Horse Diseases Equine arteritis virus Etiology Equine arteritis

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 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 (ERh. V 1) is a worldwide cause of acute febrile respiratory disease. ERh. V 1 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 ERh. V 1 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 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 Th 2 cytokine profile of CD 4 lymphocytes is associated with such allergies. Th 2 -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 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.