Chapter 19 Microbial Diseases of the Skin & Wounds PDF

Chapter 19 Microbial Diseases of the Skin & Wounds Structure of the Skin What is the role of dendritic cells found in the epidermis? Phagocytize microbes and deliver microbial antigens to lymphocytes Why is the surface of the skin inhospitable for most microbes? Salt...

Chapter 19 Microbial Diseases of the Skin & Wounds Structure of the Skin What is the role of dendritic cells found in the epidermis? Phagocytize microbes and deliver microbial antigens to lymphocytes Why is the surface of the skin inhospitable for most microbes? Salt Sweat Sebum Keratin Normal skin microbiota is able to grow and thrives in the presence of the above  Also competes with potential pathogens  Normal Microbiota of the Skin  Lipophilic Yeast Malassezia- Digest sebum Gram positive bacteria Staphylococcus, Micrococcus Staphylococcus epidermidis is the most common species Diphtheroids e.g., Propionibacterium acnes  Gram positive pleomorphic bacteria  Carbohydrate propionic acid  skin pH lowered May produce disease if penetrate epidermis or if immune system is suppressed  Normal Microbiota of the Skin Malassezia Malassezia rashes Acne Bacterial Diseases of skin include infections with: Staphylococcus Streptococcus Propionibacterium Bartonella Pseudomonas Rickettsia  Buruli Ulcer Insect bite  small painless nodule  painless swelling  increased  sudden pain  swollen finger ruptured  foul smelling liquid came out Mycobacterium ulcerans Mycolactone toxin: destroys fat & muscle cells below skin Surgeries Skin grafts Antibiotics  Rifampicin  Streptomycin Months of hospitalization Folliculitis Signs and symptoms Infection of the hair follicle, often called a pimple Called a sty when it occurs at the eyelid base Spread of infection to nearby tissues  furuncles(boil) Carbuncles: when multiple furuncles grow together Mass of inflammation and pus under thick skin Pathogen and virulence factors Most commonly caused by Staphylococcus Facultatively anaerobic, Gram-positive bacteria Tolerant of salt (10%) & desiccation 2 species commonly found on skin Staphylococcus epidermidis Staphylococcus aureus Folliculitis Staphylococcal skin infections Furuncle Carbuncle Folliculitis Pathogenesis of Staphylococcus transmitted via direct contact or by fomites Infection  blood (bacteremia)  organs beyond skin into heart, lungs and bones Epidemiology S. epidermidis lacks virulence factors but an opportunistic pathogen S. aureus transiently colonizes skin, mucous membranes, particularly nostrils. Diagnosis Isolate bacteria in grapelike clusters from pus Coagulase positive Staphylococcus aureus clot blood Treatment Antibiotics-Dicloxacillin is the dug of choice Prevention Hand antisepsis Proper procedures in hospitals to minimize MRSA  Clots blood, hides S. aureus Dissolves blood clots-spread Digests lipids  food Resistance to β lactams e.g., penicillin and cephalosporin capsule Attach biofilms to catheter etc Block IgG stems  no opsonization, no phagocytosis Disrupt CM Kills leukocytes Large holes in endothelium Scalded skin syndrome Toxic shock syndrome Staphylococcal Scalded Skin Syndrome Signs and symptoms Skin becomes red and wrinkled and forms blisters Outer epidermis peels off in sheets typically starting near the mouth spreading over the entire body Pathogen and virulence factors Some Staphylococcus aureus strains Exfoliative toxins cause the signs and symptoms of SSSS These toxins cause dissolution of intercellular bridge proteins that hold together adjoining cells Toxins carried by blood (toxemia) throughout the body Staphylococcal scalded skin syndrome Staphylococcal Scalded Skin Syndrome Pathogenesis No scarring because dermis is unaffected Death rare, may be due to secondary infections by Candida albicans, Pseudomonas aeruginosa Epidemiology Disease occurs primarily in infants and children under 5 and in the elderly and immunosuppressed. Transmitted by person-to-person spread of bacteria into cuts and abrasions Diagnosis, treatment, and prevention Diagnosed by characteristic sloughing of skin Treated by administration of intravenous antimicrobial drugs (cloxacillin) Impetigo (Pyoderma) and Erysipelas Signs and symptoms Impetigo: red patches form on the face and limbs  oozing pus filled vesicles  thick honey colored sticky crust  intense itching Usually children Numerous vesicles at various stages of development Erysipelas: infection spreads to lymph nodes  intense pain & inflammation  may be fatal Reddening of skin of face, arms or legs Red area has distinct margins Swollen local lymph nodes, pain, fever, chills Fatal if left untreated  Impetigo Erysipelas Children are usually infected with Impetigo just below the nose where the skin is abraded by frequent wiping away of mucus Impetigo (Pyoderma) and Erysipelas Pathogens and virulence factors Staphylococcus aureus & Streptococcus pyogenes Virulence factors of Streptococcus pyogenes that contribute to impetigo  M protein destabilizes complement, interferes with phagocytosis and lysis of bacterium  Hyaluronic acid capsule hides bacteria from phagocytes  Pyrogenic toxins(Erythrogenic toxins) make macrophages & TH cells make