Trypanosomiasis in horse treatment

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Trypanosomiasis in horse treatment

African horse sickness (AHS) is an insectborne, viral disease of equids that is endemic to sub-Saharan Africa.

It can be acute, subacute, or subclinical and is characterized by clinical signs and lesions associated with respiratory and circulatory impairm In endemic regions of Africa, the appearance of AHS may be preceded by seasons of heavy rain that alternate with hot and dry climatic conditions, which favor transmission by the insect (biting midge) vector. Outbreaks in central and east Africa have occas

ionally extended to Egypt, the Middle East, and southern Arabia. In 1959–1961, a major epidemic, caused by AHSV serotype 9, extended from Africa through the Near East and Arabia as far as Pakistan and India, causing the deaths of an estimated 300,000 equids. A further epidemic of the same serotype in 1965–1966 centered on northwest Africa (Morocco, Algeria, and Tunisia) but also extended briefly into southern Spain. This outbreak in Spain was eliminated by a vigorous vaccination and slaughter campaign. In July 1987, AHS caused by AHSV serotype 4 was reported in central Spain, due to the importation of infected zebra from Namibia. The outbreak lasted until the cold weather started in October 1987

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Equine trypanosomiasis is endemic in many areas of the world with high morbidity and mortality in affected populations. Trypanocides form an essential part of current treatment strategies but evidence regarding efficacy in equines is scarce. In order to inform disease management, the efficacy of three trypanocidal drugs was assessed in horses and donkeys that fulfilled 2/5 clinical inclusion criteria for trypanosomiasis in The Gambia. Selected equines received randomised treatment with either isometamidium, diminazene or melarsomine dihydrochloride and were observed for adverse drug reactions. Follow-up was performed at 1 and 2 weeks. Blood collected at each timepoint was analysed for Trypanosoma spp. using a PCR approach. Within the selected population 66% were PCR positive pre-treatment for Trypanosoma spp.. Trypanosome positive individuals responded favourably to each treatment, but clinical evaluation and PCR status post-treatment supported a superior effect for isometamidium. Melarsomine dihydrochloride had inferior efficacy to isometamidium. Immediate adverse side effects were only documented following isometamidium administration in donkeys (26%) and these were self-limiting. Diminazene had the longest duration of action as judged by PCR status. The data support the continued use of isometamidium and diminazene but not melarsomine dihydrochloride for trypanosomiasis in equines at the doses and routes of administration reported.

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A prospective randomised, open-label non-inferiority trial was performed in The Gambia on horses and donkeys that fulfilled 2/5 clinical inclusion criteria (anaemia, poor body condition, pyrexia, history of abortion, oedema). Following randomised trypanocidal treatment (diminazene diaceturate, melarsomine dihydrochloride or isometamidium chloride), animals were observed for immediate adverse drug reactions and follow-up assessment was performed at 1 and 2 weeks. Blood samples underwent PCR analysis with specific Trypanosoma sp. primers. Treatment efficacy was assessed by measuring changes in clinical parameters, clinicopathological results and PCR-status post-treatment after evaluating for bias. Using PCR status as the outcome variable, non-inferiority of isometamidium treatment was determined if the upper bound limit of a 2-sided 95% CI was less than 10%.
Results
There was a significant beneficial effect upon the Trypanosoma sp. PCR positive population following trypanocidal treatment for all groups. The findings of clinical evaluation and PCR status supported a superior treatment effect for isometamidium. Melarsomine dihydrochloride efficacy was inferior to isometamidium. There were immediate, self-limiting side effects to isometamidium in donkeys (26%). Diminazene had the longest duration of action as judged by PCR status.
Conclusions
The data support the continued use of isometamidium following careful dose titration in donkeys and diminazene for trypanosomiasis in equines using the doses and routes of administration reported.

