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Vaginal infection by Enterobacter sakazakii
  1. J Ongrádi
  1. National Institute of Dermato-Venereology, Budapest VIII, Mária utca 41, Hungary 1085; ongjos{at}hotmail.com

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    In August 2001, a 26 year old woman seen at our outpatient clinic in Budapest complained of vulvar pruritus and vaginal discharge in the preceding 2 weeks. The only risk factor she admitted was that she had bathed in the resort lake Balaton a few times a week before the onset of symptoms, when the water was unusually warm (26–28°C). Examination revealed vulvovaginitis with mucous discharge at pH 5.5. A vaginal smear showed a large number of polymorphonuclear leucocytes, Gram negative rods, but no Lactobacillus. Culture on blood agar at 37°C for 48 hours resulted in yellow pigmented, bright, tough colonies. Biochemical analysis1 verified Enterobacter sakazakii. Standard disc diffusion technique,2 on Mueller-Hinton agar (Becton Dickinson, Sparks, MD, USA) using commercial discs (Oxoid, Basingstoke, UK), revealed sensitivity to carbenicillin, netilmycin, cefazolin, ofloxacin, tetracycline, and gentamicin; limited sensitivity to erythromycin; and resistance to ampicillin, clindamycin, nalidix acid, furadantin. This pattern is common in recent isolates.3 Empirical treatment—starting before laboratory data were available—with intravaginal Pimafucort ointment (1% natamycin, 0.25% neomycin, 0.5% hydrocortisone) for 7 days resulted in a complete recovery in 2 weeks, at which time the vagina was colonised by Streptococcus agalactiae. The following week a normal Lactobacillus flora at pH 4.2 returned.

    Nearly 50 E sakazakii infections resulting in meningitis, necrotising enterocolitis, and one urine infection of newborns have been documented. E sakazakii have been recovered from their blood, spinal fluid, throat, trachea, stomach aspirates, and rectum. Newborns were premature, and fed on powdered milk formula, which is the known source of infection.3,4 The means of its contamination is not known. For affected newborns, vaginal delivery does not seem to be a risk factor, since no colonisation of the mother’s genital tract has been reported. Less than 20 isolates have been obtained from children and adults, including eight from urine and one from genital secretion. Patients had either neoplasm or other serious underlying conditions, but their clinical details were not available. In both newborns and adults occasional coinfections with Serratia marcescens, Staphylococcus aureus, Enterococcus faecalis, or Candida albicans were reported.3,5

    The normal habitat, reservoir, and pathogenesis of E sakazakii are unknown. No cultivation from environmental sources (surface water, animals, raw cow’s milk, etc) has been successful,3 except recently from the gut of fruit flies.6 The rare related species E intermedium causing urinary tract infection, was found in drinking water and soil.5 Our case strongly suggested that warm surface water was the source of infection. The unusually high thermal resistance of E sakazakii3 might contribute to its survival during the manufacture powdered milk batches.4 It is important to remember that the stomach of newborns, especially that of premature babies, lacks free acid and is less acidic than that of adults. Ingested milk preparations remaining neutral or slightly alkaline in their stomach ensure survival and subsequent infection in the alkaline intestine. This pathomechanism is similar to pH increase in vaginal infections in the lack of Lactobacillus flora. The detrimental effect of E sakazakii infection is also reflected by the fact that recolonisation by the normal flora and a pH shift towards physiological level could be achieved only gradually in our patient.

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