Most cases of Zika are asymptomatic or mild. If there are symptoms, they seldom last more than a week. Most symptomatic individuals present with fever and rash, joint pain or conjunctivitis, muscle aches, and/or headache. The incubation period is estimated to be from a few days up to a week. Rarely is hospitalization needed or death reported. Once infected, a person is immune. Symptoms overlap with those of dengue fever and chikungunya infection. Laboratory testing must be performed to correctly identify the etiology of the illness.
Guillain-Barre syndrome has been reported in patients after Zika infection. Guillain-Barre syndrome is a rare disorder of muscle weakness and possible paralysis; a form of acute motor axonal neuropathy. Most people recover over time, but sometimes paralysis is permanent. The infected patient's own immune system attacks nerve cells. Sustained motor, low visual acuity, and cognitive decline were reported in a study of patients diagnosed with Zika virus in Brazil. Very rare cases of acute myelitis and meningoencephalitis have been reported in Zika infected patients. Acute disseminated encephalomyelitis is seen much less than Guillain-Barre, but has been reported in Brazil. It damages the white matter in the brain and may last six months after Zika infection. It is an immune-mediated disease characterized by demyelination and polyfocal neurologic symptoms. Animal studies have shown that adult brain cells can be destroyed.
The greatest risk from infection with Zika occurs if a pregnant woman is infected. The earlier in her pregnancy she is infected, the greater the likelihood of damage to her fetus. Pregnancy can end in miscarriage, stillbirth, or the child may be born with severe neurological damage. The worst of this is microcephaly. Infants with microcephaly have much smaller heads than normal because their brain is damaged or stops growing. Symptoms of microcephaly include seizures, developmental delay, intellectual disability, ocular abnormalities, hearing loss, movement disorders, and difficulty feeding. The Zika virus has been identified in the amniotic fluid, placental, and brain tissue of babies with microcephaly.
Other infections, such as cytomegalovirus (CMV) or rubella virus infection, in pregnant women can also cause microcephaly. From two to twelve cases per 10,000 live births occurred in the US before Zika. Since reporting began until June 23, 2016, seven cases of babies with microcephaly or other Zika-related serous brain abnormalities have been born in the United States. Five pregnancies were lost from stillbirth, miscarriage, or termination.
From a study of 5,909 possible cases of Zika virus infected infants, there were 602 definite or probable cases who had smaller head circumference at birth. Their mothers were more likely to have had a rash during pregnancy. The infants were also four times more likely to die in the first week of life. In addition they found infants with heads of normal circumference who had neurological defects.
A study in Brazil has found that 6% of infants born of mothers with confirmed Zika infection during pregnancy had hearing loss. A child born with hearing may have hearing loss later.
Arthrogryposis (joint contractures) has also been reported in infants born with Zika virus. Musculoskeletal deformities secondary to neurological abnormalities are seen in the arms and legs. These infants also had malformations and calcifications in the cortex of the brain, as well as decreased brain volume and hypoplasia of the brainstem and cerebellum.
A study in Thailand of patients with laboratory-confirmed dengue virus antibodies and were then infected with Zika were more likely to have a higher viral load, more severe disease, and possibly greater susceptibility to Zika virus. This has implications for more congenital infections and neurological sequelae.
There is no specific antiviral treatment and no vaccine at the time of this writing.