Viro Final

Front 1

vaccines: PRRS

Back 1

killed/ MLV

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vaccines: EVA

Back 2

killed/ MLV

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Vaccines: Feline Calicivirus

Back 3

fort dodge, booster -- does not prevent carrier status

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vaccines: RHDV

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?

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vaccine: VES

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slaughter

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vaccine" FMDV

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multivalent, inactivated, adjuvant (4-6mo)
mostly killed - mostly import strategy is antigenic comparison
slaughter

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vaccine: PEE

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killed/ MLV

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vaccine: SVD

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no commercial,
inactivated strains
not suitable in countries free

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vaccine: EEE

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inactivated

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vaccine: WEE

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inactivated

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vaccine: VEE

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inactivated

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vaccine: WNV

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kelled, 2 doses, 3-6 weeks apart - annual booster

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vaccine: Japanese encephalitis

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live attenuated (equine/swine), reduce incidence, inactivated (JEVAX)- humans in endemic areas, recomended for travelers

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vaccine: CSF

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doesn't eliminate infection

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vaccine: BVD

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killed/ MLV
doesn't give complete protection
reduces infection
not long lasting - booster
vaccine can be infectoid (preg. cattle --> abortion)

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vaccine: border disease

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none

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vaccine: TGE

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MLV, inactivated, and maternal IgA

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vaccine: PHED

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no vaccine

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vaccine: PED

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no vaccine

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vaccine FECV, FIP

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non core vaccine, not recommended

Felocell FIP (Pfizer, temperature sensitive, intranasal)

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vaccine: CVE

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no treatment

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vaccine: BCE

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killed, MLV

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vaccine: Rabies

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MLV, oral/parental inactivated, oral/parental recombinant, nucleic acid

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vaccine: vesicular stomatitis

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no specific

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vaccine: BEFV

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vaccinate

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vaccine: RVF

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MLV, not approved in US, may cause abortion

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vaccine: Akabane

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inactivated, attenuated, killed
not available in US

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vaccine: NSD

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vaccine for naive animals, experimental

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vaccine: BTV

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serotype specific but adverse effects (fetal malformations, recombinations new strains of virus)

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vaccine: orbivirus

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attenuated live

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vaccine: enteric disease

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vaccine

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- After 7 weeks of age alveolar macrophage becomes more resistant to PRRS infection
-Very few visible post-mortem changes associated with PRRS.
- Majority of the signs relate to secondary infections.
- Histologically: interstitial pneumonia and lack of air spaces.

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PRRS

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PRRS transmission

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direct contact with infected animals (nose to-nose contact--virus present in the respiratory tract and tonsils); airborne; semen in some cases.
 Endemic in farms: continuous or in waves

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 Non-arthropod-borne disease; contagious viral disease of equids of low mortality; outbreaks associated with movement of horses: racetracks & breeding farms

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EVA

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 Clinical signs – incubation period 2 to 13 days (average of 7 days); fever 106o F, depression, anorexia, leucopenia, limb edema (especially hind limbs), edema of the prepuce and scrotum, lacrimation, conjunctivitis, photophobia, periorbital or supraorbital edema, nasal discharge, rhinitis, edema of the ventral body wall, urticaria, stiff gait, ataxia, icterus, dyspnea, or diarrhea may also be seen.
 More severe in very young, very old, debilitated

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EVA

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EVA DDX

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 Differntial diagnosis – equine influenza, equine herpes virus Types1 and 4, equine infectious anemia, african horse sickness, abortions caused by equine viral arteritis must be distinguished from abortions caused by equine herpes virus.

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 Acute disease: kittens 2 to 3 months of age (decline of maternal antibody)
 Large amounts of virus excretion: oronasal secretions
 Persistent infection after recovery: important carriers
 Natural transmission: aerosol, fomites

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feline calicivirus

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CS feline calicivirus

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sneezing, oculonasal discharge, fever, loss of appetite, sores around the mouth, nose, lips and palate, upper respiratory tract disease, arthritis, pulmonary edema and pneumonia.
 Recovered cats remain persistently infected and shed virus from the oropharynx possibly for life.

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 Highly contagious, acute fatal disease in European rabbits: > 2 months
 This disease affects only rabbits of the species Oryctolagus cuniculus.

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RHDV

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CS RHDV

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- Peracute infections – rabbits die suddenly within 12 to 36 hours of its onset.
- Acute infection – dullness, anorexia, congestion of the palpebral conjunctiva, neurologic signs including incordination, excitement, opisthotonos and paddling
- Subaccute infection – similar but milder symptoms, cattarhal enteritis.
- Chronic infection – persistent infections are thought to be asymptomatic.

