The Games of the XXXI Olympiad were held in Rio de Janeiro, Brazil. As a beautiful, cultural location, Brazil initially seemed as the perfect venue for the Summer Olympics. Unfortunately, as the games approached many nations became wary for the safety of their athletes if they were to attend these games. This was in part due to the fact that the World Health Organization (WHO) had declared a public health emergency related to the Zika Virus (ZIKV) previously that year, and Brazil was the country with the highest number of ZIKV-positive cases in Latin America (World Health Organization, 2016; Slavov et al., 2016). Since ZIKV is known to be an arboviral infection, visitors who contracted the infection would likely be bringing this virus back to their home nations (Slavov et al., 2016). This would be especially problematic for developing nations that were not equipped or prepared to deal with extensive outbreaks (Slavov et al., 2016).
In general, the biggest issues associated with ZIKV are not from the disease itself, but rather from secondary conditions that have been linked to it (Slavov et al., 2016). One such example is the Guillain-Barré Syndrome. The Guillain-Barré Syndrome (GBS) is an autoimmune disease in which the immune system attacks the peripheral nervous system (PNS) (NINDS, 2011). The cause of this disease is still unknown although it has been linked to bacterial or viral infections such as Campylobacter jejuni found in contaminated poultry or water, Dengue fever, and the Zika virus (Ho and Ho, 2016). In fact, GBS is called a syndrome rather than a disease because it is unclear whether a specific disease-causing agent is involved (Ho and Ho, 2016). Generally speaking, GBS is rare with only 6-40 cases per 1 million people. With the spread of the ZIKV virus, it has become more prevalent (NINDS, 2011), despite the fact that not everyone who is infected with ZIKV will develop GBS (CDC, 2016).
There are many different forms of GBS, all of which are classified depending on the part of the PNS that is involved in the condition (Genetics Home Reference, 2016). The most common form of GBS is Acute Inflammatory Demyelinating Polyradiculoneuropathy (AIDP) (Genetics Home Reference, 2016). As the name suggests, AIDP targets the myelin of neurons and degrades it. This demyelination can pose as a serious problem affecting the speed at which neurons travel.
Most neurons in the PNS are covered with Schwann cells which make up the myelin sheath of neurons (Nicholls et al., 2012). Myelin makes neurons more efficient by increasing the speed at which nerve signals are transmitted. Myelin thickens the walls of the neurons, decreasing the capacitance on the outside of the neuron (Equation 1- the relationship between the capacitance (C), the area (A) and the distance (d) is depicted). This decreased capacitance prevents charge from building up inside the neuron and hence the nerve impulse will better propagate down the axon.
Equation 1
When axons are demyelinated, the efficiency of neurons is compromised. In the AIDP demyelination process, both the cellular and the humoral immune system are seen to play a role (Ramachandran, 2016). Using electron microscopy, macrophages have been observed to remove the myelin sheath off of neurons (Ramachandran, 2016). It is very likely that humoral molecules (such as antimyelin antibodies) contribute to this process by directing the macrophages to the Schwann cells (Ramachandran, 2016). This damage to the myelin sheath results in segmental demyelination (figure 1), which increases the capacitance and results in a slower and less efficient nerve impulse.
As of now, there is no cure to GBS (Slavov et al., 2016). However, there are a number of treatments that have been seen to improve patient prognosis, including immunotherapy and supportive care (Ho and Ho, 2016). There are many studies being done regarding both ZIKV and GBS in order to try to stop the spread ZIKV and further improve the prognosis of GBS patients (Hughes and Cornblath, 2005).
Work Cited
CDC. (2016). Zika and Guillain-Barré Syndrome. [online] Available at: http://www.cdc.gov/zika/healtheffects/gbs-qa.html [Accessed 6 Nov. 2016].
Genetics Home Reference. (2016). Guillain-Barré syndrome. [online] Available at: https://ghr.nlm.nih.gov/condition/guillain-barre-syndrome#sourcesforpage [Accessed 5 Nov. 2016].
Ho, G. and Ho, M. (2016). Undergraduate Science Case Competition. 1st ed. SCINAPSE.
Hughes, R. and Cornblath, D. (2005). Guillain-Barré syndrome. The Lancet, 366(9497), pp.1653-66.
Nicholls, J., Martin, A., Fuchs, P., Brown, D., Diamond, M. and Weisblat, D. (2012). From neuron to brain. 5th ed. Sunderland, Mass.: Sinauer Associates, Inc.
NINDS. (2011). Guillain-Barré Syndrome Fact Sheet. [online] Available at: http://www.ninds.nih.gov/disorders/gbs/detail_gbs.htm [Accessed 5 Nov. 2016].
Ramachandran, T. (2016). Acute Inflammatory Demyelinating Polyradiculoneuropathy: Background, Pathophysiology, Epidemiology. [online] Emedicine.medscape.com. Available at: http://emedicine.medscape.com/article/1169959-overview#a5 [Accessed 5 Nov. 2016].
Slavov, S., Otaguiri, K., Kashima, S. and Covas, D. (2016). Overview of Zika virus (ZIKV) infection in regards to the Brazilian epidemic. Braz J Med Biol Res, 49(5).
World Health Organization. (2016). WHO statement on the first meeting of the International Health Regulations (2005) (IHR 2005) Emergency Committee on Zika virus and observed increase in neurological disorders and neonatal malformations. [online] Available at: http://www.who.int/mediacentre/news/statements/2016/1st-emergency-committee-zika/en/ [Accessed 5 Nov. 2016].