2-year 5-month-old, female, domestic shorthair cat, feline (Felis domestics).This young adult cat lived in a rural area in northern Scotland, United Kingdom, and had a history of hunting small birds. In January 2006, it became dull and anorexic for 24 hours. The cat began showing signs of distress and abdominal discomfort, then vomited yellow material. It developed seizures and died 36 hours after the onset of clinical signs. An in-contact cat was unaffected.

Gross Description:  

At postmortem examination, the cat had dilatation and thickening of several 1cm long segments of the jejunum and a 3cm long segment of the ileum.

Histopathologic Description:

Intestine (Ileum and caecum). The mucosa of the ileum is eroded and there is necrosis, with exudation of neutrophils and necrotic cellular debris into the intestinal lumen. Destruction of villi and crypts is evident. The intestinal lamina propria is extensively infiltrated with neutrophils and sheets of macrophages, producing a pyogranulomatous inflammatory reaction. Bacteria are present on the luminal surface of the mucosa and also infiltrate the lamina propria. Less severe changes are present in the caecum.

Lymph node. The subcapsular, intertrabecular and medullary sinuses of the ileocaecal lymph node are infiltrated with macrophages and lesser numbers of neutrophils, producing a pyogranulomatous inflammatory reaction, and there is focal necrosis in some areas.

Morphologic Diagnosis:  

Intestine: Enteritis, segmental, severe, necrotising, pyogranulomatous, with bacterial colonisation and invasion, consistent with enteric salmonellosis (Salmonella enteric server typhimurium, phage type DT40), domestic shorthair, feline

Ileocaecal lymph node: Lymphadenitis, moderate, multifocal, locally extensive, pyogranulomatous, consistent with salmonellosis.

Lab Results:  

Bacteriology: Salmonella enterica serovar typhimurium, phage type DT40, was recovered in profuse growth from the small intestine.

Virology: Intestinal contents were negative for feline parvovirus by the polymerase chain reaction.


Salmonella typhimurium

Contributor Comment:  

The clinical signs and pathological findings in this cat were consistent with fatal enteric salmonellosis. The isolate of Salmonella enteric server typhimurium obtained from the affected cat was phage typed as the definitive type (DT) 40. This strain is associated with wild birds, particularly finches (family Fringillidae), in North America, Europe and Scandinavia(2,4,5,8). The cat had a history of hunting wild birds, which represents the likely source of infection.

An outbreak of gastroenteritis due to S. typhimurium DT40 in cats and humans in central Sweden in 1999 was associated with infection and mortality in wild birds, notably common redpolls (Carduelis flame) and Eurasian siskins (Carduelis spinus)(8). In the United Kingdom, S. typhimurium DT40 has been isolated from European greenfinches (Carduelis chloris), house sparrows (Passer domesticus), chaffinches (Fringilla coelebs) and European goldfinches (Carduelis carduelis), in decreasing order of frequency, as well as occasionally from other species of birds(4). S. typhimurium DT40 has also been associated with epizootics of mortality in wild birds from winter 1997 to summer 1998 in eastern North America, including the Canadian Atlantic maritime provinces of New Brunswick, Novia Scotia, Prince Edward Island, Newfoundland and Labrador(2). The species most commonly affected in North America were common redpolls (Carduelis flammea), pine siskins (Carduelis pinus), purple finches (Carpodacus purpureus), evening grosbeaks (Coccothraustes vespertinus) and American goldfinches (Carduelis tristis), in decreasing order of frequency. S. typhimurium DT40 is considered to be an avian-adapted strain with a relatively narrow host range and a wide geographical distribution(5). Wild bird strains of S. typhimurium (DT2, DT40, DT41, DT56 variant, DT99 and DT195) have been isolated at relatively low frequency from domestic livestock in the United Kingdom, but appear to be uncommon in humans, cats or dogs(4).

The most common source of infection with S. typhimurium in cats is from the consumption of raw meat(6). Healthy cats, as well as sick cats without enteric disease, may carry S. typhimurium, which is a potential zoonosis, although the reported prevalence of infection varies widely(7,9). Cats may also be a source of antimicrobial resistant S. typhimurium(9). The isolate of S. typhimurium DT40 from the cat reported here was resistant to streptomycin and sulphafurazole, but sensitive to ampicillin, clavulanate-potentiated amoxicillin, enrofloxacin, chloramphenicol, furazolidone, neomycin, oxytetracycline, and trimethoprim-sulphonamide, so was not considered to be a multi-drug resistant strain.

JPC Diagnosis:  

1. Ileum: Enteritis, necrotizing and pyogranulomatous, diffuse, moderate to severe, with marked lymphoid necrosis and crypt regeneration.

