Infection due to C. indologenes in humans is a rare occurrence and is usually nosocomial. These are mainly found in soil, plants, water and foodstuffs. They are not found in human flora. Within the hospital premises, they exist in water systems and wet surfaces and can survive in chlorinated water [1].

Chryseobacterium species are gram-negative, aerobic, non-motile, oxidase positive, catalase positive, indole positive, producing a distinct yellow orange pigment due to production of flexirubin. Indole was produced in tryptophan broth. The genus Chryseobacterium belongs to the family Flavobacteriaceae. The commonly isolated species includes C. meningosepticum, C. multivorum, C. odoratum, C. breve and group IIb Chryseobacterium species which includes C. indologenes and C. gleum. Of these C. meningosepticum is the most pathogenic causing neonatal meningitis [2].

Chryseobacterium infections are frequently associated with the presence of indwelling devices like intra-vascular catheters etc., in immunocompromised patients or in patients on long-term broad-spectrum antibiotics. Factors influencing the development of Chryseobacterium infection include a suitable entry port, invasive procedures, neutropenia, production of biofilm on foreign materials, prolonged use of antibiotics and immunodeficiency [3, 4]. Infections associated with Chryseobacterium species include bacteremia, wound sepsis, indwelling device associated infections, ocular infections and intra-abdominal infections. In our patient it was associated with cellulitis, soft tissue infection and abscess formation. They are usually isolated from clinical specimens but rarely from blood as were in our case [4].

Most of the C. indologenes infections described in literature were hospital acquired and were seen in patients with underlying debilitating diseases [4–9]. Mostly our isolate is community acquired, as the sample grew Chryseobacterium from pus collected intraoperatively on the second day of admission. During the above said period, environmental surveillance samples did not grow Chryseobacterium.

Interestingly our patient was not immunosuppressed or was on any long term antibiotics or with indwelling devices, making this case unusual in presentation. Douvoyiannis et al. [10] had reported the first case of C. indologenes in a 33 day old infant in 2010. Hendaus et al. [11] reported the second case of C. indologenes infection from healthy newborn in 2013. Ours would be the third case of C. indologenes infection reported from an immunocompetent paediatric patient.

Not much data is available in literature on the choice of appropriate antibiotic for empirical treatment in C. indologenes infections [12]. This uncertainty is attributed to the wide spectrum of antimicrobial resistance, lack of gold standard susceptibility testing, unpredictable nature and non-establishment of MIC breakpoints for these organisms [13]. Further, biofilm and proteases production by C. indologenes species reduces its antimicrobial susceptibility [14]. Based on the results of SENTRY antimicrobial surveillance program during 1997–2001, the highest prevalence of Chryseobacterium was seen among the elderly. The most appropriate antibiotics that can be used for treating Chryseobacterium infections are newer fluoroquinolones (MIC 90–1 µg/ml) followed by rifampin (MIC 90–2 µg/ml). C. indologenes isolates showed adequate susceptibilities to trimethoprim-sulfamethoxazole, ciprofloxacin and piperacillin–tazobactam [15]. Variable susceptibility to vancomycin has been reported in literature [16].

Chryseobacterium indologenes is invariably resistant to aminoglycosides, shows varying degree of resistance to carbapenems, cephalosporins, piperacillin–tazobactam and are susceptible to fluroquinolones and cotrimoxazole. Based on the sensitivity pattern reported in SENTRY [15] and other literatures [9, 10, 17], there was no evident difference for community acquired isolates as compared with hospital acquired strains.

In this study, the isolate was resistant to meropenem and susceptible to imipenem by VITEK-2 systems. This could be due to different mechanisms involved in imipenem and meropenem resistance. Meropenem resistance is due to efflux systems and imipenem resistance is by porin mutations. Over expression of MexAB-OprM, an efflux system pumps out meropenem but not imipenem [18]. As the isolate was confirmed to be a MBL producer by imipenem-EDTA double disc diffusion test, all the carbapenems were reported as resistant for therapeutic purpose.

Disk diffusion methods are not reliable and thus susceptibility testing by broth micro dilution method should be performed [19].