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Microbiology in usmle 1 microbiology 1
- 1. MICROBIOLOGY IN USMLE 1 IMG. Leslie Millán Studying test prep Copyright to Leslie Millán
- 2. General Index in Bacteriology Studying section 1. Bacterial taxonomy 2. Bacterial structures or morphology 3. Stains 4. Diagnostics 5. Bacterial genetics 6. Immunity and Mechanism of action of bacteria 7. Antimicrobians, mechanism of action of antibacterial drugs
- 4. Bacterias Microbial nomenclature- naming microorganisms Taxonomy- classifying living things Identification- discovering and recording the traits of organisms so they can be named and classified
- 5. Bacterias Bacterias are unicellular microorganisms that live in the environment and in all living entities
- 8. Bacterial structure of the cell wall and membrane Kaplan medical 2018
- 9. Morphology of Bacterias Coccus Pleomorphic Bacillus or rods Spiral Branching filaments
- 10. TOXINS Toxins may aid in invasiveness, damage cells, inhibit cellular processes, or trigger immune response and damage. Structural Toxins• Endotoxin (lipopolysaccharide LPS), EXOTOXINS -Peptidoglycan -Teichoic Acids
- 11. Bacterial growth and death Kaplan medical 2018
- 12. Endospore Bacillus Clostridium Kaplan medical 2018
- 13. Stains GRAM FAST ACID India Ink Silv er stain GIEMSA Ziehl Neelsen
- 14. DIAGNOSTIC METHODS Rapid Conventional Or Direct detect Ag or pathogen Undirect : Detect Abs or subproducts like ELISA Rapid are the diagnostics made in 24h like smears, frotis reactive Abs to Ag Or Ag detection to Specific pathogen Conventional are all procedures that take more tan 24h to diagnose an infection and include: culturing, some PCR, antibiotic susceptibility and resistance.
- 15. Genetics
- 16. PLASMIDS
- 17. Genetics Microbial Genetics – General Microbiologyopen.oregonstate.education
- 18. TRASLATION
- 19. TRANSDUCTION Microbial Genetics – General Microbiologyopen.oregonstate.education
- 20. RECOMBINATION Microbial Genetics – General Microbiologyopen.oregonstate.education
- 21. MUTATIONS Silent: no change in amino acids to conform a protein. Missense: Different amino acid in protein product. Nonsense: Stop codon, no protein synthesis.
- 22. IMMUNITY
- 23. IMMUNE RESPONSE
- 24. iMMUNITY
- 26. Mechanism of action of antibiotics Kaplan medical 2018
Editor's Notes
- NOTE: To change the image on this slide, select the picture and delete it. Then click the Pictures icon in the placeholder to insert your own image.
- THE BACTERIAL STRUCTURE HAS IN MOST CASES, PEPTIDOGLYCAN, AND A CYTOPLASMIC MEMBRANE, THAT FIX THE STRUCTURE, GIVE RESISTANCE AND ALLOW INTERCHANGE WITH THE EXTERIOR DURING DIFFERENT PROCESS. AS YOU CAN SEE, MOST BACTERIAS CAN BE GRAM POSITIVE AND GRAM NEGATIVE DEPENDING ON THE GRAM STAIN.
- LPS is part of gram-negative outer membrane– Tox i c p o r t i o n i s l i p i d A: generally not released (and toxic) until death of cell (exception: N. meningitidis, which over-produces outer mem-brane fragments)–LPS is heat stable and not strongly immunogenic, so can not be converted to a toxoid –LPS is primary virulence factor in Gram negative septic shock–Mechanism: LPS activates macrophages, leading to release of TNF-alpha, IL-1, and IL-6. IL-1 is a major mediator of fever. Macrophage activation and products lead to tissue damage. Damage to the endothelium from bradykinin-induced vasodilation leads to shock. Coagulation (DIC) is mediated through the activation of Hageman factor.
- On first exposure to an allergen in a susceptible individual, antigen-presenting cells process and present allergen epitopes with major histocompatibility complex (MHC) II to T helper cells. B cells also process and present the same allergen epitope to TH2 cells, which release cytokines IL-4 and IL-13 to stimulate proliferation and differentiation into IgE-secreting plasma cells. The IgE molecules bind to mast cells with their Fc region, sensitizing the mast cells for activation with subsequent exposure to the allergen. With each subsequent exposure, the allergen cross-links IgE molecules on the mast cells, activating the mast cells and causing the release of preformed chemical mediators from granules (degranulation), as well as newly formed chemical mediators that collectively cause the signs and symptoms of type I hypersensitivity reactions. 25