JOURNAL OF CLINICAL MICROBIOLOGY, Feb. 1992, p. 261-264 Vol. 30, No. 20095-1137/92/020261-04$02.00/0Copyright C 1992, American Society for Microbiology

Clinical Significance of Staphylococcus warneri BacteremiaUSHA KAMATH,lt CAROL SINGER,'* AND HENRY D. ISENBERG2

Division of Infectious Diseases, Department of Medicine,1 and Division of Microbiology, Departmentof Pathology,2 Long Island Jewish Medical Center, The Long Island Campus for

The Albert Einstein College of Medicine, New Hyde Park, New York 11042

Received 26 July 1991/Accepted 24 October 1991

Twenty-seven episodes of bacteremia caused by Staphylococcus warneri were identified at Long Island JewishMedical Center in New York between 1984 and 1989. Fourteen of these were thought to represent truebacteremias and 13 to represent contaminants. Of the 14 true bacteremias, 5 were in pediatric and 9 were inadult patients. Eight of 14 patients (57%) had catheter-related bacteremia and 5 of 14 had bacteremia ofunknown source. There was one case of fulminant native valve S. warnedi endocarditis. All cases ofcatheter-related bacteremia, except one, were nosocomially acquired, and 75% of these patients had anunderlying immunosuppressive condition. Only 40% of patients with bacteremias of unknown source wereimmunocompromised, and S. warnedi appeared to be noninvasive in this group. Interestingly, all five of thepediatric isolates were oxacillin susceptible, although four of five were resistant to penicillin, despite the factthese patients were hospitalized an average of 29 days. In contrast, seven of nine adult isolates were resistantto both oxacillin and penicillin. The only case of native valve S. warned endocarditis occurred in a patient whohad no known underlying valvular heart disease, but had an underlying immunosuppressive condition.Identification to species level of coagulase-negative staphylococci may lead to appreciation of the importance ofbacteria such as S. warned as human pathogens.

Coagulase-negative staphylococci are now considered sig-nificant nosocomial pathogens complicating central venouscatheters, prosthetic heart valves, prosthetic joints, andneurosurgical ventricular shunts and in infants in intensivecare nurseries (1, 8, 12, 15, 20, 24-26, 28). Bacteremia withcoagulase-negative staphylococci may be associated withsignificant morbidity and mortality in hospitalized patients.Such isolates can no longer be regarded only as contami-nants (1, 21). Staphylococcus epidermidis is the most com-monly isolated species of clinical importance (18, 19, 21, 23),while data on the clinical significance of other coagulase-negative staphylococci are limited, and few are available forStaphylococcus warneri (14).

This study evaluated the clinical significance and outcomeof S. warneri bacteremia in both adult and pediatric patients,including a case of native valve endocarditis. This studydocuments the importance of S. warneri as a potentialhuman pathogen and emphasizes the value of identifyingcoagulase-negative staphylococci to the species level, par-ticularly when isolated from blood cultures in appreciablenumbers.

MATERIALS AND METHODS

The medical records of all patients with S. warneri bacte-remia between 1 January 1984 and 31 December 1989 atLong Island Jewish Medical Center were reviewed. Patientswere identified by the records of positive blood cultures inthe hospital's division of microbiology. Both adult andpediatric patients were included. The following clinical in-formation was obtained: age, sex, underlying disease, typeof catheter if bacteremia was catheter related, number ofpositive blood cultures, antibiogram of the isolate, treat-ment, and outcome of infection.

* Corresponding author.t Present address: St. Barnabas Hospital, Bronx, NY 10457.

Definitions. We classified patients into three broad catego-ries.

(i) Catheter-related infections. The onset of bacteremiaoccurred within a few days of the placement of the catheterand/or the catheter tip yielded the same organism at the timeof removal of the catheter. Catheter tips were cultured asdescribed previously (10). These patients had one or morepositive peripheral blood cultures.

(ii) Endocarditis. The patient with endocarditis had two ormore positive blood cultures with clinical evidence of en-docarditis.

