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M1 - Microbiology > Gram+ and Gram- Cocci (Kaul) - 4/26/16 > Flashcards

Gram+ and Gram- Cocci (Kaul) - 4/26/16 Flashcards

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1
Q

Discuss 4 overall characteristics of Gram+ cocci.

A
  1. Important human pathogens
  2. Adapted to living on/in humans
  3. Three genera comprise majority: Staphylococcus, Streptococcus, Enterococcus
  4. Virulence factors (factors that enable an organism to produce disease)
    - Adhesins/cell surface factors
    - Secreted enzymes/toxins
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2
Q

Describe characteristics of Staphylococci:

  • Gram Stain?
  • Skin Flora?
  • Anaerobe type?
  • Heat resistant?
  • Growth and appearance on blood agar?
  • Catalase positive or negative?

Describe catalase test.

A
  • Gram Stain? Cells in cluster (bunch of grapes)
  • Skin Flora? Normal - most abundant on our skin
  • Anaerobe type? Facultative (can grow both aerobically and anaerobically)
  • Heat resistant? Yes, resistant to heat and drying- persist on fomites; hardy bacteria - can exist on metal instruments, door knobs, beds, etc…
  • Grows well on blood agar; golden-yellow colonies
  • Catalase positive or negative? Positive (unlike streptococci)

Describe the catalase test:
- Drop H2O2 onto microscope slide. Mix in unknown bacteria (blue circle)… gram+. Mix in with H2O2. If bubbles –> staph cocci… if no bubbles –> strep cocci

  • Most common infection in cuts and wounds
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3
Q

Discuss the pathogenic strains of Staphylococci.

A

S. aureus = major pathogen (coagulase positive)

All other pathogenic strains = coagulase negative Staph (abb. CoNS or CNS); e.g. S. epidermidis, S. saprophyticus

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4
Q

Describe GENERAL CHARACTERISTICS of Staphylococcus aureus.

A
  • “Golden” colonies on agar
  • Coagulase positive (coagulase clots plasma)
  • Normal flora of anterior nares in 1/3 of people
  • Most common human pathogen
  • Ferments mannitol (if ferments mantel, turns agar yellow)

Virulence factors:

  • Protein A (binds to antibodies on Fc portion) - evades immune system
  • Microcapsule
  • Adhesins
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5
Q

Describe VIRULENCE FACTORS of Staphylococcus aureus.

S. aureus produces many exotoxins that damage membranes:

S. aureus superantigen toxins stimulate T lymphocytes

A

Virulence factors:

  • Protein A (anti-opsonin effect by binding to antibodies on Fc portion) - evades immune system
  • Microcapsule - antiphagocytic polysaccharide “microcapsule”
  • Adhesins - facilitate attachment to host cells/connective tissue

Exotoxins:

  • alpha-toxin: Hemolysins (punches holes in RBCs)
  • beta-toxin: lipase - damages membranes (basis of CAMP test used to ID Strep)
  • PVL (leukocidin): (punches holes in WBCs); produced predominantly by CA-MRSA; destroys neutrophils

Invasins (burrow into cell)

  • Staphylokinase
  • Hyaluronidase
  • Lipase
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6
Q

Describe SUPERANTIGEN TOXINS of Staphylococcus aureus.

A
  • Non-specifically crosslink MHC to TCR
  • Activates T-cells with differing specificities
  • Up to 20% of all T-cells activated!
  • Overproduction of cytokines (IL-1, IL-2, TNF)
  1. Toxic shock syndrome toxin (TSST-1) - IL-1, IL-2, TNF
  2. Enterotoxins (“food poisoning”) - nausea, vomiting, no fever
  3. Exfoliatin (“scalded skin syndrome”) - skin peels off
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7
Q

Describe EPIDEMIOLOGY of Staphylococcus aureus.

A
  • Carriage rate for healthy adults = 20-30%
  • Very common hospital-associated infection (facilitated by ability to persist on fomites)
  • Predisposition to infection include: tissue injury (surgical/battle wounds), pre-existing primary infection, diabetes, immunodeficiency, poor hygiene, nutrition
  • Infections can be localized or systemic
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8
Q

Describe CLINICAL MANIFESTATIONS of Staphylococcus aureus.