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Trypanosoma evansi is the etiological agent of the disease known as Mal das Caderas (Latin America) or surra (Asia, Africa, and Europe) in horses. This parasite, which has been reported in domestic and wild mammals, can cause considerable economic losses. The trypanosomes reproduce in the blood of the vertebrate host, and the trypomastigote forms are transmitted mechanically by bloodsucking insects from infected to uninfected animals. Hot and humid climatic conditions may contribute to outbreaks of trypanosomiasis, due to higher proliferation of insects, the main vectors of T. evansi.
Surra is the most commonly reported disease in some continents due to the favorable environment for insects. In recent years, several outbreaks or isolated cases have been reported in certain European countries, an atypical region for the disease. In Brazil, the disease was restricted to the Midwest (region of the Pantanal of Mato Grosso) for many years. However, in the last 10 years it has spread to all regions of the country, with isolated cases and outbreaks with high associated mortality. Wild animals such as capybaras (a large rodent) and coatis (member of the raccoon family) may act as reservoirs of T. evansi. Populations of these species, which are present in the same areas as these outbreaks of surra, have increased considerably in recent years.
Trypanosomiasis in horses is characterized by anemia (low red blood cell count), edema (fluid swelling) of the limbs and dependent regions, anorexia, dehydration, lethargy, fever, loss of appetite, weight loss, abortion, and incoordination, followed by paralysis of the hind limbs. Researchers divide these clinical signs in two or three stages of the disease: subacute, acute, and chronic. In the chronic stage, horses usually exhibit cachexia (chronic wasting) associated with neurologic signs and limb paralysis. Neurologic signs are the result of the parasite travelling to the brain, where it

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Trypanosoma evansi infection typically produces wasting disease, but it can also develop into a neurological or meningoencephalitis form in equids. Trypanosomiasis in horses was treated with quinapyramine sulfate, and all the 14 infected animals were recovered clinically. After clinical recovery, four animals developed a neurological form of the disease at various intervals. Two of these animals treated with diminazene aceturate recovered temporarily. Repeated attempts failed to find the parasite in the blood or the cerebrospinal fluid (CSF), but all of the animals were positive in enzyme-linked immunosorbent assay. The calculation of the antibody index (AI) in the serum and the CSF and polymerase chain reaction (PCR) analysis of the CSF and brain tissue were carried out to confirm the neuro-infection. We found PCR and AI analyses of the CSF to be useful tools in the diagnosis of the neurological form of trypanosomiasis when the organism cannot be found in the blood or CSF. The increased albumin quotient is indicative of barrier leakage due to neuroinflammation. The biochemical changes in the CSF due to nervous system trypanosomiasis include increases in the albumin quotient, total protein, and urea nitrogen. It seems to be the first report on relapse of the nervous form of trypanosomiasis in equids even after quinapyramine treatment in endemic areas.

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Prevention: Environmental insect control (sprays/repellants), avoiding wooded areas or areas with long grass/brush, and frequent tick checks are the best options. No approved vaccination options for horses exist at this time.

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Tsetse control has long been an important option for reducing the impact of African trypanosomiasis but, although many effective methods have been used, the results have seldom proved sustainable. Developments to reduce cost and environmental impact increasingly limit the choices available for control and the scale of operations has declined. Conversely, human trypanosomiasis has reached epidemic proportions in some countries. Here, Reg Allsopp argues that those tasked with managing trypanosomiasis or committed to poverty alleviation in Africa should consider large-scale, area-wide tsetse control involving all proven methods, including aerial spraying and the sterile insect technique.

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Treatment
Chemotherapy of equine trypanosomosis consists of treatment with diminazene diaceturate, isometamidium chloride, quinapyramine chloride/quinapyramine sulphate combination, suramin or melarsomine hydrochloride. Except for trypanosome strains that display an innate or acquired resistance, these drugs are able to clear the parasites from the blood circulation. However, except for T. congolense, all the other trypanosomes are known to reside mainly in extravascular spaces of many tissues and organs, including the central nervous system. Evidence is accumulating that none of the aforementioned drugs is effective in the neurological stage of the disease since none is able to cross the blood-brain-barrier in sufficient amounts . Still, a recent outbreak of surra (caused by T. evansi) in Spain was brought under control upon treatment with melarsomine hydrochloride (Cymelarsan, Merial, France) of all parasitologically confirmed and suspect animals (dromedary camels, horses, donkeys) as well as of all animals that were in direct or indirect contact with the index case The latter was a dromedary camel imported from Gran Canaria, without prior screening for surra, one-and-a-half years before the disease was detected . Another outbreak, this time of dourine (caused by T. equiperdum), occurred in Italy in 2011 and illustrates the risk of importation of equine trypanosomosis with infected animals into non-endemic countries. That outbreak was only brought under control thanks to drastic measures taken by the veterinary authorities over several years. A potential, yet undocumented, risk of importation of equine trypanosomosis into non-endemic countries is by artificial insemination with contaminated semen

