Please enter verification code
Confirm
Microbiology of Diabetic Foot Ulcer with Special Reference to ESBL Infections
American Journal of Clinical and Experimental Medicine
Volume 3, Issue 1, January 2015, Pages: 6-23
Received: Dec. 7, 2014; Accepted: Dec. 17, 2014; Published: Jan. 26, 2015
Views 3474      Downloads 349
Authors
Mohammad Zubair, Rajiv Gandhi Centre for Diabetes and Endocrinology, Faculty of Medicine, J.N. Medical College, Aligarh Muslim University, Aligarh 202002, India
Abida Malik, Department of Microbiology, Faculty of Medicine, J.N. Medical College, Aligarh Muslim University, Aligarh, India
Jamal Ahmad, Rajiv Gandhi Centre for Diabetes and Endocrinology, Faculty of Medicine, J.N. Medical College, Aligarh Muslim University, Aligarh 202002, India
Article Tools
Follow on us
Abstract
Chronic foot wounds represent an increasing burden to healthcare systems as the age of the population increases. The deep dermal tissues of all chronic wounds harbor microorganisms, however, the precise interaction between microbes in the wounds and impaired healing is unknown. With regard to antibiotic therapy, there is a lack of evidence concerning its effectiveness, optimal regimens or clinical indications for treatment. Despite this lack of evidence, antibiotics are frequently a feature of the management of chronic wounds and these patients receive significantly more antibiotic prescriptions (both systemic and topical) than age and sex-matched patients. Current guidelines for antibiotic prescribing for such diabetic foot wounds are often based on expert opinion rather than scientific fact and may present difficulties in interpretation and implementation to the clinician. Although the increasing prevalence of antibiotic resistance is widely recognized, the relationships between antibiotic resistance, chronic wound microbiology and rationales for antibiotic therapy have yet to be determined. This review discusses the role of microbes in chronic diabetic foot wounds from a clinical perspective with particular focus on the occurrence of type bacteria and their impact on such wounds and resistance pattern, Extended Spectrum Beta Lactamases [ESBL] studies with special reference to Indian studies. The evidence and role of antibiotics in the treatment of such wounds are outlined and current practice of antibiotic usage for chronic wounds in the primary care setting described. The implications of antibiotic usage with regard to antibiotic resistance are also considered.
Keywords
Diabetic Foot, India, ESBL
To cite this article
Mohammad Zubair, Abida Malik, Jamal Ahmad, Microbiology of Diabetic Foot Ulcer with Special Reference to ESBL Infections, American Journal of Clinical and Experimental Medicine. Vol. 3, No. 1, 2015, pp. 6-23. doi: 10.11648/j.ajcem.20150301.12
References
[1]
Armstrong DG, Lipsky BA. Advances in the treatment of diabetic foot infections. Diabetes Technol Ther 2004, 6(2): 167-177.
[2]
Schubert S, Heesemann J. Infections in diabetes mellitus [in German]. Immun Infekt. 1995; 23:200–204.
[3]
Gin H. Infection and diabetes [in French]. Rev Med Interne. 1993; 14: 32–8.
[4]
Joshi N, Caputo G, Weitekamp M, et al. Infections in patients with diabetes mellitus. N Engl J Med. 1999; 341: 1906–12.
[5]
Lipsky BA. Evidence-based antibiotic therapy of diabetic foot infections. FEMS Immunol Med Microbiol. 1999; 26: 267–76.
[6]
Ramakant P, Verma AK, Misra R, Prasad KN, Chand G, Mishra A, Agarwal G, Agarwal A, Mishra AK. Changing microbiological profile of pathologenic bacteria in diabetic foot infections: time for a rethink on which empirical therapy to choose?. Diabetologia 2011; 54:58-64.
[7]
Bowler PG. The 105 bacterial growth guideline: reassessing its clinical relevance in wound healing. Ostomy Wound Manage. 2003; 49(1):44–53.
[8]
Wheat LJ, Allen SD, Henry, et al. Diabetic foot infections: Bacteriologic analysis. Arch Intern Med 1986; 146: 1935-1940.
[9]
Lipsky BA, Pecoraro RE, Larson SA, et al. Outpatient management of uncomplicated lower-extremity infections in diabetic patients. Arch. Intern. Med. 1990; 150: 790-797.
[10]
Sapico FL, Witte JL, Canawati HN, et al. The infected foot of the diabetic patient: quantitative microbiology Guidelines for Diabetic Foot Infections • CID 2004:39 (1 October) 905 and analysis of clinical features. Rev Infect Dis. 1984; 6(Suppl 1): S171 6.
