Aebischer, N.

Bille, J.

Cometta, A.

Heitmann, L.

Hurni, M.

Tschan-Schild, I.

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158 Brief Reports CID 1997;25 (July)P  .017). There were statistically significant differences between duction. Host factors, especially debilitated status, appear to beimportant determinants for the clinical expression of CDAD.the patients with the CDAD and the carriers in terms of the presenceof more than three active medical problems (i.e., requiring treatmentShu-Hsing Cheng, Jang-Jih Lu, Tzuu-Guang Young,in the ICU; 65% vs. 27%; P  .05), the presence of more than threeCherng-Lih Perng, and Wei-Ming Chiunderlying diseases (65% vs. 27%; P  .05), and longer durationDepartment of Internal Medicine, Provincial Taoyuan General Hospital,of antibiotic therapy (88% vs. 45%; P  .02) (table 1).Taoyuan; Division of Clinical Pathology, Department of Pathology, Tri-A total of 68 stool specimens were positive for C. difficile, andService General Hospital, Taipei; and Department of Internal Medicine,62 of the isolates were preserved for further research. Fifty-nineChanghua Christian Hospital, Changhua, Taiwan, Republic of China(95%) of the 62 isolates, evenly distributed in CDAD group andcarrier group, were positive for toxins. PCR ribotyping yieldedReferencesfive ribotypes, and the RAPD method yielded seven types. The1. Pantosti A, Cerquetti M, Gianfrilli PM. Electrophoretic characterization ofcombination of these two methods generated eight distinctive fin-Clostridium difficile strains isolated from antibiotic-associated colitis andgerprints. The most frequently isolated type was type I (isolatedother conditions. J Clin Microbiol 1988;26:540–3.from 29 [47%] of 62 patients), which could be isolated from nine2. Wren B, Heard SR, Tabaqchali S. Association between production of toxins(53%) of 17 patients with CDAD and from two (18%) of 11A and B and types of Clostridium difficile. J Clin Pathol 1987;40:1397–asymptomatic carriers (P  .08). In addition, types II, III, IV, and401.V were variably associated with diseases. Types VI, VII, and VIII3. McFarland LV, Elmer GW, Stamm WE, Mulligan ME. Correlation of im-were recovered only from asymptomatic carriers, but the numbers munoblot type, enterotoxin production, and cytotoxin production withof isolates of these types were small. clinical manifestations of Clostridium difficile infection in a cohort ofOur data show that there was no correlation between genotypes, hospitalized patients. Infect Immun 1991;59:2456–62.4. Gu¨rtler V. Typing of Clostridium difficile strains by PCR-amplification oftoxin production, and clinical manifestations of infection. Therevariable length 16S-23S rDNA spacer regions. J Gen Microbiol 1993;was no strain-specific difference for asymptomatic carriers vs. pa-139:3089–97.tients with CDAD. The predominant type (type I) was variably5. Chachaty E, Saulnier P, Martin A, Mario N, Andremont A. Comparison ofassociated with diseases, and five of eight types were associatedribotyping, pulsed-field gel electrophoresis and random amplified poly-with diarrhea. Toxigenic C. difficile strains could be isolated bothmorphic DNA for typing Clostridium difficile strains. FEMS Microbiolfrom patients with CDAD and from asymptomatic carriers. Actu- Lett 1994;122:61–8.ally, most strains from both groups were toxigenic in vitro. The 6. Onderdonk AB, Allen SD. Clostridium. In: Murray PR, Baron EJ, Pfallerresults of our study also failed to support the belief that the patho- MA, Tenover FC, Yolken RH, eds. Manual of clinical microbiology. 6thed. Washington, DC: American Society for Microbiology, 1995:574–86.genicity of an isolate depended on strain variation and toxin pro-did not reveal any abnormalities. The erythrocyte sedimentationRight-Sided Pacemaker-Related Endocarditis Due torate was 16 mm/h, and the level of C-reactive protein was 9 mg/L.Acremonium SpeciesBlood cultures (four sets) were sterile. Findings on a transthoracicechocardiogram were normal. The patient received iv amphoteri-Fungal endocarditis is a rare complication of pacemaker place-cin B therapy (cumulative dose of 1 g).ment. We report the successful treatment of disseminated acremo-On day 45 of hospitalization, the patient’s temperature rose tonium infection associated with pacemaker-related endocarditis and39.57C and he experienced chills; blood cultures yielded Acremo-endophthalmitis in an 80-year-old male patient with no underlyingnium species. Findings