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Pathophysiology Chapter 19: Microbial Diseases of the Skin and WoundsI. Structure of the skinA. overview1. covers 2m22. varies in thickness3. replaces outer layer about once a monthB. Functions of the skin1. prevents excessive water loss2. regulates temperature3. involved in sensory phenomena4. barrier against microbial invaders5. aids in formation of vitamin D6. helps control microbial invaders through competitionC. Composed of 2 main layers1. epidermisa. superficialb. avascular – no blood vesselsc. 4-5 layers thick – depending on areas subject to abrasion-stratum basale – deepest- 1 cell layer – attached to underlying dermis-stratum spinosum – several layers of cells-stratum granulosum – typically 4-6 cell layers-stratum lucidum – present only in thick skin – 2-3 cell layers thick-stratum corneum – outer most - 20-30 layers of dead cellsd. upper layers of dead cells - filled with keratin – waterproof proteine. outer layer covered with salt and sebumf. base of epidermis mitotic 2. dermisa. below epidermisb. gives skin strength, resiliency, supportc. composed of: -cells, protein fibers, muscles (arrector pili), sweat (suderiferous) glands, oil (sebaceous) glands, nerve endings, hair follicles, vascular (blood vessels)d. below dermis-hypodermis-composed of fat and fibers-function-cushions, insulates, energy source, anchors skin to underlying tissuesD. Wounds1. trauma to any tissue of the body-cuts, scrapes, surgery, burns, bites, etc.2. allow microbes to infect deeper tissues of bodya. in most cases other body defenses eliminate infection-blood clot formed-cells divide and grow into clot-2nd line of defense kicks in-phagocytes, complement, inflammationb. can result in severe or fatal diseasesII. Norma Microbiota of the skinA. Skin microbiota normally harmless microbes present on skin, hair follicles, and in sweat ducts1. can’t be completely removed by cleansing2. body odor – bacteria breaking down sebum and producing waste (arm pits and groin)2. made of various microbesa. yeast-Malasseziab. bacteria-Staphylococcus-Micrococcus-the diphtheroids3. may produce disease-if penetrate epidermis or if immune system is suppressedIII. Bacterial Diseases of the Skin and WoundsA. Folliculitis1. signs and symptomsa. infection of hair follicleb. often called a pimplec. called a sty when it occurs at eyelid based. spread of infection into surrounding tissues can produce furunclese. carbuncles occur when multiple furuncles grow together2. pathogen and virulence factorsa. most common cause – Staphylococus-facultative anaerobic, gram-positive bacteria-cocci typically arranged in clusters-tolerant of:- up to 10% NaCl-dry conditions-solar radiation-heat up to and above 600C (1400F) for over 30 minutesb. 2 species commonly found on skin-Staphylococcus epidermis – most common – 90% of microbiota-Staphylococcus aureus – more virulent – often in nose-enzymes produced making it more virulent-coagulase – clots blood – pathogen hides in clot-staphylokinase – dissolves blood clots – pathogen released-hyaluronidase – dissolves matrix between cells – allows pathogen to spread easily-lipase – digests fat for food-β lactamase – conveys resistance to many drugsc. virulence factors-enzymes-protein A – inhibits opsonization/complement cascade-capsule – inhibits phagocytosis, chemotaxis-toxins-cytolytic toxins – disrupts plasma of cells-leukocidin – kills leukocytes -inhibitor – makes holes in blood vessels-exfoliative toxin – shed skin3. pathogenesisa. direct contact with person or fomitesb. grows into hair follicles, sebaceous glandsc. triggers fever/inflammationd. follicle enlarges and fills with puse. infection spreads into hypodermis – forms furunclef. several neighboring furuncles together – forms carbuncleg. may spread to blood-bacteremia-could lead to endocarditis, osteomyelitis, pneumonia4. epidemiologya. S. epidermis-part of normal microbiota – on all skin-seldom pathogenic-can be opportunistic pathogenb. S. aureus-not permanent resident-grows on skin, mucous membrane, moist skin folds (armpits, groin)5. diagnosis, treatment, and preventiona. diagnosis- isolation of gram-positive bacteria in grapelike clusters from pusb. treatment-Dicloxacillin – drug of choice (semisynthetic penicillin)-Vancomycin used to treat resistant strainsc. prevention- hand antisepsis-proper procedures in hospitals to minimize MRSA infectionsB. Staphylococcal scalded skin syndrome (SSSS)1. signs and symptomsa. cells of outer epidermis separateb. outer epidermis also separates from underlying tissuec. reddening/wrinkling of skin - begins near mouth spreading over entire bodyd. large blisters develop-fluid lacks bacteria/wbce. affected area peels off in sheets2. pathogen and virulence factorsa. some Staphylococcus aureus strainsb. 