During the most recent outbreak of RVF in the Ijara District of Northeastern Province, Kenya, early recognition of the disease outbreak by astute clinicians allowed for the installation of public-health measures to stem the spread of the disease.22–24
With a multitude of febrile tropical illnesses overlapping in geographical distribution with Rift Valley fever,21,25,26
the disease can be difficult to identify in the early stages of an outbreak.
Several series in the past have described general symptoms associated with RVF.9,14–20
However, for a clinician at the bedside, these descriptions are difficult to apply in recognizing disease outside of a known outbreak. The above cases illustrate the evolution of individual clinical cases. The illness in these patients was largely characterized by an early syndrome of fever, proximal large-joint arthralgias (particularly knees, elbows, and shoulders), throbbing headaches, malaise, and anorexia followed shortly thereafter by nausea, vomiting, and vague midepigastric discomfort. Only one-half of the confirmed cases had hemorrhagic manifestations (two of which were severe with hematemesis). The peak of disease severity coincided with tender hepatomegaly, scleral icterus, and delirium. This is consistent with earlier findings of hepatic necrosis noted at autopsy in two Egyptian RVF patients.8
Many infections with RVF virus are mild and often subclinical.18,20
These mild cases can often be difficult to distinguish from other mild, self-limited illnesses. In particular, the symptoms of mild disease can mimic those of malaria, and in an area with a high incidence of malaria, RVF can be difficult to identify. The symptoms and geographic distribution of RVF partially overlap with those of dengue fever. RVF is less often characterized by rash, bone pain, and myalgia than is dengue fever.9,18,27,28
Chikungunya virus, also found recently in East Africa often during times of drought,29
is also characterized by severe arthralgias, which persists for prolonged periods of time and often involves the small, peripheral joints.30–32
In endemic areas, after periods of flooding, RVF should be considered in patients with febrile illness and without evidence of malaria.
One patient in this series was found to have the late manifestation of retinal vasculitis. His syndrome was similar to that described in previous descriptions of ocular manifestations of disease.14
With a small sample size, the low number of observed late complications of disease is not unexpected. Additionally, cultural and economic limitations of the health-care system in this region may have led to an overall underreporting of late manifestations of RVF, such as encephalitis and retinal vasculitis.14,17
In this case series, we studied only a very small subset of RVF cases among the total that occurred during this outbreak. As with other, previously published RVF reports, there was undoubtedly some selection bias in the cases that came to our attention. However, the cases reported here were generally observed over a longer period of time with careful attention to patient history and the details of clinical presentation. The particular population studied in this single location may have manifested a specific set of RVFV infection-related symptoms because of a particular combination of genetic background in combination with concurrent malnutrition, anemia, or chronic dehydration. Other potential comorbidities, such as malaria, schistosomiasis, typhoid fever, hypertension, congestive heart failure, tuberculosis, and peptic ulcer disease are also common illnesses treated in this region and could have affected the patients' clinical presentations.
RVF is present in many areas of sub-Saharan Africa. The conditions that favor its epidemic spread tend to exist more commonly in rural, semi-arid, sparsely populated and underdeveloped areas. All patients seen in this series were evaluated in their local milieu using evaluation techniques available to local medical staff. The focus on history and physical examination in diagnosis reflects resources available to providers in this setting—routine, laboratory serum studies (such as complete blood counts, basic chemistry, and liver-function tests), radiographic studies, and advanced supportive-care technology were unavailable. As a result, the natural disease course was followed in its natural setting.
Currently, RVF in humans is distinguished from other febrile illnesses primarily by its epidemiological association with concurrent livestock illness. With emerging data that suggest persistent interepidemic transmission,7,33
the concurrent epizootic criterion is not sufficiently reliable in detecting human RVF. Whereas RVFV outbreaks often afflict rural sub-Saharan Africa,12,13,34
epidemics in Egypt8
and Saudi Arabia/Yemen9,10
illustrate the ability for the virus to move into presently non-endemic regions and to expand the risk of human RVFV-associated disease outside of its traditionally reported geographic range. Earlier identification of disease is a key in limiting its spread and initiating appropriate treatment of RVF-afflicted patients.35
More work will be needed in further describing the distinct manifestations of disease in humans to promote this early phase of RVF recognition.