African Horse Sickness 2024 PDF
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Uploaded by CelebratedQuasar
University of Ibadan
2024
O.O. Akinniyi
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This presentation discusses African horse sickness, covering definition, aetiology, epidemiology, transmission, pathophysiology, clinical presentation, diagnosis, treatment, and prevention and control. It appears to be an educational presentation from the University of Ibadan's Department of Veterinary Medicine. It focuses on the veterinary aspect of the disease.
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COURSE: EQUINE MEDICINE(VMD VI) Topic: African horse sickness DR. O.O. AKINNIYI University of Ibadan, Department of Veterinary Medicine 1 DEFINITION The disease is infectious bu...
COURSE: EQUINE MEDICINE(VMD VI) Topic: African horse sickness DR. O.O. AKINNIYI University of Ibadan, Department of Veterinary Medicine 1 DEFINITION The disease is infectious but non-contagious, and it kills a significant percentage of vulnerable hosts. The World Organization for Animal Health (OIE) has classified it as a notifiable viral disease due to its severity and the potential for rapid worldwide spread. Endemic in Sub-Saharan Africa African horse sickness by Dr. O.O Akinniyi 2 AETIOLOGY The African horse sickness virus (AHSV) causes African horse sickness (AHS). The AHSV is a double-stranded, nonenveloped RNA virus from the genus Orbivirus (family Reoviridae), and it resembles other Orbiviruses such as Epizootic haemorrhagic disease virus (EHDV), Bluetongue virus (BTV), and Equine encephalosis virus (EEV). It contains seven structural proteins (VP1-7) and three non-structural proteins (NS1-3). So far, 9 serotypes have been discovered. The majority are found only in Sub-Saharan Africa. Outside of Sub-Saharan Africa, Types 4 and 9 are responsible for the majority of epidemics. African horse sickness by Dr. O.O Akinniyi 3 EPIDERMIOLOGY The disease most severely affects ponies, horses, and European donkeys; mules are slightly less afflicted, and zebras and African donkeys are more resistant and often show milder symptoms, but can still be affected. Dogs are the only non-equine animal species known to get AHS, with data indicating that the route of infection may, but not necessarily, be through ingestion of infected meat. There is no preference for age or gender. There are no breed dispositions. In the natural setting, it is not a zoonotic disease. AHS is thought to be enzootic in central and eastern Africa, with yearly incursions of the disease into southern Africa. Epidemics have been documented and proven in North Africa, the Middle East, Afghanistan, Pakistan, Turkey, India, Portugal, and Spain. To date, the virus has never been documented in North America. African horse sickness by Dr. O.O Akinniyi 4 TRANSMISSION Most of it is transmitted by female Culicoides midges (Culicoides spp.) during a blood meal, which they need to reproduce. Other blood-sucking arthropods, such as mosquitoes, Stomoxys and Tabanus, which transmit a variety of blood-borne infections, could serve as possible vectors. Midges get their infection from the blood of infected donkeys, horses, mules, and zebras. Transmission of the virus to areas where it does not normally reside happens through the movement of infected animals, such as horses and zebras, as well as the transport of midges by wind or aircraft. The risk of mechanical transmission of the virus via infected needles and surgical instruments should be considered. African horse sickness by Dr. O.O Akinniyi 5 PATHOPHYSIOLOGY a) Infection and Primary Viremia: When an infected midge bites a horse, the virus is introduced into the skin. The virus initially replicates in local lymph nodes. This leads to primary viremia, where the virus enters the bloodstream for the first time. Primary viremia is usually short-lived and may not cause noticeable clinical signs. b) Secondary Viremia: Following primary viremia, the virus infects and replicates in target organs, particularly the lungs, spleen, and lymphoid tissues. This leads to a more pronounced and prolonged secondary viremia. Secondary viremia is associated with the onset of clinical signs and is when the virus can be most easily detected in blood samples. c) Endothelial Cell Damage: The virus has a particular tropism for endothelial cells lining blood vessels. Infection of these cells leads to increased vascular permeability and fluid leakage. This results in the characteristic edema seen in affected tissues, particularly the lungs. African horse sickness by Dr. O.O Akinniyi 6 PATHOPHYSIOLOGY d) Pulmonary Edema: The lungs are a primary target organ for AHSV. Severe damage to pulmonary endothelial cells leads to pulmonary edema. This causes respiratory distress and can lead to the "dunkop" or pulmonary form of AHS. e) Cardiovascular Effects: The virus also affects the heart and other blood vessels throughout the body. This can lead to myocarditis (inflammation of the heart muscle) and circulatory failure. These effects contribute to the "dikkop" or cardiac form of AHS. f) Coagulation Abnormalities: AHSV infection can cause disseminated intravascular coagulation (DIC). This leads to the formation of microthrombi (small blood clots) and bleeding tendencies. g) Immune Response: The host's immune response, while eventually protective, can contribute to tissue damage. Cytokine release and inflammatory responses can exacerbate the clinical signs. African horse sickness by Dr. O.O Akinniyi 7 CLINICAL