Like the alphaviruses, flaviviruses may cause encephalitis or a fever/ arthritis/rash syndrome, the pathogenesis and clinical features of which were described in Chapter 25, but yellow fever and dengue viruses as well as a number of tick-borne flaviviruses cause hemorrhagic fever. The striking feature of this potentially lethal syndrome is hemorrhage, which manifests as pefechiae and ecchymoses on the skin and mucous membranes (see Fig. 33-4), with bleeding from any or all of the body orifices. Examination of the blood reveals thrombocytopenia and usually leukopenia. In fatal cases the patient collapses abruptly from hypotensive shock Further details are given in Chapters 30, 32, 33, and 36.
Yellow fever is a hemorrhagic fever with a difference; the liver is the major target, with virus replicating in Kupffer cells and massive necrosis of hepato-cytes leading to a decrease in the rate of formation of prothrombin as well as to jaundice. Although most cases are mild, presenting with fever, chills, headache, backache, myalgia, and vomiting, a minority progress (sometimes after a brief remission) to severe jaundice, massive gastrointestinal hemorrhages (hematemesis and rnelena), hypotension, dehydration, proteinuria, and oliguria signaling kidney failure. Mortality from this severe form of the disease is of the order of 20-50%.
Dengue fever is typical of the painful but nonlethal fever/arthritis/rash syndrome which is the common presentation of so many arbovirus diseases: sudden onset of fever (characteristically biphasic, or "saddle back"), chills, retroorbital headache, conjunctivitis, and severe pains in the back, muscles, and joints, followed by a rash and rapid resolution. Sometimes, however, the presentation is that of a hemorrhagic fever, in which a child can die of shock within hours—hence the name dengue hemorrhagic fever/ dengue shock syndrome (DHF/DSS).
The disease is generally observed during epidemics of dengue (often type 2) in a population with a previous history of infection with another dengue serotype (e.g., type 7). The majority of the cases occur in children who can be shown to have previously acquired antibody against another type, or in young infants with maternally acquired antibodies against another type. This observation gives support to the "immune enhancement" (or "antibody-dependent enhancement") hypothesis, namely, that dengue virus, the principal target of which is cells of the monocyte/macrophage series, is opsonized by antibodies against a heterologous dengue virus serotype (which bind to the virion but do not neutralize its infectivity), hence is more avidly taken up, via Fc receptors, into the very cell in which it replicates best. Experimentally, it can readily be demonstrated that such virus-antibody complexes replicate to higher titer in macrophage cultures On the other hand, only a small minority of people with sequential infections develop DHF/DSS, and some cases of DHF/DSS have been reported in people with no prior experience of any type of dengue; thus the possibility remains that individuals differ markedly in susceptibility and/or that strains differ substantially in virulence. Oligonucleotide fingerprinting and partial gene sequencing of numerous strains of all four dengue serotypes has demonstrated the existence of a number of discernable geographic variants (topoli/pes), especially within type 2, but no major differences in virulence have been discerned.
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