VSV & BLuetongue Flashcards
(48 cards)
1
Q
What doe “Rhabdo-“ mean?
A
rod (bullet-shaped)
2
Q
What genus does Vesicular stomatitis virus belong to?
A
Vesiculovirus
3
Q
What are the physical characteristics of VSV?
A
- Enveloped
- (-)ssRNA
- 11Kb genome
- 5 distinct proteins
- G: neutralizing epitopes
4
Q
What species are affected by VSV?
A
- Horses, Cattle, Swine
- wildlife, very rare in sheep, goats, llamas, alpacas
- Zoonotic potential
5
Q
How many serogroups of VSV are there?
A
- 2 serogroups - distinct NAb
- New Jersey
- Indiana
6
Q
What is the geographical spread of VSV?
A
- Limited to the Americas
- sporadic outbreaks in US
- limited to western states since 1980s
- sporadic outbreaks in US
7
Q
How does VSV affect humans?
A
- Most cases asymptomatic
- Can cause flu-like illness
- Headache, fever, muscle aches, weakness for 3-5 days
- Rare - vesicles and encephalitis
8
Q
When does VSV occur?
A
- Seasonal variation - vector availability
- May to October
9
Q
Why is VSV important?
A
- Reportable disease
- May result in trade restrictions
10
Q
How is VSV transmitted?
A
- Direct: contact with infected animals - mucosa and skin
- Indirect: contaminated shared feed and water stations
- Blood-feeding insects:
- sandflies, black flies, biting midgets
- Biological vectors
- Associated with water sources, typically warmer months
- sandflies, black flies, biting midgets
11
Q
How do insects spread VSV?
A
- Insect pick up VSV from feeding on infected animals
- replicate the virus
- secrete it from their salivary glands when they feed again
12
Q
What are the clinical signs of VSV infection?
A
- Incubation period 2-8d
- Fever - before or same time lesions appear
- Broad tissue tropism
- Typically self-limiting, resolves in 10-14 days
13
Q
How prevalent is VSV? How fatl?
A
- Morbidity rate generally low in herd: 10-20%
- Previous exposure, underlying immunity, route of exposure
- Seroprevalence may be high - approaching 100%
- Mortality rare
14
Q
How are VSV and FMDV similar?
A
-
Identical clinical presentation to FMDV
- Excessive salivation: ptyalism )often 1st sign)
-
Vesicles, ulceration, erosion of various sizes of the oral and nasal mucosa, mucocutaneous junction of lips, sloughing of the epithelial surface of tongue
- Coronary bands, foot lesions, and lameness
- Prepuce, vulva, and teat lesions , possible 2° mastitis
- loss of appetite, reluctance to eat/drink
- Crusting lesions of the muzzle, ventral abdomen, ears, sheath, and udder
15
Q
When were significant outbreaks of VSV?
A
- 2005/2006
- 9 states, 445 premises
- 584+ equines cases
- 202+ bovine cases
- 2009
- 2 states, 5 premises
- 7+ equine cases
- 2012
- 2 states, 36 premises
- 51+ equine cases
- 2015/2016
- 823 VSV-affected premises confirmed or suspected in 8 states
- 2019
- 1144VSV affected premises confirmed or suspected in 8 states
- 2020
- 326 VSV affected premises confirmed or suspected in 8 states
- KS: 196 affected premises
16
Q
How is VSV diagnosed?
A
- REPORT to Authorities/Regulatory Veterinarians
- Samples collected FAD diagnostician
- Zoonotic - PPE should be worn when handling affected animals
- Antibody detection
- VI/PCR or active vesicular lesions
- Vesicular fluid, epithelial tags from lesions, lesion or mucosal swab
- Typically no viremia
17
Q
What are the DDx for VSV?
A
- FMDV
- SVDV
- VESV
- SVA
18
Q
How is VSV managed?
A
- No specific treatment available
- Soft feed for pain associated with oral lesions
- Cleaning wounds with mild antiseptics (prevent 2° infections)
-
Reduce exposure to vector
- Shelter/housing, insecticides, eliminate insect breeding areas
- Pasture away from moving water (streams, rivers)
- Isolate affected animals, quarantine
- Premises containing affected animals are quarantined for at leas 14 days from the onset of lesions in the last affected animal
- Biosecurity, disinfecting equipment/fomites
- Commercial vaccines not available in US
19
Q
Is there a vaccine for VSV?
