A 58-year woman with a 1 month history of diarrhea, mucoid stool and abdominal pain was referred for intractable diarrhea. Sigmoidoscopy was done in primary care clinic and showed mucosal edema, whitish patchy and less than 5mm sized multiple inflammatory papules at sigmoid colon. Enterococcus avium (E .avium) was cultured in biopsy sample. Complete resolution of the colitis with E. avium required two weeks of antibiotics and probiotics. Many E. avium cases have been reported in the blood culture. However, it has never been proven that E. avium infection has caused colitis. In addition, the endoscopic finding of E. avium colitis was not known. Herein we report our case of E. avium colitis with biopsy culture proven.

Keywords: Enterococcus avium, colitis, biopsy culture

Enterococcus avium, formerly known as “group Q streptococcus”, is a gram-positive, catalase-negative coccus-shaped organism. Enterococci are generally regarded as the normal intestinal flora of humans. It is normally found in the urogenital and intestinal tracts of human beings and animals.^1,2 Some species cause serious infections. Endocarditis, intraabdominal infections and urinary tract infections are common clinical manifestations. Most of infections are caused by either En­terococcus faecalis or E. faecium. E.avium rarely infects man. Being regarded as a pathogen of low virulence, E. avium are seen mostly in patients with underly­ing immunosuppressive conditions and are usually of a polymicrobial character because of the typically intra-abdominal source.³ Although a few case reports of E. avium infection exist, no previous cases of stool culture positive for E. avium have been reported. Herein we report a case of endoscopically document E. avium colitis with biopsy culture proven.

A 58-year woman with a 1 month history of diarrhea and abdominal pain was referred from local clinic for evaluation of diarrhea. She had dyslipidemia and taking anti hyperlipidemic agents. She had no history of diabetes mellitus, intravenous drug use, or other immunosuppressed conditions. She had no recent abroad travel history and surgical history. Her physical examination was unremarkable. The patient was alert and did not appear to be in poor physical health. Her abdomen was soft and mild hyperactive bowel sound. Her height was 160cm, and her weight was 61kg, with no recent episode of malnutrition or weight changes. On arrival our hospital, she had a still mucoid stool and abdominal discomfort with taking two weeks of antibiotics. All routine laboratory tests were within the reference ranges. Sigmoidoscopy performed in primary care clinic 2 weeks ago showed mucosal edema, whitish patchy and less than 5mm sized multiple inflammatory papules at sigmoid colon. Sigmoidoscopic finding looked like pseudomembranous colitis (Figure 1). Sigmoidoscopic tissue biopsy revealed chronic nonspecific colitis. The biopsy cultured performed at the local clinic revealed Group D Enterococcus avium. These species are susceptible to Ampicillin, gentamycin, penicillin G, Vancomycin. After 2 weeks treatment of probiotics, and ciprofloxacin, we planned to perform follow up sigmoidoscopy. Mucosal edema and multiple white inflammatory papules were improved on sigmoidoscopy (Figure 2). Follow up biopsy and stool culture was done. Biopsy revealed chronic inflammation with lymphoid follicles and stool culture result was detected normal intestinal flora. After two weeks treatment of ciprofloxacin, she returned to an outpatient clinic for follow-up. Her mucoid stool was subsides and general condition was improved. At present, patient is on regular follow up based at outpatient clinic.

Figure 1 Local sigmoidoscopy performed in 2017.7.1.

Figure 2 Follow up sigmoidoscopy after two weeks of antibiotic treatment 2017.7.27.

