Up to a million children die every year from pneumococcal infections, mainly as a result of pneumonia or meningitis. (See a recent TropIKA.net news story.) In the developed world, vaccination with pneumococcal conjugate vaccine (PCVs) is now widespread and cases of the disease usually receive effective treatment. Nine-eight per cent of pneumococcal deaths occur in developing countries. The need for vaccination programmes in those countries is abundantly clear.

Are people with sickle cell disease (an inherited disorder that is extremely common in Africans) at particular risk of contracting pneumococcal disease? The condition is known to cause an immune deficit so it seems likely to be a risk factor. Those people with SCD who live in developed countries receive prophylactic treatment with penicillin, as well as pneumococcal vaccination, and this is considered to be a major factor in the reduction of morbidity and mortality in SCD patients in these countries.

People with SCD in developing countries would, therefore seem, to be priority targets for pneumococcal vaccination programmes and they should also be receiving penicillin prophylaxis. However, this has been challenged because there are no published studies proving that children in Africa with SCD are particularly at risk of pneumococcal disease. Writing in Archives of Disease in Childhood, Stephen Obaro of Michigan State University argues that absence of evidence of this risk is not evidence of absence.

In his extensive review article (1) Dr Obaro notes the lack of reliable data as to the causes of morbidity and mortality in people with SCD living in Africa. He calls for further research into this issue. However, he believes that, “It is unlikely that African children with SCD will be at less risk from IPD [invasive pneumococcal disease] than children without this condition”. Given their compromised immune systems he argues that a full range of prophylactic measures is required for these children.

Reference
1. Obaro S (2009). Pneumococcal Disease in Sickle Cell Disease in Africa: Does Absence of Evidence Imply Evidence of Absence? Arch Dis Child; May 3.

http://adc.bmj.com/cgi/content/abstract/adc.2008.154815v1?ct=ct

Researchers say they have developed a way in which outbreaks of dengue fever could be predicted 40 weeks in advance (in Latin America and the Caribbean), and which would give some idea of their likely scale. Focusing on Costa Rica, which saw over 100 000 cases of the disease from 2003 to 2007, the researchers used sea-surface temperature anomalies related to the El Niño Southern Oscillation (ENSO) plus satellite observations of vegetation greenness.

The research team, based in Costa Rica and at the University of Miami, USA, went on to devise a mathematical model which can explain 83% of the variance in weekly dengue fever/dengue haemorrhagic fever cases when run back in time. And when run forwards in time, it can explain 64% of the variance. The researchers say their model may be used to inform national vector control programmes in Costa Rica and that it potentially scalable to the broader region of Latin America and the Caribbean.

The modelling study is published in Environmental Research Letters (1). In an interview for environmentalresearchweb lead researcher Dough Fuller said his team had also shown the model to work well in Trinidad and that a paper on this would be published later this year.

Reference
1. Fuller D. Troyo A, Beier JC (2009). El Ni˜no Southern Oscillation and vegetation dynamics as predictors of dengue fever cases in Costa Rica. Environ Res Lett; 4,1-8.

A family of proteins that helps influence the development of the parasite that causes sleeping-sickness (human African trypanosomiasis, HAT) has been identified in a study (1) reported in Nature. The authors argue that the protein family will prove a useful biomarker and may aid in the development of new treatments.

Keith Matthews and colleagues at the University of Edinburgh, UK show that the PAD (proteins associated with differentiation) family of proteins helps the parasite, Trypanosoma brucei, respond to specific environmental cues that influence its form — the parasites have a complex life cycle, and exist in different forms in mammalian and insect hosts.

The proteins are expressed on the surface of the transmission-competent ‘stumpy-form’ parasites in the bloodstream. When PAD expression is abolished, the ability to change shape in response to key environmentalcues is diminished.

A commentary (2) on the study has been published in the same issue of Nature.

References
1. Dean S, Marchetti R, Kirk K, Matthews KR (2009). A surface transporter family conveys the trypanosome differentiation signal. Nature; 459(7244):213-217.
2. Shadan S (2009). Microbiology: Signals for change. Nature; 459(7244):175.