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 Primary lesion – hepatic necrosis and splenomegaly.
- Liver: pale, with a fine reticular pattern of necrosis outlining each lobule; extensive liver necrosis  diffusely pale, yellow, gray, friable or congested.
- Spleen: black and engorged, rounded edges.
- Kidneys: very dark brown.
- Trachea: hyperemic and contains frothy, bloodstained mucus.
- Lungs: congestion and multifocal hemorrhage.
 Disseminated intravascular coagulation (DIC) is common in the terminal stages of disease, and results in hemorrhages in a variety of organs and tissues
 Hemorrhages are also common in the thymus, and petechiae may be found on the serosal membranes or viscera.
 Infarcts may be seen in most organs.
 High morbidity (30% to 100%), and high mortality (40 to 100%)

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RHDV

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DDX RHDV

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 Differential diagnosis – acute pasteurellosis, atypical myxomatosis, poisoning, heat exhaustion, enterotoxemia due to E. coli or Clostridium perfringens Type E, and other causes of severe septicemia with secondary DIC.

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control RHDV

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 Control – depopulation, disinfection, surveillance and quarantines.

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clinically it resembles FMD and if it occurred a slaughter policy would be applied; arises from waste sea food fed to pigs as garbage or finding its way to pigs from farmed-mink fed sea-food.
 Clinical signs – acute, highly contagious, febrile disease; formation of vescicles on snout, tongue, teats, oral cavity and feet, encephalitis, myocarditis, fever and diarrhea; abortion
 High morbidity; low mortality

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VES

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 Diagnosis – fever with presence of vescicles which rupture in 24-48 hours and form erosions.
 Virus isolation in swine cell cultures, various serological tests (ELISA, CFT) and electron microscopy.

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VES

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DDX VES

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 Differential diagnosis – FMD, vesicular stomatitis, swine vesicular disease

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 Control – herd quarantine, garbage cooking laws and strict slaughter program

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VES

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Picornaviridae

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Aphthovirus (foot and mouth disease), Teschovirus (porcine enterovirus 1), Enterovirus (swine vesicular disease, avian enterovirus, duck hepatitis, porcine enterovirus 2-4)

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 Low mortality; high morbidity
 7 distinct serotypes; no cross-protection; affects cloven-hoofed animals
 Inactivated at pH < 6.5 and > 11.0
 Survives in milk, milk products, bone marrow, lymph glands

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FMDV

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Transmission FMDV

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 Transmission – contact, aerosol (respiratory or oral routes), secretions and excretions from infected animal (milk and semen)

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Profuse salivation with drooling and smacking of lips, lameness (coronary band and interdigital cleft of hooves); snout and oral vesicles, fever and anorexia; incubation period 2 to 14 days

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FMDV

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Path FMDV

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 Pathology – spreads via blood stream to predilection sites in the epithelium of mouth, muzzle, feet and teats and areas of damaged skin
 Primary site of replication and infection: mucosa of respiratory tract (also in lnn.)
 Development of vesicles at predilection sites; rupture of vesicles usually within 48 hours; viremia persists for 5 days.

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PM lesions in FMDV

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 Post mortem lesions – clinically indistinguishable from other vesicular diseases in swine
 Single or multiple vesicles; white area, fluid filled blisters, red erosion, fibrin coating, dry lesions, tiger heart

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FMDV DDX

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 Differential Diagnosis – swine vesicular disease, vesicular exanthema of swine, vesicular stomatitis and bluetongue (samples of vesicular epithelium or vesicular fluid for antigen detection).

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dx FMDV

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 Diagnosis – serology (ELISA or CF test), RT-PCR

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control fmdv

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 Control – reportable in USA, depopulation, vaccine in endemic areas
 Vaccine: multivalent, inactivated, adjuvanted (4 to 6 months protection)

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pigs (Teschen disease or Talfan Disease); 13 serotypes.
 Epidemiology – world wide distribution
 Teschen disease: morbidity (50%); mortality (70-90%)
 Talfan disease: milder form (widely distributed), mortality (6%), resulting in posterior paresis

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PEE

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Tz PEE

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 Transmission – ingestion, aerosol routes, transmammary

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CS PEE

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 Pathogenesis – Virus replicates in intestinal tract and respiratory tract; rapid spread and all ages excrete virus in feces; restricted to CNS and intestines of affected pigs.
 Clinical signs – acute viral encephalomyelitis (Teshen disease), fever, anorexia, vomiting, stiffness of extremities, inability to stand, followed by tremors, nystagmus, convulsions, laryngeal paralysis, facial paralysis.

