Gram-Positive Bacteria

first-line identification method. tells you: is it gram-positive (purple) or gram-negative (pink/red)?

Gram stain

3 multiple choice options

grow bacteria on specific media to observe colony morphology and growth patterns. automated systems (like Vitek) read growth curves and run biochemical tests to quickly ID species.

cultures

3 multiple choice options

a super-fast way to ID bugs by their protein fingerprint. think of it as bacterial CSI 🕵‍♀️—very accurate and FAST

MALDI-TOF

3 multiple choice options

once ID-ed, labs test which antibiotics the bacteria is sensitive/resistant to (think MIC testing, zone of inhibition, etc.)

susceptibility testing

3 multiple choice options

cell wall: thin peptidoglycan + outer membrane

staining result: don’t retain violet → appear pink/red due to counterstain (safranin)

alcohol wash removes the crystal violet

Gram negative

3 multiple choice options

cell wall: thick peptidoglycan

staining result: retain the crystal violet → appear purple

alcohol wash can’t remove it—they hold onto that dye like their lives depend on it (because they kinda do)

Gram positive

3 multiple choice options

select all that apply:

what is in the Gram-positive cell wall?

1. peptidoglycan

2. teichoic acids

~90% of the cell wall; it's like the bricks and mortar

peptidoglycan

3 multiple choice options

give the wall structure and contribute to antigenicity (recognized by the immune system). these are species-specific; vary in amino acid content

teichoic acids

rare in Gram-positives (unlike Gram-negatives with rich outer membranes)

lipids

3 multiple choice options

THICK peptidoglycan. teichoic acids embedded in the wall. NO outer membrane, just one plasma membrane, and very little to no lipids

gram-positive bacteria

1 multiple choice option

THIN peptidoglycan. has outer membrane with LPS (lipopolysaccharide) — triggers immune responses/endotoxins, porins — transport channels. has periplasmic space between inner and outer membranes. more complex structure = more resistance to some antibiotics

gram-negative bacteria

1 multiple choice option

clusters like grapes

staphylo

3 multiple choice options

chains or pairs

strepto/entero

3 multiple choice options

Gram-positive cocci (purple, spherical). appear in clusters (think: "bunch of grapes")—that's literally what "Sstaphyl" means.

non-spore forming - can also show up as singles, pairs, or short chains, but clusters are most classic

staphylococcus spp.

3 multiple choice options

the infamous one

causes severe infections, very virulent, coagulase positive

Staphylococcus aureus

3 multiple choice options

skin flora, opportunistic, coagulase negative

Staphylococcus epidermidis

3 multiple choice options

associated with UTIs, especially in young women, coagulase negative

Staphylococcus saprophyticus

3 multiple choice options

all are normal flora, especially on the skin and mucous membranes - but they're also survivors—they can live on dry surfaces like plastic and metal (think: hospital equipment)

Staphylococcus spp

3 multiple choice options

a slimy, sticky layer made by bacteria like Staph. formed of polysaccharides, proteins, and DNA. lets bacteria stick to surfaces (like catheters, pacemakers, artificial joints). once they’re in this form, they’re protected from the immune system, antibiotics (which can’t penetrate well), and environmental stress

biofilm

3 multiple choice options

_________________ = chronic, hard-to-treat infections

S. epidermidis is notorious for forming these on indwelling medical devices

S. aureus also uses these to evade clearance, especially in prosthetic joint infections

biofilm

3 multiple choice options

a major nosocomial (hospital-acquired) pathogen. think: catheter infections, post-surgical wounds, ventilator-associated pneumonia.

Staphylococcus aureus

3 multiple choice options

breaks down hydrogen peroxide—helps escape neutrophil killing.

catalase

3 multiple choice options

converts fibrinogen to fibrin—helps form clots that shield bacteria.

coagulase

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surface protein that binds fibrinogen, promotes adhesion.

clumping factor

3 multiple choice options

"spreading factor" that breaks down connective tissue.

hyaluronidase

3 multiple choice options

cytolytic; destroy host cells.

alpha, beta, gamma, delta toxins

3 multiple choice options

destroys leukocytes, particularly neutrophils—associated with necrotizing infections.

leukocidin

3 multiple choice options

cause scalded skin syndrome (especially in neonates).

epidermolytic toxins

3 multiple choice options

heat-stable; cause food poisoning with rapid-onset vomiting.

enterotoxins

3 multiple choice options

lead to toxic shock syndrome (fever, rash, hypotension, multi-organ failure).

