Complex homoeopathy in the management of African Horse Sickness.
Niven, A. G.
putrid blood for more than two
ABSTRACT The Gauteng region of South Africa is affected by years. Any contaminated and
outbreaks of African Horse Sickness on a regular and seasonal infected substances, from
basis. This viral disease is transmitted by flies of the Culicoides mucous and snot to post mortem
spp. Fly activity and therefore the incidence of disease is related to contaminants must be
seasonal rainfall patterns. Evidence is presented that indicates adequately cleaned and
encouraging results; as indicated by below expected death rates, disinfected.
when horses are treated exclusively with homoeopathic medicines. EPIDEMIOLOGY
When combined with anti-inflammatory and or antibiotic medications The disease is endemic in
homoeopathy was unable to demonstrate significantly improved Central and Eastern Africa where
results. it is available on an annual basis
to spread mainly to Southern
Key words: African Horse Sickness. Equine. Homoeopathy. Virus. Africa. From time to time it may
spread to North Africa, the Middle
Niven AG. Complex homoeopathic treatment in the management of East and Spain. Serotype 9
African Horse Sickness. 2005 Conference of the British Association caused havoc in Iran during
of Homoeopathic Veterinarians. 1959, from where it spread to the
Persian Gulf as well as into India
INTRODUCTION was the 1855 outbreak in the and Pakistan, Turkey and
African Horse Sickness (AHS) is Cape when some seventy Afghanistan during 1960-61.
an infectious viral disease of thousand horses, making up Estimates indicated that a total of
equines caused by members of nearly forty per cent of the total some 300,000 horses were lost
the Orbivirus genus in the family equine population, succumbed to during this outbreak. Spanish
Reoviridae. Midges of the infection. Remember that we are outbreaks between 1987-90 were
Culicoides species transmit the talking about massive losses thought to have been carried by a
disease. occurring at a time when horses group of Burchell’s zebra Equus
HISTORY were of enormous importance as burchelli imported from Namibia.
The disease occurs frequently in working and transport animals. It Apart from the NE Transvaal the
most countries of sub-Saharan is not difficult to imagine the great disease is not endemic in South
Africa, and has been recorded disruption and distress. It was as Africa. The disease appears first
since the 14th century . Records early as 1900 that evidence there during early summer, Dec
of the Dutch East India Company confirming the requirement for an and Jan and gradually works its
often refer to the disease as a insect vector was established, way southwards, depending on
significant problem, including a although it was not until 1944 that climatic conditions being
reference to an outbreak in 1719, du Toit reported that the midge favourable for the breeding of the
in Cape Town where some Culicoides imicola was implicated Culicoides midges. This is
seventeen hundred horses were as the vector of AHS and a offered as the explanation for the
lost . Many explorers; including similar disease called Bluetongue disease regularly not appearing
Livingston and hunters such as in sheep. in many years in areas such as
Gordon Cumming also sustained AETIOLOGY Gauteng, Free State and the
severe losses. The pioneers of AHS viruses are classified in the Cape. Good early summer rains
early, modern Southern Africa, genus Orbivirus and family often indicate that virus will be a
including the much traveled Reoviridae. The virus has many problem during that season. In
Voortrekkers also experienced relationships with other the summer rainfall areas of
many difficulties with AHS. A orbiviruses, including those that Southern Africa, AHS enjoys
major reason for the placement cause Bluetongue in sheep and warm coastal regions and moist
of the South African Veterinary the equine encephalosis viruses. low-lying inland areas with
Institute at Onderstepoort was There are nine serotypes of the valleys and marshes. In these
Theiler’s interest in AHS; this virus. It is important to note that areas the disease begins to flare
being prevalent in the area. there are certain affinities up during February with most
Major outbreaks historically seem between some strains, such as deaths during March and April.
