and enlarged causing the lymph follicles to form raised on the roof of the pharynx. The plaques are hyperemic and begin to produce increased quantities of mucus which coats the pharynx, larynx and the trachea. The increased amount of mucus and the enlarged lymphatic tissue causes airflow to become and results in increased resistance to airflow in the more distal parts of the airways. Increased turbulence and airflow resistance causes discomfort and pain in the pharynx.
Young horses,
years of age are more susceptible to pharyngitis and pharyngeal
lymphoid hyperplasia. The lymph follicles are very pronounced in young horses.
Infection of the pharynx is transmitted through the inhalation of aerosol respiratory secretions from an infected horse, or through the direct or indirect contact with infected respiratory secretions. The clinical presentation of pharyngitis and pharyngeal lymphoid hyperplasia include coughing, poor performance, nasal and lacrimal discharge, dysphagia, and anorexia. Diagnosis is made through endoscopy revealing raised, red plaques on the roof of the pharynx and increased mucus production in the upper airways as well as pharyngeal swab for bacterial culture and blood analysis. Treatment is dependent on the type of infective agent. For bacterial infections systemic antibiotics and NSAID’s are recommended. For viral infections rest, NSAID’s and lavage of the throat with DMSO may be recommended. In cases where the hyperplasia of the lymphoid tissue is persistent or recurring cryosurgery or chemical cauterization may be used to remove the lymphoid plaques.
Prognosis for pharyngitis and pharyngeal lymphoid hyperplasia is good.
Equine Viral Rhinopneumonitis (Equine Herpes Virus)
Equine viral rhinopneumonitis, or “rhino”, is caused by the infection of the respiratory tract by equine herpes virus (EHV) type . EHV has an affinity for the endothelial cells of the respiratory tract and the endothelium of nearby . EHV infects these cells and uses the cells’ machinery to replicate new viral units. Once the host cell if full of new virus the host cell bursts, freeing the viral clones to infect neighbouring cells. The lysis of the respiratory endothelial cells causes inflammation of the respiratory tissues resulting in the influx of leukocytes, especially neutrophils. Neutrophils phagocytized infected and damaged cells in an attempt to remove the virus from the respiratory tissue, causing further inflammation and chemotaxis. Occasionally EHV type I infections can spread from the lymph nodes to the blood, causing viremia. Once in the circulation EHV type I may spread across the blood-brain barrier resulting in viral encephalomyelitis, or it may damage
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