MSSA whith h VISA phenotype -can be seen when vancomycin is used emprically in ICU for MRSA coverage ,then de escalated once MRSA was excluded (either negative nasal swab rapid PCR test in pneumonia or culure showing sensitivity to beta lactams - exposure can lead to stepwise genetic mutations( such as walKR, vraSR, or rpoB) leading to thickened cell wall in slowly growing subpopulation ........... NB: h VISA and MRSA are two distinct phenomenon as MRSA means resistance to beta lactams due to acquisition of mec gene causing altered PBPA2 , the target of beta lactams .............. when you switch according to guidelines from vancomycin to beta lactams , based on sensitivity , (هنا السؤال الأول ليه البكتريا اللى فاضلة ممتش طالما مفيش مقاومة للمضاد الحيوي Beta-lactams target active cell wall synthesis. Because stationary hVISA bacteria are growing much slower and have thick, modified walls, beta-lactams are far less lethal in the human body than in an actively dividing in-vitro sample) يبقى هنا هتلاقى علامات التحسن الإكلينيكي لكن لما تعيد المزرعة بعد 3 أيام هتلاقى منظر غير مفسر هتلاقى نفس البكتريا وكمان بحساسية أكبر لنفس المضاد الحيوي اللى فشل فى القضاء عليها antibiotic will exert selective pressure leading to elimination of MSSA population with clinical and lab improvement followed by persistant bactremia by the growing h VISA طيب ليه لما تتكاثر بالدرجة الكافية المضاد الحيوي مش هيبقى فعال ضدها In an actively growing state, its susceptibility profile shifts, making it appear vulnerable to the antibiotic that clinically failed to eradicate it in the human body ايه الغلطات اللى مفروض متعملهاش هنا (1) this can be interpreted as new infection (however careful examination will show no evidence of new lung consolidation , no pus on urine analysis ,no hidden abscess and no biofilms ) this unexplained bacterima will be investigated by blood culture which will come back showing either(1) MSSA with h VISA phenotype which is more sensitive to beta lactam (lesser MIC with the same bacterial load "phenotypic tolerance and MBC/MIC decoupling" بما أنها نفس البكتريا فى المزرعة مفيش معنى انك تدور على عدوى جديدة وبما ان الحمل البكتيري اقل مفيش اى معنى انك تدور على خراج او مكان خفى للعدوى إلا باعتبار انه ملجأ للبكتريا intracellular staph invading macrophage of non immune cells وهنا هتكون قربت جدا من الحقيقة biofilm-intracellular nicht -....ect (2) no growth when MSSA is cleared while the MSSA-h VISA not yet grew enough to appear in the culture هنا لو كملت على نفس المضاد الحيوي ل5-7 ايام هيموت البكتريا اللي هتنمو خلال الفترة دي .طيب لو استعجلت ووقفت المضاد الحيوي او حصل lag , bacterial growth was not covered by antibiotic !! IT is a clinical trap , patient may develop severe sepsis or even septic shock .this unexplained deterioration will be considered as new onset infection الأخطر هنا لما تكون دكتور شاطر وتفترض ان العدوى بما انها حصلت داخل المستشفى فهي hospital acquired pneumonia , you re introduce vancomycin for MRSA + levofloxacin as anti pseudomonal clinical deterioration will be noticed , the culture will show MSSA resistant to vancomycin (high MIC more than 2= VISA) .................. how to escape the trap ? do not reintroduce vancomycin , when empirical MRSA coverage is needed in a patient recently covered by vancomycin consider this trap , use ceftaroline ( linezolid is bacteriostatic not preferred in bacteremia , daptomycin will clear bacteremia but not the original lung infection -Delafloxacin can cover both MRSA and pseudomonas لكن زي ما قلنا امبارح مينفعش تستعمله قبل المزرعة لتتغطية العشوائية ولا ينفع تستعمله فى حالات HAP ( ONLY CAP and soft tissue infection) ..................... it is an art based on deep knowledge on microbiology , dynamic rather than static Never treat antibiotic as a hummer then you will be just a fool with a tool #foundational_microbiology #pneumonia_secrets
MSSA whith h VISA phenotype -can be seen when vancomycin is used… — Medical Notes Dr. Ayman Radwan — TG.ME
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