Spontaneous (primary) candida peritonitisrated peptic ulcer disease, traumatic in-testinal...

Spontaneous (primary)candida peritonitis

JOE SUKHABOTE MD, HUGH J FREEMAN MD

SPONTANEOUS (PRIMARY)

PERITOnitis is a form of peritonitis,usually due to a bacterial agent, with-out a recognizable source of infectionor inflammation. There is continuingdebate as to the mechanism of organ-ism entry into the peritoneal cavity, al-though the gastrointestinal tract is be-lieved to be the likely source.Spontaneous bacterial peritonitis re-mains a very serious complicating clini-cal disorder in patients with chronic

liver diseases, usually with ascites, andcauses a high mortality rate.

Although the incidence of candidainfections has increased, peritonitisdue to candida infection is very uncom-mon (1). Candida albicans may causemassive ascites by direct peritoneal in-volvement. This usually occurs in pa-tients with a pathological or artificialroute of contamination, or their pres-ence might result from an occult gas-trointestinal perforation. The usualprecipitating factors or associated clini-

cal conditions specifically associatedwith candida infection include perfo-rated peptic ulcer disease, traumatic in-testinal perforation, gastric and/orintestinal surgery and peritoneal dialy-sis.

In this report, a female patient is de-scribed with spontaneous or primaryperitonitis and ascitic fluid that cul-tured Candida species. She respondedcompletely to antifungal therapy us-ing amphotericin B with completeresolution of abdominal pain and as-cites.

CASE PRESENTATIONA 49-year-old woman initially pre-

sented in the emergency room with atwo-month history of abdominal painand fever. Approximately four monthsearlier she developed jaundice and wasdiagnosed with ‘hepatitis’, attributed toalcohol abuse. The jaundice subse-quently resolved but she developedanorexia and increasing abdominalgirth followed by the onset of diffuseand poorly localized abdominal painwith fever, chills and occasional nightsweats. Before current hospitalization,she received treatment with spirono-lactone and amoxicillin.

Initial examination revealed tem-perature of 37.8oC and slight tachycar-dia of 104 beats/min. Ascites wasevident with abdominal tenderness;rebound was present but there was nolymphadenopathy or peripheral stig-mata of chronic liver disease.

Laboratory investigations revealed:hemoglobin 115 g/L; white blood cells

BRIEF COMMUNICATION

J SUKHABOTE, HJ FREEMAN. Spontaneous (primary) candida peritonitis. CanJ Gastroenterol 1995;9(3):144-146. A 49-year-old female presented with ab-dominal pain and ascites. Subsequent investigations revealed Candida albicans inthe ascitic fluid without evidence of systemic candidiasis or a source of local in-fection in another site. Additional studies revealed no evident underlying immu-nological disorder and the gastrointestinal tract was intact. Therapy withamphotericin B led to resolution of abdominal pain and ascites with no recur-rence.

Key Words: Ascites, Bacterial peritonitis, Candida peritonitis, Immunosuppression,Primary peritonitis

Péritonite à Candida spontanée (primaire)

RÉSUMÉ : Une femme de 49 ans se présente pour douleur abdominale et ascite.Les épreuves diagnostiques révèlent la présence de Candida albicans dans le liq-uide d’ascite, sans signe de candidose systémique ni source d’infection localeprovenant d’un autre foyer. Les épreuves additionnelles ne révèlent aucun signede trouble immunologique sous-jacent et les voies digestives sont intactes. Letraitement par amphotéricine B a fait disparaître la douleur abdominale et l’as-cite, sans récurrence.

