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Small intestinal bacterial overgrowth in older people

Published online by Cambridge University Press:  15 June 2015

Syed Amer  and
Huma S Manzar
Syed Amer*
Affiliation:
Department of Internal Medicine, Mayo Clinic, Phoenix, Arizona, USA
Huma S Manzar
Affiliation:
Department of Medicine, Shadan Institute of Medical Sciences, Hyderabad, Telangana, India
*
Address for correspondence: Dr Syed Amer, Department of Medicine, Mayo Clinic, Phoenix, AZ 85054, USA. Email: drsyedamer1@gmail.com
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Summary

Small intestinal bacterial overgrowth (SIBO) is a condition in which non-native bacteria and/or native bacteria are present in increased numbers in the small bowel, resulting in excessive fermentation, inflammation or malabsorption. Patients with SIBO vary in presentation, from being only mildly symptomatic to suffering from chronic diarrhoea, weight loss and malabsorption. A number of diagnostic tests are currently available, with aspiration of the small intestinal fluid being the gold standard. Treatment encompasses a multimodal approach including treatment of the underlying disease, nutritional support and antibiotic therapy. In this review, we discuss the risk factors, clinical manifestations, diagnosis and treatment of SIBO in older people.

Keywords

small intestinal bacterial overgrowthdiarrhoeabloatingaspiratebreath testantibiotics

Information

Type
Review Article
Information
Reviews in Clinical Gerontology , Volume 25 , Issue 2 , May 2015 , pp. 81 - 85
Copyright
Copyright © Cambridge University Press 2015 

Introduction

Small intestinal bacterial overgrowth (SIBO) is defined as any condition in which part of the small bowel harbours for a long time bacterial counts over 105 colony-forming units/ml (CFU/ml). Bacterial proliferation deprives the host of macro- and micronutrients. Reference Bouhnik, Alain and Attar1 In spite of being a common cause of malabsorption, it remains an under-recognized clinical syndrome in older people. The exact prevalence is unknown, with reports varying considerably from 2.5 to 90% in older adults with lactose intolerance. Reference Almeida, Kim and Stoita2

Risk factors and predisposition to SIBO

Advanced age is an independent risk factor for SIBO. It is not clear if overgrowth results from the ageing process itself and age-related changes in intestinal motility, or if it is a consequence of achlorhydria due to underlying gastric disease or use of acid neutralizing agents. Early studies found that SIBO was a common (and often unrecognized) cause of malabsorption in the elderly population and that many patients did not have an obvious predisposing factor, such as a blind loop. Reference McEvoy, Dutton and James3 More recent studies have reported SIBO in asymptomatic elderly people residing in the community. These patients, although asymptomatic, had lower weights and body mass indices (BMI) than expected, and treatment with antibiotics increased both weight and BMI. Reference Parlesak, Klein and Schecher4 Interestingly, Mitsui et al. reported SIBO (diagnosed by glucose hydrogen breath test) in 25.6% of disabled older adults, but none in healthy older adults. Reference Mitsui, Shimaoka and Goto5 Risk factors for SIBO are summarized in Table 1. The bacteria in SIBO are similar to those found in the normal colon and certain organisms are commonly responsible (summarized in Table 2).

Table 1.

Risk factors for development of SIBO

Table 2.

Organisms in SIBO

Effects of SIBO on intestinal structure

Histological appearance of the small intestine in SIBO is usually not significantly altered. However, in some cases SIBO is associated with subtotal villous atrophy and increased cellularity in the lamina propria, which may be confused with coeliac disease. Focal areas of ulceration and erosions also may be seen. The degree of mucosal inflammation can vary from mild to severe. Epithelial cell injury and inflammation may ultimately impair absorptive function. Electron microscopy studies of experimental animals with SIBO have described enterocyte abnormalities, such as vacuolization of microvillus membranes and mitochondrial swelling. Reference Toskes, Giannella and Jervis22

Mechanism of malabsorption

Impaired absorption of nutrients in SIBO results from either maldigestion in the intestinal lumen, or from malabsorption at the level of the intestinal microvillus membrane due to enterocyte damage. Carbohydrate malabsorption in SIBO results from the intraluminal degradation of sugars by enteric bacteria leading to the production of short-chain fatty acids, carbon dioxide, hydrogen and methane, which may be associated with acidic stools, abdominal distension and flatulence. Another mechanism that leads to carbohydrate malabsorption in SIBO is by reducing the brush-border disaccharidase levels. Reference Sherman, Wesley and Forstner23

