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Acute Terminal Ileitis Mimicking Crohn's Disease Caused By Case Report Acute Terminal Ileitis Mimicking Crohn’s Disease Caused by Salmonella veneziana Daniele Dionisio, MD; * Francesco Esperti, MD; * Angela Vivarelli, MD; * Claudio Fabbri, MD; * Paola Apicella, MD;I Nicola Meola, MD, *** Patrizia Lencioni, PhD,§ and Roberto Vannucci, MDn Gastroenteritis induced by nontyphoidal Salmonella is mesenterium and adjoining small bowel (Figure 1). Stool characterized by fluid secretion and inflammatory neu- cultures established the diagnosis of Salmonella species trophil migration into the intestinal mucosa and the gut enterica subspecies enter&a serotype veneziana (11: i: lumen. l-3 Nontyphoidal Salmonella may specifically enx),‘” with negative results for mycobacteria, Clostrid- infect the terminal ileum (terminal ileitis) or the ileocecal ium di@cile toxins, fungi, parasites, adenoviruses, and area (ileocecitis), thus mimicking appendicitis and rotaviruses. For Salmonella, after incubation in selenite Crohn’s disease.*-’ Superinfection with these agents in broth (Selenite Broth, Biolife, Milan, Italy), the stool sam- relapses of inflammatory bowel disease has been ples were passed in solid SM ID medium (Salmonella reported.X In addition, Salmonella may cause appendici- Identification Agar, Biomerieux-Marcy D’Etoile, Paris, tis by direct invasion of the appendix.9 No reports of animal or human infections caused by Salmonella veneziana are currently available, although some cases of human infection have been diagnosed by stool cultures in Italy To the authors’ knowledge, no gut biopsies were taken in these cases, and nothing was known about environmental sources, clinical manifesta- tions, host predisposing factors, drug susceptibility pat- terns, or duration of microbial shedding in feces. Because of the lack of information, the natural history of infection caused by S. veneziana is not yet under- stood. This report presents a case of S. veneziana acute terminal ileitis posing problems in differential diagnosis with Crohn’s disease. A previously health 39-year-old Italian male with a 6 day complaint of watery diarrhea (3-6 stools/d; mean, 4) and remittent fever (max. 38.5”C), was referred to Pistoia Hospital because of a right-sided lower abdominal pain that had developed abruptly. His history was negative for digestive tract diseases or exposure to risk factors, includ- ing animal contacts, exotic travels, insect bites, or inges- tion of suspect food. Physical examination revealed a soft mass in the right lower abdomen with tenderness and increased bowel movements. Sonography showed a homogeneous thick- ening of the terminal ileum, with exudation involving *Infectious Diseases Unit, *Unit of Pathology, *Unit of Internal Medi- cine, ‘Laboratory for Microbiology and Virology, and ‘General Practi- tioner, Pistoia Hospital, Pistoia, Italy. Address correspondence to Dr. Daniele Dionisio, Infectious Diseases Unit, Pistoia Hospital, Piazza Giovanni XXIII 5 1100, Pistoia, Italy. E-mail: [email protected]. Figure 1. Sonography. Homogeneous thickening of the terminal ileum. 225 226 International Journal of Infectious Diseases / Volume 5, Number 4,200l Table 1. Susceptibility Pattern of the Sa/mone//e veneziena Strain DISCUSSION Drug M/C (pg/m L) Susceptibility Ileitis caused by nontyphoidal Salmonella is not infre- Amoxicillin-clavulanate 58 S Ampicillin 18 S quently reported. 4,5 Differential diagnosis with Crohn’s ktreonam 12 S disease depends on microbial isolation, on the extent and Cephalothin 18 S recurrence of fecal blood, and mainly, on typing of the Cefepime 58 S Ciprofloxacin I1 S inflammatory infiltration, which is neutrophilic in sal- Chloramphenicol 28 S monellosis, as opposed to the lymphocyte-plasmacyte, Gentamicin $4 S lmipenem 24 S and typically, granulomatous infiltration in Crohn’s dis- Meropenem 14 S ease.‘,” Mezlocillin 5 16 S The case described here is the first reported infec- Netilmicin 58 S tion attributable to S. veneziana, possibly leading to a Piperacillin 516 S Tetracycline $4 S misdiagnosis of Crohn’s disease. The role of S. ueneziana Co-trimoxezole $0.5 S was supported by the patient’s recovery following anti- MIC = minimum inhibitory concentration; S = susceptible. biotic treatment according to the results of drug sus- ceptibility testing. This was consistent with the absence of blood in the feces. France) at 36°C for 18 to 24 hours. Identification of The finding of lymphocyte-plasmacyte infiltration is colonies and drug susceptibility testing were performed difficult to explain; although, consistent with the late per- by Scepter System (Becton-Dickinson, Milan, Italy). Mini- formance of endoscopy, replacement from an initial neu- mum inhibitory concentration (MIC) results are listed in trophil infiltration