Lecture 19 Flashcards
4 genera of pyogenic cocci
Staphylococcus
Streptococcus
Enterococcus
Neisseria
(Ness)
Pyogenic
Bacteria that stimulate the formation of pus
Pus caused by
Neutrophils
Staphylococcus characteristics
Gram positive, spherical cells, arranged in clusters
No spores or flagella
Common inhabitants (microbiota) of swim and mucus membranes
Staphylococcus species
Over 40,12 of them colonize humans, 3 of major medical importance
3 staphylococcus species of major medical importance
S. aureus
S. epidermidis
S. saprophyticus
S. Aureus
Primary pathogen, facultative anaerobe, catalase positive, 10-46°C but 37°C ideal makes it good on famines
* most resistant of non-endospore forming pathogens
Can with stand 7.5 - 10 percent salt, pH 4-10, drying (thick pg layer), resistant to some antibiotics (MRSA VRSA), heat up to 60°C
S. aureus virulence factors (6)
Protein A- causes antibodies to bind f(c) region so it doesn’t stimulate an immune response
Coagulase- enzyme that clots blood, restricts blood flow to area preventing neutrophil * used diagnostically to differentiate S. aureus from other staphylococci
Hyaluronidase- digests hyaluronic acid in the basement membrane of tissues to infect deeper since non-motile aka spreading factor
Staphylokinase- digests blood clots
Lipase- digests lipids and oils on skin as nutrition and to more easily colonize skin
Penicillinase- antibiotic resistance enzyme, inactivates beta-lactam ring
S. aureus exotoxins
Hemolysins- lyse red blood cells that contain lots of protein and iron to eat
Leukocidins - lyse white blood cells
Enterotoxins- exotoxins that act on GI tract inducing nausea, vomiting, diarrhea
Toxic shock syndrome toxin (tsst)- systemic effects fever, vomiting, rash, shock from major vasodilation BP drops brain doesn’t relieve enough blood
3 types staphylococcal diseases
Localized pyogenic, systemic, toxigenic infections
Localized staph aureus infections
Invades skin through wounds, follicles, and glands
Causes abcess/boils (inflamed lesion with a core of pus) which either go away on their own or need to be drained
Furuncle
Abscess resulting from an infected hair follicle
Carbuncle
Deeper access formed by an aggregation of furuncles
Impetigo
Localized S. aureus infection, infection of the epidermis characterized by honey-crusted skin lesions
Common in newborns and young children
Systemic staph aureus diseases
Usually caused by spreading from local cutaneous infection to other sites via bloodstream
Bacteremia
Systemic staph aureus infection, the presence of viable bacteria in the blood
Osteomyelitis
Systemic Staph aureus Infection of the bone creates pus inside bone
Endocarditis
Infection of inner heart lining and values
Can cause permanent valve damage and mur murs
3 toxigenic staph aureus diseases
Food intoxication, scalded skin syndrome, toxic shock syndrome
Food intoxication
Toxigenic staph aureus disease caused by hear stable enterotoxins produced by the bacteria, associated with foods rich in carbs like cream, pastries, potato salad, processed meats
Acute vomiting
Vomiting that occurs 1-6 hours after ingestion
Scalded skin syndrome
Toxigenic staph aureus disease, grows on skin and secretes exfoliative toxin causing upper skin layer separation
Young kids + newborns prone
Toxic shock syndrome
Toxigenic staph aureus disease, first identified through tampon use, causes fever, vomiting, rash, and shock
Some women have staph aureus in the vagina that release this
Most important test for distinguishing staph aureus from other staphylococci
Catalase test, Also helps differentiate staph and streptococcus
Coagulate test
Added to rabbit serum either clumps or does not
Clumping = positive staph aureus
Negative= other staphylococcus species or streptococcus
CNS
Coagulase negative staph
Streptococcus
Gram positive, spherical/ovoid, arranged in bead-like chains
Non-spore forming non-motile
Common inhabitants of throat and nasopharynx and sometimes skin
Facultative anaerobes, catalase negative, fastidious needs enriched media,
Small round colonies that are translucent or gray
Allows for differentiation of streptococci from staphylococci
Streptococci are catalase negative
Lancefield classification system
Rebecca craighill lancefield, based on cell wall carbohydrates displayed by each, 17 different alphabetical groups A to O
Group A strep
Strep pyogenes, primary human pathogen, 95% all streptococcal diseases
Gas
Group A strep
Group B
Streptococcus agalactiae, responsible for neonatal infections, some moms have it in birth canal
Can cause neonatal meningitis and sepsis blood infection
Group D strep
Enterococcus from large intestine or fecal matter causes several human infections especially nosocomial infections and UTIs
Feces contaminates bed pans, catheters, etc
Beta hemolytic
GAS, GBS, GCS
Alpha hemolysis
Incomplete hemolysis, strep pneumonie and viridans strep
Gamma hemolysis
No hemolysis, some GDS
Strep pyogenes/group A strep
Strict parasite, inhabits throat/nasopharynx sometimes skin mucus membranes
Surface antigens: 1. C-carbohydrates unique technic acids used for Lance field, protects against lysozyme 2. M protein for fimbriae
Exoenzymes: 1. Streptokinase 2. Hyaluronidase
Exotoxins: 1. hemolysins 2. Erythrogenic toxin- exotoxin causes fever and rash in strep throat infections
Determine if impetigo caused by staph or strep
Catalase test or with microscope
Erysipelas
Infection in the dermis caused by a deep wound or incision
Forms red hot rash via mast and releasing histamine
Streptococcal pharyngitis
Localized strep pyogenes
Multiplies in tonsils or pharyngeal mucous membranes
Causes redness, edema, extreme tenderness, painful swallowing, fever, headache
Purulent exudate (pus) over the tonsils
Scarlet fever
Systemic strep pyogenes, lysogenic strain releases erythrogenic toxin causing systemic bright red rash over body (scariatina) and strawberry tongue
