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Antibiotics are medications that are prescribed for people with bacterial infections. Bacteria can cause many diseases including tuberculosis, malaria, ear infection, and gonorrhea and have become resistant to the antibiotics developed to cure them. Antibiotic resistance arises as a result of natural selection. There is variation within any population of individual, including within a population of bacterial cells. Some bacteria, even before exposure to the antibiotic, carry genes that enable them to resist it. You can develop a drug-resistant infection by selecting for the resistant bacteria within your own body or by contracting the resistant bacteria from someone else.
Tetracycline is an antibiotic used to kill bacteria that cause acne. It works to prevent translation, the production of proteins, in prokaryotes. Since the workbenches of translation, the ribosomes, differ structurally in prokaryotes and eukaryotes, this antibiotic - like all effective antibiotics - selectively kills bacterial cells and not eukaryotic host cells. One bacterial cell in a population of millions may have a different DNA sequence in the region of DNA that encodes for a protein involved in translation. If this protein enables the bacterial cell to withstand tetracycline treatment, it will survive and pass on the resistant sequence to its offspring. In this manner, those bacteria that are not killed are selected for, and resistant infections develop.
The problem of resistance in bacteria seems to have originated from medical and agricultural overuse of antibiotics. Some patients ask their doctors to give them antibiotics for a cold, cough, or the flu - all of which are caused by viruses. For example, tetracycline would not be able to kill a viral infection because the virus is using your eukaryotic ribosomes for translation and is thus unaffected by the treatment. Adding to the problem of medical overuse is that people often discontinue their prescribed antibiotics when they feel better. Not finishing all of the prescribed medication allows resistant bacteria to spread and the infection will come back, resistant to that antibiotic, in a few weeks, and another course of medication will be required. Bacteria are particularly efficient at enhancing the effects of resistance, not only because of their ability to multiply very rapidly but also because they can transfer their resistance genes, which are passed on when the bacteria replicate. In the medical setting, such resistant microbes will not be killed by an antimicrobial agent during a standard course of treatÂment. Resistant bacteria can also pass on their resistance genes to other related bacteria through "conjugation", whereby plasmids carrying the genes jump from one organism to anÂother. Resistance to a single drug can thus spread rapidly through a bacterial population. When anti-microbials are used incorrectly - for too short a time, at too low a dose, at inadequate potency; or for the wrong disease - the likelihood that bacteria and other microbes will adapt and replicate rather than be killed is greatly enhanced. Much evidence supports the view that the total consumption of antimicrobials is the critical factor in selecting reÂsistance. Paradoxically, underuse through lack of access, inadequate dosing, poor adherence, and substandard anti-microbials may play as important a role as overuse. For these reasons, improving use is a priority if the emergence and spread of resistance are to be controlled (4).
The use of antibiotic in agriculture is also on the rise. Animals such as cows and chickens are given antibiotic drugs in their feed to prevent them from becoming ill. Animals who are fighting infections do not gain as much weight. Antibiotic treated animals may harbor resistant bacteria, and eating undercooked meat from an animal infected by resistant population of bacteria can give you a drug-resistant infection.
Malaria is infection with any of four species of Plasmodium, such as P. falcifarum, P. vivax, P. ovale, P. malariae. Symptoms are fever, which may be periodic, chills, sweating, hemolytic anemia, and splenomegaly. Diagnosis is by seeing Plasmodium in a peripheral blood smear. Treatment and prophylaxis depend on the species and drug sensitivity and include chloroquine, quinine, atovaquone and proguanil, mefloquine, doxycycline, and artemisin derivatives (1). It is widespread in tropical and subtropical regions, including parts of the Americas (22 countries), Asia, and Africa. Each year, there are approximately 350-500 million cases of malaria,killing between one and three million people, the majority of whom are young children in sub-Saharan Africa. Ninety percent of malaria-related deaths occur in sub-Saharan Africa (5). Malaria is commonly associated with poverty, but is also a cause of poverty and a major hindrance to economic development .
