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Lassa Fever: An Old World ArenaVirusA brief summary of lassa fever, its history, pathology and effects on the indigenous populations. Also, lassa fever in the context of newly emerging diseases. LASSA FEVEROn January 12, 1969, a missionary nun, working in the small town of Lassa, Nigeria, began complaining of a backache. Thinking she had merely pulled a muscle, she ignored the pain and went on about her business. After a week, however, the nurse had a throat so sore and so filled with ulcers, she couldn’t swallow. Thinking she was suffering from one of the many bacterial diseases endemic to the area, her sisters administered every antibiotic they had on store in the town’s Church of the Brethren Mission Hospital. But, the antibiotics did nothing. Her fever escalated, she was severely dehydrated and blotches, hemorrhages, were appearing on her skin. She began to swell and became delirious, so they shipped her to a larger hospital, where one day later she went into convulsions and died. After a nurse who was tending to the sister came down with the same symptoms and died, the doctors in the hospital began to suspect it was a disease heretofore unseen by any of them. Autopsy on the nurse showed significant damage to every organ in the body, the heart was stopped up, with loads of blood cells and platelets piled well into the arteries and veins. Fluids and blood filled the lungs. Dead cells and lipids clogged the liver and spleen. The kidneys were so congested with dead cells and free proteins they had ceased to function. Dissecting the lymph nodes, they discovered that they were completely empty; every white blood cell had been utilized in a futile attempt to stave off the unknown microbe. A few days later, a prominent western viral researcher contracted the unknown disease and the hunt for the microbe that caused lassa fever, began in earnest.(Garrett, 1994)Lassa fever is a virus belonging to the family Arenaviridae. Genus Arenavirus, although being around for about 60 years in the form of lymphocytic choriomeningitis, has recently been brought to the public’s attention because of the large number of species known as “emerging viruses” in the genera. The genera consists mostly of new world viruses, among them the Junin, Machupo and Guanarito viruses, which cause, respectively, Argentine, Bolivian and Venezuelan hemorrhagic fevers along with a few other non – pathogenic viruses. These viruses, long hidden in the deepest recesses of rain forests, are making their presence felt as much of the rain forest and other isolated areas become more and more accessible. Lassa fever is mostly on the rise as its main vector, the rodent Mastomys natalensis, is increasing in numbers due (indirectly) to an increase in poverty and scarcity of food.(Garrett, 1994) To be specific, when the endemic region has a scarcity of food, the villagers kill and eat the larger rat, Rattus rattus, which is a main competitor of the Mastomys natalensis, thereby allowing the smaller Mastomys to flourish. The disease mainly effects the areas of western Africa, from Senegal to, of course, Zaire, although it has been exported to the United States (about 115 cases). (Southern, 1996)Lassa fever consists of two single strands of RNA enclosed within a spherical protein coat. The RNA exists as two strands designated L (for long) and S (for short). The S segment is the more abundant of the two as it codes for the major structural components such as the internal proteins and the glycoproteins, while the L segment codes for RNA polymerase and perhaps a few structural proteins. The protein coat has a number of T-shaped glycoproteins protruding from it, composed of GP (glycoprotein)2 which is the base and GP1 which is the T-bar. (Southern, 1996) This structure is what inserts itself into the receptors on the host cell. When the virus first gains entry into the cell, it quickly takes over the mechanisms of the cell to its own purpose. First it creates clones of its RNA strands, then directs the cell to make the glycoproteins on the host cell membrane. The virions bud from the cell membrane, leaving the cell intact until, finally, the production of virions exceeds the cells capabilities and the cell lyses.

Infection with Lassa virus leads, after a 10 day incubation period, to a gradual onset of fever, then full blown Lassa fever begins. First, the throat gets exceedingly sore, even to point of severe ulceration and inability to swallow or drink. In the first week anorexia, vomiting and chest pains are also common. The second week is worse. The chest pains move to the abdominal region and intractable vomiting begins followed by severe edema of the throat and neck, tinnitus (ringing in ears), bleeding from the gums and mouth, huge rashes, coughing and dizziness. During this acute phase extremely low blood pressures of To date there has been no intensive mapping of the extent of virulent Lassa distribution in Africa and there is no surveillance for spread or contraction of the established highly endemic zones.(Southern, 1996) It took a number of sick westerners to grab the attention of the developed nations before they began to investigate this illness. Now that we have discovered it and are convinced it is not an immediate danger, we have retreated to our own nations, without so much as a single rodent eradication program. As a result the disease has spread to a much larger endemic area. The feeling is that it could be controlled by proper hygienic and educational measures, but the developed world chooses to leave the dying and forgotten continent, Africa, to suffer yet another vicious and deadly disease. LITERATURE CITEDGarrett, Laurie, 1994, “Into the Woods”, The Coming Plague; Newly Emerging Diseases in a World out of Balance, 71 -99. Southern, Peter, 1996, “Arenaviridae: The Viruses and Their Replication”, Fields Virology, 1505 -1520. Sanford, Jay, “Lassa Fever”, The Merck Manual, 218 -219.


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