(iii) Bacteremia of unknown source. These patients had twoor more positive blood cultures with no definite source of S.warneri infection, no clinical evidence of endocarditis, andno other source of fever.We considered S. warneri to be a contaminant if only one

blood culture was positive, regardless of the number drawn,and there was no clear source for the bacteremia.

Patients were considered cured if signs and symptoms ofinfection were no longer present and the bacteremia wascleared.

Microbiology. Adult and pediatric isolator tubes (DuPont,Wilmington, Del.) were used to obtain all blood specimensfor culture; they were processed in accordance with themanufacturer's instructions. One 5% sheep blood agar plate(Becton-Dickinson Microbiology Systems [BBL], Cockeys-ville, Md.), two chocolate agar plates (BBL) and one Sab-ouraud agar plate (BBL) were each inoculated with approx-imately 0.3 ml of the sedimented (adult) and uncentrifuged(pediatric) specimen. The remaining 0.3 ml was added to 18ml of a special broth, previously described (11), whichpermits the growth of all medically significant anaerobes. Onisolation, S. warneri formed whitish, circular, slightly domedcolonies, 2 to 3 mm in diameter on blood and chocolate agarwithin 24 h of incubation at 35°C. Several colonies from eachprimary isolation plate were transferred to blood and Staph-ylococcus 110 (BBL) agars and held for 72 h to ensureuniformity of colonial morphology. All isolates were coagu-

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262 KAMATH ET AL.

TABLE 1. S. warneri bacteremia in pediatric patients

Bac- Underlying Type of No. of days No. of positive Antibiotic Out-teremia Patient Age Sex disease catheter catheter in blood cultures/ suscepti- Treatment comeplace no. drawn bilitya

Catheter 1 27 mo F Renal failure Subclavian 8 2/2 Penr OXs Catheter removed; no antibiotic Curedrelated 2 15 yr M Short bowel Broviac 14 1/1 Pens Ox' Catheter not removed; 14 days of Cured

syndrome appropriate antibiotic3 36 wk F Gastroschisis Broviac 12 2/2 Penr oXs Catheter removed; 3 wk of appro- Cured

priate antibiotic4 26 wk M Prematurity UV line 15 1/1 Penr OX, Catheter removed; 10 days of ap- Cured

propriate antibiotic

Unknown 5 8 days F C-section None 2/2 Penr Oxs 7 days of inappropriate antibiotic Curedsource

a Pen, penicillin; Ox, oxacillin.

lase negative and were identified as S. warneri by theStaph-Ident systems (Analytab Products, Plainview, N.Y.)and the gram-positive identification card in the AutoMicro-bic System (Vitek Systems, Hazelwood, Mo.). All isolateswere identified independently as S. warneri by Wesley E.Kloos (North Carolina State University, Raleigh). None ofthe isolates produced acid from mannose but all producedacid from mannitol, two important reactions that distinguishS. warneri from Staphylococcus lugdunensis (14). Diffusion(3) and dilution (22) susceptibility studies were performed instrict compliance with published procedures.

RESULTSTwenty-seven cases of S. warneri bacteremia were iden-

tified. According to the above definitions, 5 of 9 bacteremiasin pediatric patients and 9 of 18 in adults represented trueinfections. The remainder were considered contaminants.For purposes of analysis, the 14 patients with true bactere-mias were divided into pediatric and adult groups.

Pediatric patients. Table 1 summarizes the data on the fivepatients with S. warneri infections. The patients ranged inage from 26 weeks to 15 years, with a mean age of 39.6months. Two of these patients were male, and three werefemale. Three of five patients were immunocompromised.Four patients had catheter-related bacteremias, and one

had bacteremia of unknown origin. Of the four patients withcatheter-related bacteremia, two had Broviac catheters, onehad an umbilical vessel, and one had a subclavian catheter.The catheters were in place from 8 to 15 days, with a meanof 12.2 days. Three of four patients had their cathetersremoved. One of these three patients received no antibiotics,while the other two received antibiotics for 10 and 21 days.The single patient who did not have his catheter removedreceived 2 weeks of appropriate antibiotics and was cured.The patient with bacteremia of an unknown source received7 days of inappropriate antibiotics and recovered.The isolates from four of the five patients were resistant to

penicillin but susceptible to oxacillin. The fifth isolate wassusceptible to both penicillin and oxacillin. All isolates weresusceptible to vancomycin.