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Transmission and resulting geographical distribution
Trypanosoma brucei and T. congolense are the only species that are confined to the distribution of tsetse flies (the vector) in sub-Saharan Africa. Trypanosoma equiperdum is transmitted sexually, and T. evansi is transmitted mechanically by blood-sucking flies, vampire bats, and possibly sexually
Oral transmission of T. evansi via contaminated meat or carcasses is well documented but normally does not occur in equines Trypanosoma vivax can be transmitted both cyclically by tsetse flies and mechanically by other haematophagous flies. The global distribution of T. equiperdum, T. evansi and T. vivax is much wider, including Africa and Latin America for T. vivax, Africa, Latin America and Asia with sporadic import cases in Europe for T. evansi and worldwide, except Oceania, for T. equiperdum Most countries where trypanosomoses are endemic do not regularly report on these diseases, and as a consequence, the exact burden and area of distribution remain largely unknown. For example, a systematic review on surra shows serious discrepancy between countries reporting this disease to the World Organisation for Animal Health (OIE) and countries for which published evidence of surra exist From recent reviews on surra it becomes clear that its distribution map is based on anecdotal observations No such recent reviews exist on T. brucei, T. congolense, T. equiperdum and T. vivax in horses. However, evidence is increasingly being published on horses infected with T. evansi, T. equiperdum and T. vivax in Brazil, Ethiopia, India, Israel, Jordan, Mongolia, Nigeria, Pakistan, South East Asia, Sudan, Venezuela, etc

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Aetiology
Equine trypanosomosis is an infectious disease that is caused by several species of the genus Trypanosoma, including T. evansi, T. equiperdum, T. brucei, T. vivax, T. congolense and T. cruzi. Infections of horses with T. cruzi are very rare and are not further considered here [1]. Historically, the diseases caused by these trypanosomes are called “surra” (T. evansi), “dourine” (T. equiperdum) and “nagana” (T. brucei, T. congolense and T. vivax) but careful examination of published and unpublished data reveals that for all these three diseases, the clinical signs observed, including ventral oedema, emaciation, anaemia and neurological symptoms, can be very similar and are certainly not pathognomonic

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Equine trypanosomosis is a complex of infectious diseases called dourine, nagana and surra. It is caused by several species of the genus Trypanosoma that are transmitted cyclically by tsetse flies, mechanically by other haematophagous flies, or sexually. Trypanosoma congolense (subgenus Nannomonas) and T. vivax (subgenus Dutonella) are genetically and morphologically distinct from T. brucei, T. equiperdum and T. evansi (subgenus Trypanozoon). It remains controversial whether the three latter taxa should be considered distinct species. Recent outbreaks of surra and dourine in Europe illustrate the risk and consequences of importation of equine trypanosomosis with infected animals into non-endemic countries. Knowledge on the epidemiological situation is fragmentary since many endemic countries do not report the diseases to the World Organisation for Animal Health, OIE. Other major obstacles to the control of equine trypanosomosis are the lack of vaccines, the inability of drugs to cure the neurological stage of the disease, the inconsistent case definition and the limitations of current diagnostics. Especially in view of the ever-increasing movement of horses around the globe, there is not only the obvious need for reliable curative and prophylactic drugs but also for accurate diagnostic tests and algorithms. Unfortunately, clinical signs are not pathognomonic, parasitological tests are not sufficiently sensitive, serological tests miss sensitivity or specificity, and molecular tests cannot distinguish the taxa within the Trypanozoon subgenus. To address the limitations of the current diagnostics for equine trypanosomosis, we recommend studies into improved molecular and serological tests with the highest possible sensitivity and specificity. We realise that this is an ambitious goal, but it is dictated by needs at the point of care. However, depending on available treatment options, it may not always be necessary to identify which trypanosome taxon is responsible for a given infection.

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