Read-Only Case Details Reviewed: Sep 2008

JPC SYSTEMIC PATHOLOGY

RESPIRATORY SYSTEM

August 2023

P-B15

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 80% of the section (some slide variation), there is an exudate filling the lumina and obscuring or effacing the walls of secondary bronchi, parabronchi, and respiratory atria composed of numerous foamy macrophages, viable and necrotic heterophils, sloughed necrotic epithelial cells, fewer multinucleated cells, lymphocytes, and plasma cells, eosinophilic fibrillar material (fibrin), hemorrhage, and increased clear space (edema). Respiratory epithelium is either hyperplastic, piling up to 3 cell layers thick, attenuated, discontinuous, or necrotic, with shrunken hypereosinophilic cytoplasm and pyknotic nuclei and occasional sloughing into the lumen. Adjacent air capillaries are effaced by eosinophilic cellular and karyorrhectic debris (lytic necrosis), previously described 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.

There is a focally extensive, well demarcated area of necrosis with a sharp of necrotic tissue (infarct) that is present on some slides.

MORPHOLOGIC DIAGNOSIS: Lung: Pneumonia, necrotizing, subacute, focally extensive, marked, Australorp, chicken.

ETIOLOGIC DIAGNOSIS: Pulmonary salmonellosis

CAUSE: Salmonella Pullorum

ETIOLOGY SYNONYMS: Salmonella enterica ssp. enterica serovar Pullorum

CONDITION: Pullorum disease

GENERAL DISCUSSION:

Pullorum disease (PD) is an infectious, egg-transmitted disease of poultry, especially young chicks and turkey poults, often characterized by white diarrhea and high mortality in young birds and asymptomatic adult carriers
Caused by Salmonella Pullorum, a highly host adapted Salmonella, which is a nonmotile, gram-negative bacillus that can establish acute septicemia with lesions in multiple organs (see C-B01)
1. S. Pullorum is closely related to S. Gallinarum, the causative agent of fowl typhoid; cross-agglutinate on serologic tests due to shared antigens
2. The bacteria is resistant and can survive for months but can be destroyed by thorough cleaning and disinfection
Salmonella spp. nomenclature:
1. Genus Salmonella is composed of two species, S. enterica and S. bongori
2. Salmonella are further subtyped into subspecies and serovars
  - E.g., S. enterica subspecies enterica serovar Enteritidis, more commonly referred to as S. Enteritidis, or S. enterica subspecies enterica serovar Typhimurium, also referred to as S. Typhimurium
  - Pullorum and Gallinarum are both serovars of Salmonella enterica ssp. enterica

PATHOGENESIS:

Vertical/transovarial spread is the principal route from carrier hens to chicks
1. Infected chicks can then transmit horizontally to other birds through the digestive and respiratory systems
Other routes of transmission include adult carriers shedding organism in feces (contaminating feed, water, and the environment) or cannibalism of infected bacteremic birds
Virulence factors
1. Salmonella pathogenicity islands- Encodes virulence factors on its chromosome
2. Type III secretion system injects bacterial proteins into target cells that stimulate phagocytosis through mobilization of actin filaments
3. Flagella of most Salmonella spp. may play a role in infection, but lack of flagella in Pullorum makes their virulence highly dependent on survival and multiplication in internal tissues
4. Fimbriae (pilar adhesins) which are important for colonization and receptor-mediated endocytosis
5. 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

TYPICAL CLINICAL FINDINGS:

Chicks/Poults
1. Morbidity and mortality are high (can approach 100%); mortality usually confined to chicks and poults less than 4 weeks old
2. Reduced hatchability; some hatched birds weak or dying; sudden death
3. Sick birds are weak and can appear “sleepy” and may have anorexia, white chalky diarrhea pasting the vent, dehydration, huddling near heat sources, shrill chirping
4. Survivors may have growth retardation and be underdeveloped and/or poorly feathered; they may remain carriers
Adults
1. Often none; may see reduced egg production or an unthrifty appearance

TYPICAL GROSS FINDINGS:

Chicks
1. Pale/white 2-4 mm nodules or foci in multiple organs:
  - Lungs, liver, heart (C-B01), ventriculus wall, intestinal and cecal wall, spleen, and/or peritoneum; frequently splenomegaly
2. Petechial hemorrhages or foci of necrosis in the liver
3. White mucosa plaques in intestines; caseous cecal or intestinal core (more common in birds that die later in the course of the outbreak)
4. Swollen joints containing white to yellow viscous fluid
5. Ureters distended with urates
Adults
1. May have few or no lesions
2. Nodular myocarditis, pericarditis, or abnormal gonads; occasionally granulomas or nodules in the lungs
  - Ovary (oophoritis) with hemorrhagic, atrophic, or discolored follicles, +/- oviduct impaction
  - Testes may have white foci or nodules
3. Occasionally peritonitis or ascites

