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Systemic Pathology I > Avian Diseases, Pt. 2 > Flashcards

Avian Diseases, Pt. 2 Flashcards

1
Q

What causes Marek’s disease? What species are most affected?

A

avian alphaherpesvirus, Gallid herpesvirus type 2 (dsDNA)

chickens
- quails, turkeys, pheasants, jungle fowl

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2
Q

How is Marek’s disease transmitted? What kind of disease is it?

A

highly infectious, particularly in young chicks through feather dust, where it can remain infectious for years (inhaled)

lymphoproliferative and neoplastic - first neoplastic disease for which a vaccine was developed

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3
Q

What are the 3 serovars of Marek’s disease virus?

A

1 = oncogenic
2 = chickens
3 = turkeys

(other oncogenic virus = avian leukosis virus, a retrovirus)

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4
Q

What are the 4 phases of Marek’s disease?

A
  1. early cell-to-cell infection
  2. latent infection
  3. feather follicle shedding
  4. proliferative (lymphoma) phase
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5
Q

What happens during phase 1 of Marek’s disease?

A
  • inhalation or ingestion of infected feather dander
  • infection of respiratory epithelium and macrophages
  • viremia
  • infection of T and B cells in thymus, bursa, spleen, and BM, causing immunosuppression
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6
Q

What happens during phase 2 of Marek’s disease?

A
  • replication in T cells (CD4+), less so in B cells and CD8+ cells
  • no obvious clinical signs

(latent infection)

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7
Q

What happens during phase 3 of Marek’s disease?

A
  • lymphocytes carry virus to feather follicles
  • virus replicates in epithelial cells
  • virus shed in feather dander
  • lymphocytes also carry virus to visceral epithelium and nervous system
  • mononuclear inflammation
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8
Q

What happens during phase 4 of Marek’s disease?

A
  • some CD4+ T cells undergo neoplastic transformation
  • lymphomas develop
  • tumors are a mixture of neoplastic T cells and reactive B cells and macrophages
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9
Q

What is characteristic of classical Marek’s disease? In what 3 ways does this affect the bird?

A

neurolymphomatosis = paralysis

  • leg/wing paralysis (sciatic/brachial nerves)
  • torticollis (cervical nerves)
  • dilation of crop and respiratory signs (vagus/intercostal nerves)
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10
Q

What are the 3 other presentations of Marek’s disease other than classical?

A
  1. VISCERAL (ACUTE) - lymphomatous proliferation (tumors) in viscera and skin
  2. OCULAR LYMPHOMATOSIS - lymphocyte infiltration of iris with loss of pigmentation (grey eye)
  3. CUTANEOUS - enlarged feather follicles/nodules, erythematous legs (Alabama redleg)
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11
Q

Classical Marek’s disease:

A

paralysis - sciatic nerve

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12
Q

Classical Marek’s disease:

A

left sciatic nerve thick due to lymphocyte inflammation

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13
Q

Visceral (acute) Marek’s disease:

A

nodular lymphoblastic lesions

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14
Q

Ocular Marek’s disease:

A

grey eye - lymphocyte infiltration of iris

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15
Q

Ocular Marek’s disease:

A

grey eye, constricts pupil due to inflammation

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16
Q

Cutaneous Marek’s disease:

A

Alabama redleg - erythematous legs

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17
Q

Cutaneous Marek’s disease:

A

enlarged feather follicles/nodules

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18
Q

What are the 2 main histopathological presentations of classical Marek’s disease?

A
  1. PNS = proliferative/inflammatory with demyelination, causing paralysis; chronic without paralysis
  2. CNS = inflammatory lesions with perivascular cuffing, microgliosis, and endotheliosis
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19
Q

What is the histopathological presentation of visceral (acute) Marek’s disease?

A

lymphoid tumors with a mixture of pleomorphic lymphocytes including malignant T cells, reactive B cells, other T cells, and macrophages

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20
Q

What is the histopathological presentation of ocular lymphomatosis due to Marek’s disease?

A

lymphocyte infiltration of the iris

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21
Q

What are the 3 histopathological presentations of cutaneous Marek’s disease?

A
  1. dermatitis with lymphocytes and/or lymphomatous proliferations
  2. lymphomatous lesions around feather follicles and blood vessels
  3. IN inclusions in feather follicle epithelium
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22
Q

Classical Marek’s disease, histopathology:

A

PNS = inflammation

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23
Q

Cutaneous Marek’s disease, histopathology:

A

perivascular lymphomatous lesion

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24
Q

How is Marek’s disease diagnosed? How is it controlled? Is it zoonotic?

A

PCR, IHC
- virus isolation, IFA, viral neutralization

chicks are typically vaccinated by 1 day old

no

25
Q

Marek’s disease vs. Lymphoid leukosis:

26
Q

What causes Newcastle disease? How does it compare to others in the same family?

A

avian Paramyxovirus 1 (ssRNA)

reportable to OIE - does not cause paramyxovirus infection

27
Q

What species are most affected by Newcastle disease? What are some potential reservoirs?

A

chickens

waterfowl, psittacines

28
Q

What 2 things determine the pathogenicity of avian Paramyxovirus 1?

A

strain
1. ICPI - intracerebral pathogenicity index
2. F protein sequence - penetrates host cell membrane

(VELOGENIC - viscerotropic, neurotropic)

29
Q

What is the main way that Newcastle disease is transmitted? How else can it be transmitted?

A

ingestion of inhalation of infected secretions (feces, respiratory secretions, excretions)

  • fomites
  • vertical
30
Q

What is the pathogenesis of Newcastle disease?

