814 Proceedings of the Royal Society of Medicine 34

interpreted with extreme caution as the proportions quoted are crude rates. The figures for
London and Middlesex are taken from the reports of the respective County Medical Officers.
It is interesting, but possibly without significance, to observe that the deaths seem to follow the
pattern of London, the area from which the estate inhabitants have come, while the incidence
of new cases follows Middlesex in which county they are now living. From Table XVII it
TABLE XVII.-CouNcIL ESTATE B, RELATIONSHIP OF "INFECTED HousEs" 1930-51
Next door houses Next door but one
Actual ............ ... ... ... ... ... ... 79 62
Expected ... 65 2 60-9
Difference/Standard Error.. 1 71 0-14
5% level. ... ... ... ... ... ... ... ... 195
can be seen that on this particular estate the number of next door "tuberculous" houses does not
reach statistical significance. Further, as in 28 instances it is known that although next door
houses contained at some time tuberculous individuals there was in fact no possible connexion
between them (e.g. both were tuberculous before living on the estate), we conclude that there
is no evidence of appreciable house-to-house spread of tuberculosis on this particular estate.
Summary.-Our findings suggest that the known case of tuberculosis can, when taught the
necessary hygiene precautions, be largely neutralized as a source of infection to others; the
unknown case is a great danger and is probably the cause of tuberculous infection and consequent
disease in individuals soon after leaving school; the X-ray of doctors' referred cases is a very
important although not the only method of discovery of these unknown cases of phthisis; there
is no evidence of appreciable house-to-house spread of tuberculosis on the new housing estates
we have studied.
We wish to thank Drs. A. F. Adamson, E. Grundy, and E. W. Caryl Thomas, Medical
Officers of Health of Hendon, Wembley, and Harrow, and Drs. A. W. Anderson and W. C.
Harris for the help they have given us with the work reported, Mr. D. J. Wheeler for assistance
in the statistical analysis of the housing estate results, the General Practitioners in our areas for
their co-operation, and Miss E. Last and Miss M. Shaw for preparing tables and lantern slides.
REFERENCES
ANDERSON, A. W., and GRENVILLE-MATHERS, R. (1952) Lancet, ii, 330.
-, , and TRENCHARD, H. J. (1951) Lancet, i, 842.
COCHRANE, A. L., Cox, J. G., and JARMAN, T. F. (1952) Brit. med. J., ii, 843.
JARMAN, T. F. (1953) Brit. med. J., i, 754.
MACDOUGALL, I. A., MIKHA1L, J. R., and TATTERSALL, W. H. (1953) Brit. med. J., i, 64.
Medical Research Council (1952) Lancet, i, 775.
TRENCHARD, H. J. (1945) Lancet, ii, 842.
(1949) Lancet, ii, 956.
(1951) Lancet, ii, 539.
and GRENVILLE-MATHERS, R. (1952) Tubercle, 33, 20.

Psittacosis: Recent Epidemiological Observations

By J. C. N. WESTwOOD, M.R.C.S., L.R.C.P.
DURING 1952 psittacosis, for the second time in the history of the disease, suddenly leaped
from its position as something of a medical curiosity and became an immediate problem to the
public health services and clinicians, and received considerable publicity in the daily press.
From the time of its earliest known recognition by Jurgesson in 1874, as a clinical entity
associated with sick parrots, small sporadic outbreaks have occurred, the most notable being
that in Paris in 1892 where there were 51 known cases with 16 deaths, a high fatality rate which
continued to be associated with the disease until the introduction of antibiotic therapy. But in
1929-30 the whole position changed and the disease ceased to be a curiosity. The world was
flooded in those years with parrots derived largely from South America where, in the Argentine,
there was a very severe epidemic amongst bird dealers and the public, and what has been rather
generously termed a "pandemic" of psittacosis occurred. In 12 different countries a total of
750-800 known cases occurred with a fatality rate of 18%.
Bedson, at the London Hospital, soon demonstrated that the disease was due to a filter-passing
virus (Bedson, Western and Simpson, 1930) and subsequently knowledge of the disease was
Frapidly acquired on both sides of the Atlantic. Bedson and his colleagues worked on the
35 Section of Epidemiology and Preventive Medicine 815
biological characters of the virus, demonstrating its life-cycle and dependence on living cells
(Bedson and Bland, 1932, 1934; Bland and Canti, 1935; Bedson, 1933; MacCallum, 1936). Bedson
further developed the complement-fixation test for serological diagnosis. Rivers and his colleagues
in America worked out in detail the nature of the infection in various laboratory animals and
showed that the probable route of human infection was by the upper respiratory tract from
dust derived from the dried faces and nasal discharges of sick birds. He showed that the mouse
could be used for isolation of the virus from human sputum and that monkeys, and probably
man, could be immunized by the inoculation of live virus (Rivers, Berry and Sprunt, 1931; Rivers
and Berry, 1931).
Meanwhile Meyer and Eddie in California demonstrated that so far from being confined to
South American parrots the disease was widespread throughout domestic aviaries and that native
Australian budgerigars were also infected (Meyer and Eddie, 1933). Aviaries in Europe were
later shown also to be infected (Levinthal, 1935). Following a further demonstration by
Levinthal of infection in Australian parrots consigned to London, Burnet undertook an investiga"
tion of the disease in wild birds in Australia and showed that the true parrots, lorikeets and
cockatoos were endemically infected. The disease was normally mild with a long carrier
state. Fledglings became infected in the nest and pa'ssed the infection to their own young in
the next breeding season. Occasionally in the wild, and almost invariably, as a result of
insanitary conditions of transport, among captured birds, the host-parasite equilibrium was
upset and highly fatal epizootics occurred (Burnet, 1935).
The work of Meyer, Eddie and Burnet showed clearly that psittacine birds the world over
were a source of danger and when it was found that the fulmar petrels of the Faroe Islands were
endemically infected and a source of human cases, the field widened yet further (Rasmussen,
1938; Haagen and Mauer, 1938; Bedson, 1939). Infection has now been demonstrated in at
least 70 species of birds belonging to 10 different orders. So far in this country only pigeons,
herring gulls, black-backed gulls, and ducks have actually been incriminated.
In spite of the fact that the infection is now so widespread amongst birds the imposition in
1930 of bans on the importation of psittacines by many countries brought the human outbreak to
an abrupt end and psittacosis once more retired into obscurity. Isolated human cases continued
to occur and the biggest single source of such cases was pigeons, but the disease ceased to be
an important health problem.
However, in 1952, on the grounds that pigeons in this country were already infected so
reimportation of the virus could do no further harm, the ban on importation of psittacines was
lifted. Within two months psittacosis had re-emerged and a series of outbreaks occurred
culminating in the death of a dealer in Birmingham.
In Table I the figures obtained from examination of sera at the Central Public Health
Laboratory in 1952 are compared with those of the previous two years. In Table II is shown
the change in the distribution of bird and animal contacts. In the latter table is given the
history of association and this does not necessarily imply a causal relationship. It is not known,
for instance, whether cats or dogs can transmit viruses of this group, though one of the group
is responsible for epizootic pneumonia in cats.
These figures make it clear that birds of the psittacine family constitute a far graver threat to
their human associates than do the endemically infected native birds. The reason for this is
probably twofold. Firstly the parrot is a domestic pet usually in intimate contact with the family.
Secondly cases are nearly Rdways associated with sick birds recently purchased, birds in fact which
must be shedding huge quantities of virus so that their human contacts are exposed to very
TABLE I.-SEROLOGICAL EVIDENCE OF PSrrTACOSIS
July 1949 - June 1951 1952
Upper respiratory infections. Sera examined 1,660 1,251
Positive to psittacosis-LGV (titre 1/40 or rising) 36 52
Percentage positive . ... ... ... 2-2 4-2

