By Dr. Geoffrey Modest
There was a good review of the Zika virus from the CDC in a recent issue of NEJM (see DOI: 10.1056/NEJMra1602113).
Details:
- Epidemiology: flavivirus, discovered in 1947 in Zika rainforest in Uganda, transmitted by Aedes africanus mosquito, with seroprevalence of 6.1% back then (i.e., lots of human transmission), and with documented wide geographic distribution in Africa and Southeast Asia. Though only rare reports of cases of human illness over the next 57 years
- 2007: Outbreak in Micronesia (State of Yap) with 5000 infections in population of 6700
- 2013-4: Big outbreak in French Polynesia involving 32,000 people. Some cases of Guillan-Barre. Other outbreaks in Pacific Islands, not much more in Southeast Asia
- 2015: outbreak in Brazil, then widely spread with up to 1.3 million suspected cases, with >4300 cases of microcephaly (now officially caused by the Zika virus, per the CDC – i.e., not from insecticides, herbicides, etc.)
- By March 2016, spread to at least 33 countries and territories in the Americas. The strains of Zika in the Americas is of the Asian genotype, similar to the outbreaks in Yap, French Polynesia, though overall Zika virus has conserved its genetic structure very well over time [which is good in terms of diagnostic testing, development of vaccines, and understanding expected symptoms/sequelae]
- Transmission: many different Aedes mosquitoes likely involved in nonhuman transmission in nonhuman animals in Africa; A. aegypti and (to lesser extent) A. albopictus, have been involved in nearly all human cases. (? If A. hensilli and A. polynesiensis were involved in Yap)
- egypti likely to be the bad actor overall: it feeds primarily on humans, often bites multiple people in a single blood meal, has an almost imperceptible bite, and lives in close proximity to humans.
- Both A. egypti and A. albopictus bite primarily during the daytime, and are widely spread throughout the tropical and subtropical world. A. albopictus is more widely distributed in the eastern US and Hawaii
- But it seems that A. albopictus does not cause much problem so far, with dengue or Zika, except in Hawaii, which has had some dengue outbreaks.
- Though Zika has been identified in malaria mosquito vectors, they seem to have low potential for transmission for Zika
- Non-mosquito transmission– pretty definitely: mother-to-fetus (found in amniotic fluid in fetuses with cerebral abnormalities, found in brain tissue), but in the very few cases of peripartum transmission, not a significant problem; sexual transmission: in one case occurred before the onset of symptoms. Virus identified in sperm up to 62 days after onset of symptoms. Though blood transfusion transmission not reported, it is likely given this happens with other similar flaviviruses. Zika virus has been recovered in breast milk
- Clinical presentation: unclear incubation period, but likely <1 week (if similar to other flaviviruses). In a volunteer, febrile illness after 82 hours of subcutaneous inoculation, viremia only when symptomatic. In Yap, about 20% of people become symptomatic: macular/pruritic rash (90%), short-term fever (65%), arthralgia/arthritis (65%), conjunctivitis (55%), myalgias (48%), headache (45%), retro-orbital pain (39%), edema (19%), vomiting (10%). Also, hematospermia, dull hearing, swelling of hands/ankles, subcutaneous bleeding. In French Polynesia Guillan-Barre was found in 38 people of 28,000 who sought medical care. Also meningoencephalitis and acute myelitis. In terms of fetal outcomes, much is inferred from other infections (CMV, rubella). Most prominent effects in first trimester infections, though there is evidence that microcephaly can occur with infection late in second trimester or early third. Recent data does suggest that most infections associated with microcephaly occur between 7-13 weeks of gestation. In Brazil, fetal abnormalities were detected by ultrasound in 29% of women infected with Zika (though, note: ultrasound is not a very sensitive method to detect microcephaly). Fetal loss/death has been found in infections from 6-32 weeks gestation. Ocular anomalies in 35%
- Diagnosis: detection of viral nucleic acid in the blood is definitive, but that may be transient (mostly up to 1 week), though viral RNA has been detected in serum of pregnant women with infected fetus 10 weeks after infection. The virus-specific IgM antibody develops at the end of the first week, but may reflect cross-reaction with other flaviviruses (e.g. dengue, yellow fever). Plaque-reduction neutralization testing provides more specific Zika virus assessment.
- Prevention: use of mosquito repellent, permethrin treating of clothing, bed nets, window screens help.
(Visited 4 times, 1 visits today)