African Trypanosomiasis — photos

Symptoms and syndromes in photos

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African trypanosomiasis is confined to equatorial Africa with a patchy distribution depending upon detailed topo­graphical conditions. It is caused by two subspecies of Trypanosoma brucei. Trypanosoma brucei. gambiense infection is widespread in West and Central Africa but Trypanosoma brucei. rhodesiense is restricted to the East and East Central areas with some overlaps between the two. Slanted lines indicate Trypanosoma brucei. gambiense; solid areas Trypanosoma brucei. rhodesiense.

Distribution map of African trypanosomiasis

Distribution map of African trypanosomiasis

T.b. rnodesiense in rat blood.

Photo 1. Trypanosoma brucei rhodesiense in rat blood. Trypanosoma brucei gambiense, Trypanosoma brucei rhodesiense (and T. b. brucei of animals) are virtually indistinguishable in blood films. They are polymorphic; ie long, thin, intermediate and short stumpy forms of trypomasti-gotes may coincide. Note the small kinetoplast and free flagellum. Both subspecies from man will infect guinea pigs but only Trypanosoma brucei. rhodesiense is infective to rats. (X1250)

T.b. rnodesiense in rat blood too.

Photo 2. T.b. rnodesiense in rat blood too.

Diagram of ultrastructure of T.b. gambiense.

Photo 3. Diagram of ultrastructure of T.b. gambiense. A - free flagellum; В - micro­tubules of pellicle; С - nucleus; D - mitochondrion; E - kinetoplast; F - cyto­plasmic granule; G - reservoir; H - basal body of flagellum; I - Golgi apparatus; J - endoplasmic reticulum; К - ribosomes; L - fold of pellicle; M - attached flagellum; N - undulating membrane. (x 30000)

Tsetse fly feeding.

Photo 4. Tsetse fly feeding. The common vectors of T. b. gambiense are Glossina palpalis and G. tachinoides in West Africa. T. b. rhodesiense is associated with G. morsitans, G. swynnertoni and G. pallidipes. Other, secondary vectors have more localised distributions. (x4)

Trypanosomes in section of tsetse fly.

Photo 5. Trypanosomes in section of tsetse fly.

After ingestion by the tsetse fly, the trypomastigotes pass to the midgut. After asexual reproduction the parasites migrate forward between the peritrophic membrane and gut wall to re-enter the pharynx and proboscis. They migrate back into the salivary glands when they transform first into epimastigotes, then to the infective stage (metacyclic trypomastigotes). The section shows trypomastigotes massed at the entrance to the midgut ready to enter the proventriculus. fx 90).

Metacyclic trypanosomes in saalivary probe

Photo 6. Metacyclic trypanosomes in salivary probe.

The infective stages are passed into the bite together with the saliva when the fly next feeds. They may be observed in saliva expressed from the proboscis of the fly onto a microscope slide. (X 900)

Larva, pre-pupa and pupa of Glossina morsitans.

Photo 7. Larva, pre-pupa and pupa of Glossina morsitans. A single larva develops inside the female tsetse fly and is deposited when mature in dry soil. Here it pupates and metamorphoses to the adult. (x4)

Ecology of gambiense infection.

Photo 8. Ecology of gambiense infection. 

Gambiense trypanosomiasis is transmitted by riverine species of Glossina requiring optimum shade and humidity. Shady trees near lakes, river and pools of water are ideal habitats. The figure shows a typical site for transmission by G. palpalis in the hinterland of Liberia. Man/fly contact is intimate when villagers congregate around pools for collecting water or washing. Glossina tachinoides is second in importance to G. palpalis as a vector of sleeping sickness. Rhodesiense trypanosomiasis can occur in scrub savannah country because the Glossina vectors are less dependent on moisture. Moreover, in such terrain wild animals and domestic cattle provide alternative feeding opportunities for the fly. Trypanosomiasis is a serious disease of domestic animals, causing great economic loss and depriving human populations of much needed protein. T. vivax and T. congolense are the commonest parasites involved. Pigs may also be decimated by other species.

Bushbuck reservoirs of T. rhodesiense.

