234

Eur. J. Clin. Microbiol. Infect Dis.

infection was community-acquired. As Corynebacterium xerosis is a normal commensal of the skin, it is possible that the aspiration of the the bursitis, which preceded the hospital admission, was followed by a transient bacteremia with subsequent dissemination to the mitral vatves. Another possible source of the infection was the teeth. B. L. R C d e r * N. F r i m o d t - M ¢ l l e r Department of Clinical Microbiology, Bispebjerg Hospital, Bispebjerg Bakke 23, DK-2400 Copenhagen NV, Denmark. References 1,

Lipsky BA, Goldberger AC, Tompkins LS, Plorde JJ. Injections caused by nondiphtheria coryne-

bacteria. Reviewsof InfectiousDiseases 1982,4: 1220-1235. 2. Loeksley RM: The lowly diphtheroid: nondiphtheria corynebacterial infections in humans. Western Journal of Medicine1982, 137: 45-52. 3. Johnson WD, Kaye D: Serious infections caused by diphtheroids. Annals of the New York Academy of Sciences 1970, 174:568-576. 4. Collins MD, Cummins CS: Genus Corynebacterium. In: Sheath PHA, Mair NS, SharpeME, Holt JG (ed): Bergey's manual of systematicbacteriology. Volume 2. Williams & Wilkins, Baltimore, 1986, p. 1266--1276. 5. Gerry JL, Greenough WB: Diphtheroid endocarditis. Report of nine cases and review of the literature. Johns Hopkins Medical Journal 1976, 139: 61-68. 6. Geraci JE, Forth RJ, Ellis FH: Postoperative prosthetic valve bacterial endocarditis due to Corynebacterium xerosis. Mayo Clinic Proceedings 1967, 42: 736-743. 7. Porsehen IlK, Goodman Z, Rafal B: Isolation of Corynebacterium xerosis from clinical specimens. American Journal of ClinicalPathology1977,68: 290293.

Proteus mirabilis as a C a u s e o f Recurrent Lung Infection Fibrosis Patient

in a C y s t i c

Proteus mirabilis is rarely isolated from the bronchial secretions of cystic fibrosis patients. It is considered a transient colonizer of the bronchial secretions, generally being far outnumbered by Pseudomonas aeruginoas. To our knowledge there are no previous reports of the isolation of Proteus mirabitis as a single or overwhelmingly predominant organism during

very long periods of time in this type of patient, particularly in recurrent episodes of pneumonia

(1, 2, 3). An 18-year-old woman suffering from chronic respiratory disease since early childhood was referred to our hospital with a diagnosis of cystic fibrosis and acute respiratory tract infection. Two sweat tests revealed high chloride and sodium concentrations of over 120 meq/1. Steatorrhea and hyperamylasemia (1,084 IU/1) were also documented. During the previous two years she had been treated with tetracycline, amoxicillin and amoxicillin-clavulanate. When the patient presented to our outpatient department, Proteus mirabiIis was isolated from a homogenized sputum sample (95 % of the cells were polymorphonuclear neutrophils) in pure culture on CLED medium (Oxoid, UK), with a count of 3 x 105 CFU/ml; treatment with cotrimoxazole was started. The patients's condition worsened and she was admitted to hospital. At this time she was suffering from a productive cough, dyspnea and fever (39 °C). The leukocyte count was 24,000/ mm with neutrophilia and 13 % band forms. Chest X-ray revealed disseminated cystic bronchiectasis with multifocal pneumonia. Proteus mirabiIis was again isolated from sputum, with a count of 6 x 106 CFU/ml. The strain exhibited resistance to amoxicillin, tetracycline and cotrimoxazole. A variant of the same strain exhibited resistance to ticarcillin, cephalothin and cefazolin, and reduced susceptibility to amoxicillin-clavulanate, Aspergillus fumigatus was also isolated from the sputum. Specific anti-Aspergillus fumigatus IgE and IgG levels were significantly increased, suggesting the presence of allergic bronchopulmonary aspergillosis, a disease present in about 10 % of cystic fibrosis patients. The serological response to the homologous Proteus mirabilis strain was tested: anti-H and anti-O agglutinating antibodies were detected at titres of 1:80 and 1:320, respectively. The acute exacerbation was treated with oral ciprofloxacin (750 mg b.i.d.) for ten days. One month later there was a significant increase in anti-H antibodies (1:1,280) and maintenance of anti-O antibodies (1:320). The overall development of Proteus mirabilis counts in sputum is presented in Table 1. In June a small number (2 x l 0 2 CFU/ml) of an arginine dehydrolase-positive, lysine and ornithine decarboxylase-negative Pseudomonas strain was isolated. This was presumptively identified as Pseudomonas pseudomatlei, a species that has not previously been reported in cystic fibrosis patients. In the follow-up examination carried out at the end of June, Proteus mirabilis was again prevalent and the patient's

