Avian Dz Flashcards
Paramyxoviridae causes _____________
Newcastle Dz (APMV-1)/ Avian pneumoencephalitis
genus: avulavirus, 11 serotypes
In many countries like ________________, __________ is the biggest threat to food security because of recurring outbreaks and high mortality
Asia, Middle east, Africa, Central and South America
Newcastle Dz
International monitoring of Newcastle Dz is done by who?
FAO and OIE
Which species show no CS with Newcastle
Ducks and geese
Carrier in Migratory waterfowl
Pathotypes of Newcastle
Asymptomatic, enteric: subclinical
Lenthogenic: subclinical to mild resp.
Mesogenic: Resp. or neuro
Velogenic: Neurotropic (resp. or neuro) and vicerotropic (hemorr. intestinal lesions)
What is the new classification of Newcastle Dz?
vND, reportable
Mesogenic, velogenic neurotropic (lethal) and velogenic vicerotropic (lethal + hemorr.)
CS of Newcastle
Edema of the head (eyes)
Greenish- dark watery diarrhea
Resp. or neruo signs
Neuro. signs in protracted cases
Muscle tremors, drooping wings, dragging legs, twisted head and neck, circling, depression, inappetence, paralysis
T/F: Vx birds will have less severe signs but not protected against vND viruses
TRUE
Newcastle Dz is indistinguishable from _____________
Highly pathogenic avian influenza
Hemorrhagic internal lesions: tracheal and intestinal mucosa and proventriculus
Zoonosis of Newcastle Dz
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
Control of Newcastle
Disinfection of premises
Delay re-intro of new birds for 30d
Control insects and mice
Limit human traffic
Vx
Newcastle vx
Live (lentogenic NC virus) for commercial
Inactivated (individual bird)
Recombinant (in ovo)
Combo of live then inactivated
What are the 3 R’s with infectius bronchitis
Resp., renal, reproductive
Gallid Herpesvirus 2 causes ____________
Marek’s Dz Virus (non-resp.)
genus: mardivirus
How does GH1 differ from GH2?
GH1 (Avian Laryngotracheitis) is a resp. dz
Marek’s Dz is the most important progressive _____________ of chickens (+ turkeys) causing substantial economic loss worldwide
Lymphoproliferative dz
Acute signs of Marek’s Dz
Fowl paralysis in explosive outbreaks in young chicken with depression
Mortality without neuro signs
Enlargement of nerves (most consistent)
Classical signs of Marek’s Dz
Lymphoproliferative syndromes
Lymphomas, neuro signs
Vagus nerve: dilation of crop and gasping
Ocular Lymphomatosis (Marek’s Dz)
Graying of the iris
Pupil irregular and eccentric (partial or total blindness)
Cutaneous Marek’s Dz
Round nodular lesions on feather follicles of young
Redleg
Carcass condemned
Epidemiology of Marek’s Dz
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)
Pathogenesis of Marek’s Dz
Inhalation of skin dander/ dust → lung B cells and macros → B cells to T cells → immunesuppression → skin infection lymphos
What happens of the second week after infection of Marek’s Dz
Proliferation of T cells then death 1 w layer
T lymphomas
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)
What lesions due to in situ proliferation of T cells of Marek’s Dz lead to?
Leukemia
Significant inflamm cell resp.
Enlargement of nerves
What nerves are enlarged fro Marek’s Dz
Abdominal vagus, sciatic plexuses, brachial plexuses, coeliac plexuses, intercostal nerves
Dx of Marek’s
History, CS and gross lesions (lymphomas and nerve enlargement)
Age (not in chicks <3w, older)
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
Marek’s Dz vx
↓ the incidence of neoplastic lesions in visceral organs and neuro. Dz
Marek’s Dz control measures
Building up of flocks carrying B21 alloantigen
All-in-all-out
Cleaning/ disinfection
Retroviridae causes _________
Avian Leukosis Viruses
genus: alpharetrovirus
Lymphoid leukosis (visceral lymphomatosis)
Most common form of avian leukosis in chickens 3-7m
Lesions of Lymphoid Leukosis
Non-specific (pale comb, abdominal swelling etc)
Multi-centric tumors (discrete nodular lesions in the BF that metastasize)
__________ up to 5m of age abrogates formation of tumors for avian leukosis virus
Bursectomy
Tumors associated with lymphoid leukosis
Aggregates of B lymphoblasts
Transformation the intact bursa
Diffuse or nodular lymphoid tumors common in liver, spleen and bursa
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)
Dx of Avian leukosis virus
History, CS, histopath
Immune assays
RT-PCR and sequence analysis
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
Control of Avian leukosis virus
All-in-all-out
Hygiene, single source chicks (genetically resistant animals)
Birnaviridae causes ________________
Infectious Bursal Dz/ Gumboro Delaware Dz
genus: avibirnavirus, RNA, reportable
Infectious Bursal Dz
Severe and prolonged immunosuppression
Contagious: oral and direct contact
2 serotypes
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)
What age does IBD affect?
Most severe in chicks 3-6w
<3w subclinical infection, >6w rarely develop dz
CS of IBD
Distress, depression, ruffled feathers, anorexia, diarrhea, trembling and dehydration
Clinical dz starts @ 3-4d and immunodepressed
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
Pathogenesis of IBD
Replicates in macros and lymphos → viremia 1 in cecum and SI
Infects BF lymphos → viremia 2 and systemic dissemination
______________ survive without CS or dz with IBD
Bursectomized
Why is the stage of B cell differentiation crucial in IBD?
Only IgM bearing B cells of pre- B cells are infected
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)
How long does the IBD virus last?
> 120d in farm environ.
50d in feed, feces and water
Resists heat, cleaning and disinfection
Control of IBD
Inacvitvated by phenolic-base compounds, iodine complexes, formalin, chloramine compounds
Vx primary mode of control
