- Email: [email protected]
Actinomycosis masquerading as incarcerated incisional hernia
References 1. Rubin, R,H. 1988. Infections in the patient after renal and fiver transplantation. p. 557-583. In R. H. Rubin and L S. Young (eds.),Clinical approach to infectiens in the immunucompmmised patient.2nd ed. Hmum Press, N e w York. 2. Dworkin, R., and W. L. Drew. 1989. Therapy for herpes'virus infections in AIDS. Curr. Opinion Infect. Dis. 3:108112. 3. Goedrich, J. M. et al. 1991. Early treatment with ganciclovir to prevent eytomegalovirusdiseaseafterallogeneic bone marrow transplantation. N. Engl. L Med. 325:1601-1607. 4~ Myers, J. D., P. Ljmagman, and L. D. Fisher. 1990. Cytomegalovirus excretion as a predictor of cytomegalovirus disease after marrow transplantation: imlxrtance of cytmnegalovirus viremia. J. Infect. Dis. 162:373-380. 5. Salmon, D. et al. 1990. Predictive value of cytomegalovims viraemia for the occurrence of CMV organ involvement in AIDS. I. Med. Virol. 32:160-163. 6. Paya, C. V., A. D. Wold, and T. F. Smith. 1987. Detection of cytomegalovims infectionsin ~ other than urine by the shellvialassay and conventionalrobe cellcultures.J.Clin.Mierobiol.25:755-757. 7. Stockl, E. et al.1988. Potentialof in situhybridizationfor earlydiagnosisof productivecytomegalovims infection.L Clin.Microbiol.26:2536-2540. 8. Dankner, W. M. et al. 1990. Localization of human cytomegalovirus in peripheral blood leukocytes by in sire hybridization. J. Infect. Dis. 161:3136. 9. Zipeto, D. et al. 1992. Development and
clinical significance of a diagnostic assay based on the l~lymerase chain reaction for detection of human cytomegalovirus DNA in blood samples fixan immunocompromised patients. J. Clin. Microbiol. 30:,527-530. 10. Gerna, G. et al. 1991. Monitoring of human cytomegalovirus infections and ganciclovir treatment in heart transplant recipients by determination of viremia, antigenemia, and DNAemia. J. IlffecL DIS. 164:488--498. 11. Einsele, H. et al. 1991. Polymerase chain reaction to evaluate anfiviral therapy for cytomegalovims disease. Lancet 338:1170-1172. 12. Shibata, D. et al. 1988. Detection of cytomegalovirusD N A in imripheralblood of patients infected with human immunodefieiency virus. J. Infect. Dis. 158:1185-1192. 13. Jiwa, N. M. et al. 1989. Rapid detection of human cytomegalovims D N A in peripheral blood leukocytes of viremic transplant recipients by the pol3anaase chain reaction. Transplantation 48:7276. 14. Persing, D. H. 1991. Polymerase chain reaction: trenches to benches. J. Clin. Microbiol. 29"I281-1285. 15. Van der Bij, W. et al. 1988. Rapid immunodiagnosis of active cytomegalovims infection by monoclonal antibody staining of blood leucocytes. ]. Med. Virol. 25:179-188. 16. VanderBij, W. etal. 1988. Comparison between virm~a and antigenzmia for detection of cytom~alovirus in blood. ]. Clin. Microbiol. 26:25312535. 17. Van den Berg, A. P. ©t aL 1989. Cytomegalovirus anfigmemia as a useful
18.
19.
20.
21.
22.
23.
24.
marker of symptomatic cytomegalovi., rus infection after renal transplantation---a relx~ of 130 consecutive patients. Transplantation 48:991-995. Van der Bij, W. et al. 1989. Cytomegalovkus (CMV) antigenemia: rapid diagnosis and relationship with CMVassociated clinical syndromes in renal allogmft recipients. Transplant. Proc. 21:2061-2~ Van den Berg, A. P. etal. 1991. Antigenemia in the diagnosis and monitoring of active cytomegalovirus infection after fiver Cansplantation. J. Infect. Dis. 164:265-270 Revefio, M. G. et al. 1989. Detection of human cytomegalovirus immediate early antigen in lcukocytes as a marker of viremia in imm~ocompromised patients. L Med, Virol. 29:88-93. Erice, A. et al. 1992. Cytomegalovirus (CMV) antigenemia assay is more sensitive than sheU vial cultures for rapid detection of CMV in polymorphonuclear blood lenkocytes. J. Clin. MierobioL 30:.2822-2825, Grefte, J.M.M. et al. 1991. Thelow~ matrix protein pp65 is the principal viral antigen present in peripheral blood leukocytes during an active cytomegalovims infection. J. Gen. Virol. 73:2923-2932 Reveno, M. G. et al. 1992. Nuclear expression of the lower malfix protein of human cytomegalovirus in peripheral blood lenkocytcsof immtmocomproraised viremic patimts. J. Gen. Virol. 73:437-442 Miller, H. et al. 1991. Prospective study of eytomegalovirus antigencmia in allograft recipients. J. CIL~ Microbiol. 29:1054-1055.
