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Shigella dysenteriae, as are all Shigellae, is strictly a
human pathogen. It is spread by the fecal-oral route and is highly communicable. It is
estimated that less than 100 Shigella can start an infection, whereas it can take tens of
millions of, for instance, cholera vibrios to cause disease. Transmission is by
contaminated fingers, food, or water. Children in group care are considered to be at high
risk, because of poor hygiene and close contact. The organisms multiply in the small
intestine, then invade the large intestine. Disease is caused by the invasion of the
colonic epithelial cells and multiplication of the organisms within these cells and the
lamina propria with attendant cell death and tissue destruction. This produces acute
inflammation and ulceration of the mucosa. Shigella dysenteriae, in contrast to S.
flexneri, S. sonnei, and S. boydii, can also cause cell death by the production of
Shiga toxin, an A-B type toxin with 1 A subunit and 5 B subunits. As with other A-B type
toxins, the B subunits bind to the cell, injecting the A subunit into the cell. The A
subunit cleaves a specific adenine residue from the 28S ribosomal RNA in the 60S ribosome,
inhibiting protein synthesis and causing cell death. Hemolytic-uremic syndrome can occur
if the Shiga toxin attacks the renal endothelial cells, to which it has some affinity.
Rarely, in contrast to invasive Salmonella, is there invasion beyond the intestinal mucosa
or local lymph nodes. Invasion of the bloodstream is rare. Genes coded for by a large
"virulence" plasmid are apparently responsible for the ability of S. dysenteriae
to penetrate and multiply within cells. It is known that the organism induces its
endocytosis by epithelial cells, lyses the endocytic vesicle (the phagosome), multiplies
in the cytoplasm, and causes cell death. Shigellae are members of the family
Enterobacteriaceae. The identification of the Enterobacteriaceae is complicated and
involves a large number of tests. Of primary importance is the fermentation of lactose,
which Escherichia and Klebsiellae can accomplish, but which Shigella,
Salmonella, and Proteus cannot. Other characteristics which can
distinguish between the members of the family Enterobacteriaceae include indole, urease,
hydrogen sulfide, and gas production.
Phage Therapy for Shigella Infections
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Phage Therapy Center treats antibiotic-resistant infections. [More information...]
Additional Information About Phage Therapy for this Condition
Dubos,
R., Straus, J. H. and Pierce, C. , 1943 The multiplication of bacteriophage in
vivo and its protective effect against an experimental infection with Shigella
dysenteriae. J Exp Med 20: 161-168.
Morton, H. E. and Engely, F. B., 1945 Dysentery
Bacteriophage: Review of the Literature on its Prophylactic and Therapeutic Uses in Man
and in Experimental Infections in Animals. J Am Med Assoc 127: 584-591.
Schade, A. L. and Caroline, L. , 1943 The preparation of a
polyvalent dysentery bacteriophage in a dry and stable form. I. Preliminary Investigations
and general procedures. J Bacteriol 46: 463-473.
Schade, A. L. and Caroline, L. , 1944 The preparation of a
polyvalent dysentery bacteriophage in a dry and stable form. II. Factors affecting the
stabilization of dysentery bacteriophage during lyophilization. J Bacteriol 48: 179-190.
Schade, A. L. and Caroline, L., 1944 The preparation of a
polyvalent dysentery bacteriophagein a dry and stable form. III. Stability of the dried
bacteriophage towards heat humidity age and acididty. J Bacteriol: 243-251.
New York Times
A Stalinist Antibiotic Alternative
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Are Bacteriophages?
Evergreen State College
Phage
Therapy as Antibiotics
Biotechnology and Development Monitor
Bacteriophages:
An alternative to antibiotics?
Annual Reviews, Intelligent Synthesis of the Scientific Literature
Bacteriophage Therapy
Eliava Institute
List of Bacteriophages
Rehydration Project
Dialog on Diarrhoea
During the late 1960s, Shiga's bacillus was responsible for a series of devastating
epidemics of dysentery in Latin America, Asia and Africa. In 1967 it was detected in the
Mexican-Guatemalan border area and spread into much of Central America. An estimated half
million cases, with 20,000 deaths, were reported in the region between 1967 and 1971. In
some villages the case fatality rate was as high as 15 per cent; delayed diagnosis and
incorrect treatment may have been responsible for this high death rate. One particularly
disturbing feature was the resistance of the bacteria to the most
commonly used antibacterial drugs: sulfonamides, tetracycline, chloramphenicol and
streptomycin.
Serious epidemics due to the multiple-drug resistant S. shigae have
occurred recently in Bangladesh, Somalia, South India, Burma, Sri Lanka, Nepal, Bhutan,
Rwanda and Zaire. Each epidemic showed similar features: the disease spread rapidly in
spite of all available public health measures, attacking over 10 per cent of the
population and killing between two and ten per cent even of the hospitalised cases.
West Bengal in India has always been an endemic area for bacillary dysentery. In 1984,
greater numbers of dysentery cases started occurring and spread rapidly throughout the
state. Investigations revealed that attack rates were high, especially among young
children, and that all the shigellae isolated from stool specimens were resistant to the
commonly used drugs.
In response to the outbreak, control measures were initiated, newspapers, radio and
television carried information about the epidemic to raise public awareness; and district
level health personnel were alerted. Reports came in of increasing numbers of dysentery
cases, between two and three thousand new cases, and up to 150 deaths, a day. People began
to panic and doctors were frustrated by the ineffectiveness of conventional treatment .
Rehydration Project
Resistance to antibiotics
The epidemic spread to Calcutta, where stool samples from 382 patients showed Shiga's
bacillus in 35 per cent of cases, and different species of shigella organisms in 52 per
cent. These organisms were sensitive to nalidixic acid (96.7 per cent), gentamicin (83 per
cent), furazolidone (77.7 per cent), and; moderately sensitive to ampicillin (42.2 per
cent), kanamycin (37.4 per cent), neomycin (21.8 per cent) and cotrimoxazole (23.2 per
cent), but were resistant to other commonly available drugs and antibiotics. For most
doctors this was their first experience of coping with an epidemic of severe bacillary
dysentery and there was great confusion over the choie of antibacterial drugs and other
treatment. Nalidixic acid, although found to be most effective, was too expensive for
common use. Oral rehydration, the magic therapy for acute watery diarrhoea, was effective
in only about ten per cent of these cases, since in 90 per cent dehydration was not
serious.
Medical Information
CDC, February 5, 2003
Multidrug-Resistant
Shigella dysenteriae Type 1: Forerunners of a New Epidemic Strain in Eastern India?
Multidrug-resistant Shigella dysenteriae type 1 caused an extensive epidemic of
shigellosis in eastern India in 1984
CDC, October 2, 1987
Nationwide Dissemination of Multiply Resistant Shigella sonnei Following a
Common-Source Outbreak
In early July 1987, an outbreak of multiply resistant Shigella sonnei gastroenteritis
occurred among persons who attended the annual Rainbow Family gathering in North Carolina
(1). Since that time, four clusters of gastroenteritis due to multiply resistant S. sonnei
have been reported among persons who had no apparent contact with gathering attendees.
Association of Medical Microbiologists
Shigella
infections and bacillary dysentery |
