cases, according to retrospective inquiry, occurred in June 1899;
suspicions were aroused in July, but the diagnosis was not
established until August. The conclusion reached, after careful
investigation by Dr Jorge, the medical officer of health, that the
commencement really dated from June, is confirmed by the fact
that about that time the riverside labourers, who were first
affected, began to notice an illness among themselves sufficiently
novel to attract their attention and that of an English shipowner,
who from their description suspected plague. Through
him the suspicion was conveyed to the 'Medical Times and
Gazette, in which the suggestion of plague at Oporto was made
before any public mention of it in the town itself. The outbreak
never assumed large proportions. It gained ground by degrees
until October, after which it declined, and eventually ceased in
February 1900. No recrudescence has been officially announced.
The number of cases recorded in a population of 150,000 was 310,
with 114 deaths, representing a case mortality of 36·7%. They
were widely scattered about the town and outlying suburbs,
but no further extension occurred, except some isolated cases at
Braga, a town 35 m. distant, and one at Lisbon, in the person
of the distinguished bacteriologist, Professor Camara Pestana,
who contracted the disease in making a post-mortem at Oporto,
and died in Lisbon.
The only other appearance of plague in Europe in 1899 was on the Volga Three places were affected, namely, Kolobovka, and Krasnoyarsk, in the province of Astrakhan, and Samara, higher up the river. All three outbreaks were small and limited, and no further extension took place. A commission appointed by the Russian government pronounced the disease to be undoubtedly plague, and it appears to have been very fatal. The origin was not ascertained.
The most interesting extensions of plague in 1900 were those in Australia and Glasgow. The following towns were affected in Australia: Sydney, in New South Wales; Adelaide, in South Australia, Melbourne, in Victoria; Brisbane, Rockhampton, Townsville, Cairns and Ipswich, in Queensland; Freemantle, Perth and Coolgardie, in West Australia. In none of these, with the exception of Sydney, did plague obtain a serious hold. The total number of cases reported in Queensland was only 123, with 53 deaths. In Sydney there was 303 cases, with 103 deaths, a case mortality of 34%. The infection is supposed to have been brought from Noumea, in New Caledonia, where it was present at the end of 1899, and the medical authorities believe that the first case, which occurred on the 19th of January, was recognized. The outbreak, which hardly reached epidemic proportions, lasted about six months. That in Glasgow was on a still smaller scale It began, so far as could be ascertained, in August 1900, and during the two months it lasted there were 34 cases and 15 deaths. Once more the disease was not at first recognized, and its origin could not be traced. In 1901 plague invaded South Africa, and obtained a distinct footing both at Cape Town and Port Elizabeth. The total number of cases down to July was 760, with 362 deaths; the number of Europeans attacked was 196, with 68 deaths, the rest being natives, Malays, Indians, Chinese and negroes. With regard to Great Britain, a few ship-borne cases have been dealt with at different ports from time to time since 1896, but except at Glasgow the disease has nowhere obtained a footing on land.
Causation.—Plague is a specific infectious fever, caused by the bacillus pestis, which was identified in 1894 by Kitasato, and subsequently, but independently, by Yersin (see Parasitic Diseases). It is found in the buboes in ordinary cases, in the blood in the so-called “septicaemic” cases, and in the sputum of pneumonia cases. It may also be present in the urine. Post mortem it is found in great abundance in the spleen and liver. Nothing is known of its natural history outside the body, but on cultivation it is apt to undergo numerous involution forms Its presence in a patient is regarded as positive diagnostic proof of plague, but failure to find or to identify it does not possess an equal negative value, and should not be too readily accepted, for many instances are recorded in which expert observers have only succeeded in demonstrating its presence after repeated attempts. It is clear, from the extreme variations in the severity of the illness, that the resisting power of individuals varies greatly. According to the Plague Research Committee of Bombay, the predisposing causes are “those leading to a lower state of vitality,” of which insufficient food is probably the most important. There is no evidence that age, sex or race exercises a distinct predisposing influence. The largest incidence in Bombay was on young adults, but then they are more numerous and more exposed to infection, because they go about more than the younger and the older. Similarly, the comparative immunity of Europeans in the East may be explained by their different conditions of life. It is doubtful whether the distinction drawn between pestis minor and pestis major has a real etiological basis. Very mild cases occurring in the course of an outbreak of typical plague may be explained by greater power of resistance in individuals, but the epidemic prevalence of a mild illness preceding the appearance of undoubted plague suggests some difference or modification of the exciting cause. “It is impossible,” writes Sir Richard Thorne (Local Government Board Report, 1898–1899), “ to read the medical history of this disease in almost every part of the world without being impressed with the frequency with which recognized plague has been preceded by ailments of such slight severity, involving some bubonic enlargement of glands and some rise in body-temperature, as to mask the real nature of the malady.” Considering the great importance of arresting the spread of infection at the outset, and the implicit reliance placed upon bacteriological criteria, the aetiology of such antecedent ailments deserves more attention than has hitherto been paid to it. Of course plague does not stand alone in this respect. Epidemic outbreaks of other diseases—for instance, cholera, diphtheria and typhoid fever—are often preceded and followed by the prevalence of mild illness of an allied type; and the true significance of this fact is one of the most important problems in epidemiology. In plague, however, it is of special importance, on account of the peculiarly insidious manner in which this disease fastens itself upon a locality.
The path by which the bacillus enters the body varies. In pneumonia cases it is presumed to enter by the air-passages, and in bubonic cases by the skin. The Bombay Plague Research Committee, whose experience is unequalled, say: “ In a number of instances points of inoculation were found on the extremities of patients, from which plague cultures were obtained, and in these cases buboes were found above the point of inoculation. In the majority of instances, however, no local indication could be found marking the point at which the microbe was implanted”. From the fact that bacilli are hardly ever found in the blood of bubonic cases it may be inferred that they are arrested by the lymphatic glands next above the seat of inoculation, and that the fight—which is the illness—takes place largely in the bubo; in non-bubonic cases they are not so arrested, and the fight takes place in the general circulatory system, or in the lungs. As might be expected from these considerations, the bubonic type is very little infectious, while pneumonia cases are highly so, the patients no doubt charging the surrounding atmosphere by coughing. Whether infection can be introduced through the digestive tract by infected food is doubtful. The bacillus is non-resistant and easily killed by heat and germicide substances, particularly acids. Little is known of its toxic action; only a weak toxin has been obtained from cultures. Of the lower animals, mice, rats, guinea-pigs, rabbits, squirrels and monkeys are susceptible to the bacillus; horses, cattle, sheep, goats, pigs, dogs and cats are more or less resistant, but cats and dogs have been known to die of plague (Oporto, Daman, Cutch and Poona). In the Great Plague of London they were believed to carry the infection, and were killed in vast numbers The bacillus has been demonstrated in the bodies of fieas, flies, bugs and ants.
Clinical Characters.—One of the results of recent observation is the classification of plague cases under three heads, which have already been mentioned several times: (1) bubonic, (2) pneumonia, (3) septicaemic. (The word “pesti-caemic” is
