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

ORIGINAL RESEARCH
The Rabies Epidemic in Trinidad of 1923 to 1937: An
Evaluation with a Geographic Information System
Kameel 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 to
afflict humans with as many as 55,000 deaths annually. The case fatality rate remains the highest among
infectious 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 factors
identified in the literature were further explored such as land use/land cover, rainfall and magnetic
declination.
Results.—The bat rabies epidemic of 1923 to 1937 in Trinidad was migratory and seasonal, shifting
to new locations along a definite path. The pattern of spread appears to be spatially linked to land
use/land cover. The epidemic continues to present many unexplained peculiarities.
Conclusion.—Despite the fact that this epidemic occurred almost 7 decades ago, the application of
new tools available for public health use can create new knowledge and understanding of events. We
showed that the spatial of distribution of the disease followed a distinct pathway possible due to the use
of electromagnetic capabilities of bats.
Key words: rabies, GIS, epizootics
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 the
family Rhabdoviridae genus Lyssavirus, transmitted
through the bite of an infected mammal in which the
virus is present in the saliva.1–4
However, this is not the
only mode of transmission, as rabies can be acquired
with infected aerosolized tissue in caves inhabited by
rabid bats and in laboratory accidents.5–7
Transmission is
also possible by handling and skinning of infected car-
casses.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 as
the cause of death among 4 patients who were recipients
of organs and a vascular graft.11
A potential risk also
exists from contact with infected body fluids.12
The only
epidemic of rabies to have occurred on the island of
Trinidad was in 1929 to 1937. In that epidemic, bats, for
the first time, were identified as the mode of transmis-
sion. Bats are a major reservoir for variants of rabies
viruses and transmit the disease through biting, which
can sometimes go unrecognized.5,13–18
Support for the
effectiveness of this mode of transmission is derived
from laboratory data with silver-haired bats (Lasionyc-
teris noctivagans) and eastern pipistrelles (Pipistrellus
subflavus) that demonstrated a higher likelihood of in-
fection after superficial inoculation into cells of epider-
mal origin.19
Infection is primarily of the central nervous
system (CNS), leading to an acute progressive encepha-
lomyelitis in which most cases are fatal.
The annual number of deaths worldwide caused by
rabies is estimated to be 55,000, mostly in rural areas
of Africa and Asia, while the annual estimated cost of
rabies is $583.5 million (USD).20
Although mortality
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.
Mungrue@sta.uwi.edu).
WILDERNESS & ENVIRONMENTAL MEDICINE, 22, 28–36 (2011)

