JPC SYSTEMIC PATHOLOGY
DIGESTIVE SYSTEM
August 2021
D-B03 (NP)

Signalment (JPC #1782711):   A quail

HISTORY:  Tissue from a large flock of quail that suffered a loss of 20-50 birds over a 2-week period.  The birds seemed to be fine at night and then were found dead the next morning.  Treatment with tetracycline in the drinking water for three days appeared to stop the deaths.

HISTOPATHOLOGIC DESCRIPTION:  Small intestine: Multifocally and circumferentially, there is marked loss of normal mucosal villar architecture with replacement by a thick coagulum of necrotic debris, fibrin, hemorrhage, numerous colonies of 1x4 um bacilli, high numbers of macrophages, lymphocytes, and fewer heterophils (diphtheritic membrane).  Adjacent less affected villi are multifocally eroded, ulcerated, blunted, and/or fused, and remaining mucosal epithelial cells are often either brightly eosinophilic, angular, and shrunken with pyknotic nuclei (necrosis) or swollen with microvacuolated cytoplasm (degeneration).  Multifocally expanding the remaining lamina propria or extending transmurally through the intestinal wall are numerous heterophils, macrophages, lymphocytes, plasma cells, hemorrhage, fibrin, and edema.  Multifocally, adventitial vessels are markedly congested.   

MORPHOLOGIC DIAGNOSIS:  Small intestine:  Enteritis, ulcerative and necrotizing, subacute, diffuse, severe, with intralesional colonies of bacilli, quail, avian.

ETIOLOGIC DIAGNOSIS:  Clostridial enteritis

CAUSE:  Clostridium colinum

CONDITION:  Ulcerative enteritis

SYNONYM:  Quail disease

GENERAL DISCUSSION:

• Acute ulcerative enteritis and necrotizing hepatitis results in sudden death in young captive or wild game birds, young quail, grouse, turkeys, chickens, partridge, pigeons, pheasants; does not affect water fowl
• First described in quails “quail disease”
  • Quail (particularly bob-white quail) are among the most susceptible
• Gram positive, spore forming, pleomorphic (straight or slightly curved rods with rounded ends), anaerobic, non-motile bacterium
• Typically affects young birds, 4-12 weeks old (but can occur in adults as well)
• Outbreaks in chickens often accompany or follow coccidiosis or immunosuppressive conditions (e.g. chicken infectious anemia virus [circovirus], infectious bursal disease [birnavirus], or stress conditions)

PATHOGENESIS:

• Fecal-oral transmission: bacteria adhere to intestinal villi > cause inflammation > ulceration in small to upper large intestine > bacteria moves to liver, if bird survives > survivors and birds with active infection are carriers > shed in feces
• Localizes in liver (via portal circulation) and spleen; causes hepatic necrosis
• Toxin has not been implicated

TYPICAL CLINICAL FINDINGS:

• Similar to coccidiosis (Eimeria brunetti in chicken): Listlessness, droopy wings, anemia, diarrhea, bloody feces
• Quail usually pass distinctive white watery droppings; chronic carriers have diarrhea and emaciation
• Mortality varies with species (10% in chickens, up to 100% in quail)
• Sudden death may occur in fat, well-muscled quail with feed still in the crop
• Notable emaciation with atrophy of pectoral muscle in chronic cases

TYPICAL GROSS FINDINGS:

• Intestine (including ceca):
  • Marked duodenal hemorrhagic enteritis with small punctate mucosal ulcers surrounded by hemorrhagic halo
  • Full thickness ulceration may also occur
  • In turkeys: necrotic, diphtheritic membrane in case of extensive ulceration
  • Perforation/peritonitis may occur
  • Acute lesions are characterized by marked hemorrhagic enteritis in the duodenum
• Liver:
  • When lesions are present: large, multifocal, yellow-gray foci sometimes surrounded by a pale yellow halo
• Spleen:
  • When lesions are present: enlarged and hemorrhagic

TYPICAL LIGHT MICROSCOPIC FINDINGS:

• Intestine:
  • Acute: mucosal erosion, edema of intestinal wall, vascular congestion, heterophilic infiltration of lamina propria; lumen contains desquamated mucosal epithelium with hemorrhage, coagulative necrosis, and bacterial rods; diphtheritic membrane formation
  • Chronic: ulceration involves villi and extend into submucosa, with pseudomembrane formation; adjacent epithelial cells show coagulation necrosis
  • Vascular fibrin & bacterial thrombosis are consistent findings in both acute and chronic lesions
  • Ulcers often surrounded by granulocytes and mononuclear inflammatory cells
• Liver:
  • Centrilobular or diffuse, pinpoint coagulative hepatic necrosis with gram-positive bacteria
• Spleen:
  • Variable splenic necrosis in quail

