Malaria infections cause more than 200 million new clinical cases and approximately 400,000 deaths annually. An efficient malaria vaccine is yet to be developed and resistance has emerged against all anti-malarial treatments. The most severe form of the disease, cerebral malaria has the highest mortality rate and may result in life-long impacts such as neurological deficits on survivors. We are yet to fully understand why the clinical outcome of infection varies dramatically, ranging from asymptomatic to death, and in particular what drives cerebral malaria. To address this gap in knowledge a new research area has recently emerged and investigates the interrelationship between malaria infection and the gut microbiome. While recent studies have indicated a key role for the gut microbiome in a range of health conditions, very limited research has been conducted in this area in the context of malaria disease.
Our study utilised a mouse-model of cerebral malaria to investigate its impact on the gut microbiome. Six-week-old C57B6 mice (n=5) were infected with blood stage Plasmodium berghei parasites and a control group of mice (n=5) were injected with non-infected blood. Faecal samples were collected daily and removed from the intestine after mice were culled. To characterise bacterial communities, DNA was extracted from the faecal samples and 16S rRNA profiling and predictive functional profiling was performed.
We found significant differences in the composition of bacterial communities, including a higher abundance of the mucus-degrading genus Akkermansia in infected mice. Differences were primarily driven by treatment (infection) and time to a lesser extent. In addition to changes in the composition of the bacterial communities, we found differences in the predicted functionality of the infected mice compared to uninfected controls.
Our findings aim to pave the way for a new area of research and novel intervention strategies to modulate the severity of the disease.