Dengue Fever: Symptoms, Treatment and Prevention

dandy febricityishness Fever Symptoms, Treatment and Prevention dengue fever fever pyrexiaDengue feverishness is a disease that is triggered by a computer computer computer virus (DENV) and there are different serotypes related viruses (DENV-1, DENV-2, DENV-3, DENV-4) (Byron et al., 2009 Whitehorn et al., 2011). However they have 60-80% homology The virus belongs to the flaviviridae family genus and the flavivirus which is an aborvirus that is arthropod borne (Roach, 2002 Byron et al., 2009). Severity of dengue fever basin progress to Dengue hemorrhagic Fever (DHF) or Dengue Shock Syndrome (DSS) (Byron et al., 2009). It is an icosahedral virus that has an enveloped case-by-case stranded, positive sense genome (Byron et al., 2009 Whitethorn et al., 2011). Figure 1. Dengue virus evoluntary shoetree (Hesse, 2007) transmission arrangement of Dengue virusThe virus is transmitted through a biological vector to serviceman bloodstream from mosquito bites. The arthropod vector i s genus Aedes mosquito chiefly Aedes aegypti that is common in tropic or subtropics regions (Byron et al., 2009).Aedes albopictu is another mosquito vector. The mosquito that has acquired the virus can transmit it to un septic human for the reliever of its life (). Human being are the reservoir for the virus, mosquito bite an infected human to obtain the virus which it go forth transmit to another human being who will now become a carrier () other reservoir is monkey in the DENV virus sylvatic cycle. The virus is found in the mosquitoes salivary gland and can alike be transmitted from grown mosquito to its egg making it preserving the virus from season to season (Rolland, 1995)Figure 1. Transmission cycles of dengue virus (Byron et al., 2009)Symptoms and Clinical features of dengue feverInfection by DENV maybe asymptomatic or show a wide tend of clinical symptoms (Byron et al., 2009). Symptom are more(prenominal) punishing in children under 15 years than in adults (Byron e t al., 2009 Carlos et al., 2005). Dengue fever initiate with a senior utmost school fever whereby the body temperature increases up to (104-105) Fahrenheit within 4-5 twenty- quadruplet hours from transmittance (Guzman et al., 2002). After 2-5 days of fever a red snowstorm might appear fol pitiableed by a second severe anthesis again that looks like measles accompany by increase sputter sensitivity and discomfort (Harris et al., 2000). Other symptoms are fatigue, muscle ache, joint ache, vomiting, Nausea, swollen-headed lymph nodes, headache especi eithery on the area behind the eyes, nasal stiffness, delirious throat, coughing, retro-orbital pain, arthralgia, myalgia and gastrointestinal pain ( Byron et al., 2009 Guilarde et al., 2008). Leukopenia is common while thrombocytopenia is occasional, apt(predicate) in patients with haemorrhagic signs like petechiae, gingival bleeding and epistaxis (Guilarde et al., 2008 Kittigul et al., 2008)Pathogenesis of the Dengue virus (DE NV)Lack of animal models results to lack of knowledge of the actual pathogenesis of the virus but it anticipated it is multifactorial (Bryon, 2009).Dengue fever virus have four serotypes (homology of surface antigen) which make it hard for the tolerant system to combat and this is the tail of it virulence(Ross, 2010 Limon et al., 2005). Host genetics and background, viral genetics and host immune attitude go throughs the pathogenesis and how the immune system reacts (Sierra et al., 2007 Quinlivan, 2007 Tanaka and Mizokami, 2007 Byron et al., 2009). Once the virus access the body system through the skin epidermis Langerhans and keratinocytes cells are initially infected. However the immune system responds by producing antibodies that stick structural protein while inactivating the virus and keep macrophage infection by the virus. At this point primary infection occurs which is the dengue fever. However antibody adherence does not inactivate the virus, viral replication occurs by attaching to the cell surface entry inside the cell cytoplasm and explanation of viral