TSST-1,2: superantigens

3 multiple choice options

select all that apply:

what are some clinical diseases that come from Staphylococcus aureus?

1. pneumonia

2. bacteremia

3. skin/soft tissue infections

4. endocarditis

5. osteomyelitis

S. aureus is genetically adaptable—it gains __________________ and resistance genes easily.

virulence

3 multiple choice options

encodes PBP2a, an altered penicillin-binding protein that doesn't bind β-lactams effectively → leads to methicillin resistance. found on SCCmec, a mobile DNA element that can be transferred between strains.

mecA gene

3 multiple choice options

helps with adhesion, immune evasion

wall teichoic acid

3 multiple choice options

linked to CA-MRSA

Panton-Valentine leukocidin

3 multiple choice options

prevents neutrophil recruitment

chemotaxis inhibitory protein

3 multiple choice options

nosocomial MRSA became common in hospitals by 1990. __________________ emerged independently in people without traditional risk factors (e.g., kids, athletes, prisoners).

CA-MRSA

3 multiple choice options

⚠️ CA-MRSA outbreaks:

Detroit 1980s: mostly in IVDU

1990s onward: kids, sports teams, jails

2000s: ______________________, skin infections, even fatal outcomes

necrotizing pneumonia

3 multiple choice options

mecA → PBP2a → _________________ (key resistance mechanism)

MRSA

3 multiple choice options

#1 culprit in prosthetic device infections. normal skin flora, but gets real shady when a catheter or implant is around. forms biofilms (aka "slime") that make it super hard to treat

Staphylococcus epidermidis

3 multiple choice options

skin flora, less common in disease, but has been isolated in bacteremias

Staphylococcus hominis

3 multiple choice options

major cause of urinary tract infections (UTIs)—especially in young, sexually active women. uniquely resistant to novobiocin, which helps ID it in the lab. also linked to some GI infections

Staphylococcus saprophyticus

3 multiple choice options

doesn’t produce the same array of toxins as S. aureus. no TSST, enterotoxins, or exfoliative toxins. still pathogenic, especially when devices are involved—but more of a stealthy saboteur than an aggressive attacker

coagulase negative Staphylococcus

3 multiple choice options

CoNS, especially S. epidermidis, make a _________________________ that sticks to plastic and foreign bodies (catheters, heart valves, prosthetics). this shields bacteria from antibiotics and immune system and makes infections chronic and hard to eradicate

polysaccharide-rich matrix

3 multiple choice options

select all that apply:

what are some clinical diseases that can come with coagulase negative Staphylococcus?

1. indwelling catheters & foreign bodies

2. bacteremia

3. pneumonia

4. skin infections

Gram-positive (purple on Gram stain), spherical (cocci), and grow in pairs or chains — hence the name which means twisted chain

so when you hear "chains of purple cocci," your mind should immediately go:

Streptococci

3 multiple choice options

Gram-positive, round cocci. arranged in chains or pairs (not clusters like Staph)

Streptococci

3 multiple choice options

select all that apply:

what is the classification of Streptococci based on?

1. hemolysis on blood agar

2. antigenic composition

3. growth/biochemical features

partial hemolysis → greenish hue (e.g., S. pneumoniae, viridans group)

α-hemolytic

3 multiple choice options

complete hemolysis → clear zone (e.g., S. pyogenes, S. agalactiae)

β-hemolytic

3 multiple choice options

Lancefield grouping: based on differences in cell wall carbohydrates. Groups A, B, C, D, G

antigenic composition

3 multiple choice options

sensitivity to bacitracin, optochin, bile solubility

growth characteristics

3 multiple choice options

partial breakdown of RBCs, leaves a greenish discoloration. think S. pneumoniae, S. viridans

alpha hemolysis

3 multiple choice options

complete lysis of RBCs. results in clear zones around colonies. think S. pyogenes (Group A Strep), S. agalactiae (Group B)

beta hemolysis

3 multiple choice options

Group A = S. pyogenes → β-hemolytic

Group B = S. agalactiae (not listed here but part of Group B) → β-hemolytic

Group D = now known as Enterococcus spp.

