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Microbiology 12 |
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Microbiology 12 |
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NOTE: INFORMATION ON THIS PAGE IS INTENDED FOR EDUCATIONAL USE ONLY. FOR MEDICAL ADVICE YOU SHOULD CONSULT WITH A PHYSICIAN
The Enterics
The enterics (Enterobacteriaceae) are a large family of gram negative bacteria which inhabit animal intestines and contain some of the most medically significant genera. Certain genera such as Salmonella, Shigella and Yersinia spp. are important pathogens of the GI tract. Others, such as Escherichia and Enterobacter, are typically considered normal flora of the intestine but may also cause disease if given the opportunity or are represented by pathogenic strains.
As you will discover during our bacterial identification labs, many enterics can be differentiated by characteristic fermentation reactions and other biochemical tests. The enterics must also be differentiated from another medically important family of gram negative rods called the Pseudomonadaceae. Enterics typically ferment glucose and produce acid and gas, are oxidase negative and if motile, exhibit peritrichous flagella. In contrast, Pseudomonads are not fermentors and have a respiratory metabolism. They are also oxidase positive and exhibit polar flagella.
Representatives:
(Note: The enteric family is too vast to be considered in entirety here but a few medically important pathogens will be discussed)
For more information on enteric pathogens go to the FDA's Bad Bug Book
Escherichia coli (Named for Escherich (Germany) and inhabiting the colon)
(Many strains are normal flora of the mammalian colon. Others are important causes of travellers diarrhea, bacterial dysentery and UTI's).
E.coli is the main representative of the enteric family and is the "poster child" of microbiologists and researchers. Much of our understanding of microbial genetics and metabolism was first worked out in E. coli systems. Our knowledge of the organism in health and disease has been furthered as its entire genome has been sequenced. E. coli is commonly used in genetic engineering experiments and by the biotechnology industry. The presence of E. coli in foods, water or other substances is commonly used as an "indicator" of fecal contamination.
E. coli is a remarkably adaptable organism metabolically and physiologically. As a faculative anaerobe, it can grow in the presence or absence of oxygen. It can carry out fermentation of sugars, producing mixed acids and gas. A positive lactose fermentation test helps differentiate E. coli from the non-lactose fermenting gut pathogens, Salmonella and Shigella. E. coli can also carry out anaerobic respiration, using NO3 or N02 as final electron acceptors, which enables it to survive in an anaerobic intestinal environment. In the absence of sugar, E. coli can also metabolize the amino acid tryptophan into indole and pyruvate.
E. coli becomes established in the human colon and intestines of most endothermic animals shortly after birth. The organisms are acquired from other individuals, food or water. Resident flora are usually quite persistent but may get pushed out of the way during diarrheal disease or after taking antibiotics. E. coli is the predominant facultative anaerobe in the human colon but is outnumbered by strict anaerobes such as Bacteroides by as much as 20:1. Resident E. coli help outcompete gut pathogens and also produce a number of useful vitamins, including various B vitamins (common coenzymes) and up to 50% of vitamin K, which is involved in blood-clotting. However, a healthy individual receiving a well-balanced diet probably does not depend too heavily upon the vitamins produced by gut flora.
Over 700 strains of E. coli have been recognized, of which a small number cause disease. Strains can be distinguished by a method known as serotyping. Specific antibodies are used that react with cell wall (O) antigens, capsular (K) and flagellar (H) antigens.
Pathogenic E.coli are well known for producing forms of enteritis (see Table 1) and urinary tract infections. The diarrheal pathogens have some common strategies:
Fig. 1. E. coli attaching to intestinal epithelium by fimbriae.