Case Report Actinomycosis M a s q u e r a d i n g as Incarcerated Ineisional Hernia Sousan Sayahtaheri Aitaie, Ph.D.
Department of Pediatrics Division of l~ectious Diseases State Universityof N~, York at Bt~alo School of Medicine and The Children's Hospital Buffalo, NY 14222
I00
0196-4399/93/$0.00+ 06.00
cora isio ycosis of the greater omentmn, altboqh
Elfriede Kohout-Dutz, M.D. H. Robert Lipl~m' M.D. Vanessa Taylcc, M r ( A . ~ H a i r Hokaa Mcg~iire~ Richmomd, VA 23249
Center
Abdominal actinemycmis in a number o f fmms and is ome o f the
great imitatonin ~
lmUice. We
.:port the o f histologically ~ emeatal actinomycosis masquerading as incar-
© 1993 Elaevicr~
I~ab[iahmgCo., Inc.
ra~, shoatdbe ~ ia t h e ~ tiat d i a g ~ of an ~ ~ . C u e Report A 71-yr-old male with n o known alcohol abuse and a ~ o f smoking more than 55 ~ year was admit-
ted throught h e ~ ~
~
the initial dia~,nosis o f an umbilical and incisional hernia. The paClinical hfaombio~gyNcwslet~ 15:13,1993
tient's history included a vagotomy, antrectomy, and Billroth-I surgery for a chronic choleeystitis 25 yr prior to admission. The patient noticed a painful bulge at the base of the midline sear approximately 5 d prior to admission, the most severe pain having occurred on the last day. No nausea, vomiting, change in bowel movements, or obstructive symptoms were present. Upon admission, the physical examination revealed an afebfile patient with a blood pressure of 110/60, a pulse of 88, a respiration rate of 16, a soft scaphoid abdomen, and a tender mass below the umbilicus with some surrounding erythema. No fluctuanee or significant bowel sounds were present. The rectal exam was normal and the stool was negative for occult blood. The white blood cell count was 8.6 cells/dL; hemoglobin 13.8 g/dL; and normal differential cell count, prothrombin time, and partial thromboplastin time. An incarcerated hernia was suspected. The patient was given cefoxitin prophylactically upon admission and was taken to the operating room on the following day. At surgery, the patient had an omental abscess with gross pus inside the omental mass. The pus was cultured anaerobically and aerobically. The segment of omentum involved was resected and the abdominal cavity packed to avoid diffuse spillage into the abdomen. The bowel was not perforated and did not show any diverticula that might have perforated adherent to the mass. The direct Gram stain smear revealed gram-negative bacilli and grampositive cocci. As a result, cefoxitin was discontinued and the patient was placed on clindamycin and ceftriaxone. The pus, which appeared granular, was cultured on routine anaerobic media, including brucella agar supplemented with 5% sheep blood, vitamin K, and hemin; kamomycin-vancomycin laked blood aga~, phenyl-ethyl alcohol sheep blood aga~, and chopped meat carbohydrate broth. Following 48-h anaerobic incubation at 37°C, cultures grew only Peptostreptococcus micron and Bacteroides sp. Since there was no special request for culture for Actinomyces, the
Clinical Microbiology Newsletter 15:13,1993
Figure 1. "Sulfur" granule of the omentum. (a) H&E stain; note that the granule is enveloped by purulent exudate (x1,150). (b) 4,600x magnification of the boxed area in a; note the pronounced peripheral clubbing.
primary cultures were discarded after 4 d without the recovery of Actinomyces. Sections of omentum stained with hemotoxylin and eosin (H&E) revealed sulfur granules composed of filamentous bacteria surrounded by hyaline clubs (Fig. 1). Brown and Brenn tissue Gram stain revealed radial clusters of f'damentous bacillary organisms with right angle branching (Fig. 2), compatible with Actinomyces or Nocardia. The absence of staining by acid-fast stains favored the diagnosis of actinomycosis
The patient was started on intravenous penicillin therapy, 2 million units every 6 h for 4 wk and then discharged on oral penicillin (500 mg q 6 h) for an
© 1993 Elsevier Science Publishing Co., Inc.
0196-4399/93/$0.00 + 06.00
of the omentum. The patient was worked up with lower and upper gastrointestinal x-rays and CT scan of the abdomen for other sources of actinomycosis. No fluid collection but a thickened rectal wall were noted. Sigmoidoscopy was performed and revealed only an edematous mucosa.
