Lassa fever outbreaks have occurred in Nigeria, Liberia, Guinea, Togo, Benin, Ghana, and Sierra Leone. Cases have been imported to the US, Germany, Sweden, and the United Kingdom.
The reservoir is the rats Mastomys natalensis, M. erythroleucus, and Hylomyscus pamfi. The pygmy mouse (Mus baoulei) has recently been implicated as a reservoir species in West Africa, all of which commonly inhabit houses in Africa. Most human cases result from contamination of food with rodent urine, saliva, or feces, but human-to-human transmission can occur via exposure to the urine, feces, saliva, vomitus, or blood of infected people. Nosocomial human-to-human transmission is common when personal protective equipment is not available or not used.
Based on serologic data, indigenous people in endemic areas have a very high rate of infection—much higher than their rate of hospitalization for Lassa fever—suggesting that many infections are mild and self-limited. However, some observational studies of missionaries sent to endemic areas show they have a much higher rate of severe illness and mortality. The Centers for Disease Control and Prevention estimates that about 80% of infected people have mild disease and about 20% have severe, multisystem disease.
The incubation period for Lassa fever is 5 to 16 days.
Symptoms of Lassa fever begin with gradually progressive fever, weakness, malaise, and gastrointestinal symptoms (eg, nausea, vomiting, diarrhea, dysphagia, stomach ache); symptoms and signs of hepatitis may occur. Over the subsequent 4 to 5 days, symptoms progress to prostration with sore throat, cough, chest pain, and vomiting. The sore throat becomes more severe during the first week; patches of white or yellow exudate may appear on the tonsils, often coalescing into a pseudomembrane.
In 60 to 80% of patients, systolic blood pressure is < 90 mm Hg with pulse pressures of< 20 mm Hg, and relative bradycardia is possible. Facial and neck swelling and conjunctival edema occur in 10 to 30%.
Occasionally, patients have tinnitus, epistaxis, bleeding from the gums and venipuncture sites, maculopapular rash, cough, and dizziness.
Sensorineural hearing loss develops in 20%; it is often permanent.
Patients who recover defervesce in 4 to 7 days. Progression to severe illness results in shock, delirium, rales, pleural effusion, and, occasionally, generalized seizures. Pericarditis occasionally occurs. Degree of fever and aminotransferase levels correlate with disease severity.
Late sequelae include alopecia, iridocyclitis, and transient blindness.
Lassa fever is suspected in patients with possible exposure if they have a viral prodrome followed by unexplained disease of any organ system.
Liver tests, urinalysis, serologic tests, and possibly complete blood count should then be done. Proteinuria is common and may be massive. Aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels rise (to 10 times normal), as do lactic dehydrogenase levels.
The most rapid diagnostic test is PCR, but demonstrating either Lassa IgM antibodies or a 4-fold rise in IgG antibody titer using an indirect fluorescent antibody technique is also diagnostic.
Although the virus can be grown in cell culture, cultures are not routine. Because infection is a risk, particularly in patients with hemorrhagic fever, cultures must be handled only in a biosafety level 4 laboratory.
Chest x-rays, obtained if lung involvement is suspected, may show basilar pneumonitis and pleural effusions.
Recovery or death usually occurs 7 to 31 days (average 12 to 15 days) after symptoms begin. In patients with severe, multisystem disease, the case fatality rate is 16 to 45%.
Disease is severe during pregnancy, especially during the 3rd trimester. The case fatality rate is 50 to 92% in women who are pregnant or who have delivered within 1 month. Most infected pregnant women lose the fetus.
Ribavirin, if begun within the first 6 days, may reduce mortality up to 10-fold. Treatment with ribavirin is 30 mg/kg IV (maximum, 2 g) loading dose followed by 16 mg/kg IV (maximum, 1 g/dose) every 6 hours for 4 days, then 8 mg/kg IV (maximum, 500 mg/dose) every 8 hours for 6 days.
Anti-Lassa fever plasma has been tried in very ill patients but has not been shown to be beneficial and is not currently recommended.
Supportive treatment, including correction of fluid and electrolyte imbalances, is imperative.
For infected pregnant women, abortion reduces risk of maternal death.
Universal precautions, including use of personal preventive equipment and other measures for airborne isolation (eg, use of goggles, high-efficiency masks, a negative-pressure room, positive-pressure filtered air respirators), and surveillance of contacts are recommended when treating patients with Lassa fever.
Primary transmission of the Lassa virus from its rodent host to humans can be prevented in endemic areas by avoiding food, water, and environment contaminated by infected rodents; however, the wide distribution of these rodent hosts in Africa makes complete control of these rodent reservoirs impractical. Guidelines for cleaning up after rodents and working in areas with potential rodent excreta are available from the Centers for Disease Control and Prevention (CDC).
No vaccine for Lassa fever is available.
Lassa fever is usually transmitted by consuming food contaminated with rodent excreta, but human-to-human transmission can occur via infected urine, feces, saliva, vomitus, or blood.
Symptoms may progress from fever, weakness, malaise, and gastrointestinal symptoms to prostration with sore throat, cough, chest pain, and vomiting; sometimes to shock, delirium, rales, and pleural effusion; and occasionally to severe illness and shock.
For the most rapid diagnosis, use PCR, but antibody tests can also be used.
Lassa fever is severe during pregnancy; most infected pregnant women lose the fetus.
Ribavirin, if begun within the first 6 days, may reduce mortality up to 10-fold; supportive treatment, including correction of fluid and electrolyte imbalances, is imperative.