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.infection & immunity > Avian Dz > Flashcards

Avian Dz Flashcards

1
Q

Paramyxoviridae causes _____________

A

Newcastle Dz (APMV-1)/ Avian pneumoencephalitis
genus: avulavirus, 11 serotypes

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2
Q

In many countries like ________________, __________ is the biggest threat to food security because of recurring outbreaks and high mortality

A

Asia, Middle east, Africa, Central and South America
Newcastle Dz

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3
Q

International monitoring of Newcastle Dz is done by who?

A

FAO and OIE

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4
Q

Which species show no CS with Newcastle

A

Ducks and geese
Carrier in Migratory waterfowl

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5
Q

Pathotypes of Newcastle

A

Asymptomatic, enteric: subclinical
Lenthogenic: subclinical to mild resp.
Mesogenic: Resp. or neuro
Velogenic: Neurotropic (resp. or neuro) and vicerotropic (hemorr. intestinal lesions)

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6
Q

What is the new classification of Newcastle Dz?

A

vND, reportable
Mesogenic, velogenic neurotropic (lethal) and velogenic vicerotropic (lethal + hemorr.)

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7
Q

CS of Newcastle

A

Edema of the head (eyes)
Greenish- dark watery diarrhea
Resp. or neruo signs

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8
Q

Neuro. signs in protracted cases

A

Muscle tremors, drooping wings, dragging legs, twisted head and neck, circling, depression, inappetence, paralysis

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9
Q

T/F: Vx birds will have less severe signs but not protected against vND viruses

A

TRUE

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10
Q

Newcastle Dz is indistinguishable from _____________

A

Highly pathogenic avian influenza
Hemorrhagic internal lesions: tracheal and intestinal mucosa and proventriculus

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11
Q

Zoonosis of Newcastle Dz

A

Mild conjunctivitis: sheds ocular secretions for 4-7d (avoid contact)
Lab and vx crews most @ risk
No cases handling or consuming poultry or human-human spread

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12
Q

Control of Newcastle

A

Disinfection of premises
Delay re-intro of new birds for 30d
Control insects and mice
Limit human traffic
Vx

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13
Q

Newcastle vx

A

Live (lentogenic NC virus) for commercial
Inactivated (individual bird)
Recombinant (in ovo)
Combo of live then inactivated

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14
Q

What are the 3 R’s with infectius bronchitis

A

Resp., renal, reproductive

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15
Q

Gallid Herpesvirus 2 causes ____________

A

Marek’s Dz Virus (non-resp.)
genus: mardivirus

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16
Q

How does GH1 differ from GH2?

A

GH1 (Avian Laryngotracheitis) is a resp. dz

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17
Q

Marek’s Dz is the most important progressive _____________ of chickens (+ turkeys) causing substantial economic loss worldwide

A

Lymphoproliferative dz

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18
Q

Acute signs of Marek’s Dz

A

Fowl paralysis in explosive outbreaks in young chicken with depression
Mortality without neuro signs
Enlargement of nerves (most consistent)

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18
Q

Classical signs of Marek’s Dz

A

Lymphoproliferative syndromes
Lymphomas, neuro signs
Vagus nerve: dilation of crop and gasping

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19
Q

Ocular Lymphomatosis (Marek’s Dz)

A

Graying of the iris
Pupil irregular and eccentric (partial or total blindness)

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20
Q

Cutaneous Marek’s Dz

A

Round nodular lesions on feather follicles of young
Redleg
Carcass condemned

21
Q

Epidemiology of Marek’s Dz

A

Mature chicken have Ab
Protected first weeks of life due to progressive nature of the dz
Epizootic: sexually immature birds (2-5m), high mortality
Commercial flocks in US vx (endemic)

22
Q

Pathogenesis of Marek’s Dz

A

Inhalation of skin dander/ dust → lung B cells and macros → B cells to T cells → immunesuppression → skin infection lymphos

23
Q

What happens of the second week after infection of Marek’s Dz

A

Proliferation of T cells then death 1 w layer
T lymphomas

24
Q

Marek’s resistance to infection

A

Genetics: Carry MHC B21 halotype
Maternal Abs in chicken up to 3w
Bursectomized
Life-long carriers and shedders (5-6w after infection)

25
Q

What lesions due to in situ proliferation of T cells of Marek’s Dz lead to?