All five patients cleared their bacteremia and were consid-ered cured, including the patient with bacteremia of un-known source who received inappropriate antibiotics.

Adult patients. Table 2 summarizes the data on the nineadult patients with S. warneri bacteremia. The patientsranged in age from 33 to 77 years, with a mean age of 60.5years, and included six patients who were immunocompro-mised. Six of these patients were male, and three female.

Four patients had catheter-related bacteremia. The patientwith native valve endocarditis was a 64-year-old male withno history of congenital heart disease or rheumatic feverwho was admitted with fever, subconjunctival hemorrhages,splinter hemorrhages, multiple petechiae, splenomegaly, anda systolic murmur. Four of six blood cultures were positivefor S. warneri. Despite treatment with vancomycin andgentamicin, the patient developed a new diastolic murmur ofaortic insufficiency and deteriorated neurologically. He diedafter 15 days of hospitalization. Autopsy revealed friablevegetations on the mitral, aortic and pulmonary valvesconsistent with endocarditis. Splenic infarcts and septicemboli to the kidneys were also noted. Of the four patientswith bacteremias of unknown origin, two had localizedabscesses which grew other organisms; these lesions werenot considered the source of the S. warneri bacteremia.Of the four patients with catheter-related bacteremia, two

patients had central venous pressure lines, one had a triplelumen, and one had a Swan-Ganz catheter. The catheterswere in place from 3 to 14 days (mean, 8 days) and wereremoved in three patients at the time of onset of bactere-mias. Patients received antibiotics for a duration of 5 to 15days, with a mean of 6.7 days. All patients with catheter-related infections cleared their bacteremia and were consid-ered cured. One patient who received no antibiotics and didnot have his catheter removed also recovered.Three of the four patients with bacteremia of unknown

origin received antibiotics for 2 to 7 days, with a mean of 4days. These three patients responded to therapy. One pa-tient received inappropriate antibiotics and remained febrile2 weeks after his blood cultures were positive. One patientdied of causes unrelated to S. warneri bacteremia.

Five of the nine isolates were resistant to oxacillin andpenicillin. Three were resistant to penicillin but susceptibleto oxacillin, and one was susceptible to both penicillin andoxacillin. All nine isolates were susceptible to vancomycin.

DISCUSSIONCoagulase-negative staphylococci have emerged in recent

years as important nosocomial pathogens, with S. epidermi-dis the most frequently recognized organism in this group(27). S. warneri and other coagulase-negative staphylococcihave been recognized less frequently as significant humanpathogens (17). Additionally, S. warneri represents only 1%of the skin staphylococci in normal individuals (6). S.warneri is distinguished from S. epidermidis by its lack ofphosphatase and its ability to produce acid from trehalose(14).

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S. WARNERI BACTEREMIA 263

TABLE 2. S. warneri bacteremia in adult patients

No. of No. of posi- AntibioticBacteremia Pa- Age Sex Underlying Type of days tive blood suscepti- Treatment Outcometient (yr) disease catheter catheter cultures/no. bility.

in place drawn

Catheter 6 71 M Myelodysplastic Triple 14 1/3 Penr oxr Catheter removed; Curedrelated syndrome 15 days of ap-

propriate antibi-otic

7 33 M Parapelvic abscess CVP line 5 1/2 Penr oxr Catheter removed; Cured5 days of appro-priate antibiotic

8 77 M Stomach carci- CVP line 3 1/3 Pens Oxs Catheter removed; Curednoma with liver 7 days of appro-mets priate antibiotic

9 71 M Subtotal gastrec- Swan-Ganz 10 1/3 Penr Oxr Catheter not re- Curedtomy for ulcer; moved; no anti-colon carcinoma biotic

