The authors have prospectively applied the guidelines for expectant observation—including possible default to surgery—for more than 25 years. Through 2008, successful outcomes in about 80 patients under 9—among a much larger number of patients of all ages—had been published as a single-institution experience [8, 9].

Despite the success of this approach, vigilance is needed to avoid undertreatment. The pathogens ultimately responsible for sinusitis-related orbital cellulitis and SPA are the normal upper respiratory flora. This distinctive pathogenesis differentiates these conditions from orbital infections that arise from other sources, such as traumatic wounds, skin lesions, dacryocystitis, or dacryoadenitis. However, evolutionary trends in the general microbiome may impact sinusitis-induced SPA as well as other types of orbital infection. Widespread antibiotic use has fostered the emergence of more robust strains, such as MRSA, and immunization against specific organisms has favored competing species.

MRSA first appeared in the United Kingdom in 1961, only 2 years after the introduction of methicillin. It has since become increasingly common, even accounting for the majority of community-acquired and nosocomial Staphylococcus aureus infections in some geographical areas [10–17]. Its particular pathogenicity is not due to drug resistance per se but to production of multiple virulence factors, including exotoxins, staphylococcal enterotoxins, leukocidins, and hemolysins [18]. MRSA’s clinical impact is most obvious in microenvironments where staphylococcal species predominate, such as the skin, and MRSA is increasingly common in eyelid and orbital soft tissue abscesses that develop rapidly with or without minor surface trauma [19]. Less obvious, but increasing, is its role in microenvironments with diverse competing flora when the latter are suppressed by widespread immunization. This applies to the upper respiratory tract, and the introduction of vaccines directed against Haemophilus influenzae in 1985 and Streptococcus pneumoniae in 2003 has resulted in greater representation of S. aureus in sinus infections [15]. Accordingly, with greater antibiotic use, the prevalence of methicillin-resistant strains of S. aureus has increased. A recent meta-analysis reported a rise in the recovery of MRSA in acute rhinosinusitis from 0% in a 2006 study to 15.9% in a 2012 series [10].

Considering the pathogenesis of sinusitis-related orbital celluliti s and SPA, a commensurate increase in MRSA would be expected in these conditions. Indeed, multiple cases of MRSA-positive orbital cellulitis and MRSA-positive SPAs of sinus origin have been reported [13–15, 20–23].

Our recent analysis noted not only an increase in S. aureus strains but also an increase in Streptococcus anginosus group and group A β-hemolytic streptococcus over time [23]. These normal floras of the oral cavity and gastrointestinal tract are unique among streptococcal species in their ability to cause abscesses through a variety of virulence factors [24]. The pathogenicity of group A β-hemolytic streptococcus (S. pyogenes) is attributed to capsular elements that protect it from phagocytosis, adhesion factors that aid attachment to host cells, and enzymes that facilitate spread through host tissue layers [25].