Fat malabsorption results from bacterial deconjugation of bile acids and the toxic effect of free bile acids on the intestinal mucosa. Reference Tabaqchali, Hatzioannou and Booth24 Hydroxylated fatty acids (and free bile acids) stimulate the secretion of water and electrolytes, leading to diarrhoea. Fat malabsorption may lead to weight loss, steatorrhoea and deficiencies of fat-soluble vitamins A, D, E and K. Protein malabsorption probably results from decreased mucosal uptake of amino acids and the intraluminal degradation of protein precursors by bacteria. Reference Sherman and Lichtman25 SIBO may also be associated with a reversible form of protein-losing enteropathy. Vitamin B12 malabsorption results from anaerobes that can utilize vitamin B12 coupled to intrinsic factor. Reference Giannella, Broitman and Zamchek26 Malabsorption of vitamin B12 may result in anaemia and neurological disturbances.

Clinical features

Clinical features in SIBO can be variable ranging from the asymptomatic, to presence of only nutrient deficiencies, to extreme weight loss with failure to thrive. Classic manifestations include anorexia, bloating or flatulence, abdominal discomfort, pain and diarrhoea. Complaints in older patients may be atypical and may even resemble gradual deterioration in health, falsely attributed to ageing. Some patients may report improvement in abdominal complaints following a recent antibiotic course prescribed for an unrelated respiratory or urinary infection.

Patients with vitamin B12 deficiency can present with neurological symptoms, central or peripheral neuropathy, and symptoms of anaemia, such as fatigue, breathlessness and chest pain. Those with fat-soluble vitamin deficiency can present with night blindness (in vitamin A deficiency) and metabolic bone disease (in vitamin D deficiency). Osteoporosis is another well-recognized complication of SIBO.*Reference Stefano, Veneto, Malservisi and Corazza27, Reference Stotzer, Johansson and Mellstrom28

Diagnosis

The diagnosis of SIBO should be considered in any patient with malabsorption and a predisposing condition.

Aspiration

The gold standard test for the diagnosis of SIBO is aspiration of small intestinal fluid with culture and bacterial counts of the aspirate; presence of more than 105 CFU/ml of duodenal aspirate is considered diagnostic. However, it is time consuming, invasive and costly. Other potential problems with aspiration of small intestinal fluid include contamination of the aspirate with bacteria from the mouth, and technical difficulties with transport and culture of the aspirate.

Breath tests

Breath tests are simple and non-invasive, and therefore are more attractive than duodenal intubation or endoscopy for collecting intestinal aspirates. Moreover, older patients tolerate breath tests well. For reliable testing the patients should be advised to avoid high-fibre or carbohydrate-rich foods for at least a day prior to the test.

A glucose hydrogen breath test is safe and easy to perform in the out-patient setting. It evaluates carbohydrate malabsorption. Normally, glucose is absorbed completely in the upper small intestine; with bacterial overgrowth, however, the glucose is cleaved by bacteria into carbon dioxide and hydrogen. The hydrogen is measured in the exhaled breath (at baseline and then every 30 minutes for 2 hours); a rise of 20 parts per million (p.p.m.) above the baseline is regarded as diagnostic of SIBO. Fasting breath hydrogen levels of more than 20 p.p.m. also are considered positive. The lactulose hydrogen breath test is based on a principle similar to that of the glucose hydrogen breath test. Lactulose is a disaccharide that is not absorbed in the small intestine but is metabolized by bacteria in the proximal colon, producing a late peak in exhaled hydrogen. In the presence of bacterial overgrowth, an early hydrogen peak is observed.

Additional tests to evaluate anaemia or nutrient deficiencies and their cause may be required; faecal fat collection may help confirm steatorrhoea; radiological tests may help diagnose anatomical abnormalities such as diverticulae or fistula. Differential diagnosis of SIBO is summarized in Table 3.

Table 3.

Differential diagnosis of SIBO

Treatment

Treatment of SIBO consists of a multimodal approach including treatment of the underlying disease, nutritional support and antibiotic therapy. SIBO due to sluggish motility should be treated with medications to enhance motility to eliminate and prevent relapse. Drugs that reduce motility (narcotics, benzodiazepines, anti-motility agents) commonly prescribed to elderly patients should be discontinued. Attention should be given to the patient's nutritional state and any vitamin deficiency should be corrected.

