Massive perianal ulceration: Entamoebahistolytica and Candida albicans co-infectionMichael Davis, Emory UniversityStephen F. Templeton, Emory UniversityDavid L. Dickensheets, Cumming, GeorgiaAlexander S. Gross, Emory University

Journal Title: JAAD Case ReportsVolume: Volume 3, Number 6Publisher: Elsevier | 2017-11, Pages 553-555Type of Work: Article | Final Publisher PDFPublisher DOI: 10.1016/j.jdcr.2017.07.020Permanent URL: https://pid.emory.edu/ark:/25593/s6j24

Final published version: http://dx.doi.org/10.1016/j.jdcr.2017.07.020

Copyright information:© 2017 by the American Academy of Dermatology, Inc. Published by Elsevier,Inc.This is an Open Access work distributed under the terms of the CreativeCommons Attribution-NonCommercial-NoDerivatives 4.0 International License(http://creativecommons.org/licenses/by-nc-nd/4.0/).

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CASE REPORT

Massive perianal ulceration:Entamoeba histolytica and

Candida albicans co-infection

Michael J. Davis, BMus,a Stephen F. Templeton, MD, FAAD,b

David L. Dickensheets, MD,c and Alexander S. Gross, MDb

Atlanta and Cumming, Georgia

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Key words: amebiasis Cutis; Candida albicans; co-infection; Entamoeba histolytica.

Abbreviation used:

PAS: periodic acideSchiff

INTRODUCTIONAlthough Entamoeba histolytica, named for its

notorious tissue-lysing facility, is a major cause ofmorbidity and mortality worldwide, cutaneousinvolvement is rare. Presentation in nonendemiccountries is exceptionally rare.1 We present a caseof amebiasis cutis presenting as a deeply invasiveperianal ulceration. Delayed diagnosis, empiricuse of broad-spectrum antibiotics, and systemiccorticosteroids provided fertile ground for Candidaalbicans co-infection. This case highlights thetissue destructive nature of E histolytica and thepotential for candidiasis to potentiate this tissuedestruction.

CASE REPORTAfter a flight from India to the Unites States, a

76-year-old, nondiabetic, immunocompetent manhad rectal bleeding attributed to manualdisimpaction for constipation relief. Over the next2 weeks, he complained of abdominal discomfort,fever, and a wound around his rectum.Trimethoprim/sulfamethoxazole prescribed by anurgent care center provided no improvement. Hewas admitted to the hospital where physicalexamination found a well-circumscribed 5-cmperianal ulceration with deep necrosis and adjacenterythema. Laboratory tests on admission found awhite blood cell count of 20,600/mm3 and normalliver enzymes. Bacterial culture of the wound grewmixed skin flora. Polymerase chain reaction testfor herpes was negative. Computerized axialtomography found a soft-tissue abnormality poste-rior to the rectum without other intra-abdominal

the Department of Dermatology,b Emory University School

Medicine, Atlantaa and Cumming, Georgia.c

ing sources: None.

icts of interest: None declared.

spondence to: Michael J. Davis, BMus, 640 Linwood NE Ave

t 2, Atlanta, GA 30306. E-mail: michael.james.davis@emory.

u.

conditions. Nonspecific ulcerations of the ascendingcolon and cecum were biopsied during colonos-copy. Pathology results showed architecturallynormal inflamed colonic mucosa. The wounddramatically worsened despite broad-spectrumantibiotics. Given concern for pyoderma gangreno-sum, systemic corticosteroid therapy was initiated(Fig 1).

Corticosteroid administration did not lead toclinical improvement, and the patient’s whiteblood cell count increased to 45,000/mm3. Thedermatology department was consulted and punchbiopsies performed. Histopathology found extensivetissue necrosis and a neutrophilic inflammatoryinfiltrate (Fig 2). Also noted were scattered largeround periodic acideSchiff (PAS) stainepositivecells containing a solitary nucleus and abundantamphophilic cytoplasm characteristic of amoebictrophozoites (Figs 2 and 3). PAS-positive sporesand pseudohyphal structures indicative of yeastsuperinfection were also identified (Fig 4).

Tissue culture grew C albicans. The patient wastreated with intravenous metronidazole and oralfluconazole. Fever resolved within 48 hours. Theperianal wound underwent pulse lavage andsurgical debridement leaving a 15-cm defect withexposed coccyx. Temporary laparoscopic divertingloop ileostomy, partial primary closure, rotationflap, and skin grafting were required for woundhealing.

JAAD Case Reports 2017;3:553-5.

2352-5126

� 2017 by the American Academy of Dermatology, Inc. Published

by Elsevier, Inc. This is an open access article under the CC BY-

NC-ND license (http://creativecommons.org/licenses/by-nc-nd/

4.0/).

http://dx.doi.org/10.1016/j.jdcr.2017.07.020

553

Fig 1. Indurated erythema surrounds a rapidly expanding,deeply necrotic perianal ulceration.