Endocarditis 10 64 M Cirrhosis of liver None 4/6 Penr oxr 14 days of appro- Deathbpriate antibiotic

Unknown 11 57 M AML, urosepsis None 2/2 Penr oxr 7 days of appropri- Death (respira-source ate antibiotic tory failure)

12 56 F Alzheimers None 2/2 Penr Oxs 7 days of appropri- Curedate antibiotic

13 45 F Iliac crest and glu- None 2/3 Penr Oxs 2 days of appropri- Curedteal abscessesc ate antibiotic

14 71 F Rectal carcinoma None 2/2 PenT Oxs 8 days of inappro- Remained fe-priate antibiotic briled

a Pen, penicillin; Ox, oxacillin.b Autopsy revealed vegetations on mitral, aortic, and pulmonary valves.c Cultures grew S. aureus.d Patient remained febrile for 2 weeks after positive blood cultures.

In the 5-year period between 1984 and 1989, we identified27 episodes of S. warneri bacteremia among adult andpediatric populations, 14 (51.8%) of which were consideredclinically significant. S. warneri, like S. epidermidis, wasmost frequently associated with intravascular catheter infec-tions, representing 57% of infections in this study. Seventy-five percent of patients with catheter-related bacteremia hadunderlying immunosuppressive illnesses. Catheters were inplace for an average of 10.1 days prior to the episode ofbacteremia. All cases of catheter-related bacteremia werenosocomially acquired, except for patient 1, who had apositive blood culture after 1 day of hospitalization, althoughhe had a Broviac catheter in place for a year.The S. warneri isolates from the pediatric patients differed

from those recovered from adults by their susceptibility tooxacillin. In the pediatric patients, all isolates were suscep-tible to oxacillin and one of four was susceptible to penicillinas well, whereas three of four adult isolates were resistant toboth oxacillin and penicillin. Usually, antibiotic resistancepatterns suggest the nosocomial origin of coagulase-negativestaphylococci (5, 13), particularly in patients with indwellingintravascular catheters. It is somewhat surprising, therefore,that the S. warneri isolates from hospitalized pediatricpatients with catheter-related infections were susceptible tooxacillin. Six of eight patients had their catheters removedand received antibiotics for an average of 8.9 days. Of theremaining two patients in whom the catheters were left inplace, one received antibiotics while the other did not. Allpatients with catheter-related bacteremia were apparentlycured.

It is interesting to note that the adult case of native valve

endocarditis occurred in a patient with no known underlyingcongenital or rheumatic heart disease. Most cases of nativevalve endocarditis caused by coagulase-negative staphylo-cocci have an underlying valvular defect (2, 4, 6, 9, 16),while only one such case has been reported as due to S.warneri (6). This patient's underlying cirrhosis may havepredisposed him to serious infection with S. warneri, in viewof the increasing recognition of coagulase-negative staphylo-cocci as pathogens of immunocompromised patients (2, 8).Two of five patients with bacteremia of unknown origin

were immunosuppressed. All blood cultures were drawnwhen patients manifested signs and symptoms of infection,e.g., elevated white blood cell count and a toxic appearance.Since this was a retrospective study, it is difficult to becertain that positive blood cultures in a given individualwere, in fact, drawn at separate times. However, the generalpractice at this hospital is to draw two blood cultures atseparate times. With the exception of patient 11, who hadacute myelocytic leukemia and died secondary to respiratoryfailure, all patients were cured of their infection whether ornot the antibiotics utilized were considered appropriate.Although these patients appeared to have true bacteremias,S. warneri may cause less serious disease in immunocompe-tent individuals than in those who are immunocompromised.

This study suggests that S. warneri may be a nosocomialpathogen, especially in catheter-related infections. In immu-nocompromised patients, S. warneri may cause seriousinvasive infections, including endocarditis on native heartvalves. Although some studies have suggested that identifi-cation of coagulase-negative staphylococci may have limited

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264 KAMATH ET AL.

utility (7, 23), this study emphasizes the importance of suchanalyses in coagulase-negative staphylococcal bacteremias.

