On April 14, CI News published a PNC article headlined “Pacific paddlers blamed for Zika outbreak.”
The article reported that a recent scientific paper showed it unlikely that Zika came to Brazil during the soccer World Cup in June-July 2014 and that it probably came with Pacific paddlers to the Va‘a World Sprint Championship at Rio de Janeiro in August 2014.
The first cases of Zika in Brazil were confirmed in March 2015, by which time the outbreak was accelerating dramatically to reach a peak in July and then it rapidly subsided (see graph). Before the Brazil outbreak the only significant epidemics had been in a few Pacific island countries and territories. It was also known to have a low level presence in parts of Southeast Asia.
In June 2015 Zanluca et al. suggested the virus might have come to Brazil with the soccer World Cup (June 12 - July 13, 2014).
In October Musso, a scientist at the Malarde Institute in Tahiti, suggested that the World Cup was unlikely to be the culprit because it did not have teams from Pacific countries having had Zika. He suggested that the Va‘a Sprint was more likely with teams from French Polynesia, New Caledonia, Cook Islands and Rapanui, which had had Zika in early 2014.
In March this year Faria et al. presented genetic evidence that Zika probably arrived in Brazil between May and December 2013 and that it was camouflaged by dengue until the major outbreak got underway in March 2015.
As a result, contrary to the PNC article in CI News, Faria et al. concluded: “Our results suggest that the introduction of ZIKV to the Americas predated [the World Cup and the Va‘a Sprint].”
The arrival of Zika in late 2013 was “more consistent with the Confederations cup [15-30 June 2013]”. However, “that event ended before ZIKV cases were first reported in French Polynesia. Consequently, we believe that large-scale patterns in human mobility will provide more useful and testable hypotheses about viral introduction and emergence than ad hoc hypotheses focused on specific events.” (See graph for details.)
The study showed that all the Zika viruses in Brazil and throughout the Americas had a common ancestor very closely related to the virus that spread in French Polynesia.
The data shows that the proposed arrival period (May-December) had a three month overlap with the large outbreak in French Polynesia. During that overlap several hundred people from French Polynesia visited Brazil. Any of those travellers could have taken Zika to Brazil, just as travellers from French Polynesia took Zika to New Caledonia, Rapanui and Cook Islands.
On the other hand, the graph shows a doubling of travellers from Southeast Asian countries known to have had Zika and any of those travellers could have taken Zika to Brazil and to French Polynesia. The story is still unfolding.
Zika in the Pacific and Americas
Zika was first recorded in 1947 in a feverish monkey in Zika Forest in Uganda. It was a monkey disease spread by Aedes africanus that sometimes infected people, such that about 6% of people in Zika forest had antibodies.
During the 1950s it moved out of east Africa as a monkey disease with a few isolated cases of human infection in west Africa, India and southeast Asia.
The first human epidemic was in 2007 on Yap in the Federated States of Micronesia where antibody evidence showed 75 per cent of the population older than three years had been infected, although only 20 per cent had symptoms.
The outbreak lasted 13 weeks (April-June) and the key symptoms were a body rash and mild fever, often associated with conjunctivitis, swelling of hands or feet, and muscle and joint pain. It was initially thought to be dengue until genetic research showed it to be Zika. The virus was the Asian strain and it was spread by Aedes hensilli – Aedes aegypti was absent. It was also shown that symptoms appear about 6 days after being infected and lasted two to seven days.
Six years later in 2013 Zika arrived in French Polynesia starting a dramatic outbreak in October that peaked in December and was finished at the end of April (see graph). Although it is not known exactly how the virus arrived in Tahiti it was the Asian strain known in Southeast Asia. In French Polynesia the disease was spread primarily by Aedes aegypti, and secondarily by Aedes polynesiensis (Bossin, pers.comm. 2015/06). Elsewhere Aedes albopictus has also been an important vector of Zika.
Zika arrived in New Caledonia with visitors from French Polynesia in late November 2013, the first autochthonous cases appeared in mid-January, the epidemic peaked in April and the last case was on the 2nd August. From Tahiti Zika also spread to Rapanui for the Arts Festival in January and the outbreak lasted until 30th May. In the first week of February Zika appeared in the Cook Islands and the outbreak lasted until the end of May.