Malaria is naturally transmitted by the bite of a female Anopheles mosquito. When a mosquito bites an infected person, a small amount of blood is taken, which contains malaria parasites. These develop within the mosquito, and about one week later, when the mosquito takes its next blood meal, the parasites are injected with the mosquito's saliva into the person being bitten. After a period of between two weeks and several months (occasionally years) spent in the liver, the malaria parasites start to multiply within red blood cells, causing symptoms that include fever and headache. In severe cases, the disease worsens, leading to coma and death.
A wide variety of antimalarial drugs are available to treat malaria. In the last 5 years, treatment of P. falciparum infections in endemic countries has been transformed by the use of combinations of drugs containing an artemisinin derivative. "Severe malaria is treated with intravenous or intramuscular quinine or, increasingly, the artemisinin derivative artesunate"(3). Several drugs are also available to prevent malaria in travellers to malaria-endemic countries. Resistance has developed to several antimalarial drugs, most notably chloroquine.
Discovery of chloroquine revolutionalised the treatment of malaria, pushing quinine to the sidelines. Resistance began from 2 epicentres - Columbia (South America) and Thailand (South East Asia) in early part of 1960s. Since then, resistance has been spreading world wide and reached the Indian state of Assam in 1973. (6) 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. Most of the studies have focused on P. falcifarum infection with virtually no comparative efficacy data addressing the management of chloroquine resistant P.vivax infection. Comparing the safety and efficacy of dihydroartemisinin- piperaquine (DHP) with amodiaquine (AAQ) for the treatment of patient with malaria we can see that "DHP was more efficacious and better tolerated than AAQ for the treatment of multidrug-resistant P. falcifarum and P. vivax infection in Papua Indonesia" (4).
Three hundred and thirty-four cases of confirmed malaria seen in the Asir Central Hospital in southwestern Saudi Arabia were studied retrospectively. "Two hundred and eighty-two of these (84.4%) were Saudis and the majority (72.2%) were living in the lowlands of Tihama. Transmission was found to occur throughout the year, with peaks following the rainy season and in the summer. In Saudis, falciparum malaria is more common than vivax (97.2% vs. 2.8%), while vivax malaria is more commonly seen in expatriates(46.4% vs. 23%) The possibility of the emergence of choloquine- resistant malaria in the southwestern region of Saudi Arabia was discussed.
All malaria cases seen in hospital of Saudi Arabia for the period of 5 years were studied. 84.4% were Saudis and the remaining 15.6% were people of different nationalities. They comprised 231 males and 103 females and children. The average age was 15.9_+ 17.2 years, with a range of two month to 80 years. Children and males were affected more than females. The majority of patients were living in the lowlands of Tihama. Three hundred and two (90.4%) had falciparum malaria and the remaining 32 (9.6%) had vivax malaria" (5). Although malaria has been largely controlled in the eastern part of Saudi Arabia, transmission still occurs in the north, western and especially the southwestern region, where it is considered to be hyperendemic. (3).
This study has emphasized that malaria is still the health problem in the Asir region. However, the peaks of transmission related to rainy and hot weather, it is also connected with the geographical position of Tihama. In the lowland of Tihama the anopheline mosquito is abundant.
Secondly, disease is more common in children who are non immune and whose immunity increases as they grow up due to repeated exposure.
The study has shown that in 77% of Saudi patients falciparum malaria responded to chloroquine alone, in comparison to only 53.6 % of expatriates, most of whom were from areas known as endemic with chloroquine resistant malaria. Falsifarum malaria in Saudi Arabia has been widely considered to be chloroquine sensitive.
This retrospective study strengthens our suspicion, since it has been found that in 23% ot the patients with falciparum malaria, another drug was needed to cure malaria on clinical grounds. Chloroquine is still considered the first line treatment of uncomplicated falciparum malaria in the region. However, doctors should be alerted to the possible emergence of chloroquine resistance, and be ready to use another second drugs in cases that do not respond to chloroquine.
In conclusion we may say that chloroquine resistance to Plasmodium falciparum occurred in the areas where parasite species is endemic. Spread of resistance is determined by eco-epidemiological factors among which migration and vectorial parameters play a major role.