Este é um Blog educacional, dedicado a discussões acadêmicas sobre a Ecologia Evolutiva. Contém chamadas específicas relacionadas às disciplinas de Ecologia da Universidade Federal de Ouro Preto, e textos didáticos gerais.
Domingo, 18 de Maio de 2008
Parte 1a - Cowell 1996

Science 20 December 1996:
Vol. 274. no. 5295, pp. 2025 - 2031
DOI: 10.1126/science.274.5295.2025

Policy Forum
Global Climate and Infectious Disease: The Cholera Paradigm*
Rita R. Colwell
The author is in the University of Maryland Biotechnology Institute, 4321 Hartwick Road, Suite 550,College Park, MD 20740, USA.

Historically, infectious diseases have had a profound effect on human populations, including their evolution and culturaldevelopment. Despite significant advances in medical science,infectious diseases continue to impact human populations in manyparts of the world. Emerging diseases are considered to be thoseinfections that either are newly appearing in the population orare rapidly increasing in incidence or expanding in geographicrange (1). Emergence of disease is not a simple phenomenon,mainly because infectious diseases are dynamic. Most new infectionsare not caused by truly new pathogens but are microorganisms (viruses,bacteria, fungi, protozoa, and helminths) that find a new wayto enter a susceptible host and are newly recognized because ofrecently developed, sensitive techniques. Human activities driveemergence of disease and a variety of social, economic, political,climatic, technological, and environmental factors can shape thepattern of a disease and influence its emergence into populations.For example, travel affects emergence of disease (2), and humanmigrations have been the main source of epidemics throughout history.Trade caravans, religious pilgrimages, and military campaignsfacilitated the spread of plague, smallpox, and cholera. Globaltravel is a fact of modern life and, equally so, the continuedevolution of microorganisms; therefore, new infections will continueto emerge, and known infections will change in distribution, frequency,and severity.
Reports of disease outbreaks have been more frequent during the past few years. For example, two malaria cases were recentlyreported in New York and traced to local mosquitoes. These casesdemonstrate that the potential exists for reintroduction of malariainto areas where it is no longer endemic, such as the United States.Malaria is an old disease with the potential of re-emerging asa new disease, especially in association with climate change.
Tuberculosis (TB), according to the World Health Organization, is now the world's leading killer of adults; 30 million adultsare expected to die from TB in the next 10 years. With the spreadof HIV, coupled with deterioration of conditions in many cities,not just in developing countries, but throughout the developedworld as well, and the explosion in international travel, a resurgenceof tuberculosis has occurred in Tokyo, New York, London, and othermajor cities.
Eastern Europe and the former Soviet Union have been battling a diphtheria epidemic since 1990. More than 25,000 cases havebeen reported. In October 1995, a hemorrhagic fever of unknownorigin swept through Northeast Nicaragua (2, 3). The disease,leptospirosis, characterized by fever and internal bleeding, causedhospitalization of more than 500 Nicaraguans and infected morethan 2000 before it was identified by experts at the U.S. Centerfor Disease Control. Leptospirosis is a bacterial infection transmittedby animal urine or excrement that seeps into food and water supplies.The disease can be treated with antibiotics, and its spread canbe curtailed by methods similar to those used for cholera epidemics.
More than 500 cases of Dengue fever were reported in 1995 in the Caribbean region by the Caribbean Epidemiology Center. Dengue,and the more severe Dengue hemorraghic fever, or DHF also ragedthrough Central America between September and November 1995; Denguereports sharply increased from 23,603 to 46,532; DHF reports rosefrom 352 to 546. Other countries reporting cases of Dengue orDHF include Belize, British Virgin Islands, Barbados, Dominica,Grenada, Guadeloupe, Guiana, Jamaica, Martinique, Montserrat,Puerto Rico, St. Vincent, Trinidad, and Tobago.
In Columbia, an apparent outbreak of mosquito-borne equine encephalitis killed at least 26 people and forced 13,000 othersto seek treatment in September 1995. In November 1995, Labreablack fever, just one of a half-dozen deadly and little understoodviral diseases emerging from the rain forests from Latin Americabegan appearing.
Thus, communicable diseases are resurging. Some of the underlying causes are obvious; namely, poverty, which continues tobe a huge problem worldwide. Without latrines or indoor plumbing,increasing populations, especially those millions lacking foodand housing, create an environment for these diseases to flourish.
