The current outbreak of Zika virus in Jaipur, India has rekindled national and international interest in this mosquito-borne illness. Zika virus causes a mild fever but can also result in serious neurological complications like Guillain-Barré syndrome and microcephaly in infants born to infected mothers. While the illness is usually self-limiting, the recent outbreak in Jaipur of 29 reported cases in one month requires a task force to prevent further spread.

1. ZIKA VIRUS
SENSITIZATION FOR FACULTY AND STUDENTS
Dr. Mayank Gupta
SR, MU-4 Department Of
Medicine
SMS Medical College
Jaipur

2. INTRODUCTION
DENGUE’S COUSIN
 Zika virus infection is a mild febrile viral illness
transmitted by mosquitoes
 Zika virus is an arthropod-borne flavivirus transmitted by
Aedes mosquitoes currently “spreading explosively”
 The virus is related to other flaviviruses including dengue
virus, yellow fever virus, chikungunya and West Nile virus
 Disease has a self limiting course, sometimes associated
with congenital microcephaly and fetal loss among
women infected during pregnancy

3.  It was discovered in the Zika forest in Uganda in 1947.
 The Zika virus' incubation period is about 2 to 14 days after
the bite of an infected mosquito.
 The vast majority of infections are not contagious from
person to person.
 One out of five people may develop symptoms, but in those
who are affected the disease is usually mild and may last
between two and seven days.

4.  Two ZIKV lineages have been described, African and
Asian, with the African lineage spitted in East and
West African clusters, some authors described three
different lineages (West African, East African and
Asian).
 The Asian lineage is expanding, this lineage emerged
in the Pacific and in South America and is the
currently circulating strain.

5. ZIKA VIRUS EPIDEMIOLOGY
 The virus was first identified in a rhesus monkey in the
tropical Zika Forest in Uganda in April 1947 by the
scientists of the Yellow Fever Research Institute.
 The first human cases were reported in Nigeria in 1954.
A few outbreaks have been reported in tropical Africa
and in some areas in Southeast Asia.

6. ZIKA VIRUS EPIDEMIOLOGY
1951-1981 – Africa and Asia
• Until 1981, evidence of human infection with Zika
virus was reported from other African countries, such
as the Central African Republic, Egypt, Gabon, Sierra
Leone, Tanzania, and Uganda, as well as
in parts of Asia including Indonesia, Malaysia, the
Philippines, Thailand, and Vietnam.

7. ZIKA VIRUS EPIDEMIOLOGY
 The first major outbreak, with 185 confirmed cases, was
reported in 2007 in the Yap Islands of the Federated States of
Micronesia. (Estimated 5000 infections among the total population of 6700)
 In 2013 another large outbreak (involving 32000 persons)
was reported in French Polynesia that was thought to be
from an independent introduction of the virus from Asia than
the Yap Island outbreak.

8. ZIKA VIRUS EPIDEMIOLOGY
 In May 2015, the Pan American Health Organization
(PAHO) issued an alert regarding the first confirmed
Zika virus infections in Brazil.
 May 2015: The World Health Organization reported
the first local transmission of Zika virus in the Region
of the Americas, with autochthonous cases identified
in Brazil.

9. ZIKA VIRUS EPIDEMIOLOGY
 In July 2015 Brazil reported an association between Zika
virus infection and Guillain-Barré syndrome.
 In October 2015 Brazil reported an association between
Zika virus infection and microcephaly.
 Mosquito-borne Zika virus is suspected to be the cause of
2,400 cases of microcephaly and 29 infant deaths in Brazil
in 2015.
 By mid-February 2016, more than 4300 cases of
microcephaly had been recorded(although overreporting and
misdiagnosis probably inflated this number)

10. ZIKA VIRUS EPIDEMIOLOGY
 In December 2015, the Ministry of Health estimated
that 440,000–1,300,000 suspected cases of Zika virus
disease had occurred.
 As of 17 March 2016, 59 countries have reported
locally acquired circulation of the virus since January
2007.
 World Health Organization (WHO) declared Zika Virus
Disease as a Public Health Emergency of International
Concern (PHEIC) on 1st February 2016.