cytokines  fever, rash, shock Pathogenesis Invade where the skin’s integrity is compromised Acute glomerulonephritis Impetigo (Pyoderma) and Erysipelas Epidemiology Spread via person-to-person contact or via fomites Impetigo occurs most in children (in nurseries) Erysipelas can also occur in the elderly Diagnosis, treatment, and prevention Presence of vesicles is diagnostic for impetigo Pus in blisters filled with bacteria and white blood cells Impetigo is treated with oral and topical antimicrobials and careful cleaning of infected areas Erysipelas is treated with penicillin Prevent with proper hygiene and cleanliness Necrotizing fasciitis Caused by Group A Streptococcus (S. pyogenes) and by Staphylococcus aureus “Flesh eating” bacteria Person to person contact  enters broken skin Invasive enzymes of Streptococcus pyogenes Streptokinase: dissolves blood clot Hyaluronidase: breaks down hyaluronic acid Deoxyribonuclease: breaks down host DNA M protein: helps bacteria survive phagocytosis Streptolysin: kills neutrophils and RBCs Exotoxin A: triggers immune responses  damage to healthy tissue  Necrotizing fasciitis Streptococcus pyogenes Diagnosis, treatment, prevention Early diagnosis difficult Surgical emergency Removal of dead tissue immediately Treat with intravenous clindamycin, penicillin Necrotizing fasciitis Begins as an injury that rapidly becomes red, swollen, intensely painful and hot to touch.  Acne Pathogen  Propionibacterium acnes  Commonly found on the skin  Gram-positive, rod-shaped diphtheroids Epidemiology  Propionibacteria are normal microbiota  Typically begins in adolescence, can occur later Diagnosis, treatment, and prevention  Diagnosed by visual examination of the skin  Treated with antimicrobial and exfoliation drugs(Benzoyl peroxide)  Retinoic acid Vitamin A derivative inhibits sebum formation  A specific wavelength of UV light is also used Cat Scratch Disease Signs and symptoms Swelling of a scratch leading to fever, malaise, swollen lymph nodes Pathogen and virulence factors Bartonella henselae (Gram-negative Intracellular bacillus of skin) Endotoxin: primary virulence factor Pathogenesis and epidemiology Transmitted by cat bites, scratches Diagnosis, treatment, & prevention Diagnosed with serological testing Treated with antimicrobials-rifampicin,ciprofloxacin Pseudomonas Infection Signs and symptoms Commonly seen in burn victims Blood infection causes fever, chills, shock Blue-green color from bacterial pigment pyocyanin contributes to tissue damage Pathogen and virulence factors Pseudomonas aeruginosa is the causative agent Gram-negative bacillus Soil, decaying matter, moist areas Numerous virulence factors  Fimbriae, adhesins, capsule, toxins, enzymes OPPORTUNISTIC PATHOGEN  Pseudomonas aeruginosa Pyocyanin pigment Nail infection Pseudomonas Infection Fimbriae & adhesins: Attach to host cells, form biofilms Capsule: shields bacteria from phagocytosis, helps in biofilm formation and attachment Neuraminidase: modifies host cell receptors to make bacterial attachment better Elastase: breaks down elastic fibers, cleaves IgG & IgA Endotoxin (lipid A): fever, blood clotting, inflammation, shock Exotoxin & exoenzyme S: inhibit translation in host Pyocyanin: form superoxides that damage host cells Pseudomonas Infection Pathogenesis Infection can occur in burn victims Bacteria grow under the surface of the burn Bacteria kills cells, destroys tissue, triggers shock Debridement of burn is required for topical antimicrobials to be effective Epidemiology P. aeruginosa is inhabitant of water and soil Swimmer’s ear (otitis externa) Bacterium rarely part of the human microbiota Can infect almost any organ once inside body Pseudomonas Infection Diagnosis, treatment, and prevention Pyocyanin discoloration indicates massive infection Multi-drug resistant (MDR), resistant to antimicrobials, quats, soaps etc., lives in disinfectants Infections typically don't occur in healthy individuals Multidrug resistance due to Ability to metabolize many drugs Antiports that pump many drugs out of bacterium Ability to form biofilms Ubiquitous so can’t prevent exposure  Simultaneous use of Sulfonamide and Piperacillin  Rocky Mountain Spotted Fever Pathogenic process Pathogenic process involves damage to blood vessels! Rocky Mountain spotted fever (RMSF) Pathogen Arthropod-borne rickettsias  vector is a tick Signs and symptoms Non-itchy petechial rash starting on hands & feet  spreads to torso Organ failure can occur in severe cases Fever, nausea, vomiting, muscle pain, chills, delirium, convulsions, coma, death Pathogen and virulence factors Caused by Rickettsia rickettsii Gram negative, aerobic, obligate intracellular parasite Rickettsias do not use glucose as a nutrient Pathogen avoids digestion in phagosome by secreting an enzyme that lyses phagosome Rocky Mountain Spotted Fever Pathogenesis Dormant in salivary gland of tick until bloodmeal Bacteria reaches blood, damages blood vessels R. rickettsii does not secrete any toxins Epidemiology Transmitted via bite of infected Dermacentor tick Rodents are reservoir Diagnosis, treatment, and prevention Diagnosed with serological testing