Department of Medicine (Gastroenterology), University of British Columbia, Vancouver,British Columbia

Correspondence and reprints: Dr Hugh Freeman, ACU F-137, Vancouver Hospital (UBCSite), 2211 Wesbrook Mall, Vancouver, British Columbia V6T 1W5. Telephone (604)822-7216

Received for publication June 13, 1994. Accepted October 17, 1994

144 CAN J GASTROENTEROL VOL 9 NO 3 MAY 1995

17.0x109/L; and platelets 628x109/L.Liver chemistry tests included: totalbilirubin 16 �mol/L (normal 2 to 23);alkaline phosphatase 477 IU/L (normal30 to 110); and aspartate amino-transferase 624 IU/L (normal 5 to47). Serum amylase, glucose and im-munoglobulins were normal. Serologi-cal studies for hepatitis A, B and Cwere negative. Paracentesis revealedyellow, cloudy fluid with 5000 redblood cells and 5000 white blood cells(24% neutrophils, 32% mononuclearcells, 44% lymphocytes). Analysis ofthe ascitic fluid revealed total proteinof 27 g/L. Gram stains of the fluidshowed no organisms but peritonealfluid cultures demonstrated C albicans.The patient was treated with intrave-nous amphotericin B, and abdominalpain and ascites completely resolved.

Additional investigations to ex-clude other causes of infection as wellas to locate the source of the candida –including cultures of feces, sputum,skin, cervix, vagina, liver, cere-brospinal fluid, blood and bone marrow– were normal. Serological studies forhuman immunodeficiency virus, cy-tomegalovirus, Epstein-Barr virus, her-pes simplex virus and fungi werenegative. Radiographic examinationsof the chest and abdomen, includingbarium contrast studies of the upperand lower gastrointestinal tracts, werenormal as were ultrasound and com-puted tomography of the abdomen andpelvis (except for ascitic fluid). Fibre-optic endoscopic examinations of theupper gastrointestinal tract and colon,with biopsies of the esophagus, stom-ach, small and large intestine, werenormal. Histological evaluation of theliver revealed nonspecific lobularhepatitis with some periportal fibrosis.

DISCUSSIONC albicans and other species of Can-

dida are frequent ubiquitous microbio-logical agents on normal mucousmembranes of the mouth, vagina andintestinal tract (2). Candida specieshave also been cultured from the fecesin up to 31% of healthy subjects and inan even higher percentage of patientsreceiving broad-spectrum antibiotictreatment (3). If the organism becomes

invasive it may result in a variety ofacute or chronic, localized or widelydisseminated lesions (1). Generally,C albicans is not pathogenic in healthyhumans but it may become a virulentpathogen in immunosuppressed pa-tients or those suffering from severalmetabolic or neoplastic disorders (eg,diabetes, malignant lymphoma), inwhom it can complicate total par-enteral nutrition or follow treatmentwith antibacterial or corticosteroiddrugs (1,4). Conversely, severe andvery extensive candidiasis may result ina significant, but an entirely reversible,immunological impairment in whiteblood cell function, specifically, inneutrophil candidacidal activity; in aprevious report (3), extensive esophag-eal candidiasis was described simulat-ing changes in the acquiredimmunodeficiency syndrome. Al-though our patient had evidence ofliver disease, possibly related to prioralcohol abuse, the ascites appeared tobe due, at least in part, to infectionwith positive cultures of the peritonealfluid for C albicans. After the patientwas treated intravenously with a potentantifungal agent, amphotericin B, ab-dominal pain and ascites completelyresolved.

C albicans peritonitis is most com-monly seen as a complication of perito-neal dialysis, in perforation of anabdominal viscus or following gas-trointestinal surgical procedures (3-6).To our knowledge it has not been re-corded as a primary or spontaneouscause of peritonitis, even in patientswith chronic liver disease and ascites.Candida species are frequently isolatedfrom the peritoneal fluid of peritonealdialysis patients, in whom the organismappears to be a contaminant and cancause clinically significant peritonitisas reflected by the presence and persis-tence of fever, peritoneal signs, periph-eral leukocytosis, positive peritonealcultures for candida and purulent as-citic fluid (3). C albicans peritonitisalso occurs in 1% of renal transplant re-cipients; in these patients it is most of-ten due to an unrecognized intestinalperforation or other intraperitonealdisease. The pathogenic role of C albi-

cans peritonitis in patients with po-

lymicrobial enteric flora is poorlyunderstood. In surgical patients, can-dida has generally been isolated fromthose with a spontaneous perforationor a surgical opening in the gastrointes-tinal tract (6). It appears that isolationof Candida species has been most fre-quent from patients having surgicaltherapy for severe pancreatitis, recur-rent perforation of the gastrointestinaltract or anastomotic leakage (6);moreover, for surgical patients, mortal-ity was significantly greater in the pres-ence of Candida species infections.Aggressive antifungal treatment hasbeen recommended (3) because it ap-pears to lower mortality.

