Grossmont Microbiology Microbe Mini-talk Paper Professor H.

Valtierra

Dengue Fever Dengue fever, also known as break-bone fever due to the immense pain associated with sore muscles and tendons, is a serious viral disease caused by one of the four viral strains of Flaviviridae: Flavivirus dengue virus. The four strains (also referred to as serotypes) are commonly abbreviated as DENV -1, -2, -3 or 4. The virus threatens more than fifty million people per year with a one in one thousand rate of mortality. With dramatic growth of incidence in the past decades and cause of fifty thousand deaths per year and two million five hundred thousand at risk, dengue fever has become a major public health concern (WHO, 2009). Dengue fever comes from the family Flaviviridae and genus Flavirus. The species of the dengue virus has four strains (DENV -1, -2, -3 and 4), which are found to cause the disease (CDC, March 25, 2011). Each individual unit, or virion, of dengue virus has a core of RNA as its nucleic acid. Surrounding the genetic material is a protein coat called a capsid and superior to the capsid is an envelope of glycoprotein. Dengue virus is known for its unusually smooth envelope that gives it a golf ball type appearance (PURDUE UNIVERSITY, 2003). When the virus enters to host it has been found to inhabit hepatocytes of the liver, alveolar macrophages, and perivascular cells in the brain. Dengue fever is generally asymptomatic with the possibility of a mild fever, though some individuals, mostly children, are susceptible to a much more severe form of the virus. Dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS) are the more severe and life-threatening forms of the disease (WHO, March 25 2011). DHF and DSS cause uncontrolled internal bleeding, hepatomegaly (liver enlargement) and shock. The symptoms of the disease are defined in three stages: febrile, critical, and recovery (WHO, March 25 2011). If symptoms progress beyond a mild fever, we advance to the febrile phase of which involves a high fever (over forty celcius), retro orbital and joint pain and petechiae (red spots from broken capillaries). The febrile phase can last 2-7 days, which

proceeds to develop into the critical phase. If the critical phase occurs then the fever will break rapidly and varying circulatory problems will occur. This is due to the blood vessels becoming especially leaky causing a loss of fluid that can inhibit necessary circulatory demands and cause gastrointestinal bleeding (WHO, March 25 2011). Many patients recover either spontaneously or with the help of electrolyte therapy. Those with extreme plasma loss will not recover as easily as dengue shock syndrome ensues and can progress rapidly to profound shock and death. If the infected does not die from shock, their condition will deteriorate after a fever of two to seven days duration. Circulatory failure and death can result from the deteriorating condition. The final phase, recovery, occurs next by reabsorbing the leaked fluid back into the blood stream usually taking two to three days to achieve full absorption. If absorption occurs too fast, seizures can ensue. Recovery at this point is often times remarkable. The dengue virus is considered an arbovirus meaning that it needs and arthropod vector. The virus adapted from animals and does not need an animal reservoir. An arthropod vector of the disease, most commonly the Aedes aegypti mosquito, transmits the dengue fever (CDC, 2010). Though the Aedes aegypti mosquito is the primary vector, other species of the Aedes genus can also transmit the virus. The mosquito will bite an infected host and the virus will infect the gut of the mosquito. The virus then spreads to other organs of the body including the salivary glands (take around eight days). When the infected mosquito bites a specific host, the virus transfers from the saliva of the mosquito to the reservoir. Humans are the only reservoir of the disease, though certain primates in Africa and Asia can also act as host, but will not develop dengue hemorrhagic fever (WHO, March 25 2011). The pathogens life cycle starts out as a virion (individual viral unit). The virions glycoprotein envelope attaches to the host cells receptor and the virus and cell fuse together. Once the virus attaches to the wall and penetrates it is encapsulated by an endsome. Protons are then pumped into the endsome, changing the pH. The change in pH causes the viral proteins to change arrangement and expose the viral membrane. The proteins then shift their shape to form trimers. The trimers function is to fuse the viral membrane and endosomal membrane together, which creates a fusion pore (an opening to the inside of the cell, from inside the viral membrane). The RNA is forced out through the

fusion pore into the cytoplasm. The viruss RNA takes control of the cells viral genes and synthesizes the components of new viruses. The components are then assembled and inserted into the cell wall membrane, which it will utilize a portion as its glycoprotein envelope. The newly made virions then released and are circulated freely in the blood (Microbiology: A Systems Approach. Second Edition 2008). Over two billion people in over one hundred countries are at risk of the dengue fever (WHO, March 25 2011). It is most prominent in tropical and subtropical climates where the Aedes aegypti mosquito lives (equator belt) and has become one of the most important emerging disease problems among international travelers (WHO, March 25 2011). Dengue fever is only second to malaria for hospitalization among travelers returning from the tropics (WHO, March 25 2011). The disease is most common in infants and children, and more common among women than men. The dengue virus can be confirmed by the isolation of the virus from blood, tissue or cerebrospinal fluid or other fluids or on the basis of symptoms and examination. If the virus is greater than 5 days infected an IgM antibody test can be administered. IgM are the antibodies made by the immune system and become elevated during infection. At early infection the virus can be detected by a low white blood cell count and a positive tourniquet test (determining if the capillaries are weak). It has proven to be very difficult for to early diagnose dengue fever, often times other diseases must be eliminated as possibilities. Currently there is no vaccine or treatment available for the dengue virus. Once a person becomes infected with one serotype of the virus they develop immunity for that specific type, unfortunately they become more at risk for developing DHF and DSS in future infections of the remaining three strains. If the infected become overly dehydrated, an IV can be used to administer electrolyte therapy. Also recommended is plenty of rest and bedside care. Prevention is one of the only known was of dealing with dengue fever. When outside wear long clothing, use insect repellant, sleep under a mosquito net, remove tepid pooling water and respect the day biters.

Bibliography Cowan, Marjorie Kelly, and Kathleen Park Talara. Microbiology: A Systems Approach. McGraw-Hill Science/Engineering/Math: 2nd ed. 2008. United Nations. World Health Organization. Dengue: Guidelines for Diagnosis, Treatment, Prevention and Protocol Tropical Disease Training 2009, March 25, 2011 < http://whqlibdoc.who.int/publications/2009/9789241547871_eng.pdf> United Nations. World Health Organization. 2011. March 25, 2011 < http://www.who.int/topics/dengue/en/> CDC Centers for Disease and Prevention. September 1, 2010. March 28, 2011 < http://www.cdc.gov/dengue/clinicalLab/clinical.html> Gaidos, Susan, Richard J. Kuhn, and Michael G. Rossmann Purdue News. Scientist Solve Structure of Dengue Virus March 7, 2002: 1 par. March 28, 2011 < http://news.uns.purdue.edu/html4ever/020307.Kuhn.dengue.html>