7-year-old, spayed female, domestic shorthair cat (Felis catus).This cat was presented with general lethargy and responded initially to anti-inflammatory therapy (Rimadyl) for 24 hours. Marked swelling of the left cervical lymph node and tongue occurred after hospitalization. The animals condition worsened, with respiratory signs (rales, rapid and open mouth breathing, dyspnea). The animal eventually was unable to stand, and was euthanized. 

Gross Description:  

This cat had enlarged cervical lymph nodes with a draining lesion of the left cervical node. The left tonsil was enlarged, and there was a large area of swelling and reddening under the tongue. A pseudomembrane was over a portion of this area. All lobes of lung were markedly congested, deep reddish-purple, and just barely floated in formalin. 

Histopathologic Description:

In the lung, there are multifocal to coalescing areas of necrosis that obliterate the normal architecture. In the affected areas, the bronchioles and alveoli are filled with numerous bacteria, intact and degenerate neutrophils, fewer macrophages, fibrin, and edema fluid. Alveolar macrophages sometimes contain phagocytosed erythrocytes, necrotic cellular debris, and bacteria. The alveolar capillaries are engorged with RBCs and the necrotic foci occasionally contain fibrin thrombi. 

Morphologic Diagnosis:  

Lung: Pneumonia, necrotizing, suppurative, acute, multifocal to coalescing, moderate with intralesional bacteria colonies of Yersinia pestis.

Lab Results:  

Bacteriology: Yersinia pestis was isolated from lung. Lung was also positive on FA testing of lung swab smears for Y. pestis


Yersinia pestis

Contributor Comment:  

Plague is a zoonotic infection caused by Yersinia pestis affecting rats, mice, ground squirrels, prairie dogs, kangaroo rats, bobcats, cats, rabbits, and chipmunks. The disease has also been described in ferrets, llamas, camels, mule deer, and goats. In New Mexico, it is occasionally also seen in dogs, although most of the literature cites that dogs are resistant. In our experience, we would modify that statement to most dogs are resistant. Yersinia pestis is a pleomorphic, non-motile, non-spore forming, facultative anaerobe, gram negative, bipolar staining coccobacillus of the family Enterobacteriaceae. The organism is now more accurately classified as a subspecies of Y. pseudotuberculosis based upon DNA-DNA pairing. It is a disease of antiquity, decimating human populations at various stages in history. Plague continues to be a problem today in many parts of the world, particularly in the western United States. In the Southwest, it is seen primarily in northern New Mexico and northeastern Arizona. In New Mexico, plague is most commonly found at elevations where pi+â-¦on and juniper trees flourish. The main reservoirs are rock squirrels and prairie dogs, as well as deer mice and kangaroo rats. The principal mode of transmission of Y. pestis in mammals is via flea bite. A less common mode of transmission is ingestion of, or exposure to another animal infected with Y. pestis. Inhalation of aerosolized bacteria from animal with pneumonic plaque is a rare but effective mode of transmission also.

Cats (and dogs) acquire the disease most commonly following predation on infected rodents and lagomorphs or by bites from the preys plague-infected fleas. The season for plague in New Mexico begins in mid-May, and peaks in August, tailing off in October. However, cases occur at any time with proper conditions. In New Mexico, plague cases increase after unusually wet winter and spring weather; these conditions are conducive to increase in the rodent (and subsequently, flea) population. 

The lesions seen in Y. pestis-infected animals vary according to the mode of transmission of the organism and susceptibility of the host. The three classic clinical manifestations of Y. pestis infection include bubonic, pneumonic and septicemic plague and are seen primarily in susceptible non-rodent species. Cats submitted to our laboratory typically have some type of enlargement of tonsils, cervical lymph nodes, or both. These may or may not present as draining lesions. Exudate produced is typically mucoid, grey, and contains large numbers of bacteria. When the disease has progressed to the lungs, all lobes of both lungs will typically be deep reddish-purple, very congested, and often will sink (or just barely float) in formalin. When presented with a suspect plague case (either clinically or in the laboratory), it is important to take proper precautions with the animal. Intense and immediate flea control is paramount with these cases; in our laboratory, suspect cases are routinely sprayed liberally with an appropriate pyrethrin based insecticide prior to any examination or handling. 

Clinically, these animals usually present with some type of oral lesion, salivating, gagging, respiratory difficulty or distress, and lymph node enlargement accompanied by a high temperature. There may be a draining lesion from the cervical lymph node region or tonsils. When diagnosed early, these animals respond readily to appropriate antibiotic therapy. The disease is so common in Santa Fe County in the summer months as to commonly be one of the differentials in ADR (i.e. aint doing right) cats. This disease is of importance as a public health risk, and as one of the select agents of bioterrorism.

