: History and Epidemiology By MAX J. MILLER* History JN the history of disease, no other single disease has inspired the terror of a plague epidemic. For the suddenness of its attack, the frightfulness of its manifestations, and the multitude of its deaths it has had few equals. Such a disease, if it did occur in antiquity, could not help but have been noted in the writings of the ancients, and, certain diseases mentioned in the Bible are very suggestive of plague. Thus it is written that during the military campaign of the Philistines against the Israelites, the in- habitants of Ashdod, Goth and Ekron were attacked with tumours in their secret parts, the pestilence causing a deadly destruction. In the city of Beth-shemesh over 50,000 are related to have died. The Assyrian invasion of attempted by Sennacherib was prevented by the deaths of large numbers of his soldiers due to an epidemic of disease which is thought to have been plague. The early Greeks make no direct reference to this disease although Hippocrates wrote that all diseases associated with "Buboes' are bad. The record of plague for the first four centuries of the christian era are collected in the writings of Oribasius. In his compilation of the works of ancient authors, plague is shown to have occurred especially in , and Egypt, regions which played an important part in the history of plague in later centuries. The epidemic in Libya is described as ac- companied by an acute fever, intense pain, perturbation of the whole body, delirium, eruption of large Buboes, hard and with suppuration. This des- cription leaves no doubt as to the identity of the disease. The tirst well authenticated had its origin in Pelusium Egypt, in the year 542 A. D. From this great world trade centre it spread out over'the greater part of the populated world. Procopius, who has left a very illuminating account of this pandemic, writes that in Byzantium, where the plague lasted four months, as many as 5,000 and later 10,000 per- sons were dying each day of the disease. Plague quickly spread to , and in the latter half of the sixth century it ravaged the inhabitants of Ireland. This epidemic is thought to have been brought over from Italy with which Ireland was in constant communication. Plague struck Ireland one hundred years later and spread over into England in 664. Sporadic outbreaks of plague are recorded from the Mediterranean littoral in the 7th and 8th centuries. However, in the two hundred years preceding the 11th century the disease practically disappeared. In 1032, a, devastating epidemic of plague occurred in which spread through Asia Minor and Europe. This epidemic continued to rage in the armies of the crusaders, several of which it wiped out almost entirely. *Institute of Parasitology, McGill University, Macdonald College [183] Canadian of July 1940 [1844I ComparativeJournalMedicine *Vol.Plague:IV-No. History and Epidemiology The second great pandemic of plague occurred in the 14th century. It was, from the standpoint of its destructiveness, the most deadly the world has ever seen. It originated in in the year 1333 during a period of famine. Thirteen million persons are reported to have perished there. From China it spread through , Persia and Asia Minor, reaching in 1347, whence it was distributed to Europe and . In three years it swept over all of Europe taking the lives of at least one fourth of the entire population. England was invaded in 1348. Starting from the sea-coast towns it spread inland. Le Baker de Swynebroke has left a good account of the epidemic, and states that the death toll was so great "scarcely one in ten of either sex was left alive". This is probably an exaggeration. In London the death toll reached 100,000. Nor were the more northerly countries spared. Denmark and Norway suffered severely, and in the latter country two-thirds of the population are reported to have died. This second epidemic is commonly referred to as "the great ". During the 15th, 16th and 17th centuries, plague continued to manifest itself throughout Europe, Asia and Africa in circumscribed areas. Certain of the outbreaks appeared to be recrudescences of the disease which had become endemic, whereas others were carried over from the old endemic areas in Asia Minor. In the 18th and early 19th centuries plague prevailed mainly in Turkey, Syria and Egypt. However, it was still being carried from these countries to parts of Europe, particularly large coastal towns. Thus in 1720 it was imported into Marseilles from Tripoli, by a merchant vessel. A de- scription of the terrible conditions occurring during a plague epidemic in early times, is presented in the following short account published in 1806, of the Marseilles plague of 1720: "the houses throughout all their recesses and apartments were strewn with the dead and the dying. All the streets were covered with carcasses. The grave diggers had disap- peared. Undertakers and sextons were not to be found. About