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34 Cards in this Set
- Front
- Back
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Gram Positive cocci Staphylococci
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common inhabitant of the skin and mucous membranes.
spherical cells arranged in irregular clusters. Gram + lack spores and flagella may have capsules 31 species |
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Staphylococcus aureus
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grows in large, round, opaque colonies.
optimal temperature 37 C facultative anaerobe Withstands high salt, high temperature, extreme Ph. Produce many virulence factors Beta hemolytic |
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Enzymes S. aureus (virulence factors)
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Coagulase-coagulates blood and serum, 97% human isolates, diagnostic
Hyaluronidase- digests connective tissue Staphylokinase digests blood clots DNase digests DNA Lipases digests oils, enhances colonization on skin Penicilinase inactivates penicillin |
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S. Aureus toxins
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Hemolysin-lyse RBC
Leukocidin Lyse WBC neutrophils, macrophages Enterotoxin-induces gastrointestinal distress Exfoliative toxin separates dermis from epidermis (gas) TSST-toxic shock syndrome toxin induces fever, vomiting, shock, and systemic organ damage |
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S. aureus Pathogenesis
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Present where humans frequent can be readily isolated from fomites
Carriage rate in healthy adults 20%-60% most found in the nares Predisposition factors: poor hygiene and nutrition tissue injury, preexisting primary infections, immunodeficiency, diabetes. Increase in community acquired MRSA |
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Staphylococcal Disease cutaneous infections
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Localized cutaneous infections: invade through skin, wounds, follicles, or glands
Folliculitis-superficial inflammation of hair follicle, usually resolves on own, but can progress. Furuncle-boil; inflammation of hair follicle sebaceous gland. progresses into abscess or pustule. Carbuncle-large and deeper lesion created by aggregation and interconnection of a cluster of furuncles. Impetigo-bubble like swellings that can break and peel away, common in newborns |
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Staphylococcal Disease Systemic Infections
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Osteomyelitis- infection is established in the metaphysis; abscess forms
Bacteremia-primary origin is bacteria from another infected site or medical devices. Endocarditis possible. #1 infection of S aureus |
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Staphylococcal Disease
Toxigenic Disease |
Food intoxication- ingesting heat stable enterotoxins cause GI distress
Staphylococcal scalding skin syndrome-toxin induces bright red flush, blisters, then desquamation of epidermis TSS toxemia leading to shock and organ failure |
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4 clinical concerns and treatment
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95% have penicillinase and are resistant to penicillin and ampicillin.
MRSA methicillin resistant and S. aureus and carry multiple resistance. Some strains have resistance to all major drug groups except vancomycin Abscesses have to be surgically perforated. Systemic infections require intense lengthy therapy. |
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Streptococci (7)
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Gram positive spherical cocci arranged in long chains
Non-spore forming, non motile can from capsule and slime layers Facultative anaerobes Do not form catalase, but do have a peroxide system Most parasitic forms are fastidious require enriched media Sensitive to drying heat and disinfectants |
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Human Streptococcal pathogens
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S. pyogenes
S. agalctiae Viridens, S. mutens S. pneumonia Enteroccusfacialis |
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Streptococcal pyogenes
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Beta hemolytic
Most serious Streptococcal pathogen Strict parasite Inhibits throat, nasopharynx, occasionally skin |
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S. pyogenes surface antigens (virulence factors)
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C-carbohydrates-protect against lysozyme
Fimbriae-adherence and slime layers M-protein-contributes to resistance to phagocytosis Hyaluronic acid capsule-Provokes no immune response |
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S. pyogenes
Extracellular enzymes (virulence factors) |
Streptokinase-digests fibrin clots
Hyaluronidase DNase |
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S. pyogenes
Extracellular toxins (virulence factors) |
streptolysins-hemolysin streptolysin O (SLO) and streptolysin S (SLS) cause cell and tissue injury
Erythrogenic toxin induces fever and typical red resh Super antigens strong lymphocyte and monocyte stimulants; cause the release of tissue necrotic factor |
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S. pyogenes
Pathogenesis |
Human only reservoir
