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African Trypanosomiasis African Trypanosomiasis

Sleeping Sickness
-Trypanosoma brucei.
-Transmitted by the Tsetse fly (Glossina species - rural Africa),
African Trypanosomiasis (sleeping sickness)
-Transmitted by the Tsetse fly (Glossina species - rural Africa),
-Serious Public health problem : sub-Saharan Africa.
-About 10,000 new cases each year are reported (WHO).
-Curable - medication, but is fatal if left untreated.
Epidemiology & Risk Factors Epidemiology & Risk Factors
Two subspecies
T. b. rhodesiense (East African sleeping sickness)
< hundred cases are reported (WHO).
-Animals are the primary reservoir of infection.
-Cattle have been implicated in the spread of the disease to new -Cattle have been implicated in the spread of the disease to new
areas and in local outbreaks.
-A wild animal reservoir is thought to be responsible for sporadic
transmission to hunters and visitors to game parks.
T. b. gambiense (West African sleeping sickness)
-Most of the sleeping sickness in Africa is caused by this form of
the parasite.
-Humans are the important reservoir of infection, although the
parasite can sometimes be found in domestic animals (e.g., pigs,
dogs, goats).
-Both forms - transmitted by the bite of the Tsetse fly (Glossina
species).
-Habitat: rural areas, living in the woodlands and forests and
vegetation along streams.
Tsetse fly (Glossina spp).
vegetation along streams.
-Tsetse flies bite during daylight hours.
-Both male and female flies can transmit the infection
-Other modes of transmission are possible.
Eg. A pregnant woman can pass the infection to her unborn baby.
by blood transfusion or sexual contact (rare)
Life Cycle Life Cycle
Two stages.
First stage- peripheral circulation,
Second stage - central nervous system
T. b. rhodesiense - infection progresses rapidly.
Disease in Humans Disease in Humans
- Large sore (a chancre). Some develop a rash.
- Fever, headache, muscle and joint aches, and generalized
enlarged lymph nodes within 1-2 weeks of the infective bite.
- After a weeks infection - the parasite invades CNS - mental
deterioration and other neurological problems.
- Death ensues usually within months.
Disease in Humans contd.. Disease in Humans contd..
T. b. gambiense infection - progresses more slowly.
- At first- mild symptoms. Such as intermittent fevers,
headaches, muscle and joint aches, and malaise.
- Itching of the skin, swollen lymph nodes (winterbottom
sign posterior cervical lymph node), and weight loss
can occur. can occur.
- After 1-2 years- central nervous system involvement, with
personality changes, daytime sleepiness with nighttime sleep
disturbance, and progressive confusion.
- Other Neurologic signs - partial paralysis as well as
hormonal imbalances.
- Untreated infection rarely lasts longer than 6-7 years and
more often kills in about 3 years
-T. congolense, T. vivax and T. brucei subsp. brucei.
-T. congolense : classified 3 types
Savannah
Forest
Kilifi
African Animal Trypanosomiasis
Kilifi
-T. simiae and T. godfreyi
-All domesticated animals are affected
-Incubation period: 4 days to approx. 8 weeks
-Most cases : are chronic, but acute cases may occur.
Clinical Signs in Animals
-First sign - localized swelling (chancre) at the site of bite
-Intermittent fever, anemia, lymphadenopathy and weight loss.
-Milk yield : decreased -Milk yield : decreased
-Reproduction: abortions, premature births and testicular damage
-An acute hemorrhagic syndrome (T. vivax in Cattle): enlarged lymph
nodes, severe anemia, widespread visceral and mucosal hemorrhages
-In one outbreak: bleeding from the ears and severe weight loss.
-Serological testing screening purpose
-Microscopic Demonstration of parasite in blood, CSF or lymph
node aspirate (posterior cervical lymph node)
Diagnosis
node aspirate (posterior cervical lymph node)
-Criteria for second stage :
- observation of trypanosomes in CSF or a
- white cell count of 6 or higher.
-Other indications of second stage :
- elevated protein
- increase in nonspecific IgM in CSF.
Treatment
Species
Drug of
choice
Adult Dosage Pediatric Dosage
T. b.
rhodesiense,
hemolymphatic
stage
Suramin
1
1 g IV on days 1,3,5,14, and 21
2
20 mg/kg IV on days 1, 3, 5, 14, and 21
3
stage
T. b.
rhodesiense,
CNS
involvement
Melarsoprol
4
2-3.6 mg/kg/d IV x 3 days.
5
After 7
days, 3.6 mg/kg/d x 3 days. Give a
3rd series of 3.6 mg/kg/d after 7
days.
2-3.6 mg/kg/d IV x 3 days.
5
After 7 days,
3.6 mg/kg/d x 3 days. Give a 3rd series of
3.6 mg/kg/d after 7 days.
T. b. gambiense,
Hemolymphatic
stage
Pentamidine
6
4 mg/kg/d IM or IV x 7-10 d 4 mg/kg/d IM or IV x 7-10 d
T. b. gambiense,
CNS
involvement
Eflornithine
7
400 mg/kg/d in 4 doses x 14 d 400 mg/kg/d in 4 doses x 14
Control Measures
- No vaccine
- Minimizing contact with tsetse flies
- Protective clothing avoid bright or dark colour and light weight
- Use insect repellent - Permethrin-impregnated clothing
- Reducing the disease reservoir and controlling the tsetse fly vector
Disease reservoir: T. b. gambiense
controlling the tsetse fly vector : T. b. rhodesiense
American Trypanosomiasis American Trypanosomiasis
Chagas Disease Chagas Disease
-Brazilian physician Carlos Chagas (1909).
-Trypanosoma cruzi
-Triatomine bug (Reduviid bug/kissing bug): humans and animals
American Trypanosomiasis (Chagas Disease)
-Indoors: cracks and holes of substandard housing
-Outdoor settings :
Beneath porches
Between rocky structures
Under cement
In rock, wood, brush piles, or beneath bark
In rodent nests or animal burrows
In outdoor dog houses or kennels
In chicken coops or houses
Geographical Distribution
-Bug bite
-mother-to-baby (congenital)
Transmission
-contaminated blood products (transfusions),
-an organ transplanted from an infected donor
-laboratory accident
-contaminated food or drink (rare)
Life Cycle
Acute and Chronic phase
Acute Phase: immediately last up to a few weeks or months, parasites in blood.
mild or asymptomatic - swelling around the site of inoculation
Chronic Phase: prolonged asymptomatic form - few or no parasites in the blood.
Disease in Humans
Many remain asymptomatic for life and never develop Chagas-related symptoms
Only 20 - 30% of infected people will develop debilitating and sometimes life-
threatening medical problems
-heart rhythm abnormalities that can cause sudden death;
-dilated heart that doesnt pump blood well;
-dilated esophagus or colon, leading to difficulties with eating or passing stool.
-Immunosuppresed severe fatal disease
Disease in Animals
-Cause infection
Dog, Cat, Horse and various other domestic and wild animals
-Young animals are more susceptible
Dog: debility, anaemia and spleenomegaly -Dog: debility, anaemia and spleenomegaly
-Cat : convulsions and posterior paralysis
Diagnosis
Acute Chagas disease
- Microscopic examination: thin and thick blood smears stained
with Giemsa, for visualization of parasites.
- Isolation of the agent:
o Inoculation in specialized media (e.g. NNN, LIT) o Inoculation in specialized media (e.g. NNN, LIT)
o Inoculation into mice; and
o Xenodiagnosis: where uninfected triatomine bugs are fed on the
patient's blood, and their gut contents examined for parasites 4
weeks later.
- Molecular tools: PCR.
Chronic Chagas disease
- Patients clinical history and findings
- Endemic country
- at least two different serologic tests.
Treatment
Drug Age group Dosage and duration
Benznidazole < 12 years 10 mg/kg per day orally in 2 divided doses for 60 days
12 years or older 5-7 mg/kg per day orally in 2 divided doses for 60 days
Nifurtimox 10 years 15-20 mg/kb per day orally in 3 or 4 divided doses for 90 days
11-16 years 12.5-15 mg/kg per day orally in 3 or 4 divided doses for 90 days
17 years or older 8-10 mg/kg per day orally in 3 or 4 divided doses for 90 days
Endemic areas :
-Improved housing and spraying insecticide
Control measures
-screening of blood donars
-Early detection and treatment of cases
Amphistomiasis Amphistomiasis
Caused Caused by by aa trematode trematode (fluke) (fluke) named named gastrodiscoides gastrodiscoides hominis hominis
Infection Infection that that usually usually asymptomatic asymptomatic && affects affects small small intestine intestine..
Gastrodiscoidiasis Gastrodiscoidiasis
G G.. hominis hominis usually usually found found in in animals animals (pigs), (pigs), but but when when infects infects
humans humans can can cause cause serious serious health health problems problems && even even mortality mortality..
Also Also known known as as aa Digenean Digenean Fluke Fluke (subclass (subclass of of platyhelminths) platyhelminths)
that that affect affect mostly mostly digestive digestive tract tract..
Although Although gastrodiscoidiasis gastrodiscoidiasis not not seen seen as as aa serious serious health health threat threat
yet, yet, it it is is not not an an infection infection to to take take lightly lightly..
HISTORY HISTORY
Gastrodiscoidiasis was first brought to attention in 1939 by J.J.C. Gastrodiscoidiasis was first brought to attention in 1939 by J.J.C.
Buckley. Buckley.
Buckley described life cycle & prevalence of disease in state of Buckley described life cycle & prevalence of disease in state of
India (Assam). India (Assam).
Found in 1939 that three villages surveyed in Assam over 40% of Found in 1939 that three villages surveyed in Assam over 40% of Found in 1939 that three villages surveyed in Assam over 40% of Found in 1939 that three villages surveyed in Assam over 40% of
the population was infected. the population was infected.
Buckley: formal classification of this parasite. Buckley: formal classification of this parasite.
AGENT: AGENT:
Phylum: Platyhelminths Phylum: Platyhelminths
Class: Trematoda Class: Trematoda
Family: Amphistomidae Family: Amphistomidae
Genus: Gastrodiscoides Genus: Gastrodiscoides Hominis Hominis
MORPHOLOGY MORPHOLOGY
OVA OVA ::- -
Size Size-- --160 x 65 mcm (large). 160 x 65 mcm (large).
Shape Shape-- --Spindle Spindle- -shaped. shaped.
Color Color-- --Light brown. Light brown.
Operculum Operculum-- --Present, distinct. Present, distinct.
Content Content- - Yolk mass Yolk mass Content Content- - Yolk mass Yolk mass
ADULT ADULT
Size Size-- --5 to 10 mm long by 2 to 5 5 to 10 mm long by 2 to 5
mm wide (medium). mm wide (medium).
Shape Shape-- --Gourd Gourd- -like like
Color Color-- --Reddish Reddish
Intestinal Ceca Intestinal Ceca-- --Straight Straight
Testes Testes-- --Anterior, lobate, and Anterior, lobate, and
tandem. tandem.
Acetabulum Acetabulum-- --Very wide and Very wide and
posterior posterior
EPIDEMIOLOGY EPIDEMIOLOGY
Found Found in in Vietnam, Vietnam,
Philippines, Philippines, Bangladesh Bangladesh
and and most most commonly commonly in in
the the Assam Assam state state of of India India..
It It is is prevalent prevalent in in areas areas
that that use use "night "night soil" soil" like like
in in Southeast Southeast and and Central Central
Asia Asia..
AA few few cases cases have have been been
documented documented in in Nigeria Nigeria..
POINTS TO REMEMBER POINTS TO REMEMBER
Common Name: Colonic fluke. Common Name: Colonic fluke.
Geographical distribution Geographical distribution-- --India, Viet Nam,Philippines, Malaysia, Kasakstan. India, Viet Nam,Philippines, Malaysia, Kasakstan.
Pathogenesis: Mucosal inflammation of cecum and ascending colon. Pathogenesis: Mucosal inflammation of cecum and ascending colon.
Habitat: large intestines; cecum and colon. Habitat: large intestines; cecum and colon.
Intermediate host Intermediate host
FIRST FIRST-- --Snail. Snail.
SECOND SECOND-- --Aquatic vegetation. Aquatic vegetation.
Reservoir host Reservoir host Hogs, Napu mouse deers, Monkeys, Rats, Fish, and other fish Hogs, Napu mouse deers, Monkeys, Rats, Fish, and other fish- -
eating animals eating animals ..
Infective form Infective form-- --Metacercaria. Metacercaria.
Mode of infection Mode of infection Ingestion (vegetation found in contaminated water such as Ingestion (vegetation found in contaminated water such as
water caltrop or eating infected fish that has not been cooked properly or at all ). water caltrop or eating infected fish that has not been cooked properly or at all ).
Specimen of Choice Specimen of Choice-- --Feces Feces
CLINICAL PRESENTATION CLINICAL PRESENTATION
Parasite Parasite typical typical found found in in pigs, pigs, can can also also affect affect humans humans..
Usually Usually infection infection asymptomatic asymptomatic
Occasionally Occasionally cause cause intestinal intestinal problems problems:: diarrhea, diarrhea, fever, fever, Occasionally Occasionally cause cause intestinal intestinal problems problems:: diarrhea, diarrhea, fever, fever,
abdominal abdominal pain, pain, colic colic && increase increase in in mucous mucous production production..
In In severe severe cases cases (large (large amounts amounts of of eggs eggs present) present) tissue tissue
reactions reactions occur occur in in heart heart or or mesenteric mesenteric lymphatics lymphatics..
AA case case report report of of aa seven seven year year old old Nigerian Nigerian child child presented presented with with
features features of of malnutrition malnutrition and and anaemia anaemia and and found found to to have have G G..
hominis hominis and and Ascaris Ascaris lumbricoides lumbricoides..
DIAGNOSTIC TESTS DIAGNOSTIC TESTS
Examination of feces & detection of eggs. Examination of feces & detection of eggs.
There have not been any other tests made There have not been any other tests made There have not been any other tests made There have not been any other tests made
at this time at this time
MANAGEMENT AND THERAPY MANAGEMENT AND THERAPY
Soap Soap sud sud enema enema can can be be effective effective in in removing removing
the the worms worms (flush (flush the the flukes flukes from from the the colon colon
which which removes removes the the parasite parasite entirely entirely since since it it
does does not not reproduce reproduce within within the the host) host).. does does not not reproduce reproduce within within the the host) host)..
Proven Proven effective effective drugs drugs: : Tetrachlorothyline Tetrachlorothyline
( (00..11mg/kg mg/kg empty empty stomach) stomach)..
Preferred Preferred drug drug- - Prazinquantal Prazinquantal (less (less toxic toxic & &
eliminates eliminates most most of of parasite parasite with with 33 doses doses (at (at 25 25
mg/kg) mg/kg) in in one one day) day)..
PUBLIC HEALTH AND PREVENTION PUBLIC HEALTH AND PREVENTION
Prevention Prevention of of disease disease is is not not difficult difficult when when
simple simple sanitary sanitary measures measures taken taken..
"Night "Night Soil" Soil" should should never never be be used used as as aa fertilizer fertilizer "Night "Night Soil" Soil" should should never never be be used used as as aa fertilizer fertilizer
because because it it could could contain contain any any number number of of
parasites parasites..
All All food food should should be be washed washed thoroughly thoroughly using using
filtered filtered water water && proper proper techniques techniques to to dispose dispose of of
waste waste should should observed observed..
Coenurosis Coenurosis
Introduction Introduction
Human Human coenurosis coenurosis infection infection by by aa coenurus, coenurus,
Larval Larval stage stage of of any any one one of of four four species species of of dog dog tapeworms tapeworms:: Taenia Taenia multiceps multiceps,,
TT.. serialis serialis,, TT.. brauni brauni && TT.. glomerata glomerata..
Adults Adults worms worms live live in in the the intestines intestines of of dogs dogs && other other canines canines
Pass Pass eggs eggs which which are are then then ingested ingested by by grazing grazing animals, animals, usually usually sheep, sheep, goats, goats,
and and rabbits rabbits..
Coenurosis Coenurosis results results when when humans humans accidentally accidentally ingest ingest these these eggs, eggs, usually usually in in
contaminated contaminated fruits fruits or or vegetables vegetables..
Oncospheres Oncospheres (tapeworm (tapeworm embryos) embryos) escape escape from from the the eggs eggs && form form fluid fluid filled, filled,
bladder bladder- -like like cysts cysts called called coenurus coenurus (hence (hence the the name name of of the the disease) disease) in in
various various tissues tissues but but usually usually in in the the central central nervous nervous system system (CNS) (CNS)..
Taxonomy Taxonomy
Common name: Tapeworm Common name: Tapeworm
Kingdom: Animalia Kingdom: Animalia
Phylum: Platyhelminths Phylum: Platyhelminths Phylum: Platyhelminths Phylum: Platyhelminths
Class: Cestoda Class: Cestoda
Order: Cyclophyllidea Order: Cyclophyllidea
Family: Taeniidae, Genus: Family: Taeniidae, Genus: Taenia Taenia
Species: Species: multiceps, serialis, brauni, glomerata multiceps, serialis, brauni, glomerata
History History
The The first first infection infection due due to to T T.. multiceps multiceps.. In In 1913 1913 aa locksmith locksmith in in Paris Paris was was
suffering suffering from from convulsions convulsions and and aphasia, aphasia, loss loss of of ability ability to to speak speak or or
understand understand speech speech.. During During his his autopsy, autopsy, two two coenuri coenuri (probably (probably TT..multiceps multiceps))
were were found found in in the the brain, brain, one one being being degenerate degenerate and and the the other other containing containing 75 75
scolices scolices (knoblike (knoblike anterior anterior end end of of aa tapeworm tapeworm that that has has suckers) suckers)..
The The first first infection infection due due to to T T.. serialis serialis.. The The first first proven proven case case of of human human
coenurosis coenurosis due due to to TT.. serialis serialis was was reported reported in in aa 59 59 year year old old French French woman woman by by
The The first first infection infection due due to to T T.. serialis serialis.. The The first first proven proven case case of of human human
coenurosis coenurosis due due to to TT.. serialis serialis was was reported reported in in aa 59 59 year year old old French French woman woman by by
Bonna Bonna and and collegues collegues in in 1933 1933.. The The coenurus coenurus from from this this patient patient was was fed fed to to aa
dog dog and and seven seven characteristic characteristic scolices scolices were were obtained obtained.. The The first first infection infection in in
the the Western Western Hemisphere Hemisphere was was reported reported in in 1950 1950 in in aa two two year year old old California California
boy boy..
The The first first infection infection due due to to T T.. brauni brauni.. TT.. brauni brauni is is thought thought to to cause cause the the
African African form form of of coenurosis coenurosis.. The The first first patient patient suffering suffering from from coenurosis coenurosis
caused caused by by TT.. brauni brauni was was reported reported by by Fain Fain and and colleagues colleagues in in 1956 1956..
The The first first infection infection due due to to T T.. glomerata glomerata.. First First infection infection found found in in Nigeria Nigeria
by by Turner Turner in in 1919 1919..
Hosts Hosts
Definitive Definitive Hosts Hosts: : dogs, dogs, foxes foxes && other other canids canids..
Accidental Accidental intermediate intermediate host host:: humans humans
Intermediate Intermediate Hosts Hosts:: Sheep Sheep and and other other ungulates ungulates.. More More Intermediate Intermediate Hosts Hosts:: Sheep Sheep and and other other ungulates ungulates.. More More
specifically specifically
TT.. multiceps multiceps:: Sheep, Sheep, goats, goats, cattle, cattle, horses horses && antelopes antelopes.. Larva Larva
develops develops in in various various tissues, tissues, commonly commonly in in the the brain brain..
TT.. serialis serialis:: Rabbits, Rabbits, hares hares && rodents rodents.. Larva Larva develops develops in in
subcutaneous subcutaneous tissue tissue && intramuscular intramuscular connective connective tissue tissue..
TT.. brauni brauni:: Gerbils Gerbils.. Larva Larva inhabits inhabits subcutaneous subcutaneous tissue tissue && other other
organs organs.. Occurs Occurs in in North North Africa, Africa, Rwanda Rwanda && the the Democratic Democratic Republic Republic of of
Congo Congo..
TT.. glomerata glomerata:: Gerbils Gerbils && larva larva develops develops in in muscles muscles.. The The definitive definitive
host host in in unknown unknown..
Coenurus Coenurus
Coenurus Coenurus: : is is aa white, white, translucent translucent structure structure
varying varying from from 22- -10 10 cm cm in in the the largest largest dimension, dimension,
filled filled with with clear, clear, watery watery fluid fluid or or aa collapsed collapsed
membrane membrane with with many many protoscolices protoscolices on on its its
internal internal surface surface..
Cysts Cysts from from sc sc tissues tissues are are often often unilocular unilocular
(having (having aa single single compartment compartment or or cavity) cavity).. (having (having aa single single compartment compartment or or cavity) cavity)..
From From CNS CNS frequently frequently multilocular multilocular (with (with many many
compartments compartments or or cavities), cavities), sometimes sometimes with with
multiple multiple irregular irregular vesicles vesicles & & with with aa grape grape- -like like
appearance appearance..
Viable Viable cysts cysts have have many many (often (often hundreds) hundreds)
protoscolices protoscolices..
The The bladder bladder of of the the coenurus coenurus has has budding budding- -off off
daughter daughter bladders, bladders, either either internally, internally, floating floating in in
the the cystic cystic fluid, fluid, or or externally, externally, attached attached by by
stalks stalks..
Speciation Speciation of of coenurus coenurus is is based based on on number number && size size of of
rostellar rostellar hooklets hooklets..
However, However, aa unilocular unilocular coenurus coenurus in in the the brain, brain, eye, eye, or or
subcutaneous subcutaneous tissues, tissues, with with scolices scolices distributed distributed in in subcutaneous subcutaneous tissues, tissues, with with scolices scolices distributed distributed in in
groups, groups, is is probably probably the the larva larva of of TT.. multiceps multiceps..
Coenuri Coenuri recovered recovered from from subcutaneous subcutaneous tissues tissues (never (never
from from the the central central nervous nervous system) system) of of patients patients in in
tropical tropical Africa Africa probably probably belong belong to to TT.. brauni brauni..
Cases Cases of of coenurosis coenurosis in in the the North North American American continent continent
are are probably probably due due to to TT..serialis serialis..
Epidemiology Epidemiology
The The incidence incidence of of coenurosis coenurosis are are very very low low with with only only about about 100 100 cases cases
ever ever being being reported reported in in humans humans..
No No real real endemic endemic area area..
Coenurosis Coenurosis is is very very rare rare in in the the Western Western Hemisphere Hemisphere with with the the
majority majority of of cases cases ( (65 65%%) ) occurring occurring in in Europe Europe and and Africa Africa.. majority majority of of cases cases ( (65 65%%) ) occurring occurring in in Europe Europe and and Africa Africa..
The The distribution distribution of of the the different different species species that that cause cause coenurosis coenurosis are are
as as follows follows..
T T.. multiceps multiceps: : France, France, Africa, Africa, England, England, Brazil Brazil & & the the United United States States..
T T.. serialis serialis: : Canada Canada & & the the United United States States
T T.. brauni brauni: : North North Africa, Africa, Rwanda Rwanda & & the the Democratic Democratic Republic Republic of of Congo Congo..
T T.. glomerata glomerata: : Nigeria Nigeria & & the the Democratic Democratic Republic Republic of of Congo Congo..
Life Cycle Life Cycle
Prime Prime larval
final intermediate predilection
Adult host Larva host site
Multiceps dog Coenurus sheep central nervous Multiceps dog Coenurus sheep central nervous
(=Taenia) cerebralis system
multiceps
Multiceps dog Coenurus rabbit connective
(=Taenia) serialis tissue
serialis
T. Brauni dog Coenurus Rat SC tissue
T. Glomerata T. Glomerata Gerbils Gerbils muscles muscles
Clinical manifestations Clinical manifestations
Coenurosis Coenurosis are are variable variable and and depend depend on on the the location location of of
the the cyst cyst..
Brain Brain: : occipital occipital headaches, headaches, vomiting, vomiting, seizures, seizures,
hemiplegia, hemiplegia, monoplegia, monoplegia, and and cerebellar cerebellar ataxia ataxia.. hemiplegia, hemiplegia, monoplegia, monoplegia, and and cerebellar cerebellar ataxia ataxia..
Spinal Spinal canal canal: : Arachnoiditis Arachnoiditis
Eye Eye: : located located in in the the posterior posterior chamber,decreased chamber,decreased
vision vision..
Subcutaneous Subcutaneous && intermuscular intermuscular tissues tissues: : the the lesion lesion
presents presents as as aa mass mass which which is is sometimes sometimes painful painful
Diagnosis Diagnosis
Symptoms Symptoms
Papilledema (swelling of the optic nerve head) in the back of the Papilledema (swelling of the optic nerve head) in the back of the
retina during eye examination retina during eye examination
Moderate hypoglycorrhachia (low concentrations of blood sugar in Moderate hypoglycorrhachia (low concentrations of blood sugar in Moderate hypoglycorrhachia (low concentrations of blood sugar in Moderate hypoglycorrhachia (low concentrations of blood sugar in
the cerebral spinal fluid) with glucose concentrations below 40 the cerebral spinal fluid) with glucose concentrations below 40
mg/dl occurs in about half the cases; occasionally the glucose mg/dl occurs in about half the cases; occasionally the glucose
levels fall to values as low as 10 mg/dl. levels fall to values as low as 10 mg/dl.