Rheumatic never
Systemic strep pyogenes, if bacteria enters the bloodstream it can attach to and damage heart valves leading to heart disease and murmurs
Necrotizing fascitis
Group A strep, flesh-eating bacteria, virulent group A toxins and enzymes that destroy tissues
Strep pyogenes enters through a break in the skin
Tissues destroyed in hours
Necrotizing fasciitis progression
Cellulitis with no clear margins+ painful develops, then bullae (large blisters) form after a few hours organism releasing toxins, then gangrene which is permanent tissue death, massive tissue necrosis, systemic symptoms, multi-system organ failure
Enterococcus/group D strep
Enterococcus faecalis and faecium found in large numbers in the large intestine, normal microbiota
Cause opportunistic infections of the urinary tract, wounds and bacteremia
Endogenous from own intestines
Risk for enterococcus/strep D
Patients who have been hospitalized for prolonged periods or treated with broad spectrum antibiotics that enterococci are resistant to like VRE
Viridans streptococci
Alpha hemolysis, most numerous resident of oral cavity, nasopharynx, GI tract, and skin
Dental or surgical procedures can facilitate entrance
Strep mutans
Dental caries and tooth abscess, opportunistic
Subacute endocarditis
Blood borne bacteria settle and grow in inner heart lining and values
Viridans group can cause
Bacteremia, meningitis, and abdominal infection
Streptococcus pneumoniae/ pneumococcus
Significant human pathogen, 60-70% all bacterial pneumonias, a main cause bacterial meningitis, lancet shaped cells in diplococcus or short chains
Humans principal reservoir carrying in nasopharynx
Streptococcus pneumoniae virulence factors
Pronounced capsule present in all pathogenic strains of strep pneumoniae, 90 different capsular types found with Quellung test, subunit vaccines target capsular strains
Quellung test
Capsular swelling test using antiserum specific for a capsule type, can be used to figure out strain patient has in lungs
Strep pneumoniae vaccine for infants
Prevnar 13 for infants, 13 capsules
Strep pneumoniae vaccine for adults
23 and older
What allows strep pneumoniae to enter lower respiratory tract
Presence of compromising factors that impair mucociliary motion, cough reflex, etc
Once in the lungs the bacteria can evade non-specific host defenses like phagocytosis due to its large capsule
1 cause strep pneumoniae
Ottis media, a middle ear infection that is very common in US children, pneumococcus gains access via the Eustachian tube (connects ear to throat)
Most susceptible to strep pneumoniae
Children under 2 because of shorter rustachian tube
Neisseria
Aerobic, gram negative diplococci with flattened adjacent sides, non-spore forming and no flagella, most opportunistic colonize mucous membranes, pathogenic ones are strict parasites
Pathogenic neisseria
Strict parasite, capsules and fimbriae as main virulence factors, very fastidious
Neisseria may be cultured on
Chocolate agar containing heated blood and/or hemoglobin for enrichmen, heating breaks open blood cells for them since they’re non hemolyti
Selective media for neisseria
Thayer-martin agar containing 3 antibiotics that inhibit other microbes
2 primary pathogenic neisseria
Neisseria ghonorrhoeae
Neisseria meningitidis
Neisseria gonorrhoeae
Aka gonococcus, eriological agent gonorrhea, one of top five STDs worldwide, strictly human infection, no more than 1-2 hours on formites, asymptomatic in 10% males and 50% females
Neisseria gonorrhoeae virulence factors
Fimbriae
IgA protease- destroys the IgA secretary antibody on host mucosal surfaces
Capsule blocks phagocytosis
Endotoxin Los highly toxic
Gonorrhea in males
Infection mostly restricted to urethra causing urethritis (inflamed urethra) and painful urination
Prolific pus production
Could resolve on own, occasionally spread to prostate and epididymis leading to infertility
Gonorrhea in females
Primary site of infection is cervix but can be isolated from urethra, vagina, and rectum
Vaginal discharge, painful urination, vaginitis, urethritis, and salpingitis (inflammation of the fallopian tubes)
PID (pelvic inflammatory disease)
Gonorrhea in females can lead to
Infertility or ectopic pregnancies later in life due to scarring of fallopian tubes
Gonorrhea in new barns
Infected as pass through birth canal, eye inflammation, purulent conjunctivitis which can lead to blindness, prevented by prophylaxis afte birth using silver nitrate or other antibiotic drops
Pregnant women should he screened
New cases gonorrhea each year
500,000 every year in US
Does prior infection provide long-term immunity for gonorrhea
No, lots of strains
Neisseria meningitidis
Aka meningococcus causes epidemic cerebrospinal meningitis, highest incidence kids under 5, 2nd most common cause in adults (after strep pneumoniae), human reservoir in nasopharyny, spreads within families and communities
Neisseria meningitidis virulence factors
Capsule, fimbriae, IgA protease, endotoxin LOS
Neisseria meningitidis transmission
Aerosolized respiratory droplets especially in crowded situations
Neisseria meningitidis entrance and progression of meningitis
Enters respiratory tract, crosses mucosal barrier, enters blood stream, bacteremia allows it to travel to brain and cross BBB, establish infection in meninges
Headache, fever, nausea, vomiting, stiff neck
Endotoxin release can cause hemorrhage and shock
Meningitis mortality
100% untreated, drops to 10% with treatment
Meningitis diagnosis
CSF specimen cultured or gram stand
Meningitis vaccine?
Meningococcal vaccine, subunit vaccine using capsular polysaccharides, recommended for all ages especially during outbreaks dermis, military base, etc
Antibiotic prophylaxis for those with significant exposure to the sick
