Ruminants integument & mixed Flashcards
Schmallenberg virus infection is an infectious disease of ruminants, transmitted by insects, and characterized by
arthrogryposis hydraencephaly syndrome.
SBV / Schmallenberg virus infection was first reported in
in 2011 in Holland and Germany.
Adult cattle had very non-specific clinical signs: fever, drop in milk production, watery diarrhea.
Later: abortions, stillbirths, malformations in cattle and sheep herds
New viral RNA was discovered in samples,
named after the geographic region of the first outbreak.
Causative agent of SBV infection.
family
genus
DNA type
Schmallenberg virus (SBV)
Genus Orthobunyavirus,
family Bunyaviridae
RNA virus
Schmallenberg virus serogroup and reassortment
Simbu serogroup
reassortment of the genomes of Sathuper and Shamonda viruses
Survival of SBV in environment etc.
Survival outside the host or vector is short
Inactivated in 50-60°C 30min
Common disinfectants can inactivate
Host range of SBV.
ruminants
Cattle, sheep, goats, buffalos, roe deer, red deer
Seroprevalence of SBV in cattle in Holland:
70%
Seasonality for SBV
Most common during high season of vectors so summertime.
Transmission of SBV.
Via blood sucking insects (mostly Culicoides spp)
In utero transmission
- In small ruminants on 28th-56th day of pregnancy
- Cattle 80th-150th day of pregnancy
Result: malformation of fetuses and newborns
Clinical signs of SBV in adult cattle:
Inappetence, weight loss
Fever (>40°C)
Drop in milk production (<50%)
Watery diarrhea
Recovery in 2-3 weeks
Clinical signs of SBV in calves:
Mild illness
Diarrhea
In utero transmission: malformation of fetuses and newborns
Clinical signs of SBV in newborns/neonates:
Cattle and small ruminants affected.
Fetuses are full term or near.
Congenital neurological disorders – lack of activity, abnormal vocalization, blindness, abnormal movements etc.
Malformations in spine and limbs, mandibula
Arthrogryposis hydranencephaly syndrome (AHS): stillbirth, premature birth, mummified fetuses, arthrogryposis (joint contractures), hydranencephaly, ataxia, paralysis, muscle atrophy, joint malformations, torticollis, kyphosis, scoliosis.
Suspect SBV when…
characteristic clinical signs in ruminants at the high season of vectors and at the following calving/lambing/kidding season.
Material for diagnosis of SBV: (2)
Aborted fetuses
Blood
Lab analyses for diagnosis of SBV: (3)
RT-qPCR – for viral RNA
Serology (ELISA, virus neutralization test) for antibodies
Histopathology
Vaccine for SBV?
Vaccine is expensive, but exists.
(Zulvac SBV protects cattle two weeks and sheep three weeks after vaccination.
In pregnant ewes vaccination reduced viraemia and infection of the embryo.)
Prevention & control of SBV.
Controlling or getting rid of the vectors – insecticides and mosquito nets.
Vaccine exists but is expensive and protection is short lived (2-3 weeks).
IBK
Infectious bovine keratoconjuntivitis
Infectious bovine keratoconjuntivitis is an infectious disease of cattle, sheep and goats, caused by Moraxella bovis, and is characterized by
blepharospasm, conjunctivitis, lacrimation, and varying degrees of corneal opacity and ulceration.
Causative agent of IBK.
Infectious bovine keratoconjuntivitis caused by gram neg. Moraxella bovis.
Family Moraxellaceae
serogroups of IBK
7 serogroups
Moraxella bovoculi has also been isolated from cattle with IBK but it is not recognized as a primary agent.
Host range of IBK.
cattle, sheep, goats
Animals of all ages are susceptible
Most frequently affected: young animals
Most common ocular disease of cattle?
IBK
Reported worldwide
More common during summer and fall
Morbidity of IBK.
<80%
Risk factors: plant awns, face flies, ultraviolet radiation from bright sunlight, dry and dusty environmental conditions, shipping stress, trace mineral deficiencies (e.g. selenium and copper deficiency).
Mortality of IBK.
0%, doesn’t kill, just blinds.
Transmission of IBK.
Excretion: ocular and nasal discharge
Carriers can secrete for more than a year
Mechanial vectors – flies
Indirect contact – dust, grass
Route: via mucous membranes
IP of IBK.