2. Lymph node: Lymphadenitis, necrotizing and pyogranulomatous, diffuse, moderate to severe, with marked lymphoid necrosis.

Conference Comment:  

Lymphoid necrosis of the Peyers patches and lymph node is a prominent feature in this case, and is consistent with the pathogenesis of Salmonella, which invade M cells in the Peyers patches and epithelium of the distal small intestine, cecum, upper colon, and tonsils. Virulence factors include fimbriae (pilar adhesins), which are important for colonization and receptor mediated endocytosis; flagella which enhance movement and facilitate attachment; enterotoxins that produce secretory diarrhea by blocking closure of chloride channels; and bacterial wall lipopolysaccharides (endotoxins) that cause membrane injury and cell death. These endotoxins are composed of an O-specific side chain which is unique to each bacterial species, and a Lipid A core which activates mononuclear phagocytes and induces the production of tumor necrosis factor (TNF) and interleukin- 1 (IL-1). This, in turn, induces endothelial cells to produce IL-6 and IL-8 and induce adhesion molecules, thus participating in leukocyte recruitment. Once adhered to macrophages, the bacteria inject bacterial proteins by a type III secretion system. Salmonella sp. also induce apoptosis of macrophages by a type I secretory system which activates caspase-1. The resulting pattern of injury includes acute coagulative necrosis of enterocytes and vasculitis with thrombosis in the lamina propria, resulting in button ulcers, and the bacteria can migrate via the portal vein to the liver, causing paratyphoid nodules(3,10).

Some conference participants interpreted multinucleated giant cell macrophages in the Peyers patches as syncitial cells, which can be found feline parvovirus, a primary differential for this case. Also known as feline panleukopenia virus, feline parvovirus, like all parvoviruses, lack polymerase enzymes and are dependent on host cell DNA polymerase II, which are produced during S and early G2 phases, for replication. The resultant effects of parvovirus infection are thus greatest in tissues with a high mitotic rate, such as hematopoietic cells and dividing cells of intestinal crypts(10).

Another differential is Francisella tularensis, the causative agent for tularemia. Tularemia, a gram negative intracellular coccobacillus, is passed by several types of ticks and causes necrosis of the liver, spleen, lymph nodes, lung, and bone marrow due to thrombosis, or less commonly caseating granulomas or hemorrhagic enteritis with ulceration over Peyers patches in cats(1).


1. Cullen JM, Brown DL. Hepatobiliary system and exocrine pancreas. In: Zachary JF, McGavin MD, eds. Pathologic Basis of Veterinary Disease. 5th ed. St. Louis, MO: Elsevier; 2012:432-3.
2. Daoust PY, Busby DG, Ferns L, Goltz J, McBurney S, Poppe C, Whitney H. Salmonellosis in songbirds in the Canadian Atlantic provinces during winter-summer 1997-98. Can Vet J 41(1): 54-59, 2000
3. Gelberg HB. Alimentary system and the peritoneum, omentum, mesentery, and peritoneal cavity. In: Zachary JF, McGavin MD, eds. Pathologic Basis of Veterinary Disease. 5th ed. St. Louis, MO: Elsevier; 2012:357, 376-7.
4. Pennycott TW, Park A, Mather HA. Isolation of different serovars of Salmonella enterica from wild birds in Great Britain between 1995 and 2003. Vet Rec 158(24): 817-820, 2006
5. Rabsch W, Andrews HL, Kingsley RA, Prager R, Tschape H, Adams LG, Baumler AJ. Salmonella enterica serotype Typhimurium and its host-adapted variants. Infect Immun 70(5): 2249-2255, 2002
6. Stiver SL, Frazier KS, Mauel MJ, Styer EL. Septicemic salmonellosis in two cats fed a raw-meat diet. J Am Anim Hosp Assoc 39(6): 538-542, 2003
7. Spain CV, Scarlett JM, Wade SE, McDonough P. Prevalence of enteric zoonotic agents in cats less than 1 year old in central New York State. J Vet Intern Med 15(1): 33-38, 2001
8. Tauni MA, Osterlund A. Outbreak of Salmonella typhimurium in cats and humans associated with infection in wild birds. J Small Anim Pract 41(8): 339-341, 2000
9. Van Immerseel F, Pasmans F, De Buck J, Rychlik I, Hradecka H, Collard J-M, Wildemauwe C, Heyndrickx M, Ducatelle R, Haesebrouck F. Cats as a risk for transmission of antimicrobial drug-resistant Salmonella. Emerg Infect Dis 10(12): 2169-2174, 2004
10. Zachary JF. Mechanisms of microbial infections. In: Zachary JF, McGavin MD, eds. Pathologic Basis of Veterinary Disease. 5th ed. St. Louis, MO: Elsevier; 2012:169-70, 204-6.

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