We report on the case of a 25-year-old female with severe systemic lupus erythematosus (SLE) who presented with pancytopenia, fever, arthralgia and abdominal pain. After antibiotic treatment, the patient was afebrile for 3 days before her temperature rose again. Dyspnoea and cough pointed towards pneumonia which was confirmed by X-ray. Different antibiotics and the antimycotic agent fluconazol were given. The lupus flare was treated with high-dose prednisolone.

After a couple of days, the dyspnoea increased and mechanical ventilation became necessary. Bronchoscopy and transbronchial biopsy revealed the diagnosis of invasive aspergillosis*. Despite of an immediate treatment with amphotericin B, the patient died because of respiratory insufficiency. The literature on aspergillosis in SLE is reviewed and prophylactic, diagnostic and therapeutic options are discussed for this infectious complication which has an 80% mortality in patients with SLE.

*Checked medical dictionary; same as aspergillus below articles!

The articles below are from the SALINE IMPLANT LIBRARY at the SILICONE IMPLANT SURVIVORS SITE:

http://www.GeoCities.com/HotSprings/8689/saline.html

A case of aspergillus niger fungal colonization associated with bilateral inflatable silicone mammary implants is reported. Painful fibrous capsular contractures without clinical evidence of infection or inflammation characterized the presenting symptoms. Operative findings included a cheesy-white exudate that surrounded the implants and turbid fluid within the implants.

All specimens yielded a heavy growth of aspergillus niger. Special stains of the fibrous capsules were negative for fungal invasion.

The etiology and pathogenesis of aspergillus colonization in this patient are postulated.

In vitro and in vivo experiments were conducted to determine whether intraluminal saline in breast implants can support the growth of common wound-infecting micro-organisms over a prolonged period of time. The bacteria tested were Staphylococcus aureus, Staphylococcus epidermidis, Escherichia coli, Corynebacterium jeikeium, Enterobacter cloacae, Klebsiella pneumoniae, and Pseudomonas aeruginosa. Three fungal species also were tested: Aspergillus fumigatus, Paecilomyces variofii, and Candida albicans. In the in vitro study, four organisms survived in flasks of sterile saline for the 2 weeks in which serial cultures were performed: K. pneumoniae, C. albicans, A. fumigatus, and P. variotii.

In the in vivo study, 61 white rabbits (122 implants) received both an experimental implant inoculated with one of the test organisms and a control implant containing only sterile saline. They were sacrificed at 1-, 3-, or 6-month scheduled endpoints. None of the control implants containing sterile saline had positive cultures. In contrast, the intraluminal saline was culture positive for 7 of the 10 inoculated organisms after varying lengths of time: S. epidermidis, E. coli, E. cloacae, K. pneumoniae, P. aeruginosa, A. fumigatus, and P. variotii. Samples of capsular tissue also were cultured. Of the 122 capsular tissue specimens, 21 (17 percent) had positive cultures and surrounded both inoculated and sterile implants.

In most instances, capsules that were culture positive contained an organism different from the one that had been inoculated in the group. In only 3 cases was the same organism cultured from both the periprosthetic tissue and the intraluminal saline, and these may represent instances of the inoculated organism migrating through the implants filler valves. The data show that several types of bacteria (particularly gram-negative species) and fungi can grow and reproduce in a restricted saline environment for extended periods of time.

The survival of bacteria was evaluated in custom-made saline breast implants with integral injection ports in vitro and in 10 New Zealand White rabbits for Staphylococcus aureus, Staphylococcus epidermidis, Pseudomonas aeruginosa, and Serratia marcescens. Pseudomonas and Serratia survived in vitro in saline-filled implants and multiplied 24-fold and 22-fold, respectively, from the initial inocula of 300 colony-forming units per cubic centimeter in 21 days.

Serratia alone survived in saline implants placed on the dorsum of rabbits, proliferated 80-fold in 7 days, and tapered to 10-fold at the end of 3 weeks. Chemical analysis revealed the presence of glucose in fluid from the implants in the animal study (mean, 1.2 mg per deciliter; standard error of mean [SEM], 0.6) after 21 days and from human subjects (mean, 3.8 mg per deciliter; SEM, 1.0) after 8 months to 10 years. Serratia incubated in human breast implant fluid samples proliferated 7-fold to 30-fold greater than in the saline control in a nonaerated environment. We conclude that some bacteria are able to proliferate in saline in breast implants. Furthermore, their survival may be facilitated by a substance (i.e., glucose) that diffuses across the implant outer shell.

This report describes a case of gross contamination with the filamentous fungus P. variotii cultured from an intraluminal saline breast implant removed from a patient 14 months after implantation because of severe capsular contracture. We suspect the fungal contamination occurred when a container of saline was left open in the operating room prior to filling and placement of the implant. This case may be the first documented report of microbial growth and reproduction in the internal environment of a saline implant. We assume that organisms such as P. variotii can survive - and accumulate biomass - on the minute amounts of substrates that diffuse across an implant envelope.

NOTE: One of the women in our support group brought her intact explanted saline- filled implants to a meeting locally. They are filled with black, brackish saline with particles floating profusely in them. She is also on disability and in a wheelchair. She was a school teacher; another intelligent woman struck down in her 30's or in the prime of life.

The shells are permeable; fluid can flow in and out. See below:

This study was prompted by 5 patients (seen by O. G. Robinson, M.D.) presenting with unilateral enlargement of the breasts 4 to 9 years following augmentation mammaplasty with saline-filled implants. At exploration one breast implant was seen to be markedly enlarged when compared to the other, with a brownish yellow material that had the consistency of serum.

Studies were undertaken to determine the permeability of the silicone container to various body fluids and a study of the contained fluid itself. Protein measurements, viscosity measurements, and osmotic water permeability measurements were performed. The results were consistent with the hypothesis that these silicone implants were indeed permeable to both water, glucose, and protein. We hypothesize that the mechanism underlying this in vivo expansion is colloid osmotic swelling. Why one breast should be more involved than the other is unknown. We believe that this phenomenon is occurring more frequently than is being reported

The cause of silicone gel implant ageing and rupture is not known. Recent reports indicate the failure rate is higher than previously published, and implant ageing and rupture may be due to progressive mechanical deterioration of the outer vulcanized silicone shell. It is known that lipids are absorbed by the hydrophobic silicone elastomer, and lipid infiltration causes mechanical attenuation and possible failure of the elastomer. The purposes of this article are to analyze the silicone envelope/gel of explanted prostheses and the silicone elastomer of other medical grade silicone devices for lipid content and to suggest its possible role in implant ageing and rupture.

We assayed 33 ruptured silicone breast implant shells (mean age 13.1 years; range 8 to 26 years) and 8 medical grade silicone elastomer devices (mean age 3.7 years; range 3 months to 12 years) for evidence of lipid infiltration using thin layer chromatography. These were compared with control group assays from two nonimplanted silicone gel implants and one unused Silastic catheter. Ninety-eight percent of implants and other previously implanted silicone devices were found to have evidence of lipid infiltration compared with none in nonimplanted controls (p < 0.005).

We conclude that lipids infiltrate the outer silicone shell and may be a factor related to breast implant ageing and rupture due to progressive mechanical weakening of the outer silicone shell.