Cholera transmission: the host, pathogen and bacteriophage dynamic

30 Oct 2009

Paul Chinnock

Source: Nature Reviews: Microbiology (see original article or PDF)

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Citation: Nelson EJ, Harris JB, Morris JG Jr, Calderwood SB, Camilli A (2009). Cholera transmission: the host, pathogen and bacteriophage dynamic. Nat Rev; 7(10):693-702.

2009 Nature Publishing Group

Now is an appropriate time to step back review what science can tell us about cholera. The last few months have seen alarming outbreaks of the disease in many countries, the most publicised of which has been in Zimbabwe, where at least 4,000 people died. An article in Nature Reviews: Microbiology points out that case fatality rates in Zimbabwe were at the same level as reported in cholera outbreaks of a century ago.

The authors of the article set out to highlight the advances that have been made in understanding the interactions between the bacterium which causes cholera (Vibrio cholerae) and its human host. Also considered are the viruses (bacteriophages) with which V. cholerae its elf is often infected. Most strains of V. cholerae are in fact harmless but virulent strains can transmit their capacity to produce a toxin to other strains, and in the 1990s it was shown that this transfer of genes is brought about by bacteriophages.

Roughly half of infections with virulent strains of cholera do not lead to symptoms of the disease. Some people develop symptoms of life-threatening severity, while in others the symptoms can be quite mild. Susceptibility to the infection is therefore very variable. The article discusses the genetic and nutritional factors in the host which determine the human immune response to V. cholerae.

People who suffer symptoms often acquire immunity against subsequent infection but the mechanisms by which this is achieved remain unknown. It has recently become clear that herd immunity plays a role in slowing transmission in cholera outbreaks. There are implications for the assessment of the effectiveness of vaccines; currently the impact of herd immunity is not included in evaluations of vaccine trial data.

The authors also reviews studies conducted on V. cholerae itself. This takes up the greater part of the article. Much has been learned in recent years about the molecular mechanisms that contribute to infectivity and virulence.

Other recent research has expanded understanding of the interactions between the pathogen and its bacteriophages. The authors argue that these advances will lead in time to improvements in the capacity to control epidemics such as Zimbabwe’s. Areas recommended for further research include the impact of bacteriophage predation and how vaccines lower the susceptible pool to the point that transmission cannot be perpetuated.

Meanwhile, the authors say, and given that centralised water and sanitation systems often fail in the developing world:

“...cholera outbreaks may best be stopped at the source, by reducing human exposure to freshly passed, hyperinfectious stool. In other words, while maintaining centralized management, decentralized efforts for directed waste management at the unit of the household should be encouraged and tested. This concept highlights the crucial importance of already proven but simple household-based interventions, such as the use of narrow-mouthed jugs, chlorination of stored water and hand washing, for disease prevention”.

But how much better, one must reflect, if the infrastructure were not to fail. Access to safe water and sanitation is a human right and if this right is fulfilled then cholera as a major cause of sickness and death can be consigned to history.

Note: This article is published in a journal that is not open-access. To see the full article therefore a subscription to Nature Reviews: Microbiology is required. Readers in some developing countries who are based within institutions may be able to access it through the HINARI programme.