JPC SYSTEMIC PATHOLOGY
SIGNALMENT (AFIP#1946537): Tissue from a 4-year-old yellow-naped Amazon parrot
HISTORY: The bird became progressively docile, passive, and depressed.
MICROSCOPIC DESCRIPTION: Liver: Multifocally there are random irregularly round, variably sized (up to 1 mm diameter) areas of lytic necrosis characterized by complete loss of hepatic architecture with replacement by eosinophilic cellular and karyorrhectic debris, and heterophils, surrounded by hemorrhage, multinucleated giant cells (foreign body and Langhan’s type), epithelioid macrophages, and fewer lymphocytes and plasma cells. Multifocally, there are random foci of coagulative necrosis characterized by retention of hepatic cord and cellular architecture with increased cytoplasmic eosinophilia. Multifocally, few random hepatocytes and Kupffer cells contain intracytoplasmic gray indistinct granular coccoid bacteria. Hepatocytes surrounding areas of necrosis often have vacuolated cytoplasm and are dissociated from hepatic chords (degeneration). Diffusely, sinusoids are expanded by macrophages, heterophils and lymphocytes. Multifocally hepatocytes are mildly vacuolated and contain small aggregates of brown, granular pigment (bile, hemosiderin and/or lipofuscin). Bile ducts are prominent, mildly ectatic, and lined by hyperplastic epithelium characterized by piling up, mild anisokaryosis and increased mitotic activity (regeneration) with adjacent dilated lymphatic vessels and periductular clear space (edema).
MORPHOLOGIC DIAGNOSIS: Liver: Hepatitis, necrotizing, heterophilic and granulomatous, multifocal to coalescing, moderate, with mild bile duct hyperplasia and intracellular bacteria, yellow-naped Amazon parrot (Ochrocephala auropalliate), avian.
ETIOLOGY: Chlamydophila psittaci
ETIOLOGIC DIAGNOSIS: Chlamydial hepatitis
CONDITION: Avian chlamydiosis (birds); psittacosis (humans)
- Gram negative obligate intracellular bacteria
- Synonyms: Parrot Fever, Ornithosis
- The family Chlamydiaceae contains a single genus: Chlamydia, which includes 11 species:
- C. muridarum
- C. suis
- C. trachomatis
- C. abortus (ruminant)
- C. caviae (Guinea pig)
- C. felis (feline)
- C. pecorum (ruminants, swine, koalas)
- C. pneumoniae (human, marsupial, and amphibious origin)
- C. psittaci (avian serovar)
- C. avium
- C. gallinacea
- psittaci has 8 known fairly host specific serovars: 6 in birds and 2 in mammals
- Serovars A and F – Psittaciformes (especially cockatiels & budgerigars)
- Serovar B – Columbiformes (pigeons, doves)*low virulence
- Serovar C – Anseriformes (ducks, geese, swans)
- Serovar D – Galliformes (turkeys *highly virulent)
- Serovar E – Columbiformes and Galliformes (pigeons, turkeys)
- Zoonotic (and reportable) - Take precautions during necropsy if suspected
- Emerging disease in broiler chickens (Serovars B and D)
- Obligate intracellular gram negative bacteria (but Gram stain of no practical value, since the cell wall lacks peptidoglycan)
- Unique morphology and biphasic life cycle with two morphologically distinct forms and an intermediate form:
- Elementary body (EB): Infectious form that enters the cell
- Reticulate body (RB): Intracellular, metabolically active, replicating form that synthesizes DNA, RNA, and protein, and divides by binary fission
- Intermediate body (IB): Has a morphologic characteristic between EB and RB
- Organisms have tropism for coated pits on epithelial cells of the respiratory tract
- Inhalation or ingestion of contaminated feather dust or feces > multiply in lung, air sacs and pericardial sac within 4 hours > bacteremia within 48 hours > portals of exit (cloaca & nasal turbinates)
- The reproductive cycle: EBs attach to host cell membrane at coated pit > internalization into host cell via invagination of the host cell membrane > inhibition of phagosome - lysosome fusion > differentiation into RB > replication by binary fission > reorganization, through IBs, into new EBs > release from host cell (cell lysis or exocytosis)
- Depend on eukaryotic cells for energy
- Mitochondria are often found in juxtaposition to the psittaci inclusion
- RBs may parasitize mitochondrial ATP via a chlamydial ATP-ADP translocase
TYPICAL CLINICAL FINDINGS: (in birds)
- Diarrhea and excretion of green to yellow-green urates
- Severely affected birds may become anorectic and produce sparse, dark green droppings, followed by emaciation, dehydration and death
- Recurrent episodes of illness culminating in chronic debilitation
TYPICAL GROSS FINDINGS:
- Hepatomegaly and splenomegaly +/- necrotic foci
- Fibrinous air sacculitis, pericarditis and peritonitis
- Associated with atherosclerosis in psittacines
TYPICAL MICROSCOPIC FINDINGS:
- Acute: Multifocal coagulation/lytic necrosis
- Chronic: Granulomas and bile duct hyperplasia
- Kupffer cell hyperplasia
- Intrahepatocellular bacteria
- Spleen: Multifocal necrosis, histiocytosis, lymphoid depletion, plasmacytosis,
- Air sacs: Fibrinous exudate with heterophils and macrophages, some containing bacteria