[11]
Dang CN, Prasad YD, Boulton AJM, et al. Methicillin-resistant Staphylococcus aureus in the diabetic foot clinic: A worsening problem. Diabet Med 2003; 20(2): 159-161.
[12]
Eady EA, Cove JH. Staphylococcal resistance revisited: community acquired methicillin-resistant Staphylococcus. aureus—an emerging problem for the management of skin and soft tissue infections. Curr Opin Infect Dis. 2003; 16:103–24.
[13]
Williams DT, Hilton JR, et al. Diagnosing foot infection in diabetes. Clin Infect Dis 2004, 39(2): S83-S86.
[14]
Bendy RH, Nuccio PA, Wolfe E, et al. Relationship of quantitative wound bacterial counts to healing of decubiti. Effect of topical gentamicin. Antimicrobial Agents and Chemotherapy 1964; 4, 147–55.
[15]
Douglas WS & Simpson NB. Guidelines for the management of chronic venous leg ulceration. Report of a multidisciplinary workshop. British Journal of Dermatology. 1995; 132: 446–52.
[16]
American Diabetes Association. Consensus development conference on diabetic foot wound care. Diabetes Care 1999; 22, 1354–60.
[17]
Gardner SE, Frantz RA & Doebbeling BN. The validity of the clinical signs and symptoms used to identify localized chronic wound infection. Wound Repair and Regeneration. 2001; 9: 178–86.
[18]
Tice A, Hoaglund P, Giani G, et al. Outcomrs of osteomyelitis among patients treated with outpatient parenteral antimicrobial therapy. Am J Med 2003; 114(9): 723-728.
[19]
Lipsky BA, McDonald D, Litka PA. Treatment of infected diabetic foot ulcers: Topical MSI-78 vs. oral ofloxacin (abstract) Diabetologia 1997; 40(1): 482.
[20]
Raymakers JT, Houben AJ, et al. The effect of diabetes and severe ischaemia on the penetration of ceftazidime into tissues of the limb. Diabetic Medicine 2001; 18(3): 229-234.
[21]
Legat FJ, Maier A, et al. Penetration of fosfomycin into inflammatory lesions in patients with cellulitis or diabetic foot syndrome. Antimicrob Agents Chemother 2003; 47(1): 371-374.
[22]
Oberdorfer K, Swoboda S, et al. Tissue and serum levofloxacin concentration in diabetic foot infection patients. J Antimicrob Chemother 2004; 54(4): 836-839.
[23]
Armstrong DG, Stephan KT, Joseph, et al. What is the shelf –life of physician- mixed antibiotic-impregnated calcium sulphate pellets? J Foot Ankle Surg 2003, 42(5): 302-304.
[24]
Lipsky BA, Pecoraro RE, Wheat LJ. The diabetic foot: soft tissue and bone infection. Infect Dis Clin North Am. 1990; 4: 409–32.
[25]
Van Damme H, Rorive M, Lavery LA, et al. Amputations in diabetic patients: A plea for footsparing surgery. Acta chir Belg 2001; 101(3): 123-129.
[26]
Rauwerda JA. Surgical treatrment of the infected diabetic foot. Diabetes Metab Rs Rev2004, 20(1): S41-S44.
[27]
Tan JS, Friedman NM, Hazelton-Miller C, et al. Can aggressive treatment of diabetic foot infection reduce the need for above-ankle amputation? Clin Infect Dis 1996; 23: 286-291.
[28]
Eneroth M, Apleqvist J, Stenstrom A. Clinical characteristics and outcome in 223 diabetic foot infections. Foot Ankle Int.1997; 18:716-722.
[29]
Steed DL. The role of growth factors in wound healing. Surg Clin North Am 1997; 77: 575-586.
[30]
Hunt TK, La Van FB. Enhancement of wound healing by growth factors. N Engl J Med 1989, 321: 111-112.
[31]
Witte MB, Barbul A. General principles of wound healing. Surg Clin North Am 1997; 77: 509-528.
[32]
Park JE, Barbul A. understanding the role of immune regulation in wound healing. Am J Surg 2004; 187: 11S-16S.
[33]
Hubner G, Braucle M, Smola H, et al. Differential regulation of pro-inflammatory cytokimes during wound healing in normal and glucocorticoid-treated mice. Cytokine 1996; 8: 548-556.
[34]
Cherry GC, Hughes MA, Ferguson MWJ, et al. Wound healing: In Morris PJ, Wood WC (eds): Oxford textbook of surgery. Oxford UK: Oxford University Press, 2000. 131-159.
[35]
Carmeliet P. Angiogenesis in life, disease and medicine. Nature 2005, 438: 932-936.
