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Name some typical and atypical Gram + bacteria.
- Typical: Staphlococcus, Streptococcus, Enterococcus
- Atypical: Actinomyces, Nocardia, Streptomyces
Name some typical and atypical Gram - bacteria.
- Typical: Enterobacteriacea family
- Atypical: Chlamydia & Rickettsiae (obligate intracellular parasites)
What bacteria has NO cell wall?
Which bacteria are spore formers? Are these Gram + or -?
- Bacillus & Clostridium.
- Gram +
What bacteria stains w an Acid-Fast test? Gram + or -? What's unique about the cell wall?
- Stains weakly Gram +
- Waxy cell wall
What is a capnophile? What type of bacteria does this describe?
What are some rod-shaped Gram + bact?
Actinomyces, Nocardia, Streptomyces, Bacillus, Clostridium
What are some cocci shaped Gram - bact?
What are some Gram + facultative anaerobes?
Staphylococcus, Streptococcus, Enterococcus, Streptomyces, Bacillus (also aerobe), Actinomyces
What's an example of a Gram + obligate anaerobe?
What Gram + bact is a strict aerobe?
Classify Staphylococcus in terms of Gram
status, shape, arrangement, location in the body, optimal temperature, oxygen preferences, resistance to drying and salt and catalase production.
- - Staphylococcus:
- Gram +
- Grape-like clustering
- Optimal temp: can live between 18-40; w 37 deg as optimal growth.
- Live on skin. Also in respiratory tract. Resistant to drying (Gram + have thick Peptidoglycan layer) à can live on dry surfaces. Be careful of fomites!!
- Facultative Anaerobe
- Resistant to salts, so grow on MSA (Mannitol Salt Agar) – selective media due to salt. Differential b/c only 1 species ferments mannitol (only S. aureus) à it turns yellow due to pH change when sugar is broken down into acid
- Has enzyme “catalase” for peroxide breakdown à breaks down into O2 + H2O. Humans use peroxide as an anti-microbial. Staph can survive in the presence of peroxide. (note: Staph are
- catalase positive. Strep are catalase negative!)
Which species is coagulase positive? Which other human pathogens are coagulase positive?
- -S. aureus is coagulase +. Coagulase is enzyme tightly bound to surface of S. aureus. It reacts w
- pro-thrombin, activating clotting cascade, so bact coats itself w fibrin -> no phagocytosis. (coats itself w your own fibrin, so macrophages aren’t interested in it)
- -Yersinia pestis -> the plague!
Staphylococcus aureus: Disease, Coagulase? Catalase?
- TOXINS: food poisoning, scaled skin, TSS
- SKIN: folliculitis, furuncle, carbuncle, impetigo
- INTERNAL: bacteremia, endocarditis, osteomyelitis, pneumonia
- Coagulase +
- Catalase +
Staphylococcus epidermis: Disease, coagulase, catalase
- Bacteremia, endocarditis, surgical wounds, UTI
- Coagulase -
- Catalase +
Staphylococcus saprophyticus: disease, coagulase, catalse
- UTI and other opportunistic infections
- Coagulase -
- Catalase +
Staphylococcus lugdunensis: disease, coagulase, catalase
- Arthritis, bacteremia, endocarditis, UTI
- Coagulase -
- Catalase +
Staphylococcus hemolyticus: disease, coagulase, catalase
- Bacteremia, bone/joint, endocarditis, UTI, wound
- Coagulase -
- Catalse +
List the factors predisposing a patient to S. aureus infections.
- break in skin
- viral infxn, especially influenza
- immunodifficient (immunosuppressing drugs, diabetic patients, etc)
- patients who’ve previously had MRSA infxns (Methacyllin Resistant S. Aureus)
Name the types and characteristics of cutaneous S. aureus infections.
- follicultis -> if it gets bigger, it’s called a boil (both come from irritated hair follicles).
- If it’s down into a sweat gland, it’s called a “furuncle” (means you’re into a sebaceous gland). At this point, neighboring sweat glands get infected and tend to merge -> you get big, serious nodules.
- At this point, they’re called “carbuncles” (GIANT!) All of these are staph skin infections.
- Impetigo -> superficial skin infection. Also involves Staph and Strep. Has pus color. Mostly children infected.
