randomized controlled trial. ForeignBody Infection (FBI) Study Group. JAM A 1998; 279: I537- I54 I. 13. De Gbrgolas M, Avilts P, Vcrdejo C, Guerrcro ML. Treatment of experimental endocarditis due to methicillinsusceptible or methicillin-resistant Staphylococcus aureus with trimethoprim-sulfamethoxazoie and antibiotics that inhibit cell wall synthesis. Antimicrob Agents Chemother 1995; 39:953-957. 14. Markowitz N, Quinn EL, Saravolatz LD. Trimethoprim-sulfamethoxazole compared with vancomycin for the treatment of Staphylococcus aureus infection. Ann Intern Med 1992; I 17:390-398. 1.5. Kaatz GW, Seo SM, Barriere SL, Albrecht LM, Rybak MJ. Development of resistance to fleroxacin during therapy of experimental methicillinsusceptible Staphylococcus aureus endocarditis. Antimicrob Agents Chemother I99 I ; 35: I547- 1550. 16. Heldman AW, Harte.rt TV, Ray SC, Daoud EG, Kowalski TE, Pompili VJ, Sisson SD, Tidmore WC, vom Eigen KA. Goodman SN, Lietman PS, Petty BG, Flexner C. Oral antibiotic treatment
of right-sided staphylococcal endocarditis in injection drug users: prospective randomized comparison with pare&ml therapy. Am J Med 1996; 101:68-76. 17. Ford CW, Hamel JC, Wilson DM et al. In vivo activities of U- I00592 and U- 100766 novel oxazolidinone antimicrobial agents against experimental bacterial infections. Antimicrob Agents Chemother 1996; 40: 1508-l 5 13. 18. Drew RH, Perfect JR, Srinath L, Kurkimillis E, Dowzicky M, Talbot GH. Treatment of methicillin-resistant staphylococcus aureus infections with quinupristin-dalfopristin in patients intolerant of or failing prior therapy. For the Synercid Emergency-Use Study Group. J Antimicrob Chemother 2000; 46:775-784. 19. Sande MA, Scheld WM. Combination antibiotic therapy of bacterial endocarditis. Ann Intern Med 1980; 92:390. 20. Polk R. Optimal use of modern antibiotics: emerging trends. Clin Infect Dis 1999; 29~264-274. 21. Gengo FM, Mannion TW, Nightingale CH, Schentag JJ. Integration of pharmacokinetics and pharmacodynamics of methicillin in curative treatment of
experimental endocarditis. J Antimicrob Chemother 1984; 14:6 19-63 I. 22.. Malanoski GJ, Samore MH, Pefanis A. Karchmer AN! Staphylococ&s au-. catheter-associated bacteremia. Arch Intern Med 1995; 155:1161-1166. 23. Zeylemaker MM, Jaspers CA, van Kraaij MG, Visser MR, Hoepelman IM.
Long-term infectious complications and their relation to treatment duration in catheter-related Staphylococcus aureus bacteremia. Eur J Clin Microbial Infect Dis 20:380-384,200l. 24. Di Nubile MJ. Short-course antibiotic therapy for right-sided endocarditis caused by Staphylococcus aunzus in injection drug users. Ann lntem Med 1994; 121:873-876. 25. Tetzlaff TR, McCracken GH, Nelson JD. Oral antibiotic therapy for skeletal infections of children. J Pediatr 1978; 92:485. 26. Black J, Hunt TL, Godley PJ, et al. Oral antimicrobial therapy for adults with osteomyelitis or septic arthritis. J Infect Dis 1987; 155:968-972. 27. Cahill DW, Love LC, Rechtine GR. Pyogenic osteomyelitis of the spine in the elderly. J Neurosurg 1991; 74:878-886.
