Attitudes and Awareness of Cornea Specialists and Oculoplastic Surgeons toward Methicillin-Resistant Staphylococcus aureus Decolonization.

Background: Methicillin-resistant Staphylococcus aureus (MRSA) decolonization is widely utilized in many medical subspecialities to reduce surgical site infections, but routine ophthalmic implementation has been limited. The aim of this study was to investigate the attitudes and actual practice of corneal specialists and oculoplastic surgeons toward MRSA decolonization as a preventive measure in ophthalmic surgery. Materials and Methods: A web-based survey was sent to cornea specialists and oculoplastic surgeons to assess their knowledge, beliefs, and practices regarding MRSA prophylaxis and the use of MRSA decolonization to prevent post-operative infections. Results: A total of 180 surgeons participated in this study: 71% of respondents agreed that MRSA colonization plays a role in post-operative infection of the eye and adnexal structures; 65% stated that MRSA decolonization could help prevent MRSA infection. Although 41% of respondents would change their management in response to a positive pre-operative MRSA screening result, only 18% performed pre-operative screening. Seventeen percent of respondents indicated that they offer pre-operative decolonization for MRSA-positive patients; the most frequently applied technique was the use of nasal antibiotic agents such as mupirocin, followed by antiseptic baths. Peri-operative MRSA prophylaxis was used by 18% of respondents; pre-operative MRSA decolonization was used in conjunction by 8.5 % of respondents. Conclusions: Although MRSA decolonization has been validated in fields outside of ophthalmology, there has not been widespread adoption of this practice among oculoplastic surgeons and cornea specialists. Prospective MRSA decolonization ophthalmic studies are necessary if evidence-based management guidelines are to be developed.

The first US domestic report of disseminated Mycobacterium avium complex and anti-interferon-γ autoantibodies.

INTRODUCTION: Anti-interferon-γ (IFNγ) autoantibodies have been associated with disseminated mycobacterial infections, mostly in patients from Southeast Asia. PURPOSE: We studied an American-born, Caucasian female with M. avium complex infection of the subglottic mucosa and brain for underlying etiologies of infection. METHODS: Plasma was screened for anticytokine autoantibodies using a Luminex-based approach. The ability of patient plasma to block IFNγ-induced STAT1 phosphorylation in normal blood cells was evaluated by flow cytometry with intracellular staining. Plasma inhibition of IFNγ production and IFNγ-induced cytokines in normal and patient blood cells washed of autologous plasma was also evaluated. RESULTS: Patient plasma contained high-titer IgG anti-IFNγ autoantibodies, primarily of the IgG1 subclass. Patient but not control plasma prevented IFNγ-induced STAT1 phosphorylation and expression of the IFNγ-inducible cytokines tumor necrosis factor (TNF) α and interleukin (IL)-12 in normal blood cells. Patient blood cells washed free of autologous plasma demonstrated normal IFNγ production and response. CONCLUSIONS: Disseminated nontuberculous mycobacterial infections should always prompt immune evaluation. This first case of disseminated nontuberculous mycobacterial infection and anti-IFNγ autoantibodies in an American-born Caucasian suggests that anti-cytokine autoantibodies are not racially or regionally restricted.

Mycotic aortic aneurysm due to intravesical BCG immunotherapy: Clinical manifestations and diagnostic challenges.

A live, attenuated form of Mycobacterium bovis, bacillus Calmette-Guérin (BCG), is commonly used as intravesical immunotherapy for non-invasive urothelial bladder carcinoma. While complications are rare, dissemination can occur. A case of mycotic aortic aneurysm following BCG administration with recovery of Mycobacterium bovis in culture is reported. A review of the published experience with this problem is also presented.

Chlamydial Hsp60-2 is iron responsive in Chlamydia trachomatis serovar E-infected human endometrial epithelial cells in vitro.

Chlamydial 60-kDa heat shock proteins (cHsp60s) are known to play a prominent role in the immunopathogenesis of disease. It is also known that several stress-inducing growth conditions, such as heat, iron deprivation, or exposure to gamma interferon, result in the development of persistent chlamydial forms that often exhibit enhanced expression of cHsp60. We have shown previously that the expression of cHsp60 is greatly enhanced in Chlamydia trachomatis serovar E propagated in an iron-deficient medium. The objective of this work was to determine which single cHsp60 or combination of the three cHsp60 homologs encoded by this organism responds to iron limitation. Using monospecific polyclonal peptide antisera that recognize only cHsp60-1, cHsp60-2, or cHsp60-3, we found that expression of cHsp60-2 is responsive to iron deprivation. Overall, our studies suggest that the expression of cHsp60 homologs differs among the mechanisms currently known to induce persistence.

Ultrastructural analysis of chlamydial antigen-containing vesicles everting from the Chlamydia trachomatis inclusion.

Several chlamydial antigens have been detected in the infected epithelial cell cytosol and on the host cell surface prior to their presumed natural release at the end of the 72-96 h developmental cycle. These extra-inclusion antigens are proposed to influence vital host cell functions, antigen trafficking and presentation and, ultimately, contribute to a prolonged inflammatory response. To begin to dissect the mechanisms for escape of these antigens from the chlamydial inclusion, which are enhanced on exposure to antibiotics, polarized endometrial epithelial cells (HEC-1B) were infected with Chlamydia trachomatis serovar E for 36 h or 48 h. Infected cells were then exposed to chemotactic human polymorphonuclear neutrophils not loaded or pre-loaded in vitro with the antibiotic azithromycin. Viewed by electron microscopy, the azithromycin-mediated killing of chlamydiae involved an increase in chlamydial outer membrane blebbing followed by the appearance of the blebs in larger vesicles (i) everting from but still associated with the inclusion as well as (ii) external to the inclusion. Evidence that the vesicles originated from the chlamydial inclusion membrane was shown by immuno-localization of inclusion membrane proteins A, F, and G on the vesicular membranes. Chlamydial heat shock protein 60 (chsp60) copies 2 and 3, but not copy 1, were released from RB and incorporated into the everted inclusion membrane vesicles and delivered to the infected cell surface. These data represent direct evidence for one mechanism of early antigen delivery, albeit membrane-bound, beyond the confines of the chlamydial inclusion.