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PEE DDX

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 Differential diagnosis – pseudorabies, hemagglutinating encephalomyelitis virus of swine, bacterial diseases, intoxication

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 Control – killed and modified live vaccines available
 Teschen disease: reportable disease in many countries

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control of PEE

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Picornaviridae; Genus: Enterovirus
 Difficult to distinguish from foot-and-mouth disease; control measures, eradication costly
 Transmission – fecal-oral route (direct or indirect), ingestion of contaminated meat scraps
 Excretion of virus: nose, mouth, feces
 Clinical signs – very similar to foot and mouth disease; vesicles and erosions on snout, mammary glands, coronary band, interdigital areas

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SVD- zoonotic

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SVD DDX

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 Differential diagnosis – foot-and-mouth disease, vesicular stomatitis, vesicular exanthema of swine, chemical or thermal burns

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SVD in humans

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 SVD in humans – mild influenza-like symptoms, generalized abdominal and muscle pain, aseptic meningitis (one case), no vesicular lesions
 Diagnosis: seroconversion
 Treatment: supportive care

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SVD control

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 Prevention and Control – no vaccine, eradication programs, reportable

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Togaviridae

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enveloped, Icosahedral symmetry, agglutinate chicken erythrocytes
Viral encephalitis – Western equine encephalitis (WEE), Eastern equine encephalitis (EEE), St. Louis encephalitis (SLE), La Crosse encephalitis (LAC), Venezuelan equine encephalitis (VEE), West Nile virus (WNV)

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ZOONOTIC!
 Hosts – horses, pheasants, quail, ostriches, emus, puppies, humans
 Clinical signs (horses) – fever, anorexia, weight loss, depression, CNS signs (wide stance, droopy ears, flaccid lips, hanging head), death in 4 days.

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EEE

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DX EEE

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 Diagnosis – serology (paired serum samples); ELISA, Plaque Reduction Neutralization Assay, HI and CF
 Vaccine does not elicit IgM response
 Treatment is difficult, poor prognosis

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ZOONOTIC! Forage poisoning, cerebrospinal meningitis, corn-stalk disease, harvest disease, sleeping sickness
 Clinical signs (humans) – sudden onset of fever, headache, nausea, vomiting, anorexia, malaise, CNS signs in children (altered mental status, weakness, irritability, stupor, coma)
 Poor prognosis in children
 Diagnosis: virus in CSF, not blood
 Clinical signs (horses) – fever, depression, altered mentation, head pressing, ataxia, dysphagia, progress to paralysis, convulsions, death
 Mortality: 20-50%
 Asymptomatic: blacktail jackrabbit, kangaroo rat, Western gray squirrel, prairie dog
 Diagnosis – serology (paired serum samples), virus isolation from CFS

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WEE

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ZOONOTIC! Peste loca, derrengadera
 Epizootic/epidemic – disease in humans and horses (horses and donkeys act as amplifier); transmission by mosquito species
 Enzootic/endemic – disease in humans; natural reservoir is rodents; transmission mainly by Culex (Melanoconion) species
 Clinical signs (humans) – fever, malaise, dizziness, chills, headaches, anorexia, severe myalgia, arthralgia, nausea, vomiting, abortion (less severe than EEE and WEE)
 Diagnosis – paired sera with rising titer, ELISA IgG or IgM
 Treatment – supportive care, no vaccine available
 Prognosis – variable
 Clinical signs (horses) – fever, anorexia, depression, flaccid lips, droopy eyelids and ears, incoordination, blindness, abortion, death
 Diagnosis – virus isolation, paired sera with rising titer, ELISA (IgG or IgM)
 Treatment – supportive care; vaccine available for horses

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VEE

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ZOONOTIC! Infectious encephalitis of sheep; occurs in spring and summer; transmitted by tick (Ixodes ricinus).
 Clinical signs – prolonged viremia, biphasic fever, cerebral ataxia, tremors, hyper-excitability and paralysis
 Prevention – inactivated vaccine

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louping ill

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ZOONOTIC! Clinical disease of sheep only, parts of sub-Saharan Africa, transmitted by mosquitoes, generalized infection, hepatitis & abortion.
 Clinical signs – fever, depression, hepatitis with jaundice and subcutaneous edema
 Vaccine – combined with Rift Valley fever vaccine