[36]
Clark RAF. Wound repair: Overview amd general considerations. In Clark RAF (ed): the Molecular and Cellular Biology of wound Healing. New York: Plenum Press, 1996, pp 3-50.
[37]
Grant DS, Kleimann HK, Goldberg ID, et al. Scatter factor induces blood vessel formation in vivo. Proc Natl Acad Sci USA 1993; 90: 1937-1941.
[38]
Knighton DR, Fiegel VD. Macrophages-derived growth factors in wound healing: Regualtion of growth factor production in the oxygen microenvironment. An Rev Respir Dis 1989; 140: 1108-1111.
[39]
Andrew S. Powlson and Anthony PC. The treatment of diabetic foot infections. J Antimicrob Chemother 2010; 65 (3): 3–9.
[40]
Anandi C, Alaguraja D, Natarajan V, Ramanathan M, Subramaniam CS, Thulasiram M, Sumithra S. Bacteriology of diabetic foot lesions. Indian Journal of Medical Microbiology 2004; 22(3): 175-178.
[41]
Gadepalli R, Dhawan B, Sreenivas V, et al. A clinico-microbiological study of diabetic foot ulcers in an Indian tertiary care hospital. Diabetes Care. 2006; 29:1727-1732
[42]
Citron DM, Goldstein EJC, Merriam CV, Lipsky BA, Abtamson MA. Bacteriology of moderate-to-severe Diabetic foot infections and in vitro activity of antimicrobial agents. J. Clin Microbio 2006; 45(9):2819-2829.
[43]
Zubair M, Malik A, Ahmad J. Clinico-bacteriology and risk factors for the diabetic foot infection with multidrug resistant microorganisms in North India. Biology and Medicine. 2010: 2(4): 22-34.
[44]
Zubair M, Malik A, Ahmad J, Rizvi M, Farooqui KJ, Rizvi MA. A study of biofilm production by gram negative organisms isolated from diabetic foot ulcer patients. Biology and Medicine 2011: Vol 3 (2) Special Issue: 147-157.
[45]
Zubair M, Malik A, Ahmad J. Clinico-microbiological study and antimicrobial drug resistance profile of diabetic foot infections in North India. The Foot 2011 (March): 21(1): 6-14.
[46]
Zubair M, Malik A, Ahmad J. The impact of creatinine clearance on the outcome of diabetic foot ulcers in North Indian tertiary care Hospital. Diabetes & Metabolic Syndrome: Clinical Research & Reviews. 2011; 5(3): 120-125.
[47]
Zubair M, Malik A, Ahmad J. Study of Plasmid mediated Extended Spectrum Beta Lactamase producing Strains of Enterobacteriaceae, Isolated from Foot Infections in North Indian tertiary care hospital. Diabetes Technology and Therapeutics 2012: 12(4); 315-324.
[48]
Louie TJ, Bartlett JG, Tally FP, Gorbach SL. Aerobic and anaerobic bacteria in diabetic foot ulcers. Ann Intern Med. 1976; 85:461-463.
[49]
Lily SYN, Kwang LL, Yeow SCS, Tan TY. Anaerobic culture of diabetic foot infections: organisms and aantimicrobial susceptibilities. Ann Acad Med Singapore 2008; 37:936-939.
[50]
Sapico FL, Canawati HN, Witte JL, et al. Quantitative aerobic and anaerobic bacteriology of infected diabetic feet. J Clin Microbiol. 1980; 12:413–20.
[51]
Cooper CR Jr, McGinnis MR,. Arch. Pathol. Lab. Med 1997; 121, 798-804.
[52]
Bader M, Jafri AK, Krueger T, et al. Fusarium Osteomyelitis of the Foot in a Patient with Diabetes Mellitus. Scand. J. Infect. Dis 2003; 35 (11-12), 895-896.
[53]
Abdulrazak A, Bitar ZI, Al-Shamali AA, and Mobasher LA. Bacteriological study of diabetic foot infections. J. Diabetes Complications 2005; 19:138-141.
[54]
Raja NS. Microbiology of diabetic foot infections in a teaching hospital in Malaysia: a retrospective study of 194 cases. J Microbiol Immuno Infect 2007; 40(1):39-44
[55]
Bansal E, Garg A, Bhatia S, Attri AK, Chander J. Spectrum of microbial flora in diabetic foot ulcers. Ind J. Path Microbiol 2008; 51(2): 204-208.
[56]
Sharma VK, Khadka PB Joshi A, Sharma R. Common pathogens isolated in diabetic foot infection in Bir Hospital. Kathmandu University Medical Journal. 2006; 4; 3(15): 295-301.