I O]
Figure 2. Actinomycosis of the omentum; Brown and Brenn stain. The filaments are well demonstrated in a tissue section of the omentum (><1,150).
additional 11 mo. On follow-up visits the patient was doing well and remained asymptomafic.
Discussion
The etiology of aclinumycosis has been described at Ionglh (1). The first clinical description of human actinomycosis is credited to yon L a n g ~ in 1945. In 1877, Bollinger fn'st delineated the disease, called "lumpy jaw" in cattle because it involved the jaw bones and was believed to be caused by sulfur granule-producing fungi. In the same year, I-Iarz named this fungus Actinomyces for its appearance of filaments radiating from a central mass (2). Wolff and Israel carefully studied the organism and in 1891 described its anaerobic growth requirements (1). Their work also spawned the theory that the organism was an endogenous microbe not found outside the bodies of humans and animals. The organisms causing disease in cattle and humans were differentiated in 1940 when Erickson showed morphologic, biochemical, and serologic differences between the two strains (3). The human pathogen was renamed Actinomyces israelii, and the ammal s t r ~ was renamed Actinomyces bovis.
Since then, additional species of Actinomyces have been identified as causative agents of human disease, but A. bovis has never been isolated from humans (4). Studies of the cell wall components have led to classification of Actinomyce$ in the order Actinomycetales, which includes the genera Streptomyces and Mycobacterium. These organisms are considered normal tlova of the oral cavity and have been found on tooth surfaces, and in tonsillar crypts, vermiform appendix, colonic diverticula, and the vagina. Actinomyces are thought of as opportunistic pathogens requiring damage of the oral mucosal barrier by trauma, disease, or surgery in order to enter the tissues and cause disease. The least common form, pulmonothoracic disease, which accounts for 15% of all cases (4), may result from inhalation or aspiration of the organism via the t r a e ~ h i a l tree. "Vneeervicofaeial form of the disease is the most common, accounting for 55% of all cases (4), because the organism is normally found in the mouth. Any trauma, dental decay, tooth e x ~ , or fracture of the jaw may alk~v the oxganism to enter the adjacent ~ . The second most common form of hhe disease, abdominopelvic, accounts for 20% of all cases (5). Abdominal actinomycosis
usually results after surgery or peribration of the appendix, stomach, or colonic diverticulum, when the organism gains access to the peritoneal cavity. The disease spreads via direct extension without regard to normal tissue planes. Hematogenous or lymphatic spread is rare. In a large series of 122 patients with abdominal actinomycosis, only seven had no recent history of an acute gastrointestinal event (5). Although the disease has been described in all abdominal organs, the ileocecal region is the most commonly involved. A more recently described form of the infection is associated with intrauterine devices (IUD) (6). Duguid et al. (7) reported a much higher prevalence of Actinomyces in cervical material of women using plastic IUDs (42%) vs. those using copper IUDs (2%)~ Clinically, the abdominal form of the disease may have a variety of manifestations and has been called one of the great imitators in clinical practice. Classically, the disease progresses to form a chronic indurated abdominal mass with draining cutaneous or intraabdominal fistulas (as in this case report) associated with persistent fever, weight loss, and malaise (none of which were present in this patient). The initial phase of the disease may masquerade as cholecystitis, hepatitis, appendicitis, diverticulitis, inflammatory bowel disease, anorectal disease, peptic ulcer, or malignancy (8). The patient described here was thought to have cholecystitis and peptic ulcer disease 25 yr prior to his last hospitalization with suspected incarcerated incisional hernia that led to the diagnosis of omental actinomycosis and inflammatory bowel disease. The diagnosis of actinomycosis is rarely made clinically. A presumptive diagnosis is usually ~ on finding the classical sulfur granules in pus or on H&E stain and filamentous grampositive bacilli on Gram stain of histologic preparations. Sulfur granules are distinctive, congtoraerate masses of organisms, but aggregates of other organisms, including fungi, nocaxdia, streptomyces, and staphylococci (botryomycosis), may resemble them; imitators usually lack the characteristic clubbed peripheral fringes (1). In H&E-
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102
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© 1993 Elsevier Science Publishing Co., lrm.
