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==Overview==
==Overview==
Lassa fever is an [[acute]] [[viral hemorrhagic fever]] first described in 1969 in the town of Lassa, Nigeria, located in the Yedseram river valley.<ref>{{cite journal |author=Frame JD, Baldwin JM, Gocke DJ, Troup JM |title=Lassa fever, a new virus disease of man from West Africa. I. Clinical description and pathological findings |journal=Am. J. Trop. Med. Hyg. |volume=19 |issue=4 |pages=670-6 |year=1970 |pmid=4246571 |url=http://www.ajtmh.org/cgi/content/abstract/19/4/670}}</ref> The virus, a member of the [[virus]] family [[Arenaviridae]], is a single-stranded [[RNA virus]] and is [[zoonotic]], or animal-borne. Clinical cases of the disease had been known for over a decade earlier but not connected with this viral [[pathogen]]. The infection is [[endemic (epidemiology)|endemic]] in West African countries, and causes 300-500,000 cases annually with ~5,000 deaths.<ref name=Ogbu_2007>{{cite journal |author=Ogbu O, Ajuluchukwu E, Uneke CJ |title=Lassa fever in West African sub-region: an overview |journal=Journal of vector borne diseases |volume=44 |issue=1 |pages=1-11 |year=2007 |pmid=17378212 |doi=}}</ref> [[Outbreak]]s of the disease have been observed in Nigeria, Liberia, Sierra Leone, Guinea, and the, Central African Republic, but it is believed that human [[infection]]s also exist in Democratic Republic of the Congo, Mali, and Senegal.
Lassa fever is an [[acute]] [[viral hemorrhagic fever]] caused by Lassa virus, a zoonotic, single-stranded [[RNA virus]] that is transmitted to humans by the ''Mastomys natalensis'' rodent. Lassa fever is [[endemic (epidemiology)|endemic]] to West Africa with an annual incidence of 300,000 to 500,000 cases and a case fatality rate of approximately 5%-15%.<ref name=Ogbu_2007>{{cite journal |author=Ogbu O, Ajuluchukwu E, Uneke CJ |title=Lassa fever in West African sub-region: an overview |journal=Journal of vector borne diseases |volume=44 |issue=1 |pages=1-11 |year=2007 |pmid=17378212 |doi=}}</ref> Risk factors in the development of 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. However, clinical manifestations may progress, and patients may experience [[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 antiviral therapy with [[ribavirin]]. Ribavirin has been demonstrated to be most effective when administered intravenously early in the course of the disease (optimal efficacy when administered early within the first 6 days of symptom-onset).<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, patients should receive supportive care to adequately maintain respiratory status and [[fluid]] and [[electrolyte]] balance. While there is no vaccine against Lassa fever, avoiding infected individuals or rodents and proper handling of infected waste products are recommended for the primary prevention of Lassa fever.
Lassa fever is also the most common [[hemorrhagic fever]] that is exported beyond its endemic area to countries like the United States, the United Kingdom of Great Britain and Northern Ireland, the Netherlands, Japan, and Israel. While Lassa fever is mild or has no observable [[symptom]]s in about 80% of people infected with the virus, the remaining 20% have a severe multisystem disease. Lassa fever is also associated with occasional [[epidemic]]s, during which the [[case fatality rate]] can reach 50%.
 
==Historical Perspective==
==Historical Perspective==
The illness was discovered in 1969 when two missionary [[nurse]]s died in Nigeria, West Africa. The cause of the illness was found to be Lassa virus, named after the town in Nigeria where the first cases originated.
The first case of documented Lassa fever was reported in 1969 following the death of 2 nurses in Lassa, Nigeria.
 
