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)
Clostridium perfringens
Gram (+) bacilli
Characteristics:
- obligated anaerobes (grow better without oxygen)
- (-) catalase
- spore-producer*
- common cause of food poisoning and gas gangrene*
Virulence factors
- clostridium perfringens enterotoxin (CPE)*
(Destroys tight junctions between epithelial cells, which promotes inflammation and GI ulcers. Note: this toxin is destroyed at 72 C, so only usually seen in reheated/uncooked foods)
- alpha-toxin (lecithinase/CPAT)
(usually only seen in dirty wounds and causes myocyte swelling and necrosis)
(this is the toxin that causes myonecrosis (gas gangrene)*
Complications:
- food poisoning
- GI ulcers
- gas gangrene (myonecrosis)
- the hall mark sign is crepitus on palpation of the wound*
Treatment:
- no antibiotics, just palliative care (non-gangrene complications)
- surgical debridement/excision with IV penicillin V/clindamycin
(myonecrosis only) - hyperbaric chamber (myonecrosis only)
Clostridium botulinum (botulism toxin)
Gram (+) bacilli
Characteristics:
- obligate anaerobes
- spore forming*
Virulence factors:
- botulinum toxin*
(toxin that inhibits ACh vesicles from binding to presynaptic neuron plasma membrane via SNARE protein cleavage)
Complications:
- paralysis
- “floppy baby” syndrome (flaccid paralysis in babies due to colonizing botulinum in the GI tract)
- especially common with honey consumption in infants (<12 months)
- bulbar palsy (CN 9/10/11/12 are disabled)
Treatment:
- supportive care
- antitoxin A/B/E trivalent vaccine
- antitoxin A/B/C/D/E/F/G heptavalent vaccine
- most common exposures are due to Botox injections (subtoxins A/B ONLY) and in poorly prepared canned foods (can looks like its buldging)*
What are the 4 Ds of botulism toxicity?
Dysarthria
Dysphagia
Diplopia
Dyspnea
Clostridium tetani (tetanus)
Gram (+) Bacilli
Characteristics:
- obligate anaerobes
- spore forming
most common in ALL TYPES puncture wounds (hence why most penetration wounds often requires tetanus booster to ensure it doesn’t exist)
Virulence factors:
- tetanospasmin* (disables renshaw Cell SNARE proteins, which disables the inhibitory neuronal release of GABA seen in renshaw cells)
Complications
- generalized tetanus
- bone fractures
- sympathetic over activity
- local tetanus
- Cephalad tetanus (muscles controlled by the CNs are affected only)
- neonatal tetanus
Treatment:
- tetanus immune globulin (TIG) antitoxin
- diazepam (for muscle contractions)
- NSAIDs
- tetanus toxoid vaccine
- one clinical way to test for tetanus is the spatula test (take tongue depressor and touch the posterior pharyngeal wall. A positive sign is if the patient involuntary bites down on it instead of gagging like normal*
What is the tetanic triad?
Three symptoms most commonly seen In clostridium tetani infections
Trismus (locked-jaw)
Risus sardonicus (raised eyebrows w/ open grin)
Opisthotonos (spasms of the spinal extensors which causes arched back)
Clostridium difficle (C. Diff)
Gram (+) bacilli
Characteristics:
- obligate anaerobe
- spore forming
- non motile
most common cause for diarrhea outside of E. Coli, also is commonly seen as a 2nd infection after treating a primary one, especially with clindamycin/ampicillin
Virulence factors
- difficle toxins A/B*: (destroy enterocytes in the GI tract leading to diarrhea and increased chances of GI ulcers and psuedomembranous colitis)
Complications:
-GI ulcers
- food poisoning
- pseudomembranous colitis
- toxic megacolon
Treatment:
- oral vancomycin
- metronidazole
- fecal microbotia transplant (only in chronic recurrent cases)
Listeria monocytogenes
Gram (+) bacilli
Characteristics
- facultative intracellular (can live inside or outside cells)
- facultative anaerobic
- (+) oxidase
- (+) catalase
- non spore forming
- B-hemolysis
- *very motile (“looks like rocket tails”) (only works at 37C or lower)
common food borne infection that is in unpasteurized milk and cold deli meats
Virulence:
- *internalins (allows for adherence to gut cells (especially Cadherin) which forms vacuoles inside cells)
- *flagella: are made by flagellin protein in listeria. When extracellular, uses these to move around. In intracellular environments, uses actin molecules to move in a “tumbling” manner though the cell and into the next adjacent cell)
- *listeriolysin O (allows for bacteria in the vacuole to use host resources and generate new bacterium via binary fission
Complications
- disseminated listeriosis (listeria bacterium moving throughout blood stream)
- liver abscesses
- meningitis
- *spontanous abortion (if disseminated listeriosis reaches placenta in pregnant patient)
- granulomatosis (immune compromised and neonates only)
- neonatal sepsis and meningitis
- food poisoning
Treatment:
- IV ampicillin/ gentamicin (in non-pregnant patients with any of the complications that’s not GI tract limited)
- meropenem (used in pregnant patients)
- supportive care (if non-pregnant and only limitied to GI system)
What are three classic symptoms of neonatal listeriosis?
