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

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

1
Q

Gram+ cocci

genera, virulence factors

A

majority comprise 3 genera:

  • Staphyococcus
  • Streptococcus
  • Enterococcus

major virulence factors

  • adhesins/cell surface factors : allow to stick to host ECM
  • secreted enzymes/toxins : allow to penetrate/digest host ECM
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2
Q

Staphylococci

A
  • Gram stain : cells in clusters (bunches of grapes)
  • normal skin flora (most common bacteria on our skin)
  • facultative anaerobes (aerobes, but can also grow anaerobically)
  • hardy : resistant to heat/drying → persist on fomites
  • wound and nosocomial (hosp-acquired) infections

all are catalase+ (unlike streptococci)

S. aureus (major pathogen) is coagulase+, all others are coagulase- Staph (CoNS; CNS)

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3
Q

Staphylococcus aureus basics

A

most common human pathogen

  • normal flora in ant nares of 1/3 of ppl

predisposition to infection can be due to:

  • tissue injury (surgical/battle wounds)
  • preexisting primary infection
  • diabetes
  • immunodef
  • poor hygiene and nutrition

infections either localized or systemic

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4
Q

S. aureus

superantigen toxins

A

non-specifically link MHC to TCR

activate T cells with different specificities

  • up to 20% of all T cells activated
  • overproduction of cytokines (IL1, IL2, TNF)
  1. toxic shock syndrome toxin (TSST1)
  2. enterotoxins
  3. exfoliatin
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5
Q

Staphylococcus aureus

virulence

A
  1. cell surface virulence factors
  • protein A : (binds to Fc portion of abs) → opposite orientation req for opsonization → anti-opsonin effect to evade immune system
  • adhesins : facilitate adhesion to host cell/ECM
  • antiphagocytic polysacch microcapsule
  1. cytolytic exotoxin
  • hemolysin - lyses RBCs
  • PVL (Panton-Valentine leukocidin) - lyses leukocytes, specifically PMNs (produced predominantly by CA-MRSA)
  1. superantigen toxins : nonspecifically crosslink MHC/TCR
    * (TSST1, enterotoxin, exfoliatin)
  2. tissue “invasin” enzymes : “spreading factors” - facilitate penetration through extracellular tissue
  • staphylokinase
  • hyaluronidase
  • lipase
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6
Q

Staphylococcus aureus

common clinical manifestations

A

1. SSTIs (skin and soft tissue infections)

  • furuncles : small, pus-filled, local infections
  • carbuncles : larger skin abscesses
  • impetigo : spreading, crusted skin infection
  • cellulitis : deep skin infection

2. infection of other tissues, potentially from metastasis of superficial infections…

  • osteomylitis
  • septic joint/ septic arthritis (esp in children)
  • pneumonia
  • bloodstream infections: bacteremia, septicemia
  • acute endocarditis (freq assoc with IV drug use)

3. toxinoses

  • gasteroenteritis (from enterotoxins) → acute onset of GI distress with char projectile vomiting
  • toxic shock syndrome (TSST1 exotoxin) → high fever, sunburn like rash, multiple organ failure
  • scalded skin syndrome (exfoliatin toxin) → bullous impetigo → desquamation of epidermix
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7
Q

Staphylococcus aureus

treatment options

A
  • beta-lactamase resistant penicillins (ex. nafcillin)
    1. penicillinase-resistant penicillins (ex. oxacillin)
    2. clindamycin

**if MRSA, vancomycin is SOC antibiotic

  • vancomycin - glycopeptide
  • daptomycin - lipopeptide
  • linezolid - oxazolidone
  • ceftaroline - cephalosporin with affinity for PBP2a
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8
Q

S. aureus antibiotic resistance

A

1945: penicillin
1955: almost all S. aureus resistant due to penicillinase
enter. ..penicillinase-resistant beta-lactams (methicillin, oxacillin, nafcillin)
* bound to PBP2 (penicillin binding protein 2)

countered by…MRSA! (methicillin-resistant S. aureus)

  • made PBP2a
    now. ..vancomycin!
    but. ..VISA (intermediate), VRSA (resistant) → uncommon but growing in importance
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9
Q

Staphylococcus aureus

diagnostics

A
  1. Gram stain: Gram+ cocci in clusters
  2. culture: golden-yellow colonies
  3. catalase+
  4. coagulase+
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10
Q

Staphylococcus epidermidis

basics

A

major component of normal skin flora

  • cause wound infections through broken skin

relatively less virulent

freq involved in nosocomial infections, opportunistic infections

produces cell surface polysacch “slime” → adheres to bioprosthetic material and acts as barrier to antibiotics

most are highly resistant to oxacillins, penicillins

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11
Q

Staphylococcus epidermidis

virulence

A
  1. polysaccharide capsule adheres to prosthetic devices
  2. highly resistant to antibiotics
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12
Q

Staphylococcus epidermidis

most common clinical manifestations

A

nosocomial infections…

  1. prosthetic jts and heart valves
  2. IV lines
  3. UTIs
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13
Q

Staphylococcus epidermidis

treatment options

A

vancomycin (resistant to many antibiotics)

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14
Q

Staphylococcus epidermidis

diagnostics

A
  1. Gram stain: Gram+ cocci in clusters
  2. catalase+
  3. coagulase-
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15
Q

Staphylococcus saprophyticus

most common clinical manifestations

A

normal vaginal flora (infreq found on skin)