Case Report
Campylobac&rfetus subsp. fetus Cellulitis and Bacteremia in a Patient With Lymphoma: A Case Report and Literature Review Lawrence A. Cone MD, DSC Philip Dreisbach MD Chandra Shekar MD Luke Dreisbach MD Department of Medicine Eisenhower Medical Center Rancho Mirage, CA 92270 Correspondence and request for reprints: Lawrence A. Cone MD, DSc Eisenhower Medical Center 39000 Bob Hope DK, P#308 Ranch0 Mirage, CA 92270 Campylobacter bacteria are motile, non-spore forming, comma-shaped, gram-negative rods (1). In 1909, C. j&us subsp.fifus (formerly Mbrio fetus) was found to be associated with abortion in cattle, goats, and sheep (2) and later isolated f?om other animals and reservoirs (3-5). In cattle, it is a venereal infection transmitted by the asymptomatic bull. In 1947, Vinzent
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(6) first recovered Campylobacter organisms from a human. While C. jejuni is the most common or second most common bacterial cause of diarrhea in children and adults in the United States (2,500,OOO cases per year), and has been implicated as etiologic in 30% of patients with the Guillain-Barr6 and Miller-Fisher syndromes (7), the related organism CTfetus subsp. fetus usually causes non-intestinal diseases such as bacteremia, meningitis, septic abortion, septic arthritis, cellulitis, and endocarditis (8), often in immunocompromised hosts. Ichiyama et al. (9) recently reported three cases of C. fetus cellulitis and bacteremia and reviewed the literature, fmding an additional seven cases. Four had cirrhosis, two systemic lupus erythematosis, one diabetes and leukemia, one Paget’s disease and a parotid tumor, one aplastic anemia and
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a malignant tumor, and one lymphoma and hypogammaglobulinemia ( 1- 14). We report a second case of C. fetus cellulitis in a patient with non-Hodgkin’s lymphoma and dysgammaglobulinemia.
Case Report A 92-year-old retired white male had been diagnosed with large-cell lymphoma 8 years earlier and treated with cyclophosphamide, doxorubicin, vincristine, and prednisone, resulting in a complete clinical remission. Seven years later, recurrent lymphoma was documented and he was treated with rituximab weekly for 4 weeks. A week prior to his hospitalization at the Eisenhower Medical Center on June 10, 200 1, he noted pain, swelling, and erythema of his left leg. The positive clinical findings included a fever of 10 1OF, an area of cellulitis involving the entire
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left leg extending from the toes to just below the groin, a small bilateral axillary, and inguinal lymph nodes. Blood cultures were drawn, and empiric antimicrobial therapy was initiated with ceftriaxone 1 g iv. daily. Within 24 h, the patient felt better, the fever was gone, and the left leg was no longer tender; at 72 h, the cellulitis had largely resolved. On the fifth hospital day, C. fetus subsp. fetus was isolated from all blood cultures. By the seventh hospital day, the patient was discharged and continued on i.m. ceftriaxone for an additional week. Laboratory studies revealed a WBC of 8,60O/mm’, Hb/Hct = 1l.lg/32.7%, platelets = 225,000/mm3, IgG = 355 mg%, IgM = 423 mg%, and IgA= 87%. There was an IgG paraprotein measuring 130 mg by serum protein electophoresis. Serum calcium = 8.0 mg/dL, BUN/ treat = 5 lmg/2.6/dL, Na = 139 mmol/L, K = 3.6 mmol/L, Cl = 100 mmol/l, CO= 30 mmol/L, and glucose = 125 mg/dL. Thyroid and liver function studies and a urinalysis were normal. A chest X ray was normal, and a CT scan of the abdomen revealed widespread retroperitoneal lymphadenopatby.
Discussion A total of 10 patients infected with C. fetus subsp. fetus and cellulitis with bacteremia have been reported since 1980 (9-14), while C.jejuni has been isolated only twice (15), although the latter is probably the most common cause of bacterial invasive colitis in the United States. The laboratory differentiation of C. jejuni from C. fetus subsp. fetus is difficult and depends upon the ability of the strains to grow at different temperatures and their susceptibility to nalidixic acid. Studies by Karmali et al. ( 16) convincingly showed that C. jejuni and C. fetus subsp. fetus can also be reliably distinguished by the latter’s in vitro sensitivity to most first-, second-, and third-generation cephalosporins, in contrast to the uniform resistance of C. jqjuni to these agents. These findings stand in contrast to earlier studies by Chow et al. (17) and Butzler (18). Our patient’s dramatic response to cefiriaxone would seem to confirm the efficacy of third-generation cephalosporins in the treatment of C. fetus infection, as reported by Karmali. Systemic infection with C. fetus