Raised intracranial pressure caused by ventricular obstruction. Raised intracranial pressure caused by ventricular obstruction.
CSF examination showing nonspecific profile indicating subacute CSF examination showing nonspecific profile indicating subacute
(between acute and chronic) nonbacterial inflammation. (between acute and chronic) nonbacterial inflammation.
Imaging Imaging reveals reveals aa cystic cystic mass, mass, often often in in the the ventricles ventricles or or
in in the the subarachnoid subarachnoid space, space,
CT CT scans scans viable viable cysts cysts appear appear as as lucent lucent lesions lesions
surrounded surrounded by by aa contrast contrast- -enhanced enhanced peripheral peripheral rim rim..
Multiple Multiple echo echo MRI MRI sequences sequences reveal reveal that that the the
intensity intensity of of the the cyst cyst contents contents is is similar similar to to that that of of
the the CSF CSF..
Ventriculography Ventriculography: : CT CT or or MRI MRI may may show show dilatation dilatation of of the the
ventricles ventricles
definitive definitive diagnosis diagnosis: : gross gross microscopic microscopic examination examination of of
the the morphologic morphologic appearance appearance of of the the cyst cyst..
Papilledema: edges of optic nerve (yellow
disc in center) appear blurred & indistinct
when swollen
CT scan showing enlarged
lateral ventricles
Treatment Treatment
Only recognized treatment for coenurosis: surgical removal of cysts. Only recognized treatment for coenurosis: surgical removal of cysts.
Glucocorticoids and Anthelmintics have been used to treat coenurosis. Glucocorticoids and Anthelmintics have been used to treat coenurosis.
Traditional drugs used within these categories are as follows: Traditional drugs used within these categories are as follows:
Anthelmintics: Anthelmintics: Anthelmintics: Anthelmintics:
Praziquantel (Biltricide): Praziquantel (Biltricide):
Niclosamide (Niclocide): Niclosamide (Niclocide):
Albendazole (Albenza): Albendazole (Albenza):
Glucocorticoids: Glucocorticoids: usually used for patients with elevated intracranial usually used for patients with elevated intracranial
pressure. pressure.
Dexamethasone (Decadron) Dexamethasone (Decadron)
Prevention Prevention
Avoid Avoid eating eating fruits fruits and and vegetables vegetables that that were were
grown grown on on fields fields fertilized fertilized with with dog dog manure manure (or (or
to to avoid avoid using using dog dog manure manure in in general) general)..
Uncooked Uncooked sheep sheep (offal (offal & & brain) brain) should should not not be be
fed fed to to dogs dogs..
Dogs Dogs should should be be treated treated immediately immediately if if they they are are
suspected suspected of of having having any any sort sort of of tapeworm tapeworm..
Annelid diseases INTRODUCTION
Aquatic, terrestrial, or amphibious.
The annelids include earthworms, polychaete
worms, and leeches.
Charac. bloodsuckers & like ticks, adapted to
engorge large amounts of blood.
Phylum: Annelida
Elongated, cylindrical,
triploblastic, coelomate,
metameric protostomes
Complete gut, ventral nerve Complete gut, ventral nerve
cord, paired setae
Once divided into the classes
Polychaeta, Oligochaeta &
Hirudinea;
Now reorganized:
Class Polychaeta
Class Clitellata
Subclass Oligochaeta
Subclass Hirudinea
Class: Polychaeta
Parapodia with many
setae
Monoecious or diecious
Trochophore larva
Two Life Styles:
Sessile filter-feeders
Errant predators; head
Class: Clitellata
No parapodia, few or
no setae, monoecious no setae, monoecious
Subclass: Oligochaeta
(earthworms, Tubifex)
Few setae; no
distinct head;
mostly fresh water &
terrestrial
Subclass: Hirudinea (leeches)
Most species live in freshwater environments; some
terrestrial
Many predatory or scavengers; perhaps 25%
parasitic
Most with 34 true internal segments; outer surface
annulated
With anterior (pseudosucker) and large posterior
suckers
Most without setae
Some can swim; others cannot Some can swim; others cannot
Complete gut; sometimes with diverticulae
Some species with eyes
Sensory papillae embedded over body surface
Male reproductive system
4-80 pair of testes
Spermatozoa cemented together in seminal Spermatozoa cemented together in seminal
vesicles & enter ejaculatory ducts (2); these fuse
to form an atrium
Most species pass sperm as spermatophores;
the Hirudidae possess a penis instead
Female reproductive system
2 ovaries
Oviducts unite to form uterus
Leech Anatomy Life-cycle
Hermaphroditic
Spermatophores released onto body surface of partner
Enter tegument via histolytic enzymes; migrate through
coelomto fertilize oocytes within ovaries.
In Hirudidae, sperm placed within female gonopore by penis.
The clitellum inconspicuous & secretes rings which collect
fertilized ova as they pass anteriorly over female gonopore &
sloughed off anterior end of the body as cocoons (May-Aug.)
Young leeches hatch & exit cocoon; similar to adults
Development: some years to complete
Order: Acanthobdellida
Primitive, with 1 species (acanthobdella) on salmonids
in europe.
Setae present.
Coelom as compartments in 5 anterior segments.
Order: Gnathobdellida
Large mouth.
Non-eversible pharynx.
3 pair jaws.
Testes large and arranged in metameric pairs.
Aquatic or terrestrial.
5 annuli per segment.
Typical genera include hirudo, macrobdella, limnatis.
Hirudo medicinalis (European medicinal leech)
Hirundinaria granulosa ( Indian medical leech)
Hirundinaria zeylandica ( terrestrial leech) that attacks humans
and animals in the tropics of Asia.
Limnatis nilotica (large horse leech in Europe); members of
genus sometimes accidently ingested by various animals and
attach & suck blood along esophagus & nasopharyngeal area.
Often used for bloodletting in Europe.
Order: Pharyngobdellida
Large mouth
Non-eversible pharynx Non-eversible pharynx
Without true jaws or dentition
Testes in grape-like bunches
Mostly aquatic; some semi-terrestrial
Order: Rhynchobdellida
Mouth small, as a pore
Eversible proboscis derived from pharynx
Without jaws or dentition
All aquatic
Typical genera include Glossiphonia, Haementeria,
Placobdella
Haementeria officinalis the medicinal leech of Central and
South America
Placobdella parasitica the common turtle leech in Kansas
Hirudiniasis
Medicinal importance:
as an aid used for bloodletting.
as injurious to man, painlessly inserting their jaws in the as injurious to man, painlessly inserting their jaws in the
skin or mucus membrane of man & produce trickling blood.
Medicinal leech (Hirudo medicinalis) linked to practice of
medicine for years untold.
Use for blood letting peaked mid 1800s.
Recently by microvascular & plastic surgeons, treatment of
black eyes & varicose veins.
Some species more likely to afflict humans, Dinobdella ferox
(terrible ferocious leech) and spp. of Limnatis, Praobdella &
Myxobdella.
Medically important leeches: mostly belong to the genus Medically important leeches: mostly belong to the genus
Limnatis.
Reported from various countries in Africa, Asia, Southern
Europe & America.
Human infection with most notorious spp. Limnatis nilotica.
Habitat in small streams, springs, wells, water-troughs, ponds,
ditches.
Pathogenesis
Mucosal/ Orifical/ vesical/ Internal hirudiniasis:
mouth, genitourinary tract (vulva, vagina & urethra),
nostrils or conjunctiva. nostrils or conjunctiva.
Internal hirudinaisis common in Middle East, India &
Ethiopia.
Presence of leeches in throat & upper air passages
most common than vaginal hirudiniasis.
Small, young leeches quickly enter mouth or nostrils,
attach to wall of resp. passages, usually far back in
pharynx or larynx causing epistaxis & haemoptysis. pharynx or larynx causing epistaxis & haemoptysis.
They grow rapidly & reach a large size & do much
damage.
Normally puncture not painful, but wounds remain
open for long time, heal slowly, even not infected
with pyogenic organisms.
During biting excrete a local anaesthetic; allows it to
bite & suck blood without pain.
Secretes: Secretes:
An anticoagulant (hirudin) from salivary glands;
inhibit thrombin in clotting process.
Histamine like substances to prevent closure of
capillaries
Hyalurondinase,
Calin (a platelet aggregation inhibitor).
Continuous bleeding even after the leech has
dropped or been removed leads to anaemia & death.
Manifestations and management of internal
hirudiniasis
Clinical pictures
-Apicomplexan parasites: Genus, Babesia
-Babesia microti (rodent origin) asymptomatic and non-fatal
infection
-B. bovis and B. divergens (cattle origin) fatal infection
-Tickborne transmission (peaks infection - warm months)
Babesiosis
-Tickborne transmission (peaks infection - warm months)
-Ixodes scapularis ticks (also called blacklegged ticks or deer ticks)
-Ixodes ricinus ticks (B. divergens)
-Rhipicephalus spp (B. bigemina, B. bovis, and B. major )
-Common in tropical and subtropical areas (Asia, Africa, Central and
South America, parts of southern Europe, and Australia)
-Babesia infection - from asymptomatic to life-threatening.
.
Life Life
Cycle Cycle
-Not transmitted from person-to-person
-Through the bite of an infected tick (during outdoor activities)
-Blood Transfusion
Transmission Transmission
-Congenital
-Majority are symptom less.
-Flu-like symptoms, such as fever, chills, sweats, headache, body
aches, loss of appetite, nausea, or fatigue.
-Hemolytic anemia - lead to jaundice and dark urine.
-Severe disease (weak immune system: cancer, lymphoma, or AIDS)
Disease in Humans Disease in Humans
-Severe disease (weak immune system: cancer, lymphoma, or AIDS)
Complications of Babesiosis can include:
-low and unstable blood pressure;
-severe hemolytic anemia (hemolysis);
-very low platelet count (thrombocytopenia);
-disseminated intravascular coagulation (also known as DIC or
consumptive
coagulopathy), which can lead to blood clots and bleeding;
-malfunction of vital organs (such as the kidneys, liver, lungs, and
heart)
-death.
Disease in Animals Disease in Animals
Young naturally resistance while Older are susceptible
Cattle : B. bovis, B. divergens, B. major and B. bigemina
Horse : B. caballi and B. equi (Jaundice biliary fever)
Sheep: B. motasi and B. ovis
Dog : B. gibsoni and B. canis
Cat : B. felis Cat : B. felis
Initial stage : high fever, anorexia, depression and weakness
Terminal stage: Jaundice, haemoglobinuria and anemia
Diagnosis Diagnosis
-Blood Smear Examination:
o Small Babesiosis (B. microti) - "Maltese cross formations"
Giemsa Stain
o Large Babesiosis (B. canis, B. bigemina) Two pears hanging o Large Babesiosis (B. canis, B. bigemina) Two pears hanging
together -
Romonovski stains (methylene blue and eosin).
-Serology (IgM or IgM) False positive results
-Molecular methods PCR detection of Babesia from the peripheral blood
-Other laboratory tests : Complete blood count.
- decreased red blood cells and platelets
Lasts for 7-10 days with a combination of two prescription
medications
Atovaquone PLUS Azithromycin; OR
Clindamycin PLUS Quinine (severely ill patients).
Treatment
Drug Adult dosage (usually treat for at least 7-10 days)
Atovaquone 750 mg orally twice a day
along with
Azithromycin
On the first day, give a total dose in the range of 500-1000 mg orally; on subsequent
days, give a total daily dose in the range of 250-1000 mg
or
Clindamycin
600 mg orally 3 times a day
or
300-600 mg intravenously 4 times a day
along with
Quinine 650 mg orally 3 times a day
Diminazen (Berenil), Imidocarb or Trypan blue in Animals
-Vaccine is available for animals but not for humans
-Avoiding exposure to tick habitats is the best defense.
-Protective clothing
-Apply repellents to skin and clothing
eg. DEET (N,N-diethylmetatoluamide) skin/clothing
Control Measures Control Measures
eg. DEET (N,N-diethylmetatoluamide) skin/clothing
Permethrin - clothing/boots no skin
Amebiasis Amebiasis
-Entamoeba histolytica (dogs, rats, cats and swine)
-Entamoeba polecki (swine)
-Entamoeba dispar limited knowledge
Zoonotic interest
-more common in people who live in tropical and subtropical areas
with poor sanitary conditions
-Infected people do not always become sick.
-medication is available
Life Cycle Life Cycle
Disease in Humans
-Asymptomatic
-Common in young adults
Intestinal disease:
Mild form : mild abdominal discomfort with bloody mucous
diarrhea diarrhea
Acute form: fever, chills, bloody and mucous diarrhea
(amebic dysentery)
Extra Intestinal Disease:
Amebic liver abscess, lung, skin, genital organs, spleen, brain
and
pericardium
Disease in Animals
-Asymptomatic
-Intestinal and hepatic form occur in lower primates
and dogs
-Laboratory rodents : hamsters and jerboa are -Laboratory rodents : hamsters and jerboa are
susceptible to hepatic form guinea pig and rats are
resistant
-E. polecki: non-pathogenic in swine
Diagnosis
- Demonstration of cysts or trophozoites in feces
- Cysts are best concentrated by ZnSO4 Floatation technique
- Serological testing : ELISA, IHA, IFA and CIEP
Features E. histolytica E. polecki Features E. histolytica E. polecki
Cysts Nucleus four single
Chromatin Evenly distributed Uneven distributed
Glycogen vacuoles in
cytoplasm
frequent rare
Cytoplasmic inclusion
bodies
No Opaque & larger than
nucleus
Chromatoidal bars < 10 Upto 30
Treatment
Presentation: Drug: Adult Dosage: Efficacy
Asymptomatic cyst passage -
(luminal infection only)
Diloxanide furoate 500 mg t.i.d., 10 days 87-96%
Iodoquinol
(Diiodohydroxy
quin)
650 mg t.i.d., 20 days 95%
500 mg t.i.d, 10 days
Paromomycin
500 mg t.i.d, 10 days
OR 30 mg/kg/day in 3 doses, 5-10
days
85-90%
Invasive Rectocolitis -
(Note)
Metronidazole
750 mg t.i.d., 5-10 days
OR 50 mg/kg, 1 dose
90%
86%
Tinidazole 50 mg/kg q.d., 3 days
Amoebic Liver Abscess -
(Note)
Metronidazole
750 mg t.i.d., 5-10 days
OR 2.4 g q.d., 1-2 days
95%
Control Measures
-Good Sanitation
-Improved Sewage Disposal
-Avoid faecal excretion outdoors
-Improved Personal Hygiene -Improved Personal Hygiene
-Health Education
Giardia
History
- First observed 1681 by Anthony van Leeuwenhoek
- Described ~200 years later by Vilem Lambl
- First cultured in 1960s
- Confirmed pathogen 1970s
- One of most common intestinal parasites
- Causes Giardiasis (beaver fever) - Causes Giardiasis (beaver fever)
- > with poor water sanitation
Species details
- 5 species of Giardia
G. intestinalis/lamblia/duodenalis
G. muris in rodents, birds, reptiles
G. agilis in amphibians
G. ardae in great blue heron
G. psittaci in budgerigar
Morphology
Cyst
- Infective stage in the environment, hardy
- Persist in cold water up to several months
- egg-shaped, 8-14m by 7-10m
- Organelle duplication w/out cytokinesis
results in
four nuclei (Nu)
four median bodies (MB) four median bodies (MB)
four axonemes (Ax)
- Upon excystation, each cyst produces two
trophozoites.
Trophozoite
- Cannot survive in the environment
- Motile 4 pairs of flagella
- Pear shaped, bilaterally symmetrical
- Relatively flattened, 10-12m long
- 5-7m wide with a large sucking disk on the
anterior ventral side
- Two nuclei
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-Global disease.
-Infects nearly 2% (adults) and 6-8% (childrens) in developed
countries
-Nearly 33% of people in developing countries have giardiasis.
Geographical Distribution
Life Cycle
2 trophozoites
released per
cyst
Multiply by
binary fission
Sucking disc
used for
attachment
binary fission
every 12 h
Cyst forms in
transit to colon
Giardiasis in Humans & Animals
Manifest in 7-10 days
Lasts 2- 6 weeks
Symptoms
- Severe diarrhea
- Abdominal cramps
Common Chronic
vs.
More severe
condition
Lasts 2 months -
years
Symptoms
Host examples
E Humans
E Cats, dogs
E Cows, lamb
E Beavers, deer
- Abdominal cramps
- Bloating
- Flatulence
- Nausea
- Vomiting
May lead to
- Weight loss
- Dehydration
Symptoms
- Increased gas
- Dehydration
- Burping
- Loose stools
- Slowed growth
Giardia cysts can be excreted intermittently
-Multiple stool collections (i.e., three stool specimens collected
every other
day) increase test sensitivity.
-The use of concentration methods and Trichrome staining
Diagnosis
-Immunoassays or Rapid immune-chromatographic cartridge assays
-molecular testing (PCR) can be used to identify the subtypes of
Giardia.
Effective treatment :
-Metronidazole Adult dosage : 250 mg 3.t.d. for 5 days
Pediatric dosage : 5 mg/kg B.W. 3.t.d, for 5 days
-Tinidazole, Adult dosage : 2 g ounce
Pediatric dosage : 50 mg/kg B.W. ounce
-Nitazoxanide. Adult dosage : 500 mg 2.t.d for 3 days
Pediatric dosage : 13 yrs: 100 mg every 12 hours for 3 days;
Treatment
Pediatric dosage : 13 yrs: 100 mg every 12 hours for 3 days;
411 yrs: 200 mg every 12 hours for 3
days
Alternatives treatment :
-Paromomycin,
Adult dosage : 2535 mg/kg B.W/dose, 3 doses/day for 7 days
Pediatric dosage : 2535 mg/kg B.W/dose, 3 doses/day for 7 days
-Quinacrine
Adult dosage : 100 mg 3.t.d. for 5 days
Pediatric dosage : 2 50 mg/kg B.W., three times per day for 5
days
-Furazolidone.
Adult dosage : 100 mg 4.t.d. for 710 days
Pediatric dosage : 6 mg/kg B.W/dose, 4 doses/day for 7-10 days
Methods of Prevention
1. Good Hygiene
2. Safe Traveling/Hiking
3. Vaccines 3. Vaccines
4. Halogenation
5. Filtration
Prevention
Hygienic Practices
Wash hands thoroughly with
soap and water, especially:
E After using the bathroom
E After handling animals
1.
E After handling animals
E After touching dirt
E Before eating/preparing food
Avoid consuming contaminated
water
E Dont swallow recreational water or
drink untreated water
Prevention (cont.)
Safe Traveling/Hiking
- Be careful of drinking the water and consuming
raw foods
- If you must drink untreated water, use sand
filtration or boil the water. Sand filtration filters
are available in many outdoors-goods stores
2
.
are available in many outdoors-goods stores
Vaccines
- Not available for humans
- Available in Animals
Prevent cross-transmission
Problems: live-vaccine, must be refrigerated,
short shelf-life
3.
Prevention (cont.)
Halogenation
- Non-spore forming bacteria are very susceptible
- Protozoan cysts are resistant, therefore, used but not as effective
Filtration
4.
5 Filtration
- Most effective way of removing Giardia cysts
- Many filtration systems implement other methods of disinfection
Halogenation (see above)
Ozone - produces small amt of carcinogen, no residual
UV radiation - no residual disinfectant
- Method 1623
5
.
Method 1623
Assessment of the occurrence of Giardia and Cryptosporidium
E Surface waters
1996-influenced by Safe Drinking Water Act amendments
First developed Method 1622
E Detection of Cryptosporidium only
Combined procedure for detection of Cryptosporidiumand
Giardia
Steps:
E Filtration
E Immunomagnetic separation of oocysts and cysts
E Immunofluorescence assay
E Dye staining and contrast microscopy
Balantidiosis Balantidiosis
Balantidium coli - intestinal protozoan parasite
(largest protozoan)
Common - pigs in warmer climates,
- monkeys in the tropics
Rare - Humans
Prevalence : throughout the world,
most prevalent in tropical and subtropical developing
countries.
Transmission
Fecal-oral route.
-eating contaminated meat, fruits, and vegetables .
-drinking and washing food with contaminated water
-poor hygiene habits.
Life Cycle
Humans Humans
Most people experience no symptoms.
Severe signs and symptoms Immunocomprimised
Clinical signs :
-persistent diarrhea or dysentery,
-abdominal pain,
-weight loss,
nausea,
Disease
-nausea,
-vomiting.
If left untreated, perforation of the colon can occur.
Animals
Swine: Non pathogenic but occasionally acute fatal infections
dysentery and hemorrhages
Dog, Cat, Sheep and Cattle are also affected
Clinical signs
Balantidiasis should be considered if the patient works
closely with pigs
or
lives in or has recently traveled to a region with poor
water sanitation,
Diagnosis
water sanitation,
Balantidiosis is diagnosed by microscopic examination of
a patients feces (wet mount)
Treatment
Tetracyclines : 500 mg 4.t.d for 10 days
(Contraindicated - pregnant women and
children < 8 years of age)
(2) Metronidazole : 750 mg three times daily for 5 days
(3) Iodoquinol : 640 mg three times daily for 20 days
First, barriers between swine and humans should be established.
- Pig & human habitat separate.
Clean water is imperative.
Foods and Vegetables should be washed with clean water
Control measures
Foods and Vegetables should be washed with clean water
Proper sewage and trash removal is crucial.
Personal hygiene
Finally, asymptomatic carriers should be treated with antibiotics
along with symptomatic patients.
Coccidia Coccidia
Q Q Family Family Eimeriidae Eimeriidae (one Host Coccidia) (one Host Coccidia)
Genus:1. Eimeria Genus:1. Eimeria
2. Isospora 2. Isospora
3. Cryptosporidium 3. Cryptosporidium 3. Cryptosporidium 3. Cryptosporidium
Q Q Family Family Sarcocystidae Sarcocystidae (two Host Coccidia) (two Host Coccidia)
Genus: 1. Toxoplasma Genus: 1. Toxoplasma
2. Sarcocystis 2. Sarcocystis
Family: Eimeriidae (One host Coccidia) Family: Eimeriidae (One host Coccidia)
Mainly intracellular parasites Mainly intracellular parasites -- intestinal epithelium, intestinal epithelium,
Except Except --
-- Eimeria truncate Eimeria truncate which affect which affect kidney kidney of Geese. of Geese.
-- Eimeria stiedae Eimeria stiedae which affect which affect liver liver of rabbits. of rabbits.
The term The term coccidiosis coccidiosis is usually reserved for infections is usually reserved for infections
caused by caused by Eimeria Eimeria and and Isospora Isospora. .
Typical Life Cycle of the Coccidia Typical Life Cycle of the Coccidia
Definitive host
ingests oocyst
(sporozoites)
sporozoites
released
Sporozoites
develop
Outside Outside
Host Host
Inside Host Inside Host
Macro and microgametes
unite to form oocyst (intestines)
oocyte passed
in feces
matures to
oocyst
develop
Life Cycle Eimeria Life Cycle Eimeria
Single Host Coccidia of Domestic Single Host Coccidia of Domestic
Animals Animals
Coccidia of fowl (poultry) Coccidia of fowl (poultry)
Coccidia of Cattle Coccidia of Cattle
Coccidia of Sheep & Goats Coccidia of Sheep & Goats
Coccidia of Dogs and Cats Coccidia of Dogs and Cats
Coccidia of fowl (poultry) Coccidia of fowl (poultry)
Chicken Chicken
- Eimeria tenella (Coecal Coccidiosis)
-- Eimeria necatrix, Eimeria necatrix,
-- Eimeria acervulina, Eimeria acervulina,
-- Eimeria maxima, Eimeria maxima, -- Eimeria maxima, Eimeria maxima,
-- Eimeria mitis, Eimeria mitis,
-- Eimeria brunette Eimeria brunette..
Turkey Turkey
-- Eimeria meleagrimimis Eimeria meleagrimimis
-- Eimeria adenoeides. Eimeria adenoeides.
Geese Geese
-- Eimeria truncate Eimeria truncate : : this species affects this species affects Kidney Kidney. .
Coccidia of Cattle Coccidia of Cattle
More than 21 species have been reported More than 21 species have been reported
-- Eimeria bovis, Eimeria bovis,
-- Eimeria zuernii Eimeria zuernii
Calves from 1-6 month of age (frequently affected).
Diarrhoea is the main clinical signs. Diarrhoea is the main clinical signs.
In most severe cases the manure may contain blood,
mucus and stringy mass of tissue.
Coccidia of Sheep and Goats Coccidia of Sheep and Goats
Eimeria arloingi, Eimeria arloingi,
E.crandalli E.crandalli, ,
E.ovina E.ovina, ,
E.parva E.parva, ,
Eimeria ahsata Eimeria ahsata
Coccidia of Camels Coccidia of Camels Coccidia of Camels Coccidia of Camels
Eimeria cameli, Eimeria cameli,
Eimeria dromedarii Eimeria dromedarii..
