Rift Valley Fever, RVF
More than you wanted to know, research for a friend.
First of all RVF is not Black Water Fever. I don’t think that you implied that it was, but just to clarify, BWF is late stage Malaria with hemolysis and disseminated intravascular coagulopathy, DIC. The resulting hemoglobin in the urine turns black in acid urine, thus black water.
RVF is a viral disease also potentially mosquito born and occurring mostly in ruminating animals of Sub-Sahara Africa. It is sometimes transmitted to humans through handling infected animals and meat, somewhat synonymous to the transmission of bird flue to humans. It is also transmitted by mosquitoes of many genera.
Transmission to humans may have as the source: nasal discharge, blood, vaginal secretions post abortion, mosquitoes, infected meat, raw milk and possibly aerosols.
Distribution of RVF is limited exclusively to Africa, favoring heavy rain fall areas, and dense mosquito populations. Cases appeared in Egypt in 1977 and 1993 also in Mauritania in 1987. There have been laboratory infections in other parts of the world.
In Cattle the incubation period ranges from 1-6 days with a fever of 40-41C in calves with a 10-70% mortality. Adult cattle may show temperatures of 40-41C, experiance extreem salivation, anorexia, weakness and feted diarrhea. Abortion runs 85% and mortality 10%.
Humans experience flue like symptoms with fever, 40C, headache, muscle pain, weakness, nausea, abdominal pain and photophobia lasting 4- 7 days. More sever cases lead to retinopathy, blindness, meningo-encephalitis, patechial hemorrhages, jaundice and death.
Leisions include: focal hepatic necrosis, sub-capsular hemorrhage, congestion and swelling. Skin leisions are patechial leading to hemorrhagic echomotic swelling. Visceral and serosal hemorrhage occur as well as hemorrhagic enteritis.
Laboratory diagnosis is confirmed by inoculation of mice and hamsters. Isolation of the virus by tissue culture can be confirmed by immunofluorence. The presence of the virus can be indirectly measured by viral antigen, complement fixation and immuno diffusion. Antigen is detected by enzyme immuno-assay. These tearms all mean much the same thing. A fluorescent antigen attaches either to the invisible virus itself or to an equally invisible antigen thereby lighting up each spot where there is an attachment. The virus can be seen with an electron microscope but is too small to be seen with a light microscope. The immuno-fluorescence however is easily seen even with a limited power microscope.
Serologic testing is done on plasma samples involving procedures with names referring to similar procedures. An active infection may not be required for detection of past infection and the sample may not be as fresh. Some of these sero-testing procedures may be called IGG,IGM, our old friend fluorescent antibody, hemagglutenation inhibition, plaque reduction neutralization, complement fixation and immuno-diffusion.
Samples may consist of heperinized or clotted blood, plasma or serum, or a tissue sample.
Sanitary procedures have not been of much help in stemming the epidemics of RVF, but vaccine has. Attenuated vaccines give lasting immunity but are pathogenic to humans. Inactivated virus vaccines are safe but require two shots and need to be renewed annually, at the present stage of development.
Virus cannot be seen directly in the blood. The above testing measures view the fluorescent markers giving indirect evidence of the viral presence, the antigen or the antibody.
Virus History
Ed Jenner successfully immunized against Small Pox by vaccination with Cow Pox 1798. Dimitrii Ivanovsky identified the non filterable virus that caused mosaic disease of tobacco leaves in 1892. D’Herelle postulated a bacteriophage. Twort conceived an ultrascopic filter passing virus and the beginning doctrine of non filterable viruses. Loeffler and Frosch identified the innoculable virus of foot and mouth disease in 1898. Beijerinck in 1893 contributed and Olitsky developed a tissue culture of a virus in 1925. The virus of cattle plague was found in 1897. Walter Reed recognized the viral cause of Yellow Fever in 1900. Dengue virus was identified in 1917. The Rift Valley Fever virus was identified in 1930. It was probably the combination realization of inoculation by a non filterable virus, the recognition of a bacteriophage on bacterial culture plates and the immunization with cow pox that lead to the recognition of the invisible virus as a pathogen.
Today NASA thinks it can identify the temperature and climate changes that cause the epidemics of RVF by picturing the ocean temperature changes of El Niño in the Indian Ocean and western Pacific.