Concerning the paddler hypothesis, the outbreaks in Polynesia (French Polynesia, Cook Islands and Rapanui) all ceased more than two months before the Va‘a Sprint in Brazil which means it was extremely unlikely that any paddler or supporter carried Zika. The New Caledonian outbreak lasted to the end of July and someone could have travelled to Brazil with Zika. However, as a source for Zika in Brazil this is ruled out by Faria et al, showing that Zika arrived many months before the Va‘a Sprint.
From trivial to serious
The first report of a serious side of Zika was a March 2014 report (Oehler et al.) of a 20-fold increase of Guillain-Barré Syndrome (GBS, pronounced “gee-YAN-buh-RAY”) among 8,200 cases of Zika in French Polynesia. GBS is a complex of neurological disorders causing muscular weakness and paralysis, usually starting in the hands and feet. Its immediate cause is the auto-immune system attacking the nervous system and most victims make a complete recovery, although it can lead to fatal complications.
In Brazil in November 2015 there was an increase in newborns with microcephaly, small heads and underdeveloped brains.
Suddenly Zika “the trivial” became the most feared mosquito-borne disease for pregnant women. Retrospectively, Cauchemez et al. (March 2016) reported eight cases of microcephaly associated with the Zika outbreak in French Polynesia, which was 50x the normal rate; they concluded that the risk period was the first trimester of pregnancy.
Does Zika directly cause microcephaly? While the linkage seems obvious to the public, scientists have been cautious. However, an extensive review in April this year (Rasmussen et al.) applied a range of criteria of proof and concluded “we suggest that sufficient evidence has accumulated to infer a causal relationship between prenatal Zika virus infection and microcephaly and other severe brain anomalies.” The exact causal linkage is still under investigation.
Infections of Dengue, Chikungunya and Ross River Fever result in very extended immunity, called “life-time immunity”. Of the three diseases, Dengue is more complicated by having four serotypes: DEN-1, DEN-2, DEN-3 and DEN-4. Each serotype gives immunity against further infection by the same serotype, but not against infection by the other three; in fact, in some cases it enhances the severity to an infection by another serotype.
An infection of Zika is also expected to give “lifetime immunity,” although proving this will take a lifetime after the Yap outbreak of 2007!
When a community has a high percentage with immunity a new epidemic cannot get a foothold despite mosquitoes being plentiful. Cao-Lormeau et al (2014) concluded that herd immunity in PICs for a particular dengue serotype lasts three to four years, by which time the community immunity has been sufficiently reduced by births and immigration.
A significant outbreak and the resultant herd immunity can also protect PICs from the immediate return of Zika, and supporting this idea there have not been second outbreaks in French Polynesia, Cook Islands, Rapanui or New Caledonia.
On Rarotonga 866 people sought medical treatment. Based on the indications that only 20% of infected people have symptoms we can estimate that about 4,500 or 50 per cent of the population had Zika.
We also know that the disease was relatively trivial and many people with symptoms, including myself, did not seek medical help which means the percentage with immunity is probably well above 50 per cent. This level of herd immunity makes a renewed epidemic most unlikely, although it does not stop localised outbursts.
How long will the herd immunity last? In the worst case scenario it could have a three to four year cycle as for a particular serotype of dengue, and this would also apply to chikungunya. Unfortunately we cannot know how long the herd immunity to Zika will last, and we also have different serotypes of dengue knocking at the door.
We need to constantly reduce the number of Aedes aegypti and Aedes polynesiensis and Public Health will continue to treat every new case with “dengue-like symptoms” as a potential epidemic of Dengue, Zika or chikungunya.
The close relative, Ross River Fever charged through Fiji, Samoa and Rarotonga in 1979-1980 and we might well wonder why it has not come again.
Cauchemez et al. (2016 March) Association between Zika virus and microcephaly in French Polynesia, 2013-2014: a retrospective study. Lancet 2016 March 15. http://dx.doi.org/10.1016/S0140-6736(16)00651-6
Faria et al. (2016 March) Zika virus in the Americas: Early epidemiological and genetic findings. Science 10.1126/science.aaf5036
Musso D. (2015) Zika virus transmission from French Polynesia to Brazil. Emerg. Infect. Dis. 21, 1887.
Oehler et al. (2014) Zika virus infection complicated by Guillain-Barre syndrome – case resport, French Polynesia, December 2013. Euro. Surveill. 19(9):1-3.
Rasmussen et al. (2016 April) Zika Virus and Birth defects – Reviewing the Evidence for causality. New England Journal of Medicine.
Zanluca et al. (2015) First report of autochthonous transmission of Zika virus in Brazil. Mem Inst Oswaldo Cruz. 110:569–72.