TEST 2 Bugs 1 Part 1/2 Flashcards
Staphylococcus aureus
Catalase?
Coagulase?
Hemolytic? (Details)
Colony description
Salt?
- Catalase: Positive
- Coagulase: Positive
- B-Hemolytic (Pale/Clear area surrounding colonies on blood agar)
- Golden yellow colonies
- Grape-like clusters
- Polysaccharide capsule
- Ferments Mannitol salt (yellow)
Staphylococcus aureus
Pathogenesis for colonization:
- Adhesins = attach to collagen
- Fibronectin-binding protein = bind to clots and
Staphylococcus aureus
Pathogenesis for Invasion:
- Staphylokinase = lyse fibrin clot
- Hyaluronidase = hydrolyze hyaluronic acid. Tissue Spreading.
Staphylococcus aureus
Pathogenesis for inhibit phagocytosis:
- Polysaccharide capsule
- Protein A - bind IgG Fc.
- Coagulase - activates prothrombin to form a clot.
- Clumping factor = bound coagulase - bind fibrin to wall off abscess
Staphylococcus aureus
Pathogenesis to enhance survival:
- Catalase - Removes H2O2
- B-lactamase - cleaves penicillin
Staphylococcus aureus
Pathogenesis
Membrane-disrupting toxins:
- Cytolytic/hemolysins - alpha, beta, sigma, gamma.
- Cause eukaryotic cell pores.
- Panton-Valentine Leukocidin (PVL) - pore forming toxin encoded on plasmids in CA-MRSA strains.
Staphylococcus aureus
Pathogenesis
Exotoxins:
- TSST-1 - Superantigen that binds MHC-II without processing antigen ⇢ activated T cells ⇢ massive cytokine release (Toxic shock syndrome, TSS).
- Enterotoxins A (SEA), B(SEB), C, D, etc. Heat-Stable superantigens.
- Cause vomiting and diarrhea (food poisoning) and TSS.
Staphylococcus aureus
Infections
Pyogenic Infections
- Impetigo (bullous and non-bullous), folliculitis, styes, furuncles/boils, carbuncles, mastitis, wound infections, otitis externa.
Staphylococcus aureus
Infections
Systemic Infections
- Pneumonia (often after influenza virus infection), empyema, septicemia, septic arthritis, osteomyelitis, endocarditis.
- Endocarditis: Acute endocarditis, rapid onset of symptoms, very ill patient, often no pre-existing valve disease (i.e. NO mitral valve prolapse).
Staphylococcus aureus
Infections
Toxigenic Infections:
- Food poisoning, toxic shock syndrome, Staph. scalded skin syndrome.
-
Food poisoning
- Common in Mayonnaise
- Preformed toxins: Rapid (3-6hr) onset of nausea, vomiting, abdominal cramps and diarrhea (rare). Over in <24hr.
-
Food poisoning
Staphylococcus aureus
Toxic Shock Syndrome (TSS)
- Found commonly in Surgical Packing or hyper-absorbent tampons.
-
S. aureus produces TSST-1 or SEB/C
- Results in: High fever, rash (diffuse, red erythroderma), hypotension, vomiting, diarrhea, desquamation of palms and soles, possible multi-organ failure.
Staphylococcus aureus
Staphylococcal scalded skin syndrome (SSSS)
- Infection of umbilicus or face in < 5 year-olds.
- Exfoliative toxins ⇢ large bullae (blisters) and epithelial desquamation (intra-epidermal, stratum granulosum).
Staphylococcus aureus
Anti-staph antibiotics
- Most strains of Staph resistant to penicillin by producing penicilinase (B-lactamase), treated with anti-staphylococcal penicillins:
- Dicloxacillin, Nafcillin, oxacilin, or methicillin.
- First generation cephalosporins:
- Cephalexin
- B-lactam plus inhibitor.
What is another name for penicillinase?
B-Lactamase
What does MRSA mean?
Methicillin Resistant Staph Aureus
MRSA contain Xsomal mecA gene, what is it?