How does cutaneous S. aureus differ from Staphylococcal food poisoning?
One is colonized, one is enterotoxin.
Staphylococcal food poisoning, one of the most common foodborne illnesses, is an intoxication rather than an infection. Disease is caused by bacterial toxin present in food, rather than from a direct effect of the organisms on the patient.
Describe the virulence factors of Staphylococcus
aureus including slime layer, capsule, cell wall components, Protein A, cytolytic toxins, enterotoxins, exfoliative toxins, TSST, coagulase, catalase, hyaluronidase, staphylokinase, penicillinase.
- slime layer: helps bact stick to things; on very outer side of bact. Allows it to stick to catheters, heart valves, prosthetics, etc.
- capsule: underneath slime layer. Makes you more
- virulent. Made up of polysaccharides -> decreases phagocytosis.
- Cell wall: peptidoglycan -> activates complement, attracts monocytes and macrophages, brings in
- neutrophils (PMNs) -> pus (causes an abscess, generally internal). ALSO teichoic acid -> often how we ID strains.
- “Protein A”: built into cell wall -> binds to Fc region of IgG. Abs are binding backwards, so cant activate complement.
- Coagulase (in S. aureus only).
- Cytolytic toxins: alpha, beta, gamma, delta, PV (leukotoxic -> kills WBCs).
- Exotoxins: Cause cell damage and tissue destruction.
- Exfoliative toxins: breaks down desmosomes in epidermis. ETA and ETB
- Enterotoxins: GI tract -> some are superantigens
- (hooks up MHC to receptor without antigens present)
- TSST-1: toxic shock syndrome-1 (an exotoxin)-> a superantigen; binds to MHC II on macrophages, which in turn react w T-cell receptors -> massive release of cytokines by both macrophages and T-cells
- Superantigens: non-specifically activate T-cells. Ex: TSST: toxic shock syndrome toxin-> leads to multi-organ failure.
- Enzymes: coagulase (blood clotting), catalase (H2O2 breakdown), Hyaluronidase (hydrolyzes HA, present in acellular matrix of CT -> allows it to spread), Staphylokinase (breaks down blood/fibrin
- clots), penicillinase -> a Beta-lactam ring breaker-upper
Know the identifying features of, organisms that cause and treatment of: scalded skin syndrome
- Mostly infants, low mortality
- ID features: exfoliative toxin
- Org: Staphylococcus aureus
- Treatment: Abx, wound care, fluids
- *note MRSA
- *now Vanco resistance
- *most B-lactam resistant
Know the identifying features of, organisms that cause and treatment of: bullous impetigo
- ID features: exfoliative toxin but LOCAL unlike SSS
- Org: Staphlococcus aureus
- Tx: topical abx may be effective
Know the identifying features of, organisms that cause and treatment of: toxic shock syndrome
- ID: SUPERANTIGEN. Rapid onset fever, low bp, rash, skin falls off
- Org: Staphylococcus aureus (can also be Strep Group A)
- Tx: Abx and support
Know the identifying features of, organisms that cause and treatment of: bacteremia
- ID: varied
- Org: Staphlococcus aureus (et al)
- Tx: abx
Know the identifying features of, organisms that cause and treatment of: bacterial endocarditis
- 40-50% mortality w treatment; fatal if untreated
- ID: clot/vegetation formation - (bact, tissue, blood clotting agents), fever, fatigue, sweats, chills, joint pain
- Org: Staph aureus (main cause in ARTIFICIAL valves -also Streptococcus viridans group)
- Tx: abx
Know the identifying features of, organisms that cause and treatment of: lung abscess
- ID features: cough, fever, sputum
- Organism: many
- Tx: abx
Know the identifying features of, organisms that cause and treatment of: osteomyelitis
- ID: pain, redness, swelling. Osteonecrosis b/c abscess cuts off blood supply
- Organism: Staphylococcus aureus (et al)
- Tx: surgery, abx
Classify Streptococcus in terms of Gram status, shape, arrangement, location in the body, optimal
temperature, oxygen preferences, resistance to drying and salt and catalase production.
- -Strepto means “chains” of cocci.
- Like 37 deg.
- Normal flora of mouth.
- Most resist drying.
- Most resistant to salt, but not as much as Staph.
