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Good Bugs Gone Bad

This time of year veterinarians are often asked, “Where do the bad bugs come from?”

TheE. colistory is a good place to start.

E. colihas been a normal inhabitant of the lower intestinal track of mammals for as long as mammals have existed. Then something happened to make certain strains of the garden variety bug a serious pathogen for both man and animals.E. coliis an organism often taken for granted because it is ubiquitous in nature. The presence ofE. coliand other kinds of bacteria within the intestines of both humans and animals is necessary for health.E. coliand other bacteria provide a vital role in digestion of food and production and absorption of vitamins.E. coliin the intestine aid in the absorption of a large portion of vitamin K and B-complex vitamins from the diet. Animals born and raised “germ free,” require vitamin supplements to stay alive. Scientists useE. colias a valuable biotechnology tool because it can readily be grown and its genetic structure easily manipulated. Today, genetically alteredE. coliis used to produce valuable pharmaceuticals like insulin and high-quality vaccines.

On the nasty side of the ledger,E. colievolved into a “bug” that commonly causes diarrheal disease in young animals and humans, is a constant threat of troublesome infections on medical wards and refuses to disappear from the news as a serious food safety issue in humans.

E. coliis the abbreviated name of the bacteriumEscherichia coli.Its scientifi name is derived from the name the German scientist and pediatrician, Theodor Escherich, who first isolated and characterized the bacterium in 1885. Veterinary and medical texts estimate that approximately 0.1 per cent of the total bacterial population of an adult’s intestines (on a western diet) is represented byE. coli.

E. colicolonizes the intestinal tract of the newborn within hours of birth. A calf, for example, is exposed immediately to an environment whereE. coliis everywhere including the udder and teats of the brood cow.E. coliare consumed when the calf first suckles. In the bowel,E. coliadheres to the mucus of the lower intestine where they remain as benign residents unless transformed into one of the pathogenic or bad bugs we commonly associate with diarrhea or food poisoning by some fluke of nature.

E. colicauses disease in two ways: WhenE. colifrom the intestine gets into other tissues or organs where it does not belong, or

WhenE. coliis changed genetically, becomes pathogenic, is shed, and subsequently infects a susceptible host.

Genetic mutation is a game of chance. Consider the entire human population of the world at around five billion and the chance of something going genetically wrong somewhere. It seems almost a certainty. Now consider the same number of bacteria in close association within a gut and the possibility genetic material somehow is altered and exchanged between living cells. Again, the chances are inevitable. Add to the mix thatE. coliis very adaptable. Despite being a one-celled organism, it can respond in remarkable ways to environmental signals like chemical changes, and shifts in pH or temperature. It can move and attach itself to other cells.E. colican change the pore diameter of its outer membrane to accommodate nutrients, to exchange material with other cells, or exclude inhibitory substances like antimicrobials.

Strains ofE. coliare named and classified based on the type of surface antigens they present to the immune system.E. colihas two: the O or somatic cell antigen and the H or flagellar antigen. There are more than 700 serotypes ofE. coli. One of the more dangerous food-borne E. colistrains is O157: H7.E. coliare also classified based on the types of toxins they produce and how well they are able to invade human cells.

Once established, anE. colistrain may persist for months or years. Resident strains shift more rapidly in the wake of intestinal infections or after the use of antimicrobial treatments that alter normal flora of the gut. How and why this occurs is not well understood.

Exchange of genetic information between cells happens in several ways. There are bacterial viruses that invade bacteria that deposit genetic pieces into the genetic machinery of cells they invade. Then there are the plasmids or free-floating, naked pieces of DNA within cells that become incorporated and functional components of the bacteria’s own DNA helix, sometimes transforming the innocuousE. coli into a pathogen capable of producing potentially lethal toxins like the Shiga or Vero toxins produced byE. coli O157: H7.

If we consider the sheer number ofE. colithat exist in our environment, perhaps it is fortunate more good bugs don’t go bad. Regrettably, the food animal industry is under fire when it does.E. coli O157: H7 gets front-page coverage because of its seriousness and the association that is always drawn between animals and food. Cattle have been implicated as the most important source ofE. coli O157: H7,but pigs, horses, dogs and deer have also been incriminated in outbreaks involving foods like meat, milk, fruit juice, spinach, water, sprouts and cheese.

New strains will continue to emerge andE. coliwill forever remain both friend and foe.


E. coliadheres to the mucus of the lower intestine where they remain as benign residents unless transformed into one of the pathogenic or bad bugs by some fluke of nature

About the author


Dr. Ron Clarke

Dr. Ron Clarke prepares this column on behalf of the Western Canadian Association of Bovine Practitioners. Suggestions for future articles can be sent to Canadian Cattlemen ([email protected]) or WCABP ([email protected]).



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