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Micro Chapter 18

Micro Chapter 18. Microbial diseases of the Skin Structure of skin Epidermis Dermis Pathways into deeper tissues – hair follicles and sweat glands Normal flora – skin has many microbes present as commensals, can be opportunistic pathogen if the skin is breached. Micro Chapter 18.

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Micro Chapter 18

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  1. Micro Chapter 18 Microbial diseases of the Skin Structure of skin Epidermis Dermis Pathways into deeper tissues – hair follicles and sweat glands Normal flora – skin has many microbes present as commensals, can be opportunistic pathogen if the skin is breached

  2. Micro Chapter 18 1. These microbes are adapted to dry conditions and even the fatty acids that inhibit most other microbes. Ex. Staphylococcus and Micrococcus 2. Other genera – Corynebacterium and Propionobacterium

  3. Fig. 18.1

  4. Fig. 18.2, Impetigo

  5. Staph and Strep on blood agar

  6. Micro Chapter 18 Bacterial diseases of the skin : 1. Staphylococcal skin infections - S. Aureus, has some highly virulent strains A. Gram + cocci, catalase +, coagulase +, beta hemolytic, golden yellow colonies on nutrient agar B. The commensal staph are usually catalase and coagulase negative – S. epidermididis C. Pathogenic staph can produce dangerous toxins i. Leukocydin – kills leukocytes

  7. Micro Chapter 18 ii. Exfoliate toxin – causes skin to separate and peel away – (SSSS) – staph scalded skin syndrome (pg.), bacteriophage dependent toxin (toxemia) iii. Coagulase – fibrin clots, shield staph from phagocytes iv. Entero toxin – exotoxin that causes FBI symptoms in the intestinal tract v. Toxic shock toxin 1 – life threatening disease, toxin enters blood stream, causes symptoms of fever, vomiting, skin rash and deadly shock (originally diagnosed and associated with use of vaginal tampons – now associated with surgical procedures using packing or post childbirth complications)

  8. Micro Chapter 18Coagulase test

  9. Micro Chapter 18Rapid Staph tests

  10. Micro Chapter 18Staph: SSSS

  11. Micro Chapter 18 D. Pathogenesis on skin i. Folliculitis – infection of hair follicles (pustules) ii. Boils and carbuncles – deeper more serious infection of hair follicle – treat by lancing and draining, penicillins iii. Abscesses – deep pustular lesions, can be serious, can invade deep into tissue and causes blood stream infection (septicemia) iv. Impetigo (really a four letter word) in hospital nurseries and daycares, reason for use of hexachlorophene disinfectants

  12. Micro Chapter 18Staph: Boil, Carbuncle Staph; skin infections, danger – toxemia, septicemia

  13. Staph - Furuncle, Carbuncle

  14. Micro Chapter 18 E. Drug resistance is a real problem with Staph i. Many are penicillin resistant, artificial penicillins – methicillin resistant strains are appearing ii. Cephalosporins are used (resistant to penicillinases) iii. Vancomycin is drug of last resort, now a few strains resistant to vancomycin (Detroit area)

  15. Micro Chapter 18 Drug resistant Staph; MRSA

  16. Micro Chapter 18

  17. Micro Chapter 18 2. Streptococcal skin infections – gram + cocci, usually in chains, A. Group a beta hemolytic strep (S. pyogenes) B. Erysipelas – serious infection by Strep of the skin, can spread and even cause septicemia – treatable with penicillin type drugs

  18. Micro Chapter 18 Beta hemolytic Strep

  19. Micro Chapter 18 C. Impetigo – local skin infections (often with Staph), spread easily on contact and spreads among children in day cares (page)

  20. Micro Chapter 18 • D. Remember Strep has several virulence factors (hyaluronidase, streptokinases, • hemolysins, etc.) • E. Group a Strep – associated with the necrotizing fascitis – flesh eating Strep, • exotoxin a seems to be associated, deep tissues involved (cellulitis, myositis, • muscle coverinng – fascia) see pg 551