from rabies is considerably less in the New World.
Canada, documented 24 human rabies cases since
1924,21,22
emphasizing the global importance of this
disease. Trinidad continues to provide a habitat for a
wide variety of bats including the vampire bat. While
reports exist of bats biting humans, there has been no
confirmed human case of rabies in Trinidad since the
epidemic of 1929 to 1937.
The historical and social forces that influence disease
patterns in populations are critical in understanding the
epidemiology of diseases. While the identification of
biological processes is crucial, the contribution of other
factors such as land use, change affecting vector or host
habitats, human interaction with vectors, and climate are
also important to identify and have a geographical di-
mension. Spatial diffusion or the movement of disease
through time and space to new locations contributes to the
understanding of the social and environmental factors that
affect risk and susceptibility. While investigation of the
1929 to 1937 epidemics contributed to the further under-
standing of the biological processes, no study to date
has described the geographical patterns. The aim of
this study, therefore, is to use Geographic Information
Systems (GIS) software capabilities to identify and add a
geographical analysis of the epidemic.
Methods
A review of the literature was undertaken using the Med
Carib database and Index Medicus, using the key words
rabies, epidemic, and Trinidad. All scientific papers pub-
lished on the epidemic, as well as extracts from the
administrative reports of the Director of Agriculture for
the years 1923 to 1948, were reviewed: for example,
proceedings of the Agricultural Society of Trinidad and
Tobago, the administrative report of the Surgeon General
for the period 1925 to 1941, and the Central Board of
Health, Hints Series No 3 were also reviewed. Data were
collected on the number and location of all animal
deaths.
All available human cases were reviewed, and data
were collected on age at death, gender, and geographic
location. Before mapping case distributions, careful con-
sideration was given to all cases in the database with
regard to case definition. The nature of the lesions in the
nervous system as described by Knutti,23
together with
Negri bodies and positive animal inoculation, were the
methods used to establish the diagnosis of rabies.
Mapping and spatial analysis were conducted using
ArcGIS version 9.2. Several layers were superimposed
on the distribution map of human rabies deaths. The first
layer used represented land use/land cover for the island.
Due to the scale of this dataset, 1:150,000, and the
diversity of land use/land cover represented at the time,
it was difficult to show land use/land cover in its entirety.
For these reasons, a generalized version of this map was
created. The other dataset used was a generalized rainfall
map for Trinidad. Previous studies have demonstrated
that bats detect and use the earth’s magnetic field as an
internal compass to re-orient and find their way back to
their roosts.24
Based on this evidence, the average dec-
lination for the period under study was calculated using
information provided from the National Geophysical Data
Center (NGDC).25
The NGDC provides a free online ser-
vice that calculates magnetic declination based on date and
time and location on the earth’s surface.
Results
The data collected showed that the epidemic really began in
1923 among cattle that were dying suddenly in Debe and
Maraval. At that time, the deaths were attributed to the
ingestion 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 to
discover any poisonous weeds, particularly the local poi-
sonous plants Brinvilliers (Spigelia anthelmintica) and wild
ipecacuanha (Asclepias curassavica) or spraying of the area
with 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 disease
thought unrelated to the events of the previous years
broke out among cattle (young heifers) in St Anns, a
suburb north of Port of Spain in which animals were
dying of a peculiar disease, the chief signs being exces-
sive salivation, marked constipation, and a staggering
gait followed by paralysis.28
In spite of early interven-
tions by veterinary surgeons, all the animals died.
Preliminary investigations revealed that all the ani-
mals afflicted were left outdoors both day and night.
Stock in stables in the same environment were unaf-
fected. As a prevention strategy, healthy animals were
removed from pasture; however, some of these animals
continued to die at varying periods from the time of their
removal. It was also noticed that stock previously stabled
remained healthy, although they were placed in close
contact with those removed from pasture. Postmortem
examinations of animals that died conducted by the vet-
erinary surgeon provided a differential diagnosis that
included bulbar paralysis, botulism, and Grass tetany.
The government pathologist confirmed the disease was
botulism after discovering Clostridum boutulinus in
some of the dead animals.29
Towards the end of 1925
and early in 1926 similar reports of cattle dying were
reported in Diego Martin 4 miles west of Port of Spain.
The Rabies Epidemic in Trinidad of 1923 to 1937 29

In 1927, the disease reappeared in Diego Martin, while a
few cases were also reported in St James, a town on the
western outskirts of Port of Spain, and Laventille, 2
miles east of Port of Spain. In the same year, disease in
cattle was also reported in Couva, 28 miles south of Port
of Spain. With the exception of a few cases in Diego
Martin during the rainy season of 1928, the disease
appeared to be waning, when suddenly in August of 1929
there was resurgence in Siparia, 55 miles south of Port of
Spain, in which occurred the heaviest losses in livestock
yet.
By this time the disease had spread to new areas such
as St Joseph to the north and Fyzabad to the southeast. In
1929, 1930, and 1931, the death rate averaged over 1000
animals per year, 90% were cattle, but the deaths of
horses, mules, and donkeys, and even goats, sheep, and
pigs 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 they
reported that they were convinced the disease was botu-
lism. As a consequence, antitoxin was imported, but its
application did not seem to stop the disease. The data
were mapped using street address and geocoding, and
show both the location of all animal deaths and the
direction of spread over time (Figure 1).
The first reported case of the epidemic to occur in
humans is presented here in detail. All subsequent cases
had remarkably similar presentations. On July 16, 1929
at 10:00 AM, a 15-year-old boy was seen by the District
Medical Officer (DMO) in Siparia. He complained of
severe abdominal pains which had started about midday
4 days prior, for which his mother administered “salts”
(cathartic). Subsequently, 2 days prior to being seen he
suddenly cried out with pains in his right leg and felt
feverish. Shortly afterwards he noticed that his right leg
was weak. The day prior to being seen fever continued
and the right leg was “dead” (no voluntary movements).
On examination, his temperature was 101°F, pulse 96
beats per minute (bpm), and respiratory rate (RR) 24 per
minute; there was flaccid paralysis of the right lower
extremity with absent knee and plantar reflexes, in the
absence 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
Figure 1. Map identifying communities (cities and towns) in Trinidad with reported animal deaths between 1923 and 1929, and the direction
of spread.
30 Mungrue and Mahabir