a thousand corpses were thrown daily into the streets to putrefy until at length, a passenger could hardly walk without treading on them. In the public walks, and before the church doors, they were piled up in large heaps, men, women and children. Persons of all ages and conditions were under- going corruption, as they overspread the pavements, and filled the at- mosphere with their noxious exhalations". Plague ravaged the armies of Napoleon during his disastrous Egyptian military campaign, in the last years of the 18th century. A good account of this is presented by P. Assalini who accompanied the troops. The main purpose of his publication was, however, to refute the arguments in favour of the infectious nature of plague. During the latter half of the 19th century the levantine regions were practically free of plague, and only isolated spots throughout the world reported the disease. However, the last decade of the 19th century brought forth the third great pandemic which seeded plague throughout the entire world. Canadian iJounal of History and Epidemiology July 1940 Comparative Plague: - [18515 MedicineVo.I . [1 The early history of this pandemic takes us back to 1871, when M. Rocher reported plague in , China, while travelling there. From Yunnan it spread slowly eastward, reaching Canton in 1894 with disastrous results. From Canton it swept into Hongkong. These two centres now became foci of infection for the rest of the world. Plague reached Bombay in 1896 and spread to other parts of India. By 1904, plague was present in Australia, South Africa, western and eastern ports of South America, West Indies, Mazatlante in Mexico, San Francisco, Glasgow, Spain, and of course, China, India, Japan, Asia Minor and the Mediterranean littoral. Plague first appeared in the United States in 1900 when San Francisco suffered an epidemic which took 22 lives, and from that time until 1937 California has had at least one case of plague each year. It appeared in New Orleans in 1914 and persisted until 1921. Beaumont and Galveston, Texas, had an epidemic in 1920 with the loss of 19 lives, and Pensacola, Florida, suffered a minor epidemic the same year. In more recent years it has occurred sporadically, and only in the western states. In 1937 there were 3 cases of plague in California, one in Utah and one in Nevada. The last reported case occurred in Utah in 1939. At the present time this disease still claims a considerable number of lives in , in Fukien Province in China, in India, in Java, in , and in South Africa. Senegal in West Africa has a few cases each year, as has Egypt. South America, Brazil, , Ecuador and Argentina report cases every year. The Belgian Congo has a small plague focus, and Tanganyika, Kenya and Uganda report plague cases not in- frequently. Burma and Siam have a few plague cases each year. Other regions report it sporadically and still others are potential plague areas. In recent years with the introduction of control measures, the extent of infections in many areas has decreased. Thus, India which had 240,000 deaths from plague between 1929 and 1933, lost only 7000 lives in 1938. Java has had a steady decrease in the number of cases; in 1938, only some- what over 2000 lives were claimed by plague as compared with more than 6000 for 1936. Brazil which had 1344 cases from 1934 to 1936, had only 35 in 1937. However, in discussing a rise or fall in its intensity, the distinc- tion between rat-transmitted plague and plague carried by wild rodents must be made. In those areas where plague is dependent on wild rodents, control becomes a very difficult task. The elimination of the wild rodent population from an entire area is practically impossible, and in such syl- vatic plague areas the number of human cases depends primarily on the intimacy between the wild rodent and the human population, and the factors which lead to plague epizootics. Epidemiology Most early writers realized the contagious nature of the disease and had numerous, if erroneous, ideas regarding its cause. One of the favourite explanations was the "pestiferous emanations from the soil contaminating the air". Hecker in 1837 writes: "This disease was a consequence of violent commotions in the earth's organism". Assalini, as mentioned pre- Canadian [186] ComparativJuMediioneofelaueiHstryanPlague: History and Epidemiology Vol. IV-No.July 19407 viously, considered the disease to be non-infectious. Kircher as early as I685, however, considered the causative agent of plague to be a living entity. He writes: "Plague is in most cases a living being; for the sick man harassed by pestiferous virulence soon contracts a marvellous putre- faction which we have shown to be most apt to create worms. Now these worms propagators of plague are so small, so light, so subtile, that they elude any grasp of perception, and can be seen only under the most power- ful microscope". After reading this description it seems very likely that Kircher