Source: http://www.asmscience.org/content/concept/Entity/ASM/Microbiology/Bacteria_and_Archaea/Bacteria/Bacterial_Diseases/Bacterial_Gastrointestinal_Infections/Bacterial_Lower_Gastrointestinal_Tract_Infections/Bacterial_Large_Intestinal_Infections/Bacterial_Diarrhea/Cholera
Timestamp: 2019-04-21 02:28:54+00:00

Document:
Review of: Sick from Freedom: African-American Illness and Suffering during the Civil War and Reconstruction; Jim Downs; (2012). Oxford University Press, Oxford, England. 280 pages.
Review of: Africa in the Time of Cholera: A History of Pandemics from 1817 to the Present; Myron Echenberg; (2011). Cambridge University Press, Cambridge, UK. 232 pages.
In the summer of 1881, Robert Koch went as a delegate of the German government to London to attend the Seventh International Medical Congress. In London for the first time, Koch found himself surrounded by many interested workers who were following Lister&apos;s lead. Lister not only mentioned Koch in the speech he gave to the Pathology Section of the meeting, but also arranged for Koch&apos;s demonstration to be set up in Lister&apos;s own laboratory at King&apos;s College. Also present at the London Congress was Louis Pasteur, now at the height of his powers. At the London meeting, Pasteur was received everywhere with acclaim. He reported details of his fowl cholera studies, studies that were to lead him on the road to the major work of the last quarter of his life— the use of attenuation in the development of vaccines against infectious disease. Only a few days after he returned from his London triumph, Koch began his work on tuberculosis, work that was to make his name known, not only throughout the scientific world, but to the general public as well.
Robert Koch was about to embark on a new venture. Cholera had broken out in Egypt and threatened to move into Europe again—it had been absent since the Hamburg epidemic of 1866. One of the most dreaded diseases of humans, cholera must not be allowed to enter Europe. His work on tuberculosis, begun only two years earlier, was set aside, and he would not return to further work on this disease until 1890 when he began his controversial work on tuberculin. The mysterious appearance and disappearance of cholera was completely unexplained, but the fear of cholera was widespread and when a new epidemic spread from India to Asia Minor and Egypt in 1883, great concern was expressed in many European countries. Extensive animal inoculation studies were carried out, using monkeys, dogs, cats, chickens, and mice, looking for a suitable animal model. In all cases in which the typical clinical symptoms of cholera were present, a characteristic bacterium was found in the tissue of the intestine. Today, more than 100 years after its etiology was explained by Robert Koch, cholera remains an important public health problem.
Throughout most of Koch&apos;s career, his relationships with Pasteur were very poor. The reasons for this are complex and difficult to unravel; however, it is clear that the Pasteur-Koch controversy not only influenced the lives of these two outstanding scientists, but also had implications for the development of the microbial sciences. The reasons for this are complex and difficult to unravel; however, it is clear that the Pasteur-Koch controversy not only influenced the lives of these two outstanding scientists, but also had implications for the development of the microbial sciences. Indeed, even the name for the discipline is linked to the controversy: the Pasteur school preferred "microbiology" whereas the Koch school preferred "bacteriology". Evidence for the Pasteur-Koch controversy can be found in the scientific writings of these two savants and in their correspondence. The whole controversy has been masterfully outlined by Mollaret in 1983 and this paper is summarized briefly here. As discussed, Pasteur and Koch first met at London in 1881 at the International Congress of Medicine. Most of Koch&apos;s attacks on Pasteur were gratuitous, and can only be explained as the young upstart resenting being ignored by the grand master. Koch&apos;s co-workers, Loeffler and Gaffky, were even less polite in their articles published in the same volume of the Mitteilungen. The basis of the controversy between Koch&apos;s group and Pasteur was over the validity of Pasteur&apos;s method of attentuation.
This chapter reviews the pathophysiology of cholera, focusing on the most common and important complication, dehydration; describes the clinical features of patients with cholera; and outlines treatment for patients with this disease. The major effects of V. cholerae O1 infection are to increase active chloride and bicarbonate secretion into the intestinal lumen by crypt cells and to decrease villous absorption of sodium chloride. The majority of children with cholera and hypoglycemia have neither frank marasmus nor kwashiorkor and resemble other cholera patients in their general clinical features. Severe dehydration produces such distinctive and pronounced features that cholera is one of the few diseases in adults that can be accurately diagnosed at first sight. The major laboratory abnormalities in patients with cholera are alterations in the concentration of serum electrolytes and creatinine and the effects of hemoconcentration on other blood constituents. Although replacement of fluid lost in cholera stool remains the crucial element of treatment of cholera patients, antimicrobial therapy is an important adjunctive therapy, especially in patients with high purging rates. Antimicrobial therapy of cholera is complicated by the marked increase in multiply antibiotic-resistant strains during the last 20 years. Currently in Bangladesh, more than 90% of V. cholerae O1 isolates are resistant to tetracycline, ampicillin, and trimethoprim-sulfamethoxazole. When epidemics occur in rural areas, it is often necessary to establish temporary cholera treatment centers. The supplies required for such temporary facilities are quite straightforward, and the costs not great.
This chapter provides an overview of the history of cholera to set the scene for understanding the epidemiology and surveillance of cholera since 1970. Accounts of the spread of pandemic cholera in the 19th century are largely summaries of apparent transfer from place to place by steamship. Before 1961, the El Tor biotype of V. cholerae O1 was known to cause cases and outbreaks of cholera-like disease, but it was not generally considered to have epidemic potential. It may be reasonable to consider the first six cholera pandemics as a single continuing pandemic, even though there is no bacteriologic proof that V. cholerae O1 of the classical biotype caused the first four pandemics as well as the fifth and sixth. First, the divisions between the six pandemics are indistinct, and it is not clear that they were separated by cholera-free intervals. Second, there is recent evidence that V. cholerae O1 can persist indefinitely as a free-living organism in some natural environments; pandemics 2 through 6 may have stemmed from organisms persisting in the environment in many countries as well as from small foci of human disease. Third, the seventh pandemic, caused by a different biotype, has persisted for 33 years, longer than any of the previous pandemics; it had explosive expansions in 1970 and 1991 that might have been considered new pandemics according to methods used to describe the first six pandemics. Finally, there may now be an eighth pandemic caused by V. cholerae of a different O group.

References: V. 
 V. 
 V. 
 V. 
 V. 
 V.