1-2 different exfoliative toxins cause SSSS-causes cells of outer epidermis to separate – dissolves desmosomes3. pathogenesisa. blood carries toxins throughout body - toxemiab. no scarring b/c dermis is unaffectedc. death rate rare – but may be due to secondary infections4. epidemiologya. disease occurs primarily in infantsb. transmitted by person-to-person spread of bacteria5. diagnosis, treatment, and preventiona. diagnosed by characteristic sloughing of skinb. treated by administration of antimicrobial drugsc. widespread presence of S. aureus makes prevention difficultC. Impetigo (Pyoderma) and Erysipelas1. signs and symptomsa. impetigo-small red flattened patches – mainly on face/limbs-develops into oozing pus filled vesicles-forms honey colored crust-if spreads into lymph nodes with pain and inflammation – now erysipelasb. erysipelas-red face, arms or legs-distinct margin on red patches-swollen lymph nodes-pain-fever-chills-leukocytosis-can be fatal without treatment2. pathogens and virulence factorsa. most cases caused by S. aureusb. some cases caused by Streptococcus pyogenes-gram-positive coccus, arranged in chains-virulence factors similar to those of S. aureus-M protein – interferes with complement and phagocytosis-hyaluronic acid capsule – inhibits phagocytosis-pyrogenic toxins – cause fever, rash, shock3. Pathogenesis-bacteria invade where skin is compromised4. epidemiologya. transmitted by person to person contact or via fomitesb. impetigo occurs most in childrenc. erysipelas can also occur in elderly5. diagnosis, treatment, and preventiona. presence of vesicles filled with bacteria and wbc is diagnostic for impetigob. treat with penicillin and careful cleaning of infected areasc. prevent with proper hygiene and cleanlinessD. Necrotizing fasciitis – “flesh eating strep”1. signs and symptomsa. intense pain/swelling at site of infectionb. extremely sensitive to touchc. fever, nausea, malaise, flu-like symptomsd. drop in blood pressure – causes confusion2. pathogen and virulence factorsa. most cases caused by S. pyogenesb. various enzymes facilitate invasion of tissuesc. exotoxin A and streptolysin S also secreted-exotoxin A – causes toxemia -causes over reaction of immune system-causes tissue damage-streptolysin S-kills many kinds of human cells3. pathogenesis and epidemiologya. S.pyogenes enters through breaks in skinb. usually spread person to personc. 15% die4. diagnosis, treatment, and preventiona. early diagnosis difficult b/c symptoms are nonspecificb. treat with clindamycin and penicillinc. affected tissue must be removedE. Acne1. pathogen and virulence factors-commonly caused by Propionibacterium acne - 85% of cases-gram-positive, rod shaped diphtheriods-commonly found on skin2. pathogenesisa. grows on sebum within sebaceous glandsb. excessive oil production due to hormones stimulates growth of bacteriac. chemicals secreted attracts wbc and triggers inflammationd. wbc eat bacteria and more chemicals released with same responsee. dead bacteria/wbc and live wbc make pus – pimplef. blackhead – plug of dead/live bacteria block poreg. cystic acne pustules formed-if rupture can cause scarh. acne where sebaceous glands most numerous: face scalp, neck, chest, back, shoulders, upper arms3. epidemiologya. Propionibacteria are normal microbiotab. typically begins in adolescence but can occur later in life4. diagnosis, treatment, and preventiona. diagnosed by visual examination of skinb. treated with antimicrobial drugs/drugs causing exfoliation of dead skin cells (benzoyl peroxide)c. Accutane used to treat severe acned. new treatment uses blue-light wavelength to destroy bacteriaF. Cat Scratch Disease1. signs and symptomsa. feverb. malaisec. swelling at site of infection and nearby lymph nodes2. pathogen and virulence factorsa. caused by gram-negative bacterium Bartonella henselaeb. endotoxin primary virulence factor-Lipid Ac. can grow/reproduce in rbc and cells lining blood vessels3. pathogenesis and epidemiologya. transmitted by cat bites/scratches or blood sucking arthropodsb. grows intracellularlyc. releases endotoxin when dies – triggers inflammation4. diagnosis, treatment, and preventiona. diagnosed with