on a second transthoracic echocardiogramcondition.were normal, but a transesophageal echocardiogram showed aThree weeks before admission to the hospital, the patient wasfloating mass of 2 cm in diameter in the right atrium that wastreated with topical and systemic steroids for an unspecified in-surrounding the pacemaker wire. A new course of amphotericin Bflammatory disease of the left eye; he had had a pacemaker in placetherapy was started but had to be discontinued after a cumulativefor 3 years. At admission, the clinical examination was consistentdose of only 315 mg because of renal toxicity.with fungal endophthalmitis and he underwent vitrectomy. After 3The susceptibility of the Acremonium isolate recovered from thedays of incubation, fungal culture (on Sabouraud dextrose and brain-eye was tested (P. Troke, Pfizer Clinical Research Department, Sand-heart infusion agar) yielded Acremonium species with the character-wich, UK) with use of an agar dilution method and yielded the follow-istic fine and hyaline septate hyphae, with long awl-shaped phialidesing MICs: fluconazole, 50 mg/mL; amphotericin B, 31 mg/mL; itraco-producing one-celled oblonged conidia in clusters.nazole, 3.1 mg/mL; and voriconazole, 0.39 mg/mL. Therapy withFindings of the rest of the clinical examination were normal;voriconazole (200 mg b.i.d. orally, provided by Pfizer) was started,the electrocardiogram, a chest roentgenogram, and a WBC countand the patient became afebrile. Twelve days after this treatment wasstarted, the pacemaker and the electrode were surgically removed byright atriotomy (figure 1). Cultures of biopsy specimens from thepacemaker electrode and heart yielded Acremonium species. Histo-Reprints or correspondence: Dr. A. Cometta, Division of Infectious Diseases,pathological examination of the inflammatory tissue adherent to theCentre Hospitalier Universitaire Vaudois, 1011 Lausanne, Switzerland.wire and to the right atrium revealed fungal filaments (hyphae).Clinical Infectious Diseases 1997;25:158–60The patient received voriconazole (3 mg/kg b.i.d.) intravenouslyq 1997 by The University of Chicago. All rights reserved.1058–4838/97/2501–0029$03.00 for 7 days after surgery and orally for 5 more weeks. No adverse/ 9c33$$jy02 06-10-97 19:48:43 cida UC: CID159CID 1997;25 (July) Brief ReportsFigure 1. View of the right opened atriumof an 80-year-old man with right-sided pace-maker-related endocarditis due to Acremoniumspecies. Note that the electrode (E) is enclosedby a tissue (arrow) partially fixed to the rightatrium and to the anterior leaflet of the tricuspidvalve (T).event was reported, and the patient left the hospital 10 days after the MIC of voriconazole was low. Although the MIC results shouldbe cautiously interpreted because of a lack of standardized method-surgery. There were no signs of recurrence of the infection 2 yearsafter the device was removed. ology for susceptibility testing of filamentous fungi, treatment withamphotericin B was clinically unsatisfactory. Our patient wasEndocarditis is an uncommon complication of pacemaker place-ment and is reported in 0.15%–6% of patients [1, 2]; fungal infections cured by surgery combined with voriconazole treatment, and therewere no signs of recurrence of the infection at a 2-year follow-upare extremely rare in patients with pacemakers, and only a few caseshave been reported. The etiologic agents of pacemaker infection in- visit.This case report is important for three reasons: (1) our case ofclude Candida species [3, 4], Aspergillus species [5, 6], and, in onecase, Petriellidium (Pseudallescheria) species [7]; to our knowledge, pacemaker-related fungal endocarditis is rare, (2) to our knowl-edge, we report the first case of pacemaker-related endocarditiswe report the first case of pacemaker-related endocarditis due toAcremonium species. Invasive infections due to Acremonium species due to Acremonium species, and (3) our patient survived an episodeof fungal pacemaker-related endocarditis.can be localized, systemic, or sometimes both [8].The reported cases of acremonium endophthalmitis were sec-ondary to penetrating injuries, viral or fungal keratitis, or ocular L. Heitmann, A. Cometta, M. Hurni, N. Aebischer,surgery [9]. However, our patient did not report even a minor I. Tschan-Schild, and J. Billepenetrating injury. In the absence of such an injury, we believe Division of Infectious Diseases, Department of Cardiac Surgery,that endophthalmitis