- Catalase – (important differential test between Staph and Strep).
Identify location, pathogenicity, pigment, hemolysis
and coagulase expression for Staphylococcus
aureus vs. Staphylococcus epidermidis.
- S. aureus
- location: skin, nose
- Pathogenicity: produces toxins that cause food poisoning, scalded skin, toxic shock. Skin infxns, bacteremia, endocarditis, osteomyelitis, pneumonia
- Pigment: gold
- Hemolysis: Beta (clear)
- Coagulase +
- S. epidermidis
- Location: skin
- Pathogenicity: bacteremia, endocarditis, surgical wounds, UTI
- Pigment: None, cream
- Hemolysis: Gamma or alpha (none or incomplete)
- Coagulase -
Name the 7 groups of important Streptococci. Which of these are part of the viridans group?
- Streptococcus pyogenes: Group A (GAS) & beta
- Streptococcus agalactiae: Group B (GBS) & beta
- Streptococcus bovis: Group D (GDS)-Enterococcus & gamma (NON-hemolytic)
- Streptococcus pneumoniae: NONE & alpha
- Streptococcus mutans: NONE - Viridans & alpha
- Streptococcus mitas: NONE - Viridans & alpha
- Streptococcus salivarius: NONE - Viridans & alpha
Describe the three classification schemes used to classify Streptococci.
- SEROLOGICAL GROUPINGS
- AKALancefield groups
- looks at carbs on cell surface
- GAS, GBS, GCS, GDS
- HEMOLYTIC PATTERNS
- Based on ability to break down rbc’s
- ALPHA = Green. Partial/Incomplete Hemolysis
- BETA = Yellow/clear. Complete Hemolysis
- GAMMA = Unchanged. Non-hemolytic
- viridans = alpha-hemolytic & nonhemolytic. Group name derived from viridis “green”.
- GAS: upper resp tract (throat, skin). Can cause necrotising fasciitis. Also post infxn complications
- GBS: GI flora and urogenital tract. Mostly a concern for newborns à causes septicemia and
- meningitis. (Preg women swabbed
- for Group B strep à if she is, before she delivers, she’s given antibiotics so the baby isn’t exposed to Group B strep so no septicemia or meningitis).
- GDS: in cattle/sheep. Questionable role in colon cancer.
- S. pneumoniae: normal in upper resp tract. Pathogenic in lower resp tract: sinus infection, ear, meningitis. ID feature: used to do capsule staining -> has GIANT capsule
- Viridans group causes endocarditis.
What diseases are caused by Streptococcus pyogenes? Describe epidemiology, virulence factors, toxins, phage conversion, lysins, kinases.
- Pharyngitis – throat
- Pyoderma/impetigo – skin (impetigo involves Staph and Strep)
- Erysipelas– skin
- Cellulitis – skin/connective tissue
- Necrotizing fascitis – fascia – underlying tissue
- Toxic shock syndrome - systemic
- Endocarditis – heart
- Any type of strep: virulence factors
- have capsules
- adhesion molecules -> M-protein family (allow
- binding to epithelial cells) & F-proteins (binding host cells)
- toxins: pyrogenic (pus) SP A, B, C (pyrogenic exotoxins)
- streptolysins: S & O -> lyse WBCs and RBCs
- (these are toxins)
- streptokinase: enzyme that’s a toxin that lyses blood clots.
- Hyaluronidase: allows it to be invasive in tissue
- DNAase: “Streptodornase” enzyme that breaks down DNA. Bact being lysed at infxn site, DNA being released, makes pus viscous…ezyme makes
- exudate less viscous, so it increases virulence.
Name the suppurative streptococcal diseases and know what part of the body they infect.
- Pharyngitis: reddened pharynx with exudates generally present; cervical lymphadenopathy can be prominent
- Scarlet fever: diffuse erythematous rash beginning on the chest and spreading to the extremities; complication of streptococcal pharyngitis
- Pyoderma: localized skin infection with vesicles progressing to pustules; no evidence of systemic disease
- Erysipelas: localized skin infection with pain, inflammation, lymph node enlargement, and systemic symptoms
- Cellulitis: infection of the skin that involves the subcutaneous tissues
- Necrotizing fasciitis: deep infection of skin
- that involves destruction of muscle and fat layers
- Streptococcal toxic shock syndrome: multiorgan
- systemic infection resembling staphylococcal toxic shock syndrome; however, most patients bacteremic and with evidence of fasciitis
- Other suppurative diseases: variety of other infections recognized, including puerperal sepsis, lymphangitis, pneumonia
Name the two post-streptococcal diseases. What causes each?
