Trypanosoma
evansi (surra)
in camels: a factor in the weakening of Islam?
William G. Clarence-Smith
ABSTRACT
Trypanosoma evansi, the most lethal disease
of camels, is caused by blood parasites, which provoke serious and often fatal
anaemia. During the last few thousand years, Trypanosoma brucei brucei, causing
sleeping sickness in tropical Africa, evolved into T. evansi in the
Sudanic-Sahelian region of Africa, to the north of the tsetse belts. The new
disease was transmitted by blood-sucking flies, notably Tabanids. Camels then
carried the disease across the Sahara to Morocco around the 7th or 8th
century of the Common Era, whence Islamic armies and caravans further dispersed
it. Although the details of this process remain to be discovered, the changing
size of the parasite yields a very rough chronology. Moreover, the disease
remained largely confined to Islamdom in the Old World. As camels and equids
were fundamental to Islamic military and economic power, this disease can be
seen as having contributed to the weakening of Islamdom in its long contest
with Christendom.
Introduction
Trypanosoma evansi is the most lethal disease of camels. If
untreated, it can result in up to 90% mortality among infected animals,
although a partial resistance can build up. (Irwin 2010: 32-3; Röttcher et al.
1987; Leese 1927: 222-4) Also known by its Indian name of surra, Trypanosoma evansi
further kills horses, donkeys and mules across the tropical and sub-tropical
world, and can be fatal to dogs and elephants. It weakens cattle and buffaloes,
but does not affect humans. A single-cell parasite of the blood, it is almost
always transmitted mechanically by blood-sucking flies, notably flies of the Tabanus genus. Any kind of direct blood
contact can spread the malady, however, and vampire bats are vectors in the
Americas. The parasites destroy red blood cells, provoking serious and often
fatal anaemia. (Hoare 1972; Luckins 1988)
It is suggested here that the diffusion of Trypanosoma evansi was a factor in the decline of the Islamic
world, albeit one that has been completely neglected to date. Paradoxically,
the great initial military triumphs of the new religion created a perfect
environment for the disease to flourish. The intensification of cross-Saharan
trade by Muslims probably brought this parasitic disease from Sub-Saharan Africa
into the Mediterranean Basin in the first place. Islamic armies and caravans,
unifying the desert edges of the Old World as never before, then provided ideal
conditions for the further dispersal of T.
evansi. As the disease only penetrated into the Iberian and Russian fringes
of Europe, it contributed to the weakening of Islamdom in its multi-secular
contest with Christendom.
Semper
ex
Trypanosoma brucei, causing nagana
or sleeping sickness of animals in Africa, at some point evolved into Trypanosoma evansi. The two parasites
are morphologically virtually indistinguishable, and the evidence points firmly
to T. evansi emerging from T. brucei. Whereas T. brucei parasites undergo genetic exchange and development inside
tsetse flies, T. evansi has lost that
capacity, adapting to mechanical transmission by blood contact. T. evansi protozoa are thus clonal,
reproducing by longitudinal division. (Hoare 1972: 97-8, 582-3, 593; Luckins 1988:
137-8; Gibson 2001: 643-6)
Analysis of the DNA of the parasite’s kinetoplast reveals that this was
a ‘comparatively recent’ mutation. (Stevens et al. 1999: 110, 113) More
specifically, T. evansi parasites
‘may have evolved as clonal entities only in the last few thousand
years.’(Gibson 2001: 644) The kinetoplast is a tiny organoid, 0.6 microns long.
