Topic 8: Parvovirus diseases of Mink Flashcards
Pathogen ; Parvoviral Enteritis of Mink
present in Europe since 1950s
Parvoviridae, parvovirinae
related to FLPV and CPV2 (genus parvo)
Mink Enteritis virus, hilghy contagious
]all ages susceptible, outcome of disease depends on immune status, most serious cases in kits (young)
Pathogenesis Mink enteritis virus
similar to parvoviral infection in dog and cat
faeco-oral transmission, infrom infected faeces or environment
Viral replication in pharyngeal lymphoid tisse, vireamia, targets cells will rapid division
lymphoid cells (BM, spleen, thymus and LN) = leukopenia
Crpty cellos SI = massive viral shedding via faeces
Myocardial cells of young animals
CS of Mink enteritis virus
appear following a 5-7 day incubation
Non specific signs, fever depression, anorexia nd wight loss
acute GE, vomting, watery/bloody dra, abd pain
Dehydration
Death, high mortality, up t 80% in highly susceptible, young milk flock
Dx of Mink enteritis virus
CS are typical, and post mortem lesions
IF, antigen EILSA, PCR
Virus Isolation
Serology; VN, ELISA
Control and prevention
early in outbreak, all mink showing CS should be culled or isolated, all clinically normal mink should be vx immdiately
MVE can be prevented, vx of all mink under 2m
inactivated vx (usually a combo with MVE, botulism, Pseudomonas around 11-12 weeks)
1st does 8-9w
2nd 12 w
repeats every year after last dose
Epidemiology of Aleutian Mink Disease
since 1956, now WW Parvovirinae, Amdovirus - parvoviral infection of mustiledae - not related to MVE - plasmocytosis, ZOONOTIC!
- poor repro performance, gradual weight loss, oral and GI bleeding, renal failure and high mortality
Mainly in blue grey colour variant, but all colours may be infected
shed via faeces and urine and other excretions of persistently infected mink
Can be intrauterine, direct or indirect transmission (horizontal and vertical)
Young kits ; may die from acute interstitial pneumonia
Older mink: mainly Aleutian genotype, hypergammaglobulinemia, glomerulonephritis
Pathogenesis of Amdovirus
PO / inhaltional, lympoid tissue of the throat, viremia, x in cells with rapid division
After infection, IG levels increase markedly, but are unable to neutralise the virus, persistne infection, hypergammaIG and plasmocytosis
immune complex formation dn deposition in kidney, BVs , peri / vasculitis
Immune complex glomerulonephritis and arteritis, type III rxn
CS of Amdovirus
chronic appearance )CS persists for some weeks with incubation time of 4-6 weeks
bleeding from nose and mouth
anorexia, thirst, bloody faeces
pregnant animals, foetal damage and abortion
some neuro signs
50% mortality in Aleutian, 5% in other
PM Lesions of Amdovirus
Gross - splenomegaly, Hepatomegaly - renal changes, swelling, petechia, atrophy and pitting, glomerulonephritis - enlarged mesenteric LN Bleeding and erosions on MM uraemia
HP
- elevated plasma cell count, plasma cell infiltration of the kidneys, liver, spleen and LN
Dx of Amdovirus
CS, pathology and HP changes
PCR
Virus isolation
Serology, KJ, ID
Detection of virus, abs, immune complex
Prevention / Control of Amdovirus
no vaccine or tx
strict hygiene, steam cleaning and disinfecting pens etc
test and slaughter, eradication programs
blood test and cull all seropositive
test all breeding animals, due to intrauterine transmission
ZOONOTIC, public health risk
