Infectious Dz Lecture #1


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Professor Stringer's 1st lecture on Infectious Disease

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  • Frequently, presenters must deliver material of a technical nature to an audience unfamiliar with the topic or vocabulary. The material may be complex or heavy with detail. To present technical material effectively, use the following guidelines from Dale Carnegie Training®.   Consider the amount of time available and prepare to organize your material. Narrow your topic. Divide your presentation into clear segments. Follow a logical progression. Maintain your focus throughout. Close the presentation with a summary, repetition of the key steps, or a logical conclusion.   Keep your audience in mind at all times. For example, be sure data is clear and information is relevant. Keep the level of detail and vocabulary appropriate for the audience. Use visuals to support key points or steps. Keep alert to the needs of your listeners, and you will have a more receptive audience.
  • Infectious Dz Lecture #1

    1. 1. An Overview of Infectious Disease C. Stringer PA-C Copyright 1996-98 © Dale Carnegie & Associates, Inc.
    2. 2. Introduction <ul><li>Of diseases afflicting humans, most that are curable and preventable are caused by infectious agents. </li></ul><ul><li>An understanding of infectious diseases offers insight into medicine as whole. </li></ul><ul><li>Infectious diseases remain a major cause of death and debility of many millions of people around the world (e.g.MTB). </li></ul>
    3. 3. COURSE OBJECTIVES <ul><li>Identify the database needed to evaluate infectious diseases. </li></ul><ul><li>Understand the basic concept of host parasite interactions. </li></ul><ul><li>Acquire an understanding of immunology and vaccinations. </li></ul><ul><li>Demonstrate knowledge of the principles of anti-microbial therapy. </li></ul>
    4. 4. Innate immune response
    5. 5. Cytotoxic T-cell
    6. 6. Innate-Adaptive responses
    7. 7. The Immune System <ul><li>The immune system: an organization of cells and molecules with specialized roles in defending against infection. </li></ul><ul><li>Innate-acquired immunity are complementary systems. </li></ul><ul><li>Clinical manifestations seen in patients with either an infection, allergy, cancer or autoimmune disease. </li></ul>
    8. 8. Innate immune response <ul><li>Key components in the innate immune response include soluble and cellular factors,which are nonspecific, invariable and they lack immunologic memory. </li></ul><ul><li>The interaction of these factors allows the body to recognize and respond to foreign antigens with their elimination from the host without damaging host tissues. </li></ul>
    9. 9. Adaptive responses <ul><li>Humoral immunity relies on B lymphocytes </li></ul><ul><li>Cell-mediated immunity relies on T cells </li></ul><ul><li>T cells are divided into helper cells(CD4) and suppressor cells(CD8). </li></ul>
    10. 10. Diagnostics of ID
    11. 11. The Complement System <ul><li>The complement system enhances phagocytosis, lyses of microbes-infected cells. </li></ul><ul><li>Microbes and acute phase proteins activate the complement system. </li></ul><ul><li>The classic pathway is activated by antigen-antibody complexes </li></ul><ul><li>The alternate pathway by microbial-cell walls </li></ul>
    12. 12. Host Defense Mechanisms. <ul><li>For any infectious process to occur, the parasite and host must first encounter each other. </li></ul><ul><li>The normal human body harbors a complex microbial ecosystem: </li></ul><ul><li>The skin </li></ul><ul><li>Mucus membranes </li></ul><ul><li>The gut (enteric bacteria) </li></ul><ul><li>Generally these are commensal organisms </li></ul>
    13. 13. Three levels of Defense <ul><li>Pathogens must overcome numerous anatomic barriers: </li></ul><ul><li>such as enzymes </li></ul><ul><li>Mucus that’s directly antimicrobial or inhibt the attachment of the microbe . </li></ul><ul><li>breaches of anatomic barrier unleashes specific host defenses; innate and acquired immune responses . </li></ul>