Clinical Microbiology Newsletter 15:13,1993
PUS, SPUTUM, TISSUE
I
Examine material for "sulfur granules"
I
Stain granules or flecks of pus by Gram stain /
Gram-positive branching rods in diphtheroid-like characters Inocu ate brain heart infusion agar (BHIA) or Actinomyces maintenance media, blood agar (two plates each) and thioglycolate, supplemented with serum (0.2%)
I
Incubate anaerobically (jar or chamber) and in candle jar or CO2 incubate( /
Examine BHIA plates at 48 hours for "spider colonies'; record colony morphology
I
Examine BHIA plates at 7 and 14 days; record colony morphology I Examine thioglycolate (5-7 days); record type of growth; subculture to BHIA if typical Examine blooo. agarI {"5- 7d ay s"); record type of growth, hemolysis, colony color (red colonies characteristic of A.
odontolyticus)
I
Pick suspected colonies to BHIA and Actinomyces maintenance broth
I
Incubate 5-7 days
I Gram stain to check for pure culture i
I
I
*inoculate PYG broth
*Inoculate three BHIA slants from each broth /
Incubate148 hours
Incubate one alerobically, one anaerobically, and one in 2-5% CO2 I
Perform Igas chromatography I
Record results Examine at 5-7 days for oxygen tolerance; record degree of growth in each tube /
Perform catala[se test and Gram stain to check for pure culture
I I
Inoculate anaerobic idenlification kit
Record results and look up code/identification
Figure 3. Flow chartfor identification of Actinomyces. *Bothprocedures may not be necessary for definitive identification. Choices will depend on findings from earlier steps in theflow chart, capabilities of the laboratory, and interest of the investigator. [Reprinted with permission from H. P. Dalton (9)].
stained sections, granules are conspicuous, deep purple, round-to-oval bodies 1 to 3 lain in diameter (1) and are characteristically enveloped by purulent exudate (Fig. la). Typically, pinkish club-like structures radiate from the periphery of the granules (Fig. lb).
ClinicalMicrobiologyNewsletter15:13,1993
Grossly, the granules are hard, gritty, yellow or dull white by reflected light and light brown, translucent, or refractable by transmitted light (1). The granule represents a mineralized mass by host calcium phosphate consequent to phosphatase activity from tissue inflamma-
© 1993ElsevierScicacePublishingCo.,Inc.
tmn. The surtace ClUt>Strtg. l) are maments encased in the same polysaccharide-protein complex (1). Filaments will stain by Gomori methenamine-silvet stain, but they stain better in tissue Gram stains, for example, the Brown and Brenn Gram modification (Fig. 2). The definitive diagnosis is established by culture or direct fluorescent antibody staining. The flow chart in Figure 3 outlines the steps one might use in identifying Actinomyces from clinical material (9). Before the introduction of antimicrobial agents, actinomycosis was a serious disease causing significant disfigurement and frequently death. In 1946 Kolouch and Peltier (10) reported a 54% mortality associated with abdominal actinomycosis. In the preantimicrobial era, although various nonsurgical methods were used, surgical extirpation was the f'trst and most successful treatment (10). With the introduction of antimicrobial agents, most notably penicillin, the treatment and prognosis of actinomycosis dramatically changed. Putnum et al. (5) noted a cure rate of 16% before antimicrobials, with an improvement io 95% with penicillin therapy. Despite these impressive cure rates, most investigators recommend that treatment for actinomycosis consist of intensive and prolonged treatment with antimicrobials as well as surgical drainage and excision of the involved tissue (8). This is necessary because of the marked fibrotic tissue reaction, which has the effect of walling off the infection. Actinomyces also tend to develop into granules in the tissue, making it difficult to reach effective antimicrobial levels in the area of infection. Penicillin remains the drug of choice. Long-term treatment (6 to 12 me) with oral penicillin V (2 to 5 million U daily) after a 4- to 6-wk course of intravenous penicillin G (10 to 20 million U daily) is recommended for patients with cervicofacial, thoracic, or abdominal actinomycosis (11).
References 1. Lerncr, P. I. 1979. Actinomyces and arachnia species, p. 273-332. In G. L. Mandell, R. G. Douglas, and J. E. Ben-
0196-4399/93/$0.00+ 06.00
103
nett (eds.), Principles randpraetic~ of infectious disemcs, 3rd ed. John Wiley and Sons, New York.
2.
Rippon, J. W. 1988. Medical mycology, 3rd ed. WB Saunde~ Co., Philadelphia.
3.
Erikson, D. 1940. Pathogenic anaerobic organisms of the Actinomyces group, p. 1-63. In Medical research council special report, series no. 240. Her Majesty's Stationery Of_ rice, London. Wohlgemuth, S. D. and M. C. Gaddy. 1986. Surgical implications of actino-
4.
mycosis. South. Med. J. 79:1574--1578. 5.
6.
7.
8.
Putnmn, H. C., M. B. Dockerty, and J. M. Waugh. 1950. Abdominal actinomyco, is: an analysis of 122 cases. Surgery 28:782-800. Hager, W. D. and B. Majumdar. 1979. Pelvic actinomycosis in women using inlrauterine contraceptive devices. Am. J. Obstet. Gynecol. 133:60-63. Duguid, H. et al. 1982. Actinomyces and intrauterine devices. JAMA 248:1579-1580. Brown, J. R. 1973. Human actinomyco-
sis: a study of 181 subjects. Human Pathol. 4:319-330. 9.
