Microbiology: Gram Positive Bacteria Flashcards
Staph aureus
Gram (+) cocci bacteria that grows in stick “clusters of grapes”
- on blood agar, looks yellow-golden
Characteristics:
- facultative anaerobes
- non-motile
- non- spore forming
- (+) catalase
- (+) coagulase
- B-hemolytic
Virulence factors:
- protein-A (inhibits complement and phagocytosis by binding to Fc-IgG complex)
- biofilm production (slime layer that forms around clusters allowing colony to survive on surface. Also increases antibiotic resistance)
- TSST-1 (binds to MHC-2, causing hyper stimulation of cytokines, causing cytokine storm) “Toxic shock syndrome”
- PVL (punches holes in leukocytes killing them and triggers inflammation)
- hemolysin (punches holes in RBC killing them and using the iron to help grow S. Aureus)
- exfoliatin (causes SSSS/RItter’s disease which is red painful blisters throughout skin that are self limiting)
- enterotoxin (causes stomach flu/ food poisoning)
- most common bacterium*
Possible Complications: (only occurs during infections, not colonization)
- pimples
- feruncles (boil) and carbuncles (large boil)
- superficial impetigo
- cellulitis
- subcutaneous abscesses
- osteomyelitis
- pyomyositis
- sepsis/bacteremia
- meningitis
- epidural abscesses
- pneumonia
- infective endocarditis
Treatment:
- tetracyclines
- penicillins (have to make sure it isnt MRSA first)
- use clindamycin/vancomycin (MRSA only)
- trimethoprim sulfamethoxazole
What’s the physiological difference between MRSA and S. Aureus
MRSA has:
-Mutations in the DD-transpeptidase enzyme called mecA gene related transpeptidases (helps in trans-peptide linkage when dividing and growing)
- presence of B-lactamases (cuts the B-lactam ring on penicillins)
- can use clavulanate acid to counter this specific issue*
CAN ONLY USE VANCOMYCIN FOR MRSA
Staph. epidermidis
gram (+) cocci that grows like clusters of grapes
Characteristics
- facultative anaerobe
- non-spore forming
- non motile
- (+) catalase
- (-) coagulase
- (+) urease (shows bright pink)
- (-) mannitol fermentation
- (+) novobiocin sensitivity (cant grow)*
Virulence factors:
- biofilm producer (exopolysaccharide slime layer that adheres colonies together, fights antibiotics and immune system and allows fro spread of resistant genes)
most common bacteria on human skin, also most common contaminant in blood supplies
Complications:
- VERY common in catheter and prosthetic infections (especially prosthetic valve endocarditis)
- bacteremia/sepsis
Treatment:
- oxacillin/Nafcillin (only if methicillin-sensative)
- vancomycin (if not sensitive to methicillin)
- removal of prosthetic device
Staph. Saprophyticus
Gram (+) cocci that form clusters
Characteristics:
- facultative anaerobe
- non-motile
- non-spore-forming
- (+) catalase
- (-) coagulase
- (+) urease (turns pink)
- (-) mannitol fermentation
- (-) novobiocin sensitivity*
Virulence factors:
- biofilm producer (exopolysaccharide (EPS) slime layer that adheres colonies together, fights antibiotics and immune system and allows fro spread of resistant genes)
- most common in decaying material, contaminated meat and women urogential tract (2nd most common UTI pathogen)*
- however consuming staph. Saprophyticus DOESNT produce food poisoning.
Complications:
- UTIs
- catheter infections
Treatment:
- trimethoprim-sulfamethoxazole
- nitrofurantoin
- removal of contaminated catheters (if present)
What is the #1 pathogen for UTI’s?
E. Coli
How are struvite (small urinary stones that act similar to kidney stones just WAYY smaller) get formed by staph. Saprophyticus?
Urease enzymes hydrolysis urea into ammonia and carbon dioxide
- this is done to change urinary pH to neutral/basic vs acidic (which bacteria cannot grow easily in acidic environments)
Sometimes, especially in high magnesium diets, magnesium ions traveling through the urinary system will bind to ammonia and form magnesium ammonium sulfate stones (striuvte)
- these stones can block urinary outflow if too many build up.