JPC Diagnosis:  

Lung: Pneumonia, necrosuppurative, multifocal to coalescing, severe, with myriad extracellular coccobacilli.

Conference Comment:  

Pneumonic plague has killed more people than any other bacterial pathogen in recorded history (1), and the contributor appropriately emphasized the importance of 1) having a high index of suspicion for plague based on geographical location and clinical and gross findings, and 2) using appropriate personal protective equipment when handling suspect cases in a clinical or diagnostic setting.

The virulence of Yersinia sp. depends on its ability to invade the host and evade host immune responses. This begins in the gut of the infected flea, where Y. pestis forms a biofilm that obstructs the gut; the flea then must regurgitate before feeding, and thus infects the host that it bites. Via an elaborate gene complex, the Yop virulon, Yersinia spp. form proteins that assemble into a type III secretion system, a hollow tube that projects from the bacterial surface, binds to host cells, and injects the bacterial toxins, known as Yersinia outercoat proteins (Yops). YopE, YopH, and YopT interfere with actin polymerization inside the host cell, thus blocking phagocytosis of the bacterium. YopJ inhibits the production of inflammatory cytokines by inhibiting the signaling pathways that are activated by lipopolysaccharide.(9)

While natural Y. pestis infections still occur in humans, large outbreaks have been prevented by improved sanitation and prompt, successful antibiotic treatment of patients with the bubonic form of the disease. However, it is now apparent that that Y. pestis can acquire multidrug resistance via plasmids that are readily horizontally transmitted, and in 1995, two fatal cases of bubonic plague were caused by multidrug resistant Y. pestis. As a result, the threat of Y. pestis emergence as a deadly, multidrug resistant epidemic has prompted renewed interest in vaccination as a best line of defense against resurgent plague.(1)

Because whole cell vaccines are considered potentially unsafe and unreliable, vaccine research has focused on two antigens, F1 and LcrV. The F1 protein is a bacterial surface antigen that aids Y. pestis in evading recognition by the innate immune system; it is not essential for virulence, however, and is therefore not considered sufficient as a sole vaccine antigen. The LcrV protein is essential for virulence, and mediates insertion of a translocation pore, assembled via the type III secretion system, in the host cell membrane. Vaccines which combine both LcrV and F1 show promise against bubonic and pneumonic plague in animal models. The Brown Norway rat has emerged as a model for both human bubonic and pneumonic plague.(1)


1. Anderson DM, Ciletti NA, Lee-Lewis H, Elli D, Segal J, DeBord KL, Overheim KA, Tretiakova M, Brubaker RR, Schneewind O: Pneumonic plague pathogenesis and immunity in Brown Norway rats. Am J Pathol 174(3):910-21, 2009
2. Behr M: Clarification about plague and its diagnosis. J Am Vet Med Assoc 211(6):698, 1997
3. Cleri DJ, Vernaleo JR, Lombardi LJ, Rabbat MS, Mathew A, Marton R, Reyelt MC: Plague pneumonia disease caused by Yersinia pestis. Semin Respir Infect 12(1):12-23, 1997
4. Eidson M, Thilsted JP, Rollag OJ: Clinical, clinicopathologic and pathologic features of plague in cats: 119 cases (1977-1988). J Amer Vet Med Assoc 199:1191-1196, 1991
5. Ettestad, PE: Veterinary Epidemiologist, NM Dept Health, Personal Communication, July, 2005
6. Lappin MR: Feline zoonotic diseases. Vet Clin North Am Small Anim Pract 23(1):57-78,1993
7. Lopez T: Plague. Finding ways to stop a killer. J Am Vet Med Assoc 211(3):280-281, 1997
8. Macy DW: Plague. In: Infectious Diseases of the Dog and Cat, ed. Greene CE, 2nd ed., pp. 295-300. WB Saunders Co., Philadelphia, PA, 1998
9. McAdam AJ, Sharpe AH: Infectious diseases. In: Robbins and Cotran Pathologic Basis of Disease, eds. Kumar V, Abbas AK, Fausto N, Aster JC, 8th ed., p. 365. Saunders Elsevier, Philadelphia, PA, 2010
10. Rosser WW: Bubonic plague. J Am Vet Med Assoc 191(4):406-9, 1987
11. Watson RP, Blanchard TW, Mense MG, Gasper PW: Histopathology of experimental plague in cats. Vet Pathol 38:165-172, 2001

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3-1. Lung

3-2. Lung

3-3. Lung

3-4. Lung

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