serological testingb. treated with antimicrobialsG. Pseudomonas Infection – most common microorganism in burn victims1. signs and symptomsa. invades bloodstreamb. chills, fever, shockc. blue-green pigment - pyocyanin2. pathogen and virulence factorsa. Pseudomonas aeruginosa is causative agent-Gram- aerobic bacillus-found in soil, decaying matter, moist environmentsb. virulence factors-adhesins, toxins, polysaccharide capsule, fimbriae, biofilmc. upon cell death, large amounts of potent endotoxin releasedd. exotoxin A and exoenzymes released-inhibit eukaryotic protein synthesise. enzyme elastase-breaks down elastic fibers-degrades complement-breaks apart some immunoglobulinsf. pyocyanin-triggers 2 reactive forms of oxygen-these 2 forms contribute to tissue damage3. pathogenesisa. infection can occur in burn victimsb. burned area moist warm environmentc. bacteria grows under scabb. bacteria kills cells, destroys tissue, triggers: fever, inflammation, vasodilation, shock4. epidemiologya. P. aeruginosa rarely part of microbiota – rarely causes disease-can cause infections throughout the body once inside-infections common in burn victims and cystic fibrosis patientsb. swimmers earc. hair follicles infected from contaminated hot tubs5. diagnosis, treatment, and preventiona. diagnosis difficult-pyocyanin discoloration indicates massive infectionb. difficult to treat due to multidrug resistance-treated with aminoglycoside and antimicrobials-polymyxin – last resort due to human toxicityc. P. aeruginosa widespread - infections not typical in healthy individualsH. Rocky Mountain Spotted Fever1. signs and symptomsa. non-itchy spotted rash on trunk and appendagesb. 50% of cases get petechiae - rash develops into subcutaneous hemorrhagesc. fever, headache, muscle pain, nausea, vomitingd. severe cases – respiratory, CNS, gastrointestinal, and renal systems fail-brain infections-produces delirium, convulsions, language issues, death2. pathogen and virulence factorsa. caused by Rickettsia rickettsiab. Gram- aerobic intracellular parasitec. pathogen avoids digestion in phagosome b/c of capsuled. dies quickly outside of hoste. needs vector for transmission from host to hostf. enters cell by endocytosisg. released from phagosome – pathogen secretes enzyme – digests phagosome’s membraneh. grows/reproduces slowly – divides ever 8-12 hoursi. daughter cells released by exocytosis3. pathogenesisa. disease follows due to damage to blood vesselsb. blood leaks from bv-bp drops-tissues deprived of O2 and nutrientsc. 5% died. if survive, may experience during recovery:-paralysis of legs-gangrene-results in amputation of arms, legs, fingers, toes-hearing loss4. epidemiology-transmitted by bite of infected tick5. diagnosis, treatment, and preventiona. initial diagnosis from rash on soles and palms, sudden, fever, headacheb. diagnosis confirmed with serological testingc. diagnosis crucial b/c treatment often makes difference between life and deathd. treated with various antimicrobialse. prevention: tick repellents, avoid tick infested areas, protective clothing, remove attached ticksI. Cutaneous Anthrax1. caused by Bacillus anthracis – enters wound2. 3 typesa. gastrointestinal – rareb. inhalationc. cutaneous3. characterized by an eschar-black, painless, ulcer4. treated with antimicrobial drugs5. prevention requires control of disease in animalsa. vaccinate animalsb. destroy infected animalsc. burn or bury carcassJ. Gas gangrene1. overviewa. blood supply to tissue interrupted – called ischemiab. tissue becomes anaerobicc. necrosis sets ind. if wound infected with anaerobic Clostridium – gas gangrene develops2. signs and symptomsa. intense pain at initial site of infectionb. blackening of infected muscle and skinc. presence of gas bubbles (H2 and CO2)d. kidney failuree. shockf. death3. pathogens and virulence factorsa. caused by several Clostridium species-anaerobic Gram+ endospore Bacillus-most common cause of disease – C. perfringesb. bacterial endospores survive harsh conditions-soil, water, sewage, intestines of animals, 1-9% of healthy women’s vaginasc. vegetative cells secrete 11 toxins-lyse rbc and wbc-increases vascular permeability lowering bp-kills cellsd. rapid growth enables rapid spreading4. pathogenesis and epidemiologya. traumatic event must introduce endospores into dead tissueb. mortality rate exceeds 40%5. diagnosis, treatment, and preventiona. appearance is usually diagnosticb. rapid treatment crucial-surgical removal of dead tissue-administration