As T. evansi came to rely on
mechanical transmission, the DNA of the kinetoplast was no longer needed for
the protozoa to develop inside tsetse flies, leading to genetically
irreversible mutations. (Hoare 1972: 103-6, 568; Gibson 2001)
Hoare has often been misunderstood as having written that the mutation
giving rise to T. evansi took place
in North Africa, whereas, in reality, he indicates that the process occurred in
the Sahel-Sudanic zone of Africa, to the north of tsetse belts. Anywhere
between modern Senegal and Somalia, biting flies could have spread a mutant
form of T. brucei. Patterns of
resistance to the parasite suggest that it was the Horn of Africa, with its
notably patchy and discontinuous tsetse belts, that witnessed the birth of T. evansi. There exists a degree of
resistance to the disease among horses and donkeys in Northern Kenya, Somalia
and the Nilotic Sudan, and indigenous breeds of Somali dogs are immune. (Hoare
1972: 557, 579-80, 583-5)
If the disease did emerge in the Horn of Africa, it would easily have
spread from east to west along the Sahel-Sudanic zone to West Africa, where it
is enzootic and found particularly among camels. (Ford 1971: 92-3, 377)
Although little is known about ancient east-west trade routes in the northern
half of Africa, camels moved across the southern fringes of the Sahara by the
third or fourth century CE. (Bulliet 1975: 132-4) Caravans of donkeys, equally able
to transmit the disease, were also widely employed. (Roberts 1987: 14-15, 62-4)
The West African connection is important, because measuring parasites
underpins the theory that T. evansi
first crossed the Sahara along the western routes, arriving in Morocco. The
parasite is about 20 microns long at 5 degrees west of Greenwich, corresponding
to northern Morocco, and it increases in size eastwards from this point, to
reach some 27.5 microns in the Philippines. According to Hoare, this indicates
that Morocco was the centre of diffusion north of the Sahara. (Hoare 1972: 568,
579) This evidence on the size of parasites does not support other possible
routes, such as the Nile valley, or the short maritime crossing of the Red Sea
or the Gulf of Aden.
Moreover, parasitologists believe that T. evansi must have been brought to North Africa by camels,
because equids die more quickly than camels when they contract the disease, and
the Sahara routes are long and slow. (Hoare 1972: 583-6) A strong supporting
argument is that equids are not known to have crossed the great desert from
south to north after the introduction of camels, although they continued to
come from north to south. (Law 1980; Mahadi 1992: 120)
The diffusion of Trypanosoma evansi across Islamdom
The most likely time for T. evansi
to have entered Morocco was when camels began to cross the western swathes of
the great desert more regularly and in greater numbers. The establishment of
Islamic rule in the Maghrib, from 661 CE, is known to have resulted in a
considerable intensification of cross-Saharan traffic. (Bulliet 1975: 138-40)
Although it is possible that T. evansi’s
arrival in the Mediterranean Basin somewhat predated the arrival of Islam, the
two processes were probably intimately related. New trading connections
provided the necessary density of camels making voyages for the parasite to
survive the desert crossing and become established in its new environment. This
is in part because the disease is seasonal, often being described as a ‘summer’
plague. (Irwin 2010: 33) Seasonality is in turn closely related to the
appearance of dense swarms of flies, typically during and after heavy rainfall.
(Leese 1927: 243) Indeed, the usual Arabic word for T. evansi is dhubâb (debab), which simply means fly. (Leese
1927: 250-1)
Trading caravans provided ideal conditions for the subsequent dispersal
of T. evansi out of Morocco, together
with equids and camels in Islamic armies, whether as mounts or for logistic
purposes. (Cauvet 1926: 28-32; Irwin 2010: 151-3).
Eventually, the disease reached the furthest corners of the Islamic world, and
spilled over into the rest of Asia, probably entering the Philippines around
1900 CE. (Clarence-Smith 2010: 132)
Assuming that the malady arrived in Morocco around 700 CE, and then
marched across North Africa and Asia with absolute regularity, it would have
advanced about 650 miles, or some 1,000 kilometres, every century. However, it
is far more likely that the disease spread quite fast to modern Libya, which
may have provided an initial barrier, as Tabanid flies are rare in this arid
area. (Leese 1927: 251). Once in Egypt, however, the
disease would probably have progressed rapidly to the Indus valley, and then
more slowly across South and Southeast Asia.
