Horse Diseases Equine arteritis virus Etiology Equine arteritis virus EAV is the cause of equine vir

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Horse Diseases Equine arteritis
virus EtiologyEquine arteritis
virus (EAV) is the cause of equine viral
arteritis (EVA) that is a worldwide respiratory
disease involving abortions and often carried by
stallions..
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DiagnosisSymptoms 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.
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TreatmentLike most virus diseases, there is no
specific treatment.PreventionLittle can be
suggested past quarantine.
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RabiesRabies virus reaching
the brain is fatal for all mammals, however it is
most rare in horses.
EtiologyOf 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.
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DiagnosisHydrophobia,
biting as by a dog and frothing at the mouth are
famous signs. However, your canine teeth will not
grow. TreatmentThe
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.
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PreventionControl 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.
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Rhinopneumonitis
EtiologyEquine 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.
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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
acuteandconvalescent -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.
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TreatmentAs in most virus
diseases, there is no targeted treatment.
PreventionUse quarantine measures.
Possibly obtain a certificate before buying a
horse.
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Pneumonia of foalsImproved 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.
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EtiologyPneumonia 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.
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DiagnosisMany foals will cough,
breath abnormally and, less commonly, have
diarrhea before the age of 4 months. Many will
have pneumonia by 1-2 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.
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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 salmon-colored to orange. Several
other harmless orange R. spp. are found in soil.
Tracheal or bronqueal fluids are routinely
sampled.
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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).
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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 ?
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TreatmentPassive
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..
PreventionNo 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.
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Ulcerative lymphadenitisThis is is a mildly
contagious disease of horses characterised by
inflammation of the lymphatic vessels of
the lower limbs.
EtiologyCaused by Corynebacterium
pseudotuberculosis, a similar disease is
very common in goats and sheep.
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DiagnosisThe 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
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TreatmentCorynebacteria are
sensitive to penicillin and a host of other
antibiotics. PreventionNormal
protection of the legs against skin infections
seems adequate.
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Heaves
EtiologyHeaves 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 dust-induced asthma
that is characterized by airway neutrophilia,
mucus hypersecretion and airway obstruction.
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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.
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Heaves in horses shares many similarities with
human COPD and asthma, including lower airway
inflammation, reversible airway obstruction and
bronchial hyper-responsiveness. 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.
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DiagnosisSigns include mucopurulent
nasal discharge, dyspnea, tachypnea,
coughing,exercise intolerance and increased
expiratory effortheaving. 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.
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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.
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TreatmentDaily 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 trialPrednisone 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.
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PreventionIn 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.