Trypanosoma Evansi In Horses Biology Essay
Trypanosoma evansi is a protozoan originated in Africa that can affect a wide range of mammalian hosts, including equines. It is the most widely distributed of the pathogenic animal African trypanosomes, affecting Africa, Asia, South America and recently some outbreaks have been reported on Europe. The main clinical signs include weight loss or wasting, lethargy, enlargement of lymph nodes, edema of hind limbs and distal parts of the body, fever and anemia. Neurological involvement is responsible for lameness, characterized by reluctance to move, ataxia, weakness, incoordination, paresis of the pelvic members, paraplegia and dog-sitting position. The disease cause important economic impact due to mortality, reduced production and costs with treatment. The prevention and control are made by trypanocidals drugs, combat of the vector, animal movement control and an efficient diagnose system.
The disease named Surra in India and, amongst others, El Debab, El Gafar, Tabourit or MBori in North Africa, Mal de Caderas or Murrina in Latin America (VER COMO CITAR) is caused by the protozoal parasite Trypanosoma evansi and transmitted mechanically by the bite of hematofagous flies or bats in South America, or even through coitus, milk or by eating freshly killed infected animals (Gutierrez et al., 2010; Wang, 1998; Woo, 1977).
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It was originated in Africa and spread to South America and Asia due to importion of animals from Africa, including horses, camels and mules (Hoare, 1972). This equine trypanosomiasis has an economic importance in these regions considering the losses due to mortality, lower productivity and cost of treatment (Silva et al., 1995; Seidl et al., 1998, 2001).
Horses are susceptible animals for Trypanosoma evansi and usually develop oHweight loss or wasting, lethargy, enlargement of lymph nodes, edema of hind limbs and distal parts of the body, fever and anemia (Berlin, Loeb & Baneth, 2009; Seiler et al., 1981; Rodrigues, 2006). Neurological signs, immunosuppression and reproductive issues can also be reported in affected horses (Brun et al., 1998; VER COMO CITAR 3).
The treatment is performed by administration of trypanocidals drugs and it can be in order to cure or to prevent, depending on the active principle used or its dosage (Peregrine, 1994). Others prevention measures also include vector control, efficient diagnosis by combined serological, parasitological and molecular techniques to detect infection (Gutierrez et al.,, 2010), as well as controlled movement of animals between properties and continuous surveillance (Dávila et al., 2000; Gutierrez et al.,, 2010).
The hemoflagellate protozoan parasite responsible for the disease is specie known as Trypanosoma evansi, pertaining to the Subgenus Trypanozoon, Genus Trypanosoma, family Trypanosomatidae and Order Kinoplastida (VER COMO CITAR1).
This hemoflagellate is transmitted by hematophagus flies, mainly Tabanus sp. (Herrera et al., 2004); but other insects as the members of the genera Stomoxys, Lyperosia, Haematopota (flies), Ornithodorus (tick), Chrysops, Musca and Atylotus has also been reported to play a role in transmission (Juyal, n.d.; VER COMO CITAR2).
Efficiency of transmission is dependent on the interval between 2 successive feedings and intensity of fly challenge (Juyal, n.d.). In general, the shorter the interval between the two feedings, the greater the chances of successful transmission; since trypanosomes have a restricted survival time in the mouth parts of the vector (Hoare, 1972; Luckins, 1988). Development stages does not happen in the vectors, which means that a procyclic or insect stage does not exist in T. evansi, explained by the lack of maxicircles in the kinetoplast DNA of this parasite (Borst et al., 1987)
Transmission can be performed by vampire bats (Desmodus rotundus) in South America (Hoare 1965, 1972; Losos, 1968) and horses can also get infected through milk, during coitus (Wang, 1988) or by iatrogenic form (Juyal, n.d.). Carnivores animals can become infected after feeding on freshly-killed infected tissues (Woo, 1997), as well as oral transmission might occur during fighting (VER COMO CITAR2).