was not the site of the primary infection but Division of Cardiology, Institute of Pathology, and Department ofMicrobiology, Centre Hospitalier Universitaire Vaudois, Lausanne,rather the consequence of a hematologic spread. The filamentousSwitzerlandfungus could have contaminated the pacemaker during its place-ment in 1991.Although patients usually do not survive an episode of fungal Referencespacemaker-related endocarditis, a recent case was reported in1. Phibbs B, Marriott HJL. Complications of permanent transvenous pacing.which a 56-year-old man with pacemaker-related endocarditis due N Engl J Med 1985;312:1428–32.to candida infection survived after undergoing surgery and receiv- 2. Kugener H, Rey JL, Tribuilloy C, et al. Endocardites infectieuses suring treatment with antifungal agents [3]. In the other four cases sondes de stimulation permanentes: inte´reˆt de l’e´chocardiographie etof fungal pacemaker-related endocarditis reported, the outcome revue de la litte´rature. Ann Cardiol Angeiol (Paris) 1993;42:331–8.3. Wilson HA Jr, Downes TR, Julian JS, White WL, Haponik EF. Candidawas fatal [4–7]. Right-sided endocarditis has been diagnosed withendocarditis: a treatable form of pacemaker infection. Chest 1993;103:use of the transesophageal echocardiogram after two transthoracic283–4.approaches. Transesophageal echocardiography is significantly4. Davis JM, Moss AJ, Schenk EA. Tricuspid candida endocarditis complicat-more sensitive than transthoracic echocardiography for the recog-ing a permanently implanted transvenous pacemaker. Am Heart J 1969;nition of vegetations and paravalvular abscesses [10] in patients77:818–21.with infectious endocarditis. However, this series includes mostly5. Kramer L, Rojas-Corona RR, Sheff D, Eisenberg ES. Disseminated asper-patients with aortic and mitral endocarditis. gillosis and pacemaker endocarditis. PACE Pacing Clin ElectrophysiolThe antimicrobial treatment for acremonium infections is not 1985;8:225–9.yet well defined because of the rarity of this infection [8]. In our 6. Moorman JR, Steenbergen C, Durack DT. Aspergillus infection of a per-case, susceptibility testing of our isolate suggested resistance in manent ventricular pacing lead. PACE Pacing Clin Electrophysiol 1984;7:361–6.vitro to amphotericin B; on the other hand, this test showed that/ 9c33$$jy02 06-10-97 19:48:43 cida UC: CID160 Brief Reports CID 1997;25 (July)7. Davis WA, Isner JM, Bracey AW, Roberts WC, Garagusi VF. Dissemin- 9. Culbertson WW, Mandelbaum S. Exogenous fungal endophthalmitis. Oph-ated Petriellidium boydii and pacemaker endocarditis. Am J Med 1980; thalmology 1988;95:19–30.69:929–32.10. Birmingham GD, Rahko PS, Ballantyne F. Improved detection of infective8. Fincher R-M, Fisher JF, Lovell RD, Newman CL, Espinel-Ingroff A,endocarditis with transesophageal echocardiography. Am Heart J 1992;Shadomy HJ. Infection due to the fungus Acremonium (Cephalospor-ium). Medicine (Baltimore) 1991;70:398–409. 123:774–81.the intravenous combination of amoxicillin/clavulanate (1,000/200Pleural Empyema Due to Clostridium difficile andmg q4h) and metronidazole (500 mg t.i.d.). Follow-up cultures ofClostridium cadaverisfluid from the drain were all sterile. Therapy with metronidazolewas stopped on 12 April, and the drain was removed 1 week later.Pleuropulmonary infections with clostridial species, usuallyTherapy with amoxicillin/clavulanate was continued until 26 MayClostridium perfringens, have been reported occasionally [1]. We(during the last 2 weeks, amoxicillin/clavulanate was administereddescribe a patient with a bronchogenic cyst who developed pleuro-orally at a dosage of 500/125 mg t.i.d.). A CT scan showed nopulmonary empyema due to Clostridium difficile and Clostridiumsigns of abscesses. The leukocyte count was 8,200/mm3. Nocadaveris after surgical removal of the cyst.b-lactamase production was detected in the C. cadaveris isolate.A 33-year-old male pig farmer had had a bronchogenic cyst inThe patient was discharged from the hospital in good clinicalthe upper lobe of the left lung for 8 years. Because the cyst wascondition with a prescription for oral amoxicillin (500 mg q.i.d.).enlarging, segmental resection was performed on 31 January 1996.As of this writing (3 months later), he is clinically stable.On the sixth postoperative day, the patient developed fever withFew cases of pleural infection with C. difficile have been re-leukocytosis (leukocyte count, 17,700 cells/mm3). A chest radio-ported [2, 3]. C. cadaveris is not known to produce a toxin and isgraph revealed pleural effusion on the left side. Foul-smelling fluidconsidered to be nonpathogenic for humans and laboratory animalswas obtained via transthoracic puncture on 11 February.