Staphylococcus aureus among insulin-injecting diabetic patients. An increased carrier rate

Tuazon, C. U.

doi:10.1001/jama.231.12.1272

Cited by 48 publications

(33 citation statements)

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“…S. aureus is a common cause of both community-acquired and hospital-acquired nosocomial infections. Patients with indwelling medical devices, patients on hemodialysis, patients who use intravenous drugs, and patients with dermatologic disease and diabetes mellitus have higher rates of colonization than the general population (26,59,60), and S. aureus isolates causing infection are often endogenous in origin (16,28,39,62,64). According to the National Nosocomial Infection Surveillance System of the Center for Disease Control and Prevention, S. aureus is the most common cause of surgical site infection and the second most common cause of nosocomial bacteremia (38).…”

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confidence: 99%

c-di-GMP (3′-5′-Cyclic Diguanylic Acid) Inhibits Staphylococcus aureus Cell-Cell Interactions and Biofilm Formation

Karaolis¹,

Rashid²,

Rajanna³

et al. 2005

Antimicrob Agents Chemother

134

101

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Staphylococcus aureus is an important pathogen of humans and animals, and antibiotic resistance is a public health concern. Biofilm formation is essential in virulence and pathogenesis, and the ability to resist antibiotic treatment results in difficult-to-treat and persistent infections. As such, novel antimicrobial approaches are of great interest to the scientific, medical, and agriculture communities. We recently proposed that modulating levels of the cyclic dinucleotide signaling molecule, c-di-GMP (cyclic diguanylate [3,5-cyclic diguanylic acid], cGpGp), has utility in regulating phenotypes of prokaryotes. We report that extracellular c-di-GMP shows activity against human clinical and bovine intramammary mastitis isolates of S. aureus, including methicillinresistant S. aureus (MRSA) isolates. We show that chemically synthesized c-di-GMP is soluble and stable in water and physiological saline and stable following boiling and exposure to acid and alkali. Treatment of S. aureus with extracellular c-di-GMP inhibited cell-to-cell (intercellular) adhesive interactions in liquid medium and reduced (>50%) biofilm formation in human and bovine isolates compared to untreated controls. c-di-GMP inhibited the adherence of S. aureus to human epithelial HeLa cells. The cyclic nucleotide analogs cyclic GMP and cyclic AMP had a lesser inhibitory effect on biofilms, while 5-GMP had no major effect. We propose that cyclic dinucleotides such as c-di-GMP, used either alone or in combination with other antimicrobial agents, represent a novel and attractive approach in the development of intervention strategies for the prevention of biofilms and the control and treatment of infection.

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mentioning

confidence: 99%

c-di-GMP (3′-5′-Cyclic Diguanylic Acid) Inhibits Staphylococcus aureus Cell-Cell Interactions and Biofilm Formation

Karaolis¹,

Rashid²,

Rajanna³

et al. 2005

Antimicrob Agents Chemother

134

101

View full text Add to dashboard Cite

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“…Although limb-threatening infections in the diabetic individual are frequently polymicrobial, S. aureus is a major pathogen in these infections (6). Type 1 diabetic patients show more frequent colonization of the nose and skin by S. aureus than nondiabetic and non-insulindependent diabetic individuals (7)(8)(9). The emergence of S. aureus strains resistant to multiple antibiotics has made the treatment of staphylococcal infections especially problematic.…”

