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Bacteria Change Shape to Survive Overcrowding

One species of bacteria have developed a unique mechanism for coping with overpopulation. They change their shape. Researchers at the University of Texas, Austin, describe a newly discovered mechanism that the bacterium Paenibacillus dendritiformis uses to survive overcrowding.

P. dendritiformis is typically a rod-shaped bacterium. As it grows it produces a toxic protein, called sibling lethal factor (Slf) which kills cells of encroaching sibling colonies. However, the researchers found that sublethal levels of Slf induce some of the rods to switch Slf-resistant cocci-shaped bacteria.

When crowding is reduced and nutrients are no longer limiting, the bacteria produce another signal that induces the cocci to switch back to rods, allowing the population to spread.

Another Way for Cholera to Cause Disease

Cholera is a severe diarrheal disease typically caused by the O1 strain of the bacterium Vibrio cholerae. All pandemic O1 strains require two critical factors to cause disease: cholera toxin (CT) and toxin coregulated pilus (TCP). However, some nonpandemic strains of V. cholerae do not produce CT or TCP and yet still cause disease.

Researchers from Harvard Medical School, Brigham and Women's Hospital and the Howard Hughes Medical Institute studied one of those strains (AM-19226) which causes a rapidly fatal diarrheal disease in rabbits. Analysis of the genome showed that the bacterium lacked the genes that code for CT and TCP but instead carried a gene encoding a type III secretion system (TTSS), which other bacteria are known to use to infect host cells.

TTSS proved to be essential for AM-19226 virulence in rabbits. An AM-19226 derivative deficient for TTSS did not cause diarrhea or colonize the intestine.

"Our findings provide insight into a new type of diarrheagenic mechanism used by non-O1, non-O139 V. cholerae strains and suggests that TTSS can lead to diarrheal illness," write the researchers.

Like a Fungus in a Candy Store

While the fungal pathogen Cryptococcus neoformans can produce its own glucose during the initial establishment of infection, it inevitably needs to live off the glucose stored in its host to persist and cause disease.

C. neoformans is an emerging fungal pathogen of humans and is responsible for approximately 625,000 deaths annually among those suffering from AIDS. Researchers from Duke University and the University of British Columbia investigated how the fungus acquires the nutrients it needs to establish infection and cause disease.

"The ability of this fungus to persist in the host, coupled with its propensity to colonize the central nervous system (CNS), makes understanding of nutrient acquisition in the host a primary concern," write the researchers. They discovered that to cause lung infection the fungus could use a process known as gluconeogenesis to create its own glucose, but in order to infect the central nervous system it required a process known as glycolysis where it used glucose from the host. Inhibition of glycolysis could be a target for new drug development.

New Insect-Borne Virus

Researchers from Germany and the United States report the discovery of the first insect-associated nidovirus, which they have tentatively named Cavally virus (CAVV), during a survey of mosquito-associated viruses in Cote d'Ivoire. CAVV was found with a prevalence of 9.3%.

CAVV is the first representative of a family of nidoviruses that is distinct from the established Arteriviridae, Roniviridae and Coronaviridae families. No other nidoviruses are known to live in an insect.

Nidoviruses are known for causing severe disease in livestock, but until the 2003 outbreak of severe acute respiratory syndrome (SARS) were thought to only cause relatively mild diseases in humans, like the common cold. It is unclear whether CAVV causes disease in humans or animals or is exclusive to mosquitoes.

In a population study of CAVV in its natural habitat, the authors isolated the virus from several species of mosquitoes and tracked its prevalence and genomic diversity across a gradient of environmental disturbance, ranging from undisturbed primary forest to plantations and human settlements. The virus was found in all habitat types, and as disturbance increased, so did the prevalence of the virus: the virus was most prevalent in human settlements.


Contact: Jim Sliwa
American Society for Microbiology

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