Eimeria leuckarfi Eimeria leuckarfi, ,
Eimeria solipedum Eimeria solipedum
Coccidia of Equines Coccidia of Equines
Coccidia of Dogs and Cats Coccidia of Dogs and Cats
Eimeria canis, Eimeria canis,
Eimeria cati Eimeria cati
Isospora cati, Isospora cati,
Isospora canis, Isospora canis,
Isospora bigeminia, Isospora bigeminia, Isospora bigeminia, Isospora bigeminia,
Isospora felis Isospora felis
Imp species are:
Isospora Isospora bigemina
Isospora Isospora hominis
Isospora Isospora belli Cause infection
Coccidia of Humans Coccidia of Humans
Diagnostic stage: oocyst
Infective stage: oocyst
Pathogenesis Pathogenesis
The term The term coccidiosis coccidiosis is usually reserved for infections caused by is usually reserved for infections caused by
Eimeria and Isospora. Eimeria and Isospora.
Coccidiosis is chiefly confined to Coccidiosis is chiefly confined to young animals young animals..
Mixed infections Mixed infections are usual. are usual. Mixed infections Mixed infections are usual. are usual.
Pathogenesis is based on the Pathogenesis is based on the destruction of epithelial cells of the destruction of epithelial cells of the
intestinal mucosa intestinal mucosa (schizonts). (schizonts).
Clinical Signs Clinical Signs
Brownish to yellowish diarrhoea Brownish to yellowish diarrhoea
Abdominal pain, Abdominal pain,
Anaemia (not so often), Anaemia (not so often),
Inappetence, Inappetence, Inappetence, Inappetence,
Weakness and loss of weight may occur. Weakness and loss of weight may occur.
Lambs may die from diarrhoea or the consequent dehydration. Lambs may die from diarrhoea or the consequent dehydration.
The mortality rate usually less than The mortality rate usually less than 10 10%. The majority recover. %. The majority recover.
E. tenella E. tenella (coecal coccidiosis) of chicken reveal massive (coecal coccidiosis) of chicken reveal massive
haemorrhages in coecum (diagnostic sign). haemorrhages in coecum (diagnostic sign).
Diagnosis Diagnosis
Microscopic detection of oocyst on faecal examination. Microscopic detection of oocyst on faecal examination.
Demonstration of schizonts and oocyst on scraping of the gut. Demonstration of schizonts and oocyst on scraping of the gut.
In birds In birds the best diagnosis is based on postmortem examination of few the best diagnosis is based on postmortem examination of few
affected birds, for the following reasons: affected birds, for the following reasons:
-- The localization and type of lesions present provide a good guide of the The localization and type of lesions present provide a good guide of the
Coccidia species which can be confirmed by examination of the oocysts Coccidia species which can be confirmed by examination of the oocysts
in the faeces. in the faeces.
Treatment Treatment
+ + Should be introduced as early as possible after diagnosis has been Should be introduced as early as possible after diagnosis has been
made made
+ + The drugs are recommended to be given for two periods of three The drugs are recommended to be given for two periods of three
days in drinking water with an interval of two days between days in drinking water with an interval of two days between
treatments. treatments. treatments. treatments.
+ + The drugs of choice are: The drugs of choice are:
-- Sulphonamides (sulphaquinqxaline, sulphadimidine) Sulphonamides (sulphaquinqxaline, sulphadimidine)
-- Amprolium is used when resistant occur to Sulphonamides. Amprolium is used when resistant occur to Sulphonamides.
Prevention and Control Prevention and Control
Based on a combination of good management and the Based on a combination of good management and the
use of anticoccidial drug. use of anticoccidial drug.
Feed lots should be kept dry and clean. Feed lots should be kept dry and clean.
Treatment: Coccidiosis is usually a herd problem. Treatment: Coccidiosis is usually a herd problem.
Therefore, treatment of the whole group with Therefore, treatment of the whole group with
Sulphonamides is recommended. Sulphonamides is recommended.
Sarcocystis Sarcocystis spp. spp.
Sarcocystis suihominis
Sarcocystis bovihominis
Sarcocystis Sarcocystis
Rare human infection
predator-prey life cycle
originally identified as 2 species
intestine ~ Isospora intestine ~ Isospora
tissue ~ Sarcocystis
Taxonomic confusion
generally named after host species
Sarcocystis bovihominis
Sarcocystis suihominis
Definitive host: dog, or cat (human- accidental)
Intermediate host: cattle or pigs (ingest oocyst
travels to muscle and becomes a sarcocyst)
Sarcocystosis Sarcocystosis
travels to muscle and becomes a sarcocyst)
Infective stage: sarcocyst (muscle of cow or pig)
Diagnostic stage : oocysts or sporozoites (stool)
Life Cycle of Sarcocystis Life Cycle of Sarcocystis
Classic predator-prey life cycle
High host specificity
Gametogony + sporogony in predator,
Schizogony tissue phase in prey
little gut pathogenecity
No immunity to re-infection develops
in predators
Human Isospora now known to be S.
bovihominis or S. porcihominis
Intestinal
Disease
undercooked meat
transient mild to severe
diarrhea
excrete sporulated excrete sporulated
sporocysts
13x10 mm
4 sporozoites
Muscle Disease
ingest sporocysts (sporadic
reports)
develop sarcocysts
several 100 mm several 100 mm
compartments
sometimes thick striated
wall
muscle tenderness
episodic inflammation
Diagnosis Diagnosis
Presence of oocyst or mature sporocysts in faeces Presence of oocyst or mature sporocysts in faeces 9 to10 9 to10
days following ingestion of infected meat (ZnSO days following ingestion of infected meat (ZnSO4 4 Flotation) Flotation)
Muscular cysts in cattle and swine Muscular cysts in cattle and swine found along length of found along length of
muscle fiber muscle fiber whitish in colour, microscopic in size, shape of whitish in colour, microscopic in size, shape of
long cylinder. long cylinder. long cylinder. long cylinder.
Cysts mostly found Cysts mostly found - - cardiac muscle, cardiac muscle,
oesophagus and oesophagus and
diaphragm of cattle and swine. diaphragm of cattle and swine.
Serology (indirect IFAT & ELISA) Serology (indirect IFAT & ELISA): Muscle infection : Muscle infection
Not useful for Not useful for
Intestinal infection Intestinal infection
Sarcocystis Sarcocystis in Muscle in Muscle
Control Measures Control Measures
Prevent Cattle & Swine from grazing in those areas which are
contaminated with Dog or Human faeces
Human and Dogs : Avoid eating raw and undercooked food
Proper sewage disposal Proper sewage disposal
Health education
Veterinary Inspection at Slaughter houses
Freezing of meat reduces number of viable cysts.
^ Clarke in 1895, observed & described as "swarm spores
lying upon the gastric epithelium of mice.
^ Tyzzer ^ Tyzzer
^ 1907, C. muris (Cryptosporidium = hidden sporocysts)
^ 1912, described (morph. & L/C ) C. parvum (S. I. of lab mice)
^ The first Human cases were reported in 1976
^ 21 species are known affecting various animals,
man, birds, reptiles and fishes
^ In humans, the main causes of disease are C. parvum
and C. hominis (previously C. parvum genotype 1).
^ C. canis, C. felis, C. meleagridis, and C. muris can
also cause disease in humans
^ Prevalent in 6 continents of world serological evidence
shows 25-35% in developed countries and 65% in
developing countries
^ 80% of calves under 1 month & 62% of healthy adult
cattle are infected
^ Reported from several states of India both in human and
animals (Nath 1999; Das et al 2006; Roy et al 2006;
Ajjampur et al 2007; Muraleedharan 2009; Paul et al
2008)
Host: Mammals, birds and Rodents
Infective stage: Sporulated oocyst (2 to 10)
Predilection site: Small intestine
Excreted in: Feces of infected host
PONTS TO REMEMBER PONTS TO REMEMBER PONTS TO REMEMBER PONTS TO REMEMBER
Excreted in: Feces of infected host
Transmission: Ingestion of food/feed and
water contaminated with fecal
matter of infected man/animals,
contact with feces, bedridden
patent caregivers and child care
workers
LIFE CYCLE
Parasitophorous
Vacuole Vacuole
80%
20%
CLINICAL SIGNS IN
MAN
Immuno-competent: Asymptomatic or self-limiting
disease with profuse watery diarrhea 8-10
days, abdominal pain, nausea, low grade
fever weight loss
Immunodeficient: Severe form with 71 evacuations Immunodeficient: Severe form with 71 evacuations
/day & fluid loss, may persist for life of
individuals, respiratory and biliary tract
infection also seen
+ Common in calves less than 2 months of age
+ Diarrhea, tenesmus, anorexia & weight loss
+ In infected rodents clinical disease do not develop
+ In other animals disease seen in immuno-
IN ANIMALS
+ In other animals disease seen in immuno-
deficient cases
+ No solid evidence that animals are
important source for man
DIAGNOSIS DIAGNOSIS DIAGNOSIS DIAGNOSIS
Hard to distinguish clinically
Demonstration of sporulated thick walled oocyst in stool/ feces
by concentration technique (Sheathers solution), Zeihl-
Neelson staining
Multiple stool specimens should be tested (at least 3) Multiple stool specimens should be tested (at least 3)
Stool specimens fresh or formalin (10%) or sodium acetate-
acetic acid-formalin fixed.
Fluorescent monoclonal antibobdy technique
Culturing of oocyst
Immuno assay or ELISA based techniques and PCR
For environmental samples concentration techniques are
needed--- water (filtration)
PREVENTION
- Avoid ingestion of raw foods contaminated with
fecal matter through water
- Avoid contact with sewage or feces
contaminated water bodies contaminated water bodies
- Filtering of water before consumption is
important as chlorination is ineffective
- Pepetide based vaccine --- under trial
- Health education and sanitary practices
Welcome
In
Presentation
On
Taenia solium
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Taenia solium
&
Taenia saginata
Anjay
Roll No. 1390
Introduction
+ Taeniosis (Greek: Tainia means bend, ribbon or tape-like structure-
tape-worm)
+ A nonfatal intestinal infection of human caused by adult
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+ A nonfatal intestinal infection of human caused by adult
cyclophyllidean cestodes; Taenia saginata & T. solium.
+ Larvae (Cysticercus, cyst or bladderworm) affects many spp of animals
& man & produce a disease K/A Cysticecosis.
+ Imp meat borne obligatory cyclo anthropozoonotic helminthosis.
+ Cysticercosis designated as a biological marker of social &
economic development of a community.
History
+ 3rd century BC: Aristophanes & Aristotle; first described Cysticercosis
in pigs.
+ 1550: Parunoli; noticed Cysticercosis in human.
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+ Described in ancient Indian medical book, the Charak Sanhita
+ Hippocrates; first documented Taenia solium.
+ 1700: Audry; first report T. saginata, but unable to distinguish
proglottids of two tapeworms.
+ 1782: Goeze; first correctly distinguish T. solium from T. saginata in
treatise on helminthology.
+ 1853: Kuchenmeister indicated cysticercus as developmental stage of
T. solium.
+ 1863: Leuckart first showed experimentally proglottids of T. saginata
fed to calves developed into cysticerci in the calf's muscles.
+ Oliver, first discover that when humans ingested "bladder worms, they
developed adult T. saginata.
Cont
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developed adult T. saginata.
+ 1888: Armstrong reported NCC in a coolie from Madras, who died to
seizure & found infected with cyst on autopsy.
+ 1912: Krishnaswamy reported cysticerci related case of muscle pain &
s/c nodules with abundant cysticerci in muscles, heart & brain at
autopsy.
+ 1934: MacArthur noticed high rate of onset epilepsy related to
cysticercosis in British army deployed in India.
Taenia solium
+ Pork or Armed tapeworm.
+ Adult: Human S.I. causing
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Adult: Human S.I. causing
taeniasis.
+ Larval stage (Cysticercus
cellulose): Pig or human tissues
causing cysticercosis.
+ DH: Man
+ IH: Pig & Man
Morphology
+ Flattened ribbon-like,
+ Creamy white in color,
Adult
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+ Creamy white in color,
+ 2-7 m long,
+ 700-1000 proglottides.
+ Consist of:
+Scolex,
+Neck,
+Strobila
Scolex
Globular,
1mm.
Scolex &Neck
Cont
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4 suckers,
1 rostellum.
22-36 hooklets arranged in a double
crown
Neck
+ Narrowest part of body (5-10 mm).
+ Budding zone containing germinative
tissue.
STROBILA
Q Immature proglottids
Q Mature proglottids
Cont
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Q Gravid proglottids
Immature proglottids:
+ Transverse rectangle,
+ Located at anterior part of
body
+ Inner organs developing
+ Width>length.
Strobila of adult
tapeworm
+ Square shape,
Mid body,
Mature proglottids
Cont
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+ Mid body,
+ Reproductive systems fully
develop (hermaphroditic).
+ Testes: 150-200 follicles.
+ A centrally straight uterus,
+ 3 lobes of ovary
+ Width=length.
+ Longitudinal rectangle,
+ Posterior body,
Gravid
proglottids
Cont
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+ Most parts of repro sys
rudimentary
+ A large, branched uterus
filled with eggs
+ Branch each side 7-13.
+ Width<length.
EGG
Cont
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LIFE CYCLE
Euzoonosis or
perfect zoonosis Obligatory
cyclozoonosis
Taeniasis
Cont
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Monkey, wild boar, camel, dog, cat, fox and roden
Porcine cysticercosis
Human
cysticercosi
s
Global distribution of T. solium cysticercosis &
taeniosis
Cont
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Geographical distribution of cysticercosis &
taeniosis T. solium in India
Cont
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Clinical Manifestations
Taeniasis.
Cysticercosis: 3 types
Cont
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Cysticercosis: 3 types
Muscular/ Subcutaneous cysticercosis
Ocular cysticercosis
Neuro cysticercosis (NCC).
PORCINE CYSTICERCOSIS
Lodge anywhere in body of pig, most
commonly in muscle & s/c fat.
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Rarely associated with symptoms.
NCC in naturally infected swine showed
excessive salivation, blinking and tearing.
No degenerative stage.
Develop:
By hetero infection: eggs in contaminated food.
HUMAN CYSTICERCOSIS
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By exogenous autoinfection: Ano-oral
contamination.
By endogenous autoinfection: Reverse
peristalsis.
The larval stage infests different tissues skeletal muscle,
diaphragm, heart, peritoneum, pleura & subcutaneous tissue
(Shankar et al 1994).
Least prevalent type, but in
India with high prevalence as
10%.
Muscular / Subcutaneous Cysticercosis
Cont
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Muscle cysticercosis cause
pain & hypertrophy & dead &
calcified cysts.
Usually found in head, limbs,
neck, abdomen & back.
Movable & painless.
Extremly rare,
2.5% prevalence in some
countries
Ocular cysticercosis
Cont
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countries
Found in vitreous body or
subretina.
Proptosis, diplopia, visual
disturbance.
Died body of worm may
provokes local inflam.
causing blindness
Most prevalent & dangerous
form.
Neurocysticercosis (NCC)
Cont
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Symptoms:
Headaches, nausea, vomiting,
Blurred vision, neurologic
change,
Acute confusion, IC
pressure,
Focal neurologic deficit,
intellectual deficit.
Epilepsy (70% cases).
FORM OF NCC
4 stages of development & regression of cysticercus in CNS.
Cystic or vesicular stage:
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Viable & composed of well-defined, fluid-filled
membrane, contain scolex.
Degenerating, colloid or granular stage:
Corresponds to parasite necrosis & inflam process.
Appear as eosinophilic structures contain components
of bladder & disintegrated scolex & tissue surrounded
by multinuclear giant cells, foamy macrophages &
neutrophils.
Nodular stage:
Fibrosis develops recognized as a nodule of smaller
size than the bladder.
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size than the bladder.
Mineralization & calcification stage:
Partial dystrophic calcification of necrotic larva or
presence of cysticercal calcareous corpuscle.
Taenia saginata
Worldwide zoonotic cestode.
Beef / unarmed tapeworm.
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Larvae (Cysticercus bovis) in cattle (IH) musculature; bovine
cysticercosis
Adult worms in human (DH) SI; taeniasis.
Approx 50 million cases of infestation worldwide & 50,000
deaths (human) annually.
Economic losses in cattle production due to downgrading &/or
condemnation of carcasses as untreated infected meat an
important source of zoonosis.
Biological differences between T.
solium and T. saginata
Adult T. solium
T. saginata
Length 2-7 meters 5- 12 (24) meters
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Scolex 1 mm in diameter with
4 suckers, 1 rostellum
& 22- 36 hooklets.
2 mm in diameter, with
4 suckers but no
rostellum & hooklets.
Number of segment 700 to 1000 (< 1000) 1000 to 2000 (~ 2000)
Mature proglottid 3 lobes of ovary 2 lobes of ovary
Gravid proglottid 7-13 uterine lateral
branches on one side
15-30 uterine lateral
branches on one side
Adult T. solium
T. saginata
No. of gravid
proglottid detached
Several segments Single segment
Cont
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proglottid detached
Mode of proglottids
passing out
Passively expelled Actively migrate out
of anus
Cysticercus Scolex with hooklets
in man & pig
No hooklets on
scolex only in cattle
Disease in man Taeniasis &
Cysticercosis
Taeniasis
Egg
Spherical, 31- 43 m diameter, thick radially
striated brown embryophore. oncosphere
with 6 hooklets.
Life cycle of T. saginata
Cont
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CLINICAL SIGNS IN CATTLE
+ Oncospheres develop in skeletal & cardiac muscles
& in fat & visceral organs.
Mild symptoms: Increased pulse & respiratory rates,
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+ Mild symptoms: Increased pulse & respiratory rates,
slight increase in body temp. depending on dose of
infection.
+ Local inflammatory reactions (Oryan et al., 1998).
+ Heavy infestation by larvae
Myocarditis or heart failure.
Clinical signs in Human
+ HUMAN
Infestation with mild symptoms:
Nausea,
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Nausea,
Abdominal discomfort,
Epigastric pain,
Diarrhea,
Vitamin deficiency,
Excessive appetite or loss of appetite,
Weakness
Loss of weight
Digestive disturbances
Intestinal blockage.
DIAGNOSIS IN HUMANS
+ By finding gravid proglottides or egg in stool.
Direct fecal smear.
Cont
Taeniasis
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Brine floatation technique.
Cellophane-tape technique.
Scotch tape test.
+ Fecal concentration techniques (Kato thick
smear, Formyl ether).
+ Taenia antigens in stool.
Clinical Manifestations
Cysticercosis
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Neuroimaging / Radiological:
CT: Sensitivity and specificity over 95%.
MRI: Most accurate technique to assess degree of
infection, location & evolutionary stage of
parasites.
Electroimmunotransfer Blot:
Utilizes lentil-lectin purified glycoproteins (LL-GP) diagnosis
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Utilizes lentil-lectin purified glycoproteins (LL-GP) diagnosis
of T. solium cysticercosis based on antibody detection.
Enzyme-Linked Immunosorbent Assay
Antibody detection ELISA
Antigen detection ELISA
Dot ELISA
DIAGNOSIS OF CYSTICERCOSIS IN CATTLE
Carcass inspection:
Partial incision & inspection of target organs/muscle groups:
heart, masseters, tongue, triceps brachii & diaphragm;
search of T. saginata cysts.
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search of T. saginata cysts.
Enzyme-Linked Immunosorbent Assay
Antibody detection ELISA: 3 weeks post-infection
Antigen detection ELISA
Electroimmunotransfer Blot
Dipstick-immunoassay
Dot-ELISA
DIAGNOSIS OF CYSTICERCOSIS IN PIGS
Carcass inspection:
More sensitive to detect dead, degenerated, or calcified cysticerci;
but most likely to miss quite a number of viable cysticerci (same
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but most likely to miss quite a number of viable cysticerci (same
pinkish-red color as meat).
Partial incision & careful observation in predilection sites: heart,
masseters, tongue, & triceps brachii (Boa et al., 2002).
Tongue palpation:
Detection of T. solium cysts in live pigs by palpation and visual
inspection (high specificity (100%), but generally low sensitivity).
Electroimmunotransfer Blot :
Most sensitive and specific assays for the detection of antibodies
specific to T. solium cysticercosis in pigs
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specific to T. solium cysticercosis in pigs
Enzyme-Linked Immunosorbent Assay
Antibody detection ELISA: assay detects IgG
Antigen detection ELISA
Revised Diagnostic Criteria for NCC
Absolute:
Histological demonstration of parasite from biopsy of
brain or spinal cord lesion.
Cystic lesions with scolex on CT or MRI.
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Cystic lesions with scolex on CT or MRI.
Direct visualization of sub retinal parasite by
fundoscopy
Major:
Lesions highly suggestive of NCC on neuroimaging
Positive serum EITB for detection of anticysticercal
antibodies
Resolution of cysts after antiparasitic therapy
Spontaneous resolution of small single enhancing
lesions
Minor:
Lesions compatible with NCC on neuroimaging
Clinical manifestations suggestive of NCC
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Clinical manifestations suggestive of NCC
Positive CSF-ELISA for detection of anticysti-
cereal Ab or cysticercal Ag
Cysticercosis outside CNS
Epidemiologic:
Evidence of household contact with T solium
infection.
Individual coming from living in endemic area.
History of travel to endemic area.
Treatment
Pumpkin seed
Areca nut
Cont
Taeniasis
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Drug of choice
Drug Adult Pediatric
Praziquantel 5-10 mg/kg once 5-10 mg/kgonce
Niclosamide 2 gm once 50 mg/kg once
+ Outside nervous system:
Benign disorder not merit specific treatment
Cont
Cysticercosis
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+ Neurocysticercosis
Surgical or cyst excision or
Ventricular shunts or steroids to decrease inflam
Praziquantel
Albendazole.
GUIDELINES FOR TREATMENT OF NEURO-CYSTICERCOSIS
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ARGUMENTS
3 major arguments against use of cysticidal therapy in
NCC:
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Immediate risks because of neurologic symptoms due
to acute inflammation results from death of cysts.
Long-term prognosis of underlying seizure disorder
may worsen because of increased scarring due to acute
inflammation.
Treatment may be unnecessary since most cysts die by
themselves within a short period.
PREVENTION & CONTROL MEASURES
Public hygiene & health education.
Avoid eating raw bean-pork or beef.
Cont
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Avoid pigs or cattle eating human stool.
Sanitary inspection of slaughter.
Buying only officially inspected meat,
Carcasses irradiation.
Cooking of beef at 57
o
C, refrigeration at -20
o
C or less for 2
days, pickling meat in 25% salt solution for 5 days.
Cont
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Sanitary disposal of night soil.
Stool examination of food handlers from endemic countries
Avoid eating uncooked vegetables & fruits that cannot be
peeled while traveling in developing countries (NCC).
Adequate meat inspection: most important public health
measure practised in controlling transmission cycle of parasite.
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measure practised in controlling transmission cycle of parasite.
Mass chemotherapy (using praziquantel &/or albendazole &
praziquantel or niclosamide).
Vaccination of pigs.
Recombinant Vaccines against Cysticercosis
Cont
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Filariasis
Nine filarial nematodes - humans act as their definitive host.
Divided into 3 groups according to the niche within the body that they occupy
1. Lymphatic filariasis (Elephantiasis)
Wuchereria bancrofti, Brugia malayi, and Brugia timori.
2. Subcutaneous filariasis 2. Subcutaneous filariasis
Loa loa (the African eye worm), Mansonella streptocerca, Onchocerca volvulus
(River blindness), and Dracunculus medinensis (the guinea worm).
3. Serous cavity filariasis
Mansonella perstans and Mansonella ozzardi - serous cavity of the abdomen.
Transmitting vectors are either blood sucking insects (flies or mosquitoes)
Dracunculus medinensis. - copepod crustaceans
Lymphatic Filariasis
Wuchereria bancrofti (Culex spp.)
Brugia malayi (Mansonia spp.)
Brugia timori (Anopheles / Mansonia spp.)
Bite of
infected
mosquito
- All the parasites have similar life cycle in man
- Adults seen in Lymphatic vessels
- Offsprings seen in peripheral blood during night
Distribution
World wide - Tropical and Sub-tropical regions of
- Africa
- Asia
- Western Pacific - Western Pacific
- Parts of Central & South America
Social & Environmental Factors
Associated with
- Urbanization (Industrialization)
- Poverty, Illiteracy and Poor sanitation.
- Climate and Environment : - Climate and Environment :
- The breeding of mosquito
- Longevity (Optimum temperature 20-30
0
C & Humidity 70%)
- The development of parasite in the vector
- Sanitation, Town planning, Sewage & Drainage.
Host Factors
Man Natural Host
Age All age (6 months) Max: 20-30 years
Sex Higher in men
Migration leading to extension of infection to non-endemic
areas
Immunity may develop after long year of exposure (Basis of
immunity-not known)
Lymphatic Filariasis Endemic Countries & Territories
Endemic Countries
Global Scenario
Population
at risk : 1.2 Billion
No. of countries : > 80
Carriers : 76 Million
Diseased : 44 Million
Hydrocele : 27 Million
Lymphoedema : 16 Million
TPE : 1 Million
National Scenario
Population at risk : 45.4 C
(in 16 States & 5 UTs)
Total infected : 51.7 M
(Wb - 99.4 % and Bm - 0.6 %)
No. of diseased : 22.5 M No. of diseased : 22.5 M
Disease Manifestation
Disease manifestation range from
None
Acute-Filarial fever
Chronic-Lymphangitis, Lymphadenitis, Elephantiasis of
genitals/legs/arms
Tropical Pulmonary Eosinophilia (TPE) Tropical Pulmonary Eosinophilia (TPE)
Filarial arthritis
Epididimoorchitis
Chyluria, etc.
