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Transcript
Horse Diseases
Equine arteritis virus
Etiology
Equine arteritis virus (EAV) is the cause of
equine viral arteritis (EVA) that is a
worldwide respiratory disease involving
abortions and often carried by stallions..
Diagnosis
Symptoms are a) fever, b) swelling
(edema), most notably of the legs,
scrotum, sheath or mammary glands,
c) loss of appetite (anorexia),
d) depression, e) nasal discharge, initially
watery (serous), f) conjunctivitis that may
be accompanied by tearing down the face
and swelling around the eyes, g) skin rash
(urticaria), often localized to the cheeks
or sides of the neck, h) abortion and i)
pneumonia ± enteritis in young foals.
Treatment
Like most virus diseases, there is no
specific treatment.
Prevention
Little can be suggested past
quarantine.
Rabies
Rabies virus reaching the brain is fatal for all
mammals, however it is most rare in horses.
Etiology
Of Louis Pasteur fame, rabies virus is
transmitted from mammal to mammal by
bites. As Hollywood teaches us correctly that
the virus drives us mad when bitten by rabid
wolves or vampire bats. All mammals are
susceptible to rabies virus.
Diagnosis
Hydrophobia, biting as by a dog and
frothing at the mouth are famous signs.
However, your canine teeth will not grow.
Treatment
The Pasteur treatment is by repeated IM
injections of killed vaccine. This intent to
raise antibodies to stop the natural
infection before the virus reaches the
brain has saved many lives.
Prevention
Control of dogs by vaccine campaigns is
quite common. Poison baits against stray
dogs is another practice. Wild animals like
raccoons deserve scrutiny. Cats and of
course all other mammals are involved.
Rhinopneumonitis
Etiology
Equine rhinovirus 1 (ERhV1) is a worldwide
cause of acute febrile respiratory disease.
ERhV1 is closely related to foot-and-mouth
disease virus, and tentatively included in the
genus Rhinovirus in the family Picornaviridae.
However, it is sometimes classified as herpes
virus.
Diagnosis
Viral antigen can sometimes be detected by
immunofluorescence assay in the cytoplasm of
ERhV1 infected cells, using nasopharyngeal swabs.
A rise in serum neutralizing antibody titer between
acute—and—convalescent -phase sera confirms
diagnosis.
The disease is characterized by fever, anorexia,
nasal discharge, coughing, pharyngitis and
lymphadenitis of the head and neck. Infection is
also accompanied by viremia and long-term fecal
and urinary shedding of the virus. The respiratory
form has clinical signs very similar to equine
influenza (fever, cough, nasal discharge). Its mode
of transmission is also similar. Abortion can occur
in late pregnancy.
Treatment
As in most virus diseases, there is no
targeted treatment.
Prevention
Use quarantine measures. Possibly
obtain a certificate before buying a
horse.
Pneumonia of foals
Improved recognition of Rhodococcus
equi and Arcanobacterium haemolyticum,
formerly classified in the genus
Corynebacterium, and C.
pseudotuberculosis of ulcerative colitis
are members of the loosely defined taxon
“coryneform” bacteria. Although they are
the etiologic agents of distinct infections,
these microorganisms are often
overlooked, sometimes simply by not
taking bacteriological samples and not
having the facilities needed.
Etiology
Pneumonia in very young horses is caused
by Rhodococcus equi, a typical soil
organism that has adapted to mammalian
hosts. R. equi is common in the intestine
of adult horses. Certain farms, perhaps
overcrowded, have much higher rates of
pneumonia than others.
Diagnosis
Many foals will cough, breath abnormally and,
less commonly, have diarrhea before the age
of 4 months. Many will have pneumonia by 12 months of age. Ultrasonographic
examination of the lungs is a way to monitor
foals, permitting early detection of lung
lesions, therefore early treatment.
The common sign of R. equi in foals is a
suppurative bronchopneumonia with
extensive abscessation and suppurative
lymphadenitis. Clinical signs may include
a slight increase in respiratory rate and mild
fever.
Corynebacterium equi produces a soluble factor
(equi factor) which interacts with the
phospholipase D (PLD) toxin of C.
pseudotuberculosis, A. haemolyticum, the a-toxin
of Staphylococcus aureus, and an uncharacterized
partial hemolysin of Listeria monocytogenes to
give an area of complete hemolysis with sheep
erythrocytes. In the absence of this bacterial
solluble factor, C. equi is not hemolytic. The test is
made on an blood agar plate with a vertical streak
of R. equi perpendicular to streaks of 1 of the 3
mentioned bacteria. R. equi is a grampositive
bacillococcus or coccoid. Colonies can be salmoncolored to orange. Several other harmless orange
R. spp. are found in soil. Tracheal or bronqueal
fluids are routinely sampled.