11. PATHOGENESIS
 Pathogenesis of ZIKV is almost unknown.
 It is found that mosquito-borne flaviviruses initially
replicate in dendritic cells close to the inoculation
site and then spread to lymph nodes and the blood.
 The neurotropism and tenacity of ZIKV may explain
neurological complications such as GBS &
microcephaly in congenital ZIKV infection.

12. TRANSMISSION OF ZIKA VIRUS
VECTOR BORNE
Through mosquito bites:
 Transmitted primarily through the bite of an
infected Aedes species mosquito (A. aegypti and
A. albopictus).
 These mosquitoes typically lay eggs in and near
standing water things like buckets, bowls, animal
dishes, flower pots and vases.
 Mosquitoes that spread chikungunya, dengue, and
Zika are aggressive daytime biters. They can also
bite at night.
 Mosquitoes become infected when they feed on a
person already infected with the virus. Infected
mosquitoes can then spread the virus to other
people through bites.
Aedes aegypti
Aedes albopictus

13. TRANSMISSION OF ZIKA VIRUS
NON VECTOR BORNE:
From mother to child:
 A mother already infected with Zika virus near the time of
delivery can pass on the virus to her newborn around the
time of birth.
 It is possible that Zika virus could be passed from a mother
to her baby during pregnancy.
 To date, there are no reports of infants getting Zika virus
through breastfeeding.
 Because of the benefits of breastfeeding, mothers are
encouraged to breastfeed even in areas where Zika virus is
found.

14. TRANSMISSION OF ZIKA VIRUS
Through sexual contact:
 Dallas County Health and Human Services (DCHHS) has received
confirmation from the Centers for Disease Control and Prevention (CDC)
of the first Zika virus case acquired through sexual transmission in Dallas
County in 2016.
 The patient was infected with the virus after having sexual contact with
an ill individual who returned from Venezuela, a country where Zika virus
is present.
 Sexual transmission of Zika virus from infected women to their sex
partners has not been reported.
 Zika virus is transmissible also via blood products, laboratory exposure,
and organ or tissue transplant.

15. CLINICAL MANIFESTATIONS
 The incubation period between mosquito bite and onset
of clinical manifestations is typically 2 to 14 days.
 The illness is usually mild; symptoms resolve within 2 to 7
days.
 Once a person has been infected, he or she is likely to be
protected from future infections.
 Severe disease requiring hospitalization is uncommon,
and case-fatality rates are low.

16. SIGNS & SYMPTOMS OF ZIKA VIRUS
 Sx present in 20 -25%
80% :Asymptomatic
 Acute onset of low-grade fever (100 to 101.5°F) (65%)
with
 Maculopapular rash (90% of patients),
 Arthralgia (notably the small joints of hands and feet)
(65%) and
 Nonpurulent conjunctivitis (55%)
 Other manifestations include
myalgia (48%),
headache (45%),
retro-orbital pain (39%),
edema (19%),
vomiting (10%),
asthenia, abdominal pain,nausea,
membrane ulcerations, pruritus,
hematospermia, transient dull & metallic hearing,
subcutaneous bleeding.
 Thrombocytopenia documented in case reports only.
*Yap Island, 2007
Duffy M. N Engl J Med 2009

17. SIGNS & SYMPTOMS OF ZIKA VIRUS
 Clinical manifestations of Zika virus infection in pregnant
women are the same as those in non-pregnant adults.
 In children,it can manifest as irritability, walking with a
limp, difficulty moving or refusing to move an extremity,
pain on palpation, or pain with active or passive
movement of the affected joints.

