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Tuberculosis in resource poor countries; better access to antiretroviral therapy and isoniazid prophylaxis offer new opportunities for control [editorial]
No full textDiagnostic delay in a multi-organ tuberculosis immunocompetent patient: a case report
No full textA 67-year-old immunocompetent male presented with intermittent fever for 3 months associated with urinary incontinence, altered bowel habits and history of loss of appetite and weight. He was treated as having enteric fever at various clinics in the city by different physicians. On evaluation the patient was found to have disseminated tuberculosis with involvement of the lungs, eyes, testes, brain, bone, kidneys, liver, spleen and possibly the gastrointestinal tract. This paper reports a case of disseminated tuberculosis to many organs with significant diagnostic delay more than twelve decades after the discovery of the tuberculosis bacillus by Robert Koch
Co-trimoxazole prophylaxis in tropical countries in the era of highly active antiretroviral therapy: do we know enough?
No full textCo-trimoxazole prophylaxis in HIV-infected persons is beyond doubt one of the cheapest and most important interventions, next to antiretroviral therapy (ART), to improve survival. However, many questions, ranging from programme coverage and public health impact to individual tolerance and compliance, remain unanswered. Together with the need for more research to identify optimal ART regimens for resource-poor settings, research regarding optimal chemoprophylaxis against opportunistic infections should also remain high on the agenda
Special infectious disease risks of expatriates and long-term travelers in tropical countries. Part II: Infections other than malaria
No full textThe definitive version is available at www3.interscience.wiley.comA wide range of viral, bacterial, and protozoal diseases pose risk to long-term tropical travelers. Risk varies geographically and with lifestyle. For some infections, risk increases with duration of stay, coming to resemble that of the local population. Risk management strategies include vaccination, chemoprophylaxis, avoidance measures, and screening, where appropriate. Vaccination against hepatitis A and B, typhoid, and rabies is recommended for all long-term travelers to (sub-)tropical areas. Lowering of the vaccination threshold for Japanese encephalitis is suggested. Meningococcal disease is rare in travelers, but vaccination is safe and acceptable. The efficacy of Bacillus Calmette-Guérin (BCG) is uncertain; immunological testing avoids BCG's confounding of tuberculin testing. Diarrhea is common, and self-treatment may be recommended. Sexually transmitted infections including human immunodeficiency virus (HIV) are serious risks; education, screening, and HIV postexposure prophylaxis following involuntary exposure are recommended. Many infections are chronic or asymptomatic, and appropriate screening is recommended on return or after prolonged exposure
Visceral leishmaniasis: what are the needs for diagnosis, treatment and control?
No full textVisceral leishmaniasis (VL) is a systemic protozoan disease that is transmitted by phlebotomine sandflies. Poor and neglected populations in East Africa and the Indian sub-continent are particularly affected. Early and accurate diagnosis and treatment remain key components of VL control. In addition to improved diagnostic tests, accurate and simple tests are needed to identify treatment failures. Miltefosine, paromomycin and liposomal amphotericin B are gradually replacing pentavalent antimonials and conventional amphotericin B as the preferred treatments in some regions, but in other areas these drugs are still being evaluated in both mono- and combination therapies. New diagnostic tools and new treatment strategies will only have an impact if they are made widely available to patients
Lack of evidence for the involvement of rectal and oral trichomonads in the aetiology of vaginal trichomoniasis in Ghana
