Microbiology Flashcards
Staphylococci
GENERAL
Gram positive, Fac. Aerobe (prefer reduced O2), Normal microbiota, Extracellular pathogens, Catalase Positive , Coagulase positive
Staphylococci aureus Description
Pus-filled abscesses, almost every niche of the body
Nasal cavity, axilla, perineum
Small Capsule not important as virulent factor
Exotoxins are a major virulence factor
30% intermittently carry, 20% persistent
CA infections – carrier strain
HA – single strain around facility
Staphylococci aureus Scalded skin syndrome
in children < 5 caused by exfoliative toxin A; eta on gene or on a plasmid (exfoliative toxin B, etb) toxins are not active until they reach the skin. They cause skin problems by degrading desmoglein-1, a cadherin protein involved in holding desmosomes together.
Scalded skin syndrome Prognosis
most superficial, But in extensive infections, extensive amounts of fluid lost can lead to death. In older children the reaction is usually less severe and may only cause bullous impetigo (i.e. blisters).
Staphylococci aureus superantigen
A relatively small percentage of S. aureus produce superantigens, but when they do they usually make several different ones.
Staphylococci aureus enterotoxins
S. aureus enterotoxins (SEA, SEB, etc.) cause food poisoning, leading to vomiting (emesis) and cramping.extremely stable proteins. The onset 2-3 hours after ingesting.
Enterotoxins work?
also superantigens , but they don’t get into the bloodstream. could also be aerosolized and used as a biowarfare agent. don’t often kill people intoxication rather than an infection, since you can cook the food and kill the bacteria, but the toxin can remain.
Staphylococci aureus Infections
Follicullitis (hair follicles) Furuncles (boils)
Carbuncles (bunches of boils)- may have fever, chills. Stye (hordeoleum)
External:Sebaceous glands (Zeiss) Sweat glands (Moll)
Meibomian (or tarsal) glands infected
Chalazion – inflammation due to blockage of Meibomian gland
Bullous impetido
Blistering vesicles that crust over
Severe pneumonia w/ necrotic abscesses (secondary to flu)
Follicullitis
(hair follicles)
Furuncles
(boils)
Carbuncles
(bunches of boils)- may have fever, chills
Stye
(hordeoleum)
External: Sebaceous glands
(Zeiss)
External:Sweat glands
(Moll)
Chalazion
Chalazion – inflammation due to blockage of Meibomian (or tarsal) gland
Bullous impetido
Blistering vesicles that crust over
Staphylococci aureus Virulence Factors
Alpha-toxin/ cyolytic toxin, Panton-Valentine Leukocidin (PVL), Exfoliative Toxin, Enterotoxin, Surface-bound proteins - adhesins, fibronectin, collagen, laminin, etc.MSCRAMM, Hyaluronidase, PAMPs.
Alpha-toxin/ cyolytic toxin.
= pore-forming, beta-barrel toxin family. Cells die because they ions
Panton-Valentine Leukocidin (PVL)
PVL is a beta-toxin, but it also kills cells by forming pores in the membrane. PVL was transferred to S. aureus by a bacteriophage enhanced virulence CA-MRSA
Surface-bound proteins - Virulence Factors
adhesins bind host receptor molecules such as fibronectin, collagen, laminin, etc.
MSCRAMM
microbial surface components recognizing adhesive matrix molecules. Many anchored by a mechanism involving sortase.
Hyaluronidase:
secreted virulence factor/ enhancer - degrades hyaluronic acid in the connective tissue spaces making bacterial spread through tissues easier.
PAMPs
PAMPs cell wall components - stimulators of Toll-like receptors.
Staphylococci aureus TSST-1
TSST-1 on a pathogenicity island in the chromosome (can theoretically spread to other bacteria- a mobile genetic element) 5-25% for the fraction of S. aureus isolates that have the gene.
Staphylococci aureus Classification
Gram positive, Fac. Aerobe (prefer reduced O2), Normal microbiota, Extracellular pathogens.
