A unifying theme in the epidemiology of these diseases is found in the interface between children and the corresponding zoonotic vectors or the degree of nosocomial transmission. Overall, the disease manifestations in children resemble those in adults with notable exceptions. DSS in the first year of life, which appears to be precipitated by maternal antibody, and the swollen baby syndrome of Lassa fever are uniquely pediatric diseases. DSS from secondary dengue virus infection also appears to be a disease that preferentially affects children for unknown reasons. Independent observations of the increased incidence among girls and well-nourished children with presumed increased immune reactivity may help to clarify the underlying pathogenic mechanism for DHF/DSS in children. Pediatric viral hemorrhagic fever cases or a lack thereof also can provide a clue to the predominant mechanism of exposure and the potential vector. In hyperendemic and urban outbreaks situations caused by either yellow fever or dengue, adults usually are solidly immune, and therefore children represent the highest proportion from rodents should follow a similar pattern for the Aedes species- transmitted diseases (ie, provide ample opportunity for contact between the vector/reservoir and children). This appears to be true for lassa fever and during town-based outbreaks of Bolivian hemorrhagic fever and the tick-borne hemorrhagic fevers. The few pediatric cases noted during the outbreak of Ebola hemorrhagic fever in an otherwise susceptible population underscored the health education message that this disease was not extremely contagious without direct patient contact. Not unexpectedly, children rarely are infected with the New World arenaviruses, except as discussed, or jungle/sylvatic yellow fever, which is acquired predominantly in the forest or fields. The same appears to be true for the current epidemiology of the tick-borne hemorrhagic fevers. The possible explanations for the small number of pediatric cases observed with some of the hemorrhagic fever include lack of exposure, unrecognized or mild atypical disease, and resistance to infection. The paucity of pediatric cases is most obvious for all the hantavirus (see article Bryan et al in this issue), given the expected population distribution and epidemiology of these disease. However, we can not exclude that these illnesses simply are being misdiagnosed because clinicians are unaware of these diseases in children and the full clinical spectrum of the illness among this age group. This has been reported with Lassa fever when adult goes undiagnosed in endemic areas among uninformed physicians kilometers from physicians who otherwise are making the correct diagnosis (Frame J and Lloyd E. 1992, personal communications). In addition, the paucity of cases may be a function of nonuniform or nonexistent surveillance methodologies. Furthermore, many of these studies fail to take into account the underlying population distribution or depend on antibody prevalence studies done with unreliable or outdated assays. The occurrence of severe and fatal yellow fever in children has become evident only over the last 25 years because of systematic investigations. Other explanations for the small number of pediatric cases include that they may be buried in the background of the 5- to 10-fold higher childhood mortality in many of the countries in which these disease occur. However, we must remain wary to the probability that a mere review of case reports and case series does not provide a true assessment of the incidence of pediatric cases, particularly among diseases that occur primarily in developing countries. A myriad of factors have led to the 'emergence' of many of these viral hemorrhagic fevers that appear to be independent of our increasing recognition of these diseases attributable to improved communications and ability to obtain and transport specimens for diagnostic testing. Increasing encroachment of humans into rural areas invariably will lead to an increased frequency of contact between competent disease reservoirs/vectors and humans, as is seen with tick-borne, filoviral, flaviral, and arenaviral hemorrhagic fevers. The continued expansion of the Argentine hemorrhagic fever endemic zone is alarming in that it now encompasses more than 1 million persons. The 1987 outbreak of Rifi Valley fever in Mauritania was associated with damming the Senegal river. Societal changes partly explain the large 1996 outbreak of Lassa fever in Sierra Leone amidst economic impoverishment and civil conflict. The pandemic spread of dengue in the 20th century is linked intimately to a worldwide resurgence of A aegypti. The dependence of Middle East countries on imported livestock from East Africa explains the increasing reports of Crimean-Congo hemorrhagic fever in those countries.
|Original language||English (US)|
|Number of pages||10|
|Journal||Seminars in Pediatric Infectious Diseases|
|State||Published - 1997|
ASJC Scopus subject areas
- Pediatrics, Perinatology, and Child Health
- Microbiology (medical)