Escherichia coli O157:H7

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Escherichia coli

Scientific classification
Phylum: Proteobacteria
Class: Gamma Proteobacteria
Order: Enterobacteriales
Family: Enterobacteriaceae
Genus: Escherichia
Species: E. coli
Binomial name
Escherichia coli
T. Escherich, 1885

Escherichia coli O157:H7 is an enterohemorrhagic strain of the bacterium Escherichia coli and a cause of foodborne illness.[1] An estimated 73,000 cases of infection and 61 deaths occur each year in the United States alone.[2] Infection often leads to bloody diarrhea, and occasionally to kidney failure. Most illness has been associated with eating undercooked, contaminated ground beef, although it is also transmitted by person-to-person contact, produce, drinking unpasteurized milk or swimming in or drinking contaminated water.

Contents

[edit] Biochemistry

E. coli serotype O157:H7 is a gram-negative rod-shaped bacterium. The "O" (which is a capital O, not a zero) in the name refers to the somatic antigen number, whereas the "H" refers to the flagellar antigen. Other serotypes may cause (usually less severe) illness, but only those with the specific O157:H7 combination are reviewed here. Other bacteria may be classified by "K" or capsular antigens. (The "O" stands for ohne Hauch [Ger. “without breath”]; "H" for Hauch; and "K" for Kapsel.[3][4]) This is one of hundreds of serotypes of the bacterium Escherichia coli. While most strains are harmless and normally found in the intestines of mammals, this strain produces Shiga-like toxins, causes severe illness, and is a member of a class of pathogenic E. coli known as enterohemorrhagic Escherichia coli or EHEC. Sometimes also referred to by their toxin producing capabilities, Verocytotoxin producing E. coli (VTEC) or Shiga-like Toxin producing E. coli (STEC).

E. coli O157:H7 was first recognized as a pathogen as a result of an outbreak of unusual gastrointestinal illness in 1982. The outbreak was traced to contaminated hamburgers, and the illness was similar to other incidents in the United States and Japan. The etiologic agent of the illness was identified as a rare O157:H7 serotype of Escherichia coli in 1983. This serotype has only been isolated once before, from a sick patient in 1975.[5]

E. coli O157:H7 is markedly different from other pathogenic E. coli, as well. In particular, the O157:H7 serotype is negative for invasiveness (sereny test), elaborates no colonization factors (CFA/I or CFA/II), Doesn't produce heat stable or heat labile toxins and is non-hemolytic. In addition, E. coli O157:H7 is sorbitol negative where 93% of all E. coli ferment sorbitol.[6]. E. coli O157:H7 also lacks the ability to hydrolyze 4-methylumbelliferyl-ß-D-glucuronide (MUG)[7] and does not grow at 45ºC in the presence of 0.15% bile salts. Because of the latter characteristic this serotype cannot be isolated by using standard fecal coliform methods that include incubation at 45ºC. [7][8]

E. coli O157:H7 serotypes of are closely related, descended from a common ancestor, divergent in plasmid content more than chromosomal content, and are no more related to other shiga toxin producing strains than any other randomly chosen E. coli serotype. E. coli O55:H7 and E. coli O157:H7 are most closely related and diverged from a common pathogenic ancestor that possessed the ability to form attaching and effacing lesions. E. coli O157:H7 serotypes apparently arose as a result of horizontal gene transfer of virulence factors.[9]

Among these virulence factors are a periplasmic catalase and shiga-like toxins. Shiga-like toxins are iron regulated toxins that catalytically inactivate 60s ribosomal subunits of eukaryotic cells blocking mRNA translation and causing cell death.[10] Shiga-like toxins are functionally identical to toxins produced by virulent Shigella species.[11]. Strains of E. coli that express shiga-like toxins gained this ability due to infection with a prophage containing the structural coding for the toxin, and Non-producing strains may become infected and produce shiga-like toxins after incubation with shiga toxin positive strains[12][13] The periplasmic catalase is encoded on the pO157 plasmid and is believed to be involved in virulence by providing additional oxidative protection when infecting the host [14](11).

[edit] Transmission

The major source of infection is undercooked ground beef; other sources include consumption of unpasteurized milk and juice, raw sprouts, lettuce, and salami, and contact with infected live animals. Waterborne transmission occurs through swimming in contaminated lakes, pools, or drinking inadequately treated water. The organism is easily transmitted from person to person and has been difficult to control in child day-care centers.

E.coli O157:H7 is found on a small number of cattle farms and can live in the intestines of healthy cattle. The toxin requires highly specific receptors on the cells' surface in order to attach and enter the cell; species such as cattle, swine, and deer which do not carry these receptors may harbor toxigenic bacteria without any ill effect, shedding them in their feces from where they may be spread to humans. Meat can become contaminated during slaughter, and organisms can be thoroughly mixed into beef when it is ground into chopmeat. Bacteria present on the cow's udders or on equipment may get into raw milk. Although the number of organisms required to cause disease is not known, it is suspected to be very small.