Fig 2. Several round organismswith pale foamy, basophiliccytoplasm and a solitary nucleus characteristic of amoebictrophozoites are visiblewithin a brisk inflammatory infiltrateand surrounding necrotic debris. (Hematoxylin-eosin stain;original magnification:3400.)

Fig 3. PAS stain highlights the large unicellular protozoawithin necrotic tissue. (Original magnification: 3400.)

Fig 4. PAS stain shows a dense collection of spores,budding yeast, and pseudohyphae, characteristic ofinvasive candidiasis. (Original magnification: 3100.)

JAAD CASE REPORTS

NOVEMBER 2017554 Davis et al

DISCUSSIONWorldwide, E histolytica is a common cause of

infectious colitis and liver abscesses, and the secondleading cause of death from parasitic disease.1 Yet,cutaneous involvement is unusual.2 Much of theliterature on cutaneous disease has come fromMexico where, likely because of availability ofappropriate therapy, the incidence has significantlywaned.3 A retrospective analysis published in2012 involving 2 large Mexican institutions andcovering more than a 50-year period identified only26 cases.3 A review of 5097 patients treated in SouthAfrica for invasive amebiasis identified only 2 caseswith cutaneous disease.4 Much of the recentliterature on cutaneous amebiasis consists of rarecase reports.

E histolytica plagues communities in which thewater and food supply are contaminated by humanfeces. Infection occurs after ingestion of cysts, whichdevelop into trophozoites that colonize the intestineand feed on gut bacteria. After multiplying andencysting, the parasite is excreted into stool as bothcysts and trophozoites.1 Amebiasis cutis occurswhen virulent trophozoites from the bowel comeinto prolonged contact with traumatized skin. Thus,infants and children in diapers are at increased risk.5

Local trauma from efforts to relieve constipation mayhave precipitated our patient’s cutaneous infection.Sexual transmission is well documented, particularlyin those who practice anal intercourse.6 Notably,tracks from needle aspiration or surgical drainage ofliver abscesses can act as conduits for cutaneousdisease.3,5 Skin infection at more distant locations ismuch less common.1

Typical lesions present as one or several painfulfoul-smelling ulcers with purulent exudate and deepnecrotic bases. Ulcer margins tend to be red,well-demarcated, slightly elevated with surroundingerythema and expand at a rate of roughly 1 cm/wk.7

Trophozoites can be identified on a wet preparation

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VOLUME 3, NUMBER 6Davis et al 555

of exudate or a scraping of the wound edge and onhematoxylin-eosin staining of tissue.3,5 Tissuevisualization is enhanced with PAS or immuno-peroxidase and antilectin antibody staining.2 Theneed for extensive tissue debridement as in thecurrent case, loss of genitalia and urethra, andsubsequent reconstructive surgery are documentedsequelae of delayed diagnosis.6

Amoebic ulceration is fueled by apoptosis anddestructive proteases including hyaluronidase,collagenase, N-acetylglucosaminidase, and phos-pholipase-A.1,4 On contact, motile trophozoitescause cytolysis of host cells including neutrophils,which then release additional tissue destructiveenzymes.1 In a 2003 Lancet seminar, SamuelL. Stanley Jr suggests physicians ‘‘Think of thisprotozoan parasite as a macrophage on steroidswith pumped-up phagocytic, proteolytic, andcytolytic capabilities.’’1 It follows that concomitantuse of systemic corticosteroids fuels the protozoan’svirulence, increasing the incidence of toxicmegacolon, intestinal perforation, and liver abscess;worsening of cutaneous ulceration and candidiasisas in this case is not surprising.1

The relationship between E histolytica and gutmicrobiota is complicated; research suggests thatspecific commensals likely promote asymptomaticamoebic colonization, whereas others likelyenhance mucosal inflammation and amoebicvirulence.8 Co-infection of amoebic liver abscesseswith gut microbiota and Entamoeba dispar, a speciesof Entamoeba generally considered nonpathogenic,is well-documented.8 The literature discussingcutaneous amebiasis-bacterial co-infection is sparse;

yet, bacterial co-infection potentiating the pathoge-nicity of E histolytica in such instances has beenpostulated.5 The possibility of C albicans andE histolytica potentiating the virulence of oneanother has not been discussed previously but isintriguing especially given the histopathology in thiscase. In certain laboratory settings, the virulence ofC albicans is found to be enhanced by bacteriaincluding Pseudomonas aeruginosa, Escherichiacoli, and Staphylococcus epidermis.9 Clinically,candidemia is found to be more lethal in the settingof bacterial co-infection.10 The current casesuggests that C albicans and E histolytica are also adangerous duo.

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