Lambert, F. W. Jr., N. G. Warren, and H. P. Dalton. 1986. Actinomycetales flora respiratory specimens, p. 363365. in H.P. Dalton and H. C. Jr. (eds.), ~ v e medical microbiology. Churchill Livingstone,N e w York.
10. Kolouch, F. and L. F. P¢Itier. 1946. Actinomycosis. Surgery 20:.401-430. 11. Hart'is,L. F., P. R. Kakni, and C. E. Sclab. 1985. Actinomycosis surgical aspects. Am. Surg. 31:262-264.
i
Editors Mary Jane Feararo Paul A. Graham Josephine A. M o r e l l o ILL Zabransky @ 1993 ElsevierS~ia~cePublishingCo., Inc.
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Clinical Micf~iololy N e w ~
15:13,1993
clinical significance of a diagnostic assay based on the l~lymerase chain reaction for detection of human cytomegalovirus DNA in blood samples fixan immunocompromised patients. J. Clin. Microbiol. 30:,527-530. 10. Gerna, G. et al. 1991. Monitoring of human cytomegalovirus infections and ganciclovir treatment in heart transplant recipients by determination of viremia, antigenemia, and DNAemia. J. IlffecL DIS. 164:488--498. 11. Einsele, H. et al. 1991. Polymerase chain reaction to evaluate anfiviral therapy for cytomegalovims disease. Lancet 338:1170-1172. 12. Shibata, D. et al. 1988. Detection of cytomegalovirusD N A in imripheralblood of patients infected with human immunodefieiency virus. J. Infect. Dis. 158:1185-1192. 13. Jiwa, N. M. et al. 1989. Rapid detection of human cytomegalovims D N A in peripheral blood leukocytes of viremic transplant recipients by the pol3anaase chain reaction. Transplantation 48:7276. 14. Persing, D. H. 1991. Polymerase chain reaction: trenches to benches. J. Clin. Microbiol. 29"I281-1285. 15. Van der Bij, W. et al. 1988. Rapid immunodiagnosis of active cytomegalovims infection by monoclonal antibody staining of blood leucocytes. ]. Med. Virol. 25:179-188. 16. VanderBij, W. etal. 1988. Comparison between virm~a and antigenzmia for detection of cytom~alovirus in blood. ]. Clin. Microbiol. 26:25312535. 17. Van den Berg, A. P. ©t aL 1989. Cytomegalovirus anfigmemia as a useful
18.
19.
20.
21.
22.
23.
24.
marker of symptomatic cytomegalovi., rus infection after renal transplantation---a relx~ of 130 consecutive patients. Transplantation 48:991-995. Van der Bij, W. et al. 1989. Cytomegalovkus (CMV) antigenemia: rapid diagnosis and relationship with CMVassociated clinical syndromes in renal allogmft recipients. Transplant. Proc. 21:2061-2~ Van den Berg, A. P. etal. 1991. Antigenemia in the diagnosis and monitoring of active cytomegalovirus infection after fiver Cansplantation. J. Infect. Dis. 164:265-270 Revefio, M. G. et al. 1989. Detection of human cytomegalovirus immediate early antigen in lcukocytes as a marker of viremia in imm~ocompromised patients. L Med, Virol. 29:88-93. Erice, A. et al. 1992. Cytomegalovirus (CMV) antigenemia assay is more sensitive than sheU vial cultures for rapid detection of CMV in polymorphonuclear blood lenkocytes. J. Clin. MierobioL 30:.2822-2825, Grefte, J.M.M. et al. 1991. Thelow~ matrix protein pp65 is the principal viral antigen present in peripheral blood leukocytes during an active cytomegalovims infection. J. Gen. Virol. 73:2923-2932 Reveno, M. G. et al. 1992. Nuclear expression of the lower malfix protein of human cytomegalovirus in peripheral blood lenkocytcsof immtmocomproraised viremic patimts. J. Gen. Virol. 73:437-442 Miller, H. et al. 1991. Prospective study of eytomegalovirus antigencmia in allograft recipients. J. CIL~ Microbiol. 29:1054-1055.
Case Report Actinomycosis M a s q u e r a d i n g as Incarcerated Ineisional Hernia Sousan Sayahtaheri Aitaie, Ph.D.
