Since the outbreak of the Zika virus in South America last year…

By Global Medical Advisory Board Chairman Dr. Ken Gorson

There has been an enormous amount of information about the neurological complications associated with Zika infection which has been disseminated to the public by media outlets, research publications, recommendations from the Centers for Disease Control (CDC) and National Institutes of Health (NIH,) web postings and press releases from various organizations, including the GBS|CIDP Foundation International. We would like to place this information in proper context and clarify the current understanding of the relationship between Zika virus and GBS.
The Zika virus was first discovered in a Rhesus monkey in Uganda in 1947. The first human infection was reported in 1954 in Nigeria, and during the subsequent 60 years there have been only a handful of human cases reported; there was little attention paid to the virus because human infection was so rare and symptoms were mild and resolved without complications. During this time, the virus spread eastward to other countries in Africa and Southeast Asia, with the first major outbreak in 2007 in the Yap State of the Federated States of Micronesia (an island in the South Pacific.) There were approximately 900 cases reported, but only 19% had clinical symptoms of the infection (discussed below.) There were no neurological complications reported.

The next Zika outbreak occurred in French Polynesia in 2013, followed by smaller outbreaks in other South Pacific islands. It was during the French Polynesia outbreak that a relationship between Zika infection and GBS was first reported. In 2015, the Zika virus was detected in Brazil,
and since then the virus has spread rapidly through South and Central America, Mexico, and many islands of the Caribbean, reaching epidemic proportions, most recently in Puerto Rico. The virus has spread north to the continental United States, and as of August, 2016, there have been 29 mosquito-transmitted infections, thus far limited to the state of Florida.
Zika virus is transmitted most commonly by the bite of the Aedes Aegypti mosquito. This mosquito is very common throughout South and Central America, the Caribbean, and the lower half of the continental United States, and explains the spread of the virus north from the southern hemisphere. Currently, 70 countries have reported Zika virus infection. This mosquito primarily feeds on humans, bites during the day and night, may bite multiple people during a single meal, where the bite is often imperceptible. The mosquito reproduces in free standing
water, and may lay eggs in as little as a bottle cap of water. This, in part, explains the rapid rise in Zika infection in countries of South and Central America, where free standing water is common, combined with densely populated areas without access to screens and air conditioning (which reduce mosquito transmission.) Once an infected mosquito transmits the virus to a person, a subsequent bite of that person from another, non-infected mosquito, can infect that mosquito, which then spreads the virus with further mosquito bites to other people. This explains how people within the same family or neighborhood can become infected quickly.

Lastly, there are many “travel-related” cases. These are individuals who have traveled to regions where the virus is common (so called endemic areas,) who became infected, returned to the United States, and then developed symptoms of the infection (where non-infected mosquitoes also may bite them and spread the virus.) As of this report, there have been 2,487 travel-related cases in the United States, and 8,968 in US territories (mostly in Puerto Rico.) The virus also may be spread from a pregnant woman to the fetus and by sexual transmission, and there have
been single reports of the virus spread through platelet transfusion. During the French Polynesia epidemic, 3% of donated blood screened positive for the virus, and all US blood banks are required to screen for the virus. The symptoms of Zika virus infection can be similar to other viral infections like the flu. Symptoms are acute in onset but generally mild, and include fever, joint and muscle aches and pains, rash, malaise (an ill feeling,) headache, and conjunctivitis (pinkeye.) The symptoms resolve uneventfully, usually within a few days to a week. The diagnosis is established by blood testing that detects viral RNA or acute antibodies directed against the virus. There is no specific anti-viral treatment. Symptoms are usually managed with rest, increased fluid intake, and acetaminophen or other over the counter analgesics to treat fever and pain. Only 20% of infected individuals have symptoms of acute viral infection. The remainder do not know they have been infected, which has particular importance to women who
are pregnant or actively planning to become pregnant, as they can unknowingly spread the virus to their unborn child. It is the potential catastrophic neurological complications that follow Zika infection that have made international headlines. It is now well-established that the virus has

a particular attraction to nerve cells in the brain of the developing fetus and to peripheral nerves in adults; it is therefore considered a “neurotropic” virus. There are severe neurological complications that can occur to the developing fetus following exposure to the virus. As of August, 2016, an increased incidence of GBS or laboratory confirmation of GBS following Zika infection has been reported in 16 countries. There have been only 7 cases of GBS in the continental US, and 26 cases in US territories. What does this mean for you? First, although the risk of developing GBS after Zika infection is higher than the background rate in the general population, the risk is still very low: approximately 1 in 4000 (at least in the French Polynesian population,) and perhaps even lower if the rate is closer to what has been reported in Brazil and Columbia. Second, GBS has not been linked to asymptomatic Zika virus infection, which represents 80% of all infections. Third, in contrast to densely populated regions in South and Central America, public health experts believe the risk of Zika infection reaching epidemic proportions in the continental United States is low, as it is more likely that there will be
small, isolated outbreaks, and thus the chance of developing GBS is even further reduced. Fourth, there have been no reports of Zika-related GBS in patients who have had GBS in the past (or CIDP and other immune neuropathies,) or Zika infection worsening residual neuropathic symptoms in patients who have had GBS. Finally, there currently are no published data regarding treatment response or prognosis in patients with Zika-related GBS, but there is no reason to believe that response to therapy and recovery should be substantially different from non-Zika related cases.

There are several measures that reduce the risk of Zika infection by mosquito transmission. The CDC has recommended routine application of mosquito repellant (containing DEET or other effective agents,) wearing long-sleeve shirts and pants, removing items around the home that may hold water and serve as a breeding ground for mosquitoes, using screens on windows and doors, and air conditioning when available. Pregnant women, or those planning to become pregnant, should follow recommendations from the CDC website to further reduce
their risk of exposure.
Vaccine development against the Zika virus is underway and looks promising, but due to lack of funding from Congress, this critical research may be delayed or even halted. In addition, despite specific recommendations from the World Health Organization, there are no formal surveillance and monitoring systems in place to ascertain the nature and frequency of Zika-related GBS in the United States. We strongly suggest that you contact your congressmen to encourage him or her to urgently allocate appropriate funding for these activities.

For additional information, please contact Lisa Butler,
Executive Director, 610-667-0131, lisa.butler@gbs-cidp.org

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