Asymptomatic carriers Transmission- contact, droplets, food, fomites Portal entry, generally skin or pharynx Children predominant group for cutaneous and throat infections. Systemic infections and progressive sequelae possible if UNTREATED |
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S. Pyogenes
Skin Infections and Throat |
Impetigo-superficial lesions that break and form highly contagious crust; often occurs in epidermis in school children
NECROTIZING FASCILITUS- due to destructive enzymes and toxins STREPTOCOCCAL PHARYNGITIS- STREP THROAT |
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S. Pyogenes
Clinical Disease Systemic Infections |
Scarlet fever-strain of S. pyogenes carrying a prophage that codes for erythrogenic toxin
Septicemia Pneumonia Streptococcal toxic shock syndrome |
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Scarlet Fever
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Caused by Erythrogenic toxin
high fever bright red rash on face, trunk, inner arms, legs and tongue Eventual desquamation of epidermis Septicemia as a complication |
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S. Pyogenes Long-term complications
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Rheumatic fever- after overt or subclinical pharyngitis in children Carditis with extensive valve damage
arthritis, fever, chorea Acute glomerulonephritis nephritis, increase blood pressure, occasional heart failure, and chronic cases kidney failure |
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Group B Streptococcus agalactiae
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Resides in human skin, vagina, pharynx, large intestine
Can be transferred to infant during delivery and cause sever infection. Most prevalent cause of neonatal pneumonia, sepsis, and meningitis Pregnant women should be screened and treated Wound and skin infections and endocarditis in debilitated people. |
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Treatment (A, B)
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Penicillin
Long-term penicillin prophylaxis for people with a history of rheumatic fever or recurrent strep. Invasive dental treatment. |
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Viridans group
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Bacteremia, abdominal infections, meningitis, tooth abscesses
Most serious infection acute endocarditis Blood-borne bacteria settle and grow on heart lining and valves form biofilms (colonize) Persons with preexisting heart disease are high at risk. |
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Strep pneumoniae
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All pathogenic strains form large capsule
Major virulence factor Cause pneumonia and Otis Media 90 different capsule types have been identified Majority of child ear infection |
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Gram negative cocci Nesseriaceae
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Residents of mucous membranes of warm blooded animals.
Causes Neisseria gonorrhea Neisseria meningitis |
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Neisseria
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Gram negative diplococcic
No flagella, no spores Capsules on pathogens Pili Strict parasite, cannot survive out of host Produce catalase and cytochrome oxidase Pathogenic species are fastidious enriched media and CO2 |
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Neisseria Gonorrhoeae
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Cause gonorrhea
Virulence factors fimbriae slows down phagocytosis IGa protease cleave mucous secreting IGA |
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Neisseria Gonorrhoeae
Pathology |
Strictly human infection
Most common Maryland STD Infectious dose 100-1000 Does not survive more then 1-2 hours on fomites Extremely resistant forms emerging |
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Gonorrhea
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Infection is asymptomatic in 10% males, 50%females
Males: urethritis, yellowish discharge, scarring, infertility Females: vaginitis, urethritis, PID, most common cause of sterility, and ectopic tubal pregnancy. Extragenital infections: anal, pharyngeal, conjunctivitis, septicemia, arthritis |
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Gonorrhea in newborns
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Infected through canal
Eye inflammation, blindness Prevented by prophylaxis immediately after birth. |
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Neisseria Meningitis
Virulence factors |
Capsule
Adhesive fimbriae IgA protease Endotoxin |
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Neisseria Meningitis
Pathology |
Prevalent cause of meningitis
Human reservoir- nasopharynx 3-30% of adult population High risk individual living in close quarters, 6mos-3 yrs and 10-20yrs Very rapid onset, neurological symptoms, endotoxin causes hemorrhage and shock; can be fatal |
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Neisseria Meningitis
Clinical Diagnosis |
Gram stain CSF, blood, or nasopharyngeal sample
Culture for differentiation using biochemical testing Rapid tests for capsular polysaccharide |
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Treatment Meningitis
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IV penicillin G and cephalosporin
Prophylactic treatment of family members, medical personnel, or children in close contact with patient Primary vaccine contain specific purified capsular antigens |