to have occurred at intervals of 1&2, 3&7, 5&8 and 6&9. This The disease normally disappears
20-30 years. The most severe does, however indicate that for after the first frosts, although
a vaccine to be effective all nine cases during May and June will
P.O. Box 3301 Cramerview serotypes have to be considered. still be found in the sub tropical
2060 South Africa The virus is relatively heat stable Lowveld. With the absence of
firstname.lastname@example.org and is capable of surviving in insect vectors during most
normal winters the disease sunset and sunrise that the regional lymph nodes where it
disappears completely until the midges are most active. They finds conditions favourable to its
following rainy season when the will travel several km from their multiplication. Virus is released
cycle once again is repeated breeding sites, although factors into the blood whereby it finds
from the North. such as winds may carry them to itself infecting the target
One serotype of the virus usually adjacent areas even over some organs , namely the lungs and
dominates during an outbreak. considerable distances. In 1996 the other lymphoid tissues of the
Serotypes 1-8 may be associated a single fly trap was recorded as body. This resultant viraemia is
with more than ninety per cent catching in excess of one million associated with red blood cells
mortality, while serotype 9 is individuals in one night! We can and lasts for about four to eight
slightly less dangerous with thus begin to understand the risk days. By the third day after
mortality of about sixty five per factors that may prevail when inoculation the virus may be
cent. climatic factors are favourable to found in the spleen, lungs and
Horses are the most susceptible fly biology. The established pharynx as well as most lymph
to AHS while mules have a ideas that stabled horses will not nodes. The heart is not a primary
reduced mortality and donkeys contact the disease as the midge site for virus replication.
and zebra are most resistant. It will not go inside have been CLINICAL
is suggested that certain breeds disproved. There are times when Theiler’s original description of
of horses in the North and West the environment is so full of the four different types of disease
of Africa may have developed pregnant hungry female flies is still valid:
acquired natural resistance by needing a blood meal that they 1. The horse sickness fever
virtue of the fact that they have will find a horse somewhere, form.
been in Africa for more than two anywhere! The risk years have 2. The peracute, pulmonary or
thousand years. been clearly associated with dunkop form. The thin head!
Foals that are born from immune good early summer rains allowing 3. The cardiac, sub acute
mares gain adequate colostral excellent breeding conditions for oedematous, or dikkop form.
protection which usually protects the flies and a steady drift of The swollen head!
them until between the four and infected flies does occur from the 4. The mixed form.
six month of age, after which they North. We are faced with the Fully susceptible horses usually
are fully susceptible. Foals born prospect that in exceptionally wet develop dunkop, while those with
from susceptible mares have no years the presence of some immune awareness
protection. Dogs are highly overwhelming virus challenge develop the dikkop form. It is
susceptible to the disease both may allow disease to develop in likely however that most cases
from natural infection caused by horses that are suspected to are actually some variant of the
insect transmission and also by have normal levels of vaccination mixed form. It is interesting that
eating the meat of horses that immunity. When infection is there is some evidence that
died from the disease. However expected to be high, foals may horses who have exercised hard
Culicoides does not usually feed have to be vaccinated from three during the incubation of the
on dogs. Antibodies to AHS have months of age. The first four disease will be more likely to
also been found in elephant complete vaccination courses develop dunkop. Isolation of
Loxodonta africana but no may have to be completed before more than one serotype from an
evidence exists that they act as foals attain two years of age. infected horse has never been
reservoir hosts. AHS is Over vaccination of adult horses recorded.
infectious, but it is not may actually result in a lowered INCUBATION
contagious. The difference here immunity awareness that The duration of the incubation
is that there is a requirement for increases susceptibility to period is from 2 – 10 days
the insect to spread the virus by infection. Transmission of the although more commonly
inoculating it directly into another virus may be effected by injecting between five and seven days.
horse, rather than by direct horses using the same syringe or Dunkop. This form is seen in
transmission. Horses incubating needle. Horses that recover from fully susceptible horses,
the disease can spread the virus AHS do not become carriers of particularly foals. Also seen in
by traveling to other areas the virus. dogs. The body fever may be
provided the vector is available. PATHOGENESIS 41C or higher for up to 36 even
This was clearly demonstrated in There are many factors that 48 hours, Breathing is severely
the highly publicised outbreaks in decide the outcome in the horse compromised; mouth may be
the Cape during 2000. that is bitten by a midge infected open with the tongue extended,
CULICOIDES by AHS virus including the and the neck and head are
There are now known to be many virulence of the individual virus stretched out. Coughing is usual
species of Culicoides that are serotype and the Immune status and may be severe, even
vectors for AHS, many of them of the horse. paroxysmal. Large quantities of
being of local significance only. It After the virus is inoculated into frothy coloured fluid may escape
is during the period between the body it is carried to the from the nostrils, sometimes only
after death. May even be increased heart rate and mucosal suspicious. Marked post mortem
exercising when dramatically congestion may be seen. signs are indicative. Blood in
becomes ill with dyspnoea and Equine piroplasmosis or heparin for virus examination
death may follow quickly. Interest Biliary Fever. Many horses during the fever stages is useful.
