Infection

bacteria

BASICS

  • Diabetics are at greater risk of infection.
  • Patients with diabetes and high blood glucose levels in the peri-operative period have a much higher risk of an infection in surgery.
  • Uric acid inhibits nitric oxide release by the phagocytes (white cells).
  • Fructose loads decrease neutrophil mobility.
  • There are no new antibiotic drugs in testing at present.
  • Decreasing susceptibility to infection seems good PREVENTION.

 

IDEAS

Increased incidence of children’s respiratory infections following Easter ‘chocolate binge’.

There are no new antibiotic drugs in testing at present.

There are rising super bugs with resistance across multiple antibiotic techniques and these are in increasing prevalence across the world.

Rather than looking at drugs to manage infection it would be reasonable to reconsider our diet which may in fact be inhibiting the antibiotics from having the full effect.

High sugar content foods have the potential to be mild immunosuppressive agents right at a time when patients need to have their immunity system on “full alert”.

Cutting back dramatically on Sugar and Polyunsaturated Oils MAY improve infection outcomes. See Uric Acid effects on Nitric Oxide below and at Damage Process. There is certainly no ‘cost’ in trying this option.

Read about Hospital Food.

Read about the Metabolism

Read about the Health Issues

Food Ideas to Help Yourself

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MORE INFORMATION

Infection Risk

Patients with diabetes and high blood glucose levels in the peri-operative period have a much higher risk of an infection in surgery.

Diabetics are at greater risk of infection.

Fructose loads decrease neutrophil mobility and motility and this effect appears to be related to the uric inhibition of nitric oxide release by phagocytes. Phagocytes are the white cells that travel around the body and are involved in the whole immune process. They include neutrophils, macrophages and monocytes. There is a specific nitric oxide synthase which is involved in allowing the white cell to enter damaged tissue.

Uric acid inhibits nitric oxide release by the phagocytes and as a result is the theoretical basis for poorer white cell activity under a fructose load.

Bacterial Drug Resistance

There are rising numbers of ‘super bugs’ with resistance across multiple antibiotic techniques and these are in increasing prevalence across the world.

There are no new antibiotic drugs in testing at present.

Rather than looking at drugs to manage infection it would be reasonable to reconsider our diet which may in fact be inhibiting the antibiotics from having the full effect.

Nitric Oxide

Uric Acid has a potent inhibitory effect on Nitric Oxide Synthase which in turns affects Nitric Oxide activity.

There are three main forms of Nitric Oxide Synthase. They all act as Endothelium-Derived Relaxing Factor (EDRF) and have a vasodilatory effect through their action in the production of Nitric Oxide.

eNOS (endothelial Nitric Oxide Synthase)

  • Acts on blood vessel endothelium

iNOS (inducible Nitric Oxide Synthase)

  • Acts on white cells involved in immunity and tissue damage homeostasis
  • Phagocytes
  • Neutrophils
  • Macrophages
  • Monocytes

nNOS (neuronal Nitric Oxide Synthase)

  • Acts on the brain and may be involved in the prioritisation of blood and oxygen supply to the brain.

The effect of Uric acid reducing  Nitric Oxide bioavailability creates a variety of effects including

  • Vasoconstriction and hypertension via its effect on vascular smooth muscle cells
  • Oxidative stress in a variety of cells and particularly Adipocytes(fat cells)
  • Endothelial cells permeability changes
  • ? Immune effect by inhibiting phagocyte (white cell) activity

Read about the Damage Process

Read about the Metabolism

Food Ideas to Help Yourself

The NoFructose Handout Starter Sheet is your take away summary of this web site. Read it at the NoFructose Starter Sheet area of this web site or download it.

Please add information by going to Contribute to NoFructose.com

 

ARTICLES

 

Perioperative hyperglycemia and postoperative infection after lower limb arthroplasty.

Mraovic B, Suh D, Jacovides C, Parvizi J.J Diabetes Sci Technol. 2011 Mar 1;5(2):412-8.