"Surra" is an animal trypanosomiasis with a wide range of hosts, which vary geographically. It is pathogenic for most domestic, wild and laboratory mammals (Brun, Hecker & Lun, 1998); however, equines, camels, dogs, deer and Asian elephants are more frequently found infected by T. evansi species than buffalo and cattle (Hoare, 1972; Lun et.al, 1993). Infection can occurs in pigs with light clinical signs (Brun, Hecker & Lun, 1998) and goats experimentally infected with the parasite, showed subclinical form of the disease (Buscher et al., 2010) and also chronic infection even with nervous system involvement (Zweygarth, 1992) and arthritis (Buscher et al., 2010).
The presence of this protozoan in wild animals in a low and cryptic parasitemia suggests their importance in the maintenance of the parasite in nature (Herrera et al., 2004), offering risk to horses that live in proximity with these infected mammals, because equine species are considered highly sensitive to T. evansi (Rodríguez, 2012) and develop the severe form of the disease due to the nervous symptomatology (Silva et al., 1995a).
Trypanosoma evansi is the most widely distributed of the pathogenic animal african trypanosomes, affecting livestock and wildlife in Asia, Africa and Latin America (Luckins & Dwinger, 2004). Prevalence of the infection among horses varies greatly between geographical areas and the disease causes losses due to reduced productivity, mortality, cost of treatment (Mavadiya, Raval & Mehta, 2010) and failure of vaccination due to severe immunosuppression (Holmes, 1980).
Periodical outbreaks of trypanosomiasis have been reported from time to time throughout south East Asia and India, a country where the disease has a major impact and is endemic, particularly in low-lying areas (Juyal, n.d.). The parasite was probably introduced in South America during the sixteenth century by Spanish settlers (Hoare, 1972) and the disease has an important impact in this region because horses play a central role in extensively-managed beef cattle industry (Seidl, Moraes & Silva, 2001).T. evansi was first diagnosed in Europe in 1997 at the Canary Islands, two recent outbreaks happened in Spain in 2008 and France in 2006; but nowadays the disease is considered eventually eradicated from islands and areas previously infected except in a little area of Gran Canaria (Gutierrez et al., 2010; Rodriguez et al, 2012).
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Equine trypanosomiasis has been mainly reported in the rainy and post rainy seasons (Herrera et al., 2004; Juyal n.d.) when the flies are most numerous. Increase in flies activity is expected to increase the likelihood of T. evansi transmission and hence contribute to disease outbreaks (Juyal, n.d.).
Pathogenesis and Lesions:
The effect of Trypanosoma evansi in its host varies according to the virulence of the strain of trypanosome, specie of host, unspecific factors affecting the animal, such as other infections and general stress and local epizootiological conditions (Hoare, 1972).
The trypanosomes multiply on the bite site, on the skin and reach the blood flow and the lymphatic system, causing fever and inducing an anti-inflammatory response (Connor & Van Den Bossche, 2004).
The high parasitemia of the host is followed by fever peaks and non-parasitemic periods, characterizing the recurrent fever (Rodrigues et al., 2009). This happens due to antigenic variation of the parasite's surface; as antibodies are produced there is elimination of the current form, but new patterns of surface antigens are produced to evade the host's immune response (Lucas et al., 1992), restarting the fever.
The nature of the anemia presented by the horses is not completely elucidated (Anosa & Kaenko, 1983a,b) but the erythrocytes from the host may acquire trypanosomal antigen, which may result in immunological reaction and complement mediated destruction of erythrocytes (Juyal n.d.). Therefore, the main cause of anemia is the removal of the damaged erythrocytes from blood flow by the mononuclear phagocytic cells from spleen, bone marrow, lungs and lymph nodes (Rodrigues, 2006).
T. evansi has affinity for tissues and the inflammatory, degenerative and necrotic lesions are a result of extravascular spaces invasion by the parasite (Rodrigues et al. 2009). The lysosomal secretory proteinases, phospholipases and other hydrolytic enzymes of trypanosomes are considered potentially important factors in the development of the disease. The excretory/secretory proteases released into the blood stream may degrade the host tissue proteins and contribute to the pathogenesis (Juyal n.d.).
