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Parallels between E. coli O157 and Flesh-Eating Methicillin Resistant Staphylococcus aureus (MRSA)

Influenza Epidemic and Methicillin Resistant   Staphylococcus Aureus (MRSA)

Stock Photo

The Nation is currently experiencing two major health scares due to toxic bacteria. One derives from E. coli O157 contaminated lettuce and has caused severe diarrhea in several hundred individuals. The other epidemic is caused by toxic methicillin resistant Staphylococcus aureus (MRSA). It presents as a rapidly progressing skin abscess accompanied by significant tissue destruction or “flesh-eating.” Both epidemics could have been prevented through a more diligent and responsive Public Health Service. The time to act was when the mutant bacteria causing these respective illnesses were first identified in 1983 and 1992, respectively. At least in the case of toxic MRSA, it is not too late to mount a vigorous nationwide eradication program. Such a program will be facilitated by the availability of a simple environmental testing procedure for the presence of MRSA. The testing can also determine effectiveness of the MRSA eradication methods being employed. This article provides a brief historical account of the genesis of both types of bacteria, and outlines a community-based approach being promoted by the Institute of Progressive Medicine that is aimed at the eradication of MRSA. Information is also provided on the Staph Identification Plate for MRSA.

E. coli O157
Diarrhea caused by E. coli O157 bacteria is due in part to toxins coded by genes that are present in bacteriophages (bacterial viruses) that originated in shigella bacteria, the cause of dysentery, also a diarrheal disease. While bacteriophages commonly destroy bacteria, some are involved in the transfer of genes between bacteria, as apparently occurred between a shigella and an E. coli bacterium. The toxicity of E. coli O157 is also determined by additional genes that allow the bacteria to i) withstand the stomach’s acidity; ii) attach to and damage cells of the small intestine; and iii) destroy both red blood cells and kidney tissue. Most of these genes originally came from other bacteria and were transferred to E. coli O157 within another type of mobile genetic element termed plasmids. The unique association within an E. coli of certain specific plasmids and one or more shiga-toxin producing bacteriophages has created an extremely virulent (disease causing) E. coli. Death following infection can occur from dehydration due to uncontrolled diarrhea; anemia from gastrointestinal bleeding and red blood cell destruction; and renal failure due to toxic damage to the kidneys. The effects can last for years even after the infection has cleared.
Hundreds of strains of E. coli have been differentiated on the basis of antibody reactions with bacterial components termed “O” and “H” antigens. The O157 E. coli strain that now carries the virulent plasmids along with toxin producing bacteriophages has a specific H antigen, designated H7. Essentially, all of the toxic O157 bacteria arose from a single bacterium that became uniquely infected with specific plasmids and toxin coding bacteriophages. These events apparently occurred around 1980, since prior to that time E. coli O157:H7 bacteria were extremely rare and the diseases they now produce were unknown. In retrospect, major efforts should have been undertaken to search out and destroy these mutant bacteria when they were first identified. Instead, E. coli O157 bacteria have become disseminated worldwide and comprise a major biological threat to the nation’s food supply.
Persistent infection by E. coli O157 has become particularly common in corn fed cattle. Cows do not completely metabolize the simple starches in corn, thereby providing a rich food source for the sugar dependent growth of E. coli. Levels of E. coli in cow feces can be dramatically reduced within a few days of switching the diet to natural foliage or even to hay. This practice has been resisted by the cattle industry and, as a result, feedlot manure is commonly heavily contaminated with E. coli O157. It has especially proven difficult to avoid E. coli O157 contamination of bulk minced meat products. Cow’s milk can also become contaminated and transmit infection if the milk is not pasteurized. Water runoffs from cattle feed lots can potentially mix with the water used on crops, thereby providing an opportunity for cross contamination. The pooling and marketing of spinach and lettuce leaves in ready-to-eat plastic bags has lead to national outbreaks of E. coli O157 infection. For this to occur, contaminating bacteria need only be present on a fraction of the total crops being pooled.
A small percentage of healthy farm workers can also persistently shed E. coli O157 in feces. The lack of illness in these farm workers may be attributed to sufficient immunity against the antigens of E. coli O157 to prevent tissue damage. Anyone acquiring an active infection that causes diarrhea can also transmit illness if even a minute amount of their infected feces is inadvertently ingested by others.
The Public Health authorities have done little to stem the spread of E. coli O157. Moreover, they have not been forthright with the American public on the genesis of the problem and how, in retrospect, a more proactive E. coli O157 surveillance program should have been instituted. E. coli O157 can be differentiated from other E. coli strains using culture plates that contain sorbitol and rhamnose sugars. Multiple fecal samples can be applied to different regions of a single culture plate, bringing the reagent cost per sample to well under $1.00. Yet most cattle and feedlots are not routinely screened for E. coli O157; possibly to avoid incrimination based on an overt awareness of the problem.
The public should be informed whether the meat, milk and other produce they purchase has been specifically tested for E. coli O157, and found to be bacteria-free. It is not sufficient to simply recommend that hamburger meat be well cooked, since even handling the uncooked meat can be a source of household E. coli O175 contamination.