Ignorance about the timing of T.
evansi’s diffusion across the Islamic world contrasts with the historical
record of the introduction and spread of the disease in the Americas. In the
sixteenth century, the Spaniards brought it to Mesoamerica, together with
equids, but it did not traverse the densely forested Isthmus of Panama. Two
further independent importations, into Venezuela and the Brazilian Amazon
respectively, can be dated with some certainty to the early decades of the
nineteenth century, and the progress of the disease from coastal foci has been
charted. (Hoare 1972: 557, 560-1, 569, 587; Canelón and Meléndez 2003)
Even the limits attained by T.
evansi in Asia remain uncertain, although the prevalence of sufficient
concentrations of Tabanid flies was probably the main factor determining the
reach of the disease. The furthest north in the world that T. evansi has been recorded is around 55 degrees north,
on the
Much about T. evansi may lie
in old Islamic veterinary writings, which appeared from the mid-eighth century
CE, in Abbasid times. They were centred on horses and falcons, reflecting the
importance of hunting. (Schimmel 2003: 4) Among them was a work by Ahmad b.
al-Hasan ibn al-Ahnaf, dating from around 1100 CE, and relating to horses,
donkeys and mules. Chapter 27 dealt with the ‘emaciation, weakness and anorexia’
of equids. (Kamal 1975: 735-6) This could refer to T. evansi, although it would be necessary to consult the Arabic
text to find out more. Veterinary manuals were particularly common under Mamluk
rule in Egypt and Syria, from 1250 to 1517, when cavalry units from the
Eurasian steppe came to power. (Kamal 1975: 735; Schimmel 2003: 5) The Ottomans
had animal hospitals by the sixteenth century, funded by awqâf, charitable trusts, which may have left records. (Foltz 2006:
5)
One detailed examination of alterations in patterns of camel breeding in
the lands of Islam concerns the movement of Turkic peoples into northeastern
Iran in the eleventh century CE. Richard Bulliet argues that a cooling of the
climate in this area was the chief cause of these migrations, especially
exceptionally cold winters. (Bulliet 2009: 96-117) However, he does not
consider whether a colder climate might have reduced the number of flies
spreading T. evansi.
In the absence of studies of camel raising, the
history of equids in Islamdom may suggest the impact of the disease. Thus, the
spread of T. evansi may account for a
hitherto unexplained crisis in the equine economy of southern Arabia. There is
much evidence for horse exports to mediaeval and early modern South Asia from
ports in this area, and parts of Yemen enjoyed a great reputation for horse
breeding. (Fattah 1997: 160, 235) By the early nineteenth century, this had
ceased, and horses in Yemen were rare and of poor quality. (Greely 1975:
22) The ‘air’ of Yemen was
alleged to cause degeneracy in its equids. (Balfour 1871: II, 616) In the
1930s, horses were imported into the north and hardly ever seen in the south. (Coon 1968:
203) However, there are other
possible explanations for the crisis, such as surges of African Horse Sickness,
a viral ailment, crossing the Red Sea.
A similar straw in the wind is that Ottoman statesmen became
increasingly worried that they disposed of insufficient horses for military
purposes, as Austrian and Russian armies pressed ever further into the empire in
the eighteenth century. These fears resulted in sporadic prohibitions on horse
exports from Iraq to India, even though the Porte was also greatly concerned
about the ‘drain’ of bullion to South Asia. The Crimean War of 1854-56 caused a
renewed spurt of Ottoman anxiety. (Fattah 1997: 74-5, 105-6, 111, 160-1, 173-6,
183; Ammon 1983: 278-82; Barendse 2001: 30) Breeding of horses in the
Iraqi-Syrians borderlands prospered, however, possibly because flies were
scarce in this dry zone. Lady Blunt reported that horses were exceptionally
healthy in this region in the 1870s. (Blunt 1968: II, 263) In contrast, camel
trypanosomiasis was prevalent in the areas flooded by the Tigris and Euphrates
rivers. (Leese 1927: 224)
Conditions were less favourable in Persia, where a disease of livestock
was reported in 1876, which was later demonstrated to have been T. evansi. (Luckins 1988: 139) It was
probably no coincidence that, from around this time, prices of equids soared in
Persia, exports dwindled, and some tribes faced acute shortages of horses. (Encyclopaedia Britannica 1911: XXI, 196)
That said, drought may also have played its part.