An aspect of infectious disease, receiving relatively little attention until recently, is the environment. Malaria, currentlyclaiming about two million victims each year worldwide, couldkill an additional million people annually if global temperaturesrise, thereby allowing the parasite-bearing mosquito to spreadinto geographic areas not now affected (4). Because most emergingdisease agents are not new but are existing pathogens of animalsor humans that have been given opportunities to infect new hostpopulations, environmental and social changes--especially thoseresulting from human activities--which accelerate pathogen trafficneed to be defined (1).
Cholera as a Paradigm
Cholera offers an excellent example of how information concerning environmental factors permits better understanding of disease--notonly virulence, but equally important, transmission and epidemiology.The etymology of the term "cholera" has been in dispute for manyyears but may provide clues to understanding the disease. Choleramay have been derived from the Greek words, chole (bile) and rein(flow), meaning the flow of bile in that language (5). Otherinvestigators suggest the name comes from the Greek word cholera,which means gutter of a roof (6). The symptoms of cholera mayhave suggested to the Greeks the heavy flow of water on roof guttersduring thunderstorms. To distinguish the general term, cholera(gutter), from the disease cholera, the word "nousos" or sicknesswas added to the latter (5).
There are descriptions of a disease resembling cholera in Sushruta Samshita from India, written in Sanskrit 500 to 400 B.C.(7). Historical records tracing back 2000 years, in both Greekand Sanskrit, describe diseases similar to cholera (5). Thus,from the literature, it is clear that there was cholera before1817, when the records of the pandemics begin. However, choleraexisted on the Indian subcontinent for centuries before the firstEuropean arrived, where it was described early in the 16th century,not invading other areas until 1817. When Vasco da Gama landedon the southwestern or Malabar coast of India in 1498, as describedby Gaspar Correa, an officer of Vasco da Gama in 1503, about 20,000men of Calicut died of "a disease which struck them sudden-likein the belly, so that some of them died in 8 hours" (8).
The impact of gastrointestinal illnesses, including cholera, on military campaigns has been reviewed by Tramont and Gangarosa(9). The battles of Gallipoli, El Alamein, and other conflictswere influenced and their outcome set by diarrhoeal disease.
The first pandemic of cholera occurred from 1817 to 1823 and was fairly limited in scope and related to the two wars--the OmanWar and the war between Persia and Turkey. Before 1817, cholerawas most probably a sporadic, summertime illness, perhaps emergingin its violent epidemic form in the early 19th century.
The second pandemic (1829 to 1851) is believed to have begun in Russia, where citizens of Moscow were particularly hard hit.The pandemic spread across the Atlantic Ocean in 1832 to the Americas,initially up the St. Lawrence River and, ultimately, spreadingto New York on 23 June 1832. At the time, New York was ripe fora cholera epidemic because of its proximity to the ocean, thatis, the rivers flanking Manhattan Island had increased salinityand the city had a bad water and sanitation system (5). Thedisease spread from New York to Philadelphia in 2 weeks and subsequentlyalong the coast to New Orleans.
The second pandemic reappeared in a region of London, close to where Dr. John Snow, physician to Queen Victoria, lived. Inthe summer of 1849, John Snow determined that the spread of thedisease was connected to mixing of drinking water and sewage inBroad Street, Golden Square, and adjoining streets of London.Snow was credited with stopping the Broad Street epidemic by recognizingthat the location of deaths from cholera was near the wells onBroad Street and urging the Board of Guardians of St. James Parish,which owned the well and pump, to remove the handle of the pumpin September. By then, the epidemic had begun to wane, but thisaction probably represents the first instance on record of theimplementation of an appropriate measure to prevent the transmissionof a waterborne disease (10). Thus, John Snow is given creditfor both stopping the epidemic and proving its connection to drinkingwater. In reality, Snow never claimed that the removal of thepump handle ended the epidemic in the area of the Broad Streetpump. Snow did understand, however, that the disease was spreadmore easily by contaminated water than by person-to-person contact.He noted that the number of cholera deaths per 10,000 houses from8 July to 26 August 1854 was 315 for houses whose water was suppliedby the Southwark and Vauxhall Company and only 37 for houses suppliedby the Lambeth Company. His tracking of the death rate, as a functionof water supply, was an important observation in the understandingof the epidemiology of cholera.
A third pandemic, from 1852 to 1859, was followed by the fourth (1863 to 1879), fifth (1881 to 1896), and sixth (1899 to 1923)pandemics. From 1926 to 1960, many believed that cholera wouldnot recur in pandemic form because water supplies had been improvedworldwide. Indeed, many parts of the world did become free ofcholera. But, nature prevailed and the seventh pandemic beganin 1961 and continues to the present on six continents. A newbiovar or biotype of Vibrio cholerae caused the current pandemic--theEl Tor biotype of V. cholerae 01, which emerged in Celebes, Indonesia,in 1961. The disease caused by this organism is usually not assevere as that of the classical biotype.
