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Horse Diseases
Equine encephalites
Five kinds of viruses kill horses, people and
wild animals including birds.
Horses are especially sensitive to all of
these encephalitis viruses.
The epidemiology of these mosquito-borne
diseases is shockingly bad. One mistake
after another and why? By following
untested assumptions and accepting
opinions as facts, and by lack of funds and
interest. THOUSANDS of horses are killed
by these viruses.
Etiology
These mosquito-borne equine encephalites
are caused by:
1/ Eastern Equine Encephalitis Virus: EEEV
2/ Western Equine Encephalitis Virus: WEEV
3/ St Louis Encephalitis Virus: SLEV
4/ Venezuelan Equine Encephalitis Virus: VEE
5/ West Nile Virus: WNV
Diagnosis
Disorientation, pressing the forehead
against a wall, fever and finally crashing
into things are common symptoms shared
by many encephalitic infections and also
various hosts from rodents to humans.
Treatment
Good nursing care is the only treatment.
Prevention
A vaccine against EEE only is missing the
point. We have a
certain risk of infection by: 1/ EEEV,
2/ WEEV, 3/ SLEV,
4/ EEEV or 5/WNV. This risk—in some
regions—is high enough
to warrant a vaccination campaign.
We need 5 and have 3: WEEV, EEEV & VEEV.
Regardless of vaccine progress, we are far
behind in SURVEILLANCE AND VECTOR
CONTROL of mosquito-borne diseases, which
includes dengue (DEN 1-4). What should we
vaccinate against and why do these
pathogenic types and strains change from
year to year and place to place? The
epidemiologists went out to lunch and never
came back.
Surveillance is done by research motives
not as necessary public health routine.
Research might be after the outbreak,
whereas routine surveillance is prognostic!
We are ASSUMING virus amplifications in
horses and not other hosts. Where & when?
Immunizing all the population COULD
eradicate the pathogen.
Here is a problem: The time is short between
the warning and the vaccination application,
and then the antibody response. But this is
theory, since no warning system exists.
Now you finally see why a tremendous or
horrific CHAEMERA vaccine is needed for
horses.
THE VIRUS EPIDEMIC WILL RUN ITS
NATURAL COURSE BEFORE VACCINATIONS
CAN BE MADE. WHICH VIRUS WAS IT ??
There is nothing easy about this ! Did Virus X
come from Colombia and Venezuela by
hurricane?
Equine Infectious Anemia
Equine infectious anemia (EIA) is a highly
contagious and potentially fatal viral
disease for equines. EIAV is a retrovirus,
containing genetic RNA material, which it
uses to produce DNA. This DNA is then
incorporated into the horse’s genenome.
It’s really a case of Goodbye horse.
When horses are exposed to EIAV, many
may develop severe symptoms and die in
2-3 weeks. The initial fever may last less
than 24 hours.
Federal regulations concerning interstate
movement of horses and EIA are:
“Any reactor to an official test shall be
classified as infected with equine
infectious anemia, and shall not be
moved interstate unless:
1/ It is officially identified (officially
identified by either a lip tattoo or a neck
brand) and accompanied by a certificate
. . . and
2/ It is moved interstate, for immediate
slaughter or to a diagnostic or research
facility . . . or
Transmission
Horse flies and deer flies mechanically
transmit EIAV. Insect transmission of
EIAV is dependent on the number and
habits of the insects, the density of the
horse population, the number of times the
insect bites the same and other horses,
the amount of blood transferred and the
level of virus.
Etiology
EIA is caused by a retrovirus thereby it
relates to the autoimmune deficiency
syndrome (AIDS). Insects like horse flies
can carry infected blood. In the US, 80 %
of EIA is in the 9 southeastern states. Do
these states make a valiant attempt to
eradicate ? Of course not. Horses
recovering are lifelong carriers.
Diagnosis
The first indication that a horse was exposed
to and infected with EIAV may well be a
positive result on a Coggins annual test.
If the horse survives this first acute attack, it
will develop permanent disease with:
1/ Fever for an indeterminate period until the
onset of another episode.
2/ Petechial hemorrhages-Minute bloodcolored spots appear on the mucous
membranes.
3/ Depression-The horse appears more or less
dejected (head hangs low) and generally
listless.
Treatment
No treatment. Refer to AIDS.
Prevention
Horse quarantine and the Coggins test
constitute the means of prevention. Positive
horses are branded with 73ª on the left neck.
Negative horses should have a certificate.
ALL HORSES SHOULD BE COGGINS OR ELISA
TESTED ANNUALLY. Otherwise ALL can—in
the futre—be vaccinated (research not done !)
in order to drive out—eradicate—EIA. But
what is the risk, where ?
Equine Influenza
Equine influenza is an acute respiratory
disease of horses worldwide. Equine
influenza is represented by 2 subtypes:
1/ Influenza A/ equine 2 and
2/ virus (H3 N8 ) which is an most
important cause of respiratory diseases in
horses, and
Influenza A/ equine 1 virus (H 7 N 7 ).