Transmission & Incubation Period
Lymphatic Filariasis is transmitted by the bite of Infected
mosquito which harbours L
3
larva.
L
1
: 1-3 hours
L
2
: 3-4 days
L
3
: 5-6 days
Pre-patent period: (L
3
to Mf) Not known Pre-patent period: (L
3
to Mf) Not known
Clinical Incubation period: 8-16 months
Diagnosis
1. Demonstration of microfilarae in the peripheral blood
Thick blood smear: 2-3 drops of free flowing blood by finger
prick method, stained with JSB-II
Membrane filtration method: 1-2 ml intravenous blood filtered
through 3m pore size membrane filter
DEC provocative test (2mg/Kg): After consuming DEC, mf
enters into the peripheral blood in day time within 30 - 45
minutes. minutes.
2. Immuno-Chromatographic Test (ICT)
Circulating Filarial Antigen detection is regarded as Gold
Standard for diagnosing Wuchereria bancrofti infection.
Can detect ;
Q Amicrofilaraemic
Q Lymphoedema
Q Elephantiasis.
3. Quantitative Blood Count (QBC)
Though quick it is not sensitive than blood smear examination.
4. Ultrasonography
can locate and visualize the movements of living adult worms of W.b.
5. Lymphoscintiography
inject radio-labelled albumin or dextran in the web space of the toes.
The structural changes can be imaged using a Gamma camera.
Lymphatic dilation & obstruction can be directly demonstrated even in Lymphatic dilation & obstruction can be directly demonstrated even in
early clinically asymptomatic stage of the disease.
6. X-ray Diagnosis
X-ray are helpful in the diagnosis of Tropical pulmonary eosinophilia.
7. Haematology
Increase in eosinophil count
Clinical Manifestations
Manifestations are 2 types
1. Lymphatic Filariasis (Presence of Adult worms)
2. Occult Filariasis (Immuno hyper responsiveness)
Clinical Spectrum
None
Asymptomatic
microfilaremia
Filarial
fever
Chronic
pathology
TPE
Stages in Lymphatic Filariasis
Four stages :
+ Asymptomatic amicrofilariaemic stage
+ Asymptomatic microfilariaemic stage + Asymptomatic microfilariaemic stage
+ Stage of Acute manifestation
+ Stage of Obstructive (Chronic) lesions
1. Stage of Asymptomatic amicrofilaraemic
- Does not show mf or clinical manifestation
- Laboratory diagnostic techniques are not able to detect infected cases
2. Stage of Asymptomatic Microfilariaemic
- asymptomatic for months and years
- important source of infection
- detected by Night Blood Survey and other suitable procedures.
3. Stage of Acute Manifestation
- Acute inflammation in the lymph vessel/node of the limb & scrotum
Clinical manifestations are consisting of:
Filarial fever (ADL-DLA) Filarial fever (ADL-DLA)
Lymphangitis
Lymphadinitis
Epididimoorchitis
4. Chronic Manifestation
- takes 10-15 years.
- permanent damage to the lymph vessels.
- Initially, it starts with pitting oedema which gives rise to browny oedema leading
to hardening the tissues. Still late, hyper pigmentation, caratosis, wart like lesions
are developed. Eg. Hydrocele (40-60%), Elephantiasis of Scrotum, Penis, Leg,
Arm, Vulva, Breast, Chyluria
Tropical Pulmonary Eosinophila
- Classical clinical manifestation mf will be absent.
- result of hyper responsiveness to filarial antigens
- Seen more in males.
- Clinical signs: cough and wheezing, low grade fever, scandy sputum
with occasional haemoptysis, adenopathy and increased eosinophilia.
- X-ray shows diffused nodular mottling and interstial thickening.
Classification of Lymphoedema
Lymphoedema is classified into 7 stages on the basis
of the presence & absence of the following:
1. Oedema
2. Folds
3. Knobs
Mossy foot 4. Mossy foot
5. Disability
Stages of Lymphoedema of the Leg (Stage I)
Swelling reverses at night
Skin folds-Absent
Appearance of Skin-Smooth, Normal
Stages of Lymphoedema of the Leg (Stage II)
Swelling not reversible at night
Skin folds-Absent
Appearance of skin-Smooth, Normal Appearance of skin-Smooth, Normal
Stages of Lymphoedema of the Leg (Stage III)
Swelling not reversible at night
Skin folds-Shallow
Appearance of skin-Smooth, Appearance of skin-Smooth,
Normal
Stages of Lymphoedema of the Leg (Stage IV)
Swelling not reversible at night
Skin folds-Shallow
Appearance of skin
- Irregular,
* Knobs, Nodules * Knobs, Nodules
Stages of Lymphoedema of the Leg (Stage V)
Swelling not reversible at night
Skin folds-Deep
Appearance of skin Smooth or Appearance of skin Smooth or
Irregular
Stages of Lymphoedema of the Leg (Stage VI)
Swelling not reversible at night
Skin folds-Absent, Shallow, Deep
Appearance of skin *Wart-like Appearance of skin *Wart-like
lesions on foot or top of the toes
Stages of Lymphoedema of the Leg (Stage VII)
Swelling not reversible at night
Skin folds-Deep
Appearance of skin-Irregular
Needs help for daily activities - Needs help for daily activities -
Walking, bathing, using
bathrooms, dependent on
family or health care systems
Management of Lymphatic
Filariasis
1. Treating the infection
2. Treatment and prevention of Acute ADL attacks
Treatment and prevention of Lymphoedema 3. Treatment and prevention of Lymphoedema
Chemotherapy of Filariasis
Drugs effective against filarial parasites
1. Diethyl Carbomazine citrate (DEC)
2. Ivermectin
3. Albendazole
4. Couramin compound
Diethyl Carbomazine Citrate
(Hetrazan, Banocide, Notezine)
Mode of action: DEC do not have direct action of parasite but mediate
through host immune system.
Very effective against mf (Microfilariacidal)
Lowers mf level even in single dose
Effective against adult worms in 50%of patients in sensitive cases.
Dose: 6mg/Kg/12 days Dose: 6mg/Kg/12 days
Recent dosage: 6mg/Kg single dose
Adverse reactions are mostly due to the rapid destruction of mf which
is characterised by fever, nausea, myalgia, sore throat, cough,
headache.
No effect on the treatment of ADL
Drug of choice in the treatment of TPE.
Ivermectin
Mode of action: Directly acts on mf and no action on adults.
Very effective against mf (Microfilariacidal)
Lowers mf level even in single dose of 200g 400g/Kg body weight
No action on TPE No action on TPE
Drug of choice in Co-endemic areas of Onchocerciasis with LF.
Adverse reactions are lesser but similar to that of DEC
Microfilariae reappears faster than DEC
Albendazole
This antihelmenthic kills adult worms
No action on microfilariae
Dose: 400mg/twice day /2 weeks
With combination of DEC & Ivermectin, it enhances the action of the
drugs.
It induces severe adverse reactions in hydrocele cases due to the
death of adult worms.
Surgical Treatment
Hydrocele: Excision
Scrotal Elip: Surgical removal of Skin & Tissue,
preserving penis and testicles.
Lymphoedema (Elephantiasis): Excision of redundant
tissue, Excision of subcutaneous and fatty tissues
postral drainage and physiotherapy
Lymphatic Filariasis Control Programme
The current strategy of filariasis control (Elimination) is based on:
1. Interruption of transmission
2. Control of Morbidity
a. Chemotherapy
b. Vector control
Note:
There are three main reasons why filariasis never causes explosive
epidemics
1. The microfilariae does not multiply in the vector
2. Infective larvae do not multiply in man
3. Life cycle of the parasite is relatively long (>15 )
3. Case detection and treatment
4. In high endemic areas, Mass chemotherapy is the approach.
5. DEC medicated salt is also a form of Mass treatment using low dose
of drug over a long period of time (1-2 gm /Kg of Salt).
Lymphatic Filariasis Control Programme
of drug over a long period of time (1-2 gm /Kg of Salt).
Vector Control
Vector control involves integrated approach:
- anti larval measures,
- anti adult measures,
- personal prophylaxis.
Anti larval measures Anti larval measures
1. Chemical control
- Mosquito larvicidal oil
- Pyrosene oil
- OP compounds such as Temephos, Fenthion,
2. Removal of pistia plants
3. Minor environmental measures
Vector Control
Anti adult measures
Indoor residual spay using DDT, HCH, Pyrethrum and Dieldrin.
Personal Prophylaxis
Reduction of man mosquito contact
- mosquito nets,
- Mosquito repellents
- screening of houses, etc.
Filariasis in Animals
Cattle
Verminous haemorrhagic dermatitis : Parafilaria bovicola.
Intradermal onchocercosis : leather loss
Onchocerca dermata, Onchocerca ochengi, Onchocerca dukei. Onchocerca ochengi.
Horses Horses
Summer bleeding : hemorrhagic subcutaneous nodules in the head and upper
forelimbs,
Parafilaria multipapillosa
Dogs
Heart filariasis - Dirofilaria immitis
GNATHOSTOMIASIS
Rajagunalan S.
Roll No: 1392
Introduction
It was first described by Owen 1836 from gut of a
tiger
Etiology: Ganthostoma spinigerum
Host: Wild carnivores, Cats and Dogs Host: Wild carnivores, Cats and Dogs
Man act as paratenic host
The condition in man is characterised by
appearance of hard, non-pitting subcutaneous
swellings on the upper extremities and other parts
of the body
Prediliction site: stomach of wild
carnivores and other hosts
Eggs are ovoid and transparent possesses
a mucous plug at one ploe, shows pitted a mucous plug at one ploe, shows pitted
surface and is un-embryonated
Lifecycle
DH and man acquire infection by ingestion of fish infected with
third stage larvae
In man the larvae do not undergo any further development
In DH the adult always induces productuion of tumour like
mass in the stomach
Eggs are passed in the feaces which hatches upon contact with
water
The motile larvae are ingested by cyclops first IH
The second IH can be fish, frogs, snakes inest cyclops and
further devlopment occurs in the fleshes of these animals
DH gets infected by ingesting the infected fishes
Pathogenicity
Causes devlopment of tumour like mass in digestive tract of
DH with one or more adult worms inside mass
Gnathostomiasis interna------ not in man
In man the third stage larvae migrate in visceral organs and In man the third stage larvae migrate in visceral organs and
S/C producing intermittent or migratory swellings---
Gnathostomiasis externa
Creeping erruptions and swelling of S/C and
musclesallergic response
Swelling are hard and non pitting
Infection in Man
Can cause visceral larval migrans in any
parts of the body
Migration of larvae along SPC or brain
causes paralysis causes paralysis
Worms have been removed from urinary
baldder, respiratory tract and eye
Larvae can also cause CLM or creeping
erruptions
In animals
Tumour like mass in the stomach in DH
Diagnosis
Demonstration of characteristic larvae in
surgical specimens
A positive skin test with adult and larval A positive skin test with adult and larval
antigen helps in diagnosis
Treatment & control
Surgical removal of lesion along with worm
is the only mode of treatment.
Mebedazole in high doses can be tried in
man. man.
Proper cooking of fishes
Hydatid disease (Hydatidosis)
Echinococcus spp.
- Echinococcus granulosus
- Echinococcus vogeli
hydatid disease
- Echinococcus multilocularis - alveolar hydatid disease
- produces many small cysts
Life Cycle Life Cycle
Definitive Hosts
E. granulosus
- Dogs
- Coyotes
- Wolves
E. multilocularis
- Mostly foxes
Intermediate Hosts
E. granulosus
- Sheep
- Horses
- Camels
- Pigs
E. multilocularis
- Small rodents
- Pigs
- Humans
Morphology of Hydatid Cyst
Fibrous layer
Laminated layer
Germinal layer
Hydatid sand
Exogenous
daughter cyst
Individual proscolices Brood capsules
Hydatid sand
Daughter cyst
daughter cyst
Hydatid fluid
Pathogenesis and Clinical Picture
According to the site of cyst
1- No symptoms
Hepatic cyst (66%)
2- Obstructive jaundice
3- Rupture:
Secondary new cysts
Allergic manifestations
Anaphylactic shock
Pathogenesis and Clinical Picture
Haemoptysis, transient thoracic pain
and shortness of breath.
Pulmonary cyst (about 22%)
Cyst present within lung tissue cause:
and shortness of breath.
Cyst transforms into chronic pulmonary
abscess:
Sudden attack of cough with sputum
containing frothy blood, mucus and
hydatid material.
Pathogenesis and Clinical Picture
Brain cyst (about 1%)
Increased intracranial tension - epilepsy
Headache
Renal cyst (about 3%)
Intermittent pain & haematuria
Hydatid sand may be present in urine.
Pathogenesis and Clinical Picture
Osseous cyst (about 2%)
Bone Erosion
Trabeculae Destruction
Spontaneous Fracture Spontaneous Fracture
Fibrous layer
Laminated layer
Germinal layer
Normally hydatid cyst
wall is 3 layered
Osseous cyst wall is
one layered
Diagnosis of Hydatid Cyst
2- Computerized tomography & ultrasonography
1- X-ray imaging
2- Computerized tomography & ultrasonography
3- Aspiration cytology
Diagnosis
4- Intradermal test of Casoni
May give false positive results in 18%
May give allergic reactions
5- Serological tests
6- Molecular diagnosis
Detection of parasite DNA in patients serum
-By IHA to detect anti-hydatid antibodies in patients serum
-By ELISA to detect hydatid antigen
-By immunoelectrophoresis to detect serum antibodies against antigen 5
Treatment
1- Surgical removal
2- PAIR Technique
Percutaneous
Aspiration needle
Percutaneous
Aspiration
Injection
Reaspiration
Done under sonographic or CT guidance.
3- Medical treatment
Albendazole
Praziquantel
Control Measures
E Dogs prevent them
from getting infected
E Human - avoid ingesting
food or other substances food or other substances
contaminated with dog
feces
E Disrupt the lifecycle
Basic hygiene practices
Avoid feeding raw offal
INERMICAPSIFERIASIS
S. Rajagunalan
Roll No: 1392
Introduction
A cestode infection caused by Inermicapsifer
madagascariensis (I. cubensis and I. arvicanthidis)
It is about 27cm to 42cm long and 2.3mm width, has It is about 27cm to 42cm long and 2.3mm width, has
350 proglottids
Gravid segment encloses 150-175 capsules containing
6 or more eggs
Life cycle
Life cycle is unknown but by analogy with Rallietina it is believed
that arthropods acts as intermediate host.
It is a parasite of rodents occasionally in man.
Cases in man have been reported from Congo, Kenya, Madagascar,
Philippines, Thailand
It is believed that larval stages develop in the arthropods after
ingestion of eggs of cestodes from fecal matter of DH.
DH gets infected by ingestion of IH containing larvae
In Africa: Rodent Arthropod Rodent cycle
Outside Africa: Man Arthropod Man cycle occurs
Disease
The Parasitosis is generally unaccompanied by
clinical symptoms
Mild gastrointestinal disturbances like loss of Mild gastrointestinal disturbances like loss of
appetite, abdominal pain can be observed
Diagnosis
By examination of stool/ Feces for proglottids
Treatment and Control
The condition can be effectively treated with Niclosamide
Rodent control and environmental hygiene
Larva Migrans
DURGA PRASAD DAS
LARVA MIGRANS
Prolonged migration of immature(larval) stages of
parasitic worms in various parts of body
Migration occuurs one of 3 forms
- Cutaneous larva migrans- animal hook worms
- Visceral larva migrans- round worms of dogs & cats
- Occular larva migrans- -------------do-------------
Animals-Dogs,Cats,Pigs,Rabbits,Lambs,Cattles &
Non human primates
Human
History
Rober Lee(1874)-
- Described syndrome of cutaneous lesions by larvae of
Ancyclostoma -under name of Creeping eruption
Beaver (1956) & Beaver et al. (1952)-
- Observed larvae of dog ascarid(T.canis)-can enter
internal organs of man
- Differentiation betwwen 2 larva migrans-CLM & VLM
Transmission of Larva migrans
Animals get worm larvae
- From mother before birth
- From mother while nursing
- Oral-Ingesting worm eggs from feces in env. Oral-Ingesting worm eggs from feces in env.
- Eating other infested animals (cat eating rodents)
Human get infected
- By direct contact-penetration thr.skin
- By accidental ingesting parasitic eggs
- By eating tissues from infested animals
Common signs of Larva migrans
IN ANIMALS
- Most animals-no signs of illness
- Young animals-diarrohea (die-if worms in large no.)
- Some worm spp.-migrate to brain & sp.cord-
incordination,trembling & circling-manytimes fatal
IN HUMAN
- CLM-Raised redened tracts or lines in affected area(foot
or arm)
- VLM-Vary dependind on organs infested
- OLM-Vision problem-blindness
Cutaneous Larva
Migrans
CREEPING ERUPTION,
GROUND ITCH
Etiology
Prolonged migration in skin by-
larvae of hookworms
Ancylostoma caninum
Ancylostoma braziliensis
Uncinaria stenocephala
larvae of other nematodes
Strongyloides stercoralis Strongyloides stercoralis
Gnathostoma spinigerum
Cappillaia spp.
Eggs are found in dog or cat feces and can be contracted even through intact
skin while walking barefoot or lying on the ground
Cutaneous larva migrans-TRANSMISSION
Direct penetration of the skin by hookworm 3rd stage larvae,
which develop in the environment from eggs shed in dog or cat faeces.
Lifecycle
LIFE CYCLE OF A.caninum

Dog
&cat
Dog
&cat
SOIL
3
RD
LARVA Eggs in feces
Dermal
route
HUMAN
Epidemiology
Mostly in worm & damp climates in localites with
sandy soils-favourable for larval survial
Commonly in children-play in places polluted with
exretas of dogs & cats
In persons-work on plumbing/electrical wiring- In persons-work on plumbing/electrical wiring-
come in contact with damp soil laden with larvae
In South Asian countries- highly prevalent among
- sweet potato growers
- rice field workers
- tea picking labours
Signs and Symptoms
Invading skin-redish itchy papules
In 2-3days serpiginous channels in str.germinativum
This lesion-erythematous-then elevated & vesicular
Larvae travel under the skin a few millimeters/cms a day,
leaving itchy red trackstunnel-dry& crusty
Irritation-pruritus-scratching-pyogenic infection Irritation-pruritus-scratching-pyogenic infection
Eosinophilia in 65% children affected with creeping
eruption
Lesion-single/multiple
Foot ,ankle ,hands - most common sites
Occasionally massive infection-cutaneous lesions over
large areas of body may penetratevaginal& anal mucosa
The larvae can migrate for weeks,even months but cant
reach circulation.
Diagnosis
Detecting signs, size of skin lesions and at numerous
locations
Seeing elevated tortuous chr. of tunnels under snin.
TREATMENT
Mebendazole 100 mg BID x3 days
OR
Albendazole 400 mg OD x3 days
Visceral Larva Migrans
Toxocariasis; Ocular larva migrans; Toxocariasis; Ocular larva migrans;
Larva migrans visceralis
Visceral larva migrans
Extra intestinal migration of larval nematodes of
lower animals (dogs and cats)-
in human tissues in human tissues
chr.ed by-chronic granulomatous lesions
Etiology
Larvae of worms ( parasites) that infect the
intestines of dogs and cats.
Dog parasite - Toxocara canis
Cat parasite - Toxocara cati
Eggs produced by these worms are in the feces Eggs produced by these worms are in the feces
of the infected animals.
By larval stages of Other nematodes
Gnathostoma spinigerum
Cappillaria hepatica (of rodents)
Ascaris suum
Dirofilaria spp.
Epidemiology
Usually in children(1-5yrs)-habit of dirt eating
P.H.importance-
- GreatBritain (20.7% dogs exrete Toxocara eggs)
- INDIA (A.P.-667%,Karnatak-26.23%,T.N.-16.28%) - INDIA (A.P.-667%,Karnatak-26.23%,T.N.-16.28%)
Transmission
The feces mix with soil, allowing the infection to
spread to humans
Humans may get infected
- if they eat unwashed raw vegetables that grew in the
infected soil
- by eating raw liver - by eating raw liver
Young children with pica - at highest risk
But this infection can also occur in adults
After a person swallows the contaminated soil, the
worm eggs break open in the gastrointestinal tract
Carried throughout body to various organs, such as
the lungs, liver, and eyes
Brain, heart, and other organs can also be affected.
LIFECYCLE
Traceal migration
Occurs in puppies (few wks.-<3 months of age)
After ingestion eggs hatch in S.I. -2
nd
larva comeout
Reach liver in 2 days of infection
Pass thr. Lungs via hepatic vein,heart &pulmonary Pass thr. Lungs via hepatic vein,heart &pulmonary
artery-peak at 5 days of infection
Pass to tracheal side of lungs-migrating into
alveoli,bronchioles & trachea
Eventually swallowed-to reach somach on 10
th
day
They moult into adult
Somatic migration
Occurs on adult bitch
2
nd
stage larvae migraqte to different tissues of
body after 8days of infection
At this stage in liver,lungs and kidney-no dev.
Mobilization of larvae after 42 days of preg.
After reaching liver-larvae mpoult-3
rd
stage After reaching liver-larvae mpoult-3
rd
stage
At birth of puppies -3
rd
stage remain in lung
Here moult to 4
th
stage
By end of 2
nd
wk after birth moult to 5
th
stage
By end of 3
rd
wk after birth-adult may be
present
Symptoms
Mild infections may not cause symptoms
More serious infections may cause the following symptoms:
- Abdominal pain
- Cough
- Pica
- Fever
- Irritability
- Itchy skin (hives)
- Shortness of breath
- Wheezing
Possible Complications
Blindness/Dicreased visual activity
Encephalitis (infection of the brain)
Heart arrhythmias
Respiratory distress
Hepatomegaly
Allergic pneumonia
- Wheezing
Granulomatous lesions-in organs of children-liver,lungs,brain
sometimes eyes
Eosinophilia
- 80% cases reach 50%;somecases 90%
- Chronicity-lasts for>2yrs.
Leucocytosis (count>20,000/mm3)
Chiefly a condn of children 18months-5yrs of age
If eyes - infected (ocular larva migrans)-chorioretinitis-loss of vision and
crossed eyes(strabismus) may occur
Allergic pneumonia
Diagnosis
Demonstration of Lesions-typical granulomatous
Demonstration of larva in biopsy material
Signs of -swollen liver, rash, and lung or eye
problems problems
Tests may include:
Complete blood count
Serology for anti-Toxocara antibodies
(CFT,IFAT,IHA,ELISA)
Treatment
This infection usually goes away on its own and may
not require treatment
Some people may need anti-parasitic drugs such as
Albendazole Albendazole
Prognosis
Rare-Severe infections involving the brain or heart -
death
Prevention
De-worming dogs and cats
Preventing dogs and cats from defecating in public areas
Keeping children away from areas where dogs and cats
may defecate
Keep play areas,lawns gardens free from animal wastes Keep play areas,lawns gardens free from animal wastes
Regular disposing of pet feces & covering sand boxes
when not in use
Important - carefully washing hands after touching soil
or animals
T o kill larvae in soil spray strong salt soln. or borax
^ In 1903 Sir William Leishman reported parasite from
spleen of a soldier in England, conracted from Dum Dum,
India
^ In the same year Charles Donovan demonstrated similar
parasite from a patient suffering from Kala-azar in India.
^ The sand fly was incriminated as vector by Indian Kala-
azar commission
^ The disease is both anthroponotic and zoonotic in nature
^ Human infection is caused by about 21 of 30 species
^ Include 2 subgenera
^ L. donovani complex with three species (L. donovani, L. ^ L. donovani complex with three species (L. donovani, L.
infantum, and L. chagasi)
^ L. mexicana complex with four main species (L. mexicana, L.
amazonensis, and L. venezuelensis)
^ L. tropica; L. major; L. aethiopica; and the subgenus Viannia with
four main species (L. (V.) braziliensis, L. (V.) guyanensis, L. (V.)
panamensis, and L. (V.) peruviana)
^ Leishmaniasis is endemic in tropical, subtropical and
southern Europe
^ Commonly reported from India, Afganistan, Iran, sudan,
South America,etc.,
^ Causes three form of disease
^ Cutaneous ^ Cutaneous
^ Mucocutaneous
^ Viseral lesihmaniasis
^ Has two developmental stages
^ Amastigote- man and other animals
^ Promastigote gut of Phlebotomus
^ Host: Man, Dogs, marsupials, Rodents
^ Infective stage: Promastigote
^ Predilection site: Macrophages and RES ^ Predilection site: Macrophages and RES
^ Vector : Phlebotomus and Lutzomia
^ Transmission: Bite of infected sandfly
Bite of sandfly (Promastigote)
Enter macrophages cutaneous mainifestations
Amastigote and multiplies by binary fission
Multiplies RES of different visceral organs
(spl, liv, BM, LN, Intestine) (spl, liv, BM, LN, Intestine)
Hyperplasia and enlargement of organs (spleen)
Hematopoesis decreased (granulocytopenia, thrombocytopenia &
anemia)
Severe mucosal hemorrhages (intestine)
Ulceration and 2
0
bacterial infection diarrhea
^ Cutaneous leishmaniasis the most common form--a sore at the bite site,
which heals in a few months to a year, leaving an unpleasant looking scar
called as LCL . This form can progress to any of the other three forms.
^ Diffuse cutaneous leishmaniasis this form produces widespread skin
lesions which resemble leprosy and is particularly difficult to treat.