Department of Pediatrics Division of l~ectious Diseases State Universityof N~, York at Bt~alo School of Medicine and The Children's Hospital Buffalo, NY 14222
I00
0196-4399/93/$0.00+ 06.00
cora isio ycosis of the greater omentmn, altboqh
Elfriede Kohout-Dutz, M.D. H. Robert Lipl~m' M.D. Vanessa Taylcc, M r ( A . ~ H a i r Hokaa Mcg~iire~ Richmomd, VA 23249
Center
Abdominal actinemycmis in a number o f fmms and is ome o f the
great imitatonin ~
lmUice. We
.:port the o f histologically ~ emeatal actinomycosis masquerading as incar-
© 1993 Elaevicr~
I~ab[iahmgCo., Inc.
ra~, shoatdbe ~ ia t h e ~ tiat d i a g ~ of an ~ ~ . C u e Report A 71-yr-old male with n o known alcohol abuse and a ~ o f smoking more than 55 ~ year was admit-
ted throught h e ~ ~
~
the initial dia~,nosis o f an umbilical and incisional hernia. The paClinical hfaombio~gyNcwslet~ 15:13,1993
tient's history included a vagotomy, antrectomy, and Billroth-I surgery for a chronic choleeystitis 25 yr prior to admission. The patient noticed a painful bulge at the base of the midline sear approximately 5 d prior to admission, the most severe pain having occurred on the last day. No nausea, vomiting, change in bowel movements, or obstructive symptoms were present. Upon admission, the physical examination revealed an afebfile patient with a blood pressure of 110/60, a pulse of 88, a respiration rate of 16, a soft scaphoid abdomen, and a tender mass below the umbilicus with some surrounding erythema. No fluctuanee or significant bowel sounds were present. The rectal exam was normal and the stool was negative for occult blood. The white blood cell count was 8.6 cells/dL; hemoglobin 13.8 g/dL; and normal differential cell count, prothrombin time, and partial thromboplastin time. An incarcerated hernia was suspected. The patient was given cefoxitin prophylactically upon admission and was taken to the operating room on the following day. At surgery, the patient had an omental abscess with gross pus inside the omental mass. The pus was cultured anaerobically and aerobically. The segment of omentum involved was resected and the abdominal cavity packed to avoid diffuse spillage into the abdomen. The bowel was not perforated and did not show any diverticula that might have perforated adherent to the mass. The direct Gram stain smear revealed gram-negative bacilli and grampositive cocci. As a result, cefoxitin was discontinued and the patient was placed on clindamycin and ceftriaxone. The pus, which appeared granular, was cultured on routine anaerobic media, including brucella agar supplemented with 5% sheep blood, vitamin K, and hemin; kamomycin-vancomycin laked blood aga~, phenyl-ethyl alcohol sheep blood aga~, and chopped meat carbohydrate broth. Following 48-h anaerobic incubation at 37°C, cultures grew only Peptostreptococcus micron and Bacteroides sp. Since there was no special request for culture for Actinomyces, the
Clinical Microbiology Newsletter 15:13,1993
Figure 1. "Sulfur" granule of the omentum. (a) H&E stain; note that the granule is enveloped by purulent exudate (x1,150). (b) 4,600x magnification of the boxed area in a; note the pronounced peripheral clubbing.
primary cultures were discarded after 4 d without the recovery of Actinomyces. Sections of omentum stained with hemotoxylin and eosin (H&E) revealed sulfur granules composed of filamentous bacteria surrounded by hyaline clubs (Fig. 1). Brown and Brenn tissue Gram stain revealed radial clusters of f'damentous bacillary organisms with right angle branching (Fig. 2), compatible with Actinomyces or Nocardia. The absence of staining by acid-fast stains favored the diagnosis of actinomycosis
The patient was started on intravenous penicillin therapy, 2 million units every 6 h for 4 wk and then discharged on oral penicillin (500 mg q 6 h) for an
© 1993 Elsevier Science Publishing Co., Inc.
0196-4399/93/$0.00 + 06.00
of the omentum. The patient was worked up with lower and upper gastrointestinal x-rays and CT scan of the abdomen for other sources of actinomycosis. No fluid collection but a thickened rectal wall were noted. Sigmoidoscopy was performed and revealed only an edematous mucosa.
I O]
Figure 2. Actinomycosis of the omentum; Brown and Brenn stain. The filaments are well demonstrated in a tissue section of the omentum (><1,150).
additional 11 mo. On follow-up visits the patient was doing well and remained asymptomafic.
Discussion
The etiology of aclinumycosis has been described at Ionglh (1). The first clinical description of human actinomycosis is credited to yon L a n g ~ in 1945. In 1877, Bollinger fn'st delineated the disease, called "lumpy jaw" in cattle because it involved the jaw bones and was believed to be caused by sulfur granule-producing fungi. In the same year, I-Iarz named this fungus Actinomyces for its appearance of filaments radiating from a central mass (2). Wolff and Israel carefully studied the organism and in 1891 described its anaerobic growth requirements (1). Their work also spawned the theory that the organism was an endogenous microbe not found outside the bodies of humans and animals. The organisms causing disease in cattle and humans were differentiated in 1940 when Erickson showed morphologic, biochemical, and serologic differences between the two strains (3). The human pathogen was renamed Actinomyces israelii, and the ammal s t r ~ was renamed Actinomyces bovis.
