Week 12

• Equine Infectious Anemia Virus (swamp virus)


  Lentivirus

  Peracute or acute/chronic disease

  Inapparent, Notifiable
• Equine Infectious Anemia Virus transmission

  Blood - instruments or biting insets

  In all secretions - veneral (virus can pass through semen), in utero, milk/colostrum
• Equine Infectious Anemia Virus pathogenesis

  1. Initially infections monocytes (cannot replicate) -> replicates in macrophages in tissues
  2. Spreads to lymphocytes
  3. in circulatory system, adsorbs onto surface of RBCs (acting as antigens)
  4. Antibodies mediate phagocytosis and complement mediated lysis of RBCs
• Equine Infectious Anemia Virus clinical signs

  Anemia

  Thrombocytopenia (petechial hemorrhages, edema)

  lethargy, weight loss, enlarged spleen

  Depression ,decreased athletic performance

  Death (rare in acute cases)
• Equine Infectious Anemia Virus diagnostic tests

  Agar gel immunodiffusion

  ELISA kit (replaced AGID)

  Immunoblot

  Complement ELIsA

  Horses imported to US and Canada may require negative test certificate
• Rhabdoviridae has 4 genera of human and animal pathogens - Lyssavirus, Vesiculovirus, Ephemerovirus, Novirhabdovirus
• Lyssavirus

  Causes rabies-like disease in animals and humans (apart from true rabies caused by rabies virus)

  Bats are potential reservoirs

  Rabies virus

  Mokola virus, Lago bat virus, Duvenhage virus, Europena bat lyssavirus 1 and 2, Australian bat lyssavirus
• Vesiculovirus

  Vesicular stomatitis Indiana virus (US)

  Vesicular stomatitis New Jersey virus (US)

  Vesicular stomatitis Alagoas virus (Trinidada and Brazil)

  Vesicular stomatitis Cocal virus (Brazil)

  Spring viremia carp virus
• Novirhabdovirus

  Infectious hematopoietic necrosis virus

  Viral hemorrhagic septicemia virus
• Rhabdoviridae virion properties

  Single stranded, linear, negative sense RNA

  Enveloped

  Rod or cone shaped

  Relatively stable in the environment - can withstand alkaline pH, senetitive to UV radiation from the sun, detergent based disinfectants and iodine containing solutions, oxidizing agents, acids, aldehydes
• Rabies virus

  Infects all mammals and can result in death

  Found in all parts of the world (except Japan, New Zealand, and some Caribbean islands)

  Most rabies caused by rabid dog bites
• Rabies virus reservoirs

  Silver-haired bats in many parts of the world

  Vampire bats transmitted to cats in Central and South America
• Rabies virus urban cycle

  Dogs are reservoirs

  Predominate in areas of Africa, Asia, and Central and South America

  Can present spontaneously with the urban cycle in some parts of the world
• Rabies virus sylvatic cycle

  Virs circulates in animals in the wild

  Predominant cycle in Northern Hemisphere
• Rabies virus clinical features

  Transmission - bites from rabid animals

  Disease is similar in most species

  Incubation period - 14-90 days (even years)
• Clinical phases of rabies

  Prodromal phase (1-3 days) - aggressiveness in tame animals, day time activities in nocturnal animals, no fear of humans in wild animals, abnormalities in appetite

  Excitative phase - severe agitation and aggressivement, animal often bites any material, rabid dogs may develop typical high barking sound

  Paralytic phase - characteristized by the inability to swallow (hydrophobia, excessive salivation), paralysis beginning in the hind limbs -> complete paralysis -> death
• Rabies virus pathogenesis

  1. Replicates in muscle tissue
  2. Accesses peripheral nerves through sensory or motor nerves (binds to acetylcholine receptor at neuromuscular junction)
  3. Moves to infect CNS -> neuronal dysfunction
  4. Reached limbic system and replicates rapidly -> fury phase (seen clinically)
  5. Reaches other organs, mostly salivary glands late in the course of infection
  6. Secreted in salivary gland during fury stage of disease
• Negri bodies are diagnostic of rabies

  Eosinophilic intracytoplasmic inclusion bodies

  In neurons

  Only typical finding during histopathology
• Rabies virus diagnosis

  Tissue from at least two locations in the brain (brain stem, cerebellum, presence of negri bodies)

  Demonstration of rabies viral antigen, nucleic acid or viable virus

  Diagnosis performed only in reference laboratories (fluorescent antibody test, immunohistochemistry, ELISA)

  Detection of rabies virus after cell culture inoculation

  Molecular techniques (rtPCR)
• Rabies control

  Vaccines are available

  Rabies free countries - dogs/cats quarantined before entry into country

  Control programs in places where rabies is enzootic
• Dogs, cats, ferrets for postexposure rabies prophylaxis

  Healthy and availalbe for 10 day observations - persons should not be given vaccination unless animal develops clinical signs of rabies