Table 1. The Five Main Groups of Escherichia coli that Cause Diarrhea
Type of E. coli Enteropathogenic
(EPEC) Diarrhea in infants (outbreaks in hospital nurseries) Watery, no fever Enterotoxigenic
(ETEC) Traveler's diarrhea, infant diarrhea Watery, no fever Enterohemorrhagic (EHEC): caused
by one serotype 0157:H7 Hemorrhagic colitis Hemolytic Uremic Syndrome as a complication in
infants and the elderly Thrombotic thrombocytopenic purpura (TTP) in the
elderly Bloody or watery diarrhea Fever low grade or absent Enteroinvasive
(EIEC) Diarrhea in all ages Dysenteric (bloody) stools with inflammation and fever,
almost identical to Shigellosis Enteroaggregative (EaggEC) Chronic diarrhea in infants Persistent, watery diarrhea without inflammation or
fever
More on E. coli 0157:H7
This virulent serotype was first associated with human disease in 1982 when it was linked to two outbreaks of a severe diarrheal disease. Since then the organism has been increasingly recognized as a significant emerging pathogen. Between 1993 and 1995 alone there were 63 outbreaks and 1,735 cases of E. coli 0157:H7 in the U.S.A. Currently, about 75,000 cases are estimated to occur each year in the U.S.A. and the number of associated deaths are growing. Most outbreaks have been associated with contaminated ground beef from fast-food chains. Infections have also been traced to fruit and vegetables,contaminated by fertilizer, and to sewage-contaminated water. The emergence of the organism in the 1980's can be explained by current farming practices. "With thousands of cattle on hundreds of farms going to tens of slaughter houses to one hamburger plant, where everything is mixed together to allow cross contamination....it's no surprise that 0157:H7 emerged" (J. Kaper, University of Maryland School of Medicine in Science News, 8/4/01, Vol 160 pp. 74-76).
The entire genome of O157:H7 was sequenced in 2000. It was found that the organism carries a lot of genes that more resemble the pathogens Shigella and Salmonella than harmless strains of E. coli. For example, O157:H7 produces one of two Shiga toxins which cause severe inflammation of the colonic mucosa. Toxin production depends on the presence of a lysogenic bacteriophage. Several days after eating or drinking contaminated foods, symptoms appear along with a watery diarrhea and severe stomach cramps. The diarrhea can turn grossly bloody. In most cases the illness is self-limiting after about a week but up to 15% of cases (usually infants and the elderly) are susceptible to a complication known as Hemolytic Uremic Syndrome which can cause permanent kidney damage and may be fatal.
Uropathogenic E. coli (UPEC)
E .coli cause 90% of community-acquired and nosocomial urinary tract infections (UTI's) in anatomically normal urinary tracts. Most strains are accidentally introduced from the fecal flora as a result of lack of hygiene, sexual activity or through prolonged use of urinary catheters. UTI's are about 15 times more common in women because of a short urethra. Sexually active women may suffer from "honeymoon cystitis" whereby UPEC strains from the fecal flora are introduced into the urethra during sexual intercourse. Symptoms of cystitis include a burning pain upon urination and a frequent urge to urinate. Blood can also be visible in the urine.
UPEC produce adhesins in the form of attachment pili for the urinary tract epithelium. There is a genetic component involved in UTI's. People with cell surface receptors for the attachment pili are more likely to suffer UTI's and recurrences. Variations in the architecture of the urinary tract, related to the presence of pockets, also influences how well E. coli can colonize these areas.
Treatment & Prevention of E. coli infections
The best way to prevent E. coli infections is to minimize exposure to fecally contaminated food and water. Washing fruits and vegetables and cooking meat thoroughly is good practice. Widespread use of "tetracycline prophylaxis" to "prevent E. coli-associated traveler's diarrhea should be discouraged to avoid selecting for drug-resistant microbes. The best treatment for most E. coli enteric infections is fluid and electrolyte replacement. Notably, antibiotic therapy may actually worsen 0157:H7 infections and lead to hemolytic uremic syndrome. It appears that antibiotics stress the bacteria and trigger phage-associated production of Shiga toxin. As bacteria are lysed by viruses, the toxin travels in the blood to the kidneys.
UTI's caused by E. coli are often treated with sulfa-containing drugs such as Septra or Bactrim . Nitrofurantoin or Ciprofloxacin can be used if the patient is allergic to sulfa or if there is resistance to sulfa. Treatment is necessary to prevent ascending damage to the kidneys from the urinary bladder. Evan with treatment about a third of UTI's recur! Research is being conducted to test a hypothesis that UPEC may enter a form of dormancy during infection, perhaps in the form of a biofilm, and become less sensitive to antibiotics (Personal communication 8/15/01. Todd Steck, Ph.D. University of North Carolina, Charlotte).
