Lassa fever overview: Difference between revisions
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==Treatment== | ==Treatment== | ||
===Medical Therapy=== | ===Medical Therapy=== | ||
Intravenous (IV) [[ribavirin]] | Data on the efficacy of antiviral agents in Lassa fever are scarce. Intravenous (IV) [[ribavirin]] was previously evaluated for treatment of Lassa fever and demonstrated a reduction in mortality when administered anytime during the course of the disease, especially early within the first 6 days of symptom-onset. Ribavirin is administered intravenously for a total of 10 days using the following regimen: first, loading dose of 30 mg/kg (max. 2g) followed by a dose of 16 mg/kg (max. 1g) IV q6h for 4 days, followed by a dose of 8 mg/kg (max. 500mg) IV q8h for 6 days.<ref name="pmid3940312">{{cite journal| author=McCormick JB, King IJ, Webb PA, Scribner CL, Craven RB, Johnson KM et al.| title=Lassa fever. Effective therapy with ribavirin. | journal=N Engl J Med | year= 1986 | volume= 314 | issue= 1 | pages= 20-6 | pmid=3940312 | doi=10.1056/NEJM198601023140104 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3940312 }} </ref> In addition to antiviral therapy, management includes supportive care to adequately maintain respiratory status, as well as [[fluid]] and [[electrolyte]] balance. | ||
===Primary Prevention=== | ===Primary Prevention=== | ||
Revision as of 17:07, 4 January 2016
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Ammu Susheela, M.D. [2]; Yazan Daaboul, M.D.; Serge Korjian M.D.
Overview
Lassa fever is an acute viral hemorrhagic fever that was first described in 1969 in Lassa, Nigeria.[1] The virus is a member of the family Arenaviridae. It is a zoonotic, single-stranded RNA virus that is transmitted to humans by the Mastomys natalensis rodent. The infection is endemic in West African with an annual incidence of 300,000 to 500,000 cases and a case mortality rate of 5-15%.[2] Risk factors for Lassa fever include travel to endemic regions (West Africa), exposure to infected individuals or rodents, and occupational exposure in healthcare settings. Pregnant women, immunosuppressed patients, and young patients are at high risk of developing Lassa fever-associated complications. Following exposure, infected patients remain asymptomatic for approximately 3 to 21 days. The majority of patients experience no or mild clinical manifestations. Typically, patients first develop persistent high-grade fever and other non-specific signs and symptoms. If left untreated, the majority of cases self-resolve without intervention. However, in the minority of cases, clinical manifestations may progress to hemorrhage, deafness, edema, seizures, coma, and death. Lassa fever is usually diagnosed by detection of Lassa antibodies in the patient's serum using ELISA. The mainstay of therapy of Lassa fever is Ribavirin. The efficacy of ribavirin is most strongly observed when it is administered intravenously early in the course of the disease. In addition to antiviral therapy, patients should typically receive supportive care to adequately maintain respiratory status and fluid and electrolyte balance. While there is no vaccine for Lassa fever, avoiding infected individuals or rodents and proper handling of infected waste products are recommended for the primary prevention of Lassa fever.
Historical Perspective
The first case of documented Lassa fever was reported in 1969 following the death of 2 nurses in Lassa, Nigeria. Prior to that, similar cases in West Africa were reported and thought to be caused by Lassa fever given the clinical and epidemiological resemblance of the presentation to Lassa fever.
Pathophysiology
Lassa fever may be transmitted from either infected animals (typically rodents) or humans following exposure to body fluids and excretions/secretions from the respiratory tract or GI tract. Following transmission, Lassa virus infects the endothelium and replicates intracellularly using an L-polymerase enzyme and nucleocapsid protein NP, which synthesize ribonucleoprotein (RNP) that produces mRNA and antigenomic RNA required for transcription. NP protein helps the virus evade the host immune system. Following transcription, vascular dysfunction ensues, resulting in the development of clinical manifestations of the disease. Although all organs may potentially be infected, the liver is a common target organ, and hepatitis/hepatic necrosis is typical following Lassa fever infection.
Causes
Lassa fever is caused by the Lassa virus, a member of the zoonotic Arenaviridae family. It is an enveloped, single-stranded, bisegmented RNA virus. The natural reservoir of Lassa virus is the Mastomys natalensis rodent (multimammate rat/mouse) that sheds the virus in urine and fecal droppings.
Differentiating Lassa fever from other Diseases
Lassa fever must be differentiated from other diseases that cause hemorrhagic fever, diarrhea, muscle fatigue, such as Ebola infection, Typhoid fever, Malaria, Diphtheria, Legionellosis, Congo-hemorrhagic fever, yellow fever, and Shigellosis.