actually saw the plague bacillus which was first accurately des- cribed in 1894. The year 1894 stands for the beginning of truly intensive scientific studies on plague. In that year it was demonstrated by two men, Kitasato and Yersin, working independently at Hongkong during the plague epi- demic there, that plague was caused by a specific bacillus. Kitasato's description preceded that of Yersin by a few days, but as his first descrip- tion was incomplete, credit for the discovery has been given to Yersin by some workers, mainly French. . While the evidence for the transmission of plague from rats to man was not available until the first decade of the 20th century, the associa- tion between epizootics amongst rats and epidemics of plague in man had been recognized for many centuries. Even in the most ancient epi- demics, amongst the Israelites and the Philistines, and Sennacherib's army, disease amongst rats is noted. In the pandemic of the 14th century, epizootics amongst rats as well as amongst the domestic animals are men. tioned again and again. In fact the appearance of sick rats was often taken as an impending sign of a plague epidemic. This, of course, fitted in with the ancient theories for the causative nature: as the disease arose as a noxious principle from the soil it would naturally affect burrowing animals, which in order to escape the disease came up to the surface where they died. The hypothesis that fleas transmit plague from rat to rat and from rat to man was first proposed by Ogata in 1897, who induced plague in rodents by injecting crushed fleas removed from infected rats. Simond, in 1898, was the first to demonstrate that fleas removed from infected rats when placed on uninfected ones could transmit the infection. This was con- firmed by Verjbitski in 1903 who also showed that Ctenocephalides canis, C. felis, Leptosylla musculi and Pulex irritans could all transmit plague from rat to rat. Liston, in 1904, by using guinea pigs as flea traps was able to demonstrate that fleas infected with plague occurred in rooms where plague patients had contracted the infection, and that these fleas, when injected into susceptible animals, caused a plague infection. Thus, both from epidemiological and experimental evidence, it was definitely shown that plague could be transmitted from a susceptible rodent host to man through the intermediary of fleas. Clinically, there are three types of plague: bubonic, septicaemic and pneumonic. is characterized by an invasion of the lymph Canadian Journal of Plague: and July 1940 [1Q871 Comparative Medicine History Epidemiology Vol. IV-No. 7 L'J glands by the parasite and the consequent swelling of these tissues to form large "buboes". In the early stages the bacilli are confined to the bubo and the immediate surrounding tissues. In the septicaemic type of plague the bacilli multiply very rapidly in the blood causing an acute septicaemia which proves rapidly fatal even before the lymph glands are noticeably enlarged. is characterized by an involvement of the lungs; it may arise either secondarily to a bubonic infection, or it may be primary. It has been well established that the three types of plague are caused by the same organism, although from the epidemiological stand- point they have to be treated quite distinctly. Bubonic and septicaemic plague are acquired primarily through the bite of an infected flea, and depend for their existence on a suitable host to act as a reservoir and a suitable flea to act as a transmitter of the infection from the reservoir to man. Pneumonic plague, on the other hand, can be transmitted directly from man to man, as the expectorations and the droplet spray of coughing are contaminated with bacilli, and highly infectious. An epidemic of pneumonic plague almost invariably begins with bubonic cases that have developed a secondary lung involvement. However, once such an epidemic has started it can go on quite independently of bubonic infections, and in circumstances where a case of pneumonic plague is imported into a plague- free locality which does not have an infected rodent population, an epi- demic of pneumonic plague can readily occur. Infection of susceptible rodents by pneumonic plague patients is thought to occur but rarely. Pneumonic plague is by far the most spectacular and deadly type, and is invariably concerned in the great epidemics. It was the predominant form in the "Black Death" of the 14th century, and also the main type involved in the 1933 Manchukuo epidemic. Because of its ready trans- missibility, under certain conditions it spreads very rapidly. These con- ditions are primarily such as result in a crowding of the population into limited areas. Thus, in famines or wars, rural populace flocks to large urban centres resulting in overcrowding, ill-ventilation and poor sanita- tion; conditions which are most likely to foster an epidemic of pneumonic plague. On the other hand, because of its rapid course and high