From the pandemics of the 19th century to the recent major epidemics in South America and Africa, cholera left its mark onhuman history. In Latin America, cholera re-emerged after a 100-yeardisappearance. Cholera spread throughout parts of Africa in 1991at a catastrophic rate, killing more people than the epidemicin Latin America. According to the World Health Organization,45,159 cases and 3488 deaths in 10 African nations were reportedup to 23 July 1991. By comparison, 2618 of the 251,553 reportedcases in South America were fatal.
Vibrio cholerae non-01 serogroups were not known to cause epidemics of diarrhea; they are known, however, to cause sporadiccases and small outbreaks of diarrheas and extraintestinal infections.However, in October 1992, a dramatic event occurred. An epidemicof cholera-like disease, caused by a V. cholerae non-01 serogroupbroke out in the southern port city of Madras in southern India.Within a few months, it arose in other southern Indian citiesand reached the northeastern city of Calcutta (11). By December1992, there was an outbreak of cholera-like illness in the southerncoastal cities of Bangladesh, and the disease eventually spreadto the entire country (12, 13). The disease affected thousandsof people, mainly adults, and caused many deaths in the Indiansubcontinent. The causative agent was found to be a new serogroupof V. cholerae, defined as 0139, with the synonym Bengal, to indicatethat it was first isolated from coastal areas of the Bay of Bengal(14).
Since 1993, the serogroup V. cholerae 0139 has been reported from India, Bangladesh, Nepal, Burma, Thailand, Malaysia, SaudiArabia, China, and Pakistan (14). The V. cholerae 0139 serogroupis nearly identical to V. cholerae 01 El Tor but possesses a capsule,and the capsular layer is distinct from the lipopolysaccharide(LPS) antigen. The V. cholerae 0139 antigen includes an O-antigencapsule and lipopolysaccharide virulence determinants (15).Furthermore, there is a deletion of about 22 kb of DNA from the01 chromosome in the rfb region and an insertion of a new 35-kbregion of DNA that specifies the 0139 LPS and capsules (16).The occurrence of epidemics caused by V. cholerae 0139 is a significantturning point in the history of cholera because the evidence pointsto this strain arising as from genetic recombination and horizontalgene transfer, and the acquisition of unique DNA. The 01 antigenhas been the relied upon tag for recognition of V. cholerae epidemicstrains. Now a new serotype was associated with cholera epidemics.
Seroconversion had been reported years ago (17), that is, seroconversion between Ogawa and Inaba serotypes of the choleravibrios possessing specific O antigens. The 0139 strains havebeen shown to belong to a distinct serogroup, defined by monoclonalantibodies and polyclonal antisera that recognize only the 0139strains (18). In V. cholerae 01, the chemical basis for theserogroup-defining antigen lies in the O side chain of LPS. The0139 LPS differs from 01 LPS in that it has a short O side chainlength and different sugar composition (17). The evidence furthersuggests the V. cholerae 01 El Tor gave rise to 0139 by acquisitionof novel DNA which was inserted into, and replaced part of, theO antigen gene cluster of the recipient strain. From the sequenceof the novel DNA, two open reading frames (otn A and otn B) weredetected, the products of which showed homology to proteins involvedin capsule and O antigen synthesis, respectively. The otn AB DNAdetermines the distinct antigenic properties of the 0139 cellsurface. The otn AB DNA was not detected in 01 strains, but waspresent in two non-01 V. cholerae strains with serotypes 069 and0141 (19).
Antigenic conversion of 01 to non-01, and the reverse, in V. cholerae has been demonstrated in the laboratory (20, 21).The co-existence of Vibrio cholerae 01 and 0139 Bengal in planktonin Bangladesh has also been demonstrated (22).
In Bangladesh, the epidemic of V. cholerae 0139 started in the chars, the temporary islands off the coast of the Sundarbanarea in the southwestern coastal districts of Bagerhat. Most ofthe islands emerge at the end of the monsoon period, and migrantfishermen arrive in October to fish in the Bay of Bengal. Thechars are in remote areas, and communication with the mainlandis limited. Thus, the 0139 V. cholerae epidemic went unnoticeduntil December 1992, when it was identified in the mainland ofBagerhat; afterward it appeared in five neighboring districts.The epidemic lasted more than 4 months, and involved a total of46,965 cases and 846 deaths in the six southern districts of Bangladesh.In September 1993, 3 months after its decline in the southernareas, the epidemic moved to the northern regions of the country.It was reported that epidemic resurgence coincided with the onsetof seasonal outbreaks of Vibrio cholerae 01 in Bangladesh (23).
