Management of infection by the Zika virus
Falcao et al. Ann Clin Microbiol Antimicrob (2016) 15:57
DOI 10.1186/s12941-016-0172-y
Annals of Clinical Microbiology
and Antimicrobials
Open Access
REVIEW
Management of infection by the Zika
virus
Melissa Barreto Falcao1, Sergio Cimerman2, Kleber Giovanni Luz3, Alberto Chebabo4, Helena Andrade Brigido5,
Iza Maria Lobo6, Artur Timerman7, Rodrigo Nogueira Angerami8, Clovis Arns da Cunha9, Helio Arthur Bacha10,
Jesse Reis Alves2, Alexandre Naime Barbosa11, Ralcyon Francis Teixeira2, Leonardo Weissmann2,
Priscila Rosalba Oliveira12*, Marco Antonio Cyrillo13 and Antonio Carlos Bandeira14
Abstract
A panel of national experts was convened by the Brazilian Infectious Diseases Society in order to organize the national
recommendations for the management of zika virus infection. The focus of this document is the diagnosis, both clinical and laboratorial, and appropriate treatment of the diverse manifestations of this infection, ranging from acute mild
disease to Guillain-Barré syndrome and also microcephaly and congenital malformations.
Keywords: Zika virus infection, Guideline, Diagnosis, Therapeutics
Background
The Zika virus is an arbovirus of the genus Flavivirus, in
the family Flaviviridae, which was first identified in 1947,
in the Zika Forest in Uganda during a monitoring program on wild yellow fever [1–4]. It is related to other flaviviruses, including the viruses that cause dengue, yellow
fever and West Nile fever.
Outbreaks of the disease were first notified in the
Pacific region in 2007 and 2013, respectively in the Yap
islands and in French Polynesia, and then in the Americas (Brazil and Colombia) and in Africa (Cape Verde) in
2015 [2, 3, 5, 6]. Rapid geographical expansion has been
observed since then, with 40 countries in the Americas
reporting autochthonous transmission as sporadic cases
or outbreaks. It is also important to mention the growing
number of countries on other continents that have been
notifying occurrences of imported cases of Zika virus
infection, thus demonstrating its great potential for dissemination on a worldwide scale [7].
Through occurrences of Zika outbreaks, the central
nervous system and autoimmune complications that
*Correspondence:
12
Universidade de São Paulo, Rua Doutor Ovidio Pires de Campos, 333,
Sao Paulo, SP CEP 05403‑010, Brazil
Full list of author information is available at the end of the article
were previously reported in French Polynesia have also
come to be observed in the Americas.
Zika infection during pregnancy has been correlated
with congenital microcephaly, fetal malformations and
fetal losses. This led the Brazilian Ministry of Health to
declare a state of public health emergency of national
importance in November 2015, after observation of
changes to the epidemiological pattern of occurrences of
microcephaly in Pernambuco and other states in northeastern Brazil [8, 9].
In the light of the significant increase in the incidence
of neurological syndromes and cases of microcephaly
that were potentially related to the Zika virus, the World
Health Organization (WHO) declared an international
public health state of emergency in February 2016. To
put the importance of this event into context, this was
the fourth time that WHO has ever declared a worldwide
state of emergency in relation to a viral epidemic. The
previous decisions were made in relation to H1N1 (2009),
poliomyelitis (2014) and Ebola (2014).
On February 18, 2016, the Brazilian Ministry of Health
issued an ordinance that made it compulsory to notify
suspected cases of Zika throughout the country. This disease has thus been added to other arboviruses, such as
dengue, yellow fever, West Nile fever and chikungunya,
© 2016 The Author(s). This article is distributed under the terms of the Creative Commons Attribution 4.0 International License
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and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/
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Falcao et al. Ann Clin Microbiol Antimicrob (2016) 15:57
which were already on the national list of diseases with
compulsory notification [10].
Epidemiology
Geographical distribution
In humans, the Zika virus was first identified in Uganda
and Tanzania, in 1952 [11]. Between 1952 and 1981, a
variety of serological evidence regarding infection by this
virus was reported from countries in Africa and some
parts of Asia [4].
The first epidemic outside of Africa and Asia occurred
in 2007, in the Yap islands of Micronesia. It was estimated that more than 70 % of the population over the age
of 3 years became infected [2]. Another large outbreak
of Zika fever occurred concomitantly with a dengue epidemic (serotypes 1 and 3) in French Polynesia in 2013–
2014, affecting around 32,000 people [3].
In 2014, cases of Zika virus infection were reported
on Easter Island, which is Chilean territory [12]. In May
2015, some months after reports of increased incidence
of exanthematous febrile disease in states of northeastern Brazil, which until then were of unidentified cause,
presence of Zika virus circulation was confirmed in this
country. This was initially confirmed in Bahia on April
29, 2015, from analysis on samples from patients with an
exanthematous condition in Camaçari, Bahia, and subsequently in Rio Grande do Norte on May 9, 2015, with
identification of the Asian genotype [13, 14]. Also in
May, cases in Sumaré and Campinas (São Paulo), Maceió
(Alagoas) and Belém (Pará) were confirmed through laboratory tests. Since then, rapid expansion of the areas of
circulation and autochthonous transmission of the virus
has been observed, notably in states of the northeastern
region of Brazil. It is estimated that more than one million Brazilians became infected with the Zika virus in
2015, thus reflecting the capacity of the virus to cause
large-scale outbreaks in places where the biological vector is present.
Worldwide, the virus is now circulating in 65 countries
and territories, mostly in the Americas [15].
Transmission methods
Zika is transmitted primarily through the bites of
infected mosquitos of the genus Aedes, especially Aedes
aegypti and Aedes albopictus [16].
In humans, except for pregnant women, the period of
viremia is short and it is most frequently identified by the
5th day after the symptoms start. The RNA of the Zika
virus has been identified in blood as early as on the 1st
day, and also only up to 11 days after the disease begins.
Prolonged Zika virus RNA was detected in serum of four
symptomatic pregnant women in up to 46 days after
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symptoms onset and in one asymptomatic pregnant
woman 53 days after infection [17]. In pregnant women
Zika (...truncated)