1
Q
What are two genuses of gram positive cocci?
A
1) Staphylococcus (catalase +)
2) Streptococcus (catalase -)
2
Q
Generally describe staph aureus.
A
- 1ary pathogenic species of genus
- gram (+) cocci in clusters
- Asymptomatic carriers => ~30% of healthy ppl —» potential for carriers to spread to pts
- Responsible for wide spectrum of diseases – depending on strain
3
Q
What are the categories of the wide range of diseases caused by staph aureus?
A
1) Cutaneous infection
2) Toxin-mediated disease
3) Pneumonia
4) Foreign-associated infections
5) Bacteremia/endocarditis
4
Q
Describe cutaneous infections caused by staph aureus
A
Characteristic lesion => Localized abscess
- Bacterium + host wall off infection w/ fibrinous capsule
- Capsule prevents infiltration of phagocytes, Abs, antimicrobials
- Tx => draining abscess
- Often associated w/ presence of foreign body (splinter, suture)
5
Q
Which enzyme helps form the fibrinous capsule involved in cutaneous infections caused by staph aureus?
A
Coagulase
- An essential virulence factor
- Deposits fibrin on cell surface –» interferes w/ phagocytosis
Coagulase is used as a diagnostic factor when differentiating between different staphalococci
6
Q
Which major cytotoxic agent is released by staph aureus during cutaneous infections?
A
Alpha-toxin
- First identified member of pore-forming beta-barrel toxin family
- Knock-out strains => reduces invasiveness and virulence of infection
7
Q
What are different types of toxin-mediated diseases caused by staph aureus?
A
1) Scalded Skin Syndrome
2) Toxic shock syndrome
3) Staph food poisoning
8
Q
Describe Scalded Skin Syndrome
A
- Local infection, toxin production => systemic effects
- Epidermis sloughs off (doesn’t necessary slough where the infection is)
- Adult slough —» more localized b/c of ^ presence of Ab
- Infant slough —» widespread b/c their immune system hasn’t seen the infection before (no Abs)
9
Q
Describe Toxic Shock Syndrome
A
- Most frequent in menstruating women (but 1/3 of cases are males)
- Local infection and toxin production
- Toxins requires O2, neutral pH, high protein environment (not changing a tampon often => ideal environment for staph aureus) «—IMPORTANT!! KNOW THIS
- Symptoms: High fever, shock, vomiting, muscle-pain, renal/hepatic injury
10
Q
Describe staphylococcal food poisoning
A
- Caused by contaminated food —» ingestion of superAg toxin
- Vomiting and diarrhea
YIPPEEEE!
11
Q
What is a superantigen toxin?
A
- Ag class => cause non-specific activation of T cells
- Polyclonal T cell activation and massive cytokine release
- Produced by pathogenic microbes
Normal Ags induce .001% of T cell response —- SuperAgs induce 25%!!
12
Q
Describe staphylococcus epidermidis
A
- Prototype of SSNA (aka CNS) —» Staph species, not aureus - Coagulase-negative staph
- Normal skin flora, relatively non-pathogenic
- Allows slime/biofilm formation => adheres to implanted devices (catheters, shunts)
- Very difficult to treat! Usually have to remove device
13
Q
Describe streptococcus pyogenes (Group A strep)
A
- Can cause pharyngeal infection (LOCALIZED)
- Can cause skin/wound infections (SYSTEMIC)
- If untreated => post-strep probs (glomerulonephritis, rheumatic fever)
14
Q
Describe streptococcal pharyngitis. What is the primary virulence factor associated w/ local infection?
A
- Spreads via droplet/nasal secretions of infection person
- Several % of asymptomatic carriers
- Swollen tonsils w/ white, purulent exudate
Virulence factor
- M-protein => inhibits phagocytosis, kills PMNs, enhances adherence to epithelial cells
- Produced by bacteria
15
Q
Describe rheumatic fever
A
- Autoimmune inflammatory heart, joints, other tissue disease — may follow strep throat
- Results from Abs produced b/c of strep throat —» now attack heart
- Distinct from infective endocarditis b/c the infection itself does not attack heart, just Abs
16
Q
Describe infective endocarditis
A
- Caused by bacterial infection of heart valves
Three common bacteria:
1) Staph a.
