GI involvement in disseminated Mycobacterium genavense: endoscopy and histology

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was recommended, but the patient continued to use naproxen without change. Repeat EGD 2 months later revealed that the 5-cm gastric antral ulcer, which was now clean based, persisted (B). He refused follow-up evaluation and was subsequently hospitalized 4 months from the time of his initial presentation with emaciation, watery postprandial diarrhea, prominent halitosis, and a 60pound weight loss (despite reportedly excellent oral intake and a ravenous appetite). Repeat EGD at this time revealed mild erosive gastritis and thickened erythematous folds surrounding an ulcerated 4-cm gastrocolic fistula (C) along the distal gastric antrum. The fistula orifice (D) led to the splenic flexure of the colon (E). Repeat gastric biopsy specimens showed only benign inflammation, and a fasting serum gastrin level was normal. It was suspected that previous endoscopic treatment of the gastric ulcer was not responsible for the fistula formation because the initial

follow-up EGD revealed a clean-based ulcer. After intensive nutritional support (via surgical jejunostomy), the patient underwent a partial gastrectomy with Billroth II gastrojejunostomy and segmental transverse colon resection. The patient recovered uneventfully, his symptoms resolved, and he has regained the weight that he had previously lost. DISCLOSURE The author disclosed no financial relationships relevant to this publication. Joseph C. Yarze, MD, FACP, FACG, FASGE, AGAF, Gastroenterology Associates of Northern NY, Glens Falls, New York, USA doi:10.1016/j.gie.2011.03.1254

Commentary Gastrocolic fistula has a variety of causes including malignancy of the stomach and colon, peptic ulcer disease, foreign body ingestion, radiation, and endoscopic and surgical procedures. Symptoms can be explained by the bidirectionality of the fistulous tract: halitosis, weight loss, and diarrhea from microbial overgrowth as bacteria and their metabolic products pass retrograde from the colon into the stomach and then down the small intestine; and diarrhea with passage of recognizable foodstuffs as the small intestine is bypassed and food directly enters the colon to exit undigested. NSAIDs are well recognized to cause GI ulceration, which rarely has been documented to result in gastrocolic or even gastroaortic fistula formation. This patient exhibited particularly poor judgment in not following his physician’s recommendations to halt NSAID treatment with the result that his gastric ulcer perforated into the colon, necessitating gastric and colonic resection. His ulcer also seemed to have a mind of its own and followed the advice of Ralph Waldo Emerson not to go where the path may lead but rather to go instead where there is no path and leave a trail. The trail exited the stomach and entered the colon, but with the help of the surgeon, all turned out well in the end. Lawrence J. Brandt, MD Associate Editor for Focal Points

GI involvement in disseminated Mycobacterium genavense: endoscopy and histology 1A 34-year-old man ultimately shown to have immunodeficiency and disseminated Mycobacterium genavense associated with protein-losing enteropathy presented with cachexia and generalized weakness. Physical examination revealed a cachectic man with generalized muscle wasting and a protuberant abdomen with shifting dullness, but without tenderness, rebound, or guarding. Laboratory data showed the following: white blood cell count, 4.8 K/␮L (normal range 3.98–10.14 K/␮L); hemoglobin, 13.6 g/dL (normal range 11.2–15.7 g/dL); platelet count, 73,000/␮L (normal range 173–369 K/␮L); sodium, 134 mmol/L (normal range 135–144 mmol/L); potassium, 3.7 mmol/L (3.3–5.1 mmol/L); urea nitrogen, 25 mg/dL (normal range 8–22 mg/dL); creatinine, 0.86 mg/dL (normal range 0.56– 1.16 mg/dL); alkaline phosphatase, 153 U/L (normal range 37– 116 IU/L); alanine aminotransferase, 84 U/L (normal range 6–41 U/L); aspartate aminotransferase, 120 U/L (normal range 9–34 688 GASTROINTESTINAL ENDOSCOPY Volume 74, No. 3 : 2011

U/L); total protein, 3.9 g/dL (normal range 6.4 – 8.2 g/dL); albumin, 1.4 g/dL (normal range 2.5– 4.8 g/dL); prealbumin, 15 mg/dL (normal range 17–39 mg/dL); 24-hour stool ␣1- antitrypsin level, 93 mg/dL (normal ⬍54 mg/ dL); trace urinary protein; negative HIV test results; IgG, 377 mg/dL (normal range 642–1730 mg/dL); IgA, 20 mg/dL (normal range, 91– 499 mg/dL); IgM, less than 21 mg/dL (normal 34 –342 mg/dL); and IgE, 2.4 mg/dL (normal range 0 –90.0 IU/mL). CT scan of the abdomen and pelvis revealed nonspecific small-bowel thickening, sigmoid mucosal enhancement, and extensive mesenteric adenopathy (A). EGD revealed diffuse esophageal mucosal denudation and friability, mild thickening of the gastric and duodenal folds (B). Colonoscopy (C) showed mucosal edema, absence of vasculature, and loss of haustral folds. Biopsy specimens (D,E) revealed www.giejournal.org

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expansion of the lamina propria, which was filled with foamy macrophages that contained acid-filled bacilli, subsequently shown to be M genavense.