Enterococcus species have emerged as the major pathogens causing nosocomial infection including bloodstream, and intraabdominal infections, as well as urinary tract.^4-6 Enterococcus faecalis and Enterococcus faecium accounting for more than 90% of cases of enterococcal bacteremia. Enterococcus avium, originally called group Q streptococcus owing to the presence of the group Q antigen, were most prevalent in chicken feces.⁷ E. avium is rarely reported as a pathogen, accounting for fewer than 5% of cases of enterococcal bacteremia.⁸ The biliary tract, followed by the abdomen, is the most commonly reported site of entry. The risk factors for E avium infection include contact with animals, especially birds. Nevertheless, our patient did not have a history of eating raw chickens or contact with birds or other animals. Although these bacteria were thought to have low virulence,⁹ E avium seems to be less virulent than E. faecalis. Most of patients with bacteremia had serious underlying disease. E avium bacteremia reflecting the serious underlying disease and may be a marker of poor prognosis.¹⁰ Further studies are needed to define the pathogenesis and virulence of E avium prognosis. There have been some case reports about E avium bacteremia in Korea.¹⁰ These observations suggest that E avium bacteremia most often originated from a gastrointestinal tract source. This case is first time isolated E avium from sigmoid lesion from endoscopic document colitis. After antibiotics treatment, patients recovered from colitis completely. Compared with other Enterococci, E avium show relatively showed resistant to penicillin G and ampicillin.¹¹ Furthermore, these days, the emergence and spread of vancomycin- resistant Enterococcus species has focused greater attention on this genus.¹² Depending on the results of susceptibility testing, ampicillin, aminoglycoside, vancomycin should be considered as a treatment for E avium infection.

In summary, we herein described a case of endoscopically confirmed colitis caused by E avium infection in a immunocompetent patient.

None.

There is no conflict of interest with this manuscript.

None.

1. Mackowiak PA (1989) The enterococci: evidence of species specific clinical and microbiologic heterogeneity. Am J Med Sci 297(4): 238-243.
2. Winn WC, Allen SD, Janda WM, Koneman EW, Procop GW, et al. (2006)Gram-positive cocci. In: Koneman EW (Ed.), Koneman’s Color Atlas and Textbook of Diagnostic Microbiology. (6th edn), JB Lippincott, Philadelphia, USA, pp. 701-704.
3. Na S, Park HJ, Park KH, Cho OH, Chong YP, et al.(2012)Enterococcus aviumbacteremia: a 12-year clinical experi­ence with 53 patients. Eur J Clin Microbiol Infect Dis31(3): 303-310.
4. Dealler SF, Grace RJ, Norfolk DR (1990) Enterococcus avium septicemia in an immunocompromised patient. Eur J Clin Microbiol Infect Dis 9(5): 367-368.
5. Mohanty S, Dhawan B, Kapil A, Das BK, Pandey P, et al. (2005) Brain abscess due to Enterococcus avium. Am J Med Sci 329(3): 161-162.
6. Vergis EN, HaydenMK, Chow JW, Snydman DR, Zervos MJ, et al. (2001) Determinants of vancomycin resistance and mortality rates in enterococcal bacteremia. A prospective multicenter study. Ann Intern Med 135(7): 484-492.
7. Nowlan SS, Deibel RH (1967) Group Q streptococci. I. Ecology, serology, physiology, and relationship to established enterococci. J Bacteriol 94(2): 291-296.
8. Patel R, Keating MR, Cockerill FR, Steckelberg JM (1993) Bacteremia due to Enterococcus avium. Clin Infect Dis 17(6): 1006-1011.
9. Fisher K, Phillips C (2009) The ecology, epidemiology and virulence of Enterococcus. Microbiology 155(Pt 6): 1749-1757.
10.  Na S, Park HJ, Park KH, Cho OH, Chong YP, et al. (2012) Enterococcus avium bacteremia: a 12-year clinical experience with 53 patients. Eur J Clin Microbiol Infect Dis 31(3): 303-310.
11. Maki DG, Agger WA (1988) Enterococcal bacteremia: clinical features, the risk of endocarditis, and management. Medicine (Baltimore) 67(4): 248-269.
12. Murray BE (2000) Vancomycin-resistant enterococcal infections. N Engl J Med 342(10): 710-721.