As prolonged or excessive acid suppression may be a contributing factor for the development of symptoms of SIBO, the use of acid suppressive medication should be minimized to the lowest possible dose for the condition being treated and for the shortest duration. Any predisposing anatomical or functional abnormality should be corrected when possible.

There are no controlled trials to guide the duration of treatment or management of recurrent SIBO and recommendations are generally based on clinical experience. Antibiotics that have been found to be effective include metronidazole, rifaximin, amoxicillin, amoxicillin-clavulanate, ciprofloxacin, tetracycline and cotrimoxazole. Therapy is usually given initially for two weeks and then clinical response is assessed; it may be useful to repeat a breath test or culture of small intestinal aspirate. Many patients with an underlying anatomical or motility disorder require permanent antibiotic treatment; in such patients, it is usual to rotate antibiotic treatment every two weeks or, alternatively, to give antibiotics for two of every four weeks. Continuous treatment with a single agent can lead to antibiotic resistance or to side-effects associated with long-term use, such as peripheral neuropathy in patients given metronidazole.

The somatostatin analogue octreotide stimulates intestinal motor activity when administered at low doses. It has been reported to be effective in SIBO associated with scleroderma. Reference Soudah, Hasler and Owyang29

Probiotic therapy is a logical and attractive approach to the management of SIBO. The impact of probiotic yogurt administration for 4 weeks was studied in healthy older community subjects; normalization of the various cytokine responses and modulation of activation markers in blood phagocytes became more apparent in the group with a positive breath test. Reference Schiffrin, Parlesak and Bode30

Conclusion

Elderly patients have a higher prevalence of malnutrition. SIBO is often an under-recognized cause of malabsorption in the older population, commonly mistaken for other disorders. In any cause of malnutrition or weight loss in an elderly patient that is not fully explained, it may be worthwhile to exclude the diagnosis of SIBO. Treatment not only has the potential to improve patients’ wellbeing and quality of life, but also avoids unnecessary costs and treatment for alternate erroneous diagnoses.

Conflict of interest

The author declares that there is no conflict of interest.

