Felipedia

Yersinia pestis is the causative agent of plague, a gram-negativebacterial disease occurring principally in rodents and fleasand occasionally in non-rodent mammals including domestic catsand humans.²¹ Y. pestis is established in certain ecologicalniches worldwide, including the south-western United States.¹⁶Historically, the plague has been associated with large human epidemics, particularly in medieval Europe. Although there are historic suggestions of cats being susceptible to plague,²⁷it was not until the latter part of the 1900s that plague was recognized as a significant disease in cats and that infectedcats could serve as a threat to human health.¹⁶ Cats are rareamong carnivores in that they are unusually susceptible to diseaseafter Y. pestis exposure.

In 1999, a total of 42 plague casesin cats (Felis cattus) were confirmed from the three stateswhere plague is most common: California (7), Colorado (9), andNew Mexico (26) (C. Fritz, R. E. Enscore, and P. Reynolds, personalcommunication). Many cats may succumb to the disease withoutever being identified, or examined, or counted, often dyingin secluded areas.¹⁰ The published mortality rates for plaguein this species is approximately 33%.^9,15,26 Because of thenumber of cases of feline plague, this disease is becoming increasinglyimportant as a veterinary medical concern and as a zoonoticlink to humans.^12,14 In both cats and humans, clinical signsinclude fever, lethargy, myalgia, palpable lymphadenopathy,and anorexia with an onset 2–5 days following exposure.An average of 11.4 cases of human plague are reported each yearin the United States, and about 2,000 cases/year are reportedworldwide.¹¹ Several human plague cases in the south-westernUSA reportedly originated in cats and were transferred via catbite, scratch, or contact with infected bodily fluids, suchas respiratory droplets.^8,30–32

Fig. 5. Pharyngeal tonsil; cat No. 2. There is necrosis of lymphoid tissue and disruption of the overlying tonsillar epithelium. HE. Bar = 210 µm.
Fig. 6. Pharyngeal tonsil; cat No. 2. Same tonsil as in Fig. 5. There is intense immunolabeling of necrotic lymphoid areas. Streptavidin–biotin–peroxidase complex method, Mayer's hematoxylin counterstain. Bar = 210 µm.

Fig. 1. Lymph node; cat No. 4. Massive numbers of bacteria, admixed with macrophages and degenerate and necrotic neutrophils, expand the medullary sinus. HE. Bar = 25 µm.
Fig. 2. Lymph node; cat No. 4. Same lymph node as in Fig. 1. Numerous immunolabeled bacteria are present. Streptavidin–biotin–peroxidase complex method, Mayer's hematoxylin counterstain. Bar = 25 µm.
Fig. 3. Lung; cat No. 2. The alveolus is filled with numerous bacteria, degenerate and necrotic neutrophils, fewer macrophages, and fibrin. Note expanded alveolar wall (upper left). HE. Bar = 25 µm.
Fig. 4. Lung; cat No. 2. Note aggregates of immunolabeled bacteria. Streptavidin–biotin–peroxidase complex method, Mayer's hematoxylin counterstain. Bar = 25 µm.

Almost all carnivores that have been tested, including blackbears, raccoons, badgers, and dogs, either experimentally orin surveys for natural exposure in endemic areas mount a robustimmune response that prevents the development of clinical signsor pathologic changes.^{4–6,13,17,20,28,34} Cats and probablyblack-footed ferrets are an exception in plague susceptibilityamong carnivores.^15,26,33 Bubonic, pneumonic, and septicemicplague are technically morphologic diagnoses of Y. pestis infectionin humans.^21,23 Within veterinary medicine, these classic lesionsof plague have only been described in monkeys, cats, and black-footedferrets (see Table 2).^7,9,33 Cats incur pathologic changes analogousto human lesions, suggesting that the pathogenesis of Y. pestisin these two species is similar.

Signs appear within 1-7 days of infection, consisting of high fever (>40⁰C), lethargy, inappetence and dehydration. Bubonic plagues is characterised by marked solitary or regional painful mandibular, retropharyngeal and cervical lymphadenopathy due to severe lymphadenitis.

The lymphadenitis is characterised by haemorrhage, necrosis and perinodal oedema, and later by lymph node abscessation. Abscesses may rupture and drain thick creamy pus. The severely swollen, inflamed nodes are referred to as 'bubos'. This distribution of lymphadenopathy results from oral exposure during hunting.

Other possible signs include oral ulcers. tonsillar enlargement, ocular and nasal discharges and abdominal distension. Cats may initially present with less severe signs. Septicaemic plague, characterised by fever and septic shock, may occur with or without bubo formation.

Pneumonic plague in cats, characterised by fever, dyspnoea, oral or nasal discharges, and coughing or sneezing occurs occasionally and is usually a sequel to bubonic or septicaemic plague.

The presence of numerous intralesional bacteria is a consistentfinding in fatal plague. Each of the affected cats exhibitedenlargement and abscessation of various lymph nodes, with disseminatedpetechiation and ecchymosis as the principal pathologic manifestation.Grossly, the infection appeared to be contained within the nodes,which were swollen and hemorrhagic. However, microscopic examinationrevealed that the massive numbers of Y. pestis within the lymphnodes extended beyond the node borders; bacteria were frequentlyseen in the extranodal connective tissue. In all the cats studied,Y. pestis escaped the lymph nodes and entered the blood stream,as indicated by positive blood culture data obtained from eachcat. Plague organisms were cultured from the livers and spleensfrom some of the cats in this study at the time of necropsy.¹⁵However, the positive cultures may have resulted from hematologiccontamination; little evidence of colonization of these tissues was seen histologically. Although low numbers of bacteria were present in the spleen of four cats (Nos. 2, 4, 5, and 7), nopositive staining was found by immunohistochemistry. Too fewbacteria may have been present in replicate tissue sectionsto obtain a visible immunohistochemical reaction. Alternatively,the splenic bacteria could represent post-mortem proliferationof intestinal flora.There was widespread endothelial necrosis and loss within both venules and arterioles, especially in lymph nodes, with manysmall venules and fewer arterioles partially or completely occludedby fibrinocellular thrombi. These lesions are noted in allcats and are consistent with a fatal gram-negative sepsisand disseminated intravascular coagulopathy.

In contrast to most other carnivores, cats fail to prevent Y. pestis from multiplication within targetorgans at an early phase of the infection. Cats produce antibodiesto the fraction 1 antigen of Y. pestis and to some of its majorvirulence factors; however, this humoral response is not correlatedwith survival.¹⁵ Because early response to infection is crucial,a component of the early response mechanism may protect mostother carnivores from fatal plague infection.

A number of diseases with similar signs of lymphadenopathy, septicaemia, fever and abscessation of regional lymph nodes include cat bite abscess, bacterial lymphadenitis, FeLV, FIV, tularaemia, and rarely, anthrax

Recommended antibiotics include tetracycline, doxycycline, chloramphenicol, trimethoprim-sulphonamide, streptomycin, gentamicin and kanamycin at standard recommended doses. Recommended duration of therapy is usually for 21 days, given parenterally to minimise handling of the infected cat.

Mortality with Y. pestis infection in cats is 50% in untreated patients. Cats with septicaemic and pneumonic plague have the worst prognosis.

Plague is highly zoonotic from infected cats to humans, infection via fleas, or contact with abscess material, often leading to pneumonic plague in humans/