REFERENCES1. Anday, E., and G. Talbot. 1985. Coagulase-negative staphylo-

coccus bacteremia-a rising threat in the newborn infant. Ann.Clin. Lab Sci. 13:246-251.

2. Baddour, L., T. Phillips, and A. Bisno. 1986. Coagulase negativestaphylococcal endocarditis. Arch. Intern. Med. 146:119-121.

3. Barry, A. L., and C. Thornsberry. 1991. Susceptibility tests:diffusion test procedures,-,p. 1117-1125. In A. Balows, W. J.Hausler, Jr., K. L. Herrmann, H. D. Isenberg, and H. J.Shadomy (ed.), Manual of clinical microbiology, 5th ed. Amer-ican Society for Microbiology, Washington, D.C.

4. Caputo, G., G. Archer, S. Calderwood, M. Dinubile, and A.Karchmer. 1987. Native valve endocarditis due to coagulase-negative staphylococci: clinical and microbiologic features. Am.J. Med. 83:619-625.

5. Christensen, G., A. Bisno, J. Parisi, B. McLaughlin, M. G.Hester, and R. Luther. 1982. Nosocomial septicemia due tomultiply antibiotic resistant Staphylococcus epidermidis. Ann.Intern. Med. 96:1-10.

6. Dan, M., G. Marien, and G. Goldsand. 1984. Endocarditiscaused by Staphylococcus warneri on a normal aortic valvefollowing vasectomy. Can. Med. Assoc. J. 131:211-213.

7. Eng, R., C. Wang, A. Person, T. Kiehn, and D. Armstrong. 1982.Species identification of coagulase-negative staphylococcal iso-lates from blood cultures. J. Clin. Microbiol. 15:439-442.

8. Fidalgo, S., F. Vazquez, M. Mendoza, F. Perez, and J. Mendez.1990. Bacteremia due to Staphylococcus epidermidis: microbi-ologic, epidemiologic, clinical and prognostic features. Rev.Infect. Dis. 12:520-528.

9. Harris, L., and H. O'Shields. 1986. Coagulase-negative staphy-lococcal endocarditis: a view from the community hospital.South. Med. J. 79:1379-85.

10. Haslett, T., H. D. Isenberg, E. Hilton, V. Tucci, B. Kay, andE. M. Vellozzi. 1988. Microbiology of indwelling central intra-vascular catheters. J. Clin. Microbiol. 26:696-701.

11. Isenberg, H. D. 1983. The detection of small numbers ofmicroorganisms in seeded blood samples using lysis-centrifuga-tion, p. 19-30. In A. Balows and A. C. Sonnenwirth (ed.),Bacteremia. Charles C. Thomas, Publisher, Springfield, Ill.

12. Karchmer, A., G. Archer, and W. Dismukes. 1983. Staphylococ-cus epidermidis causing prosthetic valve endocarditis: microbi-ologic and clinical observations as guides to therapy. Ann.Intern. Med. 98:447-455.

13. Kirchoff, L., and J. Sheagren. 1985. Epidemiology and clinicalsignificance of blood cultures positive for coagulase negativeStaphylococcus. Infect. Control 6:479-486.

14. Kloos, W. E., and D. W. Lambe, Jr. 1991. Staphylococcus, p.222-237. In A. Balows, W. J. Hausler, Jr., K. L. Herrmann,H. D. Isenberg, and H. J. Shadomy (ed.), Manual of clinicalmicrobiology, 5th ed. American Socity for Microbiology, Wash-ington, D.C.

15. Liekweg, W. G., Jr., and L. J. Greenfield. 1977. Vascularprosthetic infections: collected experience and results of treat-ment. Surgery 81:335-342.

16. Lockman, D., W. Chew, and J. P. Rissing. 1983. Staphylococcusepidermidis endocarditis: a community-acquired methicillin-resistant isolate. South. Med. J. 76:1203-1204.