Epidemiology and Demographics
Lassa fever is endemic in West Africa and is rare in developed countries. The annual incidence of Lassa virus is 100,000-300,000 individuals with a case fatality rate typically reaching 1-5% but may be as high as 65% during outbreaks.[3] There is no predilection to specific age groups, gender, or race. However, young age and pregnancy are associated with increased risk of Lassa fever-associated
Risk Factors
Risk factors for Lassa fever include travel to endemic regions (West Africa), exposure to infected individuals or rodents, and occupational exposure in healthcare settings. Pregnant women, immunosuppressed patients, and young patients are at high risk of developing Lassa fever-associated complications.
Natural History, Complications and Prognosis
Following exposure, infected patients remain asymptomatic for approximately 3 to 21 days. The majority of patients experience no or mild clinical manifestations. Typically, patients first develop persistent high-grade fever and other non-specific signs and symptoms. If left untreated, the majority of cases self-resolve without intervention. However, in the minority of cases, clinical manifestations may progress to hemorrhage, deafness, abdominal/chest pain, pleural/pericardial effusions and ascites, and facial edema. Eventually, manifestations progress to include convulsions, hypovolemic shock, coma, and eventually death. The most common complications of Lassa fever are neurosensory deafness and hepatic injury, which may be a mild hepatitis or fulminant hepatic necrosis. Although prognosis of Lassa fever is generally good but development of complications, pregnancy, infancy, and immunosuppression are associated with poorer prognosis and increased risk of death.
Diagnosis
History and Symptoms
Common symptoms of Lassa fever typically include persistent, high-grade fever and other non-specific symptoms, such as headache, myalgia/arthralgia, cough, conjunctival injection, and vomiting. Less commonly, patients may present with more severe symptoms, such as GI bleeding, deafness, confusion, seizures, and coma.
Physical Examination
Persistent, high-grade fever is the most common sign on physical examination. Other common signs on physical examination include tachycardia, tachypnea, conjunctival injection, abdominal/chest tenderness, pharyngitis with tonsillar exudates, and hepatosplenomegaly.
Laboratory Findings
Acute Lassa fever is usually diagnosed by detection of IgG Lassa antibodies in the patient's serum using ELISA. Additional investigations are also required following diagnosis to monitor the course of the disease for development of complications and target organ damage.
Other Diagnostic Studies
Other diagnostic tests to confirm the diagnosis of lassa fever include reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemistry using either skin, tissue or liver tissue.
Treatment
Medical Therapy
Data on the efficacy of antiviral agents in Lassa fever are scarce. Intravenous (IV) ribavirin was previously evaluated for treatment of Lassa fever and demonstrated a reduction in mortality when administered anytime during the course of the disease, especially early within the first 6 days of symptom-onset. Ribavirin is administered intravenously for a total of 10 days using the following regimen: first, loading dose of 30 mg/kg (max. 2g) followed by a dose of 16 mg/kg (max. 1g) IV q6h for 4 days, followed by a dose of 8 mg/kg (max. 500mg) IV q8h for 6 days.[4] In addition to antiviral therapy, management includes supportive care to adequately maintain respiratory status, as well as fluid and electrolyte balance.
Primary Prevention
There is no vaccine for Lassa fever. Primary transmission of the Lassa virus can be prevented by avoiding contact with Mastomys rodents, especially in the geographic regions where outbreaks occur. When caring for patients with Lassa fever, further transmission of the disease through person-to-person contact or via nosocomial routes can be avoided by taking preventive precautions against contact with patient secretions.
References
- ↑ Frame JD, Baldwin JM, Gocke DJ, Troup JM (1970). "Lassa fever, a new virus disease of man from West Africa. I. Clinical description and pathological findings". Am. J. Trop. Med. Hyg. 19 (4): 670–6. PMID 4246571.
- ↑ Ogbu O, Ajuluchukwu E, Uneke CJ (2007). "Lassa fever in West African sub-region: an overview". Journal of vector borne diseases. 44 (1): 1–11. PMID 17378212.
- ↑ "The Centers for Disease Control and Prevention facts sheets" (PDF).
- ↑ McCormick JB, King IJ, Webb PA, Scribner CL, Craven RB, Johnson KM; et al. (1986). "Lassa fever. Effective therapy with ribavirin". N Engl J Med. 314 (1): 20–6. doi:10.1056/NEJM198601023140104. PMID 3940312.