Since then, additional species of Actinomyces have been identified as causative agents of human disease, but A. bovis has never been isolated from humans (4). Studies of the cell wall components have led to classification of Actinomyce$ in the order Actinomycetales, which includes the genera Streptomyces and Mycobacterium. These organisms are considered normal tlova of the oral cavity and have been found on tooth surfaces, and in tonsillar crypts, vermiform appendix, colonic diverticula, and the vagina. Actinomyces are thought of as opportunistic pathogens requiring damage of the oral mucosal barrier by trauma, disease, or surgery in order to enter the tissues and cause disease. The least common form, pulmonothoracic disease, which accounts for 15% of all cases (4), may result from inhalation or aspiration of the organism via the t r a e ~ h i a l tree. "Vneeervicofaeial form of the disease is the most common, accounting for 55% of all cases (4), because the organism is normally found in the mouth. Any trauma, dental decay, tooth e x ~ , or fracture of the jaw may alk~v the oxganism to enter the adjacent ~ . The second most common form of hhe disease, abdominopelvic, accounts for 20% of all cases (5). Abdominal actinomycosis
usually results after surgery or peribration of the appendix, stomach, or colonic diverticulum, when the organism gains access to the peritoneal cavity. The disease spreads via direct extension without regard to normal tissue planes. Hematogenous or lymphatic spread is rare. In a large series of 122 patients with abdominal actinomycosis, only seven had no recent history of an acute gastrointestinal event (5). Although the disease has been described in all abdominal organs, the ileocecal region is the most commonly involved. A more recently described form of the infection is associated with intrauterine devices (IUD) (6). Duguid et al. (7) reported a much higher prevalence of Actinomyces in cervical material of women using plastic IUDs (42%) vs. those using copper IUDs (2%)~ Clinically, the abdominal form of the disease may have a variety of manifestations and has been called one of the great imitators in clinical practice. Classically, the disease progresses to form a chronic indurated abdominal mass with draining cutaneous or intraabdominal fistulas (as in this case report) associated with persistent fever, weight loss, and malaise (none of which were present in this patient). The initial phase of the disease may masquerade as cholecystitis, hepatitis, appendicitis, diverticulitis, inflammatory bowel disease, anorectal disease, peptic ulcer, or malignancy (8). The patient described here was thought to have cholecystitis and peptic ulcer disease 25 yr prior to his last hospitalization with suspected incarcerated incisional hernia that led to the diagnosis of omental actinomycosis and inflammatory bowel disease. The diagnosis of actinomycosis is rarely made clinically. A presumptive diagnosis is usually ~ on finding the classical sulfur granules in pus or on H&E stain and filamentous grampositive bacilli on Gram stain of histologic preparations. Sulfur granules are distinctive, congtoraerate masses of organisms, but aggregates of other organisms, including fungi, nocaxdia, streptomyces, and staphylococci (botryomycosis), may resemble them; imitators usually lack the characteristic clubbed peripheral fringes (1). In H&E-
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© 1993 Elsevier Science Publishing Co., lrm.
Clinical Microbiology Newsletter 15:13,1993
PUS, SPUTUM, TISSUE
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Examine material for "sulfur granules"
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Stain granules or flecks of pus by Gram stain /
Gram-positive branching rods in diphtheroid-like characters Inocu ate brain heart infusion agar (BHIA) or Actinomyces maintenance media, blood agar (two plates each) and thioglycolate, supplemented with serum (0.2%)
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Incubate anaerobically (jar or chamber) and in candle jar or CO2 incubate( /
Examine BHIA plates at 48 hours for "spider colonies'; record colony morphology
I
Examine BHIA plates at 7 and 14 days; record colony morphology I Examine thioglycolate (5-7 days); record type of growth; subculture to BHIA if typical Examine blooo. agarI {"5- 7d ay s"); record type of growth, hemolysis, colony color (red colonies characteristic of A.
odontolyticus)
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Pick suspected colonies to BHIA and Actinomyces maintenance broth
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Incubate 5-7 days
I Gram stain to check for pure culture i
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*inoculate PYG broth
*Inoculate three BHIA slants from each broth /
Incubate148 hours
Incubate one alerobically, one anaerobically, and one in 2-5% CO2 I
Perform Igas chromatography I
Record results Examine at 5-7 days for oxygen tolerance; record degree of growth in each tube /
Perform catala[se test and Gram stain to check for pure culture
I I
Inoculate anaerobic idenlification kit
Record results and look up code/identification
Figure 3. Flow chartfor identification of Actinomyces. *Bothprocedures may not be necessary for definitive identification. Choices will depend on findings from earlier steps in theflow chart, capabilities of the laboratory, and interest of the investigator. [Reprinted with permission from H. P. Dalton (9)].
stained sections, granules are conspicuous, deep purple, round-to-oval bodies 1 to 3 lain in diameter (1) and are characteristically enveloped by purulent exudate (Fig. la). Typically, pinkish club-like structures radiate from the periphery of the granules (Fig. lb).