SSTIs, Infections, Toxinoses

A

Most common clinical presentation is SSTIs (skin, soft tissue infections):

  1. Furuncles: small PUS-filled local infections
  2. Carbuncles: larger skin abscesses
  3. Impetigo: spreading, crusted skin infection
  4. Cellulitis: deep skin infection

Infections of other tissues, potentially from metastasis of superficial infections:

  1. Osteomyelitis: S. aureus = most common cause of bone infections in children
  2. Septic joint/septic arthritis: especially in children
  3. Pneumonia: often follows viral flu infections, particularly in hospitalized patients
  4. Acute endocarditis: frequently associated with IV drug abuse (rapid onset of vegetation on valve –> can embolize to other tissue including lungs or brain)
  5. Bloodstream infections: Bacteremia and Septicemia

Toxinoses:

  1. TSS from TSST-1 exotin results in high fever, sunburn-like rash and multi-organ failure
  2. “Food poisoning” or gastroenteritis from enterotoxins - ingestion of heat stable enterotoxins formed riectly from contaminated food; acute onset of GI distress –> projectile vomiting
  3. Scalded Skin Syndrome - exfoliatin toxin induced bright red flush, blisters (bullae) –> bullous impetigo –> desquamation of epidermis
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9
Q

Describe ANTIBIOTIC RESISTANCE to Staphylococcus aureus.

A

1945: Penicillin
1955: Almost all S. aureus resistant to penicillin (due to penicillinase - cleaved beta-lactam ring of penicillin, inactivating it)

Anti-staphylococcal “penicillinase-resistant” beta-lactams developed - methicillin, oxacillin, nafcillin

MRSA (methicillin resistant S. aureus) emerges! SJDFKLSDF :(

Vancomycin - glycopeptide
VISA (Vancomycin Intermediate S. aureus) and VRSA (Vancomycin Resistant S. aureus) - relatively uncommon but growing in importance

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10
Q

Describe ANTIMICROBIAL TREATMENT for Staphylococcus aureus.

A

Can’t use penicillin - completely resistant

Can use:

  • Beta lactamase resistant penicillins (Nafcillin)
  • Vancomycin - glycopeptide
  • Daptomycin - lipopeptide
  • Linezolid - oxazolidone
  • Ceftaroline - cephaolosporin with affinity for PBP2a
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11
Q

Describe GENERAL CHARACTERISTICS, VIRULENCE, COMMON CLINICAL MANIFESTATIONS, TREATMENT OPTIONS, and DIAGNOSTICS of Staphylococcus epidermidis.

A

GENERAL:

  • Major component of normal skin flora
  • Cause wound infections through broken skin

DIAGNOSTICS:

  • Gram stain: Gram positive cocci in clusters
  • Catalase positive
  • Coagulase negative

VIRULENCE:

  • Relatively less virulent
  • Produces cell surface polysaccharide “slime” - adheres to bioprosthetic* materials and acts as barrier to antibiotics

COMMON CLINICAL MANIFESTATIONS:
- Frequently involved in nosocomial and opportunistic infections - catheters or medical devices, IV lines

TREATMENT OPTIONS:

  • Vancomycin
  • Most are HIGHLY RESISTANT to penicillins and oxacillins
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12
Q

Describe GENERAL CHARACTERISTICS, VIRULENCE, COMMON CLINICAL MANIFESTATIONS, TREATMENT OPTIONS, and DIAGNOSTICS of Staphylococcus saprophyticus.

A

GENERAL:
- Normal vaginal flora (infrequently found on skin)

DIAGNOSTICS:

  • Gram stain: Gram positive cocci in clusters
  • Catalase positive
  • Coagulase negative
  • Novobiocin resistant

COMMON CLINICAL MANIFESTATIONS:
- UTI, cystitis in women

TREATMENT OPTIONS:

  • Pencillin G
  • Distinguished from other CoNS and S. aureus by its natural resistance to novobiocin
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13
Q

Describe characteristics of Streptococcus.

