Common Bacterial Pathogens Flashcards
Staphylococcus aureus
- Gram (+), cocci
- 30% of people carry it and are asymptomatic
- Mostly carry in anterior nares and perineum
- Protein A: binds Fc portion of Ab (prevent opsonization & phagocytosis)
- Coagulase: cleaves fibrinogen –> fibrin formation around bacteria; walled off
- Adherence: fibronectin binding proteins
- Alpha toxin: damages tissues & interferes with phagocytosis & killing
- Can be Pen-r, Meth-r, and (lately) Vanc-r
Can cause…
• Cutaneous infection: boils, abscesses, folliculitis, wound infections. Occur commonly with foreign body infections (problem because body focuses on the FB and not the staph)
• Scalded Skin: exfoliating (serine protease specific for a protein involved in integrity of desmosome (holds skin keratinocytes together and to BM). Can go systemic if immune system sucks (baby)
• TSS: Some staph strains can produce a super antigen that binds APC & Tcell and co-stim receptors –> massive Tcell activation, inflammation, cytokine release (TNFa, IL-2, IFNg); frequent in menstruating women (but 1/3 case are in men); local infection environment must be just right - high O2, neutral pH, high protein. Can happen with contaminated food
• Pneumonia: esp with immunocompromised pts. Mostly common with hospital acquired pneumonia, not pts presenting in clinics
• Bacteremia (bug goes systemic after local skin/soft tissue infection
• Endocarditis
Staphylococcus epidermidis
Staph Epidermidis
Classic SSNA; CNS (Coagulase NEGATIVE)
Part of normal flora, but assoc w/ infections in FB
Produces slime (glycocalyx); allows biofilm formation (matte of cells on substrate, stay stuck to each other and objects)
Difficult to treat: AB-r, hard to get drugs into biofilm
What 3 bacteria are most commonly found in endocarditis?
Staph aureus
Strep viridans
CNS staph (e.g. Staph Epidermidis)
Streptococcus pyogenes
GAS: Gram (+) cocci, coag negative
produce a variety of hydrolytic enzymes that act in concert to break down tissue and damage or kill phagocytic cells (spread through tissues)
- Pharyngeal infection = strep throat; M protein inhibits phago & killing by PMNs and enhances adherence to cells; Recurrence b/c of 70 serotypes (antigenic at M protein); normal flora in some ppl
- Skin & wound infection: cellulitis - spreading inf of cut & sub cut
- Glomerulonephritis: follows skin / pharyngeal GAS infection. Strep Ag-Ab complexes are deposited in the kidney and accumulate at the BM. Self-limiting, complement-mediated damage to the kidney results.
- Rheumatic fever: production of Abs after GAS pharyngitis that cross react to host myocardium and heart valves –> progressive Ab-mediated damage to these tissues –> fever and inflammation of the heart, joints, and other tissues. Heart tissue itself is NOT colonized by the infecting Streptococcal organisms, making the disease distinct from infective (bacterial) endocarditis- a true bacterial infection of the heart valves (e.g., Staphylococcus epidermidis).
Contrast skin infections of S. aureus and Strep pyogenes
Staph aureus is more likely to produce an abscess, whereas strep pyo is more associated with a spreading cellulitis infection (spreading from cut to sub cut.)
Streptococcus pneumoniae
• G+ diplococci; “pneumococcus”
• Normal flora in UR tract of up to 40% of healthy people
• Non-invasive: Pneumonia (one of the most frequent causes of bacterial pneumonia in all age groups, world-wide). Sinusitis, otitis media, bronchitis
• Invasive disease: Meningitis, bacteremia/septicemia, pneumonia with septicemia
• Pathogenic b/c antiphagocytic polysaccharide CAPSULE (at least 91 distinct antigenic types) and recovery/immunity due to anticapsular antibody
• Predisposing factors: young or old, alcoholism (e.g., mucocillary defect), respiratory viral infection
• Vaccines: adults (pneumovax, PPSV23, “pneumonia vaccine”) provides measurable (but by no means complete) protection against INVASIVE disease in elderly and immunocompromised adults. Ironically, does NOT provide protection against pneumonia.
Children: Important since kids under 2 can’t make Ab to polysaccharide alone just yet (vaccine is protein+polysac) Hepta-valent (Prevnar) and newer 13-valent (Prevnar 13) vaccines in kids are remarkably successful at reducing disease; confers a degree of “herd immunity” on unvaccinated individuals. Rather unexpectedly, widespread vaccination of kids also reduced vaccine-type pneumococcal carriage across all age groups. Some studies suggest efficacy is threatened by “serotype replacement”.