- theoretically, any urease (+) bacterium could do this, just staph. Saprophyticus is the most common in UTIs*
Strep. Pneumoniae
Gram (+) diplococci/ lancet shaped bacteria
Characteristics
- facultative anaerobe
- non-motile
- non-sporeforming
- a-hemolytic
- (+) optochin sensitive
- (-) catalase negative
- (+) bile soluble*
Virulence factors:
- polysaccharide capsule (make it easier to attach to mucosa and make it harder to be engulfed by phagocytes. CANNOT be virulent without this)*
- biofilm producer (exopolysaccharide (EPS) slime layer that adheres colonies together, fights antibiotics and immune system and allows for spread of resistant genes)
- pneumococcal surface protein A (PspA)
(inhibt is complement cascade and inhibtors opsonization - IgA protease (destroys IgA antibodies and prevents FcIgA binding in mucosa phagocytes
- autolysin (bacteria breaks down and releases internal components, increasing inflammation)
- pneumolysin (binds to cholesterols in cell membranes which forms pores and ultimately cell lysis)
- most common pneumoniae pathogen, especially in smokers*
- produces “rusty brown” sputum usually*
Complications:
- rhinosinusitis: (fever/facial pain/headaches)
- middle ear infection (otitis media): (pain and earaches with building tympanic membrane)
- mastoiditis (spreading of otitis media into the mastoid sinuses)
- meningitis
- pneumonia
- bacteremia/sepsis: (in chronically untreated pneumonia where the pathogen crosses the alveolar wall into blood stream)
- pneumococcal endocarditis
- septic arthritis
Treatment:
- PPV23 vaccine (used in adults)
- PCV13 vaccine (used in infants)
- penicillin G/V and cephalosporins
- fluroquinolones
- ceftriaxone
- amoxicillin/ clavulanate acid
Types of hemolysis
Alpha = Partial (looks green)
Beta = complete (looks clear)
Gamma = none (looks yellow)
What are the common ways to be immunosupressed?
Being elderly or an infant (>60 or <5)
Having HIV/AIDs
Having diabetes
Having cancer
Abusing alcohol
Smoking cigarettes
Sickle cell disease
Functional asplenia
Being pregnant
What two conditions make bacteremia/sepsis more likely and more dangerous to stop?
Spleen failure/rupture/surgery (splenectomy)
Sickle cell disease
Strep. Pyogenes (GAS)
Gram (+) chained- cocci
Characteristics:
- facultative anaerobe
- non-spore forming
- non-motile
- B-hemolytic
- (+) bacitracin sensitivity*
- (+) catalase
- (+) PYR enzyme (pyrrolidonyl arylamidase)*
Virulence factors:
- hyaluronic acid capsule (helps bind to mucosa and prevent mucosal phagocytosis)
- M protein* (aids in host cell attachment and inhibits phagocytosis. Also antibodies to this protein is what causes rheumatic fever in some cases since it mimics cardiac myosin/glycogen)
- hyaluronidase (destroys hyaluronic acid and increases inflammation and enables hematogenous spread)
- streptolysin O/S (causes hemolysis of RBC’s and releases iron which promotes bacterial growth)
- streptococcal pyrogenic exotoxins (SPE:A/B/C)
(SPE A and C are superantigens, which binds to MHC 2 and forms a cytokine storm. Results in TSS)
Complications:
- TSS
- bacteremia/sepsis
- pneumonia
- infective endocarditis
- meningitis/ brain abscesses
- strep throat
- Scarlett fever* (blanching “sandpaper-like” rashes, strawberry tongue, circumoral pallor)
- impetigo (“crushed honeycomb-like” lesions)
- Erysipelas
- cellulitis
- necrotizing fasciitis
- glomerulonephritis (most common after impetigo infections, and is caused by type 3 hypersensitivity with streptocccal antigens)
