EC Microbiology

Introduction: Patients who have diabetes mellitus (DM) are more susceptible to infections than those without DM. Due to the defects
seen in the immunity, the course of the infections and increased prevalence of infections are seen more in this group. Cellular and
humoral immunity show disturbances. Diabetic polymorphonuclear cells and diabetic monocytes/macrophages also tend to show
decreased functions. Higher glucose environment tends to attract certain microorganisms causing infections that affect multiple
organs and organ systems, eventually leading to morbidity and mortality of the patients.

Aim of the Work: The review summarizes the physiopathology, associated mechanisms that make DM patients susceptible to devel-
oping infections, and major infections seen with diabetes mellitus.

Methodology: This article is a comprehensive review of PUBMED from the year 1999 to 2017.

Conclusion: Novel treatment options and methods to prevent infectious diseases in diabetic patients can be better understood if
proper knowledge about immune dysfunctions during hyperglycemia is known. This can, in turn, improve the outcome of treatment
of these infectious diseases.

Keywords: Type 2 Diabetes; Immunity; Immune Dysfunction; Hyperglycemia

1. American Diabetes Association. “Standards of medical care in diabetes-2016: summary of revisions”. Diabetes Care 39.1 (2016): S4-S5.
2. Casqueiro J., et al. “Infections in patients with diabetes mellitus: A review of pathogenesis”. Indian Journal of Endocrinology and Metabolism 16.1 (2012): S27.
3. Mishra M and Fomusi Ndisang J. “A critical and comprehensive insight on heme oxygenase and related products including carbon monoxide, bilirubin, biliverdin and ferritin in type-1 and type-2 diabetes”. Current Pharmaceutical Design 20.9 (2014): 1370-1391.
4. Petersen M C., et al. “Regulation of hepatic glucose metabolism in health and disease”. Nature Reviews Endocrinology 13.10 (2017): 572.
5. Ndisang J F., et al. “Insulin resistance, type 1 and type 2 diabetes, and related complications 2017”. Journal of Diabetes Research (2017).
6. Abu-Ashour W., et al. “Diabetes and the occurrence of infection in primary care: a matched cohort study”. BMC Infectious Diseases 18 (2018): 67.
7. Carey IM., et al. “Risk of Infection in Type 1 and Type 2 Diabetes Compared With the General Population: A Matched Cohort Study”. Diabetes Care 41 (2018): 513.
8. Bartelink ML., et al. “Infections in patients with type 2 diabetes in general practice”. Diabetes Research and Clinical Practice 40 (1998): 15.
9. Martin ET., et al. “Diabetes and Risk of Surgical Site Infection: A Systematic Review and Meta-analysis”. Infection Control and Hospital Epidemiology 37 (2016): 88.
10. Latham R., et al. “The association of diabetes and glucose control with surgical-site infections among cardiothoracic surgery patients”. Infection Control and Hospital Epidemiology 22 (2001): 607.
11. Wiseman JT., et al. “Predictors of surgical site infection after hospital discharge in patients undergoing major vascular surgery”. Journal of Vascular Surgery 62 (2015): 1023.
12. Furnary AP., et al. “Continuous intravenous insulin infusion reduces the incidence of deep sternal wound infection in diabetic patients after cardiac surgical procedures”. The Annals of Thoracic Surgery 67 (1999): 352.
13. Boreland L., et al. “The effectiveness of tight glycemic control on decreasing surgical site infections and readmission rates in adult patients with diabetes undergoing cardiac surgery: A systematic review”. Heart Lung (2015): 4.
14. Haug JB., et al. “Bloodstream infections at a Norwegian university hospital, 1974-1979 and 1988-1989: changing etiology, clinical features, and outcome”. Clinical Infectious Diseases 19 (1994): 246.
15. Geerlings SE and Hoepelman AI. “Immune dysfunction in patients with diabetes mellitus (DM)”. FEMS Immunology and Medical Microbiology 26.3-4 (1999): 259-265.
