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Enterococcus gastritis
HUMAN PATHOLOGY
Volume 34, No. 9 (September 2003)
ENTEROCOCCUS GASTRITIS HALA M. T. EL-ZIMAITY, MD, JACQUELINE RAMCHATESINGH, MD, JILL E. CLARRIDGE, PHD, SUHAIB ABUDAYYEH, MD, MICHAEL S. OSATO, PHD, AND DAVID Y. GRAHAM, MD Helicobacter pylori infection is the most common cause of gastritis with its associated sequelae. Gastritis secondary to other bacteria is rare. This report describes Enterococcus-associated gastritis in a 59year-old diabetic man. Nine months after receiving treatment for H. pylori-associated gastritis, he underwent endoscopy to confirm H. pylori eradication and to evaluate the status of previously seen ulcers. Mucosal biopsy specimens revealed severe active but focal gastritis adjacent to gram-positive coccobacilli in short to long chains with no H. pylori. Culture grew an Enterococcus similar to E. hirae and E.
durans. No treatment was given, and endoscopy done 2 months later showed complete resolution of the gastritis and absence of H. pylori or enterococci. Our patient’s gastritis represents a previously undescribed manifestation of Enterococcus infection. It is possible that the presence of NSAID gastric mucosal injury and diabetes predisposed this individual to the development of transient Enterococcus gastritis. HUM PATHOL 34:944-945. © 2003 Elsevier Inc. All rights reserved. Key words: Helicobacter pylori, gastritis, Enterococcus. Abbreviations: NSAID, nonsteroidal anti-inflammatory drug.
Enterococci are part of the normal bowel flora of both humans and animals1 and are currently the second-leading cause of nosocomial infections,2,3 particularly among debilitated patients and those with severe underlying illness.4,5 Enterococcal infections have generally been associated with infections in the urinary tract, wounds, bacteremia, endocarditis, meningitis, and arthritis, as well as contamination of intravenous or intra-arterial lines.1,3,6 Enterococcus durans and E. hirae are uncommon human pathogens.7 We describe a patient with active gastritis associated with an Enterococcus species biochemically related to E. hirae and E. durans.
showed complete resolution of the previously seen gastritis and no change in the intestinal metaplasia in the antrum. Parietal cells were plentiful in the corpus. Gastric cultures at the second endoscopy grew an Enterococcus species biochemically related to E. hirae and E. durans. Susceptibility testing showed that the organism was susceptible to vancomycin, tetracycline, clarithromycin, and amoxicillin (minimum inhitory concentration [MIC], ⱕ1 mg/L) and resistant to metronidazole (MIC, 256 mg/L).
CASE REPORT A 59-year-old diabetic man presented with substernal chest pain. He had a history of coronary artery disease, myocardial infarction, percutaneous transluminal coronary angioplasty, and osteoarthritis of both the left and right knees. The pain was relieved with antacids. Upper endoscopy revealed nonsteroidal anti-inflammatory drug (NSAID) gastropathy with small (3 mm) gastric and pyloric ulcers/erosions. Gastric biopsy spedicmens revealed chronic active gastritis with active Helicobacter pylori infection. There was extensive intestinal metaplasia of the antrum. The patient received a 2-week course of quadruple therapy consisting of omeprazole, metronidazole, bismuth, and tetracycline. He was lost to followup. Nine months later he underwent endoscopy to confirm H. pylori eradication and to evaluate the status of the previous gastropathy/ulcers. He had no gastrointestinal complaints at the time of endoscopy. Endoscopy revealed multiple antral erosions. Biopsy specimens were obtained from the normalappearing mucosa of the antrum and corpus for histology, rapid urease testing, and culture. Histology showed focal active gastritis (Fig 1) associated with the presence of diplococci in short to long chains on the mucosal surface (Fig 2). No H. pylori were seen, and the intervening mucosa not directly associated with the diplococci showed no acute inflammation. The patient received no specific treatment. Repeat endoscopy was done 3 months later and was normal except for mild NSAID gastropathy. Gastric biopsy specimens