17. Lowy, F., and S. Hammer. 1983. Staphylococcus epidermidisinfections. Ann. Inter. Med. 99:834-839.

18. Martin, M., M. Pfaller, and R. Wenzel. 1989. Coagulase nega-tive staphylococcal bacteremia: mortality and hospital stay.Ann. Intern. Med. 110:9-16.

19. Moyer, M., L. Edwards, and L. Fraley. 1983. Comparativeculture methods on 101 intravenous catheters. Arch. Intern.Med. 143:66-69.

20. Neihart, R., J. Fried, and G. Hodges. 1988. Coagulase negativestaphylococci. South. Med. J. 81:491-500.

21. Ponce de Leon, S., and R. Wenzel. 1984. Hospital-acquiredbloodstream infections with Staphylococcus epidermidis. Re-view of 100 cases. Am. J. Med. 77:639-643.

22. Sahm, D. F., and J. A. Washington II. 1991. Antibacterialsusceptibility testing: dilution methods, p. 1105-1116. In A.Balows, W. J. Hausler, Jr., K. L. Herrmann, H. D. Isenberg,and H. J. Shadomy (ed.), Manual of clinical microbiology, 5thed. American Society for Microbiology, Washington, D.C.

23. Sewell, C., J. Clarridge, E. Young, and R. Guthrie. 1982.Clinical significance of coagulase-negative staphylococci. J.Clin. Microbiol. 16:236-239.

24. Shurtleff, D., E. Foltz, R. Weeks, and J. Loeser. 1974. Therapyof Staphylococcus epidermidis: infections associated with spi-nal fluid shunts. Pediatrics 53:55-62.

25. Sidebottom, D., J. Freeman, R. Plalt, M. Epstein, and D.Goldmann. 1988. Fifteen-year experience with blood streamisolates of coagulase-negative staphylococci in neonatal inten-sive care. J. Clin. Microbiol. 26:713-718.

26. St. Geme, J. W., III, L. M. Bell, S. Baumgart, C. Angio, and M.Harris. 1990. Distinguishing sepsis from blood culture contam-ination in young infants with blood cultures growing coagulase-negative staphylococci. Pediatrics 86:157-162.

27. Stillman, R., R. Wenzel, and L. Donowitz. 1987. Emergence ofcoagulase negative staphylococci as major nosocomial bloodstream pathogens. Infect. Control. 8:108-112.

28. Verhoef, J., and A. Fleer. 1983. Staphylococcus epidermidisendocarditis and Staphylococcus epidermidis infection in anintensive care unit. Scand. J. Infect. Dis. Suppl. 41:56-63.

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Letters to the EditorCLEARVIEW Chlamydia Test for Detection of Chlamydiae

in Cervical Specimens

In their evaluation of the CLEARVIEW Chlamydia test, arapid immunoassay for the direct detection of Chlamydiatrachomatis from cervical specimens, Stratton et al. (1)reported that 14 of 677 (2%) cervical specimens failed tomigrate in the CLEARVIEW test. We conducted a studybetween February and May 1991 in which 23 private gyne-cologists volunteered to participate. Each woman visitingtheir clinics during that period was asked to participate, andif consent was given a cervical specimen was then system-atically taken, unless cervical bleeding was too heavy. Aquestionnaire was filled out by every patient included in thestudy. We used the CLEARVIEW test to analyze thecervical samples.Nine hundred and thirty cervical specimens were ana-

lyzed; 22 (2.4%) were positive and 17 (1.8%) failed to migratein the CLEARVIEW test and were considered uninterpret-able. We compared characteristics of these 17 women tothose of either positive or negative women. There was nodifference in the permeabilities of the cervixes. No lubricantwas used with the vaginal speculum by the physicians whotook the uninterpretable specimens, except, rarely, somewater. The mean delays between sampling and laboratorytesting did not differ between uninterpretable specimens andnegative or positive ones. In 58% of the uninterpretablespecimens (versus 9.5% of the positive and 12.8% of thenegative specimens), swab-induced bleeding was reported,and in 31.3% (versus 4.8% of the positive and 9% of thenegative), spontaneous bleeding (menses or metrorrhagia)

was noted. This suggests that the presence of blood on theswab may prevent the migration of the extracted specimen inthe CLEARVIEW test. However, no bleeding was reportedin 35% of the uninterpretable specimens. A possibility whichcould be investigated is the presence of cervical mucus onthe swab. Further research is needed to establish all thereasons for the failure to migrate in the CLEARVIEW testand the best conditions of use for this test.

