus consists of
a network of uniformly distributed chromatin strands giving a fine reticu lar appearance. It
stains a reddish p urple colour and contains several darker staining nucleoli.
Early normoblast. There is a very close resemblance between this cell and the pronormoblast;
it varies from 10 to 16 !J.m in diameter. The nucleus is relatively large, stains deeply and the
chromatin strands are thicker than in the pronorm oblast, giving a coarser appearance; generally
no nucleoli are to be seen.
Intermediate normoblast. In this cell , which is from 8 to 14 1-l-m in d iameter, the cytoplasm
shows a polychromatic staining reaction, i.e. a tendency to take both the basic and acid stains,
ATLAS OF HAEMATOLOGY
thus giving a purple tint which becomes more acidophilic as the cell matures, due to
haemoglobin appearing. The nucleus occupies a relatively smaller part of the total and decreases
in size as the cell ages; it now stains deeply and the chromatin is arranged in clumps.
Late normoblast. The cytoplasm of this cell , although acidophilic, may show a faint
polychromatic tint. The cell varies from 8 to 10 fJ.m in diameter. The nucleus is small and may
still show very coarse clumped chromatin which disappears as the nucleus shrinks and is
eventually seen as a homogenous blue-black structureless mass . As the cell matures the nucleus
is commonly eccentric, occasionally lobulated and is eventually lost by extrusion, fragmentation
or dissolution.
R eticulocyte . This is a young erythrocyte which still has a content of fine basophilic reticulum
which can be demonstrated with a supravital stain such as brilliant cresyl blue. When stained
by any of the Romanowsky methods these cells exhibit a diffuse pale basophilia. In normal
blood the reticulocyte content is from 0.02 to 2% . This cell is flat and disc-shaped and as it loses
its basophilic reticulum it develops into a mature red cell or erythrocyte.
Erythrocyte. This is a biconcave cell which shows a moderate variation in size, from 6.7 to 7.7
fJ.m with a mean of 7.2 fJ.m, is readily distorted because of its flexibility; hence the variations in
shape seen in stained blood films. It exhibits an eosinophilic reaction when stained by the
Romanowsky methods, the staining being deep at the periphery and gradually lessening
towards the centre because of the biconcavity of the cell. This pale central area is commonly
known as the area of central pallor and occupies less than one-third of the diameter of the
normal erythrocyte, but this may vary according to the staining technique. Cells with a normal
haemoglobin content are described as being normochromic.
MEGALOBLASTIC ERYTHROPOIESIS
Megaloblasts are not present in normal marrow. Their occurrence is due to disturbance of cell
growth and maturation caused by d eficiency of vitamin B 12 and/or folic acid. The maturation of
the megaloblastic series is similar to that of the normoblastic series but there are morphological
differences at each stage. Megaloblastic erythropoiesis is frequently accompanied by
abnormalities in development of the myeloid and megakaryocyte series. A moderate increase in
the number of haemohistioblasts and haemocytoblasts also occurs.
T he earliest cell in this series, in transition from the haemocytoblast is the promegaloblast and
maturation develops through early, intennediate and late megaloblast to the macrocyte. The
morphological differences from the normoblastic series affect the cell size and the appearance of
the nucleus.
The cell size is larger and the cytoplasm more abundant in comparison to normoblasts at
equivalent stages of maturation:
I. Promegaloblast
2. Early megaloblast
3. !ntelmediate megaloblast
4. Late megaloblast
5. Macrocyte
20 to
18 to
16 to
12 to
9 to
30 fJ.m
25 fJ.m
20 f).m
15 fJ.m
12 fJ.m
The nucleus is larger in comparison to the normoblast at all stages of development. The
chromatin has a more open pattern, being arranged in a fine reticular fashion giving the nucleus
a stippled appearance . This is often quite well marked in the intermediate stage and may still be
present in the late megaloblast. As the cell matures the clumping of the chromatin is much less
obvious than in normoblasts at the corresponding stages. Nuclear maturation lags behind
DEVELOPMENT OF T HE BLOOD CELLS
cytoplasmic haemoglobinisation with the result that megaloblasts with eosinophilic cytoplasm
may still show nuclei with fine reticular chromatin. One of more Howell-Jolly bodies may be
present in the late stages.
Promegaloblasts and early megaloblasts may constitute over SO% of the erythroid series in the
marrow in a severe megaloblastic anaemia.
LEUCOPOIESIS
THE MYELOID (GRANULOCYTIC) SERIES
Mature granular leucocytes are cells with cytoplasmic granules which give either a neutrophilic,
eosinophilic or basophilic reaction to the Romanowsky stains. Because of their lobula ted
(segmented) polymorphic nuclei these cells are referred to as polymorphonuclear leucocytes
(polymorphs). When used without qualification, the term 'polymorph ' refers to a mature
neutrophil leucocyte.
The myeloblast is the first recognisable cell of the granulocytic series from which the
promyelocyte, and then by progression, the myelocyte, the metamyelocyte, the non-segemented (stab)
forms and finally the mawre (segmented) granular leucocytes develop. Specific granules which
determine the nature of the mature cell, i.e. neutrophil, eosinophil or basophil begin to appear
at the promyelocyte stage and are fully differentiated in the myelocyte. Mitotic divisions occurs
up to the myelocyte stage, the normal metamyelocyte being incapable of mitosis.
The neutrophil (polymorphonuclear) series
Maturation of this cell type is characterised by the development of specific cytoplasmic granules
and changing of the staining reaction of the cytoplasm from basophilic to eosinophilic at which
stage the granules take an admixture of both staining elements. As the nucleus ripens it
becomes lobulated. There is also the development of motility and phagocytosis.
Myeloblast. Variation in the size of this cell is between 15 to 20 JJ.m. The cytoplasm may be
non-granular or may exhibit a few azurophil granules depending on the stage of development. It
is moderately deep blue in staining reaction which m ay be uneven, often being somewhat
lighter in the perinuclear region. The nucleus is round or oval and occupies about four-fifths of
the total cell area. The nuclear chromatin is arranged in fine strands which stain a reddishpurple colour and give an even, reticular appearance. There may be up to six nucleoli but two
to five are usual; they are of medium size and are generally sharply defined with a well-marked
chromatin border.
Promyelocyte. This cell, which is from 22 to 25 JJ.m in diameter, resembles the myeloblast
except that the cytoplasm contains granules (azurophil granules) which stain from blue to
reddish purple. The nuclear chromatin is somewhat coarser than in the myeloblast and
although nucleoli are still present they are less well defined.
Myelocyte. The differences between this cell and the promyelocyte are that the cytoplasmic
granules have now assumed their neutrophilic character and no nucleoli are discernible. The
cell is from 18 to 20 JJ.m in diameter, although at the very early stage it may be as large as 25
JJ.m. At this earlier stage the cytoplasm stains light blue and the cytoplasmic nuclear ratio is
increased. The cytoplasm progressively acquires a pinkish hue and in the mature form is
predominantly or completely pink. The nucleus is round or oval and the nuclear chromatin is in
the form of thick strands which stain deeper than in the promyelocyte.
Metamyelocyte. At this stage of development the cytoplasm is pink and contains fine
10
ATLAS OF J-IAEMATOLOGY
neutrophil granules resembling the myelocyte. The nucleus is smaller and slightl y indented
(kidney-shaped); there can be considerable variation in the size of this cell , from 14 to 20 j.lm.
Juvenile (non-segmemed) neutrophil leucocyte. Usually smaller than the metamyelocyte, this cell
has a deeply staining u-shaped nucleus in which the chromatin is coarse and clumped. They are
often described as 'stab' (rod-like) for ms.
Mature (segmented) neutrophil leucocy te. The diameter of this cell is from 12 to 14 j.lm, the pink
cytoplasm containing numerous fine neutrophil granules which are evenly distributed. Its
nucleus is lobulated, the number of lobes, which may overlap, varying from two or five ; they also
show variation in size and shape and are connected by thin chromatin strands, the nuclear
chromatin being arranged in larger clumps. Some neutrophi ls of the female have a nuclear
appendage with a well-defined head shaped like a drumstick attached to one nuclear lobe by a
thin chromatin strand . Such appendages do not occur in the neutrophils of the male.
The eosinophil (polymorphonuclear) series
This cell series develops through the same stages as the polymorphonuclear neutrophil series.
Apart from the large eosinophilic cytoplasmic granules which common ly have a reddish-orange
colour and which are apparent at the myelocyte stage, the cells have the same structural
characteristics as their neutrophil counterparts
The mature eosinophil leucocyte averages 16 j.lm in d iameter. Its nucleus is usually bi-lobed
and the large cytoplasmic granules do not overlap it as a general rule. These cells are very
fragile and are often damaged during the spreading of blood films, leaving the nucleus
surrounded by free granules.
T he basophil (polymorphonuclear) series
In this series the cells are characterised by the presence of large, round , deeply basophilic
staining grunules. Otherwise this cell type progresses through the same stage as the neutrophil
and eosinophil series.
The mature basophil leucocyte varies from 14 to 16 j.lm in diameter; its cytoplasm stains pink
and contains numerous large granules which tend to overlie the nucleus and obscure detai l but
do not pack the cytoplasm as do the granules of the eosinophil leucocyte. The nucleus of the
mature cell is usually bi-lobed.
Mast cell (tissue basophil)
These cells which develop from the histioblast are not found in human peripheral blood. They
are present in bone marrow in which tissue they may be numerous in cases of aplastic anaemia,
chronic blood loss, anaphylaxis and tumours of the lymphoid tissue involving the bone marrow.
This cell type differs from the true basophil in that its granules are insoluble whereas the
granules of the basophil leucocyte are soluble to a large degree in methyl alcohol. The granules
are much more numerous, coarser and stain deeply basophi lic; they exhibit a metachromatic
staining reaction to toluidine blue . The nucleus of this cell is usually round, not bi-lobed as in
the basophil leucocyte. It is a large cell, usually from 20 to 25 j.lm in diameter and may be
elongated.
1
DEVELOPMENT OF THE BLOOD CELLS
11
THE LYMPHOCYTIC SERIES

L ymph ocytes develop mainly in the lymp hoid tissues of the body, e.g. lymph nodes, lymphoid
follicles of the spleen and gastrointestinal tract, tonsils and other sites. Throughout the marrow
there are a number of small , primary lymphoid follicles.
Lymphoblasl. The primitive cell of this series is the lymphoblast from which large and small
lymphocytes develop. This cell , which resembles the myeloblast in general struct ure is
approxi mately I S to 20 1-'-m in diameter. It has non-granu lar cytoplasm which stains deep blue
at the periphery a nd a lighter colour centrally. The nucleus is large, usually occupying
four-fifths of the cell area and the nuclear chroma ti n is arranged in a reticular fashion and tends
to be stippled . As a general rule only one or two nucleoli arc present.
Prolymphocyte. This cell is smaller than its precursor and usuall y has a broad band of blue
staining cytoplasm, the nuclear chromatin tends to be clumped and no definite nucleolus can be
seen. As the transition from the lymph oblast to the lymphocyte is brief the term
'prolymphocyte' is of no great significance.
Large lymphocyte. Variation in the size of this cell is commonly fro m 12 to 16 1-'-m in diameter.
Its cytoplasm is fairly abu ndant and stains a sky-blue colour and there may be a few small,
sharply-defined azurophil cytoplasmic granu les present. The densely staining nucle us is round
or may be slightly indented and the chromatin tends to be clumped .
Small lymphocyte. This cell varies from 9 to 12 1-'-m in diameter and except for the difference
in size a nd the sca nty cytoplasm which is generall y little more than a narrow rim around the
large nucleus it is identical to the large lymphocyte.
THE MONOCYTIC SERIES

This cell typ e is formed mainly in the sp leen a nd lymphoid tissues and to a much lesser extent
in the bone marrow.
M onoblast. This primitive cell which is from 18 to 22 1-'-m in diameter is very similar in
appearance to the myeloblast except that the cyto plasm is usually lighter in colour and the
nuclear chromatin less definite . Several nucleoli may be visible.
Promonocyte. The size of this cell is variable, usually approximately 20 IJ..m in diameter. Its
cytoplasm which stains grey-blue may contain fine azuroph il granules. The nucleus is large and
generally convolu ted giving a folded appearance; the chromatin is usually loose, resembling a
netwo rk and no definite nucleoli arc visible.
Monocyte. The diameter of this large cell is gene rally from IS to 18 1-'-m with cytoplasm which
stains a grey-bl ue colour an d often described as having a ground glass appearance. Fine
azurophil granu les and vacuoles may be present in the cytoplasm . The nucle us is generally
round or kidney-shaped, bu t may be lobulated with two or more lobes, the chromatin being
arranged in skein-like strand s .
THE PLASMA CELL SERIES
The p lasma cell is thought to be a derivative of the stem cell (haemohistioblast) although o ther
cell types have been named as its precursor.
Plasmablast. The primitive cell of this series, closely resembling the lylJ)phoblast in size,
shape and staining reactio~ , has an average size of 18 IJ..m. No cytoplasmic gra nula tion is visible
and it is difficult to resolve the nucleoli although up to six may be present.
Pro plasma cell. Exhibiting considerable variation in size, from 1S to 25 IJ..m the cytoplasm has
12
a deep blue colour, is non-granular and usually shows a pale perinuclear halo. The nucleus is
generally eccentric but may be situated centrally within the cytoplasm. The nuclear chromatin
appears to be in the form of a loose mesh; several nucleoli may be discernible and are usually
more obvious than in the plasmablast.
Plasma cell. This mature cell varies in size, generally between 14 and 20 f-lm and has a deep
blue staining non-granular cytoplasm which may contain one or more vacuoles even in the
normal state. The nucleus is eccentric and small in relation to the size of the cytoplasm and
generally a clear perinuclear halo can be seen. In paraffin embedded sections from wellpreserved material, the chromatin is often clumped towards the margin of the nucleus in a
so-called cartwheel fashion. This appearance is not found in blood or marrow smears. Plasma
cells with two or m ore nuclei are a common finding in the marrow in chronic inflammatory
conditions and plasma cell myeloma. This is probably due to mitotic division of the nucleus
without corresponding division of the cytoplasm; the chromatin structure is usually denser in
these multiple nuclei.
THE MEGAKARYOCYTE SERIES AND PLATELET FORMATION
Megakatyoblasts. The primitive cell of this series varies from 25 to 30 J-lm in diameter ; its
cytoplasm, which stains intensely blue, is generally just an irregular rim to the large nucleus
which is usually oval or kidney-shaped. The nuclear chromatin is poorly defined and con tains
several deep blue staining nucleoli which are usually indefinite. In normal marrow, this cell
comprises less than 1 per cent of all the megakaryocyte series and is therefore difficult to find.
Megakaryoblasts with two, three or four nuclei may be seen, due to mitotic division of the
nucleus without corresponding division of the cytoplasm; this is a perfectly normal fi nding.
Promegakatyocyte (basophilic megakatyocyte). This cell is much larger than the
megakaryoblast; the cytoplasm which may exhibit a finely granular appearance, has a basophilic
staining reaction to the Romanowsky m ethods. The nucleus is large and usually indented, its
chromatin appearing as coarse, intertwining, deeply staining strands against a lighter stained
background.
Megakatyocyte (granular megakaryocyte). This is the largest cell found in marrow and can be
up to 100 f-lm in diameter. The cytoplasm is bulky and contains many azurophil granules which
are well marked against a pale stained background. The cell margin is irregular and in the late
stages of maturation (budding megakaryocyte) will show differentiation of granular platelets in
pseudopodia-like structures. The nucleus of this cell is small in comparison to the volume of
cytoplasm; it is usually multilobed or indented, with chromatin which is arranged in coarse,
deeply staining strands.
Platelets. These are small fragments of cytoplasm which have become detached from t he
periphery of the megakaryocyte. They are usually from 2 to 3 f-lm in dia meter bu t may range
from 1 to 4 f-lm. The cytoplasm stains light blue and contains a central area of azurophil
staining material.
3. Normal haematological values
18
Term s commonly used to describe anom alies and artefacts

seen in red blood cells in stained preparatio ns
Acanthocytes. These are red cells with fine projections from the surface. They occur as an
inherited abnormality associated with abnormal phospholipid metabolism.
Anisocywsis. This term is used to denote variation in cell size.
Anulocytes. Due to a lowered haemoglobin conrent these eryt hrocytes exhibit a large area of
central pallor.
Basophilic stippling. These small blue granules arc formed by condensation of basophilic
substance within the cy toplasm giving it a stippled appearance . In conditions such as severe
anaem ia these granules may be quite coarse .
Burr cells. T hese cells have several poinred projections resembling t he b urrs of certa in plants.
T hey are poikilocytes and are readily confused with crenated forms.
Cabot ,-ings. In some forms of severe anaemia these appear as purplish rings in the centre or
near the periphery of ery throcytes. L ike H owell-Jolly bodies they are nuclear remnants.
Crenated red blood cells. This artefact is usually due to fault y drying of a blood film.
Echinocytes. These cells have spicules evenly distribu ted over the su rface of the red cell as the
result of alteration of intra- and extracellular environment. The term is synonymous with Burr
cell .
Elliptocywsis. This is a form of poikilocytosis and is a heredi tary anomaly where a large
number of elliptical erythrocytes are present.
Heinz bodies. Polymerisation and precipitation of denatured haemoglobin molecules result in
Heinz bodies which are best demonstrated when supravitall y stained by methyl violet.
H owell-Jolly bodies. These are n uclear remnants and appear as dense blue inclusions. They
may be single or multiple, as a rule are commonly near the periphery of the cell and may be up
to 1 f.Lm in diameter. Both Howell-Jolly bodies and Cabot rings are found in blood films
following splenectomy and occasionally in dyshaem opoietic states such as megaloblastic anaemia
and the leu kaemias, but Cabot rings are fou nd less frequentl y than H owell-Jolly bodies.
Hypochromia. This denotes a decrease in the intensity of staining which may vary from only a
sligh t increase in size of t he area of central pallor to a very large area surrounded by a small ri m
of haemoglobinised cytoplasm.
Lepwcyte. This is a thin hypochromic cell of normal d iameter and decreased MCV.
Commonly fou nd in thalassaemia.
Microcytes. These are smaller and paler than normal ery th rocy tes.
Microspherocytes. Erythrocytes of spherical form, these cells are smaller t han normal
erythrocytes and because of their spherical shape do not exhibit an area of central pallor. They
are present in haemolyt ic diseases.
Pincered cells. These are erthrocytes which appear as if part of their substance had been
indented by pincers. This appearance probably represen ts the process of fragmentation.
Poikilocywsis. T hese are irregularly shaped ery throcytes . T his term includes such alterations
in shape as burr cells, elliptocytes, pear- and tear-shaped cells and sickle cells.
Polychromasia. This denot es that the cell is ta king both the basic and the acid dyes due to
alteration in the haem oglobin conten t of t he erythrocyte, the cell exhibiting much t he same
colouration as seen in the intermediate stage of erythropoiesis. In t his instance the cytoplasm
has lagged behind the nucleus in maturation and has not completely lost its ribonucleic acid .
Pyknocyte. Distorted and contracted red cells similar to the echinocyte.
Schiswcytes. These are the products of red cell fragmentation and ma ny take a triangular or
THE RED CELL SERIES
l
~
19
small elliptical form with indentation, or may appear as irregularly crenated cells. They are
common in haemolytic anaemia.
Sickle cells. In cases of haemolytic anaemia (sickle-cell anaemia) this anomaly occurs, many of
the erythrocytes exhibiting a definite sickle-shape and taking the stain much more heavily than
the surrounding erythrocytes.
Siderocytes. These are erythrocytes which contain one or more unevenly distributed ironcontaining granules, demonstrated by a positive Prussian Blue reaction. They are sometimes
discernible as basophilic dots in films stained by the Romanowsky methods and may then be
referred to as Pappenheimer bodies. These cells are found in peripheral blood in disorders
associated with impaired haemoglobin synthesis, e.g. thalassaemia and lead poisoning. They are
also present in blood following splenectomy where this has been undertaken for the treatment
of certain haemolytic conditions.
Spherocytes. Spheroidal cells occuring in many types of haemolytic anaemia including
hereditary spherocytosis, immune haemolytic anaemia and in burns.
Stomatocytes. These are red cells in which the central biconcave area appears as a slit rather
than a circular concavity. Large numbers of this type of red cell have been noted in an
uncommon type of hereditary haemolytic anaemia.
Target cells. In these cells there is a rounded central area of normally stained cytoplasm
surrounded by a clear lightly stained area which in turn is surrounded by a normochromic
peripheral ring.
20
Fig. 1 Marrow film Normoblastic erythropoiesis

Left: The cell types seen are:
( I) Transitional stage between pronormoblast and early normoblast. (2, 3) Early normoblasts. (4, 5, 6) Transitional
forms between early and intermediate normoblasts. (7; 8, 9) Intermediate normoblasts, of which (9) is the metaphase
stage of mitosis. ( 10) Late normoblast. Leishma11 stailz x 1200
Right: This field shows intermediate and late normoblasts and one lymphocyte (L). Leishma11 stai11 x 1200
THE RED CELL SERIES
I
I
'f
Fig. 2 Marrow film Normoblastic hyperplasia

pNb- pronormoblast; INb- intermediate normoblast; ENb - early normoblast; L - lymphocyte; Stab- nonsegmented polymorphonuclear leucocyte.
In this illustration the majority of the cells are normoblasts in varying stages of development. The lymphocytes are
useful for comparison of nuclear structure and intensity of staining. In this condition the myeloid-erythroid ratio is
markedly decreased . May-Griit~wald-Giemsa stai11 x 1200
21
22
Fig. 3 Marrow film Macronormoblastic hyperplasia

In this condition the normoblasts are larger than their normal counterparts of similar age, but in all other respects,
including nuclear structure, they are normal in appearance . Leislrma11 stain x I 200
Fig. 4 Marrow film Iron deficiency anaemia

There is marked erythroid hyperplasia present in this specimen , the increase being mainly in the more mature forms of
normoblasts, which are smaller than normal. This is often described as rnicronormoblastic hyperplasia. The cytoplasm
of the normoblasts is decreased, the cell borders are raggedand their staining reaction irregular. M ay-Gronwald-Giemsa
stai11 x 1200
THE RED CELL SERIES
23
Fig. 5 Marrow film Iron deficiency

The Prussian Blue reaction stains haemosidcrin blue. In this preparation there is absence of stainable haemosiderin.
Absent stainable ha~mosiderin is a sensitive indication of iron deficiency. ?russian Blue reaction, cozmterstained Methyl
R ed x 800
Fig. 6
M arrow film
Left: Howell-Jolly bodies. Small, densely staining dark blue particles are seen in the polychromatic cytoplasm of the
late megaloblasts. These bodies are most often seen following splenectomy but are also present in blood from the
leukaemias and dyshaemopoietic conditions such as megaloblastic anaemia, as in this example . Leishman stai1z x 1200
Right: Basophilic stippling. Basophilic stippling is demonstrated as very fine pin-point cytoplasmic granules and is
often associated with toxic conditions, e.g. lead poisoning and d yshaemopoietic states such as megaloblastic anaemia
and thalassaemia. Polychromasia is also present and is seen as a diffuse light blue staining in several erythrocytes. These
are normally present in small numbers in the peripheral blood where they stain as reticulocytes (Fig. 21) . Leishman
stain x 1200
24
Fig. 7 Blood film Normal erythrocytes

Cells are of uniform size and shape with a normal haemoglobin concentration. One cell, centre of field, reveals a small
area of central pallor which is less than one-third of the total cell volume . Wright's stain x 1200
THE RED CELL SERIES
25
Fig. 8 Blood film Abnormal erythrocytes

These fields from a case of pernicious anaemia, show anisocytosis, macrocytosis (Mac), poikilocytosis (Poik), an
intermediate normoblast (INb) and a late normoblast (L Nb) with a Howell-Jolly body (HJ). This composite illustration
along with Figure 9 serves to show how a number of red cell anomalies may occur in an individual patient. Leishma11
stai11 X 1200
26
Fig. 9 Blood film Abnormal erythrocytes

This demonstrates some of the red cell anomalies found in the blood in pernicious anaemia, such as anisocytosis,
macrocytosis (Mac), poikilocytosis (Poik), and polychromasia (Pol). Also present is an intermediate megaloblast (1Mb)
and a late normoblast (LNb) with polychromatic cytoplasm. In the right-hand illustration is a late normoblast in which
the nucleus is pyknotic and gives the impression that it is beginning to break up. Leishman stain x 1200
THE RED CELL SERIES
27
~8~
(]~
6J
3
~
s:
HJ
scJ
F ig. 10 Blood film Pernicious anaemia (und er treatment)

This illustration shows poikilocytosis, anisocytosis, polychro masia (Pol), basophilic stippling (BS), a normoblast with
polychrom atic cytoplasm and a H owell-Jolly body (HJ). Also seen are several schistocytes (Sc) and a normoblast in
mitosis, a piece of the nucleus of which has broken away; t his would have been seen eventually as a H owell-Jolly body.
Note t he hypochromia of the red blood cells due to deficient hacmoglobinisation. Leishman stain x 1200
28
Fig. 11 Blood film

Left: Hereditary spherocytosis. The spherocytes are small, round, deeply staining erythrocytes. In the lower portion of
the illustration a late normoblast can be seen. Leishma11 stai11 x 1200
Right: Elliptocytosis. Over 50% of the erythrocytes present have a moderate or pronounced elliptical form. Leishma11
stai11 x 1200
THE RED CELL SERIES
Fig. 12 Blood film Spherocytosis

