Category Archives: Caribbean

El Niño and Possibly New World Primates Contributed to Zika Explosion

by Michelle Ziegler

The explosion of Zika-related birth defects this past year came out of the blue. Zika has been known since the 1940s but was seen as a mild dengue-like illness (Fauci & Morens, 2016). Leaving aside how and why microcephaly has appeared so dramatically, it is undeniable that Zika’s emergence and transmission in the Americas have been unusually rapid and extensive.

Aedes aegypti from Tanzania (Source: Muhammad Mahdi Karim, 2009, GNU Free Documentation License)

Two papers published in December focusing on the Aedes mosquito vectors begin to shed light on how Zika was able to be established so quickly and pervasively. Zika utilizes the same tropical mosquito Aedes aegypti as dengue; it was once known as the yellow fever mosquito. It is also the vector of the chikungunya virus.

As first observed in West Africa many years ago, Zika epidemics followed a chikungunya epidemic by a couple years. Chikungunya was the emerging infectious disease of 2013, the year that Zika is believed to have arrived in South America (Fauci & Morens, 2016). Unrecognized by public health workers at the time, a Chikungunya epidemic was simultaneously chugging along under the radar in at least Salvador, the capital of the Bahai state of Brazil, during the peak of Zika epidemic of 2015 (Cardoso et al, 2017).

El Niño 2015-2016

In the first study by Cyril Caminade and colleagues at the University of Liverpool modeled Zika transmission in the two critical vector species in the Americas, the tropical Aedes aegypti found primarily in South America and the temperate Aedes albopictus found in the southern United States. It is thought that Zika transmits better from A. aegytpi but more research is needed to fully understand the differences. They developed a two vector, one host model where the climate is a variable to compare the effect of climate patterns on Zika transmission. They ran these simulations for each vector individually and together against historic climate data sets.

When they compared the worldwide distribution of the vectors and climate, they were able to show that all of the countries where Zika has been reported were predicted in their model. Ominously, South America was the most friendly region in the world for Zika (Caminade et al, 2016). The model for Zika produced a map that correlates extremely well with the global distribution of dengue. Due to the overlap of A. aegypti and A. albopictus territory, they found a high probability that Zika would transmit well in most of the southern United States.

Risk of Zika transmission based on their models A. winter of 2015-2016 B. Risk over the last 50 years. (Caminade et al, 2016)

The global climate anomaly known as El Niño is known to impact mosquito-transmitted diseases, so they had a particular interest in comparing the 2015-2016 El Niño to historic data sets. The map shows the predicted Ro (reproduction number) for Zika around the world in 2015-2016  and in the bar graph compared to the last 50 years. The conditions for Zika were the best for the last 50 years. Other hot spots that did not experience a Zika epidemic, like India, did have a record year for dengue. They also note that the African hot spot for ideal transmission conditions corresponds and to Angola where there was a Yellow Fever outbreak. In short, it was a very good year for Andes aegypti! And now, as of January 2017, Yellow Fever had added to their misery in a Brazil.

A Sylvatic Reservoir? 

Understanding if Zika will establish a sylvatic reservoir in South America is of vital importance for projections and mitigation of future Zika epidemics in Brazil and elsewhere in South America. Zika was initially detected in a sentinel monkey in Uganda and has since been detected in a wide variety of smaller primates in Africa and Asia. Using a model originally proposed for dengue they were able to show that primates with rapid birth rates and short lifespans are ideal for establishing sylvatic Zika. In primates with short life span, five years or less, and rapid birth rates, the establishment of a sylvatic reservoir is “nearly assured” (Althouse et al, 2016). They predict that a primate population as small as 6,000 members with 10,000 mosquitoes could support a sylvatic reservoir (Althouse et al, 2016). Ironically, since infection rate is dependent upon bites per primate, a small primate population with a large mosquito population is better at maintaining the reservoir than a large primate population. Old World monkeys like the African Green Monkey, a known African host of Zika, are already established in free-living troops in South American forests.  While A. aegypti favors human environments, A. albopictus prefers forested environments and has been spreading in Brazil.  It could be a prime candidate for a bridging vector between a sylvatic and domestic Zika cycle. Studies on Zika vulnerability and incidence in all South American primates has to be a priority. Our ability to manage Zika in the future depends on it.


Caminade, C., Turner, J., Metelmann, S., Hesson, J. C., Blagrove, M. S. C., Solomon, T., et al. (2016). Global risk model for vector-borne transmission of Zika virus reveals the role of El Niño 2015. Proceedings of the National Academy of Sciences of the United States of America, 201614303–28.