Modified penicillin-binding proteins (PBSs, transpeptidase).
What is HA-MRSA treated with?
(Hospital Acquired)
Treated with Vancomycin, linezolid, daptomycin, or ceftaroline.
Describe CA-MRSA
- Less antibiotic resistance than HA-MRSA.
- More virulent and more invasive (PVL).
- Treated with trimethoprim-sulfamethoxazole (Bactrim).
Where did Methicillin- and vancomycin-resistant S. aureus acquire this trait from?
Enterococcus plasmid
Describe B-Lactamases?
- Major mechanism of antibiotic resistance in Gram-negative pathogens.
- Synthesized in cytoplasm and secreted into periplasm.
- Gram-positives synthesize in cytoplasm and secrete them extracellularly.
- Most are on plasmids.
What are the Three types of B-Lactamases?
- Penicillinases inactivate penicillins
- Extended-spectrum B-Lactamases (ESBLs) inactivate most B-lactams except for carbapenems.
- Carbapenemases (e.g., OXA, KPC, metallo-B-lactamase) inactivate carbapenems.
Define Bacteriostatic
Agents inhibit bacterial growth while the agent is present. Rely on the immune system (of an immunocompetent person) to aid the bacteriostatic agent and clear the infection.
Define Bactericidal?
Agents kill bacteria but are bacteriostatic under some conditions, e.g., in biofilms.
Staphylococcus epidermidis
Catalase?
Coagulase?
Urease?
Hemolytic? (Details)
Colony description
Capsule type
Notable Sensitivity?
- Catalase: Positive
- Coagulase: Positive
- Urease: Positive
- Hemolytic? Non-Hemolytic (gamma-hemolysis) salt tolerant.
- White Colonies, arranged in grape-like clusters.
- Polysaccharide Capsule
- Novobiocin sensitive
Staphylococcus epidermis Basics?
- Normal Skin flora. Contaminants blood cultures
- Opportunistic pathogen
- Grows on mannitol salt but does not ferment mannitol ⇢ red.
- Capsule and biofilms.
Staphylococcus epidermidis Infection
- Catheter or prosthetic device infections (hip implant, heart valve). Endocarditis of artificial valves.
- Endocarditis in people with indwelling IV catheters or IV drug users.
- Vancomycin is the drug of choice.
Staphylococcus saprophyticus traits
- Catalase: Positive
- Coagulase: Negative
- Novobiocin resistant
- Differentiate from S. epidermidis with novobiocin.
- Nitrite negative on urine dipstick
- Opportunistic pathogen.
- Sexual activity (honeymooner’s cystitis)
- Normal Vaginal and GIT flora
S. saprophyticus common disorder?
- UTIs (uncomplicated cystitis/pyelonephritis) in adolescent females, often newly sexually active. Treated with UTI antibiotics.
What are common UTI antibiotics?
Fluoroquinolones, Bactrim, Nitrofurantoin
Streptococcus pneumoniae traits?
Catalase, Hemolysis, shape, capsule, sensitivity, solubility, antigens, respiration and fermentation.
- AKA, Pneumococcus
- Catalase: Negative
- A-Hemolytic (green colony on blood agar under room air)
- Lancet-shaped diplococcus
- Polysaccharide capsule
-
Optochin sensitive (P disk)
- Used to differentiate S. pneumoniae from a-hemolytic Viridans Strep.
- Bile Soluble (cellular autolysin is activated by bile salts).
- No Lancefield antigens
- Facultative anaerobe, but ferments in the presence of O2.
How to type Streptococcus pneumoniae?
Use capsular Abs = Quelling reaction
Where does S. pneumoniae colonize?
Throat and nasopharynx ⇢ resp. droplet (aerosol) spread.
How does S. pneumoniae inhibit phagocytosis?
Capsular polysaccharide (90 serotypes) inhibits phagocytosis unless specific Ab is present.
How does S. pneumoniae increase adherence to mucosal surfaces?
IgA protease cleaves secretory IgA.