REFERENCE

1. Stratton, N. J., L. Hirsch, F. Harris, L. M. de la Maza, and E. M.Peterson. 1991. Evaluation of the rapid CLEARVIEW Chlamydiatest for direct detection of chlamydiae from cervical specimens.J. Clin. Microbiol. 29:1551-1553.

Josiane WarszawskiLaurence MeyerDepartment of EpidemiologyINSERM U292H6pital de Bicetre94275 Le Kremlin-BicetreFrance

Philippe WeberCentre de Diagnostic du Galile77200 Torcy-Marne la VallkeFrance

Ed. Note: The authors felt that no response was necessaty.

Significant Infection Caused by Staphylococcus warneri

Kamath et al. recently reported 27 episodes of bacteremiacaused by Staphylococcus warnei identified in their institu-tion between 1984 and 1989 (5). Among the nine truebacteremias in adult patients, there was one case of commu-nity-acquired native valve endocarditis in a 64-year-old manwithout known valvular heart disease. The patient died after2 weeks of medical therapy, and autopsy revealed mitral,aortic, and pulmonary valve vegetations as well as splenicinfarcts and septic renal emboli. Cirrhosis was cited as a

possible predisposing disease. One previously reported caseof native valve endocarditis caused by S. warneri followingvasectomy in a 32-year-old man without known valvularheart disease was cited (3). This patient required aortic valvereplacement in addition to medical therapy for cure. Smallvegetations and ulcerative destruction of the noncoronarycusp of the aortic valve were found at surgery. No predis-posing cause for infection was identified. On the basis ofthese two cases, the authors concluded that S. warneri maycause serious, invasive infection.

Considerable additional data support the pathogenic roleof S. warneri. Five additional cases of native valve en-docarditis have been reported: one was a well-characterized

case report (8) and four were from two series which reportedcases of native valve endocarditis caused by coagulase-negative staphylococci (2, 4). I reported a community-acquired episode which occurred in a 66-year-old man

without valvular heart disease (8). He required both aorticand mitral valve replacements. Extensive destruction ofboth valves and an aortic valve ring abscess were found atsurgery. No significant predisposing cause was evident.Caputo et al. reported three cases in which S. waneri was

isolated from patients meeting strict criteria for native valveendocarditis (2). All of these isolates were community ac-

quired. Etienne and Eykyn reported one case caused by S.warneri in their series of 35 patients with native valve en-

docarditis caused by coagulase-negative staphylococci (4).S. waneri has also been reported to have caused three

cases of hematogenous vertebral osteomyelitis (1, 6, 8). Oneof these infections was attributed to an infected Hickmancatheter (1), whereas the others were caused by community-acquired bacteremias. In addition, occult infection with S.warneri has recently been implicated as the etiological agentin three cases of femoral anastomotic pseudoaneurysmsassociated with prosthetic vascular grafts (7).

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Vol. 30, No. 8

LETTERS TO THE EDITOR 2217

It is clear that S. warnen has the potential to causesignificant community-acquired and nosocomial infections.In particular, native valve endocarditis may present asacute, aggressive disease, requiring a combined medical andsurgical approach because of valve destruction or abscessformation. Routinely identifying clinically significant isolatesof coagulase-negative staphylococci to the species level willclarify the frequency and spectrum of disease caused bythese increasingly important pathogens.

REFERENCES1. Bryan, C. S., J. T. Parisi, and D. G. Strike. 1987. Vertebral

osteomyelitis due to Staphylococcus warnen attributed to aHickman catheter. Diagn. Microbiol. Infect. Dis. 8:57-59.