[57]
Ako Nai AK, Ikem IC, Akinloye OO, Aboderin AO, Ikem RT, Kassim OO. Characterization of bacterial isolates from diabetic foot infections in Ile-Ife, Southwestern Nigeria. 2006; 16(3): 158-164.
[58]
Sotto A, Bouziges N, Jourdan N, Richard JL, Lavigne JP. In vitro activity of tigecycline against strains isolated from diabetic foot ulcers. Pathlogie Biologie 2007;55: 398-406.
[59]
Alavi MA, Khosravi AD, Sarami A, Dashtebozorg A, Montazeri EA. Bacteriologic Study of Diabetic Foot Ulcer. Pak J Med Sci 2006; 23(5): 681-684.
[60]
Tascini C, Piaggesi A, Tagliaferri E, Iacopi E, Fondelli S, Tedeschi A, Rizzo L, Leonildi A, Menichetti F. Microbiology at first visit of moderate-to-severe diabetic foot infections with antimicrobial activity and a survey of quinolone monotherapy. Diab Res Clin Prac. 2011; 94: 133-139.
[61]
Umadevi S, Kumar S, Joseph NM, Easow JM, Kandhakumari G, Srirangaraj S, Raj S, Stephen S. Microbiological study of diabetic foot infections. Indian Journal of Medical Specialities 2011; 2(1):12-17.
[62]
Tiwari S, Pratyush DD, Dwivedi A, Gupta SK, Rai M, Singh SK. Microbiological and clinical characteristics of diabetic foot infections in Northern India. J Infect Dev Ctries. 2012; 6(4): 329-332.
[63]
Day MR, Armstrong DG. Factors associated with methicillin resistance in diabetic foot infections. Journal of Foot and Ankle Surgery. 1997; 36: 322–5.
[64]
Cosgrove SE. & Carmeli, Y. The impact of antimicrobial resistance on health and economic outcomes. Clinical Infectious Diseases 2003; 36, 1433–7.
[65]
Murugan. S, R. Bakkiya Lakshmi, P.Uma Devi and K.R.Mani (2010). Prevalence and Antimicrobial Susceptibility pattern of Metallo beta lactamase producing Pseudomonas aeruginosa in Diabetic Foot Infection. International Journal of Microbiological Research, 1(3); 123-128Wilson R. Upward trend in acute anaphylaxis continued in 1998–9. British Medical Journal 2000; 321, 1021.
[66]
Knothe H, Shah P, Krcmery V, et al. Transferable resistance to cefotaxime, cefoxitin, cefamandole and cefu- roxime in clinical isolates of Klebsiella pneumoniae and Serratia marcescens. Infection 1983; 11: 315–317.
[67]
Sirot DJ. Sirot R. Labia A. et al. Transferable resistance to third- generation cephalosporins in clinical isolates of Klebsiella pneumoniae: identification of CTX-1, a novel beta-lactamase. J. Antimicrob. Chemother 1987; 20:323–334.
[68]
Brun-Buisson C, Legrand P, Philippon A, et al. Transferable enzymatic resistance to third-generation cephalosporins during nosocomial outbreak of multiresistant Klebsiella pneumoniae. Lancet 1987; ii:302–306.
[69]
Philippon A, Labia R, Jacoby G. Extended-spectrum beta- lactamases. Antimicrob. Agents Chemother 1989; 33:1131–1136.
[70]
Bush KG. Jacoby A, and Medeiros AA. A functional classification scheme for beta-lactamases and its correlation with molecular structure. Antimicrob. Agents Chemother 1995; 39:1211–1233.
[71]
Bradford PA. Extended-spectrum beta-lactamases in the 21st cen- tury: characterization, epidemiology, and detection of this important resis- tance threat. Clin. Microbiol. Rev 2001; 14:933–951.
[72]
Ambler RP, Coulson AF, Frere JM, et al.. A standard numbering scheme for the class A beta-lactamases. Biochem. J 1991; 276: 269–270.
[73]
Jacoby GA. Extended-spectrum beta-lactamases and other enzymes providing resistance to oxyimino-beta-lactams. Infect. Dis. Clin. N. Am. 1997; 11:875–887.
[74]
Sykes RB, Bush R. Physiology, biochemistry and inactivation of beta-lactamases. 1982. 155–207. In R. B. Morin and M. Gorman (ed.), The chemistry and biology of beta-lactam antibiotics, vol. 3. Academic Press, London, England.
[75]
Paterson DL, Hujer KM, Hujer AM, et al. Extended-spectrum beta-lactamases in Klebsiella pneumoniae bloodstream isolates from seven countries: Dominance and widespread prevalence of SHV- and CTX-M-type beta-lactamases. Antimicrob. Agents Chemother 2003; 47:3554–3560.
