micro lecture 4

ch 19 pathogenic gram-positive bacteria
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ch 19 pathogenic gram-positive bacteria
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Staphylococcus structure & physiology
-facultative anaerobic
-nonmotile staphlyococci
staphlyococcus is tolerant of?
-salt tolerant
-tolerant of desiccation, radiation, heat
staphylococcus can survive on
environmental surfaces
2 species of staphylococcus assoc. w diseases in humans:
staphlyococcus epidermidis

staphlyococcus aureus
staphylococcus epidermidis:
___________ of human skin
______________ infections
-microbiota of human skin
-opportunistic
staphylococcus aureus:
-_________ microbiota of _____________
-more ___________ strain
-Normal microbiota of mucous membranes (20% of population)
-More virulent strain
staphylococcus aureus: pathogenicity results from three features:
-structural defenses against phagocytosis
-production of enzymes
-production of toxins
Structural defenses against phagocytosis:
protein A
bound coagulase
slime layers (capsule)
production of enzymes:
hyaluronidase
staphylokinase
lipases
B-lactamase
production of toxins:leukocidins exfoliative toxins toxic shock syndrome toxin enterotoxinsStaphylococcus aureus primarily found:only in moist skin foldss. aureus can grow in what tracts of humansupper respiratory GI UGS. aureus is harbored by what carriersasymptomatic actives. aureus is transmitted bydirect contact fomitesstaphylococcal diseases vary depending on:site of infection immune state of host strain virulences. aureus noninvasive disease:staphylococcal food poisioningstaph. cutaneous diseases:impetigo folliculitis SSS sty furuncle carbuncles. aureus systemic diseases: result when staphylococci enter deeper tissuesTSS bacteremia endocarditis pneumonia osteomyelitisstaph. food poisoning: food sources: signs & symptoms: pathogenesis: treatment/prevention:-high protein foods made w hand contact that require no add. cooking -nausea, vomiting, diarrhea -ingestion of enterotoxin-contaminated food -ORS, proper handling, refrigeration, heatingfolliculitisinfection of hair folliclesstyfolliculitis of an eyelashimpetigocrusting pustulesfuruncle(boil) hard, tender, red nodule, extension from follicle in to surrounding tissuecarbuncle-several furuncles coalasce -extends to deeper tissues -fever -chills -pus dischargingscalded skin syndromeredness loss of skin exfoliative toxinssystemic diseasesTSS bactermia acute bacterial endocarditistoxic shock syndrome TSS-some staph. strains produce TSS toxin -bacteria grow in wound or abraded vagina & TSS toxin absorbed in blood -produces fever, vomiting, rash, low blood pressure ---> shockbacteremiastaphylococci enter bloodstream & travel to heart, lungs, boneacute bacterial endocarditisdamage to heart liningstaph. aureus: diagnosis treatment prevention-detecting staph. in pus or blood -drainage, debridement of wounds -antimicrobial therapy -MRSA serios problem, intially only HA but now CA -decolonization -hand antiseptisgroup A streptococcus: streptococcus pyogenes structure & physiology-Facultative anaerobes -Cocci arranged in pairs or chains -Lancefield classification: serotype Agroup A streptococcus: streptococcus pyogenes epidemiolgy-typically infects pharynx or skin -often causes disease when normal microbiota are depleted, large infecting dose occurs, or person is immunocompromised -spreads via respiratory dropletsgroup A streptococcus: streptococcus pyogenes pathogenicity-Hyaluronic acid capsule: "invisibility cloak" -M proteins -Hemolysins called streptolysins -Hyaluronidase, streptokinases -Lysogenized bacteria produce pyrogenic toxins that cause immune cells to release cytokines stimulating fever, rash, and shock -C5a peptidase destroys C5agroup A streptococcal diseases:pharyngitis scarlet fever rheumatic fever pyoderma erysipelas necrotizing fasciitispharyngitis"strep throat" -inflammation of pharynx w pus patches, cervical lymphadenopathy, fever -might disseminate to laryngitis or bronchitisscarlet fever can occur followingstreptococcal pharyngitis infections when infection involves lysogenized strainscarlet fever ___________ triggers rash also known as?pyrogenic toxins "strawberry tongue"rheumatic fever-complication of untreated streptococcal pharyngitis -autoimmune response against heart antigens -inflammation damages heart valves, muscle, skin, joints, nervous tissue -treatment: anti inflammatory medspyodermaimpetigo along w s. aureus pus producing lesion