2. Caputo, G. M., G. L. Archer, S. B. Calderwood, M. J. Dinubile,and A. W. Karchmer. 1987. Native valve endocarditis due tocoagulase-negative staphylococci. Clinical and microbiologic fea-tures. Am. J. Med. 83:619-625.

3. Dan, M., G. J. R. Marien, and G. Goldsand. 1984. Endocarditiscaused by Staphylococcus warneri on a normal aortic valvefollowing vasectomy. Can. Med. Assoc. J. 131:211-213.

4. Etienne, J., and S. J. Eykyn. 1990. Increase in native valveendocarditis caused by coagulase negative staphylococci: anAnglo-French clinical and microbiological study. Br. Heart J.64:381-384.

5. Kamath, U., C. Singer, and H. D. Isenberg. 1992. Clinicalsignificance of Staphylococcus wamren bacteremia. J. Clin. Mi-crobiol. 30:261-264.

6. Karthigasu, K. T., R. A. Bowman, and D. I. Grave. 1986.Vertebral osteomyelitis caused by Staphylococcus warneri. Ann.Rheum. Dis. 45:1029-1030.

7. Seabrook, G. R., D. D. Schmitt, D. F. Bandyk, C. E. Edmiston,C. J. Krepel, and J. B. Towne. 1990. Anastomotic femoralpseudoaneurysm: an investigation of occult infection as an etio-logic factor. J. Vasc. Surg. 11:629-634.

8. Wood, C. A., D. L. Sewell, and L. J. Strausbaugh. 1989. Vertebralosteomyelitis and native valve endocarditis caused by Staphylo-coccus warnei. Diagn. Microbiol. Infect. Dis. 12:261-263.

Craig A. WoodDivision of Infectious DiseasesDepartment of MedicineHahnemann University, Mail Stop 461Broad and Vine StreetsPhiladelphia, Pennsylvania 19102

Author's ReplyWe appreciate Dr. Wood's comments regarding our arti-

cle. Dr. Wood correctly refers to a case of native valve

endocarditis due to S. waneri that he reported (3). As in ourstudy, his patient had no evidence of prior valvular heartdisease. Caputo et al. described 21 patients with native valveendocarditis caused by coagulase-negative staphylococci(1). Of the 16 isolates studied, 3 were S. wameen. However,14 of the 21 patients had preexisting valvular or congenitalheart disease. It is not clear whether the three cases of S.waneri endocarditis occurred in patients without preexist-ing valvular heart disease. Similarly, Etienne and Eykynreported 35 cases of native valve endocarditis due to coag-ulase-negative staphylococci, of which 1 was due to S.wameri (2). Seventy-four percent of these patients hadsome underlying cardiac abnormality. The authors do notcomment on whether the patient with S. waneri endo-carditis had preexisting valvular or congenital heart dis-ease.

Again, we regret not including Dr. Wood's case report.His comments serve to further emphasize the potentialimportance of S. waneri as a human pathogen.

REFERENCES

1. Caputo, G. M., G. L. Archer, S. B. Calderwood, M. J. Dinubile,and A. W. Karchmer. 1987. Native valve endocarditis due tocoagulase-negative staphylococci. Clinical and microbiologic fea-tures. Am. J. Med. 83:619-625.

2. Etienne, J., and S. J. Eykyn. 1990. Increase in native valveendocarditis caused by coagulase-negative staphylococci: anAnglo-French clinical and microbiological study. Br. Heart J.64:381-384.

3. Wood, C. A., D. L. Sewell, and L. J. Strausbaugh. 1989. Vertebralosteomyelitis and native valve endocarditis caused by Staphylo-coccus warneri. Diagn. Microbiol. Infect. Dis. 12:261-263.

Usha KamathDivision of Infectious DiseasesSt. Bamabas HospitalBronx, New York 10457

Carol SingerDivision of Infectious DiseasesDepartment of MedicineLong Island Jewish Medical CenterNew Hyde Park, New York 11042

Henry D. IsenbergDivision of MicrobiologyDepartment of PathologyLong Island Jewish Medical CenterNew Hyde Park New York 11042

VOL. 30, 1992