Staphylococci aureus Diagnostic
Catalase Positive
Coagulase positive (activates pro-thrombin)
Agglutination +
Beta-Hemolytic (clear on BAP)
carotenoid pigment – appear more golden than other staph (more white color)
Staphylococci aureus (ACUTE Infection)
ACUTE Infective endocarditis (heart valves)- bulky vegetations platelets attach and fibrinogen is converted to fibrin, plasma proteins bind to these components. A vegetation is a complex biofilm.
Staphylococcal toxic shock syndrome
Staphylococcal toxic shock syndrome & tampons- a toxin called Toxic Shock Syndrome Toxin-1 or TSST-1.
Staphylococci epidermidis Description
Colonizes skin
Coagulase negative
Carriage rates ~100%
Staphylococci epidermidis Infections
Indwelling catheters/ medical advices
15-40% prosthetic valve endocarditis
Ensure not a contaminant
Staphylococci epidermidis Virulence Factors
Thick Capsule
Exotoxins are not as important
Staphylococci epidermidis Classification
Gram positive Fac. Aerobe (prefer reduced O2) Normal microbiota Extracellular pathogens Catalase positive Coagulase negative
Streptococci General
Range from harmless oral to flesh eating, Faculative anaerobes, Fastidious, grow on BAP, classify by the hemolysis & Lancefield antigen (carbohydrate antigen), Catalase negative (unlike staph), oxidase negative (not Neisseria)
Staphylococci saprophyticus Description
Urinary Tract Infections
(second to E coli)
Colonizes GI tract, perineum
Coagulase negative
Streptococci pyrogenes Description
Superantigens, Streptolysin O Titers (SLO), Streptolysin S Titers (SLS)
Streptococci pyrogenes Infections
Pharyngitis, Scarlet Fever Puerperal Sepsis,
Erysipelas, Septicemia, Tonsilitis, Cellulitis, Impetigo, Ecthyma, Necrotizing Fasciitis (NF), TSS, Acute Rheumatic Fever,Acute Glomerulonephritis, PANDAS
Streptococci pyrogenes Virulence Factors
Hemolysins,Hyalurinic acid capsule,M protein, Lipoteichoic Acid, Strep pyrogenic exotoxin A (SpeA, SpeB),Streptokinase:
Streptococci pyrogenes Classification
Group A Strep
Beta-hemolytic
Superantigens
stimulate a much larger fraction of the overall T cell population than would a normal antigen.
Streptolysin O Titers (SLO)
oxygen sensitive, so you grow colonies below the surface of the agar to see it
Streptolysin S Titers (SLS)
oxygen stable, you see hemolysis surrounding the oxygen colonies
Pharyngitis (exudative)
Pharyngitis (exudative) 5-15yo, spread by droplets, 2-4 day incubation, tx to prevent ARF (not AGN).Enlarged, painful cervical lymph nodes, fever > 101F
Scarlet Fever Puerperal Sepsis
1800s – Semmelweis & handwashing endometritis-puerperal fever- childbed fever)
Erysipelas
cellulitis characterized by fiery-red erythema w/ rapidly advancing well-demarcated edges, often on the cheeks – pain, fever, lymphadenopathy, children & elderly
Impetigo
Most common in children, may follow insect bites. Skin infecions associated w/ AGN, weeping vesicles that crust over (pictures of children – near their mouth)
Ecthyma
deep impetigo, pustular capsule & ulceration
Necrotizing Fasciitis (NF)
40-70% mortality, rapid spread (1 in/hr), early signs: flu, brawny edema, extreme pain out of proportion to the size of the lesion, spreading erythema, eccumosis, purple bullae can cause toxic shock, crescendo pain (ramping up the degree of pain)
Treatment: debridement, use of antibiotics, IV fluids, cardiac output
Clindamycin (inhibits proteins, does not breakdown cells walls to release more toxins to activate the immune system)
TSS –
TSS – widespread shock that blanches when pressure is applied
Acute Rheumatic Fever
Jones criteria: early signs: erythema marginatum, subcutaneous nodules
Hyalurinic acid capsule
antiphagocytic, no antibodies against S pyrogenes capsule (see a halo in india ink)
M protein
a sortase-anchored surface protein, C terminal is conserved, N-terminus is the basis for serotyping; M is a major phagocytic factor, binds fibrinogen to mask bacteria from the immune system
M protein also functions as an adhesion
Lipoteichoic Acid:
adhesion (mucosal) PAMP (not as strong as LPS)
Strep pyrogenic exotoxin A (SpeA, SpeB) =
superantigens cytokine storm (TSS)
Streptokinase:
converts plasminogen plasmin & dissolves clots
Streptococcal pyrogenic exotoxin B
SpeB, potent protease
C5a peptidase –
specific for C5a peptidase, specific for C5a and also degrades IgG
Streptococci pyrogenes Treatment:
Treatment: Penicillin (no resistance so far)
Allergies clindamycin, azithromycin
IVIG – some use against superantigens?