• Antibiotic resistance: emerging pencillin resistance due to alterations of penicillin-binding proteins
Enterococcus
- Part of normal flora
- Very AB resistant (e.g. VRE), so must distinguish from strep to treat effectively!
- Common inf sites: UTI, surgical wounds, biliary tract, anything that touches colon
- Often a mixed infection w/ anaerobes (e.g., perforated colon spills into peritoneum) –> neutral bug gets into bad spot and is resistant to AB
3 general characteristics of Clostridia
- Gram (+) rods: most common species
- STRICT anaerobes (die in O2)
- Spore formers (hard to kill)
Clostridium difficile
- Part of normal flora in 10% of ppl
- Typically nosocomial infection: after pt comes in, give ab, kill normal flora, c diff proliferates (in 10% of people)
- Causes diarrhea & pseudomembranous colitis
- Resistant to most common AB
- Spores are not killed by sani
- Produces two discrete toxins: entertoxin and cytotoxin, which together are responsible for the observed pathology and symptoms.
- Treat q/ metronidazole for 14 days
- You can culture from stool, but some strains don’t make toxin. Dx with ELISA for toxin (some hospitals use PCR)
Clostridium tetani
- Common in soil and GI tract of animals (importance of spores b/c bacteria would die)
- Local infection (anaerobic) and toxin production
- Retrograde axonal transport of TOXIN to CNS
- Toxin blocks inhibitory interneurons in CNS resulting in “spastic paralysis” (lockjaw b/c masseter is most sensitive)
- Vaccine (inactive toxoid) used to induce production of protective anti-toxin antibody
- Antitoxin = Passive immunization with tetanus-immune human IgG to treat non-immune individuals with clinical signs of tetanus (won’t reverse damage but will prevent new damage)
- Newborns can be affected if mom is not immunized
Clostridium botulinum
- Common in soil and GI tract of animals (importance of spores)
- Preformed toxin in food –> circulation; Toxin block ACh transmission at NM junctions –> flaccid paralysis
- Especially common in home canned products (process removes O2, bacteria grows); kill by cooking
Compare and contrast the 4 food poisoning bacteria
????Staphylococcal, ETEC, Clostridial ?????
Clostridium perfringens
- Wound infections, esp crush –> compromised blood flow to tissues –> low-O2 environment in the devitalized tissue –> anaerobe grows
- While growing in the wound, the bacterium produces “alpha toxin” (phospholypase enzyme), and several other damaging enzymes and toxins.
- Alpha toxin kills phagocytic cells and muscle tissue. Disease can range from cellulitis (outer skin), fasciitis (deeper), to myonecrosis/gas gangrene (killing muscle, invading dead tissue)
- Gram stain shows lack of PMN and dead muscle cells (soup)
- Food poisoning via enterotoxin (exotoxin that affects the gut). Bugs grow in cooling food, ingest the bugs, they make enterotoxin in small int; toxin disrupts tight junctions between endothelial cells in the ilium resulting in a dysregulation of fluid transport.
- Can be normal flora (won’t notice damage from low level alpha toxin)
Escherichia Coli
- CLASSIC Gram (-) rod
- Part of normal GI flora
- Disease by endogenous or acquired (ingestion)
- MANY strains causing varying pathogenicity
• GI disease: many strains, typically from contaminated food & water, AB might be needed.
ETEC = “traveler’s diarrhea,” special adherence to human gut, produce toxin that disrupts electrolyte balance; self-limiting, manage fluids
• UTI: typically isolates from GI tract. Travel from urethra –> bladder –> kidney; special strains getting into the wrong place
Special adherence AND interaction with bladder & kidney epithelium, typically B-hemolytics
• Abdominal infection: release of colon contents into peritoneal cavity via surgery, wound, cancer, etc. Thus, usually MIXED infection with other gut anaerobes (seldom alone)
Pseudomonas aeruginosa
- Very common environmental bacterium; most individuals are highly resistant to infection.
- Infections of traumatic injuries, surgical wounds, and especially BURNS. Opportunistic pathogen often affecting immunocompromised patients
- Hospital-acquired infections (UTIs, pneumonia, less frequently associated with intravascular catheter-related infections). Treat with specialized AB that covers P. aeruginosa
- Early in life, CF pts have chronic lung infections b/c of viscous mucus in lungs keeping bugs down (usually Staph A), controlled with AB
- By age 15-20, all CF pts are chronically infected w/ P. aeruginosa b/c resistant to ABs (like those used to combat Staph A)
- Protected from phagocytosis by viscous lung secretions, bacteria’s mucoid exopolysaccharide, bacterial toxins (Exotoxin A & hemolysin)
- Lung damage from toxins and host response
- Treatment difficult b/c INTRINSIC drug resistance & drug accessibility
- Frequently the cause of death in CF pts