often on exposed skinerysipelasinfection & inflammation on lymph nodes surrounding streptococcal infection of superficial skin layers -bacteria can stread to bloodstream causing bacteremia & streptococcal TSSnecrotizing fasciitis-streptococci enter body, spread along fascia -secrete enzymes & pyogenic toxins that destroy tissue: exotoxin A exotoxin B -destruction is rapid-several cm per hour -treatment: debridement or amputationexotoxin Atriggers overactive immune response that further damages healthy tissueexotoxin Bprotease that destroys tissue (fascia, muscle, fat)group a streptococcal diagnosisskin infections w presence of gram-pos. streptococci *rapid strep test* against antigens used to diagnose respiratory infectionsgroup a streptococcal treatmentpenicillins cephalosporins erythromycin to prevent complicationsgroup a streptococcal preventionantibodies against M protein provide protection but multiple strains existalpha-hemolytic streptococci: viridans group-lack group specific carbohydrates & cannot be grouped by lancefield system -usually *alpha hemolytic* inhibit mouth, pharynx, GI tract, genital tract, urinary tract -*opportunistic pathogens*streptococcus mutans is most common cause ofdental caries -biofilm forms dental plaque -can cause *endocarditis* if enters bloodstrept. pneumoniae structure & physiologydiplococcus alpha hemolytic lacks lancefield antigensStrept pneumoniae pathogenesisgreat at "hiding" hyaluronic acid capsule *phosphorylcholine* in cell wallStrept pneumoniae epidemiologynormal inhabitant of URT, cofactors involved w disease -most common in children & elderlystrept. pneumoniae diagnosis treatment prevention-gram stain of sputum of CSF -still responsive to most antibiotics -*PSV* -23 strain conjugate vaccinepneumococcal disease-pneumoncoccal pneumonia -sinusitis & otitis media -bacteremia -endocarditis -pneumococcal meningitispneumococcal pneumonia*primary typically pneumonia* -bacteria inhaled into damaged lungs -symptoms: abrupt onset of high fever, chills, productive cough w bloody septum, chest painsinisitis & otitis media sometimes occur following: ____________ symptoms:viral infections -pain -pressurepneumococcal meingitis spread to meninges following: symptoms:bacteremia, sinusitis, or otitis media -fever -headache -stiff neck -nausea -vomiting -convulsions -comahighest mortality ratepneumococcal megingitismost common disease caused by S. pneumoniaepneumococcal pneumoniabacillus anthracis-large bacillus -zoonosisbacillus anthracis produces ___________ & __________ _________endospores anthrax toxinsInhalational (pulmonary) anthrax: resembles what? -most _________.initially resembles pneumonia; most fatalGastrointestinal anthrax: __________ lesions in what?ulcerative lesions in GI tractCutaneous anthrax: producesproduces ulcers called *eschars*bacillus anthracis responds well to _______ if caught earlyAbxbacillus anthracis prevention in humans requires control in:animals: vaccine -burn/burt carcassesclostridium: aerobic or anaerobic? __________- ________ bacillus __________ in soil, water, & _____ tracts of animals & humansAnaerobic, endospore-forming bacillus Ubiquitous in soil, water, and gastrointestinal tracts of animals and humans Endospores allow for survival in harsh conditionsclostridium: __________ allows for survival in harsh conditionsendosporesclostridium perfringens: pathogenesis & disease-*food poisoning*: spores germinate in contaminated foods & produce enterotoxin ----> cramping & diaarhea -*gas gangrene*: spores germinate in wound w dead tissue & produce toxins that perpetuate conditions & cause nercrosisclostridium perfringens: food poisoning prevention & treatment-proper storage -reheating -self limitingclostridium perfringens: gas gangrene prevention & treatment-proper wound care -antitoxin -antibiotics surgery-oxygenclostridium difficile epidemiology-common member of intestinal microbiota -*opportunistic pathogen*clostridium difficile pathogenesis & disease-C. difficile sporulates, produces 2 exotoxins and hyaluronidaseclost. difficile overgrows causing:hemorrhagic death of intestinal wallclost. difficile minor infections result in:self-limiting explosive diarrheaclost. difficile serious cases can cause:pseudomembranous colitisclost. difficile diagnosis:Isolation of organism from feces or presence of toxins by immunoassayclost. difficile: prevention treatment-proper hygiene limit nosocomial infections -minimizing antibiotic use -Discontinue causative antimicrobial drug -Serious