The Rabies Epidemic in Trinidad of 1923 to 1937: An Evaluation with a Geographic Information System

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WILDERNESS & ENVIRONMENTAL MEDICINE, 22, 28–36 (2011)

ORIGINAL RESEARCH

The Rabies Epidemic in Trinidad of 1923 to 1937: AnEvaluation with a Geographic Information SystemKameel Mungrue, MBBS, MPH, FRIPH, MBA; Ron Mahabir, BSc, MSc

From the University of the West Indies, St Augustine, Trinidad and Tobago.

Background.—Rabies, although not preeminent among current infectious diseases, continues toafflict humans with as many as 55,000 deaths annually. The case fatality rate remains the highest amonginfectious diseases, and medical treatments have proven ineffective.

Objective.—This study analyzes the rabies epidemic of 1929 to 1937 in Trinidad from a geograph-ical perspective, using Geographic Information System (GIS) software as an analytical tool.

Setting.—A small island developing country at a time when infectious diseases were rampant.Methods.—A review of the literature was undertaken, and data were collected on the occurrence of

disease in both animal and humans populations and mapped using GIS software. Several factorsidentified in the literature were further explored such as land use/land cover, rainfall and magneticdeclination.

Results.—The bat rabies epidemic of 1923 to 1937 in Trinidad was migratory and seasonal, shiftingto new locations along a definite path. The pattern of spread appears to be spatially linked to landuse/land cover. The epidemic continues to present many unexplained peculiarities.

Conclusion.—Despite the fact that this epidemic occurred almost 7 decades ago, the application ofnew tools available for public health use can create new knowledge and understanding of events. Weshowed that the spatial of distribution of the disease followed a distinct pathway possible due to the useof electromagnetic capabilities of bats.

Key words: rabies, GIS, epizootics

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Introduction

High mortality rates have been associated with epizoot-ics. Rabies, one of the oldest recognized zoonotic dis-eases, is caused by ribonucleic acid (RNA) viruses in thefamily Rhabdoviridae genus Lyssavirus, transmittedthrough the bite of an infected mammal in which thevirus is present in the saliva.1–4 However, this is not theonly mode of transmission, as rabies can be acquiredwith infected aerosolized tissue in caves inhabited byrabid bats and in laboratory accidents.5–7 Transmission islso possible by handling and skinning of infected car-asses.7,8 Human-to-human transmission other than by

corneal transplantation has not been well docu-mented,9,10 although, in 2004, rabies was identified ashe cause of death among 4 patients who were recipients

Corresponding author: Kameel Mungrue, MBBS, MPH, FRIPH,MBA, Faculty of Medical Sciences, Dept of Paraclinical Sciences,University of the West Indies, St Augustine, Trinidad (e-mail: Kameel.

f organs and a vascular graft.11 A potential risk alsoexists from contact with infected body fluids.12 The onlypidemic of rabies to have occurred on the island ofrinidad was in 1929 to 1937. In that epidemic, bats, for

he first time, were identified as the mode of transmis-ion. Bats are a major reservoir for variants of rabiesiruses and transmit the disease through biting, whichan sometimes go unrecognized.5,13–18 Support for the

effectiveness of this mode of transmission is derivedfrom laboratory data with silver-haired bats (Lasionyc-teris noctivagans) and eastern pipistrelles (Pipistrellussubflavus) that demonstrated a higher likelihood of in-fection after superficial inoculation into cells of epider-mal origin.19 Infection is primarily of the central nervoussystem (CNS), leading to an acute progressive encepha-lomyelitis in which most cases are fatal.

The annual number of deaths worldwide caused byrabies is estimated to be 55,000, mostly in rural areasof Africa and Asia, while the annual estimated cost of

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The Rabies Epidemic in Trinidad of 1923 to 1937 29

from rabies is considerably less in the New World.Canada, documented 24 human rabies cases since1924,21,22 emphasizing the global importance of this

isease. Trinidad continues to provide a habitat for aide variety of bats including the vampire bat. While

eports exist of bats biting humans, there has been noonfirmed human case of rabies in Trinidad since thepidemic of 1929 to 1937.