Cardoso, C. W., Kikuti, M., Prates, A. P. P. B., Paploski, I. A. D., Tauro, L. B., Silva, M. M. O., et al. (2017). Unrecognized Emergence of Chikungunya Virus during a Zika Virus Outbreak in Salvador, Brazil. PLoS Neglected Tropical Diseases, 11(1), e0005334–8.

Althouse, B. M., Vasilakis, N., Sall, A. A., Diallo, M., Weaver, S. C., & Hanley, K. A. (2016). Potential for Zika Virus to Establish a Sylvatic Transmission Cycle in the Americas. PLoS Neglected Tropical Diseases, 10(12), e0005055–11.

Fauci, A. S., & Morens, D. M. (2016). Zika virus in the Americas—yet another arbovirus threat. New England Journal of Medicine, 374(7), 601–604.

Famine and Epidemic Anthrax, Saint-Domingue (Haiti), 1770

Map of Haiti, (Source: Wikipedia Commons, 2008 CIA World Factbook)

Earthquakes have brought devastation on the Port-au-Prince region many times in the last 300 years. The 1770 earthquake was stronger and relatively as destructive as the 2010 quake (Ker, 2010). It also was centered near Port-au-Prince and to the west of the city.   Ship captain accounts of the earthquake in the Boston Evening-Post from 9 July 1770 make it clear that the quake destroyed the buildings throughout the southern peninsula causing landslides, a tsunami and liquefaction of the valley where Port-au-Prince stands. A 100 family village called Croit De Bouquets was reported to have sunk and disappeared. Despite the destruction Spanish trade restrictions barring the importation of meat or fish remained in place. Famine followed throughout the western part of the island.

To compound the disaster, an epizootic broke out among their cattle. Here we have a rare description of what followed from Michel-Placide Justin, written about 1825:

“… The unfortunate slaves in the north of Saint-Domingue therefore experienced the most frightful famine. The dependencies of Fort Dauphin, that of Gros-Morne, [and] of Jean Rabel, were devastated. Codfish being entirely unavailable, the Spaniards whose hattes [… ‘cattle ranch’] or pastures were being thinned out daily by a terrible epizootic [“épizootie”], sought to salt or smoke all their ill or dead animals; and they [then] brought them into French establishments. These meats, known as tassau in the colonies, which the Negroes avoided eating when they could get [uncontaminated] salted beef or codfish, spread to the slaves the communicable agent [“germe“] of the disease with which they [the meats] were infected [“infectées’]. A type of epidemic disease [“peste“] , called anthrax [“charbon“], spread throughout all the neighboring dwellings of the Spanairds or the routes they frequently used, and in those where the Negroes had bought this tassau. Within six weeks, more than 15,000 white and black colonists perished of this terrible disease, and its ravages did not stop until the government, the magistrates, and the inhabitants themselves had all joined their efforts to repel the scourge introduced into the colony by Spanish greed.

But the numerous and rapid deaths caused by the disease were not all: at least 15,000 Negroes perished of hunger, and the escape of slaves increased in the northern dependency, causing serious fear for security of the colony…” (Morens, 2002:1160).

The mortality counts here may not be very accurate (Morens, 2002). There are no known records or more contemporary accounts for comparison. Perhaps the most important point is that Justin estimated that as many people died from the epidemic as the famine. Both are credited with killing 15,000. I have not been able to find a good mortality estimate for the earthquake itself either.

Its not uncommon for famine to follow natural disaster. The loss of buildings destroys food stores and flooding destroys crops in the field. In this case we have colonial powers taking advantage of the situation by continuing to enforce trade regulations despite the famine. We have to remember that the colonial powers were not shy about using biological warfare to their advantage, so taking advantage of a natural disaster would have seemed strategic. Justin’s account specifically says that people didn’t want to eat the contaminated meat, but it was all that was available to them. It is a good reminder that in times of famine people will eat food that they know will make them sick.

The relationship between famine and infectious disease is a topic I hope to explore in more detail here at Contagions in time. There is a direct relationship between the two; malnutrition severely weakens the immune system making people more vulnerable to contracting and dying of infectious disease.

Cutaneous anthrax (Source: Wikipedia commons/CDC)

The identity of the disease called charbon here is not as clear as the translation implies. Anthrax is a disease that has been compared to coal from ancient times; the term anthrax derives from the Greek word for charcoal. As you can see from the image to the left, cutaneous anthrax produces an ulcer with a  charcoal black center. The cutaneous lesions are really the only visible characteristic of anthrax. The problem comes in, as Morens (2002: 1181) notes, that charbon “was sometimes applied nonspecifically to other human diseases producing skin lesions, including not only dark or violaceous lesions of any sort but also plague and smallpox”.