Moving to South Asia, strong resistance to the parasite demonstrated by
bovids prompts a suggestion that the disease had been present for a long time.
(Leese 1927: 223) However, this is insufficient to justify Hoare’s claim that T. evansi dated back to ‘the remote
past’ or ‘time immemorial,’ given that he notes that a qualified bovid immunity
to T. evansi could be acquired in as
little as twenty years. (Hoare 1972: 555, 581).
The numerous names for the malady in the nineteenth century again
suggest that the disease had been present for many generations. Griffith Evans,
the scientist who discovered the parasite in 1880, noted that the common
Hindustani term was surra, meaning
‘rotten’ or ‘withered.’ (Evans 1881: 1-2, 84) Although it was this term that
entered the literature, a plethora of other names were in use. Some twenty were
recorded in the northwest of British India alone, where both camels and equids
were present in significant numbers. (Leese 1927: 224)
It may be that T. evansi
spread during the Delhi Sultanate of the thirteenth century CE, when a Mamluk
cavalry regime greatly strengthened links with the Islamic world. A Middle Eastern
or Inner Asian origin for the disease is certainly propounded, inasmuch as the
word surra allegedly derives from the
Arabic word for epilepsy, sara‘. (Phillott 1911: 39) This derivation
may be spurious, however, as there is no indication that speakers of Arabic
ever used this word to designate T.
evansi. (Adel Aulaqi, personal communication) Nevertheless, the fact that
an Arabic etymology was suggested probably reflected the belief that the
disease reached South Asia from the Middle East, either traveling with camel
and equid caravans, or brought by horses coming by sea.
Colonial triumphalism: quarantine, entomology
and drugs
As Western colonialists triumphed over Islam from the 1750s, the new masters
of the world developed techniques with which to fight T. evansi. Although the disease was by no means eradicated, control
improved the West’s military and economic position in the lands of Islam. In
particular, from the beginning of the British conquest of India in the
mid-eighteenth century, horses and camels played a significant part in Western
military campaigns over a vast area. (Cauvet 1926: 42-52; Bulliet 1975: 237-58)
At the same time, inroads into the malady formed part of a broader scientific
justification for formal and informal imperialism.
Simply knowing more about the disease was an important step forward.
European scientists first observed trypanosomes in the blood of trout and frogs
in 1843, leading up to Griffith Evans’ great discovery in the Punjab in 1880.
India’s Imperial Bacteriological Laboratory then investigated T. evansi extensively in its early
years. (Ware 1961: 25, 32) This helped to avoid incorrect diagnosis, for
example by confusing T. evansi in
horses with equine piroplasmosis [horse tick fever; Texas fever], caused by two
other protozoan blood parasites, Babesia
equi and Babesia caballi,
transmitted by blood-sucking ticks. (Lloyd 1987: 433-5)
Early twentieth-century successes in preventing the entry of T. evansi into areas of European
settlement were mainly due to rapid diagnosis, followed by the slaughter of
infected animals, and the imposition of strict quarantine. Imported camels were
responsible for outbreaks in Namibia [German South West Africa], the United
States, and Western Australia in the decade of the 1900s. In none of these
three cases was T. evansi allowed to gain a permanent foothold. (Hoare 1972:
560; Leese 1927: 223; Reid 2002: 223; Röttcher et al. 1987: 464)
Preventing transmission by insects was a second measure, although it did
not take Western scientific advances for local peoples to make the connection
between biting flies and infection. In what is today northern Nigeria, smoke
and herbal remedies served to discourage flies from biting animals in the
1820s. (Law 1980: 81-2) Evans noted that Punjabis blamed biting flies for
spreading T. evansi, although he
himself equivocated, opining that infected water was the ultimate source.