From the Departments of Medicine and Pathology, Veterans Affairs Medical Center, and Baylor College of Medicine, Houston, TX. Accepted for publication April 9, 2003. Address correspondence and reprint requests to Hala M. T. El-Zimaity, MD, Department of Medicine, V.A. Medical Center (111D), 2002 Holcombe Blvd., Houston, TX 77030. © 2003 Elsevier Inc. All rights reserved. 0046-8177/03/3409-0017$30.00/0 doi:10.1016/S0046-8177(03)00287-9
DISCUSSION Gastric acidity is the main factor determining gastric bacterial flora.8-10 At pH ⬎4, the more acid-tolerant bacteria, such as Lactobacillus and Streptococcus, proliferate, whereas more complex flora proliferate at high pH values.8 Certain bile-resistant organisms (eg, fecal streptococci, enterobacteria, and fecal bacteroids) have been described in the resident gastric flora of achlorhydric patients9 and infrequently in transient hypochlorhydria, such as that following treatment with drugs to inhibit acid secretion.10 Nonetheless, active gastritis is typically not associated with colonization associated with poor acid output.8-12 The presence of histological damage suggests the presence of a pathogen. We have reported a case of asymptomatic enterococcal gastritis limited to the mucosa. Enterococcus is a subgroup of group D streptococci that are differentiated from other streptococci by their ability to grow in the presence of
FIGURE 1. Focal active gastritis. (Carbol fuchsin/Alcian blue/ hematoxylin and eosin; original magnification ⫻ 10.)
944
CASE STUDIES
Our patient’s gastritis represents a previously undescribed manifestation of Enterococcus infection. In this instance the infection was asymptomatic and resolved spontaneously. It is unknown where the infection originated, possibly from poorly prepared food, such as chicken. It is also possible that the mucosal damage caused by the NSAIDs provided a focus for the infection to gain a foothold. Despite the presence of diabetes and a documented enterococcal gastritis, the patient recovered uneventfully. Finding the infection was purely a chance observation. It is unknown how often such events occur and how often an acute but selflimited bacterial gastritis may be responsible for upper gastrointestinal complaints. REFERENCES
FIGURE 2. Diplococci in short to long chains on the mucosal surface. (Carbol fuchsin/Alcian blue/hematoxylin and eosin; oil immersion.)
40% bile and their ability to hydrolyze esculin. In general, enterococci are of low virulence and are differentiated from non-enterococci by their resistance to penicillin. The genus Enterococcus is composed of 12 species: E. avium, E. casseliflavus, E. durans, E. faecalis, E. faecium, E. gallinarum, E. hirae, E. malodoratus, E. mundtii, E. pseudoavium, E. raffinosus, and E. solitarius.3 E. faecalis is most common, being present in up to 90% of clinical isolates.13 E. hirae is a common component of the intestinal flora of several domestic animal species and is known to cause infections in rats and birds. It has also been found in foods of animal origin and in water. E. durans is a rare inhabitant of the gut except in preruminant calves and young chickens.14 Infections in humans associated with E. hirae and E. durans have been rarely reported and when present are usually nosocomial.7