DIAGNOSTIC TESTS:

• Presumptive diagnosis with typical gross lesions (ulcerations in ceca and intestine, hepatic necrosis, and enlarged hemorrhagic spleen)
• Final diagnosis - Detection by culture or PCR of liver, spleen, intestinal contents
• Fluorescent antibody: Highly specific
• Cytological findings - Bacilli occasionally contain 1um, oval, sub-terminal spores

DIFFERENTIAL DIAGNOSIS:

• Coccidiosis: Often seen or confused with ulcerative enteritis; does not cause focal liver necrosis or an enlarged hemorrhagic spleen
• Hemorrhagic enteritis in turkey poults (avian adenovirus type 2): Intranuclear inclusion bodies
• Necrotic enteritis (Clostridium perfringens type G): No liver lesions, quail not affected; causitive subtype associated with NetB gene positivity (recently reclassified as perfringens type G) which is responsible for producing pore forming compound; clinically and pathologically indistinguishable from C. colinum
• Histomonas meleagridis: Produces caseous cecal cores and necrotic targetoid hepatic lesions; histomonads visible in liver and spleen histologically; does not induce small intestinal lesions

COMPARATIVE PATHOLOGY:

• The invasive or enterotoxigenic clostridia causing diseases in animals include:
  • colinum: Ulcerative enteritis in young game birds, turkeys, chickens and psittacines
  • perfringens: Classified into 7 major types (A, B, C, D, E, F, and G), based on the production of major lethal toxins; all C. perfringens types produce alpha toxin:
    • Type A produces alpha toxin only; yellow lamb disease
    • Type B produces alpha toxin, beta toxin, and epsilon toxin; lamb dysentery/hemorrhagic enteritis
    • Type C (D-B02) produces alpha toxin and beta toxin; “struck” in adult sheep
    • Type D (N-B01, U-B06) produces alpha toxin and epsilon toxin; pulpy kidney/overeating disease and encephalomalacia in sheep and goats
    • Type E produces alpha toxin and iota toxin; enterotoxemia, canine hemorrhagic gastroenteritis
    • Type F produces alpha toxin and perfringens enterotoxin; human food poisoning and diarrhea
    • Type G produces alpha toxin and NetB toxin; poultry necrotic enteritis
  • haemolyticum (D-B17): Bacterial icterohemoglobinuria (Bovine bacillary hemoglobinuria) or Redwater disease (cattle)
  • novyi: Black disease (sheep); malignant edematous disease in other animals
  • chauvoei (M-B01): Blackleg (cattle and sheep)
  • septicum (D-B04): Braxy (sheep); malignant edematous infection in other species; necrotizing dermatitis in poultry
  • spiroforme: Spontaneous, antibiotic-induced enterotoxemia in rabbits
  • villosum: Subcutaneous abscesses (cats)
  • difficile: Antibiotic-induced enterocolitis (hamsters, rabbits, guinea pigs); naturally occurring enterocolitis (swine and foals)
  • piliforme(D-B06): the only gram negative Clostridium sp.; Tyzzer's disease; multiple animal species; liver, intestine, and heart

REFERENCES:

1. Abdul-Aziz T, Fletcher OJ, Barnes HJ. Avian Histopathology. 4^th Jacksonville, FL: AAAP, Inc.; 2016:326.
2. Crespo R, Franca MS, Fenton H, Shivaprasad HL. Galliformes and Columbiformes. In: Terio KA, McAloose D, Judy St. Leger J, ed. Pathology of Wildlife and Zoo Animals, Cambridge, MA Academic Press; 2018: 761-762.
3. Fulton RM. Ulcerative Enteritis. In: Boulianne M, ed. Avian Disease Manual. 8^th Jacksonville, FL: AAAP Inc.;2019:111-113.
4. Shivaprasad HL, Uzal F, Kokka R, Fisher DJ, McClane BA, and Songer AG. Ulcerative Enteritis-Like Disease Associated with Clostridium perfringens Type A in Bobwhite Quail (Colinus virginianus). Avian Diseases. 2008;52(4):635-40.
5. Rood JI, Keyburn AL, Moore RJ. NetB and necrotic enteritis: the hole movable story. Avian Pathol. 2016;45(3):295-301.
6. Uzal FA. Ulcerative Enteritis. In: Swayne DE, ed. Diseases of Poultry. Vol 1. 14th ed. Hoboken, NJ: John Wiley & Sons, Inc; 2020:967-971.

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