DISCLOSURE: All authors disclosed no financial relationships relevant to this publication. This submission was supported by the www.giejournal.org

Intramural Research Programs of the NIDDK, NIAID, and NIH. Manish Arora, MD, Digestive Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland/University of Maryland, Baltimore, Maryland, Gulbu Uzel, MD, Immunopathogenesis Section, National Institute of Allergy and Infectious DisVolume 74, No. 3 : 2011 GASTROINTESTINAL ENDOSCOPY 689

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eases, National Institutes of Health, Bethesda, Maryland, Yvonne R. Shea, MD, Microbiology Section, National Institutes of Health, Bethesda, Maryland, David E. Kleiner, MD, Laboratory of Pathology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, Steven M. Holland, MD, Immunopathogenesis Section, National Institute of Al-

lergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, Theo Heller, MD, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA doi:10.1016/j.gie.2011.04.021

Commentary Atypical mycobacterial infection was described in the mid-1950s, although it was the AIDS epidemic that brought these nontuberculous mycobacteria to the familiarity of most clinicians. In 1959, the botanist Ernest Runyon grouped these organisms into 4 groups: photochromogens, which develop pigments in or after being exposed to light (eg, Mycobacterium kansasii); scotochromogens, which become pigmented in darkness (eg, Mycobacterium scrofulaceum); nonchromogens, a group of prevalent opportunistic pathogens that includes Mycobacterium avium complex (MAC) as well as M genavense; and finally, the rapid growers (eg, Mycobacterium fortuitim). M genavense, described by Bottger et al in 1992, is a fastidious organism that has a slow growth rate in liquid media, requiring 3 to 12 weeks to be identified. Although it can grow on solid media, it does not grow on standard solid media like Lowenstein-Jensen. M genavense infections occur only rarely in persons other than AIDS patients, although all patients infected with this organism are immunocompromised. M genavense resembles MAC in its clinical infection patterns and is a good organism to keep in mind when faced with an AIDS patient who has diarrhea, fever, and lymphadenopathy. Interestingly, M genavense is common in birds, especially passerines (which include songbirds and sparrows) and psittacines (which include parrots and parakeets). We must wage war against M genavense, the name of which derives from Geneva, the source of the first isolate. But must we respect the conventions also named after the same city in this battle? There are 4 Geneva conventions (and 3 protocols), which set the standards for humanitarian treatment of the victims of war and were conceived by Henri Dunant after his witnessing the horrors of war at the Battle of Solferino in 1859. I would treat the patient as humanely and kindly as possible and bring all force to bear to annihilate the invader. John F. Kennedy said “Mankind must put an end to war before war puts an end to mankind.” In this case, a battle won will enable man’s survival . . . and we can then deal with the immunocompromise that allowed the invasion to occur. Lawrence J. Brandt, MD Associate Editor for Focal Points

A case of beef tapeworm (Taenia saginata) infection observed by using video capsule endoscopy and radiography (with videos) A 50-year-old Japanese man was referred for treatment of cestodiasis. He was asymptomatic, and all laboratory study results were normal, including hemoglobin, albumin, liver biochemical profile, and basic metabolic panel. The patient first noticed excretion of proglottids in his stool while living in Indonesia 3 years earlier, at which time he was treated with an anti-helminthic agent. One month later he again noticed proglottids in his stool. Two years later, he was diagnosed as having a GI stromal tumor and had a partial gastrectomy. After mentioning to his surgeon that he passed proglottids in his stool he was referred for evaluation. A small bowel series was performed with water soluble radiopaque contrast medium, and meandering tapeworm movement was observed (A; Video 1, available online at www.giejournal.org). An excreted proglottid was captured, and counting of its uterine branches under the microscope, it was determined to be Taenia saginata; excretion of the scolex 690 GASTROINTESTINAL ENDOSCOPY Volume 74, No. 3 : 2011

was not confirmed. Videocapsule endoscopy (Endo capsule EC-1; Olympus Medical Systems, Tokyo, Japan) was performed to determine whether there were any residual parasites. Indeed, residual tapeworm in the video capsule endoscopy (B; Video 2, available online at www.giejournal.org) and appeared similar to that seen on the radiologic study. DISCLOSURE All authors disclosed no financial relationships relevant to this publication. Naoki Hosoe, MD, PhD, Hiroyuki Imaeda, MD, PhD, Center for Diagnostic and Therapeutic Endoscopy, Susumu Okamoto, MD, PhD, Rieko Bessho, MD, Riko Saito, MD, Yosuke Ida, MD, Division of Gastroenterology and Hepatology, Department of Internal Medicine, Seiki Kobayashi, PhD, Dewww.giejournal.org