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subsp. fetus is most frequently diagnosed in men over the age of 50 years with underlying liver disease, malignancy, or hematologic disorders (8). C. fetus also has a remarkable ability to cause a relapsing or prolonged bacteremia without endocarditis (14), perhaps secondary to the absence of opsonizing antibodies and effective phagocytosis in infected individuals (19,20). Our patient with significant dysgammaglobulinemia was predisposed to infection by C. fetus spp. fetus likely due to his lymphoma and an inability to generate C. fetus-specific antibody. It is also of interest to note that commercial gamma globulin does not contain functional opsonic antibody to C. fetus (14) and would probably not be an effective additional treatment in hypogammaglobulinemic and dysgammaglobulinemic patients. Although thrombophlebitis has sometimes been associated with C. fetus subsp. fetus cellulitis (10,12,2 l), this was not so in our patient. While staphylococcal and streptococcal infections are most often the etiology of septic thrombophlebitis, gram-negative organisms such as C. fetus subsp. fetus, Aeromonas hydrophi/a, and Bacteroides sp. have also been implicated as causing thrombophlebitis, particularly in the debilitated host (12). Failure to respond to nafcillin, vancomycin, linezolid, or dalfopristin/daunapristin should suggest a gram-negative infection. The source of infection in patients infected with C. fetus subsp. fetus is often obscure. Only on rare occasions can the organism also be isolated in stool, and contact with large, domestic animals or chickens occurs in less than a third of all patients (22). Gastrointestinal symptoms are rare, and our patient also lacked these epidemiologic associations. Nevertheless, serotyping and more recently phenotypic and genotypic methods for subtyping isolates from humans, poultry, and cattle imply that the source of C. fetus subsp. fetus is still believed to be in the intestine and introduced by contaminated food (23,24). The organism subsequently enters the circulatory system and becomes deposited in the soft tissues. The highmolecular-weight surface proteins act as a capsule and appear as a major virulence factor (19,20). Coupled with the previously mentioned humoral defects,
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the situation resembles the known association of multiple myeloma and chronic lymphocytic leukemia with sepsis secondary to bacterial pathogens due to deficient antibody production. Although mortality due to C. fetus bacteremia can be as high as 26%, successful treatment of C. fetus infections has been achieved with most newer cephalosporins, aminoglycosides, tetracycline, macrolides, and chloraphenicol, but the organisms are resistant to some cephalosporins, penicillin, rifampin, imipenem/cilastatin, aztreonam, quinolones, and vancomycin (16). Our patient’s response to ceftriaxone was prompt and complete. There is no evidence of recurrence 7 months after treatment.
References I.
Penner JL. The genus Catnpylobacter: a decade of progress. Clin Microbial Rev 1988; 1:157:172.
2. Smibent RM. The genus Campylobacter Annu Rev Microbial
1978;32:673-709.
3. Blaser MJ, Taylor DN, Feldman RA. Epidemiology of Campylobacterjejuni infections. 176.
Epidemiol Rev 1983; 5: l57-
4. Tribe GW, Frank A. Campylobacter
in monkeys. Vet Ret 1980; 106:365-371.
5. Vogt RL, Sours HE, Barrett T, Feldman RA, Dickinson RJ, Witherell L. Campylobacter enteritis associated with contaminated water. Ann Intern Med 1982; 961292-296.
6. Vinzent R, Dumas J, Picard N. Septicemie grave au tours de la grassesse du a vibrio II avortement consecutif. Bull Acad Natl Med (Paris) 1947; 3 I :90-92. Nachamkin I, Allos BM, Ho T. Campylobacter species and Guillain-Barre syndrome. Clin Microbial Rev 1998; l l:SSS-567. Guerrant RL, Lahita RG, Winn WC Jr, Roberts RB. Campylobacteriosis in man: pathogenic mechanisms and review of 9 I bloodstream infections, Am J Med 1978; 65584-65592. lchiyama S, Hirai S, Minami T, Nishiyama Y, Shimizu S, Shimokata K, Ohta M. Campylobacterfetus ssp. fetus cellulitis associated with bacteremia in debilitated hosts. Clin Infect Dis 1998; 271252-255. IO. Schmidt U, Chmel H, Kaminski Z, Pen P. The clinical spectrum of Campylobacterfetus infections: report of five cases and review of the literature. Q J Med 1980; 196:43 l-442.
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16. Karmali MA, De Grandis S, Fleming PC. Antimicrobial susceptibility of Campylobacter jejuni and Campylobacterfetus subsp. fetus to eight cephalosporins with special reference to species differentiation. Antimicrob Agents Chemother 1980; 18:948-95 I.
II. Righter J, Wells WA, Hart GD, McNeely DJ. Relapsing septicemia caused by Campylobacterfetus subsp. fetus. Can Med Assoc J 1983; 128:686-689. 12. Carbone KM, Heinrich MC, Quinn TC. Thromobophlebitis and cellulitis due to Campylobacterfetus subsp. fetus. Medicine (Baltimore) 1985; 65:244250.
17. Chow AW, Patten V, Bednorz D. Susceptibility of Campylobacterfetus to twenty-two antimicrobial agents. Antimicrob Agents Chemother 1978; 13:416-418.