No full textOBJECTIVE: To investigate the possible involvement of human trichomonads (Pentatrichomonas hominis and Trichomonas tenax) other than Trichomonas vaginalis in the aetiology of vaginal trichomoniasis. METHODS: Vaginal swabs taken from women attending antenatal clinics were tested for Trichomonas vaginalis by traditional assays (wet-mount microscopy and InPouch culture) and nucleic acid amplification (polymerase chain reaction). These swabs were also tested for the presence of P hominis and T tenax by nucleic acid amplification. Oral and rectal swabs from these women were tested for T tenax and P hominis respectively. Data on sociodemographic characteristics, sexual and anogenital hygiene practices likely to seed P hominis and T tenax into the vagina were collected by a questionnaire. RESULTS: 93% (161) of the 173 samples in which T vaginalis was detected by wet preparation or culture was evaluable by PCR. Of this, T vaginalis was detected in 94% (152) by T vaginalis-specific PCR. Neither P hominis nor T tenax was detected in any of the vaginal swab samples. These included nine samples for which T vaginalis had been detected by wet preparation or culture, but were negative by T vaginalis nucleic acid amplification. P hominis and T tenax were not detected in any of the rectal and oral swabs, respectively. CONCLUSION: In this group of women, there was no evidence for the involvement of trichomonads other than T vaginalis in the aetiology of vaginal trichomoniasis
Evidence for intramacrophage growth phase of Mycobacterium ulcerans
No full textMycobacterium ulcerans is the etiologic agent of Buruli ulcer (BU), an emerging tropical skin disease. Virulent M. ulcerans secretes mycolactone, a cytotoxic exotoxin with a key pathogenic role. M. ulcerans in biopsy specimens has been described as an extracellular bacillus. In vitro assays have suggested a mycolactone-induced inhibition of M. ulcerans uptake by macrophages in which its proliferation has not been demonstrated. Therefore, and uniquely for a mycobacterium, M. ulcerans has been classified as an extracellular pathogen. In specimens from patients and in mouse footpad lesions, extracellular bacilli were concentrated in central necrotic acellular areas; however, we found bacilli within macrophages in surrounding inflammatory infiltrates. We demonstrated that mycolactone-producing M. ulcerans isolates are efficiently phagocytosed by murine macrophages, indicating that the extracellular location of M. ulcerans is not a result of inhibition of phagocytosis. Additionally, we found that M. ulcerans multiplies inside cultured mouse macrophages when low multiplicities of infection are used to prevent early mycolactone-associated cytotoxicity. Following the proliferation phase within macrophages, M. ulcerans induces the lysis of the infected host cells, becoming extracellular. Our data show that M. ulcerans, like M. tuberculosis, is an intracellular parasite with phases of intramacrophage and extracellular multiplication. The occurrence of an intramacrophage phase is in accordance with the development of cell-mediated and delayed-type hypersensitivity responses in BU patients
Molecular investigation of recurrent tuberculosis in patients from Rwanda
No full textSETTING: Pulmonary tuberculosis (TB) patients enrolled in four provinces of Rwanda. OBJECTIVE: To determine the cause of recurrent TB. DESIGN: Serial Mycobacterium tuberculosis isolates obtained from patients with recurrent TB from January 2002 to September 2005 were genotyped by spoligotyping and mycobacterial interspersed repetitive unit-variable number of tandem repeat (MIRU-VNTR) typing. Drug resistance was determined by phenotypic susceptibility testing and sequencing of rpoB, katG, inhA and embB genes. RESULTS: Among 710 culture-positive TB patients enrolled in the study, initial drug susceptibility testing results were available for 638. Sixty-nine of these had multidrug-resistant (MDR) TB and 569 were non-MDR-TB. Among the MDR-TB patients, 22 had follow-up isolates after cure (n = 12) or chronic infection (n = 10). The DNA patterns of sequential isolates from 4 of the 12 previously cured MDR-TB patients were different, indicating re-infection. DNA patterns of isolates from the remaining 8 previously cured and 10 chronic MDR-TB patients were identical, suggesting reactivation and treatment failure, respectively. Among the non-MDR-TB patients, disease recurrence was observed in one case; this was determined to be due to reactivation after initial mixed infection. CONCLUSION: These results document a high treatment failure/reactivation rate for MDR-TB and suggest that re-infection within 2 years may not be a common cause of recurrent TB in this setting