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systemic pathology > Unit 4- Avian > Flashcards

Unit 4- Avian Flashcards

1
Q

Lead Toxicosis

A

Ingestion of lead, low pH from grains increases availability and toxicity, waterfowl, raptors, and loon

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2
Q

Bird Lead Susceptibility

A

Lead stays in gizzard and is ground down over time

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3
Q

Lead Dynamics

A

Ingested, attaches to albumin and RBC in blood, ubiquitous with long term deposition, neurotropism, excreted in bile, urine, milk, and skin

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4
Q

Lead Pathogenicity

A

Inhibits hemoglobin synthesis enzymes, inhibits nucleotidase weakening RBC, disrupts neuron and astrocyte metabolism, disrupts vascular endothelium metabolism

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5
Q

Lead Toxicosis Clinical Signs

A

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

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6
Q

Lead Toxicosis Histopathology

A

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

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7
Q

Lead Toxicosis Diagnosis

A

Antemortem lead levels in blood, postmortem lead levels in liver, kidney and bone, species specific values

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8
Q

Gout

A

Renal gout, visceral gout, or articular gout, urate crystals in renal tubules or serosal and synovial surfaces

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9
Q

Gout Causes

A

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

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10
Q

Acute Gout

A

Renal and visceral, little to no inflammation

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11
Q

Chronic Gout

A

Articular with granulomatous inflammation

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12
Q

Gout Pathogenesis

A

Hyperuricemia, monosodium urate tophi precipitation on renal tubules and visceral and synovial surfaces, attempted phagocytosis by macrophages, renal tubular epithelial necrosis, inflammation, and fibrosis

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13
Q

Gout Clinical Signs

A

Little to no clinical signs for acute, difficulty flying and perching with inflamed feet for articular

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14
Q

Renal Gout Gross Findings

A

Enlarged kidneys with patchy/streaky appearance, ureters dilated and filled with urate calculi

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15
Q

Visceral Gout Gross Findings

A

Chalky patches on serous membrane of pericardium and hepatic capsule

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16
Q

Articular Gout Gross Findings

A

Swollen joints and tendon sheaths with chalky deposits, rupture of synovial membrane and skin

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17
Q

Tophi

A

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

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18
Q

Gout Diagnosis

A

Chalky matertial and tophi, tophi can be stained for calcium with GMS and Von Kossa, but are water soluble

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19
Q

Fowl Diphtheria

A

Infectious laryngotracheitis, gallid herpesvirus type 1, alphaherpes, domestic chickens most common, peasants, peafowl, and turkeys

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20
Q

Infectious Laryngotracheitis Pathogenesis

A

Highly contagious, aerosols, syncitial cell formation, necrosis of tracheal mucosa, cellular immune response, latent carriers in trigeminal nerve ganglion

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21
Q

Epizootic Infectious Laryngotracheitis

A

Highly pathogenic form

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22
Q

Endemic Infectious Laryngotracheitis

A

Low pathogenic form

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23
Q

Infectious Laryngotracheitis Clinical Signs

A

High morbitidy moderate mortality, coughing, sneezing, head shaking, gasping for air, expectoration of bloody mucus

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24
Q

Infectious Laryngotracheitis Gross Findings

A

Tracheal mucosal necrosis and hemorrhage, occlusive pseudomembranes filling tracheal lumen, sinusitis, conjunctivitis, seromucous exudate

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25
Q

Infectious Laryngotracheitis Histopathology

A

Tracheal mucosal necrosis, fibrinonecrotic psuedomembrane, syncitial cell formation, intranuclear inclusion bodies, mucosal ulceration, inflammation, squamous metaplasia

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26
Q

Infectious Laryngotracheitis Diagnosis

A

PCR, IFA, IHC, EM, isolation, serology not helpful because can’t distinguish between infection and vaccine Ab

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27
Q

Infectious Laryngotracheitis Control

A

Vaccine, hygiene

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28
Q

Marek’s Disease

A

Gallid herpesvirus 2, dsDNA, chickens most affected

29
Q

Marek’s Disease Pathogenesis

A

Highly infectious, chicks susceptible, feather dust and dander, lymphoproliferative

30
Q

Marek’s Disease Serotypes

A

1 oncogenic, 2 common in chicken, 3 in turkey

31
Q

Marek’s Disease Development

A

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

32
Q

Classic Marek’s Disease

A

Neurolymphomatosis, paralysis, torticollis when cervical nerves are infected, dilatation of crop and respiratory signs

33
Q

Visceral Marek’s Disease

A

Acute, lymphomatous tumors in viscera and skin

34
Q

Ocular Lymphomatosis

A

Leukocyte infiltration of iris and loss of pigmentation causing grey eye

35
Q

Cutaneous Marek’s Disease

A

Enlarged feather follicles, alabama redleg from erythematous legs

36
Q

Classic Marek’s Disease Histopathology

A

Proliferative or inflammatory with demyelination causing paralysis in PNS, inflammatory with perivascular cuffing, microgliosis, and endotheliosis in CNS