This illustration is from a film of blood from a patient who had been severely burned. The extremely small spherical
cells are erythrocytes which have been affected by heat. This condition is sometimes referred to as thermal haemolytic
anaemia. May-Griin wald-Giemsa stain x 1200
29
30
ATLAS OF H AEMATOLOGY
()
riZ
~~
k
8
Fig. 13
GBG
~ODa
8~u
Po;k
\)
Blood film
Lefc: Poikilocytosis and schistocytosis. The erythrocytes show marked poikilocytosis (Poik) and schistocytosis (Sc)
also anisocytosis, polychromasia (Pol) and hypochromia. From a case of thalassaemia minor. May-Griinwald-Giemsa
scain x 1200
Righc: Poikilocytosis and macrocytosis . Pear-shaped, tear-shaped and small irregular poikilocytes (Poik) are seen, and
also numerous rnacrocytes (Mac). From a case of pernicious anaemia. May-Griinwald-Giemsa scain x 1200
THE RED CELL SERIES

/
Fig. 14 Blood film

Left: Poikilocytosis and macrocytosis. This illustrates the alteration in shape of the erythrocytes. Poikilocyte (Poik),
sickle cell (S) and macrocyte (Mac). Leishman stain x 1200
Right: H ypochromia and target cells. In this extreme example of hypochromia (Hyp) a large area of central pallor is
seen in many of the erythrocytes . Four target cells (T ) are present; these have a normochromic centre separated from
the normochromic peripheral ring by a broad unstained band. L eishman stain x 1200
31
32
Fig. 15 Blood film Target cells

These cells exhibit a rounded central area of normal staining surrounded by a clear lightly stained area, which is
surrounded by a normochromic peripheral ring . Target cells are commonly associated with chronic liver disease.
Wright's stain x 1200
Fig. 16 Blood film

Left: Anisocytosis. This illustration demonstrates the marked inequality in size of the erythrocytes. Leishman stain x
1200
Right: H ypochromia. In this condition there is a marked decrease in the intensity of staining of the erythrocytes. Many
of the cells show a large area of central pallor surrounded by a darker rim at the periphery of the cell. This is referred to
as ring staining. A target cell is present at uppel' right of the field. Leishman stain x 1200
I
THE RED CELL SERIES
33
F ig. 17 Blood film Pincer ed cells

This illustration shows a curious type of erythrocyte which is occasionally seen in cases of hereditary haemolytic
anaemia and also in cases of haemolytic anaemia resembling hereditary spherocytosis. Several of the erythrocytes have
an indented appearance as if they had been gripped by pincers. May-Griinwald-Giemsa stain x 1200
Fig. 18 Blood film D imorphism

In this condition both macrocytic and hypochromic microcytic anaemia exist at the same time. In this example the
macrocytosis is not as pronounced as in pernicious anaem ia and does not overshadow the associated iron deficiency .
Wright's stai1z x 1200
34
Fig. 19 Blood film Stomatocytes

In these red cells the central biconcave area appears as a slit rather than a circular concavity. This may be a congenital
abnormality but may also be present in severe liver disease. May-Griinwald-Giemsa stain x 1200
Fig. 20 Blood film M acrocytic a naemia of pregnancy
Left: The blood picture is similar to that seen in pernicious anaemia; marked oval macrocytosis, anisocytosis and
poikilocytosis are all present. May-Grii11wald-Giemsa stain x 1200
Right: This illustration , from the same patient, shows the appearance after treatment with folic acid. Many of the
erythrocytes exhibit varying degrees of polychromatic staining which indicates a satisfactory response to therapy. Note
also the late normoblast in this field. May-Griinwald-Giemsa stain x 1200
THE RED CELL SERIES
35
Fig. 21 Blood film Haemolytic anaemia

Preparation from a patient suffering from idiopathic acquired haemolytic anaemia. Polychromatic cells and microcytic
cells are prominent. Note the intermediate and late normoblasts. May-Grii11wald-Giemsa staill x 1200
Fig. 22 Blood film Sickle-cell anaemia

The bizarre-shaped red blood corpuscles include elongated narrow types with rounded and pointed ends; they are sickle
or oat-shaped and tend to take the stain to a heavier degree than the other erythrocytes. May-Grii11wa/d-Giemsa stai11
X / 200
36
Fig. 23 Blood film Acanthocytosis

In this film , practically all of the red cells have fin e projections from the surface. This appearance differs from burr cells
(Fig. 34) in that the projections are more filamentous. May-Griir~wald-Giemsa stam x 1200
Fig. 24 Blood film Polychromasia, nucleated red blood cells

This illustrations show large polychromatic cells staining blue grey and nucleated red blood cells. May-Griilzwald-
Giemsa stain
1200
THE RED CELL SERIES
37
Fig. 25 Blood film Haemolytic disease of the newborn

The prominent feature in this preparation is that of polychromatic cells and nucleated red blood cells. May-Griillwald-
Giemsa stai11 x 1200
Fig. 26 Blood film H aemolytic uraemic syndrome

In this illustration there are many polychromatic cells, nucleated red blood cells, and prominent burr cells. May-
Griillwald-Giemsa stai11 x 1200
38
Fig. 27 Blood film Microangiopathic haemolytic anaemia

In this condition, contracted and distorted cells, some of which are irregular and angular in shape are illustrated. These
are known as triangular or helmet cells. Red cell fragments, some with spinous processes and polychromatic cells
(bottom left), are also present. Wright's stain x 1200
THE RED CELL SERI ES
39
..
Fig. 28 Blood film Howell-Jolly bodies

Howell-Jolly bodies are nuclear remnants appearing as small round, densely staining, dark purple particles, commonly
near the periphery of the cell. They are seen most often following splenectomy, but are occasionally present in
dyshaemopoietic states such as megaloblastic anaemia and leukaemia. May-Griinwald-Giemsa stain x 1200
.,
. .
-
--e ee
a .
It
..
-- ~~
Fig. 29
Blood film
Reticulocytes from a case of hereditary spherocytosis (acholuric jaundice)
Left: The basophilic granules and filaments are clearly defined in this preparation stained with Brilliallt Cresyl Blue
X 1200
Right: This film has been stained with Brilliant Cresyl Blue and counterstained with L eishman and clearly demonstrates
the microspherocytes. The filaments and granules are not so well differentiated as in the fi lm which has not been
counterstained . x 1200
40
,I
F ig. 30 Blood film Heinz bodies

Deep purple bodies are seen, some lying close to the periphery of the red cells and others attached to the outer surface.
Several bodies may be present in the same cell, but when large they are usually found singly. T he large bodies can be
up to 1 JJ.m in diameter. Heinz bodies are the result of polymerization and precipitation of denatured haemoglobin
molecules. Methyl Violet. x 1200
F ig. 31 Blood film Siderocytes (Pappenhe imer bodies)

Many of the erythrocytes show varying numbers of iron-containing granules which are deep blue in colour; the
individual granules can be up to 2 JJ.m in diameter. Prussian Blue reaction, May-Griirzwald-Giemsa stairz X 1200
THE RED CELL SERIES
41
Fig. 32 Blood film H owell-Jolly bodies

Howell-Jolly bodies can be seen near the periphery of the cell. This preparation is from a post-splenectomy patient who
developed megaloblastic anaemia. Macrocytes containing H owell-Jolly bodies are illust rated. May-Grii11wa/d-Giemsa
srai1z x 1200
Fig. 33 Blood film Ro ulea ux formation

T his illustration demonst rates the phenomenon of running together of the red blood cells to form aggregates resembling
piles of coins wh ich is known as rouleaux formation. It is sometimes difficult to distinguish between t rue agglut ination
and rouleaux formatio n when the latter appears in a marked degree , forming compact masses very similar to the
appcaran~e gzven by true agglutination ( Fig. 40). Rou leaux formation is seen in conditions where the albumi n:
globulin serum protein balance is disturbed, as occurs in multiple myeloma o r when too concentrated a cell suspension
is used. Le1shma11 stai11 x 1200
42
Fig. 34 Blood film Burr cells

This illustration shows the contracted red blood cells with spiny surface projections which are often referred to as 'burr'
cells because of their resemblance to the burrs from certain plants. T hese cells are deformed poikilocytes and are
commonly seen in blood fil ms from patients with chronic renal failu re. Leishman stai11 x 1200
THE RED CELL SERIES
43
Fig. 35 Blood film Thalassaemia ma jor

T he red cells vary greatly in size, are distorted in shape and contain little pigment. The haemoglobin outlines the
periphery of the cell. Target cells are present, as are distorted nucleated red blood cells. Bizarre poikilocytes and
distorted red cell remnants are also present. Leishman stain x 1200
'
44
Fig. 36 Blood film T halassaemia minor

The red cells exhibit hypochromia , anisocytosis, moderate poikilocytosis and microcytosis. Target cells are also present,
as are basophilic stippled cells in lower part of the field, left centre. Leishman stain x 1200
Fig. 37 Blood film Basophilic stippling

This shows fine basophilic stippling in three of the red cells present in this illustration. The blood film was prepared
from a patient suffering from lead poisoning. May-Griinwald-Giemsa stain x 1200
THE RED CELL SERI ES
45
..
Fig. 38 Blood film Haemoglobin 'H' inclusions

The small fine inclusions in the red cells appear after incubation with Brilliant Cresyl Blue and contrast with the more
coarse basophilic granules of the reticulocytes. Brilliam Cresy/ Blue x 1200
Fig . 39 Blood film Haemoglobin 'C'

The red cells exhibit anisocytosis and poikilocytosis as well as targeting with some hypochromia. These morphological
changes are usually associated in t his condition with minimal anaemia. May-Griinwald-Giemsa stain X 1200
46
Fig. 40 Blood film Autoagglutination

The red cells have formed clumps or aggregates, the shape of the agglutinated masses being quite distinguishable from
the intertwining columns seen in rouleaux formation (Fig. 33). This specimen is from a patient suffe ring from cold
agglutinin disease. Leishma11 stai11 x 1200
THE RED CELL SERIES
F ig. 41 Bloo d film Autoagglutination

In this illustration there is agglutination of both erythrocytes and neutrophil leucocytes. The leucocytes appear to be
much smaller than in Figure 40; this is due to the pressure o n these cells by the surrou nding masses of erythrocytes.
Leishma11 stail1 x 1200
47
48
Fig. 42 Necro biotic c hanges and inclusion bodies- Red cell series
This series of illustrations shows necrobiotic changes and inclusion bodies in the red cell series, as follows: A, Band C,
necrobiotic change in late normoblasts; in C the nucleus has been in the prophase stage of mitosis but has become
necrotic. D is a late stage of mitosis in a normoblast which is necrotic.
E and F depict single and multiple Howell-Jolly bodies in a late normoblast and a normocyte, whereas G, Hand I
show Howell-Jolly bodies in macrocytes. Note also the polychromasia of many of these cells. J , K , L , M and N are
examples of Cabot rings which , like Howell-Jolly bodies, are nuclear remnants. N is an example where the ring is at the
periphery of the cell , whereas the others show an outer band of cytoplasm. K and M have double rings. All of these
cells show fine basophilic stippling and K, M and N also contain Howell-Jolly bodies. Cabot rings are seen following
splenectomy and in dyshaemopoietic states such as megaloblastic anaemia and leukaemia.
0 , P , Q and R show basophilic stippling in varying degrees of coarseness, this phenomenon being associated with
toxic states such as lead poisoning and dyshaemopoietic states, e.g. megaloblastic anaemia and thalassaemia.
Polychromasia is also present in several of the cells. Leishmau scaiu x 1200
THE RED CELL SERIES
49
Fig. 43 Blood film H ypcrscgmentcd neutrophil leucocytcs

Normally the nucleus of the segmented ne utrophils have less than five lobes. Increased segmentation as illustrated is
usually the first morphological abnormality to appear in a developing megaloblastic state. M ay-Griilzwald-Giemsa stai1z
X
/200
I,
--
50
Fig. 44 Marrow film Megaloblast series

L eft: Shows an early megaloblast (EMb) with indistinct nucleoli and an intermediate megaloblast (1Mb) and late
megaloblasts (LMb). May-Griinwald-Giemsa stain X 1200
Right: This field illustrates an early megaloblastic (EMb) and an early megaloblast in the anaphase stage of mitosis, also
intermediate (1Mb) and late (LMb) megaloblasts. May-Griinwald-Giemsa stain X 1200
THE RED CELL SERIES
51
Fig. 45 Marrow film Megaloblastic erythropoiesis

This illustrates early and intermediate megaloblasts and also an early myeloblast in the anaphase stage of mitosis. Note
the typical spongy stippled appearance of the nuclei , and in the early megaloblasts, some definite nucleoli and shadow
necleoli . May-Griirzwald-Giemsa stairz x 1200
Fig. 46 M arrow film Mega loblast series

A is an example of an early megaloblast, the nucleus of which is large and spongy and the cytoplasm basophilic. B is an
intermediate form and should be compared with A, when it will be seen that the nucleus is smaller and that the
cytoplasm is becoming polychromatophilic. C, D and E are all late m egaloblasts; note the acidophilic cytoplasm and
that the nucleus is becoming smaller and denser in its staining properties. In E the nucleus is being expelled . D shows
several Howell-Jolly bodies. F is a typical macrocyte. Leishmarz stairz x 1200
52
ATLAS OF HAEM ATO LOGY
Fig. 47 Marrow film Megaloblas t series

Left : A megaloblast in the anaphase stage of mitosis; also a promeylocyte (pMy). M ay-Griinwald-Giemsa stain
X 1200
Right : This composite field shows two intermediate megaloblasts and two late megaloblasts, one of which shows a
Howell-Jolly body and the other twinning of the nucleus. May-Griinwald-Giemsa Stain x 1200
THE RED CELL SERIES
53
Fig. 48 Marrow film Stages of mitosis

Immature haemopoietic cells in early prophase (A) (the nuclear membrane (NE) is still apparent), early metaphase
(B), metaphase-anaphase (C), anaphase (D ), anaphase-telophase (E), telophase (F). Also illustrated is a pair of
daughter cells (G). L eishman stain x 1200
54
ATLAS OF HAEMA TO LOGY
Fig. 49 Early megaloblast

The nucleus is of premature appearance with pronounced nucleoli and no chromatin condensation. The cytoplasm
contains large mitochondria, lysosomal granules and numerous free ribosomes. The cell exhibits marked nuclear
crythroplasmic asynchrony. Glutaraldehyde, urauy lacetate, lead cirate x 18 200
THE RED CELL SERIES
55
Fig. 50 Marrow film Megaloblastic anaemia

Left: Several early megaloblasts (EMb), which vary in size, are present along with a typical promyelocyte (pMy).
Right: Shows a large early megaloblast (EMb) in which shadow nucleoli can be resolved; also present are two late
megaloblasts (LMb). Note also the variation in size of the red blood corpuscles. May-Grii11wa/d-Giemsa
Szai11 x 1200
56
THE RED CELL SERIES
57
Fig. 51 Megaloblastic anaemia

A. M arrow film. This field shows numerous megaloblasts at various stages of development, from the
promegaloblast to the late megaloblast. Note that in the more primitive cells, to the top and left of the field,
shadows of nucleoli are still apparent. May-Griinwald-Giemsa szain x 1200
B. Marrow aspirate section. This section of marrow is from the same aspirated specimen as field A and
shows the marked shrinkage and distortion which takes place during fixation and processing of the tissue. While it
would still be possible to give an opinion on the type of cells present it could not be stated definitely that the
large cells are megaloblasts. Haemalum & Eosin x 800
C . Marrow trephine needle biopsy. This is a section from a trephined specimen from the same case of
megaloblastic anaemia. The gross distortion and disruption of the cells, due to fixation and decalcification, make a
definitive diagnosis impossible. The large pleomorphic cells with large nuclei mimic the appearance of malignant
epithelial cells. This pseudo-carcinomatous appearance is a well known artefact in histological rather than
cytological specimens in megaloblastic erythropoiesis. For this reason the diagnosis of megaloblastic erythropoiesis
should be based on cytological rather than histological preparations. H aemalum & Eosin x 800
58
Fig. 52 Marrow film Megaloblastic erythropoiesis

This illustrates frank megaloblastic erythropoiesis. An early megaloblast, intermediate and late megaloblasts are
illustrated, as well as one megaloblast in mitosis. The early and intermediate forms exhibit a stippled appearance
of the nucleus which becomes more coarse at the late megaloblast stage. May -Gnl11wald-Giemsa stai11 x 1200
T HE RED CELL SERIES
59
F ig. 53 Marrow Erythrophagocytosis

Erythrophagocytosis seems to be common to primitive marrow cells of all types as shown in this series of
illustrations. A shows a giant erythroblast with a bi-lobed nucleus. B is a p rimitive monoblast. C the cell shown
here is a lymphoblast the nucleus of which h as been compressed by an ingested erythrocyte. D is a myeloblast
which shows toxic granulation in addition to the ingested erythrocyte. E shows two mast cells, the lower of which
contains two ingested erythrocytes. May-Griinwald-Giemsa stain x 1200
Fig. 54 Marrow film Erythroleukaemia (Di Guglielmo's disease)

Left: There is a complete absence of cells of the myeloid series, all the cells p resent being of erythroblastic origin.
Note the early and late erythroblasts with multiple nuclei, and also the mitotic forms. May -Griinwald- Giemsa x 500
Right: At the top of this illustration a late normoblast with twin nuclei can be seen and lying in close proximity is
an atypical late normoblast with a four lobed nucleus which shows 'megaloblastoid' changes. Lower in the field
are several primitive cells of erythroblastic potentiality, one of which has a twin lobed nucleus. May -GninwaldGiemsa stain x 1200
60
':1 ,'~ -~
~"
Fig. 55 Marrow film E rythroleukaemia (D i Guglielmo's disease )

All the cells in this composite illustration belong to the erythroblastic series and several in varying stages of
development exhibit multiple nuclei . At bottom left, a cell which is either a proerythroblast or an early
normoblast has twin nuclei and also peculiar vacuolation of the cytoplasm, while at bottom right there is an
atypical late normoblast with four distinct nuclei showing megaloblastoid change. M ay-Griinwald-Giemsa stain
X 1200
Fig. 56 Marrow film Ery throleukaemia (Di Gug lielmo's disease)

The Periodic Acid-Schiff Reaction commonly shows strong diffuse and granular positivity in the abnormal
erythroblasts depicted here from a case of erythrolcukacmia. Periodic A cid- Schiff (PAS) x 1200
THE RED CELL SERIES
61
F ig. 57 S pleen Norm al

A non-reactive lymphoid follicle is shown with its arteriole. Compare the amount of lymphoid tissue with that in
Figures 78 and 256. Haemalwn & Eosin x 50
. . .'"\ .... '
~,..
;.,A
':""
F ig. 58 Sternal m a rrow aspira te section Norma l

L eft : In this biopsy specimen, no bone trabeculae or fat spaces are present. Compare th is with Figure 59.
H aema/um & Eosin x 150
R ight : In this mass of haemopoietic tissue, only a few cells are readily distinguishable. Near the bottom margin
there is a large megakaryocyte and slightly to the right of it, two mitotic figu res can be seen. Several late
normoblasts are easily distinguished by their dark-blue nuclei and red cytoplasm. Haemalum & Eosin x 450
62
Fig. 59 Vertebral marro w section Normal

T his shows bone trabeculae, fat spaces and haemopoietic tissue in normal proportions. Haema/wn & Eosin x 40
..
r.....
/
Fig. 60 Ma rrow Trephine needle biopsy specimen Aplastic anaemia

This shows a marked increase in the proportion of fat cells along with a corresponding marked decrease in the
proportion of haemopoietic cells; only a very occasional blood cell is present between the fat spaces. Compare this
illustration with Figure 58. Haemalum & Eosin x 90
THE RED CELL SERIES
63
F ig. 61 Spleen Polycythaemia rubra vera

This shows sinusoidal congestion, with some swelling of the sinusoidal lining cells seen in the h igh power (right).
Red cells and leucocytes are prominent in the 'red pulp'. Extra-medullary haemopoiesis is not a feature.
H aemalum & Eosin x 55, x 120
Fig. 62 Bone biopsy Polycythaemia rubra vera

This specimen exhibits a markedly hyperplastic marrow. The marrow spaces are completely filled with
haemopoietic, leucopoietic tissue as well as megakaryocytes. Haemalum & Eosiu x 100, x 350
I' IN , 6.1 Mur row film
S ideroblastic anaemia
1,1'/t : This illustration, at low magnification, shows numerous erythroblasts (sideroblasts) containing large
qunntitics of siderotic granules. Prussian Blue reaction, cowuerstained Neutral Red x 120
Ri~:lu : I Iigh magnification reveals sideroblasts showing the cytoplasmic Perls positive granules, and also the
perinuclear arrangement of the iron deposits in 'ringed sideroblasts'. Prussian Blue reaction, coumerstained Neutral
Red x 1200
THE RED CELL SERIES
65
Fig. 64 Rin ged sidero blast

The perinuclear mitochond ria contain large quantities of non-cr ystalline iron-containing material termed
'ferruginous m icelles'. To the right of the nucleus the centrosome and well resolved golgi complex are visible.
Osmium tetroxide, lead citrate x 8500
l llSet: At higher magnification a typical mitochondrion is seen con taining the 'ferruginous micelles'. Osmium
tetroxide, lead citrate x 22000
~--Jl----------~------~------~----------~--~~==~==~~~
l
66
Fig. 65 Spleen Erythroleukaemia (Di Guglielmo's disease)

Upper field : The red pulp contains many abnormally large cells which show a tendency to occur in groups within
sinusoids. Haemalum & Eosin x 120
Lower field: The cells vary considerably in size, they have basophilic cytoplasm and large vesicular nuclei with
fine chromatin strands. The cell to the right of the centre containing two nuclei is probably an atypical
normoblast showing megaloblastoid change. Haemalwn & Eosin x 600
T HE RED CELL SERIES
67
F ig. 66 Bone marrow Congential dyserythropoiesis