PRESENTATION Natural infections have an incubation period of 5 to 7 days. There are four clinical forms of the disease: Pulmonary ("dunkop"): per acute form Cardiac ("dikkop"): Subacute form Mixed: the most common type Horse sickness fever: mildest form All forms have an intermittent fever of 40° to 41° C (105-106° F). African horse sickness by Dr. O.O Akinniyi 8 CLINICAL PRESENTATION Pulmonary ("dunkop"): per acute form The peracute type of AHS arises in naive animals and is the most severe form of AHS, with a death rate of 95%. Fever is accompanied by laboured breathing, acute coughing paroxysms, and a profuse nasal discharge of yellowish serous fluid and froth. Once foam appears In the nostrils, death follows rapidly. Profuse perspiration, severe weakness, and a stumbling stride lead to recumbency. Death usually occurs after a total course of 4 to 5 days. In surviving animals, severe respiratory distress lasts for several weeks. This is the form of AHS that naturally arises in dogs. African horse sickness by Dr. O.O Akinniyi 9 CLINICAL PRESENTATION Cardiac ("dikkop"): Subacute form The cardiac form of the disease is typically characterised by fever, oedema of the head, neck, and chest, supraorbital fossae, petechial haemorrhages in the eyes, ecchymotic haemorrhages on the tongue, and colic. In these cases, the mortality of infected animals may exceed 50%. African horse sickness by Dr. O.O Akinniyi 10 CLINICAL PRESENTATION Mixed: Most common form The mixed form is the most prevalent form of the disease, and it is a combination of the cardiac and pulmonary forms. Mild pulmonary symptoms are followed by oedema and heart failure in the first place. In the second, oedema and subclinical cardiac dysfunction are followed by dyspnoea, nasal discharge, and death. Death occurs frequently within three to six days. African horse sickness by Dr. O.O Akinniyi 11 CLINICAL PRESENTATION Horse sickness fever: the mildest form This is the mildest form of AHS and the form that most commonly affects donkeys and zebras, with an incubation period of 5 to 9 days. The temperature gradually rises to 104° F over four days before returning to normal. Mild clinical signs of the cardiac and pulmonary forms may occur. African horse sickness by Dr. O.O Akinniyi 12 DIAGNOSIS Clinical signs. Haematology – leucopenia, thrombocytopenia, elevated haematocrit. Serology. Virus isolation, antigen capture ELISA, PCR. Necropsy. African horse sickness by Dr. O.O Akinniyi 13 TREATMENT African horse sickness does not have a specific treatment. Supportive care and treatment of disease complications should be offered. Nonsteroidal anti-inflammatory drugs (NSAIDs) for pain relief and fever reduction, antimicrobials to combat secondary bacterial infection, and corticosteroids to help stabilise cell membranes and protect vascular membrane integrity have all been used as supportive therapy. It is critical that all affected horses rest because exertion can result in death. This rest period should last at least one month after the clinical signs have stopped. There is a 5% likelihood of survival for the pulmonary or peracute form; a 50% chance of survival for the cardiac or subacute form; and a 30% chance of survival for the mixed form. African horse sickness by Dr. O.O Akinniyi 14 PREVENTION AND CONTROL Vaccination Senegal and South Africa are the primary producers of AHS vaccines Administered Subcutaneously. Once a year in endemic areas. There is cross protection between serotype 6 (included in the vaccine) and serotype 9 There is cross protection between serotype 8 (included in the vaccine) and serotype 5 South Africa vaccine: course consists of two doses: one with serotypes 1, 3, and 4, followed by a second dose with serotypes 2, 6, 7, and 8 provided three weeks later (serotypes 5 and 9 are absent in the two doses). Repeated yearly. Senegal vaccine: The Senegalese vaccine contains all 7 serotypes (1, 2, 3, 4, 6, 7, and 8) in a single dose. Unlike the two-dose system with separate serotype combinations, this vaccine is typically administered as a single dose containing all 7 serotypes. Annual boosters are usually given as a single dose, again containing all 7 serotypes.. African horse sickness by Dr. O.O Akinniyi 15 PREVENTION AND CONTROL Vector control Stabling equids at night from 2-4 hours before sunset to 2-4 hours after sunrise in vector-proof housing. Move only during daylight. Using insect repellents Stable in insect-free stalls. Decontamination Effective disinfectants, namely, virkon, acetic acid, bleach, formalin, β- propiolactone, acetyl-ethyleneimin derivatives. African horse sickness by Dr. O.O Akinniyi 16 Normal supraorbital fossae (white arrow) African horse sickness by Dr. O.O Akinniyi 17 Cardiac form: Oedema and distention of the supraorbital fossae (red arrow) African horse sickness by Dr. O.O Akinniyi 18 Cardiac form: Note the severe supraorbital fossa swelling and chemosis in this AHS-affected horse African horse sickness by Dr. O.O Akinniyi 19 PREVENTION AND CONTROL Cardiac form: Horse, skeletal muscle. There is marked intermuscular edema African horse sickness by Dr. O.O Akinniyi 20 Pulmonary form: Sclera haemorrhage African horse sickness by Dr. O.O Akinniyi 21 Pulmonary form; Discharge from the nostrils African horse sickness by Dr. O.O Akinniyi 22 PREVENTION AND CONTROL Pulmonary form: Abundant froth draining from the nostrils reflects severe pulmonary edema African horse sickness by Dr. O.O Akinniyi 23 Pulmonary form; Discharge from the nostrils African horse sickness by Dr. O.O Akinniyi 24