1. Howe RA, Brown NM, Spencer RC: The new threats of Gram positive pathogens: Re-emergence of things past. J Clin Pathol 49:444-449, 1996 2. Hoffmann SA, Moellering RC Jr: The enterococcus: “Putting the bug in our ears.” Ann Intern Med 106:757-761, 1987 3. Vemuri RK, Zervos MJ: Enterococcal infections: The increasing threat of nosocomial spread and drug resistance. Postgrad Med 93:121-128, 1993 4. Tornieporth NG, Roberts RB, John J, et al: Risk factors associated with vancomycin-resistant Enterococcus faecium infection or colonization in 145 matched case patients and control patients. Clin Infect Dis 23:767-772, 1996 5. Lucas GM, Lechtzin N, Puryear DW, et al: Vancomycin-resistant and vancomycin-susceptible enterococcal bacteremia: Comparison of clinical features and outcomes. Clin Infect Dis 26:1127-1133, 1998 6. Stevenson KB, Murray EW, Sarubbi FA: Enterococcal meningitis: Report of four cases and review. Clin Infect Dis 18:233-239, 1994 7. Gilad J, Borer A, Riesenberg K, et al: Enterococcus hirae septicemia in a patient with end-stage renal disease undergoing hemodialysis. Eur J Clin Microbiol Infect Dis 17:576-577, 1998 8. Hill M: Normal and pathological microbial flora of the upper gastrointestinal tract. Scand J Gastroenterol Suppl 111:1-6, 1985 9. Borriello SP, Reed PJ, Dolby JM, et al: Microbial and metabolic profile of achlorhydric stomach: Comparison of pernicious anaemia and hypogammaglobulinaemia. J Clin Pathol 38:946-953, 1985 10. Karmeli Y, Stalnikowitz R, Eliakim R, et al: Conventional dose of omeprazole alters gastric flora. Dig Dis Sci 40:2070-2073, 1995 11. Carboni M, Guadagni S, Pistoia MA, et al: The microflora of the gastric juice after Billroth I and Billroth II partial gastrectomy. Scand J Gastroenterol 21:461-470, 1986 12. Husebye E, Skar V, Hoverstad T, et al: Fasting hypochlorhydria with gram-positive gastric flora is highly prevalent in healthy old people. Gut 33: 1331-1337, 1992 13. Thornsberry C: Emerging resistance in clinically important grampositive cocci. West J Med 164:28-32, 1996 14. Devriese LA, Laurier L, De Herdt P, et al: Enterococcal and streptococcal species isolated from faeces of calves, young cattle and dairy cows. J Appl Bacteriol 72:29-31, 1992
945
Volume 34, No. 9 (September 2003)
ENTEROCOCCUS GASTRITIS HALA M. T. EL-ZIMAITY, MD, JACQUELINE RAMCHATESINGH, MD, JILL E. CLARRIDGE, PHD, SUHAIB ABUDAYYEH, MD, MICHAEL S. OSATO, PHD, AND DAVID Y. GRAHAM, MD Helicobacter pylori infection is the most common cause of gastritis with its associated sequelae. Gastritis secondary to other bacteria is rare. This report describes Enterococcus-associated gastritis in a 59year-old diabetic man. Nine months after receiving treatment for H. pylori-associated gastritis, he underwent endoscopy to confirm H. pylori eradication and to evaluate the status of previously seen ulcers. Mucosal biopsy specimens revealed severe active but focal gastritis adjacent to gram-positive coccobacilli in short to long chains with no H. pylori. Culture grew an Enterococcus similar to E. hirae and E.
durans. No treatment was given, and endoscopy done 2 months later showed complete resolution of the gastritis and absence of H. pylori or enterococci. Our patient’s gastritis represents a previously undescribed manifestation of Enterococcus infection. It is possible that the presence of NSAID gastric mucosal injury and diabetes predisposed this individual to the development of transient Enterococcus gastritis. HUM PATHOL 34:944-945. © 2003 Elsevier Inc. All rights reserved. Key words: Helicobacter pylori, gastritis, Enterococcus. Abbreviations: NSAID, nonsteroidal anti-inflammatory drug.
