These three groups are small, Gram-negative bacilli with similar morphological and cultural features. The organisms are essentially animal parasites that under certain conditions are transmitted to man, sometimes directly and sometimes through intermediary insect vectors, these are certain species of fleas and ticks. The infections are therefore, zoonoses. Each group gives rise to its own particular disease manifestations. The organisms implicated in human infections were commonly known as Pasteurella pestis, Pasteurella psestatuberculosis, Pasteurella multocida (sometime it know as Pasteurella septica) and Pasteurella tularensis. However as a result of improved knowledge, the group has recently been classified into three different genera. These are Yersinia (pestis, pseudo-tuberculosis and entercolitica), Pasteurella multocida and Franciselia (tularensis)
Yersinia pestis is the cause of plague in rats and man. Yersinia pseudotuberculosis is a parasite of guinea-pigs and other rodents, causing a fatal disease in those animals and sometimes, though rarely, a severe typhoid-like illness in persons who come into contact with infected animals. It is also one of the causes of acute mesenteric lymphadenitis in children and of erythema nodosum sometimes associated with this disease. Pasteurella multocida is responsible for ‘haemorrhagic septicaemia' in a wide range of animals and birds. It has been known as an important cause of animal disease since the time of Louis Pasteur who isolated it from chickens suffering from 'fowl cholera' and used it to develop an effective attenuated vaccine. But only in recent years has it been recognised as causing various forms of infection m man, in particular, superficial and deepseated septic infections following dog and cat bites Francisella tularensis is the cause of tularaemia. The infection is transmited directly from animal to animal or from animal to man but may also be spread by ticks, or through polluted drinking water. Human tularaemia manifests itself as a prolonged febrile illness sometimes with local ulcerative lesions and glandular involvement. Laboratory infection is readily acquired.
YERSINIA PESTIS (Pasteurella Pestis)
Yersinia pestis is a small ovoid Gram-negative bacillus, 1.5 pm by 0.7 Ian, showing pleomorphism, i.e. extreme variation in size and shape, under certain conditions of culture. True capsules are formed in living tissues but are less readily seen in culture. When stained with methylene blue the stain is taken up more densely at both ends— bipolar staining.
The organisms are non-motile and non-sporing. Growth occurs aerobically and anaerobically but Yersinia pestis is somewhat sensitive to oxygen and small inocula may not grow readily on ordinary culture media incubated aerobically. The optimum temperature for growth is 27°C which is unusual for parasitic organisms. Unlike the other members of the genus, Yersinia pestis grows poorly at 37°C. The plague bacillus is essentially a parasite of rodents.
In certain parts of the world burrowing animals such as gerbilles and voles act as chronic carriers and provide a continuing reservoir of infection that may be transmitted by fleas to more susceptible animals of the same species and to other species of rodent such as bandicoots, marmots and squirrels. These animals suffer from outbreaks of plague, and fleas from them may attack man and give rise to sporadic cases of human plague.
This form of plague in .man occurs in rural areas as a result of endemic infection in wild rodents and is referred to as 'wild plague' (previously known as syllabic plague). It tends to affect such persons as farmers and trappers who are likely to come into contact with infected animals.
More serious for man is the spread of infection to rats especially the species of black rat known as Rattus rattus that flourishes in and around human habitation. This constitutes the most important source of infection for man and outbreaks of human plague following epizootics in rats (domestic plague) have in the past sometimes developed into pandemics.
HISTORY OF PLAGUE
Human plague was introduced into Europe from Asia in the 13th century when infected black rats with their flea colonies spread westwards by land and sea with the returning crusaders. This led to the great pandemic known as the Black Death. During the years 1347 to 1348 about a quarter of the population of Europe succumbed to the Plague. For two centuries after this pandemic had subsided the infection remained enzootic in the rats in Europe and continued to give rise to outbreaks of human plague until in 1665 there occurred the last major epidemic in England, the Great Plague.
