Unit 4- Avian Flashcards
Lead Toxicosis
Ingestion of lead, low pH from grains increases availability and toxicity, waterfowl, raptors, and loon
Bird Lead Susceptibility
Lead stays in gizzard and is ground down over time
Lead Dynamics
Ingested, attaches to albumin and RBC in blood, ubiquitous with long term deposition, neurotropism, excreted in bile, urine, milk, and skin
Lead Pathogenicity
Inhibits hemoglobin synthesis enzymes, inhibits nucleotidase weakening RBC, disrupts neuron and astrocyte metabolism, disrupts vascular endothelium metabolism
Lead Toxicosis Clinical Signs
Reluctance to fly, weakness, ataxia, flaccid neck in geese, roof shape wings, bile stained feathers around cloaca, emaciation, facial edema, impacted food in GI, lead in gizzard, reticular pattern in kidneys
Lead Toxicosis Histopathology
Fibrinoid necrosis of vessels, hemorrhage, and secondary ischemia or hemorrhage, intracytoplasmic inclusion bodies, acute tubuloepithelial degeneration and necrosis in kidneys or nephropathy and fibrosis if chronic
Lead Toxicosis Diagnosis
Antemortem lead levels in blood, postmortem lead levels in liver, kidney and bone, species specific values
Gout
Renal gout, visceral gout, or articular gout, urate crystals in renal tubules or serosal and synovial surfaces
Gout Causes
Impaired excretion of uric acid by kidneys due to dehydration, renal disease, post renal obstruction, nephrotoxins, nephropathogenic viruses, high protein overproduction of uric acid, and defects in uric acid metabolic enzymes
Acute Gout
Renal and visceral, little to no inflammation
Chronic Gout
Articular with granulomatous inflammation
Gout Pathogenesis
Hyperuricemia, monosodium urate tophi precipitation on renal tubules and visceral and synovial surfaces, attempted phagocytosis by macrophages, renal tubular epithelial necrosis, inflammation, and fibrosis
Gout Clinical Signs
Little to no clinical signs for acute, difficulty flying and perching with inflamed feet for articular
Renal Gout Gross Findings
Enlarged kidneys with patchy/streaky appearance, ureters dilated and filled with urate calculi
Visceral Gout Gross Findings
Chalky patches on serous membrane of pericardium and hepatic capsule
Articular Gout Gross Findings
Swollen joints and tendon sheaths with chalky deposits, rupture of synovial membrane and skin
Tophi
Clusters of needle shaped birefringent crystals, pathognomonic of gout, associated with tissue necrosis and inflammation in acute form, surrounded by heterophilic and granulomatous inflammation in chronic
Gout Diagnosis
Chalky matertial and tophi, tophi can be stained for calcium with GMS and Von Kossa, but are water soluble
Fowl Diphtheria
Infectious laryngotracheitis, gallid herpesvirus type 1, alphaherpes, domestic chickens most common, peasants, peafowl, and turkeys
Infectious Laryngotracheitis Pathogenesis
Highly contagious, aerosols, syncitial cell formation, necrosis of tracheal mucosa, cellular immune response, latent carriers in trigeminal nerve ganglion
Epizootic Infectious Laryngotracheitis
Highly pathogenic form
Endemic Infectious Laryngotracheitis
Low pathogenic form
Infectious Laryngotracheitis Clinical Signs
High morbitidy moderate mortality, coughing, sneezing, head shaking, gasping for air, expectoration of bloody mucus
Infectious Laryngotracheitis Gross Findings
Tracheal mucosal necrosis and hemorrhage, occlusive pseudomembranes filling tracheal lumen, sinusitis, conjunctivitis, seromucous exudate
Infectious Laryngotracheitis Histopathology
Tracheal mucosal necrosis, fibrinonecrotic psuedomembrane, syncitial cell formation, intranuclear inclusion bodies, mucosal ulceration, inflammation, squamous metaplasia
Infectious Laryngotracheitis Diagnosis
PCR, IFA, IHC, EM, isolation, serology not helpful because can’t distinguish between infection and vaccine Ab
Infectious Laryngotracheitis Control
Vaccine, hygiene
Marek’s Disease
Gallid herpesvirus 2, dsDNA, chickens most affected
Marek’s Disease Pathogenesis
Highly infectious, chicks susceptible, feather dust and dander, lymphoproliferative
Marek’s Disease Serotypes
1 oncogenic, 2 common in chicken, 3 in turkey
Marek’s Disease Development
Phase 1 cell to cell infection after inhalation, viremia, immune cell infection, phase 2 latency in t cells, phase 3 replication in feather follicle epithelium, shedding in dander, spread to visceral epithelium and nervous system, phase 1 proliferative lymphoma
Classic Marek’s Disease
