An outbreak of lymphocutaneous sporotrichosis among mine-workers in South Africa

BACKGROUND The largest outbreak of sporotrichosis occurred between 1938 and 1947 in the gold mines of Witwatersrand in South Africa. Here, we describe an outbreak of lymphocutaneous sporotrichosis that was investigated in a South African gold mine in 2011. METHODOLOGY Employees working at a reopened section of the mine were recruited for a descriptive cross-sectional study. Informed consent was sought for interview, clinical examination and medical record review. Specimens were collected from participants with active or partiallyhealed lymphocutaneous lesions. Environmental samples were collected from underground mine levels. Sporothrix isolates were identified by sequencing of the internal transcribed spacer region of the ribosomal gene and the nuclear calmodulin gene. PRINCIPAL FINDINGS Of 87 male miners, 81 (93%) were interviewed and examined, of whom 29 (36%) had skin lesions; specimens were collected from 17 (59%). Sporotrichosis was laboratory-confirmed among 10 patients and seven had clinically-compatible lesions. Of 42miners with known HIV status, 11 (26%) were HIV-infected. No cases of disseminated disease were detected. Participants with 3 years’ mining experience had a four times greater odds of developing sporotrichosis than those who had been employed for >3 years (adjusted OR 4.0, 95%CI 1.2–13.1). Isolates from 8 patients were identified as Sporothrix schenckii sensu stricto by calmodulin gene sequencing while environmental isolates were identified as Sporothrix mexicana. CONCLUSIONS/SIGNIFICANCE S. schenckii sensu stricto was identified as the causative pathogen. Although genetically distinct species were isolated from clinical and environmental sources, it is likely that the source was contaminated soil and untreated wood underground. No cases occurred following recommendations to close sections of the mine, treat timber and encourage consistent use of personal protective equipment. Sporotrichosis is a potentially re-emerging disease where traditional, rather than heavily mechanised, mining techniques are used. Surveillance should be instituted at sentinel locations.http://www.plosntds.orgam201

Laboratory tests performed 2 weeks before or after the fungal diagnostic test for patients with proven, probable or possible laboratory-diagnosed endemic mycoses in South Africa, 2010–2020.

Laboratory tests performed 2 weeks before or after the fungal diagnostic test for patients with proven, probable or possible laboratory-diagnosed endemic mycoses in South Africa, 2010–2020.</p

Distribution of endemic mycoses in South Africa by province from 2010 to 2020.

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Endemic Mycoses in South Africa survey.

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Frequency of laboratory-diagnosed endemic mycoses (proven, probable and possible) per year in South Africa from 2010–2020, n = 682.

Frequency of laboratory-diagnosed endemic mycoses (proven, probable and possible) per year in South Africa from 2010–2020, n = 682.</p

Demographic and clinical characteristics of patients with proven, probable or possible laboratory-diagnosed endemic mycoses in South Africa (2010–2020), n = 682.

Demographic and clinical characteristics of patients with proven, probable or possible laboratory-diagnosed endemic mycoses in South Africa (2010–2020), n = 682.</p

Flow chart showing levels of certainty for cases of endemic mycoses reported in South Africa from 2010–2020, n = 682.

Flow chart showing levels of certainty for cases of endemic mycoses reported in South Africa from 2010–2020, n = 682.</p

Two echinocandin-resistant Candida glabrata FKS mutants from South Africa

Echinocandins are recommended as first-line agents to treat invasive infections caused by Candida glabrata since this organism is inherently less susceptible to azoles. However, resistance to echinocandins has been described in C. glabrata due to amino acid changes in the hotspot regions of the FKS1 and FKS2 genes. In this report, we describe the first two South African C. glabrata isolates with echinocandin resistance mediated by mutations in the FKS2 gene. Both isolates were cultured from urine specimens from private-sector patients