Drug Resistance in Yemen [Archives:1997/45/Health]

The world over, many people are faced with a relatively recent happening; bacterial strains which were once curable have become resistant to pharmaceuticals. There are threats of new disease outbreaks if the drug resistant strain is not beaten. People who are uninformed about alternative medicines to take or who only consult a pharmacist and not a specialist could soon find himself buying ineffective drugs. This might generate a good turnover for the pharmacist but the patient is largely unsatisfied and takes the blame out on the lack of medical assistance. Having recently come over from Italy and working in collaboration with microbiological centres in Italy and Canada, I am not surprised to see the same problem surface in Yemen. Certain brand named drugs have been on the market for years and the bacteria they are supposed to fight are no longer affected by it. This is because the continued use of the same drug allows the bacteria to develop a means which makes it possible to grow even in the drug’s presence. On many occasions drugs might even be prescribed for the common flu which should be allowed to follow its own course unless there are bacterial complications. Cases in Yemen have developed where people have been prescribed ampicillin for example to fight the virus only to find that the same flu symptoms linger on in spite of the drug use because the person has not followed a full course treatment with the drug. If a full course treatment isn’t followed there is a good chance that the harmful bacteria would have a chance to become resistant to any drug. To get by, scientists add substituent chemical groups or side chains to the drug so that it maintains its overall capacity to fight illnesses; since the drug molecule is no longer the same the bacteria does not recognize it and has had no chance of developing a resistance to it. The drugs referred to are antibiotics and in many places the selling of these across the counter without proper prescriptions only aggravates an already existing problem. The patient may have had a simple bacterial infection which could have been overcome by a steady dose of a specific drug, but if he buys a brand which has been out on the market for many years that bacterial strain may have had the chance to become unaffected by the drug. The patient may be partially blamed. He may be unaware of recent drug synthesis developments or be advised wrongly on the part of a physician advising him to treat the infection where there is no clear proof of the exact bacteria causing the ailment. The pharmacist should encourage the patient to visit a laboratory and get a bacterial smear before he continues with any further unspecific treatment. The patient should also visit a specialist, one who is more keen on finding the specific symptoms behind a particular infection and who knows a proper cure. But often enough its all to easy for the individual to say that he had been advised on using a particular drug without having had the causing agent identified. Worse still are faulty diagnoses by clinicians who prescribe a drug for an infection that the drug has minimal if not any effect. Such might be the case for patients with urinary infections who are prescribed drugs aimed for the upper respiratory tract. E. Coli bacterial resistant strains to tetracycline are a common nuisance now whereas years ago anybody suffering from a mild attack of “car sickness” years ago could have taken a healthy dose of a tetracycline and the bug would disappear. Strep throats are another common nuisance where the streptococcus bacteria have had many years to develop resistance. Now and then cases of diseases such as tuberculosis which was thought to have been dominated by antibiotics have reappeared because the old remedy prescribed in the 50s is no longer as effective. Malarial resistant strains to recent drugs have occurred making it more difficult to wipe it out completely. To understand resistance the layman has to understand the antibiotics main means of action until now which has largely been to inhibit the cell wall synthesis in the bacteria. Muraminic acid, a chemical component of the bacterial cell wall would have been inhibited and the bacteria cell wouldn’t be able to go very far before its daughter cells would not be viable. This is because the bacteria without a cell wall cannot contain its inner fluid or cytoplasm and so does not survive. Bacteria divide by fission. Today microbiologists have had to become more defensive because so-called “smart bacteria” are able to block that inhibitor making that drug action useless. So the advent of using friendly plasmids came about, small DNA rings which could be incorporated into the bacterial genome or onto the the genetic material of the bacteria. The plasmid would contain information which would block the cellular activity of the bacteria producing a specific enzyme such as a ligase. Bacteria produce enzymes like ligase which are emitted into the blood circulation causing damage to the host organ by digesting the connective tissue that makes it up. As a result, the new bacteria with the transplanted plasmid would reproduce and produce new cells that would no longer produce the harmful enzyme. but the problem does not end here because a permanent solution to a particular bacterial infection has yet to be found. Scientists have combined antiobiotics drugs to increase or potentiate their effect. Such is the case for the sulfomethoxy drugs which block or inhibit the folic acid synthesis in bacteria. That acid is primarily important for the bacterial metabolism. Malaria is particularly difficult because of an intermediate parassite host, the Anopheles mosquito, which will always transport the malarial protozoan, until it is completely wiped out. This would be an unlikely event and even if the host were wiped out there’s nothing to prevent another blood-sucking insect from taking its place eventually. So science has to keep on searching for an always more efficient means of preventing diseases or infections caused by micro-organisms.
By: Martin Dansky, B.Sc.

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