Neurolymphomatosis, paralysis, torticollis when cervical nerves are infected, dilatation of crop and respiratory signs
Visceral Marek’s Disease
Acute, lymphomatous tumors in viscera and skin
Ocular Lymphomatosis
Leukocyte infiltration of iris and loss of pigmentation causing grey eye
Cutaneous Marek’s Disease
Enlarged feather follicles, alabama redleg from erythematous legs
Classic Marek’s Disease Histopathology
Proliferative or inflammatory with demyelination causing paralysis in PNS, inflammatory with perivascular cuffing, microgliosis, and endotheliosis in CNS
Visceral Marek’s Disease Histopathology
Lymphoid tumors with mixture of lymphocytes
Cutaneous Marek’s Disease Histopathology
Dermatitis and lymphomatous proliferation around feather follicles and blood vessels, intranuclear inclusion bodies around feather follicle epithelium
Marek’s Disease Diagnosis
Isolation, IFA, neutralization, PCR, IHC
Newcastle Disease
Avian paramyxovirus, ssRNA, reportable to OIE, does not cause paramyxovirus infection, chickens and varying strains and pathogenicity
Newcastle Transmission
Ingestion or inhalation of infected secretions, fomites from feces, velogenic strain is vertically transmitted and kills chicks
Newcastle Disease Pathogenesis
Replicates in mucosa of upper respiratory and intestine, viremia by binding to RBC, infects spleen and bone marrow, spreads to CNS and other organs
Velogenic Strains
Can be viscerotrophic or neurotrophic
Viscerotrophic Velogenic Newcastle Disease
Lethal to all ages, green diarrhea, weakness, anorexia, prostration, tremor
Neurotrophic Velogenic Newcastle Disease
More lethal in chicks, decrease in egg production, respiratory signs, nervous signs, weakness, tremor, torticollis, paralysis
Newcastle Gross Lesions
Necrotizing gastroenteritis and hemorrhage in VVND, or pneumonia and encephalitis in NVND
Newcastle Diagnosis
OIE does isolation and qPCR, hemagglutination in unvaccinated flocks, immunochromatographic strips
Newcastle Control
Live attenuated vaccines, hygiene
Newcastle Zoonosis
Rare, self limiting conjunctivitis, fever and headache
Bornavirus Disease
Avian bornavirus,, ssRNA, Macaw wasting disease, Psittacine Proventricular dilatation, proventricular dilation, neuropathic gastric dilatation, progressive neurologic disease of psittacines and geese
Bornavirus Pathogenesis
Autonomic nerves of upper and middle GI as well as CNS, inoculation or respiration and migration to nervous ganglia, retrograde axonal, psittacine carriers common
Bornavirus Clinical Signs
weight loss, crop stasis, proventricular dilatation, regurgitation, maldigestion, starvation, CNS signs, death
Bornavirus Gross Findings
Emaciation, flaccidity and dilation of GI, undigested seed in feces, no GI lesions if exclusively CNS, cardiomegaly, hydropericardium
Bornavirus Histopathology
Infiltrates in myenteric plexus, ganglia, peripheral nerves, brain, spinal cord, heart, adrenals, demyelination and perivascular cuffing in CNS
Bornavirus Diagnosis
Plucked feathers, IHC
Salmonellosis
Salmonella enterica, typhimurium, songbirds and garden birds, fecal oral cycle from bird feeders, vertical transmission of chickens
Songbird Salmonellosis Clinical Signs
Abnormally tame, weak, stay on feeders
Songbird Salmonellosis Gross Findings
Esophagitis, fibronecrotizing multifocal, necrosis, fibrinonecrotic pseudomembrane, gram - rods, emaciation, arthritis
Songbird Salmonellosis Diagnosis
Crop swap and liver tissue culture
Salmonellosis Control
Bring down feeders to reduce contact and crowding
Salmonellosis Zoonosis
Humans, cats
Mycoplasmosis
Finch strain, chronic respiratory disease, infectious sinusitis, house finch conjunctivitis, spread from west to east
Mycoplasmosis Pathogenesis
Direct contact transmission, targets ocular and nasal mucosa, adhesion to epithelium, cellular damage, inflammation, carriers
Mycoplasmosis Clinical Signs
Swollen eyelids, emaciation, predation
Mycoplasmosis Diagnosis
PCR, difficult to culture
Trichomoniasis
Wild birds, trophozoite protozoa, trichomonosis, canker in dove and pigeon, frounce in raptos
Trichomoniasis Pathogenesis
Crop milk, feeders, and regurgitated material transmission, tropism to oral cavity, esophagus, and cranial bones, binary fission replication, damage to mucosa and bones
Trichomoniasis Clinical Signs
Weakness, fluff, lack of predator response, regurgitation, crust around beak, emaciation
Trichominiasis Gross Findings
Caseous canker material in lumen of esophagus, thickened esophageal wall