2) Viridans Strept
3) Coagulase-negative staph
17
Q
Describe streptococcus pneumoniae
A
- G(+) cocci in pairs
- In normal flora of 40% of healthy pop’n
- Pathogenesis related to ability to grow and evade host defenses:
1) Antiphagocytic polysaccharide capsule
2) Recovery/immunity due to anticapsular Ab development
3) Multiple antigenic types of capsule
18
Q
What are the diseases caused by streptococcus pneumoniae? Classify according to invasiveness
A
Non-invasive:
- Pneumonia
- Sinusitis, otitis media, bronchitis
Invasive:
- Meningitis
- Bacteremia/septicemia
19
Q
Which factors predispose a person to pneumonia?
A
1) Young and old
2) Alcoholism
3) Respiratory viral infection
20
Q
Which types of vaccines exist against pneumonia? Separate according to age.
A
Adults:
- 23-valent vx (you’ll hear pts call it the “pneumonia vaccine”)
- Technically also 13-valent, but Gill doesn’t say this (ACIP recommends in kids/adults)
Kids:
- 7-valent vx (not recommended by ACIP anymore)
- 13-valent vx (recommended by ACIP)
Gill needs to update his vx info — recommendations have changed
21
Q
Describe enterococcus faecalis and E. faecium
A
- Primary causes of enterococcal infections
- Often nosocomial infections
- Common sites: urinary tract, surgical wounds, biliary tract
- Important to differentiate from other streptococci b/c of antibiotic tx resistance
22
Q
Which genus is classified as gram-positive rods?
A
Clostridium!!!
23
Q
How are Clostridia classified?
A
1) Strict anaerobes
2) Endospore-formers
24
Q
Describe Clostridium difficile
A
- Typically a nosocomial infection
- in normal flora of 10% of healthy ppl
- Resistant to most common antibiotics
- Spores NOT KILLED by alcohol-based hand sanitizers!! (HOLY FRICKIN MOLY!!!)
25
How is C. Diff disease acquired?
- In hospitals
- Associated w/ or follows antibiotic use (Clindamycin, etc.) b/c normal GI flora is suppressed => C. Diff grows!!
- Can also be transmitted from an infected person to another person
26
Go read the C. Diff case history!!
It will help you understand the progression of C. Diff
SERIOUSLY!! GO READ IT! NOW
27
Describe C. Tetani
- Comes from soil/animals (think spore transmission)
- Local infection and toxin production
- Retrograde transport of toxin to CNS
- Toxin blocks interneurons in CNS (Spastic paralysis!!! LOCK-JAW!)
Also, maternal and neonatal tetanus (b/c of unhygienic deliveries and umbilical cord care)
28
Describe C. Botulinum
- Comes from soil/animals (spore transmission)
- The preformed toxin in food circulated in body --->> blocks Ach transmission at neuromuscular junctions => FLACID PARALYSIS
- Common in home-canned foods
29
Describe C. perfringens
- In wound infections (cellutis, fasciitis, myonecrosis) => bacteria produces alpha-toxin, and other damaging enzymes/toxins
- Alpha-toxin kills phagocytes and muscle tissue
- In food poisoning: produce enterotoxin in vitro ==> disrupts tight junctions between endothelial cells in ilium (dysregulation of fluid transport)
30
What are two types of gram-negative rods?
1) E. coli
| 2) Pseudomonas aeruginosa
31
Describe E. Coli
- Many different strains
- Normal in large intestine flora
Causes GI disease:
- many strains vary in severity
- typically from contaminated food/water
- Antibiotics can/cannot be used (depends on strain)
- Traveler's diarrhea (toxin disrupts electrolyte balance in gut, managed by fluid replacement)
32
Describe E. Coli in UTIs
- Endogenous fro GI tract
- Access UT via uretha -->> bladder --->> kidney
- Certain strains can adhere to cells, interact w/ bladder epithelial cells, or are hemolytic
33
Describe E. Coli in abdominal infections
- Release/escape of contents of colon to peritoneal cavity/adjacent tissues
- B/c of surgery, wounds, colon cancer
- Often associated w/ anaerobic bacteria
34
Describe Pseudomonas Aeruginosa
- A very common environmental bacterium --- most ppl are highly resistant to it
- Infections caused by traumatic injuries, surgical wounds, burns (especially BURNS)
- Also associated w/ chronic lung infection in pts w/ CF
35
Describe Pseudomonas Aeruginosa in cystic fibrosis
- Nearly all CF pts 15-20 yo are infected
- Facilitated by resistance to anti-staph drugs (makes it difficult to treat)
- Lung damage b/c of bacterial toxins
- PA is protected from phagocytes
Frequently the COD in pts w/ CF
36
What is a type of gram-negative (diplo)cocci?