The historical and social forces that influence diseaseatterns in populations are critical in understanding thepidemiology of diseases. While the identification ofiological processes is crucial, the contribution of otheractors such as land use, change affecting vector or hostabitats, human interaction with vectors, and climate arelso important to identify and have a geographical di-ension. Spatial diffusion or the movement of disease

hrough time and space to new locations contributes to thenderstanding of the social and environmental factors thatffect risk and susceptibility. While investigation of the929 to 1937 epidemics contributed to the further under-tanding of the biological processes, no study to dateas described the geographical patterns. The aim ofhis study, therefore, is to use Geographic Informationystems (GIS) software capabilities to identify and add aeographical analysis of the epidemic.

ethods

review of the literature was undertaken using the Medarib database and Index Medicus, using the key words

abies, epidemic, and Trinidad. All scientific papers pub-ished on the epidemic, as well as extracts from thedministrative reports of the Director of Agriculture forhe years 1923 to 1948, were reviewed: for example,roceedings of the Agricultural Society of Trinidad andobago, the administrative report of the Surgeon General

or the period 1925 to 1941, and the Central Board ofealth, Hints Series No 3 were also reviewed. Data were

ollected on the number and location of all animaleaths.All available human cases were reviewed, and data

ere collected on age at death, gender, and geographicocation. Before mapping case distributions, careful con-ideration was given to all cases in the database withegard to case definition. The nature of the lesions in theervous system as described by Knutti,23 together withegri bodies and positive animal inoculation, were theethods used to establish the diagnosis of rabies.Mapping and spatial analysis were conducted using

rcGIS version 9.2. Several layers were superimposedn the distribution map of human rabies deaths. The firstayer used represented land use/land cover for the island.

iversity of land use/land cover represented at the time,t was difficult to show land use/land cover in its entirety.or these reasons, a generalized version of this map wasreated. The other dataset used was a generalized rainfallap for Trinidad. Previous studies have demonstrated

hat bats detect and use the earth’s magnetic field as annternal compass to re-orient and find their way back toheir roosts.24 Based on this evidence, the average dec-ination for the period under study was calculated usingnformation provided from the National Geophysical Dataenter (NGDC).25 The NGDC provides a free online ser-

vice that calculates magnetic declination based on date andtime and location on the earth’s surface.

Results

The data collected showed that the epidemic really began in1923 among cattle that were dying suddenly in Debe andMaraval. At that time, the deaths were attributed to theingestion of oleander leaves.26 In April of the same year,cattle continued to die, which attracted concern and encour-aged further investigation. After a careful inspection todiscover any poisonous weeds, particularly the local poi-sonous plants Brinvilliers (Spigelia anthelmintica) and wildipecacuanha (Asclepias curassavica) or spraying of the areawith insecticides, the cause of death was attributed to so-dium chloride poisoning.27 In the following year (1924),further reports of deaths among cattle in the same loca-tion (Maraval) went unrecorded. In July 1925, a diseasethought unrelated to the events of the previous yearsbroke out among cattle (young heifers) in St Anns, asuburb north of Port of Spain in which animals weredying of a peculiar disease, the chief signs being exces-sive salivation, marked constipation, and a staggeringgait followed by paralysis.28 In spite of early interven-ions by veterinary surgeons, all the animals died.

Preliminary investigations revealed that all the ani-als afflicted were left outdoors both day and night.tock in stables in the same environment were unaf-ected. As a prevention strategy, healthy animals wereemoved from pasture; however, some of these animalsontinued to die at varying periods from the time of theiremoval. It was also noticed that stock previously stabledemained healthy, although they were placed in closeontact with those removed from pasture. Postmortemxaminations of animals that died conducted by the vet-rinary surgeon provided a differential diagnosis thatncluded bulbar paralysis, botulism, and Grass tetany.he government pathologist confirmed the disease wasotulism after discovering Clostridum boutulinus inome of the dead animals.29 Towards the end of 1925nd early in 1926 similar reports of cattle dying were

30 Mungrue and Mahabir

In 1927, the disease reappeared in Diego Martin, while afew cases were also reported in St James, a town on thewestern outskirts of Port of Spain, and Laventille, 2miles east of Port of Spain. In the same year, disease incattle was also reported in Couva, 28 miles south of Portof Spain. With the exception of a few cases in DiegoMartin during the rainy season of 1928, the diseaseappeared to be waning, when suddenly in August of 1929there was resurgence in Siparia, 55 miles south of Port ofSpain, in which occurred the heaviest losses in livestockyet.