Vibrio cholerae serogroup 0139 Bengal completely displaced V. cholerae serogroup 01 in Calcutta in January 1993, and an epidemicof V. cholerae 0139 followed in March to May 1993 (13). Theorganism first caused a large outbreak of cholera-like illnessin Madras in October 1992. Initially, cases were clustered ina suburban area 16 km north of the city limit. Similar strainswere isolated a month later from other parts of India; for example,Madurai, Vellore, and Calcutta. Interestingly, V. cholerae 01El Tor entered India almost concurrently in Calcutta and Madrasin 1964 and spread rapidly over wide areas, outnumbering preexistingclassical V. cholerae 01 in India. By 1966, El Tor had almostcompletely replaced classical cholera. In parallel in Calcutta,the 0139 serogroup appeared on or about 20 November 1992 and quicklyreplaced V. cholerae 01 El Tor by December 1992 (13).
The data suggest that V. cholerae 01 began to be displaced in the southern coastal areas of Bangladesh in 1991 or even earlier.The epidemic that included the coast of southern India and WestBengal (India) arose from a single clone, and the Indian outbreakswere of the same origin (24).
Five major rivers of the Indian subcontinent flow through into the Bay of Bengal. These rivers all carry large amounts ofagricultural and industrial waste and thus provide nutrients sufficientto convert the coastal waters to eutrophic conditions. Brackishwater extends some distance upriver for all rivers.
All Vibrio spp. that are pathogenic are adapted to salinities between 5 per mil and 30 per mil. Salinities favorable for growthof V. cholerae are found primarily in inland coastal areas andestuaries, but the bacterium thrives in seawater as well. PathogenicV. cholerae grows in water with low salinity if the water temperatureis relatively high and organic nutrients are present in high concentrations(25, 26, 27), that is, high concentrations of organic nutrientscan compensate to a degree for lack of salt. Similarly in freshwater, the presence of divalent cations can compensate for Na+ (27). Survival of V. cholerae in seawater for more than 50days has been demonstrated (28).
Vibrio cholerae can survive under unfavorable environmental conditions in a dormant state; that is, it is viable but nonculturable(29). Representing a spore-like stage, without formation ofa true spore coat, dormant cells can survive changes in temperature,salinity, or availability of organic matter, as do the spore-formingbacteria, Bacillus spp. (30). Viable but nonculturable organismsremain infectious (31). V. cholerae cells, when viable but nonculturable,are small and spherical (32), but apparently can be resuscitatedby heat shock (33). Viable but nonculturable V. cholerae contributeto the occurrence of seasonal epidemics because V. cholerae canpersist for a long time in the aquatic environment; reintroductionof the organism by infected humans is not necessary. Furthermore,V. cholerae is a microbial inhabitant of brackish water and estuarineecosystems; that is, it is autochthonous, as has been demonstratedby Xu et al. (34). In addition to elucidation of the salinityrequirement and range for V. cholerae, many pathogenic Vibriospp. are associated with chitinaceous zooplankton and shellfish,and also can survive on fish and shellfish (27, 35, 36).
The association of V. cholerae with zooplankton has proven to be a key factor in deciphering the global nature of choleraepidemics. V. cholerae preferentially attaches to chitinaceousplankton, for example, copepods, and can be detected in zooplanktonin cholera endemic regions. Ocean currents sweeping along coastalareas thereby translocate plankton and their bacterial passengers.
The Origin of Cholera
The history of cholera reveals a remarkably strong association with the sea. The great pandemics followed coastlines of theworld oceans. As with acute communicable diseases in general,endemicity of cholera carries the potential of epidemic flare-ups,and pandemicity is always a threat, especially in developing countrieshaving poor sanitation, lack of hygiene, and crowded living conditions.These factors have long been recognized as characteristic of environmentsin which diarrhoeal diseases flourish.
