Aspergillus fumigatus is an increasingly prevalent opportunistic fungal pathogen of various immuno-compromised individuals. It has the ability to filament within the lungs forming dense intertwined mycelial balls. These morphological characteristics resemble those of microbial biofilms, which are matrix enclosed microbial populations, adherent to each other and/or to surfaces or interfaces. The purpose of this paper is to review some recent experiments that indicate the potential biofilm forming capacity of A. fumigatus in vitro. Initially it was established that conidial seeding density is important for stable biofilm development. In the optimized model conidial germination and filamentous growth characteristics were not observed until 8 h, after which a multi-cellular population expanded exponentially forming a thick structure (approx. 250 microm). Calcofluor white staining of this revealed the presence of extracellular polymeric matrix material, which increased as the biofilm matured. Subsequent antifungal sensitivity testing of this structure showed that azoles, polyenes and echinocandins were ineffective in reducing the cellular viability at therapeutically attainable concentrations. Microarray and real-time PCR analysis demonstrated the up-regulation of AfuMDR4 during multicellular growth and development, which may account the recalcitrance observed. Overall, A. fumigatus appears to possess the classical elements of biofilm growth, namely multicellularity, matrix production and sessile resistance. This controversial approach to understanding the biology of A. fumigatus infection may provide crucial information on how to treat this pathogenic fungus more effectively.
A 7-valent pneumococcal conjugate vaccine (PCV7) has gained licensure and has proven successful in the USA for preventing pneumococcal disease and reducing the incidence of antibiotic-resistant pneumococcal strains. The ability, therefore, to accurately monitor the likely effect of the introduction of PCV7 vaccine on invasive pneumococcal disease in the UK is essential. Serotyping and multilocus sequence typing was performed on invasive isolates of Streptococcus pneumoniae (n=645) from Scotland during 2003. The information gained from this was used to evaluate serotype coverage by the vaccine and the relationship between serotypes. In the present study, invasive pneumococcal disease in Scotland was caused by 33 different serotypes, consisting of 150 sequence types. Overall, 48.4% of the isolates were of serotypes included in the PCV7. Pneumococci were most frequently associated with sequence types 9, 124, and 162. PCV7 would provide protection in 71.8% of infants under 5 years of age against the serotypes in the vaccine. There was limited evidence of the potential for capsule switch among currently circulating invasive pneumococci. The successful implementation of a suitable vaccination programme should lead to a reduction in invasive pneumococcal disease in the UK as well as a reduction in antibiotic resistance of pneumococcal strains.
Of the 10 most common STs, 6 coexisted with a single serotype each. Vaccine coverage in all age groups was 94.9% for the 23-valent polysaccharide vaccine and 50.7, 55.4, and 64.1% for the 7-, 9-, and 11-valent Pnc vaccines, respectively. For those under the age of 2 years, 79% coverage would be provided by the 7-, 9-, and 11-valent Pnc vaccines.
Sixty-seven serotype 14 pneumococci, isolated from invasive disease in Scotland during the first 6 months of 2003, were characterized. Serotype 14 pneumococci accounted for 18 . 2 % of the total number of cases. Serotyping, multilocus sequence typing and antibiotic susceptibility testing revealed 10 different sequence types (STs), predominantly ST 9 and ST 124; most ST 9 pneumococci were erythromycin-resistant whilst those of ST 124 were not.
The common cold is a very prevalent infection in humans, with adults having two to five colds each year and schoolchildren suffering between seven and 10 colds per year (34).
MicrobiologyMore than 200 different types of virus are responsible for human upper respiratory tract infections (34). The most common are rhinoviruses (30-50% of all colds), followed by coronaviruses (10-15% of all colds). Influenza viruses cause 5-15% of colds.
PathophysiologyThe symptoms of the common cold are a result of viral infection of the upper airway. The incubation 151
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