A
  • Gram-positive spherical/ovoid cocci arranged in long chains; commonly in pairs
  • ~25 species
  • CATALASE NEGATIVE (distinguishing factor from Staph)
  • Most parasitic forms are fastidious and require enriched media (not hardy)
  • Sensitive to drying and heat (not hardy like staph)
  • Aerotolerant anaerobes (facultative anaerobes)
  • Natural habitat = mucous membranes (abundant in normal flora of oral cavity, GI, respiratory, and GU tracts)

Classification based on (1) hemolysis pattern on blood agar and (2) cell wall antigen

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14
Q

Characterization technique 1: Compare the three different types of hemolysis.

A
  1. Beta-hemolysis = complete erythryocyte destruction (bright yellow halo)
  2. Alpha-hemolysis = Erythrocytes damaged by peroxide, hemoglobin turns green/brown
  3. Gamma-hemolysis = No hemolysis
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15
Q

Characterization technique 2: What are Streptococcus Lancefield Groups?

A
  • Serological classification (dependent on antigen)
  • Based on antigenic cell wall polysaccharide called C-substance
  • Groups A-U: Reaction w/ specific antisera tested in a slide agglutination assay; common human pathogens: Groups A, B, D, and “none” (no Lancefield Group)

*REVIEW

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16
Q

Describe VIRULENCE FACTORS, COMMON CLINICAL MANIFESTATIONS, and EPIDEMIOLOGY of Group A Streptococci (GAS): S. pyogenes

A

VIRULENCE FACTORS:
- M-protein (~80 types!): essential for infection; highly variable antigenic –> prevents activation of complement by alternate pathway; anti-phagocytic

  • Hemolysins: Oxygen-sensitive [Streptolysin O = SLO]; Oxygen-stable [Streptolysin S]
  • Streptococcal pyrogenic exotoxins (SPE) A, B, C (some strains)
  • Erhtyrogenic toxin: SPE = streptococcal pyrogenic exotoxin, a superantigen toxin –> causes rash of Scarlet fever
  • Exoenzymes: Streptokinase - dissolves clots by activating plasmin

COMMON CLINICAL MANIFESTATIONS:

  1. Streptococcal pharyngitis “strep throat”: purulent inflammation in pharynx; can be associated with scarlet fever (toxin mediated skin rash)
  2. Streptococcal skin infections: impetigo (crusted skin infection) or erysypelas (redness) –> cellulitis or more severe necrotizing fasciitis
  3. Streptococcal toxic shock syndrome: superantigen pyrogenic toxin mediated shock and multi-organ failure

Post-infection sequelas of untreated infections - antibody-mediated:

  • Acute Rheumatic Fever: antibodies to M protein are thought to cross-react with heart tissue and damage heart valves; (2-3 weeks after pharyngitis)
  • Acute glomerulonephritis: injury to kidney (1 week after pharyngitis or skin infection)

EPIDEMIOLOGY:

  • Inhabits throat, nasopharynx, occasionally skin in humans
  • Transmission - contact, droplets, food
  • Spreads easily in crowded environments
  • Portal of entry generally skin or pharynx
  • Children predominant group affected for cutaneous/throat infections (~30% all bacterial pharyngitis in children due to GAS)
  • Systemic infections/progressive sequelae possible if untreated
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17
Q

Describe characteristics of Group B Streptococci: S. agalactiae

A
  • Normal flora of female repro tract
  • Leading cause of neonatal sepsis
  • Women routinely screened and treated for GBS colonization prior to delivery
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18
Q

How do you distinguish Group A Streptococci from Group B Streptococci?

A

Bacitracin Sensitivity

Group A Strep won’t grow (inhibition)
Group B Strep is resistant to bacitracin

19
Q

Describe characteristics and clinical manifestations of alpha-hemolytic Viridans Group Streptococci.

