Rhabdoviridae

General Characteristics

•Members of the family Rhabdoviridae (Greek rhabdos ,rod) have characteristic rod shapes.

•Viruses in this family possess a

  Ø     linear

  Ø     non - segmented

  Ø     single - stranded RNA genome of negative polarity encased in a ribonucleoprotein complex.

•Rhabdoviruses of vertebrates are bullet - shaped or cone - shaped while those infecting plants are generally bacilliform.

•Replication occurs in the cytoplasm (with the exception of nucleorhabdoviruses). Newly synthesized nucleocapsids acquire envelopes from the plasma membrane as virions bud from the cell.

•They are rapidly inactivated by

  Ø    heating at 56 ° C

  Ø    treatment with lipid solvents

  Ø    exposure to UV light.

•Virions are stable in the pH range 5 to 10.

•Average size of these viruses is about 100nm.

The family Rhabdoviridae comprises six genera:

1.Vesiculovirus,

2.Lyssavirus,

3.Ephemerovirus,

4.Cytorhabdovirus,

5.Novirhabdovirus

6.Nucleorhabdovirus

Rhabdoviruses usually contain five major proteins:

1. A large RNA - dependent RNA polymerase (L),

2.A surface glycoprotein (G),

3.A nucleoprotein (N),

4.A protein component of the viral polymerase (P)

5.A matrix protein (M).

Role of G protein

The G protein forms the surface peplomers which

interact with host cell receptors, facilitating endocytosis

of the virion.

In addition, the G protein induces virus - neutralizing antibodies and cell – mediated immunity.

Rabies

The best known and most important member of the Rhabdoviridae is rabies virus, a Lyssavirus (Greek Alyssa , rage or fury).

This viral infection, which affects the central nervous system of most mammals including humans, is invariably fatal.

•Most clinical cases are due to infection with rabies virus (genotype 1).

•Classical rabies caused by genotype 1 lyssavirus is endemic on continental land masses with the exception of Australia and Antarctica.

Epidemiology

Two epidemiologically important infectious cycles are

Recognized.

1.urban rabies in dogs  

2.sylvatic rabies in wildlife.

•More than 95% of human cases are the result of bites from rabid dogs.

•Although virus may be transmitted through scratching and licking, transmission usually occurs through bites.

•Infected animals may excrete virus in their saliva for some time before the onset of clinical signs.

Pathogenesis

 

•Following introduction into the tissues, virus enters peripheral nerve endings. There may be limited replication locally in myocytes or other tissue cells.

•The virus is transported to the central nervous system by retrograde axoplasmic flow and becomes widely disseminated in nervous tissue by intra - axonal spread.

•Although rabies viral antigens are highly immunogenic, immune detection is delayed because intracellular transport prevents contact with the cells of the immune system in the early stages of infection.

•Clinical signs develop following neuronal damage caused by viral replication.

•Virus spreads centrifugally within nerve cell processes and is released at axon terminals where it infects many non – nervous tissues including the salivary glands.

Clinical signs

•The incubation period  ( Normally 3 to 8 weeks ), which is highly variable and can be of many months duration, is influenced by various factors including

  Ø  host species

  Ø  virus strain

  Ø  The quantity of virus in the inoculum

  Ø  The site of introduction of the virus.

•The clinical course in domestic carnivores, which usually lasts for days, may encompass prodromal, furious (excitative) and dumb (paralytic) phases.

•In the prodromal phase, affected animals are often confused and disorientated; wild animals may lose their natural fear of humans.

•The furious phase is characterized by an increase in aggressiveness and hyper excitability, and there is a tendency to bite at inanimate objects and at other animals. Affected animals may roam over long distances.

•In dumb rabies, muscle weakness, difficulty in swallowing, profuse salivation and dropping of the jaw are the usual features.

Diagnosis

•History

•Signs and symptoms

•Clinical examination

•Ante mortem diagnostic tests for rabies are not generally used except in humans where saliva is examined by PCR.

•Rabies virus is particularly abundant in Ammon ’ s Horn of the hippocampus, cerebrum, cerebellum and medulla.

•The preferred method of diagnosis is the direct fluorescent antibody test (FAT) on acetone – fixed brain tissue smears.

•CSF (cerebrospinal fluid)analysis.

•Negri bodies

                Negri bodies are eosinophilic, sharply outlined inclusion bodies found in the cytoplasm of nerve cells containing the virus of rabies.

They consist of ribonucleic protein produced by the viruses

Control

•Urban rabies can be effectively controlled by vaccination and restriction of dog and cat movement and by the elimination of stray animals.

•Commercial vaccines available for the immunization of domestic carnivores by parenteral inoculation contain inactivated virus (genotype 1) and are potent and safe.

Bovine ephemeral fever

•This arthropod - borne viral disease of cattle and water buffalo occurs in tropical and subtropical regions of Africa, Asia and Australia.

•The virus causes subclinical infection in many other ruminant species including Cape buffalo, wildebeest, waterbuck and deer.

Clinical Signs

•Fever usually lasting only 1-2 days.

•Disease tends to be severe in

  Ø   well - fed animals

  Ø   high - yielding dairy cows.

•Affected animals become

  Ø   Depressed

  Ø   Anorexic

  Ø   lame

  Ø   constipated.

•Incubation period is typically 3 to 5 days.

•Milk production drops dramatically.

•Muscle stiffness and ruminal stasis may develop.

•Pregnant animals may abort.

•Recumbency may be accompanied by salivation and ocular and nasal discharge.

Diagnosis

Diagnosis of bovine ephemeral fever is usually based

on clinical signs. Neutrophilia, increased plasma fi brinogen and

decreased plasma calcium levels are commonly

present.

Treatment

•The disease is of short duration and affected animals usually recover after a few days.

•Anti - inflammatory drugs such as phenylbutazone, flunixin meglumine and ketoprofen have proved useful for treatment.

•Intravenous or subcutaneous administration of calcium borogluconate is recommended.

Control

•Vector control is usually impractical in endemic areas.

•Control is based on the use of vaccines, both inactivated and attenuated.