A

Leukemia
Significant inflamm cell resp.
Enlargement of nerves

26
Q

What nerves are enlarged fro Marek’s Dz

A

Abdominal vagus, sciatic plexuses, brachial plexuses, coeliac plexuses, intercostal nerves

27
Q

Dx of Marek’s

A

History, CS and gross lesions (lymphomas and nerve enlargement)
Age (not in chicks <3w, older)

28
Q

DD of Marek’s DZ

A

Avian leukosis
Neuro symptoms, @ least 3w, T lymphomas, Herpesvirus, several species vx in MD
Tumors in bursa, .14w, B lymphomas, acute, chickens, vertical trans, retrovirus in AL

29
Q

Marek’s Dz vx

A

↓ the incidence of neoplastic lesions in visceral organs and neuro. Dz

30
Q

Marek’s Dz control measures

A

Building up of flocks carrying B21 alloantigen
All-in-all-out
Cleaning/ disinfection

31
Q

Retroviridae causes _________

A

Avian Leukosis Viruses
genus: alpharetrovirus

32
Q

Lymphoid leukosis (visceral lymphomatosis)

A

Most common form of avian leukosis in chickens 3-7m

33
Q

Lesions of Lymphoid Leukosis

A

Non-specific (pale comb, abdominal swelling etc)
Multi-centric tumors (discrete nodular lesions in the BF that metastasize)

34
Q

__________ up to 5m of age abrogates formation of tumors for avian leukosis virus

A

Bursectomy

35
Q

Tumors associated with lymphoid leukosis

A

Aggregates of B lymphoblasts
Transformation the intact bursa
Diffuse or nodular lymphoid tumors common in liver, spleen and bursa

36
Q

Avian leukosis virus transmission

A

Congenital due to virus in oviduct → chicks shed virus in meconium and feces
Horizontal by direct contact, saliva and contaminated environ.
Transovo (not impt)

37
Q

Dx of Avian leukosis virus

A

History, CS, histopath
Immune assays
RT-PCR and sequence analysis

38
Q

Immunity and prevention of Avian leukosis virus

A

Maternal Abs low and disappear by 4-7w
Infected chicks have high levels of Abs (persistently infected)
Roosters in germ line transmission of endogenous retroviruses

39
Q

Control of Avian leukosis virus

A

All-in-all-out
Hygiene, single source chicks (genetically resistant animals)

40
Q

Birnaviridae causes ________________

A

Infectious Bursal Dz/ Gumboro Delaware Dz
genus: avibirnavirus, RNA, reportable

41
Q

Infectious Bursal Dz

A

Severe and prolonged immunosuppression
Contagious: oral and direct contact
2 serotypes

42
Q

Serotype 1 of IBD

A

Pathogenic in young Ab- free chickens
Classic or standard with 10-50% mortality (worldwide)
Variant: no mortality (worldwide)
Very virulent: 50-100% mortality (Europe, Asia, SA)

43
Q

What age does IBD affect?

A

Most severe in chicks 3-6w
<3w subclinical infection, >6w rarely develop dz

44
Q

CS of IBD

A

Distress, depression, ruffled feathers, anorexia, diarrhea, trembling and dehydration
Clinical dz starts @ 3-4d and immunodepressed

45
Q

Lesions of IBD

A

3-4d after infection, BF enlarged up to 5x → edema, hyperemia, prominent longitudinal striations
Hemorrhage, necrotic foci through parenchyma
Virulent: lymphos in spleen, thymus and BM
BF atrophic, kidneys enlarged

46
Q

Pathogenesis of IBD

A

Replicates in macros and lymphos → viremia 1 in cecum and SI
Infects BF lymphos → viremia 2 and systemic dissemination

47
Q

______________ survive without CS or dz with IBD

A

Bursectomized

48
Q

Why is the stage of B cell differentiation crucial in IBD?

A

Only IgM bearing B cells of pre- B cells are infected

49
Q

Dx of IBD

A

IF (smears and secretions of BF) - Ag 3-4d after infection
RT-PCR
EM of bursal specimens
Cell cx: chicken lymphoblastoid cells (14d)

50
Q

How long does the IBD virus last?

A

> 120d in farm environ.
50d in feed, feces and water
Resists heat, cleaning and disinfection

51
Q

Control of IBD

A

Inacvitvated by phenolic-base compounds, iodine complexes, formalin, chloramine compounds
Vx primary mode of control

.infection & immunity (12 decks)

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