[4]. However, C. cadaveris bacteremia (in two immunocomprom-Culture of the material yielded two anaerobic gram-positive spore-ised patients) and C. cadaveris–associated spontaneous bacterialforming rods with different colony morphologies and odors. Withperitonitis have been described [5, 6]. Aspiration of aerosol fromuse of the API 20A system (bioMe´rieux, Marcy l’Etoile, France) andanimal material while handling dead piglets seems to be a logicalgas chromatography, the isolates were identified as C. difficile andexplanation for our patient’s pulmonary infection. The severity ofC. cadaveris (the identity of the latter isolate was confirmed by Dr.his infection with two anaerobic organisms that are both consideredM. McTeague, Wadsworth Anaerobe Laboratory, Los Angeles). Theto be of little pathogenic importance, with destruction of a wholeC. difficile strain produced cytotoxin B. The Etest (AB BIODISK,lung despite adequate antimicrobial therapy, is remarkable.Solna, Sweden) showed that both organisms were susceptible toWe believe that the C. cadaveris isolate persisted after 4 weeksamoxicillin/clavulanate and metronidazole. Therapy with iv amoxicil-of therapy because of its capacity to sporulate. The persistence oflin/clavulanate (1,000/200 mg t.i.d.) was started on 11 February.C. cadaveris despite adequate therapy was not described in theOn 19 February, the patient developed a bronchopleural fistula. Athree previously mentioned case reports [5, 6]; those patients allsecond thoracotomy was performed on 21 February. The rest of thedied of complications during hospitalization, which obscured theleft lung was found to be necrotic, and pneumonectomy was per-possible role of C. cadaveris. We conclude that the pathogenicityformed. Intravenous metronidazole (500 mg t.i.d.) was added to theof C. cadaveris needs further study.patient’s regimen of amoxicillin/clavulanate. Cultures of fluid fromthe thoracic drain were repeatedly negative after antimicrobial therapyVirginia Stolk-Engelaar, Jeroen Verwiel, Ger Bongaerts,was initiated. The drain was removed on 1 March, antibiotic therapyVic Linsen, Leon Lacquet, and Anton Coxwas stopped, and the patient was discharged from the hospital.Department of Medical Microbiology, University Hospital Nijmegen;Four days later, he returned to the hospital with fever and painand University Lungcentre Dekkerswald, Nijmegen, the Netherlandson the left side of the thorax. A chest radiograph revealed a normalpleural cavity but enlarged cardiac contours. An echocardiogram Referencesrevealed a 5-cm pericardial effusion. A third thoracotomy with1. Bekemeyer WB. Clostridial infections of the lungs and pleura. South Medpericardiotomy was performed on 25 March for debridement fol-J 1986;79:1393–7.lowed by drainage and daily rinsing with 5% povidone-iodine.2. Smith LDS, King EO. Occurrence of Clostridium difficile in infections ofCulture of the pleural fluid yielded only C. cadaveris; the isolateman. J Bacteriol 1962;84:65–7.was susceptible in vitro to amoxicillin/clavulanate and metronida- 3. Simpson AJH, Das SS, Tabaqchali S. Nosocomial empyema caused byzole. The pericardial fluid was sterile. The patient again received Clostridium difficile. J Clin Pathol 1996;49:172–3.4. Willis AT. Characteristics of the pathogenic and related clostridia. In: WilliaAT, ed. Anaerobic bacteriology: clinical and laboratory practice. Boston:Butterworths, 1977:111–66.5. Gucalp R, Motyl M, Carlisle P, Dutcher J, Fuks J, Wiernik PH. ClostridiumReprints or correspondence: Dr. Virginia Stolk-Engelaar, Department ofcadaveris bacteremia in the immunocompromised host. Med Pediatr On-Medical Microbiology, University Hospital Nijmegen, P.O. Box 9101, 6500col 1993;21:70–2.HB Nijmegen, the Netherlands.6. Herman R, Goldman IS, Bronzo R, McKinley MJ. Clostridium cadaveris:Clinical Infectious Diseases 1997;25:160an unusual cause of spontaneous bacterial peritonitis. Am J Gastroenterolq 1997 by The University of Chicago. All rights reserved.1058–4838/97/2501–0030$03.00 1992;87:140–2./ 9c33$$jy02 06-10-97 19:48:43 cida UC: CID

Right-Sided Pacemaker-Related Endocarditis Due to Acremonium Species

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