Does early antibiotic use in horses with ‘strangles’ cause metastatic Streptococcus equi bacterial infections?

Streptococcus equi (Streptococcus equi ssp. equi) is a Lancefield group C Streptococcus that causes ‘strangles’, a highly contagious purulent lymphadenitis and pharyngitis of members of the family Equidae. In most cases, S. equi infection in horses causes a transient lymphadenopathy of the mandibular and retropharyngeal lymph nodes, with subsequent abscessation (Foreman 1999; Sweeney et al. 2005). Although the disease is associated with significant morbidity, most infected horses ultimately recover. However, in some cases, metastatic dissemination develops. This is sometimes referred to as ‘bastard strangles,’ a perhaps unfortunate and archaic term that has become embedded in the veterinary literature, first having appeared in the early 19th century (Slater 2003). Spread of the S. equi organism has been reported to many organs and tissues of the horse’s body, including, but not limited to, the lungs, mesentery, liver, and brain (Ford and Lokai 1980; Spoormakers et al. 2003). There appears to be a belief, and some authors have stated, that the institution of antimicrobial therapy in the treatment of S. equi infections of horses is contraindicated prior to maturation of the submandibular abscesses that are typical of the clinical course of the disease, as the use of such therapy may enhance the frequency of multifocal abscesses (Beech 1979). The reason(s) for concerns about antibiotics are speculative. Early observers rather accurately, if colourfully, described the pathobiology of metastatic abscessation: “... for want of properly effecting suppuration, the humours frequently settle, or are translated to the lungs, the fleshy bowels or falling on the fleshy part of the hindquarters ... which sometimes kill the horse...” (Bartlett 1777). It has more recently been suggested that antibiotics such as procaine penicillin G may somehow affect the bacterium in such a way as to result in an inadequate host immune response (Bryans and Moore 1972; Beech 1979; Clabough and Scrutchfield 1987; Sweeney 1987; Timoney 1993; Semrad 1999). For example, one such hypothesis suggests that antibiotics alter bacterial protein synthesis, thereby reducing immunogen levels, resulting in a suboptimal immune response, thereby allowing for dissemination of the bacterium (Sweeney et al. 2005). Alternatively, another hypothesis is that, since penicillin works on the bacterial cell wall, it somehow prevents the horse from developing immunity, allowing for spread of the infection (Beech 1979). However, and perhaps remarkably so, given the persistence of the belief in the veterinary literature, there appears to be no clinical or experimental evidence to support the supposition that treatment with antimicrobial agents at any stage in the course of the clinical disease ‘strangles’ increases the prevalence of metastatic dissemination of the organism. One of the first references suggesting that increased incidence of disseminated S. equi infections were associated with antimicrobial therapy appears to come from a publication on streptococcal disease in human medicine, in which 2 veterinary authors gave their ‘clinical observations’ of such an association in horses (Foreman 1999; Sweeney et al. 2005). These observations appear to have been perpetuated in subsequent publications. There appear to be no prospective studies comparing horses treated with antimicrobials to untreated horses. Even the prevalence of ‘bastard strangles’ is unknown. In 4 cases of horses suffering from cerebral damage due to metastatic S. equi abscesses, confirmed antemortem by MRI, and by post mortem examination, no antibiotics were used in any of the cases before neurological complications were identified (Spoormakers et al. 2003). Perhaps paradoxically, and particularly so given the concerns about antibiotics in the treatment of strangles, longterm (2–6 month) antimicrobial therapy with procaine penicillin G has resulted in clinical resolution of internal abscesses in many animals (Rumbaugh 1978).