A

CHARACTERISTICS:

  • Large complex group (S. mitis, S. mutans, S. oralis, S. salivarus, S. sanguis, S. milleri)
  • Widespread residents of the oral cavity - gums and teeth
  • Not very invasive; dental or oral surgical procedures facilitate entrance

CLINICAL MANIFESTATIONS:

  • Dental caries
  • Subacute Endocarditis: blood-borne bacteria settle and grow on heart lining/valves –> persons with pre-existing heart disease = high risk (have to be treated w/ antibiotics before getting any dental procedure)
20
Q

Describe CHARACTERISTICS of alpha-hemolytic Streptococcus pneumonia.

Not Group D

A
  • Causes 30-60% of all bacterial pneumonias
  • Small, “lancet-shaped” cells arranged in pairs and short chains
  • Aka pneumococci
21
Q

Describe VIRULENCE FACTORS of alpha-hemolytic Streptococcus pneumoniae.

A
  • Polysaccharide capsule (very important virulent factor)
  • Antiphagocytic and antigenic
  • Over 85 capsule serotypes
  • Capsule = virulence factor; heavily encapsulated forms are more frequently associated with severe, invasive disease
  • S. pneumoniae secretes pneumolysin and autolysin (lyse host cells)
22
Q

Describe EPIDEMIOLOGY of alpha-hemolytic Streptococcus pneumoniae.

A
  • Normal flora in nasopharynx in carriers; infections = endogenous (carriers can get infected)
  • Very delicate, does not survive long outside humans
  • Young children, elderly, immune compromised, alcoholics, those with other lung diseases or viral infections, smokers, persons living in close quarters are predisposed to pneumonia

The spleen = especially important in clearance of the organism from bloodstream and asplenics have greatly increased sensitivity to infection.
- Patients with sickle cell disease (damaged spleen) or those who have had a splenectomy = susceptible

23
Q

Describe CLINICAL MANIFESTATIONS of alpha-hemolytic Streptococcus pneumoniae.

A
  1. Lobar pneumonia: whole lobe is infect and filled with pus - overwhelming inflammatory response
  2. Otitis media (ear infection): gains access to middle ear by way of eustacian tube; most frequent bacterial infection in children
  3. Meningitis: common cause of adult bacterial meningitis; characteristics nuchal rigidity (stiff neck)
  4. Bacteremia and Sepsis: High mortality rates in adults up to 60% in elderly; asplenic patients = susceptible
24
Q

Describe S. pneumoniae LAB TESTS.

A
  • When you plate them out, the blood agar will appear green (b/c of incomplete hemolysis).
  • Sensitive to optochin (how you differentiate from Viridans group)
  • Lysis by bile acids (grow bacteria overnight, add bile salts and deoxycholate… it will lyse S. pneumoniae but not Viridans Group)
  • Quellung reaction (if you mix pneumoniae with bacteria… you’ll see swelling around it)
25
Q

Describe S. pneumoniae ANTIBIOTIC RESISTANCE.

A
  • All Streptococcus are sensitive to pencillin EXCEPT S. pneumoniae (resistant)
  • Intermediate level resistance now common
  • Resistance mediated by altered PBP acquired by genetic transmission from environmental streptococci - cannot cross BBB to treat CNS-meningitis
  • Resistant strains of S. pneumoniae sensitive to 3rd generation cephalosporins (i.e., cefotaxime and ceftriaxone)
26
Q

Describe S. pneumoniae VACCINE.

A

1983: Pneumovax (PPV): protects against 23 serotypes (including strains known to be responsible for 85-90% infections including common penicillin resistant strains); recommended for adults older than 65 years and older
2010: Prevnar (PCV13): Immune response to polysaccharide-only vaccines limited in children; recommended for all children under 5 years of age

27
Q

Describe characteristics of Group D Streptococci: S. bovis.

A
  • Component of normal gastrointestinal flora and can grow in 40% bile
  • “Nonenterococcal Group D strep”
  • Non-hemolytic (gamma-hemolysis) or alpha-hemolytic
  • Bacteremia caused by S. bovis associated w/ GI malignancy and COLON CANCER
  • Now called S. gallolyticus
28
Q

Describe CHARACTERISTICS and EPIDEMIOLOGY of Enterococci.