In historical treatises on cholera, sea-borne transportation of cholera provides the prevailing theory of dissemination. Initialcases characteristically occur along coastal areas, among fishermenor boatmen, and outbreaks were commonly ascribed to ships arrivingfrom cholera-epidemic areas (8) and, more recently, to dischargeof ballast water from ships arriving in a port in Peru from acholera endemic region. The invasion of V. cholerae El Tor, abiotype of cholera, into India was believed "likely to have beencarried by the sea-route ... into Calcutta" (37). The early recordsshow an association with bad water, usually taken from riversor swampy areas, or marshes, where flow of streams was much reduced.All six pandemics of the last century are believed to have startedin "Hindoostan," now known as Bangladesh, and to have been causedby the classical biotype V. cholerae of the 01 serotype (38).The most recent pandemic of 1961 continues today.
The seventh pandemic was different from the six previous ones, in that authorities claimed that it originated in Indonesiaand that the cause was V. cholerae 01 El Tor. After its appearancein Indonesia in 1961, the disease spread to East Pakistan (Bangladesh)in 1963, India in 1964, the former U.S.S.R. in 1965 to 1966, andAfrica in 1970 to 1971. But, the greatest surprise was in 1991when the seventh pandemic struck South America, first in Peruin the port city of Chancay, 60 km north of Lima. The next dayan outbreak was reported from Chimbote, a seaport 400 km northof Chancay. Spread of the outbreak was rapid, and by 7 February1991, confirmed cases were reported along the Peruvian coast fromthe Chilean to the Ecuadorean border, 2000 km distant (39).The near simultaneous appearance of cholera along such a greatdistance of coastline cannot easily or logically be explainedby ballast discharge from a single ship in Lima. More likely,the plankton blooms that occurred were triggered by a climaticevent, the most logical being El Niño, which brings rain andan influx of nutrients from land and warm sea surface temperatures.These factors have already been associated with initiating planktonblooms. Because phytoplankton blooms can be measured by satelliteimagery (40) and zooplankton blooms quickly follow phytoplanktonblooms (41, 42), conditions associated with a cholera outbreakor epidemic can be monitored by satellite. Because a single copepodcan carry up to 104 cells of V. cholerae (30), a massive bloom can provide an infectiousdose in the brackish water of tidal rivers. An infectious dosehas been reported to be 103 V. cholerae cells, on the basis of human volunteer studies (31,43). It has been shown that several copepods, with V. choleraecells attached to the surface and in the gut (45), can carrythe requisite infectious dose for clinical cholera. That is, acolonized copepod may contain up to 104 cells of V. cholerae. During a plankton bloom, several copepodsmay be ingested in a glass of water, if there is no treatmentof the water supply, as is the case in villages in Bangladesh,India, and many other cholera endemic countries (45). The chanceof consuming this Vibrio capsule increases during periods whenthe concentration of copepods in the water is high, that is, attimes of plankton blooms.
Thus, as was the case in the earlier pandemics, spread of the disease was rapid and far flung. In Peru, as early as 12 February1991, epidemics were reported from communities 50 to 150 km inland,and by 20 February cases were reported in the Andean highlands.Characteristic of the seventh pandemic, as in earlier pandemics,coastal towns and fishing villages were affected in the LatinAmerica outbreaks during 1990 to 1991.
The disease in Latin America has abated, but remains endemic, as elsewhere in the world where cholera has occurred. Peru,alone, suffered more than 300,000 victims, of which almost 1%died. In 1991, 21 African countries reported a total of 153,367cases and 14,000 deaths. In contrast, during 1994, tribal conflictsin the Central African nation of Rwanda claimed more than 500,000lives and thousands of Rwandans fled to Zaire, Burundi, and Tanzania.About 50,000 Rwandan refugees contracted cholera in the refugeecamps, and many thousands died.
Cholera pandemics visited North America (United States and Canada) regularly in the 1800s. The first epidemic broke out inCanada in April 1832, and 2208 died from cholera in Quebec by2 September 1832 (38, 46).
In Bangladesh and India, many of the cholera outbreaks have been geographically localized, demonstrating the occurrence ofthe disease is typically seasonal (47) and correlates with tidalestuaries and riverine systems. Outbreaks in Naples in 1973 andin Portugal in 1974 were traced to uncooked and inadequately cookedseafood, respectively.
The characteristic geographic occurrence of cholera and the speed with which it can be spread were reported more than a centuryago (46). The implications of the geographical patterns of thisdisease (with respect to origin of the disease), however, werenot pursued until recently, when new methods revolutionized thefield of environmental microbiology. Epifluorescent microscopyand hybridoma production of monoclonal antibodies now permit directdetection of V. cholerae with the use of fluorescent-labeled monoclonalprobes. Gene probes, colony hybridization, and polymerase chainreaction (PCR) methods are highly selective and allow detectionof a few cells in water samples (48). With the use of monoclonalantibodies, improved fluorescent dyes, epifluorescent microscopy,and equipment for concentration of samples, as few as one to twocells of V. cholerae per liter of water can be detected and confirmedby PCR. Fluorescent-labeled RNA probes also provide a sensitivemethod for detection and enumeration, if used simultaneously withthe direct viable count procedure (49).
