JPC SYSTEMIC PATHOLOGY
Signalment (JPC #1492950): Australorp chick
HISTORY: Two chicks became sick shortly after the new owner moved the brooder. Gross pathology included a yellow, solid, 3 mm nodule in the right lung and an abscessed umbilicus that was adhered to the gut.
HISTOPATHOLOGIC DESCRIPTION: Lung: Affecting approximately 40% of the section, filling the lumina and obscuring or effacing the walls of secondary bronchi, parabronchi, and respiratory atria, there is a mucinous exudate composed of numerous foamy macrophages, viable and degenerate heterophils, sloughed necrotic epithelial cells, fewer multinucleated cells, lymphocytes and plasma cells, fibrin, hemorrhage, and edema. Respiratory epithelium is either hyperplastic and up to 3 cell layers thick, attenuated, discontinuous, or necrotic, with shrunken hypereosinophilic cytoplasm and pyknotic nuclei, with occasional sloughing. Adjacent air capillaries are effaced by eosinophilic cellular and karyorrhectic debris (lytic necrosis) and similar inflammatory cells, fibrin, edema, and hemorrhage. Multifocally, perivascular and interlobular septa are moderately expanded by fibrin, increased clear space and ectatic lymphatics (edema), and low numbers of similar inflammatory cells. Diffusely, blood vessels are moderately congested.
MORPHOLOGIC DIAGNOSIS: Lung: Pneumonia, necrotizing, subacute, focally extensive, marked, Australorp, chicken.
ETIOLOGIC DIAGNOSIS: Pulmonary salmonellosis
CAUSE: Salmonella Pullorum
ETIOLOGY SYNONYMS: Salmonella enterica serovar Gallinarum biovar Pullorum; Salmonella enterica ssp. enterica serovar Gallinarum-Pullorum
CONDITION: Pullorum disease
- Pullorum disease (PD), historically referred to as bacillary white diarrhea, is a highly host adapted septicemic disease affecting primarily chickens and turkeys; rare in the U.S. commercial poultry industry and is now primarily a disease of backyard flocks
- Salmonellae (Enterobacteriaceae family) are gram negative, 0.5-0.8 x 1-3.5 um, motile bacilli
- All Salmonella are pathogenic
- The genus Salmonella comprises two species, bongori and S. enterica
- The names of serotypes are capitalized, not italicized
- The main species that cause disease in humans and domestic animals is enterica; there are six subspecies of S. enterica which include enterica, salamae, arizonae, diarizonae, indica, and houtenae
- Salmonella Pullorum is classified as a single species (Salmonella enterica enterica serovar Gallinarum-Pullorum); PD is caused by S. Pullorum and fowl typhoid is caused by S. Gallinarum
- Chickens and turkeys are important natural hosts of PD; the disease principally affects chicks and poults, typically 2-3 weeks old
- Additional species affected include pheasants, quail, ducks, peacocks, guinea fowl, sparrows, and parrots
- Morbidity and mortality are highly variable and influenced by age, strain of bird, nutrition, flock management, concurrent diseases, and route and dose of exposure
- Routes of transmission
- Vertical (transovarial) via contamination of ovules before ovulation, contamination of ovum following ovulation, and shell penetration
- Horizontal via feed/water/litter contamination, contact, and cannibalism of infected birds
- Virulence factors
- Salmonella pathogenicity island 2 (SPI2) 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
- Fimbriae (pilar adhesins) which are important for colonization and receptor mediated endocytosis
- Infection is primarily spread by carrier hens to chicks via infected eggs as a result of contamination of the ovum prior to or following ovulation; surviving birds become carriers
- Ingestion > Salmonella interacts with 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
- Infections in species other than chickens and turkeys seldom cause significant disease
TYPICAL CLINICAL FINDINGS:
- Morbidity and mortality are high; mortality is usually confined to chicks 2-3 weeks old
- Anorexia, white chalky diarrhea, dehydration
- Dyspnea, blindness, and joint swelling (tibiotarsal, humeroradial)
- Survivors may be greatly retarded in growth, underdeveloped, and poorly feathered
- Often none; reduced egg production or fertility
- Diarrhea, anorexia, dehydration in severe cases (uncommon)
TYPICAL GROSS FINDINGS:
- Lesions vary from few in acute cases to disseminated lesions in chronic cases
- Enlarged and congested liver, spleen, and kidneys (acute)
- Pale/white 2-4mm nodules or foci in the lungs, liver, heart, pancreas, and ventriculus
- Caseous cecal cores; fibrinous pericarditis, serositis; caseous material in the yolk sac
- Swollen joints (tibiotarsal) containing yellow viscous fluid
- Adults may have few or no lesions.