Passive immunization with the IV
administration of hyperimmune (HI)
plasma is a generally effective way to
reduce the incidence of damage and
deaths. Up to 8 liters of blood can come
from a donor horse made hyperimmune
(as in a slaughterhouse) and all really
needed is a heavy centrifuge (4 sterile
bottles of 500 ml each).
Active immunization would be much
better to control R. equi pneumonia on
enzootically infected farms by the
active immunization of mares and their
foals with a protective antigen rather
than by the IV administration of a large
volume of plasma. Such experimental
attempts have been generally
unrewarding and vaccines against
R. equi infections are not currently
available. Do you know why not ?
Treatment
Passive immunization with IV
hyperimmune plasma or serum can be
effective depending on the immune status
of mare and its foal. Otherwise a wide
range of antibiotic applications are
successful, e. g., terramycin..
Prevention
No commercial vaccine is available, which
is amazing news. This might come around
to: Company X is not going to make that
vaccine unless guaranteed X thousands of
sales.
Ulcerative lymphadenitis
This is is a mildly contagious disease of
horses characterised by inflammation of
the lymphatic vessels of the lower limbs.
Etiology
Caused by Corynebacterium
pseudotuberculosis, a similar disease is
very common in goats and sheep.
Diagnosis
The disease is due to infection of skin
wounds, which is followed by infection of
lymphatic vessels and the development of
abscesses along their course. The
following signs are seen:
·
Infected wound on the lower limb
·
Swelling and pain
·
Lameness
·
Subcutaneous nodules particularly
around the fetlock
·
Ulcers
Treatment
Corynebacteria are sensitive to
penicillin and a host of other antibiotics.
Prevention
Normal protection of the legs against
skin infections seems adequate.
Heaves
Etiology
Heaves is a chronic obstructive pulmonary
disease (COPD) that may result from severe
cases of influenza, but much more often it
develops as an allergic response to fungus
spores and dust in bad hay. Equine heaves is
an mould endotoxin-containing, organic dustinduced asthma that is characterized by
airway neutrophilia, mucus hypersecretion
and airway obstruction.
In COPD, clara cell degranulation and loss,
necrosis of type 1 alveolar epithelial cells with
replacement by type II alveolar epithelium,
and the presence of intraepithelial lamellar
inclusion bodies can occur. Larger airways
have focal loss of ciliated epithelium, with
epithelial metaplasia and hyperplasia.
Heaves is not an infectious disease like the
other viral and bacterial diseases discussed
here. Mainly, it is caused by horses eating
mouldy hay. Black patches in the bailed green
hay are areas filled with fungal spores. This
mouldy hay might have been bailed when
wet.
Heaves in horses shares many similarities
with human COPD and asthma, including
lower airway inflammation, reversible airway
obstruction and bronchial hyperresponsiveness. Heaves is an allergic
response to environmental allergens. A Th2
cytokine profile of CD4 lymphocytes is
associated with such allergies. Th2-type
lymphocytes, mast cells and eosinophils are
considered the primary effector cells leading
to allergic airway inflammation in the lungs
of horses with heaves. However, heaves,
unlike asthma, is characterized by neutrophil
recruitment into airway secretions after
antigenic stimulation.
Diagnosis
Signs include mucopurulent nasal
discharge, dyspnea, tachypnea, coughing,
exercise intolerance and increased
expiratory effort—heaving. The horse has
obvious difficulty in expiring. Wheezes
and expiratory crackles are heard upon
thoracic auscultation. Weight loss,
cachexia and hypertrophy of the external
abdominal oblique muscles may occur in
severe cases. Neutrophilia is frequent.
The clinical classification of COPD separates
affected horses into stages one to five. Stage
1/ Includes horses with a history of COPD,
but no clinical signs. Stage 2/ Horses have
occasional cough and seasonal improvement.
Stage 3/ Horses exhibit coughing and
exercise intolerance with some seasonal
improvement. Stage 4/ Horses have
persistent respiratory dysnea (shortness of
breath) and dysnea at rest. Stage 5/ horses
have severe dysnea and tachycardia (rapid
pulse). Percent saturation of arterial blood is
little studied.
Treatment
Daily administration of i.v. dexamethasone
(0.1 mg/kg) to COPD challenged horses
caused a significant reduction of airway
obstruction within 3 days with improvement
in a 10-day trial
Prednisone or prednisolone may be
considered for continued maintenance once
obstruction is relieved because prolonged use
of dexamethasone or triamcinolone has side
effects like laminitis. However, the value of
prednisone or prednisolone is questioned in
horses.
Prevention
In many cases, producing or buying good
hay may very well allow escape from
heaves. Overpopulations of horses that
turn pastures to dust are to be avoided of
course. Reduce dust. The proper care of
buildings and reasonable sanitation end
the story. A sprinkler truck for the race
track is a nice touch.