JPC SYSTEMIC PATHOLOGY

CARDIOVASCULAR SYSTEM

April 2022

C-B01 (NP)

 

Signalment (JPC #1947994):  5-week-old Rhode Island Red chicken

 

HISTORY:   None

 

HISTOPATHOLOGIC DESCRIPTION:  Heart:   The ventricular and septal walls are diffusely and transmurally thickened 2-4 times normal by large numbers of infiltrating macrophages and few lymphocytes, and heterophils/granulocytes that separate and replace cardiac myocytes.  Similar inflammatory cells infiltrate the endocardium and epicardial adipose tissue and multifocally form irregular tags and nodules that protrude from the epicardial surface.  Macrophages often have large vesiculate nuclei and foamy, pale eosinophilic cytoplasm.   Remaining cardiac myocytes are often pale and have swollen, vacuolated cytoplasm (degeneration), or have fragmented sarcoplasm with loss of cross striations and pyknotic nuclei (necrosis).   Multifocally, arteriolar walls are disrupted and replaced by intensely eosinophilic fibrillar material (fibrin), necrotic debris, and few degenerate inflammatory cells (necrotizing vasculitis).   

 

MORPHOLOGIC DIAGNOSIS:  Heart:   Pancarditis, histiocytic and granulocytic, diffuse, severe, with necrotizing vasculitis and myocardial degeneration and necrosis, Rhode Island Red, chicken, avian.

 

ETIOLOGIC DIAGNOSIS: Myocardial salmonellosis 

 

CAUSE:  Salmonella enterica subsp. enterica serovar Pullorum

 

CONDITION:  Pullorum disease

 

SYNONYMS:   Bacillary white diarrhea, white diarrhea

 

GENERAL DISCUSSION:  

• Infectious, egg-transmitted disease of poultry affecting especially young chicks and turkey poults, often characterized by white diarrhea and high mortality in young birds and by asymptomatic carriers 
• Pullorum disease (PD), historically referred to as bacillary white diarrhea, is a highly host adapted acute septicemic disease affecting primarily chickens and turkeys (especially chicks and poults); eliminated from commercial poultry industry in the U.S. today, now primarily a disease of backyard flocks or in developing countries establishing a poultry industry
• Salmonella sp. nomenclature:

• Salmonellae (Enterobacteriaceae family) are gram negative, 0.5-0.8 x 1-3.5 um,  motile bacilli, however, the Pullorum and Gallinarum serovars are characteristically nonmotile
• The genus Salmonella is composed of two species, S. bongori and S. enterica
• The names of serotypes are capitalized, not italicized
• The main species that cause disease in humans and domestic animals is S. enterica; there are six subspecies of S. enterica which include enterica, salamae, arizonae, diarizonae, indica, and houtenae 
• Only 1 subspecies of S. enterica (S. enterica subspecies enterica) causes disease in warm-blood animals; different serotypes cause different diseases

• PD is caused by Salmonella enterica subspecies enterica serovar Pullorum (i.e. S. Pullorum) and fowl typhoid is caused by S. Gallinarum; they share antigens and cross-agglutinate on serologic tests
• The bacteria is rather resistant and can survive for months; can be destroyed by thorough cleaning and disinfection
• Morbidity and mortality (distinctively high compared to other serovars) are highly variable and influenced by age, strain of bird, nutrition, flock management, concurrent diseases, and route and dose of exposure
• Notifiable disease to the World Organisation for Animal Health (OIE)
• Other avian species (quail, pheasants, ducks, peacocks, and guinea fowl) are also susceptible

 

PATHOGENESIS:  

• Routes of transmission

• Vertical (transovarial) is the principal route- by carrier hens to chicks via contamination of ovules before ovulation, contamination of ovum following ovulation, and shell penetration; surviving birds become asymptomatic carriers, harboring bacteria in splenic macrophages and reproductive tract
• Horizontal via feed/water/litter contamination, cannibalism of and contact with infected birds through digestive system; adult carriers can shed the organism in their feces