fatality, and therefore the absence of infective carrier cases, it responds readily to proper preventive measures, which consist mainly of rapid isolation and destruction after death of patients and all objects that they may have contaminated, together with isolation and observation of persons with whom they may have come into contact. Thus, when an outbreak of pneu- monic plague occurs on an isolated farm several or perhaps all the in- dividuals located there may contract the infection. However, the epidemic is usually localized and the disease will not spread unless it is by actual human contact. As will be discussed later, this is not the case in bubonic plague epidemics where the disease is not dependent on human contact with a plague patient for acquiring the infection, but rather on contact with infected rodents. As was pointed out above, bubonic and septicaemic plague infections are acquired by the bite of an infected flea. Fleas usually become infected of July 1940 [188][CanadianJournalComparative Medicine Plague: HistoryHsoy anddEpemlgyEpidemiology Vol. IV-No. 7 by feeding on diseased rodents. Direct transmission from man to man by the "human" flea, Pulex irritans, which may have played a role in the epidemiology of plague infections in previous times, is not particularly important now. However, that this type of transmission may still occur in parts of the world is suggested by the findings of Girard et al (1932), who showed that in Tananarive, fleas (principally Pulex irritans) were comparat;ively numerous in buildings, and on the bodies of natives and Europeans in plague free areas. Among rodents, rats have played the most important role in the transmission of plague, and it is because of the unhappy circumstance that rats are particularly susceptible to plague infections that the disease is at the present time world-wide. Plague is readily transferrable from country to country by infected rats on board ship, and it was in this manner that plague was spread to every continent following the epidemic in China and India at the close of the last century. It almost invariably happens that prior to outbreaks of bubonic plague an epizootic occurs among the rodent population. And it is readily un- derstandable why with large numbers of rats dying of plague, hungry infected fleas leaving the rat corpses would readily bite humans and thus pass on the infection. However, it is not as easy to explain the cause of plague epizootics among rats. It is possible that when the rat population increases to a point where the food supply is inadequate, they have a les- sened resistance to disease and succumb to plague more readily. On the other hand, the Indian Plague Commission considered that plague epi- zootics depended not on the number of rats but rather on the number of fleas, and that factors which were suitable for the rapid multiplication of fleas fostered epizootics. It has also been pointed out that the species of rat may have a considerable bearing on the spread of human plague. Thus, Rattus rattus, the black rat, is considered a much more effective vector of plague than Rattus norvegicus, the brown rat, because the former lives in closer association with man, and harbors Xenopsylla cheopis which readily bites man. The brown rat, on the other hand, rarely invades the habitable parts of dwellings and harbors mainly Ceratophyllus fasciatus which rarely bites man. Raybaud (1933) and Guiart (1937) believe that the almost corn?lete absence of human plague from Europe is due to the displacement of the black rat by the brown rat. The role of insects other than fleas in the transmission of plague has received considerable attention. Nuttal showed that bed-bugs could harbor the bacilli in the alimentary tract but that the bite of such bugs did not transmit plague. Hunter (1905) shiwed that in bed-bugs the plague bacilli disappeared in a few days. Flu (1916) demonstrated that plague bacilli could grow in the stomach of mosquitoes. However, all attempts to transmit the infection to guinea pigs by the bites of infected mosquitoes failed. According to Russo (1938) all stages of the flesh-eating flies offer favourable conditions for the multiplication and diffusion of the plague bacillus. Faddeeva (1932) demonstraLted that the nymphs and adults of the tick Argas persicus were readily infected with plague bacilli, Canadian Journal of Plague: and July 1940, Comparative Medicmne HistoryHty Epidetmiolo Vol. IVJu194No. 7 L and that they remained infective for 110 days as demonstrated by-injecting suspensions of crushed ticks into susceptible hosts. De Raadt proved that human head lice became infected by feeding on plague patients. He in- fected five rodents by the inoculation of the crushed contents of the lice. Investigators in the Western United States have demonstrated that lice and ticks in nature become infected with plague, and when crushed and injected into susceptible hosts can transmit the infection. It