    14. 14. Immunology <ul><li>The immune system has two arms: innate immunity, which is nonspecific and immediately available; And acquired immunity, which develops over time (adaptive) to specific antigens. </li></ul><ul><li>The immune system consist of the immune cells, and the central and peripheral lymphoid structures. </li></ul>
    15. 15. Immunology
    16. 16. Innate immune response <ul><li>Key components in the innate immune response include cellular and soluble factors,which are nonspecific, invariable and they lack immunologic memory. </li></ul><ul><li>The interaction of these factors allows the body to recognize and respond to foreign antigens with their elimination from the host without or with minimal damage to host (native) tissues. </li></ul>
    17. 17. Immunology (Innate) <ul><li>The skin-mucosal surfaces serves as the first line of defense of the innate immune system. </li></ul><ul><li>Complement, acute phase proteins, natural killer cells, phagocytic wbc’s and certain cytokines provide additional protection (second line of defense). </li></ul>
    18. 18. Innate immune response. <ul><li>Nutrition </li></ul><ul><li>Age: very young-old </li></ul><ul><li>Fever </li></ul><ul><li>Immunization </li></ul><ul><li>Immunocompromised: </li></ul><ul><li>Diabetes, pregnancy </li></ul>
    19. 19. Host and the parasite
    20. 20. Humans and the Environment
    21. 21. Host and parasite
    22. 22. The Febrile response <ul><li>Fever is defined as a state of elevated body temperature that is mediated by hypothalamus (TRC). </li></ul><ul><li>Fever is usually a physiologic response to infection or inflammation </li></ul><ul><li>Malignancies </li></ul><ul><li>Autoimmune disorders </li></ul><ul><li>Allergies </li></ul>
    23. 23. The febrile response <ul><li>Many immunologically disorders, such as SLE-RA </li></ul><ul><li>Many drug reactions are associated with fever and/or rash </li></ul><ul><li>Endocrine disorders like thyrotoxicosis, adrenal insuffiency, pheochromoctyoma can also produce fever. </li></ul>
    24. 24. Fever of unknown origin <ul><li>Nosocomial FUO: fever not manifest on admission and requiring 3-days of evaluation, including blood cultures. </li></ul><ul><li>Neutropenic FUO: fever on several ocassions with absolute neutrophil count (ANC) < 500 with incubating blood cultures. </li></ul><ul><li>HIV-Associated FUO: fevers over a period > 4 weeks with outpatient evaluation or 3-day hospitalization. </li></ul>
    25. 25. Diagnostic approach <ul><li>General lab workup includes: </li></ul><ul><li>CBC with peripheral smears </li></ul><ul><li>Cultures of urine, stool and blood </li></ul><ul><li>PPD </li></ul><ul><li>ANA, Rheumatoid factor </li></ul>
    26. 26. Diagnostic approach <ul><li>Syphilis serology </li></ul><ul><li>LFT’S </li></ul><ul><li>Thyroxine-calcium level </li></ul><ul><li>HIV test. </li></ul><ul><li>Additional diagnostic test depend on the clincal setting e.g CT scans, endoscopy, BX, echocardiograms, gallium scans, etc. </li></ul>
    27. 27. Clinical Pathogens <ul><li>Mycobacterium are a group of obligate aerobes, rod shape bacilli that stain weakly (acid alcohol) gram positive. </li></ul><ul><li>Atypical mycobacteria (MOTT) like MTB have high lipid cell wall content and are recognized by their growth and response to light </li></ul><ul><li>M. kansasii-Marinum, M. Scrofula, MAC complex, M. Fortuitum-Chelonei. </li></ul>
    28. 28. Clinical Pathogens <ul><li>Chlamydiae obligate intracellular parasites closely related to gram negative bacteria </li></ul><ul><li>The three chlamydial species known to cause disease: </li></ul><ul><li>C.trachomatis, C. pneumonia and C. psittaci. </li></ul>
    29. 29. Clinical Pathogens <ul><li>Gram- bacteria contain a endotoxin, a potent inducer of cytokines and are associated with fever, bacteremia, and septic shock. </li></ul><ul><li>Gram-negative cocci that cause disease in humans are N. menigitidis, N. gonorrhea (diplococci), and Moraxella catarrhalis species. </li></ul>
    30. 30. Gram- rod (klebsiella)
    31. 31. Clinical Pathogens <ul><li>H. influenzae and other haemophilus species may cause sinusitis, otitis, bronchitis, epiglottis, pneumonitis, cellulitis, arthritis, and endocarditis. </li></ul><ul><li>Pneumonia is one of the more common infections of adults caused by H influenzae type b. </li></ul><ul><li>The enteric bacteria are large gram- rods that include E. coli, Klebsiella, Serratia, Salmonella, Shigella, Proteus and Enterobacter. </li></ul>