By this time the disease had spread to new areas suchas St Joseph to the north and Fyzabad to the southeast. In1929, 1930, and 1931, the death rate averaged over 1000animals per year, 90% were cattle, but the deaths ofhorses, mules, and donkeys, and even goats, sheep, andpigs were recorded. Only 2 of the cases occurred in dogs.At this time a full description of the disease was avail-able, resulting in a diagnosis of ascending myelitis. Post-mortem and laboratory findings were forwarded to re-search workers on botulism in the United States, and theyreported that they were convinced the disease was botu-lism. As a consequence, antitoxin was imported, but its

Figure 1. Map identifying communities (cities and towns) in Trinida

application did not seem to stop the disease. The datawere mapped using street address and geocoding, andshow both the location of all animal deaths and thedirection of spread over time (Figure 1).

The first reported case of the epidemic to occur inhumans is presented here in detail. All subsequent caseshad remarkably similar presentations. On July 16, 1929at 10:00 AM, a 15-year-old boy was seen by the DistrictMedical Officer (DMO) in Siparia. He complained ofsevere abdominal pains which had started about midday4 days prior, for which his mother administered “salts”(cathartic). Subsequently, 2 days prior to being seen hesuddenly cried out with pains in his right leg and feltfeverish. Shortly afterwards he noticed that his right legwas weak. The day prior to being seen fever continuedand the right leg was “dead” (no voluntary movements).On examination, his temperature was 101°F, pulse 96beats per minute (bpm), and respiratory rate (RR) 24 perminute; there was flaccid paralysis of the right lowerextremity with absent knee and plantar reflexes, in theabsence of clonus. All modalities of sensation were in-tact, and the remainder of his examination was normal.The diagnosis was ascending myelitis.30–32 The patient

ith reported animal deaths between 1923 and 1929, and the direction

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was referred but his parents preferred for him to die athome rather than at hospital. The DMO visited the pa-tient at home on the following day and recorded that hewas surprised to find that the paralysis had spread to theleft lower extremity. The patient’s bladder was greatlydistended as he did not pass urine that day nor did he passstool. His temperature rose to 103°F, pulse to 100 bpm,and RR to 26 per minute, yet he continued to be alert. For2 days he maintained a temperature of 102°F, but hisbreathing became very labored, he had difficulty swal-lowing, and salivation was profuse; as such he died at4:00 AM on July 20, 1929. The diagnosis of acute anterioroliomyelitis was vigorously defended and apparentlyas confirmed by pathological reports. By the end of929, there were 13 such cases. Table 1 summarizes byear, number of cases, incidence rate per 100,000 pop-lation, gender and age distribution of 72 of the 89 caseshich occurred during 1929 to 1937; mortality was00%. Reliable data for the remaining 17 cases could note recovered.The distribution of human cases from 1929 to 1937

as mapped at the community level using geocodingFigure 2). Eight maps were produced to show the pro-ression and direction of spread by year starting with therst set of cases in 1929. Each subsequent map is anggregate of all cases up to that year. A key to theistribution of cases by communities as mapped in Fig-re 2 is provided in Table 2. The adjacent island ofobago 22 miles north never recorded any cases.The mapped human deaths were overlaid on a land

se/land cover map showing forest, urban, swamp, rice,ocoa, coffee, banana, and citrus (Figure 3). No reportedases occurred in forested areas, although they providedn ideal habitat for vampire bats. In addition, in urbanreas, mainly Port of Spain and San Fernando, noeaths were reported, which may be partly attributedo better housing conditions, annoyances such as

