But you do recall, don't you, that during that epidemic most of the
infected were immigrants from Australia and New Zealand. Where health
care was and to a large degree is today something not affordable by
any but the very rich.?

Of course it was then. as I pointed out, as it is now a minority based
problem. And today, when you throw in the down low homosexuals, you
got trouble in River City.

Good one Martin........lol

Daily Trust (Abuja)

16 March 2008
Posted to the web 17 March 2008
Musa Simon Reef

Resistance to anti- malarial drugs in patients is becoming a worrisome
phenomenon in Nigeria. It has posed serious challenge of combating malaria
in most parts of the world.

Since the early 60's there has been marked resistance by malaria parasites
to chloroquine, the best and most widely used drug for treating malaria,
has been less efficacious. Newer anti-malarial drugs were discovered later,
but all these drugs are either expensive or have undesirable side effects.
Moreover after a variable length of time, the parasites, especially the
falciparum species, have started showing resistance to these drugs also.
Drug resistance, by definition, is the ability of the parasite species to
survive and/or multiply despite the administration and absorption of a drug
given in doses equal to or higher than those usually recommended but within
the limit of tolerance.

Resistance to chloroquine: Discovery of chloroquine revolutionalised the
treatment of malaria, pushing quinine to the sidelines. Resistance began
from two epicentres - Columbia (South America) and Thailand (South East
Asia) in early 1960s. Since then, resistance has been spreading world wide
and reached the Indian state of Assam in 1973. Resistance is conferred by a
stable mutation which is transferred to the progeny. It involves multiple
mutations which means that resistance need not be complete - it may be
partial also.

Resistance to quinine: Chloroquine resistance has brought this drug back to
the limelight. Quinine remains quite effective even after extensive use.
Reports of resistance to quinine are rare, but cases have been reported
from Thailand and East Africa. High degree of resistance to quinine is not
common. For reasons not known clearly, it has been difficult to induce
quinine resistance in experimental conditions. Efficacy of quinine can be
increased by adding tetracycline group of drugs. Poor compliance is a major
drawback of this drug.

Resistance to mefloquine: Sporadic cases of mefloquine resistance have been
reported from Thailand and Kenya. Structurally it is close to quinine and
hence cross resistance with quinine is common. Resistance develops when the
parasite is able to efflux the drug. Initially it was given at dose of
15mg/kg and was combined with sulfadoxine/pyrimethamine to reduce emergence
of resistance. This approach did not succeed in Thailand probably due to
the already existing high grade resistance to sulfa/pyrimethamine. Later
the dose was increased to 25 mg/kg. Even at this dose efficacy of
mefloquine is only 50 per cent in Thailand. Since it is easy to induce
resistance for mefloquine due to its prolonged half life, its use should be
limited, especially since it has cross resistance to quinine. To prevent
development of resistance to this valuable drug, it has been suggested that
mefloquine should always be used in combination with another antimalarial,
like pyrimethamine/ sulphadoxine.

Resistantace test: Four basic methods are involved in testing malaria for
drug resistance: in vivo tests, in vitro tests, molecular characterization,
and animal models. Of these, only the first three are routinely done.

In vivo tests, patients with clinical malaria are administered a dose of an
anti-malarial drug under observation and monitored over time for either
failure to clear parasites or for reappearance of parasites. In vitro
tests, blood samples from malaria patients are obtained and malaria
parasites are exposed to different concentrations of anti-malarial drugs in
the laboratory. Some methods call for adaptation of parasites to culture
first, while others put blood directly from patients into the test system.
Molecular characterization: For some drugs (chloroquine, SP and similar
drugs, atovaquone), molecular markers have been identified that confer
resistance. Molecular techniques, such as polymerase chain reaction (PCR)
or gene sequencing can identify these markers in blood taken from
malaria-infected patients.

Dr. Lawal Abdulrahman, who works in private hospital in Abuja, explained
that several factors are responsible for the increased resistance of
malaria to drugs. One factor he identified is the presence of fake drugs in
the country. He noted that despite the aggressive campaign against fake
drugs, several drugs, especially malaria drugs still find their ways into
the markets. Abdulrahman advocates strict adherence to the genuine drugs to
avoid patients being administered with fake drugs.

Another medical practitioner, Solomon Agbese, said the prevalence of
resistance of malaria to certain drugs may be attributed to the abuse of
drugs by patients. It is based on this abuse of the malaria drugs on the
part of patients, that hospitals have adopted the task of ensuring that
patients suffering from malaria are adequately treated.

According to the PLoS Medicine study, "most of the fakes examined as part
of Operation Jupiter contained no artesunate, and some contained a wide
range of potentially toxic active ingredients. Also of grave concern was
the fact that counterfeiters sometimes included dangerously small amounts
of artesunate in the tablets. This may be done to foil screening tests of
drug quality, but these doses are too low to be efficacious, yet high
enough to contribute to malaria parasites becoming resistant to this class
of drugs."

It is this small amount of artesunate found in fake drugs, according to Dr.
Paul Newton of the University of New York, that has led to increased
resistant of the disease to the malaria parasite

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