of antitoxin and penicillinc. prevent with proper cleaning of wounds IV. Viral diseases of skin and woundsA. Many viral diseases systemic in nature-these diseases can result in signs and symptoms in the skin-poxvirus, herpes infections, warts, chickenpox, shingles, Rubella, measles, Roseola, cocksackie viral infections, erythema infectiosumB. Diseases of poxviruses1. poxviruses that cause human diseasesa. smallpox - humanb. orf, cowpox, and monkeypox - animal2. smallpox 1st human disease eradicated3. signs and symptoms – progresses through series of stagesa. flat reddened maculesb. become raised sores – papulesc. fill with clear fluid – vesiclesd. fill with pus – pustules or poxe. dry and form crustf. possible scarring b/c dermis involvedg. fever (up to 1070F), malaise, delirium, prostration, possible blindness if infects eye4. pathogens and virulence factorsa. caused by Orthopoxvirus (variola virus) – DNA virusb. replicates in cytoplasmc. produces proteins that interfere with interferon, inflammation, and complementd. human pox virus – variola only infects human cellse. those of cows, sheep, goats, monkeys can – with prolonged exposure/close contact – infect humans5. pathogenesisa. smallpox virus-close contact-virus inhaled or person has contact with dried crust-dried crust can remain active for up to 2 years-virus replicates in respiratory tract-spread via blood and lymph throughout body-lesions occur in about 12 days after exposure-40% fatality rateb. other poxviruses-spread by direct contact-do not move through body-infection of humans mild6. epidemiologya. 2 strains-variola major –severe-20-40% mortality rate or higher-variola minor – mild-less than 1% mortality rateb. smallpox vaccine discontinued-increase in monkeypox cases over past decade-smallpox vaccine conveyed immunity to monkeypox also7. diagnosis, treatment, and preventiona. by visual examination – distinctive poxb. confirmed by inoculation of fertilized chick eggsc. treatment requires immediate vaccination for exposed people-prevents diseased. once disease develops – no treatment e. vaccine discontinued in 1980’sf. military personnel and some healthcare providers immunizedC. Herpes infections1. signs and symptomsa. skin lesions appear approximately 1 week after infection-on lips or genitalia-itchy, red, painful lesionsb. flulike symptoms – fever, malaise, muscle achec. recurrence of lesions is common in a bout 2/3’s of patientsd. can occur in other locations-herpes gingivostomatitis – oral cavity (inside mouth)-herpetic pharyngitis – throat-herpes gladiatorum – occurs anywhere on athletes-fingers where the skin is broken and virus enters – called a whitlowe. after primary infection-virus moves to base of nerve and becomes latent-may reactivate due to immune suppression-stress, illness, too much sun, menstrual cycle, trauma2. pathogen and virulence factorsa. caused by human herpes viruses 1 and 2-HHV1 – oral-HHV2 – genital-both can occur in either locationb. produce various proteins that act as virulence factors-glycoproteins in plasma membrane aid in fusion of virus to cells-some inactivate complement IgG3. pathogenesisa. lytic cycle-attachment-entrance-replication-assembly (in nucleus)-virus acquires its envelope from nuclear membrane as it exits-exit-exocytosis-cell lysisb. active lesions contagious-can be asymptomatic and shed virus (mainly HHV2)c. virus infects/reproduces in epithelial cellsd. produces inflammation/cell deathe. painful lesions on skin resultf. syncytium – fusion of infected/uninfected cells-how virus spreads-how virus avoids humoral immune systemg. by age 2 80%of children have HHV14. epidemiologya. spread between mucous membranes of mouth and genitalsb. can be inactive for yearsc. sometimes virus inserts itself into chromosome-can cause mutation-can cause some types of cancerd. can cause encephalitis, meningitis, pneumoniae. herpes infections in adults not life threateningf. herpes in newborns-virus can cross placenta-baby can acquire virus as passes through birth canal-mother with oral herpes can kiss baby-infection can be severe-mortality rate 30% if cutaneous/oral-mortality 80% if CNS infected-if gets in eye during birth, can cause blindness5. diagnosis, treatment, and preventiona. diagnosis made by presence of characteristic lesionsb. immunoassay reveals presence of viral antigensc. chemotherapeutic drugs help control disease d. topical drugse. no curef. prevention – caution/protectionD. Warts1. signs and symptomsa. benign epithelial