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  http://news.sciencemag.org/sciencenow/2010/01/13-01.html

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). http://en.wikipedia.org/wiki/1770_Port-au-Prince_earthquake

Cholera’s Chain of Infection

Cholera is the pandemic that just won’t go away. Worse yet, it preys on us when we are at our most vulnerable, after a natural or man-made disaster. We know how to prevent it but in times of natural disaster or in areas where infrastructure is inadequate, those conditions can be hard to maintain. A review of cholera’s chain of infection illustrates the challenges  of containing cholera.

The Organism

Vibrio cholerae (Public domain courtesy of Dartmouth Electron Microscopy Facility).

Scientific name: Vibrio cholerae

Common names: cholera, Asiatic cholera

The causative agent of cholera is Vibrio cholerae, a facultative, gram-negative bacterium. There are 155 known serogroups, differentiated by their O antigen. Only two serogroups, O1 and O139, are responsible for all epidemic and endemic cholera. The O1 serogroup can be further differentiated into three serotypes, Ogawa, Inaba, and (rarely) Hikojima, that can themselves be divided into two biotypes (genotypes), classical and El Tor (Faruque, Albert, & Mekalanos, 1998). V. cholerae O139, which is responsible for the on-going epidemic in Bangladesh and India, evolved from the El Tor biotype of serogroup O1 (Heymann, 2004). This chain of infection is restricted to serogroups O1 and O139, which have epidemic potential.

There are two major virulence factors of pathogenic V. cholerae. The primary virulence factor is cholera toxin responsible for the rice water diarrhea. The toxin gene is carried by a lysogenic bacteriophage (bacterial virus) ensuring that this mobile toxin gene will continue to create new pathogenic strains (Nelson et al, 2009). Haiti’s current outbreak by an altered El Tor strain with a classical B toxin gene is an example of the bacteriophage’s effect on V. cholerae‘s diversity. Biofilms are important in both the intestinal and aquatic environments.  V. cholerae’s other major virulence factor, toxin co-regulated pilus, binds together islands of bacteria (Nelson et al, 2009). Another bacteriophage carries an  island of antibiotic resistance genes (Nelson et al, 2009). However, antibiotics are usually not critical to cholera treatment because its not an invasive pathogen.

Reservoir

Cholera lifecycle between aquatic and human reservoirs. Source: Nelson et al, 2009. Click to enlarge.

There are two reservoirs for V. cholerae O1 and O139: humans and the aquatic environment. Humans are considered the primary reservoir and can be asymptomic carriers (Heymann, 2004). These bacteria are considered hyperinfective immediately upon release from the human body as defined by a significantly lower infectious dose required to cause an infection (Nelson et al, 2009). It has been shown that V. cholerae changes its gene transcription pattern shortly before release from the intestine as part of its ‘escape response’ to prepare it for survival in the aquatic environment (Nelson et al, 2009).

V. cholerae exists in both fresh water, such as the Ganges River delta, and marine environments.  In the Ganges River delta, where V. cholerae has been endemic for centuries (at least), it exists in wide variety of serotypes, toxigenic and non-toxigenic,  though only toxigenic O1 El Tor and O139 serotypes are found in symptomatic patients (Nelson et al, 2009).  An aquatic reservoir exists in Bangladesh where V. cholerae O139 has been shown to be a strain adapted to flourish in an environment changed by global warming (Koelle, Pascule, & Yunus, 2005). A poorly defined reservoir exists in the Gulf of Mexico associated with shellfish. Two cases of V. cholerae O1 were identified in a couple who ate poorly cooked shellfish after Hurricanes Katrina and Rita in Louisiana in 2005 (Straif-Bourgeois et al., 2006)

Portal of Exit

The portal of exit from the human reservoir is from the anus in fecal waste. Faruque et al. (2006) has shown that humans shed fragments of V. cholera biofilm into the environment. Symptomatic patients begin shedding hyperinfectious bacteria from before diarrhea begins and continue to shed for one to two weeks (Nelson et al, 2009). Asymptomatic cases are believed to shed bacteria for only a day (Nelson et al, 2009).  The portal of exit from the aquatic reservoir is in water used for drinking or food preparation, or in contaminated shellfish (Heymann, 2004).