^ Mucocutaneous leishmaniasis commences with skin ulcers which spread
causing tissue damage especially to nose and mouth.
^ Visceral leishmaniasis the most serious form and potentially fatal if
untreated. a markedly enlarged spleen\
^ PKDL- seen after cure
^ Dogs may exhibit lesions similar to that of visceral
and Cutaneous leishmaniasis
^ Lesions are also seen in equines, donkeys
^ Clinical signs
^ Physical exam may show signs of an enlarged spleen, liver, and
lymph nodes. The patient may have been bitten by sandflies, or
was in an area known for leishmaniasis.
^ Tests that may be done to diagnose the condition include: ^ Tests that may be done to diagnose the condition include:
^ Biopsy of the Spleen, Bone marrow and culture
^ Lymph node biopsy and culture
^ Direct agglutination assay
^ Indirect immunofluorescent antibody test
^ Montenegro skin test
^ Skin biopsy
^ No vaccine available
^ Can be treated with pentavalent antimonial
compounds and amphoteracin B
^ Vector control measures
^ Reduce the reservoirs and exposure vectors
Paragonimiasis
Chronic disease caused by Paragonimus
westermani (lungs), P. szechuanensis &
several other related spp.
Characterized by cough, chest pain, rusty
sputum & hemoptysis (P. westermani ) &
subcutaneous nodules (P. szechuanensis).
By eating raw crayfish & freshwater crab.
Paragonimus westermani infection occurs in Asia Central-
West Africa South America.
Morphology
Adult worm:
Monoecious, two
suckers & parallel
reproductive organs,
Eggs: Golden brown,
ovate, operculate, 80-
120 48-60 m.
Metacercariae: round
or ovate. Diameter
300-400 m, 1-3
layers of cyst wall.
Life cycle
DH: Man, cat, dog, pig, lion, leopard, wolf & other mammals.
1
st
IH: Fresh water snail (Pleuroceridae & Thiaridae).
2
nd
IH: Fresh water crabs and cray fishes.
Infective stage: Metacercaria Infective stage: Metacercaria
Human infection:
Ingestion of raw or improperly cooked fresh water crabs
& cray fishes
Ingestion of raw meat from bild boar (immature worm)
Contamination of food, kitchen utensils & hands during
preparation.
Pathology and Symptomatology
Adults inhabit lungs & other organs
also.
Pathological lesions 4 stages:
1. Invading and migrating stage: 1. Invading and migrating stage:
1. After excystation adolescents penetrate
intestinal wall & migrate to lungs.
2. Suppurative stage:
bleeding & infiltration of neutrophils &
eosinophils surrounding worms form a capsule,
abscess.
3. Cystic stage:
Cyst wall formed due to progressive fibrosis of
surrounding tissue.
Contain chocolate or rusty thick fluid with eggs
and Charcot-Leyden crystals, which looks like and Charcot-Leyden crystals, which looks like
sesame paste.
Patients cough out rusty sputum when the cyst
communicates with bronchioles.
4. Fibrous-scar stage:
Worms dead or escape from cyst. The exudate &
pus expelled or absorbed & replaced by fibrous-
scar tissue.
Clinical manifestation
Paragonimiasis may be classified into 4 types :
1. Pulmonary type: symptoms resemble pulmonary
tuberculosis with low fever, loss of appetite, night
sweating, chest pain, loss of weight & rusty sputum.
2. Brain type: manifests epilepsy, hemiplegia,
monoplegia, aphasia, visual disturbance &
resembles cerebral cystycercosis.
3. Abdominal type: abdominal pain diarrhea or
dysentery with blood, mucus & ova in faeces.
4. Subcutaneous type: wandering & painless
subcutaneous nodules.
Diagnosis
1. Sputum examination: eggs (90%), eosinophils and Charcot-Leyden
crystal.
(1) Alkali digestive method (10%NaOH),
(2) Direct sputumsmear.
2. Stool examination: eggs (15-40%). 2. Stool examination: eggs (15-40%).
(1) Alkali digestion ,
(2) Water sedimentation method,
(3) Direct fecal smear.
3. Biopsy for Subcutaneous type: typical eosinophilous granuloma
with eggs, larvae &adult worm.
4. CT for brain type.
5. Immunological tests for reference: Intracutaneous test, ELISA,
Dot-ELISA, Weston blot, IHA and RIA etc
Treatment and Prevention
1. Treatment:
Drug of choice is praziqantel.
Other effective drugs include hexachloroparaxylol, bithionol.
2. Prevention: 2. Prevention:
(1) Health education,
(2) Avoid eating raw fresh water crabs and crayfishes.
(3) Avoid sputum &stool getting into water.
Chlonorchiasis a chronic parasitosis caused
by clonorchis sinensis, inhabit human
intrahepatic ducts.
Chlonorchiasis
Characterized by hepatomegaly, vague pain
of upper abdomen, lassitude & tiredness.
Acquired by ingestion of raw or
inadequately cooked freshwater fish or
shrimp.
Morphology
+Adult worm
Flat, elongated worm, 10-
15 3-5 mm, monocious,
two suckers.
Most characteristic feature
branched testis in branched testis in
posterior third of body &
relative small ovary before
them.
+Eggs
The smallest one of the
eggs of human parasites
(27.3-35.1 11.7-12.9 m)
Yellow brown operculated,
with a fully embryonated
miracidia in it.
Distribution
+ Endemic areas are Asia including Korea, China, Taiwan,
and Vietnam.
+ Occasionally reported in non-endemic areas (including
the United States).
Life Cycle
1st intermediate host: snail
2nd intermediate host: numerous 2nd intermediate host: numerous
freshwater fish
Definitive hosts ingest metacerariae
Humans and animals (dogs, pigs, cats, rats)
Clinical Manifestation
Incubation period: 1-2 months
Most person with mild infections asymptomatic, only
eggs can be found in feces eggs can be found in feces
Severe infections:
onset is insidious, with intestinal manifestations like
viral hepatitis, hepatomegaly, neurasthenia, person
with heavy worm loads may suffer from biliary
angina and obstructive icteric.
Acute symptoms:
Appear when heavy primary infection
Sudden onset, chill, high fever, slight jaundice,
hepatomegaly, eosinophilia, a few patients have hepatomegaly, eosinophilia, a few patients have
splenomegaly & weeks later, enter chronic stage.
Continuous reinfection:
Cirrhosis & portal hypertension.
In children may cause malnutrition growth
development disturbance, even dwarf.
Complications
Acute or chronic cholecystitis, cholangeitis &
cholelithiasis are most common complications
Portal liver cirrhosis: portal hepertension result in Portal liver cirrhosis: portal hepertension result in
upper gastrointestinal bleeding
Cholestatic cirrhosis
Pancreatitis
Primary carcinoma of liver &
cholangiocarcinoma.
Diagnosis
Blood routine test: eosinophilia, anemia in
severe infection.
Eggs examination: Eggs examination:
o Simple faecal smear.
o Stool concentration technique increase positive
rate.
o Duodenal aspiration: raise chance of finding
eggs.
Immunological Test
Skin test: positive rate 97.9%, 99.5%
coincide with result of faeces. coincide with result of faeces.
PHA: positive rate 53.7%, 80% coincide
with the result of faeces.
ELISA: positive rate 98.3%, 93.5%
coincide with result of faeces
Treatment
Pathogenic Treatment
Praziquantel best choice of drug for therapy
Dose: 15-25mg/kg, three times a day, for 2 days, Dose: 15-25mg/kg, three times a day, for 2 days,
the total dose is 90-150mg/kg
Another choice of drug is Albendazole
Prevention & control
Health education
Environmental modification
Reformof traditional farming and fishing techniques Reformof traditional farming and fishing techniques
Mass screening and chemotherapy
Management of domestic animals are needed in developing
control strategies to decrease spreading
Controlling the use of "night soil" (fertilizer contaminated with
human feces), used to fertilize fish ponds
Avoid eating raw fish and using contaminated water for
consumption.
Paragonimiasis
Rajagunalan S.
Roll no: 1392
Introduction
Synonyms: Pulmonary Distomisis, Endemic hemoptysis,
Lung fluke infection
Caused by members of the genus Paragonimus
Disease is prevalent in West Africa, south America and Disease is prevalent in West Africa, south America and
Indian subcontinent
Includes 9 species infective to man
P. westermani (recognised in 1880 so most data are on it)
P. heterotremus
P. mexicanus
P. africanus
P. skrjabini (dog and cat)
Life cycle
Predlictionsite: Lungs
Host;
Man and other mammals (carnivore)
Penetrate thru intestine peritoneum---
diaphragm--- pleura form pair encyst
Produce 1000-2000 eggs/day shed via
expecvtorant or in faeces (swalloed)
In inapparent host like wild boar remain In inapparent host like wild boar remain
without development and it act as a
partenic host
Eggs reaching water develop to miracidium
First intermediate host: Snails
Release cercariae stage
Second intermediate host:
Crab or Cray fish
Muscles and gills ---- Metacercaria
(P. skrjabini --- frog)
Disease in Man & Animals
Migration causes considerable damage and parasite may
be lodged in ectopic sites (brain, SPC, thoracic muscles,
S/C and organs)
Abdominal pain, fever, diarrhea, pleural effusion,
chronic cough, angina, blood tinged sputum
Diagnosis
Symptoms and endemicity
Often mistaken as TB Often mistaken as TB
Eggs in sputum, feces, pleural effusions and
biopsy ---- reddish brown operculate eggs
ELISA and PCR
Control
Proper cooking of crabs or cray fishes
Mass treatement in endemic areas
Sanitary practices and eliminate stray dog and Sanitary practices and eliminate stray dog and
cats
Use of molluscicides
Heterophyiasis
&
Metagonimiasis
Rajagunalan S.
Roll no: 1392
Introduction
A fluke infection caused by members of the family
Heterophyidae
Disease is prevalent in Japan and Korea, middle east, Disease is prevalent in Japan and Korea, middle east,
turkey and spain
Includes 10 species infective to man
Important ones being
Heterophyes heterophyes
H. nocens
Metagonimus yokogawai
Life cycle
First intermediate host: snails
Release cercariae stage
Second intermediate host: fresh and
brackish water fishes
Cercariae encyst and forms
metacrecaria by penetration thru
scales into the musculature scales into the musculature
Host; Ingesting Raw Fish
Heterophyes: man, cat, dog, foxes & other
fish eating animals and birds
Metagonimus yokogawai; man, cat, dog,
swine, pelicans & other fish
eating animals and birds
Release egg containing Miracidium
Predlictionsite: small intestine
Disease in Man & Animals
Mild infections are asymptomatic
Huge parasitic load causes irritation of intestinal Huge parasitic load causes irritation of intestinal
mucosa- superficial necrosis, chronic Diarrhea,
colic and nausea
Aberrant egg in organ causes granuloma-
myocardium and brain
Diagnosis
Observation for parasitic egg in fecal matter
Eggs of Heterophyes, Metagonimus, Clonorchis Eggs of Heterophyes, Metagonimus, Clonorchis
and Opisthorchis are virtually indistinguishable
Adult flukes are used for identification after
deworming
Control
Health education
Proper cooking of fishes
Proper disposal of excreta Proper disposal of excreta
Never feed cat and dog with raw fishes
Opisthorchiasis
Rajagunalan S.
Roll no: 1392
Introduction
Caused by
Opisthorchis viverrini,
O. felineus,
O. pseudofelineus
Difficult to differentiate from the Clonorchis spp., L/C also
similar to it
Prevalent in Thailand, Vietnam, Siberia Kazakhstan
Life cycle
Host;
Man, dog, cat and other fish eating animals
Migrate thru the bile duct from duodenum
can live upto 20 yrs
Egg contain fully devloped miracidium Egg contain fully devloped miracidium
First intermediate host: Snails
Release cercariae stage
Second intermediate host:
Fishes
penetrate and encyst to form
metacercaria (s/c or base of fin)
Predlictionsite: bile duct
Disease in Man & Animals
Hepatomegaly and pericholangitis
Dilatation of duct with hyperpalsia, desquamation and Dilatation of duct with hyperpalsia, desquamation and
infiltration with connective tissue
Diarrhea, moderate jaundice, flatulence, cephalgia
In chronic cases biliary stasis --- cholangitis
Hepatic carcinoma and cholangiocarcinoma can occur
Diagnosis
Observation for parasitic egg in fecal matter
ELISA with monoclonal antibody ELISA with monoclonal antibody
Control
Proper cooking of fishes
Proper disposal of excreta Proper disposal of excreta
Diagnosis and TTT of patients
Health education
Thankyou !!!
SPARGANOSIS
Human infection by plerocercoid larvae of Spirometra spp.
Diesing first named the Sparganumgenus of cestodes in 1854
Patrick Manson first reported sparganosis and the species
Sparganum mansoni in China in 1882
MORPHOLOGY-Much similar to Diphyllobothrium spp.
Small-medium sized tapeworms
Adults-pink coloured-in S. I. of wild carnivores,cats & dogs
Systematics of Spirometra-still controversial
Several spp. Recognized-
S.mansonoides
S.mansoni
S.erinaeci
S.felis
Epidemiology
Found mainly in East & South-east Asia, Japan& Indo-china
Lesser extent-in Africa,Europe,Australia , North & South
America
Ocular sparganosis - especially prevalent in China and Vietnam
The highest numbers of cases occur in Korea and Japan The highest numbers of cases occur in Korea and Japan
Man acquires Sparganosis by
Ingestion of infected Cyclops containing plerocercoid thrugh
drinking water
Consuming frogs,snakes or rodents having plerocercoid
Penetration of cutaneous tissue,specially orbit by plerocercoid
from poultices of infected flesh of frogs/snakes
Ingestion of pig meat-Feral pig meat in Australia
Lifecycle
Symtoms
Plerocercoids- not highly pathogenic to man
Sometimes Parasite-discomfort/uneasy feeling (while migrating under
skin)
Occasionally abscesses-at site of larva located
Migration to the brain results in cerebral sparganosis, while
migration to the eyes results in ocular sparganosis
Degenerated larvae-intense local inflammation & necrosis but no Degenerated larvae-intense local inflammation & necrosis but no
fibrous tissue
Infected persons-
Local induration
Periodic giant utricaria
Oedema
Erythema
Accompanied by chills,fever & high eosinophilia
Occular infection-painful oedematous conjuctivitis with lacrimation
Diagnosis
By finding larvae in lesions
AntisparganumELISA
CT and MRI scans (Diagnosis of cerebral sparganosis -characteristic finding
tunnel signin MRI images)
Treatment
Immature forms of Spirometra spp. -resistant to praziquantel and
mebendazole mebendazole
Currently no recommended drug therapy for sparganosis.
Surgical removal of the complete sparganumis the best treatment
Prvention
By eating properly cooked flesh of I.H. (In endemic areas)
By drinking boiled or properly filtered water
RAILLIETINIASIS
Main spp.as agent of dis. in Man
Raillietina celebensis
D.H.-Rodents(Rats)
Size-maxm. 40 cm x 2.5 mm >500 proglottids Size-maxm. 40 cm x 2.5 mm >500 proglottids
Suckers-not spinose (uncommon in this genus)
Gravid proglottids-300-400 eggcapsules with upto 4 eggs each
R.demerariensis
In both rodents & howling monkeys
Size-23 cm -12mt 320-5000 proglottids
Gravid proglottids 75-250 eggcapsules with 7-9(12)eggs each
Shaped like grains of rice
Other spp.-R. asiatica,R.formosana,R.garisoni,R. siriraji
Lifecycle
Infective stage- Cysticercoids
D.H.-Rodents(Rats) & howling monkeys
I.H.-Arthropod (probably an ant or beetles)
Raillietina Eggs ingested by I.H.(Insects)
Infective stage- Cysticercoids
D.H.-Rodents(Rats) & howling monkeys
I.H.-Arthropod (probably an ant or beetles)
Raillietina Eggs ingested by I.H.(Insects)
Develop into Cysticercoids in tissues of I.H.
New adult worms in I.H.
Insect (I.H.) eaten by D.H.(Rodents)/Human
Epidemiology
Resorvoirs-rodents
Transmission-Man becomes infected by accidentally
ingesting food contaminated with arthropod infected with
cysticercoids
Distribution
R.celebensis recovered in children in south estern R.celebensis recovered in children in south estern
Africa,Australia,Iran,JapanMauritus,thePhilippines,Taiwan,
& Turkistan region of Asia
Infection common in rodents
In Taiwan ---Rattus norvegicus(54%) R.rattus(9%)
In India(Bombay)-R.rattus(5%) Bandicota bengalensis(7%)
R.demerariensis-neotropical spp.-found in
Cuba,Ecuador,Guyana,& Honduras
Largest endemic focus-parish of Tumbaco (Ecuador)
Disease in Man
Primarily in children
In Ecuador-
Digestive upsets (nausea,vomiting,diarrhoea,colic)
Nervous disorders (headaches,prsonality change,convulsion) Nervous disorders (headaches,prsonality change,convulsion)
Circulatory disorder (tachycardia,arrhythmia,lipothymia)
General disorders (wt loss, retarded growth)
In Philippines-
Human infection-usually asymptomatic
Parasite expelled spontaneously by infected individual
DIAGNOSIS
Proglottids -observedin fecal matter
-resemble grains of rice (frequently mistaken)
Free capsules found in feces-as result of disintegration of
proglottids
Differential diagnosis
Raillietina spp- scolex has hooks
Inermicapsifer- scolex unarmed Inermicapsifer- scolex unarmed
CONTROL
Large scale treatment-not warranted
(Human infection so infrequent)
Burning & annual treatment of fields (where cotton rat lives)
Individual control-hygienic handling of food(to prevent
contamination of infected insects)
Strongyloidiasis
Strongyloides stercoralis
Common in tropical and subtropical areas
Strongyloides fuelleborni Strongyloides fuelleborni
Limited to Africa and Papua New Guinea
Threadworm
Adult
Rhabditifor
m Larvae
(non-infective
2 mm long intestinal worm
Filariform
Larvae
(penetrating
)
(non-infective
form)
(pathogenic form)
2 mm long intestinal worm
L1: 0.3 mm long
L3: 0.6 mm long
+The size and shape of the worm are
dependent on whether its parasitic or
free-living.
Free-living females 1 mm by 60 m
Parasitic females 2.2 mm by 45 m
Eggs 55 m by 30 m
- Found worldwide
- An estimated 50 to 100 million cases
- Favors warmer tropical and subtropical climates
- Endemic in sub-Saharan Africa, Latin America, southeast
Asia & the southeastern United States
Symptoms
- Commonly asymptomatic
- But symptoms may include:
1. Gastrointestinal (diarrhea, abdominal
pain, malabsorption)
2. Respiratory (coughing, wheezing)
3. Dermatologic (ground itch, rash ,
larva currens)
3. Dermatologic (ground itch, rash ,
larva currens)
4. Anaemia
+ Immunosuppressed patients:
Q Disseminated strongyloidiasis
Q Hyperinfection:
Intestinal perforation
Hemorrhagic pneumonia
Shock, sepsis, gram-
negative meningitis
Eosinophilia may be limited
Diagnostic Testing
Stool
- Microscopic: S. sterocoralis larvae is
the definitive diagnosis
- Ova usually not seen (only helminth to - Ova usually not seen (only helminth to
secrete larva in the feces)
Stool wet mount (direct exam)
Larva seen via direct examination of stool
+SEROLOGY
ELISA
Most sensitive method (88-95%) Most sensitive method (88-95%)
+ IMAGING
Treatment
+ The drug of choice is
thiabendazole.
+ Alternatives :
+ Albendazole.
+ Ivermectin.
Prevention
Q Community education on Good personal hygiene can reduce
the risk of strongyloidiasis.
Q Adequate public health services and sanitary facilities
provide good control of infection provide good control of infection
Q Emphasis should be placed on the importance of:
Washing of hands
Disposing of human faeces in a sanitary way
Wearing covered footwear when outside
Swimmers itch
Duck itch, Cercarial dermatitis, and
Schistosome cercarial dermatitis
A short-term Immune reaction occurring in
the skin of humans that have been infected the skin of humans that have been infected
by water-borne Schistosomatidae.
Symptoms-itchy, raised papules
- commonly occur within hours of infection
- do not generally last more than a week.
Important
The schistosomatidae - give rise to swimmers itch -----
should not to be confused with
Genus Schistosoma, which infect humans and cause the
serious human disease schistosomiasis,
Larval stages of thimble jellyfish (Linuche unguiculata) - Larval stages of thimble jellyfish (Linuche unguiculata) -
give rise to seabather's eruption.
Seabather's eruption
- mostly occurs in salt water,
- on skin covered by clothing or hair,
whereas swimmer's itch
- mostly occurs in freshwater,
- on uncovered skin
Etiology
The schistosomatidae genera most commonly associated with
swimmers itch in humans are
- Trichobilharzia
- Gigantobilharzia.
Trematodes in these groups normally complete their life cycles
in water birds.
Also by schistosome parasites of non-avian vertebrates, such Also by schistosome parasites of non-avian vertebrates, such
as Schistosomatium douthitti, which infects snails and rodents.
Other taxa reported to cause reaction include
Bilharziella polonica and Schistosoma bovis.
In marine habitats, especially along the coasts, swimmers itch
can occur as well.
In Australia, the so called "pelican itch" is caused by cercariae
of the genus Austrobilharzia employing marine gastropods of
the genus Batillaria (B. australis) as intermediate hosts.
Causal Agent
Caused by the cercariae of certain species of
schistosomes whose normal hosts are birds and
mammals other than humans.
These cercariae seem to have a chemotrophic
reaction to secretions from the skin and are not as
host-specific as other types of schistosomes.
They attempt to, and, sometimes may actually, enter They attempt to, and, sometimes may actually, enter
human skin.
The penetration causes a dermatitis which is usually
accompanied with intense itching,
but the cercariae do not mature into adults in the
human body.
Cases of cercarial dermatitis can occur in both fresh
and brackish water environments
One species of schistosome often implicated
Austrobilharzia variglandis,- whose normal hosts are ducks.
The snail, Nassarius obsoletus, is the intermediate host for
this species and can be found at marine beaches in
temperate climates.
Cercarial dermatitis should not be confused with Cercarial dermatitis should not be confused with
seabather's eruption, which is caused by the larval stage of
cnidarians (e.g., jellyfish). The areas of skin affected by
seabather's eruption is generally under the garments worn
by bathers and swimmers where the organisms are trapped
after the person leaves the water.
Cercarial dermatitis occurs on the exposed skin outside of
close-fitting garments
LIFE CYCLE
Hosts of avian schistosomes can be either year-round
resident or migratory birds, including seagulls, shorebirds,
ducks, and geese.
Adult worms are found in the blood vessels and produce
eggs that are passed in the feces .
On exposure to water, the eggs hatch and liberate a ciliated
miracidiumthat infects a suitable snail (gastropod)
intermediate host . intermediate host .
The parasite develops in the intermediate host to produce
free-swimming cercariae that are released under
appropriate conditions and penetrate the skin of the birds
and migrate to the blood vessels to complete the cycle .
Humans are inadvertent and inappropriate hosts; cercariae
may penetrate the skin but do not develop further .
A number of species of trematodes with dermatitis-
producing cercariae have been described from both
freshwater and saltwater environments, and exposure to
either type of cercaria will sensitize persons to both.
Can swimmer's itch be spread from
person-to-person?
Swimmer's itch is not contagious and cannot be
spread from one person to another.
Who is at risk for swimmer's itch?
Anyone who swims or wades in infested water
may be at risk. may be at risk.
Larvae are more likely to be present in shallow
water by the shoreline.
Children are most often affected because they
tend to swim, wade, and play in the shallow
water more than adults.
Also, they are less likely to towel dry themselves
when leaving the water.
Symptoms of Swimmer's Itch
Some common Symptoms of Swimmer's Itch :
Small reddish pimples .
Tingling, burning, or itching of the skin
Small Blisters Small Blisters
Fever.
Treatment of Swimmer's Itch
Treatment is by application of medications to ease the itch
if inflammation is severe, preparations containing
corticosteroids.
Since the cercariae need about 15 minutes to penetrate the
skin. the risk of exposure is reduced by drying the skin
immediately after swimming, but it is best to avoid bathing immediately after swimming, but it is best to avoid bathing
where anyone has previously picked up swimmers' itch.
Take shallow lukewarm baths with three tablespoons of baking
soda in the water.
Anti-itch creams or ointments, such as those containing
calamine lotion
Take colloidal oatmeal baths.
Oral antihistamines .
Apply cool compresses.
Control
Avoid swimming in areas where swimmers' itch is a
known problem.
Rinse exposed skin with fresh water immediately after
leaving the water. Then vigorously dry your skin with a
towel.
Avoid swimming near or wading in marshy areas where
snails are commonly found.
Towel dry or shower immediately after leaving the
water.
Do not attract birds (e.g., by feeding them) to areas
where people are swimming.
Encourage health officials to post signs on shorelines
where swimmer's itch is a current problem.