Eating contaminated meat (especially ground meat) or produce that has not been cooked sufficiently to kill E. coli O157:H7 can cause infection. Contaminated foods look and smell normal.

[edit] Signs and symptoms

E. coli O157:H7 infection often causes severe, acute bloody diarrhea (although nonbloody diarrhea is also possible) and abdominal cramps. Usually little or no fever is present, and the illness resolves in 5 to 10 days. It can also be asymptomatic.

In some people, particularly children under 5 years of age and the elderly, the infection can cause hemolytic uremic syndrome, in which the red blood cells are destroyed and the kidneys fail. About 2%–7% of infections lead to this complication. In the United States, hemolytic uremic syndrome is the principal cause of acute kidney failure in children, and most cases of hemolytic uremic syndrome are caused by E. coli O157:H7.

[edit] Diagnosis

A stool culture can detect the bacterium, although it is not a routine test and so must be specifically requested. The sample is cultured on sorbitol-MacConkey (SMAC) agar, or the variant cefeximine potassium telluride sorbitol-MacConkey agar (CT-SMAC). However, like all cultures, diagnosis is slow using this method, and more rapid diagnosis is possible using PCR techniques. Newer technologies using fluorescent and antibody detection are also under development.

[edit] Surveillance

E. coli O157:H7 infection is nationally reportable in the USA and Great Britain, and is reportable in most U.S. states. HUS (hemolytic-uremic syndrome) is also reportable in most US states.

[edit] Treatment

Most people recover without antibiotics or other specific treatment in 5–10 days. There is no evidence that antibiotics improve the course of disease, and it is thought that treatment with some antibiotics may precipitate kidney complications.[15] Antidiarrheal agents, such as loperamide (imodium), should also be avoided.

Hemolytic uremic syndrome is a life-threatening condition usually treated in an intensive care unit. Blood transfusions and kidney dialysis are often required. With intensive care, the death rate for hemolytic uremic syndrome is 3%–5%.

[edit] Prognosis

The majority of infections resolve completely. Those who develop hemolytic uremic syndrome suffer more long-term consequences. 3–5% of those with HUS die, causing about 61 deaths annually in the USA. One third of this group have abnormal kidney function many years later, and a few require long-term dialysis. Another 8% of this group develop other lifelong complications, such as high blood pressure, seizures, blindness, paralysis, and, if surgery is required to remove part of the bowel, additional procedure-related side-effects.

There are currently long term studies continuing in Walkerton, Ontario, looking at the long term effects of E. coli O157:H7 after approximately 2500 people were infected through the municipal water system in May 2000.

[edit] Costs

The pathogen results in an estimated 2,100 hospitalizations annually in the United States. The illness is often misdiagnosed; therefore, expensive and invasive diagnostic procedures may be performed. Patients who develop HUS often require prolonged hospitalization, dialysis, and long-term follow-up.

[edit] Prevention

[edit] Agricultural

In January 2007 Canadian bio-pharmaceutical company Bioniche announced it has developed a bovine vaccine capable of reducing O157:H7 in cattle by over 99%. http://www.cnxmarketlink.com/en/releases/archive/January2007/10/c4698.html

Beef processing is the most common point of contamination, when during the slaughtering process the contents of intestines mix with the meat and bacteria flourish in the warm, moist conditions. If the infected parts are then ground, the bacteria goes from the surface of the cut to the interior of the ground mass. Thus, ground beef is more likely to be a source of infection than steak. In steak only the surface area of a cut is exposed during rendering, and cooking the outside affects the entire exposed portion. In ground beef, however, bacteria is mixed throughout the meat mass, requiring the entire mass to be heated thoroughly to eliminate the pathogen. Additionally, in the production of ground beef, meat from multiple cows is often ground together, enabling contamination from a single cow to infect an entire lot of ground beef.

Accordingly, elimination of infection is unlikely until preventative measures either reduce the number of cattle that carry E.coli O157:H7 or reduce the contamination of meat during slaughter and grinding.

[edit] Culinary and dietary

Cooking all ground beef and hamburger thoroughly, using a digital instant-read meat thermometer, will eliminate the organism. Ground beef should be cooked until a thermometer inserted into several parts of the patty, including the thickest part, reads at least 72°C (160°F).

When preparing meat, it should be kept separate from other foodstuffs, and all surfaces and utensils which come into contact with raw meat should be washed thoroughly before being used again. Hand washing is similarly important. Placing cooked hamburgers or ground beef on an unwashed plate that held raw patties can transmit infection.