Table 1. The distribution of human rabies cases in Trinidad, 1

Year 1929 1930 1931

No. of cases 13 3 4Incidence rate (per 100,000 pop.) 3.7 0.7 1.0Gender

Males 8 2 2Females 5 1 2

Age0–15 9 1 316–30 4 0 131–45 0 2 0� 46 0 0 0

oise, and better lighting. On the other hand, there was h

n almost identical overlap of the occurrence of deathsnd cultivation sites for cocoa, coffee, banana, and citrusroduction. Several factors may explain this finding: (1)ultivation sites provide farm animals for prey by hema-ophagous bats; (2) cultivation sites lack predators suchs snakes, hawks, and carnivorous bats; (3) poor housingllows easy access to humans by bats; and (4) poorousing encourages children and adolescents to spendore time outdoors, increasing their exposure to bats.ver half of the deaths (38) occurred in the age group 0

o 15 years.Trinidad is situated 11° north of the equator and has 2

easons, the rainy season during the months of June toovember and the dry season from December to May.verage rainfall was overlaid on the distribution of ra-ies cases (Figure 4); however, no relationshipsmerged. Although the epidemic lasted 9 years, thereere no deaths reported in the months of November orecember as shown in Figure 5.Spatial and temporal distribution of cases demon-

trated that the epidemic progressed along a northeast-rly direction (Figure 6). At the time of the epidemic,agnetic declination was calculated as 5°59’ W chang-

ng by 0°7’ W/year. The forward progression of thepidemic was approximately at right angles to magneticorth. In addition, the mean width of the outbreak was.5 km, and the forward annual velocity ranged from 7.5o 30 km/yr, with a mean of 12.5 km/yr.

iscussion

he major finding of the study was disease among ani-als followed a hierarchical diffusion pattern; ie, the

isease among animals started in an urban setting andpread over time to medium-sized towns, then to smallerowns, mainly along the western half of the island in aoutherly direction. On the other hand, disease among

9 to 1937

1932 1933 1934 1935 1936 1937 Total

5 0 7 21 4 15 721.2 0 1.6 4.8 3.4 3.4

3 0 3 8 1 10 372 0 4 13 3 5 35

2 0 5 9 1 8 383 0 1 3 1 6 190 0 1 6 1 1 110 0 0 3 1 0 4

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umans started in small towns, continued to affect small

32 Mungrue and Mahabir

Figure 2. Distribution of human deaths caused by rabies, 1929 to 1937.

The Rabies Epidemic in Trinidad of 1923 to 1937 33

towns but followed a diagonal pathway to the northeasttip of the island. The use of GIS technology capabilitiescan now link the epidemic model and the spatial diffu-sion model to predict the movement of an epidemic andthus identify likely communities at risk. The benefit of

Table 2. The number of human deaths in Trinidad caused by

Location 1929 1930 1931 1932

Siparia 8 1Rousillac 1 3Fyzabad 2San Francique 2Oropouche 3Mayo 1Gran Couva 1 1Beunos-Ayres 1Parry Lands 1BrazilGuanapoMaturiteSanta CruzValenciaTalparoTocoBicheSan JuanVega De Oropouche

Figure 3. Distributions of human rabies death

these capabilities includes strategic planning, such as theavailability of hospital beds, health-care professionals,equipment, and supplies required for an impending out-break, as well as preventive interventions like immuni-zation of communities at highest risk.

ies, by location, 1929 to 1937

1933 1934 1935 1936 1937 Total

942231211

3 33 31 1

12 127 71 1

4 412 12

1 13 3

rab

s superimposed on to land use/land cover.