IP: 2-3 days
Initial clinical signs of IBK. (3)
Photophobia
Blepharospasm
Epiphora
Later signs of IBK. (3)
Ocular discharge may become mucopurulent
Conjunctivitis, with or without varying degrees of keratitis
Corneal ulcers
Appetite may be depressed.
In severe cases: corneal rupture and permanent blindness.
Material for diagnosis of IBK.
Ocular swabs – get to the lab within 2 hours!
Lab analyses for diagnosis of IBK.
Microbial culture
PCR
Tx of IBK.
Tx: self-limiting dz
but ABs may be useful to prevent scarring.
In early cases: topical treatment
Later: parenteral treatment
Ancillary:
Place animal inside – out of sun light
Eye patches
Prevention & control of IBK.
Fly control
Vaccines – efficacy?
Enzootic bovine leukosis (EBL) is a contagious disease of cattle, caused by retrovirus, and characterized by
lymphocytosis and lymphosarcoma.
Causative agent of Bovine lymphosarcoma.
genus
family
DNA type
Bovine leukemia virus (BLV)
Genus Deltaretrovirus,
family Retroviridae
RNA retrovirus
Bovine leukemia virus is Closely related to
the human T-lymphotropic virus type 1 HTLV-I.
Oncogenic!
Bovine leukemia virus survival in environment:
Does not survive long outside the organism.
In milk 1°C 3 days, in 10°C 48h
Inactivated by UV radiation
Common disinfectants can inactivate
Host range of Bovine lymphosarcoma.
Age demo?
cattle
Uncommon in cattle <2 years of age.
More common in big herds
Milk cattle > beef cattle – higher age on average.
Where in the world if Bovine lymphosarcoma found?
Reported in Canada, USA, some European countries and South America.
Eradicated in Estonia.
Notifiable disease
Morbidity of BLV.
Morbidity <80%
Transmission of BLV.
Excretion: blood, milk, tumor masses.
Virus is present mostly in lymphocytes.
Direct contact
Iatrogenic transmission
Insects? potentially mechanically.
Congenital infection
Route: through mucous membranes
Clinical course of bovine leukemia virus infection.
Primary infection: flu-like syndrome (in 1-4 weeks)
Persistent infection: immune dysregulation (several months/years)
Persistent lymphocytosis: weakness, opportunistic infections (years)
Tumoral stage of disease: 5-10% animals make it to this point.
Clinical signs of BLV.
Clinically presented in older animals (4-8 years) (long incubation period).
No clinical signs during initial stage of infection and persistent lymphocytosis.
Lymphosarcoma tumors in many sites developing rapidly.
Characterized by loss of body weight, inappetence, pallor, weakness, and loss of milk production.
Enlargement of all superficial lymph nodes (75-90%)
Abomasal ulceration
Congestive heart failure
Paresis and paralysis due to neural involvement.
Stertor due to enlargement of retropharyngeal lymph nodes.
Eventually weak and recumbent
IP of BLV.
IP: 4-5 years
Forms of sporadic bovine leukosis ( the congenital form of disease caused by BLV).
Sporadic bovine leukosis (congenital) has three forms:
Juvenile calf lymphosarcoma
Thymic lymphosarcoma
Cutaneous lymphoma
Post mortem signs of BLV.
LNs and other tissues are infiltrated by neoplastic cells (Abomasum, heart, spleen, intestine, liver, kidney, omasum, lung, uterus).
Lymphosarcoma may appear as yellow-tan, discrete nodular masses or a diffuse tissue infiltrate.
Diffuse: enlarged, pale organ and can be easily misinterpreted as a degenerative change.
Material for diagnosis of BLV. (2)
Blood
Milk
Lab analyses for diagnosis of BLV. (3)
Identification of the agent – culture, PCR
Antibodies – serology
Histology
Tx of Bovine lymphosarcoma
no treatment
Prevention & control of BLV.
Eradication: test-and-slaughter!
Eliminate blood contamination
Colostrum feeding for antibodies
Thorough cleaning and disinfection of used equipment
Dehorning: cautery or other bloodless methods should be used
Change rectal sleeves between cows
Single use, disposable needles (IM)
Fly control