cannot be excluded. Table 1. Serotyping was carried out at the Centre for Findings reported here may further the understand- Pathogenic Enterobacteria, Department of Experimental ing of the natural history of infection caused by S. Pathology, University of Pisa, Pisa, Italy, by using slide veneziana by substantiating the harmful role of the agent agglutination with polyvalent and monovalent anti-0 and in humans and providing some insight into the spectrum anti-H sera (Sanofi Pasteur, Milan, Italy). of the clinical and pathologic manifestations. Moreover, Stools were negative for either manifest or occult the data suggest that such a microbial etiology should blood. Results of chest radiography, electrocardiogram, not be ruled out, even if only lymphocyte-plasmacyte serum immunoglobulins, as well as serum antibodies for infiltration is documented. Possible correlation of this Salmonella and Brucella were negative. Biochemical tests finding with the late stage of infection is of interest and showed a white blood cell increase (13,8OO/p,L with deserves further study. 74.7% neutrophils) and markedly raised inflammatory indices. Combination treatment with standard intravenous piperacillin-tazobactam and amikacin led to the disap- ACKNOWLEDGMENT pearance of fever within 24 hours. During the subsequent days the white cell count returned to normal and the fre- The authors thank Dr. Paola Valentini (Centre for Pathogenic Enterobacteria,Department of Experimental Pathology,University quency and consistency of stool improved, but tenderness of Pisa,Pisa, Italy) for technical advice and information about S. still was evoked in the right lower abdomen. At that time veneziana infection. antibiotics were changed to standard intravenous ciprofloxacin. Four weeks after the clinical onset, lower endoscopy REFERENCES revealed swelling and hyperemia in the mucosa of the 1. Miller SI, Pegues DA. Salmonella species, including Salmo- terminal Ileum, which showed a stiff wall. Biopsy samples nella typbi. In: Mandell GL, Bennett JE,DoIin R, eds. MandeIl, were taken from the site and examined by light Douglas, and Bennet’s principles and practice of infectious microscopy. Focal ulcerations with edema and a marked diseases. 5th ed. Philadelphia: Churchill Livingstone, lymphocyte-plasmacyte infiltration involving the sub- 2000:2344-2363. mucosa were observed. No granulomas were found. 2. Galyov EE, Wood MW, Rosqvist R, et al. A secreted effec- tor protein of Salmonella dublin is translocated into The patient was discharged without diarrhea and eukaryotic cells and mediates inflammation and fluid with negative stool cultures on day 31 after the clinical secretion in infected ileal mucosa. Mol Microbial 1997; onset. Five weeks later the abdominal tenderness disap- 25:903-912. peared, and a normalized sonographic pattern of the ter- 3. Darwin KH, Miller VL. Molecular basis of the interaction of minal ileum was documented. During the l&month Salmonella with the intestinal mucosa. Clin Microbial Rev 1999;12:405-428. follow-up, the inflammatory indices rapidly returned to 4. Deutsch A, Wasserman D, Ruchelli E, Johnson J, Broussard normal, and the patient was in good health, with no signs DL. An uncommon presentation of Salmonella. Pediatr of either clinical or laboratory relapse. Emerg Care 1996; 12:285-287. Sulmonella veneziana Ileitis Resembling Crohn’s Disease / Dionisio et al 227 5. Balthazar EJ, Charles HW, Megibow AJ. Salmonella- and 9. Van Noyen R, Selderslaghs R, Bekaert J, Wauters G, Vandepitte Shigella-induced ileitis: CT findings in four patients. J Com- J. Causative role of Yersiniu and other enteric pathogens in put Assist Tomogr 1996; 20:375-378. the appendicular syndrome. Eur J Clin Microbial Infect Dis 6. Puylaert JB, Vermeijden RJ, van der Werf SD, Doombos L, 1991; 10:735-741. Koumans RK. Incidence and sonographic diagnosis of bacterial 10. Popoff MY, Le Minor L. Antigenic formulas of the Salmo- ileocaecitis masquemding as appendicitis. Iancet 1989; 2:&4-86. nella serovars. WHO Collaborating Centre for Reference 7. Dagash M, Hayek T, Gallimidi Z,Yassin K, Book JG. Transient and Research on Salmonella. Paris, France: Institut Pasteur, radiological and colonoscopic features of inflammatory 1997. bowel disease in a patient with severe Salmonella gastro- 11. Tanaka M, Riddell RH, Saito H, Soma Y, Hidaka H, Kudo H. enteritis. Am J Gastroenterol 1997; 92:349-351. Morphologic criteria applicable to biopsy specimens for 8. Weber P Koch M, Heizmann WR, Scheurlen M, Jenss H, Hart- effective distinction of inflammatory bowel disease from mann E Microbic superinfection in relapse of inflammatory other forms of colitis and of Crohn’s disease from ulcerative bowel disease. J Clin Gastroenterol 1992; 14:302-308. colitis. Stand J Gastroenterol 1999; 34:55-67. .
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