Gram Positive Cocci: Catalase Negative Flashcards
Enterococcus General
Environment, transmission, significance, morph
Environment: facultative anaerobe, GI tract, grows more in normal flora eliminated by antibiotics
Transmission: endogenous, person to person
Significance: about 17 species, usually E. faecalis or E. faecium
GPC: pairs and short chains, cells may be elongated
Can grow in extreme conditions (alkaline, high temps, NaCl)
Enterococcus Lancefield Typing
What is it?
Antigen: carbohydrate structural component of cell wall
Rebecca Lancefield: identification of streptococci by precipitation reaction with homologous antiserum
Enterococcus: Virulence Factors
3
Surface adhesins: colonization and edherence to heart valves, renal epithelial cells
Enzymes: cytolysin: protein that inhibits G+ bacteria, hyaluronidase: spread in tissue
Antibiotic resistance: to vancomycin
Enterococcus: Infections
3
Nossocomial: UTI, bacteremia
Peritonitis: after surgery or trauma
Endocarditis: inflammation of heart valve linings (surface adhedsin virulence factor!)
Enterococcus Infection: Endocarditis
Symptoms, entry, and spread
Infection is IN the heart, not from another site and traveling through blood - actually coming from heart
Symptoms: flu, fever, chills, heart murmur, fatigue, aching, night sweats, swelling in feet, legs or abdomen
Entry and Colonization: transient bacteremia common, mucosal surface is diseased
- Vascular endothelium is resistant to bacteremia, *bacteria initially stick to platelet and fibrin aggregates
*
Spread: vegetation formations, cytokine release and tissue damage
Endocarditis Virulence Factors
2
Adherance to thrombotic vegetation or valve endothelium
Replicate the valve surface to avoid detection
Streptococcus Species General
G+ cocci in pairs or short chains, can be lancet shaped
Use hemolysis to identify
Streptococcus pyogenes Background
Group A Strep (GAS)
Where, transmission, clinical
Where: transient colonization skin, URT of humans
Transmission: person to person, droplets, breaks in skin direct contact or fomites
Clinical: pharyngitis, skin or pyodermal infections, sepsis
Streptococcus Virulence Factors
4
Capsule: resists phagocytosis
M proteins: resists phag., adhere and invade host cells
Teichoic/lipoteichoic acid: adhere and invade
Exotoxins
Streptococcus pyogenes Exotoxins
3
Streptococcal pyrogenic exotoxin: superantigen, necrotizing fasciitis and strep toxix shock syndrome
Streptolysin S and O: hemolysin, lyses blood cells, S version is why hemolyzed on SBA
Streptokinase: lyse blood clot and fibrin, spreads microbe
Streptococcus pyogenes Pharyngitis
Pharyngitis: 2-4 days, abrupt sore throat, fever, headache
Scarlet fever: diffuse rash, strawberry tongue, lasts 5-7 days
Streptococcus pyogenes Pyoderma
Impetigo, cellulitis
Erysipelas: acute spreading red lesion, face and lower extremities, upper layer of skin
Seen in mostly elders
Streptococcus pyogenes Necrotizing Fasciitis
Deep subcutaneous muscle and fat breakdown in fascial plane (right above muscle layer)
Comes in through a break in the skin
Surgery to remove infection
Streptococcal Toxic Shock Syndrome
Initial strep infection goes to shock, organ failure
Patients often have necrotizing fasciitis, bacteremic
Post-Strep Sequelae
And why
Rheumatic fever: inflammatory affecting heart, joints, can lead to damaged heart valves, disability, embolic stroke, endocarditis, heart failure
Why: molecular mimicry, response to microbe cross reacts with host antigens, autoimmunity
- Follows pharyngitis, not cutaneous infection
- Young children
Acute glomerulonephritis: inflammation of glomeruli, edema, hypertension, hematuria, proteinuria, sequealae of both pharyngitis and cutaneous
Streptococcus agalactiae Background
Group B Strep (GBS), where, transmission, clinical, virulence
Where: normal flora, female genital tract, lower GI tract, 1 in 4 pregnant women
Transmission: person to person, endogenous
Clinical: neonatal/postpartum infection
Virulence factor: capsule, adhesions
Streptococcus agalactiae Infections
Neonatal disease
Earl onset: vertical transmission from mother, bacteremia, pneumonia, meningitis
Late onset: exogenous source, mostly meningitis
Pregnant women: post partum endometritis, wound infection, UTIs
Other: at risk if older, diabetes, heart disease || bacteremia, pneumonia, skin, soft tissue, bone, joint infections, UTIs
Streptococcus agalactiae Prevention
Neonatal: screened for colonization
Chemoprophylaxis for all women at high risk or already colonized
Intrapartum temp of at least 38 C
Membrane rupture 18 hours before delivery
Vaginal or rectal culture positive
Streptococcus pneumoniae Background
Where, transmission, clinical
Where: nasopharynx or oropharynx, common in children
Transmission: person to person droplet, endogenous
Clinical: meningitis, pneumonia, otitis media, bacteremia
Streptococcus pneumoniae Virulence Factors
3
Protein adhesions
Pneumolysin that creates pores in cells so pathogen can spread into sterile tissue
Capsule for resisting phag
Streptococcus pneumoniae Infections
Pneumonia: 25-60% all pneumonia, sudden chills, fever, chest pain, cough, pleural fluid effusion problems, cloudy lungs on x ray
Otitis media: inflammation of middle ear, 75% of children get it within 3 years of life
Streptococcus pneumoniae Prevention
Vaccines available
Composed of polysaccharide antigen fused with a protein carrier molecule
The protein carrier is a stronger antigen that enhances effectiveness of vaccine because original polysacch. antigen can be weak
Viridans streptococci Background
Where, transmission, clinical
Where: normal mouth flora, GI tract, female genital tract
Transmission: exogenous
Clinical: opportunistic
Viridans Infections
Subacute bacterial endocarditis: prosthetic valves at risk, slow course of disease, S. sanguis and S. mitis
Dental caries and gingivitis: S. mutans
Gastrointestinal carcinoma: S. gallolyticus
Antibiotic Resistance and General Prevention
Enterococci are antibiotic resistant, some GBS are vancomycin resistant
S. pneumoniae gaining some resistance too
Mostly just antibiotic treatments, clean wounds, keep hygiene/
