Campylobacter infection is the leading cause of bacterial gastroenteritis worldwide, yet life-threatening complications are extremely rare. We present a 32-year-old previously healthy man who presented with dysentery from Campylobacter jejuni, which was complicated by cecal perforation and secondary bacterial peritonitis

Betrner, Weston

Jain, Seema

Olevian, Dane

Yadav, Dhiraj

English

The Research Repository @ WVU (West Virginia University)

Faculty Scholarship 2019 Cecal Perforation in the Setting of Campylobacter jejuni Infection Seema Jain Weston Betrner Dane Olevian Dhiraj Yadav Follow this and additional works at: https://researchrepository.wvu.edu/faculty_publications  Part of the Anatomy Commons, and the Pathology Commons Downloadedfromhttps://journals.lww.com/acgcrbyBhDMf5ePHKav1zEoum1tQfN4a+kJLhEZgbsIHo4XMi0hCywCX1AWnYQp/IlQrHD35y8U/jUqeEwJ8JqglcOOaaKl+NhYMphARYM5etAp0mI=on04/06/2020Downloadedfromhttps://journals.lww.com/acgcrbyBhDMf5ePHKav1zEoum1tQfN4a+kJLhEZgbsIHo4XMi0hCywCX1AWnYQp/IlQrHD35y8U/jUqeEwJ8JqglcOOaaKl+NhYMphARYM5etAp0mI=on04/06/2020ACG CASE REPORTS JOURNALCASE REPORT | COLONCecal Perforation in the Setting of Campylobacterjejuni InfectionSeema Jain, MD1, Weston Bettner, MD2, Dane C. Olevian, MD3, and Dhiraj Yadav, MD, MPH21Department of Internal Medicine, University of Pittsburgh Medical Center, Pittsburgh, PA2Department of Gastroenterology, Hepatology and Nutrition, University of Pittsburgh Medical Center, Pittsburgh, PA33Department of Pathology, Anatomy, and Laboratory Medicine, West Virginia University, Morgantown, WVABSTRACTCampylobacter infection is the leading cause of bacterial gastroenteritis worldwide, yet life-threatening complications are extremelyrare. We present a 32-year-old previously healthy man who presented with dysentery from Campylobacter jejuni, which wascomplicated by cecal perforation and secondary bacterial peritonitis.INTRODUCTIONCampylobacter is the leading cause of bacterial gastroenteritis worldwide, withCampylobacter jejuni being themost common speciesto cause illness. Typically, C. jejuni causes acute self-limited gastroenteritis. However, 10%–20% of culture-confirmed cases in theUnited States require hospitalization.1 Acute enteric complications are uncommon and include mesenteric adenitis, pseudomem-branous colitis, massive gastrointestinal bleeding, ischemic bowel disease, and bowel perforation.1,2 Colonic perforation is ex-ceedingly rare; only a handful of reported cases exist, primarily in the context of toxicmegacolon.3,4We present a case of enterocolitissecondary to C. jejuni complicated by cecal perforation.CASE REPORTA32-year-old previously healthyman presentedwith 4 days of fevers, bilateral lower quadrant abdominal pain, and bloody diarrhea afterreturning from a 9-day trip to Japan. Stools were initially watery but progressed to a bloody, currant-jelly consistency.Hewas febrile up to39.5°C before presentation. He presented to the emergency department 1 day after returning from his trip, where he was febrile to 38.2°Cand tachycardic to 108beats perminute.Abasicmetabolic panel and complete bloodcountwere remarkable formildhyponatremiaof 132mmol/L andmildhypokalemiaof 3.3mmol/L; no leukocytosiswas evident. Stool sampleswereobtained, andhewasdischargedona3-daycourse of azithromycin for the treatment of dysentery. Within 12 hours, however, he re-presented with severe right lower quadrantabdominal pain. Abdominal and pelvic computed tomography (CT) scan demonstrated acute enterocolitis consisting of moderatelydistended, thickened,fluid-filled loopsof thedistal ileumandcolon,mostprominent in the righthemicolonandcecum(Figure1).Reactivemesenteric lymph nodes up to 1.5 cm in the right lower quadrant and diffuse mesenteric edema were also demonstrated.The patient was given intravenous fluids and discharged. Despite 2 days of adherence to azithromycin therapy, he had persistentsymptoms and so presented to the infectious disease clinic. Stool nucleic acid amplification testing had by then returned positive forC. jejuni with negative results for other bacterial pathogens. He was admitted for initiation of intravenous meropenem, givena concern for macrolide resistance.On admission, he remained tachycardic and developed a leukocytosis to 12.63 109 cells/L with neutrophil predominance. On day 2of admission, he developed a new singultus with an abdominal examination demonstrating rebound and guarding. His laboratoryresults were remarkable for a newbandemia of 22%and a fall in his albumin from3.8 to 2.8 g/dL. An abdominal x-ray revealed free airunderlying the diaphragm (Figure 2).ACG Case Rep J 2019;6:e00268. doi:10.14309/crj.0000000000000268. Published online: December 5, 2019Correspondence: Seema Jain, MD, UPMC Montefiore Hospital, N-715, 200 Lothrop St, Pittsburgh, PA 15213 (jains5@upmc.edu).ACG Case Reports Journal / Volume 6 acgcasereports.com 1The patient underwent an