Sleeping Sickness: Human Sleeping Sickness | Animal Sleeping Sickness


Sleeping sickness is also known as African human trypanosomiasis, is a vector-borne parasitic disease. It is caused by infection with protozoan parasites happiness to the genus Trypanosoma. They’re transmitted to humans by glossina bites that have nonheritable their infection from men or animals harboring human pathogenic parasites. They are transmitted to humans by glossina bites that have nonheritable their infection from individuals or animals harboring human infective parasites.

Forms of Human Sleeping Sickness

  • Trypanosoma Brucei Gambiense is found in central and west Africa. This form presently accounts for over ninety-eight of reported cases of sleeping sickness and causes a chronic infection. Someone can be infected for months or maybe years while not major signs or symptoms of the illness. Once additional evident symptoms emerge, the patient is commonly already in a complicated illness stage wherever the central system is affected.
  • Trypanosoma Brucei Rhodesiense is found in southern and eastern Africa. This form represents two of according to cases associated causes an acute infection. 1st signs and symptoms area unit observed some months or weeks after infection. The malady develops quickly and invades the central system. Only African nation presents each type of the disease, however in separate zones.

Another form of trypanosomiasis happens primarily in Latin America. It’s referred to as American trypanosomiasis or Chagas disease. The causative organism belongs to a different Trypanosoma taxonomic group and is transmitted by a different vector.


Animal Sleeping Sickness

Other parasite species and sub-species of the Trypanosoma genus are infective to animals and cause animal trypanosomiasis in wild and stock. In cattle, the unwellness is termed Nagana. Trypanosomiasis in domestic animals, significantly in cattle, could be a major obstacle to the economic development of affected rural areas. Animals will host the human microorganism parasites, particularly rhodesiense, of that domestic and wild animals, are a vital reservoir. Animals may also be infected with gambiense and act as a reservoir to a lesser extent. But the precise epidemiologic role of the animal reservoir within the gambiense type of the illness isn’t however well known.


  • Mother-to-child infection: the trypanosome will cross the placenta and infect the fetus.
  • Mechanical transmission through alternative blood-sucking insects is possible. However, it’s tough to assess its epidemiologic impact.
  • Accidental infections have occurred in laboratories as a result of pricks with contaminated needles.

  In the initial stage, the trypanosomes multiply in connective tissue tissues, blood, and bodily fluid. This is often additionally known as a haemo-lymphatic stage that entails bouts of fever, headaches, joint pains, and haptic sensation. In the second stage, the parasites cross the barrier to infect the central nervous system. This is often referred to as the neurological or meningo-encephalic stage. Usually, this is often once a lot of visible signs and symptoms of the disease appear: changes in behavior, confusion, sensory disturbances, and poor coordination. Disruption of the sleep cycle, which provides the illness with its name, is a vital feature. While not treatment, sleeping sickness is considered fatal though cases of healthy carriers are reported.



Diagnosis is made in 3 steps:

  1. Screening for potential infection: This involves using serological tests (only obtainable for T.b.gambiense) and checking for clinical signs – particularly swollen cervical lymph nodes.
  2. Diagnosing by establishing whether or not the parasite is present in body fluids.
  3. Staging to see the state of disease progression. This entails examining the humor obtained by lumbar puncture.

Diagnosis should be created as early as possible to avoid getting to the neurological stage to elude risky and challenging treatment procedures. The long, comparatively asymptomatic 1st stage of T. b. Gambians’ sleeping sickness is one in all the explanations why a complete, active screening of the population in danger is suggested, to identify patients at an early stage and reduce transmission by removing their status of a reservoir. Complete testing needs a severe investment in human and material resources. In Africa such resources square measure typically scarce, particularly in remote areas wherever the disease is generally found. As a result, some infected people might die before they can ever be diagnosed and treated.



The type of treatment depends on the illness stage. The medication used in the primary step is safer and more comfortable to administer than those for the second stage. Also, the earlier the sickness is known, the higher the prospect of a cure. The assessment of treatment outcome needs follow of the patient up to twenty-four months and entails laboratory exams of body fluids together with cerebrospinal fluid obtained by spinal puncture, as parasites might stay viable for long periods and reproduce the sickness months when treatment.

Treatment success within the second stage depends on medicine that crosses the blood-brain barrier to achieving the parasite. Such drugs are hepatotoxic and complicated to administer.

Drugs used in first stage treatment:

  • Pentamidine: used for the treatment of the primary stage of T.b. gambiense sleeping sickness. Despite non-negligible undesirable effects, it’s usually well tolerated by patients.
  • Suramin: used for the treatment of the primary stage of T.b. rhodesiense. It provokes specific undesirable effects, as well as the track and allergic reactions.

 Drugs used in second stage treatment:

  • Melarsoprol: it is used for the treatment of each gambiense and rhodesiense infections. It’s derived from arsenic and has several undesirable facet effects. The most dramatic of that is reactive encephalopathy (encephalopathic syndrome) which may be fatal. An increase in resistance to the drug has been observed in many foci, significantly in Central Africa. It’s presently suggested as the first-line treatment for the rhodesiense type and as second-line for the gambiense type.
  • Eflornithine: It is only effective against T.b. gambiense. The regimen is complicated and difficult to use.
  • Nifurtimox: It simplifies the employment of eflornithine by reducing the duration of treatment and therefore the number of IV perfusions, however, unfortunately, it’s not been studied for T.b. rhodesiense. Nifurtimox is registered for the treatment of American trypanosomiasis however not for human African trypanosomiasis. However, once safety and effectivity information provided by clinical trials, its use together with eflornithine has been included within the “WHO List of Essential Medicines” and is presently counseled as first-line treatment for the gambiense type. Each medicine is provided free of charge by who to endemic countries with a kit containing all the fabric required for its administration.

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