VIRAL DISEASE OF HORSE WHICH HAS MAINLY DUNKOP AND DIKKOP FORM
SLIDE IS PREPARED BY A VET STUDENT
AHS IS A VERY FATAL DISEASE OF EQUINES ALL OVER THE WORLD.
TREATMENT IF NOT GIVEN AT PROPER TIME, DEATH RATE IS VERY HIGH
2. INTRODUCTION
• African horse sickness is a devastating disease that causes great suffering
and many fatalities amongst horses in sub-Saharan Africa.
• African horse sickness is a highly infectious and deadly disease caused by
African horse sickness virus.
• It commonly affects horses, mules, and donkeys.
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3. AETIOLOGY
• Reoviridae---Orbivirus—AHSV.
• Nonenveloped, spherical virions; 80 nm in diameter.
• Virions possess 3 concentric capsid layers, all icosahedral: outer, middle, and inner
capsids.
• Genome consists of dsRNA, divided into 10-12 segments.
• Cytoplasmic replication, with formation of large intracytoplasmic perinuclear
inclusion bodies.
• Synonym- Dunkop and Dikkop, Equine Plague
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4. SUSCEPTIBLE HOST
• The common hosts of this disease are horses, mules, donkeys, and zebras.
• However, elephants, camels, and dogs can be infected, as well, but often
show no signs of the disease.
• Dogs usually contract the disease by eating infected horse meat, although a
recent report has been made of the disease occurring in dogs with no known
horse-meat ingestion.
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5. TRANSMISSION
• The most important vector for AHS in endemic areas is the biting
midge Culicoides imicola, which prefers warm, humid conditions.
• Larvae do not carry the virus, and long, cold winters are sufficient to break
epidemics in nonendemic areas.
• Not zoonotic
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6. INCUBATION PERIOD
• Incubation period is usually 7–14 days, but may be as short as 2 days.
• For the purposes of the OIE Terrestrial Code, the infective period for AHSV
shall be 40 days for domestic horses.
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7. PATHOGENESIS
• Bite of insect takes virus into subcutaneous tissue.
• Then migration to nearest lymph node and then to systemic circulation.
• Mainly deposits on heart and lungs along with systemic deposition.
• Then the virus localised in places will produce many lesions .
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8. CLINICAL SIGNS
There are four principal manifestations of disease.
• In the majority of cases, the subclinical cardiac form is suddenly followed by
marked dyspnea and other signs typical of the pulmonary form
• A nervous form may occur, though it is rare .
• Animals that recover from AHS develop good immunity to the infecting serotype
and partial immunity to other serotypes.
• Morbidity and mortality vary with the species of animal, previous immunity and the
form of the disease .
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9. 1. Subclinical form (Horse sickness fever)
Fever (40–40.5°C/104°F–105°F) .
Mild form; general malaise for 1–2 days.
Very rarely results in death.
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10. 2. Subacute or cardiac form/Dikkop Form
• Mainly called as Dikkop Form.
• Fever (39–41°C/102–106°F)
• Swelling of the supraorbital fossa, eyelids, facial tissues, neck, thorax, brisket
and shoulders
• Mortality usually 50% or higher; death usually within 1 week
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11. 3. Acute respiratory or pulmonary form/Dunkop Form
• Mainly called as Dunkop Form.
• Fever (40–41°C/104–106°F) .
• Dyspnea, spasmodic coughing, dilated nostrils with frothy fluid oozing out .
• Redness of conjunctivae .
• Nearly always fatal; death from anoxia within 1 week .
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12. 4. Mixed form (cardiac and pulmonary)
• Both organs get damaged.
• Occurs frequently.
• Pulmonary signs of a mild nature that do not progress, edematous swellings
and effusions .
• Mortality: about 70–80% or greater .
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13. Lesions
Respiratory
• interlobular edema of the lungs
• hydropericardium, pleural effusion
• edema of thoracic lymph nodes
• petechial haemorrhages in pericardium
• mucosa and serosa of small and large intestines
may exhibit hyperemia and petechial hemorrhages.
Cardiac
• subcutaneous and intramuscular gelatinous edema.
• epicardial and endocardial ecchymoses;
myocarditis .
• haemorrhagic gastritis .
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29. DIAGNOSIS
• Virus isolation
• Cell cultures, such as baby hamster kidney-21 (BHK-21), monkey stable (MS) or African green monkey kidney (Vero) or insect cells (KC)
• Intravenously in embryonated eggs
• Intracerebrally in newborn mice
• Virus identification
• Enzyme-linked immunosorbent assay (ELISA) – rapid detection of AHSV antigen in blood, spleen and supernatant from cell culture
• Virus neutralization (VN) – until recently the ‘gold standard’ for typing as well as identifying virus isolates, but takes 5 days RT-PCR is a highly sensitive technique
that allows the detection of a very low number of copies of RNA molecules Real-time PCR – detects all 9 serotypes
• AHSV typing
• VN test has been the method of choice for typing as well as the ‘gold’ standard test for identifying AHSV’s isolated from the field using type specific antisera
Development of a type-specific gel-based RT-PCR and real-time RT-PCR using hybridization probes for identification and differentiation AHSV genotypes provides a
rapid typing method for AHSV in tissue samples and blood.
• There is a good correlation between the results obtained with the type-specific RT-PCR and the VN test, however, the sensitivity of these assays is lower than that
obtained with the diagnostic group-specific real-time RT-PCR Typing of nine AHSV types has also been performed with probes developed from a set of cloned full
length VP2 genes
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30. PREVENTION AND CONTROL
• In endemic areas horses are vaccinated using attenuated live polyvalent
vaccines.
• Immunity is serotype specific.
• Horses should be protected from flies during disease outbreaks.
• U.S.A: A sixty-day quarantine on all horses imported from Africa, Asia, and
the Mediterranean.
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