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The pathogenesis of fibrous capsular contracture after augmentation mammaplasty is still debated. One hypothesis implicates low-grade bacterial infections as a cause. The presence of a staphylococcal biofilm in a patient with recurrent capsular contracture was previously reported. A comparative, prospective, blinded, clinical study of implants and capsules removed from patients with or without significant capsular contracture was conducted to investigate the association of biofilm contamination, breast implants, and capsular contracture. Capsule and implant samples obtained during explantation were tested by routine microbiological culture, sensitive broth culture (after maceration and sonication), and scanning electron microscopy. Clinical parameters were correlated with microbiological findings. A total of 48 implant and/or capsule samples were obtained from 27 breasts during a 22-month period. Of the 27 breasts, 19 exhibited significant contracture (Baker grade III/IV). The mean duration of implantation was 9.2 years (range, 0.4 to 26.0 years). Routine swab cultures obtained at the time of explantation were negative for bacterial growth for all samples. The sensitive broth culture technique yielded 24 positive samples (50 percent, n = 48). An analysis of capsules demonstrated that 17 of 19 samples obtained from patients with significant contracture were positive, compared with only one of eight samples obtained from patients with minimal or no contracture (p = 0.0006). Fourteen of the 17 positive cultures from significantly contracted breasts yielded coagulase-negative staphylococci, mainly, species of the Staphylococcus epidermidis group. The presence of coagulase-negative staphylococci was also significantly associated with capsular contracture (p = 0.01). There was no significant difference in the frequency of culture positivity for saline versus silicone implants (p = 0.885). Scanning electron microscopy confirmed the presence of extensive biofilm on implants and within capsules.Biofilm, in particular, S. epidermidis biofilm, was detected for a significant proportion of patients with capsular contracture. This implicates biofilm disease in the pathogenesis of contracture, and strategies for its prevention should be explored.

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The risk of perinatal transmission of hepatitis C virus (HCV) from a cohort of 95 human immunodeficiency virus (HIV)-negative intravenous drug users (IVDU) is described, 89 of whom were positive for antibodies to HCV (anti-HCV). Infection, defined as the presence of HCV RNA in a serum sample collected from an infant at any time during follow-up, was detected in six of 63 (9.5%) infants born to HCV antibody-positive viraemic mothers. No mother who was HCV RNA negative at delivery transmitted HCV to her infant. Hepatitis C virus antibodies became undetectable in uninfected infants by 15 months, but persisted in all HCV-infected infants throughout follow-up. An abnormal alanine aminotransferase (ALT) level was observed on at least one occasion in all HCV-infected infants and in six occasions in uninfected infants. Two of the six HCV-infected infants became HCV RNA negative during follow-up by 27 and 29 months. Both of these infants had a large ALT elevation (mean peak ALT 398U l-1) at around 12 months of age. Analysis of a range of potential risk factors revealed that maternal HCV RNA load was important in predicting transmission, but suggested that other factors play a role in perinatal transmission from mother to child. No difference was found between mothers who transmitted HCV to their infants and those who did not for HCV genotype, duration of drug use, duration of methadone use, methadone dose, history of alcohol abuse, past hepatitis B virus (HBV) infection, mode of delivery, maternal and gestational age, birth weight and incidence of breast-feeding. Mothers who transmitted HCV to their infants had a longer duration between membrane rupture and delivery than the mothers who did not transmit (P = 0.03). HCV RNA was not detected in breast milk and colostrum samples from 38 viraemic mothers, including two who transmitted HCV to their infant.

Viral recurrence is universal after transplantation for hepatitis C infection. This may lead to difficulties in differentiating allograft dysfunction caused by chronic rejection from hepatitis C virus (HCV) recurrence. Cases of severe cholestatic hepatitis have also been reported in conjunction with reinfection of the graft with HCV. Patients receiving transplants for HCV-related liver disease were studied before and after transplantation by HCV RNA quantitation of serial serum samples. Four major clinical patterns of HCV recurrence could be distinguished posttransplantation: group 1, asymptomatic hepatitis with no significant symptoms; group 2, cholestatic hepatitis with centrilobular ballooning; group 3, hepatitis leading to chronic allograft rejection; and group 4, persistently normal serum aminotransferase levels. Pretransplantation viral load was shown to be an important indicator of disease severity because the group 2 patients had significantly higher pretransplantation viral loads than patients in group 1 (P ‫؍‬ 0.01) and group 4 (P ‫؍‬ 0.005). The group 2 patients also had persistently significantly higher posttransplantation viral loads than the patients in group 1 (P ‫؍‬ 0.01) and group 4 (P ‫؍‬ 0.02), whereas patients who developed chronic allograft rejection showed marked decreases in serum HCV RNA before retransplantation. Patients from group 4 had the lowest viral loads after transplantation. These results show that persisting graft cholestasis due to HCV is associated with persistently high HCV RNA levels compared with other etiologies of graft dysfunction. Prospective studies are needed to determine whether such quantitation may be diagnostically helpful in distinguishing the different patterns of HCV-related graft dysfunction observed after liver transplantation.

Abstract:Background. Chemical carcinogens induce squamous cell carcinoma (SCC) of the head and neck by targeting the p53 and the retinoblastoma (pRb) pathways. Human papillomavirus (HPV) might have an etiologic role in these cancers at particular sites. Few studies have compared cell cycle protein expression in HPV-positive and HPV-negative tumors in this region.Methods. Fifty tonsil SCCs were analyzed for HPV by PCR and for expression of cell cycle proteins (p53, pRb, p16, p27 KIP1 , and cyclinD1) by immunohistochemistry. Results. HPV was present in 42%; almost all were type 16. There were statistical associations between HPV positivity and reduced expression of pRb and cyclinD1, overexpression of p16, and younger patient age. Tumor with down-regulated p27 tended to have down-regulated pRb and p21.Conclusions. HPV-positive tonsil SCCs have distinct molecular pathways. Their association with younger patient age suggests that they are biologically distinct from HPV-negative tumors.

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