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ScienceWeek
MICROBIOLOGY: CHITIN AND CHOLERA
The following points are made by D.H. Bartlett and F. Azam (Science 2005 310"1775):
1) The ancient human pathogen Vibrio cholerae resides in oceanic, estuarine, and freshwater aquatic environments, where it often attaches to and feeds on chitin, the most abundant polymer on Earth after cellulose, and the most abundant polymer in the marine environment [1]. Chitinous substrates include arthropods and their molts and fecal pellets, some diatoms, and fungi, which are spread over wide geographic and spatial ranges in rivers, estuaries, and oceans.
2) The connection between this bacterium and chitin has been a long-standing concern to health scientists for two reasons. First, this association increases the microbe's resistance to acids such as those secreted by the lining of the stomach. Thus, if ingested by drinking contaminated water or improperly cooked shellfish, there is an increased possibility that the microbe will cause cholera, a potentially devastating intestinal infection [2]. Second, V. cholerae biofilms that develop on single chitin-containing plankton may rise to the level of an infectious dose [3]. More recently it has been shown that attachment to chitin is favored by V. cholerae bacteria that express a surface protein that is also required for infecting humans [4].
3) New work [5] adds a new reason to worry about the V. cholerae-chitin connection: the phenomenon of microbial competence, the ability of a bacterium to directly take up DNA present in the environment by the process known as natural DNA transformation. V. cholerae is already renowned for its ability to absorb new genes into its genome. But this feature has previously been attributed to bacterial cell-to-cell contacts (conjugation) or virus-mediated events (transduction). Even the cholera toxin genes themselves are shared among serotypes and biotypes of V. cholerae via bacterial viruses. The discovery of DNA transformation in V. cholerae provides a new mechanism for this organism to effectively acquire genes for adapting to its aquatic habitat or infecting its human host.
4) Meibom et al[5] developed the hypothesis of competence in V. cholerae after observing that chitin induced the production of a protein appendage known as a type IV pilus, a structure sometimes associated with DNA-uptake ability in other bacteria. Chitin oligosaccharides, as well as natural chitin from crab shells, stimulate transformation of bacteria to antibiotic resistance and restore their ability to synthesize amino acids. Components of the type IV pilus are required for competence. The authors examined the role of a chitin-induced gene that regulates natural transformation in other bacteria and compared the genotypes of competence-positive and -negative strains of V. cholerae. In an series of genetic experiments, they elucidated three separate regulatory circuits in the bacterium that control transformation. These pathways are stimulated by (i) the availability of chitin; (ii) a lack of nutrients, or by some other stress; or (iii) a sufficiently high bacterial population.
References (abridged):
1. K. L. Meibom et al., Proc. Natl. Acad. Sci. U.S.A. 101, 2524 (2004)
2. J. Castro-Rosas, E. F. Escartin, Int. J. Food Microbiol. 102, 195 (2005)
3. R. R. Colwell, Science 274, [2025] (1996)
4. G. Reguera, R. Kolter, J. Bacteriol. 187, 3551 (2005)
5. K. L. Meibom, M. Blokesch, N. A. Dolganov, C.-Y. Wu, G. K. Schoolnik, Science 310, 1824 (2005)
Science http://www.sciencemag.org
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Related Material:
ENSO AND CHOLERA: A NONSTATIONARY LINK RELATED TO CLIMATE CHANGE?
X. Rodo et al (University of Barcelona, ES) discuss climate change and cholera, the authors making the following points:
1) A main issue at the center of the current debate on climate change is the impact that any anthropogenic-induced changes will have on human society (1,2). Of considerable importance among these impacts are those affecting human health, particularly the spread and intensification of water-born (1,3-5) and vector-born diseases (1). A central difficulty that precludes quantitative assessment of these impacts arises from the lack of studies comparing past and present dynamics of infectious diseases over sufficiently long time periods relevant to climate change. For endemic diseases with a long history, such as cholera in Bangladesh, the existence of historical records and on-going surveillance programs make such a comparison possible.
2) Studies of climate and disease so far have been limited to two main areas: the exploration of links between temporal patterns of disease and the interannual variability of climate, mainly El Nino/Southern Oscillation (ENSO), and the building of scenarios for the geographical spread of disease with climate change. The former addresses only interannual variability; it does not address long-term change. Thus, for endemic diseases such as cholera, one key question has been overlooked. Has the interannual variability of climate become a stronger driver of disease dynamics in recent decades? Currently, there is considerable interest in the consequences of climate change for the interannual variability of climate itself, particularly for ENSO and associated phenomena. In this context, the question of a nonstationary link between climate variability and disease dynamics is central to address the effect of climate change.
3) In summary: The authors present quantitative evidence for an increased role of interannual climate variability on the temporal dynamics of an infectious disease. The evidence is based on time-series analyses of the relationship between ENSO and cholera prevalence in Bangladesh (formerly Bengal) during two different time periods. A strong and consistent signature of ENSO is apparent in the last two decades (1980-2001), while it is weaker and eventually uncorrelated during the first parts of the last century (1893-1920 and 1920-1940, respectively). Concomitant with these changes, the Southern Oscillation Index (SOI) undergoes shifts in its frequency spectrum. These changes include an intensification of the approximately 4-yr cycle during the recent interval as a response to the well documented Pacific basin regime shift of 1976. This change in remote ENSO modulation alone can only partially serve to substantiate the differences observed in cholera. Regional or basin-wide changes possibly linked to global warming must be invoked that seem to facilitate ENSO transmission. For the recent cholera series and during specific time intervals corresponding to local maxima in ENSO, this climate phenomenon accounts for over 70% of disease variance. The authors suggest this strong association is discontinuous in time and can only be captured with a technique designed to isolate transient couplings.