==Pathophysiology==
==Pathophysiology==
Lassa virus is [[zoonosis|zoonotic]] ([[transmission|transmitted]] from animals). The [[natural reservoir|reservoir]], or [[definitive host|host]], of Lassa virus is a rodent known as the "multimammate rat" of the [[genus]] Mastomys. It is not certain which [[species]] of Mastomys are associated with Lassa; however, at least two species carry the virus in Sierra Leone. Mastomys [[rodent]]s breed very frequently, produce large numbers of [[offspring]], and are numerous in the savannas and forests of West, Central, and East Africa. In addition, Mastomys generally readily colonize human homes. All these factors together contribute to the relatively efficient spread of Lassa virus from infected rodents to humans.
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==
==Causes==
Lassa fever is caused by the ''Lassa virus'', a member of the [[Arenaviridae]] family; it is an [[enveloped virus|enveloped]], single-stranded, bisegmented [[RNA]] virus. [[viral replication|Replication]] for Lassa virus is very rapid, while also demonstrating temporal control in replication.  There are two [[genome]] segments.  The first step involved is making [[messenger RNA|mRNA]] copies of the negative-sense [[genome]].  This ensures that there are adequate [[protein]]s, which are required for [[replication]].  The N and L proteins are made from the mRNA produced.  The -ve sense genome then makes vcRNA (viral circular RNA) copies of itself which are positive-sense.  The vcRNA is a [[template strand|template]] for producing -ve sense progeny but mRNA is also synthesized from it.  The mRNA synthesized from vcRNA [[translation (biology)|translates]] the [[G proteins|G (spike) proteins]] and Z proteins.  Thus, with this temporal control, the spike proteins are produced last, making the infection further undetected by the [[host (biology)|host]] [[immune system]].
Lassa fever is caused by the [[Lassa virus]], a member of the zoonotic [[Arenaviridae]] family. It is an [[enveloped virus|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==
==Differentiating Lassa fever from other Diseases==
Clinically, Lassa fever [[infection]]s are difficult to distinguish from other [[viral hemorrhagic fever]]s such as [[Ebola]] and [[Marburg virus|Marburg]], and from more common [[febrile]] illnesses such as [[malaria]].
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.<ref name=CDC>{{cite web | title = The Centers for Disease Control and Prevention facts sheets | url =http://www.cdc.gov/vhf/lassa/pdf/factsheet.pdf }}</ref> 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==
Individuals at risk are those who live or visit areas with a high [[population]] of Mastomys rodents infected with Lassa virus or are exposed to infected humans. Hospital staff are not at great risk for [[infection]] as long as protective measures are taken.
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==
==Natural History, Complications and Prognosis==
The most common [[complication]] of Lassa fever is [[deafness]]. Various degrees of deafness occur in approximately one-third of cases, and in many cases [[hearing loss]] is permanent. [[Spontaneous abortion]] is another serious complication. Approximately 15%-20% of patients hospitalized for Lassa fever die from the illness. However, overall only about 1% of [[infection]]s with Lassa virus result in death. The death rates are particularly high for women (greater than 80%) in the [[third trimester]] of [[pregnancy]], and for [[fetus]]es, about 95% of which die in the uterus of infected pregnant mothers.
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 pain|abdominal]]/[[chest pain]], [[pleural effusion|pleural]]/[[pericardial effusion|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 [[deafness|neurosensory deafness]] and [[hepatitis|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==
==Diagnosis==
==History and Symptoms==
===History and Symptoms===
Lassa fever after an [[incubation period]] of six to twenty-one days, an acute illness with [[multiorgan]] involvement develops [[gastrointestinal]], neurological and [[pulmonary]] 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]], [[seizure]]s, and [[coma]].
==Physical Examination==
 
Lassa fever is commonly associated with [[fever]] on physical examination at admission. At advanced stages of the disease, physical examination findings are more pertinent and often include unstable vital signs, such as [[tachycardia]] or relative [[bradycardia]], [[hypotension]], and [[tachypnea]]. Physical examination may also be remarkable for [[abdominal tenderness]] and distension and neurological impairment.
===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 tenderness|abdominal]]/chest tenderness, [[pharyngitis]] with tonsillar exudates, and [[hepatosplenomegaly]].
 
===Laboratory Findings===
===Laboratory Findings===
There is a range of [[laboratory]] investigations that are performed to diagnose the disease and assess its course and [[complication]]s. [[ELISA test]] for [[antigen]] and [[IgM]] [[antibodies]] gives 88% [[sensitivity]] and 90% [[specificity]] for the presence of the infection. Other laboratory findings in Lassa fever include [[lymphopenia]] ([[low white blood cell counts]]),  [[thrombocytopenia]] (low [[platelet]]s), and elevated [[aspartate aminotransferase]] ([[AST]]) levels in the blood. Lassa fever can also be found in [[cerebrospinal fluid]]. The virus itself may be cultured in 7 to 10 days. [[Immunohistochemistry]] performed on tissue specimens can be used to make a [[post mortem]] diagnosis. The virus can also be detected by [[reverse transcriptase polymerase chain reaction]] ([[RT-PCR]]); however, this method is primarily a research tool.<ref>Lassa Fever Encephalopathy: Lassa Virus in Cerebrospinal Fluid but Not in Serum
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.
Stephan Günther, Boye Weisner, Andreas Roth, Thomas Grewing, Marcel Asper, Christian Drosten, Petra Emmerich, Jochen Petersen, Martin Wilczek and Herbert Schmitz
 
