|Clinical Guidelines and Treatment Manual (MSF, 1993, 319 p.)|
|Chapter 6 - Parasitic diseases|
African trypanosomiasis = sleeping sickness
- African trypanosomiasis is caused by a flagellated protozoan, which is transmitted to humans by the tsetse fly (Glossina spp)
- There are two species of the parasite, each having a different geographical distribution:
· Trypanosoma brucei gambiense (West Africa)
· T. b. rhodesiense (East Africa)
Clinical manifestations of infections with the two species are similar, except that T. b. rhodesiense infections tend to run a more rapid course.
- Primary stage: sometimes a painless chancre appears at site of bite. Incubation period very variable (days to years).
- Blood stage: fever, adenopathy, hepatosplenomegaly and facial edema. Presence of trypanosomes in blood and in lymph: gland puncture, blood film
- Cerebral stage: chronic meningoencephalomyelitis
· "Sleeping sickness": psychiatric, motor and sensory signs
· Disturbed sleep pattern: hepatosplenomegaly and adenopathy may resolve, blood film becomes negative for trypanosomes, specific serology positive, CSF (raised numbers of lymphocytes (> 5/mm3), raised protein, sometimes presence of trypanosomes, CATT test on serum, Elisa or CSF).
- Other manifestations: T. b. rhodesiense infections may be complicated by a fatal myocarditis.
A trypanosomiasis control program must only be conducted in coordination with national health authorities. Consult specialized documents or monographs. Elements:
- Active case detection and treatment.
- Vector control.
- Notification of cases to health authorities (surveillance).
The choice of regimen is based upon the results of CSF examination. If CSF is normal, the disease is considered to be in the blood stage. Abnormal CSF indicates cerebral involvement.
Therapy should of course follow national guidelines. Refer also to the WHO monograph (Technical Report Series 739).
Where resistance to melarsoprol develops, use nifurtimox according to national guidelines or DFMO.
Ameriacan trypanosomiasis = Chagas' disease
Disease caused by Trypanosoma cruzi, transmitted to humans through the feces of infected reduviid bugs, which live in cracks in walls. T. cruzi infects humans via skin lesions (scratches, or bug bite) or mucus membranes, especially the conjunctivae.
- Incubation:10 to 20 days
- Acute phase:
· Chagoma: chancre, often on face
· Unilateral edema of the eyelid and adenopathy
· Persistent fever, generalized adenopathy
· Acute myocarditis: chest pain, CCF
· Meningoencephalitis: paralyses, convulsions
- Chronic phase (after a long latent period):
· Chronic cardiomyopathy: arrythmias, CCF, angina
· Megacolon, megaesophagus
- Acute phase:
· blood slide: often difficult to find the parasite.
· Xenodiagnosis: examination of the feces of reduvid bugs that have fed upon the patients blood.
- Chronic phase: serology.
Treatment (dispensary - hospital)
- In spite of progress, treatment for T. cruzi infections is not entirely satisfactory. The drug of choice is at present: nifurtimox(PO): 8 to 10 mg/kg/d divided in 3 doses x 3-4 months.
· No alcohol during therapy (Antabuse effect)
· Give prednisone ou prednisolone (PO): 1 to 2 mg/kg/day at the same time and taper off gradually.
NB: this use of corticosteroids is controversial: some sources
claim it can exacerbate the disease.
Side effects (may be severe): gastritis, agitation, convulsions, tremor, paraesthesiae.
· Contraindications: pregnancy, history of convulsions.
- benzonidazole(PO): 5 to 8 mg/kg/day x 30 days.
· Side effects: rash, peripheral neuritis
Indications for therapy
- Both drugs are active during the acute phase.
Only benzonidazole has an effect during the chronic phase.
- Give supportive treatment of convulsions, CCF and pain.
- Mosquito nets.
- Vector control (insecticides): residual insecticides.
- Improved housing: plastered walls, corrugated iron rooves, cemented floors all reduce the vector habitat (thatch, small cracks in mud).