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34 Mungrue and Mahabir

The spatial findings of our study also raise alternativeexplanations and several questions. Pawan explained theepidemic by suggesting (1) the flight or transit in sloopsand other vessels of infected bats from the mainland toTrinidad and (2) the infection of bats in Trinidad bysome latent, unrecognized “carrier” of the disease.33 Amore affordable explanation may now lie in the conceptof compartmentalization, whereby specific virus variantswithin a genotype tend to perpetuate among particularhosts in different geographic areas. Such associationsmay last for decades or longer.34 This is against theackground that the last reported case of rabies in Trin-dad prior to the epidemic was in 1912, a 17-year gap.eographic features, such as mountains and rivers, may

reate physical barriers to animal movement and pro-ote localized viral evolution in specialized host nic-

es.35 Also, the emergence of viral variants may occur

Figure 4. Distribution of human rabies

02468101214

Jan Feb Mar Apr May Jun July Aug Sep Oct Nov Dec

Month

No of cases

Figure 5. Distribution of cases by month, 1929 to 1937.

with extension of the host range.36 Notwithstanding,movements of infected animals to new unaffected areashave the potential to produce explosive, sustainable out-breaks.34

Although much travel was conducted between theislands of Trinidad and Tobago, approximately 22 milesacross the Caribbean Sea, the epidemic never reachedTobago. The outbreak is further characterized by manypeculiarities, the first of which was the apparent discon-nect between disease events occurring in animals andhumans. The first phase of the outbreak between 1923and 1931 was characterized predominantly by animalinfections, and the first documented human case was notrecorded until 1929. The disease occurring in animalsand man was not established as the same until September10, 1931, after much wrangling between veterinariansand physicians. Thus disease events in humans may haveoccurred but were misdiagnosed, particularly as acutepoliomyelitis. However, during the period 1925 to 1928,there were 7, 2, 0, and 0 reported cases of infantileparalysis or acute poliomyelitis, and there were no re-ported deaths from either acute poliomyelitis or ascend-ing myelitis. Lastly, several questions remain unan-swered such as why did the pattern of human diseaseoccur in only one direction without recurring in previ-ously infected areas. It is unlikely that all rabies infected

ths superimposed onto rainfall (inches).

bats in a particular area would have succumbed as Pawan

sup

The Rabies Epidemic in Trinidad of 1923 to 1937 35

himself showed survival after inoculation with infectedbrain extract.33 This raises the question, does survivalthen alter behavior or does the immunologic responseconfer incapability to further transmission? It appearsfrom the data that the epidemic ended at the northeastcoast of Trinidad, as all 15 cases that occurred in 1937occurred in that region of the island. This epidemicclearly established that bats were the mode of transmis-sion, and therefore, as the epidemic ended, it suggeststhat no susceptible bats remained.

During the period from July 16, 1929 to September 27,1929, 13 cases of rabies occurred in humans with 100%mortality. On the other hand, there was only 1 reportedcase of acute poliomyelitis in February 1929. Thisprompted the governor, on September 21, 1929, to de-clare acute poliomyelitis, encephalitis lethargic, and ce-rebrospinal fever, infectious diseases of the nervous sys-tem, as compulsory notifiable diseases. The immediatepublic health reaction was an intense investigation ofsanitary conditions of all premises and the surroundingenvironment where cases had occurred. Despite promptmeasures to have all nuisances removed and the sanitaryconditions improved, the epidemic did not abate.

Rainfall records for the period May to June in 1927 to1929 did not reveal an epidemiological association withdisease distribution, and there was no apparent seasonalvariation in cases except that there were no reported

Figure 6. Distribution of rabies

cases during the months of November and December

(Figure 4). This may be attributed to the use of decora-tive lights in houses and on trees, and the playing ofmusic during the festive seasons of both Diwali andChristmas, which occur during these months.

Our findings support the assertions that bat rabies ismigratory and seasonal, shifting to new colonies along aquite definite path.37 The epidemic progressed in a north-easterly direction and approximately at right angles tothe line of declination which approximates the earth’smagnetic field in Trinidad.

In conclusion, the only epidemic of rabies in Trinidadnot only established for the first time the transmission ofrabies by hematophagous (vampire) bats but continues toprovide peculiarities that even presently remain unex-plained. The bat rabies epidemic of 1923 to 1937 inTrinidad was migratory and seasonal, and its spatialdiffusion appears to have been linked to land use/landcover. The pattern of spread appears to be spatiallylinked to land use/land cover.

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