emergent exploratory laparotomy,which revealed cecal perforation complicated by gross fecalcontamination of the abdomen. Peritoneal cultures wereobtained, and an ileocolic resection with a side-to-side ileoco-lonic anastomosis was performed. Pathology demonstrated ac-tive enterocolitis with ulceration, patchy mild crypt distortion,transmural colonic perforation, and acute serositis (Figure 3).There was no evidence of chronic mucosal injuries such asgranulomas, transmural chronic inflammation, or mural scar-ring, arguing against an underlying diagnosis of inflammatorybowel disease. Intraoperative cultures grew pan-sensitive En-terococcus faecalis,whereas blood cultures remained negative.Hewas treated with 8 days of meropenem overlapped with 3 daysof gentamicin for empiric treatment of C. jejuni. Antibiotictherapy was extended with an additional 4 days of piperacillin-tazobactam to complete treatment of E. faecalis.Postoperatively, hishemoglobindropped from12.2 to7.5g/dLoverthe course of 4 days with no overt gastrointestinal bleeding. A CTscandemonstrated a largehematoma in the right lowerquadrant ofthe retroperitoneum without active contrast extravasation on an-giogram. The patient then underwent a repeat exploratory lapa-rotomy that revealed a large clot in the pelvis near the anastomosis,whichwas evacuated; no active source of bleedingwas seen, andhishemoglobin stabilized thereafter. He subsequently developeda postoperative ileus and briefly required total parenteral nutrition.He was discharged on hospital day 16 with negative pressurewound therapy. He was evaluated in the clinic 2 weeks after dis-charge with significant improvement in his symptoms.DISCUSSIONCampylobacter jejuni infection typically causes acute self-limited gastroenteritis or colitis with symptoms lasting 1 day to1 week. The most common symptoms are crampy abdominalpain, malaise, fever, and diarrhea, with stools that can rangefrom loose to watery to bloody.2 The cornerstone of treatment,as for any diarrheal illness, is fluid and electrolyte replacement.5In a meta-analysis of 11 small randomized trials, antimicrobialtherapy, when started early in the disease course, reduced du-ration of symptoms by 1.3 days.6 Antimicrobial therapy istypically reserved for patients with severe symptoms such ashigh fever, massive or bloody diarrhea, or symptoms persistingfor more than 1 week. Owing to increased rates of fluo-roquinolone resistance, macrolides are considered first-linetherapy when antimicrobials are warranted.5Identifying and treating patients at risk for enteric complica-tions ofC. jejuni infection is challenging as complications are sorare. Only a handful of cases of perforation from C. jejuni in-fection have been reported. In previous cases of perforation,patients had suddenworsening of their abdominal examinationalong with concurrent fevers and increasing leukocytosis beforethe development of toxic megacolon.3,4,7 Similarly, our patienthad an ongoing systemic inflammatory response despite ade-quate fluid resuscitation and antimicrobial therapy as his ab-dominal examination progressed to an acute abdomen.Persistent systemic inflammatory response criteria in concor-dance with other inflammatory laboratory markers despiteadequate initial therapymay, therefore, be helpful in identifyingpatients at risk for toxicity who warrant serial examinations orrepeat imaging. Our patient developed a new leukocytosis onadmission followed by a bandemia and hypoalbuminemia ap-proximately 12 hours before his surgical resection. C-reactiveprotein was not checked for our patient but may have been anadditional helpful tool for risk stratification, as markedly ele-vated C-reactive protein was noted in 2 cases of bowel perfo-ration secondary to C. jejuni.7,8Figure 1. Abdominal and pelvic computed tomography showingdistended and thickened fluid-filled loops of distal ileum and colon.Figure 2. Abdominal x-ray showing large volume pneumo-peritoneum with diffuse distended and dilated loops of the smallbowel and numerous air-fluid levels.ACG Case Reports Journal / Volume 6 acgcasereports.com 2Jain et al Cecal Perforation in C. jejuniIn most of the previously reported cases of intestinal perfo-ration from C. jejuni infection, colonic dilation, particularly inthe form of toxic megacolon, was a harbinger for perforation,although perforation in the absence of marked distension hasalso been reported.7 In our case, the initial CT exhibitedmoderate colonic distension, particularly in the right hemi-colon. On further review of the initial CT, a punctate focus offree air was seen adjacent to the liver, which was not formallyreported (Figure 4). This finding suggests a sentinel micro-perforation that could have preceded macroscopic complica-tions and highlights the importance of imaging review withradiology. To our knowledge, no other study has noted thisfinding.An additional risk factor for enteric