- Few misshapen, discolored, cystic ova; fibrinous peritonitis, perihepatitis, pericarditis
- Occasionally granulomas or nodules in the lungs, testes, and pancreas
TYPICAL LIGHT MICROSCOPIC FINDINGS:
- Peracute: Severe vascular congestion of multiple organs (liver, spleen, kidneys)
- Acute to subacute lesions:
- Lung: Necrotizing interstitial pneumonia with necrosis with mixed inflammation
- Liver: Multifocal necrotizing hepatitis
- Heart and ventriculus have the most characteristic lesions: Necrosis with mixed inflammatory infiltrates (heterophils, lymphocytes, plasma cells) and replacement by histiocytes that may form nodules
- Lung: Necrotizing pneumonia (+/- nodules)
- Pancreas: Necrosis with similar nodular 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
- Fibrinoheterophilic to caseous oophoritis, salpingitis, orchitis
ADDITIONAL DIAGNOSTIC TESTS:
- Isolation and identification of Pullorum
- PCR assay based on ratA gene differentiates between Gallinarum and S. Pullorum (absent on genome of S. Pullorum)
- Salmonella Gallinarum (Fowl typhoid): Similar clinical signs and lesions; associated with both young and adult chickens and turkeys; isolation and identification to differentiate from Pullorum
- Salmonella Typhimurium: Broad range pathogen; produces liver, spleen, and intestinal lesions that cannot be distinguished grossly or histologically from those of PD; need isolation and identification to differentiate from Pullorum
- Salmonella enterica arizonae: Turkeys are most commonly affected; produces similar systemic disease; need isolation and identification to differentiate from S. Pullorum
- Marek’s disease (alpha herpesvirus; gallid herpesvirus-2): Nodules that may appear identical grossly; histologically similar to chronic stages of PD
- Lung: Aspergillus, other fungi; other Salmonella spp.
- Heart: Marek’s disease (alpha herpesvirus)
- Liver: Yersinia pseudotuberculosis (shares some antigenic relationships)
- Swollen joints: Mycoplasma synoviae, Staphylococcus aureus, Pasteurella multocida, Erysipelothrix rhusiopathiae
- S. Pullorum is not commonly associated with disease in other animals because it is highly host specific
- 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
- Anderson LA, Miller DA, Trampel DW. Epidemiological investigation, cleanup and eradication of pullorum disease in adult chickens and ducks in two small-farm flocks. Avian Dis. 2006;50(1):142-147.
- Barrow PA, Jones MA, Smith AL, Wigley P. The long view: Salmonella — the last forty years. Avian Pathol. 2012;41(5):413-420.
- Barrow PA, Neto OCF. Pullorum disease and fowl typhoid—new thoughts on old diseases: a review. Avian Pathol. 2011;40(1):1-13.
- Batista DFA, de Freitas Neto OC, de Almeida AM, et al. Molecular identification of Salmonella enterica Enterica serovar Gallunarum biovars Gallinarum and Pullorum by a duplex PCR assay. J Vet Diagn Invest. 2016;28(4): 419-422.
- Batista DFA, de Freitas Neto OC, Lopez PD, et al. Polymerase chain reaction assay based on ratA gene allows differentiation between Salmonella enterica enterica serovar Gallinarum biovars Gallinarum and Pullorum. J Vet Diagn Invest. 2013;25(2):259-262.
- Chappell L, Kaiser P, Barrow P, Jones MA, Johnston C, Wigley P. The immunobiology of avian systemic salmonellosis. Vet Immunol Immunopathol. 2009;128(1-3):53-59.
- Fulton RM, Boulianne M. Salmonellosis. In: Boulianne M, ed. Avian Disease Manual. 7th Jacksonville, FL: The American Association of Avian Pathologists; 2013.
- Henderson SC, Bounous DI, Lee MD. Early events in the pathogenesis of avian salmonellosis. Infect Immun. 1999;67(7):3580-3586.
- Shivaprasad HL, Barrow PA. Pullorum disease and fowl typhoid. In: Saif YM, ed. Diseases of Poultry. 13th ed. Ames, IA: Blackwell Publishing; 2008:678-693.