Most doctors and hospitals also fail to routinely test the feces of patients presenting with diarrhea for E. coli O157. A reason frequently cited is that there are no specific therapies for the diseases caused by these bacteria. Infected patients are often misdiagnosed as having another illness and are subjected to inappropriate testing and therapeutic endeavors. The overall annual incidence of severe E. coli O175 infections in the United States is variously estimated to be in the order of 30-50,000. With more specific testing, this number would likely be much higher.
Any future eradication program for E. coli O157 has to be tempered by the recent finding that the shiga-coding bacteriophages and harmful plasmids have been transmitted to other E. coli strains. The industry emphasis is being placed on the potential use of bacteriophages that would kill food-contaminating bacteria. With little public debate, the Food and Drug Administration (FDA) recently approved the spraying on processed meats and salads, of bacteriophages that selectively kill listeria bacteria. This action is widely seen as a forerunner to approving E. coli destroying bacteriophages. Given the potential capacity of bacteriophages to transmit genes between bacteria, FDA should proceed cautiously with such a program. Full consideration should first be given to alternative, more natural methods such as simply adjusting the diets of cows being brought to slaughter. Mandatory testing of the food supply for E. coli O157 should also be instituted.
Flesh-Eating Toxic MRSA Bacteria.
A somewhat parallel situation to E. coli O157 exists with the emergence of a flesh-eating strain of methicillin resistant Staphylococcus aureus (MRSA). In 1932, a leukocyte (white blood cell) killing toxin was identified in some strains of Staphylococccus aureus (golden staph) by Drs. Panton and Valentine. It was subsequently termed the PVL (Panton-Valentine-Leukocidin) toxin. Similar to the shiga-toxin genes of E. coli O157, the PVL gene was also transmitted to an MRSA by a bacteriophage.
Staphylococcus infections were a growing problem until the commercial availability of penicillin in the mid 1940’s. The success of using penicillin to kill staph was relatively short lived, however, since certain strains of staph carried a plasmid that produced a penicillinase, a penicillin destroying enzyme. By the early 1960’s most strains of Staphylococccus aureus carried this plasmid and were resistant to penicillin. However, they were susceptible to a newly developed synthetic penicillin-like antibiotic called methicillin, which is unaffected by penicillinase. Over time, MRSA bacteria appeared leading to the need for newer antibiotics for which resistance also progressively developed. Methicillin resistance is carried by a transmissible genetic element termed Mec that codes for a modified penicillin binding protein non-reactive with methicillin. This element can also transmit genes conferring resistance to various other antibiotics. To a large extent, multiple antibiotic resistant MRSA have only infected hospitalized patients who were already sick and did not pose a major threat to healthy individuals. Most of the hospital acquired staph infections can still be controlled using vancomycin as an antibiotic of last resort.
What should have provoked immediate major concern was the report from Australia in 1992 of MRSA bacteria that were producing PVL-like toxin. Even in1995, there were still only 10 hospitalized cases in Australia attributed to this emerging strain of highly toxic Staphylococccus aureus. Ten years later in 2005, there were over 35,000 hospitalized cases in Australia with this strain of staph. It has spread worldwide and in many countries is now the major cause of hospital acquired infections.
Largely due to hospitals discharging infected patients, toxic MRSA bacteria have now entered the community. They can harmlessly reside on the skin surface, including the hands and especially on the moist inner lining of the nose, armpits and groin areas. They can also survive on clothing and towels, desk tops, floors and other items. Toxic MRSA induce inflammatory disease only when they gain entry into the tissues. This can occur because of trauma of the skin, as in accidents, contact sports and even normal child play; because of an associated skin disease such as eczema, psoriasis or herpes infections; or because of an accompanying cold or bout of influenza.
Increasingly, there are community reports of MRSA outbreaks, which are almost invariably due to a PVL toxin producing MRSA. They can progress rapidly from a small abscess to widespread muscle invasive disease. Surgeons report on the ghastly sight of dissolving MRSA infected tissue justifying the annotation of a flesh eating bacteria. Limiting the body spread of toxic MRSA infections can sometimes require major surgical excisions, including amputations.
Toxic MRSA infections are contributing to many hospital deaths and extended patient stays. Discharged infected patients are not being warned of the risks they pose to family members. Up to 9% of healthcare providers may now carry toxic MRSA from their workplace to their home. They have not been fully alerted to their unwitting role in placing their family and friends at risk. Even family pets can become ill from acquiring MRSA infections, thereby spreading the risk of infection to veterinarians.
While the so called community acquired MRSA bacteria are still susceptible to many of the antibiotics that are ineffective on the less toxic (PVL negative) MRSA, it is predictable that multiple-antibiotic-resistant, flesh eating staph will soon appear. All that is required is for the complex Mec gene complex conferring resistance to multiple antibiotics in non-toxic MRSA to exchange with the simpler Mec gene complex currently in PVL positive MRSA. Vancomycin resistant staph bacteria have recently been identified and the gene for this resistance may too pass into a toxic MRSA. When these events occur, mankind will surely be confronted with increasing numbers of MRSA associated deaths occurring in previously healthy individuals. That is, unless society takes immediate action.
