Focus–specific clinical profiles in human African trypanosomiasis caused by <i>Trypanosoma brucei rhodesiense</i>

&lt;p&gt;&lt;b&gt;Background:&lt;/b&gt; Diverse clinical features have been reported in human African trypanosomiasis (HAT) foci caused by &lt;i&gt;Trypanosoma brucei rhodesiense&lt;/i&gt; (&lt;i&gt;T.b.rhodesiense&lt;/i&gt;) 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.&lt;/p&gt; &lt;p&gt;&lt;b&gt;Methods/Principal Findings:&lt;/b&gt; We 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 &lt;i&gt;T.b.rhodesiense&lt;/i&gt; 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 &lt;i&gt;T.b.rhodesiense&lt;/i&gt; 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).&lt;/p&gt; &lt;p&gt;&lt;b&gt;Conclusions/Significance:&lt;/b&gt; We 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 &lt;i&gt;T.b.rhodesiense&lt;/i&gt; HAT has much relevance for both improvement of disease management and the identification of new drug therapy.&lt;/p&gt

Immunological aspects of viral infections of the nervous system

No abstract available

AIDS-neurological complications

No abstract available

Human immunodeficiency virus infection of the nervous system

No abstract available

Viral encephalitis

Acute viral encephalitis may be caused by a wide range of viruses but the most important is herpes simplex encephalitis (HSE) because of its severity, especially if untreated, and its good response to specific treatment with acyclovir. The outcome of any CNS viral infection is dependent on both the immune status of the host and the virulence of the infecting virus. In evaluating a patient with suspected viral encephalitis there are 3 essential steps, namely the identification of a true parenchymal virus infection of the brain rather than a non–infective encephalopathy, the distinction of an infectious viral encephalitis from an acute disseminated encephalomyelitis (ADEM), and then the determination, where possible, of the specific virus involved. In practice, the precise viral cause of the encephalitis may never be established. Analysis of the CSF for herpes simplex virus (HSV) DNA using the Polymerase Chain Reaction (PCR) has been a significant advance in the diagnosis of HSE as this test has a very high sensitivity and specificity especially with appropriate sample timing. It is essential to commence early treatment with intravenous acyclovir in patients suspected of having HSE because of the remarkable safety and efficacy of this drug and the dangers of delaying potentially effective treatment of life threatening disease. This review outlines the general management approach in patients suspected of having viral encephalitis

Review of "Clinical Neuroimmunology" ed. by J.A. Aarli, W.M.H. Behan and P.O. Behan

No abstract available

An alternative form of melarsoprol in sleeping sickness

Human African trypanosomiasis (HAT), or sleeping sickness, is a major threat to human health throughout sub-Saharan Africa. Almost always fatal if untreated or inadequately treated, a commonly used drug for treating late-stage HAT, and the only drug for late-stage Trypanosoma brucei rhodesiense, is intravenous melarsoprol, which kills 5% of patients receiving it. Melarsoprol cyclodextrin inclusion complexes have been tested in a highly reliable mouse model of HAT. These complexes increase the oral bioavailability of melarsoprol making them effective orally and both curative and nontoxic in doses that are equivalent to those of intravenous melarsoprol. It is argued that a small clinical trial of this drug in HAT is justified to potentially improve the outcome of patients with late-stage rhodesiense disease

Management of motor neurone disease

No abstract available

AIDS-neurological complications

No abstract available