A microbial aetiology of acne has been suggested since the beginning of the last century. There is considerable evidence, circumstantial at best, which suggests that micro-organisms, particularly Propionibacterium acnes, are important in the pathogenesis of acne vulgaris. However, it is still unclear whether P. acnes is actually a causal agent in the development of noninflamed or inflamed acne lesions. Based on a review of the microbiological data on normal and acne-affected skin, we propose that P. acnes neither initiates comedogenesis nor has a role in the initiation of inflammation in inflamed acne lesions.

Acne vulgaris is a common disease that carries an enormous financial and psychosocial impact. Androgens, excessive sebum production, ductal hypercornification, changes in the microbial flora, as well as inflammation and immunological host reactions are considered the major contributors to acne pathogenesis. Despite extensive research on acne pathogenesis, the exact sequence of events and their possible mechanisms leading to the development of a microcomedone and its transformation into an inflamed lesion has remained unclear. There is a significant amount of in vitro evidence suggesting a possible pathogenetic role for Propionibacterium acnes in comedogenesis as well as inflammation in inflammatory acne. However, the microbiological data from non‐inflamed as well as inflamed acne lesions, cultured individually, do not entirely support the hypothesis that these micro‐organisms are actually responsible for their initiation. There appears to be comedones and inflamed lesions in which there is no clear evidence of Propionibacterium acnes involvement. Considering this microbiological data, alongside the in vitro evidence, we have tried to delineate the possible sequence of events and their mechanisms, leading to the development of a microcomedone and its transformation into an inflamed lesion. Based on the available literature we have analysed the evidence of both non‐inflamed as well as inflamed acne lesions occurring in the absence of Propionibacterium acnes from the pilosebaceous follicles. We propose that the development of an inflamed acne lesion depends on an imbalance between the pro‐inflammatory and anti‐inflammatory pathways rather than the incitement of inflammation by Propionibacterium acnes.

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Acute pharyngitis is one commonest reasons for patients to visit the family physician, 80-90% of cases are caused by viruses particularly adenovirus. The most important bacterial cause is group A streptococcus, which is responsible for about 15% of all cases. Because of the time required to confirm the presence of group A streptococci using throat cultures many commercial antigen detection tests for the rapid identification of group A streptococci directly from throat swabs have been developed utilizing the latex agglutination principle and a result is available within 5 minutes. Objective: The purpose of this study was to determine the value of using rapid detection procedure (Reveal color strep A test, Murex) for group A streptococci directly from throat swabs. Material and Method: Data from 200 patients with sore throat attending one of the Public Medical Centers in Amman over 6 month period May 1998-January 1999. Both throat swabs and cultures were taken and throat swabs were subjected using (Reveal color strep A test) for rapid detection. The culture results were interpreted and reported by microbiologist. Data were analyzed by calculating the number of positives and negatives for both swabs and cultures, the specificity, sensitivity and predictive value were determined. Results: The usefulness of latex test was as follows: Sensitivity 87%, Specificity 98.2%, Predictive value positive 90%, and Predictive value negative 97.6%. Conclusion: Using tests for the rapid identification may help in establishing a policy for sore throat management in general practice by avoiding unnecessary cultures and antibiotic prescription