growths on skin or mucous membranesb. can form on many body surfaces – toes, fingers, face, trunk, elbow, genitalsc. most are harmless/painless2. pathogens and virulence factorsa. various papillomaviruses cause wartsb. infect cutaneous or mucosal tissuec. causes epithelial cells to divided. produces wartse. some become part of cell’s chromosomes-triggers action of oncogenes-can cause cancer3. pathogenesisa. cells develop vacuoles around nucleusb. cytoplasm becomes densec. incubation period – 3-4 monthsd. can precipitate cancers in the following areas-head, neck, anus, vagina, penis, oral (mouth)-80% of all cervical cancers due to HPV4. epidemiologya. infects through abrasions/cuts in skinb. transmission-direct contact-childbirth-fomites-autoinoculation- spread to genital area by sexual intercourse5. diagnosis, treatment, and preventiona. diagnosed by observationb. usually regress over timec. various techniques to remove warts -surgery, freezing, cauterization, laser, chemicals6. new warts can develop due to latent viruses7. prevention difficult-for genital warts – abstinence or mutual monogamyE. chickenpox (varicella) and shingles1. signs and symptomsa. highly contagiousb. incubation period – 2-3 weeks after exposurec. fever, lesions on back and trunk that spread across body (can include mouth, vagina, anus penis, pharynxd. begin as maculese. 2-3 days become papulesf. become fluid filled vesicles on red baseg. dry up and crust over in few daysh. more lesions will then appeari. virus becomes latent within sensory nervesj. reappears as shingles in 15-20% of individuals who had chickenpox-shingles lesions localized to skin along infected nerve-burning sensation, numbness, itchiness, intense pain-may remain for months/years2. pathogen-Varicella-zoster virus (VZV) causes both diseases3. pathogenesisa. begins in mucous membrane of respiratory tract-moves into liver, spleen, lymph nodes via blood and lymph fluid-eventually moves to skin via bloodb. fever, rash, malaisec. virus shed through respiratory droplets and fluid in lesion-shed before and during symptoms-dry crust not infectiveb. virus becomes latent in nerve ganglia-reactivated VZV causes shingles4. epidemiologya. chickenpox occurs mostly in children-disease more severe in adults -immune system more developed therefore bigger reactionb. risk of shingles increases with agec. individual with shingles can cause another individual to get chickenpox5. diagnosis, treatment, and preventiona. diagnosis based on characteristic lesionsb. treatment based on relief symptoms-do not give aspirin to children/adolescents with symptoms of chickenpox-can cause Reyes syndromec. vaccine available against chickenpox and shinglesF. Rubella-aka German measles or 3 day measles-generally harmless/mild-not to be confused with rubeola – more severe1. signs and symptomsa. children develop mild rash (flat, pink/red spots - macules)b. swollen lymph nodesc. can cross placenta-result in birth defects or death of fetus2. pathogen and pathogenesisa. caused by rubella virusb. spread by respiratory secretions-enters respiratory tract/infects cells-travels throughout body by bloodc. causes errors in DNA replication3. epidemiologya. spreads through respiratory secretionsb. infects only humansc. virus shed for about 2 weeks before the rash and 2 weeks after rash d. most severe form in fetus under 20 weeks4. diagnosis, treatment, preventiona. diagnosis made by observation of rash and serological testingb. not treatmentc. vaccine available-aimed at preventing rubella infections in pregnant womenG. Measles (Rubeola/red measles)1. Signs and symptomsa. fever, sore throat, headache, dry cough, conjunctivitis b. Koplik’s spots appear after 2 days of illness-look like grains of salt with red halo – in mouthc. red raised lesions appear on head and spread over bodyd. rare complications-pneumonia, encephalitis, subacute sclerosing panencephalitis-SSPE – slow progressive disease of CNS – personality changes, loss of memory, muscle spasms, blindness, eventually death2. pathogen and virulence factorsa. caused by measles virus (Morbillivirus)b. adhesion and fusion proteins help virus avoid immune recognition3. pathogenesisa. infects cells of respiratory tractb. spread throughout body by bloodc. immune response to infected cells causes most symptomsd. immunocompromised patients can die4. epidemiologya. highly contagiousb. spread via respiratory dropletsc. humans only host5. diagnosis, treatment, and preventiona. diagnosis