This disorder is characterised by bizarre nuclear abnormalities of erythrocyte precursors as illustrated. A E & F
illustrate the pronounced multinuclearity commonly found in type III. B illustrates b inuclearity and intranuclear
chromatin bridging with megaloblastOid features, commonly found in type I. C & D illustrate the binuclearity
usually associated with type II. There is frequentl y an overlap of morphological features in types I and II. M ayGriinwald- Giemsa stain x 1200
~~~--~ '----------------~--------~~~-----------------------------------
68
Fig. 67 S pleen Acquired haemolyt ic anaemia

The lymphoid follicles have prominent germinal centres. The red pulp is engorged with b lood. Compare with
Figure 57. H aema/um & Eosin x 60
Fig. 68 Spleen Acquired haem olytic anaemia

This composite illustration is of high-power fields from the same spleen as Figure 67, showing the congested
sinusoids and the presence of haemosiderin pigments in histocytes.
Left : Haemalum & Eosin x 450
Right: ?russian Blue reaction, coumerstained Newral R ed x 450
r
THE RED CELL SERIES
69
F ig. 69 Liver Haemolytic anaemia

Kupffer cells contain large quantities of stainable iron whereas hepatocytes do not. Prussian Blue x 500
Fig. 70 Liver Hae mochromatosis

Left : Yellow-brown granules of varying size a re seen .in the cytoplasm of many of the parenchymal cells with the
Eosin stain. Haemalum & Eosin x 400
Right : Prussian Blue reaction emphasizes the enormous amount of haemosiderin which has been deposited.
Prussian Blue x 400
70
Fig. 71 Liver Sickle-cell anaemia

Veins and sinusoids are packed with red cells, the distorted shape of which is clearly seen in the high power field
(right). Note also the cloudy swelling and fatty change in the liver cells, resulting from anoxia . Haemalum & Eosin
X }20, X 800
Fig. 72 Liver Transfusion siderosis

Note the contrast between the coarse granules in the parenchymal cells and the fine diffuse distribution in
Kupffer cells lining the greatly d istended sinusoids. ?russian Blue reaction, cormterstained N ewral Red x 350
THE RED CELL SERIES
71
Fig. 73 Gastric mucosa

Normal (left) and in pernicious anaemia (right). Compare the thickness of the mucous membrane, and the number
and length of the glands. In each instance the muscularis mucosae can be seen at the lower margins. H aema/um &
Eosin x 35
Fig. 74 Gastric mucosa

The central illustration is of normal mucous membrane whereas those to the left and right are from a case of
pernicious anaemia. The normal glands contain numerous parietal cells (arrow) but no Paneth cells, which may be
numerous in pernicious anaemia (right, arrow). Note also the presence of goblet cells in surface epithelium and
glands in pernicious anaemia, i.e. metaplasia to intestinal epithelium has occurred. Inflammatory foci are also
present and include plasma cells with Russell bodies (left, arrow). H aema/um & Eosin x 120
l
1
5. The white cell series
70
Fig. 71 Liver Sickle-cell anaemia

Veins and sinusoids are packed with red cells, the distorted shape of which is clearly seen in the high power field
(right). N ote also the cloudy swelling and fatty change in the liver cells, resulting from anoxia. Haemalwn & Eosin
X /20, X 800
Fig. 72 Liver Transfusion siderosis

Note the contrast between the coarse granules in the parenchymal cells and the fine diffuse distribution in
Kupffer cells lining the greatly d istended sinusoid s. ?russian Blue reaction, cormterstained Neutral Red x 350
THE RED CELL SERIES
71
Fig . 73 Gas tric mucosa

Normal (left) and in pernicious anaemia (right). Compare the thickness of the mucous mem brane, and the number
and length of the glands. In each instance the muscularis mucosae can be seen at the lower m argins. H aemalum &
Eosin x 35
Fig. 74 Ga stric mucosa

T he central illustration is of normal mucous membrane wher eas those to the left and right arc from a case of
pernicious anaemia. The normal glands contain numerous parietal cells (arrow) but no Paneth cells, which m ay be
numerous in pernicious anaemia (right, arrow). Note also the presence of goblet cells in surface epithelium and
glands in pernicious anaemia, i.e. metaplasia to intestinal epithelium has occurred. Infla mmatory foci are also
present and include plasma cells with Russell bodies (left, arrow). H aemalum & Eosin x 120
74
Fig. 75 Maturation of the neutrophil p olymorphonuclear leucocyte

A. Myeloblast. This shows the typical, uneven staining, basophilic cytoplasm which contains a few azurophil
granules; the staining reaction is lighter in the perinuclear region. The nucleus, which occupies four-fifths of
the total cell area, shows fine chromatin strands which are stained reddish-purple. Three pale blue nucleoli,
with sharply defined chromatin borders, are discernible.
B . Promyelocyte. At this stage of development the cell can be either larger, as in this example, or smaller than
its precursor; azurophil cytoplasmic granules are now evident and the nucleo-cytoplasmic ratio is diminished.
The nuclear chromatin appears to be coarser, and nucleoli, although still present, are not well defined.
C. Myelocyte. This example is intermediate between the promyelocyte and the fully developed m yelocyte in
that the cytoplasm still contains azurophil granules, although in a large area they have now assumed their
neutrophilic character and the cytoplasm is beginning to show a pinkish (acidophil) hue.
D . Myelocyte. The granules are now typical in neutrophil character and the cytoplasm is more acidophilic in
staining reaction. The nucleus is smaller than that of the promyelocyte, contains masses of chromatin and is
indented (kidney-bean shaped) which indicates progression to the metamyelocyte stage.
E. Metamyelocyte. This cell is smaller than the myelocyte and the nucleus is now reniform in shape. The
cytoplasm is pink and contains numerous neutrophil granules.
F. Juvenile (non-segmented) neutrophil.leucocyte. The nucleus has attained the typical U-shape of this stage of
development and contains coarse clumps of chromatin. The cytoplasm is typical in colour and granularity.
G. Transitional stage between F and H . The nucleus is beginning to attain its lobulated appearance while all
other features of this cell are similar to those of the mature form.
H. Mature (segmented) neutrophil leucocyte. This is a typical example of the final stage of development. The
cytoplasm displays the n eutrophil granules and pink staining reaction. The nucleus has three definite lobes
and coarse clumping of chromatin is obvious.
Note. From the promyelocyte stage to the final stage in the normal development of cells in this series there is a
gradual diminution in size. It should, however, be borne in mind that the developmental process is continuous
and therefore cells will be found which are intermediate to the stages depicted. Leishman stain x 1200
THE WHITE CELL SERIES
Fig. 76 Marrow film Neutrophil le ucocyt e series

In the centre of the field there is a promyelocyte (pMy). The upper two cells are neutrophil metamyelocytes
(mMy). Above and below the promyelocyte are myelocytes (My) and bottom left neutrophil polymorphs. May Griinwald-Giemsa szain x 1200
75
76
Fig. 77 Marrow film Neutrophil leucocyte series

A promyelocyte, myelocyte and several non-segmented neutrophil leucocytes. May -Griinwald-Giemsa stain
X 1200
Fig. 78 Marrow film Giant m e tamyelocytes

This illustrates an abnormality in the developing granulocytes seen in megaloblastic erythropoiesis . The
illustrations show giant metamyelocytes with large U -shaped nuclei, some of which are irregular in outline. These
giant for ms result from asynchronism between the development of the nucleus and the cytoplasm. I t is possible
that the large hypersegmented neutrophil leucocytes seen in peripheral blood, in some cases of megaloblastic
anaemia, are derived from these giant metamyelocytes, several of which are nearing the juvenile stage of
development. May-Griinwald-Giemsa stain x 1200
77
Fig. 79 Blood film Normal

This is a typical field of a blood fi lm from a normal person; two neutrophil polymorphonuclear leucocytes and one
lymphocyte can be seen. M ay-Griiuwald-Giemsa staiu x 1200
Fig. 80 Blood film P olymorpho nuclear neutrophilleucocytes to show the female sex chromatin
The characteristic 'drumsticks' found in the fema le neutrophil leucocytes are shown in A, B and C . A thin strand
of chromatin joining the head to a nuclear lobe can be clearly seen. In D , E and F 'small clubs' are present such
as may be seen in neutrophil leucocytes from the male. These should not be confused with d rumsticks. Leishman
stain x 1200
78
Fig. 81 Blood film Polymorphonuclear leucocytosis

This demonstrates the multilobular appearance of the nuclei of these mature neutrophil leucocytes. MayGriinwald-Giemsa stain x 1200
Fig. 82 Blood film Autoagglutination of polymorphonuclear leucocytes and erythrocytes

This illustrates sheets of leucocytes which have coalesced by the pressure from surrounding masses of
agglutinated erythrocytes; the leucocytes appear to be smaller than normal due to this pressure. This appearance
is occasionally seen as an artefact at the margins of blood films due to faulty spreading. Leishman stain x 1200
79
.t.a,
rPc:
..
Fig . 83 Blood film Polymorphonuclear leucocytosis with toxic granulation

There is an increase in the number of polymorphonuclear leucocytes, some of which a re not fully developed. Note
also that the granules are much coarser and that Ll-teir staining reaction is more acidophilic than in normal
neutrophil leucocytes. May-Griinwald-Giemsa stain x 1200
Fig . 84 Blood film C hediak- S teinbrink-Higashi a noma ly or gia n t gr a nulation of le u cocyt es

At top left a lymphocyte containing a large coarse and small granule; bottom left, a mature basophil with giant
granules and several smaller granules. Centre, a mature eosinophil containing granules of varying size; top right
and bottom right, mature neutrophil polymorphs containing sparse an d coarse granules . May-Gnlnwald-Giemsa
stain x 1200
80
Fig. 85 Blood film Leucocyte alkaline phosphatase

This blood film has been subjected to the modified azo-dye cytochemical technique. Numerous coarse granules
giving a heavy dark brown precipitate are seen in the cytoplasm of the neutrophil polymorphs. This indicates
intense alkaline phosphatase activity. This specimen was prepared from a case of polycythaemia rubra vera.
M odified azo-dye cycochemicalteclmique x 1200
'
Fig. 86 Blood film Pelger-Huet's anomaly
Stab forms and bisegmented Pelger neutrophil leucocytes are shown. The cytoplasm of these cells is less granular
than that of the cells depicted in Figure 87, but the coarse chromatin and pouch-like appearance of the
bisegmented nucleus of the mature cells are similar. M ay-Griinwald- Giemsa stain x 1200
81
F ig. 87 Blood film P elger - Huet 's anomaly

Left: Two bisegmented Pelger neutrophil leucocytes are shown. Leishman stain x 1200
Right: One bisegmented Pelger neutrophil leucocyte and two stab forms are seen . The nuclei of the Pclger cells
are small and thick with lumpy coarse chromatin. The cytoplasm shows coarse granulation which is a common
feature in the Pelger cell. Leishman stain x 1200
Fig.88 Blood film ( d efibrinated specimen ) Syst emic lupus erythema tos u s
T he LE cells are neutrophil polymorphonuclear lcucocytes with large opaque structureless basophil ic cytoplasmic
inclusions which have displaced the nuclei, these now appearing to be wrapped round the inclusions. The rosette
form shown at bottom left precedes the mature LE cell and consists of several polymorphs around free lysed
nuclear material. M ay-Griinwald-Giemsa stain x 1200
82
ATLAS OF HAEM ATO LOGY
Fig. 89 Neutrophil polymorph

T his cell exhibits the typical features of the mature neutrophil polymorph: marked chromatin condensation,
segmented nucleus, cytoplasmic granulation, glycogen particles and pinocytosis. Glwaraldehyde, urany l acetate,
lead citrate x 18 200
!o
83
l
I
Fig. 90 Blood film Myeloid leukaemoid reaction

In this illustration a marked increase in the total white cell count is obvious (total count, !03 x 10 9 / 1).
Myelocytes and immature myeloid cells are apparent. This is the usual type of myeloid leukaemoid r eaction, the
patient suffering from a non- leukaemic disorder. The peripheral blood picture resembles that of leukaemia
(marked elevation of total white cells or the presence of immature cells or both). May -Griinwald-Giemsa stain
X J200
84
Fig. 91 B lood fil m Acute undifferentiated le ukaem ia- MO

In this preparation practically all of the cells present are atypical 'blast' cells, the nuclei of which have a fine
structure, their nucleoli being pale with no thickening of the chromatin at the circumference. The majority of the
cells have a narrow border of basoph ilic cytoplasm. From this preparation it is not possible to state whether these
very primitive cells are of lymphoblastic, myeloblastic or monoblastic origin. Leishman stain x 1200
85
CLASSIFICATION OF ACUTE LEUKAEMIAS

The variability in the morphological features of acute leukaemias has resulted in the
development of several systems of classification.
The generally accepted scheme is the French-American-British (FAB) classification. Two
groups of acute leukaemia, lymphoblastic and myeloid, are sub-divided into three and six
groups.
Lymphoblastic leukaemia. L ymphoblastic leukaemia is divided into three types, Ll, L2,
and L3, according to the occurrence of individual cytological features and the degree of
heterogeneity in the leukaemia cell population.
Classification
Cell type( s)
Ll
Microlymphoblasts
L2
Large undifferentiated
lymphoblasts
Burkitt type
L3
Characteristics
Small microlymphoblasts, nucleoli often not present or small and
inconspicuous.
L arge more undifferentiated cell. Nucleoli are nearly always present and
vary in size and number.
Large cell with an oval to round regular nucleus with one or more
prominent vesicular nucleoli. Prominent cytoplasmic vacuolation in the
majority of cells, identical to that described in Burkitt lymphoma cells.
Myeloid leukaemia. Myeloid leukaemia is divided into six main types, accordin g to the
direction of differentiation along one or more cell lines and the degree of maturation. Ml, M2,
and M3 show predominantly granulocytic differentiation. M4 shows both granulocytic and
monocytic differentiation, MS predominantly monocytic differentiation and M6 p redominantly er ythroblastic differentiation.
Classification
Cell type(s)
Characteristics
Ml
Myeloblasts
M2
Myeloblasts,
promyelocytes
Myelocytes
H ypergranular
promyelocytes
Promyelocytes,
myelocytes,
promonocytes,
monocytes
Monoblasts
Monoblasts,
promonocytes,
monocytes
Erythroblasts
Non-granular myeloblasts usually containing one or more distinct

nucleoli.
Maturation beyond the promyelocyte stage. Cells containing Auer rods
are common.
M3
M4
MS (a)
MS (b)
M6
The majority of the cells are promyelocytes with a characteristic pattern

of heavy granulation.
Both granulocytic and monocytic differentiation are present in varying
proportions.
Poorly differentiated monoblastic.

Differentiated monoblasts, promonocytes and monocytes.
Bizarre erythropoiesis. Erythroblasts with multiple lobation of the

nucleus, multiple nuclei, nuclear fragments, giant forms and megaloblastic features.
Megakaryoblast leukaemia
I~
Classification
Cell type(s)
M7
Megakaryocytes
C h a racteristics
Acute megakaryoblast leukaemia in which immature megakaryocytes
with abnormal platelets are prominent.
~ ~~L--------------------~----------------------~--------~----------------------------------~
r
86
Fig. 92 Marrow film Acute myeloid leukaemia - Ml

Non-granular myeloblasts with lack of granulocytic different iation . May-Gnlnwald-Giemsa stain x 1200
THE WH ITE CELL SERIES
87
Fig. 93 Marrow film Acute myeloid leukaemia - M2

There is some degree of maturation beyond the promyelocyte stage with dysplastic forms. May -Gnlnwald-Giemsa
scain x 1200
Fig. 94 Marrow film Acute m yeloid le ukaemia - M3

The cells are predominantly promyclocytcs with prominent coarse granulations. May-Gnlnwald-Giemsa scain x
1200
88
Fig. 95 Blood film Acute myelomonocytic leukaemia - M4

The cells in this illustration are primitive cells of the monocyte series, monoblast and promonocyte (left centre),
and primitive cells of th e myeloid series promyelocyte and myeloblasts (lower right). May-Gnl11wald-Giemsa stai11
X 1200
Fig. 96 Marrow film Acute m yelomonocy tic leukaemia - M4

The cells in this illustration are primitive cells of the myeloid and monocyte series. Monoblasts top left and
myeloblasts bottom righ t. May -Grii11wald-Giemsa scain x 1200
89
Fig. 97 Ma rrow film Acute monobla stic leuka emia- MS (b )

This illustrates proliferat ion of cells of the monocytic series at various stages of development, monoblasts and
promonocytes with variation in size and nuclear configuration. May -Grii11wald-Giemsa stai11 x 1200
Fig. 98 M a rrow film Erythroleukaemia - M6

At low magnification (left) and high magnification (right) the bizarre nature of erythropoiesis is evident. There is
complete absence of cells of the m yeloid series. Erythroblasts with multiple lobation of the nucleus and multiple
nuclei are present. May-Grii11wald-Giemsa staill x 1200
90
Fig. 99 Blood film Myelodysplastic syndrome

The blood film exhibits macrocytosis and anisopoikilocytosis. Large platelets are present on the right of the field.
May-Gninwald-Giemsa scai11 x 1200
Fig. 100 Marrow film Myclodysplastic syndrome

Left : Erythroid hyperplasia with dyserythropoiesis and megaloblastoid features. M ay-Griinwald-Giemsa stain
X 1200
Right: Promyelocytes with sparse granules and hypogranularity of myelocytes. May-Gninwald-Giemsa stain
X 1200
THE W HITE CELL SERIES
Fig. 101 Marrow film Acute myeloid leukaemia- M2

In this illustration the chief cells are myeloblasts with variable nucleo-cytoplasmic ratios. Their nuclei are large,
with smooth finely stranded chromatin, and contain nucleoli. Promyelocytes, some of which possess azurophil
granules, but with otherwise similar characteristics to the myeloblasts are also present. May -Gninwa/d-Giemsa
stain x 1200
91
92
Fig. 102 Blood film Acute myeloid le ukaemia- M2

In the low power illustration (top left) the cells are seen to be all of the same cell type. Higher magnification
illustrates many m yeloblasts with moderately deeply basophilic cytoplasm. Some of the myeloblasts exhibit fine
cytoplasmic vacuolation and a spongy reticular appearance. Both the myeloblasts and promyelocytes show
irregular indentation and folding of the nucleus and these cells are sometimes referred to as paramyeloblascs and
parapromyelocyces. May -Grii11wa/d-Giemsa stain x 600, x 1200
..
Fig. 103 Blood film Acute myeloid leukaemia- M2

Numerous myeloblasts (Myb) which vary considerably in size are present in this composite illustration. Also
present are prom yelocytes (pMy), myelocytes (My) and a metamyelocyte (mMy). The main featu res of this
illustration are the complete lack of mature granular cells, and the many cells with giant nucleoli, which are
common in this condition. M ay-Grtlnwald-Giemsa stain x 1200
93
94
Fig. 104 B lood film Acute m yeloid leukaemia Auer rods - M2

Several of the myeloblasts, in this composite illustration, contain single or multiple rod-shaped structures in their
cytoplasm; these are known as Auer bodies. These bodies are probably fo rmed by the coalescence of cytoplasmic
granules in leukaemic myeloblasts. May-Gnlnwald-Giemsa stain x 1200
95
Fig. 105 Blood film Acute myeloid le ukaemia

With the staining method depicted here the nucleoli of the myeloblasts give a positive (blue) staining reaction,
against the rose pink stained nucleus, and are more clearly delineated. Chromozrope-Giemsa scaiu x 1200
Fig. 106 Blood film Rieder cells in leukaemia

All the primitive leucocytes illustrated exhibit lobular division of their nuclei; most are bi- or trifoliate. The lobes
are separated by deep clefts. Cells with such a nuclear configuration are known as R ieder cells and are frequently
seen in blood films in acute leukaemia. M ay-Grrluwald- Giemsa scaiu x 1200
96
ATLAS OF HAEM ATOLOGY
-----------------------------------------------------------------------
Fig. 107 B lood film Acute myeloid le ukaemia - M 1

The cells in this illustration are of the same type, myeloblasts of varying size with basophilic cytoplasm; irregular
shaped nucleus with nucleoli. May -Griinwald-Giemsa stain x 1200
F ig. 108 Marr ow film Acute myeloid le ukaemia- M 1

Marrow film from the patient whose blood film is illustrated in Figure 107 . The marrow is heavily infiltrated with
myeloblasts similar in morphology to that of the blood film. The myeloblasts are larger with a spongy appearance
of the nucleus compared with the myeloblasts in the peripheral blood film. May -Griinwald-Giemsa stain x 1200
THE W H ITE CELL SERIES
97
Fig. 109 Marrow film Acute myeloid leukaemia- Ml

This illustration demonstrates the Sudan Black positivity of the myeloblasts from the same marrow sample as
Figure 108. The stain detects lipids. Sudan Black, and coumerstained L eishman stain x 1200
Fig. 110 Marrow film Promyelocytic leukaemia- M3

In this illustration the majority of the immature cells exhibit cytoplasmic granulation ranging from fine to coarse.
T he nucleus of the prom yelocytes appear more immature than in the normal promyelocyte. May -GrtlnwaldGiemsa stain x 1200
98
Fig. 111 Blood film Blast cell transformed chronic myeloid leukaemia
This preparation is from a patient in whom chronic myeloid leukaemia has undergone b last cell transformation,
the blood picture now resembling .that of acute myeloblastic leukaemia. Many primitive myeloid cells are present
but more mature cells are also noted in the illustration (left). It is of interest that in spite of the acute
transformation the total platelet count remained elevated as evidenced by the many platelets seen in this
illustration; note the several giant forms. May -Griinwald-Giemsa stain x 500
Fig. 112 Marrow film Acute myeloid leukaemia in remission

The marrow is active and exhibits hyperplastic-macro-normoblastic erythropoiesis. The previous myelobhistic
infiltration has been cleared and myelopoiesis is normal, no increase in blast cells being noted. May -GriinwaldGiemsa stain x 1200
Fig. 113 Blast cell

This cell shows no features of differentiation but it was taken from a patient with acute myeloblastic leukaemia.
Glutaraldehyde, ura11yl acete, lead citrate x 18 200
'
99
100
Fig. 114 Marrow film Chronic m ye loid leukaemia

There is a marked increase in the cells of the myeloid series; many myelocytes (M y), metamyelocytes (mMy),
non-segmented (Stab) and segmented (Neut) neutro phil leucocytes are present. A haemohistioblast (R), an
eosinophil (Eos), and a basophil (Bas) leucocyte are also shown. L eishma11 s1ai 11 x 1200
THE WHITE CEL L SERIES
101
Stab
9 0
mM,
Stab'(Y
rnMy
0e
0
S tab
Stab
(iycl
Neut
F ig. ll 5 Blood film C hronic m yeloid leukaemia

' Marked proliferation of the cells in the myeloid series is demonstrated . M yelocytes (My) and metamyelocytes
(mMy) are seen in addition to numerous non-segmented and segmented neutrophil leucocytes. M ay- GninwaldGiemsa stain x 1200
102
Fig. 116 Marrow film Myeloid leukaemia

The cytoplasmic granules of the neutrophil myelocytes show a blue positive peroxidase reaction. Peroxidase
reaction, coumerstained L eishman stain x 1200
Fig. 11 7 Marrow film Myeloid leukaemia

In this preparation the peroxidase method was modified and the granules of the eosinophil myelocytes give a
positive reaction of a translucent yellow-green colour with a blue margin, whereas the granules of the neutrophil
myelocytes give a blue positive reaction. Peroxidase reaction, counterstained Leishman stain x 1200
103
Fig. 118 Blood film Chronic myeloid leukaemia

This illustration demonstrates the Sudan Black positivity of the granules of the myeloid series. The more mature
cells show a heavier reaction than the more primitive cells. Many free granules are scattered throughout the film ,
due to r upture of cells during spreading. Sudan Black and M ethyl R ed x 200, x 800
104
Fig. 119 Blood film Tra n sforming o r accelerated phase, chronic m yeloid leukaemia
This illustrates increasing cellular immaturity of the myeloid ser ies with an increase in atypical promyelocytes,