Avoid unpasteurized milk, juice, and cider. Commercial juice is almost always pasteurized, and juice concentrates are also heated sufficiently to kill pathogens.

Fruits and vegetables should be washed thoroughly, especially those that will not be cooked. Children under 5 years of age, immunocompromised persons, and the elderly should avoid eating alfalfa sprouts until their safety can be assured. Methods to decontaminate alfalfa seeds and sprouts are being investigated.

Contaminated water should be boiled at a rolling boil for at least one minute (longer at higher altitudes) before consumption. Care while swimming to avoid ingestion of potentially contaminated water can reduce the chances of infection.

Proper hand washing after using the lavatory or changing a diaper, especially among children or those with diarrhoea, will reduce the risk of transmission. Anyone with a diarrheal illness should avoid swimming in public pools or lakes, sharing baths with others, and preparing food for others.

[edit] Opportunities

Learning more about the ecology of this organism in cattle and other ruminants may help in devising methods to decrease its prevalence in food animals. Learning how this pathogen contaminates produce items could lead to measures that would increase their safety. Decreasing the incidence of these infections would decrease HUS, the major cause of kidney failure in children in the United States. Transmission in day care centers highlights need for better infection-control practices.

(adapted from two public domain sources[1], [2])

[edit] See also

[edit] References

  1. ^ Karch H, Tarr P, Bielaszewska M (2005). "Enterohaemorrhagic Escherichia coli in human medicine.". Int J Med Microbiol 295 (6-7): 405–18. PMID 16238016. 
  2. ^ Questions & Answers: Sickness caused by E. coli, Centers for Disease Control and Prevention.
  3. ^ See Kauffmann-White-Schema in the German Wikipedia.
  4. ^ Dorlands Medical Dictionary, entry for "O antigen".
  5. ^ Riley L, Remis R, Helgerson S, McGee H, Wells J, Davis B, Hebert R, Olcott E, Johnson L, Hargrett N, Blake P, Cohen M (1983). "Hemorrhagic colitis associated with a rare Escherichia coli serotype.". N Engl J Med 308 (12): 681–5. PMID 6338386. 
  6. ^ Wells, J. G., B. R. Davis, I. K. Wachsmuth, L. W. Riley, R. S. Remis, R. Sokolow, and G. K. Morris. 1983. Laboratory investigation of hemorrhagic colitis outbreaks associated with a rare Escherichia coli serotype. J. Clin. Microbiol. 18:512-520.
  7. ^ a b Doyle, M. P., and J. L. Schoeni. 1984. Survival and growth characteristics of Escherichia coli associated with hemorrhagic colitis. Appl. Environ. Microbiol. 48:855-856.
  8. ^ Szabo, R. A., E. C. D. Todd, and A. Jean. 1986. Method to isolate Escherichia coli O157:H7 from food. J. Food Prot. 49:768-772.
  9. ^ Whittam, T. S., I. K. Wachsmuth, and R. A. Wilson. 1988. Genetic evidence of clonal descent of Escherichia coli O157:H7 associated with hemorrhagic colitis and hemolytic uremic syndrome. The Journal of Infectious Diseases 157:1124-33.
  10. ^ Reisberg, R., S. Olsnes, and K. Eiklid. 1981. The cytotoxic activity of shigella toxin. J. Biol. Chem. 256:8739-8744.
  11. ^ Calderwood, S. B., F. Auclair, A. Donohue-Rolfe, G. T. Keusch, and J. J. Mekalanos. 1987. Nucleotide sequence of the shiga-like toxin genes of Escherichia coli. Proc. Natl. Acad. Sci. USA 84:4364-4368.
  12. ^ O'Brien, A. D., J. W. Newland, S. F. Miller, and R. K. Holmes. 1984. Shiga-like toxin-converting phages from Escherichia coli strains that cause hemorrhagic colitis or infantile diarrhea. Science 226:694-696.
  13. ^ Strockbine, N. A., L. R. M. Marques, J. W. Newland, H. W. Smith, R. K. Holmes, and A. D. O'Brien. 1986. Two toxin-converting phages from Escherichia coli O157:H7 strain 933 encode antigenically distinct toxins with similar biologic activities. Infect. Immun. 53:135-140.
  14. ^ Brunder, W., H. Schmidt, and H. Karch. 1996. KatP, a novel catalase-peroxidase encoded by the large plasmid of enterohaemorrhagic Escherichia coli O157:H7. Microbiology 142:3305-3315.
  15. ^ Walterspiel, J. N.; Morrow, Ardythe L.; Cleary, T. G.; Ashkenazi, S (2003). "Effect of subinhibitory concentrations of antibiotics on extracellular shiga-like toxin I". Infection 20: 25-29. Retrieved on 200-01-07. 

[edit] External links

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