In 1984, Xu et al. (50) developed an immunofluorescence method for the detection of V. cholerae serovar 01 in aquatic samplesand enrichment broths. A polyclonal antibody was used in subsequentexperiments, and fluorescein-isothiocyanate-conjugated, antirabbitglobulin-goat serum and rhodamine-isothiocyanate-conjugated, bovineserum albumin were used as a background stain. Detection of V.cholerae 01 with this fluorescent antibody system was significantlymore successful than with culture methods.
A field trial of the fluorescent antibody detection was conducted in which 52 water samples were collected in and around Matlab,Bangladesh, during April and May 1982. Only seven samples werepositive for V. cholerae 01 by conventional culture, after examinationof 3431 individual colonies for 01 antigen by slide agglutination(51). In contrast, the fluorescent antibody staining methodallowed detection of V. cholerae 01 in 51 of the 52 samples. Theseven samples that were positive by culture were also positiveby staining. Surprisingly, recovery by culture of V. cholerae01 was not possible at early stages of enrichment when cells couldbe detected by fluorescent antibody staining; that is, V. cholerae01 cells could be observed, but overgrowth blocked isolation ofthose cells in culture. V. cholerae 01 was, indeed, present, butnot recovered in culture.
Subsequently, a series of microcosm experiments were carried out and the phenomenon described above was discovered, namely,that V. cholerae 01 and related human pathogenic bacterial speciesenter into a viable but nonculturable state, and commonly do soin environmental samples (30). Thus, it was now possible toexplain why direct viable counts by epifluorescent microscopyconsistently were significantly higher than corresponding platecounts. The assumption that all V. cholerae 01 cells die off ordecay in the environment was no longer valid. Because immunofluorescentmicroscopy and, subsequently, molecular genetic probes are sensitivein detecting V. cholerae 01 in environmental samples, this microorganismcan now be readily detected and enumerated in samples where culturemethods fail or are inadequate, not to mention time-consumingand expensive.
Viability and pathogenicity of V. cholerae in the viable but nonculturable state was initially demonstrated using membranechambers submerged in semitropical waters at Bimini, Bahamas,and ligated illeal loop assays (52). Subsequently, retentionof pathogenicity for humans was demonstrated in volunteer feedingexperiments, where it was found that from nonculturable vibriospositive cultures could be demonstrated (31, 53), providingevidence that nonculturable V. cholerae can maintain pathogenicpotential, even after long-term residence in the environment (53).
Recently, optimization of the direct fluorescent antibody test in kit form, using a monoclonal antibody, as proposed by Braytonet al. (54) and Tamplin et al. (55), has been achieved. Thekit provides a simple method for detection of V. cholerae withina few minutes and is both inexpensive and convenient for fielduse, requiring neither refrigeration of the reagents nor incubationof the reaction (56, 57).
For a bacterium capable of attachment to, and colonization of surfaces, surface specificity often is critical. V. cholerae,however, offers multiple recognition sites, including not onlythe intestinal mucosa and brush border cells of the mammaliangut, but also the hindgut mucosa of blue crabs, which containchitin. Shellfish feeding on planktonic crustaceans are colonizedby V. cholerae in natural water systems (58, 59). The associationof V. cholerae with planktonic crustacean copepods is influenced,and likely controlled, by physical and chemical characteristicsof the environment. V. cholerae may also survive in associationwith aquatic vegetation; for example, water hyacinths and theblue-green bacterium, Anabena, as well as other zooplankton andcrustacean invertebrates in the aquatic environment (60, 61,62, 63, 64, 65, 66).
Seasonal outbreaks of cholera in Bangladesh are geographically related, and the outbreaks are often local (30, 67, 68).Isolates of V. cholerae with diverse seasonal distribution werefound to host different phage types (69). This evidence indicatesthat outbreaks lack a common source and likely have a broad distributionas a result of tidal ebb and flow and seasonal flooding.
Recent work on genetic fingerprinting has confirmed that the organism is multiclonal and that some clones are endemic in differentgeographical regions (70).


publicado por Sérvio Pontes Ribeiro às 15:46
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