Streptococci pneumonia Infections
Common cause of pneuomonia w/ better prognosis (fewer toxins)
Streptococci pneumonia Virulence Factors
Quelling (swelling) reaction due to antibody-induced stabilization of pneumococcal capsular material.
Streptococci pneumonia Classification
Alpha-hemolysis (green)
Streptococci agalctiae Description
Group B Strep
Beta-hemolysis
Streptococci agalctiae Infections
Used to be the most predominant cause of septicemia & meningitis in neonates
-Major cause of pregnancy-related morbidity
-Testing/treating pregnant mothers reduced disease (screening at 35-37 weeks gestation)
Group B infections have increased in nursing homes
Streptococci agalctiae Virulence Factors
Major VFs: CAPSULE Capsular Serotypes I-V (serves as an antiphagocytic factor)
Adhesions: alpha-protein & fibrinogen-binding proteins.
Surface Beta protein binds factor H, down-regulates complement deposition
B-hemolysin can damage cells
PG, LTA, Group B carbohydrates increase cytokine secretion while the capsule does not
Streptococci agalctiae Classification
Group B Beta-Hemolysis (clear) Diplococci Bacitracin resistant Hydrolysis of bile esculin CAMP factor: a GBS factor that synergizes w/ S aureus to increase lysis of RBCs
Streptococci viridans: Description
S. mitis
S. mutans
S. sanguis
S. salivarius
Part of the normal oral microbiota (dental plaque called biofilm)
Alpha hemolytic
Can grow at acidic pH
Streptococci viridans: Infections
S. mitis
S. mutans
S. sanguis
S. salivarius
Subacute – long duration infective endocarditis - Suffice it for now to say that these infections usually form on valves damaged in some way, such as by acute rheumatic fever, or prosthetic valves.
Streptococci viridans: Virulence Factor
S. mitis
S. mutans
S. sanguis
S. salivarius
Not very virulent
Cause transient bacteremia every time you brush your teeth
Can cause endocarditis
Have adhesins for fibronectin, fibrin, other host proteins that accumulate on injured calces
Streptococci viridans: Classification
S. mitis
S. mutans
S. sanguis
S. salivarius
Alpha-hemolysis (green)
No Lancefield Group
Distinguish from enterococci by ability to grow in 0.5% NaCl
Distinguished from pneumococci by ability to resit optochin
Enterococcus Faecalis / faecium are the main ones Description
Formerly known as Group D Streptococcus
Commensal of GI tract
Alpha or gamma hemolytic
Enterococcus Faecalis / faecium are the main ones Infections
Antibiotics alter the dyanimic in favor of enterococci, that are tolerant to a variety of antibiotics.
Increasing the pH may increase enterococci
Leading cause of nosocomial infections
30% VRE.
Can gain access to lymphatics of blood.
Enterococcus Faecalis / faecium are the main ones Virulence Factors
Do not make many toxins
Extremely proficient in taking up DNA and passing it along to other species
VRE brought vanc resistance to strep
Enterococcus Faecalis / faecium are the main ones Classification
Group D
Alpha or gamma hemolytic
Can grow as high salt, 45C, bile esculin positive