cases treated with more specific antibiotics: vancomycin or metronidazole -Fecal bacteriotherapyclost. botulinum strains produce:7 distinct botulinum neurotoxinsclost. botulinum: bind: prevent:neurons muscle contractions: *flaccid paralysis*foodborne botulism:-intoxication from consuming toxin in home-canned foods or preserved fish -Weakness, double vision, progressing to asphyxiation -Slow recovery from growth of new nerve cell endings -antibiotics are NOT effective!infant botulismfrom ingestion of endospores -Crying, constipation, "failure to thrive" -Paralysis and death are rarewound botulism-frmo contamination of wound by endospores -Weakness, double vision, progressing to asphyxiationclost. botulinum diagnosis-symptoms are diagnostic -culturing confirmsclost. botulinum: treatment-Induce vomiting or wash intestinal tract to remove Clostridium -Administer neutralizing antibodies against botulism toxin -Supportive care -Administer antimicrobial drugs in infant and wound botulism cases in addition to antitoxin and supportive careclost. botulinum: preventionproper canning of food infants under 1yr should not consume honeyclost. tetani epidemiology-Spores present in soil, dust, and GI tract of animals and humans -IV drug users @ risk -Trivial injuries -More prevalent in developing countriesclost. tetani pathogenesis & disease-Tetanospasmin toxin (tetanus toxin) released when C. tetani cells die -Potent neurotoxin causes tetany or continuous muscle contractions beginning with: trismus (lockjaw), risus sardonicus, opithotonus -Unrelenting contraction of the diaphragm can cause deathclost. tetani: diagnosis treatment prevetion-physical exam, medical and immunization history, signs and symptoms -Cleansing of wounds to remove endospores -Administer TIG -Administer antimicrobial drugs -Active immunization with tetanus toxoid -DTaP and Tdaplisteria monocytogenes-Large, Gram positive bacillus -Found in soil, water, and animals -Psychrophilic -Usually foodborne, causing mild or asymptomatic infections -Immunocompromised and elderly more at risk -Pregnant women can transmit to fetuslisteria monocytogenes: pathogenesis-Intracellular pathogen: grows in phagocytes in gallbladder -Invades phagocytes, produces listeriolysin O which helps avoid digestion escapes phagosome, reproduces in phagocytes, actin tails allows for cell-to-cell spread -In immunocompromised, can cause meningitis or septicemia -In fetuses, can lead to miscarriages, stillbirth or terminally ill infantslisteria monocytogenes: prevention treatment-Proper cooking & handling, reheating of food -Ampicillin for severe casesmycoplasma pneumoniaelacks cell walls, pleomorphic -sterols in membrane -causes: *primary atypical pneumonia* -"walking pneumonia" -Inhalation of droplets -Common in children and young adults -Patients often infectious without signs or symptomsCorynebacterium diphtheriae: epidmiology-Colonizes skin and respiratory, GI, urinary, and genital tracts -Transmitted from person to person via respiratory droplets or skin contactCorynebacterium diphtheriae: pathogenesis-*Diphtheria toxin* = A-B exotoxin acquired via lysogeny inhibits polypeptide synthesis -*Pseudomembrane* can cause asphyxia -Toxemia can result targeting organsCorynebacterium diphtheriae: diagnosis prevention treatment-Pseudomembrane present -antibiotics and antitoxins -DTaP vaccine; Tdap boostermyobacterium-non-endospore-forming pathogen -cell walls contain waxy lipid: *mycolic acid* -w cord factor, prevents destruction by lysosomes or macrophages -resists gram straining, dessicationtuberculosis-not highly virulent -90-95% infections cleared by immune system -Global pandemic 1/3 of world's population infected -Leading causing of death in HIV infected individuals -Prevalence in US is 10,000 annually; occurring mostly among foreign-born individuals -MDR and XDR strainsclinical tb divided into:-*Primary tuberculosis* results from the initial infection with M. tuberculosis -*Secondary tuberculosis* (reactivation or reinfection) results from reestablishment of active infection after period of dormancy -*Disseminated (extrapulmonary) tuberculosis* results when infection spreads throughout the bodytuberculosis diagnosis treatment prevention-tuberculin skin test identifies exposure -chest x rays shows active disease -AFS of sputum -common antimicrobials ineffective -combination therapy -Attenuated M. bovis strain is used in BCG immunization in other countries -Avoid inhaling respiratory droplets from TB patients