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Home \ INFEQUUS \ Equine rhinitis virus



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Differential diagnosis of infectious diseases of equidae

Equine rhinitis virus disease information
Disease
Equine rhinitis virus

Synonyms
Erbovirus A

Agents
Equine rhinitis B virus
 Acronym: ERBV
 Type: Virus
 Family: Picornaviridae
 Gender: Erbovirus
Equine rhinitis A virus
 Acronym: ERAV
 Type: Virus
 Family: Picornaviridae
 Gender: Aphtovirus

Clinical signs
Fever Cough Anorexia Bronchitis Pharyngitis Nasal discharge Lymphadenopathy Immunosuppression Hyperfibrinogenemia Loss of performance Oedema in the limbs

Equine rhinitis virus

Etiology

Within the Picornaviridae family there are twospecies that affect equids: the equine rhinitis A virus and the equine rhinitisB virus. These viruses, discovered in the 60s and 70s, were initially includedin the same genus called Rhinovirus,differentiating four groups according to their characteristics: equine rhinovirus-1,equine rhinovirus-2, equine rhinovirus-3 and acid-stable equine picornavirus. Laterthe equine rhinovirus type 1 was renamed Equine Rhinitis A Virus (ERAV) beingclassified within the genus Aphthovirus,the other three were included in a new genus called Erbovirus, considering three serotypes of Equine Rhinitis B Virus(ERBV-1, ERBV -2 and ERBV-3). They are viruses with single-stranded RNA and theviral particles have a size of about 30 nm in diameter.


Epidemiology

Seroprevalencesclose to 100% have been described in adult horses for both viruses worldwide.The serotypes ERBV-1 and ERBV-2 have been isolated worldwide, while theserotype ERBV-3 only in Australia, Japan and the United Kingdom. The primaryinfection in the case of ERAV usually occurs between 3 and 9 months of age,while in ERBV it occurs between 4 and 6 months. The transmission of ERAV occursby inhalation of aerosols from respiratory secretions and urine. It is thoughtthat the infection by ERBV is produced by direct or indirect contact with nasalsecretions or aerosols.


Pathogeny

ERAV can be isolated from oral and nasopharyngeal secretions, plasma and urine. The main route of excretion seems to be urine, through which large amounts of the virus are secreted for long periods while excretion through nasopharyngeal secretions and the presence in plasma descends between one and two weeks after infection when neutralizing antibodies develop. ERAV replicates in the upper respiratory tract producing a process of viremia later, colonizing the urinary system where it is established persistently.
/b>The place where ERBV replicates is unknown, supposing that it could vary depending on the phenotype since other acid-stable picornaviruses do so in the gastrointestinal system. In addition to producing respiratory signs ERBV could cause modulation of the immune response and consequently an increase in the duration or severity of infections caused by other pathogens. Persistent infection in this virus has also been documented for periods of up to two years.


Clinical signs

The signs produced by ERAV are variable, producing fever (1 to 3 days), anorexia, serous to mucopurulent nasal discharge, pharyngitis, bronchitis, cough and lymphadenopathy. Other signs associated with systemic infection are poor performance, temporary immunosuppression and elevated levels of plasma fibrinogen.
ERBV infection can cause fever, serous nasal discharge, anorexia, lower limbs oedema and inflammation and pain of lymph nodes of the head and neck.


Diagnosis

The diagnosis can be carried out directly demonstrating the presence of the virus through viral isolation or detection of viral RNA by RT-PCR from nasopharyngeal swabs or urine in the case of ERAV or indirectly detecting increased specific antibodies against these viruses.


Treatment

There is no specific antiviral therapy and the treatment must be symptomatic.


Prevention and control

There is only one vaccine against ERAV with a conditional license in the United States, and no other vaccine against ERAV or ERBV has been commercially developed.


Public Health Considerations

There is evidence of infection in humans by ERAV both naturally and experimentally. The infection could be acquired by direct contact with infected horses, although it would not produce clinical signs or transmission between humans.


References