Besides causing the disease, the trypanosome is also responsible for producing severe immunosuppression in the host, which makes it more susceptible to secondary infections and produce poor response to viral and bacterial vaccines (Holmes, 1980).
The protozoan has a predilection to the equine central nervous system tissues, where it infiltrates and disseminates, causing severe and potentially fatal clinical disease (Berlin, Loeb & Baneth, 2009)
Post mortem Lesions:
In the necropsy, the gross lesions tend to be nonspecific, and may include wasting or emaciation of the carcass, subcutaneous edema, signs of anemia, enlargement of the spleen and lymph nodes, and petechiae on some internal organs.
Muscle atrophy may be noted, particularly in the hindquarters. Hydrothorax and ascites are sometimes seen. The lungs may also be affected; congestion, consolidation, edema, emphysema, hemorrhages and pneumonia have been reported. Cardiac lesions including hydropericardium, pericarditis and evidence of cardiomyopathy or myocarditis occur in some animals.
The cerebral hemisphere may be swollen and the gyri flattened. There may be severe edema and malacia, with the white matter becoming yellow, gelatinous and friable. Subpial hemorrhages may be also present.
Histologically, it is possible to observe at the lymph nodes and the spleen, lymphoid follicle hyperplasia, erythrophagocytosis and hemosiderosis (Pimentel, 2009).
At the liver, periportal mononuclear infiltrate, hypertrophy and hyperplasia of Kupffer cells, centrilobular necrosis and hemosiderosis are commonly observed (Rodrigues et al. 2005).
In muscles, there is hyalin necrosis, alternating by regeneration of myofibers, mononuclear cells and hemosiderosis (Pimentel, 2009).
In the brain can be observed varying degrees of non-suppurative meningoencephalitis affecting the white and gray substances. Typically, there are broad perivascular cuffs of mononuclear inflammatory cells including large lymphocytes and hystiocytic cells and some plasma cells. Some of these plasma cells present eccentric nuclei and large eosinophilic cytoplasmatic globules (Russel corpuscles), giving the cell a morula aspect (Mott cells) and can be found randomly between the cellular infiltrate. It can also be noticed extensive areas of edema and malacia (Seiler et al. 1981; Pimentel, 2009).
At the bone marrow, perivascular cuffs and meningitis can occasionally occur (Seiler et al. 1981; Pimentel, 2009).
Surra has an incubation period of 5 to 60 days and can be an acute, subacute or choric disease; horses will normally die rapidly, but in some cases, clinical signs may persist for months or they can carry T. evansi subclinically (ver como citar3).
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Common clinical signs include weight loss or wasting, lethargy, enlargement of lymph nodes, edema of hind limbs and distal parts of the body, fever and anemia (Berlin, Loeb & Baneth, 2009; Seiler et al., 1981; Rodrigues, 2006). The increase on the parasitemia is followed by a peak of fever, which can be as high as 44o C (Gill, 1977).
Skin issues can also be observed as rash, urticarial plaques and loss of hair. Petechial hemorrhages of the mucous membrane (eyelids, nostrils and anus) are described too (VER COMO CITAR 1, 2 E 3). Besides that, other symptoms have been reported in horses, such as infertility, abortions and/or stillbirths (ver como citar 3).
Neurological symptoms occur in advanced cases, where the protozoa invade the central nervous system (Brun et al., 1998; VER COMO CITAR 3). This fact is responsible for lameness and is characterized by reluctance to move, ataxia, weakness, incoordination, paresis of the pelvic members, paraplegia and horses can adopt dog-sitting position (Rodrigues, 2006). Other neurological signs such as head tilting, circling, hyperexcitability, blindness, proprioceptive deficits and paddling movements have also been seen (ver como citar 3).
Anemia, which is usually microcytic normochromic (Silva et al., 1995), is the main outcome of infection and consequently, the resistance to develop it, as well as control of parasitemia, reflect the degree of tolerance to infection by the host (Trail et al., 1990). Development of several erythrocytes abnormalities have been reported (Silva et al., 1995). Immunosuppression is one of the consequences of the disease (Holmes, 1980) due to mild leukopenia with relative lymphocytosis and monocytosis and a decrease in the neutrophil count (Silva et al., 1995).