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wesselbron

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WNV

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ZOONOTIC! Infects humans, birds (amplifying host), horses and other mammals; transmitted via mosquitoes (primarily Culex spp.)
 Family: Flaviviridae; Genus: Flavivirus (single stranded RNA)
 Clinical signs (large animals) – ataxia progressing to paresis, fever, horizontal nystagmus, torticollis, recumbency, vocalization, mild to moderate, diffuse, non-suppurative meningoencephalitis
 Clinical signs (horses) – paralysis of lips, facial muscles, or tongue, head tilt, difficulty swallowing, sound sensitive, blindness, drowsiness, flu-like, anorexia, depression, muscle and skin twitching, hyperesthesia, propulsive walking, weakness, ataxia, recumbency, seizures

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ZOONOTIC! Disease mainly of humans; waterfowl (reservoir hosts); pigs (amplifying hosts); wide geographical distribution in Asia; transmitted by mosquitoes.
 Family: Flaviviridae; Genus: Flavivirus (enveloped, single stranded RNA virus)
 Clinical signs (horses) – fever, impaired locomotion, stupor, teeth grinding, blindness, and coma; death is rare
 Clinical signs (pigs) – exposure early in pregnancy more harmful, birth of stillborn or mummified fetuses; neurological signs and death (piglets); infertility and swollen testicles (boars).

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japanese encephalitis

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JApanese encephalitis DDX

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 Differential diagnosis (horses) – WEE, EEE, other viral encephalitides, Hendra, rabies, neurotoxins, toxic encephalitis
 Differential diagnosis (swine) – myxovirus-parainfluenza 1, coronavirus, menangle virus, porcine parvovirus, PRRS
 Diagnosis – Viral isolation (blood, spinal cord, brain, CSF), rise in titer, virus neutralization, HI, IF, CF, ELISA, cross reactivity of Flaviviruses
 Treatment – no effective treatment, supportive care

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hog cholera, peste du porc, colera porcina, virusschweinepest
 Family: Flaviviridae; Genus: Pestivirus (lipid-enveloped RNA virus)
 Transmission – ingestion (contaminated garbage or meat products), direct contact, fomites, aerosol, semen, vectors.
 Clinical signs – acute disease; Huddling, dullness, high fever (105oF), anorexia, erythema, cyanosis, petechiae, staggering, weakness, convulsions, poor reproductive (performance, abortions, stillbirths, deformities)

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CSF

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DDX/ DX / TX of CSF

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 Differential diagnosis – porcine reproductive and respiratory syndrome (PRRS), porcine circovirus associated disease, salmonellosis, erysipelas, leptospirosis, Aujeszky’s disease (pseudorabies), African swine fever
 Diagnosis – clinical signs (septicemia, high fever, purple discoloration of the skin or ears), detect virus, antigens, nucleic acids, (tissue samples--tonsils, spleen, kidneys, distal ileum, blood), ELISA, direct immunofluorescence, virus neutralization
 Treatment – no treatment should be attempted; actions needed will be directed by State and/or federal animal health authorities

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primarily cattle, but can cause clinical signs in pigs, sheep, goats, alpacas, deer, reindeer, and bison.
 Three forms of disease:
 Acute form: BVD
 Protracted form: Mucosal disease (arising from Persistent infection)
 Persistent infectious form:
- One of the main reservoirs for the virus (shed several billion virions a day)
- Contact with a PI animal: more of a risk for transmitting virus and causing infection than an acutely infected animal

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BVD

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pathogenesis of BVD

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 ncp BVDV: wider distribution throughout the host than cp BVDV.
 ncp BVDV induces humoral response whereas cp BVDV induces cell-mediated immune response.
 Low Virulent Strains:
- Primary replication: tonsils and nasal mucosa & spread to lymph nodes, spleen and thymus; highest number of antigen: six days post-infection.
 High Virulent Strains:
- Primary replication: tonsils and lymph nodes--much more antigen present and spreads much faster; can also spread to T-cell-dependent areas and even bone marrow. Will eventually spread to almost all organs
 Persistent viremia: produced if infected with ncp-BVDV due to its ability to inhibit interferon 1.
- Inhibition of interferon 1 decreases cell’s ability to fight the virus.
 BVDV 1 strain (classical isolates): used in vaccines and diagnostic tests
 BVDV 2 strain (atypical isolates): increased virulence and tissue distribution; associated with thrombocytopenia and hemorrhagic syndrome.

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transmission of BVD

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contaminated semen, transplacental, embryo transfer, modified live vaccine (infects fetus of pregnant cow), fomites, vector borne (horse flies, stable flies, head flies, face flies), environment (shed in feces).