myelocytcs and basophi ls. May-Gn111wald-Giemsa scai11 x 1200
I 05
Fig. 120 Marrow film Myelomonocytic leukaemia- M4

The majority of the cells in this composite illustration are primitive cells of the myeloid and monocyte series. The
azurophilic granulation in many of the cells indicate their myeloid potential whereas the agranular primitive cells,
best seen in fie ld C , exhibit a more grey-blue cytoplasmic staining reaction and their nuclei show the more open
arrangement of chromatin pattern; both these feature~ arc typ ical of the primitive cells of the mo nocyte series.
Note the large nucleoli in several of the cells, especially in the h istioblast in the upper left margin of field A. The
myelocyte (left of centre, fie ld C ) contains nu merous small Auer bodies . (See also I." ig . I 2 1.) Jllay- UriinnaldGiemsa srai11 x 1200
--
106
Fig. 121 Marrow film Myelomonocytic leukaemia- M4

These illustrations from the same marrow as depicted in Figure 120 and illustrating similar features also show
pronounced erythroid hyperplasia. This is sometimes called Di Guglielmo's syndrome when referring to cases of
leukaemia in which erythroid hyperplasia and abnormal erythroblasts are a feature. In field A several abnormal
erythroblasts are present; one in the centre of the field shows erythrophagocytosis. At the upper left margin there
is a monoblast with azurophilic granulation of the cytoplasm and at the upper right margin a large promyelocyte.
Field B contains a monoblast, a promyelocyte and an abnormal erythroblast. Field C consists mainly of cells of
the erythroid series, although a giant polymorphonuclear leucocyte is present in the upper part of the field. At the
lower right quadrant a large polyploid erythroblast can be seen and to the left margin there is an erythroblast with
a reniform nucleus resembling that of a metamyelocyte. All the cells in field D, including the cell in mitosis, are
of the erythroid series. (See also Figs. 54, 55 and 56.) May -Griinwald-Giemsa slain x 1200
107
Fig. 122 Marrow film . Eosinophilia

The majority of the cells in this preparation are of the eosinophil granulocyte series at all stages of maturation.
This marrow specimen was aspirated from a patient with mycosis fungoides. The b lood picture from the same
case is shown in Figure 314. May-Griinwald-Giemsa stain x 1200
F ig. 123 Blood film Eosinophilia

These illustrations show numerous segmented eosinophil leucocytes, several of which contain two pouch-shaped
nuclear Jobes. May -Griinwald-Giemsa stain x 1200
108
c
Fig. 124 Basophil le u cocyte d evelopme nt
Compare this series with mast cells ( tissue basophils) as shown in f-igurL I '3 H. A is an example of a basophil
promyelocyte. B shows a basophil myelocyte (right) and to the left a transit ional stage between A and B . C shows
a basophil metamyelocyte, a nd D a mature basophil leucocyte. Note that the cytoplasm of the basophil leucocyte
is pink and that the large granules overlie and mask the nucleus, frequently making it diffic ult to decide which
stage of maturation .a cell has reached. Leishma11 stai11 x 1200
Fig. 125 Marrow film C hronic myeloid leukaemia

This illustration shows a marked increase in the number of basophil leucocytes. In addition to the mature
basophils several immature forms with large coarse granules and multiple nucleoli arc present. Leishma11 srai11 x
1200
109
Fig. 126 F e moral m arrow C hronic m yeloid le ukaemia

This illustratio n shows almost complete replacement of hacmopoietic tissue by tumour. Huemalum & Eosi11 x 120
Fig. 127 Femoral marrow Myeloid leukaemia

Lej1: This is a typical example of the acute form of this disease. Only primitive cells can be seen, several of which
are in varying stages of mitosis (arrow). Haemalum & Eosi11 x 450
Righi: In the chronic disease, both immature and segmented cells arc seen, most of the cells with small dark
nuclei are normoblasts. Haemalum & Eosi11 x 450
-_
11 0
Fig. 128 M arrow section Chronic myeloid leukaemia

The prominent features of this preparation are eosinophilia and the presence of Charcot Leyden crystals.
H aemalum & Eosin x I 200
Fig. 129 Spleen Normal

A non-reactive lymphoid follicle has a b ilobed appearance with the arteriole between the two halves. Haemalum &
Eosin x 50
THE WHITE CELL SERI ES
11 1
Fig. 130 Spleen Acute m yeloid le uka emia

The margin of a lymphoid follicle (bottom right) abuts on red pulp which contains many p rimitive cells and very
few mature granulocytes. Haemalum & Eosin x 450
Fig. 131 Heart Acute myeloid le ukaemia

Left: This shows a massive infiltration of the heart muscle and epicardial fat by immature myeloid cells.
Haemalum & Eosin x 120
Right: T his high magnification confirms that all the infiltrating cells are primitive myeloid cells. Haemalum &
Eosin x 450
11 0
A 'IIA ~IIl
t,..
I ll l ,y m p h node M yeloid meta plasia

ti ,IIIIIIIJHtkl it tclb arc seen in the distended sinusoid and in an adjacent medu llary cord. A megakaryocyte,
""'""'hht ~ l' uno cosinophils, a t different stages of maturation, arc readily visib le. Other immature myeloid cells
1111 JIH'\Cill. 1/acmalron & Eosin x 400
Fig. 133 Liver Norma l

A single portal tract can be seen in the right half of the field; in it the portal vein containing erythrocytes lies
adjacent to a small bile duct. Two central hepatic veins are present to the left of the field. Haemalwn & Eosin
X /20
11 3
Fig. 134 Liver Chronic m yeloid leukaemia

The sinusoids show the characteristic diffu se infiltration common in th is disease. Note that there is pressure
atrophy of the parenchym al cells. Haemalum & Eosin x 120
Fig. 135 Liver Acute m yeloid leukaemia

This is a typical example of the liver in acute myeloid leukaemia; the sinusoids contain great numbers of primitive
cells, many of which a re large; no mature granulocytes a re seen. Haemalum & Eosin x 450
11 4
Fig. 136 Skin Acute m yeloid leukaemia

The upper illustration shows densely packed foci of cells in the dermis. At high power it is seen that there is little
variation in the size and staining reaction of the cells. The diagnosis was confirmed by haematological
examination. Haemalum & Eosin x 100, x 475
115
F ig. 137 Lym p h nod e C hronic g r a nulocytic leukaemia

Most of the cells are pr imitive mem bers of the myeloid series and cannot really be identified further . However a
megakaryocyte and several cosinophils are clearly visible. H aema/um & Eosin x 500
..
v
11 6
ATLAS O F HAEMATOLOGY
Fig. 138 Marrow fi lm Mast cells

.\1\ast cells or tissue basophils arc not normally fou nd in bone marrow but may be seen in cases of aplastic
anaemia, chronic blood loss, anaphylaxis, and tumours of the lymp hoid tissue involving bone marrow. These cells
arc larger and do not have the rounded appearance of mature basophil lcucocytcs; the granules arc also larger and
can be seen best in cells which have been slightly flauened during the spreading of the film. T he nucleus of a
mast cell is always pale in colo ur and although the granules are deeply basophilic when stained by the routine
blood stains they show marked metachromasia when sta ined with toluidine blue. Leishman stall/ x 8UU
Fig. 139 M a rrow fi lm s Tissue m ast cell leukaemia

A. It is ob,ious that there is a marked increase in the number of mast cells in this preparation. The granules of
the cells arc deeply basophilic and there is difficu lty in resol ving individual granules. M ay-Gn11twald-Giemsa
stain x 800
B. The metachromatic granules arc easi ly resolved when stained by toluidine blue, this identifying the cells.
T oluidine LJ/ue srain x 800
'
'
T H E WHITE CELL SER IES
LYMPHOBLAST
MONOBLAST
PROLYMPHO C YTE
PROMO NOCYTE
LARGE
11 7
PLASMABLAST
t
PR OPLASMA C EL L
SMAll
LYMPH OCYTES
MONOCYTE
PLASMA CE LL S
F ig. 140 M aturation of lymphocytes, m onocytes and plasma cells

This composit.: illustration of developing lymphocytes, monocytcs and plasma cells demonstrates the differences
in size, staining reaction, nuclear configll ration and chromatin structure at various stages of maturation . For
fu rther details of development in each cell series see Figures 141 , 180 and 20 1. l .ei.<hma>l .<t ai11 x 121111
---
11 8
ATLAS OF H AEMATO LOGY
Fig. 14 1 Maturation of the lymphocyte

Fr<;>m the left, the cells present are as follows. A lymphoblast containing a large nucleus surrounded by a narrow
rim of basophilic cytoplasm; even at this stage of development the resemblance to the mature lymphocyte is
obvious. Next in sequence is a prolymphocyte which is smaller than its precursor and shows a shadow nucleolus
within the large nucleus. The other illustration shows mature lymphocy tes in peripheral blood. Lcishmau staiu
X 1200
Fig. 142 Blood film Infectious mononucleosis

Preparation from a patient with severe infectious mononucleosis and associated grossly elevated heterophil
antibody titre. T he atypical lymphocytes vary considerably in size with irregular outlines flowing around the
adjacent red cells. The abundant basophilic cytoplasm in some cells contain fine eosinophilic granules (lower cell,
middle illustration) others exhibit marked vacuolation (right lower cell). Leishmau staiu x 1200
Fig. 143
Blood film
119
Infectious mononucle osis
This composite illustrates the atypical features which lymphocytes may exhibit in this condition. T he nuclei are
lobulated or kidney s haped. The chromatin , which is in coarse strands, is irreg ularly dis tribu ted , giving a mottled
appearance. ote the variation in size of these abnormal lymphocytes, and that the cytoplasm tends t o be more
basophilic than normal. May-Grii11wa/d-Giemsa srai11 x 1200
Fig. 144
Blood film
Lymphocytes in viral pneumonia
A exhibits a lymphocytosis, t he field being devoid of granular cells. x 600. B & C shows marked variation in size
and shape. D-H exhibit abnormal cytoplasmic and nuclear features- in particular, nuclear indentation and
c ~ toplas mic vac uolation. May-Griimvald-Giemsa stain x 1200
,---
--
--
---
120
AT L AS OF H AEMATOLOGY
Fig. 145 Blood film Neonata l c ytomega lovirus infec tion

This illustrates bizarre lymphoid cells of va rying maturity (centre and upper left field ), normoblastosis and
thrombocytopenia . The stressed neonate frequently exhibits normoblastosis and thrombocytopenia, not indicating
marrow pathology. May-Grrlnwald-Giemsa stain x 1200
Fig . 146 Blood film Alder - Reilly a nomaly

Red cytoplasmic inclusions shaped like a dot or comma surrounded by vacuoles a re present in both the
lymphocytes illustrated. These inclusions in blood lymphocytes arc sometimes refe r red to as Ciasser's cells. This
preparation was from a t:hild ~11ffering from mucopol ysaccharidosis. May-Grrlnwald-Gicmsa .(taiu x 1200
Fig . 147 B lood and m a rrow fi lm s Waldcnstro m 's macroglobulina emia

L eft: This blood film shows large lym phocytes with lobulated, indented and irregularly shaped nuclei. No
gran u lar cells are p resent. J\lfay-Gnluwald-Gicmsa staiu x 800
Right : T hi s fi lm of marrow exhibits a marked increase in lymphocytes, many of which have scanty or absent
cytoplasm. There is also a decrease in erythroid and m yeloid cells. Several plasma cells arc present. M ayGriimuald- Giemsa staiu x 800
121
122
Lymphoblastic leukaemia
Classification
Cell typ e( s)
L1
L2
Microlymphoblasts
Large undi fferentiated
lymphoblasts
Burkitt T ype
L3
Fig. 148 Marrow film Acute lymphoblas tic leukae mia - Ll

The cells in this illustration are small lymphoblasts with a h igh nuclear-cytoplasmic ratio and indistinct nucleoli.
These are often described as microlymphoblasts. May -Gnlnwald-Giemsa sea in x I 200
T H E WHITE CELL SERIES
Fig. 149 Marrow film Acute lymphoblastic le ukaemia- L2

The lymphoblasts are large with more cytoplasm compared to the cells illustrated in Figure 148. Prominent
nucleoli varying in size and number are also present in these cells. May-Gnlnwald-Giemsa srain x 1200
Fig. ISO Marrow film Acute lymphoblastic le ukaemia - L3

The prominent features in this illustration are the heavily vacuolated large lymphoblasts. These cells are
morphologically similar to those found in Burkitt's lymphoma. May-Griinwald- Giemsa stain x I 200
123
124
ATLAS OF HAEMATO LOGY
Fig. 151 Marrow film Acute lymphoblastic le ukae mia- L 2

The predominant cells in th is illustration arc lymphoblasts. These cells arc very similar in size and general
appearance to myeloblasts, but have coarser, more deeply staining nuclear chromatin , and nucleoli arc less
obvious. (See Figs. 276- 278.) May -Griinwald-Giemsa srain x 1200
THE WHITE CE LL SERIES
125
Fig. 152 Blood film Acute lymphoblastic leukae mia- L2

The cells are predo minantl y large lympho blasts with nucleoli of var ying size. M ay-G riimuald-Giemsa stai11 x 1200
126
Fig. 153 Blood fi lm Acute lym phoblastic leukaemia- L2

The predominating cells in this illustration are lymphoblasts; these cells possess round, oval or indented nuclei
containing coarse granular or stippled chromatin and also one or two poorly defined nucleoli. The agranular
cytoplasm is moderately basophilic and, in several of the cells, is seen to contain fine vacuoles. May-GninwaldGiemsa stain x 1200
..
Fig. 154 Blood fi lm Acute lymphoblastic leukaemia

The lymphoblasts show strong and coarse PAS positivity, with moderately large discrete cytoplasmic granules,
arranged in a pe rinuclear manner. Two neutrophil polymorphonuclear leucocytes containing very large amounts
of PAS positive material are also present (lower left) Periodic Acid-Schiff r PAS ) x 1200
T H E WHITE CELL SERI ES
...
'
~
ttl
~
1)1,
OJ
~t .
t\
Ce .:>o
c. o
127
'i
t.:l
c.
(I.
OJ
?
F ig. ISS E -rosetting T - ceil acute lympho blastic le uka emia
T he lymphoblasts arc surrounded by sheep red cells forming rosettes, thus confirming the T-cell phenotype.
Leishman stain x 500, x I 200
Fig. 156 M a rrow film Subacute lymphocytic le uka emia

These ill ustrations show a marked increase in the num ber of small lymphocytes, and also seve ral lym phoblast and
prolymphocytes. L eishman stain x I 200
128
Fig. 157 Blood film Subacute ly mphocytic le ukae mia

Th is composite illustration shows a predominance of the cells of the lym phocytic ser ies. L ym phocytes at all stages
of development a rc presen t, ranging from the lymphoblast to the matu re sma ll lymphocyte. M ay-GriimualdGiemsa srain x 600, x 1200
129
Fig. 158 Blood film Prolymphocytic leukaemia

A well marked increase in the total white cell count is obvious, the cells being mainly prolymphocytes and a small
percentage of lymphoblasts. May-Gnlmuald- Giemsa stai11 x 500
Fig. 159 Blood film Prolymphocytic leukaemia

This higher magnification of a field taken from Fig. 158 illustrates the prolymphocytes with indented nuclei and
shadow nucleoli; lymphoblaHs with large distinct nucleoli. \1ay - Gnl11wald-Giemsa srai11 x I 200
130
Fig. 160 B lood film Prolym phocy tic le ukae mia

Coarse PAS positivity is shown in some of the cells with discrete small cytoplasmic granules. The three
neutrophil polymorphs contain large amounts of PAS positive material. This preparation was taken from the same
patient as shown in Figs. 158 and 159. Periodic Acid-Schiff f PAS ) x 900
Fig. 16 1 Marrow film Chronic lymphocytic le ukaemia

'In this preparation, there is a marked predominance of mature small lymphocytes, in addition to which, several
immature and mature neutrophil and eosinophil leucocytes are present. Leishman srailz x 1200
THE WH ITE CELL SER IES
131
Fig. 162 Marrow section C hronic lymphocytic leukae mia

Apart from the m egaka ryocyte in the centre of the fie ld all the cells are mature small lymphocytes. H aema/um &
osi11 x 500
Fig. 163 Blood film Chronic lymphocytic leukaemia

Note the marked uniformity of the cell type. Medium-sized lymphocytes with light-blue cytoplasm and smaller
lymphocytes with a very narrow rim of dark-blue cytoplasm are seen. Several of the larger cells show indentation
of the nucleus, which is a common find ing in this condition. M ay-Grtl11wald-Giemsa stai11 x 1200
132
Fig. 164 Blood film Chronic lymphoc ytic leukaemia

The majority of the cells are medium sized lymphocytes with inden tation of the nucleus and light blue cytoplasm.
M ay-Gnl11wa/d-Giemsa srai11 x 1200
Fig. 165 Blood film Large granular lymphocytic leukaemia

The lymphocytes are much larger in size than the lymphocytes illustrated in Figs . 163 and 164. The striking fea tures
arc the large red cytoplasmic granules, abundant, cytoplasm and variation in size and shape of the nucle us. May Gnillwald-Giemsa srai11 x 1200
T H E WHITE CELL SERIES
Fig. 166 Ly mphocyte

Thb cell appears quite active, the cytoplasm contains numerous free ribosomes, some mitochondria and some
\ trands of rough endoplasm ic reticulum. There is a relatively large nucleus with only moderate chromatin
condensation around the nuclear membrane. Several nuclear pores arc seen in tangential section. A Golgi
uppnratus is present at the bottom of the illustration. A prominent centriole is seen below the nucleus.
Ul111araldehyde, uranyl acetate, lead citrate x 26 000
133
134
Fig. 167 Lymph node Infectious mononucleosis

The architecture of the cortex is obscured so that only an ill defined follicle can be seen (left). Vascularity is
increased by pro liferation of post-capillary venules (centre). The polymorphic nature of the inter-follicular
infiltrate with lymphocytes, plasma cells and immature lymphoid cells is seen at h igh magnification ( right).
Haemalum & Eosi11 x 25, x 250, x 450
Fig. 168 Femoral marrow Lymphocytic leuka emia

This illustration shows almost complete replacement of the marrow tissue by a mass of tumour cells; only a few
fat cells which are seen as clear spaces remain. Ha emalum & Eosi11 x I 20
135
Fig. 169 Femora l m a rrow Ly mphoc ytic leukaemia

A high-power view of par.t of the fie ld seen in Fig. 168, showing the almost completely lymphocytic nature of the
infiltrate. ote that many similar cells are present in the venule shown in the upper part of the illustration.
Ha ema/um & Eosin x 450
Fig. 170 Lymph node (left)' and spleen ( right) Lymphocytic le ukae mia
Both tissues show obliteration of the normal architecture by masses of cells of the lymphocyte series. Haema/wn
& Eosin x 40, x 120
..... ._.
136
ATLAS OF H AEMAT OLOGY
Fig. 171 Testic ular biopsy T -cell acu te lymph oblastic leukaemia
The interstitial tissue between atrophic seminiferous tubules is heavily infilt rated with small lymphocytes. Many
of the nuclei have an irregular configuration. Haemalwn & Eosin x 300
Fig. 172 Liver Acute lymphoblastic leukaemia

The distribution of the infiltrating cells is predominantly periportal although several small groups can be seen
lying in the sinusoids . Haemalum & Eosin x 120
137
Fig. 173 Blood film Leukaemic reticuloendotheliosis ('h air y' cell le uka emia)
This illustrates the characteristic hairy lymphocytes, found in this condition. T he grey-blue cytoplasm exhibits
irregular villi resulting in an irregular serrated ' ha iry' edge and also pseudopodia! extensions. May-Griinwa/dGiemsa srain x 1200
Fig. 174 Blood film Leuka emic reticuloendotheliosis ('ha iry' cell leukaemia)
The irregular cy toplasm ic villi of the lymphocytes, similar to F i~. 171 is illustrated in this preparation. May Griinwald-Giemsa .<rain x 1200
138
Fig. 175 Blood film Leukaemic reticulocndotheliosis ('hairy' cell leukaemia )

Tartrate-resistant positive acid phosphatase reaction in hairy lymphocytes. Acid phosphatase reaction and M ethyl
Green x 1200
I
Fig. 176 Imprint from spleen Leukaemic reticuloendotheliosis ('h airy' cell leukaemia)
In this imprint from the spleen some of the cells exhibit weak to moderate tartrate resistant positive acid
phosphatase reaction and one cell, stro ng activity. Acid phosphatase reacrion and Merhyl Green x 900
THE W H ITE CELL SER I ES
139
Fig. 177 Blood film Leukaemic reticuloendotheliosis

There are pseudopodia projecting from the cell surfaces, corresponding with the hairs seen on light microscopy .
Glutaraldehyde, ura11yl acetate, lead citrate x 10 350
140
Fig . 178 S pleen L e ukaemic r e tic ulocndo the liosis

Left: This section reveals absence of germinal centres and a diffuse infiltration of the red pulp by lymphoid cells.
H aema/um & Eosin x 125
Right: T he appearance suggests a well-di fferentiated lymphocytic lymphoma, the main problem being that the
typical 'hairy' cells are impossible to identify in histological sections. Haema/um & Eosin x 600
Fig. 179 Liver Leukaemic retic uloe ndotheliosis

Left: This section shows sinusoidal infiltration with lymphoid cells. H aemalum & /:"Min x 125
Right: The lymphoid nature of the cells is seen; but typical 'hairy' cells can not be identified. Haema/wn & Eosin
X 600
141
Fig. 180 Maturation of the m o nocyte

F rom the left, this sh ows a primitive cell which provides a link between the haemohistioblast (stem cell) and the
monoblast. A monoblast, the cytoplasm of wh ich exhibits the typical no n-granular pale grey-blue staini ng reaction
common to this cell type; nucleoli arc present but are only resolved with d ifficu lty. The other two cells are a
promonocyte which has a typical large con\'Oiuted nucleus, and a mature monocyte with an indented (kidneyshaped) nucleus. Leishma11 srailt x 1200
F ig. 181 M a rrow film Monocytcs

Top left: The monocyte present is larger than normal, the nucleus is d eeply indented and the cytoplasm contains
man~ very large azurophilic granules. Granulation of this type is oft en present in monocytic leukaemia . I.eishma11
S/CI/11 X 1200
Bottom hft: Two monoblasts arc seen , both of which show distinct nucleoli and a deep-blue cytoplasm. T he other
cells p resent arc mature monocvtcs. l.ershma/1 srai11 x 1200
RiKht: This illustration is typical of the variation in size and shape of mature monocytes which are fo und in the
marrow or blood in monocytic leukaemia. Note that several of the cells show fine granulation. Leishma11 srailt
X / 200
142
Fig . 182 M arro w film M onocytes

L eft : A large promonocyte (pMon) which is coarsely granular and appears to be necrobiotic is shown. The other
cells present are monocytes of normal size. Inset shows a monocyte in prophase stage of mitosis, the cytoplasm of
which is markedly granular. The size of the cells in this illustration can be compared with the normal la rge
lymphocyte ( L ). L eishman stain x 1200
Right: Shows a monoblast (Mon. b) and several monocytes (Mon) which vary considerably in size, the largest of
which has a deeply indented nucleus. Leishman srai11 x 1200
143
Fig. 183 Marrow film Monocytes

Top left: A typical promonocyte. The cell is large and the cytoplasm appears to have both azurophilic and
basophilic granulation which is probably due to either break-up of or damage to, the cytoplasm. Leishma11 stai11
X
1200
Top right : This monocyte has three nuclear lobes which do not appear to be joined; the cytoplasm is filled with
coarse azurophilic granules. Leishma11 staill x 1200
Cemre left: Shows a monocyte in the prophase stage of mitosis, and also a monocyte of normal size with a
segmented nucleus. Leishma11 s1ai11 x 1200
Cemre right: T he anaphase stage of mitosis is clearly seen in this monocyte. Leislmtall s1ai11 x I 200
The two large cells in the lower part of the illustration are monocytes which are normal in all appearances except
size. Leishma11 s1ai11 x 1200
144
Fig. 184 Blood film Monocytes

The monocytes present are typical of the wide variation in size and nuclear configuration wh ich is to be found in
monocytic leukaemia. The cell at centre righ t migh t at first gla nce be mistaken fo r a plasma cell if it were not for
the fact that many cells showing this appearance are found in the blood in cases of monocytic leukaemia. Leishman
stai11 X I 200
Fig. 185 Blood film Monocytes

This composite illustration shows two extremely large monocytes, the one on the left having a nucleus which
takes up practically the whole of the cell area. The cell on the r ight is in early prophase m itosis. The other cells
present a re three monocytes and one promonocyte. r:ine granules can be seen in several of the cells. Leishman
stain x I 200
THE W H ITE CELL SER I ES
145
Fig. 186 Ma rrow film - Monocytic leukaemia- M S (b)

Marked proliferation of cells of the monocyte series is the main fea ture of this illustration. M onocytes at all stages