Groups C & G = less common in humans, sometimes zoonotic

Lancefield grouping based on surface antigens

3 multiple choice options

Gram-positive cocci in chains

β-hemolytic on blood agar (clear zones around colonies). bacitracin-sensitive (vs. Group B strep)

S. pyogenes

3 multiple choice options

surface protein; major virulence factor. inhibits phagocytosis.

molecular mimicry: antibodies can cross-react with heart tissue → rheumatic fever 😬

M protein

3 multiple choice options

superantigens that cause fever, rash, toxic shock, and scarlet fever

streptococcal pyrogenic exotoxins

3 multiple choice options

hemolysins that destroy RBCs and WBCs

streptolysins O and S

3 multiple choice options

oxygen-labile and antigenic → ASO titer (used to diagnose recent strep)

streptolysin O

3 multiple choice options

classic in kids: fever, sore throat, swollen tonsils with exudates, tender anterior cervical lymph nodes. rapid test → detects Group A carbohydrate antigen

why treat? prevent rheumatic fever, not just relieve symptoms

pharyngitis

3 multiple choice options

caused by deep tissue spread or toxin release

invasive infections

3 multiple choice options

rapid tissue death ("flesh-eating bacteria"), surgical emergency

necrotizing fasciitis

3 multiple choice options

caused by SPE toxins, sandpaper rash, strawberry tongue, and circumoral pallor. happens after strep pharyngitis

scarlet fever

3 multiple choice options

SPEs act as superantigens. sudden high fever, hypotension, multi-organ failure. like Staph but associated with bacteremia and tissue necrosis

Streptococcal Toxic Shock Syndrome

3 multiple choice options

strep throat is super common in kids and can lead to acute rheumatic fever (autoimmune, from M protein mimicry) and post-streptococcal glomerulonephritis (immune complex-mediated, can follow pharyngitis or impetigo)

💊 treatment: _____________________ (even if symptoms resolve—rheumatic fever is the main thing we're preventing)

penicillin

3 multiple choice options

S. pyogenes on beast mode.

rapid progression, intense pain, out of proportion to appearance. skin turns red → purple → black.

needs surgical debridement + IV antibiotics. often associated with streptolysin O, SPE toxins, and M protein

flesh eating bacteria

3 multiple choice options

Gram-positive cocci in chains or pairs (often appear as lancet-shaped diplococci under the microscope). α-hemolytic on blood agar→ greenish discoloration due to partial hemolysis. optochin-sensitive and bile-soluble→ lab tests used to distinguish from S. viridans

Streptococcus pneumoniae

3 multiple choice options

#1 virulence factor in Streptococcus pneumoniae: ___________________

helps it evade phagocytosis (slick like Teflon 🧼). there are over 90 capsule serotypes, which is why we need vaccines like:

PCV13 (pediatric conjugate vaccine)

PPSV23 (adult polysaccharide vaccine)

polysaccharide capsule

3 multiple choice options

S. pneumoniae is the #1 cause of 🫁 ____________________ especially in the elderly, smokers, or post-viral illness

“rust-colored sputum”, sudden onset fever, lobar consolidation. can lead to sepsis if untreated

community-acquired pneumonia

3 multiple choice options

S. pneumoniae is the #1 cause of 👂 _________________

major cause in children (top 3 with H. influenzae and M. catarrhalis). ear tugging, fussiness, fever

otitis media

3 multiple choice options

S. pneumoniae is the #1 cause of 👃 _________________

purulent nasal discharge, facial pain/pressure. often post-viral URI in kids and adults

sinusitis

3 multiple choice options

select all that apply:

what other serious infections (especially in immunocompromised, elderly, or asplenic patients) can be caused by S. pneumoniae?

1. bacteremia → sepsis

2. meningitis

3. endocarditis

4. peritonitis, skin infections

treatment for S. pneumoniae: often started with _________________________ for meningitis/pneumonia

amoxicillin or high-dose amoxicillin-clavulanate for otitis or sinusitis

resistance is rising, esp. to macrolides (e.g., azithromycin), so susceptibility testing matters

ceftriaxone

3 multiple choice options

Gram-positive cocci arranged in pairs, short chains, or sometimes singly

often mistaken for strep morphologically, but was previously classified as Group D Streptococcus

Enterococcus spp.

3 multiple choice options

E. faecalis = ~80-90% of human infections

E. faecium = 5-10% (but this one tends to be more drug-resistant 💀)

Enterococcus spp.

