may cause Guillain-Barre syndrome, a disorder in which the
body's immune system attacks part
of the nervous system, new research
suggests. Blood samples from 42 patients
diagnosed with Guillain-Barre
syndrome during a Zika virus
outbreak in French Polynesia provide
the first hard evidence that the
mosquito-borne Zika virus might cause this severe neurological
disorder, researchers said. "The risk for a Zika-infected
individual of developing Guillain-Barre
syndrome is small -- less than [one]
case per 1,000 Zika infections. So,
individuals with acute Zika infection
should not be greatly alarmed by the fear of developing of Guillain-Barre
syndrome," said researcher Dr. Hugh
Willison. He's a professor of
neurology at the University of
Glasgow College of Medical,
Veterinary and Life Sciences in Scotland. The study can't prove cause-and-
effect, but as Zika cases increase,
health officials need to plan to deal
with the rise in cases of Guillain-
Barre syndrome as well, he said. Zika virus infections in pregnant
women have been linked to a birth
defect called microcephaly, a
condition in which the brain and skull
are significantly underdeveloped.
Since the Zika epidemic began last spring, it's believed there have been
more than 5,600 suspected or
confirmed cases of microcephaly in
Brazil, the World Health Organization
reported Friday. "Since Zika infection may affect
millions of persons, there will be a
surge of Guillain-Barre syndrome
cases for health services to cope
with, even though the risk is small,"
Willison added. Despite the new findings, one expert
said "it is difficult to conclusively
prove Zika virus infection in all of
these patients, because many also
had been infected with the closely
related dengue virus, which is common in French Polynesia. And
interpretation of the antibody tests
was difficult," said David Smith, a
clinical professor at the University of
Western Australia in Perth. "We need to look closely at future
cases of Guillain-Barre syndrome
occurring in Zika-affected areas to
gather more data so we can better
estimate the risk," Smith said. Guillain-Barre syndrome was
uncommon in this study -- less than
0.1 percent of the people estimated
to be infected with Zika virus -- and
may turn out to be rarer than that,
said Smith, who co-authored an accompanying journal editorial. "Zika virus is very likely to be able to
trigger Guillain-Barre syndrome, but
we don't yet know exactly how low
that risk is," he said. "This does not
alter the advice about the precautions
people should take to avoid mosquito exposure when traveling to Zika-
affected areas." The report was published in the Feb.
29 online edition of The Lancet. From October 2013 to April 2014,
French Polynesia experienced the
largest Zika outbreak reported to
date. About 32,000 people saw a
doctor about a Zika virus infection. Guillain-Barre syndrome is the
leading cause of non-trauma
paralysis, according to the study
authors. Symptoms develop quickly
and include weakness in the legs and
arms, muscle weakness and pain, the U.S. National Institute of
Neurological Disorders and Stroke
says. The syndrome is usually triggered by
an infection, such as herpes,
influenza or dengue fever, the
researchers said. To see if there was a link between
Guillain-Barre syndrome and Zika,
researchers compared three groups
of patients. One group had 42
patients with Guillain-Barre
syndrome. Another group had 98 patients who were in the same
hospital but didn't have a fever (the
"control" group). And the third group
had 70 patients diagnosed with Zika
infection but who didn't have Guillain-
Barre syndrome. Most patients with Guillain-Barre
syndrome (88 percent) reported
symptoms of Zika about six days
before neurological symptoms
appeared, the study found. The most
common symptoms of Zika include fever, rash, joint pain, or
conjunctivitis ("pink eye"). Blood tests showed that 100 percent
of the people with Guillain-Barre
syndrome showed a specific immune
system response for Zika. By
comparison, just 56 percent of those
in the control group with the non- fever illness showed this response,
the study said. Most people with Guillain-Barre
syndrome -- 95 percent -- also had
signs of past dengue infection. A
majority of patients in the other two
groups also showed signs of past
dengue infection. Dengue is another mosquito-borne illness and it's
endemic to the area, the study
authors noted. They added that past
infection with dengue didn't increase
the risk of Guillain-Barre syndrome
among patients with Zika. All of the Guillain-Barre syndrome
patients likely had a type of the
disorder called acute motor axonal
neuropathy, the study authors said.
In addition, those with Zika-related
Guillain-Barre syndrome recovered faster than is expected. Among the patients with Guillain-
Barre syndrome, 16 were admitted to
the intensive care unit, and 12
needed breathing assistance.
Patients were hospitalized for about
11 days, but those in intensive care remained for an average of 51 days,
the study found. Three months after
leaving the hospital, 57 percent of the
patients were able to walk without
assistance. None of the patients died,
the investigators reported. Based on the experience in French
Polynesia, Willison estimates that the
risk of Guillain-Barre syndrome in the
general population during the
outbreak in French Polynesia was
0.24 per 1,000 Zika virus infections. That works out to 24 people per
100,000 infections, according to
Willison. "Public health officials, neurologists
and critical care and emergency
medicine specialists need to be alert
to the likely rise in Guillain-Barre
syndrome cases that will occur in
other parts of the world that are currently going through epidemics of
acute Zika infection," Willison said. Since it first surfaced last spring, the
virus has spread to over 34 countries
and territories in Latin America and
the Caribbean. The World Health
Organization now estimates there
could be up to 4 million cases of Zika in the Americas in the next year. SOURCES: Hugh Willison, M.D.,
professor, neurology, University of
Glasgow College of Medical,
Veterinary and Life Sciences,
Institute of Infection, Immunity and
Inflammation, U.K.; David Smith, clinical professor, School of
Pathology and Laboratory Medicine,
University of Western Australia,
Perth; Feb. 29, 2016, The Lancet, online
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