of development are present; several show multi lobulation of their nucleus including one cell with a quinquefoliate
nucleus at the lower right part of the illustration. These features are reminiscent of the nuclear changes seen in
Rieder cells. (See Fig. 106.) M ay-Gnlnwald-Giemsa stain x 1200
146
Fig. 187 Blood film Monocytic leukaemia- MS (b)

This illustration shows massive proliferation of monocytes in varying stages of maturity. Several of these cells
show fine cytoplasmic granules which are normally found only in immature cells of this type. L eishman srain
X /200
THE WH I TE CELL SERIES
147
F ig. 188 Marrow film Acute monocytic leukaemia - MS (a)

L eft: The marrow is heavily infiltrated by immature cells of the monocytic series, May-Grunwald-Giemsa stai1z
X
900
Right: The non-specific esterase stain is positive in all cells illustrated, indicating the monocytic origin of the
cells. Combined chloroacetate esterase/non-specific esterase, coumersrained Methyl Green x 900
Fig. 189 Blood film Chronic monocytic le ukaemia

This illustrates a marked increase in the number of mature monocytes, exhibiting variation in size and nuclear
configuration. Leishman stain x 1200
148
'
A
# .,.~'f. (
.,;,>!
'' -J.
v~;~~f
;_~
/~
...,
Fig. 190 M o n ocyte

Th is large cell has an irregular nucleus with a single cleft containing cytoplasmic organelles. There is a moderate
amount of chromatin condensation around the nuclear membrane. The cytoplasm appears active, with
mitochondria, several short strands of rough endoplasmic reticulum and a variety of secretory granules, small in
size and with varying electron-density. In addition, there are free ribosomal granules. Glwaraldehyde, uranyl
acetate, lead citrate x 14 000
THE W H ITE CELL SER IES'
149
Fig. 191 Femoral marrow Monocytic leukaemia

There is almost complete replacement of the normal haemopoietic tissue by tumour. The majority of the cells in
the blood vessel, seen at the lower right of the field, are monocytes . Ha emalum & E osin x 120
Fig. 192 Femoral m a rrow Monocytic leukaemia

This is a high-power magnification of the field shown in Fig. 191. The cells present are almost entirely monocytes
and normob1asts. Haemalum & Eosin x 450
150
Fig. 193 Liver Monocytic le ukae mia

The distribution of the infiltrating cells may be either periportal (left), as in lymphocytic leukaemia, or diffuse
(right), as in myeloid leukaemia; mixtures of these two patterns m::y be seen . H aemalum & Eosin x 120
THE W H ITE CELL SER IES
151
:: . ~ ~-~~;:r :~: .
Fig. 194
Lung
Monocytic leukaemia
A sma ll vein ( top left) and a cap illary of an interalveolar septum (bottom left) are p lugged with masses of tumour
cells which are id entifiable at h igh magnificat ion ( righ t) as either m onoblasts o r mon ocytes. Haemalu m & Eosin
X
/20,
400,
800
152
Fig. 195 Skin Monocytic leukaemia

The dermis is densely infiltrated by tumo ur cells with resulting pressure atrophy of a hair shaft. T he monocytic
nature of the cells is clearly seen in the high-power field. T his mater ial is from the same case as Fig. I Yl.
Haema/um & Eosin X 200, X 800
Fig. 196 Marrow film Sea blue histiocytosis

The characteristic cell infilt rating the marrow is ill ustrated . T his is a large ret iculoendothelial cc.:ll with a single
eccentric nucleus. The cytoplasm contains a large n umber of sea blue g ranules. Leishman stain x 600
l)j
Fig . 197 Marrow film Niemann-Pick's disease Foam cells

These cells (monocytes), which are commonly round or ovoid, are filled with small hyaline droplets which give
a foamy or honeycomb appearance. Compare this appearance with the wrinkled cytoplasm of the Gaucher cell
( Fij(. I <lR). {,,t .<IIIIW/1 .<l cJ/11 X '}()()
Fig. 198 M arrow film Gaucher's disea se

The Gaucher cells (monocytes) have a distinctive large oval or round shape with one or more small eccentrically
placed nuclei. The cytOplasm has a laminated appearance with numerous blue fibri llae and open spaces from
which the lipid kerasin has been removed by the alcohol in the staining reagent. The Gaucher cell may also
exh ibit a foamy appearance, in which case the lipid material is contained as droplets, and in this form the cells
have a much greater resemblance to the foam cells found in Niemann-Pick's disease t Fig. I117). / ,,,,/ullc/11 .I aut
X /200
154
Fig. 199 Spleen Gaucher's disease

The capsule (top) and a trabecula (bottom) arc separated by a mass of pale cells in pseudo-follicular arrangement.
Note the widely distended sinusoids. Haemalwn & Eosin x 40
Fig. 200 Spleen Gaucher's disease

The characteristic Gaucher cells are large histiocytes with abundant pale pink foamy cytoplasm, the foamy
appearance being due to the lipid kerasin having been dissolved from the cells during the processing of the tissue.
Haemalum & E osin x 450
THE W H ITE CEL L SERIES
! 55
Fig. 20 1 M a t u r a t i on of the p l asm a cell

From left to right, the upper row s ho ws two plasmablasts, the firs t being the more primitive and the second
commenci ng to take on the characteristics of t he proplasma cell although it still s hows s hadow nucleoli. The next
cell is a proplasma cell; the nucleus has now taken up an eccen tric position and no nucleoli are obvious. Note that
in all these cells a perinuclear halo can be seen. The lower illustrations arc all of mature plasma cells, o ne o f
which is binucleate. note that in the other t wo cells the nuclei have assumed an eccentric position . Leishman stain
X
/ 200
F i g. 202 M a rrow film D yspr ote inaemia

T his composite illustration shows t he typical 'flaming' appearance which is to be seen in many of th e p lasm a cells
in this disorder. M ay- G riinwa/d-Giemsa stain x 1200
156
Fig. 203 B lood film P lasm a cell myeloma

This illustrates rouleau formation of the red .cells which is a characteristic finding in the blood film in plasma cell
myeloma and associated dysproteinaemias. May -Gnlnwald-Giemsa stain x 1200
~,
,,
Fig. 204 Mar row fil m (>lasma cell myeloma

The marrow is grossly infiltrated with plasma cells at all stages of maturation but in particular many large
plasmablasts are present. M ay-Gninwald-Giemsa stain x 300
Fig. 205 Marrow film Plas ma cell m yeloma

High power magnificat ion of a field taken from Fig. 2<H confi rming the presence of plasmablasts. Nucleoli a re
clearly seen in the nucleus of the plasmablasts. May-Gnlnwald-Giemsa srain x 1200
Fig. 206 Marrow film Plas ma cell m yeloma

T he marrow is heavily infiltrated with plasmablasts indicating the acute proliferative nature of this type of the
disease. May-Gnlnwald-Gicmsa stain x I 200
157
158
Fig. 207 M arrow film Plas m a cell m yeloma

This illustrates a proplasma cell (top) and mature plasma cells (lower part of the field). The background staining
is due to the high level of circulating immunoglobulin. May -Gnlnwald-Giemsa stain x 1200
Fig. 208 M arrow film Plasm a cell m yelom a

There is a complete absence of any white cell type other than plasma cells. The eccentric position of the nucleus
is well seen in these myeloma (plasma) cells which show considerable variation in size. Note the binucleate forms.
Leishman stain x 600
159
Fig. 209 Marrow film Plasma cell m yeloma

l .efl: A binucleate plasma cell is present, also a plasma cell in metaphase stage of mitosis. Leis/mum sraut x 600
Right: This shows a giant plasma cell with five n uclei; compare this cell for size with the normal sized plasma cell
in contact with it at bottom right. Leishma11 stai11 x 1200
160
Fig. 210 Marrow film Plasma cell myeloma

This illustration shows several immature plasma cells in which nucleoli can be seen; they have coarse cytoplasmic
granules which are commonly seen in this condition. The mature plasma cells, which predominate, show
clumping of the nuclear chromatin and several of these cells also exhibit granules. Two binucleate fo rms are
present. Leishma11 stai11 x 1200
161
Fig. 211 Bone marrow Plasma cell myeloma

In this touch preparation plasma cells vary considerably in size and shape, but are readily recognisable by the
nuclear structure, its eccentric position and pale staining paranuclear regio n. Occasional b inucleated cells are seen.
Thionine stain x 1200
Fig. 212 Femoral marrow Plasma cell m yeloma

T his marrow consists almost entirely of cells of one type, identifiable in the high-power fi eld as p lasma cells.
Haemalum & Eosin x 200, x 600
162
Fig. 213 Bone marrow Plasma cell myeloma

Three views of the same field in which amyloid has been fo rm ed within a deposit of the tumour. T his is
confirmed in the Congo Red preparation (centre) when this is examined under polarised light the amyloid displays
green birifringence (r ight). H aemalum & Eosin, Congo Red, Congo Red polarised, x 250
163
Fig. 214 Blood film Plasma cell leukaemia

The majority of cells in this blood film are plasma cells. This occurs in the end stage of plasma cell m yeloma,
plasma cells appearing in the peripheral blood. May-Griinwald- Giemsa stain x 1200
Fig. 21 5 Blood film Plasma cell leukaemia

This composite illustration shows several plasma cells, and also intense rouleaux formation and agglutination of
the red blood cells. The patient exhibited signs and symptoms suggestive of leukaemia, and plasma cells were
repeatedly seen in blood films, as was also a moderate leucocytosis and signs of anaemia. L eishman stain x 1200
164
F ig. 216 M a r row film Plasm a cell m yeloma

This illustration shows marked variation in the size of the plasma cells. The nuclei exhibit indentation and
lobulation similar to that seen in Rieder cells in acute leukaemia ( Fig . 106). May -Gnlnwald-Giemsa stain x 1200
Fig. 21 7 Marrow film Plasm a cell myeloma

These cells illustrate two of the malformations which are found in plasma cells in myeloma. The cytOplasm
exhibits some vacuolisation and many fus iform bodies similar to Auer bodies. May -Grllnwald-Giemsa stain
X /200
..
165
F ig. 218 Marrow Plasm a cell abnorm alities

The illustration at top left shows a large binucleate plasma cell, and also part of a smalle r cell wi th a single
nucleus. Both of these cells contain many large azurophilic granules which are frequently referred to as SnapperSchneid inclusion bodies. This and the subsequent three illustrations which show b inucleate plasma cells with
peculiar mottling of the cytoplasm and what appears to be basophilic granulation are all from a case of plasma cell
myeloma. Leishma11 stai11 x 1200
F ig. 219 Ma r row Plasm a cell abnorma lities

rrom left to righ t: a cell in the metaphase stage of mi tosis wh ich exhibits azurophil granulation of the cytoplasm;
a necrobiotic plasma cell; a binucleate cell in which cytoplasmic vacuoles are beginning to appear; a typical Mott
cell and a cell with marked reticulation of the cytoplasm, in both of which the nuclei are pyknotic. (M ott cells are
plasma cells which exhibit large clear globules within the cyto plasm .) Leishma11 staill x 1200
166
ATLAS O F H AEM ATO LOGY
Fig. 220 Marrow film Plasm a cell m yelo m a

At this low power magnification extremely large plasma cells a re noted. These cells are extraordinari ly large when
compared with the megakaryocyte (lower right). May -Griinwald-Giemsa stain x 300
Fig. 221 Bone m ar row P ost cy tot oxic t her ap y

Lej1. At low magnification -a very striking gelatinous change in the marrow is noted with an increase in the
proportion of fat cells. Haemalum & Eosin x 30
Right: At higher magnification this change Is even more striking, with small islets of hacmopoietic cells
between the fat spaces. This specimen was taken from a patient who had received long- term chemotherapy for
multiple myeloma. Haema/um & Eosin x 120
167
Fig. 222 P lasm a cell

Note the eccentric nucleus with peripheral chromatin clumping. There are some mitochondria present, but the
main cytoplasmic feature is the tight layering of rough endoplasmic reticulum in a concentric fashion. Some small
vacuoles are present. The two rod- like structures to the left of the nucleus are azurophil crystals. Glutaraldehyde,
uranyl acetate, lead citrate x 14 000
168
Fig. 223 Blood film Lcuco-erythroblastic reaction

The erythrocytes exhibit an isocytosis and poikilocytosis. Nucleated red cells are also present. The total white cell
count is elevated with a shift to the left, myelocytcs, metamyclocytes and a myeloblast arc seen. M ay-GnlllwaldGiemsa stain x 600, x 1200
'\
169
Fig. 224 Blood film Leuco-erythroblastic anaemia

This composite illustration depicts the immature myeloid cells found in the peripheral blood in leucoerythroblastic anaemia. The term leuco-ery throblastic a11aemia describes the abnormality seen in the blood
resulting from infiltration of the bone marrow by foreign or abnormal tissue. This anaem ia is characterised by the
occurrence of immature myeloid cells, and also nucleated red cells as shown in G . This example is from a case of
myelofibrosi s. May-Gnlmvald-Giemsa stain x 1200
Fig. 225 Rib Myelosclerosis

T he bone trabeculae are markedly increased in size and number. The haemopoietic tissue, though reduced in
amount, is of normal appearance. Haemalum & l!osi11 x 40
170
ATLAS OF H AEMAT OLOGY
Fig. 226 Trephine needle biopsy Bone Acute m ye lofibrosis

The amount of haemopoietic tissues is reduced (upper), shows increased stainable reticulin fib res (centre), and an
increase in atypical megakaryocytes (lower). Haemalum & Eosin x 40, x 450, Gordon & Sweec, cow11erscained
Neucra/ R ed x 40
171
Fig. 227 Trephine Needle Biops y Bone M yelofibrosis

At an intermittent stage in the disease reticulin stained fibres are much increased with atrophy of haemopoietic
tissue. Haemalum & Eosin x 40, Gordon & S weet, coumerscained Neutral R ed x 40
Fig. 228 Vertebra l m a rrow Myelofibrosis

In this advanced example, the bone trabeculae are atrophic and the haemopoietic tissue has been completely
replaced by rather loose fibrous tissue. Haemalrtm & Eosin x 40
..,
172
Fig. 229 Spleen Myelofibrosis

Sinusoids are distended; the only identifiable haemopoietic cells are megakaryocytes. Haemahm1 & Eosin x 50,
X 250
Fig. 230 Liver Myelofibrosis

There is diffuse infiltration of the sinusoids by cells of many types, including a giant cell (left). Haemalwn &
Eosin x 120
173
Fig. 231 Liver Myelofibrosis

High-power illustration of pan of the field in Fig. 210, showing the haemopoietic nature of the cells. The giant
cell is a megakaryocyte and many normoblasts can be recognised ; it is difficult to determine the precise nature of
the other cell types. Ha emalum & Eosin x 450
6.
The megakaryocyte series
176
Fig. 232 Megakaryoblasts

Left: The upper example is a typical megakaryoblast. Note the large nucleus with scanty indefinite chromatin, and
also that as in many cells of this type nucleoli cannot be resolved. T he cytoplasm is scanty and deeply basophilic.
The lower cell is developing to the promegak'a ryocyte stage, its nucleus is small in comparison to the cytoplasm,
the chromatin structure shows a more definite pattern and remnants of several nucleol i can be seen . The
cytoplasm is less basophil ic than in the previous cell. Leishma11 stai11 x 1200
Right: Both cells are at the same stages of development as those at the left; each have three nuclei due to division
by mitosis without corresponding division of the cytoplasm. This is a common finding and cells with two, three or
four nuclei are seen more often than megakaryoblasts with a single nucleus. Leishma11 stai11 x 1200
THE MEGAKARYOCYTE SER I ES
Fig. 233 Marrow fi lm Megakaryoblasts

The megakaryoblast may have several nuclei. Examples are shown here with two, three and four nuclei, all of
which exhibit numerous definite nucleoli. T hese arc especially well seen in the binucleate cell at bottom left.
177
178
Fig. 234 M a rrow fi lm M egakaryobla sts

Left: Note the coarse chromatin network of the nucleus and the basophi lic cytoplasm. While it is not possible to
state definitely that nucleoli can be seen, several pale blue areas of irregular size are present and these may be
nucleoli. This cell is in the early prophase stage of mitosis. May-Griinwald-Giemsa stain x 1200
Right: This cell is in the metaphase stage of mitosis; the cytoplasm is losing its basophilic properities. MayGriillwald- Giemsa stain x 1200
THE MEGAKARYOCYTE SERIES
179
Fig. 23 5 Marrow film Megakaryocytes

Both of the cells shown arc much smaller than normal granular megakaryocytcs. This is often the case in
conditions where there is a marked increase in the n umber of cells of this type. For size, compare with Figures
237 and 238. Leishman stain x I 200
Fig. 236 Marrow film Atypical Megakaryocytes

L eft: Promegakaryocyte (basoph ilic megakaryocyte). Note the numerous tiny vacuoles in the cytoplasm of this
ce ll. Leishman stain x I 200
Right: Promegakaryocyte. T h is cell is developing towards the granular megakaryocyte b ut the cytoplasm has not
com pletely lost its basophi lic p roperties . The cytoplasm contains rosette-shaped vacuoles. The changes present in
these two illustrations are usually seen in cases of ch ronic leukaemia and aplastic anaemia. L eishman swilt x I 200
180
Fig. 237 Marrow film Megakaryocyte

This granular megakaryocyte gives the impression that it might be on the point of ingesting a neutrophil
leucocyte, the elongated tag of cytoplasm being a pseudopodium. Leishman stain x 1200
F ig. 238 Marrow film Megakaryocyt cs

Left: This illustration shows a basophilic megakaryocyte which has ingesteda neutrophil polymorphonuclear
leucocyte. Leishman stain x 1200
Right: A granular megakaryocyte has ingested a neutrophil leucocyte. Leishman stain x 1200
(Note that the ingested leucocyte in both illustrations is in the same plane of focus as the cytoplasm of the
megakaryocyte. Had these cells been ly ing under or over the cytoplasm, they would not have been in the same focal
plane at this high magnification. )
T HE MEGAKARYOCYTE SERieS
Fig. 239 Marrow film Megakaryocyte

This illustration shows a granular megakaryocyte with nuclear h ypersegmentation . From a case of pernicious
anaemia. M ay-Gnlnwald-Giemsa stain x 1200
Fig. 240 Marrow film Idio pathic thrombocythaemia

Left : In this low-power illustration, megakaryocytcs, clumps of platelets and fragments of megakaryocyte
cytoplasm can be seen. May-Griinwald-Giemsa stain x 400
Right: This shows well-marked clumping of platelets. M ay- Griinwald- Giemsa stain x 1200
181
182
Fig. 241 Marrow film Thrombocythae mia

L ej1: A gross increase in the number of megakaryocytes. May-Griinwa/d-Giemsa sea in x 200
Right: At high-power magnification large sheets of platelets are apparen t. M ay-Gnlnwald-Giemsa s1ai11 x 1200
Fig. 242 Bone biopsy Thrombocythacmia

L ej1: The marrow is h yperplastic with a gross increase in the number of mcgakaryocytes, the majority of which
appear normal. H aemalum & Eosin x 200
Righ1: The gross increase in the number of mcgakaryocytcs is confirmed by the positive PAS reaction which
demonstrates the well ma rked megakaryocytic hyperplasia. Periodic Acid-Sclziff rPAS J x 200
183
Fig. 243 M a rrow film Atypica l m egakaryocytes Thrombocytha emia

Left: Promcgakaryocyte. Note the large spongy n ucleus with a suggestion of several nucleoli. May-GnlnwaldG iemsa stain x 1200
Right: M egakaryocyte con taining numerou s nuclei which d o not appear to be attached to o ne another . Compare
th i~ wuh Figure 239, which shows hypcrscgmentation of the nucleus. M ay-Gnlnwald-Giemsa stain x 1200
Fig. 244 Blood film H aemorrhagic thrombocythaemia

N umerous platelets are easily identifiable in this illustration , many of them show abno rmalities of mo rphology;
pltuclcts with irregular outlines and giant forms arc pr.:sent. The erythrocytes show h ypochromia and
uni~ocy tosis. There is also an increase in polymorphonuclear leucocytes. May-Gnlnwald-Giemsa stain x 1200
184
Fig. 245 Blood film Thrornbocythaernia .

Numerous platelets varying in size and shape are apparent in this illustration . May -Griinwald-Giemsa stain
X /200
Fig. 246 Blood film Giant platelets

This composite illustration shows platelet anisocytosis; a marked increase in the average platelet diameter is
obvious. T he field to the right shows a platelet which is almost equal in size to the accompanying neutrophil
leucocyte. May -Grzlnwald-Giemsa stain x 1200
185
Fig. 247 Blood film Giant platelets

Platelet anisocytosis is present in this illustration, as ar e giant platelets, top left and bottom right-the marked
increase in platelet diameter is obvious when compared with the diameter of the red cells and neutrophil
polymorphs. May-Gnlnwald-Giemsa stain x 1200
Fig. 248 Blood film Megakaryocyte fragments

In this illustration the lightly stained megakaryocyte fragment s are obvious. An atypical myeloblast, neutrophil
polymorph, and nucleated red b lood cell are present in this field. This blood sample was from a patient with
t ~:rminal myelofibrosis. May -Gnlnwald-Giemsa stain x 1200
186
ATLAS OF HAEMAT OLOGY
F ig. 249 Blood film Thrombocythaemia

This illustration is from a specimen of b lood from a patient with th rombocythaemia associated with splenic
hypofun ction . An isocytosis, ta rget cells and schistocytes are all present. Note also the numerous pla te lets wh ich
show co nsiderable variation in size. M ay-Gnlnwald-Giemsa stain x 1200
Fig. 250 Blood film Pla t e let sa te llitis m in t hro mbocyth aemia
T his composite ill ustration ind icates the polymor phonuclear leucocytosis wh ich is often associated with
thrombocythaem ia. The apparent satcll itism of platelets to the neutrophil lcucocytes is seen in blood preparation s
made from a specimen which has stood for some time prior to the fi lm being spread. This phenomenon is also
seen in thicker pa n s of the preparation, especiall y at the margins of the film. May -Gnlnwald-Gw nsa stain x 1200
T HE MEGAKARYOCYTE SER IES
187
Fig. 251 Blood film Platelet aggregates

Two areas of platelet aggregates a re evident. Note the variatio n in size of the platelets. Platelets clump readily and
may be seen in blood films as aggregates. May -Grrlnwald-Giemsa stain x 1200
Fig. 252 Marrow film Idiopathic thrombocytopenia

In this condition there is a marked increase in the number of mcgakaryocytes which are non-platelet producing.
Many young for ms of these cells arc usually present. The illustration is a typical example of the low-power
microscopic appearance in this condition. L eishman stain x 120
ems
1200
.. ,...
--
__
188

In this condition megakaryocytes appear in increased numbers. No platelet budding and a tendency towards
immaturity with some lack of granu larity of the megakaryocytes is evident. May -Griinwald-Giemsa stain x 400

No platelet budding is evident. The megakaryocyte lower righ t exhibits nuclear hypersegmentation and the
megakaryocyte top left exhibits fine vacuolation of the cytoplasm. May-Gnlnwald-Giemsa stain x 500
T l-IE MEGAKARYOCYTE SERIES
189
F ig. 255 B one biopsy Megakaryocyt ic h yperplasia

Left : At low magnification, it is evident that there is a well marked increase in the number of megakaryocytes.
Haemalum & Eosin x 100
Right: High magnification confi rms the megakaryocytic hyperplasia. Most of these cells do not exhibit any
abnormal features. Haemalum & Eosin x 350
Fig. 256 Spleen Idiopa thic thrombocytopenia

Left: This field shows the characteristic development of germinal centres in lymphoid follicles which, although of
normal size, are increased in number. H aemalwn & Eosin x 40
Right: This is a high-power view showing increased numbers of neutrophil and eosinophilleucocytes in the
splenic pulp. A megakaryocyte can be seen in a sinusoid at upper left. Haemalwn & Eosin x 450
190
Fig. 257 Sternal marrow section Megakaryoblast leukaemia-M 7

There is a great increase in the n umber of immature megakaryocytcs which, even at this low magnification, show
much variation in morphology. H aemalum & Eosin x 120
Fig. 258 Sternal marrow section Megakaryoblast leukaemia - M 7

This is a high-power illustration from the same section as Figure 2'57 . Note the high nucleo-c~ . ~>plasmi c ratio in
several of the megakaryocytes, and also the abnormal lobulation of their nuclei. Haemalum & l.:'osin x 450
191
F ig. 259 Budding megaka r yocyt e

This megakaryocyte, surrounded by erthrocytes, is in the process of producing platelets. Glutaraldehyde, ura11yl
acetate, lead citrate x 6720