• Virulence factors

• Salmonella pathogenicity island 2 (SPI2)- gene that allows for survival and intracellular multiplication via type III secretion system which is key for uptake by macrophages where the organism replicates in the phagosome (unable to multiply inside these cells in ducks, accounting for their resistance to PD)
• Flagella of most Salmonella spp. may play a role in infection, but lack of flagella in S. Pullorum makes their virulence highly dependent on survival and multiplication in internal tissues
• Fimbriae (pilar adhesins) which are important for colonization and receptor-mediated endocytosis
• A large plasmid is essential to S. Pullorum 

• Plasmids: transmissible extrachromosomal DNA elements that may promote survival and virulence

• Ingestion > Salmonella adheres to mucosal epithelial cells and microfold cells (M cells) overlying lymphoid tissue > penetration of microfold cells > presentation to macrophages > organism survives, replicates, and is disseminated within macrophages > invasion to internal organs (may preferentially target the Bursa of Fabricius)

 

TYPICAL CLINICAL FINDINGS:

Chicks  

• Morbidity and mortality are high; mortality is usually confined to chicks and poults, peaking at 2-3 weeks old (egg-transmitted disease); greatest loss predominantly chicks and poults less than 4 weeks old
• Anorexia, white chalky diarrhea with pasting of the vent, dehydration, huddling near heat sources, shrill chirping, appear “sleepy”, weakness
• Dyspnea, blindness, and joint swelling/lameness (tibiotarsal and humeroradial)
• Mortality usually very high and can approach 100%, or conversely may be low and go unrecognized
• Survivors may be greatly retarded in growth, underdeveloped, and poorly feathered, and many remain carriers

Adults  

• Often none; reduced egg production, fertility, or hatchability; unthrifty
• Diarrhea, anorexia, dehydration in severe cases (uncommon)

 

TYPICAL GROSS FINDINGS:  

Chicks

• Lesions vary from few in acute cases to disseminated lesions in chronic cases (some may die with no gross lesions)
• Occasionally dead birds feel wet; pasted white feces in vent area
• Enlarged and congested liver, spleen, and kidneys (acute)
• Pale/white 2-4mm nodules or foci in the lungs (P-B15), liver, heart, gizzard wall, intestinal or cecal wall, spleen, and peritoneum
• Thickened pericardium containing yellow to fibrinous exudates
• Frequently petechial hemorrhages or foci of necrosis in the liver
• Caseous cecal cores (caseous exudate in the lumen of the ceca- this occurs more in birds that die later in the course of the outbreak)
• Swollen joints (tibiotarsal) containing white to yellow viscous fluid; occasional finding
• Splenomegaly
• Ureters distended with urates
• Omphalitis (navel infection)

Adults

• Adults may have few or no lesions
• Few misshapen, discolored, cystic ova that contain oily to caseous material in a thick capsule; less frequently, oviduct impaction, peritonitis, or ascites
• Occasionally caseous granulomas or nodules in the lungs, heart, pericardium, and testes
• Fibrin-covered, misshapen, or atretic ovaries (oophoritis)
• Fibrin on both the heart and coelomic viscera
• Testes:   White foci or nodules
• Adipose tissue:   Small cysts with yellow caseous material embedded in the abdominal fat or attached to GI serosa
• Pericarditis with thickened, opaque pericardium +/- myocarditis

 

TYPICAL LIGHT MICROSCOPIC FINDINGS:  

Chicks

• Peracute:  Severe vascular congestion of multiple organs (liver, spleen, kidneys)
• Acute to subacute lesions:  

• Lung:  Necrotizing interstitial pneumonia with mixed inflammation 
• Liver:  Multifocal necrotizing hepatitis

• Chronic:  

• Heart (C-B01) and ventriculus have the most characteristic lesions:  Necrosis with mixed inflammatory infiltrates (heterophils, lymphocytes, plasma cells) and replacement by histiocytes that may form nodules
• Heart

• Acute:   Myofiber necrosis, heterophilic myocarditis
• Chronic:   Dense infiltrates of large histiocytes (with large vesiculate nuclei and foamy pale eosinophilic cytoplasm) that replace cardiac myocytes and form nodules that protrude from epicardial surface

