Avian Dz Flashcards

(52 cards)

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
Marek's resistance to infection
Genetics: Carry MHC B21 halotype Maternal Abs in chicken up to 3w Bursectomized Life-long carriers and shedders (5-6w after infection)
25
What lesions due to in situ proliferation of T cells of Marek's Dz lead to?
Leukemia Significant inflamm cell resp. Enlargement of nerves
26
What nerves are enlarged fro Marek's Dz
Abdominal vagus, sciatic plexuses, brachial plexuses, coeliac plexuses, intercostal nerves
27
Dx of Marek's
History, CS and gross lesions (lymphomas and nerve enlargement) Age (not in chicks <3w, older)
28
DD of Marek's DZ
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
Marek’s Dz vx
↓ the incidence of neoplastic lesions in visceral organs and neuro. Dz
30
Marek’s Dz control measures
Building up of flocks carrying B21 alloantigen All-in-all-out Cleaning/ disinfection
31
Retroviridae causes _________
Avian Leukosis Viruses *genus: alpharetrovirus*
32
Lymphoid leukosis (visceral lymphomatosis)
Most common form of avian leukosis in chickens 3-7m
33
Lesions of Lymphoid Leukosis
Non-specific (pale comb, abdominal swelling etc) Multi-centric tumors (discrete nodular lesions in the BF that metastasize)
34
__________ up to 5m of age abrogates formation of tumors for avian leukosis virus
Bursectomy
35
Tumors associated with lymphoid leukosis
Aggregates of B lymphoblasts Transformation the intact bursa Diffuse or nodular lymphoid tumors common in liver, spleen and bursa
36
Avian leukosis virus transmission
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
Dx of Avian leukosis virus
History, CS, histopath Immune assays RT-PCR and sequence analysis
38
Immunity and prevention of Avian leukosis virus
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
Control of Avian leukosis virus
All-in-all-out Hygiene, single source chicks (genetically resistant animals)
40
Birnaviridae causes ________________
Infectious Bursal Dz/ Gumboro Delaware Dz *genus: avibirnavirus, RNA, reportable*
41
Infectious Bursal Dz
Severe and prolonged immunosuppression Contagious: oral and direct contact 2 serotypes
42
Serotype 1 of IBD
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
What age does IBD affect?
Most severe in chicks 3-6w <3w subclinical infection, >6w rarely develop dz
44
CS of IBD
Distress, depression, ruffled feathers, anorexia, diarrhea, trembling and dehydration Clinical dz starts @ 3-4d and immunodepressed
45
Lesions of IBD
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
Pathogenesis of IBD
Replicates in macros and lymphos → viremia 1 in cecum and SI Infects BF lymphos → viremia 2 and systemic dissemination
47
______________ survive without CS or dz with IBD
Bursectomized
48
Why is the stage of B cell differentiation crucial in IBD?
Only IgM bearing B cells of pre- B cells are infected
49
Dx of IBD
IF (smears and secretions of BF) - Ag 3-4d after infection RT-PCR EM of bursal specimens Cell cx: chicken lymphoblastoid cells (14d)
50
How long does the IBD virus last?
>120d in farm environ. >50d in feed, feces and water Resists heat, cleaning and disinfection
51
Control of IBD
Inacvitvated by phenolic-base compounds, iodine complexes, formalin, chloramine compounds Vx primary mode of control