Introduction
E Caused by Thelazia callipaeda (eyeworm, conjunctival
spirurosis)
E Found in the eyelids, tear glands, lacrymal ducts, of the
dog, rabbit, cattle and other mammals including man dog, rabbit, cattle and other mammals including man
E First described by Ralliet and Henry in 1910
E Common in Japan, China, Thailand, Korea, Russia and
India
Representative species
E Thelazia anolabiata
DH: Brazilian birds Intermediate hosts: Not known Distribution: South America
E Thelazia bubalis
DH: Water buffalo IH: Not known Distribution: India
E Thelazia californiensis
Definitive hosts: Dog, Cat, occasionally Human, sheep Intermediate hosts: Lesser house fly (Fannia) Distribution: Western North America
Thelazia callipaeda (sometimes called "Oriental eyeworm") E Thelazia callipaeda (sometimes called "Oriental eyeworm")
Definitive hosts: Dog, Cat and Human; occasionally from Wolf, Raccoon , Red Fox Intermediate hosts: Fruit flies
Distribution: Asia and Europe
E Thelazia gulosa
Definitive hosts: Yak and Cattle Intermediate hosts: Face fly Distribution: Asia, Europe, and North America
E Thelazia lacrymalis
Definitive hosts: Horse and Cattle Intermediate hosts: Face fly Distribution: Asia, Europe, Middle East, North America and South America
E Thelazia rhodesii
Definitive hosts: Cattle, Buffalo, Bison and sometimes Horse IH: Flies (Face fly) Distribution: Africa, Asia, and Europe
Morphology
E Male will be of 4.5 to 13 mm length
E Female will be of 6.2 to 17 mm length
E Worms are creamy white thread like
E Eggs are ovoid transparent and are fully embryonated
when laid
Lifecycle
E The eggs develop into first stage larvae (L1) in conjunctiva of DH.
E When a tear-feeding fly feeds, it ingests larvae.
E Once inside the fly, the L1 larvae "hatch" from the egg membrane and penetrate the gut
wall.
E Remain in the hemocoel for 2 days, and then invade either the fat body or testes of the
flies.
E Larvae develop into third stage larvae (L3).
E L3 migrates to the head of the fly, and is released in or near the eye of a new DH
E In eye, L3 larvae develop to the L4 larval stage and into adults in about 1 month.
Pathogenesis & pathology
E Presence of worm in conjunctiva causes damage in
tissues of eye
E Causes excessive lacrymation
E Movement of worm in eye causes irritation, E Movement of worm in eye causes irritation,
scarification and opacity
Infection in man and animals
E Excessive lacrymation
E Pain and foreign body sensation in the eye
E Scarification and opacity of conjunctiva
E Paralysis of lower eyelid seen as a complication E Paralysis of lower eyelid seen as a complication
Diagnosis
E Demonstration of creamy white and thread like
worms in the conjunctival sac or across the cornea
E Specific diagnosis by examination of worm E Specific diagnosis by examination of worm
removed from the eye by forceps
Treatment and control
E Removal of worm by forceps after application of
topical anesthesia --- effective method
E Corneal opacity if develops it is irreversible E Corneal opacity if develops it is irreversible
E Preventive measures like fly control can be adopted
Caused by Dioctophyma renale
Also called as Giant Kidney Worm
Goeze first demonstrated the parasite in the kidney of a dog in Goeze first demonstrated the parasite in the kidney of a dog in
1782
Man gets infection by ingestion of raw or inadequately cooked
infected fish or frog
Disease is characterized by renal colic and haematuria.
Adult worm inhabits the pelvis of the kidney (Right mostly)
They are cylindrical and are blood red in colour
Male will be of 14-20 cm long and 4-6mm diameter. Female Male will be of 14-20 cm long and 4-6mm diameter. Female
will be 20 -100 cm long and 5-12 mm dia.
Eggs will be ellipsoidal and brownish yellow
DH: man and large number of animals like mink, dog, wolf,
racoon, ox cat, seal
IH: Aquatic oligocheates
Paratenic host: fishes and frogs Paratenic host: fishes and frogs
Infective stage: infective larva of D. renale
Transmission: ingestion of fishes & frog harboring larvae
Dogs are important reservoir host
Eggs are voided in the urine of DH
Egg -----L1 in water---- ingested by IH---- egg hatch ----- L1 develop in the
coelom---- moults twice and formL3 in 4 months--- ingested by fishes and
frogs----- larva encyst in the mesentry without development----- Dh ingest frogs----- larva encyst in the mesentry without development----- Dh ingest
fishes or paratenic host ---- cyst releases larva ---- penetrates stomach
and moults in the submucosa and reach liver ---pass into peritoneal cavity
and reach kidney--- pelvis--- adult
Only kidney is involved
Adult worm by virtue of its presence damages the
parenchymatous tissue of the kidney and causes formation
of folded capsules of folded capsules
Renal colic and haematuria occurs
Parasite may block ureter or urethra
Observing for the presence of characteristic eggs showing
two celled embryo with a thick and deeply sculptured egg
shell in urine
Surgical removal is recommended for treatment Surgical removal is recommended for treatment
Thorough cooking of the fishes
Proper hygienic practices
TOXOPLASMOSIS History History History History
Toxoplasma gondii is an obligate intracellular protozoan
Toxoplasmosis (G:Toxon-arc + plasma-form + osis-dis)
It derives its name from a North African rodent the gondii,
from which it was first isolated in 1908 .
First case of a congenitally infected human baby was reported
in 1923 in 1923
Discovery of dye test by Sabin and Feldman in 1948
In 1969, life cycle of parasite was discovered with its
definitive host, cats and other felines.
INTRODUCTION INTRODUCTION INTRODUCTION INTRODUCTION
A congenitally and postnatally acquired coccidial zoonosis
Classified as Saprozoonoses and Cyclozoonoses
Toxoplasmosis (G:Toxon-arc + plasma-form + osis-dis) Toxoplasmosis (G:Toxon-arc + plasma-form + osis-dis)
Host Host Host Host
Life cycle is completed in two classes of hosts.
Definitive Host: Cat & wild felines of genera Felix & Lynx , members of
the family Felidae such as mountain ions, ocelots, margays, bob cats,
Bengal tigers, etc.
Intermediate Host: Human, mice and non-feline hosts (goat, sheep, pig,
cattle, buffalo, etc.). cattle, buffalo, etc.).
Infective stage:Tachyzoites, tissue cysts and oocysts of Toxoplasma gondii.
CAT-Complete host
Transmition
Transmission Transmission Transmission Transmission Transmission Transmission Transmission Transmission
- The parasite is transmitted by three known modes,
- Carnivorism
- faeco-oral
- congential
- Due to ingestion of occysts excreted in the faeces of cats or by ingestion of
undercooked meat harboring tissue cysts.
- Approximately 5-35% of pork, 9-60% of lamb and 0-9% of beef contain T. - Approximately 5-35% of pork, 9-60% of lamb and 0-9% of beef contain T.
gondii.
- Trans-placental transmission to fetus from a mother infected is common.
Only a small proportion (less than 0.1%) of human acquire infection
congenitally.
- Can also be transmitted through milk, semen, organ transplants and
blood /leucocyte transfusions
Life Cycle Life Cycle
Epidemiology and Public Health Epidemiology and Public Health Epidemiology and Public Health Epidemiology and Public Health
Toxoplasma gondii infection in human is widespread throughout the world
including India
Approximately 500 million human beings are estimated to have
antibodies to T. gondii.
Oocyst formation, however- greatest in the domestic cat.
. Oocysts can be mechanically transmitted by invertebrates such
as flies, cockroaches and earthworms and by run off of rain and melting
snow.
Epidemiology and Public Health Epidemiology and Public Health Epidemiology and Public Health Epidemiology and Public Health
Epizootiologic data indicate
Cats become infected during the preweaning period.
Their prey -- bird, rodent, rabbit or other small mammal,
Aborted Foetuses and foetal membranes from sheep and other animals -
a good source of infection for carnivorous birds and mammals. a good source of infection for carnivorous birds and mammals.
Only a few cats may be involved in the spread of T. gondii because they
can excrete millions of resistant oocysts within 1 to 2 weeks.
Cats usually acquire good immunity to reshedding of oocysts.
Epidemiology and Public Health Epidemiology and Public Health Epidemiology and Public Health Epidemiology and Public Health
Factors determine the degree of natural spread of T. gondii
Environmental conditions
Aultural habits of the people
Animal fauna.
Mothers of congenitally infected children do not give birth to
infected children in subsequent pregnancies.
Infection occurs only when the consumed meat is not cooked
properly
because tissue cysts are destroyed at 70
o
C.
Freezing also kills most cysts but cannot be relied upon for the
destruction of all cysts of T. gondii in meat.
In India, the ingestion of food and water contaminated
with oocysts is probably the main source of infection
Incubation Period Incubation Period Incubation Period Incubation Period
10 to 23 days after ingesting
contaminated meat,
5 to 20 days after exposure to infected 5 to 20 days after exposure to infected
cats.
CLINICAL PICTURE CLINICAL PICTURE CLINICAL PICTURE CLINICAL PICTURE
In ANIMALS In ANIMALS In ANIMALS In ANIMALS
Acute, Subacute Chronic forms-clear differiantion difficult
Abortion is the most important clinical manifestation .
Can cause foetal death and resorption or retention, mummification,
abortion, still birth and birth of weak young in sheep, goats and possibly
pigs.
Transplacental infection can occur when nonimmune animals become
infected during pregnancy infected during pregnancy
Acute dis-diarrohea,lymphoadenopathy & hepatic lesions
Encephalitis and occular lesions develop gradually
Swine, dog & cat-fever,poorgrowth,hepatitis,encephalitis,pneumonia
No clinical disease -in Cattle
Virtually all forms of clinical disease seen in man can occur in dogs, cats and
several species of wildlife.
New world monkeys and marsupials are highly susceptible to T. gondii and
most of these infected animals die of overwhelming toxoplasmosis.
CLINICAL PICTURE CLINICAL PICTURE CLINICAL PICTURE CLINICAL PICTURE
In In In In HUMAN HUMAN HUMAN HUMAN
Asymptomatic
Acquired symptomatic
Congenital forms Congenital forms
Clinical picture Clinical picture Clinical picture Clinical picture
In HUMAN
CONGENITAL FORMS
Congenital infection occurs only once when a woman becomes infected for
the first time during pregnancy, resulting in the wide spectrum of clinical
disease in the newborn.
Mild disease may consist of slightly diminished vision
Sseverely diseased children may have the full tetrad of signs : Sseverely diseased children may have the full tetrad of signs :
retinochoroiditis, hydrocephalus, convulsions & intracerebral
calcificiation.
Most common sequel of congenital toxoplasmosis - ocular disease.
Except for an occaiosnal involvement of entire eye, almost always confined
to the posterior chamber.
T. gondii proliferates in the retina, which leads to inflammation in the
choroid and is correctly designated as retinochoroiditis.
The lesions of ocular toxoplasmosis are fairly characteristic in humans.
Clinical picture Clinical picture Clinical picture Clinical picture
In HUMAN
AQUIRED SYMPTOMATIC FORMS
May be localized or generalized,
Lymphadenitis - most frequently observed clinical form of human
toxoplasmosis.
Although any node may be involved, the most frequently involved are the
deep cervical nodes.
When infected these nodes are tender and discrete, but not painful, the When infected these nodes are tender and discrete, but not painful, the
infections resolve spontaneously in weeks or months.
Lymphadenopathy may be associated with fever, malaise and fatigue, muscle
pain, sore throat and headache.
Although the condition may be benign, its diagnosis is vital in pregnant
women because of the risk to the foetus.
Encephalitis is an important manifestation of toxoplasmosis in
imunosuppressed patients.
Clinically, the patients may have headache, disorientation, drowsiness,
hemiparesis, reflex change and convulsions and many may become comatose.
Clinical picture Clinical picture Clinical picture Clinical picture
In Immunocompetent individuals
Usually asymptomatic.
10-20% lymphadenitis or flulike ( fever, malaise, myalgia,
headache, sore throat, and rash).
Rarely myositis, myocarditis, pneumonitis and neurologic signs
including facial paralysis, encephalitis
Uveitis, often unilateral, can be seen in adolescents and young
adults; the result of an asymptomatic congenital infection or the
delayed result of a postnatal infection.
Clinical picture Clinical picture Clinical picture Clinical picture
Immunocompromised individuals
Toxoplasmosis is often severe.
Neurologic disease is the most common sign,
particularly in reactivated infections.
Symptoms are:
Encephalitis, Encephalitis,
Necrosis from multiplication of the parasite can cause multiple
abscesses in nervous tissue, with the symptoms of a mass lesion.
Chorioretinitis, myocarditis and pneumonitis
CULTIVATION CULTIVATION CULTIVATION CULTIVATION
Tissue cell line cultures support the multiplications of
Toxoplasma gondii
Normal murine alveolar
Peripheral macropahges cell line Peripheral macropahges cell line
Till now, this coccidian has not been successfully
cultivated in any cell-free culture medium.
Toxoplasmosis during pregnancy Toxoplasmosis during pregnancy Toxoplasmosis during pregnancy Toxoplasmosis during pregnancy
Toxo is a part of TORCH syndrome.
It is not a cause of habitual abortion.
Only pregnant women with primary active infection leads to
congenital toxo.
Development of active immunity once, protects subsequent Development of active immunity once, protects subsequent
pregnancies.
Rate of Transmission Rate of Transmission Rate of Transmission Rate of Transmission
If infection within 23 months before conception - 1% or below
risk of transmission but a high risk of miscarriage
The first trimester - 15% chance but Severity of disease in neonate
is more
Second trimester - 25% risk Second trimester - 25% risk
Third trimester - 65% chance but Severity of disease in neonate is
less usually asymptomatic
ANIMAL MODELS ANIMAL MODELS ANIMAL MODELS ANIMAL MODELS
Common laboratory animals being used- Mice Hamsters & rabbits
Route of infection-Intraperitoneal- most commonly used followed
by the intracutaneous, subcutaneous and even the inhalation.
Mice - commonly used laboratory animal for routine maintenance Mice - commonly used laboratory animal for routine maintenance
of strains of T. gondii by serial passages through intra-peritoneal
route.
Toxoplasma may appear in the blood within 4 hours of inoculation.
It disappears from the circulation shortly but persists for weeks
together in the tissues of the internal organs such as spleen, liver
and other organs.
Mouse is also commonly used for diagnostic purposes by the
isolation of the parasite from the clinical specimens.
DIAGNOSIS DIAGNOSIS DIAGNOSIS DIAGNOSIS
May be established by
Serological tests,
Polymerase chain reaction (PCR),
Histological demonstration of the parasite and/or its
antigens (i.e. immunoperoxidase stain), antigens (i.e. immunoperoxidase stain),
Isolation of the organism
Serological tests Serological tests Serological tests Serological tests
Detection of either antibodies specific to T. gondii or
toxoplasma antigen in the serum and other body fluids.
Of these, the enzyme linked immunosrbant assay
(ELISA) and agglutination tests are commonly used
some of these are commercially available in one form or some of these are commercially available in one form or
the other.
MODIFIED AGGLUTINATION TEST
Sabin-Feldman dye test - most specific for the diagnosis
of toxoplasmosis
Serodiagnosis Serodiagnosis Serodiagnosis Serodiagnosis
Presence of IgMantibodies or a four fold rise in IgG
titres at 2-3 wks interval indicates a relatively recent
infection.
Significant levels of IgMantibodies indicate - infection
acquired within the past 3 months.
IgG antibodies usually appear within 1 to 2 wks of IgG antibodies usually appear within 1 to 2 wks of
infection, peak within 1 to 2 months, fall at variable
rates, and usually persist for life
The titer does not correlate with the severity of illness
Specific Toxoplasma Antibody Tire : Some interpretations
Antibody Titre
IgM IgG IFA/Dye IgG and IgM
IgM-IFA > 1:80 Single high titre Rising titers at IFA/Dye Titre < 1:1000
IgM-ELISA > 1:256 IFA > 1:1000 3 week interval IgM-IFA/ELISA Negative
Recent Acute Probably Recent Definite Recent Exclude Recent Recent Acute Probably Recent Definite Recent Exclude Recent
Infection Acute Infection Acute Infection Acquired Infection
Blood test procedure flow chart Blood test procedure flow chart Blood test procedure flow chart Blood test procedure flow chart
blood test
positive
sample sent to lab for further testing
negative
positive to
current infection
positive to
previous infection
not immune
expert advice
about risks and
further action
immune
not at risk
from toxo
take precautions
because preg
could be at risk
from toxo
treatment
scans/further
tests to see if baby
is infected
Confirmatory test
Toxoplasma Serological Profile (TSP)
TSP
differentiate between recently acquired and chronic
infection,
is superior to any single serological test. is superior to any single serological test.
TSP consist of -
Sabin-Feldman Dye Test (DT)
Double sandwich IgMELISA or IgM-immunosorbent (IgM-
ISAGA) , IgA ELISA, IgE ELISA,
AC/HS test.
Sabin-Feldman Dye Test (DT)
DT is a sensitive and specific neutralization test in which live organisms
are lysed in the presence of complement and the patient's IgG T. gondii-
specific antibody
A positive DT establishes that the patient has been exposed to the parasite.
A negative DT essentially rules out prior exposure to T. gondii (unless the patient A negative DT essentially rules out prior exposure to T. gondii (unless the patient
is hypogammaglobulinemic).
In a few patients, IgG antibodies might not be detected within 2 to 3 weeks after
the initial exposure.
In rare cases of toxoplasmic chorioretinitis and toxoplasmic encephalitis in
immunocompromised patients have been documented in patients negative for
T.gondii-specificIgGantibodies.
Differential agglutination (AC/HS)
Uses two antigen preparations that express antigenic determinants
found in early acute infection (AC antigen) or in the later
stages of infection (HS).
Ratios of titers using AC versus HS antigens are interpreted as acute,
equivocal, non-acute patterns of reactivity or non-reactive. equivocal, non-acute patterns of reactivity or non-reactive.
The acute pattern may persist for one or more years following
infection.
This test is useful in helping differentiate acute from chronic infections
but is best used in combination with a panel of other tests (e.g.: the
TSP).
Avidity Test
The functional affinity of specific IgG antibodies is initially low after
primary antigenic challenge and increases during subsequent weeks
and months.
Protein-denaturing reagents including urea are used to
dissociate the antibody-antigen complex. dissociate the antibody-antigen complex.
The avidity result is determined using the ratios of antibody titration
curves of urea-treated and untreated serum
Avidity test is an additional confirmatory diagnostic tool in
the TSP for those patients with a positive and/or equivocal IgMtest
or acute and/or equivocal pattern in the AC/HS test.
Polymerase Chain Reaction (PCR) Polymerase Chain Reaction (PCR) Polymerase Chain Reaction (PCR) Polymerase Chain Reaction (PCR)
Used to detect T. gondii DNA in body fluids and tissues.
Used to diagnose congenital, ocular, cerebral and disseminated
toxoplasmosis.
PCR performed on amniotic fluid has revolutionized the diagnosis
of fetal T. gondii infection of fetal T. gondii infection
PCR has allowed detection of T. gondii DNA in brain tissue,
cerebrospinal fluid (CSF), vitreous and aqueous fluid,
bronchoalveolar lavage (BAL) fluid, urine, amniotic fluid and
peripheral blood
Histologic Diagnosis Histologic Diagnosis Histologic Diagnosis Histologic Diagnosis
A rapid and technically simple method is the detection of
T. gondii in air-dried, Wright-Giemsa-stained slides of
centrifuged sediment
The presence of multiple tissue cysts near an
inflammatory necrotic lesion probably establishes the
diagnosis of acute infection or reactivation of latent diagnosis of acute infection or reactivation of latent
infection.
It is often difficult to demonstrate tachyzoites in
conventionally stained tissue sections. The
immunoperoxidase technique, which uses antisera to T.
gondii, has proven both sensitive and specific
Isolation of Isolation of Isolation of Isolation of T. T. T. T. gondii gondii gondii gondii
Isolation of T. gondii by mouse inoculation from blood or body
fluids establishes that the infection is acute. fluids establishes that the infection is acute.
TREATMENT TREATMENT TREATMENT TREATMENT
Sulfonamides and pyrimethamine (Daraprim) are two
drugs widely used for therapyp of toxoplasmosis.
They act synergistically by blocking the metabolic pathway
involving p-amino benzoic acid and the folic folinic acid cycle,
respectively.
Prevention and control
Hands should be washed be washed with soap and
water after handling meat
Meat should be cooked thoroughly (70
o
C) before
consumption.
Cats should not be fed uncooked animal tissues,
Gloves should be worn while gardening and eleaning
cat litter trays.
At present there is no vaccine
but there is a good possibility of developing one
because most animal species and man acquire good
immunity against clinical toxoplasmosis after
postnatal infection
Trichinellosis
Taxonomy
Kingdom: Anamalia
Phylum: Nematoda
Class: Adenophorea
Order: Trichocephalida
Family: Trichinellidae Family: Trichinellidae
Genus: Trichinella
Species: spiralis
* 10 different subspecies of Trichenella spiralis
General Facts
- Infect a wide range of mammalian hosts
- Endemic in Japan and China
- Top carnivores are usually infected - Top carnivores are usually infected
- Smallest nematode of humans
- Trichinella spiralis is the worlds largest intracellular parasite.
- Humans get infected eating raw or undercooked meat
Trichinela spirals
10 different subspecies designated as T1 T10
- T. spiralis (T1)
- T. nativa (T2)
- T. britovi (T3) - T. britovi (T3)
- T. pseudospiralis (T4)
- T. nelsoni (T7)
- T. papaue (T9)
- T. zimbabwelensis (T10)
Geographic distribution
Worldwide
Most common in parts of Europe and the United States.
Definitive Host
Almost any species of mammal can get affected
- Humans
- Pigs/boars
- Bears
- Walruses
- Tasmanian devil
- Raccoon dogs
Domestic pigs are the main reservoir host for T.
spiralis
Morphology
Male
1.5 mm in length
Female
Larvae
36 m in diameter
twice the size of
males
0.08 mm long
7 m in diameter
Life Cycle Life Cycle in picture
sword-like stylet
Transmission
~ Ingesting raw or undercooked meat that
contains the parasite
Clinical Signs in Humans
Dysentery due to invasion by adult worms
Cause pain as they invade muscle tissue; there may
also be edema (swelling), delirium, cardiac and
pulmonary difficulty, pneumonia, nervous disorders, pulmonary difficulty, pneumonia, nervous disorders,
deafness and delayed or lost reflexes
Fever can also be caused
Many cases are never diagnosed because of the
vagueness of the symptoms
Clinical Signs in Humans Cont.
Severe symptoms include:
High fever
severe muscle pain
skin rash skin rash
headaches
swelling of eyelids, face, or extremities
More Clinical Signs in Humans
Patients may develop neurologic manifestations - second week
of infection and provoke distress.
Headache, vertigo and tinnitus, deafness, aphasia, convulsions,
and abnormalities related to peripheral reflexes
Generally, patients are alert but apathetic, affects their behavior,
causing them to become irritable.
Other neurologic symptoms such as meningitis, encephalitis,
and/or hemiplegia may develop in relation to diffuse damage of
brain tissue due to occlusion of arteries or to granulomatous
inflammation
Complications
Stillbirths in pregnant women
Hearing loss
Weight disorders
Loss of hair and nails
Disturbance of menstruation Disturbance of menstruation
Muscle stiffness
Death may occur from heart failure or central nervous
system failure
Trichinellosis is rarely detected clinically in animals.
In case of heavy burden, the following signs are seen:
Diarrhea,
Anorexia,
Clinical Signs In Animals
Anorexia,
Fever,
Weakness
myositis causing unwillingness to move.
Diagnosis
A blood test or muscle biopsy
Xenodiagnosis - lab rat is fed with a suspected piece of
tissue
DNA tests amplified with PCR have found T. spirals.
ELISA test
Treatment
Symptoms can be treated with aspirin and
corticosteroids
Thiabendazole can kill adult worms in the intestine;
however, there is no treatment that kills the larvae. however, there is no treatment that kills the larvae.
Immunity for this parasite appears to be lifelong.
Neurological symptoms need to be treated with steroids
due to inflammation.
Control & Prevention
Cook pork thoroughly (also flesh of bear, walrus, wild pigs)
Cook all garbage fed to hogs
Freezing is effective if carried out properly. The freezing
requirements differ with the size of the meat. Pieces not exceeding 6
inches in thickness require 20 days at 5F, 10 days at -10F, 6 days inches in thickness require 20 days at 5F, 10 days at -10F, 6 days
at -20F. Larger pieces require longer periods. Quick freezing and
storage for 2 days is effective.
Cook wild game meat thoroughly.
Freezing wild game meats, may not effectively kill all the worms.
This is because the species of trichinella that typically infects wild
game is more resistant to freezing than the species that infects pigs.
These organisms are characterized by having
Jointed legs
Arthropod : (Phylum Arthropoda)
Body segments
A hard outer covering or exoskeleton made of chitin
Classification
Phylum Arthopoda contains Classes :
E 1 Insecta (insects)
E 2 Arachnida (spiders, mites, ticks, scorpions,
etc),
E 3 Chilopoda (centipedes ),
E 4 Diplopoda (milipedes)
E 5 Crustacea (crabs, shrimp, lobsters, water
fleas, etc).
Myiasis
Acariasis
Tick paralysis
Scabies
Pentastomiosis
Arthropod : Imprtant zoonotic diseases
Pentastomiosis
Tungiasis
Arthropod borne allergies
Myiasis
E Infection of a fly larva (maggot) in human
tissue.
E This occurs in tropical and subtropical areas.
E People typically get the infection when they E People typically get the infection when they
travel to tropical areas in Africa and South
America.