UTI's can be prevented by the following:
Shigella spp. (Named for Shiga of Japan)
Species include Shigella sonnei, S. boydii, S. flexneri, and S. dysenteriae
Shigella spp are non-motile, non-lactose fermenting rods which produce hydrogen sulfide and indole from tryptophan. The organisms are primarily transmitted via fecally-polluted water and foods. Shigella can also be sexually-transmitted by the oral-fecal route. Cases of sexually-acquired Shigella among gay men in San Francisco have been increasing over the past year.
Shigella are very infectious pathogens that produce an acute disease called bacillary dysentery or Shigellosis. As few as 10 organisms may be needed to initiate an infection.. Within a day or two symptoms typically include abdominal cramps, vomiting, fever and diarrhea. Stools may be markedly bloody. The disease is produced when Shigella infect cells of the colonic mucosa. A plasmid is required for attachment and entry into host cells. The organisms kill intestinal epithelial cells by spreading from cell to cell by elongated host actin filaments.. This event causes a great deal of inflammation. Some strains produce Shiga toxin which causes severe abdominal cramps and frequent, bloody stools. The toxin is associated with Hemolytic Uremic Syndrome as seen in infections with E. coli O157:H7. Ampicillin and Bactrim may shorten symptoms and sheeding of the organisms in the feces.
Salmonella spp. (Named for Salmon, U.S.A)
Salmonella share ~90% homology with E. coli & should be considered the same species but this is not likely to gain acceptance.
Currently the genus Salmonella is separated into three major species designations;
Organisms can be typed by antibodies against the cell wall (O) antigen and by their susceptibility to different bacteriophages. The organsims are motile and many express two different flagellar (H ) antigens, a phenomenon known as phase variation. Salmonellae do not ferment lactose and typically produce H2S (although S. typhi produces little or no H2S).
Gastroenteritis
Salmonellae of animal origin are a common cause of gastroenteritis in humans. Salmonellae are found in wild and domestic animals, especially poultry, in eggs and on their shells. Chickens can transmit S. enteritidis transovarialy to their eggs (the idea an uncracked egg is unsafe is incorrect). Birds and reptiles shed Salmonellae and people should be aware of this fact if these animals are kept as pets. Alfalfa sprouts have also been important sources of Salmonella outbreaks in the U.S. Cross-contamination or recontamination of cooked foods from raw foods is a common cause of Salmonella outbreaks.
High risk people that are especially susceptible to foodborne illness include infants, the elderly pregnant women and persons with suppressed immune systems. Such people should avoid products containiing raw or undercooked eggs; frozen or liquid pasturerized eggs should be used instead.
The incubation period for Salmonella enteritis is between 8-72 hours. Illness last several days to a week.
Symptoms include vomiting, diarrhea, headache, nausea, abdominal pain and fever.Symptoms are probably due to invasion of mucosal cels and phagocytes. Most people recover but an infected person continues to shed bacteria for up to 3 months. In 1-3% cases chronic carriers she dbacteria > 1 yr. The disease can become systemic and lethal in IMS'd patients.
Typhoid fever is caused by Salmonella typhi, which possesses a Vi (virulence) capsular antigen and produces little or no H2S. S. typhi only exhibit one form of flagellum. The organisms enter the GI tract via fecal contamination. Incubation is longer than for typhimurium : 1 wk-1 month. Invasion phase rarely marked by diarrhea. The bacilli penetrate the intestinal lining and are taken up, but not destroyed, by macrophages. The bacteria can then disseminate in the blood to other parts of the body and a rose-colored rash typically appears. Bacteria multiply in spleen & liver & are released into blood in high numbers. S. typhi also infects Peyer's patches (lymphoid tissue) of the small intestine which can lead to intestinal rupture. ~10 % mortlality rate. Most symptoms are due to endotovin. The organism is maintained by asymptomatic human carriers, who typically carry the bacilli in their gall bladders and may excrete large numbers of bacteria in their feces. Carriers often need removal of the gall bladder and extended treatment with antibiotics to eliminate Salmonellae.