18. CLINICAL FEATURES: ZIKA VIRUS COMPARED TO
DENGUE AND CHIKUNGUNYA
Rabe, Ingrid MBChB, MMed “Zika Virus- What Clinicians Need to Know?” (presentation, Clinician Outreach and
Communication Activity (COCA) Call, Atlanta, GA, January 26 2016)

19. COMPLICATIONS
Neurologic Complications
 A temporal and geographic relationship has been observed
between Guillain–Barré syndrome and Zika virus
outbreaks in the Pacific and the Americas.
 In the outbreak in French Polynesia, 38 cases of Guillain–
Barré syndrome occurred among an estimated 28,000
persons who sought medical care. (odds ratio, >34)
 However, a direct causal relationship has not yet been
definitively established.
 Meningoencephalitis and acute myelitis complicating Zika
virus infection also have been reported.

20. COMPLICATIONS
Adverse Fetal Outcomes/congenital zika syndrome
 Intrauterine Zika virus infection in pregnant women has been associated with
microcephaly and fetal loss (in the first trimester).
 Centers for Disease Control and Prevention (CDC) guidance has recommended
that microcephaly be defined as an occipitofrontal circumference below the third
percentile for gestational age and sex.
 The findings of Zika virus RNA in the amniotic fluid and in the brain tissue of
fetuses and infants with Microcephaly, provide strong evidence linking
microcephaly to maternal Zika virus infection.
 Greatest risk of microcephaly is in the first trimester and it is estimated to be
0.88% when we assumed an 80% overall ZIKV infection rate and 100%
overreporting of microcephaly cases, to 13.2%, when we assumed a 10% ZIKV
infection rate and no overreporting.
 Thus the risk of microcephaly varies directly with the rate of infection & is
uncertain.

21. CONGENITAL ZIKA SYNDROME

22. Infant with Microcephaly Associated with
Maternal Zika Virus Infection, as Compared
with a Typical Newborn.
Microcephaly

23.  In case reports of microcephaly, documented maternal Zika virus infection
most often occurred between 7 and 13 weeks of gestation, but in some cases
it occurred as late as at 18 weeks of gestation.
 Fetal abnormalities detected by ultrasonography were present in 29% of
women with Zika virus infection during pregnancy.
 Early fetal loss & fetal death have been noted in association with maternal
infection that occurred between 6 and 32 weeks of gestation.
 In addition, OCULAR INVOLVEMENT has been observed among infants with
congenital infection including-
focal pigment mottling,
chorioretinal atrophy, and
optic nerve abnormalities(hypoplasia and severe cupping of the optic disk).

24. DIAGNOSIS
 The diagnosis should be suspected in individuals with typical clinical
manifestations and relevant epidemiologic exposure.
 The mainstays of the routine diagnosis of Zika virus infection are the
detection of viral nucleic acid by RT-PCR and the detection of IgM
antibodies by IgM-capture enzyme-linked immunosorbent assay
(MAC-ELISA).
 For individuals within the first 7 days after onset of symptoms, the
diagnosis of Zika virus infection may be established via RT-PCR of
serum for detection of Zika virus RNA.
 RT-PCR is positive only for a brief window (3 to 7days).

25. DIAGNOSIS
 For individuals, four or more days after the onset of symptoms, the
diagnosis of Zika virus infection may be established by Zika virus
serologic testing (Zika virus IgM and neutralizing antibody titers
that are ≥4-fold higher).
 Serologic testing for dengue virus infection and chikungunya virus
infection should also be pursued.
 The considerable cross-reactivity of flavivirus antibodies presents
major challenges for the interpretation of serologic test results.
 The plaque reduction neutralization test (PRNT), the most specific
test used to differentiate antibodies of closely related viruses, can
be used to help verify MAC-ELISA results.(costly).

26. DIAGNOSIS
 The greatest challenge with serologic crossreactivity
arises from the “original antigenic sin”phenomenon
(particularly problematic in areas in which dengue is
endemic; dengue and Zika viruses may be
cocirculating).
 Even the PRNT cannot reliably establish a diagnosis in
such patients.
 Zika virus RNA can be detected longer in urine than in
serum; if verified, this would extend the period during
which a definitive diagnosis of Zika virus infection can
be established by RT-PCR(but data is limited).