--
".....
'
..
190
ATLAS OF HAEMATOI.OGY
_.;
rrt
>
.,.
:>:>-
~
0
Q
-1
rrt
-\ ()
Fig. 260 Platelet

This platelet has been sectioned in its largest diameter. The marginal bundle of m icrotubules is seen almost in its
entirety. The open canalicular system is seen clearly and secretory gran ules are present. Close to the m arginal
bundles there are sm all collections of cytoplasmic granules; these may be either glycogen granules or granules
containing platelet phospholipid. In the centre of the platelet there is a vacuole containing several membranous
structures. Glutaraldehyde, ura11y l acetate, lead citrate x 31 200
7.
Phase contrast microscopy
This system enables the observer to study Jiving cells and reveals detail in objects of little
contrast. Such intra-cellular components as nuclear chromatin, chromosomes, nucleoli,
mitochondria, the centrosome and specific cytoplasmic granulation are clearly revealed free
from the artefacts which may be produced during fixation and staining. Cell motility can
also be studied with ease.
Although the phase contrast microscope has wide application in the study of normal and
leukaemic leucocytes in the Jive state, it has not, as yet, revealed any characteristic
abnormality or distinctive features in leukaemic cells. There is no doubt, however, that this
system is the greatest advance in microscopy since the electron microscope.
Figures 261 to 280 are examples of leucocytes photographed under phase contrast
conditions, and show detail which would not have been discernible under bright field
conditions or in stained preparations. Good examples of this can be seen by comparing
Figures 276 to 278 with Figure 153, all of which were prepared from the same specimen of
blood from a case of acute lymphoblastic leukaemia. Compare also Figures 271 to 273 with
Figure 102, all of which are from specimens of blood in the same case of acute myeloid
leukaemia.
PHASE CONTRAST MICROSCOPY
195
Jill(. 26 1 Blood: fresh wet preparation Neutrophil (polymorphonuclear) leucocyte

The extreme motility of this cell is obvious. N ote the cytoplasmic processes into which the granules are flowing,
the best examples being G , H , I and J. Interval time between exposures, 5 minutes. Phase comrast x 1200
196
Fig. 262 Blood: fresh wet prepara tion Eosinophil and neutrophil (polymorphonuclear) leucocytes
T he difference in size of the two types of cytoplasmic granule is well demonstrated. Note also the greater motility
of the neutrophil leucocyte and the elon gated cytoplasmic p rocesses of this cell. Interval time between exposures,
3 minutes. Phase com rast x 1200
PHASE CONTRAST MI CROSCOPY
197
tllg. 263 B lood: fres h wet preparation Eosinophil {polymorphonuclear) leucocyte

This preparation demonstrates the motility of the eosinophil which is shown thrusting its way between the
nci!(hbouring red blood corpuscles. Note how the granules, which are well defined, flow into the cytoplasmic tags
(pseudopodia) . In F, G , H, I and J a platelet, showing alteration in shape, can be seen. It should also be noted
thor defini te nucleoli are present in the nuclear lobes of the eosinophil leucocyte. These illustrations were taken at
') minute intervals and should be compared with F igure 264, which is of the same type of cell taken at 30-second
lr1rc rvnl s, in which the movement appears to be more limited. Phase comrast x 1200
198
F ig. 264 Blood: fresh wet preparation Eosinophil (polymorph onuclear) leucocyte
Interval time between exposures, 30 seconds. Compare this series with Figure 263 when it will be noted that even
at this much shorter time lapse the motility of the cell and movement of the granules is obvious. The change in
shape of the cell is seen as it thrusts its way between the red b lood corpuscles. Phase comras1 x 1200
PI lASE CONTRAST MICROSCOPY
199
:n
11hf. 265 Blood: fresh wet preparation Phagocytosis of platelet by n e utrophil polymorphonuclear
hmcocytc Haemorrhagic thrombocythaemia
I hl~c illustrations were taken at two-minute intervals, while the temperature of the preparation was maintained at
17 C . A, a neutrophil leucocyte which appears, by the projection of its cytoplasm, to be moving towards a platelet
(11rrmu) which is lying in contact with a crenated erythrocyte. B , the leucocyte has moved closer to the platelet
lltlll it b obvious, by the position of the cytoplasmic pseudopodia, that it is traversing in the direction of the
pltottlct. C, the platelet is now attached to the margin of the leucocyte. D , the platelet is lying within the cytoplasm
111 tlw leucocyte and the neutrophil granules are flowing around it. E , phagocytosis is now completed and the
lrllwtyl c is moving out of the field; note the elongated cytoplasm filled with granules. Phase comrast x 2500
\A TO LOGY
Fig. 266 Blood: fresh wet preparation Phagocytosis of p latelet by neutrophil polymorphon uclear
leucocytye Haemorrhagic thrombocythaemia
The temperature of the preparation was maintained at 42c while this series of illustrations was made at twominute intervals. Compare with Figure 265. A, shows two platelets (arrowed ) with elongated protrusions, one of
which is indicated by a white arrow, and also an elongated neutrophil leucocyte. B , shows that the p latelet (with
arrow) has been engulfed and now lies within the cytoplasm of the leucocyte. C, the leucocyte is now moving
towards the upper margin of the field and the engulfed platelet can be clearly seen. Note that the platelet
indicated by the black arrow remains in a constant position in all three illustrations. Phase contrast x 1200
F ig. 267 Blood: fresh wet preparation P h agocytosis of platelet by n eutrophil polymorphonu clear
leucocyte Haemor r h agic t hrombocyth aem ia
These illustrations should be compared with Figure 265 as in this instance the temperature was raised to 42c, at
which temperature the leucocyte has become much more rapidly motile and exhibits a more elongated appearance.
A, shows a leucocyte almost in contact with a platelet, while B, taken two minutes later, shows the p latelet lying
within the cytoplasm. Phase contrast x 1200
PHASE CONT RAST M I CROSCOPY
201
Fig. 268 Blood: fresh wet preparation Polymorphonuclear le ucocytosis

The increased motility of these cells with much pseudopodia formation is demonstrated. Note also the aggregation
of the cells at B and C, after which they start to separate again . Interval time between exposures, 5 minutes.
Phase comrasc x 1200
202
F ig. 269 Blood: fresh wet preparation Eosinophilia in m ycosis fungoides

Four eosinophil leucocytes are seen lying in close proximity to one another. It is obvious, by the alteration in
shape of these cells, that they are highly motile. Interval time between exposures, 2 minutes. Phase comrast x
1200
Fig. 270 Blood: fres h wet preparation Basophilleucocytes

The basophil leucocyte seen in fields A and B has a single lobed n ucleus, whereas the cell in fie ld C has a bilobed
nucleus. The cell illustrated in A and B was kept under observation for 15 minutes, during which time the only
apparent movement was in the disposition of the granules. Numerous small vacuoles are seen in the cytoplasm;
these are probably the result of granules having been expelled. The archoplasm is obvious in the cell in fie ld C;
it lies at the cleft of the bilobed nucleus. Phase comrast x 1200
203
Fig. 271 B lood: fresh wet preparation Acute myeloid leukaemia

All the cells in this pair of sequence illustrations are leukaemic myelocytes; the cell at the upper right of the field
is progressing to the metamyelocyte stage and appears to be more motile than the others. T he lower cell of the
group shows, in addition to the granules, clumping of mitochondria. Note the well-resolved nucleoli and nuclear
membranes in all these cells. Exposure interval between fields A and B was 5 minutes. Phase comrast x 1200
204
F ig. 272
Blood: fresh wet preparation Acute myeloid leukaemia
The cell depicted in this series of illustrations is a myelocyte which, at 5-minute intervals between exposures,
shows limited amoeboid movement. A cytoplasmic protrusion can be seen at the right of the cell, into which the
granules are flowing. Phase comrast x 1200
F ig. 273 Blood: fresh wet preparation Acute myeloid leukaemia

Fields A , B and C all show leukaemic myelocytes in which there is clumping of the mitochondria. The cell in
field B also shows a relatively clear archop lasm. Fields D , E and F are examples of metamyelocytes from the same
preparation of blood. Phase contrast x 1200
me
205
Fig . 274 Blood: f resh wet preparation Neutrophil (poly morphonuclear), leucocyte and lymphocyte
T he marked contrast in motility of these two cell types is well seen, the lymphocyte exhibiting only slow
amoeboid movement against the very vigorous movement of the polymorph. Interval time between exposures, 2
minutes. Phase comrasc x 1200
206
F ig. 275 B lood: fresh wet preparation Lymphocyte

The slow amoeboid movement of the lymphocyte is well demonstrated. Note the rather thick cytoplasmic
processes producing pseudopodia formation. As these processes extend, the nucleus appears to move in the same
direction. The lighter area at the indentation of the cytoplasm into the nucleus is the centrosome and the dark
material below it is the mitochondria. The two platelets present also appear to exhibit extending cytoplasmic
p rocesses. Interval time between exposures, I minute. Phase comrast x I 200
PHASE CONTRAST MIC ROSCOPY
207
Fig. 276 Blood: fresh wet prepar a tion Acute lymphoblastic leukaemia
This illustrated sequence shows the limited amoeboid movement of several leukaemic lymphoblasts. Note the
large nucleoli, the well m arked nuclear membranes and the high nucleo-cytoplasmic ratios of these primitive cells.
The cell in the upper right part of the fie ld shows only a faint shadow of the cytoplasmic outline, due to pressure.
The mitochondria are well resolved in this cell and appear to be lying in relationship to the archoplasm; this
feature is most obvious in field C . Interval time between exposures, 10 minutes. Phase comrasr x 1200
""
:!<
..,
"'~
,.
'
'
208
Fig. 277 Blood: fres h wet preparation Acute lymphoblastic leukaemia

The cells shown in this illustrated sequence are all lymphoblasts . The cell at the upper part of the field shows
active movement and when each frame is compared it will be noted that there is quite a marked alteration in the
configuration of the nucleus between A and D . All the cells show well resolved nucleoli also the high nucleocytoplasmic ratio typical of this cell type. Interval time between exposures, 10 minutes. Phase co111rasr x 1200
Fig. 278 B lood: fresh wet preparation Acute lymphoblast ic leukaemia

This composite illustration shows numerous leukaemic lymphoblasts which vary considerally in size; the larger,
more primitive, cells have a broader rim of cytoplasm than the smaller, more mature cells. The nuclei of all these
cells contain either one or two large nucleoli. Several of the cells show cytoplasmic protrusions, indicating that the
cells were motile. Phase contrast x 1200
209
fig. 279 Blood: fresh wet preparation Monocyte

Compare this series with Figures 261 to 264, when the diminished motility of this cell type will be obvious. The
kidney-shaped nucleus shows definite nucleoli which would not be apparent in a similar cell in a stained
preparation. Above the nuclear indentation is a dark granular mass which is the mitochondria. Interval time
between exposures, I minute. Phase contrast x 1200
- - -~.....
~ ~
~-
_,
2 10
Fig . 280 Blood: fresh wet preparation H a emorrhagic thrombocythae mia

Three polymorphonuclear leucocytes arc seen converging o n a platelet mass; one of the cells is vacuolated as if
containing some foreign matter. Phase comrast x 1200
Fig. 281 Blood: fre sh wet preparation Fibrin formation

Long slender fibrin strands arc seen adjaccm the red cells during the process of blood coagu lation. Phase
comrast x 1200
8.
The blood parasites
212
Hepatic cycle
(Exo-erythrocytic)
Fig. 282 Asexual cycle (schizogony) of th e malarial parasite

Erythrocytic and hepatic (exo-erythrocytic) cycles.
THE BLOOD PARASITES
213
ra>
. . .
4
10
!'; :N ;
:: .....~:.
~ ~- .
11
12
Fllo(. 283 Malaria The asexual cycle (schizogony) of Plasmodium v iva x

'f'h b is the pa rasite which causes benign tertian ma laria.
I . i\s n rule merozoi tes are not seen adhering to red blood corpuscles .
.!. Trophozoite- early.
I. T rophozoitc-'signet ring' stage.
I 7. The trophozoites show increase in size, alteration in shape, protrusion of pseudopodia and depositton of
~(o lde n -y ellow pigment.
H. Schiwnt stage.
!l , Segmentation of schizont, forming rosette of sixteen m erozoites; note the golden-yellow pigment in the centre
nl the rosette, and also the enlargement of the red blood corpuscle .
The presence of Schi.iffner's dots in 3- 9 should also be noted . (Schi.iffner's dots are bright red staining particles
which arc a diagnostic feature of some value. They lie within the red b lood corpuscles, but separate from the
pnrn~ itcs and should not be confused with pigment granules which lie within the parasite. )
I0. M erozoites are liberated after ruptu re of the red blood corpuscle.
I I . Macrogametocyte (female ), see sporogony Figure 287 .
12. Mic rogarnetocyte (male), see sporogony Figure 287.
/ ,,t</11/UI// .<tail/ X / 200
2 14
Q
4
'
!I
,-
(1:)
, 10
.~
I!
11
12
Fig. 284 Malaria The asexual cycle (schizogony) of Plasmodium malariae

T his is the parasite which causes benign quartan malaria.
I. As a rule merozoites are not seen adhering to red b lood corpuscles.
2, 3. Early stage of trophozoites-rings.
4-7. D eveloping stages of trophozoites showing amoeboid appearance, pseudopodia and abundant golden-brown
pigment. T he characteristc 'band' form of trophozoite is seen in 6.
8. Schizont stage.
9. Segmentation of schizon t, forming rosette of eight m erozoites; note that the red blood corpuscle is not enlarged
as in the cycle of Plasmodium vivax (Fig. 283).
I0. Merozoites are liberated after rupture of the red blood corpuscle.
II. MacrogametOcyte (female), see sporogony, Figure 287.
12. Microgametocyte (male), see sporogony, F igure 287. It should be noted that no Schiiffner's dots are present in
this form.
!I
,,
THE BLOOD PARASITES
215
, o,,
-
OQ
~
5
6
~0
Q Ot)o 10-
oo. ~
0 0
0 ""

~.
11
~ed
tin
"
12
Jllg. 285 Malaria The asexual cycle (schizogony) of Plasmodium falciparum

This is the parasite which causes estivo-autumnal malaria (malignant tertian malaria).
I. Merozoite adhering to red blood corpuscle.
2. Trophozoite-early, more than one parasite may be seen in a red cell.
}, Trophozoite and Maurer's dots in red cell. (Maurer's dots are characteristic grey-b lue staining particles, and
nrc n useful diagnostic feature. These dots are not p igment granules, with which they should not be confused.)
'' Trophozoite-'signet ring' stage.
'J, 6, 7. Trophozoite increasing in size; the parasites now contain golden-brown p igment.
R. Schizont stage.
9. The schizont becomes segmented and a large number of merozoites are formed.
I 0. The red cell ruptures and the merozoites are liberated.
I I . Macrogametocyte (female crescent).

12. M icrogametocyte (male crescent).
S1ngcs II and 12 are characteristic of Plasmodium falciparum. Note that in this type of malaria, stages I, 2, 3, 4,
I I nnd 12 occur in the circulating blood, whereas stages 5- l 0 occur in the red blood corpuscles in the internal
1>rguns.
l.t'ishma11 stai11 x 1200
'
2 16
Oocyst
development
Ookinete
Exflagellation
Oocyst ruptured
Fig. 286 Sexual cy,cle (sporogony) of th e m a laria l par asite in the body and stomach of the mosquito
See Figure 287.
THE BLOOD PARASITES
8
7
,- ----,
\ '
9
I_ _____ J
rig. 287 Mala ria Sexual cycle (sporogony) of mala rial parasites in stom ach a nd body of t h e
mosquito
I . M icrogametocyte showing exflagellation, i.e. extrusion of microgametes which penetrate and fertilise the
macrogametocyte 2.
3. Ookinete or zygote (ferti lised macrogametocyte).
I, 2, and 3 occur in the stomach of the mosquito.
4. Ookinete as it penetrates the stomach wall.
5. Sporocyst (oocyst) as in stomach wall of mosquito.
6. Sporoblasts inside sporocyst.
7. Transformation of sporoblasts into sporozoites.
8. Oocyst rupturing and sporozoites being liberated, many will enter the salivary gland of the mosquito and be
injected intO human blood when the insect bites.
9. Sporozoite attached to surface of human red blood corpuscle.
l .eishma11 s1ai11 x 1200
nosquito
21 7
2 18
Fig. 288 Blood film Be nign te rtia n malaria

In this composite illustration three roselle forms are present, the rosette at top left being the most typical and
sixteen merozoites can be counted . All other parasites present are variations of the trophozoite stage. Note that all
the red blood corpuscles containing parasites of the Plasmodium vivax sho\\' well defined SchlifTner's dots. Muy Griinwald-Giemsa s1ai11 X 1200
Fig. 289 B lood film Benign tertian and m aligna nt tertian m a laria mixed infection
In this illustration the thick ring form of P. vivax (centre upper right) and the thin ring form of P. falciparum
(bottom left) are present. The patient had previously undergone splenectomy and H owell-Jolly bodies are present
in the red cells left centre and upper right of field. The double chromatin dots of the ring forms of P. falciparum
arc present in the cell, bottom cent re of field. May -Gnlnwald-Giemsa stain x 1200
THE BLOOD PARASITES
219
II
Fig. 290 Blood film Malignant tertian mala r ia

Left: To the left of the centre a merozoite of Plasmodium falciparum is seen attached to a red blood corpuscle. All
other parasites present are trophozoites of the 'signet ring' fo rm. May-Grzinwald-Giemsa stain x 1200
Right: In this thick blood preparation from the same case, several macrogametocytes are present. May-GriinwaldGiemsa stain x 1200
Fig. 291 Liver M a laria

This illustration shows two foci of exo-erythrocytic malarial parasite (Plasmodium viv ax ) sporozoites developing
in parenchymal cells of the liver. See Figure 282. Haemalum & Eosi11 x 1000
:nt
Ill
220
Fig. 292 Liver Mala ria

The sinusoids are distended by swollen Kupffer cells, the cytoplasm of which contain characteristic granules of
malarial pigment. Haemalum & Eosin x 450
Fig. 293 Spleen Malaria

The red pulp contains reticulo-endothelial cells with prominent nuclei. Black or dark brown granules of malarial
pigment are seen in histiocytes and in erythrocytes. Haema/um & Eosin x 450
THE BLOOD PARASITES
221
Fig. 294
Left: Marrow film Leishmaniasis
The cytoplasm of the monocytes contains numerous Leishmania donov ani.
R ight: ( Leishmania) C ulture preparation NNN (Nicolle, Novy a nd MacNeal) media
This illust rates the promastigote fo rms with a dark staining trophonucleus and si ngl.: free fiagellum arising from
the anterior end of the kinetoplast. In culture these form s tend to agglomerate in clusters o r rosettes with the
flagella centrally directed. M orphologically L. tropica, L. braziliensis and L. donova ni are indistinguishable from
each other. M ay-Griinwald-Giemsa stain x 1200
Fig. 295 Skin Leishmaniasis

Left: Large cl umps of histiocytes, surrounded by a dense in fi ltrate of lymphocytes and plasma cells, occupies the
dermis. Haemalwn & Eosin x 130
Right : At high magnification, numerous parasites, Leishmania donovani, are seen in the cytoplasm of the enlarged
histiocytes. Haemalum & J:'osi11 x 11 00
222
l
Fig. 296 Blood film T rypa nosomiasis
The parasites are between the red cells in which the flagellum and darkly staining kinetoplast are seen . The
average size of the parasite is 25 ~11n long and 2 ~11n thick. The parasite Try panosoma rhodesiene is the causative agent
of acute sleeping sickness and is transmitted to man by the Glossina morsitmzs (tsetse fl y) . Leishman stain x 1200
Fig. 297 Lymph node s mea r Histoplasm a capsula tum

Left : Free fungi. L eishman stain x 1000
R ight: A large monocyte with numerous phagocytised fungi. The nuclei and capsules of the parasites are visible.
Leishman stain x I 000
THE BLOOD PARASITES
223
.,
4'1
.,
,. '
1\\)
.~.~~
".
:nt
I'
''
- - _,#
'
~
,.
Fig. 298 Blood film (thick drop preparation) Filariasis Wuchereria bancrofti
The microfilaria, which is found in the blood, is covered by an outer sheath and the body cells, which d o not
reach to the end of the graduall y tapering tail, have darkl y staining nuclei. (The filariae, which a rc the adult
parasites, are threadwo rms and belong to the class Nematoda. They cause elephantiasis and lymphangitis and
are found in the lymphatic vessels in these conditions. The larvae, known as microfil ariae, are about 300 ~t m
long, 7~t m th ic k and arc transmiued by the Culex and other mosyuiwcs. ) A/ay-Griimvalci-Giemsa stall/
X
300,
900
.....
'
I
.. ,. .....
; I! ... ; .
., ....
. ..
... ,::.
et
.\
'
,, 4
. ;~
Fig. 299 Blood film (thick drop preparation) Filariasis Acanthocheilonema Dipetalonema
This type of microfiaria is sho rter than Wuchereria bancroft!, has no sheath and the nuclei extend as far as the tip
of the tail. May-Grzlnwald-Giemsa stain x 300
9. Tumours of lymphoid tissue and other

neoplasms
The Rappaport classification of non-Hodgkin lymphomas used in the last edition has been
superceded in the literature and in practice by the Kiel classification in Europe and by the
Lukes-Collins classification in North America. It is relatively early to place a lesion in
either of these classifications because the majo r differences between them are
terminological. This is shown in T able 1.
The Working Formulation produced on behalf of the US National Cancer I nstitute for
'clinical usage' is based on morphological appearances but it is difficult to compare the
Formulation with either the Kiel or Lukes- Collins classifications. The practical value of the
Formulation has yet to be assessed: it is being used in some cancer clinics as an alternati ve
to the Rappaport classification. The two are compared in T able 2.
The nomenclature for the various forms of H odgkin's disease continues to be the Rye
modification of the L ukes-Butler classification: lymphocytic predominant, nodular sclerosis,
mi xed cellularity and lymphocytic depleted. The name used in this text for the
characteristic cell of the disease reflects the name of the disease itself rather than other
eponyms.
226
T a ble 1
Patholog ical classifica tions of non-Hodg kin's ly m p h o m as.
KI EL
LUKES & COLLINS
RAPPAPORT
B or T cell, small lymphocyte

(CLL)
L ymphocytic, well differentiated
Low grade
Lymphocytic:
CLL, B or T cell
Hairy cell leukemia
Mycosis fungoides & Sezary
syndrome
T-zone lymphoma
T cell, mycosis fungoides &

Sezary syndrome
T cell, immunoblastic sarcoma
Histiocytic
L ymphoplasmacytoid
B cell, plasmacytoid lymphocyte
Plasmacytic
B cell, plasmacytoma
Plasmacytoma
Centrocytic
*B cell, small or large cleaved

follicle centre cell
Lymphocytic, poorly
differentiated
Mixed cell
B cell, large non-cleaved follicle

centre cell
Histiocytic
B cell, small non-cleaved Burkitt

or non-Burkitt
T cell, convoluted lymphocyte
L ymphocytic, poorly
differentiated
*Centroblastic-centrocytic
Unclassified
High grade
Centroblastic
Lymphoblastic:
8 -lymphoblastic, Burkitt type
T -lymphoblastic, convoluted
cell type
Unclassified
Immunoblastic:
With or without plasmablastic
or plasmacytic differentiation, B
or T cell type
U cell
B or T cell, immunoblastic
sarcoma
Unclassifiable
*May be diffuse and/or follicular
Many T cell tumours arc not classifiable
Undifferentiated
T UMOURS OF LYMPHOID T ISSUE & OTHER NEOPLASMS
Table 2 Classification of non-Hodgkin lymphomas in clinical use.

NCl WORKING FORMULATION
RAPPAPORT
Low grade
A. Small lymphocytic
CLL
Plasmacytoid
Well-differentiated lymphocytic, diffuse
B. Follicular, small cleaved cell
Poorly differentiated lymphocytic, nodular
C. Follicular, small cleaved and large cell
Mixed lymphocytic/histiocytic, nodular
lmermediace grade
D. Follicular, predominamly large cell
Histiocytic, uodular
E. Diffuse, small cleaved cell
Poorly differemiated lymphocytic, diffuse
F. Diffuse, small and large cell
M ixed lymphocytic/histiocytic, diffuse
G. Diffuse, small aud large cell
H istiocytic, diffuse
H igh grade
H. Large cell, immunoblastic
Histiocytic, diffuse or undifferentiated, diffuse
plasmacytoid
clear cell
polymorphous
