Micro- Rabe

• Typical: Staphlococcus, Streptococcus, Enterococcus
• Atypical: Actinomyces, Nocardia, Streptomyces

• Typical: Enterobacteriacea family
• Atypical: Chlamydia & Rickettsiae (obligate intracellular parasites)

Mycoplasma

• Bacillus & Clostridium.
• Gram +

• Mycobacterium
• Stains weakly Gram +
• Waxy cell wall

• Thrives in CO2
• Strep

Actinomyces, Nocardia, Streptomyces, Bacillus, Clostridium

Chlamydia

Staphylococcus, Streptococcus, Enterococcus, Streptomyces, Bacillus (also aerobe), Actinomyces

Clostridium

Nocardia

• - Staphylococcus:
• Gram +
• Cocci/round
• 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!)

• -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!

• TOXINS: food poisoning, scaled skin, TSS
• SKIN: folliculitis, furuncle, carbuncle, impetigo
• INTERNAL: bacteremia, endocarditis, osteomyelitis, pneumonia
• Coagulase +
• Catalase +

• Bacteremia, endocarditis, surgical wounds, UTI
• Coagulase -
• Catalase +

• UTI and other opportunistic infections
• Coagulase -
• Catalase +

• Arthritis, bacteremia, endocarditis, UTI
• Coagulase -
• Catalase +

• Bacteremia, bone/joint, endocarditis, UTI, wound
• Coagulase -
• Catalse +

• break in skin
• viral infxn, especially influenza
• immunodifficient (immunosuppressing drugs, diabetic patients, etc)
• patients who’ve previously had MRSA infxns (Methacyllin Resistant S. Aureus)

• 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.

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.

• 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

• 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

• ID features: exfoliative toxin but LOCAL unlike SSS
• Org: Staphlococcus aureus
• Tx: topical abx may be effective

• ID: SUPERANTIGEN. Rapid onset fever, low bp, rash, skin falls off
• Org: Staphylococcus aureus (can also be Strep Group A)
• Tx: Abx and support

• ID: varied
• Org: Staphlococcus aureus (et al)
• Tx: abx

• 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

• ID features: cough, fever, sputum
• Organism: many
• Tx: abx

• ID: pain, redness, swelling. Osteonecrosis b/c abscess cuts off blood supply
• Organism: Staphylococcus aureus (et al)
• Tx: surgery, abx

• -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).

• 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 -

• 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

• 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”.

• LOCATION
• 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.

• 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.

• 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

• 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.

• -agglutination & blood agar test
• - Can treat w penicillin or cephalosporin.

• 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)
• Epidemiology:
• - 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

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

• -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

• - 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.