TABLE II.-ANIMAL AND BIRD CONTACTS OF POSITIVE CASES

1949-51 1952
Pigeons ...... .............
... 12 3
Chickens ................... ... 5 2
Blackbird - 1
Sick cats .-.. ... ... ... ... ... ... 2
Healthy dog .......... ... ... ... 2
" Many birds" ... ... ... ... ... ... 1
Budgerigar .1 13
Parrot .1 17
No history of contact .17 11
36 52
816 Proceedings of the Royal Society of Medicine 36
heavy doses in the dust disturbed from plumage and the floors of cages. The rarity of man-to-man
spread of the disease strongly suggests that such large doses are, in fact, necessary in order to
establish infection. Prolonged intimate contact with sick birds other than psittacines is unusual
except in the case of pigeon-fanciers, and even then the contact is not likely to be so close.
Although man-to-man spread of the disease is rare there have been in the past some severe
and highly fatal epidemics of this nature and in nearly all the reported cases the outbreak has
first involved the nursing and medical staff directly responsible for the treatment of the first
case. One such outbreak in Louisiana led to disease in 19 hospital contacts with 13 deaths. In
some of these outbreaks it has not proved possible to trace the origin of the first case back to
a bird and the suspicion has arisen that there may be human strains of the virus which have
adopted man as their primary host. To establish such a contention with any certainty is, of
course, extremely difficult, but it is interesting to note in Table II the number of cases who
denied any contact with animals or birds. Viruses belonging to the same group have now been
isolated from pneumonia in mice, meningo-encephalitis in opossums, pneumonia in cats, enteritis
in calves, infectious abortion in ewes, and lymphogranuloma venereum in man. Thus the viruses
are widely distributed throughout the mammalian as well as the bird kingdom and it is not
a priori improbable that "humanized" pneumonia strains may exist-or may come to do so in
the future. Work on this problem is greatly hampered at present by the absence of any criterion
by which strains of virus of different origins may be distinguished with certainty, but the problem
itself is biologically an interesting one arid from an epidemiological point of view its implications
could be far-reaching.
REFERENCES
BEDSON, S. P. (1933) Brit. J. exp. Path., 14, 267.
(1939) Proc. Sixth Pacif. sci. Congr., 5, 353.
and BLAND, J. 0. W. (1932) Brit. J. exp. Path., 13, 461.
(1934) Brit. J. exp. Path., 15, 243.
WEsTERN, G. T., and SIMPSON, S. L. (1930) Lancet, i, 235; 345.
BLAND, J. 0. W., and CANTI, R. G. (1935) J. Path. Bact., 40, 231.
BURNET, F. M. (1935) J. Hyg., Camb., 35, 412.
HAAGEN, E., and MAUER, G. (1938) Zbl. Bakt., 143, 81.
LEVINTHAL, W. (1935) Lancet, i, 1207.
MACCALLUM, F. 0. (1936) Brit. J. exp. Path., 17, 472.
MEYER, K. F., and EDDIE, B. (1933) Proc. Soc. exp. Biol., N.Y., 30, 484.
RASMUSSEN, R. K. (1938) Zbl. Bakt., 143, 89.
RIvERs, T. M., and BERRY, G. P. (1931) J. exp. Med., 54, 105; 119; 129.
.- , and SPRUNT, D. H. (1931) J. exp. Med., 54, 91.