The best clue we have is that the contagion came to humans from a cattle epizootic by ingestion. The Spanish, presumably in the eastern half of the island, were taking advantage of the situation by harvesting beef from dead and diseased animals. Morens notes that salted or smoked meat is usually ate without further cooking.

The differential diagnosis has pretty much always been between anthrax and plague. Smallpox doesn’t cause epizootics, so it can be ruled out.  Individual large mammals, like camels, can be infected with plague but it doesn’t cause epizootics. Gastrointestinal plague is usually caused by eating raw meat, like raw camel liver (apparently a Middle Eastern tradition). How well Yersinia pestis would survive salting or smoking is unclear; it doesn’t produce endospores. On the other hand, the spores of anthrax can easily survive salting, smoking and even incomplete cooking. Anthrax spores can survive 140ºF and harsh chemicals (Morens, 2002). Anthrax was a fairly common disease of livestock in the colonial period (Morens, 2003).

Further support for the diagnosis of anthrax comes from 1775 reports that the same disease reoccurred in milder epizootics in Saint-Domingue yearly from 1772-1775 (Morens, 2002 & 2003). Each outbreak had the same epizootic and epidemic characteristics involving both cattle and humans. These Caribbean outbreaks contributed to the characterization of anthrax as a distinct disease by French scientists (Morens, 2003).  To this day, anthrax is considered to be hyperendemic in Haiti.

Morens DM (2002). Epidemic anthrax in the eighteenth century, the Americas. Emerging infectious diseases, 8 (10), 1160-2 PMID: 12396933

Morens DM (2003). Characterizing a “new” disease: epizootic and epidemic anthrax, 1769-1780. American journal of public health, 93 (6), 886-93 PMID: 12773345

Ker, Richard. (13 Jan 2010) Haiti Could Have Been Even Worse. ScienceNOW

Thomas Truxes, (Feb 1, 2010) Earthquake at Port-au-Prince, June 3, 1770. [Excerpt from the Boston Evening-Post, July 9, 1770]

See also: “1770 Port-au-Prince earthquake” (last modified 22 Feb 2011).

Clonal origins of Haiti’s Cholera epidemic

Haiti had been free of cholera for 50 years when the earthquake struck in January 2010. The destruction of Haiti’s infrastructure by the earthquake made it vulnerable to infectious disease outbreaks but it was hoped that cholera would pass it by. As we all know by now, this unfortunately has not been the case. Cholera has spread extensively throughout the country and it is feared that with the vast infrastructure damage, it will become entrenched in Haiti.

Finding the source of the epidemic has been politically sensitive locally and internationally. While locals may be quick to accuse outsiders of increasing their misery, determining the exact origin of the bacteria is necessary to understand the outbreak and determine long-term response. Spread of Vibrio cholerae from the South American outbreak that started in Peru in 1991 or the gulf shore of the United States has been ruled out. Several groups have produced results that point toward a south Asian origin but no one has been able to conclusively prove that it came from Nepalese peacekeepers who have shouldered most the blame to date.

A forthcoming report by Ali et al in the April issue of Emerging Infectious Disease confirms a recent clonal origin for specimens taken within the first three weeks of the epidemic. Of the specimens  taken from 19 diarrhea patients in St Mark’s hospital, Artibonite, 16 patients had the altered El Tor biotype of  Vibrio cholerae O1 Ogawa with the classical cholera B toxin gene. Genetic analysis was unable to pinpoint an origin location for this strain. The lack of VNTR diversity suggests a clonal expansion of a point-source outbreak along the Artibonite river. Ali et al do not believe that this strain could have come from a long-standing environmental reservoir in Haiti because of the lack of diversity and the relatively recent origin of the El Tor  biotype.

Ali, A., Chen,Y.,  Johnson, J.A,  Redden, E., Mayette, Y.,   Rashid, M.H.,  Stine, O.C., and Morris,  J.G. (2011). Recent Clonal Origin of Cholera in Haiti. Emerging Infectious Disease, 17 (4 — April) : 10.3201/eid1704.101973

Expedited release of this article can be found here (as of Feb 20, 2011).

Enserink M (2011). Epidemiology. Despite sensitivities, scientists seek to solve Haiti’s cholera riddle. Science (New York, N.Y.), 331 (6016), 388-9 PMID: 21273460