Treated with antibiotics-doxycycline Prevented with the use of tick repellents and avoidance of tick-infested areas Cutaneous Anthrax Caused by Bacillus anthracis Facultatively anaerobic, endospore forming rod Endospores shed by infected animal  enter wound in skin  solid skin nodule  capsule prevents phagocytosis  3 toxins kill cells in affected area Eschar: black, painless, crusty, swollen ulcer characteristic of anthrax Anthrax = charcoal Cutaneous Anthrax Virulence factors Endospore, capsule, 3 anthrax toxins Portal of entry Direct contact of endospores with wounded skin Signs & symptoms Localized itching  raised lesions  painless black eschar in 7 – 10 days Treatment & Prevention Ciprofloxacin is the treatment Prevention is by vaccination of livestock Vaccine is for high-risk personnel  6 doses with annual boosters Gas Gangrene Signs and symptoms Death of muscle, connective tissue Spreading black necrosis Gas bubbles/froth Swelling, pain Rapid treatment crucial! Pathogens Caused by several Clostridium species Anaerobic, Gram-negative, endospore forming bacilli C. perfringens is most often isolated Bacterial endospores survive harsh conditions Gas Gangrene Virulence factors Endospore, 11 toxins, rapid growth & cell division Portal of entry Endospores introduced into tissue via surgical incision, gunshot, puncture, crushing trauma etc Signs & symptoms Increased pain & swelling, fever, foul smelling drainage from tissues, crepitation (crackling sound), tachycardia  if untreated, shock, coma, death Incubation Less than 24 hours to 3 days Diagnostics, Treatment & Prevention Appearance diagnostic, prompt cleaning of wounds & dead tissue, antitoxin, antibiotics (clindamycin, penicillin) Viral Diseases Smallpox – Variola virus First human disease to be globally eradicated Diseases progress through a series of stages Flat, red Pus filled pox Lesion filled with pus Raised sore Dried crust Lesion ruptures, becomes crusty Clear fluid Lesion penetrates dermis Lesion filled with fluid Smallpox – Variola virus Poxviruses are enveloped dsDNA viruses Virulence: proteins inhibit interferon, complement, inflammation Portal of entry: Smallpox infection occurs by inhalation of virus in droplets/dried crusts where virus infective for 2 yrs Viruses replicates in respiratory tract  spreads via blood & lymph nodes  lesions in skin 12 days after infection Pathogenesis Close contact necessary for spread of virus Diagnosis, treatment, and prevention Treatment requires immediate vaccination Smallpox- Variola Smallpox virus Herpes Infections Slow-spreading skin lesions whitlow Recurrence of lesions is common Caused by human herpesviruses 1& 2 Produce various proteins that act as virulence factors Portal of entry mucus membranes of mouth or genitals Malaise, fever, muscle pain precedes blisters Blisters break  tender ulcer  many weeks to heal Painful lesions caused by inflammation and cell death Warts Lesions caused by papillomaviruses Transmitted via direct contact and fomites Individuals can spread viruses among locations on their own body Various techniques to remove warts New warts can develop as a result of latent viruses Chickenpox & Shingles Chickenpox Varicella zoster virus (VZV) Highly contagious Infection spreads from respiratory tract to skin via blood and lymph Lesions on back & trunk that spread across body Virus becomes latent within sensory nerve ganglia “teardrops on rose petals” rash Shingles or Herpes zoster Occurs following reactivation of the VZV Lesions are localized to skin along infected nerve Pain may last after lesions have healed Measles (Rubeola) Characterized by Koplik's spots measles virus fatal in children Respiratory tract  lymph nodes & blood Sore throat, fever, headache, dry cough, conjunctivitis Human is the only host Rubella German measles or 3-day measles Rubella virus Congenital infection can result in birth defects or death of fetus Infection spreads from the respiratory tract throughout the body via the blood Fungal Infections (Mycoses) Dermatophytoses: Cutaneous Mycoses Cutaneous fungal disease caused by dermatophytes Grows on skin, hair and nails and use keratin as nutrient source Trigger destruction of living tissue by immune system Remain localized to epidermis, dermis, hypodermis Ringworm Athlete’s foot and “Jock itch” Athlete’s foot Ringworm Diseases by Protozoan Parasites Leishmania Female Sandfly Leishmaniasis Cutaneous: large, painless skin lesions Mucocutaneous: Skin lesions enlarge to encompass mucous membranes Visceral: Parasite is spread by macrophages throughout body  Infected macrophages stimulate inflammatory responses  FATAL Leishmania is the causative agent transmitted by female sand flies Kala azar( visceral): Protozoan in liver, spleen, bone marrow, lymph nodes  fever, weight loss, anemia  Disease by an Arachnid (Mite) Sarcoptes scabiei Itch mite on skin Scabies Itching blisters occur where female mites lay eggs Mites transmitted via prolonged body contact Diagnosis made by observing mites, eggs, or fecal matter in skin samples or characteristic burrows Treated with mite-killing lotions and cleaning of contaminated items Prevented only by good personal