E People traveling with untreated and open
wounds are more at risk for getting myiasis.
E Fly larvae need to be surgically removed by
a medical professional.
Causal Agent:
E Myiasis is infection with the larval stage (maggots) of
various flies.
E Flies in several genera may cause myiasis in humans.
E Dermatobia hominis is the primary human bot fly.
Cochliomyia hominovorax is the primary screwworm fly E Cochliomyia hominovorax is the primary screwworm fly
in the New World
E Chrysoma bezziana is the Old World screwworm.
E Cordylobia anthropophaga is known as the tumbu fly.
E Flies in the genera Cuterebra, Oestrus and Wohlfahrtia -
-animal parasites that also occasionally infect humans.
Epidemiology
E Usually occurring in tropical and subtropical areas.
E There are several ways for flies to transmit their larvae
to people.
E Some flies attach their eggs to mosquitoes and wait for
mosquitoes to bite people.
E Their larvae then enter these bites. E Their larvae then enter these bites.
E Other flies' larvae burrow into skin.
E These fly larvae are known as screwworms.
E They can enter skin through people's bare feet when
they walk through soil containing fly eggs or attach
themselves to people's clothes and then burrow into
their skin.
E Some flies deposit their larvae on or near a wound or
sore, depositing eggs in sloughing-off dead tissue.
Distribution
E Myiasis occurs in tropical and subtropical areas.
E These can include countries in Central America,
South America, Africa, and the Caribbean Islands.
Life cycle Life cycle
E Adults of Dermatobia hominis are free-living flies.
E Adults capture blood-sucking arthropods (such as mosquitoes) and lay eggs on their
bodies, using a glue-like substance for adherence.
E Bot fly larvae develop within the eggs, but remain on the vector until it takes a
blood meal from a mammalian or avian host.
E Newly-emerged bot fly larvae then penetrate the host's tissue.
E The larvae feed in a subdermal cavity for 5-10 weeks, breathing through a hole in E The larvae feed in a subdermal cavity for 5-10 weeks, breathing through a hole in
the host's skin.
E Mature larvae drop to the ground and pupate in the environment.
E Larvae tend to leave their host during the night and early morning, probably to
avoid desiccation.
E After approximately one month, the adults emerge to mate and repeat the cycle.
E Other genera of myiasis-causing flies (including Cochliomyia, Cuterebra, and
Wohlfahrtia) have a more direct life cycle, where the adult flies lay their eggs
directly in, or in the vicinity of, wounds on the host.
E In Cochliomyia and Wohlfahrtia infestations, larvae feed in the host for about a
week, and may migrate from the subdermis to other tissues in the body, often
causing extreme damage in the process.
Myiasis Transmission
E Infection from accidentally ingesting larvae
E From having an open wound or sore
E Through nose or ears.
E People can also be bitten by mosquitoes, ticks,
or other flies that harbor larvae.
People can also be bitten by mosquitoes, ticks,
or other flies that harbor larvae.
E In tropical areas, where the infection is most
likely to occur, some flies lay their eggs on
drying clothes that are hung outside.
Signs and symptoms
E A lump will develop in tissue as the larva
grows.
E Larvae under the skin may move on occasion.
E Usually larvae will remain under the skin and
not travel throughout the body. not travel throughout the body.
E Is having myiasis common?
E People with untreated and open wounds are
more likely to get myiasis
Treatment
E The larvae need to be surgically removed by a
medical professional.
E Typically, the wound is cleaned daily after the
larvae are removed.
Proper hygiene of wounds is very important E Proper hygiene of wounds is very important
when treating myiasis.
E Sometimes medication is given, depending on
the type of larva that causes the problem.
Prevention
E Taking extra care going to tropical areas and spending a
lot of time outside.
E Covering skin to limit the area open to bites from flies,
mosquitoes, and ticks.
E Use of insect repellant and follow Travelers Health
guidelines.
E In areas where myiasis is known to occur, protect yourself by
using window screens and mosquito nets.
E In areas where myiasis is known to occur, protect yourself by
using window screens and mosquito nets.
E In tropical areas, iron any clothes that were put on the line
to dry.
E Should any body be concerned about spreading infection
to the rest of his household?
E No. Myiasis is not spread from person to person. The only
way to get myiasis is through flies, ticks, and mosquitoes.
SCABIES
Causal Agent:
E Sarcoptes scabiei var. hominis, the human itch mite, is in the
arthropod class Arachnida, subclass Acari, family Sarcoptidae.
E The mites burrow into the upper layer of the skin but never
below the stratum corneum.
The burrows appear as tiny raised serpentine lines that are E The burrows appear as tiny raised serpentine lines that are
grayish or skin-colored and can be a centimeter or more in
length.
E Other races of scabies mites may cause infestations in other
mammals, such as domestic cats, dogs, pigs, and horses.
E It should be noted that races of mites found on other animals
may cause a self-limited infestation in humans with temporary
itching due to dermatitis; however they do not multiply on the
human host.
Scabies mite life cycle
Life Cycle
E Sarcoptes scabiei undergoes four stages in its life cycle: egg, larva, nymph
and adult.
E Females deposit 2-3 eggs per day as they burrow under the skin .
E Eggs are oval and 0.10 to 0.15 mm in length and hatch in 3 to 4 days.
E After the eggs hatch, the larvae migrate to the skin surface and burrow into
the intact stratum corneum to construct almost invisible, short burrows called the intact stratum corneum to construct almost invisible, short burrows called
molting pouches.
E The larval stage, which emerges from the eggs, has only 3 pairs of legs and
lasts about 3 to 4 days.
E After the larvae molt, the resulting nymphs have 4 pairs of legs .
E This form molts into slightly larger nymphs before molting into adults.
E Larvae and nymphs may often be found in molting pouches or in hair follicles
and look similar to adults, only smaller.
Life Cycle
E Adults are round, sac-like eyeless mites. Females are 0.30 to 0.45 mm long and 0.25
to 0.35 mm wide, and males are slightly more than half that size.
E Mating occurs after the active male penetrates the molting pouch of the adult female
E Mating takes place only once and leaves the female fertile for the rest of her life.
E Impregnated females leave their molting pouches and wander on the surface of the
skin until they find a suitable site for a permanent burrow.
While on the skins surface, mites hold onto the skin using sucker-like pulvilli attached E While on the skins surface, mites hold onto the skin using sucker-like pulvilli attached
to the two most anterior pairs of legs.
E When the impregnated female mite finds a suitable location, it begins to make its
characteristic serpentine burrow, laying eggs in the process.
E After the impregnated female burrows into the skin, she remains there and continues
to lengthen her burrow and lay eggs for the rest of her life (1-2 months).
E Under the most favorable of conditions, about 10% of her eggs eventually give rise
to adult mites.
E Males are rarely seen; they make temporary shallow pits in the skin to feed until they
locate a females burrow and mate.
Transmission of Scabies
E Occurs primarily by the transfer of the impregnated
females during person-to-person, skin-to-skin contact.
E Occasionally transmission may occur via fomites (e.g., E Occasionally transmission may occur via fomites (e.g.,
bedding or clothing).
E Human scabies mites often are found between the
fingers and on the wrists.
Scabies Transmission
E Transmission occurs primarily by the transfer of the impregnated females
during person-to-person, skin-to-skin contact.
E Occasionally transmission may occur via fomites (e.g., bedding or
clothing).
E Human scabies mites often are found between the fingers and on the
wrists.
Human scabies is caused by an infestation of the skin by the human itch E Human scabies is caused by an infestation of the skin by the human itch
mite (Sarcoptes scabiei var. hominis).
E The adult female scabies mites burrow into the upper layer of the skin
(epidermis) where they live and deposit their eggs.
E The microscopic scabies mite almost always is passed by direct,
prolonged, skin-to-skin contact with a person who already is infested.
E An infested person can spread scabies even if he or she has no symptoms.
E Humans are the source of infestation; animals do not spread human
scabies
Epidemiology
E Persons At Risk
E Scabies can be passed easily by an infested person to his
or her household members and sexual partners.
E Scabies in adults frequently is sexually acquired.
E Scabies is a common condition found worldwide; it affects E Scabies is a common condition found worldwide; it affects
people of all races and social classes.
E Scabies can spread easily under crowded conditions
where close body and skin contact is common.
E Institutions such as nursing homes, extended-care facilities,
and prisons are often sites of scabies outbreaks.
E Child care facilities also are a common site of scabies
infestations.
Crusted (Norwegian) Scabies
E Some immunocompromised, elderly, disabled, or debilitated persons
are at risk for a severe form of scabies called crusted, or Norwegian,
scabies.
E Persons with crusted scabies have thick crusts of skin that contain large
numbers of scabies mites and eggs.
E The mites in crusted scabies are not more virulent than in non-crusted
scabies; however, they are much more numerous (up to 2 million per
The mites in crusted scabies are not more virulent than in non-crusted
scabies; however, they are much more numerous (up to 2 million per
patient).
E Because they are infested with such large numbers of mites, persons
with crusted scabies are very contagious to other persons
E In addition to spreading scabies through brief direct skin-to-skin
contact, persons with crusted scabies can transmit scabies indirectly
by shedding mites that contaminate items such as their clothing,
bedding, and furniture.
E Persons with crusted scabies should receive quick and aggressive
medical treatment for their infestation to prevent outbreaks of scabies.
E However they do not multiply on the human host.
Symptoms in man
E The parasite pierces the skin to suck lymph and feed on
epidermal cells of hands, wrists, elbows, area around
mammary nipples and naval, penis and buttocks.
E The mites cause marked irritation resulting in intense itching
and scratching, which aggravates the condition. and scratching, which aggravates the condition.
E Scratching may cause secondary pyoderma which is
detrimental to mites.
E Usually there is absence of pruritus signs for first two or three
weeks following infection.
E Then pruitus appears which is associated with an urticarial
response.
E Scabies transmitted from animals to man is self limiting and
disappears after leaving a transient pigmentation.
Symptoms in animals
E Sarcoptic mange in animals is initially characterized by
erythema which may be unnoticed,
E but later on a popular dermatitis is evident.
Skin becomes dry and thickened, there is loss of hair E Skin becomes dry and thickened, there is loss of hair
(alopecia)
E Secondary infection (pyoderma)
E Self multiplication occur
E Formerly, scabies was frequently recorded during war
time among horses which were exposed to adverse
hygienic conditions.
Diagnosis
E Based upon
customary appearance
distribution of the the rash
presence of burrows.
E Whenever possible, diagnosis should be confirmed by
identifying the mite or mite eggs or fecal matter (scybala).
This can be done by E This can be done by
carefully removing the mite from the end of its burrow using the
tip of a needle or
by obtaining a skin scraping to examine under a microscope for
mites, eggs, or
mite fecal matter (scybala).
E However, a person can still be infested even if mites, eggs,
or fecal matter cannot be found;
E Fewer then 10-15 mites may be present on an infested
person who is otherwise healthy.
Treatment
E It is important to remember that the first time a person gets
scabies they usually have no symptoms during the first 2 to 6
weeks they are infested; however they can still spread scabies
during this time.
E Treatment also is recommended for household members and
sexual contacts, particularly those who have had prolonged
direct skin-to-skin contact with the infested personreinfestation.
E Products used to treat scabies are called scabicides because E Products used to treat scabies are called scabicides because
they kill scabies mites; some also kill mite eggs.
E Scabicide lotion or cream should be applied to all areas of
the body from the neck down to the feet and toes.
E In addition, when treating infants and young children,
scabicide lotion or cream also should be applied to their entire
head and neck because scabies can affect their face, scalp,
and neck, as well as the rest of their body.
E The lotion or cream should be applied to a clean body and
left on for the recommended time before washing it off.
E Clean clothing should be worn after treatment.
CONT..
E Bedding, clothing, and towels used by infested persons anytime
during the three days before treatment should be
decontaminated by washing in hot water and drying in a hot
dryer, by dry-cleaning, or by sealing in a plastic bag for at
least 72 hours.
E Scabies mites generally do not survive more than 2 to 3 days
away from human skin.
E Because the symptoms of scabies are due to a hypersensitivity E Because the symptoms of scabies are due to a hypersensitivity
reaction (allergy) to mites and their feces (scybala), itching still
may continue for several weeks after treatment even if all the
mites and eggs are killed.
E If itching still is present more than 2 to 4 weeks after
treatment or if new burrows or pimple-like rash lesions continue
to appear, retreatment may be necessary.
E Skin sores that become infected should be treated with an
appropriate antibiotic prescribed by a doctor.
E Use of insecticide sprays and fumigants is not recommended
Prevention & Control
E Scabies is prevented by avoiding direct skin-to-skin contact
with an infested person or with items such as clothing or
bedding used by an infested person.
E Scabies treatment usually is recommended for members of the
same household, particularly for those who have had
prolonged skin-to-skin contact.
E All household members and other potentially exposed persons
should be treated at the same time as the infested person to
E All household members and other potentially exposed persons
should be treated at the same time as the infested person to
prevent possible reexposure and reinfestation.
E Bedding and clothing worn or used next to the skin anytime
during the 3 days before treatment should be machine washed
and dried using the hot water and hot dryer cycles or be dry-
cleaned.
E Items that cannot be dry-cleaned or laundered can be
disinfested by storing in a closed plastic bag for several days
to a week.
E Scabies mites generally do not survive more than 2 to 3 days
away from human skin. Children and adults usually can return
to child care, school, or work the day after treatment.
CONT
E Persons with crusted scabies and their close contacts,
including household members, should be treated rapidly and
aggressively to avoid outbreaks.
E Institutional outbreaks can be difficult to control and require
a rapid, aggressive, and sustained response. a rapid, aggressive, and sustained response.
E Rooms used by a patient with crusted scabies should be
thoroughly cleaned and vacuumed after use.
E Environmental disinfestation using pesticide sprays or fogs
generally is unnecessary and is discouraged.
ACARIASIS
Infestation with ticks & mites Infestation with ticks & mites
TICKS:ORDER PARASITIFORMES
E Metastigmata - Ticks
Argasidae : Soft Ticks
Ixodidae : Hard Ticks
E Mesostigmata - Mites
ex.Pneumonyssus, Ornithonyssus
Hard tick
Note: scutum
on its back
Male(left) Male(left)
Female
(right)
Gnathosoma of hard ticks.
(a) dorsal view.
(b) Ventral view.
Note hypostome (). pedipalps ().
The mouthparts is composed of
chelicerae() and hypostome.
TICKS
E Soft Ticks - Argasidae
Argas , Ornithodoros, Otobius Otobius
E Hard Ticks - Ixodes
Dermacentor Dermacentor , , Rhipicephalus Rhipicephalus Dermacentor Dermacentor , , Rhipicephalus Rhipicephalus
Tick Paralysis
Important as vectors of other diseases
Rocky Mtn. Spotted Fever / Tick Fevers
Ehrlichia
Babesia (&other red blood parasites)
Lymes Dz.
Classification of ticks
According to the number of hosts they require during their life
cycle, ticks are classified into three categories :
1. One host ticks
E In these ticks all the three instars engorge on the same animal
and two ecdyses also take place on the same host. E.g. Boophilus
annulatus. annulatus.
2. Two host ticks
E IN these ticks larva engorges and moults on the host and nymph
drops off after engorgement to moult on ground and then imago, so
produced, seeks a new host, e.g. Rhipicephalus evertsi.
3. Three host ticks
E These require different hosts for every instar, they drop off
each time after having engorged and moult on the ground .e.g.
Ixodes ricinus.
The relationships with diseases
Direct impairment:
1 sting and blood sucking
2 tick paralysis (caused by the poison of ticks to
nervous system) nervous system)
Tick paralysis
E A disease affecting man and animals
E Characterized by an acute ascending flaccid motor paralysis.
E The condition may be fatal if ticks are not removed before onset of
respiratory paralysis. respiratory paralysis.
E Adult ticks, chiefly females but occasionally nymphs, of genus lxodes
are particularly associated with this condition,
E but other ticks specially Dermacentor andersoni and Ambylomma
and Argas persicus have also been reported to cause the disease.
E The motor paralysis is due to failure of release of acetylcholine
at the neuromuscular junction as somatic motor fibers are
blocked by the toxin liberated by ticks.
E The toxin is elobrated by the ticks ovaries and secreted by
salivary glands.
Tick paralysis
E Rapid onset-
malaise,vaige body pain, lassitude,cephalgia,irritability &
slight or no fever
E In a few hour ascending paralysis with muscular E In a few hour ascending paralysis with muscular
incordination
E Ataxia,disphagia & motor paralysis bilateral
sometime localised
E Death due to respiratory paralysis
E Most recover-paralysis subsides after removal of ticks
E Children affected more
Prevention & control of Ticks
E Agrasid ticks best controlled by destroying their nests or lairs.
E Infested native nests should be burned or
E Floor & walls plastered to eliminate cracks & crevices
E Spray with BHC or DDT E Spray with BHC or DDT
E Ixodid ticks elliminaqted by exterminating their rodent hosts &
destroying their habitats
E Infested grounds,houses & animals-sprayed with chlorinated
hydrocarbons
E Acaricides of choice-
Arsenic(.16-.2%)
Butacarb(.05%)
E ASTIGMATA-genera
E Sarcoptes
mange mite-all species
extreme pruritis/crusts
MITES
extreme pruritis/crusts
E Notoedres/Otodectes
ear mites-felids & canids
E Knemidokoptes
beak/skin mite - birds
MITES
E PROSTIGMATA
E Demodex
Follicle mite - all
species
E Trombiculids-
chiggers
E ORDER ACARINI
species
Often nonpathogenic
immunosuppressed
E Cheyletiella
Walking dandruff
canids/felids/lagomorp
E ORDER ACARINI
Oribatid Mites
intermed. Host for
tapeworms
potential livestock
MITES
E A number of parasitic mites transmit disease in man.
E Dermanyssus gallinae (Duges, 1834), commonly known as
red mite of poultry, attacks the fowl and pigeon.
E Human beings may also be infested when mites migrate
into bedroom and attack human bed causing skin lesions.
MITES
into bedroom and attack human bed causing skin lesions.
E Ornithonyssus bursa (Berlese, 1888), often called tropical
fowl mite, attack man and cause pruitus.
E This species can not survive for longer than ten days
away from a brid host.
E It is commonly found in Southern Africa, India, China,
Australia, Colombia, Panama and the United States.
Cont..
E Allodermanyssus sanguinus (Hisst, 1914) - blood-sucking mite &
commonly c/a house mouse mite- causes rickettsial pox of man.
E Fur mites of dogs (Cheylitiella Yasguri) and cats and rabbit mite (C.
parasitivorax) cause pruritus or dermatitis in man. They do not produce
lesions in the infested animals.
E Various species of chiggers, primarily of the genera Eutrombicula
and Neotrobicula, causes dermatitis in man.
Various species of chiggers, primarily of the genera Eutrombicula
and Neotrobicula, causes dermatitis in man.
E Their larvae attack many host species including man and transmit
trombiculosis.
E In nymphal and adult stages they are completely free living but their
numbers depend on the quantity of larvae that manage to survive by
living on various vertebral hosts.
E Dermatoses caused by
N. antumnalis in Central Europe
E. alfreddugesi in South America.
Cont..
E Nature-
mites usually live close to man
feeding on his stored products
cause allergic dermatitis or general allergies. cause allergic dermatitis or general allergies.
E Important of these are respiratory and contact
allergies.
E The mites and their excreta, debris and dust constitute
specific allergens which sensitize man and cause
bronchial asthma and rhinitis, mostly in children.
CONTROL
E Ventilation
E Cleanliness
E Fumigation
E Other acaricidal treatment E Other acaricidal treatment
Of storage places and products
Pentastomid infections
+ Pentastomids commonly known as tongue-worms
+ worm like parasites of respiratory system of snakes,
canines and human beings canines and human beings
+ whereas their immature forms (nymphs) are present in
domestic and wild herbivorous animals.
+ The species of public health importance belong to
genera Linguatuala and Armillifer.
Linguatula serrata
+ Occurs in nasal and respiratory passage of dog, fox and wolf
+ More rarely in man, horse, goat and sheep (Frohlich 1779).
+ The parasite is tongue shaped, slightly convex dorsally and
fiattened ventrally
Dog and man are infected by eating infected animals especially + Dog and man are infected by eating infected animals especially
sheep and cattle.
+ Local conditions leading to sharing of water sources with snakes and
susceptible mammals, facilitate the life cycle and increase possibility
of human infections.
+ Human infection with an adult is rare but a number of larval
infections have been reported from Africa, Southern and Wstern
Asia, Jamaica and USSR.
Armillifer spp.
+ A.ormillatus (Wyman, 1847) A. grandis and A. monilliformis have
been found in man.
+ Adult parasites occur in lungs, trachea and nasal passage of
snakes in Africa.
+ Its intermediate hosts - a variety of mammals including wild + Its intermediate hosts - a variety of mammals including wild
game, rodents and even man.
+ Human infections with Armillifer species occurs as a result of
+ drinking water contaminated with pentratomid eggs excreted by
infected snakes or
+ handling infected snakes or by eating undercooked flesh of
infected snakes.
+ Human infection with the larvae and nymph is fairly
common in Africa, particularly in the Republic of Congo.
Life cycle of Pentastomids
+ Adult female pentastomids produce several million fully
embryonated eggs, which pass out in the faeces.
+ The hatched larva is oval and tailed.
+ Its intermediate hosts are various fish, amphibians, reptiles or rarely
mammals. mammals.
+ After ingestion, the larva hatches and penetrates intestine and
migrate randomly in the body and lodged in lungs, liver and nymph
nodes where they metamorphose into a nymph.
+ The nymph is infective to definitive host, when eaten by the latter,
+ it penetrates the hosts intestine and bores into lung, where it
matures.
+ A definitive host that eats egg, can also serve as intermediate host.
Symptoms of Pentastomiasis
+ Two types of pentastomiosis have been reported from
human beings.
Visceral pentastomiosis results when eggs are eaten and + Visceral pentastomiosis results when eggs are eaten and
nymphs develop in various internal organs
+ Nasopharyngeal pentastomiosis results when nymphs that
are eaten locate in the nasopharynx.
Visceral pentastomiosis
+ Caused by A. armillatus -reported from liver, spleen, lungs,
eyes and mesenteries of people of Africa, Malaysia, the
Philippines, Java and China (Donges, 1966; Self et al., 1972, 1975).
+ Most infections cause few symptoms.
However, infection of spleen, liver or other organs causes + However, infection of spleen, liver or other organs causes
some tissue damage.
+ Occular involvement may cause vision damage.
+ The host response to nymphs is often highly inflammatory
(Self, 1972).
+ Experimentally produced heavy infections in rodents may
kill them.
Nasopharyngeal pentastomiosis
+ The nymph of L. serata cause this condition by invading the
nasopharyngeal space of human beings.
+ The condition is known as marara or halzoun.
+ A few minutes to half an hour or more after eating, there is
discomfort
A prikling sensation deep in the throat and pain may later + A prikling sensation deep in the throat and pain may later
extend upto ears.
+ Oedematous congestion of face, tonsils, larynx, Eustachian
tubes, nasal passages, conjuctiva and lips is sometimes marked.
+ Nasal and lachrymal discharges, episodic sneezing and coughing,
dyspnoea, dysphagia, dysphonia and frontal headache are
common.
+ Complications like absecesses in the auditory canal, facial swelling
or paralysis and sometimes asphyxiation and death may also occur
(Sachacher et al., 1969).
Prevention and control
E
+ The epidemiology of pentastomiosis depends on cultural
food patterns.
+ Nymphs are ingested when visceral organs of domestic
herbivores are consumed raw or undercooked.
+ Controlling the infection
Proper cooking of such infected visceral organs
Oiling of drinking water
Fleas
Life cycle
Tungiasis
E Causal agent in man: Tunga penetrans (Sand flea
or jigger or higoe flea)
E Hosts:The flea may attack pigs, monkeys and E Hosts:The flea may attack pigs, monkeys and
baboon.
E Nature:male fleas are free living whereas females
bury itself in the skin.
E Distribution: Africa, South of Sahara and few
tropical countries of South America.
Life cycle
E The female flea lays up to 20 eggs at a time out of
which larvae hatch in two days.
E These larvae are elongate, slender, maggot like
creatures
E and develop into pupal stage which finally turn into
adult.
Symptoms of Tungiasis
E Heavy infestation in man causes severe
inflammation, usually affecting feet.
E Infected individuals become restless, loose condition
and spoil their coats by biting and scratching.
Other fleas
E Various fleas of animals (dog and cat fleas) may
attack man if normal hosts not available.
E Ctenocephalides canis and C. felis -frequently attack
man. man.
E May transmit
Yerscinia pestis in man
on rare occasions, the tapeworms
Hymenolepis diminuta
Dipylidum caninum.
E Chicken flea, Ceratophyllus gallinae occasionally attack
man to produce skin reactions.
Prevention and control
E Control of fleas is difficult but temporarily, use
of insecticides is recommended.
E As a means of prevention, stout shoes should be
worn in infected area.
ARTHROPODE ALLERGENS
E Sensitization to allergens and a subsequent development of disease
only occurs after prolongedexposure to allergens that may take place
by inhalation, by skin contact or by ingestion (Colloff etal., 1992).
E In essence all species of arthropods are candidates for medically relevant
allergens.
E Arthropods secrete or excrete allergens provoking two different types
of allergic diseases: atopy and insect venom allergy (Mygind et ul.,
1996; Miiller & Mosbech; 1993).