Diagnosis of Trypanosoma evansi is based on demonstrating either the parasite or parasite antigens, or antibodies directed against the trypanosomes (Brun et al., 1998).
Identification of the agent can be made by direct microscopic examination in blood samples, wet blood films, stained thick smears, stained thin smears, lymph node biopsies or edema fluid. However it can be difficult to find T. evansi in the samples, especially in mild or subclinical cases (ver como citar 2 e 3), in this case detection can be improved with parasite concentration techniques including mini axon-exchange chromatography, hemolysis methods that use sodium dodecyl sulphate to destroy erythrocytes and by hematocrit centrifugation or the dark-ground/phase-contrast buffy coat technique.
Circulating antigen detection in blood serum is also a way to detect active infection, these methods include latex agglutination, enzyme-linked immunosorbent assays (ELISAs) and immunochemistry. Several attempts to develop such tests have not yet reached a satisfactory level to be recommended for routine diagnosis (Desquesnes, 1996); the absence of circulating trypanosome cannot exclude the possibility of a true infection (Rodriguez et al., 2012). Therefore detection of trypanosomal DNA using polymerase chain reaction is more sensitive than parasitological examination, but it can also give false-negative results when the parasitemia is low (Rodriguez et al., 2012).
Animal inoculation studies in rats or mice may occasionally be used to diagnose the parasite. These tests are very sensitive and can detect low levels of trypanosome, but they are also time consuming (ver como citar2).
The demonstration of specific antibodies for the diagnosis of T. evansi infections is commonly done through ELISAs, card agglutination (CAT/T.evansi), latex agglutination, immune trypanolysis test and indirect immunofluorescent antibody test (IFAT) (ver como citar 2 e 3). All serological tests have not been validated or standardized, and cross-reaction can occur with other trypanosomes or else, some serological test may not detect some variants of the organism (e.g. type B in Kenya).
It should be kept in mind that no single diagnostic test is 100% sensitive and 100% specific and therefore combined use of different tests (serological, parasitological and molecular) is recommended to detect the presence of Trypanosoma evansi (Gutierrez et al., 2010).
A good combination of micro-hematocrit centrifugation technique for microscopic identification of the parasite with CATT/T. evansi for serological testing; including re-evaluation of seropositive animals which didn't show the parasite with a more sensitive method to confirm or exclude infection, was reported as an efficient diagnose method in Europe (Gutierrez et al., 2010).
Diseases that cause edema, anemia, wasting and/or neurological signs should be considered in a differential diagnose, such as African horse sickness, equine viral arteritis, equine infectious anemia, equine babesiosis and chronic parasitism.
In horses with encephalitis, the diseases: equine herpesvirus type 1 myeloencephalopathy, Eastern, Western or Venezuelan equine encephalitis, equine protozoal myeloencephalitis, West Nile virus infection and rabies should also be considered.
Treatment and Prognosis:
Treatment of surra is based on the drugs suramin, diminazene, quinapyramine and cymelarsan and the choice of drug, dosage and route of application depend on the management in a given area as well as on the chemosensitivity of the trypanosome strain (Brun et al., 1998).
The success of the treatment relies on good nutrition and amount of exercise to which the animal is submitted, besides the use of an efficient trypanocidal drug. Animals chronic infected usually present iron metabolic disorder and commonly demonstrate irreversible cases (Connor & Van Den Bossche, 2004; Rodrigues, 2006).
The treatment of surra can be in order to cure or to prevent, depending on the drug that will be administered or its dosage (Peregrine, 1994). The curative drugs are used when there is low incidence of disease and just few cases occurs, on the other hand, preventive drugs are necessary when horses are under constant risk or when the disease reaches a large amount of animals during the year (Silva et al.,2002).
