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 the ‘urticarial stage’. Plaques do not always form but if they do, they are a reliable indicator of the nature of the disease. The onset of paralysis marks the third stage of the disease. Often this begins in the nose and face. It then spreads to affect the rest of the body and can result in complete paralysis affecting all the limbs. The course of the disease may take as long as 2 years and mortality can be as high as 70%.
The relationship between T. equiperdum, T. evansi, and T. brucei remains uncertain. Molecular evidence indicates that T. equiperdum and T. evansi independently diverged from T. brucei on several occasions. According to Cuypers et al. (2017), T. equiperdum arose from an East African T. brucei ancestor whilst T. evansi derives from a West African T. brucei ancestor.
Trypanosoma equiperdum is primarily a tissue parasite and not usually present in the circulating blood, but it occurs in smears taken from the genitalia or plaques. Diagnosis has traditionally relied on serological complement fixation tests and in some countries where dourine is endemic, they are mandatory. However, such tests will not reliably distinguish T. equiperdum from other trypanosomes such as T. evansi and T. brucei – which is hardly surprising because they are all closely related.
4.2.2.6 Trypanosoma cruzi
Trypanosoma cruzi causes Chagas disease – a potentially fatal infection that afflicts around 11 million people in the New World from Argentina to the southern United States of America. In addition, owing to migration, the disease now occurs in many other parts of the world with important foci in Canada, North America, Europe, and Australia. The name Chagas disease derives from that of Carlos Chagas who first described the parasites in 1910. Chagas initially believed that the parasites underwent schizogony within their mammalian host and hence named them Schizotrypanum cruzi – ‘cruzi’ derives from the famous Oswaldo Cruz Institute in Brazil. Subsequently, it became clear that the parasite’s life cycle does not include schizogony and most workers now refer to it as Trypanosoma cruzi.
In addition to humans, T. cruzi infects many domestic and wild mammals including dogs, cats, bats, rats, and armadillos. This makes disease control difficult because there are numerous potential reservoirs of infection. Trypanosoma cruzi infections are especially common among animals that utilise burrows and hollow trees because these are ideal dwellings for the insect vectors. The parasite is transmitted by blood‐feeding reduviid bugs (Order Hemiptera, Family Reduviidae, Sub‐Family Triatominae) that because of their appearance are sometimes called cone‐nosed bugs. Over 130 species of reduviid bug can act as vectors but only those living near humans are medically important. Although Chagas disease now occurs in many countries, the lack of suitable vectors limits its potential for transmission outside Central and South America. There is therefore concern over the potential for vector species to disperse by air or sea (the bugs can survive for weeks without feeding) to other countries with luggage or farm produce. Trypanosoma cruzi can infect several other blood‐feeding invertebrates. These include the bed bug (Cimex lectularius; Order Hemiptera, Family Cimicidae), the argasid tick Ornithodoros moubata and the medicinal leech Hirudo medicinalis. However, these are probably not important in the transmission of the parasite to humans. Trypanosoma cruzi can also infect vampire bats, but it is uncertain whether they transmit the parasite in their bite. During the acute phase of infection, the parasite occurs within the saliva of dogs, so it is clearly a possibility. However, whether a very ill bat would be capable of flying and feeding is uncertain.
The life cycle of T. cruzi differs from that of the other trypanosome species discussed so far in that it involves stercorarial transmission from the invertebrate vector to the vertebrate host (i.e., via the faeces rather than the saliva/bite). Reduviid bugs often defecate during or immediately after feeding, and they void the infective metacyclic stage trypanosomes with their faeces. The bugs feed at night and they often bite their victims around the face. They have therefore gained the common name of kissing bugs. On waking, the natural reaction is to rub/scratch at the bite site, and this rubs the parasite‐infected faeces into the wound site. However, most infections result from bug faeces contaminating the victim’s fingers and from there transferring to the eyes and mucous membranes where the parasites can penetrate more easily. We can also become infected from organ transplants and the use of contaminated blood during transfusions (Ries et al. 2016). In endemic areas, where the likelihood of acquiring T. cruzi infection from a blood transfusion is high, haematologists sometimes treat donated blood with gentian violet. This kills the parasites, but as the blood infuses through the tissues of the recipient, it also has the unfortunate effect of turning the patient purple temporarily. There are isolated reports of oral transmission of T. cruzi that date back many years. These arise through consuming food contaminated with infected bug faeces. They were considered rare oddities, but this mode of transmission is apparently becoming more common (Robertson et al. 2016). Furthermore, oral transmission tends to result in acute infections that may prove rapidly fatal. Congenital infection via the placenta is possible and can result in spontaneous abortion or serious disease of the infant at birth. Reservoir animals can acquire infections through being bitten, as well as from consuming bugs containing the parasites and from food contaminated with their faeces.
Once T. cruzi enters a suitable mammalian host, the trypomastigotes invade both phagocytic and non‐phagocytic cells. Indeed, they are apparently capable of invading all nucleated cells. However, most of the pathology arises from their invasion of smooth, cardiac, and skeletal muscle cells, nerve cells, and cells comprising organs such as the liver, spleen, and lymphatics. Within a host cell, the parasites develop within a parasitophorous vacuole. The mechanism by which a trypomastigote enters a host cell varies between cell types and may involve active invasion by the parasite and passive internalization through