A

Characteristics:

  • Group D antigen
  • Genetically distinct from Streptococci but sometimes still referred to as “Group D Strep”
  • Nonhemolytic (gamma-hemolysis) or alpha-hemolytic, infrequently may be beta-hemolytic
  • E. faecalis and E. faecium most clinical relevant species (cause >90% of enterococcal infections

Epidemiology:

  • component of normal GI flora
  • Not very virulent but have become significant nosocomial pathogens due to multidrug resistant phenotype
  • Resistant to chemical agents and persist on fomites
  • Rarely cause disease in normal health individuals
  • Cause opportunistic urinary or biliary infections/intra-abdominal abscesses in immune compromised individuals
  • Lead to endocarditis or bacteremia/sepsis
29
Q

Describe ENTEROCOCCAL RESISTANCE: intrinsic and acquired.

A

Intrinsic resistance:

  • Low concentrations of aminoglycosides
  • Beta-lactams (including cephalosporins)
  • Clindamycin
  • Fluoroquinolones
  • Trimethoprim-sulfamethoxazole

Acquired resistance:

  • High concentrations of aminoglycosides
  • Tetracycline
  • Ertyrhomycin
  • Rifampin
  • Vancomycin - very common in E. faecium (genes encoding regulated resistance present on transposable element)

Treating Enterococci is so difficult in clinic because they are resistant. You don’t see them as often but still… when you do, it’s difficult.

30
Q

Discuss how to identify Enterococci (2).

A
  1. Bile Esculin hydrolysis: ability to grow in 40% bile and hydrolyze esculin –> turn sol’n from orange to black
  2. Enterococci are salt resistant: grow in 6.5% NaCl broth; differentiates Group D strep (S. bovis) from enterococci
31
Q

Discuss how to treat Enterococci.

A

Sensitivity testing needed:
1st line: Ampicillin + gentamycin or penicillin + streptomycin
2nd line: Vancomycin or other gram (+) targeting drugs

Multidrug resistant VRE: i) Pristinamycin (dalfopristin + quinupristin); ii) Linezolid

32
Q

Describe Gram (-) cocci characteristics: Neisseria

A
  1. N. gonorrhoeae (gonococci) - 2nd most common STI in US
  2. N. meningitidis (meningococci) - one of the most common causative agents for bacterial meningitis

Neisseria species characteristics:

  • Gram-negative, kidney-shaped, diplococci
  • Aerobic
  • Sensitive to heat and drying (like pneumococci)
  • Pyogenic cocci (infections characterized by formation of pus)
  • LOS (instead of LPS) - since shorter CHO side chains
  • Encode iron-binding proteins: have specific receptors for transferrin (found in blood) and lactoferrin (found in mucosal cells) – able to scavenge iron from these host proteins
  • IgA Protease = virulence factor
  • Transcytosis possible - entering epithelial cell on mucosal side and exiting from basal surface into submucosal space
  • Like pneumococci, they are sensitive/delicate - when you are trying to collect samples, have to work quickly and put them on media quickly b/c will die outside human host
33
Q

Describe characteristics of N. gonorrhoeae.

A
  • Unlike meningococci, gonococci = UNENCAPSULATED
  • EXTREMELY SENSITIVE TO NORMAL HUMAN SERUM (very little capacity to multiply in blood stream) / contrast to meningococci
  • Ferment glucose only
34
Q

Describe EPIDEMIOLOGY and PATHOGENESIS of N. gonorrhoeae.

A
  • Sexually transmitted disease
  • Incident rate highest in late teens/young adults
  • Attack mucous membranes (GU, eye, rectum, throat)
  • Suppuration (pus) and fibrosis
  • Many infected individuals = asymptomatic, esp. females
35
Q

Describe CLINICAL MANIFESTATIONS of N. gonorrhoeae.