A
- Commercial vaccines are NOT available in the US
20
Q
What is the triad of Vesicular Diseases?
A
- Vesicles
- Fever
- Lameness
- All vesicular diseases are clinically indistinguishable
- All require testing to confirm diagnosis
21
Q
What Family and Genus are Bluetongue Virus part of?
A
- Reoviridae
- REO - Respiratory, enteric orphan viruses
- Orbivirus - BTV, EHDV
22
Q
What are the characteristics of BTV?
A
- dsRNA 19kb
- Nonenveloped
- Segmented genome - 10
- >26 different serotypes worldwide
- >13 in US
23
Q
What is BTV?
A
- Non-contagious infectious arthropod-borne viral disease of domestic and wild ruminants (known for >100y)
- Geographical restriction due to climate and environmental conditions needed to support Culicoides biting midge vectors
- In US: C. sonorensis and insignis
- detected in southern and western states
24
Q
What type of vector are biting midges for BTV?
A
- Biological vector:
- virus replicates in midge
- vector becomes infected by blood from an infected ruminant
- Etiological cycle between vector and susceptible ruminant
25
Why are *Culicoides* biting midges important?
* \>1400 species worldwide
* Different species transmit BTV, EHDV (many other viruses) in distinct global ecosystems
26
How is BTV transmitted?
* Virus has high affinity for blood cells
* initially all blood cells than only erythrocytes
* NO replication in RBC
* **Prolonged viremia in presence of NAb**
* Not persistent, generally \< 60 days
* May be up to 11 weeks in cattle
* Can contribute to year-round transmission
* **Primary Route: Vector**
* Virus in secretions/excretions minimal
* direct/indirect/aerosol transmission unlikely
* Semen from viremic bulls potential source through natural breeding or AI
* Transplacental transmission in cattle reported
27
What animals are primarily effected by BTV? Mortality?
* Most common in sheep - principally European sheep reeds
* Peracute to chronic course
* **Mortality rate highly variable** 2-90%
* Peracute: may die within 7-9 d
* severe pulmonary edema, dyspnea, frothing from nostrils
* Chronic: may die after 3-5 seeks
* secondary bacterial infections
* Mild cases usually recover rapidly
28
What production losses does BTV cause?
* Deaths
* unthriftiness
* wool breaks
* Reproductive losses
29
What are the clinical signs of BTV in sheep?
* Incubation: 4-6 days
* Fever (105-107.5F)
* Listless/depression, reluctance to move
* edema of lips, nose, face, submandibular region, eyelids, ears
* Congestion/hyperemia of mouth, nose, nasal cavities, conjunctiva, and coronary bands
* lameness, hoof defects
* Serous nasal discharge (mucopurulent) dyspnea
* **Sore muzzle**
* **Blue tongue**
* some have severe edema and cyanosis of tongue
* Reduced appetite, erosions/ulcers can occur in oral cavity
* Dermatitis may result in abnormal wool growth
* Muscle loss, torticollis
30
What is the pathogenesis of BTV that allows for the clinical signs in sheep?
* Vascular endothelial damage
* Increased capillary permeability, intravascular coagulation
* edema, congestion, hemorrhage, inflammation, necrosis
31
What is the pathogenesis and clinical signs of BTV in cattle?
* C/S rare but similar to sheep:
* Fever
* Increased respiratory rate
* lacrimation
* salivation
* stiffness
* Oral vesicles and ulcers
* hyperesthesia
* dermatitis
32
What are the clinical signs of BTV in pregnant cattle/sheep?
* May abort or deliver malformed calves/lambs
* infection in early gestation
* Cerebral malformation
* Hydranencephaly, ,porencephaly
* Ataxia and blindness at birth
33
What are the clinical signs of BTV in WTD and pronghorn?
* Severe hemorrhagic disease leading to sudden death
34
What are the characteristic lesions of BTV found at necropsy?
* **Petechiae, ecchymoses, or hemorrhage in wall and base of pulmonary artery**
* **Focal necrosis of papillary muscle of left ventricle**
* Ulcers/hemorrhage/necrosis in oral cavity, tongue, esophageal groove, and omasal folds
* SQ, IM and LN **edema and hemorrhage,** skeletal myonecrosis and hemorrhage, myocardial and intestinal hemorrhage, pleural and pericardial effusion, pulmonary edema, pericarditis, and pneumonia
* **Characterized by vascular permeability, thrombosis and tissue infarction**
35
How is BTV diagnosed?
