Parasitology. Alan GunnЧитать онлайн книгу.
rapid and aggressive form of MCL (Olivier and Zamboni 2020).
4.2.2 Genus Trypanosoma
All members of this genus are parasites of vertebrate animals, and they are almost all transmitted by invertebrate vectors. Asexual reproduction usually takes place in both the vertebrate host and the invertebrate vector (i.e., the parasites are heteroxenous). However, in mechanically transmitted trypanosomes, such as Trypanosoma evansi, there is no development outside the vertebrate host. There is evidence of sexual reproduction (or something like it) occurring in the invertebrate host in some trypanosome species. Trypanosoma equiperdum is something of an exception to this general lifestyle because it is a sexually transmitted parasite of horses and other equine species. Nevertheless, most of the genus Trypanosoma are heteroxenous and two distinct groups are identifiable based on where they develop within their invertebrate host. Those developing within the anterior regions of the gut and transmitted when the vector bites exhibit ‘anterior station’ development and belong to the ‘Salivaria’ group. Species developing in the vector’s hindgut and transmitted via its faeces exhibit ‘posterior station development’ and belong to the ‘Stercoraria’ group. Both groups include species of medical and veterinary importance (Table 4.4; Figure 4.6). It should come as no surprise that the taxonomy of trypanosomes undergoes regular rearrangements. It is highly likely that some well‐known species are actually ‘sub‐species’ or ‘synonyms’, but for the sake of comparison with past literature we have retained the most common species’ names.
In several trypanosome species, the kinetoplast is modified or lacking entirely. This has had a dramatic effect on their subsequent spread and evolution. In the case of Trypanosoma brucei, the development of the mitochondrion undergoes down regulation within the vertebrate host. However, the mitochondrion is fully functional during the procyclic stage that develops in the tsetse fly vector (Figure 4.7). The partial loss of kinetoplast DNA (dyskinetoplastidy) or its complete loss (akinetoplastidy) means that the mitochondria cannot fully function, and therefore the parasite can only develop within its vertebrate host. Consequently, trypanosomes lacking a kinetoplast and those in which it is only partially functional must rely on mechanical vector transmission or sexual transmission. However, this was not an evolutionary ‘retrograde step’ because these modes of transmission broke the link with the African tsetse fly belt and allowed the parasites to spread to other countries. Dyskinetoplastidy arises naturally in wild trypanosome populations by mutation, in response to treatments with certain anti‐trypanosome drugs (e.g., triacetylbenzene hydrochloride [TBG]), and through long‐term in vitro culture.
Table 4.4 Examples of Trypanosoma species of medical and veterinary importance.
| Parasite | Transmission Group | Vector/means of transmission | Host |
|---|---|---|---|
| Trypanosoma brucei brucei | Salivaria | Tsetse flies (Glossina spp.) | Ruminants (cause of ‘nagana’) |
| Trypanosoma brucei gambiense | Salivaria | Tsetse flies (Glossina spp.) | Humans (cause of ‘sleeping sickness’). No important animal reservoir of infection |
| Trypanosoma brucei rhodesiense | Salivaria | Tsetse flies (Glossina spp.) | Humans (cause of ‘sleeping sickness’). Reservoir of infection in cattle, wild game, lions, hyena etc. |
| Trypanosoma congolense | Salivaria | Tsetse flies (Glossina spp.) | Cattle, pigs, wild game. Cause of ‘nagana’ |
| Trypanosoma evansi (Trypanosoma brucei evansi) | Salivaria | Tabanid and other biting flies (mechanical transmission) | Horse, cattle, pigs, dogs, rodents. Cause of ‘surra’ |
| Trypanosoma equinum (synonym of T. evansi) | Salivaria | Tabanid and other biting flies (mechanical transmission) | Horses, donkeys, cattle, dogs Cause of ‘mal de caderas’ |
| Trypanosoma equiperdum (Trypanosoma brucei equiperdum) | Salivaria | Sexual transmission | Horse, asses. Cause of ‘dourine’ |
| Trypanosoma cruzi | Stercoraria | Reduviid bugs (e.g., Triatoma infestans) | Humans (cause of Chagas Disease). Reservoir of infection in many domestic and wild animals |
| Trypanosoma theileri | Stercoraria | Tabanid flies | Cattle |
Figure 4.6 Diagrammatic representation of some Trypanosoma species. All are drawn to the same magnification. (a) Trypanosoma brucei. (b) Trypanosoma vivax. (c) Trypanosoma congolense. (d) Trypanosoma equinum. (e) Trypanosoma equiperdum. (f) Trypanosoma evansi. Note the small size and lack of a free flagellum in Trypanosoma congolense.
Source: Reproduced from Cameron, (1934) © Copyright A and C Black Ltd.
Figure 4.7 Tsetse fly Glossina spp. (a) Adult fly. There are currently 23 described species of tsetse flies, and they vary in size from 6 to 16 mm in length. Their coloration consists mostly of the shades of brown and grey. When alive, the eyes of tsetse flies are usually dark brown, unlike those of tabanid flies in which the eyes often brightly coloured. Two characteristic features of tsetse flies are that they fold their wings completely flat when at rest and their mouthparts project forwards from their head. (b) Mouthparts of a tsetse fly. The mouthparts are lowered when the insect feeds. There are two thick palps that serve sensory and protective functions. The robust central labium is equipped with terminal teeth that facilitate skin penetration; the bite of a tsetse fly is extremely painful.
4.2.2.1 Trypanosoma brucei
Trypanosoma brucei is responsible for the disease Human African Trypanosomiasis (HAT), or more colloquially, ‘sleeping sickness’ and the wasting disease in cattle known as ‘nagana’. It was often stated that HAT is invariably fatal in the absence of treatment. However, it is now apparent that some people remain asymptomatic after contracting an infection (Kennedy and Rogers 2019) although it