October 2015

Signalment (JPC #2317341):  Slide A:  Pilot black snake 

HISTORY:  This snake was found dead after a brief period of inactivity.


  1. 1.  Liver:  Affecting 70% of normal tissue architecture are random, multifocal to coalescing areas of coagulative necrosis (characterized by loss of differential staining with retention of tissue architecture), lytic necrosis (characterized by loss of tissue architecture with replacement by karyorrhectic and cellular debris, hemorrhage, few heterophils, macrophages, and lymphocytes), and hepatocyte degeneration (characterized by cytoplasmic swelling and vacuolization). There are multifocal areas of hepaocellular loss and Kupffer cell hyperplasia.  Multifocally necrotic areas contain many extracellular, intravascular or intrahistiocytic 10-20um diameter amoebic trophozoites with a thin cell wall, abundant granular to vacuolated basophilic cytoplasm with rare phagocytized necrotic debris, and a 5-7um round to oval nucleus with marginated chromatin and a lightly basophilic karyosome.  There are scattered colonies of 1 x 2um coccobacilli.  Multifocally the tunica media and tunica adventitia of blood vessels are expanded and replaced by heterophils and eosinophilic and karyorrhectic cellular debris (vascular necrosis), and contain few previously described trophozoites and inflammatory cells.
  2. Mesentery: The fibroadipose tissue is moderately expanded by clear space and dilated lymphatics (edema), fibrin, hemorrhage, few degenerate heterophils, and karyorrhectic debris (lytic necrosis).  Multifocally, there are many scattered colonies of coccobacilli.
  3. Kidney with spermatic ductules: Multifocally separating and surrounding tubules are variably sized areas of hemorrhage.  There are multifocal areas of vascular necrosis in intermediate and large vessels, and rare ameobic trophozoites within or adjacent to affected vessels.  Diffusely, tubular epithelium is sloughed or elevated off the basement membrane (autolysis) and there are numerous scattered colonies of 2 um cocci (postmortem overgrowth).


  1. Liver:  Hepatitis, necrotizing, random, acute, multifocal to coalescing, moderate, with vascular necrosis, and extracellular and intracellular amoebic trophozoites and coccobacilli, pilot black snake (Elaphe obsoleta), ophidian.
  2. Mesentery: Steatitis, necrotizing, acute, diffuse, moderate, with necrotizing vasculitis, hemorrhage, fibrin, and edema.
  3. Kidney: Hemorrhage, multifocal, moderate with vascular necrosis and rare amoebic trophozoites. 

ETIOLOGIC DIAGNOSIS: Amoebic hepatitis

CAUSE: Entamoeba invadens

Signalment (JPC #1296472):  Slide B:  Snake


HISTOPATHOLOGIC DESCRIPTION:  Colon:  There is diffuse loss of mucosal architecture with replacement by a coagulum of fibrin, hemorrhage, and eosinophilic and karyorrhectic cellular debris (lytic necrosis), admixed with  few macrophages, heterophils, lymphocytes, and plasma cells, as well as moderate numbers of 10-20um diameter amoebic trophozoites with a thin cell wall, abundant granular to vacuolated basophilic cytoplasm, with a 5-7um round to oval nucleus with marginated chromatin, and a lightly basophilic karyosome.  Necrosis, inflammation and amoebic trophozoites extend into the submucosa, tunical muscularis and serosa.  Transmurally, the colon is expanded by clear space and dilated lymphatics (edema).  Multifocally blood vessel walls within necrotic areas are discontinuous and replaced with necrotic debris, fibrin and edema (vascular necrosis) and often contain small fibrin thrombi and/or amoebic trophozoites.  There is diffuse mesenteric fat atrophy.    

MORPHOLOGIC DIAGNOSIS:  Colon:  Colitis, necrohemorrhagic, acute, diffuse, severe, with many extracellular and intravascular amoebic trophozoites, edema, and mesenteric fat atrophy, snake, ophidian.


CAUSE:  Entamoeba invadens

Signalment (JPC #2317380):  Slide C & D:  Golden lion tamarin (Leontopithecus rosalia)



  1. 1.  Colon:  Multifocally, affecting 70% of normal tissue architecture, there is multifocal to coalescing lytic necrosis characterized by loss of mucosal architecture with replacement by abundant eosinophilic and karyorrhectic cellular debris and fibrin admixed with neutrophils, lymphocytes, macrophages, hemorrhage, and numerous colonies of 1 x 2um basophilic bacilli which often fill crypts.  Necrosis and inflammation multifocally extends through the tunica muscularis into the submucosa.  Within necrotic areas, there are few 10-25um diameter amoebic trophozoites with clumped to globular basophilic cytoplasm, and an eccentric, 3-4um diameter nucleus with a karyosome.  Colonic crypts are variably necrotic with epithelial cells that are sloughed or shrunken with hypereosinophilic cytoplasm and pyknotic nuclei, or ectatic and filled by abundant eosinophilic cellular and karyorrhectic luminal debris (crypt abscess) admixed with numerous filamentous bacteria.  There is diffuse mesenteric fat atrophy.
  2. Duodenum: Focally within an ectatic submucosal lymphatic, there is a cross section of a larva nematode surrounded by few degenerate inflammatory cells.  The nematode has a 1-2um cuticle, paired lateral alae, coelomyarian-polymyarian musculature, an indistinct digestive tract, and lacks a reproductive tract. 
  3. Multiple sections throughout the esophagus, stomach and small intestine: No significant lesions.

Slide D:  PAS:  Colon:  There are multiple PAS-positive amoebic trophozoites within the necrotic mucosa. 


  1. Colon:  Colitis, necrotizing, subacute, multifocal, moderate, with crypt necrosis, crypt abscesses, few PAS-positive amoebic trophozoites  and multifocal colonies of bacilli, golden lion tamarin (Leontopithecus rosalia), nonhuman primate.
  2. Duodenum, lymphatic: Larval nematode, focal. 


CAUSE:  Entamoeba histolytica

CONDITION:  Amoebiasis









Other causes of colitis in primates:

Other causes of gastroenteritis in snakes:



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