based on signs of measlesb. serological tests confirmc. no treatment availabled. immunization available as part of MMR vaccinee. frequent cause of death in other countriesH. Other viral rashes1. Erythema infectiosuma. caused by erythrovirus of family Parvoviridaeb. respiratory disease that manifests as a rash-begins on cheeks/spreads to arms, thighs, buttocks, and trunkc. also referred to as fifth diseased. in adults – may suffer anemia, joint pain, miscarriagee. no treatment2. Roseolaa. caused by human herpes virus 6 (HHV -6)b. characterized by rose-colored rashc. abrupt fever, sore throat, enlarged lymph nodes, faint pink rash on neck, face, trunk, thighsd. herpes virus (HHV6)3. coxsackievirus infectiona. caused by coxsackie A virusesb. produces lesions similar to herpes infections - occur in mouth and pharynx (herpangina)c. also causes hand-foot-and-mouth diseased. sore throat, vomiting, pain in swallowingV. Mycoses of the hair, nails, and skinA. Mycoses are fungal diseasesB. Most are opportunistic pathogensC. Mycoses classified by infection location1. superficial – on the surface2. cutaneous – in the skin3. subcutaneous - in hypodermis and muscles4. systemic – affect numerous systems-affect numerous systemsD. Superficial mycoses1. occur on hair, nails, and outer skin layers2. most common fungal infections3. acquired by direct contact with hyphae or spores4. examples: Piedra and Pityriasis5. signs and symptomsa. piedra-firm irregular nodules on hair shaft-2 kinds: black and whiteb. pityriasis versicolor-hypo or hyperpigmented patches of scaly skin-interferes with melanin production -on arms, trunk, shoulders6. pathogens and virulence factorsa. Piedraia hortae causes black piedra-Central and South America and Southeast Asiab. Trichosporon beigelii causes white piedra-worldwide: tropics and subtropicsc. Pityriasis caused by Malassezia furfur-worldwide-feeds on oil produced by skin7. pathogenesis and epidemiologya. superficial fungi produce keratinase – dissolves keratinb. do not penetrate tissuec. do not trigger immune responsed. fungi often transmitted via hair brushes and combse. in immunocompromised patients can penetrate tissues and become systemic8. diagnosis, treatment, and preventiona. piedra diagnosed by appearance; treated by shaving infected hairb. pityriasis identified by green color under ultraviolet light; treated with antifungal topical or oral drugsc. avoid contact with infected person and contaminated fomitesE. Cutaneous mycoses1. some fungi that grow in the skin manifest as cutaneous lesions2. dermatophytoses are cutaneous infections caused by dermatophytes-grow on hair, skin, nails-trigger immune response-cell mediated immune responses damage deeper tissue3. signs and symptomsa. ringworm-circular, scaly patchesb. athlete’s foot -scaly, red, itchy, burning, stinging rash between toes/on foot4. pathogens-3 genera of fungi responsible for most dermatophytoses5. pathogenesisa. use keratin as foodb. colonize hair, skin, nailsc. trigger destruction of living cells by immune systemd. infection requires traumatic introduction to deeper tissuese. rarely becomes systemic6. epidemiologya. recurrent infections commonb. classified by natural habitats: human, animals, soil7. diagnosis, treatment, and preventiona. diagnosed by clinical observationb. KOH preparation of skin or nail samples confirms diagnosisc. ltd. infections treated with topical agentsd. widespread infections treated with oral drugsF. Wound mycoses1. some fungi grow in deep tissues but do not become systemic2. fungi eventually grow into epidermis to produce skin lesions3. chromoblastomycosisa. caused by 4 species of ascomycete fungib. itchy, scaly, painless lesions that progressively worsenc. become wart-like or tumor-liked. develops fibrous tissue, inflammation, and abscessese. can spread throughout body4. phaeohyphomycosisa. caused by 30 genera of fungib. prevalent in indoor environmentsc. acquired when spores enter woundsd. rare cases, invades braine. diagnosis-microscopic examination, spinal tap for CSF, biopsy5. mycetomasa. caused by several genera soil fungib. tumorlike lesions on skin, fascia, and bones of hand and feetc. found worldwide but prevalent in equatorial regionsd. wear protective clothinge. pathogenesis-hard nodules form at wound site-local swelling-ulcerated lesions produce pus-oily fluid released with spores and hyphae-spreads to more tissues-destroys bone-causes deformityf. diagnosis-microscopic examination-symptomsg. treatment-surgery/possible