Continuous bladder irrigation in the monoplace hyperbaric chamber: Two case reports.

INTRODUCTION: Radiation-induced hemorrhagic cystitis is a serious side effect of radiation therapy. Anemia requiring transfusion can ensue. Treatment methods include bladder irrigation, fulguration, and hyperbaric oxygen (HBO2) therapy. Failure of treatment leads to cystectomy associated with a high risk of severe complications (42%) and mortality (16%). Continuous bladder irrigation (CBI) is often required to prevent further clot formation. HBO2 supports the healing process of radiation cystitis. In patients requiring CBI, the time in HBO2 can help cause clot accumulation and obstruction. We describe a method of providing CBI in a monoplace hyperbaric chamber. MATERIALS AND METHODS: An IV to catheter adapter is used, allowing an IV pump to control CBI flow into the chamber. Drainage is collected in an extra-large (2- to 5-liter) bag. The rate is set so the volume does not exceed the bag's capacity. The bag is placed in a manner that precludes spilling and allows monitoring of outflow. RESULTS: CBI was successfully maintained. Brief cases are presented and issues discussed. SUMMARY/CONCLUSIONS: CBI is easily maintained in a monoplace hyperbaric chamber, with readily available equipment allowing for uninterrupted CBI of hemorrhagic cystitis. HBO2 helps mitigate the potential side effects of other interventions in a previously irradiated area.

Lipooligosaccharides containing phosphorylcholine delay pulmonary clearance of nontypeable Haemophilus influenzae.

Nontypeable Haemophilus influenzae (NTHi) causes pulmonary infections in patients with chronic obstructive pulmonary disease and other mucociliary clearance defects. Like many bacteria inhabiting mucosal surfaces, NTHi produces lipooligosaccharide (LOS) endotoxins that lack the O side chain. Persistent NTHi populations express a discrete subset of LOS glycoforms, including those containing phosphorylcholine (PCho). In this study, we compared two NTHi strains with isogenic mutants lacking PCho for clearance from mice following pulmonary infection. Consistent with data from other model systems, populations of the strains NTHi 2019 and NTHi 86-028NP recovered from mouse lung contained an increased proportion of PCho+ variants compared to that in the inocula. PCho- mutants were more rapidly cleared. Serial passage of NTHi increased both PCho content and bacterial resistance to clearance, and no such increases were observed for PCho- mutants. Increased PCho content was also observed in NTHi populations within non-endotoxin-responsive C3H/HeJ and Toll-like receptor 4 null (TLR4-/-) mice, albeit at later times postinfection. Changes in bacterial subpopulations and clearance were unaffected in TLR2-/- mice compared to the subpopulations in and clearance from mice of the parental strain. The clearance of PCho- mutants occurred at earlier time points in both strain backgrounds and in all types of mice. Comparison of bacterial populations in lung tissue cryosections by immunofluorescent staining showed sparse bacteria within the air spaces of C57BL/6 mice and large bacterial aggregates within the lungs of MyD88-/- mice. These results indicate that PCho promotes bacterial resistance to pulmonary clearance early in infection in a manner that is at least partially independent of the TLR4 pathway.

Streptococcus pneumoniae forms surface-attached communities in the middle ear of experimentally infected chinchillas.

BACKGROUND: Streptococcus pneumoniae (pneumococcus) causes respiratory and systemic infections that are a major public health problem worldwide. It has been postulated that pneumococci persist in vivo in biofilm communities. METHODS: In this study, we analyzed whether pneumococci form biofilms in vivo, and if so, whether biofilms correlated with bacterial persistence. Chinchillas were infected with S. pneumoniae TIGR4 and euthanized at varying times after infection, after which the superior ear bullae were excised and examined by culture and microscopy. RESULTS: Dense material, resembling the biofilms of other otitis media pathogens, was visible in the middle ear as late as 12 days after infection. Scanning electron microscopy revealed bacteria within an electron-dense matrix, similar to pneumococcal biofilms formed in vitro. Viability staining revealed groups of viable diplococci, as well as viable and nonviable host cells, attached to a fibrous matrix that was positive when stained with propidium iodide. Cryosections of biofilms were treated with polyclonal antibodies against the pneumococcal surface components pneumococcal surface protein A family 2, pneumococcal surface protein C, choline-binding protein, and neuraminidase, coupled with appropriate secondary antibody conjugates. Immunofluorescent staining showed the presence of pneumococcal communities within the material recovered from the middle ear chamber. CONCLUSIONS: On the basis of these data, we conclude that pneumococci form biofilms in vivo and that this process may be intertwined with the formation of neutrophil extracellular traps. These findings provide new insights into the potential causes of antibiotic treatment failure and bacterial persistence in chronic pneumococcal otitis media.