thus seems that while the transmission of plague by infected arthropods other than fleas is conceivable, it is purely accidental and probably occurs by virtue of the crushed tissues of the carrier being rubbed into a wound, or by mechanical transmission on its mouth parts. Regarding the transmission of plague by fleas it can readily be under- stood that not all species are equally efficient or important as transmitters of the disease. Thus a flea that will bite humans readily would be more important as a transmitter that one that bites them only rarely. More- over, some fleas are better incubators of the disease and are more readily infectible, and would therefore be more important vectors of the disease. However, the studies of several investigators, particularly Bacot and Martin, and more recently Eskey, have shown that the most important factor determining the importance of a flea as a plague vector is not particularly the ease with which it is infected, but rather the readiness with which it infects other hosts. This brings us to the question of how plague is transmitted by fleas. Simond, as early as 1898, had suggested that infection occurred through contamination of the puncture wound by rubbing in of the faecal particle deposited by the flea while feeding. Other methods suggested later were mechanical transmission by the contaminated proboscis of the flea, ex- cretion of the plague bacillus in the saliva, or ingestion of the infected flea. Finally, it was suggested that the host could become infected through regurgitation into the puncture wound while the flea feeds. Normally this last phenomenon cannot occur because of the active valvular chamber, the proventriculus, at the proximal end of the stomach, which closes that organ completely. Infection by saliva or through ingestion of fleas was soon experi- mentally ruled out. Bacot and Martin (1914) showed that infection by faecal particles could occur, but pointed out, that the bacilli tend to lose their virulence in the stomach of the flea, and that the number of bacilli passed in the flea faeces are relatively few and tend to dry up rapidly. Although Eskey (1938) found that plague bacilli could remain viable in flea faeces for long periods, he also does not believe that they are im- portant in the transmission of plague because fleas seldom defaecate when feeding. Bacot and Martin discovered, however, that fleas in which the bacillus culture had formed a large plug, completely or partially block- ing the proventriculus, could transmit plague. This occurred by virtue of the blood that is being sucked in as the flea feeds, not being able to pass through to the stomach, and therefore being regurgitated back into the puncture wound carrying with it plague bacilli. Eskey found that go90]C190]CompanadianparativeMedicneloMeina Plague:lgu:HHistory anda Epidemiology Vol. IV-No.July 19407 only those fleas which were "blocked" could transmit the infection by bite. Fleas partially "blocked" are even more dangerous as plague car- riers as they can still transmit the infection, and as they can ingest some blood, live longer. Hirst (1923) found that Xenopsylla cheopis, the tropical rat flea, was "blccked" more readily by plague bacilli than any other species of flea. Eskey (1938) confirmed the findings of Hirst, and showed that this species was also more readily infectible, and that it succumbed to the infection more readily. The fact that plague was rapidly fatal to X. cheopis while other flea species could survive with an infection for much longer periods of time, is, as pointed out by Eskey, of considerable epidemiological im- portance. A potential plague area with X. cheopis as the principal flea would have a comparatively severe but short lived epidemic if plague was introduced. On the other hand, if, for example, Ceratophyllus fasciatus was the principal rat flea in the area, the epidemics would be of longer duration but with relatively few plague cases. Climate appears to have considerable influence on the presence of plague both through determining the rate of flea propagation and the course of plague infections in fleas. It also influences the distribution of flea species. Estrade (1935) and others have found that the optimum survival temperature for X. cheopis was between 80° and 930F. and the optimum relative humidity between 85 and 95 per cent. Below 80 per cent humidity they lived only a few hours. Hirst showed that in certain parts of India, where plague was comparatively rare, it was due to the fact that the principal flea present was X. astia,, and that this flea was not a particularly good transmitter of plague unless the temperature was low. Eskey comparing the occurrence of plague in Guayaquil, Ecuador, with that in San Francisco, California, points out that in the former, where X. cheopis was the only flea found, 364 cases occurred annually over a period of 22 years when the disease was continually present. On the other hand, in