amputations-follow with 1-3 years of antifungal treatment6. sporotrichosisa. caused by dimorphic ascomyceteb. subcutaneous infection usually limited to arms and legsc. occurs as fixed cutaneous or lymphocutaneous sporotrichosisd. also called rose-gardener’s diseasee. found in tropics, Latin America, Mexico, Africa, warm moist areas of USf. pathogenesis-painless nodular lesions at site-pus filled discharge-remains localized –does not spread-moves into lymph/lymphatic system but does not enter bloodg. diagnosis-microscopic examination, patient history, clinical signsh. treatment – topical and/or oral antifungal drugsVI. Parasitic Infestations of the skinA. Leishmaniasis1. disease of skin and oral mucous membrane2. intracellular parasitic protozoan3. signs and symptomsa. cutaneous- produces large painless skin lesions around bite woundb. mucocutaneous -skin lesion enlarges to encompass mucous membranes (mouth, soft palate, or nose)c. visceral-parasite spread by macrophages throughout body-inflammation, weight loss, fever, anemiad. if not treated - fatal4. pathogen and virulence factors-Leishmania causative agent-protozoan transmitted from dogs/rodents to humans by bite of female sand flies5. pathogenesis and epidemiologya. parasite infects macrophagesb. spread to liver, spleen, bone marrow, lymph nodesa. infected macrophages stimulate inflammatory responsesb. Leishmaniasis endemic in parts of tropics and subtropics-includes: Central and South America, Central and southern Asia, Africa, Europe, Middle East6. diagnosis, treatment, and preventiona. diagnosed by microscopic identification of protozoab. most cases heal without treatmentc. antimicrobials are needed for severe infectionsd. prevention involves reducing exposure to reservoir host-insect repellants, insecticides, protective clothing, nettingB. Scabies - arachnid1. signs and symptomsa. characterized by intense itching and rash at infection site-webbing between fingers, skin folds (wrist, elbows, knees, genitals)b. can get secondary infection with Staph or Strep2. pathogen and virulence factorsa. the mite Sarcoptes scabiei is causative agentb. damages nerve endings c. triggers inflammation3. pathogenesis and epidemiologya. female adults live up to month in skinb. lay eggs-what produces itching blistersc. incubation period – 4-6 weeksd. transmitted via prolonged bodily contacte. epidemics occur among people in crowded conditions4. diagnosis, treatment, and preventiona. physical examb. skin scraping with mites/eggsc. treated with mite killing lotions and cleaning of contaminated itemsd. immunity does not develope. prevented only by good personal hygienePathogenesis – the origin and development of a diseaseVirulence factors – enzymes, toxins, etc. that can affect ability of pathogen to infect and cause diseaseEpidemiology – study of occurrence, distribution, and spread of disease in humansFacultative anaerobe – bacteria that can live with or without oxygenCoccus/cocci – round shaped bacteriaBacillus/bacilli – rod shaped bacteriaStrep – bacteria arranged in chainsStaph – bacteria arranged in grape like clustersGram positive – cell wall has thick layer of peptidoglycan containing teichoic acids; stains purpleGram negative – cell wall has thin layer of peptidoglycan, external membrane, and a periplasmic space between; has Lipid A in cell membrane – released when dies – can be harmful to humans; stains pinkFomite – inanimate objects used to transfer pathogens (towel, glass, pencil, bed sheets, etc.)Antisepsis – the inhibiting or killing of microorganisms on skin or tissue by use of chemical antisepticExfoliate – to slough offSerological testing – tests carried out using blood samplesImmunoassay – a test used to detect the presence or quantity of a substance (like a protein)based on its capacity to act as an antigenProtein A – inhibits opsonization, therefore it is antiphagocyticLipid A – an endotoxin – release from dead bacterial cell can trigger vasodilation, fever, inflammation, blood clotting, shockComplement – plasma proteins – acts as chemotactic attractants, trigger inflammation, fever, and ultimately effect the destruction of foreign cellsFimbriae – sticky extensions of bacterial cell – used for attachment Malaise – feeling of general discomfortLeukocidin – kills wbc – therefore it is antiphagocyticM protein – interferes with complement and phagocytosis – associated with group A streptococcus ................
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