• Pericardium, pleuroperitoneum, synovium, serosa and mesentery

• Acute/subacute:   Heterophilic inflammation and fibrin
• Chronic:   Histiocytic and lymphoplasmacytic inflammation

• Lung:  Necrotizing pneumonia (+/- nodules)
• Pancreas:  Necrosis with similar nodules of inflammatory cells
• Ceca:  Mucosal necrosis with caseous cores composed of necrotic debris, fibrin, and heterophils
• Liver:  Hepatocellular necrosis; mixed heterophils and lymphocytes; chronic passive congestion if cardiac lesions are present
• Omphalitis, ophthalmitis, catarrhal bronchitis, and catarrhal enteritis

Adults 

 

ADDITIONAL DIAGNOSTIC TESTS:  

• Isolation and identification of S. Pullorum required for final diagnosis because clinical signs and gross lesions can resemble those by a variety of other bacteria, especially S. Gallinarum); time-consuming test
• Serology- can cross agglutinate with S. Gallinarum

 

DIFFERENTIAL DIAGNOSIS:  

For gross lesions: 

• Marek’s disease (gallid herpesvirus 2, I-V13, N-V08) and avian leukosis virus (avian retrovirus):  Similar white nodules in the heart and other viscera
• Salmonella enterica subsp. Arizonae (S-B01):  Acute or chronic egg-transmitted infection; primarily in turkeys with highest mortality in the first 3-4 weeks of life  
• Paratyphoid disease:  Caused by any of the non-host adapted Salmonellae, especially S. typhimurium and S. enteritidis
• Septicemic/localized coliform, staphylococcal, streptococcal, and Pasteurella multocida infections
• Mycoplasma synoviae, Staphylococcus aureus, Pasteurella multocida and Erysipelothrix rhusiopathiae cause similar synovitis

 

COMPARATIVE PATHOLOGY:  

• S. Pullorum is not commonly associated with disease in other animals because it is highly host specific; other species can be infected (pheasants, quail, ducks, peacocks, guinea fowl, sparrows, parrots, and rarely ostriches) but play an insignificant role in epidemiology of disease
• S. Pullorum has been described as a naturally occurring or experimental infection in mammals including chimpanzees, rabbits, guinea pigs, chinchillas, pigs, kittens, foxes, dogs, swine, mink, cows, and wild rats
• S. Pullorum is zoonotic but of little concern

 

REFERENCES:   

1. Barrow PA, Jones MA, Smith AL, Wigley P. The long view: Salmonella — the last forty years. Avian Pathol. 2012;41(5):413-420.
2. Barrow PA, Freitas Neto OC. Pullorum disease and fowl typhoid – new thoughts on old diseases: A review. Avian Pathol. 2011;40(1):1-13.
3. Chappell L, Kaiser P, Barrow P, Jones MA, Johnston C, Wigley P. The immunobiology of avian systemic salmonellosis. Vet Immunol Immunopathol. 2009;128(1):53-59.
4. Crespo R, Franca MS, Fenton H and Shivaprasad HL. Galliformes and Columbiformes. In: Terio KA, McAloose D, St. Leger J, eds. Pathology of Wildlife and Zoo Animals. San Diego, CA; Elsevier; 2018:759.
5. Fulton RM. Salmonellosis. In: Boulianne M, ed. Avian Disease Manual. 8th ed. Jacksonville, FL; AAAP Inc.; 2019:101-104.
6. Gast RK, Porter Jr RE. Salmonella Infections. In: Swayne DE, ed. Diseases of Poultry. 14th ed. Hoboken, NJ: John Wiley & Sons, Inc.; 2020:719-753.
7. Lu Y, Chen S, Dong H, Sun H, Peng D, Liu X. Identification of genes responsible for biofilm formation or virulence in Salmonella enterica serovar pullorum. Avian Dis. 2012;56(1):134-143.
8. Shivaprasad HL, Barrow PA. Pullorum disease and fowl typhoid. In: Saif YM, ed. Diseases of Poultry. 13th ed. Ames, Iowa: Blackwell Publishing; 2013:678-693.

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