Bacterial Pathogens Flashcards
Staphylococcus aureus
- gram+ cocci (in clusters)
- anterior nares and perineum
- cutaneous infections
- toxin-mediated disease (superantigens) (staphylococcocal toxic shock syndrome)
- hospital acquired pneumonia
- foreign body infections
- bacteremia/endocarditis
- resistant to penicillin, methicillin, and soon vancomycin
What bacteria is involved in toxic shock syndrome?
Staphylococcus aureus
superantigen toxin –> activation of T-cells –> systemic manifestations
What bacteria is involved in hospital acquired pneumonia?
Staphylococcus aureus
What bacteria is involved in cutaneous infections creating a local abscess?
Staphylococcus aureus
fibrinous capsule that prevents attack by phagocytes
Staphylococcus epidermidis
- gram+ cocci
- prototypical SSNA
- produces slime/glycocalyx
- allows adherence to foreign bodies
- requires removal of device
Streptococcus pyogenes (Group A Strep)
- gram+ cocci (usually in chains or pairs)
- pharyngitis
- skin/wound infections (cellulitis)
- post-strep diseases (glomeruloephritis, rheumatic fever)
How does pharyngitis occur?
- M protein expressed by strep pyogenes adheres bacteria to epithelial cells and prevents phagocytosis
How does post-strep glomerulonephritis occur?
- immune complex formation of strep antigen-antibody complexes deposit in kidneys (BM)
How does post-strep rheumatic fever occur?
- self-reactive antibodies in response to pharyngeal infection of group a strep
Streptococcus pneumoniae
- gram+ cocci in pairs
- noninvasive pneumonia, sinusitis, otitis media, bronchitis
- invasive meningitis, bacteremia, septicemia
- antiphagocytic capsule
- young/old, alcoholics, respiratory viral infection
Viridans streptococci
- infective endocarditis
- abundant in mouth
- deposit on damaged heart valves using dextrans for adherence
What causes infective endocarditis?
Viridans streptococci
Enterococcus faecalis/faecium
- gram+ cocci
- enterococcal infections of urinary tract, surgical wounds, biliary tract, endocarditis
- acquired resistance, especially to vancomycin
What are common causes of UTIs?
Enterococcus faecalis/faecium and E. coli
What are the most common gram+ rods?
Clostridium:
- strict anaerobes
- form endospores
- hospital acquired diarrhea/colitis (c diff)
- tetanus (c tetani)
- botulism (c botulinum)
- gangrene (c perfrignens)
Clostridium difficile
- gram+ rods
- most common hospital acquired
- diarrhea and colitis
- antibiotics can cause, esp clindamycin
- produce enterotoxin and cytotoxin
- res to a lot of antibiotics
Clostridium tetani
- gram+ rods
- found in soil
- anaerobic local infection and toxin prod
- block of inhibitory neurons in CNS –> constant constriction
Clostridium botulinum
- gram+ rods
- found in soil
- ingested in anaerobic conditions (canned, undercooked food)
- toxin is preformed
- toxin blocks Ach transmission –> paralysis
What causes spastic paralysis?
Clostridium tetani
What causes flaccid paralysis?
Clostridium botulinum
Clostridium perfringens
- gram+ rods
- wound infections; dec blood flow and low oxygen environments –> produces alpha toxin to kill phagocytic cells and muscle (causes cellulitis, gangrene)
- food poisoning from enterotoxin –> dysregulation of fluid transport
Escherichia coli
- gram- rods
- most common to acquire resistance through plasmids
- GI: diarrhea from adherence to intestinal mucosa and toxins that mess up electrolyte balance
- UTI: adherence to bladder epithelium; hemolytic
- Abdominal: colon to peritoneal cavity; (wounds, colon cancer)
Pseudomonas aeruginosa
- gram- rods
- really resistant
- wounds, esp burns
- lung infection w/ CF: stasis of fluids in lungs get infected
- hospital acq infections: UTIs, pneumonia, catheter-related
Neisseria gonorrhea
- gram- diplococci
- gonorrhea and conjunctivitis
- pilus-mediated: adherence and inhibits neutrophil attack
- inflammation of mucosal surface
- res to penicillin and FQ
Bacteroides fragilis
- anaerobic bacteria
- typically in abscess
- mixed infection (aerobic bacteria metabolize o2 to make anaerobic more habitable)
- tissue-destructive enzymes, anti-phagocytic capsule, prod of superoxide dismutase
Chlamydia trachomatis
- obligate intracellular
- trachoma: chronic conjuctivitis
- genital infections
- neonatal infections
Mycoplasma pneumoniae
- lacks a cell wall
- causes pneumonia
- penicillins not effective (since no cell wall)
- adheres to respiratory epithelial cells and produces h2o2 and superoxide dismutase –> damage tissue
Gram+ cocci
- Staphylococcus aureus
- Staphylococcus epidermidis (SSNA, CNS)
- Streptococcus pyogenes
- Streptococcus pneumoniae
- “Viridans” Streptococci
- Enterococccus faecalis,
- Enterococcus faecium
Gram+ rods
- Clostridium difficile
- Clostridium tetani
- Clostridium botulinum
- Clostridium perfringens
Gram- rods
- Escherichia coli
- Pseudomonas aeruginosa
Gram- cocci
- Neisseria gonorrhoeae
Anaerobic bacteria
- Bacteroides fragilis
- all Clostridium
Obligate intracellular bacteria
- Rickettsia
- Chlamydia trachomatis
Lacks a cell wall
- Mycoplasma pneumoniae
What are ways that bacteria can produce toxins?
- secrete outside of cell
- inject with needle like apparatus
- lysis of bacteria
- LPS
What are mechanisms of action of toxins?
- break down ECM or degrade debris in necrotic tissue
- insert into membranes and create pores –> lysis
- superantigens: activate T cells and lots of cytokine prod
- inhibit protein synth
- modify intracellular signaling
- inhibit neurotransmitter release
What are ways for toxins to enter cells?
- act extracellularly
- cross PM using membrane parts as receptors or being endocytosed
