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Epidemiology and Pathology

The causative organism of plague, Yersinia (Pasteurella) pestis, belongs to the group of bacteria producing hemorrhagic septicemias (pasteurellosis) in animals. It is a short, plump, nonmotile, gram-negative coccobacillus, which is bipolar with Wayson's stain.

Rats and other small rodents are the natural hosts for plague, but the species varies in different parts of the world. In endemic areas of Mongolia and Manchuria, the marmot is the principal reservoir and the disease is not infrequent among marmot trappers. In Kurdistan and the Central Asian republics of the former Soviet Union, mice, sisels, and jerboas are the carriers. In Africa it is gerbils and muridae, in California and neighboring states ground and rock squirrels, chipmunks, and prairie dogs, and in South America wild guinea pigs ("cuis") and other rodents of' the pampas that maintain the infection.

Some of these wild rodents are relatively resistant to plague and form permanent foci: even susceptible species become refractory during hibernation, thus also maintaining a reservoir of the organism. The link between wild and domestic rodents is usually the brown sewer rat (Rattus norvegicus), which is a great traveler and frequents city sewers and docks (and, since ancient times, is the ship-borne rat). The domestic black rat (Rattus rattus), the usual source of human infection, is very susceptible to plague and dies in great numbers during an epizootic.

However, although wild and domestic rodents are the chief reservoirs for plague, the disease is usually transmitted by fleas, of which Xenopsylla cheopis, the rat flea, is the most important. Transmission is also possible when infected rodents are eaten, or when plague bacilli are inhaled from their skins. During an epidemic, several species of animals, especially cats, become infected in this way, but fortunately for man the dog is usually not susceptible. When an infected rat dies, usually in its burrow, the fleas leave the carcass and seek out another host (rat or man) and the disease is transmitted once again as the new host is bitten. Direct transmission can also occur from man to man by fleas or lice.

Epidemics of sylvatic plague occur occasionally among wild rodents and then spread to domestic rat populations, requiring about 3 weeks to reach a peak and fading in approximately 2 months. Although most infected animals will die, enough are sufficiently resistant to become carriers and maintain the reservoir from which the infection spreads. There is a definite seasonal pattern to plague, with most patients infected during warm dry periods when fleas are most numerous and humans and the natural hosts are most likely to come into proximity with one another. Thus, in the United States peak months of infection are May through October.

Epidemics in man usually involve the bubonic form of the disease, but there is always a small number of patients with primary septicemic plague or secondary pneumonic plague. The most highly contagious form is primary pneumonic plague, which is transmitted by the inhalation of airborne organisms in droplets or sputum from an infected patient; less commonly, it may be acquired from cadavers or the carcasses of infected animals, or by accidental laboratory exposure.

The lesions seen in plague are the result of the local and systemic effects of plague endotoxins, several of which cause peripheral vascular collapse. Disseminated intravascular coagulation (DIC) is often the fatal complication, more frequently in children than in adults. Local lesions are characterized by a marked proliferation of Yersinia bacilli, which cause an extensive protein and mucopolysaccharide effusion in tissue, initially without inflammatory cells or vascular lesions. Later there is toxin-induced necrosis of tissue without actual bacterial invasion; this causes vascular destruction with resultant hemorrhage. In the final stage, which may occur during or shortly after necrosis, there is a slight neutrophilic infiltrate. Although the plague bacilli are actively phagocytized by macrophages, they are not killed; instead their bacillary toxins destroy the phagocytes, producing a diffuse amphophilic coagulum.

The pathology of plague is characterized by lymphangitis, lymphadenitis (bubo formation), and bacteremia, with spread of infection to the lung and other organs. Once Y. pestis enter the body tissues they are rapidly carried to the regional lymph nodes where they multiply in vast numbers. Thus, in bubonic plague the lymph nodes draining the primary site of infection swell from edema and hemorrhage, forming the primary bubo, which often becomes necrotic (Fig. 24.2). Adjacent nodes become matted together and the edema and hemorrhage extend into the surrounding tissues and skin. If the patient lives 10 days or longer, hemorrhagic purulent material which has formed within the bubo may burst through the skin. Alternatively, the bubo may regress without eruption or draining.

Fig. 24.2 Discharging left femoral bubo in a pregnant woman with uncomplicated bubonic plague which responded well to chloramphenicol therapy. (From Doerr and Siefert: Tropical Pathology, 1995).

In fatal cases, septicemia rapidly ensues, with extensive damage to the endothelium of blood vessels and lymphatics. Hemorrhages occur in many parts of the body, both in the skin and beneath mucous and serous membranes. Blood-stained collections of fluid develop in the pleural and peritoneal cavities. Marked visceral congestion involves the liver, spleen, heart, brain, meninges, and other organs. The spleen is often considerably enlarged. The heart is dilated and flabby, with severe toxic softening of the myocardium and hemorrhages beneath the endocardium and pericardium.

In patients with secondary pneumonic plague which develops as a sequel to bubonic plague, the lungs initially show a more diffuse involvement than is seen in the early stages of primary pneumonic plague. The lungs may be filled with blood and edema fluid; if the patient lives long enough, scattered areas of consolidation appear. Although pulmonary hemorrhage and edema are the dominant findings, the bacteria and necrosis are more frequent in the interstitium than in the alveoli.

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