  21. Micro Chapter 18Page 539.2

  22. Micro Chapter 18 • 3. Clostridium perfringens – gram+ anaerobic spore forming rod shaped bacteria • A. Gas gangrene – (pg. 549) infection occurs after skin is punctured, the organism • produces an alpha toxin that kills cells, and then dead cells are substrate for • more growth, more toxin, more dead tissue, rapid spreading of disease • B. Treat with debridement of dead tissue and hyperbaric chamber (get oxygen deep into tissues), penicillin type antibiotic • C. Can grow in high protein food that is low in oxygen and causes FBI • (enterotoxin) gravies, stews, thick meat dishes - out of temperature for too long

  23. Micro Chapter 18 • gangrene

  24. Micro Chapter 18 • Hyperbaric set up

  25. Micro Chapter 18 • 4. Leprosy – Hansen’s disease, Mycobacterium leprae, stains acid fast like tubercle bacilli, • strict human parasite, not able to culture it, was cultured in Armadillos so that it could be • studied and antigens harvested for evaluation and development of ?vaccine? • A. Not very virulent, slow progression • B. Tuberculoid form, minor skin damage, but can cause nerve damage • C. Lepromatous form, gross disfigurement – see page 552 lepromas • D. See checkpoint 18.6

  26. Micro Chapter 18 • Leprosy; awful

  27. Micro Chapter 18 • Viral infections • 1. Warts – papillomas , many different viruses • 2. Variola – smallpox, see text - biological warfare and mandatory vaccination? • 3. Varicella – chickenpox, and shingles • Warts Variola Varicella

  28. Micro Chapter 18 a. Chickenpox is relatively mild childhood disease b. Herpes type virus, acquired by respiratory system and then localizes in the skin c. Forms vesicles in skin, fill with pus, and then rupture d. Chickenpox in adults can be serious and if acquired early in pregnancy can cause serious fetal damage e. Since it is a herpes type virus can become latent, later it can erupt into serious disease in adults called shingles i. Latent in peripheral nerve ganglia ii. Triggers can be stress or aging, the virus outbreak occurs along the peripheral nerves, about the waist and even face and scalp very painful iii. Immunocompromised patients, may be fatal f. Vaccine now seems effective

  29. Micro Chapter 18 • 4. Herpes simplex viruses – HSV-1 and HSV-2 • A. H4. Herpes simplex viruses – HSV-1 and HSV-2 • A. HSV – 1 cold sores (fever blisters) most acquire it infancy, respiratory or oral route, • latent virus activated by stress, UV light etc., • B. HSV – 2 similar virus spread by sexual contact – genital herpes – 1 cold sores (fever blisters) most acquire it infancy, respiratory or oral route, • latent virus activated by stress, uv light etc., • B. HSV – 2 similar virus spread by sexual contact – genital herpes

  30. HSV 1, HSV 2

  31. Measels • 5. Rubella – german measles, mild childhood disease • A. Good vaccine available (MMR.) Checkpoint 18.8, pg 563 • B. Can pass placental barrier and cause serious deformities or death of fetus • 6.Rubeola – red measles, good vaccine available (MMR), some children are not vaccinated in the inner city areas, see measles outbreaks • A. Can be very serious disease in infants and elderly • B. Secondary bacterial infections are a problem (pneumonia)

  32. MeaselsRash Congenital rubella

  33. Micro Chapter 18 • Dermatophytes – fungal infections of the skin – griseofulvin, miconazole sse pg 568, checkpoint • 18.11 • 1. Mycosis – fungal infection • 2. Cutaneous infection – dermatophytes grow on moist skin using keratin in skin as substrate • 3. Tineas or ringworms scalp – tinea capitis, tinea cruris – groin, tinea pedis- feet (athletes foot) • 4. Tricophyton spp., Microsporium spp., Epidermophyton spp.

  34. Micro Chapter 18, Scalp ringworm

  35. Micro Chapter 18, Ringworm of body

  36. Micro Chapter 18 – tinea pedis

  37. Micro Chapter 18: Tricophyton, M. canis, Epidermophyton

  38. Micro Chapter 18 • Candida albicans – yeast infection, candidiasis, in infants causes thrush, common cause of • vaginitis - miconazole, clotrimazole

  39. Micro Chapter 18 Eye diseases: 1. Conjunctivitis – Trachoma Chlamydia trachomatis 2. Neonatal conjunctivitis by Chlamydia and N. gonnorrhea 3. Viral - adenoviruses

  40. Fig. 18.21, Neonatal conjunctivitis

  41. Fig. 18.22 Trachoma

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