Parasitology. Alan Gunn

2013). In addition, although the trypanolytic activity of normal human serum normally kills T. congolense, some strains are resistant to it (Van Xong et al. 2002).

      Trypanosoma congolense is of primary concern for its effect on domestic cattle, and it is a major cause of economic loss to cattle farmers throughout the affected regions. It is less harmful to other domestic animals and wild game. In susceptible cattle, T. congolense causes similar symptoms to T. brucei. Therefore, when farmers say that their animals are suffering from ‘nagana’, it could mean that either parasite is the cause. In addition, co‐infections are common. The disease may manifest itself in acute, chronic forms and mild forms. In the acute form, the disease causes anaemia, emaciation and a high parasitaemia in the peripheral circulation. The liver, lymph nodes and spleen enlarge, haemorrhages occur in the heart muscle and kidneys, and the infected animal may die in within 10 weeks of becoming infected. In the chronic form, the symptoms are less severe, and it may be difficult to find the parasites in the blood. There is enlargement of the lymph nodes and liver and signs of degeneration in the kidney, but the infected animal can recover after about a year. In mild infections, it may not be obvious that T. congolense is present. The pathology caused by T. congolense differs from that of T. brucei in that the parasites remain within the circulatory system and the central nervous system is not affected. Anaemia is the most characteristic feature of T. congolense infection and results from the destruction of red blood cells in the liver and spleen although other mechanisms (e.g., inflammatory processes) may also be involved (Noyes et al. 2009). Indigenous breeds of cattle, such as N’dama, are not resistant to T. congolense but have a genetic ability to limit the development of anaemia (Naessens 2006).

      4.2.2.3 Trypanosoma evansi

      Trypanosoma evansi is monomorphic, 14–33 μm in length and 1.5–2.2 μm in width and morphologically indistinguishable from Trypanosoma equinum, Trypanosoma equiperdum and the slender forms of T. brucei. Molecular evidence suggests that there are two distinct type strains of T. evansi, type A and type B, and there are further strains within each type. Types A and B are distinguished by differences in the minicircles in the kinetoplast DNA. Type A is the most common and widespread form whilst type B occurs in camels in Kenya and Ethiopia. Molecular analyses suggest that both strains probably arose independently from West African T. brucei brucei (Cuypers et al. 2017). If true, this is unexpected because currently, Type B T. evansi only occurs in Eastern Africa.

      Trypanosoma evansi has an extremely wide distribution and occurs in Africa, Asia, and Central and South America. It is particularly pathogenic in horses, but it also causes considerable morbidity and mortality in camels, cattle, pigs, dogs, and cats. It also parasitizes many wild animals such as deer, tapir, and capybara. It is usually mechanically transmitted by biting flies such as tabanids and stable flies. Trypanosoma evansi does not reproduce in its insect vectors and they act only as a ‘dirty syringe’. In South America, vampire bats can act as both hosts and mechanical vectors of T. evansi. Under experimental conditions, Raina et al. (1985) infected both dogs and mice by feeding them meat containing T. evansi. The extent to which oral infections occur naturally is, however, uncertain. Reproduction takes place asexually by longitudinal binary fission within the mammalian host.

      The disease caused by T. evansi is commonly known as ‘surra’ – which is the Hindi word for ‘rotten’ or ‘emaciated’ although other terms are also used such as el debab in many Arabic‐speaking countries. It causes the death of many thousands of animals every year and a great deal of morbidity (Aregawi et al. 2019). Horses are particularly susceptible to infections, and there are claims that the inoculation of even a single parasite can prove fatal. The disease is often acute in horses and the animal dies within a few weeks to 2 months. Chronic infections lasting over a year may also occur but also often end with the death of the horse. Surra causes anaemia, emaciation, and oedema that may vary from urticarial plaques on the neck and flanks to widespread swelling of the legs and lower body. The plaques may subsequently become necrotic and bleed whilst encephalitis and demyelination can occur in the brain and spinal cord that results in staggering and paralysis. Affected animals may also express abnormal behaviour such as hyperexcitability, head tilting, and circling.

      Surra is also an important cause of morbidity and mortality in camels in which it tends to be a chronic wasting disease. Characteristic features of infection include fever, anorexia, and the development of oedema. Cattle can be severely affected when exposed to T. evansi for the first time, but in endemic areas, the disease in cattle tends to be subclinical and reduce productivity rather than cause major morbidity and mortality. Dogs are susceptible to an acute and rapidly fatal form of the disease that causes nervous signs that are like those of rabies.

      4.2.2.4 Trypanosoma equinum

      Trypanosoma equinum and T. evansi are synonymous: T. equinum is neither a separate species nor a sub‐species of T. evansi. However, there are morphological differences between T. evansi and T. equinum: T. evansi expresses both kinetoplastic and dyskinetoplastic forms (i.e., ones retaining only fragments of kinetoplastid DNA) but T. equinum lacks a kinetoplast (i.e., it is ‘akinetoplastic’). This was one of the reasons for separating them, but molecular studies indicate that genetically they are the same.

Despite the molecular evidence, we will follow the older parasitology textbooks in dealing with them as though they are two distinct species. This is because the literature often provides different accounts of them in terms of their host range and pathology. Trypanosoma equinum only occurs in various South American countries where it causes a disease commonly known as ‘mal de caderas’ in Spanish and ‘mal de cadeiras’ in Portuguese – which translates as illness of the hips. Trypanosoma equinum is principally a parasite of horses. It infects other equids and a variety of domestic and wild animals (e.g., capybara), but these do not tend to suffer severe disease. It is mechanically spread by biting flies, such as tabanids, and in swampy areas where these flies are most numerous, T. equinum is a particular problem.

      Unlike surra, mal de caderas normally causes a chronic disease in horses. The condition develops over a period of months but usually has a fatal outcome. Symptoms begin with a fever and loss of weight and then the hindquarters become progressively weaker (hence the name ‘mal de caderas’) resulting in staggering and then an inability to walk. Horses can also exhibit conjunctivitis, the eyelids become oedematous (filled with fluid), and transient plaques form on the neck and flanks. In addition, the kidneys, brain, and spinal cord show signs of inflammation and necrosis.

      4.2.2.5 Trypanosoma equiperdum

      Trypanosoma equiperdum is monomorphic and morphologically indistinguishable from T. equinum. It exhibits dyskinetoplastidy – that is, it retains only fragments of kinetoplastid DNA. It parasitizes a range of equids although it affects the domestic horse (Equus cabalus) more severely than asses, donkeys etc. Some strains infect dogs and one can establish laboratory cultures in rats and mice. It is a sexually transmitted disease and causes a condition called ‘dourine’: a word deriving from the Arabic for ‘unclean’. The use of horses in agriculture and warfare spread T. equiperdum around the world. However, following breeding programmes aimed at eliminating infected horses, it currently has a restricted distribution in parts of Africa, Asia, southern Europe, and South America.

      Dourine typically manifests itself in three stages. The first stage begins with swelling of the genitalia. There is patchy depigmentation of the penis and vulva, and there is vaginal discharge in mares. The horse may also exhibit a slight fever and loss of appetite. After about a month, the second stage of the disease begins with the development of circular fluid‐filled (oedematous) plaques 2.5–10 cm in diameter underneath the skin. They usually form on the flanks although they can develop on any part of the body. The plaques may last a few hours or days after which they disappear and then reappear again later. Because of the rash‐like swellings, this is called