3 multiple choice options

not their strong suit. they're not toxin-producing showboats like S. aureus or S. pyogenes. but they thrive under pressure, like low nutrient environments, high antibiotic use 💊, and damaged mucosal barriers

virulence

3 multiple choice options

Enterococcus:

multi-drug resistance, especially to vancomycin (→ VRE = vancomycin-resistant enterococci), _______________, and aminoglycosides in some strains

penicillins

3 multiple choice options

live naturally in soil, water, food, and human gut flora (especially the colon)

Enterococci are __________________ → they strike when barriers are down (e.g., ICU, catheter use, immunosuppression)

opportunists

3 multiple choice options

Enterococcus is consistently ranked #2 or #3 most common ____________________ (right behind E. coli and S. aureus)

hospital-acquired infections

3 multiple choice options

select all that apply:

what are some infections that Enterococcus can cause?

1. UTIs

2. bacteremia

3. endocarditis

4. intra-abdominal & pelvic infections

5. wound Infections

select all that apply:

what are some rare infections Enterococcus can cause?

1. meningitis

2. respiratory tract infections

Enterococcus may _____________________ with other organisms—especially in polymicrobial infections like intra-abdominal abscesses. ➕ think: Enterococcus + E. coli = big problem for abdominal sepsis

synergize

organisms that stain purple with Gram stain (thick peptidoglycan wall ✅), thrive without oxygen, and tend to be spore-forming rods, especially in the Clostridium genus

Gram positive anaerobes

3 multiple choice options

anaerobic = oxygen is toxic to them, spore-forming = hard to kill (heat-resistant, survive in soil/dust), and Gram-positive bacilli = long rods under the microscope

Clostridium spp.

3 multiple choice options

select all that apply:

what are the key species in Clostridium spp.?

1. Clostridium botulinum

2. Clostridium difficile

3. Clostridium tetani

4. Clostridium perfringens

toxins are their superpower. these bugs don't rely on invading tissues like Staph or Strep—they drop toxins that wreck you from the inside out.

virulence

3 multiple choice options

found in soil, water, dust, and animal GI tracts. spores are everywhere, especially in natural environments

Clostridium botulinum

3 multiple choice options

Clostridium botulinum produces neurotoxins that block ______________ release at the neuromuscular junction. this leads to flaccid paralysis

acetylcholine

3 multiple choice options

select all that apply:

what are some botulism presentations?

1. foodborne botulism

2. wound botulism

3. infant botulism

associated with honey ingestion (infants under 1 year should NOT eat honey!)

floppy baby syndrome

3 multiple choice options

tetanospasmin toxin inhibits inhibitory neurotransmitters (GABA & glycine) in CNS→ causes uncontrolled muscle contraction (spastic paralysis)

Clostridium tetani

3 multiple choice options

entry via wounds (esp. dirty puncture wounds). incubation: hours to months. CNS symptoms - trismus (lockjaw), spasms, rigidity, and headache. autonomic NS symptoms - arrhythmias, profuse sweating, and fluctuating BP

tetanus

3 multiple choice options

contains tetanus toxoid, which is a lifesaver in global health. boosters are needed every 10 years.

DTaP/Tdap vaccine

3 multiple choice options

most commonly isolated Clostridium species (20-40% of isolates). anaerobic, spore-forming, gram-positive bacillus. it's a common environmental and GI inhabitant, but when it turns up the heat, it's dangerous.

Clostridium perfringes

3 multiple choice options

Clostridium perfringens produces α-toxin (a phospholipase) → destroys cell membranes, causes hemolysis, and tissue necrosis. the destruction is what gives you ________________—a rapid, smelly, tissue-melting disaster

gas gangrene

3 multiple choice options

select all that apply:

what are the clinical manifestations of Clostridium perfringens?

1. wound infections

2. intestinal disorders

3. systemic disease

asymptomatic colonization: not all carriers have disease. watery diarrhea: classic early sign.

pseudomembranous colitis = raised yellow-white plaques of dead cells and bacteria in the colon. toxic megacolon: colon dilation + inflammation = life-threatening.

Clostridium difficile

3 multiple choice options

C. difficile is a hospital and LTCF superstar. risk factors include broad-spectrum antibiotics like clindamycin, ______________________, or cephalosporins. these wipe out your normal flora → C. diff takes over.

fluoroquinolones

3 multiple choice options