San Francisco, where the number of X. cheopis was only half that found in Guayaquil, and where the rats also harbored Ceratophyllus fascia- tus and Leptosylla segnis, only 278 cases occurred over a period of 7 years. Eskey explains the lower number of plague cases in San Francisco on the basis of the low X. cheopis index of rats, which in turn, he believes, is dependent on the climate. It might be mentioned at this point that even in regions where the climate is unsuitable for the propagation of a certain species of flea, artificial temperatures brought about by modern heating conveniences permit these fleas to exist. Thus the tropical rat flea has now apparently established itself in Iowa, Minnesota, Indiana and Illinois, as well as in the Coastal cities. Regarding the transmission of plague by fleas in the absence of rats, Long and Mostajo (1934) state that unexpected and out of season cases of plague in Peru nearly always occur in cotton and sugar estates where large amounts of sacking are imported, together, they believe, with in- fected fleas. They present the history of plague appearing in Peruvian ports following the arrival of a vessel from Calcutta loaded with jute sack- ing, and state that numerous fleas, mainly X cheopis were recovered from Canadian Journal. of 1940 Comparative Mecticine Pau:ndVol.Plague: History IV--No.and Epidemiology7 JvolLI19[1911 the sacking. Girard and Estrade (1934) point out that in Madagascar in- fected X. cheopis living in the debris of ground rice after their rat hosts had died are responsible for human infection. They state that infected fleas were recovered from the debris. In recent years plague investigators have been giving considerable attention to plague occurring in wild rodents. This plague, which is epidemiologically distinct, from the plague in rats, has been given the name sylvatic (selvatic) plague by Jorge (1928). Sylvatic plague has been known for centuries in Central Asia where it was observed that severe epizootics occurred annually among a rodent termed the tarabagan, and that hunters coming in contact with infected animals would often contract the disease. However, until the close of the last century, sylvatic plague was almost entirely confined to Asia. At that time plague was carried to sea ports in every continent; diseased rats leaving the ships, infected local rats, and, where conditions were suitable, the infection was eventually transferred to the wild rodent population. Once the wild rodents became infected a permanent endemic plague focus was established. Numerous species of rodents have proved susceptible to plague, and each area has its own peculiar fauna which acts as a reservoir of infection, and also whose distribution controls the distribution of the disease. Areas most suitable for sylvatic plague infections are characterized by large, sparsely settled tracts bearing a thriving rodent population. One of the important new regions that has become an endemic area of sylvatic plague is the western United States, and at the present time plague has been recovered from rodents in the following ten states: California, Oregon, Washington, Nevada, Utah, Idaho, Montana, Arizona, Wyoming and New Mexico. The infection first became established in the ground squirrels of California, and from them was transferred to other rodents till at the present time at least 30 species and sub-species have been found to suffer from spontaneous plague. They include ground squirrels, marmots, prairie dogs, tree squirrels, chipmunks, several of the native rats and mice, and the cottontail rabbit. In South America important sylvatic plague areas occur in the pampas region of the Argentine, and in portions of Peru and Ecuador. There the rodents principally involved are the "cuis" (Cavia and Galea). An ar- boreal rodent (Graomys griseoflavus) has also been found to suffer from severe plague epizootics in the pampas territories. An extensive sylvatic plague area exists along the Bolivia-A-rgentine frontier where rodents, of the genus Sylvilagus are principally concerned. The Union of South Africa has extensive areas of sylvatic plague, and there the principal rodents involved are the gerbilles (Tatera and Desmo- dillus) and the multimammate mouse (Mastomys coucha). In Southern where large areas of sylvatic plague occur, the rodents principally concerned as reservoir hosts are ground squirrels (Citellus pygmaeus), gerbilles (Meriones meridianus), and the jerboa (Dipus sagitta.) The large sylvatic plague area in Central Asia including and Transbaikalia, has already been referred to, as has the principal rodent of and July 1940 [192] ConadieComparativeMJournaldMedcf Plague: Historytran Epidemiology Vol. IV-No. 7 involved, the tarabagan (Arctomys bobac). In Manchukuo, ground squir- rels are the chief hosts of sylvatic plague. Sylvatic plague occurs periodically in epizootic form, with large numbers of rodents dying of the disease. This has been observed in every