Fever
Respiratory distress
Granulomatosis infantiseptica (broadly spread red rashes with small pale nodules in the rash spots)
Bacillus anthracis
Gram (+) bacilli
Characteristics:
- spore-forming
- y-hemolysis
- non motile
- facultative anaerobe
- often shows up as “Medusa head” colonies when plated*
- affects skin, GI tract or lungs (lung is worse)*
Virulence factors:
- *poly-D-Glutamic acid capsule: (anti-phagocytic capsule which once the spores/ bacterium are consumed once by a phagocyte, it cannot be consumed again(impossible))
- *lethal factor: part of anthrax toxin, is a zinc Metalloprotease which cleaves PK 1/2 inside immune cells. Causes NADPH exhaust and cell lysis/apoptosis
- *edema factor: part of anthrax toxin, is a ADP ribosyl-transferase protein which actually stimulates Protein kinase A (PKA) function. Disables cell functions and prevents cytokine release.
- protective antigen: (part of anthrax toxin, binds to immune cell surfaces via ANTxR1 and forms a pore/channel)
Complications:
- total organ failure
- spetic shock
- GI ulcers
- eschar wounds
Diagnosis:
- very challenging, but is usually PCR assays or anti-protective antigen immunoglobulin assays
Treatment:
- *IV anthrax antitoxin
- *IV ciprofloxacin, clindamycin/linezolid and Raxibaxumab (binds to Protective antigen)
- having antibodies to ANTxR1 makes someone immune*
What are the steps to forming a spore?
1) “mother cell” copies its genome and separates it from the original genome
2) the “mother cell” forms a wall around the new spore genome, allow the plasma membrane to form around the spore
3) the plasma membrane forms a “cell-within-cell” appearance of the spore called a forespore
4) the forespore is engulfed by the cell wall and loses water, gains calcium and diplcolinic acid (forespore becomes endospore), and the mother cell dies
5) the endospore is released from the lysis mother cell and can live for over 1000 years before dying.
3 forms of anthrax
1) cutaneous anthrax
- spore comes into contact with open skin wound.
- painless red bumps will form until rupture.
- once rupture occurs, produces classic “Eschar” (black necrotic large wounds that are painless)
- symptoms are minor at best and the eschar wounds are usually enough to diagnose
2) GI anthrax
- spore comes into contact with GI via undercooked meat that was exposed to spores
- can form eschar wounds in the GI system
- hemoptysis/ ab pain/ nausea/vomiting/ blood diarrhea are the symptoms
3) respiratory anthrax (woolsorters disease) most dangerous form
- spores are inhaled and enter the pulmonary system
- NO eschar in the lungs, seen in the mediastinal lymph nodes ONLY
- causes pulmonary hemorrhages and necrosis of mediastinal lymph nodes rather quickly and leads to septic shock
- high fever, low BP/tachycardia, widening of th mediastinum and hemoptysis are the symptoms
Bacillus cereus
Gram (+) bacilli that is waxy in appearance
Characteristics:
- motile
- aerobic only*
- (+) catalase
- B-hemolytic*
- spore-former
usually only food poisoning unless patient is immunocompromised
Virulence factors:
- *cereulide: toxin that induces emetic effects when it is exposures to GI tract, is also heat resistant 1-5 hrs
- *enterotoxin: destroys intestinal epithelium tissues which induces mass secretion of electrolytes and water (diarrhea) 8-18 hrs
Complications: (usually only in immunocompromised)
- bacteremia/sepsis
- osteomyelitis
- menignoencephalitis
- endocarditis
- keratinits/ endophthalmitis (inflammation of the external and internal eye respectively)
Treatment:
- supportive care only
- antibiotics vancomycin or gentamicin (ONLY in sepsis/bacteremia complications, NOT from GI contained infections)
What are the three external factors that initiate spore forming and release from spore forming pathogens?
