Overview
African trypanosomiasis, also known as African sleeping sickness or sleeping encephalitis, is a zoonotic parasitic disease transmitted by Trypanosoma brucei through the bite of the tsetse fly (commonly known as the tsetse fly), and it is rampant in the southern part of the Sahara in Africa, with the prevalence rate as high as 80% in some endemic areas.
African trypanosomiasis is divided into two types: Gambian trypanosomiasis is distributed in the western and central parts of the country, so it is also known as Central and West African trypanosomiasis. Rhodesian trypanosomiasis is found in the eastern part of the country, so it is also known as East African trypanosomiasis.
Patients may initially experience fever, rash, edema and enlarged lymph nodes, followed by inflammation of the brain and meninges. East African trypanosomiasis can deteriorate rapidly and the brain is affected earlier and more often than in West African trypanosomiasis. In the later stages of the disease, other neurological symptoms may slowly appear, and lethargy may gradually increase, eventually leading to coma and death, hence the name “sleeping encephalitis”.
Patients with high fever should be treated as soon as possible, and can usually recover with appropriate medication and treatment.
Causes
African trypanosomiasis is caused by Trypanosoma brucei. Trypanosoma brucei gambiae causes Gambian trypanosomiasis, and Trypanosoma brucei rhodesiense causes Rhodesian trypanosomiasis. The main source of transmission of Gambian trypanosomiasis is the patient, because most of them are chronic, and there are asymptomatic carriers, some domestic animals such as cattle, pigs and wildlife such as antelopes can also be storage hosts. The main reservoir hosts for Rhodesian trypanosomiasis are domestic animals and wildlife such as African antelopes, lions, hunting dogs, monkeys, etc. Patients can also be the source of infection.
Symptoms
The basic process after the invasion of two kinds of trypanosomes into the human body includes: the local primary reaction stage caused by the local proliferation of trypanosomes and the hemolymphatic stage of dissemination in the body, as well as the meningitis stage of invasion into the central nervous system.
1. Primary reaction stage
About one week after being bitten by the tsetse fly, the local skin swells and a red spot appears in the center, which is the chancre of trypanosomes. Lymphocytes, histiocytes and a small number of eosinophils and macrophages can be seen infiltrating the subcutaneous tissue at the site of the “chancre”. Sometimes trypanosomes are seen. The localized skin lesions become self-limiting and can subside after about 3 weeks.
2. Hemolymphatic stage
After the trypanosomes enter the blood and intertissue lymphatic fluid, they can exist in the blood and lymphatic system for a long time, causing extensive lymph node enlargement, in which lymphocytes, plasma cells and macrophages proliferate, and trypanosomemia occurs 5 to 12 days after infection. As the antigens on the surface of the worms mutate at intervals, the specific antibodies produced lose their effect, thus leading to the alternating rise and fall of the number of trypanosomes in the blood. The interval is 2 to 10 days. The peak of the hemorrhagic fever may last for 2 to 3 days, accompanied by fever, headache, arthralgia, limb pain and other symptoms. The fever lasts for several days and subsides on its own. The temperature may rise again after a few days. In this period, generalized lymph node enlargement may occur, especially in the back of the neck, submandibular, groin and other obvious places. Enlargement of the lymph nodes in the posterior triangle of the neck (Winterbottom’s sign) is characteristic of Gambian trypanosomiasis. Other signs include deep sensory hypersensitivity (Kerandel’s sign). In addition, myocarditis, epicarditis and pericardial effusion may occur. Meningitis, cerebral cortical congestion and edema, neuronal degeneration, and glial cell proliferation. The main clinical symptoms are personality changes and a state of aphonia. Abnormal reflexes occur, such as deep sensory hypersensitivity, ataxia, tremor, spasticity, and lethargy and somnolence.
The course of the disease due to the two types of trypanosomes is not the same. Trypanosoma gambiae has a chronic course, which may last from months to years, during which there may be several fevers, but the symptoms are mild. Sometimes there are no acute symptoms, but central nervous system abnormalities may occur; Rhodesian trypanosomiasis has an acute course of 3 to 9 months. Patients tend to present with significant wasting, high fever and exhaustion. Some patients die before the central nervous system is invaded.
Examination
1. Pathogen examination
Smear examination method can be used, take the patient’s blood smear staining microscopic examination. When the number of worms in the blood is high, the trypanosomes are mainly of elongated type, and when the number of worms in the blood is reduced due to the immune response of the host, the stubby and short type is predominant. Lymphatic fluid, cerebrospinal fluid, bone marrow aspirate, lymph node aspirate can also be taken for smear examination.
2. Serologic diagnostic methods
Enzyme-linked immunosorbent assay (ELISA), indirect fluorescent antibody test and indirect hemagglutination test are commonly used.
3. Molecular biology methods
In recent years, PCR and DNA probe technology have been applied to the diagnosis of trypanosomiasis with high specificity and sensitivity. In addition, animal inoculation is also a useful examination method.
Diagnosis
Trypanosomal “chancre”, irregular fever, severe headache, drowsiness, lethargy, enlarged lymph nodes, and tachycardia in individuals from endemic areas of Africa are helpful in the diagnosis. Confirmation of the diagnosis depends on the discovery of the causative agent.
Differential diagnosis
Trypanosomal “chancre” should be differentiated from other insect bites, cellulitis or pyoderma. The lymphohemorrhagic stage should be differentiated from febrile illnesses such as malaria, typhoid fever, regression fever, and viral hemorrhagic fever. The advanced stage should be differentiated from cerebral malaria, viral encephalitis, the acute phase of bacterial meningitis, tuberculous meningitis, neurosyphilis, and various types of meningitis or meningoencephalitis characterized by an increase in mononuclear cells in the cerebrospinal fluid. It should be noted that the disease is occasionally associated with a positive serologic test for syphilis.
Treatment
Therapeutic agents: Sulforaphane is effective in the early stages of the disease. Other drugs include pentamidine and melarsenol (melarsenol). In cases where the central nervous system has been involved, organic arsenic must be used.
Prognosis
The prognosis is good if there are no abnormalities in the cerebrospinal fluid. Those with obvious abnormal cerebrospinal fluid have a poor prognosis, with a cure rate of only 30%. Both types of human trypanosomiasis, untreated, can be fatal.
Prevention
Control of Gambian trypanosomiasis is based on screening and treating large numbers of asymptomatically infected persons, especially those with enlarged lymph nodes, as well as treating patients and improving livestock management. Personal protection should be strengthened when entering untreated tsetse fly breeding areas. This includes wearing long-sleeved tops and long-legged pants, brightly colored clothing, mosquito nets for sleeping, and insect repellents, all of which can defend against tsetse fly infestation. Tsetse fly eradication: Changing the breeding environment for vector insects, such as clearing undergrowth, spraying insecticides and other measures.