Lassa fever is an acute viral hemorrhagic fever caused by the Lassa virus and first described in 1969 in the town of Lassa, in Borno State, Nigeria, in the Yedseram river valley at the south end of Lake Chad. Clinical cases of the disease had been known for over a decade but had not been connected with a viral pathogen. The infection is endemic in West African countries, and causes 300,000–500,000 cases annually, with approximately 5,000 deaths. Outbreaks of the disease have been observed in Nigeria, Liberia, Sierra Leone, Guinea, and the Central African Republic, but it is believed that human infections also exist in Democratic Republic of the Congo, Mali, and Senegal. The primary animal host of the Lassa virus is the Natal Multimammate Mouse (Mastomys natalensis), an animal indigenous to most of Sub-Saharan Africa. The virus is probably transmitted by contact with the feces or urine of animals accessing grain stores in residences.
Virology
Genome: Lassa fever is caused by the Lassa virus, a member of the Arenaviridae family; it is an enveloped, single-stranded, bisegmented RNA virus.
Replication for Lassa virus is very rapid, while also demonstrating temporal control in replication. There are two genome segments. The first replication step is transcription of mRNA copies of the negative- or minus-sense genome. This ensures an adequate supply of viral proteins for subsequent steps of replication, as proteins known as N and L are translated from the mRNA.
Receptors: The Lassa virus gains entry into the host cell by means of the cell-surface receptor the alpha-dystroglycan (alpha-DG), a versatile receptor for proteins of the extracellular matrix. It shares this receptor with the prototypic arenavirus lymphocytic choriomeningitis virus. Receptor recognition depends on a specific sugar modification of alpha-dystroglycan by a group of glycosyltransferases known as the LARGE proteins.
Vectors:
Lassa virus is zoonotic (transmitted from animals), in that it spreads to man from rodents, specifically multi-mammate rats (Mastomys natalensis). This is probably the most common rodent in equatorial Africa, ubiquitous in human households and eaten as a delicacy in some areas.[citation needed] In these rats infection is in a persistent asymptomatic state. The virus is shed in their excreta (urine and feces), which can be aerosolized. In fatal cases, Lassa fever is characterized by impaired or delayed cellular immunity leading to fulminant viremia. Infection in humans typically occurs via exposure to animal excrement through the respiratory or gastrointestinal tracts. Inhalation of tiny particles of infective material (aerosol) is believed to be the most significant means of exposure.
Prevalence:
The dissemination of the infection can be assessed by prevalence of antibodies to the virus in populations of:
•
Sierra Leone 8–52%
•
Guinea 4–55%
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Nigeria approx. 21%
Studies show up to half a million cases of Lassa fever per year in West Africa, with 5000 resulting in death.
Like other hemorrhagic fevers, Lassa fever can be transmitted directly from one human to another. It can be contracted by an airborne route or with direct contact with infected human blood, urine, or semen. Transmission through breast milk has also been observed.
Medical aspects: Prevention:
Control of the Mastomys rodent population is impractical, so measures are limited to keeping rodents out of homes and food supplies, as well as maintaining effective personal hygiene. Gloves, masks, laboratory coats, and goggles are advised while in contact with an infected person. Researchers at the USAMRIID facility, where military biologists study infectious diseases, have a promising vaccine candidate. They have developed a replication-competent vaccine against Lassa virus based on recombinant vesicular stomatitis virus vectors expressing the Lassa virus glycoprotein. After a single intramuscular injection, test primates have survived lethal challenge, while showing no clinical symptoms.[8]
Symptoms
In 80% of cases the disease is inapparent, but in the remaining 20% it takes a complicated course. It is estimated that the virus is responsible for about 5,000 deaths annually. The fever accounts for up to one third of deaths in hospitals within the affected regions and 10 to 16% of total cases.
After an incubation period of six to twenty-one days, an acute illness with multiorgan involvement develops. Non-specific symptoms include fever, facial swelling, and muscle fatigue, as well as conjunctivitis and mucosal bleeding. The other symptoms arising from the affected organs are:
Gastrointestinal tract , Nausea,Vomiting (bloody),Diarrhea (bloody),Stomach ache,Constipation, Dysphagia (difficulty swallowing),Hepatitis,Cardiovascular system,Pericarditis, Hypertension, Hypotension, Tachycardia (abnormally high heart rate), Respiratory tract,Cough,Chest pain,Dyspnoea,Pharyngitis,Pleuritis, Nervous system,
Encephalitis,Meningitis,Unilateral or bilateral hearing deficit,Seizures.
