Is Zika virus the definitive culprit in cases of Microcephaly?

The World Health Organisation (WHO) situational report shows that 62 countries and territories have reported cases of mosquito-borne Zika virus transmission since 2007. The report added that cases of person-to-person transmission of the Zika virus were reported in 11 countries from February 2016 (WHO, 2016). The world was alarmed at the beginning of 2016 by the sudden and explosive emergence of a Zika virus outbreak in the majority of Latin American and Caribbean countries, with estimated cases of 440 000–1 300 000 in Brazil alone (PAHO, 2016). Zika virus is thought to have led to more than 11,000 deaths and nearly 4,000 cases of microcephaly in Brazil since the start of the outbreak in May 2015 (WHO, 2016).The American Centers for Disease Control and Prevention (CDC) reported 150 cases if Zika virus in 2014, which is a very small number for its population, compared to the outbreak in 2015. The outbreak in May 2015 was unprecedented and is reported to have resulted in more than 1 million cases, with 4,000 suspected cases of microcephaly, and 270 confirmed cases that health officials believe are linked to the Zika virus (CDC, 2016). Microcephaly is described as a rare congenital disease that is linked with incomplete brain development and causes babies to be born with unusually small heads and, in the majority of cases, brain damage(Gyawali, et al., 2016).Zika virus related microcephaly has now been reported in 20 countries or territories and WHO recently predicted that as many as four million people might be infected with the virus (WHO, 2016). By January 2016, A total of 3,530 suspected microcephaly cases had been reported by January 2016 compared to 4,000 suspected cases of microcephaly reported in May 2015, many of which occurred in infants born to women who lived in or had visited areas where Zika virus transmission was occurring. The birth prevalence of microcephaly in Brazil increased sharply during 2015–2016 with the largest increase occurred in the Northeast region, where Zika virus transmission was first reported in Brazil (CDC, 2016). The Zika virus, linked in Brazil to the birth defect microcephaly, was first identified in the Ugandan Zika forest in 1947. The initial review of literature for this book shows that the Zika virus spread slowly to other parts of Africa, and eventually appeared in Southeast Asia. The evidence from the review also shows the current globalization of the Zika epidemic began on the Pacific island of Yap in the Federated States of Polynesia. The virus subsequently spread into French Polynesia where microcephaly and other congenital abnormalities were observed in the infants of women who were pregnant when they contracted the disease. The epidemic rapidly spread to the Cook Islands and Easter Island, Brazil, Caribbean Islands, the Americas and many other parts of the globe. In May 2016, the WHO tests confirmed two hundred cases of Zika virus with 7,557 suspected cases in the African island chain of Cape Verde. Cape Verde is an Atlantic archipelago that is about 350 miles (570km) west of Senegal and which has historic ties to Brazil (Icheku, 2016, who, 2016, Davis, 2016). Aim and objective of the book Until the recent WHO reported cases, there was no documented evidence of Zika-associated to microcephaly in any part of Africa, where the virus originated. This raises the question as to what is the connection between Zika virus and microcephaly. In other words, is mosquito-borne infection actually the cause of the defects in babies born to Zika-virus-infected mothers? The answer to that question could provide essential clues as to why microcephaly leading to birth defects suddenly appeared in Africa 70 years after Zika virus was first discovered in 1947. The aim of this book is to provide a single document that evaluates current evidence linking Zika virus to microcephaly in an epidemiological context of the disease and thus provide possible explanations as to why there was no microcephaly in Africa between 1947 and 2016. The objective is divided into the following five chapters of the book: Chapter 1 focuses on Zika virus transmission by exploring the scientific studies that implicated Aedes aegypti mosquitosas the main vector transmitting the Zika virus. The chapter discussed the most common symptoms of Zika virus but noted that most people infected with Zika virus would have no symptoms or fall ill; only one in five of the people infected with the disease become symptomatic. Thus, the chapter argues that the asymptomatic nature of Zika virus has public health implication. For example, those who are asymptomatic and those who are in the incubation period of Zika virus could potentially donate infected blood or exchange contaminated body fluid, thereby, increasing human to human transmission of the disease. The chapter also uses Table 1.1 to illustrate four categorises of Zika virus transmission. For example, category 1 shows area with new introduction or re-introduction with ongoing Zika virus transmission; category 2 identified area either with evidence of virus circulation before 2015 or area with ongoing transmission that is no longer in the new or re-introduction phase, but where there is no evidence of interruption; category 3 involves area with interrupted transmission and with potential for future transmission and category 4 shows area with established competent vector but no known documented past or current transmission. Also, chapter 1 explores the modes of Zika virus transmission (Vector-borne and non- vector-borne transmission) and reinforces the view that mosquitoes are not the only means of Zika virus transmission. Thus, the chapter uses figure 1.3 to illustrate the vector and non-vector modes of Zika virus transmission cycle. The cycle starts when humans are bitten by an infected mosquito followed by viral replication in humans and viremia. The transmission cycle shows that Zika virus can spread to the reproductive organs and can be transmitted during sexual intercourse. Pregnant women who are infected with the Zika virus can also transmit the virus to their unborn child or the fetus during pregnancy. The Zika virus can then be transmitted from an infected person back to mosquitoes through subsequent mosquito bites. Lastly, the cycle continues when the Zika virus replicated in the mosquitoes and transmitted back to humans. Chapter 2 focuses on the epidemiology of Zika virus with a view to documenting the incidence and geographical distribution of the virus. The chapter traced the origin of Zika virus to the first isolated in 1947 from a febrile sentinel rhesus monkey in the Zika forest in Uganda, where it got its name. The virus spread slowly to other parts of Africa and eventually appeared in Southeast Asia before the current globalization of the Zika virus epidemic, which started on the Pacific island of Yap in the Federated States of Polynesia in 2007.The chapter demonstrates that the Zika virus epidemic that started on the Pacific island