The Journal of Infectious Diseases , Vol. 184, No. 3 (Aug. 1, 2001), pp. 345-349</ref> In West Africa, where Lassa is most prevalent, it is difficult for doctors to diagnose due to the absence of proper equipment to perform tests. <ref>{{cite journal|last=Mojeed|first=Momoh|title=Molecular Diagnostics For Lassa Fever At Irrua Specialist Teaching Hospital, Nigeria: Lessons Learnt From Two Years Of Laboratory Operation|journal=Plos Neglected Tropical Diseases|date=14 Nov. 2012.|accessdate=15 November 2012}}</ref> Research has been done in the last few year, by a team of specialists, in order to diagnose the Lassa fever on a [[molecular]] level.<ref>Ehichioya, Deborah U.; Asogun, Danny A.; Ehimuan, Jacqueline; Okokhere, Peter O.; Pahlmann, Meike; Ölschläger, Stephan; Becker-Ziaja, Beate; Günther, Stephan; Omilabu, Sunday A. Tropical Medicine & International Health. Aug2012, Vol. 17 Issue 8, p1001-1004. 4p. DOI: 10.1111/j.1365-3156.2012.03010.x. </ref>
===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==
==Treatment==
==Medical Therapy==
===Medical Therapy===
[[Ribavirin]], an antiviral drug, has been used with success in Lassa fever patients. It has been shown to be most effective when given early in the course of the illness. Patients should also receive supportive care consisting of maintenance of appropriate [[fluid]] and [[electrolyte]] balance, oxygenation and [[blood pressure]], as well as treatment of any other complicating [[infection]]s.
Management of Lassa fever includes supportive care and administration of intravenous (IV) [[ribavirin]]. Data on the efficacy of antiviral agents in Lassa fever are scarce. 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 [[transmission]] of the Lassa virus from its [[host]] to [[humans]] 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 [[nosocomial routes]] can be avoided by taking preventive precautions against contact with patient secretions and educating people comes under primary prevention.
===Primary Prevention===
===Future or Investigational Therapies===
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.
Researchers at the [[USAMRIID]] facility, where military [[biologist]]s study [[infectious disease]]s, have a promising [[vaccine]] candidate. They have developed a [[Virus#Replication|replication]]-competent [[vaccine]] against Lassa virus based on [[recombinant]] vesicular [[stomatitis]] [[Vesicular stomatitis virus|virus]] [[vector]]s expressing the Lassa virus [[glycoprotein]]. After a single [[Intramuscular|intramuscular injection]], test primates have survived lethal challenge, while showing no clinical [[symptom]]s.<ref>{{cite journal |author=Geisbert TW, Jones S, Fritz EA, ''et al'' |title=Development of a new vaccine for the prevention of Lassa fever |journal=PLoS Med. |volume=2 |issue=6 |pages=e183 |year=2005 |pmid=15971954 |doi=10.1371/journal.pmed.0020183}}</ref>
 
Siga Technologies is developing an [[antiviral drug]] that has been shown effective in treating experimentally infected guinea pigs. In a study conducted at the [[USAMRIID|U.S. Army Medical Research Institute of Infectious Diseases (USAMRIID)]], treatment with ST-193 once a day for 14 days resulted in significant reduction in [[mortality]] (71% of the animals survived at the low dose), whereas all untreated animals and those treated with [[ribavirin]] died within 20 days of the [[infection]].<ref>{{cite press release
| url = http://www.siga.com/press/051507.html
| title = SIGA Passes First Hurdle with Lassa Fever Antiviral ST-193}}</ref>
==References==
==References==
{{Reflist|2}}
{{Reflist|2}}
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Latest revision as of 18:08, 18 September 2017

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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 caused by Lassa virus, a zoonotic, single-stranded RNA virus that is transmitted to humans by the Mastomys natalensis rodent. Lassa fever is endemic to West Africa with an annual incidence of 300,000 to 500,000 cases and a case fatality rate of approximately 5%-15%.[1] Risk factors in the development of 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. However, clinical manifestations may progress, and patients may experience 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 antiviral therapy with ribavirin. Ribavirin has been demonstrated to be most effective when administered intravenously early in the course of the disease (optimal efficacy when administered early within the first 6 days of symptom-onset).[2] In addition to antiviral therapy, patients should receive supportive care to adequately maintain respiratory status and fluid and electrolyte balance. While there is no vaccine against 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.

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

Management of Lassa fever includes supportive care and administration of intravenous (IV) ribavirin. Data on the efficacy of antiviral agents in Lassa fever are scarce. 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.[2] 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

  1. 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.
  2. 2.0 2.1 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.
  3. "The Centers for Disease Control and Prevention facts sheets" (PDF).


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