complications may be thevirulence of theC. jejuni isolate. Drug-resistantC. jejuni speciesare associated with an increased risk for invasive illness anddeath.9 Our patient may have grown a multidrug-resistant or-ganism because he did not respond tomacrolide therapy within48 hours, and his C. jejuni isolate revealed doxycycline re-sistance on send-out testing; unfortunately, other sensitivitieswere not reported. Resistance would have been unexpected,however, because rates of macrolide resistance for C. jejunispecies from Japan are stably low.10 In patients failing to re-spond to conventional macrolide therapy, especially thosecontracting disease in regions with higher rates of drug-resistant C. jejuni, such as Thailand, Africa, and Mexico, esca-lation to a carbapenem or aminoglycoside should be consid-ered.2 Our case demonstrates an atypical life-threateningcomplication of colonic perforation in a common illness thatis usually self-limiting.DISCLOSURESAuthor contributions: S. Jain andW. Bettner wrote and revisedthe manuscript. DC Olevian provided the histological images.D. Yadav edited the manuscript, revised the manuscript forintellectual content, and is the article guarantor.Financial disclosure: None to report.Informed consent was obtained for this case report.Received June 25, 2019; Accepted September 23, 2019REFERENCES1. Kirkpatrick BD, Tribble DR. Update on human Campylobacter jejuniinfections. Curr Opin Gastroenterol. 2011;27(1):1–7.2. Allos CM, Iovine NM, Blaser MJ. Campylobacter jejuni and related species.In: Bennett JE, Dolin R, Blaser MJ (eds). Mandell, Douglas, and Bennett’sPrinciples andPractice of InfectiousDiseases. 8th edn. Elsevier: Philadelphia,PA, 2015, pp 2485–93.3. Kummer AF, Meyenberger C. Toxic megacolon as a complication ofCampylobacter jejuni enterocolitis. Schweiz Med Wochenschr. 1998;128(41):1553–8.Figure 4. Abdominal and pelvic computed tomography showingpunctate focus of free air adjacent to liver (arrow).Figure 3. (A) Histological examination of the terminal ileum showing neutrophilic inflammation and superficial mucosal ulceration (arrow)overlying prominent Peyer’s patches with acute and organizing serositis (star) secondary to the nearby colonic perforation. Histologicalexamination of the cecum showing the (B) colonic mucosa which shows widespread evidence of acute colitis, including cryptitis, cryptabscesses, and expansion of the lamina propria by mixed inflammatory cells. There is patchy, mild crypt architectural distortion (star),including irregular and branched crypts (center). However, well-developed features of chronic mucosal injury are absent. The edge of anadjacent ulcer with fibrinopurulent exudate is shown at left (arrow), and (C) there is a transmural defect present (star) that is associated withulceration, transmural neutrophilic inflammation (arrow), edema, focal necrosis, and acute serositis.ACG Case Reports Journal / Volume 6 acgcasereports.com 3Jain et al Cecal Perforation in C. jejuni4. Vyas SK, Law NN, Hill S, et al. Toxic megacolon with late perforation inCampylobacter colitis—A cautionary tale. Postgrad Med J. 1993;69(810):322–4.5. Shane AL, Mody RK, Crump JA, et al. 2017 Infectious Disease Society ofAmerica Clinical Practice Guidelines for the Diagnosis andManagement ofInfectious Diarrhea. Clin Infect Dis. 2017;65(12):e45–80.6. Ternhag A, Asikainen T, Giesecke J, Ekdahl K. A meta-analysis onthe effects of antibiotic treatment on duration of symptoms caused byinfection with Campylobacter species. Clin Infect Dis. 2007;44(5):696–700.7. Fischer J,Mackay B,WakemanC. Caecal perforation in the absence of toxicdilatation in Campylobacter colitis. ANZ J Surg. 2013;83:583–4.8. Jassim SS, Malik A, Aldridge A. Small bowel perforation: An unusual case.Grand Rounds. 2011;11:17–9.9. Helms M, Simonsen J, Olsen KEP, et al. Adverse health events associatedwith antimicrobial drug resistance in Campylobacter species: A registry-based cohort study. J Inf Dis. 2005;191(7):1050–5.10. Gibreel A, Taylor DE. Macrolide resistance in Campylobacter jejuni andCampylobacter coli. J Antimicrob Chemother. 2006;58(2):243–55.Copyright:ª 2019 The Author(s). Published byWolters Kluwer Health, Inc. on behalf ofThe American College of Gastroenterology. This is an open-access article distributedunder the terms of the Creative Commons Attribution-Non Commercial-No DerivativesLicense 4.0 (CCBY-NC-ND), where it is permissible to download and share the workprovided it is properly cited. The work cannot be changed in any way or used com-mercially without permission from the journal.ACG Case Reports Journal / Volume 6 acgcasereports.com 4Jain et al Cecal Perforation in C. jejuni

Cecal Perforation in the Setting of Campylobacter jejuni Infection

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Cecal Perforation in the Setting of Campylobacter jejuni Infection

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