Photo 9. Bushbuck reservoirs of T. rhodesiense. A reservoir of T. rhodesiense was long suspected in wild animals. The first species found infected with this trypanosome was fhe bushbuck (Tragelaphus scriptus), but other species of game animals have since been found to harbour parasites.

Trypanosomal chancre.

Photo 10. Trypanosomal chancre.

The bite reaction, the earliest clinical lesion, is known as a 'trypanosomal chancre'. It resembles a boil but is usually painless. Fluid aspirated from the nodule con­tains actively dividing trypanosomes.

Trypanosomal rash.

Photo 11. Trypanosomal rash. In fair­skinned individuals each peak of fever may be accompanied by a remarkable skin eruption in the form of annular patches of erythema.

Temperature chart in a patient with trypanosomiasis.

Photo 12. Temperature chart in a patient with trypanosomiasis.

Irregularly occurring episodes of pyrexia are often associated with the rash. Trypanosomes appear in the blood one to three weeks after infection. They may be scanty in gambiense but are commonly numerous in rhodesiense infection which is usually a more fulminating disease. 1 - headache; 2 - trypanosomal chancre; 3 - oedema of 1. eyelid; 4 - rash; 5 - rash.

Cervical lymphadenopathy — keloid scars following attemted excision.

Photo 13. Cervical lymphadenopathy — keloid scars following attemted excision. Enlargement of lymphatic glands, especially in the posterior triangle of the neck ('Winterbottom's sign') is an important clinical feature of T. gambiense infection, and calls for diagnostic puncture of the gland.

Gland puncture.

Photo 14. Gland puncture. Gland puncture can provide early diagnosis of trypanosomiasis.

Trypanosomes in gland fluid.

Photo 15. Trypanosomes in gland fluid. The trypanosomes are easily identified as actively motile organisms in the wet preparation of aspirated gland juice. Their identity can be confirmed by staining. (xl250)

Sleeping sickness.

Photo 16. Sleeping sickness. 

In the absence of treatment, the patient with gambiense infection becomes progressively more wasted and comatose, finally showing the classical picture of sleeping sickness as the CNS becomes involved. Rhodesiense infection often leads to death from toxic manifestations before CNS changes are evident. This Ghanaian child was diagnosed as having sleeping sickness during a smallpox control campaign; she was very somnolent but not cachetic.

Lumbar puncture.

Photo 17. Lumbar puncture. This procedure should be carried out to determine whether the CNS has been invaded. In such instances, the CSF will reveal a lymphocytic pleocytosis, an increased protein content and trypanosomes may be found in stained films of the centrifuge deposit. In T. rhodesiense infection invasion of the CNS may occur within four to eight months, whereas several years usually elapse before meningoencephalitis develops in gambiense disease.

Quantitative IgM radial diffusion assay.

Photo 18. Quantitative IgM radial diffusion assay. IgM values are raised both in the blood and the CSF in trypanosomiasis. This is an important diagnostic finding both for individuals and for field surveys. Other valuable serological aids are the CFT and FAT. (From left: well l-55mg%; well 2-110mg%; well 3-220mg%; well - 4 patient's serum 170mg%)

Microscopic changes in brain.

Photo 19. Microscopic changes in brain. 

The leptomeninges are congested, there may be oedema and small haemorrhages are commonly present. The basic pathological change is a meningoencephalitis in which perivascular cuffing with round cells is often pronounced. Scattered irregularly through the brain substance there occur large eosinophilic mononuclear cells with eccentric nuclei known as morula cells of Mott. (X 90)

Morulla cell.

Photo 20. Morulla cell. The morula cell of Mott is an IgM-producing plasma cell as shown in this preparation treated with anti-IgM antibody, (x 900)

Cycle in vertebrate hosts.

Photo 20. Cycle in vertebrate hosts.

A. Trypomastigote stages (2) of Trypanosoma brucei gambiense or rhodesiense are produced in the blood and tissue spaces of man when he is bitten by a tsetse fly. The parasites may be found in various glands (3) as well as in the blood. B. Trypomastigotes ingested by the tsetse fly transform into epimastigotes (4) which divide (5) during a complicated migration in the fly, eventually forming metacyclic trypomastigotes (6). These can infect another man or reservoir animals (C) in which the blood and tissues are invaded as in man (2).



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