Hospitals are beginning to recognize the added costs of caring for patients that acquire infections within their facilities. While there is some movement towards improved hospital infection control, the problem will persist as more infected patients will be coming from the community. The community needs to reverse the MRSA epidemic and to possibly achieve a total eradication of MRSA. The key to eradication is the simplicity of detecting MRSA that, at least for the environment, can be legally performed by the lay public. This will allow for frequent monitoring of both commercial and private locations. Positive findings will indicate the need for decontamination of the premise using disinfecting solutions and non-chemical methods.
The Institute of Progressive Medicine, a component of the newly formed Progressive University, is promoting these actions through its charitable activities. It has evaluated an inexpensive Staph Identification Plates for MRSA that is available at cost from the Institute and may soon be marketed by other suppliers. Each plate comprises a thin layer of agar on clear plastic that allows for the selective growth of staphylococcus. The layer is protected by a removable transparent plastic lid. Areas can be sampled by gently touching the agar against the surfaces and replacing the lid. The plates are stored for up to 2 days and observed for the growth of golden colored staphylococcus colonies. Methicillin resistance due to the modified penicillin binding protein is indicated by a precipitation reaction surrounding the staphylococcus colonies.
Routine testing using these plates or comparable methods needs to be performed in children playgrounds, athletic locker and equipment rooms, hotels suites, and certainly in hospitals and healthcare clinics. Volunteers willing to assist in such testing are currently being recruited by the Institute. With the impending likelihood of legal suits, major institutions will need to assure those entering their facilities that they have an MRSA “Infection Prevention Program” that should clearly include repeated testing for MRSA. The Institute is willing to help such institutions by providing details on testing and recommending decontamination methods.
The Staph Identification Plates for MRSA should be given expedited FDA approval to allow personal testing. These will allow for the prompt identification and treatment of active lesions. All healthcare providers, individuals at risk for trauma or with a preexisting skin disease should also know their MRSA carrier status. Until the plates or similar methods are approved for personal diagnostic use, individuals will need to rely on licensed clinical laboratories. The cost of testing should, however, be in the range of $2.00.
Any person colonized or actively infected with an MRSA infection needs to be advised that they are a potential source of infection of others. Newly diagnosed patients should be questioned as to where they may have acquired their infection and the premises checked for MRSA. Until the State Governments designate MRSA infections as a reportable disease, the Institute of Progressive Medicine may be able to assist in the tracking of sources of infection.
Educational programs should be available through the internet and other media. These programs will encourage everyone to follow basic hygiene measures including frequent hand washings; avoidance of sharing personnel items, such as towels and non-sanitized equipment; covering, or at least regular cleansing of all exposed active skin lesions; and other measures being compiled by the Institute. Means of reducing MRSA in healthy carriers and the use of both short and long acting disinfectants along with other procedures for destroying MRSA in the environment are currently under review by the Institute and will be reported separately.
Early signs of a possible or proven active MRSA skin infection need to be immediately addressed by cleansing and application of an antiseptic or broadly acting antibiotic. Pus should not be allowed to accumulate beneath the skin and may need to be drained. Consideration should be given by the FDA to re-allow the use of established products such as mercurochrome, gentian violet and silver dressings. Prescription only products such as “triple dye” used routinely on newborn babies’ umbilical cords should be made available as over-the-counter products.
Some physicians are resorting to non-antibiotic therapies in use prior to the discovery of penicillin. One approach is to systemically stimulate polymorphonuclear cells, a major defense component against staph infections. The Institute is assembling a staph task force that includes both mainstream and less traditional physicians to help evaluate both old and new therapeutic approaches to staph infections. Members of the task force will be available to provide advice to other physicians as requested.
E. coli O157 and toxic MRSA are only two of the many types of infectious illnesses threatening mankind. In addition to conventional infectious agents, compelling data exist for widespread infection by stealth-adapted viruses that are not effectively recognized by the immune system. Although not yet considered a problem by Public Health authorities, these viruses pose a far bigger problem that those of E. coli O157 and toxic MRSA. It is easier to empower the public to test for bacteria than viruses. Mobilizing a national effort to deal with toxic MRSA may, however, greatly facilitate the task of recognizing and dealing with the growing epidemic of complex neurological and neuropsychiatric illnesses caused by stealth-adapted viruses.
For additional information on these topics, including the availability of the Staph Identification Plates for MRSA, please contact the Institute of Progressive Medicine by e-mail to s3support@mail.com
By: W. John Martin, M.D., Ph.D., Institute of Progressive Medicine

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