Extreme temperatures
Exposure to radiation
Extreme dryness
Corynebacterium diphtheria
Gram (+) rod that looks similar to a club
Characteristics:
- Aerobic*
- non-spore formers*
- (+) Albert stain* (looks green with blue spots known as (metachromatic granules)
- (+) cystine-telluride blood agar* (can ONLY grow on this agar, will look BLACK)
most commonly seen in immunocompromised or unvaccinated patients
Virulence factors:
- diphtheria toxin* (DT) (CAN ONLY be produced once a B-prophage infects the bacterium colonies, allows DT genome to be encoded in the bacterium and can now produce it. Destroys cells by binding to host cells (B subunit) and inhibits protein synthesis by binding to EF2 factors on ribosomes (A subunit) and disrupts E site activity.
Complications:
- pharyngeal diphtheria (necrosis of pharyngeal tissue once the bacteremia can produce DT toxins, forms a GRAY PSEUDOMEMBRANE in the pharynx)
- this kills by asphyxiation, when the membrane falls off and lodges into the bifurcation of the trachea
- cutaneous diphtheria
- myocarditis
- acute tubular necrosis
- peripheral nerve demyelination (almost always affects oculomotor and phrenic nerves first if it occurs)
Treatment:
- penicillin G w/ erythromycin (if allergic erythromycin will lower symptoms)
- diphtheria antitoxin (if ELEKs test is positive)
- toxoid vaccine (to prevent DT affects (diphtheria is asymptomatic without it))
- part of DTaP shots
What is the ELEKs test?
The test used in positive cultures of diphtheria, to determine if that species of diphtheria has been activated to produce DT toxin
Uses a standard agar plate with antitoxin filter paper over it
- if the species is (+) for DT formation, will react and make bands of visible precipitation’s of toxin: antibody complexes
Nocardia
Gram (+) bacilli that branches in filament shapes
Characteristics:
- aerobic*
- acid-fast/ Ziegler’s-Nielsen stain* (stains red)
- non-motile
- non spore forming
- (+) catalase*
- (+) urease*
- white/yellow/orange when cultured*
- really only seen symptomatic cases in immunocompromised patients*
Virulence factors:
- cord factor*( inhibits phagolysosome fusion)
- superoxide dismutase and catalase (breaks down ROS species produced by neutrophils)
Complications: really only in immunocompromised patients
- pulmonary nocardiosis (caused by N. Asteroides)
- dissemeinated nocardiosis
- meningitis
- cutaneous nocardiosis (caused by N. Brasiliensis)
- granuloma necrosis (caseous form)
Treatment:
- *sulfonamides (TMP-SMX)
- imipenem/amikacin IV bolus (ONLY in severe disseminated infections)
Actinomyces Israelii
Gram (+) bacilli with branching filaments
Characteristics:
- anaerobic*
- non motile
- non-spore former
- not acid fast/ Ziegler’s-Nielsen staining (will stain blue)*
- (-) catalase*
- (-) urease*
- can only grow on blood agar w/ molar tooth like colonies*
very common oral cavities pathogen that only becomes an issue in immunocompromised patients
Complications: only seen in immunocompromised patients usually
- cervicofacial actinomycosis (breech in oral mucosa allows pathogen into blood stream. Forms abscesses in sinuses and osteomyelitis in maxilla)
- will release yellow “sulfur-like” pus and granules
- actinomycosis otitis media (otitis media caused by actinomycosis)
- respiratory actinomycosis
- pelvic inflammatory disease (common in women with IUD placement)
Treatment:
- pencillin G
- doxycycline/clindamycin (penicillin allergy therapy)
- remove IUD (in presence of PID)