One of the most serious complications after major orthopedic surgery is deep wound or periprosthetic joint infection. Various risk factors for infection after hip and knee replacement surgery have been reported, including patients’ comorbidities and surgical technique factors. We investigated whether hyperglycemia and diabetes mellitus (DM) are associated with infection that requires surgical intervention after total hip and knee arthroplasty.

We reviewed our computerized database for elective primary total hip and knee arthroplasty from 2000 to 2008. Demographic information, past medical history of patients, perioperative biochemistry, and postoperative complications were reviewed. Patients were divided into two groups: infected group (101 patients who had surgical intervention for infection at our institution within 2 years after primary surgery) and noninfected group (1847 patients with no intervention with a minimum of one year follow-up. The data were analyzed using t, chi-squared, and Fisher’s exact tests.

There were significantly more diabetes patients in the infected group compared with the noninfected group (22% versus 9%, p < .001). Infected patients had significantly higher perioperative blood glucose (BG) values: preoperative BG (112 ± 36 versus 105 ± 31 mg/dl, p = .043) and postoperative day (POD) 1 BG (154 ± 37 versus 138 ± 31 mg/dl, p < .001). Postoperative morning hyperglycemia (BG >200 mg/dl) increased the risk for the infection more than two-fold. Non-DM patients were three times more likely to develop the infection if their morning BG was >140 mg/dl on POD 1, p = .001. Male gender, higher body mass index, knee arthroplasty, longer operative time and hospital stay, higher comorbidity index, history of myocardial infarction, congestive heart failure, and renal insufficiency were also associated with the infection.

Diabetes mellitus and morning postoperative hyperglycemia were predictors for postoperative infection following total joint arthroplasty. Even patients without a diagnosis of DM who developed postoperative hyperglycemia had a significantly increased risk for the infection.

 

Increasing risk of prosthetic joint infection after total hip arthroplasty.

Dale H, Fenstad AM, Hallan G, Havelin LI, Furnes O, Overgaard S, Pedersen AB, Kärrholm J, Garellick G, Pulkkinen P, Eskelinen A, Mäkelä K, Engesæter LB. Acta Orthop. 2012 Oct;83(5):449-58. doi: 10.3109/17453674.2012.733918.

The risk of revision due to infection after primary total hip arthroplasty (THA) has been reported to be increasing in Norway. We investigated whether this increase is a common feature in the Nordic countries (Denmark, Finland, Norway, and Sweden).

The study was based on the Nordic Arthroplasty Register Association (NARA) dataset. 432,168 primary THAs from 1995 to 2009 were included (Denmark: 83,853, Finland 78,106, Norway 88,455, and Sweden 181,754). Adjusted survival analyses were performed using Cox regression models with revision due to infection as the endpoint. The effect of risk factors such as the year of surgery, age, sex, diagnosis, type of prosthesis, and fixation were assessed.

2,778 (0.6%) of the primary THAs were revised due to infection. Compared to the period 1995-1999, the relative risk (with 95% CI) of revision due to infection was 1.1 (1.0-1.2) in 2000-2004 and 1.6 (1.4-1.7) in 2005-2009. Adjusted cumulative 5-year revision rates due to infection were 0.46% (0.42-0.50) in 1995-1999, 0.54% (0.50-0.58) in 2000-2004, and 0.71% (0.66-0.76) in 2005-2009. The entire increase in risk of revision due to infection was within 1 year of primary surgery, and most notably in the first 3 months. The risk of revision due to infection increased in all 4 countries. Risk factors for revision due to infection were male sex, hybrid fixation, cement without antibiotics, and THA performed due to inflammatory disease, hip fracture, or femoral head necrosis. None of these risk factors increased in incidence during the study period.

We found increased relative risk of revision and increased cumulative 5-year revision rates due to infection after primary THA during the period 1995-2009. No change in risk factors in the NARA dataset could explain this increase. We believe that there has been an actual increase in the incidence of prosthetic joint infections after THA.

More to follow.