proteins (Rothman, 2010 Byron et al., 2009). Subsequently the virus enters the blood stream and results ( primary viremia) where it will attach various tissue macrophages in various organs belike macrophages within the spleen (Bracken, 2005 Byron et al., 2009). As the virus replication expands to macrophages, monocytes, acknowledger cells, lift marrow, the viral load of DENV increases (Chang et al., 2002 Burke and Kliks, 2006). Viral replication efficiency determines the viral load which can be measure in blood to determine the severity of the infection (Hesse, 2000 Halstead, 2003 Green and Rothman, 2006 Byron, 2009). Infected cells die through programmed cell death and to some extend by necrosis (Byron et al., 2009 Chakravarti et al., 2006). Necrosis causes release of toxins which triggers clotting and fibrinolytic systems. Based on bone marrow stromal severity of infection, IL-6, IL-8, IL- 10, and IL-18 levels hemopiosis is inhibited reduce blood thrombogenicity (Byron et al., 2009 Chao et al., 2009). Viral load and viral tropism will increase resulting to severe thrombocytopenia and platelet dysfunction which cause capillary fragility, easy bruise and also gastrointestinal mucosal bleeding which are features of DHF while the infection triggers development of specific antibody and cellular immune response against DENV (Nachman, 2008 Chang et al., 2002). Ig antibodies adjudge to the virus during secondary infection thereby eliciting the infection by increase the viral load (Nachman, 2008 Byron et al., 2009) If another different serotype invades the body, the immune system combats it the alike way as it did previously due to minor difference bounty within various serotypes (Bryon, 2009 Huerre et al., 2001). Moreso, the dengue viruses have M proteins that assist in apoptosis of their target cell. Furthermore upon macrophage invasion, DENV, it triggers the pro-inflamm atory cytokines release as well(p) as other mediators by antigen presenting cells, cross reactive T-cells of low and high avidity, HLA and endothelial cells of the immune system which compromise abnormal homeostasis and tissue permeability (Byron et al., 2009 Carlos et al., 2005). This slows down virus elimination and can cause a more severe secondary infection, such(prenominal) as DHF or DSS (Byron et al., 2009).Figure 2 Proposed pathogenicity of dengue virus (Byron et al., 2009).Diagnosis of dengue feverDengue fever is diagnosed based on the clinical symptoms. Test and examination to recognize the DENV can be done through antibody titre of the DENV (Jesse et al., 2004 Hesse, 2007). Another method is by doing a white blood cell count which is very low in infected patient (Jesse et al., 2004 Hesse, 2007 Ross 2010).Blood test to detect DENV via serology and ELISA to identify IGM antibodies (Hesse, 2007 Byron et al., 2009 Whitehorn et al., 2011). Carrying out a liver function test ( ALT and AST) which is raise in infected individuals (Byron et al., 2009).Further laboratory tests like polymerase chain chemical reaction can be done for the virus types, specifically RT-PCR which identify viral ribonucleic acid in patient samples (blood,liver,CFS) and can be modified to three-figure RT-PRC or using a Taqman probe when dealing with small quantities Of RNA (Hesse, 2007 Ross, 2010). Immunohistochemistry using antidengue monoclonal antibodies to identify viral RNA (Jesse et al., 2004)Prevention fag be done by shielding away from the Aedes mosquitoe and also reducing the mosquito population by covering the body through raiment to reduce chances of mosquito bites. Mosquitoe nets can be utilize (Argawal et al., 1998 Byron et al., 2009). Moreso travelling in times or to areas where mosquitoes are absent (An et al., 2004).Usage of mosquitoe repellents is also essential. In high jeopardy areas, hose opening should be closed (windows, doors etc.) (Byron et al., 2004). E liminating water stagnant by covering them as well as putting insecticides can butcher the mosquitoe (Argawal et al., 1998 Byron et al., 2009). Moreso still water collecting containers like drums, flowerpots