The selection of the drug treatment depends also on availability of medicines; in Europe animals are treated mostly with melarsomine (CymelarsanÂ®) (Gutierrez et al., 2010) which is a relatively new drug, developed less than 10 years ago (Raynaud et al., 1989). Diminazine remains the mainstay drug for treatment in India because of the non-availability of some of the others drugs (Juyal, n.d.); as well as happens in South America, where diminazine is also the mainly used drug because of non-availability of others. This medicine has a high therapeutic action for most domestic species when compared to the other drugs (Rodrigues, 2006).
Tuntasuvan et al. (2003), showed that treating horses and mules with a 3,5 mg/Kg dose of diminazine is efficient, due to the removal of the parasites from peripheral blood. However, on a second treatment with the same drug and dose, 50% of the equines remained positive. Besides that, the medicine demonstrated slight or high toxicity for those animals. Nowadays, Silva et al. (2004) recommends the dose of 7mg/kg of diminazene to treat horses infect by T. evansi.
After treatment is likely that the parasites may reaper on blood flow because of the resistance to the drug by the agent or because of the incapacity of the medicine to pass the blood-brain barrier, when the protozoan is occulted on the liquor (Monzon et al., 2003).
Prevention and Control:
Prevention and control of equine trypanosomiasis has an economic importance considering the losses due to mortality, lower productivity and cost of treatment (Silva et al., 1995; Seidl et al., 1998, 2001). In endemic areas, this disease is usually controlled by efficient detection and treatment of infected animals and prevention of health animals, using chemotherapeutics or chemoprophylactics drugs (ver como citar 2; Rodrigues, 2006; Peregrine, 1994).
Besides the use of medicines, the vector control is also important to prevent the disease through traps impregnated with insecticides and pour on preparations to repel the insects (Silva et al., 2002). Although the latter, is not so useful since most cases of T. evansi happens during the wet season when the treatment is likely to be washed off (Seidl et al., 2001).
The control of animal's movement and import is more efficient in preventing the disease than controlling vectors or wild reservoirs of trypanosomiasis (Dávila et al., 2000). Quarantine and evaluating of animals must be carried out before they can be relocated to a surra-free area, considering that occasional introduction of T. evansi into countries free of the parasite has most often resulted in the parasite becoming endemic (Hoare, 1972; Gutierrez et al., 2010). Establishing continuous surveillance measures is also a good strategy because re-infection of animals from an unknown reservoir cannot be ruled out (Gutierrez et al., 2010).
For properties with small amount of horses, healthy animals in endemic areas can be confined to stables during the day to prevent get infected, as the vector insects preferentially feeds in sunlight and the parasite do not live long at the insect (ver como citar 2).
Hopes for the development of conventional vaccines are limited, due to the trypanosome's ability to escape the host immune response through antigenic variation (Juyal, n.d.).
Morbidity and Mortality:
Severe outbreaks can occur when the disease is insert into a disease-free area or susceptible animals are moved to an endemic area (Hoare, 1972); morbidity rates as high as 50-70% can be seen, with comparable mortality (ver como citar 2).
The severity of the disease can vary with the strain of T. evansi and with host factors including stress, concurrent infections and general health (Hoare, 1972); however, equine species are considered as highly sensitive to T. evansi (Rodriguez et al., 2012).
A study performed by Seidl et al. (2001) in South America comparing the adoption of no control strategy, year round curative control strategy and wet season curative strategy showed that when horses are left untreated, 13% of loss of horses in the region occurred; however when year round curative strategy was performed, resulted in the migration of these losses by almost 90% and when a curative strategy was administered only during the rainy season, 81% fewer horses deaths is seen than when no control was adopted.
Equine trypanosomiasis must be prevented and controlled considering the economic impact caused by impairing equine reproduction, locomotion and endurance, reducing horse's use and consequently profit. An integrated approach involving quickly and efficient techniques of diagnosis, greater availability of drugs in developing countries, researches about parasite resistance against different active principles, development of effective and practical methods of vector control and studies about the role of wild animals in the epidemiology of the disease are essential to develop a good strategy to combat the disease.
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