in food may remain reasonable harbour dormant or sub clinical Post mortem samples from
although they may take grass affection of biliary fever. There is spleen, lung or lymph nodes
into mouth and hold this without a well-recognised clinical maintained at 4C are important.
chewing it. The prognosis is that connection between AHS and an Virus may be identified by
less than 5% will recover. acute flare up of biliary fever. complement fixation, and other
Dikkop. In this form the disease Particular care must be taken to specialised immune typing
may develop more slowly: establish, or rule out, the techniques,
Swelling of the supraorbital fossa presence of biliary parasites Serotyping is carried out via virus
may be the first sign as a large during cases suspicious of AHS. neutralising testing,
bulge above the eyes, Swelling of It is likely that many mild cases of Recovered horses have high
head and or neck may develop, AHS have eventually succumbed complement fixation antibody
Fever often is not the first sign to an overwhelming and acute titres. Many new and more rapid
that is seen but where it does flare up of biliary as the immune testing methods will be available
occur it may last up to six days system becomes suppressed by very soon. Many owners and
before reducing. Oedema of the the virus. All fever cases in veterinarians become irritated by
head and neck usually appears horses must have biliary the time required to confirm a
later as disease develops, but the considered as a part of the diagnosis of AHS, but it is time
earlier that it does develop disease process. consuming and difficult to speed
worsens the prognosis. PATHOLOGY up.
Petechiation of the mucosa of the Dunkop. Severe pulmonary DIFFERENTIAL DIAGNOSIS
eyes and mouth are not good oedema is the most significant It is not possible for even
signs. Colic may be present and finding. The lungs are very experienced clinicians to
affected animals may be restless heavy, fluid oozes out of them differentiate the horsesickness
and paw the ground. when they are cut. It may appear fever form of the disease from
Mortality rate is about fifty per that the horse has drowned. many other diseases that cause
cent with death occurring about Hydrothorax with several liters of fevers in horses. Equine
four days after the start of the slightly yellow, congealing fluid encephalosis has many
fever. Swallowing may be difficult may be found in the thorax. Froth epidemiological factors in
and water and food particles may and fluid are in evidence all common with AHS:
drip out of the nose. through the trachea and bronchi. fever, oedema supraorbital fossa
Mixed form. This is the most May be haemorrhages in heart. swellings.
commonly diagnosed form at Lymph nodes show some TREATMENT
post mortem although rarely enlargement. Spleen is normal or There is no specific treatment but
diagnosed clinically. The slightly enlarged. The glandular some guidelines: TLC is very
temptation for the clinician is to stomach is markedly congested, important. Horses respond well
try to be more specific. All of the Dikkop. Oedema of the to lots of quiet attention.
signs noted above are possible. subcutaneous tissues of the head Movement should be restricted
The Dikkop form may be evident and neck, including between the as transport increases chances
then a rapid change to Dunkop muscles. This is yellow, thick and of death. An absolute minimum of
takes place. Mortality rate is gelatinous. In some cases this stress appears to be important
about seventy per cent. will include tissues of the back, and an exhausting therapeutic
Horsesickness fever. This is an chest and shoulders. The tongue system that includes tubing and
interesting situation where horses is often hugely swollen, cyanotic multiple invasive techniques may
that are immune to particular and contains numerous small be counter productive.
serotypes of the virus become petechial haemorrhages. Lungs Recovered horses must not work
affected by one of the other show only slight congestion or for six weeks.