was referred but his parents preferred for him to die at
home rather than at hospital. The DMO visited the pa-
tient at home on the following day and recorded that he
was surprised to find that the paralysis had spread to the
left lower extremity. The patient’s bladder was greatly
distended as he did not pass urine that day nor did he pass
stool. His temperature rose to 103°F, pulse to 100 bpm,
and RR to 26 per minute, yet he continued to be alert. For
2 days he maintained a temperature of 102°F, but his
breathing became very labored, he had difficulty swal-
lowing, and salivation was profuse; as such he died at
4:00 AM on July 20, 1929. The diagnosis of acute anterior
poliomyelitis was vigorously defended and apparently
was confirmed by pathological reports. By the end of
1929, there were 13 such cases. Table 1 summarizes by
year, number of cases, incidence rate per 100,000 pop-
ulation, gender and age distribution of 72 of the 89 cases
which occurred during 1929 to 1937; mortality was
100%. Reliable data for the remaining 17 cases could not
be recovered.
The distribution of human cases from 1929 to 1937
was mapped at the community level using geocoding
(Figure 2). Eight maps were produced to show the pro-
gression and direction of spread by year starting with the
first set of cases in 1929. Each subsequent map is an
aggregate of all cases up to that year. A key to the
distribution of cases by communities as mapped in Fig-
ure 2 is provided in Table 2. The adjacent island of
Tobago 22 miles north never recorded any cases.
The mapped human deaths were overlaid on a land
use/land cover map showing forest, urban, swamp, rice,
cocoa, coffee, banana, and citrus (Figure 3). No reported
cases occurred in forested areas, although they provided
an ideal habitat for vampire bats. In addition, in urban
areas, mainly Port of Spain and San Fernando, no
deaths were reported, which may be partly attributed
to better housing conditions, annoyances such as
noise, and better lighting. On the other hand, there was
an almost identical overlap of the occurrence of deaths
and cultivation sites for cocoa, coffee, banana, and citrus
production. Several factors may explain this finding: (1)
cultivation sites provide farm animals for prey by hema-
tophagous bats; (2) cultivation sites lack predators such
as snakes, hawks, and carnivorous bats; (3) poor housing
allows easy access to humans by bats; and (4) poor
housing encourages children and adolescents to spend
more time outdoors, increasing their exposure to bats.
Over half of the deaths (38) occurred in the age group 0
to 15 years.
Trinidad is situated 11° north of the equator and has 2
seasons, the rainy season during the months of June to
November and the dry season from December to May.
Average rainfall was overlaid on the distribution of ra-
bies cases (Figure 4); however, no relationships
emerged. Although the epidemic lasted 9 years, there
were no deaths reported in the months of November or
December as shown in Figure 5.
Spatial and temporal distribution of cases demon-
strated that the epidemic progressed along a northeast-
erly direction (Figure 6). At the time of the epidemic,
magnetic declination was calculated as 5°59’ W chang-
ing by 0°7’ W/year. The forward progression of the
epidemic was approximately at right angles to magnetic
north. In addition, the mean width of the outbreak was
4.5 km, and the forward annual velocity ranged from 7.5
to 30 km/yr, with a mean of 12.5 km/yr.
Discussion
The major finding of the study was disease among ani-
mals followed a hierarchical diffusion pattern; ie, the
disease among animals started in an urban setting and
spread over time to medium-sized towns, then to smaller
towns, mainly along the western half of the island in a
southerly direction. On the other hand, disease among
humans started in small towns, continued to affect small
Table 1. The distribution of human rabies cases in Trinidad, 1929 to 1937
Year 1929 1930 1931 1932 1933 1934 1935 1936 1937 Total
No. of cases 13 3 4 5 0 7 21 4 15 72
Incidence rate (per 100,000 pop.) 3.7 0.7 1.0 1.2 0 1.6 4.8 3.4 3.4
Gender
Males 8 2 2 3 0 3 8 1 10 37
Females 5 1 2 2 0 4 13 3 5 35
Age
0–15 9 1 3 2 0 5 9 1 8 38
16–30 4 0 1 3 0 1 3 1 6 19
31–45 0 2 0 0 0 1 6 1 1 11
Ն 46 0 0 0 0 0 0 3 1 0 4

