A major problem with the Enterococci is that they are very resistant to antibiotics and have ability to survive in harsh environments in community and persist in hospital settings (1). Because of this, they become important in health facility based settings (2). According to World Health Organization (WHO) report in 2017, vancomycin resistant Enterococci (VRE) is one of the most resistant bacteria in their “Global Priority list of antibiotic-resistant bacteria” (3). In the same manner, the Center for Disease Control and Prevention (CDC) has classified Enterococci among bacteria with a threat level of serious (4).
Currently, VRE are the cause of one-third and one fifth of all health care associated infections in the United States and in some European countries respectively (5). VRE are well known in causing different enterococcal infections such as infective endocarditis, bacteremia, urinary tract infection, intra-abdominal and pelvic infections, surgical wound infections, and very rarely Central nervous system (CNS) infection (6, 7). Many of these infections originate from intestinal flora of colonized individuals (8).
Enterococci are enteric bacteria that are commonly recovered in feces collected from humans and from a variety of mammals as well as birds, reptiles and insects. The relative importance of Enterococcus as a pathogen has increased with the occurrence of high-level resistance to multiple antimicrobial drugs, such as ampicillin and vancomycin (9–13).
Vancomycin is the primary alternative drug to penicillin (plus an aminoglycoside) for treating enterococcal infections (13). It is active against most Gram positive bacteria and is considered as a drug of ‘last resort’. However, nowadays Enterococcus spp that are resistant to vancomycin are emerged and spreading all over the world (12).
The term Vancomycin Resistant Enterococci (VRE) includes several combinations of enterococcal species including E. faecium (77%) and E. faecalis (9%), with the remaining 14% of isolates representing species rarely known in causing serious infections like E. gallinarum, E. casseliflavus, E. avium, and E. raffinosus (10, 14).
Vancomycin resistant Enterococci was first encountered in clinical isolates in England and France in 1986 as E. faecium, followed the next year by isolation of Vancomycin Resistant Enterococcus faecalis in the United States (15). They have become an important cause of serious invasive healthcare-associated infections globally (6, 7).
The emergence of VRE has alarmed the global infectious diseases community due to its tendency for colonization of the gastrointestinal (GI) tract and transfer of its resistance gene to Methicillin resistant Staphylococcus aureus (MRSA) to form a vancomycin-resistant Staphylococcus aureus (VRSA) isolate. Besides, VRE have different selection pressures for proliferation and rapid expansion of its resistant populations (16). Furthermore, few options are left for management of diseases caused by VRE, and hence causing increased mortality on infected individuals (12, 14). VRE now represent approximately one third of Enterococcus isolates (17).
Asymptomatic VRE gut colonization precedes infection with susceptible hosts. Such susceptible hosts are patients who are exposed to multiple and prolonged courses of antimicrobial agents like Human Immunodeficiency virus (HIV) infected individuals, severely ill, hospitalized for long lengths of stay (LOS), living in a long-term care facility, located in close proximity to another colonized or infected patient, or hospitalized in a room previously occupied by a patient colonized with VRE (2, 18, 19). Colonization is often obtained by vulnerable hosts in an environment with increased rate of patient colonization with VRE (20).
Vancomycin-resistant enterococci can persist in the environment for elongated periods (> 1 week), can contaminate almost any surface, and can be transferred from colonized or infected individual to another by health care workers (9, 13). Transmission of VRE can occur through direct contact with colonized or infected patients, indirect contact via the hands of healthcare workers, via contaminated personal protective equipment (PPE), environmental surfaces or from animals to human through food chain (21, 22). Usually colonization with VRE precedes infection, and the duration of colonization may be extremely extended ranging between 7 weeks and 3 years (22).
Colonization with VRE increases the risk of developing infection up to 5–10 folds (20). Whether VRE colonization leads to infection depends on the health status of the patient. Whereas immunocompetent patients colonized with VRE are at low risk for infection, weakened hosts such as HIV infected patients, patients with hematologic disorders, transplant recipients, or severely ill patients have an increased likelihood of developing infection following colonization (19, 20).
Compromised immune system of HIV infected patients increases the chances of acquiring various opportunistic infections (23). These individuals are at increased risk of developing infections, including infections caused by resistant bacteria pathogens (24). VRE is an important opportunistic bacterial pathogen causing significant morbidity and mortality in immunocompromised individuals like HIV patients (8, 25).
The prevalence of VRE was reported in Europe, Asia, Australia, South America and some African countries (1, 5, 24, 26). However, there is no sufficient data available on the prevalence and risk factors of VRE in developing countries like Ethiopia. Therefore, this study was conducted with the aim of determining the prevalence of vancomycin resistant enterococci gut colonization and its associated factors among HIV infected patients on Anti-Retroviral Therapy (ART).