[76]
Huang ZM, Mao PH, Chen Y, et al. Study on the molecular epidemiology of SHV type beta-lactamase-encoding genes of multiple-drug-resistant Acinetobacter baumannii. Zhonghua Liu Xing Bing Xue Za Zhi. 2004; 25:425–427.
[77]
Datta N and Kontomichalou P. Penicillinase synthesis controlled by infectious R factors in Enterobacteriaceae. Nature.1965; 208: 239–241.
[78]
Jacoby GA, Medeiros AA. More extended-spectrum beta- lactamases. Antimicrob. Agents Chemother 1991; 35:1697–1704.
[79]
Sougakoff W S. Goussard GG, Courvalin P. Plasmid- mediated resistance to third-generation cephalosporins caused by point mutations in TEM-type penicillinase genes. Rev. Infect. Dis 1988; 10:879–884.
[80]
Du Bois SK, Marriott MS and Amyes SG. TEM- and SHV-derived extended-spectrum beta-lactamases: relationship between selec- tion, structure and function. J. Antimicrob. Chemother. 1995; 35: 7–22.
[81]
Baraniak A, Fiett J, Hryniewicz W, et al. 2002. Ceftazidime-hydrolysing CTX-M-15 extended-spectrum beta-lactam- ase (ESBL) in Poland. J. Antimicrob. Chemother. 50:393–396.
[82]
Bush KC. Macalintal, B. A. Rasmussen, et al.. Kinetic interactions of tazobactam with beta-lactamases from all major structural classes. Antimicrob. Agents Chemother 1993; 37:851–858.
[83]
Yan JJ, Ko WC, Tsai SH, et al. Dissemination of CTX-M-3 and CMY-2 beta-lactamases among clinical isolates of Escherichia coli in southern Taiwan. J. Clin. Microbiol 2000; 38:4320–4325.
[84]
Mathur P, Tatman A, Das B, et al. Prevalence of ESBL gram negative bacteria in a tertiary care hospital. Indian J Med Microbiol 2002; 115:153-7.
[85]
Babypadmini S, Appalaraju B. Extended-spectrum β -lactamases in urinary isolates of Escherichia coli and Klebsiella pneumoniae - prevalence and susceptibility pattern in a tertiary care hospital. Indian J Med Microbiol 2004; 22:172-4.
[86]
Shobha KL , Ramachandra L, Rao G, et al. Extended Spectrum beta-Lactamases (ESBL) in gram negative bacilli at a tertiary care hospital. Journal of Clinical and Diagnostic Research 2009; 3:1307-1312.
[87]
DiPiro JT, Cue JI. Single-agent versus combination antibiotic therapy in the management of intra-abdominal infections. Pharmacotherapy 1994; 14:266–72.
[88]
Macgregor RR, Graziani AL, Samuels P. Randomized, doubleblind study of cefotetan and cefoxitin in post-cesarean section endometritis. Am J Obstet Gynecol 1992; 167:139–43.
[89]
Karchmer AW. Mandell GL, Bennett JE, et al. Principles and Practice of Infectious Diseases, 4th ed. New York: Curchill Livingstone, 1995: 247–64.
[90]
Martin C, Cotin A, Giraud A. Comparison of concentrations of sulbactam–ampicillin administered by bolus injections or bolus plus continuous infusion in tissues of patients undergoing colorectal surgery. Antimicrob Agents Chemother 1998; 42:1093–7.
[91]
Wise R, Donovan IA, Andrews JM. Penetration of sulbactam and ampicillin into peritoneal fluid. Antimicrob Agents Chemother 1983;24:290–292.
[92]
Schwiersch U, Lang N, Wildfeuer DA. Concentration of sulbactam and ampicillin in serum and the myometrium. Drugs 1986; 31:26–8.
[93]
Seabrook GR, Edmiston CE, Schmitt DD. Comparison of serum and tissue antibiotic levels in diabetes-related foot infections. Surgery 1991;110:671–7.
[94]
Sapico RL. Foot infections in patients with diabetes mellitus. J Am Pediatr Med Assoc 1989;79: 482–485.
[95]
Grayson ML, Gibbons GW, Balogh K, et al. Probing to bone in infected pedal ulcers. JAMA. 1995; 27:721–3.
[96]
Clinical Practice Guideline-2007. Médecine et maladies infectieuses 37 (2007) 14–25.
ADDRESS
Science Publishing Group
1 Rockefeller Plaza,
10th and 11th Floors,
New York, NY 10020
U.S.A.
Tel: (001)347-983-5186