  Rabid or suspected rabid - immediately vaccinate

  Unknown - consult public health officials
• Raccoons, skunks, foxes, and most other wild carnivores; bats


  Regarded as rabid unless animal is proven negative by laboratory test

  Consider immediate vaccination
• Livestock, horses, rodents, rabbits and hares, and other mammals 


  Consider individually

  Consult public health officials

  Bites almost never require rabies postexposure prophylaxis
• Vesiculovirus

  Viruses of horses, cattle, swine, and humans; some have been isolated from fish (eels, carp, perch, pike, salmonids, flounders

  Causes vesicular stomatitis

  Notifiable

  Disease caused by antigenically related but distinct viruses
• Vesiculovirus clinical features

  Incubation period: 1-5 days

  Excessive salivation and fever is the first sign in cattle and horse

  Lameness = first sign in swime

  Vesicles: tongue(most pronounced in horses), oral mucosa, teats, coronary bands (cattle and swine)
• Vesiculovirus pathogenesis

  Virus enters through mucosal or skin abrasions (bites by arthropods or bruises from roughage)

  Viremia does not occur in many animals apart from swine

  Virus replicates in intraepithelium of mucoase and skin leading to edema and vesicles filled with fluid
• Vesiculovirus epidemiology

  Transmission - biting insets (sand flies in tropics and subtropics; black flies, houseflies, mosquitos)

  Virus stable for many days in the environment (milking machine parts, water troughs, soil and vegetation)

  In tropical and subtropical sountries (epizootic appear every 2-3 years)

  New Jersey and Indiana viruses are most common in North America
• Vesiculovirus diagnosis

  Clinically indistinguishable from other vesicular disease of swine and cattle

  Vesicular lesions in horses are only characteristic of vesicular stomatitis virus infections

  Viruse can be recovered from vesicular fluid or tissue scrapings from lesions

  Virus isolation and rtPCR are methods of choice

  Only reference laboratories can do diagnostic testing
• Picornaviridae

  Aphtovirus - Foot and mouth disease

  Enterovirus - Swine vesicular disease virus

  Teschovirus - Porcine teschovirus 1-11

  Cardiovirus - Encephalomyocarditis virus

  Erbovirus, Kobuvirus, Hepatovirus, Parechovirus
• Picornoviridae virion properties

  Non-enveloped, single-stranded, positive sense RNA Viruses

  Icosahedral symmetry

  Genomic RNA is infections

  Stable in mucus and feces, can withstand strong sunlight, unstable in aerosols

  High humidity favors survival for several hours

  Sodium carbonate is an effect disinfectant
• Foot and mouth disease virus 


  Picornoviridae, Aphthovirus

  7 distinct serotypes, not cross protective

  Notifiable disease

  Inactivated at pH below 6.5 and above 11

  Survives in milk, milk products, bone marrow

  Disease of cloven-hoofed animals, vesicular disease
• Foot and mouth disease virus clinical signs

  Incubation period: 2-12 days

  Early clinical signs include fever, excessive salivation, and nasal discharge (cattle)

  Lesions, initially vesicles, on the buccal area and in buccal cavity (snout in pigs)

  Vesicles on the coronary bands and interdigital space

  Lesions on teats -> decreased milk production

  Abortion, death in young animals

  Recover in two weeks unless secondary infections arise
• Foot and mouth disease virus clinical signs in sheep and goats

  Mild, if any - fever, oral lesions, lameness

  Make recognition of infection and prevention of spread difficult
• Foot and mouth disease virus causes major socio-economic losses due to loss of livestock production and limitation of international trade in livestock and animal products
• Foot and mouth disease virus morbidity and mortality

  Morbidity 100% in susceptible animal population

  Mortality less than 1% - higher in young animals infected with highly virulent virus strains, animals generally destroyed to prevent spread
• Foot and mouth disease virus transmission

  Respiratory aerosols - mild temperatures and high humidity, survives 1-2 days in human respiratory tract

  Direct contact - ingestion of infected animal parts, artifical insemination, biologicals, hormones

  Indirect contact via fomites
• Foot and mouth disease virus transmission to humans

  Very rare, develop mild clinical signs

  Ingestion of unprocessed milk of dairy products from infected animals

  Type O, C, rarely A

  Acts as a transmitter to animals - harbors virus in respiratory tract for 1-2 days; contaminated boots, clothing, vehicles; spread to susceptible animals
• Foot and mouth disease virus clinical diagnosis

  Clinically, vesicular disease are indistinguishable

  Salivation, lameness with vesicles requires further testing

  Tranquilization may be necessary to complete examination (pigs)
• Foot and mouth disease virus sample collection for testing

  Before collecting or sending any samples, the proper authorities should be contacted

  Notify authorities and wait for instructions before collecting samples

  Samples should only be sent under secure conditions and to authorized laboratories to prevent the spread of the disease
• Foot and mouth disease virus laboratory diagnosis

  Virus isolation and detection (vesicular fluid)

  Antigen or nucleic acid detection

  ELISA and virus neutralization