area where sylvatic plague occurs. As in rats, the infection is transmitted from one animal to another through the bites of fleas, and many observers believe that the flea may retain its infection and transmit it a considerable length of time after the host has died. Eseeva and Firsov (1932) dem- onstrated that infected fleas could overwinter in squirrel burrows, and Buichov (1935) considers the natural cycle of plague epizootics among squirrels in Transbaikalia to be as follows: during the pre-hibernation period the squirrels contract the infection, but they develop an immunity which keeps the disease in check until they start to hibernate. At that time their.resistance is greatly weakened, and they succumb to the disease; the dead bodies are removed by the larvae of Lucilia, and when new squir- rels invade the nests they are attacked by the infected fleas of the dead rodents and acquire the infection. It appears as if sylvatic plague may exist in some rodents as a latent infection, and that these rodents act as reservoirs of the infection which occurs in an epizootic form only when the resistance of the rodent population is lowered. The fact that sylvatic plague occurs in regions that are sparsely settled reduces the possibility of human infections. However, under certain con- ditions sylvatic plague can be responsible for initiating periodic epidemics of human plague. This is well demonstrated in east-central Asia where the fur of the tarabagan is widely sought. Hunters, making annual trips to the sylvatic plague areas, invariably bring the infection back home and often initiate serious epidemics. In South Africa the principal re- servoir of sylvatic plague is the gerbille. However, it rarely comes in contact with man and transmission from the gerbille to man is affected through the intermediary of the multimammate mouse which is semi- domesticated and lives both in the country and in the outskirts of towns. It is thought to become infected when it invades the burrows of gerbilles that have died of plague and thus become exposed to the infected fleas re- maining in the burrows. In the Volga-Ural steppes the rodent Meriones meridianus comes in contact with man during the harvest of certain wild cereals which it stores for the winter. A great danger in sylvatic plague is the transfer of the infection from wild rodents to rats, for an epizootic among rats almost always results in some cases of human infection, whereas this does not necessarily occur in epizootics among wild rvodents. In the United States, as sylvatic plague continues to spread eastward it may eventually reach the densely populated eastern section of the country where as Hampton (1940) states, "through a reversal of the original sequence of spread, the disease may become epidemic in any city near the approaching danger zone which has a suf- ficiently high population of rats and a sufficiently high flea index to proviLue favourable conditions for human infection. This "reversal of the sequence of spread" appears to occur in Peru and Ecuador where it is Canadian Jou-nal of July 1940 F Comparative Medicine PagePlague HHistory adEpidemiolo:gy Vol. IV-No. 7 1931 believed that human infections are acquired from rats which in turn become infected by the fleas of the "cuis". With gradual extension of sylvatic plague areas in the United States it could only be a matter of time when the wild rodents in western Canada acquired plague infections. Large areas in the western provinces are ideal for the propagation of sylvatic plague both from the geographical and the rodent host standpoint, and a communication recently received from F. A. Humphries*. states that a specimen of Cittelus r. richardsonii, locally called "gopher", has been found in Alberta suffering from spontaneous plague. "Gophers" as well as other susceptible rodent hosts are common in many regions in the west and unless drastic control measures are taken, there is a grave likelihood that sylvatic plague may become widespread throughout western Canada. *Bacteriologist, Laboratory of Hygiene, Kamploops, B. C.

.V~~~

Sterilzation of Farm Dairy Uensils C. K. JoHNS,* rHE importance of adequate sterilization of farm dairy utensils has 1been preached for many years. Despite all that has been said and writ- ten on the subject, the bacteriological condition of these utensils on many farms shows all too clearly the need for better care. Numerous investigations have proven that milk picks tip more bacteria from poorly cared for utensils than from any other single source. Yet despite all the information available, there are still many people connected with the dairy industry who fail to realize this. When high counts and souring are encountered, there is a tendency to over-emphasize cooling. It lPresented at Annual Conference, Ontario Health Officers Association, Toronto June 13, 1940. *Division of Bacteriology and Dairy Research, Science Service, Dominion Department of Agriculture. Ottawa.