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On May 26, this report was posted as an MMWR
Dispatch on the MMWR website (http://www.cdc.gov/mmwr).
On May 3, 2005, CDC received a report of severe illness in four patients
who had received solid organ transplants from a common donor. All four organ
recipients subsequently were found to have evidence of infection with lymphocytic
choriomeningitis virus (LCMV), a rodent-borne Old World arenavirus. Preliminary
findings from the ensuing investigation indicate the source of infection likely
was an infected hamster in the donor’s home. This report summarizes
the ongoing investigation and provides information on exposure risks and possible
In early April, in Rhode Island, a woman with a medical history remarkable
only for hypertension and 1 week of headache had sudden onset of hemiplegia
caused by a stroke, followed by brainstem herniation and brain death within
3 days. A thorough evaluation was not suggestive of infection.
Family members of the woman consented to donation; organs and tissues
were recovered, including the liver, the lungs, both kidneys, both corneas,
and skin. Within 3 weeks after transplantation, the four persons who received
the liver, lungs, and two kidneys had abnormalities of liver function and
blood coagulation, and dysfunction of the transplanted organ. Signs, symptoms,
and clinical laboratory test results varied in these patients and included
fever, localized rash, diarrhea, hyponatremia, thrombocytopenia, hypoxia,
and kidney failure. Three of the four organ recipients died, 23-27 days after
transplantation. The fourth patient, a kidney recipient, survived. Histopathologic
findings varied in the four cases, but hepatocellular necrosis was common
to all three decedents on autopsy. The two cornea recipients were asymptomatic.
Skin was not transplanted.
When the cause of illness among the recipients was not identified through
extensive diagnostic testing and suspicion of transplant-transmitted infection
arose, tissue and blood samples from the donor and recipients were sent from
the Rhode Island Department of Health and the Massachusetts Department of
Public Health to CDC. LCMV was identified as the cause of illness in all four
organ recipients; diagnosis was made in tissues from multiple organs through
immunohistochemical staining, reverse transcriptase-polymerase chain reaction
(RT-PCR), enzyme-linked immunosorbent assays (i.e., IgM capture and indirect
IgG), and viral culture on Vero E6 cells. Sequencing of the virus genome confirmed
its identity as LCMV. Based on the diagnosis of LCMV infection, the surviving
kidney transplant recipient was treated with intravenous ribavirin and reduction
in his immunosuppressive drug regimen; the patient improved clinically.
To determine the source of LCMV infection, investigations were conducted
at the hospitals involved in organ recovery and transplantation and at the
coordinating organ procurement organization. Interviews also were conducted
at locations where the donor had spent substantial time in the month preceding
Interviews with hospital and organ bank staff members revealed no likely
sources of LCMV infection in the hospital or organ-recovery settings. Environmental
assessment at locations the donor frequented (e.g., home and work) revealed
limited opportunities for exposure to wild rodents; the sole location noted
with rodent infestation was a garden shed at her home. Interviews with family
members of the donor determined that a pet hamster had been acquired recently.
The hamster was cared for primarily by another family member. No illnesses
compatible with LCMV had been reported in the donor or family members during
the month preceding the donor’s death. Further investigation of the
source of infection, including rodent traceback, is ongoing.
Family members of the donor were tested for LCMV antibodies. The family
member who cared for the hamster had specific IgM and IgG antibodies to LCMV.
No other family member had detectable IgG or IgM antibodies to LCMV. All available
donor tissues were tested, and no evidence of LCMV was determined by serology,
immunohistochemistry, RT-PCR, or viral culture. However, the pet hamster was
determined positive for LCMV by virus isolation, RT-PCR, and immunohistochemistry.
Genetic sequencing to enable comparison of patient and rodent virus isolates
Rhode Island Hospital, Providence; Rhode Island Dept of Health. New
England Organ Bank, Newton; Massachusetts General Hospital, Brigham and Women’s
Hospital, Boston; Massachusetts Dept of Public Health. Infectious Disease
Pathology Activity, Special Pathogens Br, Div of Viral and Rickettsial Diseases,
Div of Healthcare Quality Promotion, National Center for Infectious Diseases;
EIS officers, CDC.
LCMV infection usually is either asymptomatic or causes mild self-limited
illness in otherwise healthy persons. LCMV can cause aseptic meningitis, but
the infection is rarely fatal.1 Infection during pregnancy can
result in vertical transmission of the virus from mother to fetus; LCMV infection
during the first or second trimesters can lead to severe illness in the fetus.2 Serologic studies conducted in urban areas of the United States have
indicated that prevalence of LCMV infection among humans is approximately
5%.3,4 The house mouse (Mus musculus)
is the primary reservoir for LCMV, with a prevalence of infection of 3%-40%;
a high degree of focality often is noted.3,5,6 However, other types
of rodents (e.g., hamsters or guinea pigs) can be infected after contact with
infected house mice7; these rodents also have been implicated in
human infection. Animals can become ill or can be asymptomatic. Infection
in humans occurs primarily through exposure to secretions or excretions of
Human-to-human transmission of LCMV has not been reported, with the
exception of vertical transmission from an infected mother to fetus.2 A large outbreak associated with pet hamsters sold by a single distributor
was reported in 1975, when 181 symptomatic cases among persons with hamster
contact were identified in 12 states; no deaths occurred.9 In 2003,
a cluster of solid organ transplant-associated meningoencephalitis deaths
in Wisconsin was investigated and determined to be associated with LCMV infection.
In that investigation, testing of donor tissues did not reveal any evidence
of infection,10 and no exposures to rodents were found. Acute LCMV
infection in an organ donor is thought to be a rare event.
In the case described in this report, neither the donor nor the infected
family member had illness characteristic of LCMV infection. In the organ recipients,
transplantation of LCMV-infected organs in the setting of immunosuppression
likely increased disease severity. Although most persons infected with LCMV
do not exhibit symptoms and the risk for LCMV infection from pet rodents is
considered low, persons (especially pregnant women) should be aware of the
possible risks associated with LCMV infection. Persons can minimize risk of
LCMV infection from pet rodents by being attentive to proper hand hygiene
and environmental cleaning. Additional information on handling pet rodents
is available at http://www.cdc.gov/healthypets/animals/pocket_pets.htm. Additional information on LCMV is available at http://www.cdc.gov/ncidod/dvrd/spb/mnpages/dispages/lcmv.htm.
Health-care providers should be aware that LCMV can be transmitted through
organ transplantation. Any unexpected infectious syndromes in recipients after
solid organ or tissue transplantation should trigger concern about the possibility
of transplant-associated transmission of an infectious agent. Although such
instances are rare, providers should alert the associated organ procurement
organization, tissue bank, and public health authorities when such events
are suspected. The lifesaving benefits from transplanted organs outweigh the
potential risk for unidentified infectious diseases; opportunities to increase
donation should be encouraged.
REFERENCES: 10 available
Lymphocytic Choriomeningitis Virus Infection in Organ Transplant Recipients—Massachusetts,
Rhode Island, 2005. JAMA. 2005;294(2):173–174. doi:10.1001/jama.294.2.173
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