In the absence of an obvious sourceof infection, fungal peritonitis, includ-ing C albicans peritonitis, appears to beexceedingly rare. A diabetic with renalfailure and prolonged broad-spectrumantibiotic treatment complicated byfungal peritonitis has been recorded al-though the specific organism in this pa-tient was not noted (7). Combinationintraperitoneal and intravenous treat-ment with amphotericin B has beenrecommended (7) for fungal peritonitisalthough no studies to date have care-fully explored an optimal treatmentregimen for candida peritonitis.

A number of fungal organisms mayrarely cause peritonitis, usually in thesetting of an immunodeficiency state.These include peritoneal histoplasmo-sis (8), coccidioidomycosis (9) and dis-seminated cryptococcal infections(10). In some patients these may mimicneoplastic disease, be associated withdisseminated granulomatous inflam-matory disease or lead to a fatal out-come. Recognition of fungal agents,particularly C albicans, may be signifi-cantly improved if ascitic fluid is sub-mitted in blood culture bottles. If C

albicans is detected, treatment consistsof a search for the infection source aswell as intravenous antifungal treat-ment.

REFERENCES1. Myerowitz RL, Pazir GJ, Allen CM.

Disseminated candidiasis: changes inincidence, underlying diseases andpathology. Am J Clin Pathol1977;68:29-38.

CAN J GASTROENTEROL VOL 9 NO 3 MAY 1995 145

Candida peritonitis

2. Noble MA, Chan V, Mangal AK,Carter CJ, Whittaker JS, Freeman HJ.Candida esophagitis in a malehomosexual with evidence of aserum-associated inhibitor ofneutrophil candidacidal activity.A case of ‘pseudo-AIDS’. Can JGastroenterol 1987;1:33-5.

3. Bayer AS, Blumenkrantz MJ,Montgomerie JZ, Galpin JE, CoburnJW, Guze LG. Candida peritonitis.Report of 22 cases and review of theEnglish literature. Am J Med1976;61:832-40.

4. Reeves KO, Ripepi AC, Carter RE,Williams TW. Candida peritonitis in a

quadriplegic. Treatment withamphotericin B. South Med J1972;65:325-8.

5. Solomkin JS, Flohr AB, Quie PG,Simmons RL. The role of Candida inintraperitoneal infections. Surgery1980;88:524-30.

6. Calandra T, Bille J, Schneider R,Mosimann F, Francioli P. Clinicalsignificance of candida isolated fromperitoneum in surgical patients. Lancet1989;ii:1437-9.

7. Runyon BA. Surgical peritonitis andother diseases of the peritoneum,mesentery, omentum, and diaphragm.In: Sleisenger MH, Fordtran J, eds.

Gastrointestinal Disease,Pathophysiology, Diagnosis,Management, vol 2, 5th edn.Philadelphia: WB Saunders, Ltd,1993:2004-14.

8. Reddy P, Gorelick DF, Brasher CA,Larsh H. Progressive disseminatedhistoplasmosis as seen in adults.Am J Med 1970;48:629-36.

9. Saw E, Shields SJ, Comer TP,Huntington RW. Granulomatousperitonitis due to cocidioides immitis.Arch Surg 1974;108:369-71.

10. Clift SA, Bradsher RW, Chan CH.Peritonitis as an indicator ofdisseminated cryptococcal infection.Am J Gastroenterol 1982;77:922-4.

146 CAN J GASTROENTEROL VOL 9 NO 3 MAY 1995

SUKHABOTE AND FREEMAN

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