Direct detection and identification of Mycobacterium ulcerans in clinical specimens by PCR and oligonucleotide-specific capture plate hybridization

SummaryClinical diagnosis of Mycobacterium ulcerans infection is currently accepted as sufficient basis for treating the disease. Inadequate laboratory resources in the highly endemic areas of Africa often limit possibilities for in-country confirmation of clinical judgement. We analysed records of 99 Buruli ulcer (BU) patients diagnosed clinically and treated surgically at Amasaman Health Centre in Ghana, for whom post-treatment diagnostic laboratory tests were performed. Comparison of clinical diagnoses with test results obtained by an in-country laboratory on samples of excised tissue showed a high specificity of clinical judgement. Among lesions with three laboratory tests (microscopy for acid fast bacilli, culture and IS2404 polymerase chain reaction) done, 94% tested positive at least once and 83% twice. Thus correct clinical diagnosis of BU by well trained health workers is achievable, although the quality of clinical diagnosis should be monitored by intermittent testing in national reference laboratories. However, being retrospective, this study did not permit sensitivity and negative predictive value analysis.

Section: Discussionsupporting

confidence: 87%

Diagnosis of Mycobacterium ulcerans infection (Buruli ulcer) at a treatment centre in Ghana: a retrospective analysis of laboratory results of clinically diagnosed cases

Mensah-Quainoo

Yeboah-Manu

Asebi

et al. 2008

“…Identi®cation using a polymerasechain reaction is much more sensitive and more feasible. Several such tests have now been described (Portaels et al 1997;Ross et al 1997;Guimaraes-Peres et al 1999). Restriction fragment length polymorphism of M. ulcerans strains was reported using the pTBN12 probe (Jackson et al 1995).…”

Section: Introductionmentioning

confidence: 99%

Susceptibility to development of Mycobacterium ulcerans disease: review of possible risk factors

Stienstra

Graaf

Meerman

et al. 2001

SummaryMycobacterium ulcerans disease, also known as Buruli ulcer (BU), is a disease of subcutaneous fat tissue. BU is prevalent in riverine and swamp areas of the tropical zone in Africa, Asia and South America, and a few scattered foci in Australia. The mode of transmission of M. ulcerans has not been fully elucidated, but inoculation into the subcutaneous tissues probably occurs through penetrating skin trauma. BU has not been linked with HIV infection. Antimycobacterial drug treatment is ineffective, and treatment is surgical. Patients eventually develop scars and contractures, with resulting disabilities, and the disease imposes a large burden on affected populations. The incidence of BU has dramatically increased in West African countries over the last decade. There is an urgent need for research into host and environmental risk factors for BU in order to develop effective strategies to combat this disease. We review possible genetic host susceptibility factors for BU that are relevant in other mycobacterial diseases: natural resistance-associated macrophage protein-1 (NRAMP-1), HLA-DR, vitamin D 3 receptor, mannose binding protein, interferon-gamma (IFN-c) receptor, tumour necrosis factor alpha (TNF-a), interleukin (IL)-1a, 1b and their receptor antagonists; and IL-12. Schistosoma haematobium infection is highly endemic in many BU foci in West Africa, with a striking increase in transmission after river dams were constructed. This observation, and the observations from interaction of schistosomiasis and tuberculosis, have fuelled our hypothesis that schistosomiasis is a risk factor for BU by driving the host immune response towards a predominantly Th-2 pattern, away from a Th-1 preponderant protection against mycobacterial infection. If the latter hypothesis is con®rmed, enhanced schistosomiasis control should impact on BU.

“…DNA was amplified by a nested PCR specific for the genus Mycobacterium (De Beenhouwer et al 1995). Identification of the amplified DNA was performed by OSCPH (Oligonucleotide-specific capture plate hybridization) as previously described (Portaels et al 1997).…”

Section: Detection and Identification Of Mycobacteria By Pcr-oscphmentioning

confidence: 99%

Mycobacterium ulcerans infection in a child from angola: diagnosis by direct detection and culture

Rüsch-Gerdes²,

Richter³

et al. 1998

SummaryBuruli ulcer, caused by Mycobacterium ulcerans, is a chronic ulcerative skin disease, found predominantly in central and west Africa and Australia. A boy of 2.5 years of age from Angola was admitted to our hospital with severe kwashiokor and a large ulcer with undermined edges on the left side of the thorax. Further examination revealed anaemia, hypoproteinaemia, bacterial superinfection of the ulcer and intestinal parasites. Histological analysis showed acid-fast bacilli and histopathological changes typical of Buruli ulcer. M. ulcerans was detected by PCR and culture. The patient was treated by surgical excision of diseased skin, followed by split-skin grafting. He also received antibiotic therapy (ciprofloxacin, clarithromycin, rifabutin, and dapsone). After six months, the child was discharged from hospital in good condition. This is the first published case of Buruli ulcer from Angola.keywords Buruli ulcer, Mycobacterium ulcerans, Angola correspondence Dr W. Bär,