Mode of Transmission

Whether the reservoir is human or aquatic, the primary mode of transmission is ingestion of water or food prepared with water containing V. cholerae. During an outbreak, there can be hand-to-mouth communication of V. cholerae (Heymann, 2004). Rare epidemics and sporadic cases of V. cholerae O1 have been contracted from eating poorly cooked shellfish in waters that have not been contaminated with sewage (Heymann, 2004). It is also a category B bioterrorism agent for water contamination (Boatwright & Greenfield, 2005).

Portal of Entry

The portal of entry is through the mouth in contaminated water or food.

Susceptible hosts

Previous infection produces variable immunity depending on the initial infection biotype (Heymann, 2004). Herd immunity appears to be a protective factor in endemic areas but its nature is not well understood.  In endemic areas hospitalizations are highest among young children, peaking around age 2 years (Nelson et al, 2009). In epidemics where there is no herd immunity cholera infects all age groups (Nelson et al, 2009).

V. cholerae responds differently to the human ABO blood groups. Paradoxically, blood group O has a lower risk of infection but those who are infected have more serious symptoms and worse outcomes (Nelson et al, 2009). The mechanism(s) at play here are not well understood. Blood group O’s “low prevalence in the Ganges River delta suggests that there is selection against this phenotype in a cholera-endemic area” (Nelson et al 2009: 694).

Vulnerable populations include anyone put at risk by dehydration.  This would include all infants, young children, pregnant women, the elderly, and people with other health conditions where hydration levels must be closely monitored. Fluid losses can be has high as 1 liter per hour causing rapid, severe dehydration and metabolic acidosis (Nelson et al, 2009).

Vaccine trials are underway. There is no approved cholera vaccine for the United States.

References

Boatwright, D. T. & Greenfield, R. A. (2005). Bioterrorism and threats to water safety: cholera and cryptosporidiosis. In Biodefense: Principles and Pathogens (pp. 587-618). Bronze, M. S. & Greenfield, R.A. (Eds). Norfolk, England: Horizon Bioscience.

Faruque SM, Albert MJ, & Mekalanos JJ (1998). Epidemiology, genetics, and ecology of toxigenic Vibrio cholerae. Microbiology and molecular biology reviews : MMBR, 62 (4), 1301-14 PMID: 9841673

Faruque SM, Biswas K, Udden SM, Ahmad QS, Sack DA, Nair GB, & Mekalanos JJ (2006). Transmissibility of cholera: in vivo-formed biofilms and their relationship to infectivity and persistence in the environment. Proceedings of the National Academy of Sciences of the United States of America, 103 (16), 6350-5 PMID: 16601099

Heymann, D. L. (Ed.). (2004). Cholera and other Vibroses: I. Vibrio cholerae serogroups O1 and O139. In Control of Communicable Disease Manual. (p. 103-111). 18th ed. Washington, DC: American Public Health Association.

Koelle, K., Pascual, M., & Yunus, M. (2005). Pathogen adaptation to seasonal forcing and climate change Proceedings of the Royal Society B: Biological Sciences, 272 (1566), 971-977 DOI: 10.1098/rspb.2004.3043

Nelson EJ, Harris JB, Morris JG Jr, Calderwood SB, & Camilli A (2009). Cholera transmission: the host, pathogen and bacteriophage dynamic. Nature reviews. Microbiology, 7 (10), 693-702 PMID: 19756008

Straif-Bourgeois, S., Sokol, T, Thomas, A, Ratard, R, Greene, KD, Mintz, E, et al. (2006). Two cases of toxigenic Vibrio cholerae 01 infection after hurricanes Katrina and Rita – Louisiana, October 2005, Morbidity & Mortality Weekly Report, 55, 31-32.

For more information see:

Todar, Kenneth. (2011) Vibrio cholerae and Asiatic Cholera, Todar’s Online Textbook of Bacteriology, retrieved February 2011.