V___O1.9, 1990

235

Table 1: Bacterial counts in sputum.

Date January

10 17 F e b r u a r y 15 March 15 April 15 June 20 28 July 15 August 15

Proteus mirabilis

Pseudomonas maltophilia

Treatment

3x105 6 x 106 1 × 104 < 102 5 × 104 1 x 108 1 × t0 4 < 102 3 × 104

1 X 102 7 x 105 3 x 103

cotrimoxazole ciprofloxacin ciprofloxacin -

condition had worsened. The patient was treated with oral ciprofloxacin for three weeks. Five days after the beginning of therapy, the number of Proteus mirabilis d e c r e a s e d significantly, but a Pseudomonas maltophilia strain appeared in low,numbers. At the end of treatment Proteus mirabilis had been completely replaced by an abundant growth of Pseudomonas maltophilia. Nevertheless, by the time the last follow-up examination was performed, Proteus mirabilis had reappeared once more. The presence of Proteus mirabilis in cystic fibrosis patients has been frequently disregarded until now. In our patient Proteus mirabilis was previously isolated in 1984 in urine and in 1987 in a sputum sample, and was present in the stools at the time we treated her. AspergiIlus fumigatus can produce chronic necrotizing pneumonia with features similar to those of bacterial infection (4), but the clinical course of the illness of our patient was closely related to the Proteus mirabilis counts and the use of ciprofloxacin. This case documents for the first time the possibility of long-term carriage and chronic lung infection with acute exacerbations caused by Proteus mirabilis in a cystic fibrosis patient.

M. O j e d a - V a r g a s 1 A. Pacheco 2 M. E l i a 1 R. V i l l a v e r d e 1 F. B a q u e r o 1. 1Servicio de Microbiologia, and 2Servicio de Neumologia, Hospital Ram6n y Cajal, Instituto National de la Salud, 28034 Madrid, Spain.

References 1. 2. 3. 4.

H a i b y N: Microbiology of lung infections in cystic fibrosis patients. Acta Paediatrica Scandinavica 1982, 301, Supplement C: 33-54. Thomassen MJ: Cystic fibrosis: a review of pulmonary infections and interventions. Pediatric Pulmonology 1987, 3: 334-351. R u b i o T: Infection in patients with cystic fibrosis. American Journal of Medicine 1986, 81, Supplement 1A: 73-77. Elliot J A , Milne LJR, Commlng D: Chronic necrotising pulmonary aspergillosis treated with itraconazole, Thorax 1989, 44: 820-821.

In Vitro Activity of Cefpirome (HR810) against Enterococcus Species Cefpirome (HR810) is a new semi-synthetic cephalosporin for parenteral use which has been reported to have an expanded spectrum of activity that includes problem pathogens such as enterococci (1, 2). In the present study we investigated the in vitro effect of cefpirome and other cephalosporins against strains of Enterococcus faecalis and Enterococcus faecium. In more detailed kill kinetic studies we investigated the effect of cefpirome in combination with gentamicin against a small number of Enterococcus faecalis strains. These effects were monitored using optical density changes and adenosine triphosphate (ATP) assessment. Twelve clinical isolates of Enterococcus faecalis and six clinical isolates of E n t e r o c o c c u s faecium were tested against cefpirome, cefotaxime (both supplied by Roussel Laboratories, UK) ceftazidime, cefuroxime (both supplied by Glaxo, UK), ceftizoxime (Wellcome, UK) and ampicillin (Beecham Laboratories, UK). MIC values were determined on DST agar (Oxoid, UK) containing twofold dilutions of antibiotic. Bacterial inocula of 107-108 CFU/ml were transferred to the agar plates with a multipoint