In recent years, this has been the most common form of transmission of yellow fever in Africa.Concern exists about yellow fever spreading to southeast Asia, where its vector A. aegypti already occurs. Pathogenesis
After transmission from a mosquito, the viruses replicate in the lymph nodes and infect dendritic cells in particular. From there, they reach the liver and infect hepatocytes (probably indirectly via Kupffer cells), which leads to eosinophilic degradation of these cells and to the release of cytokines. Apoptotic masses known as Councilman bodies appear in the cytoplasm of hepatocytes.Fatality may occur when cytokine storm, shock, and multiple organ failure follow. Diagnosis
Yellow fever is most frequently a clinical diagnosis, based on symptomatology and travel history. Mild cases of the disease can only be confirmed virologically. Since mild cases of yellow fever can also contribute significantly to regional outbreaks, every suspected case of yellow fever (involving symptoms of fever, pain, nausea, and vomiting 6–10 days after leaving the affected area) is treated seriously.If yellow fever is suspected, the virus cannot be confirmed until 6–10 days following the illness. A direct confirmation can be obtained by reverse transcription polymerase chain reaction, where the genome of the virus is amplified. Another direct approach is the isolation of the virus and its growth in cell culture using blood plasma; this can take 1–4 weeks.Serologically, an enzyme-linked immunosorbent assay during the acute phase of the disease using specific IgM against yellow fever or an increase in specific IgG titer (compared to an earlier sample) can confirm yellow fever.
It compares well to jejunal aspirates in making the diagnosis of bacterial overgrowth. Carbon-13 (13C) and carbon-14 (14C) based tests have also been developed based on the bacterial metabolism of D-xylose. Increased bacterial concentrations are also involved in the deconjugation of bile acids. The glycocholic acid breath test involves the administration of the bile acid 14C glycocholic acid, and the detection of 14CO2, which would be elevated in bacterial overgrowth.However, some physicians suggest that if the suspicion of bacterial overgrowth is high enough, the best diagnostic test is a trial of treatment. If the symptoms improve, an empiric diagnosis of bacterial overgrowth can be made.There is insufficient evidence to support the use of inflammatory markers, such as fecal calprotectin, to detect SIBO. Treatment
Treatment strategies should focus on identifying and correcting the root causes, where possible, resolving nutritional deficiencies, and administering antibiotics. This is especially important for patients with indigestion and malabsorption. Although whether antibiotics should be a first line treatment is a matter of debate. Some experts recommend probiotics as first line therapy with antibiotics being reserved as a second line treatment for more severe cases of SIBO. Prokinetic drugs are other options but research in humans is limited. A variety of antibiotics, including tetracycline, amoxicillin-clavulanate, metronidazole, neomycin, cephalexin and trimethoprim-sulfamethoxazole have been used; however, the best evidence is for the use of rifaximin, a poorly-absorbed antibiotic.