serotypes, against which they fluid. Mucous membranes of Control of biliary parasites may
may have some cross protection caecum, colon and rectum may often be important although care
immunity. This is generally a be markedly affected with must be observed with toxic
milder form of disease. Fever of congestion and petechiae. drugs. Antibiotics are not
39-40C lasting between one and DIAGNOSIS indicated and may be toxic.
five days. Fever of unknown This is not always as simple as it There is growing evidence that
origin during an AHS outbreak seems, but: the standard homoeopathic medicines provide
should always be handled with epidemiology is important. The most success.
suspicion. Transient non-specific right time of the year, the right VACCINATION
signs, including loss of appetite, area, other cases in the area. Onderstepoort produces in
any increased respiratory rate, Clinical signs such as swellings, excess of 150,000 doses of AHS
fever and respiratory distress are vaccine per year. The horse
population of South Africa is formulate specific vaccination locally. Those individuals at
probably in the region of 300,000 schedule for them. particular risk; including those
animals. Since routine FOALS under 3-y-o may be dosed
vaccination became widespread In most cases colostrum provides repeatedly. The nosodes are
the numbers of clinical cases a very effective means for usually combined with the
have dropped very significantly. immunising foals. The foal gains following remedies believed to be
There are two different live protection that is directly related capable of immune modulation;
vaccines, one against serotypes to the degree of protection that Acid-phos, Bapt, Cinch, Echi,
1,3,4 & 5; the second against the mare herself enjoys. In most Eleuth, Ferr, Gins, Nat-m, Sulph
serotypes 2,6,7 & 8. These are cases this protection will last the and Thuj. Over the last ten years
normally given three weeks apart foal only for 2-4 months, rarely thousands of individuals have
beginning from July, well before six months. In view of the been managed in this manner
the expected AHS season. thoroughbred breeding season with very few reported cases of
Serotype 9 is not included as this this means that most foals will infection. Many of these horses
is very rare in South Africa and require vaccination in Dec or Jan have received nosodes in the
does get good cross protection before the peak season for face of serious outbreaks. The
from number six. Vaccination disease occurs. immunity thus gained does not
reactions such as transient Foals and yearlings should be last until the next season in some
depression and fever are rare but vaccinated twice during their first individuals.
do occur and on occasion, even and second years of life. TREATMENT
blindness, encephalitis and other CONTROL Many remedies, sourced from
neurological disorders may be It is a significant factor that in Natura labs have been applied
associated with fatal most normal seasons, stabling of including Acon, Am-c, Ant-t, Apis,
consequences. There have been horses from four pm until nine am Arn, Ars, Bell, Beryl, Bry, Calen,
four cases in laboratory workers seems to offer some slight Cocc, Echi, Gels, Hyper, Laur,
handling the vaccine where loss protection against disease due to Led, Lob, Nat-s, Nosode, Phos,
of vision was a factor. It is a reduction in Culicoides activity. Scut, Sil, Sulph and Queb. The
important to follow the Extensive applications of registered medicines ECO-
recommended vaccine schedule insecticides also have to be HEAL® and ECO-LUNGS® are
closely. There has to be a considered during seasonal fly administered orally in high
balance between not working activity. potency every hour at 5ml each.
horses hard during the second Pro-active. Owners have the It is important that the animals
week following vaccination and right to be a nuisance by receive lots of quiet TLC
allowing them to self destruct in advising, even insisting, that their throughout this period. They do
the paddock. The owner must neighbours also follow all control respond to good nursing.
exercise some common sense in suggestions. There is nothing Transport to hospital is
this regard. Many racehorse more irritating when following a associated with decreased
trainers do not vaccinate as they routine AHS control plan to learn success rates.