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confidence: 99%

The Pathogenesis of Staphylococcus aureus Infection in the Diabetic NOD Mouse

Rich

Lee

2005

Diabetes

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Although Staphylococcus aureus is a major pathogen implicated in diabetic foot infections, little is known about the pathogenesis of this disease. A model of S. aureus infection in the hindpaw of nonobese diabetic (NOD) mice was developed. The experimental infection was exacerbated in diabetic mice (blood glucose levels >19 mmol/l) compared with nondiabetic mice, and the diabetic animals were unable to clear the infection over a 10-day period. Insulin-mediated control of glycemia in diabetic mice resulted in enhanced clearance of S. aureus from the infected tissue. Diabetic mice showed reduced tissue inflammation in response to bacterial inoculation compared with nondiabetic NOD animals, and this was consistent with the novel finding of significantly decreased tissue levels of the chemokines KC and MIP-2 in diabetic mice. Blood from nondiabetic and diabetic NOD mice killed S. aureus in vitro, whereas the bacteria multiplied in blood from diabetic mice with severe hyperglycemia. The impaired killing of S. aureus by diabetic mice was correlated with a diminished leukocytic respiratory burst in response to S. aureus in blood from diabetic animals. This animal model of hindpaw infection may be useful for the analysis of host defects in innate immunity that contribute to recalcitrant diabetic foot infections. Diabetes 54:2904 -2910, 2005 D iabetes afflicts ϳ16 million individuals in the U.S., and it is estimated that 2 million of these individuals will eventually develop chronic foot ulcers and infections (1). The most common cause of hospitalization for diabetic patients is foot infections (1), and the susceptibility of the diabetic host to these infections is multifactorial. Diabetes results in numerous physiologic perturbations in the host such as neuropathy and vasculopathy, and these can play a prominent role in the development of the diabetic foot (2).Staphylococcus aureus is the predominant pathogen in nonlimb-threatening foot infections, particularly in diabetic patients who have not yet received antimicrobial therapy (3-5). Although limb-threatening infections in the diabetic individual are frequently polymicrobial, S. aureus is a major pathogen in these infections (6). Type 1 diabetic patients show more frequent colonization of the nose and skin by S. aureus than nondiabetic and non-insulindependent diabetic individuals (7-9). The emergence of S. aureus strains resistant to multiple antibiotics has made the treatment of staphylococcal infections especially problematic. Methicillin-resistant S. aureus strains have become increasingly prevalent among both nosocomial and community-acquired infections (10,11). Recently, S. aureus isolates resistant to vancomycin, one of the antibiotics of last resort, were recovered from patients with chronic foot ulcers (12,13). Although the increased susceptibility of diabetic patients to bacterial infections is well established, the chronicity associated with these infections remains poorly understood.Many investigations have focused on the nonobese diabetic (NOD) mouse as a...

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“…Type-1 diabetic patients show more frequent colonization of the nose and skin by S. aureus than non-diabetic and non-insulin-dependent diabetic individuals [22]. Some studies involved chronic stimulation of rabbits with TSST-1 resulting in impaired systemic glucose tolerance.…”

Section: Staphylococcal Infectionsmentioning

confidence: 99%

Skin Infections in Diabetes: A Review

AK¹,

Bhatt²

2016

J Diabetes Metab

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Diabetes mellitus (DM) constitutes a growing concern to world population due to the devastating effects of its chronic complications. An estimated number of people with diabetes are projected to rise from 171 million in 2000 to 366 million in 2030. Glucose intolerance is the intermediate stage between normal glucose tolerance and diabetes. It results in ketoacidosis and hyperglycemia causing immune dysfunction. Patients with diabetes mellitus are therefore predisposed to cutaneous infections. If remain unnoticed, undiagnosed in the early stages or not treated properly such infections may get complicated and can even prove lethal. It therefore becomes imperative to recognize signs and symptoms of such infections and approach them appropriately or refer the patient to a diabetologist or dermatologist. Our review literature is a comprehensive communication involving several cutaneous infections that manifest more frequently, with greater severity; or with an elevated risk for complications in patients with diabetes mellitus.

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Staphylococcus aureus among insulin-injecting diabetic patients. An increased carrier rate

Cited by 48 publications

References 0 publications

c-di-GMP (3′-5′-Cyclic Diguanylic Acid) Inhibits Staphylococcus aureus Cell-Cell Interactions and Biofilm Formation

c-di-GMP (3′-5′-Cyclic Diguanylic Acid) Inhibits Staphylococcus aureus Cell-Cell Interactions and Biofilm Formation

The Pathogenesis of Staphylococcus aureus Infection in the Diabetic NOD Mouse

Skin Infections in Diabetes: A Review

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