- Inclusion body-like microcolonies may be seen in affected cells of many organs, particularly in serosal membranes
- Elementary body (EB): Spherical, 0.2-0.3 um body composed of a highly electron dense nucleoid at the periphery, clearly separated from the electron dense cytoplasm
- Reticulate body (RB): 0.5-2.0 um, binary fission characterized by “hour-glass” profiles
- Intermediate body (IB): 0.3-1.0 um diameter bodies with a central electron dense core, radially arranged nucleoid fibers surrounding the core and tightly packed cytoplasmic granules at the periphery
- Inside the host cell, organisms are present within endosomes
ADDITIONAL DIAGNOSTIC TESTS:
- Isolation of the organism from tissue, feces or swabs
- Microscopy (wet mounts or histology): Giemsa (dark purple), Gimenez, modified Gimenez (PVK stain) red, or Macchiovello
- Visible on phase contrast and dark-field illumination microscopy
- Serology, EM, immunofluorescence, ELISA, immunohistochemistry, strain specific monoclonal antibodies
- PCR identification of host-specific serovar may help pinpoint source of infection
- Hepatic necrosis in psittacine birds:
- Pacheco’s disease (alphaherpesvirus): Intranuclear hepatocellular inclusions
- Polyomavirus (Budgie Fledging Disease): Glassy intranuclear inclusions
- Salmonellosis (Salmonella ) and colibacillosis (E. coli): Hepatocellular necrosis with necrogranulomas
- Reoviral hepatitis: Hepatocellular necrosis without inclusion bodies
- Lead toxicosis: Eosinophilic, acid-fast, intranuclear inclusions
- Mycobacteriosis (MAIC): Acid-fast, intracellular bacilli
- In poultry, similar signs and lesions may be caused by the following diseases:
- Fowl cholera (Pasteurella multocida)
- Mycoplasmosis: gallisepticum (chronic respiratory disease/infectious sinusitis of turkeys); M. meleagridis (air sacculitis)
- Salmonellosis - Typhimurium (paratyphoid); S. Pullorum (Pullorum disease); S. Gallinarum (fowl typhoid)
- Adenovirus: Hemorrhagic enteritis of turkeys
- Humans: Zoonotic disease; influenza-like symptoms; pneumonia
- Ruminants: abortus: sporadic bovine encephalomyelitis, pneumonia, polyarthritis of calves, conjunctivitis, and sporadic abortion; abortions, including ovine enzootic abortion (necrotizing placentitis in ewe, hepatic necrosis in fetus)
- Has been reported to cause bronchopneumonia in experimentally challenged calves
- Cats: felis: conjunctivitis (also C. psittaci and C. felis)
- Guinea pigs: caviae: Guinea Pig Inclusion Conjunctivitis (GPIC); can also cause rhinitis and genital tract infections
- Dogs: Keratoconjunctivitis, bronchopneumonia, and reproductive problems (limited number of case reports)
- Wild hawks (Buteo ) in California – unknown Chlamydia spp. isolated, most similar to C. psittaci
- Turkeys – psittaci strain B was isolated from bilaterally swollen and inflamed nasal glands
- Chlamydia pecorum: causes enteritis in calves <10 days old (see N-B05 for encephalitis manifestations of sporadic bovine encephalomyelitis)
- Intestinal tract is the natural habitat and may be the portal of entry for systemic infections resulting in hepatitis, arthritis, encephalitis and pneumonia
- Enteritis in calves – even asymptomatic animals have a 48% reduction in growth rate; these animals had conjunctival hyperemia, increased serum globulin and decreased plasma albumin and insulin-like growth factor-1 suggesting that these asymptomatic infections may be the reason why in some calves feed-additive antibiotics aid in growth promotion.
- Pathogenesis: ingestion > adsorbs to brush border of enterocytes at the tips of intestinal villi (these cells are in G1 which is what Chlamydia requires for multiplication) > enters the cell via pinocytosis > multiplication in the supranuclear region > host cell degenerates > released into gut lumen and lamina propria > infects endothelial cells of lacteals > systemic travel
- Goblet cells, enterochromaffin cells, and macrophages additionally infected > macrophages spread systemically
- Gross lesions are most common in the terminal ileum; mucosal edema, congestion, petechiae, +/- ulceration
- Histologically, chlamydial inclusions are demonstrated within host cell cytoplasm using: Giemsa, Jimenez, Macchiavello or immunoperoxidase staining; crypts may be dilated with inflammatory exudate; lymphoid follicles in Peyer’s patches are necrotic.
- Chlamydia suis: associated with conjunctivitis, rhinitis, pneumonia, enteritis, reproductive disorders, and asymptomatic infections in swine.
- Recognized in the intestinal mucosa of normal and clinically ill swine
- Gnotobiotic pigs experimentally inoculated with suis had moderate diarrhea, anorexia, weakness, and body weight loss.
- Microscopically, there was necrosis and exfoliation of enterocytes on the apical half of villi leading to villous atrophy in the distal jejunum and ileum; there was also mild lymphangitis and perilymphangitis.
- Chlamydial organisms replicated within small intestinal villus enterocytes, large intestinal enterocytes, lamina propria, submucosa, and mesenteric lymph nodes.
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