Cingles Info

Sparse Lessons from Clusters of Fatal Virus in Transplants
By Jeff Minerd, MedPage Today Staff Writer
Reviewed by Rubeen K. Israni, M.D., Fellow, Renal-Electrolyte and Hypertension
Division, University of Pennsylvania School of Medicine
May 25, 2006
ATLANTA, May 25 - In December 2003, four organ transplant recipients developed
fever, abdominal pain, diarrhea, altered mental states, seizures, and multiple
organ failures. All four patients had received grafts from the same donor, and
all died.
In April 2005, the same illness struck four more transplant patients with a
single donor in common. This time, one of the patients-whose immunosuppressive
regimen had been stepped down and who had received antiviral
medication-survived.
Today, the cause of these mysterious deaths was reported to be lymphocytic
choriomeningitis virus (LCMV), a usually benign virus harbored by rodents,
according to Matthew J. Kuehnert, M.D., of the CDC, and more than half-a-dozen
fellow researchers from across the country.
The virus affected the transplant patients so virulently and fatally because of
their immunosuppressed state, Dr. Kuehnert and colleagues said in the May 25
issue of the New England Journal of Medicine.
An investigation of the two clusters of deaths revealed that, in each, every
organ recipient was infected with the same unique strain of LCMV. Though the
virus was never isolated from either donor, the donor in the 2005 cluster had a
pet hamster infected with the same viral strain that killed the patients who
received her organs.
"The coincidence in timing and the phylogenetic matching of the strains within
each cluster leave little doubt about the interpretation," said C.J. Peters,
M.D., of the University of Texas Medical Branch, Galveston, in an accompanying
editorial.
About 5% of U.S. adults have antibodies to LCMV, the investigators said. Humans
become infected with the usually harmless virus by direct contact with rodents
or by aerosolized droplets of their urine or feces. The common house mouse is
the most usual source of infection, but pet hamsters and lab rats can also
transmit the virus to humans, they said.
There are little data on how a physician should respond when confronted with a
virulent LCMV infection in a transplant patient, the investigators said.
However, the experience with the one patient in the current report who survived
suggests that stepping down the patient's immunosuppressive drug regimen and
adding an antiviral such as Rebetol (ribavirin) may be helpful, they said.
As far as preventing future LCMV infections in transplant patients, there aren't
many good options, the authors said. Screening potential donors before their
organs are harvested would use up precious time, and no currently available
assay is fast or sensitive enough for the job, they said.
Similarly, "the determination of a history of ownership of a pet rodent is
neither sensitive nor specific to LCMV infection," Dr. Peters said in the
editorial.
"One obvious way to reduce the risk of human infection with LCMV is to have
suppliers of pet rodents screen their colonies for the infection," Dr. Peters
suggested. By reducing infection of pet owners, this measure would in turn
reduce the risk to transplant patients, Dr. Peters argued.
"Such screening seems justified," Dr. Peters said, "given the serious nature of
LCMV disease and the particular risk to fetuses: LCMV infection in pregnant
women is an increasingly recognized cause of hydrocephalus, mental retardation,
and chorioretinitis in newborns."
http://www.medpagetoday.com/Surgery/GeneralSurgery/tb/3408