Gram-positive bacteria are the most common causative organisms both for exogenous and endogenous endophthalmitis. In the Endophthalmitis Vitrectomy Study, 100 % of Gram-positive organisms were susceptible to vancomycin [1]. Thus, vancomycin is the most widely used glycopeptide antibiotic used for empiric coverage of Gram-positive organisms in endophthalmitis. Multidrug-resistant bacteria especially vancomycin-resistant Enterococcus (VRE) and methicillin-resistant Staphylococcus aureus (MRSA) are emerging as an increasing threat in ophthalmology with increasing reports of these organisms causing endophthalmitis [2–7]. Further, there are also reports of prophylactic use of vancomycin either in the irrigating solution or intracamerally during the cataract surgery that would possibly increase the chances of developing drug resistance [8–10]. The diagnosis and management of these rarer infections poses a major challenge as these infections closely resemble the infections caused by Staphylococcus aureus but do not respond to the standard treatment for endophthalmitis. One has to have a high index of suspicion for these infections that may present with endogenous or exogenous endophthalmitis associated with severe intraocular inflammation.

The exogenous endophthalmitis due to VRE and MRSA is quite rare, and there are only isolated published case reports and few case series. The Gram-positive bacteria reported in Endophthalmitis Vitrectomy Study were all susceptible to vancomycin [1]. The reported incidence of MRSA-induced exogenous endophthalmitis has been reported to vary between 1.56% and 41% in different reported series (Table 9.1). A recent series reported a statistically significant increase in the trend toward microbial resistance against a variety of antibiotics including methicillin [6].

There is no series reporting the incidence of MRSA-related endogenous endophthalmitis. HoV et al. [13] have recently reported the largest series on eight patients with endogenous methicillin-resistant S. aureus who had a virulent disease course.

MRSA: These organisms may be present on the ocular surface, thus increasing the chances of acquiring infection. The culture swabs taken from the ocular surface of patients scheduled for cataract surgery in Uganda showed 31.9 % (29/91) methicillin-resistant coagulase-negative Staphylococcus (MRS) and 27.6 % (8/29) methicillin-resistant S. aureus (MRSA), respectively. All Gram-positive bacterial isolates were sensitive to vancomycin [14].

Infections caused by methicillin-resistant S. aureus (MRSA) strains, in general, have been reported to be seen in health care (hospital-acquired MRSA [HA-MRSA]) as well as in the community-based setting (community-acquired MRSA [CA-MRSA]). The intraocular infections are mostly HA-MRSA. S. aureus has a tendency to develop resistance to methicillin due to the presence of penicillin-binding protein coded for by a mobile genetic element called methicillin-resistant gene. In the last few years, this gene has continued to evolve so that many MRSA strains are becoming resistant to several antibiotics including oxacillin, penicillin, and amoxicillin. Many antibiotic-resistant genes and toxins are bundled and get transferred together to be passed on to other bacteria that enhance the development of resistant strains of MRSA [14, 15].

VRS: Vancomycin is a very commonly used antibiotic against most Gram-positive bacteria including Staphylococcus, Streptococcus, as well as Bacillus species. In addition, it is also effective against methicillin-resistant coagulase-negative Staphylococcus and methicillin-resistant Staphylococcus aureus (MRSA) infections. Vancomycin is a glycoprotein that binds irreversibly to D-alanyl-D-alanine moieties of the N-acetylmuramic acid (NAM) and N-acetylglucosamine (NAG) peptides that inhibit the synthesis and cross-linking of the NAM/NAG polymers. These polymers form the backbone of the cell wall. The mechanism of acquiring vancomycin resistance includes conversion of D-Ala-D-Ala to the depsipeptide D-Ala-D-Lac or to D-Ala-D-Ser, which in turn results in altered cross-linkages in the peptidoglycans of the cell wall contributing to the development of resistance to vancomycin [16].