buckets should be eliminated (Byron et al., 2009) furthermore the beingness wellness Organisation have made efforts to enforce correct disposal of these items via chemical methods and environmental management ( military personnel Health Organisation Media Centre, 2002 Argawal et al., 1998 Byron et al., 2009). Improving company dengue virus vector control programs and moreso monitoring and surveillance should be done in grade to determine the control measures effectiveness (World Health Organisation Media Centre, 2002)Currently there is no vaccine against the dengue fever virus but there is ongoing research to develop vaccine against the virus (Byron et al., 2009). One promising vaccine been worked on is a live attenuated virus vaccine named West Nile virus, which is measles based virus to eradicate dengue (World Health Organisation Media Centre, 2002). This vaccine have been used in Thailand although there is no evidence that it can combat all four serotypes of dengue in order to avoid complications of dengue fever (DHF and DSS) (Argawal et al., 1998 Byron et al., 2009 World Health Organisation Media Centre, 2002).TreatmentTreatment for dengue virus is not specific, to care for symptoms like dehydration, the patient must rest and bury copious amount of fluids, intravenous electrolytes is given to compensate the dehydration (Jesse et al., 2004 Hesse, 2007). For high fever, joint pain and headache antipyretic drugs like Acetaminophen (Tylenol) and codeine should be administered (Jesse et al., 2004 Hesse, 2007 Byron et al., 2009). Moreso drugs such as corticosteroids or carbazochrome sodium sulfonate are administered in order to inhibit the increase capillary permeability as well as stopping plasma leakage (Byron et al., 2009). Asprin and non-steroidal should be administered under doctor inadvertence for anti- inflammatory purposes (Byron et al., 2009). Treatment can reduce the deathrate rate from 20% to 1% (Jesse et al., 2004 Hesse, 2007 Byron et al., 2009).EpidemiologyDengue fever has re-emerged since 20 years ago accompanied by an expansion in geographic distribution thereby change magnitude the epidemic, moreso with the upcome of hyperendemicity (Debarati and Schimmer, 2005). An estimation by the World Health Organisation of about 2.5 gazillion people are affected by the dengue virus each year. World Health Organisation estimated, that yearly there are 50-100 meg cases per year with more than 500 000 cases of hospital admission with 15,00 deaths (World Health Organisation, 2002 Debarati and Schimmer, 2005 ). Dengue fever endemic has increase from 9 countries in 1970 to 100 countries currently (Debarati and Schimmer, 2005 World Health Organisation, 2002 ). The first dengue fever epidemics occurred in 1779-1780 in continent s like Africa, Asia and South America (). Recently in 1998, there was a pandemic in United States resulting to less than 1% fatality rate. The mortality rate ranges from 1-10 % (Debarati and Schimmer, 2005 Byron et al., 2009). Increasing expansion of the disease all over the manhood is due to increase in population as well as lack of vector control programs (Gubler et al., 2004 Hesse, 2000). However due to control and safety measures the number of cases is increasing from travellers who are carrying the virus from high risk areas such as sub-tropical and tropical region (Byron et al., 2009).Figure 3. Global epidemiology of Dengue virus (LaRive, 2008).Global cases and outbreaks of dengue feverIn Venezuela, 2007 there was an outbreak of 80,000 dengue fever cases in which 6,000 persisted to DHF. In the same year above 890,000 cases were report in America of which 26,000 persisted to DHF the route of transmission being endemic and from travellers ( Byron et al., 2009 World Health Orga nisation Media Centre, 2002). Most recent outbreak occurred in 2005 in Brownsville Texas with 25 reported cases and 16 DHF (Whitethorn et al., 2011) The virus was also transmitted to neighbouring read Tamaulipas where there was 1251 case reported in which 223 had DHF (Bebarati and Schimmer, 2005 Whitehorn et al., 2011).