First of all RVF is not Black Water Fever. I don’t think that you implied that it was, but just to clarify, BWF is late stage Malaria with hemolysis and disseminated intravascular coagulopathy, DIC. The resulting hemoglobin in the urine turns black in acid urine, thus black water.
RVF is a viral disease also potentially mosquito born and occurring mostly in ruminating animals of Sub-Sahara Africa. It is sometimes transmitted to humans through handling infected animals and meat, somewhat synonymous to the transmission of bird flue to humans. It is also transmitted by mosquitoes of many genera.
Transmission to humans may have as the source: nasal discharge, blood, vaginal secretions post abortion, mosquitoes, infected meat, raw milk and possibly aerosols.
Distribution of RVF is limited exclusively to Africa, favoring heavy rain fall areas, and dense mosquito populations. Cases appeared in Egypt in 1977 and 1993 also in Mauritania in 1987. There have been laboratory infections in other parts of the world.
In Cattle the incubation period ranges from 1-6 days with a fever of 40-41C in calves with a 10-70% mortality. Adult cattle may show temperatures of 40-41C, experiance extreem salivation, anorexia, weakness and feted diarrhea. Abortion runs 85% and mortality 10%.
Humans experience flue like symptoms with fever, 40C, headache, muscle pain, weakness, nausea, abdominal pain and photophobia lasting 4- 7 days. More sever cases lead to retinopathy, blindness, meningo-encephalitis, patechial hemorrhages, jaundice and death.
Leisions include: focal hepatic necrosis, sub-capsular hemorrhage, congestion and swelling. Skin leisions are patechial leading to hemorrhagic echomotic swelling. Visceral and serosal hemorrhage occur as well as hemorrhagic enteritis.
Laboratory diagnosis is confirmed by inoculation of mice and hamsters. Isolation of the virus by tissue culture can be confirmed by immunofluorence. The presence of the virus can be indirectly measured by viral antigen, complement fixation and immuno diffusion. Antigen is detected by enzyme immuno-assay. These tearms all mean much the same thing. A fluorescent antigen attaches either to the invisible virus itself or to an equally invisible antigen thereby lighting up each spot where there is an attachment. The virus can be seen with an electron microscope but is too small to be seen with a light microscope. The immuno-fluorescence however is easily seen even with a limited power microscope.
Serologic testing is done on plasma samples involving procedures with names referring to similar procedures. An active infection may not be required for detection of past infection and the sample may not be as fresh. Some of these sero-testing procedures may be called IGG,IGM, our old friend fluorescent antibody, hemagglutenation inhibition, plaque reduction neutralization, complement fixation and immuno-diffusion.
Samples may consist of heperinized or clotted blood, plasma or serum, or a tissue sample.
Sanitary procedures have not been of much help in stemming the epidemics of RVF, but vaccine has. Attenuated vaccines give lasting immunity but are pathogenic to humans. Inactivated virus vaccines are safe but require two shots and need to be renewed annually, at the present stage of development.
Virus cannot be seen directly in the blood. The above testing measures view the fluorescent markers giving indirect evidence of the viral presence, the antigen or the antibody.
Virus History
Ed Jenner successfully immunized against Small Pox by vaccination with Cow Pox 1798. Dimitrii Ivanovsky identified the non filterable virus that caused mosaic disease of tobacco leaves in 1892. D’Herelle postulated a bacteriophage. Twort conceived an ultrascopic filter passing virus and the beginning doctrine of non filterable viruses. Loeffler and Frosch identified the innoculable virus of foot and mouth disease in 1898. Beijerinck in 1893 contributed and Olitsky developed a tissue culture of a virus in 1925. The virus of cattle plague was found in 1897. Walter Reed recognized the viral cause of Yellow Fever in 1900. Dengue virus was identified in 1917. The Rift Valley Fever virus was identified in 1930. It was probably the combination realization of inoculation by a non filterable virus, the recognition of a bacteriophage on bacterial culture plates and the immunization with cow pox that lead to the recognition of the invisible virus as a pathogen.
Today NASA thinks it can identify the temperature and climate changes that cause the epidemics of RVF by picturing the ocean temperature changes of El Niño in the Indian Ocean and western Pacific.
posted by Clancy Hughes | 4/25/2006 05:12:00 PM
0 Comments:
Post a Comment
<< Home