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Arenaviruses Follow-up

  • Author: Sandra G Gompf, MD, FACP, FIDSA; Chief Editor: Pranatharthi Haran Chandrasekar, MBBS, MD  more...
 
Updated: Oct 05, 2015
 

Deterrence/Prevention

Recognition of a case of Lassa fever or any of the South American Arenavirus infections is crucial from both infection control and epidemiologic standpoints. Suspected cases should be reported immediately to local public health authorities.

Rodent control

Unlike plague, in which a rodent die-off can cause an increased risk of a human outbreak, the rodents carrying arenaviruses do not become ill or shed the virus in their urine.

Aggressive rodent control (eg, trapping, rodent poisons) and avoidance of high-density rodent areas are the most important preventative maneuvers.

Procedures to avoid rodent droppings and exposure include properly disposing of trash and clutter, moving woodpiles away from residences, properly airing out cabins and buildings prior to reoccupation, and avoiding creating dust when cleaning buildings with signs of rodent infestation.

Nosocomial spread prevention

Person-to-person spread has been problematic within hospitals where Lassa fever is endemic

Patients should be placed in a single room with isolated negative-pressure airflow. Isolation should be continued until multiple blood or urine specimens are negative for the virus.

All tests with arenaviruses should be conducted in special laboratories with BSL4 containment.

Arenavirus vaccination

No commercially available vaccines are available to prevent Arenavirus infection in the United States.

In one study with Lassa virus, a recombinant vaccinia virus that expressed Lassa virus glycoprotein was found to be efficacious in primates.

Field trials with an attenuated Junin virus vaccine have shown an efficacy of 95% with minimal side effects. This vaccine also may be protective against Machupo virus because of cross-antigenicity but not against Guanarito or Sabia viruses.

Anecdotal information suggests that antigenically similar but nonpathogenic arenaviruses may be protective against Lassa fever in monkeys.

Management of contacts of imported cases of Lassa fever

Initially, imported cases of Lassa fever were treated with supportive care under conditions of total isolation. More recently, simple barrier nursing techniques have been found to be effective in preventing transmission to health care personnel. Guidelines have been developed to establish a level of risk for Lassa fever based on the degree of exposure to an index case. Similar criteria can be used for risk of exposure to South American hemorrhagic fever viruses.

High-risk: These activities include unprotected contact with index case body fluids or excreta (eg, mouth-to-mouth kissing; sharing food, liquids, or eating utensils; sexual intercourse[6] ; needle sticks). High-risk exposures usually precipitate ribavirin prophylaxis; closely monitor the contact for fever and/or illness and measure for seroconversion beginning on day 0 and on day 15.

Medium-risk: Activities that are medium-risk include unprotected contact with surfaces that probably were contaminated or possible unprotected contact with index case body fluid or excreta (eg, drawing blood or handling lab slides containing unfixed specimen, handling bed sheets or bed pans, or perceived skin or mucosal contact with the aerosolized respiratory secretions from an index case). Medium-risk exposures trigger public health officials to monitor exposure for 21 days after the last exposure. If a fever of 38.3°C or higher occurs, intravenous ribavirin should be given and diagnostic studies of Lassa virus obtained. If the fever is low grade, other criteria, such as aminotransferase levels, should be used to determine action.

Low-risk: These exposures include unprotected contact with the index case with little chance of exposure to body fluids/excreta (eg, examining index case without gloves or being within several feet of the case when a cough or sneeze occurs). Patients with low-risk exposures should be monitored for 21 days after the last exposure. If fever is higher than 38.3°C and aminotransferases are elevated, based on clinical judgment, further action (including hospitalization with or without ribavirin) may be indicated.

No risk: Such exposure includes proximity of the index case without direct contact to potentially contaminated objects (eg, brief visit to patient's room without contact or handling blood or secretions with gloves).

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Complications

LCM virus infection

CNS complications beyond aseptic meningitis include encephalitis and may involve cranial nerve palsies and/or damage to the autonomic nervous system. Hypoglycorrhachia can be found.

Non-CNS complications include orchitis, myocarditis, alopecia, and small-joint arthritis. These develop, if at all, late in the illness, during the recurrence of fever.

Intrauterine infection with LCM virus has been described. Infection may manifest as hydrocephalus and/or chorioretinitis with persistent spastic pareses and death within several years.

Lassa fever

Eighth-nerve deafness, which can be bilateral and thought to be immune-mediated, is observed in as many as one third of patients. Recovery of hearing occurs in approximately 50% of patients, but the deafness can be permanent.

Maternal and fetal losses during Lassa fever infection are substantial. Maternal mortality rates can approach 30% and may be reduced with abortion. Fetal loss rates are close to 90% and are not affected by the trimester of infection.

Cerebellar ataxia, pericarditis, orchitis, and uveitis may be observed.

Renal or hepatic failure is generally not observed.

South American hemorrhagic fevers

In addition to severe hemorrhagic or CNS complications, convalescence in survivors can be quite prolonged, with weight loss, hair loss, and autonomic instability.

As with Lassa fever, South American hemorrhagic fevers have substantial effects on the developing fetus.

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Prognosis

LCM virus infection

Survival with recovery from LCM virus infection is the rule.

Lassa fever

Hemorrhagic features are mild and rarely of prognostic significance.

Risk factors for increased mortality are facial and/or neck edema, elevated aminotransferases, and increased viremia. With these in combination, the mortality rate can be higher than 80%.

South American hemorrhagic fevers

Mortality rates can be higher than 30%.

Risk factors for mortality include a pronounced bleeding diathesis, severe neurologic deterioration, and shock.

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Contributor Information and Disclosures
Author

Sandra G Gompf, MD, FACP, FIDSA Associate Professor of Infectious Diseases and International Medicine, University of South Florida College of Medicine; Chief, Infectious Diseases Section, Director, Occupational Health and Infection Control Programs, James A Haley Veterans Hospital

Sandra G Gompf, MD, FACP, FIDSA is a member of the following medical societies: American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Coauthor(s)

Kevin M Smith, MD Fellow in Infectious Disease and International Medicine, University of South Florida College of Medicine

Kevin M Smith, MD is a member of the following medical societies: American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Ulyee Choe, DO Fellow, Department of Infectious Diseases, University of South Florida College of Medicine

Ulyee Choe, DO is a member of the following medical societies: American College of Physicians, American Osteopathic Association, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Joseph F John, Jr, MD, FACP, FIDSA, FSHEA Clinical Professor of Medicine, Molecular Genetics and Microbiology, Medical University of South Carolina College of Medicine; Associate Chief of Staff for Education, Ralph H Johnson Veterans Affairs Medical Center

Joseph F John, Jr, MD, FACP, FIDSA, FSHEA is a member of the following medical societies: Charleston County Medical Association, Infectious Diseases Society of America, South Carolina Infectious Diseases Society

Disclosure: Nothing to disclose.

Chief Editor

Pranatharthi Haran Chandrasekar, MBBS, MD Professor, Chief of Infectious Disease, Program Director of Infectious Disease Fellowship, Department of Internal Medicine, Wayne State University School of Medicine

Pranatharthi Haran Chandrasekar, MBBS, MD is a member of the following medical societies: American College of Physicians, American Society for Microbiology, International Immunocompromised Host Society, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Additional Contributors

Daniel R Lucey, MD, MPH, MD, MPH 

Daniel R Lucey, MD, MPH, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author Larry I Lutwick, MD, to the development and writing of this article.

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