Enterococci are part of the normal bowel flora of both humans and animals1 and are currently the second-leading cause of nosocomial infections,2,3 particularly among debilitated patients and those with severe underlying illness.4,5 Enterococcal infections have generally been associated with infections in the urinary tract, wounds, bacteremia, endocarditis, meningitis, and arthritis, as well as contamination of intravenous or intra-arterial lines.1,3,6 Enterococcus durans and E. hirae are uncommon human pathogens.7 We describe a patient with active gastritis associated with an Enterococcus species biochemically related to E. hirae and E. durans.
showed complete resolution of the previously seen gastritis and no change in the intestinal metaplasia in the antrum. Parietal cells were plentiful in the corpus. Gastric cultures at the second endoscopy grew an Enterococcus species biochemically related to E. hirae and E. durans. Susceptibility testing showed that the organism was susceptible to vancomycin, tetracycline, clarithromycin, and amoxicillin (minimum inhitory concentration [MIC], ⱕ1 mg/L) and resistant to metronidazole (MIC, 256 mg/L).
CASE REPORT A 59-year-old diabetic man presented with substernal chest pain. He had a history of coronary artery disease, myocardial infarction, percutaneous transluminal coronary angioplasty, and osteoarthritis of both the left and right knees. The pain was relieved with antacids. Upper endoscopy revealed nonsteroidal anti-inflammatory drug (NSAID) gastropathy with small (3 mm) gastric and pyloric ulcers/erosions. Gastric biopsy spedicmens revealed chronic active gastritis with active Helicobacter pylori infection. There was extensive intestinal metaplasia of the antrum. The patient received a 2-week course of quadruple therapy consisting of omeprazole, metronidazole, bismuth, and tetracycline. He was lost to followup. Nine months later he underwent endoscopy to confirm H. pylori eradication and to evaluate the status of the previous gastropathy/ulcers. He had no gastrointestinal complaints at the time of endoscopy. Endoscopy revealed multiple antral erosions. Biopsy specimens were obtained from the normalappearing mucosa of the antrum and corpus for histology, rapid urease testing, and culture. Histology showed focal active gastritis (Fig 1) associated with the presence of diplococci in short to long chains on the mucosal surface (Fig 2). No H. pylori were seen, and the intervening mucosa not directly associated with the diplococci showed no acute inflammation. The patient received no specific treatment. Repeat endoscopy was done 3 months later and was normal except for mild NSAID gastropathy. Gastric biopsy specimens
From the Departments of Medicine and Pathology, Veterans Affairs Medical Center, and Baylor College of Medicine, Houston, TX. Accepted for publication April 9, 2003. Address correspondence and reprint requests to Hala M. T. El-Zimaity, MD, Department of Medicine, V.A. Medical Center (111D), 2002 Holcombe Blvd., Houston, TX 77030. © 2003 Elsevier Inc. All rights reserved. 0046-8177/03/3409-0017$30.00/0 doi:10.1016/S0046-8177(03)00287-9
DISCUSSION Gastric acidity is the main factor determining gastric bacterial flora.8-10 At pH ⬎4, the more acid-tolerant bacteria, such as Lactobacillus and Streptococcus, proliferate, whereas more complex flora proliferate at high pH values.8 Certain bile-resistant organisms (eg, fecal streptococci, enterobacteria, and fecal bacteroids) have been described in the resident gastric flora of achlorhydric patients9 and infrequently in transient hypochlorhydria, such as that following treatment with drugs to inhibit acid secretion.10 Nonetheless, active gastritis is typically not associated with colonization associated with poor acid output.8-12 The presence of histological damage suggests the presence of a pathogen. We have reported a case of asymptomatic enterococcal gastritis limited to the mucosa. Enterococcus is a subgroup of group D streptococci that are differentiated from other streptococci by their ability to grow in the presence of
FIGURE 1. Focal active gastritis. (Carbol fuchsin/Alcian blue/ hematoxylin and eosin; original magnification ⫻ 10.)
