Arenaviruses Follow-up

  • Author: Sandra G Gompf, MD, FACP, FIDSA; Chief Editor: Burke A Cunha, MD   more...
 
Updated: May 20, 2011
 

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 and 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 and 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, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Specialty Editor Board

Daniel R Lucey, MD, MPH  Chief, Fellowship Program Director, Department of Internal Medicine, Division of Infectious Diseases, Washington Hospital Center; Professor, Department of Internal Medicine, Uniformed Services University of the Health Sciences

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

Disclosure: Nothing to disclose.

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

Disclosure: eMedicine Salary Employment

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

Disclosure: Nothing to disclose.

Eleftherios Mylonakis, MD  Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital

Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Chief Editor

Burke A Cunha, MD  Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital

Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

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