Hantavirus diseases, dengue and yellow fever are described separately. Cause Viruses belonging to several families. For Ebola and Marburg viruses, humans have been infected from contact with tissues of diseased non-human primates monkeys and apes and other mammals, but most human infections have resulted from direct contact with the body fluids or secretions of infected patients.
The family Flaviviridae include dengueyellow feverand two viruses in the tick-borne encephalitis group that cause VHF: Omsk hemorrhagic fever virus and Kyasanur Forest disease virus. In September scientists writing in the journal PLOS Pathogens reported the isolation of a member of the Rhabdoviridae responsible for 2 fatal and 2 non-fatal cases of hemorrhagic fever in the Bas-Congo district of the Democratic Republic of Congo.
The non-fatal cases occurred in healthcare workers involved in the treatment of the other two, suggesting the possibility of person-to-person transmission. The pathogen that caused the cocoliztli epidemics in Mexico of and is still unknown, and the epidemic may have been bacterial rather than viral.
In most VHFs, it is likely that several mechanisms contribute to symptoms, including liver damage, disseminated intravascular coagulation DICand bone marrow dysfunction.
In DIC, small blood clots form in blood vessels throughout the body, removing platelets necessary for clotting from the bloodstream and reducing clotting ability. For filoviral hemorrhagic fevers, there are four general mechanisms for pathogensis.
The first mechanism is dissemination of virus due to suppressed responses by macrophages and dendritic cell antigen presenting cells.
The second mechanism is prevention of antigen specific immune response. The third mechanism is apoptosis of lymphocytes. The fourth mechanism is when infected macrophages interact with toxic cytokinesleading to diapedesis and coagulation deficiency.
From the vascular perspective, the virus will infect macrophages, leading to the reorganization of the VE-cadherin catenin complex a protein important in cell adhesion. This reorganization creates intercellular gaps in endothelial cells.
The gaps lead to increased endothelial permeability and allow blood to escape from the vascular circulatory system.
The reasons for variation among patients infected with the same virus are unknown but stem from a complex system of virus-host interactions. Dengue fever becomes more virulent during a second infection by means of antibody dependent enhancement.
After the first infection, macrophages display antibodies on their cell membranes specific to the dengue virus. Diagnosis[ edit ] Definitive diagnosis is usually made at a reference laboratory with advanced biocontainment capabilities. The findings of laboratory investigation vary somewhat between the viruses but in general there is a decrease in the total white cell count particularly the lymphocytesa decrease in the platelet count, an increase in the blood serum liver enzymesand reduced blood clotting ability measured as an increase in both the prothrombin PT and activated partial thromboplastin times PTT.
The hematocrit may be elevated.
The serum urea and creatine may be raised but this is dependent on the hydration status of the patient. The bleeding time tends to be prolonged. Prevention of viral hemorrhagic fever With the exception of yellow fever vaccine neither vaccines nor experimental vaccines are readily available.
Prophylactic preventive ribavirin may be effective for some bunyavirus and arenavirus infections available only as an investigational new drug IND. VHF isolation guidelines dictate that all VHF patients with the exception of dengue patients should be cared for using strict contact precautions, including hand hygiene, double gloves, gowns, shoe and leg coverings, and faceshield or goggles.
Airborne precautions should be utilized including, at a minimum, a fit-testedHEPA filter-equipped respirator such as an N maska battery-powered, air-purifying respirator, or a positive pressure supplied air respirator to be worn by personnel coming within 1,8 meter six feet of a VHF patient.
Groups of patients should be cohorted sequestered to a separate building or a ward with an isolated air-handling system.
Environmental decontamination is typically accomplished with hypochlorite e.Symptoms may appear anywhere from 2 to 21 days after contact with the virus, with an average of 8 to 10 days. Many common illnesses can have these same symptoms, including influenza (flu) or malaria.
EVD is a rare but severe and often deadly disease. Recovery from EVD depends on good supportive. Viral hemorrhagic fever; Synonyms: viral haemorrhagic fever: Two nurses standing near Mayinga N'Seka, a nurse with Ebola virus disease in the outbreak in Zaire.N'Seka died a few days later due to severe internal hemorrhage.: Specialty.
Background Limited clinical and laboratory data are available on patients with Ebola virus disease (EVD).
The Kenema Government Hospital in Sierra Leone, which had an existing infrastructure for. Background Limited clinical and laboratory data are available on patients with Ebola virus disease (EVD).
The Kenema Government Hospital in Sierra Leone, which had an existing infrastructure for. Jul 24, · Ebola virus is one of at least 30 known viruses capable of causing viral hemorrhagic fever syndrome.
(See Pathophysiology and Etiology.) Although agents that cause viral hemorrhagic fever syndrome constitute a geographically diverse group of viruses, all of those identified to date are RNA viruses with a lipid envelope, all are .
Attenuated strains of HHS Select Agents and Toxins excluded from the requirements of 42 CFR part COXIELLA BURNETTI. Coxiella burnetii Phase II, Nine Mile Strain, plaque purified clone 4 (effective ) Lipopolysaccharide (LPS) phase variation is the .