Streptococcus equi Infections in Horses: Guidelines for Treatment, Control, and Prevention of Strangles

Abstract

Abscessation, particularly of the retropharyngeal lymph nodes, may result in obstruction of the upper respiratory tract. The enlarged lymph nodes may compress the phar-ynx, larynx, or trachea, necessitating a tracheostomy in se-vere cases. Temporary laryngeal hemiplegia, resulting from damage to the recurrent laryngeal nerve from enlargement of either the retropharyngeal or anterior cervical lymph nodes, may also contribute to dyspnea. Four of 15 horses with complicated strangles had upper respiratory tract ob-struction requiring tracheostomy, and death was attributed to the obstruction in 2 of these. 1 Dysphagia may also occur as a result of lymph node enlargement or guttural pouch empyema. Pathogenesis S equi enters via the mouth or nose and attaches to cells in the crypt of the lingual and palatine tonsils and to the follicular-associated epithelium of the pharyngeal and tubal tonsils. There is no evidence for colonization prior to pen-etration but rather the organism reaches the deeper tissues of the tonsil within a few hours. Ligands responsible for binding may include the exposed surface proteins SzPSe, Se73.9, and Se51.9. FNZ, a fibronectin binding protein pro-duced by S zooepidemicus, is also produced by S equi but without a C terminal anchor and so it may not be function-al. 2 A few hours after infection, the organism is difficult to detect on the mucosal surface but is visible within cells of the epithelium and subepithelial follicles. Translocation oc-curs in a few hours to the mandibular and suprapharyngeal lymph nodes that drain the pharyngeal and tonsillar region. Complement-derived chemotactic factors generated after interaction of complement with bacterial peptidoglycan at-tract large numbers of polymorphonuclear neutrophils, al-though gross evidence of abscessation is not visible for 3 to 5 days after S equi enter the lymph node. 3 Failure of neutrophils to phagocytose and kill the streptococci appears to be due to a combination of the hyaluronic acid capsule, antiphagocytic SeM protein, Mac protein, and other unde-termined antiphagocytic factors released by the organism. This culminates in accumulation of many extracellular streptococci in the form of long chains surrounded by large numbers of degenerating neutrophils. Final disposal of bac-teria is dependent on lysis of the abscess capsule and evac-uation of its contents. Streptolysin S and streptokinase may also contribute to abscess development and lysis by damaging cell mem-branes and activating the proteolytic properties of plasmin-ogen. Although strangles predominantly involves the upper airways, including the guttural pouches and associated lymph nodes, metastasis to other locations occasionally oc-curs. Spread may be hematogenous or via lymphatic chan-nels, which results in abscesses in lymph nodes and other organs of the thorax and abdomen. This form of the disease has been known as ''bastard strangles.'' Metastasis to the brain has also been recorded. 4 Bacteremia occurs on days 6 to 12 in horses inoculated intranasally with virulent S equi.