References (abridged):
1. Watson, R. T. , Zinyowera, M. C. & Moss, R. H. (1998) IPCC Special Report on The Regional Impacts of Climate Change: An Assessment of Vulnerability (Cambridge Univ. Press, Cambridge, U.K.)
2. Huq, S. S. (2001) Science 294, 1617
3. Colwell, R. R. (1996) Science 274, 2025-2031
4. World Health Organization. (1996) Regional Health Report 1996 (W.H.O., Geneva).
5. Brandling-Bennett, A. D. & Pinheiro, F. (1996) Emerging Infectious Diseases 2, 59-61
Proc. Nat. Acad. Sci. 2002 99:12901
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Related Material:
ON THE GENOMICS OF THE CHOLERA PATHOGEN
Notes by ScienceWeek:
Cholera is an ancient disease, an acute infection by the bacterium Vibrio cholerae involving the entire small bowel, the infection characterized by profuse watery diarrhea, vomiting, muscular cramps, dehydration, and collapse. Death may follow in a few hours after the first bacterial invasion. The disease is endemic in portions of Asia, the Middle East, Africa, South and Central America, and the Gulf Coast of the US.
The group of bacteria known as the "vibrios" are found in marine and surface waters, and are among the most common bacteria in surface waters worldwide. The organisms are curved aerobic rods possessing a polar flagellum, the rod 2 to 4 microns long and approximately 1 micron in diameter.
V. cholerae and related vibrios produce a heat-labile protein *enterotoxin (mol. wt. 84,000) consisting of 2 subunits. One of the subunits enters cells, yields increased levels of *cyclic adenosine monophosphate (cAMP), and results in prolonged hypersecretion of water and electrolytes.
The following points are made by Victor J. DiRita (Science 2000 289:1486):
1) modern epidemiology originated in the work of John Snow (1813-1858), whose careful study of cholera victims led him to discover the waterborne nature of this disease [*Note #1]. Cholera also played a part in the foundation of modern bacteriology: 40 years after Snow's seminal discovery, Robert Koch (1843-1910) developed the germ theory of disease subsequent to his identification of V. cholerae as the pathogen responsible for cholera [*Note #2].
2) The complete genome sequence of the 2 circular chromosomes of V. cholerae was recently reported by J. Heidelberg et al (Nature 406:477 2000). This team discovered a total of 3885 lengths of DNA that encode proteins ("open reading frames"): 2770 open reading frames (2.9 million nucleotide base pairs) on the larger chromosome-1, and 1115 open reading frames (1.1 million nucleotide base pairs) on the smaller chromosome-2. Slightly more than 50 percent of these open reading frames encode proteins homologous to proteins of known function; the remainder encode proteins without ascribed functions or that are not homologous to any known protein. In addition to factors of potential importance for pathogenicity, the V. cholerae genome apparently contains genes encoding metabolic proteins, *transporters, and regulatory proteins appropriate for a free-living organism adapted to niches outside of the human intestine.
3) The V. cholerae that normally inhabits aquatic environments is not pathogenic. However, acquisition of virulence factors enables this microbe to colonize the intestinal *mucosa of human hosts, where the microbe releases cholera toxin (enterotoxin), which causes rapid release of water and electrolytes from intestinal epithelium, and which results in severe and often fatal diarrhea. Cholera continues to be a scourge throughout much of the world, with 7 global epidemics ("pandemics") recorded since 1817. In 1991, for the first time in 100 years, cholera arrived in the Western Hemisphere from its focal center in Asia. Cases were first reported in Peru, and epidemics throughout South and Central America rapidly followed.
4) The author (DiRita) concludes: "The postgenomic era of V. cholerae research has begun, and the challenge for investigators will be to use the genomic sequence information to probe more deeply into all aspects of the life-style of this fascinating, frightening, and often frustrating microbe."
Science http://www.sciencemag.org
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Notes by ScienceWeek:
enterotoxin: In general, any toxin specific for cells of the intestinal mucosa (see below).
cyclic adenosine monophosphate (cAMP): An important intracellular "messenger" substance involved in various aspects of cell regulation and protein synthesis.
Note #1: In 1854, John Snow demonstrated the transmission of cholera from contaminated water by analyzing disease rates among citizens served by the Broad Street Pump in London's Golden Square. Snow stopped the further spread of the disease by removing the pump handle from the polluted well.
Note #2: Koch devised techniques for culturing bacteria outside the body, and formulated the rules for demonstrating whether or not a bacterium is the cause of a disease. He identified the bacteria responsible for tuberculosis, cholera, and other diseases. He demonstrated that rats are vectors of bubonic plague and that sleeping sickness is transmitted by the tsetse fly. He received the Nobel Prize for Physiology or Medicine in 1905. He began his scientific life as a country doctor in a rural village.
transporters: (transport proteins) Proteins (or enzymes) instrumental in transporting materials across biological membranes or within a biological fluid (e.g., blood).
mucosa: In general, a multilayer tissue lining various tubular structures in the body (e.g., the intestine).
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