TYPICAL LIGHT MICROSCOPIC FINDINGS:

From Shivaprasad, Rev Sci Tech, 2000

Chicks
1. Peracute: Severe vascular congestion of multiple organs (e.g., liver, spleen, kidneys)
2. Acute to subacute lesions: Multifocal fibrinonecrotic and mixed inflammatory lesions in multiple organs:
  - Heart (C-B01) and ventriculus most characteristic: Multifocal myofiber necrosis with heterophilic (and lesser lymphoplasmacytic) inflammation
  - Liver: Fibrinonecrotic hepatitis with mixed inflammation; occasionally granuloma formation
  - Spleen: Fibrinous exudation in the vascular sinus
  - Lung: Necrotizing interstitial pneumonia with mixed inflammation
  - Cecum: Necrotic and caseous luminal debris, mucosal necrosis with heterophilic inflammation
  - Fibrinosuppurative serositis
  - Other lesions: Fibrinoheterophilic panophthalmitis or synovitis
  - Can commonly see fibrinosuppurative and pyogranulomatous oomphalitis (inflammation of the yolk sac) with bacteria
3. Chronic: Inflammation more commonly lymphoplasmacytic and histiocytic
  - Heart and ventriculus: Inflammation replaced by histiocytes, forming sheets and nodules
  - May also see chronic passive congestion within the liver, with hepatocyte degeneration and centrilobular interstitial fibrosis
Adults
1. Fibrinoheterophilic to caseous oophoritis or salpingitis or orchitis in males
2. May see catarrhal bronchitis, enteritis, interstitial pneumonia, or nephritis

ADDITIONAL DIAGNOSTIC TESTS:

Positive agglutination test (plate or tube)
Definitive diagnosis requires isolation and identification of S. Pullorum
Serology (can cross agglutinate with S. Gallinarum)

DIFFERENTIAL DIAGNOSIS:

Gross lesions:
1. Lung: Aspergillus spp., other fungi; other Salmonella spp.
2. Heart: Marek’s disease (alpha herpesvirus)
3. Liver: Yersinia pseudotuberculosis (shares some antigenic relationships), Escherichia coli
4. Swollen joints: Mycoplasma synoviae, Staphylococcus aureus, Pasteurella multocida, Erysipelothrix rhusiopathiae, Escherichia coli
5. White diarrhea: Chilling
6. Omphalitis (navel infection): Occurs in young birds, often with diarrhea; Staphylococcus aureus, Escherichia coli, Proteus sp.
Histologic lesions
1. Salmonella Gallinarum (Fowl typhoid): Similar clinical signs and lesions, but typically a disease that affects both young and adult chickens and turkeys; unlike S. Pullorum, this disease continues for months; often cross-agglutinates with S. Pullorum; isolation and identification to differentiate from S. Pullorum
2. Salmonella Typhimurium (Paratyphoid): Broad host-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 S. Pullorum
3. Salmonella enterica ssp. Arizonae (S-B01): Young turkey poults are most commonly affected; produces similar systemic disease but more commonly develop ophthalmitis and post-infection ocular atrophy; need isolation and identification to differentiate from S. Pullorum
4. Marek’s disease (H-V01, I-V13, N-V08; alpha herpesvirus): Nodules may appear identical grossly; histologically similar to chronic stages of PD

COMPARATIVE PATHOLOGY:

S. Pullorum is uncommonly associated with disease in other animals (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 disease
1. Gallinaceous species are reservoirs of S. Pullorum and S. Gallinarum
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:

Crespo R, Franca MS, Fenton H, Shivaprasad HL. Galliformes and Colubriformes. In: Terio KA, McAloose D, St. Leger J, eds. Pathology of Wildlife and Zoo Animals. London, UK: Academic Press; 2018:759.
Fulton RM, Boulianne M. Bacterial Diseases. In: Boulianne M ed. Avian Disease Manual. 8^th ed. Madison, WI: Omnipress; 2019:100-104, 193, 198-199, 204.
Fenton H, McManamon, Howerth EW. Anseriformes, Ciconiiformes, Charadriiformes, and Gruiformes. In: Terio KA, McAloose D, St. Leger J, eds. Pathology of Wildlife and Zoo Animals. London, UK: Academic Press; 2018:712.
Shivaprasad HL. Fowl typhoid and pullorum disease. Rev Sci Tech. 2000 Aug;19(2):405-24.
Smith DA. Palaeognathae: Apterygiformes, Casuariiformes, Rheiformes, Struthioniformes; Tinamiformes. In: Terio KA, McAloose D, St. Leger J, eds. Pathology of Wildlife and Zoo Animals. London, UK: Academic Press; 2018:648.
Stanton JB, Zachary JF. Mechanisms of microbial disease. In: Zachary JF, ed. Pathologic Basis of Veterinary Disease. 6th ed. St. Louis, MO: Elsevier; 2016:202-203.