37
Q

Visceral Marek’s Disease Histopathology

A

Lymphoid tumors with mixture of lymphocytes

38
Q

Cutaneous Marek’s Disease Histopathology

A

Dermatitis and lymphomatous proliferation around feather follicles and blood vessels, intranuclear inclusion bodies around feather follicle epithelium

39
Q

Marek’s Disease Diagnosis

A

Isolation, IFA, neutralization, PCR, IHC

40
Q

Newcastle Disease

A

Avian paramyxovirus, ssRNA, reportable to OIE, does not cause paramyxovirus infection, chickens and varying strains and pathogenicity

41
Q

Newcastle Transmission

A

Ingestion or inhalation of infected secretions, fomites from feces, velogenic strain is vertically transmitted and kills chicks

42
Q

Newcastle Disease Pathogenesis

A

Replicates in mucosa of upper respiratory and intestine, viremia by binding to RBC, infects spleen and bone marrow, spreads to CNS and other organs

43
Q

Velogenic Strains

A

Can be viscerotrophic or neurotrophic

44
Q

Viscerotrophic Velogenic Newcastle Disease

A

Lethal to all ages, green diarrhea, weakness, anorexia, prostration, tremor

45
Q

Neurotrophic Velogenic Newcastle Disease

A

More lethal in chicks, decrease in egg production, respiratory signs, nervous signs, weakness, tremor, torticollis, paralysis

46
Q

Newcastle Gross Lesions

A

Necrotizing gastroenteritis and hemorrhage in VVND, or pneumonia and encephalitis in NVND

47
Q

Newcastle Diagnosis

A

OIE does isolation and qPCR, hemagglutination in unvaccinated flocks, immunochromatographic strips

48
Q

Newcastle Control

A

Live attenuated vaccines, hygiene

49
Q

Newcastle Zoonosis

A

Rare, self limiting conjunctivitis, fever and headache

50
Q

Bornavirus Disease

A

Avian bornavirus,, ssRNA, Macaw wasting disease, Psittacine Proventricular dilatation, proventricular dilation, neuropathic gastric dilatation, progressive neurologic disease of psittacines and geese

51
Q

Bornavirus Pathogenesis

A

Autonomic nerves of upper and middle GI as well as CNS, inoculation or respiration and migration to nervous ganglia, retrograde axonal, psittacine carriers common

52
Q

Bornavirus Clinical Signs

A

weight loss, crop stasis, proventricular dilatation, regurgitation, maldigestion, starvation, CNS signs, death

53
Q

Bornavirus Gross Findings

A

Emaciation, flaccidity and dilation of GI, undigested seed in feces, no GI lesions if exclusively CNS, cardiomegaly, hydropericardium

54
Q

Bornavirus Histopathology

A

Infiltrates in myenteric plexus, ganglia, peripheral nerves, brain, spinal cord, heart, adrenals, demyelination and perivascular cuffing in CNS

55
Q

Bornavirus Diagnosis

A

Plucked feathers, IHC

56
Q

Salmonellosis

A

Salmonella enterica, typhimurium, songbirds and garden birds, fecal oral cycle from bird feeders, vertical transmission of chickens

57
Q

Songbird Salmonellosis Clinical Signs

A

Abnormally tame, weak, stay on feeders

58
Q

Songbird Salmonellosis Gross Findings

A

Esophagitis, fibronecrotizing multifocal, necrosis, fibrinonecrotic pseudomembrane, gram - rods, emaciation, arthritis

59
Q

Songbird Salmonellosis Diagnosis

A

Crop swap and liver tissue culture

60
Q

Salmonellosis Control

A

Bring down feeders to reduce contact and crowding

61
Q

Salmonellosis Zoonosis

A

Humans, cats

62
Q

Mycoplasmosis

A

Finch strain, chronic respiratory disease, infectious sinusitis, house finch conjunctivitis, spread from west to east

63
Q

Mycoplasmosis Pathogenesis

A

Direct contact transmission, targets ocular and nasal mucosa, adhesion to epithelium, cellular damage, inflammation, carriers

64
Q

Mycoplasmosis Clinical Signs

A

Swollen eyelids, emaciation, predation

65
Q

Mycoplasmosis Diagnosis

A

PCR, difficult to culture

66
Q

Trichomoniasis

A

Wild birds, trophozoite protozoa, trichomonosis, canker in dove and pigeon, frounce in raptos

67
Q

Trichomoniasis Pathogenesis

A

Crop milk, feeders, and regurgitated material transmission, tropism to oral cavity, esophagus, and cranial bones, binary fission replication, damage to mucosa and bones

68
Q

Trichomoniasis Clinical Signs

A

Weakness, fluff, lack of predator response, regurgitation, crust around beak, emaciation

69
Q

Trichominiasis Gross Findings

A

Caseous canker material in lumen of esophagus, thickened esophageal wall

systemic pathology (12 decks)

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