A
  1. Genitourinary tract infections
    - Urethritis in men and women
    - Cervicitis in women –> PID or salpingitis (infertility due to salpinigitis in 20%)
  2. Pharingitis and rectal infections
  3. Opthalmia neonatorum
    - Routine prophylaxis with erythromycin ointment or silver nitrate
    - High risk babies treated with ceftriaxone
  4. Bacteremia can cause disseminated infection
    - Rare b/c gonococci multiply poorly in bloodstream (unlike meningococci) - better in bone
    - Could result in septic arthritis or scattered skin lesions
36
Q

Describe DIAGNOSIS of N. gonorrhoeae.

A

Take pus specimen (intracellular? extracellular?

Smear should be pink b/c gram (-).

Culture - grown on thayer-martin medium (blood agar plate in which the blood has been lysed so its brown not red… all the nutrients are available… in this chocolate agar, you have antibiotics that suppress growth of normal flora but allow Neisseria to grow)

  • Grow better under enhanced CO2 conditions
  • Oxidase-positive

Use NAATs (nucleic acid amplification tests) to ID

37
Q

Describe TREATMENT for N. gonorrhoeae.

A
  • Antibiotic resistance in gonococci
  • Resistance to penicillin, tetracycline, quinolones
  • 20-30% of new cases being PPNG (penicillinase-producing) or TRNG (tetracycline resistant) or QRNG (quinolone resistant)

Current guideline recommendations:
1st line: IM Ceftriaxone therapy + azithromycin or doxycycline to cover possible concomitant chlamydial infection

38
Q

Describe VIRULENCE FACTORS of N. meningitides.

STRUCTURE

A
  • IgA protease, endotoxin, capsule
  • Main difference between N. meningitidis and N. gonorrhoeae is the presence of antigenic CAPSULE (13 serogroups, with serogroups A, B, C, Y and W-135 causing most infections)
39
Q

Describe the EPIDEMIOLOGY of N. meningitidis

A
  • EPIDEMIC WAVES in closed communities (schools, military barracks)
  • Carrier rate ~5-10%
  • Found in NASOPHARYNX of carriers
  • Can infect young and healthy individuals
  • Infants (6 mo - 2 yrs) particularly susceptible to meningococcal infections
  • RAPID ONSET and progression within 12-24 hrs (can affect young, healthy individuals)
  • Vaccination available
40
Q

Describe the CLINICAL MANIFESTATIONS of meningococci.

A
  • Rapidly multiplying N. mengitidis in bloodstream
  • Spiking fevers, chills, joint and muscle pain
  • Petechial rash

If develops into meningitis:

  • Puss filled CSF (you’ll see organism in CSF)
  • Systemic inflammation
  • Severe headache, stiff neck, sensitivity to light, vomiting

Alternatively, if develops into fulminant septicemia/meningococcemia

  • LOS-mediated septic shock
  • Frequently seen in fants
  • Large purplish blotchy hemorrhages
  • Disseminated intravascular coagulation (DIC)
  • Adrenal collapse (Waterhouse-Friderichsen syndrome)
41
Q

Describe the TREATMENT for meningococci.

A

Bacterial meningitis = MEDICAL EMERGENCY

Antibiotic treatment usually started before definitive diagnosis.

Third generation cephalosporin - ceftriaxone or cefotaxime

Large IV dose of penicillin G or ampicillin (corticosteroid sometimes given for inflammatory reaction)

Prophylatic rifamin tx of anyone who come in close contact w/ patient

42
Q

Describe the CLINICAL DIAGNOSIS for meningococci.

A

Gram stain CSF, blood, skin, nasopharyngeal samples

Oxidase positive

Culture for differentiation

How to differentiate between N. meningitidis and N. gonorrhoeae?

  • Sugar tests…
  • Glucose/maltose for N. meningitidis
  • Glucose for N. gonorrhoeae

Rapid latex agglutination tests for capsular antigen.

43
Q

Describe the VACCINE for meningococci.

A

Tetravalent conjugate vaccines (MCV4)

  • Polysaccharides conjugated to diptheria toxoid
  • Contains capsular polysaccharides A, C Y, W-135

M1 - Microbiology (23 decks)

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