Week 2 -Strep Flashcards
what are Streptococcus and Enterococcus
-members of the Streptococcaceae family
-catalase negative , can give weak positive if media is from blood
-pairs and chains - nicer chains in broth
-facultative anaerobes but cant use oxygen for respiration can be aerotolerant aerobes
-BH strains produce exotoxins that damage RNCs
-use fermentative processes for metabolism with lactic acid end product
-can be capnophilic
-need more nutrition than Staph, have poor growth on plain TSA media but enhanced growth media with lysed blood like chocolate
what is the cellular morph of Strep
-GPC in pairs and chains
-GPDC only if Streptococcus pneumoniae and growing colonies on plate
-elongated vs spherical cells
what is the cell wall structure of strep
-just like all other GP with peptidoglycan/teichoic acid
-common c polysaccaride - used for Lancefield grouping and for extracting cell wall AG (C carb) to react with AB causing agglutination
Viridans and S pneiumo dont have the C carb so other tests are done.
There is a NH strep group with the same Lancefield grouping so you need more tests for that category.
What occurs in Alpha hemolysis
hemoglobin is reduced to methemoglobin which is why the area surrounding the colonies will look green
what are variations that can occur in hemolysis slide 15
-S anginosus - is A, N, and BH
-Enterococci are NH but can be BH or AH
-Group B Strep have a very small BH while some are NH
what are Group A streptococcus and where are they found
Streptococcus pyogenes
-most virulent
-fastidious
-humans are ONLY known reservoir - UPT, skin
-Transient flora is in the vaginal tract
-can be asymptomatic but must always be treated
what are the Structural virulence factors associated with GAS
Capsule - has hyaluronic acid the same as humans and therefore doesnt recognize the foreign response
M protein - promotes attachment to membrane surfaces - skin. The protein is attached to peptidoglycan which extends to the cell surface interfering with phagocytosis
Protein F- fibronectin binding protein works with lipoteichoic acid to attach to host epithelial cells . Fibronectin responsible for cell adhesion, growth and wound healing
Lipoteichoic acid+M protein+Protein F = secure attachment of Streptococcus to oral mucosal cells
what are the extracellular products responsible for virulence factors for GAS
Streptolysin O - oxygen labile only active in ANO conditions
-causing BH in ana
-lyses PLTs, RNC, leuks,
-immunogenic - formation of AB by host - test with Anti-streptolysin O test (ASOT)
Streptokinase - lyses fibrin clots used as a clot buster
Streptolysin S (oxygen stable)
-lyses lueks, RBC
-non immunogenic
-causes the BH around GAS in BA in o2
Pyrogenic Exotoxins
-super AG, erythrogenic toxin
-interacts with class II MHC to produce IL-1 tumor necrotizing factor
-scarlet fever
-DNAses
Hyaluronidase
-separates connective tissues and spreads the infection
What is the clinical significance of GAS
- pharyngitis/tonsillitis - Strep throat
-droplet or close contact
-throat culture - gold standard
what are some other infections caused by GAS other than strep throat
Pyodermal Infections - skin disease that has pus
Impetigo - vesicular and pustular facial infections
-highly contagious
-especially in warm weather
-may be cause by S pyogenes or S aureus
Cellulitis -deeper
-Erysipelas - older people
-Spreading skin lesions very erythematous
Scarlet fever
-rash that spreads on chest to trunk and extremities after the throat infection so it is secondary
what is necrotizing fasciitis, symptoms and risk factors
soft tissue infection
Type 1 - polymicrobial
Type 2 - GAS AH, BH or MRSA
-flesh eating disease, necrosis of skin, fat and fascia.