Plague disappeared spectacularly from Europe during the 17th and 18th centuries. This may have been due to natural spread of the brown (sewer) rat (Rattus norvegicus) from Asia into Europe so that it largely, displaced the black rat except around the sea ports where shipping continued to re-introduce the black rat from abroad. Rattus norvegicus although highly susceptible to plague does not frequent human dwellings to the same extent as Rattus norvegicus and its fleas are therefore attack man directly. Improvements in standard of house building, leading to the more general exclusion of rats from homes,
May also played an important part in the elimination of plague from Europe. The decline in the decline in the incidence of human plague was interrupted by a major outbreak in Hong Kong in 1894 that led new pandemic, the main centers of being North and West India where, during 1904, over one million persons are known to have died of plague. Plague-infected rats were carried by ships to most of the major sea ports of the world whence they subsequently spread the infection to the indigenous rodent population of the countries concerned,
The plague bacillus was first described in 1894 by Yersin at the time of the Hong Kong outbreak. During the following years of the pandemic a great deal or experimental and investigational work was carried out by a number of Governmental Plague Commissions including the British Plague Commission that investigated the Bombay outbreak. These studies resulted in a much greater understanding of the nature of the disease, the mode of spread and ways in which it may be controlled.
ln recent years urban plague has become a rarity and rural bubonic plague is limited to sporadic outbreaks in endemic areas. However, as long as plague exists in rodents in many areas or the world a constant surveillance has to be maintained to prevent its spread to more populated areas especially those where living conditions are still below standard and where rats and their ectoparasites can flourish. The incidence of plague in endemic areas such as India was greatly reduced following the widespread use of DDT in the control of malaria.
PATHOGENESIS OF HUMAN PLAGUE
The virulence of the plague bacillus is related to certain factors that protect it from phagocytosis, the main one being the capsular (envelope) anti-gen, Two somatic antigens V and W when present also play a part in enabling the organism to resist phagocytosis in the absence of a visible capsule (Burrows and Bacon, 1956). Aggressive factors that enhance spreading and increase capillary permeability have been demonstrated in extracts of tissues of experimentally infected animals.
No exotoxin has been identified but suspensions of dead plague bacilli and extracts of them produce local necrotic lesions and general toxaemia when inoculated into laboratory animals. This protein endotoxin appears to act on the peripheral vascular system and causes gluey to the liver and kidneys. There are two severe forms of human plague, bubonic plague and pneumonic plague. In bubonic plague the lymph nodes draining area of the flea bite become infected.
The adeiutis results in painful swellings or buboes in the inguinal, axillary or cervical regions depending on the site of the bite. From these primary buboes the plague bacilli may spread through the body. In the absence of antibiotic therapy there is a case fatality of 25 to 50 per cent, occasionally it is no more than a localized infection.
In pneumonic plague there is a severe haemorrhagic bronchopneumonia, the sputum contains numerous plague bacilli, septicaemia develops and in the absence of antibiotic therapy the outcome is invariably fatal. Septicaemic plague may also occur primarily as well as a complication of bubonic or pneumonic Plague.
Plague is confirmed by demonstrating the plague bacillus in fluid from buboes in the case of bubonic plague, in the sputum in pneumonic plague and by blood culture when generalized infection is suspected. The bubo is punctured with a hypodermic syringe and some of the exudate withdrawn. A film is made and stained with methylene blue. The characteristic bacilli showing bipolar staining can be confirmed as Y. pestis by culturing some of the exudate on blood agar to obtain a pure culture for further investigation, and by inoculating the material on to the nasal mucosa of guinea-pigs or white rats.
Similarly in pneumonic plague sputum is examined microscopically, culturally and by animal inoculation. In septicaemic plague the bacilli may be demonstrated in blood culture or from smears of spleen tissue at post movie's examination. Identification of characteristic colonies is made by various cultural and bio-chemical tests and by demonstrating the ability of the bacilli to form chains in broth culture and 'stalactite' growth from oil drops layered on the surface of fluid medium.
Chemotherapy should be started without waiting for confirmation of the diagnosis. Tetracycline in large doses is the drug of choice for both bubonic and pneumonic plague.
Yersinia pestis contains many antigens, somatic, heat-stable antigens and a heat-labile capsular antigen. The effectiveness of plague vaccine is not well established but is thought to depend to a large extent on the presence of the capsular protein. Both live vaccine, prepared from a virulent strains of Yersinia pestis and vaccine from inactivated virulent cultures are available but immunity resulting from their use is of short duration and revaccination is necessary after some months.