Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

Avian Diseases, Pt. 2 Flashcards

(59 cards)

Start Studying
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Classical Marek’s disease:

A

paralysis - sciatic nerve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Classical Marek’s disease:

A

left sciatic nerve thick due to lymphocyte inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Visceral (acute) Marek’s disease:

A

nodular lymphoblastic lesions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Ocular Marek’s disease:

A

grey eye - lymphocyte infiltration of iris

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Ocular Marek’s disease:

A

grey eye, constricts pupil due to inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Cutaneous Marek’s disease:

A

Alabama redleg - erythematous legs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Cutaneous Marek’s disease:

A

enlarged feather follicles/nodules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

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

A

lymphocyte infiltration of the iris

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Classical Marek’s disease, histopathology:

A

PNS = inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Cutaneous Marek’s disease, histopathology:

A

perivascular lymphomatous lesion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

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

Study These Flashcards
A

PCR, IHC
- virus isolation, IFA, viral neutralization

chicks are typically vaccinated by 1 day old

no

25
Marek's disease vs. Lymphoid leukosis:
26
What causes Newcastle disease? How does it compare to others in the same family?
avian Paramyxovirus 1 (ssRNA) reportable to OIE - does not cause paramyxovirus infection
27
What species are most affected by Newcastle disease? What are some potential reservoirs?
chickens waterfowl, psittacines
28
What 2 things determine the pathogenicity of avian Paramyxovirus 1?
strain 1. ICPI - intracerebral pathogenicity index 2. F protein sequence - penetrates host cell membrane (VELOGENIC - viscerotropic, neurotropic)
29
What is the main way that Newcastle disease is transmitted? How else can it be transmitted?
ingestion of inhalation of infected secretions (feces, respiratory secretions, excretions) - fomites - vertical
30
What is the pathogenesis of Newcastle disease?
- 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
How does viscerotropic velogenic Newcastle disease present?
- acutely lethal, kills chickens of all ages - weakness, anorexia - green diarrhea - prostration, tremors, torticollis, paralysis, opisthotonus - death flock mortality can reach 100%
32
How does neurotrophic velogenic Newcastle disease present?
- 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
Neurotrophic velogenic Newcastle disease:
torticollis
34
What gross lesions present in visceral and neurotropic velogenic Newcastle disease?
VVND = necrotizing gastroenteritis and hemorrhage at junctions NVND = pneumonia and/or encephalitis
35
What 3 histopathological presentations are common with visceral velogenic Newcastle disease?
1. necrotizing gastroenteritis 2. hemorrhages in junctions of the esophagus, proventriculus, and gizzard 3. GALT necrosis
36
What 2 histopathological presentations are common with neurotropic velogenic Newcastle disease?
1. interstitial pneumonia 2. non-suppurative encephalitis with lymphocyte perivascular cuffing, endotheliosis, and inclusion bodies
37
Newcastle disease, CNS:
spheroids - swollen axons and demyelination
38
Newcastle disease, CNS:
neuronal necrosis - red = dead, pyknotic nuclei
39
Newcastle disease, neuronal inclusion bodies:
40
Newcastle disease, CNS (cerebellum):
pink neuronal inclusion bodies
41
Newcastle disease, CNS:
neuronal inclusion bodies - IN and IC
42
How does the OIE diagnose Newcastle disease? What else can be done?
virus isolation and qPCR NVSL panel - hemagglutination for unvaccinated flocks - IHC - immunochromatographic strips
43
How is Newcastle disease controlled?
- vaccines: live attenuated in water, aerosol, eye/nose droplets, beak dipping; inactivated - hygiene/biosecurity
44
Is Newcastle disease zoonotic?
yes, but rare - immunosuppression increases risk - veterinarians, processing plant employees, lab workers, and vaccination crews are most susceptible
45
What are the 3 major clinical signs of Newcastle disease in humans?
1. self-limiting conjunctivitis* 2. excessive lacrimation, eyelid edema, subconjunctival hemorrhage, unilateral/bilateral reddening 3. generalized infection - fever, headache, chills
46
What causes Bornavirus disease? What are some other names?
avian Bornavirus (ABV) - ssRNA virus with nuclear replication - Macaw wasting disease - Psittacine Proventricular Dilatation Disease - Proventricular Dilatation Disease - Neuropathic gastric dilatation
47
What 2 species are most affected by Bornavirus disease?
1. Pisttacines, canaries, finches 2. Canada goose
48
What does avian Bornavirus target?
- autonomic nerves of the upper and middle GI: esophagus, crop, proventriculus, gizzard, duodenum - CNS: cerebellum, cerebrum, brainstem
49
What is thought to be the infection route of Bornavirus disease? What happens after infection?
- trauma/inoculation in skin - fecal-oral, respiratory migration to nervous ganglia (and CNS in Canada goose) with retrograde axonal transport
50
What are the 6 common clinical signs of Bornavirus disease?
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
Bornavirus disease, radiography:
flaccidity and dilation of proventriculus, ventriculus, and crop
52
What are 4 common postmortem gross findings of Bornavirus disease?
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
Bornavirus, GI:
dilatation - proventriculus, ventriculus, crop
54
What 3 places do lymphocytes and plasma cells infiltrate in Bornavirus disease?
1. myenteric plexus, ganglia, and peripheral nerves 2. brain and spinal cord 3. heart and adrenal glands
55
What histopathology is characteristic in the CNS in Bornavirus disease?
demyelination and perivascular cuffing with Purkinje cell necrosis
56
Bornavirus disease, CNS:
encephalitis - mononuclear perivascular cuffs
57
Bornavirus disease, PNS:
neuritis - perivascular cuffs of lymphocytes and fewer macrophages and plasma cells
58
Bornavirus disease, PNS (ganglia):
ganglioneuritis - lymphocytes with fewer macrophages and plasma cells
59
How is Bornavirus disease diagnosed?
- ANTEMORTEM: qPCR plucked feathers - clinical signs and gross findings - histopathology and IHC neuron is dark due to nuclear replication

Systemic Pathology I (25 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions