Meadow, I had a BMX (cancer on one side, the pathology on the other benign) in Jan 2015 and developed an infection in the "healthy" breast pretty much immediately post op--a reddened patch was evident right after surgery. At that point, it was watch and wait, and when the breast continued to need a drain long past the other, the PS did a last ditch attempt to deal with it by removing the implant, bathing it and the surgical area in antibiotics and replacing the implant and putting me on oral antibiotics. It seemingly worked, but 2 months later the breast exploded with infection and I wound up in the hospital for a week, had to have the implant removed and was put on IV antibiotics for a total of 3 weeks. At the hospital I started treatment with an infectious disease doc. I was blaming myself for going back to work too soon, but she had the kindness to let me know that the infection (which was an antibiotic resistant "super staph" type) was likely introduced by contaminated surgical instruments or hands, since it originated deep in the tissue, behind the implant. That experience was much worse than the actual BMX. I had a lot of tissue damage, and have not attempted reconstruction and likely will not, as I have no desire to repeat that. I did one-step implants specifically to limit my downtime and hospital exposure--so much for that! What I have learned in the couple of years since is the scary frequency of hospital acquired infection. It happens to people who have all kinds of surgery, but is especially prevalent with reconstruction. Hospital "super bugs" are incredibly common, and the frustrating thing is that so much of this is preventable with proper sterilization and use of simple checklists to limit patient infection risk. Some hospitals have better rates of infection that others, and I have read some papers/articles that recommend the use of specialized stand-alone surgery centers or breast surgery only facilities since it can help reduce the likelihood of the presence of super bugs so common in general hospitals (you do need to research the individual center's infection rate, though). Numerous posters here have recommended the Center for Restorative Breast Surgery in New Orleans as they specialize in restoration, and repairing difficult problems. I know it is a long way, but perhaps a consult with them? If you use the search feature on this site, search under the center name or NOLA for threads about it. They have helped many people who were told by their plastic surgeon that nothing could be done. If I ever choose to give it another go, I would go there.

Hi,

I had two nasty infections following Fat Grafting. Both times I about 300cc of pus removed from my chest. I had antibiotics during surgery, specifically Vancomycin. This may be outside the comfort zone of many here on these boards, but I managed to get rid of the infections, and successfully prevented future infections so that I finally completed my Reconstruction by having Intravenous High Dose Vitamin C in addition to the antibiotics. IV Vitamin C kills bacteria through production of Hydrogen Peroxide(H2O2) in the tissue spaces. Healthy cells can handle exposure to H2O2, but abnormal cells and bacteria can not. Look at the studies I am attaching. I get Intravenous Vitamin C at my Naturopath, where I would get 50 to 75 grams of Vitamin C in a two hour infusion. I only got the infections with surgeries where I didn't get the Intravenous High Dose Vitamin C, where I only used the antibiotics.

Ascorbic acid dynamics in the seriously ill and injured.

Long CL1, Maull KI, Krishnan RS, Laws HL, Geiger JW, Borghesi L, Franks W, Lawson TC, Sauberlich HE.

Author information

1

Department of Surgery, Carraway Methodist Medical Center, Birmingham, Alabama 32234, USA.

Abstract

BACKGROUND:

In addition to the known beneficial effects of ascorbic acid on wound healing and the immune response, it is also a potent extracellular antioxidant. Recent work in septic rats suggests that high-dose ascorbic acid total parenteral nutrition (TPN) supplementation may protect cells from free radical injury and improve survival. In this study, we determined ascorbic acid levels in the immediate post-injury/illness period and evaluated the ability of early short-term high levels of ascorbic acid in TPN to normalize plasma levels.

MATERIALS AND METHODS:

Ascorbic acid levels were determined in 12 critically injured patients and 2 patients with severe surgical infections. Each patient received TPN supplemented with increasing doses of ascorbic acid over a 6-day period. Therapeutic responses were determined by plasma and urine measurements using high-pressure liquid chromatography.

RESULTS:

The initial mean +/- SEM baseline plasma ascorbic acid concentration was depressed (0.11 +/- 0.03 mg/dl) and unresponsive following 2 days on 300 mg/day supplementation (0.14 +/- 0.03; P = 1.0) and only approached low normal plasma levels following 2 days on 1000 mg/day (0.32 +/- 0.08; P = 0.36). A significant increase was noted following 2 days on 3000 mg/day (1.2 +/- 0.03; P = 0.005).

CONCLUSION:

We confirmed extremely low plasma levels of ascorbic acid following trauma and infection. Maximal early repletion of this vitamin requires rapid pool filling early in the post-injury period using supraphysiologic doses for 3 or more days.

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Abstract

Neutralised ascorbic acid is found to exert a strong bactericidal action on Pseudomonas aeruginosa suspended in isotonic phosphate buffer at pH 7.1. Both the bactericidal and bacteriostatic action of ascorbic acid are antagonised by magnesium ions. In the absence of complex formation between magnesium and ascorbic acid it is concluded that ascorbic acid acts by competing with the magnesium binding sites in the cell wall, cell membrane or ribosomes. Using the chequer-board titration method the synergistic action of ascorbic acid and erythromycin is determined; such a potentiation of erythromycin is also adversely affected by magnesium ions. P. aeruginosa cells, washed and suspended in isotonic phosphate buffer containing ascorbic acid, became increasingly susceptible to the action of polymyxin, erythromycin, chloramphenicol, neomycin and tetracycline. It is suggested that ascorbic acid alters the cell surface to render it increasingly permeable to these antibiotics.

Vitamin C Kills Mycobacterium tuberculosis

Ricki Lewis, PhD

May 22, 2013

Vitamin C kills drug-sensitive, multidrug-resistant (MDR), and extensively-drug resistant (XDR) strains of Mycobacterium tuberculosis in culture as a result of prooxidant effects, according to a report published online May 21 in Nature Communications.

The new work builds on the long-standing observation that vitamin C is toxic to M tuberculosis, a Gram-positive bacterium. Experiments in the 1930s showed that only 6% of guinea pigs exposed to the bacteria and given tomato juice became infected compared with 70% of guinea pigs not given the vitamin C–rich juice. In vitro experiments conducted in 1950 confirmed the effect of the vitamin on bacterial cultures, and a study in 2011 correlated vitamin C content of various medicinal plants with antibacterial effects.

In the current study, Catherine Vilcheze, PhD, from the Department of Microbiology and Immunology, Howard Hughes Medical Institute, Albert Einstein College of Medicine, Bronx, New York, and colleagues conducted dose–response experiments, determining that 2 mM is the bactericidal level for drug-sensitive, MDR, and XDR bacteria. The effect was not seen when the bacteria were cultured in an anaerobic chamber. M tuberculosis is much more sensitive to the prooxidant effects of the vitamin than other Gram-positive and Gram-negative bacteria.

Analysis of transcription patterns revealed that the vitamin-exposed cells accumulated ferrous ions, which is consistent with the known bactericidal mechanism of vitamin C. The vitamin reduces ferric to ferrous iron, and the ferrous ions react with oxygen to produce hydroxyl radicals, which are a type of reactive oxygen species. The hydroxyl radicals damage guanine residues in DNA, causing cell death.

On the basis of these data, the researchers suggest that adding vitamin C to treatment regimens might shorten the time that chemotherapy is necessary, which is currently from 6 to 24 months. Noncompliance with chemotherapy fuels selection of drug-resistant bacterial strains. The findings also suggest that drug developers might look for the prooxidant effects of drug candidates.

"The dramatic killing of drug-susceptible, MDR and XDR M. tuberculosis strains by [vitamin C] in vitro argues for further studies on the benefits of a high [vitamin C] diet in TB-treated patients and on the development of bactericidal drugs based on [reactive oxygen species] production," the researchers conclude.

The authors have disclosed no relevant financial relationships.

Nat Comm. Published online May 21, 2013. Abstract

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Cite this article: Vitamin C Kills Mycobacterium tuberculosis - Medscape - May 22, 2013.