Neisseria gonorrhoeae
37
Describe Neisseria gonorrhoeae
- Causes gonorrhea and conjunctivitis (leading to blindness) of infants born to gonorrhea (+) moms
- PILI: key to infectivity
- Pili interfere w/ killing of bacteria by PMNs --- Ab develops to pili prevents infection
- Prolong infection => scarring/fibrosis (urethra (men/women), cervix => infertility in women)
38
Describes anaerobes
- Found in normal flora but killed by O2
- Found in colon, mouth (e.g. gums, tongue), female genital tract, skin
- Usually cause disease as a mixed infection (lung/colon abscesses)
Treatment:
More effective - metronidazole
Less effective - aminoglycosides
39
Describe Bacteroides fragilis
- Common in colon flora, aerotolerant
- Cultured from anaerobic abscess below diaphragm
- Considered to be a prototypical endogenous anaerobic pathogen
40
What are the virulence factors associated w/ bacteroides fragilis?
1) Tissue-destructive enzymes
2) Capsule
3) Superoxide dismutase
41
What is a type of intracellular bacteria?
Chlamydia trachomatis
42
What is a type of bacteria w/o cell walls?
Mycoplasma pneumoniae
43
Which diseases are caused by chlamydia trachomatis?
1) Trachoma
2) Genital infections
3) Neonatal infections
44
Describe trachoma that is caused by chlamydia trachomatis
- Chronic infection of conjunctiva
- Causes scarring and blindness
- Endemic in parts of Asia/Africa
45
Describe the genital infections caused by chlamydia trachomatis
- Common STI
- Non-gonococcal urethritis (men) and urethritis, cervicitis, and PID (women)
LEADS TO neonatal infections in mom is infected
- Neonatal conjunctivitis, pneumonia
- Screening and treatment in pregnant women decreases incidence
46
Describe mycoplasma pneumoniae
- Produces common form of pneumonia (10%): atypical pneumonia --- found in younger ppl (5-20yo)
- Adheres to respiratory epithelial cells
- Bacterial growth is extracellular
- Bacteria produce H2O2 and superoxide radical => UH OH! serious damage
47
Describe mycoplasma pneumonia as it presents in pts
- Generally mild
- AKA: walking pneumonia
- Spread by respiratory secretions
- Fever, headache, malaise, non-productive cough, check/body aches, fatigue
- Recovery slow --- over 1-4 weeks
48
Describe mycoplasma pneumonia on a cellular level
- Culture difficult to grow => slow
- Causes inflammation/thickening of interstitium (tissue around air sacs of lungs)
- Lab diagnosis via serological tests
- Gram stain used primarily to RULE-OUT other bacteria
Treatment: b/c bacteria lack cell wall/shape => cell wall-active antibiotics not effective
D&D Unit 3
flashcards
Decks in class (12)
# Cards
-
Bacteria Structure and Function (complete)42
-
Host-Microbe Interactions (complete)15
-
Bacterial Genetic Variation (complete)29
-
Common Bacterial Pathogens (complete)48
-
Microbial Toxins (complete)28
-
Antibacterial Agents: Introduction14
-
Antibacterial Agents: Cell Wall Synthesis Inhibition35
-
Antibacterial Agents: Protein Synthesis Inhibitors0
-
Antibacterial Agents: Inhibitors of DNA Function0
-
Mechanisms of Antibiotic Resistance (complete)32
-
Clinical Antibiotic Use17
-
What kills what? (complete)14