Others are: A/equine/Miami/1/63 isolate
are currently circulating in horse
populations.
Three distinct types of influenza virus have
been isolated from horses since 1956. These
are represented by the following prototype
strains: influenza A/ equine/Prague/1/56
(H7N7), influenza A/ equine/Miami/1/63
(H3N8), and influenza A/ equine/Jilin/1/89
(H3N8). Jilin is from China. Isolation of a
H7N7 virus has only been reported twice
since 1977.
Racehorses from Miami, Florida (FL) and
New Orleans, Louisiana (LA) returning to the
north like New York (NY) say in March will
routinely have outbreaks by the barn load as
most are not vaccinated due to ignorance and
tradition.
Etiology
Equine influ enza, type A, includes viruses
infecting man, birds and swine. Type A
influenza viruses are divided into subtypes
according to the surface antigens,
hemagglutinin and neuraminidase. Two
subtypes are known to cause disease in
equids (H7N7 or equi-1 and H3N8 or equi-2).
These differ from the subtypes that cause
infection in man (H1N1, H2N2 and H3N2).
All the known subtypes (H1 to H15 and N1 to
N9) have been isolated from aquatic birds
that therefore seem to be natural reservoirs.
Diagnosis
Poor performance, a hacking dry cough,
depression, anorexia, fever, nasal discharge,
enlarged and tender submandibular and
retropharyngeal lymph nodes are notable
symptoms.
Treatment
Wait a month without stressing the
recovering horse.
Prevention
There should be no trouble at all since good
vaccines are available.
Potomac Horse Fever
Etiology
Potomac horse fever (PHF)--equine
monocytic ehlichiosis—is a worldwide
disease associated with river valleys and
caused by Ehrlichia risticii. See Int J Syst
Bacteriol 1985, 35: 524-526. The life cycle
of Ehrlichia risticii includes fluke larvas in
snails and aquatic insects. For E. equi see
Am J Vet Res 1975, 36: 85-88 and Int J
Syst Bacteriol 1988, 38: 220-222.
Diagnosis
Affected horses might develop diarrhea, fever
and usually died unless treated promptly with
tetracycline or similar antibiotics.
The infected horse will go off his feed and
develop fever. Low blood pressure and low
blood counts develop. Intracellular bacteria
will be seen in Giemsa blood smears. Severe
diarrhea and painful colic may ensue. The
horse may become severely dehydrated
requiring IV fluids. It may founder.
Infected mares may abort with inflammation
of the placenta. Many horses test seropositive
without signs of illness.
Treatment
Terracycline works.
Prevention
A vaccine has been available
since 1987.
Sarcocystosis
All mammals have Sarcocystis species or
something close so the name equine
protozoal myeloencephalitis is absurd. These
coccidian genera of the phylum Apicomplexa
are Besnoitia, Cystoisospora, Frenkelia,
Hammondia, Neospora, Sarcocystis and
Toxoplasma.
Horses are simply hosts like many other
mammals. Infections in raccoons or possums
need not be different. Schizonts and
merozoites, but no sarcocysts, are found in
horses. Similar histopathologic lesions of
S. neurona are seen in cats, mink, raccoons,
skunks and so on.
Etiology
The opposum (Didelphis virginiana) is the
definitive host. The definitive host becomes
infected by ingesting mature intramuscular
cysts (with bradyzoites) from infected
intermediate hosts. This stage can also be called
merozoites. Bradyzoites penetrate the lamnia
propria of the small intestine and form gametes.
By sexually reproducing in the intestinal wall of
the opossum, S. neurona produce fragile
sporulated oocysts, which often rupture before
being passed in the feces. Shedding of oocysts
occurs for weeks to months. Sporocysts are not
infectious to definitive hosts. Animals other than
possums may be unknown final hosts.
Diagnosis
Ataxia and incoordination can be present in
one limb or all of the other limbs. Damage to
lower motor neurons of the spinal cord or
brainstem can result in muscle atrophy.
Obscure lameness may be the only
abnormality. Signs of cranial nerve
dysfunction may be present in over 10% of
EPM cases, including atrophy of the temporal
masseter muscles, atrophy of the tongue,
vestibular signs, facial nerve paralysis,
laryngeal hemiplegia, and dysphagia.
Treatment
Usual treatment involves once daily oral
administration of sulfadiazine (20 mg/kg)
and pyrimethamine (1 mg/kg). Most
treatment regimens very expensive.
Diclazuril, a benzeacetonitrile coccidiostat
for poultry, has anti-S. neurona activity.
Toltrazuril and triazine are other
coccidiostats. Ponazuril, another anticoccidial
compound has a dosage regimen of 5 mg/kg
body weight given orally, once per day, for 28
consecutive days.
Prevention
No prevention is presented.