E Imp- inhalant allergens causing atopic disease.
E Atopy is a so-called Type-I allergy: IgE-mediated and with immediate
phenomena (Mygind et ul., 1996).
ALLERGENS &ARTHROPODES
E Atopic diseases are
Allergic Asthma, Atopic dermatitis, and Allergic rhinitis.
E Prevalence of atopic disease in relation to arthropods -considerable (up to80% )
Exposure to arthropod allergens - more extensive in domestic as compared to
occupational environment. reasons: (a) humidity higher
(b) the exposure period is longer
E The exact nature and intensity of additional occupational exposure to arthropod
allergens depend on the type of working environment.
E In general, indoor exposure to arthropod allergens has increased in the last 20 years
due to energy saving campaigns, leading to less ventilation and resulting in improved (more
humid) conditions for arthropods (Wickman et al., 1993).
E In essence the office and hospital environment are comparable to the domestic
environment
Occupational environment
E Some occupations result in a massive exposure to certain allergens, inducing specific work-
related allergies.
E As high risk occupations
E Pest exterminator (In atopics in general population sensitization to carpet beetles
amounts atopic disease to 35% (Klaschka and Rudolph, 1980).
E Employees of insect and mite laboratories (a high incidence of due to allergens of
the grain weevil , larvae of the bee moth locusts chironomid midges and cockroaches)
E Farmers and other workers in the food processing industry
(Dairy farmers -now a days abundantly allergic to storage mites; shipping workers -asthma due
to grain mites and insects )
E Workers in the silk industry (Silk worm derived atopic disease -Prevalence 12-52% )
E Sewage handlers (Asthma caused by sewer flies Psychoda alternata )
(compiled from Moscato and Dellabianca, 1994, Kagen, 1990).
MANAGEMENT &CONTROL
E Establishment of hygienic exposure limits for sensitization and for the
development of allergic symptoms.
E Until now thesethreshold levels - established for mites and cockroaches only.
E Allergen management programs are effective if allergen concentrations
remain below these thresholds.
For the allergens produced by other arthropods no hygienic thresholds have E For the allergens produced by other arthropods no hygienic thresholds have
been established- aim at the maximum reduction technically possible
E Mite allergen exposure is measured in settled dust as mite allergen
concentration, number of mite bodies, or guanine concentration
E The threshold level for the development of an acute asthma attack in
miteallergic persons is 10 pg of Der p I or 3.0 mg of guanine per gram
settled dust, or 500 mites per gram bed dust (Platts-Mills and de Weck, 1989).
E Threshold level for sensitization to cockroaches -at 2-8 ng Bla g I1 allergen
per gram dust
MANAGEMENT &CONTROL
E Pest extermination
E Removal of pests with or without pesticides forms the heart of a management plan for
arthropodallergens.
E Effective pesticides against mites and cockroaches include benzyl benzoate,
chloropyrifos,and synthetic pyrethroids
E Unwashable objects, such as furniture, may also be treated with pesticides against house
dust mites, in combination with moist cleaning, including vacuum cleaning to remove the dust mites, in combination with moist cleaning, including vacuum cleaning to remove the
loosened dirt.
E Reduction of inhalant allergens
E The remaining allergens have to be removed, e.g. by thorough wet or moist cleaning,
before a clinical effect becomes evident
E Inactivation of arthropod allergens is attempted by application of tannine or tannate
formulations to textiles.
E The effectiveness of this procedure has been studied with RAST inhibition tests.
E Management in the occupational environment
E To prevent allergic manifestations due to work, different Partners-in-Care are called for.
E Fundamentally, five partners are responsible for the well-being of the employee at work: architectand
building engineer, facility manager, manager of the organisation, the medical services of theorganisation,
and the employee themself
INTRODUCTION
Synonym: Guinea worm.
Etiology: Dracunculus medinensis.
The guinea worm is one of the best historically
documented human parasites. documented human parasites.
The parasite was named Medina as it was
common in Medina by Avicenna.
The role of cyclops as vectors for transmission of
infection to man was dscovered in 1870 by
Fedtshenko.
DISTRIBUTION
In 1986, there were an estimated 3.5 million
cases of Guinea worm in 20 endemic nations
in Asia and Africa. ( Carter Center, 2011).
The number of cases has been reduced by
more than 99% to 3,190 in 2009, of them four
African countries will be Sudan, Ghana, Mali African countries will be Sudan, Ghana, Mali
and Ethiopia.
In India, states like AP, Gujarat, Karnataka,
MP, Maharastra, Rajasthan, TN its prevalent.
LIFE CYCLE
Definitive Host: Man.
Intermediate Host: Cyclops.
Infective Stage: Third stage larvae of
D.medinensis
Transmission: Oral. Transmission: Oral.
CLINICAL MANIFESTATION
Stinging papule at the site of entry of entry of
the parasites.
Lesions over a few days develops into blister.
Fever. Fever.
Nausea.
Vomiting.
Incapaciation.
In animals.
Course and clinical manifestation is very similar
to those seen in human beings.
In dogs, there have been clinical cases of purulent In dogs, there have been clinical cases of purulent
skin nodules caused by D.insignis
Diagnosis
Cephalic end of parasite
emergence.
Radiologic examination
ELISA.
TREATMENT
No specific treatment
available.
Age old remedy is to pull out
the parasite onto a stick.
Surgical removal.
CONTROL
Prevention is the best approach.
Bore holes and hand dug wells.
Water filters and piping.
Clean water source.
Educating people.
INTRODUCTION
Synonym: Capillariosis.
Etiology:
C. philippinensis ( Intestinal capillariasis).
Transmitted through ingestion of infected fish.
Man is the definitive host. Man is the definitive host.
C. hepatica.(Hepatic capillariasis ).Transmitted
through infected soils
C. aerophila (Pulmonary capillariasis).
Transmitted through infected soil
DISTRIBUTION
C. philippinensis : Philippines, Thailand, sporadic
cases found in UAE, India, Spain, Indonesia.
C. hepatica: Found in all continent. C. hepatica: Found in all continent.
C. aerophila: North America, Europe, Former
Soviet Union, Australia, Chile and Uruguay.
LIFE CYCLE OF C. PHILLIPINENSIS
LIFE CYCLE OF C. HEPATICA
LIFE CYCLE OF C. AEROPHILA
Adult lay eggs in lungs
Eggs are coughed up and
swallowed by host
Eggs passed in the faeces
Larvae hatch in the
intestine and migrate to Eggs passed in the faeces
Larvae develops into
infective stage
Suitable host eats the
mature eggs
intestine and migrate to
lungs
CLINICAL MANIFESTATION
C. philippinensis: Serious and fatal disease if not
treated in time.
Abdominal pains.
Intermitten diarrhoea.
Death occurs due to heart failure Death occurs due to heart failure
C. hepatica
Hepatomegaly.
Morning fever, nausea, vomiting.
Spleenomegaly.
C. aerophila
Coughing
Mucoid or sometimes blood tinged
expectorant.
Fever. Fever.
Dyspnea.
Moderate eosinophillia.
C.phillipinensis has not been found in land animals but
only fish eating birds are natural host, though it is not
known whether it causes symptoms in them.
C. hepatica causes infection in rodents.
Hepatitis
Splenomegaly
Eosinophilla Eosinophilla
C.aerophila most severe in foxes, causes
Rhinitis
Tracheitis
Bronchitis
Diagnosis
C. philippinensis: finding eggs, larvae and/or adult
worms in the stool, or in intestinal biopsies.
In severe infections, embryonated eggs, larvae, and
even adult worms can be found in the feces.
C. hepatica:
Demonstrating the adult worms and/or eggs in liver
tissue at biopsy or necropsy.
C. aerophila:
Demonstrating eggs in stool or in lung biopsy.
Treatment
Mebendazole and albendazole.
Control
Refrain from eating raw fish.
Washing of hand, food and eating them raw
should be avoided.
Strict hygiene rule should be followed.
INTRODUCTION
Synonym: Hepatic distomiasis, fasciolosis.
Etiology: Fasciola hepatica and Fasciola
gigantica.
Live fluke acquired by eating raw vegetables. Live fluke acquired by eating raw vegetables.
(Water cress is classic).
3-4 month prepatent period.
Sheep & Cattle are reservoir.
DISTRIBUTION
F. hepatica Europe, America (specifically the south
and west), Australia more temperate areas.
F. gigantica Asia and Africa more tropical areas.
2.4 million people infected.
180 million people are at risk.
A lot of cases are probably not reported, especially in
Africa (note question marks). Africa (note question marks).
This is mostly in the developing countries, and not
developed ones, as a neglected disease, it has largely
been eliminated from the developed world and so is
largely forgotten in the developing world.
In India in 1997 a case of Fascioliasis was reported
from Assam. (Narain et al).
MORPHOLOGY
Adult worms are large
leaf-like, 20 to
30 mm in length.
At the anterior end, At the anterior end,
distinct conical
projection is observed.
F. gigantica
F. hepatica
THE FASCIOLA LIFE CYCLE
CLINICAL MANIFESTATION
The triad of fever, hepatomegaly, and
eosinophilia in endemic area suggests
fascioliasis.
Symptoms and signs are associated with biliary
obstruction and cholangitis. obstruction and cholangitis.
Acute epigastric pain, pruritus, and jaundice are
common.
Worms in human infections may be frequently
found in ectopic foci.
In Animals.
Disease of herbivores.Sheep most susceptible followed
by Cattle.
Acute form:
Destroying hepatic tissues, haemorrhages, hematomas,
periferal inflammation.
In massive infection Sheep may die.
Chronic form.
Progressive anaemia, weakness, loss of appetite.
Submandibular edema i.e. bottle jaw.
DIAGNOSIS
Stool examination.
ELISAIgG serology >95%sensitive
Imaging
Treatment:
Triclabedazole drug of choice.
Artemether has been shown to be effective in a
rat model of fascioliasis .
Nitazoxanide.
MEASURES SHOULD BE TAKEN TO
PREVENT INFECTION BY THE FLUKES
Control of aquatic plant industry.
Wash aquatic plants in vinegar.
Health Education.
Clean water. Clean water.
DICROCOELIASIS
Synonym: lancet fluke, small liver fluke.
Etiology: Dicrocoelium dendriticum.
Digenean trematode.
Part of the Dicrocoeliidae family of liver flukes. Part of the Dicrocoeliidae family of liver flukes.
DISTRIBUTION
Most of Europe and Asia
North America
South America
Australia
North Africa North Africa
alkaline soils that are
favorable environments
for reproduction and
survival of the
intermediate hosts
MORPHOLOGY
6-10 mm long
1.5-2.5 mm wide
Pointed ends
LIFE CYCLE
CLINICAL MANIFESTATION IN MAN AND
ANIMALS
Clinical symptoms are not usually manifested
even in heavy infections.
However they may show anemia, edema,
emaciation,and in advanced cases, cirrhosis, and emaciation,and in advanced cases, cirrhosis, and
scarring of the liver surface.
DIAGNOSIS
Adult dicrocoelia recovered in the liver post
mortem.
Stool examination.
Immuno-diagnostic techniques.
Immuno-flourescence precipitation. Immuno-flourescence precipitation.
Passive haemoagglutination test.
Complement fixation.
ELISA.
TREATMENT
Anti-helminthic drugs like benzimidazole and pro-
benzimidazole derivatives.
No treatment has been proven effective.
Control
Husbandry practices (dont allow to graze at night or early in Husbandry practices (dont allow to graze at night or early in
the morning)
Try and control snail and ant populations (difficult/expensive)
Test the soil to see whether it could be suitable for the
intermediate hosts
As humans we should avoid the urge to nibble or suck on grass
which may have ants on it.
ECHINOSTOMIASIS
Synonym: Echinostomadiosis
Etiology: Echinostoma ilocanum.
First described by Garriso in 1907.
Tubangi in 1931 showed Norway rat act as a Tubangi in 1931 showed Norway rat act as a
reservoir host.
The infection in dog was reported by Chen and
Canton.
DISTRIBUTION
Endemic to South East Asia such as
Mainland China
Taiwan.
India.
Korea.
Malaysia.
In India
Maji et al reported a case of E. malaynum in 1993.
Grover et al reported a case of E. ilonacumin 1998.
MORPHOLOGY
Tegument covered with spines.
Testes are lobed.
Eggs are operculated, straw colored.
LIFE CYCLE
Definitive Host: Man and other animals.
First IH: Planorbid snails.
Second IH: Fresh water mollusc.
Infective stage: Metacercariae.
Transmission: Eating raw infected freshwater Transmission: Eating raw infected freshwater
mollusc.
CLINICAL MANIFESTATION IN MAN AND
ANIMALS
Heavy infection may cause
Diarrhoea
Flatulence
Colic pain Colic pain
Severe anaemia
Edema.
DIAGNOSIS
Stool examination.
TREATMENT
Praziquantel, Albendazole, Mebendazole. Praziquantel, Albendazole, Mebendazole.
CONTROL
Population educated about the parasites
Biological controls.
FASCIOLOPSIASIS
SUBMITTED BY:
JOY LALMUANPUIA
ROLL NO: 1391
INTRODUCTION
Etiology: Fasciolopsis buski
Synonyms: Ginger Fluke, Intestinal Fluke.
First reported by Busk in London 1843, was
found in the duodenum of a sailor. found in the duodenum of a sailor.
Life cycle in human first describe by Barlow in
1925.
Duodenal digenetic trematode.
Family: Fasciolidae.
DISTRIBUTION: SOUTH-EAST ASIA
The prevalence of fasciolopiasis is related to
growing water plants and feeding pigs on water
plants.
In India cases have been reported from states such
as- as-
Delhi (Mahajan et al 2010).
Bihar (Rai et al 2007).
U.P. and Maharastra (CD alert 2005).
Assam, W.B., A.P., Nagaland, Meghalaya, Mizoram and
Tripura. (Parija, 1990).
Fasciolopsis Fasciolopsis Fasciolopsis Fasciolopsis buski buski buski buski: :: : is endemic in China (Taiwan), South is endemic in China (Taiwan), South is endemic in China (Taiwan), South is endemic in China (Taiwan), South- -- -East East East East
Asia, Asia, Asia, Asia,
Malaysia and India. Malaysia and India. Malaysia and India. Malaysia and India.
MORPHOLOGY
Adult worm
Like a ginger piece
Big muscular trematode
Have strong suckersventral >> oral
Egg
Biggest( largest helminth egg)
Ovoid
Minute operculum Minute operculum
Yellowish
LIFE CYCLE OF FASCILOPSIS BUSKI
1. Site of inhabitation: small intestine.
2. Infective stage: metacercaria.
3.Infective mode: eating raw water plants with
metacercariae.
4. Medium of water plants: chestnut, water bamboo 4. Medium of water plants: chestnut, water bamboo
and caltrop.
5. Intermediate hosts: Planorbis snail.
6. Reservoir host: pig.
7. Life span: 1-4 years.
CLINICAL MANIFESTATION IN MAN AND
ANIMALS
Abdominal pain
Acute intestinal obstruction
Anemia Anemia
Generalized edema
In extreme cases death may occur.(Jay, 2005).
DIAGNOSIS DIAGNOSIS DIAGNOSIS DIAGNOSIS
Stool Stool Stool Stool examination examination examination examination:
1. Direct fecal smear
2. Water sedimentation method
Treatment Treatment Treatment Treatment and and and and Prevention Prevention Prevention Prevention: :: : Treatment Treatment Treatment Treatment and and and and Prevention Prevention Prevention Prevention: :: :
The treatment of the patients, carriers and pigs
Drug of choice is Praziqantel. Other effective drugs
include Hexachloroparaxylol, Bithionol,
Nitazoxanide.
Control Control Control Control
(1) Health education.
(2) Deal with night soil. (2) Deal with night soil.
(3) Avoid feeding pigs on raw water plants.
HYMENOLEPIASIS INTRODUCTION
Synonyms: Dwarf tapeworm, rat tapeworm.
Etiology: H.nana and H.diminuta.
Smallest tapeworm infecting man.
Found worldwide.
Mainly among children.
Only human tapeworm that can complete its
life cycle in a single host.
Man can harbor both the adult and larval
stages of the parasite.
LIFE CYCLE OF H.NANA
Host: Life cycle is completed in a single host,
Man, rat, mouse.
Infective stage: Eggs of H.nana.
Transmission: External autoinfection.
Internal autoinfection.
Person to person through food
and water contaminated with
eggs.
LIFE CYCLE OF H.DIMINUTA
Rat tapeworm.
Common parasite of rats and mice.
Accidental human infections.
Differs from Hymenolepis nana in life cycle
because it requires an intermediate host. because it requires an intermediate host.
2 Hosts
Larval stage: cysticercoid is passed in fleas
Adult stage: in rats and mice and accidentally in
humans especially children who accidentally ingest
infected fleas.
CLINICAL MANIFESTATION IN MAN
AND ANIMAL
Symptoms are produced due to patients immunological
response to the parasite
Asymptomatic for light worm burden
Headache
Dizziness
Anorexia
Pruritus of the nose and anus Pruritus of the nose and anus
Abdominal pain
Pallor
Desquamation of intestinal epithelial cell or as serious as
necrosis may occur
Regulatory immunity will eventually limit the infection.
Clinical manifestations are minimal and non-specific
for H. diminuta.
DIAGNOSIS
Demonstration of characteristic ova in the stool.
Proglottids are not recovered because they undergo
degeneration prior to passage.
Treatment
Praziquantel Drug dosage is higher than that of Praziquantel Drug dosage is higher than that of
taeniasis because of resistant cysticercoids in
intestinal tissue.
Control.
Improve personal hygiene and sanitary measures.
DIPYLIDIASIS INTRODUCTION
Synonyms: Dog tapeworms, dipylidiosis,
cucumber tapeworms.
Etiology: D.caninum.
Found wherever there are dogs and fleas. Found wherever there are dogs and fleas.
Mainly affects young children.
LIFE CYCLE
Definitive host: Man, dog, cat.
Intermediate host: Dog flea,cat flea.
Infective stage: Cystecercoid larvae of
D.caninum.
Transmission: ingestion of fleas infected with Transmission: ingestion of fleas infected with
cysticercoid larvae.
In Man:
Diarrhoea and colic.
Erratic appetite and insomnia.
The infection is often asymptomatic.
In Animals In Animals
Anal irriatation or irritation
Diagnosis:
Demonstration of eggs in faeces.
Treatment:
Praziquantal.
Control:
The prevention of the disease through hygiene The prevention of the disease through hygiene
when handling the dog and in the consistent flea
control and deworming the dog.
DIPHYLLOBOTRIASIS DIPHYLLOBOTRIASIS DIPHYLLOBOTRIASIS DIPHYLLOBOTRIASIS INTRODUCTION
Synonym: Broad tapeworms, fish tapeworms.
Etiology: D. latum.
Common in fish eating carnivores.
It is a cosmopolitans species found in
temperate zones.
LIFE CYCLE
Definitive host: Man and other fish eating
mammals.
First IH:Copepods and cyclops
Second IH: Fresh water fish.
Infective stage: Pleocercoid larvae.
Transmission: oral.
Symptoms:
diarrhea, abdominal pain, vomiting, weight loss, fatigue,
constipation and discomfort.
Pernicious anemia caused by tremendous
absorption of Vitamin B12 by worm -
Vitamin B12 needed to make RBC.
In animals not clinically apparent.
Infection with small number of larvae may not
cause major damage but with large number of
larvae may cause death of animals
DIAGNOSIS
Microscopic examination of feces for the
characteristic operculated eggs.
Treatment:
Praziquantel
Niclosamide.
Control
prevention of water contamination both by
raising public awareness of the dangers of
defecating in recreational bodies of water and
by implementation of basic sanitation
measures.
INTRODUCTION
Schistosomiasis is an ancient diease of man.
Recorded in as early as 1250 B.C. (Parija, 1990).
Eggs were demonstrated in 20
th
Dynasty
mummy by Ruffer in 1910. mummy by Ruffer in 1910.
Bilharz first demonstrated adult worm in
mesenteric vein of man in Cairo in 1851.
Synonyms- Bilharziasis, Katayama syndrome.
6 species of human schistosomes
Schistosoma japonicum
S. mansoni
S. haematobium S. haematobium
S. intercalatum
S. mekongi
S. malayi
DISTRIBUTION:WORLD WIDE
600 million people are exposed to the risks of
schistosomiasis of whom 200 million are
infected. Schistosomiasis is after malaria the
most important parasitic disease of mankind.
In India cases of Schistosomiasis have been In India cases of Schistosomiasis have been
reported from
Gimvi (Godgil and Shah, 1952).
Assam ( Narain et al, 1994).
Jabalpur ( Agarwal et al, 2000).
Chattisgarh ( Agarwal et al, 2000).
MORPHOLOGY
Adult
Male (15 mm length) < female (22 mm)
Oral sucker < ventral sucker
2 paralleled guts form a blind caecum in the 2 paralleled guts form a blind caecum in the
posterior ends
Gynecophoric canal (male) in which female
repose.
Egg
Ovoid and non-opeculate
74~106 m 55~80 m
Contains one miracidium
Bear a minute lateral knob.
S. japonicum S. japonicum S. japonicum S. japonicum S. mansoni S. mansoni S. mansoni S. mansoni S. haematobium S. haematobium S. haematobium S. haematobium
Schistosome egg Schistosome egg Schistosome egg Schistosome egg
LIFE CYCLE
EPIDEMIOLOGY
Source of infection: humans and mammals
(especially cattle) infected by schistosome.
Route of transmission: three major factors are
responsible for the occurrence of
schistosomiasis
The method of disposal of human excreta The method of disposal of human excreta
The presence of the snail intermediate host
The contact with cercaria-infected water
Susceptibility : everyone is susceptive.
Especially peasant and fisherman.
S.HEAMATOBIUM (UROGENITAL)
In urinary schistosomiasis damage
to the urinary tract is revealed by
blood and schistosome eggs in the
urine.
Eggs which get stuck in the tissues
may calcify and lead to the
formation of granulomas and
superinfections. superinfections.
Urination becomes painful and is
accompanied by progressive
damage to the bladder, ureters and
then the kidneys.
Bladder cancer is common in
advanced cases.
Macrohematuria: A sample of
normal urine and blood-
containing urine from a child
suffering from urinary
schistosomiasis
1. Site of inhabitation: Pelvic and messenteric
plexuses.
2. Infective stage: Cercaria.
3.Infective mode: Penetration of skin by
infective cercaria.
4. Intermediate hosts: Different species of snails
belonging to the genus Bulinus
S. mansoni (Intestinal Schistosomiasis)
Main lesion found in intestinal wall.
In acute cases-
Fever.
Diarrhoea. Diarrhoea.
Abdominal pain, weight loss.
Chronic cases-
Persisten diarrhoea.
Abdominal pain with hepatomegaly or
splenomegaly
1.Site of inhabitation: Messenteric veins.
2. Infective stage: Cercaria.
3.Infective mode: Penetration of skin by
infective cercaria.
4. Intermediate hosts: Snails of Biomphalaria
spp.
SCHISTOSOMA JAPONICUM (ASIATIC
SCHISTOSOMIASIS)
Acute Schistosomiasis
Clinical manifestations come out after 4 to 8 weeks of
infection, similar to the time from egg to adult worm
(40 days)
Fever: intermittent, maintain weeks to months Fever: intermittent, maintain weeks to months
Allergic reaction:urticaria, angioneuroedema,
enlargement of lymph nodes and eosinophilia
Digestive syndromes: abdominal pain, diarrhea with
pus and blood, constipation or diarrhea
Hepatosplenomegaly.
Chronic Schistosomiasis
Asymptomatic: most person are
asymptomatic
Symptomatic: the most common syndrome is
abdominal pain with intermittent diarrhea.
hepatosplenomegaly
1.Site of inhabitation: Portal vein system.
2. Infective stage: Cercaria.
3.Infective mode:Penetration of skin by
infective cercaria. infective cercaria.
4. Intermediate hosts: Snails of Oncomelania spp.
DIAGNOSIS
Parasitological
diagnosis (etiological,
definitive diagnosis)
Demonstrating eggs by
stool examination
Stool examination after
Schistosoma eggs in the stool
Stool examination after
concentration
(sedimentation)
Rectal biopsy eggs-
demonstration
Urine examination
Schistosoma eggs in the stool
Urine is collected in empty beer bottles
for further analysis (courtesy
WHO/TDR
DRUG TREATMENT
Praziquantel is the best choice of drug for the
therapy of schistosomiasis
Dose:
chronic schistosomiasis
10mg/kg, tid. Po, for 2 days, total 60mg/kg 10mg/kg, tid. Po, for 2 days, total 60mg/kg
Acute schistosomiasis
10mg/kg,tid. po,for 4 days, total 120mg/kg
Vice reaction: slight and short.
Oxamniquine: effective in a single dose, but
only against S. mansoni
PREVENTION
Control of the source of infection:
Treat the patients and domestic animal at the
same time.
Cut off the route of transmission: Cut off the route of transmission:
Snail control
Sanitary disposal of human excreta
Protect of susceptive people:avoid the contact
with schistosome-infected water.
Provision of safe, adequate water supply and
sanitation
A researcher using a scoop to search for
freshwater snails which are intermediate
hosts in the schistosomiasis cycle.
A scoop being used to collect freshwater snails
which are intermediate hosts in the
schistosomiasis cycle

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