Micro- Rabe

Name some typical and atypical Gram + bacteria.

Typical: Staphlococcus, Streptococcus, EnterococcusAtypical: Actinomyces, Nocardia, Streptomyces

Name some typical and atypical Gram - bacteria.

Typical: Enterobacteriacea familyAtypical: 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?

MycobacteriumStains weakly Gram +Waxy cell wall

What is a capnophile? What type of bacteria does this describe?

Thrives in CO2Strep

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 +Cocci/roundGrape-like clusteringOptimal 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) � can live on dry surfaces. Be careful of fomites!!Facultative AnaerobeResistant 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) � it turns yellow due to pH change when sugar is broken down into acidHas enzyme �catalase� for peroxide breakdown � breaks down into O2 + H2O. Humans use peroxide as an anti-microbial. Staph can survive in the presence of peroxide. (note: Staph arecatalase 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 wpro-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, TSSSKIN: folliculitis, furuncle, carbuncle, impetigoINTERNAL: bacteremia, endocarditis, osteomyelitis, pneumoniaCoagulase +Catalase +

Staphylococcus epidermis: Disease, coagulase, catalase

Bacteremia, endocarditis, surgical wounds, UTICoagulase - Catalase +

Staphylococcus saprophyticus: disease, coagulase, catalse

UTI and other opportunistic infectionsCoagulase -Catalase +

Staphylococcus lugdunensis: disease, coagulase, catalase

Arthritis, bacteremia, endocarditis, UTICoagulase -Catalase +

Staphylococcus hemolyticus: disease, coagulase, catalase

Bacteremia, bone/joint, endocarditis, UTI, woundCoagulase -Catalse +

List the factors predisposing a patient to S. aureus infections.

break in skinviral infxn, especially influenzaimmunodifficient (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 morevirulent. Made up of polysaccharides -> decreases phagocytosis.Cell wall: peptidoglycan -> activates complement, attracts monocytes and macrophages, brings inneutrophils (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 ETBEnterotoxins: 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-cellsSuperantigens: 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/fibrinclots), penicillinase -> a Beta-lactam ring breaker-upper

Know the identifying features of, organisms that cause and treatment of: scalded skin syndrome

Mostly infants, low mortalityID features: exfoliative toxinOrg: Staphylococcus aureusTreatment: 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 SSSOrg: Staphlococcus aureusTx: 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 offOrg: 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: variedOrg: 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 untreatedID: clot/vegetation formation - (bact, tissue, blood clotting agents), fever, fatigue, sweats, chills, joint painOrg: 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, sputumOrganism: manyTx: abx

Know the identifying features of, organisms that cause and treatment of: osteomyelitis

ID: pain, redness, swelling. Osteonecrosis b/c abscess cuts off blood supplyOrganism: 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. aureuslocation: skin, nosePathogenicity: produces toxins that cause food poisoning, scalded skin, toxic shock. Skin infxns, bacteremia, endocarditis, osteomyelitis, pneumoniaPigment: goldHemolysis: Beta (clear)Coagulase +
S. epidermidisLocation: skinPathogenicity: bacteremia, endocarditis, surgical wounds, UTIPigment: None, creamHemolysis: 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) & betaStreptococcus bovis: Group D (GDS)-Enterococcus & gamma (NON-hemolytic) Streptococcus pneumoniae: NONE & alpha Streptococcus mutans: NONE - Viridans & alphaStreptococcus 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 surfaceGAS, GBS, GCS, GDS
HEMOLYTIC PATTERNS Based on ability to break down rbc�sALPHA = Green. Partial/Incomplete HemolysisBETA = Yellow/clear. Complete HemolysisGAMMA = Unchanged. Non-hemolytic viridans = alpha-hemolytic & nonhemolytic. Group name derived from viridis �green�.
LOCATIONGAS: upper resp tract (throat, skin). Can cause necrotising fasciitis. Also post infxn complicationsGBS: GI flora and urogenital tract. Mostly a concern for newborns � causes septicemia andmeningitis. (Preg women swabbedfor Group B strep � 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 capsuleViridans group causes endocarditis.

What diseases are caused by Streptococcus pyogenes? Describe epidemiology, virulence factors, toxins, phage conversion, lysins, kinases.

Pharyngitis � throatPyoderma/impetigo � skin (impetigo involves Staph and Strep)Erysipelas� skinCellulitis � skin/connective tissueNecrotizing fascitis � fascia � underlying tissueToxic shock syndrome - systemicEndocarditis � heart
Any type of strep: virulence factorshave capsulesadhesion molecules -> M-protein family (allowbinding 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 makesexudate 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 prominentScarlet fever: diffuse erythematous rash beginning on the chest and spreading to the extremities; complication of streptococcal pharyngitisPyoderma: localized skin infection with vesicles progressing to pustules; no evidence of systemic diseaseErysipelas: localized skin infection with pain, inflammation, lymph node enlargement, and systemic symptomsCellulitis: infection of the skin that involves the subcutaneous tissuesNecrotizing fasciitis: deep infection of skinthat involves destruction of muscle and fat layersStreptococcal toxic shock syndrome: multiorgansystemic infection resembling staphylococcal toxic shock syndrome; however, most patients bacteremic and with evidence of fasciitisOther 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. pyogeneseCan 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 IIIImmunopathology. 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)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-pregnantwomen 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. mutanso Streptococcus sanguis � not as acidogenic or acidouric as S. mutans, but may lay the groundwork o Streptococcus salivarius � found in saliva and ontongue � may make scaffold for other bacteriao 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� diplococciOn a stringGram +HUGE capsule for virulence. Has toxin called �pneumolysin� (paralyzes cilia in resp. tract you aren�t moving bact then, so they bind and causefurther 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.