I. L ymphoblastic, convoluted
Poorly differentiated lymphocytic, d iffuse
non-convoluted
J.
Small non-cleaved cell Burkitt
Poorly differentiated lymphocytic, diffuse
227
228
Fig. 300 Lymph node Normal

Note the size of the lymphoid follicles in cortex (left) and the p resence of lighter-staining germinal centres in
many of them. Reticular fibres are most numerous between the follicles (right). Note that no lymphoid tissue
occurs outside the capsule. H aema/um & Eosin x 60, Gordon & Sweet coumerstained Neutral R ed x 40
Fig. 301 Lymph node Normal

This shows a high power illustration of a germinal centre (left) and the mantle of small lymphocytes to the right.
The lightly stained areas within the germinal centre represent histiocytes which are always prominent in normal
germinal centres. Haema/wn & Eosin x 250
T UMOU RS OF LYMPHO ID TISSUE & OTH ER NEOPLASMS
229
F ig. 302 Lymph node Follicular h yperplasia

At low magnification , the increase in the size of the lymphoid follicles is seen, each of them having a mantle of
mature lymphocytes. Even at this magnifica tion , histiocytes can be ident ifi ed as the relatively clear spaces in the
centres of the follicles. H aemalum & Eosin x 30
Fig. 303 Lymph node Follicular H yp erplasia

T he d etails of individual cells can be seen in this touch preparation from the same node as in F igure 302. The
difference in nuclear morphology of mature lymphocytes and follicle centre cells is readily seen; both centrocytes
and centroblasts can be distin guished and the occasional ce.ntroblast is in mitosis (arrow). The ovoid outline of the
nucleus of the histiocyte contrasts with the much more rounded outline of the centroblasts. Many fragments of
nuclear debr is are seen in the cytoplasm. M ay-Gnlnwald-Giemsa x 1200
lt .
II
230
Fig. 304 Lymph node Toxoplasmosis

Left: The cytoplasm of the histiocyte contains nuclear debris and distorted ring forms, probably organisms.
Haemalum & Eosi11 x 1200
Right: Clusters of eosinophilic structures, probably organisms and apparently intracellular. Haemalw11 & Eosi11 x
1200
TUMOURS OF LYMPHOID TISSUE & OTHER NEOPLASMS
23 1
Fig. 305 Lymph node Malignant lymphoma, diffuse

This illustration shows the pattern which occurs in any lymphomatOus process when the follicular structure has
been completely obliterated by the pro liferating tumour cells. I t is no t possible tO make any statement about the
cell type at this magnification. H aemalum & Eosin x 35
Fig. 306 Lymph node Follicular lymphoma

This shows the pattern in any lymphomatous process of follicu lar type: follicles are both larger and less clearly
defined than no rmal: a mantle layer may or may not be present. The reticular content of the follicles is not
increased. Haemalum & Eosin x 40, Gordon & Sweet x 40
232
Fig. 307 Lymph node Malignant lymphoma, diffuse

This is a lesion of lymphocytic type. The monomorphic nature of the lesion and the frequency of nuclei with
ang.ular outline is well seen. Occasional centroblastic nuclei (arrow) have prominent nucleoli, and two histiocytes
with plentiful cytoplasm are also seen (top right). Haemalum & Eosin x 450
Fig. 308 Skin Malignant lymphoma

The deep dermis and subcutaneous fat are diffusely infiltrated with small lymphocytes, many of which have the
angular nuclei of cleaved cells. H aemahmr & Eosin x 50, x 500
233
Fig. 309 Iliac crest marrow Trephine specimen Malignant lymphoma, lymphocytic
The haemopoietic tissue has been replaced by a mass of tumour cells. The marrow picture in this condition is
indistinguishable from that of lymphocytic leukaemia (see Figs. 168 and 169) Haemalum & Eosin x 120, x 800
234
Fig. 310 Blood film Follicular lymphoma

These cells are larger than the mature lymphocyte. The nuclear structure is coarse and in several cells there is
marked clumping of chromatin; the nuclear outline is kidney-shaped or, in some cases, deeply indented . Nucleoli
are not well demonstrated by this staining method (see F igs. 323 and 324). L eishman stain x 150, x 1200
Fig. 311 Lymph node Lymphoplasmaeytoid lymphoma

This is a diffuse lesion in which mature lymphocytes and mature plasma cells are seen in more or less equal
numbers. Haema/um & Eosin x 400
TUMOURS OF LYMPHOID T ISSUE & OTHER NEOPLASMS
Fig. 312 Lymph node Malignant lymphoma, T-zone

At low magnification the contrast between the compressed non-neoplastic tissue (top) and the paler staining
neoplastic tissue is seen. There is also a suggestion of increased vascularity. The reticulin stain confirms this.
Ha emalum & Eosin x 25, Gordon & Sweet x 64
li
Fig . 313 Lymph node Touch preparation Maligna nt lymphoma, T -zone

The convoluted T -cell nuclei produce the apparent clefts in this preparation. May-Griimvald-Giemsa stain x
1200
235
236
Fig. 314 Skin My cosis fungoides

There is diffuse involvement of superficial and mid-dermis with a polymorphic infiltrate including small
lymphocytes and large cells. Haema/um & Eosin x 120
Fig. 315 Skin Mycosis fungoides

Details of the cellular infiltrate: note that some of the large cells appear to have bilobed nuclei . Haemalum &
Eosin x 675
237
F ig. 316 S kin Mycosis fungoides

This thionin-stained section shows the close association between the tumour cells and epidermal epithelium, a
characteristic feature of this disease. Methacrylate -embedded x 1200
Fig. 317 Skin M ycosis fungoides

The true nature of the large atypical lymphoid cell is revealed-a T -cell with a characteristic convoluted nucleus.
Electron micrograph x 20 000
Fig. 318 Lymph node Malignant lymphoma, follicula r

A narrow band of mature lymphocytes runs vertically in the centre of the field. On either side of it, there is
tumour tissue showing marked pleomorphism with centrocytes and centroblasts (small and large cells of follicle
centre type). H aemalum & Eosin x 400
Fig. 319 Lymph node Malignant lymphoma, centrocy tic

This is a touch preparation in which the great majority of tumour cells are small, often with cleaved nuclei. The
presence of an occasional centroblast or large cell (arrow) is quite usual in this condition. M ay-Cnlnwald- Giemsa
stain x 1200
239
Fig. 320 Lymph node Malignant ly mpho m a, centroblastic/centrocytic

Most of the cells are centroblasts or centrocytes: only a few small lymphocytic nuclei can be seen. Haemalum &
Eosin x 450
Fig. 321 Ly mph node Centrocytic lym phoma

This is a touch preparation from a similar case to Figure 320. The relative sizes of the nuclei of mature small
lymphocytes (arrow) and of the tumour cells are seen. Note also the outline of the nuclei and the much looser
arrangement of the chromatin in the centrocytes, a few of which are cleaved. May -Griinwald-Giemsa x 1200
240
Fig. 322 Bone biopsy Malignant lymphoma, lymphoblastic

Left: This illustrates intensive lymphoid infiltration of the bone marrow. Haemalum & Eosin x 125
Right: At higher magnification the predominant lymphoid cells are all of the small cleaved type. Ha emalum &
Eosin x 600
Fig. 323 Blood film Maligna nt Lymphoma, lympho blastic

This illustrates large abnormal lymphoid cells, some of which have a cleaved nucleus. Giant single nucleoli are
also present in some of the n uclei. May-Gnlnwald-Giemsa stain x 1200
TUMOURS OF LYMPHOID T ISSUE & OTH ER NEOPLASMS
241
Fig. 324 Blood film Malignant lymphoma, lymphoblas tic

The majority of the cells in this illu stration are lymphoid cells. These show a large single n ucleolus eccentrically
placed and obvious as a blue coloured area around which is a dense rim of chromatin. Brilliam Cresy/ Blue,
coumerstained May-Griinwald-Giemsa stain x I 200
242
Fig. 325 Lymph node Burkitt's lymphoma

The normal architecture of the node has been completely replaced, most of the cells present are tumour cells;
clear spaces, giving the 'starry sky' appearance, are occupied by histiocytes. Haemalum & Eosin x 40
Fig. 326 Lymph node Burkitt's lymphoma

A: Section. High-power view of part of the lesion shown in F igure 325. The tumour cells resemble
lymphoblasts. Several mitotic figures can be seen. The histiocytes contain intracytoplasmic nuclear debris.
Haema/um & Eosin x 400
B: Touch preparation . The characteristic cytoplasmic vacuolation of the tumour cells is well seen. Two or three
nucleoli can be seen in some of the cells. Giemsa x 1200
Fig. 327 Blood film Burkitt's lymphoma

This ill ustration from the leukaemic form of the disease shows typical Burkitt's lymphoma cells . Leishmmz stai11
X /200
243
244
Fig. 328 Lymph node Immunoblastic sarcoma

The node is diffusely replaced by masses of large cells. Haemalum & Eosin x 50
Fig. 329 Lymph node Immunoblastic sarcoma

The tumour cells have amphophilic cytoplasm which is pyroninophilic. T he large nuclei have prominent nucleoli
and are occasionally seen in mitosis. Haemalum & Eosin x 400, M ethyl-Green-Pyronin x 400
245
Fig. 330 Lymph node Signet r ing cell lymphoma

This diffuse lesion consists of large cells with markedly vacuolated cytoplasm. The resemblance to a poorly
. differentiated mucus-secreting carcinoma is obvious but all stains for proteoglycans are negative. Haemalum &
Eosin x 35, x 450
F ig. 33 1 Liver Malignant histiocytosis

T his material shows distention of the sinusoidal spaces by large cells with fairly clear cytoplasm. The liver cells
contain hemosiderin granules. Erythrophagocytosis is seen in many of the histiocytes. The nuclei of these cells
vary considerably in appearance, some being very large, and occasional cells are binucleated. Haemalum & Eosin
X /00, X 400
246
F ig. 332 Lymph node Hodgkin's disease, lymphocytic predominant

The normal architecture has been lost, by masses of lymphocytes with small numbers of Hodgkin cells, one of
which contains four nuclei. Also present are eosinophils and lymphocytes. Haemalum & Eosin x 450
Fig. 333 Lymph node Hodgkin's disease, mixed cellularity

Lefc: The normal architecture is lacking, due to diffuse infiltration, but n o fib rosis is present in this early lesion.
Haema/um & Eosin x 40
Right: Even at this low magnification, multinucleate cells arc recognisable. A focus of recent necrosis is seen in
the upper part of the field. Haemalr1111 & Eosin x 120
247
Fig. 334 Ly mph node Hodgkin's disease, mixe d cellular ity

This is a high-power view of Figure 333; the polymorphic nature of the cells is illustrated by the presence of
Hodgkin cells, one of which contains four nuclei . Also present are eosinophils and lymphocytes. Haemalum &
Eosin x 450
Fig. 335 Lymph n ode Hodgkin's disease, mixed cellularity

In this touch preparation a Hodgkin cell with multilobulated nucleus is seen in the centre of the fie ld. There is a
considerable amount of very pale staining cytoplasm. May-Griinwald-Giemsa stain x 1200
248
Fig. 336 Bon e biop sy Hodgkin's disease

A: At low-power magnification it is obvious that the haemopoietic tissue has been replaced by tumour in which
several different types of cell are present. Ha emalum & Eosin x 120
B: In this high-power field Hodgkin cells predominate. Haemalum & Eosin x 400
C: Three reticulum cells are surrounded by numerous eosinophils. Haemalum & Eosin x 400
249
Fig. 337 Lymph node Hodgkin's disease, nodular sclerosin g

Well-defined bands of collagenous tissue separate nodules of the lesion. Both the capsule and the interior of the
node are affected. The high power view shows the mixed cellular makeup of the lesion, lymphocytes, eosinophils
and large (Hodgkin) cells being present. Many of the latter are of the lacunar variety with very little cytoplasm
visible; in this particular example, multinucleated Hodgkin cells were very uncommon. Haema/um & Eosin x 25,
X 400
Fig. 338 Ly mph node Ho d gkin's disease, nodular sclerosin g

This is a touch preparation from the node illustrated in Figure 337. A very large, multinucleated Hodgkin cell is
seen in the centre surrounded by a variety of mononuclear cells. Distorted mature lymphocytes are recognizable
by their deeply staining relatively structureless nuclei. Note the very large amount of very pale staining cytoplasm
in the H odgkin cell. When compared with Figure 339, the very close relationship between the giant cells in the
two varieties of the disease is obvious. May-Grii11wa/d-Giemsa stain x 1200
250
Fig. 339 Lymph node Hodgkin's disease, lymphocytic depleted

As in Hodgkin's disease, lymphocytic predominant (Fig. 332) the normal architecture has been lost. Hodgkin
cells are much m ore numerous than in Figure 334, but lymphocytes and eosinophils are still seen . Haemo/um &
Eosin x 120, x 450
TUMOURS Of' LYMPHOID TISSUE & OTHER NEOPLASMS
25 1
Fig. 340 Lymph node Malignant Lymphoma, undifferentiated

This field is representative of the microscopic appearance of the entire node. The normal tissue is completely
replaced by a mass of undifferentiated lymphoid cells, with numerous mitotic figures (arrows). Haemalum & Eosin
X 450
Fig. 341 Lymph node M a lignant lymphoma, undiffe rentia ted

This shows a great excess of reticular fibre s, many of which surround single or small groups of cells. Gordon &
Sweet, counterstained Neutral Red x I 20
252
Fig. 342 Marrow films Metastatic tumour cells

L eft: This shows large foam y cells which are probably mucus-secreting carcinoma cells from the stomach. They
exhibit the clumped arrangement often seen in metastatic tumours invading the marrow. Leishman stain X 900
Right: These discrete. metastatic cells arc derived from a bronchial carcinoma. Note the multiple and giant
nucleoli also the pale staining marrow. Leishman stain x 900
In both cases the haematologists' findings were confirmed at autopsy.
253
Fig. 343 Marrow film and section Metastatic carcinoma

Left: The upper field consists entirely of tumour cells of unknown origin. At higher magnification (lower field) the
cells have similar morphological appearances to those seen in Figure 346. May-Grunwald-Giemsa stain x 200, x
800
Right: Section, the upper fie ld illustrates the well marked infiltration of the marrow with tumour, cells. These are
shown in great detail in the lower right field. Haemalum & Eosin x 200, x 600
252
/>
H AEM ATOLOGY
-, ~
Fig. 344 Marrow film M etas t a t ic cells from a ca se o f a d e nocarcinoma of prost ate
Left: A group of large cells with hyperchromatic nuclei and scanty cytoplasm is present in this fie ld.
Right: High-power magnification reveals the high nucleo-cytoplasmic ratio of these malignant cells. The large
nuclei show an obvious chromatin pattern and several contain pale blue nucleoli. A trephine specimen (Fig. 345)
from this case shows the adenocarcinomatous nature of the tumour. May -Griinwald-Giemsa stain x 200, x 800
255
Fig. 345 Iliac crest marrow Trephine specim en Secondary carcinoma

A: This shows the extent of the specimen obtained by this technique. The excessive number of small trabeculae
towards the centre of the specimen represent newly-formed bone. Haemalum & Eosi11 x 6
B: Most of the tumour in this field shows an adenocarcinomatous pattern. Osteoblastic activity can be seen along
the margins of trabeculae of bone (bottom right). Haema/um & Eosi11 x 80
C: In this field the tumour is less well differentiated. Such a portion as this is illustrated in Figure 344.
Subsequent investigation disclosed that the pri mary tumour was in the prostate. Haemalw11 & Eosi11 x 400
256
Fig. 346 Marrow film Metastatic cells from a case of bronchial ca rcinoma
Left: It is obvious that the cells of this large group are not of haemopoietic origin, although in some respects they
resemble primitive cells of either the lymphocyte or monocyte series. May -Griinwa/d-Giemsa stain x 200
Right: At high-power magnification it becomes more obvious that these invading undifferentiated cells resemble
lymphoblasts. A few of the cells at the periphery of the group show a narrow, uneven rim of cytoplasm. May Gnlnwa/d-Giemsa Stain x 800
Autopsy examination confirmed that the primary tumour was an anaplastic bronchial carcinoma of the small cell
type.
Fig. 347 M arrow aspirate section Secondary carcinoma

This material, taken from the same patient as that in Figure 346, illustrates the appearances, in a section, of a
small cell anaplastic bronchial carcinoma. Haema/um & Eosin x 200, x 800
T U MOU RS OF LYMPHOID T ISSUE & OTH ER NEOPLASMS
257
F ig. 348 Iliac crest marrow Trephine specimen Metastatic anaplastic carcinoma of unknown
origin
The undiffer entiated nature of the tumour is apparent (left). Groups of tumour cells are seen to be surrounded by
a reticulum framework (right). H aemf! lum & Eosin x 350, Gordon & Sweet, coumerstained Neutral R ed x 350
Fig. 349 Iliac crest marrow T r ephine needle biopsy Metastatic tumou r cells
This illustrates the ill-defi ned metastatic tumour cells in contrast to small lymphocytes and an eosinophil. Wright's
stain x 1000
10. Non-haemopoietic cells, artefacts and

other abnormalities
II
Artefacts may be encountered in any blood film or marrow smear and unless these are
recognised they may lead to hazards in diagnosis. T hey can be due to improper manipulation
during the spreading of the preparation and/or faulty fixation.
The large primitive cells, eosinophils, basophils and mast cells are those most likely to exhibit
artefactual changes in smears of marrow becau se of their size or fragile nature .
260
Fig. 350 Osteoblasts in marrow film

This illustration shows several osteoblasts surrounded by haemopoietic cells. This is due to the dislodgement of the
osteoblasts during the puncturing of the bone by the needle in the collection of the marrow specimen. The basophilic
cytoplasm appears to be granular due to the many ribosomes which take the stain and to the mitochondria which remain
unstained. Note the eccentric position of the nuclei. Leishman stai11 x 1200
1
I
NON-HAEMOPOIETIC CELLS, ARTEFACTS & OTHER ABNORMALITIES
261
tain
Fig. 351 Blood fi lm

This preparation shows a group of epithelial cells surrounded by a ring of pink staining material which has been formed
by lysed red cells. The epithelial cells have prominent nuclei and their cytoplasm appears to be wrinkled and folded.
Note the bacteria lying over and adjacent to these cells, which in all probability are from the mouth, having been
introduced to the slide during the making of the blood film. May-Griinwald-Giemsa stain x 600
262
ATLAS OF HAEMATOL OGY
Fig. 352 Blood film

Left: Crenated red blood corpuscles. These forms are artefacts produced by allowing the blood film to dry
slowly. Fluid passes from the red cells into the surrounding plasma which becomes increasingly hypertonic as
drying proceeds, thus allowing the red cells to shrink irregularly. L eishman stain x I 200
Right: Distorted red blood corpuscles. This artefact is due to faulty spreading of the film. L eishman stain x
1200
ON-HAEMOPO IETIC CELLS, ARTEFACTS & OTHER ABNORMALITIES
263
Fig. 353 Necrobiosis, vacuolation and nuclear hypersegmentation of the granular series
A shows a myeloblast with irregular staining of both cytoplasm and nucleus which contains a giant nucleolus. B is
a necrotic myeloblast, but in this instance it is not possible to differentiate between the nucleus and cytoplasm
although the granules can still be resolved. C is a promyelocyte which exhibits a peculiar clumping of the nuclear
chromatin, also dissolution of the cytoplasmic granules. D and E are examples of leucocytes with mitotic nuclei
which are undergoing necrotic change. F shows a peculiar lumpiness of the nuclear segments which appear to be
auached by fine bridges: compare this with J, where the nuclear segments are completely separated. G shows
hypersegmentation; two separated nuclei can be seen and the cell is much larger than usual. H to L (necrobiosis):
all show irregular staining, clumping of the nuclear chromatin and vacuolation of the cytoplasm. M ay- GnluwaldGiemsa sriau x I 200
264
Fig. 354 Marrow film My eloid leukaemia

Many of the p rimitive cells of the myeloid series, in this illustration, reveal evidence of heavy azurophilic
granulation similar to that described in Alder 's con stitutional granulation anomaly. It will be noted that there is a
'haziness' in all these fields, as if the illustrations were slightly out of focus, and also that the cells have stained
lighter than usual; this phenomenon is due to the specimen h aving been retained for some time prior to fixation
and staining. The cells are, therefore, in the process of degeneration . M ay - Gru11wald -G iemsa stai11 x 1200
NON-HAEMOPOIETI C CELLS, ARTEFACTS & OTHER ABNORMALITIES
265
Fig. 355 Blood film Morphological chang es in leucocytes in hyposplenism

These cells of the myeloid, lymphocyte and monocyte series were all encountered in a blood film from a patient
with thrombocythaemia and hyposplenism. A is a promyelocyte, the nucleus of which contains a definite
nucleolus. The cytoplasm is stippled with coarse azurophil granules. B and C are both myelocytes, the cytoplasm
of C being much more granu lar than that of B. D to H are all monocytes, the nuclei of which show marked
lobulation . The cytoplasm of several of these cells shows fine or coarse vacuolation. I to L are all immature
lymphocytes which show multilobulation of their nuclei and the example at I shows three peculiar pr ojections at
the left margin of its nucleus. May-Grunwa ld-Giemsa stain x 1200
OF HAEMAT OLOGY
Fig. 356 Artefacts

A. Fixation artefact in marrow smear: there is a loss of definition and also disruption of cytoplasm. These changes
are most often encountered when the smear has been subjected to heat prior to, or during, fi xation . B and C.
' Basket cells' are commonly seen in smears o r films, especially where there is a high mononuclear count. I n B, the
nucleus remains intact whereas in C, both the cytoplasm and the nucleus have been damaged in spreading the
film. D . In this primitive cell the cytoplasm has been fragmented and at first glance the fragments simulate
Leishmania donO'Uarzi. E and F . 'Smear cells': this artefact is most likely to be encountered where there is a high
mononuclear count and is caused by a still greater pulling out of the cytoplasm as already seen in B. G . Denuded
nuclei: in this illustration the cells are large lymphocytes. This artefa ct is frequently seen in blood films in
lymphocytic leukaemia. May-Grrlrzwald-Giemsa stain x 1200
NON-HAEMOPO !ET!C CELL S, ARTEFACTS & OTHER ABNORMALITIES
267
Fig. 357 Artefacts

A. Agglutination, rouleaux formation and air bubbles due to faulty spreading of blood film. The bubbles of air lie
under the erythrocytes and give the appearance of crystals; there is a complete loss of cell borders except in one or
two instances. B . In this illustration strands of cytoplasm of disrupted white cell entangle several e rythrocytes. C.
There is a total loss of definition in both red and white cells in this preparation, probably due to excessive heat
prior to fixation. D . Crushing of cells: this appearance is most likely to be encountered at the margins of the
preparations and such areas should be avoided when screening films. E, F, G and H. Elongation and disruption of
the cytoplasm of primitive cells due to undue pressure being employed in spreading smears. I. This primitive
granular cell, most likely a promyelocyte, has been distorted during spreading. The cytoplasm has been
compressed around the nucleus and pulled out at the lower margin giving it a vacuolated appearance. J, K and L.
These are examples of disrupted eosinophils at various stages of maturation. M. This is a distorted basophil
leucocyte which has been crushed and spread out, thus releasing the basophil granules and now resembling a mast
cell. May -Gninwald-Giemsa scai11 x 1200
268
...
Fig. 358 Blood film Stain deposit as artefact
The appearance of stain deposit can simulate Howell-Jolly bodies and other red cell inclusions. Careful
manipulation of the fine focusing mechanism will confirm tliat the deposit is on a different focal plane from the
cells. M ay-Griinwald-Giemsa stain x I 200
NON-HAEMOPOIETIC CELLS, ARTEFACTS & OTHER ABNORMALITIES
269
Fig. 359 Blood film Fibres as artef act

Fibres are most often introduced by inefficient cleansing of the glass slide or cover glass. May-Gnlnwald-Giemsa
stain x 800
Index
Acanthochielonema dipetalonema, 223

Acanthocytes, 18, 36
Acholuric j~undice, 39
Acute leukaemias see Leukaemia , acute
Agglutination, 46, 47, 78 , 163, 267
Alder-Reilly anomaly, 120, 264
Alkaline phosphatase, leucocyte, 80