ClinicalMicrobiologyNewsletter15:13,1993
Grossly, the granules are hard, gritty, yellow or dull white by reflected light and light brown, translucent, or refractable by transmitted light (1). The granule represents a mineralized mass by host calcium phosphate consequent to phosphatase activity from tissue inflamma-
© 1993ElsevierScicacePublishingCo.,Inc.
tmn. The surtace ClUt>Strtg. l) are maments encased in the same polysaccharide-protein complex (1). Filaments will stain by Gomori methenamine-silvet stain, but they stain better in tissue Gram stains, for example, the Brown and Brenn Gram modification (Fig. 2). The definitive diagnosis is established by culture or direct fluorescent antibody staining. The flow chart in Figure 3 outlines the steps one might use in identifying Actinomyces from clinical material (9). Before the introduction of antimicrobial agents, actinomycosis was a serious disease causing significant disfigurement and frequently death. In 1946 Kolouch and Peltier (10) reported a 54% mortality associated with abdominal actinomycosis. In the preantimicrobial era, although various nonsurgical methods were used, surgical extirpation was the f'trst and most successful treatment (10). With the introduction of antimicrobial agents, most notably penicillin, the treatment and prognosis of actinomycosis dramatically changed. Putnum et al. (5) noted a cure rate of 16% before antimicrobials, with an improvement io 95% with penicillin therapy. Despite these impressive cure rates, most investigators recommend that treatment for actinomycosis consist of intensive and prolonged treatment with antimicrobials as well as surgical drainage and excision of the involved tissue (8). This is necessary because of the marked fibrotic tissue reaction, which has the effect of walling off the infection. Actinomyces also tend to develop into granules in the tissue, making it difficult to reach effective antimicrobial levels in the area of infection. Penicillin remains the drug of choice. Long-term treatment (6 to 12 me) with oral penicillin V (2 to 5 million U daily) after a 4- to 6-wk course of intravenous penicillin G (10 to 20 million U daily) is recommended for patients with cervicofacial, thoracic, or abdominal actinomycosis (11).
References 1. Lerncr, P. I. 1979. Actinomyces and arachnia species, p. 273-332. In G. L. Mandell, R. G. Douglas, and J. E. Ben-
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nett (eds.), Principles randpraetic~ of infectious disemcs, 3rd ed. John Wiley and Sons, New York.
2.
Rippon, J. W. 1988. Medical mycology, 3rd ed. WB Saunde~ Co., Philadelphia.
3.
Erikson, D. 1940. Pathogenic anaerobic organisms of the Actinomyces group, p. 1-63. In Medical research council special report, series no. 240. Her Majesty's Stationery Of_ rice, London. Wohlgemuth, S. D. and M. C. Gaddy. 1986. Surgical implications of actino-
4.
mycosis. South. Med. J. 79:1574--1578. 5.
6.
7.
8.
Putnmn, H. C., M. B. Dockerty, and J. M. Waugh. 1950. Abdominal actinomyco, is: an analysis of 122 cases. Surgery 28:782-800. Hager, W. D. and B. Majumdar. 1979. Pelvic actinomycosis in women using inlrauterine contraceptive devices. Am. J. Obstet. Gynecol. 133:60-63. Duguid, H. et al. 1982. Actinomyces and intrauterine devices. JAMA 248:1579-1580. Brown, J. R. 1973. Human actinomyco-
sis: a study of 181 subjects. Human Pathol. 4:319-330. 9.
Lambert, F. W. Jr., N. G. Warren, and H. P. Dalton. 1986. Actinomycetales flora respiratory specimens, p. 363365. in H.P. Dalton and H. C. Jr. (eds.), ~ v e medical microbiology. Churchill Livingstone,N e w York.
10. Kolouch, F. and L. F. P¢Itier. 1946. Actinomycosis. Surgery 20:.401-430. 11. Hart'is,L. F., P. R. Kakni, and C. E. Sclab. 1985. Actinomycosis surgical aspects. Am. Surg. 31:262-264.
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Editors Mary Jane Feararo Paul A. Graham Josephine A. M o r e l l o ILL Zabransky @ 1993 ElsevierS~ia~cePublishingCo., Inc.
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