The etiology, epizootiology, pathogenesis, and clinical presentation of strangles are described. Streptococcus equi, the causative organism, is highly host-adapted to Equidae and shows no antigenic variation. Protective immunity apparently is mediated by a combination of serum opsonic and nasopharyngeal mucosal humoral responses. Vaccines based on M protein or inactivated bacterial suspensions may reduce the clinical attack rate by 50%, a level of protection much lower than that produced during recovery from strangles.