Amyloid, plasma cell myeloma, 162
Anaemia
aplastic, 10, 62, 179
haemolytic, 29, 33, 35, 68, 69
acquired, 29, 35, 68
hypochromic microcytic, 33
iron deficiency, 22, 23, 33
leucoerythroblastic, 168, 169
macrocytic, 25, 26, 30, 32, 33
pregnancy, 34
megaloblastic, 9, 18, 23, 39, 41, 48, 55-57
microangiopathic, 38
pernicious, 25, 26, 27, 30, 71
sickle cell, 19, 35, 70
sideroblastic, 64
Anaphase stage, mitosis, 50- 53, 143
Anaphylaxis, 10
Anaplastic carcinoma, 257
Anisocytosis, 18, 25, 26, 27, 30, 32, 34, 44, 45, 168
Anisopoikilocytosis, 90
Anomalies
Alder-Reilly, 120, 264
Chediak-Steinbrinck-Higashi, 79
Pelger-Huet, 80, 81
red cell, 18, 19, 25 et seq., 48, 266-289
Anulocytes (ring staining), 18, 32
Aplastic anaemia, 10, 62, 179
Archoplasm, 202 , 207
Artefacts, 18, 19, 48, 266-269
Auer bodies, 94, 105, 164
Autoagglutination, 46, 47, 78
Azurophil granules, 7, 9, 11, 12, 74 et seq.
Basket cells, 266

Basophilia 8, 108
Basophilic megakaryocytes, 12, 179, 180
Basophilic reticulum (reticulocytes), 8, 39
Basophilic stippling, 18, 23, 27, 44, 48
Basophils
count, IS
granules, 9, 10, 45, 79, 108, 116, 267
leucocyte, 10, 108

development , 10, 108
phase contrast, 202
metamyelocyte, 108
myelocyte, 15, 108
polymorphonuclear series, 10, 108
promyelocyte, 108
tissue, 10, 116
Benign quartan malaria, 214
Benign tertian malaria, 213, 218
Blast cells, 84
see also various types

Blood
acanthocytosis, 18, 36
acute lymphoblastic leukaemia, 125, 126, 127
phase contrast, 207, 208
acute myeloid leukaemia , 92-96
acute myelomonocytic leukaemia , 88
acute undifferentiated leukaemia , 84
anisocytosis, 18, 25-27, 30, 32, 34, 44, 45, 168
autoagglutination, 46, 47, 78
cell development, 7, 20, 74 et seq.
chronic lymphocytic leukaemia , 131, 132
large granular, 132
chronic monocytic leukaemia, 147
chronic myeloid leukaemia, 98, 101, 103, 104
terminating in acute phase, 98
cytomegalovirus infection, neonatal, 120
E-rosetting, 127
elliptocytosis, 18, 28
eosinophilia, I 07
phase contrast, 202
fibrin formation, phase contrast, 210
filariasis, 223
follicular lymphoma, 234
giant platelets, 184, 185
haemorrhagic thrombocythaemia , 183
phase contrast, 199, 200, 210
hereditary spherocytosis, 28, 39
hypochromia, 18, 27 , 30-33, 40, 45
infectious mononucleosis, 118, 119
leucocytosis, 78, 79, 186
phase contrast, 201
leucoerythroblastic reaction, 168
leukaemic reticuloendotheliosis, 137, 138, 139
lymphoma, malignant lymphoblastic, 240, 241
lymphosarcoma cells, 234
macrocytosis, 25, 26, 30, 31, 33, 34,90
malaria, 212-219
271
272
INDEX
Blood (contd)
monocytes, 144-154
phase contrast, 209
monocytic leukaentia, 146
myelodysplastic syndrome, 90
myeloid leukaemoid reaction, 83
normal, 7, 10, 11, 12, 14, 15 , 24, 77
parasites, 212-223
pernicious anaentia, 25-27, 30
plasma cellleukaentia, 163
plasma cell myeloma, 156
platelet satellism, 182, 186
poikilocytosis, 18, 25-27, 30, 31 , 34, 43, 44, 45, 168
polychromasia, 26, 27, 30, 34-38, 48
polymorphonuclear leucocytosis, 78, 79, 186, 201
prolymphocytic leukaentia, 129, 130
schistocytosis, 30
spherocytosis, 28 , 29, 39
stomatocytes, 19, 34
subac ute lymphocytic leukaentia, 128
systentic lupus erythematosus, 81
target cells, 19, 31, 32, 43,44
thalassaemia, 30, 43, 44
thrombocythaentia, 184, 186
trypanosontiasis, 222
viral pneumonia, lymphocytes, 119
Brilliant cresyl blue stain, 8, 39
Budding megakaryocyte, 12
Burkitt's lymphoma, 242, 243
Burkitt-type lymphoblastic leukaentia, 122, 123
Burr cells (echinocytes), 18, 36, 37, 42
Cabot rings 18, 48

Carcinoma
anaplastic, 257
secondary, bone marrow, 252-257
Cell motility, 9, 193, 195-210
Central pallor, 8, 9, 24, 31 , 32
Centrosome, 193, 195, 206
Charcot Leyden crystals, 110
Chediak-Steinbrinck-Higashi anomaly, 79
Chromatin, 7, 74, 80, 81, 193
female sex, 14, 71
Chromosomes, 193
Chronic leukaentia see Leukaemia, chronic
Congo red staining, 162
Crenated red cells, 18, 262
Crystals, Charcot Leyden, 110
Cytomegalovirus infection, neonatal, 120
Cytoplasntic granules, 7, 9, 10, 23, 64, 74 et seq., 132
phase contrast, 193, 195-204
Daughter cells, 53
DiGuglielmo's disease, 59, 60, 66, 89
Differential counts
leucocyte 16
marrow, 16
Dimorphism, 33
Dissolution of nucleus, 8
Distorted red blood cells, 262, 267

Drumstick chromatin, 10, 77
Dyserythropoiesis, congenital, 67
Dyshaemopoietic states, 18
see also individual disorders

Dysproteinaemia, ISS
E-rosetting, T-cell leukaemia, 127

Early cells
megaloblasts, 8-9, 50-51, 54-58
normoblasts, 7, 16, 20-22
Echinocytes (burr cells) 18, 36, 37, 42
Electron microscopy
blast cell, 99
leukaemic reticuloendotheliosis, 139
lymphocyte, 133
megakaryocyte, budding, 191
megaloblast, early, 54
monocyte, 148
neutrophil polymorph, 82
plasma cell, 167
platelets, 192
sideroblast, 65
Elliptocytosis, 18, 28
Eosinophilia, 107
phase contrast, 202
Eosinophils
count, IS
granules, 9, 10, 79, 102, 107, 118
phase contrast, 196- 198, 202
leukocyte, 10, 102, 107
phase contrast, 196-198, 202
myelocyte, 10, 15, 75, 102
polymorphonuclear series, 10
promyelocyte, 22
Epithelial cells, as artefact, 261
Erythroblasts, 8, 18, 59, 60, 106
Erythrocytes, 8, 24
abnormal, 8, 18, 23, 25-48
agglutinated, 78
see also Red cells
Erythroleukaentia, 59, 60, 66
Erythrophagocytosis, 59, 106
Erythropoiesis, 7-9, 20
megaloblastic, 8-9,51 , 57,58
normoblastic, 7-8, 20
Estivo-autumnal malaria, 215, 218, 2 19
Extrusion, nucleus, 8, S I
Ferruginous micelles, 64, 65

Fibres, as artefact, 269
Fibrin formation, phase contrast, 210
Filariasis, 223
Flanting plasma cells, ISS
Foam cells, Niemann-Pick disease, 153, !54
Follicular lymphoma, 231 , 234, 238
blast cell phase, 240, 241
malignant, 238
Fragmentation , nucleus, 8, 48
INDEX
Gasser's cells, 120

Gastric mucosa
normal, 71
pernicious anaemia, 71
Gaucher cell, !53, !54
Gaucher disease, !53, !54
Germinal centres, lymphoid follicle , 189, 228
Giant cells
metamyelocytes, 76
platelets, 98, 184, 185
Giant granulation, leucocytes, 79
Glandular fever, 118, 119, 134
Golgi complex, 65
Granular leucocytes, 9, 74 ecseq.
Granularmegakaryocytes, 12, 179-181
Granulation. toxic, 79
Granules
azurophil, 7, 9, 11 , 12, 74 ec seq.
basophil, 9, 10, 45, 79, 108, 116, 267
cytoplasmic, 9, 10, 23, 64, 74 ec seq., 132
eosinophil, 9, 10, 79, !02, 107, 118, 196- 198 ,202
iron-containing, 19, 40, 64, 65, 68, 69
metachromatic, 116
neutrophil, 9, 74 ecseq., 195, 196, 199-201
Perls, 64
Granulocytic series, 9, 74 ec seq.
273
follicular, 229
macronormoblastic, 22
micronormoblastic, 22
normoblastic, 21
H ypersegmentation
neutrophil leucocyte, 49, 66
nucleus, 181, 263
H ypochromia, 18, 27, 30-33,40,45
Hypochromic microcytic anaemia, 33
Hypoplasia, marrow, 62
H yposplenism, 265
thrombocythaemia, 186
Idiopathic thrombocythaemia, 181

Idiopathic thrombocytopenia, 187, 188, 189
Immunoblastic sarcoma, 244
Immunoglobulin, 158
Intermediate cells
megaloblast, 8, 26, S0-52, 56-58
normoblast, 7-8, 16, 20- 22
Iron deficiency 22, 23, 33
Juvenile neutrophil leucocytes, 10, 21, 74 ec seq.
Haemachromatosis, 69
Haematological values, normal, 14-15
Haemocytoblasts, 7, IS
Haemoglobin, 14, 24, 40
45
H,45
Haemoglobinisation, 8
Haemohistioblasts, 7, 11, 15, 22
Haemolytic anaemia, 29, 33, 35, 68, 69
acquired, 29, 35, 68
thermal, 29
Haemolytic disease, newborn, 37
Haemolytic uraemic syndrome, 37
Haemorrhagic thrombocythaemia, 183, 199, 200, 210
Haemosiderin, 23, 64, 68-70
Hairy cell leukaemia, 137-140
Halo, perinuclear, 7, 12, 155
Heart , myeloid leukaemia, 111
Heinz bodies, 18, 40
Hepatocytes, 69
Hereditary spherocytosis, 28, 39
Histioblasts, 7, 10, 11, 105
Ilistiocytosis
malignant, 245
sea blue, !52
1/iscop/asma capsu/acum , 222
Hodgkin's disease, 246-250
lymphocytic depleted, 250
lymphocytic predominant, 246
mixed cellularity, 246, 247
nod ular sclerosing, 249
Howell-Jolly bodies, 9, 18, 23, 25, 27, 39, 41, 48, 51,
52, 218, 268
H yperplasia
erythroid, 22, 90
Kupffer cells, 69, 70, 220
c,
Large lymphocytes, 11, 117, 118, 132

Late cells
megaloblasts, 8, 50, 51, 52, SS -57
normoblasts, 8, 16, 20, 22, 28
L E cells, 81
Lead poisoning, basophilic stippling, 23 , 44, 48
Leishmania donovani, 221
Leishmaniasis, 221
Leptocytes, 18
Leucocytes
alkaline phosphatase, 80
basophil, 10, 16, 108
count, 14-15
eosinophil, 10, 102, 107, 196-198,202
granular , 9, 74 ec seq.
morphological changes, 265
neutrophil, 9, 10, 47, 49, 74 ec seq., 195, 196, 199201
Leucocytosis, 78, 79, 186
phase contrast, 20 I
with toxic granulation, 79
Leucoerythroblastic anaemia, 168, 169
Leucoerythroblastic reaction, 168
Leucopoiesis, 9
Leukaemia
hairy cell, 137-140
mast cell, 116
megakaryoblastic, 85, !90
monocytic, 145-152
.~ I
.I
274
i
I
II
INDEX
'I
Ii
i
I
I
I
Leukaemia (coned )
myeloid, 85- 106, 203, 204, 264
myelomonocytic, 88, 105, 106
plasma cell, 163
prolymphocytic, 129, 130
promyelocytic, 97
Rieder cells, 95, 145
Leukaemia, acute
classification, 85
lymphoblastic, 85, 122- 127, 136
classification, 85 , 122
phase contrast 207, 208
monoblastic, 89
monocytic, 147
myeloid , 85, 87-89, 9 1-97, 98, Ill, 113, 114
phase contrast;203, 204
myelomonocytic, 88, 105, 106
undifferentiated, 84
L eukaemia, chronic
granulocytic, II 5
lymphocytic, 130-135, 266
myeloid , 100, 101, 103, 108-1 10, 113
blast cell transformed, 98
transforming (accelerated), 104
Leukaemic reticulendotheliosis, 137- 140
Leukaemoid reaction, 83
Liver
acute lymphoblastic leukaemia, 136
chronic myeloid leukaemia , 11 3
haemochromatosis, 69
haemolytic anaemia, 69
leukaemic reticuloendotheliosis, 140
malaria, 2 19, 220
malignant histiocytosis, 245
monocytic leukaemia, ISO
myelofibrosis, 172, 173
normal, 112
sickle cell anaemia , 70
transfusion siderosis, 70
Lung, monocytic leukaemia, l SI
Lupus erythematosus, systemic, 81
Lymph nodes
Burkitt's lymphoma, 242
chronic granulocytic leukaemia, II 5
follicular hyperplasia, 229
follicular lymphoma, 231
glandular fever, 134
histoplasmosis, 222
Hodgkin's disease, 246, 247, 249, 250
lymphocyte depleted, 250
lymphocyte predominant , 246
mixed cellularity, 246, 247
nodular sclerosing, 249
immunoblastic sarcoma, 244
lymphocytic leukaemia, 170
lymphoplastoid lymphoma, 234
malignant lymphoma , 231,232,235,238,239,240,
251
myeloid metaplasia, 112
normal, 228
signet ring cell lymphoma , 245
toxoplasmosis, 230
Lymphoblastic leukaemia , acute, 122-7, 136, 207, 208
classification, 85, 122
Lymphoblasts, II , 59,1 17,1 18, 122-129

Lymphocytes, 7, I I , IS, 20, 21 , 117 et seq.
count, IS
development, 117, 118
large, I I, 11 7, 118, 132
maturation, 117, 118
small , I I, 117, 118
T-cell , 127, 136
viral pneumonia, 119
Lymphocytic leukaemia
chronic, 130, 131 , 132
large granular, 132
lymph node, 135
marrow, 130, 131, 134, 135
spleen, 135
. subacute, 127, 128
Lymphocytosis, viral pneumonia, 119
Lymphoid follicles, II, 61, 68, 110, Ill , 189, 228
hyperplasia, 229
see also Follicular lymphoma
Lymphoid tissue, I I
neoplasms, 225-250
L ymphoma
Burkitt 's, 242, 243
follicular, 23 1, 234, 238
lymphocytic, 140
lymphoplastoid , 234
non-Hodgkin, classification, 225-227
signet ring cell , 245
see also Hodgkin's disease; Malignant lymphoma
Macrocytes, 8, 25, 26,30-32,34, 41 ,5 1

Macrocytic anaemia, 25, 26, 30, 32, 33
pregnancy, 34
Macrocytosis, 25, 26, 30, 31, 33, 34, 90
Macroglobulinaemia, Waldenstriim's, 121
Macronormoblastic hyperplasia, 22
Malaria, 212-220
asexual cycle, 2 12-2 15
benign quartan , 2 14
benign tertian, 213, 218
estivo-autumnal, 215, 218, 2 19
malignant tertian, 2 15,2 18,219
pigment, 213 - 220
sexual cycle, 216-21 7
Malignant histiocytosis, liver , 245
Malignant lymphoma, 232
centroblastidcentrocytic, 239
centrocytic, 238, 239
diffuse, 23 1, 232
follicular , 238
lymphoblastic, 240-24 1
lymphocytic, 140, 232 , 233
T-zone , 235
undifferentiated, 25 I
Malignant tertian malaria, 215, 218, 2 19
Marrow
acute lymphoblastic leukaemia, 122- 124
I!
,~,w~~~-=----~------------------------------~~
INDEX
acute monocytic leukaemia, 147

acute myeloid leukaemia , 86, 87, 9 1, 96- 98
in remission, 98
aplastic anaemia, 62
basophils, I08
chronic lymphocytic leukaemia, 130, 131, 134, 135
chronic myeloid leukaemia, 100, 108-110
counts, differential, IS
DiGuglielmo's disease, 58, 59
dysproteinaemia, ISS
eosinophilic, 107
erythroleukaemia, 58, 59
erythrophagocytosis, 59
Gaucher's disease, 153
Hodgkin'~ disease, 248
hyperplasia, 21 , 22,62
idiopathic thrombocythaemia, 18 1
idiopathic thrombocytopenic purpura, 187, 188
iron defi ciency anaemia, 22
leishmaniasis, 221
lymphocytic leukaemia, 134, 135
macronormoblastic hyperplasia, 22
malignant lymphoma, lymphocytic , 233
mast cell leukaemia, 11 6
megakaryoblastic leukaemia, 190
megakaryoblasts, 177, 178, 187, 190
megakaryocytes, 179-183, 187- 190
hyperplasia, 189
megaloblastic anaemia, 55, 57
metastatic tumour cells, 252-257
micronormoblastic hyperplasia, 22
monocytes, 141-143, 145, 147, 149
monocytic leukaemia, 147, 149
myelofibrosis, 170, 171
myeloid leukaemia, 102, 109, 264
myelomonocytic leukaemia, 88, lOS, 106
myelosclerosis, 169
neutrophil leucocyte series, 74-76
Niemann-Pick disease, 153
normal, 61, 62
normoblastic erythropoiesis, 20
normoblastic hyperplasia, 21
osteoblasts, 260
plasma cell myeloma, 156-162
polycythaemia rubra vera, 63
post-cytoxic therapy, 166
promyelocytic leukaemia, 97
sea blue histiocytosis, 152
secondary tumours, 252-257
sideroblastic anaemia, 64
thrombocythaemia, 182, 183
Mast cell, 7, 10,116
leukaemia, 116
Maturation
lymphocyte, 117, 118
monocyte, 117, 118etseq., 14 1
neutrophil polymorponuclear leucocyte, 9, 74
plasma cell, 11, 117, 15 5
Mature neutrophil leucocytes, 9, 10, 74 et seq.
Maurer's dots, 215
Mean corpuscular haemoglobin concentration, 14
Mean corpuscular volume, 14
Megakaryoblastic leukaemia, 85, 190
Megakaryoblasts, 8, 12 , 176, 178, 187
275
Megakaryocytes, 12 , 15, 61, 170, 172, 173, 179-183,

187- 19 1
atypical , 170, 179, 181 - 183, 185
basophilic, 12 , 179, 180
budding, 12, 191
count, 15
frag ments, 185
granular, 12 , 179-181
nuclear hypersegmentation, 181
series, 12
Megakaryocytic hyperplasia , 182, 189
Megaloblastic anaemia, 9, 18, 23, 39, 41 , 48, 55-57
Megaloblastic erythropoiesis, 8- 9, 51
Megaloblasts
early,8,9,50,51,54-58
intermediate, 8, 26, S0-52, 56- 58
late, 8, 50, 51, 52, 55-57
series , 8, 50- 57
Membrane, nuclear, 50, 53, 203
Metachromatic granules, 10, 116
Metachromatic staining, 10, 116
Metamyelocytes, 9-10, 15 , 22, 74, 76, 93, 101, 203,
204
basophil, 108
early form , 15
giant, 76
neutrophil , 10, 74
Metaphase, mitosis, 20, 53
Metastatic tumour cells, marrow, 252-257
Methyl violet, 18, 40
Microangiopathic haemolytic anaemia, 38
Microcytes, 18, 35
Microcytic anaemia, hypochromic, 33
Microcytosis, 44
Microfilaria, 223
Microlymphoblasts, 122
Micronormoblastic hyperplasia, 22
Microspherocytes, 18, 39
Mitochondria, 62, 193, 203, 204, 207
Mitosis, 9, 48 et seq.
anaphase, 50-53, 143
daughter cells, 53
metaphase, 20, 53
in monocytes, 142- 144
prophase, 48, 53 , 142, 143, 144
telophase, 53
Monoblasts, 11, 59, lOS, 106, 117 et seq.
Monocytes, 7, 11, 15, 117, 118 ec seq., 148
abnormal, 141 - 147
count, 15
development, 117, 118 et seq., 141
maturation, 117, 11 8 et seq., 141
mitosis, 141- 144
phase contrast, 209
Monocytic leukaemia, 144, 145-147, 149- 152
Mononucleosis, infectious, 118, 119, 134
Morphological changes, leucocytes, 265
Motility, cell , 9, 193, 195-2 10
Mott cell, 165
Mucopolysaccharidosis, 120
Mycosis fu ngoides, 107 , 202 , 236, 237
Myeloblasts, 7, 9, 59, 74 et seq.
count, 15
Myelocytes, 9- 10, 15,74 et seq.
--
276
INDEX
Myelocytes (comd )
basophil, 10, IS, 108
count, 15
eosinophil , 10, 15, 75, 102
count, 15
neutrophil , 9, 10, 15, 74 et seq.
count, 15
Myelodysplastic syndrome, 90
Myelofibrosis, 170, 173
Myeloid-erythroid ratio, 15, 21
Myeloid leukaemia, 85, 86, 98, 100-106, 108-111, 113,
114
acute, 85, 86, 87, 91 .:97, 98, 111, 113, 11 4
chronic, 98, 100, 101, 103, 104, 108- 110, 113
Myeloid Jeukaemoid reaction , 83
Myeloid metaplasia, lymph node, 112
Myeloma
multiple, 41
plasma cell, 12, 156-162, 164
Myelomonocytic leukaemia, 88, 105, 106
Myelosclerosis, 169
Necrobiosis
granular series, 263
red cell, 48
Neutrophils
count, 15
granules, 9, 74 et seq.
leucocyte, 9, 10, 47, 74 et seq.
hypersegmented, 49
non-segmented, 9, 10, 21 , 74 et seq.
phase contrast, 195, 196, 199-201
series, 9, 10, 74 et seq.
myelocyte, 9, 10, 15, 74 et seq.
polymorph, 15, 74 el seq., 82
maturation, 9, 74
phase contrast, 195, 196, 199-201
segmented, 9, 10, 49, 74 et seq.
Niemann-Pick disease, 153
Non-segmented neutrophilleucocytes, 9, 10, 21 , 74 et
seq.
Normoblastic erythropoiesis, 7-8, 20
Normoblastic hyperplasia, 21
Normoblastosis, 120
Normoblasts, 7, 20-22, 173
count, 15
early, 7, 15, 20-22
intermediate, 7, 8, 15, 20-22, 25
late, 8, 15, 22, 25, 26, 28, 48, 59, 60, 6 1
Nucleoli, 7, 9, 50, 51, 74 et seq.
giant, 240, 241, 252
phase contrast, 203, 204, 207, 208
Nucleus
chromatin, 193
envelope, SO, 53, 203
extrusion, 51
hypersegmentation, 181, 263
membrane, 50, 53, 203
remnants, 18, 48
see also Howell-Jolly bodies
Osteoblasts, 260
Packed cell volume, 14

Pallor, central, 8, 19, 24, 31, 32
Paneth cells, 71
Pappenheimer bodies, 19,40
Paramyeloblasts, 92
Parapromyelocytes, 92
Parasites
filarial, 223
histoplasma, 222
ieishmania, 221
plasmodia, 2 12-220
trypanosoma, 222
Pelger-Huet's anomaly, 80, 8 1
Perinuclear halo, 7, 12, ISS
Periodic acid-Schiff, 126, 130, 182
Perls granules, 64
Pernicious anaemia, 25-27, 30, 71
Peroxidase reaction, I 02
Phagocytosis, 9, 59, 199, 200
Phase contrast microscopy, 193, 195-210
Phosphatase, alkaline, 80
Pincered cells, 18, 33
Plasma cells, 7, 11, 12, 15,117,121,155-167
abnormalities, 164, 165
count, IS
development, 11, 117, ISS
flaming, 155
leukaemia, 163
maturation, 11 , 117, 155
myeloma, 9, 156- 162, 164
series, 11, 12, 117, 155-167
Plasmablasts, 11 , 117, 155 -157
Plasmodiumfalciparum, 215, 218
Plasmodium malariae, 2 14
Plasmodium vivax, 213, 218, 2 19
Platelets, 12, 15, 98, 181-187, 192, 199,200,206,2 10
aggregates, 187
count, 15
formation , 12
giant, 98, 184, 185
satellitism, 182, 186
Poikilocytosis, 18, 25-27, 30, 31, 34, 43-45, 168
Poisoning, lead, basophilic stippling, 23, 44, 48
Polychromasia, 18, 23 , 26, 27, 30, 34-38, 48
Polycythaemia rubra vera, 63, 80
Polymorphic nuclei, 9, 74 et seq.
Polymorphonuclear leucocytes, 9, 15, 74 et seq.
agglutination, 78
Polymorphonuclear leucocytosis, 78, 79, 186, 201
thrombocythaemia, 186
toxic granulation, 79
Polymorphs, 9, 15, 71
eosinophil, I 5
INDEX
neutrophil, 15, 75, 82

non-segmented, 9, 10, 21, 74 el seq.
segmented, 9, 10, 49, 74 ez seq.
Pregnancy, macrocytic anaemia, 34
Prolymphocytes, 11, 15, 52, 57, 117, 118, 127
Prolymphocytic leukaemia, 129, 130
Promegakaryocytes, 12, 176, 179, 180, 183
Promegaloblasts, 8, 9, 57
Promonocytes, 11, 117, 141-147
Promyelocytes, 9, 15, 22, 74 ez seq., 90, 93
basophil, 108
count, IS
eosinophil, 22
Promyelocytic leukaemia, 97
Pronormoblasts, 7, 15, 20, 21
Prophase stage, mitosis, 48, 53, 143, 144
Proplasma cell, 11 - 12, 117, !55, 158
Pr ussian blue reaction, 19,68-69
Pseudopodia, !95-197, 199,200,206
Purpura, idiopathic thrombocytopenic, 187, 188, 189
Pyknocytes, 18
Red cells
agglutination, 46, 47, 78, 163, 267
anomalies/artefacts, 18, 19, 25 ez seq ., 48, 266-289
distortion , 262, 267
values, 14
see also various r.ypes

Remnants, nuclear, 18, 48
Reticulocytes, 8, 14, 39, 45
Reticuloendothelial system, 7
Reticulum
basophilic (reticulocytes), 8, 14, 39, 45
cells, 248, 249
Ribonucleic acid , 5
Rieder cells, 95, 145, 164
Ring staining, 18, 32
Ringed sideroblasts, 64, 65
Romanowsky methods, 8
Rouleaux formation, 41, 163, 210, 251, 267
Russell bodies, 71
Sarcoma, immunoblastic, 245

Satellitism, platelet, 182, 186
Schistocytes, 18, 19, 27, 30,186
Schistocytosis, 30
Schiiffner's dots, 213, 218
Sea blue histiocytosis, !52
Secondary carcinoma, marrow, 252 - 257
Segmented neutrophilleucocytes, 9, 10, 49, 74 el seq.
Sex chromatin, female, 14, 77
Sickle cell anaemia, 19, 35, 70
Sickle cells, 19, 35, 70
Sideroblastic anaemia, 64
Sideroblasts, 64, 65
Siderocytes, 19, 40
Siderosis, transfusion, 70
277
Skin
leishmaniasis, 221
malignant lymphocytic lymphoma, 232
monocytic leukaemia, !52
mycosis fungoides, 236, 237
myeloid leukaemia, 114
Small lymphocytes, 11, 117, 118
Smear cells, 266
Snapper-Schneid inclusion bodies, 165
Spherocytosis, 19, 29
hereditary, 28, 39
Spleen
acquired haemolytic anaemia, 68
acute myeloid leukaemia, Ill
erythroleukaemia, 66
Gaucher's disease, 154
idiopathic thrombocytopenic purpura, 189
leukaemic reticuloendotheliosis, 138, 140
lymphocytic leukaemia, 135
malaria, 260
myelofibrosis, 172
myeloid leukaemia, I l l
normal, 61, 110
polycythaemia rubra vera, 63
Splenectomy, 18, 39, 41, 218
Stab (non-segmented) granular leucocytes, 10, 15, 21,
74 ec seq.
Stain deposit, as artefact, 268
Stem cells, 7, II, IS, 22
Stippling, basophilic, 18, 23, 27, 44,48
Stomatocytes, 19, 34
Subacute lymphocytic leukaemia, 127, 128
Sudan black stain, 103
Supravital staining, 8, 18
Systemic lupus erythematosus, 81
T-cells, 237
lymphoblastic leukaemia, 136
E-rosetting, 127
Target cells, 19, 31, 32, 43, 44
Telophase stage, mitosis, 53
Testes, T-celllymphoblastic leukaemia, 136
Thalassaemia, 19, 48
major, 43
minor, 30, 44
Thermal haemolytic anaemia, 29
Threadworms, 223
Thrombocythaemia, 182- 184
haemorrhagic, 183, 199, 200, 210
hyposplenism, 186
idiopathic, 181
polymorphonuclear leucocytosis, 186
Thrombocytopenia, 120
Thrombocytopenic purpura, idiopathic, 187, 188, 189
T oluidine blue stain, 10, 116
Toxic granulation, leucocytosis, 79
Toxoplasmosis, 230
T ransfusion siderosis, 70
Trypanosoma rhodesimse, 222
Trypanosomiasis, 222
278
INDEX
Undifferentiated neoplasms
acute leukaemia, 84
malignant lymphoma, 251
Uraemia, haemolytic syndrome, 37
Vacuolation
granular series, 263
plasma cells, 165
Viral pneumonia, lymphocytes, 119
Waldenstrom's macroglobulinaemia, 121

Wuchereria bancrofti, 223
Contents
1. Introduction
2. Development of the blood cells 5

3. N ormal haematological values
4. The red cell series
13
17
5. The white cell series 73

6. The megakaryocyte series 175
7. Phase contrast microscopy 193

8. The blood parasites 211
9. Tumours of lymphoid tissue and other neoplasms 225
10. Non-haemopoietic cells, artefacts and other abnormalities
Index
271
259

Atlas Hematologie Crop

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DEVELOPMENT OF THE BLOOD CELLS

DEVELOPMENT OF T HE BLOOD CELLS

DEVELOPMENT OF THE BLOOD CELLS

THE LYMPHOCYTIC SERIES

THE MONOCYTIC SERIES

THE MEGAKARYOCYTE SERIES AND PLATELET FORMATION

3. Normal haematological values

Term s commonly used to describe anom alies and artefacts

THE RED CELL SERIES

Fig. 1 Marrow film Normoblastic erythropoiesis

THE RED CELL SERIES

Fig. 2 Marrow film Normoblastic hyperplasia

Fig. 3 Marrow film Macronormoblastic hyperplasia

Fig. 4 Marrow film Iron deficiency anaemia

THE RED CELL SERIES

Fig. 5 Marrow film Iron deficiency

Fig. 7 Blood film Normal erythrocytes

THE RED CELL SERIES

Fig. 8 Blood film Abnormal erythrocytes

Fig. 9 Blood film Abnormal erythrocytes

THE RED CELL SERIES

F ig. 10 Blood film Pernicious anaemia (und er treatment)

Fig. 11 Blood film

THE RED CELL SERIES

Fig. 12 Blood film Spherocytosis

THE RED CELL SERIES

Fig. 14 Blood film

Fig. 15 Blood film Target cells

Fig. 16 Blood film

F ig. 17 Blood film Pincer ed cells

Fig. 18 Blood film D imorphism

Fig. 19 Blood film Stomatocytes

Fig. 20 Blood film M acrocytic a naemia of pregnancy

THE RED CELL SERIES

Fig. 21 Blood film Haemolytic anaemia

Fig. 22 Blood film Sickle-cell anaemia

Fig. 23 Blood film Acanthocytosis

Fig. 24 Blood film Polychromasia, nucleated red blood cells

THE RED CELL SERIES

Fig. 25 Blood film Haemolytic disease of the newborn

Giemsa stai11 x 1200

Fig. 26 Blood film H aemolytic uraemic syndrome

Griillwald-Giemsa stai11 x 1200

Fig. 27 Blood film Microangiopathic haemolytic anaemia

THE RED CELL SERI ES

Fig. 28 Blood film Howell-Jolly bodies

Reticulocytes from a case of hereditary spherocytosis (acholuric jaundice)

F ig. 30 Blood film Heinz bodies

F ig. 31 Blood film Siderocytes (Pappenhe imer bodies)

THE RED CELL SERIES

Fig. 32 Blood film H owell-Jolly bodies

Fig. 33 Blood film Ro ulea ux formation

Fig. 34 Blood film Burr cells

THE RED CELL SERIES

Fig. 35 Blood film Thalassaemia ma jor

Fig. 36 Blood film T halassaemia minor

Fig. 37 Blood film Basophilic stippling

THE RED CELL SERI ES

Fig. 38 Blood film Haemoglobin 'H' inclusions

Fig . 39 Blood film Haemoglobin 'C'

Fig. 40 Blood film Autoagglutination