- Post-streptococcal disease: comes after S. pyogenese
- Can get rheumatic fever -> 3% untreated. Make Ab that cross reacts w heart valves. You get a heart murmur. Most common cause of innoculus heart murmur. Type II immunopathology -> Ab bind to heart valve and valve is damaged.
- Can get Glomerulonephritis:Type III
- Immunopathology. You get Ab-Antigen complexes in kidneys. Ab is NOT to kidney, it’s to bact and other x-reacting factors.
How is Streptococcus pyogenes diagnosed and treated?
- -agglutination & blood agar test
- - Can treat w penicillin or cephalosporin.
Name the diseases caused and epidemiology of S. agalactiae and S. bovis.
- S. agalactiae:
- Neonatal disease (early-onset and late-onset disease w meningitis, pneumonia, bacteremia), infxns in pregnant women (endometriosis, wound infxns, UTIs), and other adults (bacteremia, pneumonia, bone and joint infections, skin and soft-tissue infections)
- - asymptomatic colonization of upper resp tract at GI tract
- - early-onset disease acquired by neonates from mother during pregnancy or at time of birth
- - neonates at higher risk for infection if 1) premature rupture of membranes, prolonged labor, preterm birth, or disseminated maternal group B strep disease and 2) mother is without type-specific antibodies and low complement levels
- - women w genital colonization are at risk for postpartum disease
- - men and non-pregnant
- women w diabetes mellitus, cancer, or alcoholism
- S. bovis:
- Malignancies of GI tract
Describe the role of Streptococci in the oral cavity. How does this relate to endocarditis?
In mouth: Strep are acidogenic (make acid) and acidouric (tolerate acid). May lay groundwork for other pathogens. Strep salivarius (normally in tongue and in saliva -> may make a scaffold).
- The oral Streptococci have a role in plaque and caries. When these bacteria are knocked loose (during dental procedures) they can go to the heart. There they will form clumps called vegetations, consisting of bacteria, platelets and fibrin. Patients with heart damage or artificial valves are particularly at risk.
- o Streptococcus mutans – acidogenic AND acidouric
- o Streptococcus sobrinus – highly cariogenic – used to be grouped with S. mutans
- o Streptococcus sanguis – not as acidogenic or acidouric as S. mutans, but may lay the groundwork
- o Streptococcus salivarius – found in saliva and on
- tongue – may make scaffold for other bacteria
- o Streptococcus mitis – least important to caries
Describe the arrangement, shape, Gram staining patterns of S. pneumonia. What diseases are
caused by S. pneumoniae? Give this organism’s common name. What is the role of the capsule for this organism? What treatment strategies are effective (drug and vaccine)?
- -Strep pneumonia:
- Round/coccoid -> have characteristic
- “lancet-shaped” diplococci
- On a string
- Gram +
- HUGE capsule for virulence. Has toxin called “pneumolysin” (paralyzes cilia in resp. tract you aren’t moving bact then, so they bind and cause
- further infection).
- These are becoming penicillin resistant now. What about vaccines against the polysacchrides/carbs on outside of bact? -> this vaccine is given to +65 and 2 and younger patients.
Pneumonia: acute onset with severe chills and sustained fever; productive cough with blood-tinged sputum; lobar consolidation
Meningitis: severe infection involving the meninges with headache, fever, and sepsis; high mortality and severe neurologic deficits in survivors
Bacteremia: more common in patients with meningitis than with pneumonia, otitis media, or sinusitis; overwhelming sepsis in asplenic patients
Enterococcus is closely related to Streptococcus.
Name the clinical features, epidemiological features, normal location, virulence factors and treatment.
- - Cause abdominal infections after surgery
- - Very few virulence factors
- - Infxn VRE: Vancomysin Resistant Enterococci. Emerged in mid-2000s. Although enterococcus has few virulence factors, it’s SUPER drug resistant.