27. DIAGNOSIS OF CONGENITAL ZIKA
 Exclusion of the “TORCH” (toxoplasmosis, other infections, rubella,
cytomegalovirus, herpes simplex virus-2 or neonatal herpes simplex) infections is
needed for the diagnosis of congenital Zika syndrome.
 Reliable testing regimens for the diagnosis of prenatal and antenatal Zika virus
infection have not been established.
 Amniotic fluid- tested positive by RT-PCR in instances of congenital Zika virus
infection; (sensitivity unknown).
 Cord blood can be tested by RT-PCR and MAC-ELISA (sensitivity unknown).
 Ultrasonography is not a highly sensitive means of detecting microcephaly.
 Ultrasound findings may be detected as early as 18 to 20 weeks gestation.
 The key ultrasound findings suggestive of fetal infection are microcephaly
(suggested by head circumference more than two standard deviations below the
mean) and intracranial calcifications (cerebellum, intraocular, brain).

29. PRECAUTION & PREVENTION

31. PRECAUTION & PREVENTION
 There is no vaccine for prevention of Zika virus
infection.
 Individuals in areas with risk for transmission
should take measures to avoid mosquito bites
including-
personal protection;
environmental control measures.

32. 4 S OF ZIKA VIRUS

33. MANAGEMENT
 There is no commercial vaccine or specific antiviral drug treatment for
Zika virus infection.
 Management consists of rest and symptomatic treatment including
drinking fluids to prevent dehydration and administration
of Paracetamol to relieve fever and pain.
 Aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDS) should
be avoided until dengue infection has been ruled out, to reduce the risk
of hemorrhage.
 NSAIDS should also be avoided in pregnant women at ≥32 weeks of
gestation to minimize risk for premature closure of ductus arteriosus.

34. THE CURRENT OUTBREAK OF ZIKA VIRUS IN SHASTRI NAGAR, JAIPUR HAS
REKINDLED NATIONAL & INTERNATIONAL INTEREST IN THIS SELF
LIMITING MOSQUITO BORNE VIRAL ILLNESS DUE TO A STAGGERING 29 CASES
REPORTED AS ON OCTOBER 10TH 2018 IN A SHORT SPAN OF LAST ONE
MONTH

35. CONCLUSION
 Zika virus is a mosquito-borne arboviral infection, though self limiting has
shot to limelight because of the associated grave neurological
complications like CONGENITAL ZIKA SYNDROME & GUILLAIN–BARRÉ
SYNDROME.
 Congenital zika syndrome is diagnosed by ultrasound (low sensitivity)
done at 18 to 20 weeks of gestation by detecting fetal microcephaly.
 No evidence suggests that pregnant women are more susceptible to Zika
V infection or experience more severe disease during pregnancy.
 Endemic to South and Central America, this virus has now broken the
barriers and has invaded our very own PINK CITY, jolting out ID experts
nationally and internationally to form a task force in preventing its
further spread.

36. REFERENCES
 http://zikavirusnet.com/epidemiology.html
 http://www.cdc.gov/zika/transmission/
 http://www.redaccionmedica.com/contenido/images/zika%20servicio%20de%20salud%2
0de%20dallas.pdf
 http://www.health.govt.nz/our-work/diseases-and-conditions/zika-virus
 http://www.vox.com/2016/1/28/10861094/microcephaly-zika-virus-birth-defect-pregnancy
 http://www.paho.org/hq/index.php?option=com_content&view=article&id=9183%3A2015-
preguntas-frecuentes-virus-fiebre-zika&catid=8424%3Acontent&Itemid=41711&lang=en
 http://www.medicinenet.com/zika_virus/article.htm
 http://www.health.govt.nz/our-work/diseases-and-conditions/zika-virus
 http://www.microbiologyinfo.com/zika-virus-structure-genome-symptoms-
transmissionpathogenesis-diagnosis/
 Zika Virus, Lyle R. Petersen, M.D., M.P.H., Denise J. Jamieson, M.D., M.P.H., Ann M.
Powers, Ph.D., and Margaret A. Honein, Ph.D., M.P.H. DOI: 10.1056/NEJMra1602113