of Yap was the first known presence of the Zika virus case outside of Africa and Southeast Asia. The chapter uses figures and tables to show that the wide geographical distribution of the Zika virus and demonstration that the disease spread to French Polynesia, New Caledonia, Cook Islands, and Easter Islands before cases were reported in Brazil in 2015. Chapter 2 also explores globalisation and the risk for Zika virus spread and argued that increased globalisation continues to pose a risk for Zika virus spread. For example, there is clear evidence of a well-established association between global travels and the acquisition or transmission of infectious diseases. The chapter demonstrated that in 2015, there were 9.9 million flights from Brazilian to destinations in North America, Europe, Asia, and Africa. This has public health implication given that the incubation period for Zika virus is 3 to 14 days from the bite of Aedes species mosquito. Travelers and humanitarian health workers returning from affected areas in Brazil may be incubating the virus and become infectious after returning to their home countries. Chapter 3 reviewed the evidence linking Zika virus to microcephaly and Guillain–Barré syndrome (GBS) given that the World Health Organization report of March 2016, claimed that there was a scientific consensus that the mosquito-borne Zika virus was a cause of the neurological disorder Guillain–Barré syndrome (GBS) and of microcephaly and other congenital brain abnormalities. The review is important given that the decisions about causality require a clear understanding of the association of Zika virus complications to guide public health actions. The chapter demonstrated there had been a remarkable increase in cases of microcephaly and other congenital abnormalities in Brazil between 2015 and mid-2016. The table 3.7 was used in the chapter to demonstrate that as of March 2017, 31 countries or territories reported microcephaly and other congenital abnormalities potentially linked to Zika virus infection. Chapter 4 reviewed the evidence linking Microcephaly to birth defect in Africa and found that other factors may beat play in the Zika virus related microcephaly. The chapter discussed the evidence, which suggested that the emergence in 2014 of the microcephaly increase in Brazil occurred within certain "contexts and contingencies." Environmental degradation, poor sanitation and continued use of larvicidal chemicals in the drinking water of families were blamed for the sudden increase microcephaly.These evidence may provide a clue as to why the increase cases of Microcephaly were mostly reported in the Northwest of Brazil where the factors mainly prevalent. As for the absence of microcephaly in Africa, Chapter 4 examines a phenomenon called herd immunity that seems to offer the most plausible explanation. Herd immunity becomes a type of indirect protection from infectious disease, occurring when a significant percentage of a population has become immune to an infection, thereby providing a measure of protection for individuals who are not immune and thus decreasing the number of new infections. Given that the virus is unable to infect the same person twice; the presence of immune system generating antibodies to kill the virus and the epidemic reaching a stage where there are too few people left to infect for transmission to be sustained. The chapter concluded with a warning that until the apparent association between Zika virus infection and microcephaly is either established or disproved, women should be cautious in planning to conceive a baby or to travel to a Zika-endemic country if already pregnant (Gyawali et al. 2016). Chapter 5 will start with the premise that the World Health Organisation is better placed to identify critical areas of public health research; implementation and coordination of global fight against the Zika virus epidemic. Thus, it will explore WHO's Zika Virus Research Agenda that sets out to support the generation of evidence needed to strengthen essential public health guidance; actions to prevent; limit the impact of Zika virus and its complications. The chapter is also based on the premise that research and evidence are the foundations for sound health policies. It will, therefore, explore systematic review of evidence and the use of research evidence to inform Zika virus related public health policies and practices. The readers of this book may be delighted to know that both eheAmerican Centers for Disease Control and Prevention (CDC) and the World Health Organisation (WHO) are driving and encouraging the use of research evidence to underpin public health policy in the global fight against the Zika virus epidemic. Chapter 6 discussedrecommendations for public health interventionsto prevent the global spread Zika virus infection, given that there is no cure, no vaccine or prophylactic treatment for the disease. The chapter recommended primary preventive interventions such as promotion avoidable travel to countries where Zika virus is prevalent especially pregnant women or those planning to get pregnant; use of mosquitoes repellent; practicing safe sex, etc. The chapter also recommended secondary interventions such as reduction of mosquito breeding sites in outdoor and indoor and symptomatic treatment based on a good hydration, pain relief, and anti-histamines for the pruritic rash. Lastly, the chapter examined the scope of current research to developeZika virus vaccines and argues that effective vaccines development is crucial in the fight against the Zika virus infection. In conclusion, the book provided a summary of the current evidence linking Zika virus to microcephaly in historical context, 1947 to 2016 and offered possible explanations as to why there were no cases of microcephaly in Africa for 70 years. The summary of the possible explanations are: the possibility of chemical, Pyriproxyfen, used in a State-controlled programme aimed at eradicating disease-carrying mosquitoes; possibility of existence of inequalities in the low-income countries in the Americas, which are currently ignored in the microcephaly narrative and the possibility of herd immunity occurring in Africa that may haveprovided protection against the Zika virus infection. Lastly, table and maps were used in this book to reinforce and add value to the textual information. They were also used to draw attention to spatial relationships in the global distribution of Zika virus. Their use allows lengthier information in the book to be described in pictures and tabular forms and more memorable because they have colours and in shapes. Also, the table and maps helped to present spatial relationships in a way that is more striking; given that they show the intensity of the Zika virus transmission and global spread. Once the spatial relationships were established, the book was then able to analyse them and used texts to explain the underlying causes of the disease and its complications, which in turn informed the recommended public health interventions.