JPC SYSTEMIC PATHOLOGY
Signalment (JPC #2131712): Three‑week‑old broiler cockerel.
HISTOPATHOLOGIC DESCRIPTION: Lung: Focally affecting over 60% of the section, parabronchial and air vesicle lumina are variably occluded by numerous lymphocytes and histiocytes, abundant necrotic debris, few viable and degenerate heterophils, hemorrhage, and sloughed epithelial cells. Multifocally, the parabronchial and air vesicle respiratory epithelium is either hyperplastic or attenuated. The affected interstitium is expanded by numerous macrophages, lymphocytes and plasma cells that also obscures air capillary profiles. The lamina propria of the mesobronchus, and to a lesser extent, an adjacent secondary bronchus, are multifocally expanded by increased numbers of lymphocytes and plasma cells that form lymphoid aggregates (hyperplastic bronchial-associated lymphoid tissue). The bronchial respiratory epithelium is hyperplastic, piling up to 3 layers thick, with numerous mitotic figures (regeneration) and occasional loss of cilia. Numerous basophilic, round 2‑5um cryptosporidia either line the ciliated surface of the bronchial epithelium or are within parabronchial lumina
MORPHOLOGIC DIAGNOSES: Lung: Bronchopneumonia, proliferative, subacute, lymphohistiocytic, focally extensive, moderate, with numerous apical protozoa, etiology consistent with Cryptosporidium spp., chicken, avian
ETIOLOGIC DIAGNOSES: Cryptosporidial bronchopneumonia
CAUSE: Cryptosporidium baileyi
- Respiratory disease is most common in birds, while enteric disease is more common in other species
- Cryptosporidium spp. develops intracellularly at an extracytoplasmic location within the brush border membrane of host epithelial cells (parasitophorous vacouole).
- Although it can be a primary pathogen, Cryptosporidium is usually opportunistic, infecting young and immunocompromised animals
- Avian Cryptosporidium spp. do not infect mammals
- C. baileyi infects the digestive tract (cloaca, bursa of Fabricus), the upper and lower respiratory tracts, and the eyelids
- Broiler chickens may develop resistance to reinfection with C. baileyi; There is evidence that cell mediated immunity is more important in resistance than circulating antibody
- Enterocyte tropism mediated by ligand-receptor interactions (Cryptosporidium sporozoite ligand) and GP900 adherence factor
- Cytolysis due to parasite or T cell and macrophage mediated products
- Sporulated oocysts are inhaled or ingested> sporozoites are released by excystation> attach to epithelial brush border> merogony - asexual multiplication within epithelial cells forming first and second generation merozoites> schizonts formed by: 1) asexual multiplication; 2) gametogony - sexual formation of male (microgamonts) and female (macrogamonts) gametes> oocyst wall formed> sporogony – formation of infective sporozoites within oocyst wall> oocyst infective when released in feces or discharge from upper respiratory tract
- There are two kinds of oocysts formed: thin-walled and thick-walled; Both sporulate within the host cell
- Autoinfection occurs via thin walled oocysts; Thick walled oocysts are shed in nasal secretions and feces
TYPICAL CLINICAL FINDINGS:
- Nasal and ocular discharges; Swollen sinuses
- Coughing, sneezing, dyspnea, rales
- Morbidity and mortality may be high
TYPICAL GROSS FINDINGS:
- Swelling of the nasal sinus mucosa
- Respiratory tract mucosal congestion
- Gray or white mucoid exudate on mucosal surface
- Lungs may be congested and edematous, and may have extensive consolidation
- Moderate to severe tracheitis, pneumonia, and air sacculitis
TYPICAL MICROSCOPIC FINDINGS:
- 2-8 um, apicomplexan protozoa that colonize gastrointestinal and respiratory epithelium at the brush border surface in vertebrates
- Epithelial hyperplasia
- Thickened mucosa by mononuclear cells with some heterophils
- Loss of cilia
- Discharge of mucocellular exudate into the airways
- Cryptosporidium found within the ciliated region of trachea and bronchi
- Affected air sacs contain large numbers of protozoa within respiratory epithelium and similar changes
- In the GI tract, there is villar blunting and loss, causing osmotic diarrhea
- Cryptosporidium spp. attach to host cell glycocalyx
- Located within a parasitoferous vacuole (derived from host microvilli) lined by glycocalyx
- Development is intracellular but extracytoplasmic
- Attachment zone contains feeder organelle
- Loss of microvilli at site of attachment; Organisms are associated with loss of microvilli and formation of a pedestal
ADDITIONAL DIAGNOSTIC TESTS:
- Cytology - fecal smears stained with red carbon fuscin or Giemsa
- Fecal flotation – Sheather’s sucrose solution, zinc sulfate, sodium chloride
- Phase-contrast, interference phase-contrast microscopy – touch impressions
- Fluorescent staining with auramine O or fluorescein-labeled antibody
- Acid fast stains
- EM, TEM
Respiratory: Concurrent infection with bacterial, viral, or fungal organisms is common:
- Infectious bronchitis (Coronavirus)
- Infectious laryngotracheitis (Gallid herpes-1)
- Newcastle disease (Paramyxovirus-1)Avian influenza (Orthomyxovirus)
- Infectious coryza (Haemophilus paragallinarum)
- Escherichia coli
- Pasteurella multocida
Bursitis: Bursal cryptosporidiosis is commonly seen in chickens with Infectious Bursal Disease (Birnavirus) or chicken anemia virus (Circovirus).
- Cryptosporidium parvum: small intestine (all mammals); freely transmissible among mammals, but does not infect vertebrates in other Orders; usually clinically inapparent; intractable diarrhea in young or immunocompromised
- C. muris: gastric mucosa (ruminants, dogs, cats, rats, mice)
- C. wrairi: jejunum, ileum, cecum (guinea pigs)
- C. cuniculus: small intestine (rabbits)
- Pulmonary cryptosporidiosis reported in SIV-infected Rhesus Macaques
- C. muris-like infection reported in stomach of Cynomolgus Monkeys
- C. andersoni infection reported to cause proliferative abomasitis in cattle
- C. baileyi: digestive tract (cloaca, bursa of Fabricus) and upper and lower respiratory tracts (birds); most common in chickens, but also infects turkeys, ducks, geese, gallinaceous birds, ratites, raptors, and psittacines. Intestinal infection is asymptomatic in chickens and turkeys.
- C. meleagridis: small intestine; associated with diarrhea, unthriftiness, and moderate mortality (turkeys, quail)
- C. serpentis and C. crotali - proliferative gastritis in snakes, atrophic gastritis in lizards
- C. spp. associated with aural-pharyngeal polyps in iguanas
- C. nasorum associated with severe wasting in stomach and intestine
- Severe fatal infections occur in Arabian foals with CID; non-human primates infected with SIV
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