15-year-old male castrated Maine Coon cat, (Felis cats).1-week history of lethargy and anorexia. The cat presented recumbent and minimally responsive; it went into respiratory arrest the next morning and was euthanized.
The liver and spleen contain numerous 0.5 mm white nodules. Most lymph nodes are enlarged and mottled red and white.
Lymph nodes and spleen have multifocal coalescing areas of necrosis containing macrophages and a few neutrophils. The spleen also has numerous aggregates of mast cells.
Lymphadenitis and splenitis, necrotizing, granulomatous, multifocal, severe.
Hematocrit: decreased (21)
This is a case of tularemia caused by Francisella tularensis. The organism was not cultured from the tissues but its presence was confirmed by PCR. Francisella tularensis is a potential agent of bioterrorism and is a reportable disease.
Francisella tularensis is a gram-negative bacterial rod and a facultative intracellular pathogen of macrophages. The organism is difficult to grow in artificial media and the diagnosis is best confirmed by PCR.
Francisella tularensis is the cause of the disease tularemia. Tularemia has a worldwide distribution and affects a variety of mammals, birds, amphibians and fish. The organism is maintained in the environment by various terrestrial and aquatic mammals, primarily rabbits and rodents, and is transmitted by a variety of arthropods including ticks, mites, blackflies, fleas, mosquitoes and lice.(2) The organism may also be transmitted by contact with infected vertebrates, by inhalation of feces-contaminated dust, or ingestion of insufficiently cooked infected carcasses. Human infections usually result from skinning or dressing rabbits, and rabbits are the source of infection in 90% of human cases.(4)
Gross lesions of tularemia are multifocal white spots in liver, spleen and lymph node varying in size from pinpoint to several millimeters. Microscopic lesions are multifocal to confluent areas of necrosis with a mild influx of macrophages and neutrophils.
1. Spleen: Splenitis, necrotizing, multifocal to coalescing, severe.
2. Lymph nodes: Lymphadenitis, necrotizing, multifocal to coalescing, severe.
Tularemia, a zoonotic disease also known as rabbit fever or deer-fly fever, has a worldwide distribution, is currently listed as a category A select bioterrorism agent and is thus a reportable disease in the U.S.(5) Two main biovars have been described. The more virulent biotype A (F. tularensis subsp. tularensis) ferments glycerol and spreads (predominantly in North America) via ticks and hemophagous insects (mosquitoes and biting flies). The primary tick vectors described in the U.S. include the wood tick (Dermacentor andersoni), the American dog tick (Dermacentor variabilis), the Pacific coast tick (Dermacentor occidentalis) and the lone star tick (Amblyomma americanum). The less virulent biotype B (F. tularensis subsp. holarctica) does not ferment glycerol, exhibits a complex aquatic epidemiology and is more common in Eurasia, where infection usually occurs due to ingestion of infected prey or water contaminated by rodents. Type A strains are typically responsible for clinical disease in rabbits, cats and humans.(1,3) F. tularensis has an extensive host range, and infections in more than 200 animal species (primarily mammals, but also birds, fish, amphibians, and reptiles) have been reported. Infection rates appear to demonstrate seasonal variability; cases are reported most frequently from May to August, likely due to the activity of arthropod vectors.(5)
F. tularensis can pass transovarially within tick vectors, which are infected for life.(3) Additionally, the bacterium can survive for weeks to months in water, soil, and decaying animal carcasses.(5) Bacteria are typically inoculated into the host during tick feeding/defecation or following ingestion of infected rabbits or rodents. Dogs appear to be fairly resistant while cats and rabbits are susceptible. The infectious dose can be quite low; inhalation or parenteral inoculation of 10 to 50 colony-forming units can induce clinical disease, while 108 colony-forming units are required for oral infection. F. tularensis persists within macrophages where it inhibits phagosome-lysosome fusion; the bacterial capsule is thought to be important in intracellular survival.(1,3) Necrosis generally centers upon lymphoid tissue within the spleen and lymph nodes, although lesions within the liver and lungs (especially if bacteria are inhaled) are also commonly described.(3,5) The gross lesions associated with F. tularensis (foci of splenic, lymph node and hepatic necrosis and/or pyogranulomatous inflammation) are indistinguishable from lesions associated with yersiniosis. Histologically, Yersinia spp. often form large colonies, while F. tularensis coccobacilli are typically found within macrophages,(6) although individual bacterial were not readily apparent in this case.
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3. Greene CE. Francisella and Coxiella infections. In: Greene CE, ed. Infectious Diseases of the Dog and Cat. 4th ed. St. Louis, MO: Elsevier Saunders; 2012:476-482.
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5. Spagnoli ST, Kuroki K, Schommer SK, Reilly TJ, Fales WH. Pathology in practice. Francisella tularensis. J Am Vet Med Assoc. 2011;238(10):1271-1273.
6. Valli VEO. Hematopoietic system. In: Maxie MG, ed. Jubb, Kennedy, and Palmer's Pathology of Domestic Animals. Vol 3. 5th ed. Philadelphia, PA: Saunders Elsevier; 2007:297-299.