(Evans 1881: 8-9) Research on tsetse-borne trypanosomes helped to focus scientific
attention on flies, and the role of Tabanids in passing on T. evansi was first scientifically described in 1901. (Hoare 1972:
571)
Veterinarians then concentrated on insect control. Australia’s Northern
Territory, home to significant numbers of camels and horses, was seen as
vulnerable to spread from Indonesia’s ponies. This led to experiments with
‘large fly-proof stables,’ and washing animals with an emulsion of castor oil
and soda. (Bulletin of the Imperial
Institute, 12, 1914: 116) In northwestern British India, ‘mosquito
curtains’ were found to be effective experimentally, but not practically. Other
strategies were avoiding areas where flies were known to abound, burning
greenwood fires to windward of stock, covering vulnerable areas on beasts with
sacking, and ‘clumping’ animals to improve their own herd defences. Biological
control was tried, using hornets and dragon-flies against flies, and chalcids
against eggs. (Leese 1927: 242, 247-9)
As the sheer abundance and variety of biting flies made insect control
difficult, chemical treatments moved to the fore. Alfred Lingard first
demonstrated the specificity of arsenic in treating trypanosomiasis in India.
(Ware 1961: 37) Combinations of arsenic and antimony soon proved effective,
especially if the disease was quickly diagnosed. (Leese 1927: 218, 241-2, 247,
254) The main drug to emerge was Suramin, also called Naganol or Bayer 205.
India’s Imperial Bacteriological Laboratory reported in 1927 that it had
achieved a 94% success rate, when administering Naganol ‘by the intra-thecal
route.’ (Ware 1961: 39) Injected intravenously as a prophylactic, Naganol
protected the equids of Burma’s military police in the 1930s. (Rippon 1961: 70)
Chemical treatments are no magic bullet, however, and the tendency has
been for T. evansi to remain enzootic
in its domain. Resistance has built up in camels to Suramin, and to the more
recently introduced Quinapyramine family of drugs. (Röttcher et al. 1987:
466-7; Wernery and Kaaden 2002: 280-2) After initial successes, there followed
decades of stagnation in the production of new trypanocides, and research and
experimentation have remained inadequate. (Touratier 1999)
Conclusion
For the emergence of surra
from the mists of the deep past, historians will have to remain reliant on
other disciplines. Better techniques of analyzing the DNA of the parasite’s
kinetoplast may enable more precise dates to be attributed to when this scourge
arose in Africa, as well as more exact locations of origin. (Canelón and
Meléndez 2003) Taking more measurements of the size of the parasites might also
suggest an improved chronology for its dispersion. Whether archaeologists can
throw light on this conundrum remains to be seen.
For documented history, and especially for the period of the growth and
decline of Islamdom, the focus for new research should be on veterinary
materials, particularly those in Arabic, Persian, Turkish, Armenian, and other
regional languages. This requires considerable linguistic skill, and depends on
painstakingly gathering fragmentary scraps of surviving evidence. Moreover,
there is a need to carefully interpret the formulations of Islamicate
veterinarians, who worked in conditions preceding the scientific revolution.
Concerning the central suggestion of this paper, namely that T. evansi undermined the economic and
military efficacy of Islamic states in their contest with the West, this paper
has not been able to do more than formulate a working hypothesis. There is a
need to scour documents that reveal official or mercantile preoccupations about
the state of camels and equids. The most promising sources are probably
military in nature, with an emphasis on horses, but the proverbial Arab love of
camels may also yield useful results.
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