are convinced that side effects, that adjoining properties contain REMEDIES
relating to work intolerance are twenty unvaccinated horses. Where the opportunity exists for
much higher than believed. Future. Plans for a new, more personal therapy the following
There is no doubt in my own efficient, dead vaccine with less remedies; Acon, Am-c, Ant-t, Ars,
mind that exercising young toxicity are encouraging. The use Beryl, Cocc, Led, Lob, Phos, Sil,
horses during vaccination is of DNA probes may simplify Sulph in combination with AHS-
dangerous. It is likely that many diagnosis in the near future. Nosode give at present the best
horses require three or more HOMOEOPATHY chance of success. These may
complete courses of vaccine The author has extensive be given orally on the hour for
before developing good personal experience in the four doses followed by treatment
immunity. This does explain why prevention and treatment of AHS every two hours. They may also
many of the actual clinical cases with and without the use of be given by injection four times
seen involve 2 and 3 year olds. It homoeopathic remedies. As a daily. In my opinion the injectable
is possible that regular annual direct result of that experience route gives consistently better
and repeated vaccination of older the following protocol for disease results. Low potency Apis and
individuals may be associated prevention has been found to be Crat may also be considered
with a drop in antibody levels, of value. where oedema is persistent.
leaving them more susceptible to PREVENTION Individuals that have survived the
infection. It may be important to The AHS nosode in the first twelve hours of the disease
vaccinate older animals; whose combined potencies of 6X and have a less than 10% risk of
vaccination history is known 12X may be given three times at death. In one outbreak five
every second year. The practice three day intervals, by injection or horses affected by AHS and
of blood testing individuals in July orally, in the summer; usually as treated with standard methods all
may give an indication of how to the first cases are recorded died. The next five horses treated
only with homoeopathy all Note: Remedies mentioned are:
recovered. Success rates have Acon Aconitum napellus M'FADYEAN, J., 1900. African
been found to be equivalent to Am-c Ammonium carbonicum horse-sickness. Journal of
those obtained with standard Ant-t Antimonium tartaricum Comparative Pathology, 13, 1-20
veterinary care when remedies Apis Apis meliffica DU TOIT, R.M., 1944. The
transmission of blue tongue and
have been combined with either Arn Arnica montana
anti-inflammatory, antibiotic or Ars Arsenicum album v
MIRCHAMSY, H. & HAZRATl, A.,
corticosteroid drugs. Carefully Bell Atropa belladonna 1973. A review on aetiology and
selected individual remedies Beryl Berylium metallicum pathogeny of African horsesickness.
formulated along classical Bry Bryonia alba Archiv Institut Razi, 25, 23-46.
prescribing patterns have also Calen Calendula officinalis DAVIES, F.G. & OTEINO, s., 1977.
yielded disappointing results. The Coc-c Coccus cacti Elephants and zebras as possible
administration of corticosteroids Crat Crataegus rhipidophylla reservoir hosts for African horse
sickness virus. The Veterinary
consistently causes euthanasia. Echi Echinacea angustifolia
Record, 100, 291-292.
CONCLUSION Gels Gelsemium sempervirens vii
BOSMAN, P., BRUCKNER, G.K. &
There is sufficient clinical Hyper Hypericum perfoliatum PAUL, A., 1995. African horse
evidence for the value of Ip Cephaelis acuminata sickness surveillance systems and
homoeopathy in the management Laur Prunus laurocerasus regionalisation/zoning: the case of
of AHS to warrant further Led Ledum palustre South Africa. Revue Scientifique et
investigation. Lob Lobelia inflata Technique, 14,645-653.
ACKNOWLEGEMENT Nat-s Natrium sulphuricum BROWN, C.C., MEYER, R.P.
GRUBMAN, M.J., 1994. Presence of
The work Infectious Diseases of Nosode AHS-nosode
African horse sickness virus in equine
Livestock; Oxford University Phos Phosphorus tissues, as determined by in situ
press, edited by JAW Coetzer Scut Scutellaria hybridization. Veterinary Pathology,
and RC Tustin vol 2 pages 1231 Sil Silicea 31, 689-694.
1246 is important. Sulph Sulphur THEILER, A., 1921. African horse
ECO-HEAL; Alexecovet Pty Ltd. Queb Aspidospermum sickness (pestis equorum). Scientific
P.O. Box 1600 Northcliff 2115, South REFERENCES Bulletin, 19, 1-29.
Africa. Acon 30CH, Apis 6X, Arn Natura labs. P.O. Box 86, Howard
30CH, Bell 30CH, Cal 2X, Echi i Place, 7450 South Africa.
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2X, Hyper 30CH, Laur 2X, Nat-s Horsesickness, Perdesiekte, Pestis
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