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51 Cards in this Set
- Front
- Back
Which are the typical gram-positive bacteria? |
Bacillus anthrasis, streptococcus Pneumoniae |
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Which are the typical gram negative bacteria? |
N. Gonnorhea, Pseudomonas aergunosa, E. Coli, vibrio cholera |
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Which is the most clinically relevant acid-fast bacteria? |
mycoplasma tubercolisis |
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Which is the most clinically relevant "gram less" bacteria. |
Mycoplasma pneumonia (and many other organisms of the Mycoplasma genus) |
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Describe the steps of gram staining. What additional steps need to be taken for complex staining organisms? |
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Describe in general the characteristics of gram positive bacteria |
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Diagram the structure of the plasma membrane an cell wall of a gram positive bacterium. |
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Diagram the structure of the plasma membrane an cell wall of a gram negative bacterium. |
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Describe the structure of LPS |
Can induce immune mediated damage endotoxic shock. |
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Describe the key features and significance of the O-antigen |
O antigen is the most variable among species and can be modified by environment. Differentiates bacterial serotypes. |
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Describe the mechanisms of bacitracin, penicillin, cephalonsporin and vancomycin. |
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Contrast the advantages of a bacterium being gram negative vs. gram positive. |
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Describe the structure of Acid fast-staining organisms. |
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What are characteristics of "Gramles" bacteria? Give examples of these organisms. |
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What are the common structures that are recognized by the immune system to activate inflammatory signaling? |
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Describe the structure of lipopolysaccharide. |
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Describe the different classes of bacteria with respect to growth temperature and pH preference. What are factors that affect growth rate? |
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Contrast hardy bacteria with fastidious bacteria. What are key requirements for growth? |
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Which trace metals are required for bacterial growth? What are the main 4 classes of iron transporters found in bacterial cells? |
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Describe the pathogenicity and growth of S. Ares.What are the cell surface virulence factors expressed and when? What are the secreted virulence factors expressed and when are they expressed? |
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Why does growth state matter? |
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What are Robert Koch's postulates and what are they used for? |
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What are the three categories of bacteria with which humans interact? Give two examples of how an organism might with from one to another. |
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What are some of the functions os commensal bacteria? |
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Distinguish between infection and disease. What is virulence and how is it typically measured? |
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What are the steps necessary for bacterial infection? |
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Describe the pattern of disease with respect to the magnitude of symptoms for N. Gonnorhea, bacillus anthracis, and C. Difficile for men and women. |
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What are persister cells and how do they arise? Is this state permanent or transient. |
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What are the two major ways by which bacteria cause disease? |
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What are the phases of bacterial growth? |
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What are the steps in the six link chain? |
The six-linked chain is a sequence that comprise physician-patient interactions, which are: + history-taking + physical exam + differential diagnosis + tests/investigations + provisional/definitive diagnosis + management |
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Describe broadly the role of Neutrophils, basophils, eosinophils, mast cells, macrophages and dendritic cells in immunity. |
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Describe the role of natural killer cells in immunity. |
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Describe the role of effector B cells, Memory B cells, T helper cells and cytotoxic T cells in immunity. |
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Describe the appearance of malaria on a CBC. What is a common symptom? |
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Describe the structures of peptidoglycan and techioc acid. What are their constituents? Where do they occur? |
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Describe the structure and identifying features of Staphyloccoci. How could you differentiate it from another bacterium? |
