Anaemia in human African trypanosomiasis caused by &lt;i&gt;Trypanosoma brucei rhodesiense&lt;/i&gt;

Chisi, John; Misiri, Humphreys E; Zverev, Yuriy; Nkhoma, A; Sternberg, Jeremy M.

doi:10.4314/eamj.v81i10.9232

Cited by 27 publications

(20 citation statements)

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“…The level of human infections has been on the decline, while the data for domestic animal infections is scanty. [19][20][21][22] The present study has also confirmed that both human and animal infections are likely to be caused by the Trypanosoma brucei subspecies in and around Nkhotakota Wildlife Reserve. Cases of trypanosomiasis have been reported in tourists and soldiers that have visited some of Malawi's wildlife reserves.…”

Section: Discussionsupporting

confidence: 78%

Polymerase chain reaction identification of <i>Trypanosoma brucei rhodesiense</i> in wild tsetse flies from Nkhotakota Wildlife Reserve, Malawi

et al. 2017

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BackgroundTrypanosoma brucei rhodesiense is the causative agent of acute human African trypanosomiasis. Identification of T. b. rhodesiense in tsetse populations is essential for understanding transmission dynamics, assessng human disease risk, and monitoring spatiotemporal trends and impact of control interventions. Accurate detection and characterisation of trypanosomes in vectors relies on molecular techniques. For the first time in Malawi, a molecular technique has been used to detect trypanosomes in tsetse flies in Nkhotakota Wildlife Reserve. MethodsA polymerase chain reaction (PCR) technique was used to identify the serum resistance associated (SRA) gene of T. b. rhodesiense in tsetse flies. Of 257 tsetse flies that were randomly caught, 42 flies were dissected for microscopic examination. The midguts of 206 flies were positive and were individually put in eppendorf tubes containing phosphate-buffered saline (PBS buffer) for DNA extraction. Internal transcribed spacer (ITS)-PCR was first used to isolate all trypanosome species from the flies. TBR PCR was then used to isolate the Trypanozoon group. T. brucei-positive samples were further evaluated by SRA PCR for the presence of the SRA gene.

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Section: Discussionsupporting

confidence: 78%

Polymerase chain reaction identification of <i>Trypanosoma brucei rhodesiense</i> in wild tsetse flies from Nkhotakota Wildlife Reserve, Malawi

et al. 2017

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“…Consistent with the studies in animals, human trypanosome infections also result in substantial hemolysis and release of free Hb [50]. While Hp initially binds all free Hb, the clearance of the Hp–Hb complex would result in a significant drop in Hp levels to the point where Hpr would become a major Hb-binding protein.…”

Section: Discussionsupporting

confidence: 66%

Hemoglobin Is a Co-Factor of Human Trypanosome Lytic Factor

et al. 2007

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Trypanosome lytic factor (TLF) is a high-density lipoprotein (HDL) subclass providing innate protection to humans against infection by the protozoan parasite Trypanosoma brucei brucei. Two primate-specific plasma proteins, haptoglobin-related protein (Hpr) and apolipoprotein L-1 (ApoL-1), have been proposed to kill T. b. brucei both singularly or when co-assembled into the same HDL. To better understand the mechanism of T. b. brucei killing by TLF, the protein composition of TLF was investigated using a gentle immunoaffinity purification technique that avoids the loss of weakly associated proteins. HDL particles recovered by immunoaffinity absorption, with either anti-Hpr or anti-ApoL-1, were identical in protein composition and specific activity for T. b. brucei killing. Here, we show that TLF-bound Hpr strongly binds Hb and that addition of Hb stimulates TLF killing of T. b. brucei by increasing the affinity of TLF for its receptor, and by inducing Fenton chemistry within the trypanosome lysosome. These findings suggest that TLF in uninfected humans may be inactive against T. b. brucei prior to initiation of infection. We propose that infection of humans by T. b. brucei causes hemolysis that triggers the activation of TLF by the formation of Hpr–Hb complexes, leading to enhanced binding, trypanolytic activity, and clearance of parasites.

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“…rhodesiense infection [30], [44] or has been attributed to other parasitic infections or malnutrition [45], [46], [47]. The high rate of anaemia in HAT cases in Malawi (including a subset of the Nkhotakota patients in this study) has been previously reported [48]. Marked differences in other HAT presenting signs and symptoms between study sites allowed us to establish T.b.…”

Section: Discussionmentioning

confidence: 55%

Focus–Specific Clinical Profiles in Human African Trypanosomiasis Caused by Trypanosoma brucei rhodesiense

MacLean

Odiit²,

Chisi

et al. 2010

PLoS Negl Trop Dis

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BackgroundDiverse clinical features have been reported in human African trypanosomiasis (HAT) foci caused by Trypanosoma brucei rhodesiense (T.b.rhodesiense) giving rise to the hypothesis that HAT manifests as a chronic disease in South-East African countries and increased in virulence towards the North. Such variation in disease severity suggests there are differences in host susceptibility to trypanosome infection and/or genetic variation in trypanosome virulence. Our molecular tools allow us to study the role of host and parasite genotypes, but obtaining matched extensive clinical data from a large cohort of HAT patients has previously proved problematic.Methods/Principal FindingsWe present a retrospective cohort study providing detailed clinical profiles of 275 HAT patients recruited in two northern foci (Uganda) and one southern focus (Malawi) in East Africa. Characteristic clinical signs and symptoms of T.b.rhodesiense infection were recorded and the degree of neurological dysfunction determined on admission. Clinical observations were mapped by patient estimated post-infection time. We have identified common presenting symptoms in T.b.rhodesiense infection; however, marked differences in disease progression and severity were identified between foci. HAT was characterised as a chronic haemo-lymphatic stage infection in Malawi, and as an acute disease with marked neurological impairment in Uganda. Within Uganda, a more rapid progression to meningo-encephaltic stage of infection was observed in one focus (Soroti) where HAT was characterised by early onset neurodysfunction; however, severe neuropathology was more frequently observed in patients in a second focus (Tororo).Conclusions/SignificanceWe have established focus-specific HAT clinical phenotypes showing dramatic variations in disease severity and rate of stage progression both between northern and southern East African foci and between Ugandan foci. Understanding the contribution of host and parasite factors in causing such clinical diversity in T.b.rhodesiense HAT has much relevance for both improvement of disease management and the identification of new drug therapy.

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Anaemia in human African trypanosomiasis caused by <i>Trypanosoma brucei rhodesiense</i>

Cited by 27 publications

References 0 publications

Polymerase chain reaction identification of <i>Trypanosoma brucei rhodesiense</i> in wild tsetse flies from Nkhotakota Wildlife Reserve, Malawi

Polymerase chain reaction identification of <i>Trypanosoma brucei rhodesiense</i> in wild tsetse flies from Nkhotakota Wildlife Reserve, Malawi

Hemoglobin Is a Co-Factor of Human Trypanosome Lytic Factor

Focus–Specific Clinical Profiles in Human African Trypanosomiasis Caused by Trypanosoma brucei rhodesiense

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