16. Peleg AY., et al. “Common infections in diabetes: pathogenesis, management and relationship to glycaemic control”. Diabetes/Metabolism Research and Reviews 23.1 (2007): 3-13.
17. Price CL., et al. “Methylglyoxal modulates immune responses: relevance to diabetes”. Journal of Cellular and Molecular Medicine 14.6b (2010): 1806-1815.
18. Amano H., et al. “Impairment of endotoxin-induced macrophage inflammatory protein 2 gene expression in alveolar macrophages in streptozotocin-induced diabetes in mice”. Infection and Immunity 68 (2000): 2925.
19. Al-Mashat HA., et al. “Diabetes enhances mRNA levels of proapoptotic genes and caspase activity, which contribute to impaired healing”. Diabetes 55 (2006): 487.
20. Mazade MA and Edwards MS. “Impairment of type III group B Streptococcus-stimulated superoxide production and opsonophagocytosis by neutrophils in diabetes”. Molecular Genetics and Metabolism 73 (2001): 259.
21. Graham PL., et al. “A U.S. population-based survey of Staphylococcus aureus colonization”. Annals of Internal Medicine 144 (2006): 318.
22. Donders GG. “Lower Genital Tract Infections in Diabetic Women”. Current Infectious Disease Reports 4 (2002): 536.
23. Ray D., et al. “Prevalence of Candida glabrata and its response to boric acid vaginal suppositories in comparison with oral fluconazole in patients with diabetes and vulvovaginal candidiasis”. Diabetes Care 30 (2007): 312.
24. Hostetter MK. “Handicaps to host defense. Effects of hyperglycemia on C3 and Candida albicans”. Diabetes 39 (1990): 271.
25. Ferguson BJ. “Mucormycosis of the nose and paranasal sinuses”. Otolaryngologic Clinics of North America 33 (2000): 349.
26. Hodgson KA., et al. “Altered macrophage function is associated with severe Burkholderia pseudomallei infection in a murine model of type 2 diabetes”. Microbes Infect 13 (2011): 1177.
27. Wiersinga WJ., et al. “Melioidosis”. The New England Journal of Medicine 367 (2012): 1035.
28. Ozer A., et al. “Advanced glycation end products facilitate bacterial adherence in urinary tract infection in diabetic mice”. Pathogens and Disease (2015): 73.
29. Restrepo BI., et al. “Cross-sectional assessment reveals high diabetes prevalence among newly-diagnosed tuberculosis cases”. Bulletin of the World Health Organization 89 (2011): 352-359.
30. Edmonds M. “The treatment of diabetic foot infections: focus on ertapenem”. Vascular Health and Risk Management 5 (2009): 949.
31. Preshaw PM., et al. “Periodontitis and diabetes: a two-way relationship”. Diabetologia 55.1 (2012): 21-31.
32. El-Zayadi A and Anis M. “Hepatitis C virus induced insulin resistance impairs response to anti-viral therapy”. World Journal of Gastroenterology 18 (2012): 212-224.
33. Stanley TL and Grinspoon SK. “GH/GHRH axis in HIV lipodystrophy”. Pituitary 12 (2009): 143-152.
34. Dube MP. “Disorders of glucose metabolism in patients infected with human immunodeficiency virus”. Clinical Infectious Diseases 31 (2000): 1467-1475.
35. Brown TT., et al. “Anitretroviral therapy and the prevalence and incidence of diabetes in a multicenter AIDS Cohort study”. Archives of Internal Medicine 165 (2005): 1179-1184.
36. Hertel J., et al. “A structural basis for the acute effects of HIV protease inhibitors on GLUT4 intrinsic activity”. Journal of Biological Chemistry 279 (2004): 55147-55152.
37. Lee GA., et al. “The effects of HIV protease inhibitors on carbohydrate and lipid metabolism”. Current Infectious Disease Reports 6 (2004): 471-482.
38. Woerle HJ., et al. “Mechanisms for the deterioration in glucose tolerance associated with HIV protease inhibitor regimens”. Diabetes 52 (2003): 918-925.
39. Fleishman A., et al. “Effects of a nucleoside reverse transcriptase inhibitor, stavudine, on glucose disposal and mitochondrial function in muscle of healthy adults”. The American Journal of Physiology-Endocrinology and Metabolism 292 (2007): E1666-E1673.