+ Spherical cocci + Arranged in irregular grape like clusters + Gram-positive + Ferments mannitol salt (yellow staining) + Beta-hemolytic (bright-yellow in the midst of red) + Catalase test positive (bubbles) + Coagulase test positive (the culture coagulates) + All staphylococci produce catalase (note that no streptococci produce catalase → you can use a “catalase test” to differentiate staph from strep. Hydrogen peroxide + staph = oxygen bubbles) + Catalase degrades H2O2 into O2 and H2O and is an important virulence factor + Bacteria that make catalase can survive the killing effect of H2O2 within neutrophils |
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How does catalase and superoxide dismutase contribute to bacterial anaerobic growth? |
Allows degradation of ROS => protects the bacteria from: Immune attacks (neutrophils, macrophages) Products of aerobic respiration |
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What are the toxigenic disease caused by S. Aureus? |
Staph food poisoning Scalded Skin syndrome Toxic Shock syndrome |
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Describe the symptoms, progression and prognosis for toxigenic disease caused by S. Aureus: Food poisoning |
Staph food poisoning: Acute onset (0.5-7hr) Short duration Vomit > diarrhea Cause: Emetic protein |
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Describe the symptoms, progression and prognosis for toxigenic disease caused by S. Aureus: Scalded Skin syndrome |
Scalded Skin Syndrome Dermal layer separated from intercellular junctions Occurs mainly in young children Cause: Exfoliatin protein (ETA, ETB) - proteases! |
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Describe the symptoms, progression and prognosis for toxigenic disease caused by S. Aureus: Toxic shock syndrome |
Toxic Shock Syndrome Typical of septic shock: high fever, chills, vomiting, diarrhea, sunburn-like rash, sore throat, muscle pain, exfoliation of basilar layer of epidermis of palms and soles, hypotension and shock resulting in multi-organ failure Cause: Toxic Shock Syndrome Toxin (TSST-1) |
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Describe the symptoms, progression and prognosis for inflammatory/invasive disease caused by S. Aureus: Skin and Tissue infections |
Impetigo, pyoderma |
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Describe the symptoms, progression and prognosis for inflammatory/invasive disease caused by S. Aureus: Staphylococcal pneumonia |
May follow viral respiratory infection, especially influenza in children, or occur in postoperative patients. |
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Blood stream invasion (bacteremia) |
Can follow any localized lesion Systemic responses: chill, rigor, joint pain. Can have metastatic seeding or organs, with abscess formation: Heart valves: endocarditis Bone and joints: osteomyelitis and septic arthritis |
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Describe the cell wall and and surface component, secreted enzyme and secreted toxin virulence factors of S. Areus |
Cell wall and surface components: Gram + cell wall Surface bound and secreted coagulase (Converts fibrinogen to fibrin protecting bacteria from phagocytes) Protein A- binds to Fc portion of antibodies and inhibits Fc-mediated phagocytosis Secreted Enzymes Catalase- H2O2--> H2O and O2 Superoxide dismutase Hyaluronidase → promote invasion Staphylokinase → promote invasionLipases → promote invasion Secreted Toxins Cytolytic Toxins- lyse host cells by forming pores in or interfering with membranesLeads to release of cellular mediators that cause further damage |
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Describe exfoliative, enterotoxin and any other toxins associated with S. Areus |
Exfoliative toxins ETA and ETB: serine proteases that promote breakage of desmosomes (cell-cell junctions) in epidermisCan also act as super antigens Staphylococcal Enterotoxins: 8 serotypes (classified by antigens present on bacteria) Heat and acid-stable Cause vomiting/emesis Cause toxic shock-like syndrome by functioning as super antigens (Superantigen - class of antigens that cause non-specific activation of T-Cells and massive cytokine release) TSST-1:Toxin that is associated with most or all menstrual-associated cases of toxic shock syndrome (Acts a super antigen) |
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Explain the mechanisms by which S. Aureus evades host immunity. |
Several mechanisms + Surface bound and secreted coagulase Converts fibrinogen to fibrin protecting bacteria from phagocytes + Protein A- binds to Fc portion of antibodies and inhibits Fc-mediated phagocytosis + Secreted Catalase- converts hydrogen peroxide to water and oxygen, preventing immune system attacks with ROS |
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Describe the evolution of how S. aureus acquired antibiotic resistance. |
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What are the predisposing factors for invasive S. Areus disease and what are the possible treatments? |
Invasive diseases:Most often caused by local lesion leading to infection via a break in the dermal layerSharp objects (scissors, knives, needles, etc.)Sports (wrestling mats [very common], and other full contact sports) Major cause of hospital-acquired infections |
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What are the predisposing factors for toxigenic S. Aureus disease and what are the possible treatments? |
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