Describe S. pneumoniae’s membrane-disrupting toxin:
- Pneumolysin O = Pore-forming hemolysin from autolyzed S. pneumo. Activates complement, damages resp. epithelium ⇢ productive cough + blood.
Most common cause of sepsis in children with sickle cell disease and dysfunctional spleen?
Streptococcus pneumoniae
Pneumococcal pneumonia results in what kind of pneumonia? and what are it’s symptoms?
-
Lobar pneumonia
- Blood-tinged, rusty sputum
- Major cause of death
- Blood cultures often positive.
-
Meningitis
- Preceded by Bacteremia
- Otitis media and sinusitis
What are the two vaccines for Streptococcus pneumoniae?
-
Pneumococcal conjugate vaccine or PCV13 (Prevnar13)
- Vax for kids
-
Pneumococcal polysaccharide vaccine or PPSV23
- Adult vax
Treatments for S. pneumoniae
- Macrolides, cephalosporin, and fluoroquinolones are used as alternatives to penicillin for pneumonia, otitis media, and sinusitis.
- Cefotaxime or ceftriaxone (3rd gen) for meningitis.
Streptococcus pyogenes traits?
Catalase, Hemolysis, shape, capsule, sensitivity, grouping, reservoir, solubility, antigens, respiration and fermentation.
- Catalase: negative
- B-Hemolytic
- Arranged in chains
- Hyaluronic acid capsule (aids in cellulitis)
- Bacitracin sensitive (A disk)
- Lancefield Group A
- Reservoir: Human oropharynx
- Facultative anaerobe, but ferments in the presence of O2.
How do you differentiate Streptococcus pyogenes from other B-hemolytic Strep.?
-
Use Bacitracin to differentiate.
- S. pyogenes is sensitive to penicillin G.
Streptococcus pyogenes
Pathogenesis for adhesion/colonization:
- M proteins = immunogenic fimbriae adhesins
- Protein F - binds fibronectin
Streptococcus pyogenes
Pathogenesis for Invasion:
- Hyaluronidase = hydrolyze hyaluronic acid. May help tissue spreading.
- Streptokinase = breaks down fibrin clot by activating plasminogen.
Streptococcus pyogenes
Pathogenesis to inhibit phagocytosis:
Hyaluronic acid capsule = antiphagocytic but nonimmunogenic polysaccharide.
Streptococcus pyogenes
Pathogenesis - Immune interference:
- C5a peptidase - interferes with PMN attraction (reduce inflammation)
- M Proteins - draw factor H to inhibit the alternative complement pathway (inhibiting C3b formation) and opsonization.
Streptococcus pyogenes
Pathogenesis - Membrane-disrupting toxins:
- Streptolysin O = a hemolysin that stimulates anti-streptolysin O (ASO) titer.
- Erythrogenic toxins A and C (SPE-A and SPE-C) = pyrogenic superantigens ⇢ fever, rash, T cell proliferation and B cell suppression. Phage encoded. TSS.
Streptococcus pyogenes
Suppurative Infections:
- Erysipelas
- Impetigo (non-bullous) - honey-crusted skin lesions ( versus S. aureus bullous impetigo).
- Strep throat
- Cellulitis
- Necrotizing Fasciitis
- Osteomyelitis, puerperal sepsis.
Streptococcus pyogenes
Toxin-Mediated Diseases:
- Scarlet fever: Strep throat + sandpaper rash + “strawberry tongue”.
- Toxic shock syndrome (with bacteremia).
Streptococcus pyogenes
Poststreptococcal sequelae:
-
Acute glomerulonephritis
- Pharyngitis or impetigo
-
Rheumatic fever
- Sequela to untreated GAS pharyngitis only (not impetigo). Abs cross-react between M protein and heart muscle or joint antigens ⇢ damage (autoimmune, molecular mimicry).
Streptococcus pyogenes
Treatment:
- Penicillin G
- Penicillin V
- Erythromycin
- Penicillinase-resistant penicillin: in skin infections where Staph could be the responsible organism.
