Dengue Disease: Difference between revisions

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[http://wwwnc.cdc.gov/travel/yellowbook/2010/chapter-5/dengue-fever-dengue-hemorrhagic-fever.aspx] 4. Retrieved 2010-12-23Center for Disease Control and Prevention. "Chapter 5 – Dengue Fever (DF) and Dengue Hemorrhagic Fever (DHF)". 2010 Yellow Book..
[http://wwwnc.cdc.gov/travel/yellowbook/2010/chapter-5/dengue-fever-dengue-hemorrhagic-fever.aspx 4]. Retrieved 2010-12-23Center for Disease Control and Prevention. "Chapter 5 – Dengue Fever (DF) and Dengue Hemorrhagic Fever (DHF)". 2010 Yellow Book..

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University of Oklahoma Study Abroad Microbiology in Arezzo, Italy[1]

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Etiology/Bacteriology

Taxonomy

Group = Group IV positive-sense ssRNA virus | Order = Unassigned | Family = Flaviviridae | Genus = Flavivirus | species = Dengue Virus

NCBI Taxonomy: (DENV-1) (DENV-2) (DENV-3) (DENV-4) Genome: Dengue Virus

Description

Dengue (pronounced DENgee) viruses belong to the family Flaviviridae, genus Flavivirus. There are four serotypes: DENV-1, DENV-2, DENV-3, and DENV-4, which belong to a larger, heterogeneous group of viruses called arboviruses. This is an ecological classification, one which implies that transmission between vertebrate hosts, humans, is dependent on hematophagous arthropod vectors. Dengue fever is transmitted by the bite of an Aedes mosquito infected with a dengue virus. The mosquito becomes infected when it bites a person with dengue virus in their blood. It can’t be spread directly from one person to another person. Dengue fever is a painful, debilitating mosquito-borne disease. This virus is related to the viruses that cause West Nile infection and yellow fever. Each year, an estimated 100 million cases of dengue fever occur worldwide, with most of these cases occurring in tropical areas of the world. [1]

The Dengue Virus is considered an Old Disease, which goes back to the Chin Dynasty (AD 265–420), where it was first recorded. There are reports of epidemics of dengue-like illnesses in the French West Indies in 1635 and in Panama in 1699. By the late 1700s, the disease had a worldwide distribution in the tropics: Indonesia, Egypt, and in 1780 in Philadelphia. From the late 1700s to World War II, repeated epidemics of dengue illness occurred in most tropical and subtropical regions of the world.

Pathogenesis

Transmission

Dengue virus infections come from the bite of an infected Aedes mosquito. These mosquitoes usually live between the latitudes of 35 degrees North and 35 degrees South below an elevation of 1,000 metres (3,300 ft).[6] Mosquitoes become infected when they bite infected humans, and later transmit infection to other people they bite. The two main species of mosquito, Aedes aegypti and Aedes albopictus, have been responsible for 95% of cases of dengue transmitted, however other mosquito species such as A. albopictus, A polynesiensis and several A. scutellaris may also transmit the disease.[6] Humans are the primary host of the virus, but it may also circulate in nonhuman primates.[13] An infection may be acquired via a single bite.[4] After taking a blood meal from an infected person, the virus infects the cells lining the mosquito's gut. About 8–10 days later, the virus spreads to other tissues including the mosquito's salivary glands and is subsequently released into its saliva. The virus has no effect on the mosquito, which remains infected for life. Dengue may also be transmitted via infected blood products and through organ donation.[16][17]

Infectious dose, incubation, and colonization

Epidemiology

Virulence factors

Dengue

Like all Gram negative bacteria, EHEC outer membranes have an outer facing leaflet of lipopolysaccharide (LPS). LPS consists of lipid A, core polysaccharide, and O-Antigen, which consists of 40-80 repeating subunits of 4 sugars that in the case of E. coli O157:H7 is unique to the O157 serogroup, containing N-acetyl-d-perosamine, l-fucose, d-glucose, and N-acetyl-d-galactose. The core polysaccharide essentially is conserved in all E. coli ecotypes. Lipid A is the toxic component of LPS, also known as endotoxin, which is a heat-stable toxin. Lipid A consists of a phosphorylated disaccharide of glucosamine linked by a beta-1,6 linkage and modified by fatty acids, in addition to the first ketodeoxyoctanoate of the core polysaccharide. Endotoxin is released by cell lysis rather than being secreted. Endotoxin is less potent and less specific than exotoxins. Endotoxin can cause fever, hemorrhagic shock, and diarrhea.

Clinical features

Diagnosis

Treatment

Prevention

Host Immune Response

The virus has an incubation period of 4-10 days after the bite from an infected mosquito. Symptoms usually last for 2-7 days post incubation. The next 24-48 hours of the critical stage can be lethal; proper medical care is needed to avoid complications and risk of death. The warning signs to look out for occur 3-7 days after the first symptoms. [2]

References

Created by Brandon Kitchens, students of Tyrrell Conway at the University of Oklahoma.

1 Karriem-Norwood, Varnada, MD. "Dengue Fever: Symptoms, Causes, and Treatments." WebMD. WebMD, 20 Sept. 2012. Web. 24 July 2015

2Martina, B. E. E., Koraka, P., & Osterhaus, A. D. M. E. Dengue virus pathogenesis: An integrated view. Clinical Microbiology Reviews 22, 564–581 (2009). doi:10.1128/CMR.00035-09


4. Retrieved 2010-12-23Center for Disease Control and Prevention. "Chapter 5 – Dengue Fever (DF) and Dengue Hemorrhagic Fever (DHF)". 2010 Yellow Book..