- Rapid strep test w/ symptoms can confirm GAS strep throat, however the only way to be certain is cultures from the throat swab (since it can be a false positive (A.K.A another pathogen is causing the strep throat, but since GAS is peacefully colonizing there, it can be labeled falsely as the culprit))*
Treatment:
- penicillin G
- ceftriaxone/ azithromycin (if allergic to B-lactams)
Acute rheumatic fever symptoms
J: joint inflammation
O: heart damage w/ new heart murmur
N: Nodules in elbows/knees/forearms
E: Erythema Marginatum (rash w/ very thick, sharp, red margins)
S: Sydenham Chorea (rapid involuntary hand movements)
suppose to be JONES with the O replaced by a heart symbol
Strep. agalactiae (GBS)
Gram (+) chained-cocci
Characteristics:
- facultative anaerobe
- non-motile
- non spore forming
- B-hemolytic
- (-) bacitracin sensitivity*
- (-) catalase
- (-) PYR enzyme*
- (+) hippurate test* (blue appearance in test)
- (+) CAMP factor* (plate with s. Aureus to form a cross like shape on blood agar (vertical line is aureus, horizontal line is GBS) an “arrow” will show up on the GBS line due to CAMP factor)
Virulence factor:
- polysacchride capsule* (helps bind to mucosal cells and prevent phagocytosis, this capsule is rich in Sialic acid also, which makes it especially challenging for infant immune systems to catch)
- most dangerous and common in BABIES*
Complications:
- chorioamnionitis (infection of the chorion/amnion of fetus in infected pregnant vaginas
- UTIs
- cystitis (urinary bladder inflammation)
- neonatal pneumonia and inflammation
- bacteremia/sepsis (especially in neonates)
- neonatal meningitis
- septic arthritis
Treatment:
- penicillin G/ ampicillin
- ceftriaxone/vancomycin (in allergic patients)
should give interpartum antibiotics to mothers that are 2-3 hrs pre delivery to lower chances of neonatal infections
Step. Viridans
Gram (+) cocci w/ 6 subtypes
- S. Anginosus
- S. Mitis
- S. Sanguinis
- S. Salivarius
- S. Mutans
- S. Intermedius
Characteristics:
- (-) catalase
- a-hemolysis
- (-) optochin sensitivity
- (-) bile soluble
most common mouth infections (Mitis/mutans), the most common source of subacute IE (Sanguinis), and the most common cause of brain abscesses (intermedius)
Virulence factors:
- *dextrans (mutans/mitis and Sanguinis only)
( allows platelets, fibrin and its own bacterial cells to bind together and form aggregates. Often end up on heart values and produce infective endocarditis (sanguinis) or dental plaques (mutans/mitis))
Complications:
- bacteremia/sepsis (common complication from dental work for patients with bad dental hygiene)
- Infective endocarditis (subacute)
(Complication from bacteremia/sepsis and is most common on mitral value) - septic emboli attacks
- *viridans group step. Shock syndrome
(a subset of septic shock found most commonly in children who are on central venous catheters)
Treatment:
- penicillin G/ Ampicillin
Enterococcus (group D strep)
Gram (+) cocci
most common bacteria found in the gut and common in hospital-acquired infections among immunocompromised
Two species:
- enterococcus faecalis (most common and found usually in feces)
- enterococcus faecium
Characteristics:
- facultative anaerobes
- non-spore forming
- motile
- (-) catalase
- extremophile*
- (+) PYR enzyme*
- gamma-hemolysis (sometimes alpha-hemolysis)*
- can grow on sodium chloride cultures*
- (+) bile-soluble*
Complications: (only affects immunosuppressive patients)
- Infective endocarditis
- bacteremia/sepsis
- UTIs (especially in catheter patients
- cystitis
- biliary tract infections
- cellulitis
Treatment:
- penicillin/ampicillin (facalis only)
- gentamicin/streptomycin (facalis only)
- vancomycin (all faecium and resistant strains of facalis)
- linezolid/Daptomyocin/tigecycline (VRE ONLY)
