Results of aerobic culture and antibiogram in 105 patients with acute bacterial pharyngitis

To study throat culture and antibiogram results in treatment of acute pharyngitis. 105 Patients with acute phartngitis were included in this prospective study. From all of the patients throat culture and gram-stained smear were provided. Antibiogram was done in patients with posit throat culture. 63 Patients of 105 patients [59%] gave negative throat culture and gram stained smear from pharyngeal secretions. 20 Patients [19%] have positive throat culture and gram stained smear. 12 Patients [12%] have positive throat culture and negative gram stained smear. Therefore 32 patients [31%] of 105 patients have bacterial pharyngitis. Fever, pharyngeal and tonsillar purulent exudates and adenopathy in patients with positive throat [31%] was more common than patients with negative throat cultures [69%]. The most common cause of bacterial pharyngitis was group A betahemolytic streptococcus. Antibiogram findings revealed that bacterial pharyngitis such as streptococcal, staphylococcal and pneumococcal were completely resistant penicillin, Amoxicillin and Ampicillin that are used routinely in out patient clinics, and on the other hand were sensitive to unusual antibiotics in treatment of acute bacterial pharyngitis. Including Doxycicline, Vancomycin and Erythromycin and they are better alternatives

Coagulating like conditions thrombophilia

Fluidity of blood inside the vessels on one hand, and formation of thrombus just at the site of vessel injury on the other hand, is the result of an exact interactive equilibrium of multiple procoagulant and anticoagulant factors, and their activators and inhibitors. Destruction or stimulation of endothelial cells and platelets, and contact of blood and platelets with subendothelial tissues are among the main procoagulant factors. Integrity and function of endothelial cells, washing property of blood stream, fibrinolysis system [plasminogen] and thrombomodulin system, protein C and antithrombin are the most important anticoagulant factors. Dysfunction of procoagulant factors leads to bleeding tendency, whereas dysfunction of anticoagulant factors causes predisposition to the thrombosis [thrombophilia]. Despite recent progresses, we can only diagnose half of hereditary thrombophilias, among these, the factor V Leiden, antithrombin deficiency; protein C deficiency and protein S deficiency are more common. Elevation of plasma factor VIII levels has been considered as a common but weak risk factor for hereditary thrombophilia. Mutation of prothrombin G20210A which leads to elevation of prothrombin levels, has the same importance as the factor VIII elevation. Presence of hereditary thrombophilia in an individual does not inevitably end up in the formation of pathologic thrombosis, for clinical presentation of thromboembolic syndromes, coincidence of one [or more] hereditary thrombophilia along with one [or more] acquired thrombophilia [such as pregnancy, immobility, surgery, OCP use] are usually evident. Individuals with hereditary thrombophilia are more prone to the recurrence of thrombosis than normal individuals, so long term use of anticoagulant drugs in such patients is recommended. Screening for hereditary thrombophilia must be considered when [1] there is not an acceptable acquired risk factor for thrombosis in history and physical examination; [2]venous thrombosis before age 40, [3]recurrent thrombosis, [4]arterial thrombosis before age 30, [5]family history of thrombosis, [6]thrombosis in unusual sites such as mesenteric or cerebral veins