- After Rheumatic fever:
- continuous prophylactic antibiotics to prevent repeat strep throat.
- Clindamycin when:
- Necrotizing fasciitis
- Streptococcal toxic shock syndrome
Non-bullous impetigo (pyoderma, impetigo contagiosa)
- Most commonly caused by S. aureus, second most common S. pyogenes.
- Contagious, superficial infection
- Primarily young children
- Poor personal hygiene
- “honey colored” crusted lesions
- Be careful: Nephrogenic GAS can lead to post-streptococcal glomerulonephritis.
Describe Erysipelas:
- Type of Cellulitis
- Superficial erythematous and edematous lesions.
- Fiery red (salmon red) advancing erythema.
- Superficial erythematous and edematous lesions.
- Mainly caused by GAS
- Be careful: Sometimes, erysipelas cannot be reliably distinguished from cellulitis. Patients that have systemic manifestations (fever/chills) should be treated with parenteral therapy to cover S. aureus.
Streptococcal disease complication
- Pharyngitis: “Strep throat” exudates (suppurative) on tonsils (children 5-15 yrs).
- Scarlet fever: Complication of strep pharyngitis that occurs when the infecting strain is lysogenized by a bacteriophage that produces a pyrogenic exotoxin.
Streptococcus agalactiae
Group B Strep (GBS)
- Catalase: Positive
- Diplococci in chains
-
B-Hemolytic
- Incomplete hemolysin = CAMP factor (Positive)
- CAMP test (>zone of hemolysis with S. aureus + hydrolyze Hippurate = ID
- Incomplete hemolysin = CAMP factor (Positive)
Streptococcus agalactiae Infections in adults
Asymptomatic carriage, mild febrile illness or UTI that can lead to amnionitis or endometritis in Pregnant women.
Streptococcus agalactiae Infections in Neonate:
-
Early onset (1-6 days) = Resp. problems, sepsis, pneumonia, meningitis.
- Acquired in utero or at delivery.
- Most common in premature infants
-
Late onset (≥7 days) = septicemia and meningitis.
- Acquired postpartum
- Low mortality rate (<20%)
What are the three species of Viridans Streptococci?
- S. salivarius
- S. mutans
- S. sanguinis
Viridans Streptococci normal environment?
Normally found in oral, GI, GU tract microbiota.
Viridans Streptococci can be responsible for what two issues?
-
SUBACUTE Endocarditis: May follow Dental trauma if have damaged heart valves.
- Caused by S. sanguinis
-
Dental caries, tooth abscesses and periodontitis.
- S. mutans causes dental plaque and dental caries through production of dextran biofilm.
Streptococcus bovis traits
- a or no Hemolysis
- Lancefield group D
- Important members:
- S. gallolyticus
- S. Infantarius
- Colonizes the GI tract. Normal.
- No growth in 6.5% NaCl
- Strongly associated with Colorectal cancer
Enterococcus species that I need to know.
E. faecalis and E. faecium
Enterococcus traits:
- Catalase: Negative
- a, B, or no hemolysis
- Normal in GI tract and vaginal microbiota.
- Vancomycin resistance = modification of cell wall peptidoglycan pentapeptide precursor from -D-Ala-D-Ala to -D-Lactate-D-Lactate.
- Grows in bile, and is bacitracin resistant.
Define nosocomial
Originating in a hospital
Enterococcus infection
- Significant nosocomial agents.
- Cause septicemia, wound infections, and UTI.
- Esp. in patients with urinary or intravascular catheters.
- Cause septicemia, wound infections, and UTI.
- Subacute endocarditis in patients with previously damaged hearts following urinary or GI tract manipulations.
Enterococcus Treatment
- Relatively resistant to cell wall agents.
- Penicillin & vancomycin
- Bacteremia: Often use synergistic therapy
- Vancomycin/gentamycin
- Ampicillin/gentamycin
- Vancomycin-resistant enterococcus (VRE)
- Dangerous hospital acquired infection
- Linezolid, Daptomycin.