-lots of cases without breaks in skin
-invasive - can kill in 12 hours
Type 3- gas, gangrene due to clostridium
if on genitals it is called Fournier gangrene
Risk factors high if
-weak immune system, health issues
-cuts in skin
-if you had chicken pox or viral infections that cause a rash
-steroid use that suppress immune function
Symptoms
-starts suddenly after injury
-pain get better after 24 hours and then worse
-skin in red, swollen and hot
-fever,chiils, nausea and vomiting
Streptococcal Toxic Shock Syndrome - GAS
-invasive
-shuts down entire organ system
-unknown portal of entry can be injury
-Lympadenitis –infection of lymph gland
-Lymphangitis –infection/inflammation of the lymph channels
-Puerperal sepsis (infection of uterine lining) usually during or after delivery
what are GAS Post infection Disorders
-complications because of immune response
Rheumatic Fever
-happens a month after pharyngitis
-fever, inflammation of the heart, joints and blood vessels
-if you get repeated infections youll have valve damage
-sequelae: rhematic heart disease
Acute Glomerulonephritis (AGN)
-after cutaneous or pharyngeal infection
-AG-AB complex deposits in the glomeruli causing damage
What is the theory behind why GAS post infection disorders occur
-Cross reactivity between strep antigens and heart tissue
-toxicity from bacterial exotoxins and invasion of heart tissues
how do we identify GAS
- small /medium with large BH - due to streptolysin O which is oxygen labile
-GP cocci in chains
-catalase negative
-hippurate hydrolysis negative
-NG in 6.5% NaCl
-bacitracin sensitive
-PYR positive
-fastidious - needs blood or other enrichment
-test with PathoDx for BHS
-Lancefield grouping for A
Do we do AST on GAS,GBS, GCS and GGS
-S pyogenes (GAS) and S agalactiae (GBS) is susceptible to penicillin
-D test is peni alternative or if pt on erythromycin or clindamycin on MG with 5% SB
-Etest or M.I.C. Evaluator :not at TMI for sterile sites
What is the D zone test
-erythromycin and clindamycin are popular for pt allergic to peni need to test for both
-test for msr gene which is an efflux pump and doesnt impact clinda
-test for erm gene which codes for 23S rRNA methylation causing erythromycin resistance and clindamycin resistance which can be constitutive or inducible
-presence of the methylase enzyme confers resistance to clindamycin
-seen as decreased zone size (antagonism) to clindamycin where the two ABtics interact = D formation on the agar because theyll be side by side 12mm apart -MH with blood
-you can do this test with Staph but the discs will be 15mm apart with reg MH
-So if erythromycin is testing as resistant, you need to test it to see if it is resistant due to the erm gene since if it is, you can’t use clindamycin as well.
-we don’t do BHS AST on the Vitek, you need to perform this manually
what is the E test/M.I.C.E
-not a diffusion method
-plastic strip with antimicrobial concentration with MIC reading scale
-full dilutions on white side and half dilutions on black side
-forms a ZOI
How do we treat GAS
- no vaccine since hyaluronic acid in Strep capsule is also found in humans
-peni, eryt, clinda, cephalo are used
-treat pharyngitis aggressively so you dont get Rheumatic Fever ,and AGN
-Skin infections - drainage, debridement (remove pus and infective tissues) and abtic therapy
-Prophylactic penicillin therapy- prevents Rheumatic Fever, endocarditis . This is done before dental surgery can be given to those with STT or NF infections
Streptococcus agalactiae –Group B streptococcus (GBS)
What do type is it and characteristics, virulence factors
- Acid stable polysaccharide in the cell wall so C -AG is used to ID
Virulence Factors
***Capsule- sialic acid - prevents phagocytosis and inhibits activation of complement system. but is ineffective after opsonization. This process allows molecules to have stronger binding to cell surface receptors on phagocytes and NK cells . If the AG is coated with opsonins it can bind to immune cells
Extracellular products
hemolysin
CAMP factor
Enzymes (neuraminidase, DNAse, and protease)
where does GBS live and how is it identified on a plate
- naturally found in female genital tract and male urethra
-pharynx and gastrointestinal tract
-plate shows large colony with narrow zone usually BH can be NH
-GPC in chains
-Catalase Nege
-Lancefield B grouping
-PYR neg
-CAMP positive
-Bacitracin Resistant
-Hippurate hydrolysis positive
what are GBS clinically significant
- most common cause of newborn death less than 7 days old
-high mortality rate
-women become colonized at time of delivery causing the newborn to be colonized as it comes down the birth canal
-infections within first 3 days presenting as pneumonia or meningitis with bacteremia
-rare for late onset- it would an unknown infection source
-in adults - UTI, endocarditis , endometriosis
How are specimen collected and processed from pregnant women for GBS
-screened at 35-37 weeks
-vaginal-rectal perineal swab
-swab in Todd Hewitt broth (red) with gentamicin and nalidixic acid leave the swab overnight in the media
-incubate overnight and subculture onto CNA CO2 or chromogenic media Brilliance GBS
What is Brilliance GBS
-mix of chromogens, inhibins, and antibiotics
-grows GBS and inhibits the rest
- pink colonies are presumptive GBS
-confirm ID with PathoDx