    32. 32. Clinical Pathogens <ul><li>Most pseudomonas infections are nosocomial, except for the peculiar risk of infection in IVDA. </li></ul><ul><li>P. Aeruginosa is the most commonly encountered nosocomial species and may cause osteomyelitis, Malignant external otitis, CNS infections, skin-soft tissue infections, and PVE. </li></ul>
    33. 33. Pathogenic Organisms
    34. 34. Infectious Organisms
    35. 35. Clinical Pathogens <ul><li>Occasionally, important infections of gram-positive rods include Anthrax, listeria, Tetanus, C. diphtheria Bacillus cereus and Clostridia. </li></ul><ul><li>Gram+ cocci are a much more common source of infections in particular the streptococci, e.g., pharyngitis, pneumonia, rheumatic fever, impetigo, and endocarditis. </li></ul>
    36. 36. Clinical Pathogens <ul><li>Anaerobic bacteria are primarily commensals, which inhabit the skin, the mouth, the gut and the female genital tract. </li></ul><ul><li>They usually cause infection when displaced from their normal sites into tissues or closed body spaces e.g lung, CNS, visceral “gut” perforation, bacteremia,or endocarditis. </li></ul>
    37. 37. Clinical Pathogens <ul><li>Mycoplasmas smallest free-living organisms, commonly found in plants, animals and humans. </li></ul><ul><li>The biologic properties of mycoplasmas, resistance to beta-lactam antibiotics, and their adhesion to host cells,result from the lack of a cell wall, in that they have a cell membrane. </li></ul>
    38. 38. “The fungus among us”
    39. 39. Mycoses
    40. 40. Clinical Pathogens <ul><li>Fungi appear either as rounded,budding forms (yeast like) or hyphae (molds). </li></ul><ul><li>Most fungi that are pathogens for humans are saprophytes in nature. </li></ul><ul><li>Some pathogens e.g cryptococcus, candida, pneumocystis, fusarium virtually never cause serious disease in the normal host. </li></ul><ul><li>Endemic fungi e.g histoplasma, aspergilla are more aggressive in the immunocompromised. </li></ul>
    41. 41. Clinical Pathogens <ul><li>Rickettsia are small gram negative obligate intracellular bacteria : </li></ul><ul><li>Typhus group </li></ul><ul><li>RMSF </li></ul><ul><li>Ehrlichiosis </li></ul><ul><li>Q FEVER. </li></ul>
    42. 42. Clinical Pathogens
    43. 43. “ I see something crawling”
    44. 44. What’s that sore
    45. 45. Clinical Pathogens <ul><li>Spirochetes of clinical importance </li></ul><ul><li>Treponema (Syphilis) </li></ul><ul><li>Leptospira (rat urine) </li></ul><ul><li>Borrelia(tick-borne) species are frequent causes of diseases. </li></ul>
    46. 46. Pathogens
    47. 47. If it’s crawling it’s alive
    48. 48. Clinical Pathogens
    49. 49. Laboratory Diagnosis <ul><li>Direct visualization: microscopy-staining can diagnose bacteria, mycobacteria </li></ul><ul><li>Candida through KOH prep </li></ul><ul><li>India ink cryptococci </li></ul>
    50. 50. Laboratory Diagnosis <ul><li>Tzanck’s smear zoster or simplex. </li></ul><ul><li>Diagnosis by microbial antigen detection via serology e.g chlamydia, mycoplasma,legionella,syphilis </li></ul><ul><li>IFA or EIA for influenzae, Hep B, RSV and Adenovirus </li></ul><ul><li>PCR and BDNA can identify viruses-bacteria. </li></ul>
    51. 51. Important Terms
    52. 52. Antimicrobials
    53. 53. Extended Spectrum PCN’s
    54. 54. Fluoroquinolones
    55. 55. Mechanism of Action
    56. 56. Mechanism of Action
    57. 57. The Bacteria Strike Back
    58. 58. Site of Action of ATB agents
    59. 59. Microbial Susceptibility
    60. 60. ANTI-MICROBIALS/ANTI-INFECTIVES <ul><li>Augmentin (Amoxicillin/Clavulanate) </li></ul><ul><li>Zosyn ( Piperacillin/Tazobactam) </li></ul><ul><li>Ticarcillin, Nafcillin, Dicloxacillin </li></ul><ul><li>Mezlocillin. Oxacillin, Methicillin </li></ul><ul><li>Pipercillin </li></ul><ul><li>Cloxacillin </li></ul><ul><li>Qxacillin </li></ul>
    61. 61. CEPHALOSPORIN <ul><li>1 st Generation-Kaflux. Valoof </li></ul><ul><li>2 nd Cefixime, </li></ul><ul><li>3 rd Rocephin, Fortaz </li></ul><ul><li>4 th Omnicef, Suprax </li></ul>