13. Francioli P, Herzstein J, Grob JP, Vallotton JJ, Mombelli G, Glauser MP. Campylobacterfetus subspecies fetus bacteremia. Arch Intern Med 1985; 145:289-292.
18. Butzler JP. Infection with camplobacters, p. 2 14-239. In JD Williams (ed.), Modem topics in infection. William Heinennann Medical Books, Ltd., London.
14. Neuzil KM, Wang E, Hass DW, Blaser M J. Persistance of Catnpylobacterfetus bacteremia associated with absence of opsonizing antibodies. J Clin Microbial 1994; 32:1718-1720.
KL. Pathogenesis of Campylobacter fetus infections. Failure to bind C3b explains serum and phagocytosis resistance. J Clin lnvestig 1988; 8 I : l4341444. 21. Blasius C, Ullmann U, Achinger R. Vibrio-fetus sepsis bei thrombophlebitis. Zbl Bakteriol, I Abt Orig 1970; 2 14: I 7-22. 22. Bokkenheuser V. Mbrio fetus infection in man. Am J Epidemiol 1970; 91:400-
409. 23. Nachamkin I, Ung H, Patton CM. Analysis of HL and 0 serotypes of Campylobacter strains by the flagellin gene typing systems. J Clin Microbial 1996; 34:277-28 I. 24. Nielsen EM, Engberg J, Fussing V,
19. Blaser MJ, Pei Z. Pathogenesis of Campylobacterfetus infections. Critical role of high molecular weight S-layer proteins in virulence. J Infect Dis 1993; 167:372-377.
IS. Spehnan DW, Davidson N, Buckmaster ND, Spicer WJ, Ryan P. Campylobacter bacteremia: a report of 10 cases. Med J Aust 1986; 154:503-505.
Petersen L, Brogren C-H, On SLW. Evaluation of phenotypic and genotypic methods for subtyping Campylobacter jejuni isolates from humans, poultry,
20. Blaser MJ, Smith PF, Repine JE, Joiner
Case Report
A Case Report of Abdominal Wall Actinomycosis Prolonged Use of an Intrauterine Device Actinomyces can be found in the oral cavity, peritonsillar fossa, and intestinal tract flora of humans. However, these microorganisms rarely cause disease and are seldom reported as pathogens. When this microorganism is pathogenic, it causes fistulas and sinuses and may appear as an abdominal mass or abscess. The abdominal mass can be confusing diagnostically, since it initially may be thought to be a malignant process requiring surgical intervention and resection (2). The computed tomography (CT) scan is the most useful diagnostic modality. Penicillin, arnoxicillin, tetracycline, and sulfonamides are effective against these infections.
Cavit CSl, MD Department of General Surgery AlBU Izzet Baysal Medical School Bolu, Turkey
Meltem Cijl, MD Department of Public Health Ankara University Medical School Ankara, Turkey
Levent Albayrak,
MD
Department of Pathology Ankara Numune Research and Teaching Hospital Ankara, Turkey
Introduction Abdominal-wall actinomycosis is a rare disorder in which the diagnosis is usually missed preoperatively. It is a suppurative granulomatous soft-tissue infection caused by a gram-positive, anaerobic, non-acid-fast, tilamentous bacterium of the genus Actinom?ces (1). In the past, Actinomvces spp. have been misclassified as fungi due to their iilamentous branching appearance that mimics hyphae.
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Case Report A 48-year-old woman presented with complaints of weight loss, intermittent low-grade fever, and a mass localized to the left lower abdominal quadrant which she had noticed initially 2 weeks prior to admission. The patient also had an IUD which had been inserted 17 years ago and also presented with
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a history of occasional malodorous vaginal discharge for the past year. The blood pressure was 1 lo/70 mmHg, pulse rate 112 beats/min, and body temperature 37.8”C. Further examination showed no abnormalities except for the painhrl irregular mass with a 5-cm diameter. Laboratory findings were as follows: hemoglobin level, 11.6 g/dL; white cell count, 7.7 x 1O3/mm’; erythrocyte sedimentation rate, 80 mm/h; serum glucose, 79 mg/dL (normal = 75-115); blood urea, 24 mg/dL (Normal = ll37); blood creatinin, 65 umol/L (normal = 50- 120); serum albumin, 4 1 g/L (normal = 38-54); aspartate amino transferase, 16 U/L (normal = <37); gamma glutamyl transferase 23 U/L (normal = ~50); and alkaline phosphatase, 132 U/L (normal = 98-279). Urine analysis and culture were normal. The mass, which was palpated on the front abdominal wall, was initially thought to be a malignant process. However, abdominal ultrasonography
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