References

1 Bouhnik, Y, Alain, S, Attar, A et al. Bacterial populations contaminating the upper gut in patients with small intestinal bacterial overgrowth syndrome. Am J Gastroenterol 1999; 94: 1327–31.Google Scholar
2 Almeida, JA, Kim, R, Stoita, A et al. Lactose malabsorption in the elderly, role of small intestinal bacterial overgrowth. Scand J Gastroenterol 2008; 43: 146–54.Google Scholar
3 McEvoy, A, Dutton, J, James, OF. Bacterial contamination of the small intestine is an important cause of occult malabsorption in the elderly. Br Med J (Clin Res Ed) 1983; 287: 789–93.Google Scholar
4 Parlesak, A, Klein, B, Schecher, K et al. Prevalence of small bowel bacterial overgrowth and its association with nutrition intake in non-hospitalised older adults. J Am Geriatr Soc 2003; 51: 768–73.Google Scholar
5 Mitsui, T, Shimaoka, K, Goto, Y et al. Small bowel bacterial overgrowth is not seen in healthy adults but is in disabled older adults. Hepatogastroenterology 2006; 53: 82–85.Google Scholar
6 Goldstein, F, Wirts, CW, Kowlessar, OD. Diabetic diarrhea and steatorrhea: Microbiologic and clinical observations. Ann Intern Med 1970; 72: 215–18.Google Scholar
7 Kahn, IJ, Jeffries, GH, Sleisenger, MH. Malabsorption in intestinal scleroderma: correction by antibiotics. N Engl J Med 1966; 274: 1339–44.Google Scholar
8 Tursi, A, Brandimarte, G, Giorgetti, G. High prevalence of small intestinal bacterial overgrowth in celiac patients with persistence of gastrointestinal symptoms after gluten withdrawal. Am J Gastroenterol 2003; 98: 839–43.Google Scholar
9 Pearson, AJ, Brezechwa-Ajdukiewicz, A, McCarthy, CF. Intestinal pseudo-obstruction with bacterial overgrowth in the small intestine. Am J Dig Dis 1969; 14: 200–5.Google Scholar
10 Pereira, SP, Gainsborough, N, Dowling, RH. Drug-induced hypochlorhydria causes high duodenal bacterial counts in the elderly. Aliment Pharmacol Ther 1998; 12: 99–104.Google Scholar
11 Browning, GG, Buchan, KA, Mackay, C. The effect of vagotomy and drainage on the small bowel flora. Gut 1974; 15: 139–42.Google Scholar
12 Gunnarsdottir, SA, Sadik, R, Shev, S et al. Small intestinal motility disturbances and bacterial overgrowth in patients with liver cirrhosis and portal hypertension. Am J Gastroenterol 2003; 98: 1362–70.Google Scholar
13 Lembeke, B, Kraus, B, Lankisch, PG. Small intestinal function in chronic relapsing pancreatitis. Hepatogastroenterology 1985; 32: 149–51.Google Scholar
14 Strid, H, Simren, M, Stotzer, PO et al. Patients with chronic renal failure have abnormal small intestinal motility and a high prevalence of small intestinal bacterial overgrowth. Digestion 2003; 67: 129–37.Google Scholar
15 Husebye, E, Skar, V, Hoverstad, T et al. Abnormal intestinal motor patterns explain enteric colonization with gram-negative bacilli in late radiation enteropathy. Gastroenterology 1995; 109: 1078–89.Google Scholar
16 Henriksson, AE, Blomquist, L, Nord, CE et al. Small intestinal bacterial overgrowth in patients with rheumatoid arthritis. Ann Rheum Dis 1993; 52: 503–10.Google Scholar
17 Weinstock, LB, Klutke, CG, Lin, HC. Small intestinal bacterial overgrowth in patients with interstitial cystitis and gastrointestinal symptoms. Dig Dis Sci 2007; 53: 1246–51.Google Scholar
18 Parodi, A, Paolino, S, Greco, A et al. Small intestinal bacterial overgrowth in rosacea: clinical effectiveness of its eradication. Clin Gastroenterol Hepatol 2008; 6: 759–64.Google Scholar
19 Sabate, JM, Jouet, P, Harnois, F et al. High prevalence of small intestinal bacterial overgrowth in patients with morbid obesity: a contributor to severe hepatic steatosis. Obes Surg 2008; 18: 371–77.Google Scholar
20 Pimentel, M, Wallace, D, Hallegua, D et al. A link between irritable bowel syndrome and fibromyalgia may be related to findings on lactulose breath testing. Ann Rheum Dis 2004; 63: 450–52.Google Scholar
21 Resmini, E, Parodi, A, Savarino, V et al. Evidence of prolonged orocecal transit time and small bowel bacterial overgrowth in acromegalic patients. J Clin Endocrinol Metab 2007; 92: 2119–24.Google Scholar
22 Toskes, PP, Giannella, RA, Jervis, HR et al. Small intestinal mucosal injury in the experimental blind loop syndrome. Light- and electron-microscopic and histochemical studies. Gastroenterology 1975; 68: 193–203.Google Scholar
23 Sherman, P, Wesley, A, Forstner, G. Sequential disaccharidase loss in rat intestinal blind loops: Impact of malnutrition. Am J Physiol 1985; 248: G626–32.Google Scholar
24 Tabaqchali, S, Hatzioannou, J, Booth, CC. Bile salt deconjugation and steatorrhoea in patients with the stagnant loop syndrome. Lancet 1968; 2: 12–16.Google Scholar
25 Sherman, P, Lichtman, S. Small bowel bacterial overgrowth syndrome. Dig Dis 1987; 5: 157–71.Google Scholar
26 Giannella, RA, Broitman, SA, Zamchek, N. Competition between bacteria and intrinsic factor for vitamin B. Gastroenterology 1972; 62: 255–60.Google Scholar
27Di Stefano, M, Veneto, G, Malservisi, S, Corazza, GR. Small intestinal bacterial overgrowth and metabolic bone disease. Dig Dis Sci 2001; 46: 1077–82.Google Scholar
28 Stotzer, PO, Johansson, C, Mellstrom, D et al. Bone mineral density in patients with small intestinal bacterial overgrowth. Hepatogastroenterology 2003; 50: 1415–18.Google Scholar
29 Soudah, HC, Hasler, WL, Owyang, C. Effect of octreotide on intestinal motility and bacterial overgrowth in scleroderma. N Engl J Med 1991; 325: 1461–67.Google Scholar
30 Schiffrin, EJ, Parlesak, A, Bode, C. Probiotic yogurt in the elderly with intestinal bacterial overgrowth: endotoxaemia and innate immune functions. Br J Nutr 2009; 101: 961–66.Google Scholar
Figure 0

Table 1. Risk factors for development of SIBO

Figure 1

Table 2. Organisms in SIBO

Figure 2

Table 3. Differential diagnosis of SIBO