Buruli ulcer, caused by Mycobacterium ulcerans is a serious condition that seems to be increasing in several parts of Africa. It is also found in southeastern Australia. How the infection is transmitted is unclear, though it is generally believed that M. ulcerans is an aquatic pathogen and that humans are infected through contact with certain aquatic environments (swamps and slow-flowing water). But now Australian research [1] has suggested that wild mammals may play an important role.

The researchers collected a range of environmental samples from a small town endemic for the disease and from areas with few or no reported incident cases. M. ulcerans DNA was detected in soil, sediment, water residue, aquatic plant biofilm and terrestrial vegetation collected in the endemic area, with higher levels in the faeces of two species of possum than in other samples. (Possums are small arboreal marsupial mammals, native to Australia.)

Systematic testing of possum faeces detected M. ulcerans DNA in 41% of faecal samples collected in the endemic town, compared with less than 1% of faecal samples collected from non-endemic areas. Capture and clinical examination of live possums in the endemic area revealed that 38% and 24% of the two species respectively had laboratory-confirmed M. ulcerans skin lesions and/or M. ulcerans-positive faeces. Whole genome sequencing also revealed an extremely close genetic relationship between human and possum M. ulcerans isolates.

These findings raise the possibility that mammals are an environmental reservoir for Buruli ulcer infection but further research will be necessary, particularly in Africa. The Australian researchers note that there has been research in West Africa, which failed to detect M. ulcerans in the organs or faeces of rodents and shrews, but clearly the issue deserves further attention.

Reference
1. Fyfe JAM, Lavender CJ, Handasyde KA, Legione AR, O’Brien CR, et al. (2010). A Major Role for Mammals in the Ecology of Mycobacterium ulcerans. PLoS Negl Trop Dis 4(8): e791. Available online: http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0000791
2. Vandelannoote K, Durnez L, Amissah D, Gryseels S, Dodoo A, et al. (2010). Application of real-time PCR in Ghana, a Buruli ulcer-endemic country, confirms the presence of Mycobacterium ulcerans in the environment. FEMS Microbiol Lett 304: 191–194.
3. Durnez L, Suykerbuyk P, Nicolas V, Barriere P, Verheyen E, et al. (30 April 2010) The role of terrestrial small mammals as reservoir of Mycobacterium ulcerans in Benin. Appl Environ Microbiol.

Anyone who studies the life sciences beyond a certain level is required to learn the details of the metabolic pathway known as the Krebs cycle. Named after its discoverer Hans Krebs and also called the tricarboxylic acid (TCA) cycle, the process is central to metabolism and provides most of the energy used by the vast majority of living things …but not the malaria parasite. Recently published research by US molecular biologists [1] has confirmed earlier suspicions that Plasmodium falciparum meets its energy needs by a very different process.

An article in US News features an interview with one of the research team, Kellen Olszewski, who explains that the breakdown of sugar by the malaria parasite is completely disconnected from the Krebs cycle; it is instead fed by the amino acids glutamine and glutamate and is a branched rather than a cyclical pathway: “The parasite has basically taken the standard textbook circular cycle and broken it in half, running one half in the normal direction and the other backwards. This turns the textbook model on its head”.

Nothing similar has so far been found in any other parasite. The research represents a major step forward in understanding of energy and biosynthetic processes in Plasmodium parasites. This new knowledge may in time make possible the identification of potential drug targets, leading to the development of new malaria treatments.

Reference
1. Olszewski KL, Mather MW, Morrisey JM, Garcia BA, Vaidya AB, Rabinowitz JD, Llinás M (2010). Branched tricarboxylic acid metabolism in Plasmodium falciparum. Nature; 466(7307):774-778.

Protecting women against malaria is regarded as a priority. Pregnant women are more vulnerable to the disease, which can also harm their unborn children. However, research in Mumbai, India apparently suggests that men there are more likely than women to have malaria. The records were analysed of 30,000 patients presenting to hospitals with malaria-like symptoms. [Men were in the majority, for which there could be several possible explanations.] It was found that 12% of men but only 6% of women were infected.

Dr Shobhona Sharma, one of the researchers, told the Hindustan Times that: “In children, both sexes are affected by the parasite in the same manner, but the moment one goes to the pubertal age group, men tend to show and experience the symptoms more than women. We think the hormones testosterone and oestrogen may be influencing the way immune cells react when exposed to the parasite”.

The research team’s work has yet to be formally published but the same group, using mice, have reported a gender difference in response to malaria infection [1].

Reference
1. Basant A, Rege M, Sharma S, Sonawat HM (2010). Alterations in urine, serum and brain metabolomic profiles exhibit sexual dimorphism during malaria disease progression. Malar J;9:110.