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

towns but followed a diagonal pathway to the northeast
tip of the island. The use of GIS technology capabilities
can now link the epidemic model and the spatial diffu-
sion model to predict the movement of an epidemic and
thus identify likely communities at risk. The beneﬁt of
these capabilities includes strategic planning, such as the
availability 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.
Table 2. The number of human deaths in Trinidad caused by rabies, by location, 1929 to 1937
Location 1929 1930 1931 1932 1933 1934 1935 1936 1937 Total
Siparia 8 1 9
Rousillac 1 3 4
Fyzabad 2 2
San Francique 2 2
Oropouche 3 3
Mayo 1 1
Gran Couva 1 1 2
Beunos-Ayres 1 1
Parry Lands 1 1
Brazil 3 3
Guanapo 3 3
Maturite 1 1
Santa Cruz 12 12
Valencia 7 7
Talparo 1 1
Toco 4 4
Biche 12 12
San Juan 1 1
Vega De Oropouche 3 3
Figure 3. Distributions of human rabies deaths superimposed on to land use/land cover.

The spatial findings of our study also raise alternative
explanations and several questions. Pawan explained the
epidemic by suggesting (1) the flight or transit in sloops
and other vessels of infected bats from the mainland to
Trinidad and (2) the infection of bats in Trinidad by
some latent, unrecognized “carrier” of the disease.33
A
more affordable explanation may now lie in the concept
of compartmentalization, whereby specific virus variants
within a genotype tend to perpetuate among particular
hosts in different geographic areas. Such associations
may last for decades or longer.34
This is against the
background that the last reported case of rabies in Trin-
idad prior to the epidemic was in 1912, a 17-year gap.
Geographic features, such as mountains and rivers, may
create physical barriers to animal movement and pro-
mote localized viral evolution in specialized host nic-
hes.35
Also, the emergence of viral variants may occur
with extension of the host range.36
Notwithstanding,
movements of infected animals to new unaffected areas
have the potential to produce explosive, sustainable out-
breaks.34
Although much travel was conducted between the
islands of Trinidad and Tobago, approximately 22 miles
across the Caribbean Sea, the epidemic never reached
Tobago. The outbreak is further characterized by many
peculiarities, the first of which was the apparent discon-
nect between disease events occurring in animals and
humans. The first phase of the outbreak between 1923
and 1931 was characterized predominantly by animal
infections, and the first documented human case was not
recorded until 1929. The disease occurring in animals
and man was not established as the same until September
10, 1931, after much wrangling between veterinarians
and physicians. Thus disease events in humans may have
occurred but were misdiagnosed, particularly as acute
poliomyelitis. However, during the period 1925 to 1928,
there were 7, 2, 0, and 0 reported cases of infantile
paralysis 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 disease
occur in only one direction without recurring in previ-
ously infected areas. It is unlikely that all rabies infected
bats in a particular area would have succumbed as Pawan
Figure 4. Distribution of human rabies deaths superimposed onto rainfall (inches).
0
2
4
6
8
10
12
14
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.

himself showed survival after inoculation with infected
brain extract.33
This raises the question, does survival
then alter behavior or does the immunologic response
confer incapability to further transmission? It appears
from the data that the epidemic ended at the northeast
coast of Trinidad, as all 15 cases that occurred in 1937
occurred in that region of the island. This epidemic
clearly established that bats were the mode of transmis-
sion, and therefore, as the epidemic ended, it suggests
that 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 reported
case of acute poliomyelitis in February 1929. This
prompted 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 immediate
public health reaction was an intense investigation of
sanitary conditions of all premises and the surrounding
environment where cases had occurred. Despite prompt
measures to have all nuisances removed and the sanitary
conditions improved, the epidemic did not abate.
Rainfall records for the period May to June in 1927 to
1929 did not reveal an epidemiological association with
disease distribution, and there was no apparent seasonal
variation in cases except that there were no reported
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 of
music during the festive seasons of both Diwali and
Christmas, which occur during these months.
Our findings support the assertions that bat rabies is
migratory and seasonal, shifting to new colonies along a
quite definite path.37
The epidemic progressed in a north-
easterly direction and approximately at right angles to
the line of declination which approximates the earth’s
magnetic field in Trinidad.
In conclusion, the only epidemic of rabies in Trinidad
not only established for the first time the transmission of
rabies by hematophagous (vampire) bats but continues to
provide peculiarities that even presently remain unex-
plained. The bat rabies epidemic of 1923 to 1937 in
Trinidad was migratory and seasonal, and its spatial
diffusion appears to have been linked to land use/land
cover. The pattern of spread appears to be spatially
linked to land use/land cover.
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The Rabies Epidemic in Trinidad of 1923 to 1937: An Evaluation with a Geographic Information System