A
  • ingestion/inhalation of infected secretions
  • virus replicated in the mucosa of the upper respiratory and/or intestine
  • virus spreads by hematogenous route (primary viremia) adhered to RBC
  • virus infects spleen and BM
  • virus spreads hematogenously to CNS and/or other organs (secondary viremia)
  • virus is shed through respiratory secretions, excretions, or feces
31
Q

How does viscerotropic velogenic Newcastle disease present?

A
  • acutely lethal, kills chickens of all ages
  • weakness, anorexia
  • green diarrhea
  • prostration, tremors, torticollis, paralysis, opisthotonus
  • death

flock mortality can reach 100%

32
Q

How does neurotrophic velogenic Newcastle disease present?

A
  • acutely lethal, kills chickens of all ages
  • sharp decrease in egg production
  • weakness, anorexia
  • RESPIRATORY SIGNS: difficulty breathing, wheezing, gurgling, conjunctivitis
  • NERVOUS SIGNS: prostrations, tremors, torticollis, paralysis, opsthotonus
33
Q

Neurotrophic velogenic Newcastle disease:

A

torticollis

34
Q

What gross lesions present in visceral and neurotropic velogenic Newcastle disease?

A

VVND = necrotizing gastroenteritis and hemorrhage at junctions

NVND = pneumonia and/or encephalitis

35
Q

What 3 histopathological presentations are common with visceral velogenic Newcastle disease?

A
  1. necrotizing gastroenteritis
  2. hemorrhages in junctions of the esophagus, proventriculus, and gizzard
  3. GALT necrosis
36
Q

What 2 histopathological presentations are common with neurotropic velogenic Newcastle disease?

A
  1. interstitial pneumonia
  2. non-suppurative encephalitis with lymphocyte perivascular cuffing, endotheliosis, and inclusion bodies
37
Q

Newcastle disease, CNS:

A

spheroids - swollen axons and demyelination

38
Q

Newcastle disease, CNS:

A

neuronal necrosis - red = dead, pyknotic nuclei

39
Q

Newcastle disease, neuronal inclusion bodies:

40
Q

Newcastle disease, CNS (cerebellum):

A

pink neuronal inclusion bodies

41
Q

Newcastle disease, CNS:

A

neuronal inclusion bodies - IN and IC

42
Q

How does the OIE diagnose Newcastle disease? What else can be done?

A

virus isolation and qPCR NVSL panel

  • hemagglutination for unvaccinated flocks
  • IHC
  • immunochromatographic strips
43
Q

How is Newcastle disease controlled?

A
  • vaccines: live attenuated in water, aerosol, eye/nose droplets, beak dipping; inactivated
  • hygiene/biosecurity
44
Q

Is Newcastle disease zoonotic?

A

yes, but rare
- immunosuppression increases risk
- veterinarians, processing plant employees, lab workers, and vaccination crews are most susceptible

45
Q

What are the 3 major clinical signs of Newcastle disease in humans?

A
  1. self-limiting conjunctivitis*
  2. excessive lacrimation, eyelid edema, subconjunctival hemorrhage, unilateral/bilateral reddening
  3. generalized infection - fever, headache, chills
46
Q

What causes Bornavirus disease? What are some other names?

A

avian Bornavirus (ABV) - ssRNA virus with nuclear replication

  • Macaw wasting disease
  • Psittacine Proventricular Dilatation Disease
  • Proventricular Dilatation Disease
  • Neuropathic gastric dilatation
47
Q

What 2 species are most affected by Bornavirus disease?

A
  1. Pisttacines, canaries, finches
  2. Canada goose
48
Q

What does avian Bornavirus target?

A
  • autonomic nerves of the upper and middle GI: esophagus, crop, proventriculus, gizzard, duodenum
  • CNS: cerebellum, cerebrum, brainstem
49
Q

What is thought to be the infection route of Bornavirus disease? What happens after infection?

A
  • trauma/inoculation in skin
  • fecal-oral, respiratory

migration to nervous ganglia (and CNS in Canada goose) with retrograde axonal transport

50
Q

What are the 6 common clinical signs of Bornavirus disease?

A
  1. weight loss - no movement or digestion of food
  2. crop stasis, proventricular/ventricular dilatation, regurgitation
  3. undigested material in feces
  4. starvation
  5. CNS signs - ataxia, loss of predator reflex
  6. death
51
Q

Bornavirus disease, radiography:

A

flaccidity and dilation of proventriculus, ventriculus, and crop

52
Q

What are 4 common postmortem gross findings of Bornavirus disease?

A
  1. emaciation
  2. falccidity and dilation of proventriculus, ventriculus, and crop
  3. lack of muscular grinding of seeds - undigested material in feces
  4. possible cardiomegaly and hydropericardium
53
Q

Bornavirus, GI:

A

dilatation - proventriculus, ventriculus, crop

54
Q

What 3 places do lymphocytes and plasma cells infiltrate in Bornavirus disease?

A
  1. myenteric plexus, ganglia, and peripheral nerves
  2. brain and spinal cord
  3. heart and adrenal glands
55
Q

What histopathology is characteristic in the CNS in Bornavirus disease?

A

demyelination and perivascular cuffing with Purkinje cell necrosis

56
Q

Bornavirus disease, CNS:

A

encephalitis - mononuclear perivascular cuffs

57
Q

Bornavirus disease, PNS:

A

neuritis - perivascular cuffs of lymphocytes and fewer macrophages and plasma cells

58
Q

Bornavirus disease, PNS (ganglia):

A

ganglioneuritis - lymphocytes with fewer macrophages and plasma cells

59
Q

How is Bornavirus disease diagnosed?

A
  • ANTEMORTEM: qPCR plucked feathers
  • clinical signs and gross findings
  • histopathology and IHC

neuron is dark due to nuclear replication

Systemic Pathology I (25 decks)

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