Sunday, October 24, 2021

Answer to Case 658

Answer to the Parasite Case of the Week 658: Trypanosoma brucei

Given the travel history and rapid onset of symptoms, T. b. rhodesiense is the most likely parasite present. This case shows very high parasitemia with numerous trypomastigotes seen on the patient's thick blood film. Here is the corresponding thin blood film, highlighting some of the key diagnostic features:

Note that the motile flagellate form (i.e., the trypomastigote) of T. brucei divides by binary fission in the peripheral blood. This is in contrast to Trypanosoma cruzi, the cause of American trypanosomiasis (a.k.a. Chagas disease), in which it is the non-motile tissue amastigote form that divides. Amastigotes are not seen with T. brucei infection.  

When seen in the peripheral blood, the trypomastigotes of T. brucei need to be differentiated from those of T. cruzi - particularly when the travel history is not known. Humans can also have transient asymptomatic parasitemia with some of the zoonotic trypanosomes.

So what are the next steps? 
If there was a concern for mixed trypanosomiasis/malaria, then examination of a thin film (and/or PCR) would be indicated, as suggested by Murtadha Maradun Mohammad.

If we are uncertain of the infecting Trypanosoma subspecies (e.g., if the patient was in Uganda where both T. b. rhodesiense and T. b. gambiense are present), then we could also perform serology or PCR as noted by John Markantonis and Harsha Sheorey.

Importantly, LS noted that examination of the CSF would be the next step once we have confirmed the diagnosis, since detection of parasites in the CSF would change the treatment regimen. 

You can read about the treatment regime for early and late (CNS) stage Rhodesian trypanosomiasis HERE. The only approved therapy for late stage Rhodesian is melarsoprol, an arsenic-containing compound that causes encephalopathic reactions in 5–10% of patients. When this occurs, there is a ~50% case-fatality rate (!) 

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