944
CASE STUDIES
Our patient’s gastritis represents a previously undescribed manifestation of Enterococcus infection. In this instance the infection was asymptomatic and resolved spontaneously. It is unknown where the infection originated, possibly from poorly prepared food, such as chicken. It is also possible that the mucosal damage caused by the NSAIDs provided a focus for the infection to gain a foothold. Despite the presence of diabetes and a documented enterococcal gastritis, the patient recovered uneventfully. Finding the infection was purely a chance observation. It is unknown how often such events occur and how often an acute but selflimited bacterial gastritis may be responsible for upper gastrointestinal complaints. REFERENCES
FIGURE 2. Diplococci in short to long chains on the mucosal surface. (Carbol fuchsin/Alcian blue/hematoxylin and eosin; oil immersion.)
40% bile and their ability to hydrolyze esculin. In general, enterococci are of low virulence and are differentiated from non-enterococci by their resistance to penicillin. The genus Enterococcus is composed of 12 species: E. avium, E. casseliflavus, E. durans, E. faecalis, E. faecium, E. gallinarum, E. hirae, E. malodoratus, E. mundtii, E. pseudoavium, E. raffinosus, and E. solitarius.3 E. faecalis is most common, being present in up to 90% of clinical isolates.13 E. hirae is a common component of the intestinal flora of several domestic animal species and is known to cause infections in rats and birds. It has also been found in foods of animal origin and in water. E. durans is a rare inhabitant of the gut except in preruminant calves and young chickens.14 Infections in humans associated with E. hirae and E. durans have been rarely reported and when present are usually nosocomial.7
1. Howe RA, Brown NM, Spencer RC: The new threats of Gram positive pathogens: Re-emergence of things past. J Clin Pathol 49:444-449, 1996 2. Hoffmann SA, Moellering RC Jr: The enterococcus: “Putting the bug in our ears.” Ann Intern Med 106:757-761, 1987 3. Vemuri RK, Zervos MJ: Enterococcal infections: The increasing threat of nosocomial spread and drug resistance. Postgrad Med 93:121-128, 1993 4. Tornieporth NG, Roberts RB, John J, et al: Risk factors associated with vancomycin-resistant Enterococcus faecium infection or colonization in 145 matched case patients and control patients. Clin Infect Dis 23:767-772, 1996 5. Lucas GM, Lechtzin N, Puryear DW, et al: Vancomycin-resistant and vancomycin-susceptible enterococcal bacteremia: Comparison of clinical features and outcomes. Clin Infect Dis 26:1127-1133, 1998 6. Stevenson KB, Murray EW, Sarubbi FA: Enterococcal meningitis: Report of four cases and review. Clin Infect Dis 18:233-239, 1994 7. Gilad J, Borer A, Riesenberg K, et al: Enterococcus hirae septicemia in a patient with end-stage renal disease undergoing hemodialysis. Eur J Clin Microbiol Infect Dis 17:576-577, 1998 8. Hill M: Normal and pathological microbial flora of the upper gastrointestinal tract. Scand J Gastroenterol Suppl 111:1-6, 1985 9. Borriello SP, Reed PJ, Dolby JM, et al: Microbial and metabolic profile of achlorhydric stomach: Comparison of pernicious anaemia and hypogammaglobulinaemia. J Clin Pathol 38:946-953, 1985 10. Karmeli Y, Stalnikowitz R, Eliakim R, et al: Conventional dose of omeprazole alters gastric flora. Dig Dis Sci 40:2070-2073, 1995 11. Carboni M, Guadagni S, Pistoia MA, et al: The microflora of the gastric juice after Billroth I and Billroth II partial gastrectomy. Scand J Gastroenterol 21:461-470, 1986 12. Husebye E, Skar V, Hoverstad T, et al: Fasting hypochlorhydria with gram-positive gastric flora is highly prevalent in healthy old people. Gut 33: 1331-1337, 1992 13. Thornsberry C: Emerging resistance in clinically important grampositive cocci. West J Med 164:28-32, 1996 14. Devriese LA, Laurier L, De Herdt P, et al: Enterococcal and streptococcal species isolated from faeces of calves, young cattle and dairy cows. J Appl Bacteriol 72:29-31, 1992
945