Describe the structure of the skin and mucous membranes and the Lecture 29 chapter 21 ways pathogens can invade the skin Skin inhospitable to most microbes Dry Perspiration and sebum contain nutrients salt inhibits microbes Lysozyme hydrolyzes peptidoglycan Fatty acids inhibit some pathogens Defensins are antimicrobial peptides found on the skin also found in the mucous membranes especially the GI tract mucous consists of sheets of tightly packed epithelial cells These cells are attached at their bases to a layer of extracellular material called the basement membrane Many of these cells secrete mucus Other mucosal cells have cilia and in the respiratory system the mucous layer traps particles including microorganisms which the cilia sweep upward out of the body microbial populations Also the membranes of the eyes are mechanically washed by tears and the lysozyme in tears destroys the cell walls of certain bacteria Mucous membranes are often acidic which tends to limit their Pathogens can enter through broken skin and parasitic larvae can enter through intact skin directly Provide examples of normal skin microbiota and state the general locations and ecological roles of its members On skin surfaces certain aerobic bacteria produce fatty acids from sebum these acids inhibit many microbes and allow better adapted relatively resistant to drying and to relatively high salt bacteria to flourish concentrations staphlycocci and micrococci skin contains relatively larger number of gram pos bacteria bacteria on the skin tend to be grouped in small clumps more moisture on body higher pop of microbes They metabolize sweat gland secretions and are the main contributes to body odor Differentiate Staphylococci from Streptococci and name several skin infections caused by each Staphylococci skin infections Gram low GC cocci in clusters Coagulase an enzyme clots fibrin in blood divide in those that do coagulase and those that dont majority of skin flora consists of coagulase doesn t coagulase S epidrmidis very common on skin may represent 90 of normal microbiota streptococcal skin infections only pathogenic if skin barrier is broken catheter the most pathogenic is S aureus also produces extracellular Causes all pathogenic S aureus are Coagulase enzymes and toxins Located in nasal passages sometimes Folliculitis pimples hair follicle infection styes eyelash carbuncles if a furnucle cannot be walled out by the body s furuncles boils pus abscess immune system and more tissue becomes progressively invaded and a hard deep round inflammation under skin occurs Scalded skin syndrome toxin produced by staph that makes the skin peel in sheets Associated with TSS Toxic shock syndrome TSS from highly absorbent tampons left in too long Impetigo highly contagious skin infection in children pathogen usually enters through minor break in skin Toxemias occur when toxins enter bloodstream Gram Low GC cocci in chains Hemolysins beta alpha and gamma hemolysis lyse cells esp Beta hemolytic strep is classified into groups according RBCs hemolytic enzymes and surface antigens Group A most important Many virulence factors s pyogenes Many prophages carry virulence factors Groups B C O M protein prevents activation of the complement and allows to microbe to evade phagocytosis and killing by neutrophils Also helps bacteria adhere to and colonize mucous membranes extracellular enzymes hyalurondiase dissolves the hyaluronic acid in connective deozyribonucleases degrades DNA dtreptolysis lyses RBCs and toxic to neutrophils toxins streptokinases dissolve blood clots tissue M protein on surface anti complement anti phagocytosis Causes Impetigo isolated pustules Fewer cases than staph caused impetigo Erysipelas s Pyogenes skin errupts in red patches Can enter bloodstream causing sepis Caused by group A beta hemolytic Strep toxin Invasive Group A Streptococcal Infection Streptokinases Hyaluronidase Exotoxin A superantigen acts as a superantigen causing the Cellulitis Necrotizing fasciitis flesh eating severe and rapid tissue damage List the causative agent mode of transmission and clinical symptoms immune system to contribute to damage of Pseudomonas dermatitis otitis externa and acne Aerobic gram negative rods that are widespread in water and soil Gram negative rods Five groups Unusual metabolism grow on traces of organic substance in Most prominent species P aeurginosa soap liner adhesive Environmental soils and water Opportunists P aeurginosa has an endotoxin and grows in dense Cause biofilms which contributes to its frequency in nosocomial infections of indwelling medical tubes or devices Oppurtunists for people with serious cystic fibrosis Concerns in hospitals is how easy this bacteria can grow in flower vases mop water and diluted disinfectants Pseudomonas dermatitis self limiting rash 2 wks duration swimming pool sauna hot tub where a lot of people use and so it makes the water more alkaline and the chlorine becomes less effective hair follices open wider facilitating the entry of bacteria Hot Tub Rash Pseudomonas Folliculitis Hot water makes the Wound and skin infections Otitis externa swimmer s ear Burn patient infections oppurtunists Infections have a characteristic of blue green pus pyocynanin Acne caused by when skin cells are shed at higher rate than normal and they combine with sebum and this mix clogs pores List the causative agent mode of transmission and clinical symptoms of these skin infections warts smallpox chickenpox shingles cold sores measles rubella Warts or papillomas caused by papollomavirus benign skin growths causes by viruses smallpox pox variola transported by respiratory route chickenpox varicella result of an initial infection with the herpesvirus varicella zoster transported by respiratory route pus filled vesicles Latency dorsal root ganglion viral DNA No viral antigens are expressed on surface of nerve so cytotoxic T cells aren t stimulated shingles herpres zoster immune system peripheral nerves to skin several months or years Painful dermal infections dermatomes latent varicella zoster virus decades later the virus can be reactivated by stress or lower Reactivation of latent VZV releases viruses that move along Postherpetic neuralgia severe burning or pain persists for Prevention Live attenuated vaccine Acyclovir antiviral drug may lessen symptoms herpes simplex virus HSV divided into HSV 1 2 transmitted primarily by oral or respiratory routes Cold sores or fever blisters vesicles on lips
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