* Consistent clinical signs and pathology
* **VI/PCR**
* **whole blood in anticoagulant**
* Spleen, ln, bone marrow
* Antibody response detected 7-14dpi, generally lifelong
* AGID, ELISA
* Identity of isolate (serotype)
* can be performed on both virus and Ab
36
How is BTV managed?
* No specific treatment
* Rest, soft food, husbandry
* Controlling secondary infections
* **Vaccination**
* **Control of vectors**
37
What is the BTV vaccine?
* Modified live virus (MLV) and Inactivated vaccines commercially available
* In US:
* **monovalent (BTV 10) MLV** vaccine available for use in **sheep**
* **MLV vaccine can cause abortion or malformation of fetuses when given in the first half (ewe) or first trimester (cow) of pregnancy**
* Vaccination with different serotypes does _NOT provide consistent cross-protection_
* MLV vaccines should **NOT be used during** ***Culicoides*** **season:**
* insects may transmits the vaccine virus
* potential for reassortment, new viral strains
38
does BTV undergo genetic shift?
* Genetic shift by reassortment of gene segments during infection of insects or animals with more than 1 strain/serotype of BTV
39
What are some concerns about the future of BTV?
* Climate changes: increased range of environment supportive of the vector?
* Additional emerging serotypes?
* different species virulence
* origin of virus
40
What are the characteristics of Epizootic hemorrhagic disease virus (EHDV)
* dsRNA virus
* Nonenveloped
* Segmented genome
* \>10 different serotypes worldwide
41
What is EHDV?
* Non-contagious infectious arthropod-borne viral disease of domestic and wild ruminants
* Historically, a disease of WTD in NA - rarely a clinical disease of cattle
* Ibaraki virus - outbreak in Japan 1959
* **Emerging disease in cattle**: OIE notifiable since 2008
* Biological vector: *Culicoides biting midge*
* Immunological cross-reactivity with BTV
* Seasonal due to vector
* **REPORTABLE**
42
What animals are hosts to EHDV
* **WTD most important**
* Morbidity and Mortality may be as high as 90%
* varies between years and geographical locations
* Other wild ruminants may seroconvert:
* mule deer, pronghorn, black-tailed deer, red deer, elk, moose, bighorn sheep
* Cattle: subclinical infection common, outbreaks rare
* ***Culicoides*** sp. **transmit** virus to ruminants after external extrinsic period of 10-14 days
43
What is the Pathogenesis of EHDV
* Viremia can be prolonged \> 50d in the presence of NAb
* Virus associated with RBC
* Virus infects endothelium all tissues affected
44
What are the clinical signs of EHDV in WTD?
* Incubation: 5-10d
* Fever, weakness, reduced appetite, excessive salivation, head and neck edema, hyperemia of conjunctiva and mucus membranes of oral cavity, coronitis, stomatitis
* Prolonged disease: ulcers on dental pad, hard palate, and tongu
* Terminal: excessive bleeding, bloody diarrhea, hematuria, death
45
What are the clinical signs of EHDV in cattle
* Incubation: 5-10d
* Acute disease similar to BTV;
* fever, reduced appetite, conjunctival edema, redness and crusting of nose and lips, oculonasal discharge, stomatitis, salivation, lameness, tongue edema, oronasal erosion, dyspnea, coronitis, difficulty swallowing
* Abortions/stillbirths reported
* Mortality low (\<10%)
46
What lesions are common in WTD with EHDV
* Widespread hemorrhage and edema
* especially in heart and GIT
47
jHow is EHDV diagnosed?
* REPORTABLE
* Differentials:
* WTD: BTV, FMDV
* Cattle, BTV, BVDV, FMDV, IBR, VSV, MCFV
* FAD investigation
* **VI/PCR**
* **whole blood in anticoagulant**
* spleen, lungs, ln, liver
* Serology: paired serum samples
* AGID, ELISA, SN
48
How is EHDV managed?
* Control Vector
* insecticides, repellents on susceptible ruminants, management of *culicoides* breeding areas
* NO VACCINE commercially available for preventing EHDV in US