UTIs and cystitis in women

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16
Q

Staphylococcus saprophyticus

treatment options

A

penicillin G

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17
Q

Staphylococcus saprophyticus

diagnostics

A
  1. Gram stain: Gram+ coccie in clusters
  2. catalase+
  3. coagulase-
  4. novobiocin resistant
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18
Q

Streptococcus

A

Gram+ spherical/ovoid cocci arranged in long chains, commonly in pairs

approx 25 species

catalase-

most parasitic forms are fastidious → require enriched media

sensitive to drying/heat

aerotolerant anaerobes

classified based on:

  • hemolysis pattern
  • cell wall antigen
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19
Q

hemolysis

A

beta-hemolysis : complete erythrocyte destruction

alpha-hemolysis : RBCs damaged by peroxide → Hb turns green/brown

gamma-hemolysis : no hemolysis

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20
Q

Streptococcus Lancefield groups

A

serological classification based on antigenic cell wall polysacch: C substance (carbohydrate substance)

react with specific antisera in slide agglutination assays

  • Groups A-U exist
  • common human pathogens: Groups A, B, D, none
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21
Q

Strep pathogen classification based on

  • hemolysis
  • sensitivity/resistance
  • C substance group
A

beta hemolytic

  • bacitracin sensitive → S. pyogenes : Group A streptococci
  • bacitracin resistant → S. agalactiae : Group B streptococci

alpha hemolytic

  • optochin sensitive → S. pneumoniae (“non Lancefield” streptococci)
  • optochin resistant → Viridans group, ex. S. mitis (“non Lancefield” streptococci)

gamma hemolytic

  • S. bovis : Group D streptococci
22
Q

S. pyogenes; Group A Streptococci

virulence

A

M protein (80 types)

  • key for virulence
  • highly variable

streptolysin O and S (lyse RBCs)

pyrogenic superantigen exotoxins:

invasin: streptokinase (allows to penetrate/colonize host)

23
Q

S. pyogenes; Group A Streptococci

most common clinical manifestation

A
  1. pharyngitis (“strep throat”) : purulent infl in pharynx
    * can be assoc withscarlet fever
  2. skin infections : impetigo, erysypelas → cellulitic or necrotizing fasciitis
  3. streptococcal toxic shock syndrome : mediated by superantigen pyrogenic toxin → leads to multi organ failure

post-infection sequellae (antibody-mediated)

heart and joint: rheumatic fever

  • 2-3 weeks after pharyngitis
  • myocarditis, arthritis, fever, chorea

kidney: glomerulonephritis

  • 1 week after pharyngitis or skin infection
  • hematouria, fluid retention/hypervolemia
24
Q

S. pyogenes; Group A Streptococci

epidemiology

treatment

A

inhabits human throat, nasopharynx, occasionally skin

  • entry usually through skin or pharynx

transmitted via contact, droplets, food → easily spread in crowded environments

cutaneous/throat infection : mostly children

if not treated quickly, systemic infection and progressive sequellae possible

tx

penicillin G

if skin infection: penicillinase-resistant renicillins (oxacillin) since it may be staphylococci

25
Q

S. pyogenes; Group A Streptococci

diagnostics

A

Gram stain: Gram+ cocci in chains

catalase-

beta-hemolytic

bacitracin-sensitive

26
Q

S. agalactiae; Group B Streptococci

virulence

A

normal flora of female repro tract

leading cause of neonatal sepsis

  • women are routinely screened and treated for GBS colonization prior to deliver
27
Q

S. agalactiae; Group B Streptococci

most common clinical manifestation

A

neonatal meningitis

neonatal pneumonia

neonatal sepsis

28
Q

S. agalactiae; Group B Streptococci

epidemiology and treatment

A

penicillin G

29
Q

S. agalactiae; Group B Streptococci

diagnostics

A
  • Gram stain:
  • catalase-
  • beta-hemolytic
  • bacitracin-resistant
30
Q

Viridans group streptococci

virulence

A

include many species

barring S. pneumonia, most are lumped together as “Viridans” streptococci (green on agar)

widespread residents of oral cavity : gums and teeth

  • dental oral procedures can facilitate entrace (otherwise not too invasive)

clinical manifestations

  • dental caries
  • subacute endocarditis
31
Q

Viridans group streptococci

most common clinical manifestation

A

subacute endocarditis

dental caries

32
Q

Viridans group streptococci

treatment

A

penicillin G

33
Q

Viridans group streptococci

diagnostics

A

Gram stain:

catalase-

alpha-hemolytic

optochin-resistant

34
Q
  • S. pneumoniae*
  • ​*virulence
A

causes 30-50% of all pneumonia

small, “lancet-shaped” cells arranged in pairs, short chains

aka pneumococci

normal flora in nasopharynx in carriers, doesn’t survive long out of this environment (infections often endogenous)

predisposed: young, elderly, immunocompromised, smokers, ppl living in close quarters
* esp sickle cell and/or splenectomy!

polysacch capsule (> 85 serotypes)

  • antiphagocytic, antigenic
  • virulence factor: heavy encapsulation → more freq assoc with severe, invasive disease

pneumolysin, autolysin

35
Q
  • S. pneumoniae*
  • ​*most common clinical manifestations
A

1. lobar pneumonia : pneumococci aspirated into lungs → induce infl response

2. otitis media : inner ear infection; most common bacterial infection in children

3. meningitis : characterisitic nuchal rigidity

4. bacteremia/sepsis

  • high mortality rates in adults (up to 60% in elderly)
  • esp hits asplenic patients
36
Q

S. pneumoniae

treatment

A

used to be treatable by penicillin → now intermed resistance is common

  • resistance mediated by PBP
  • resistant strains sensitive to 3gen cephalosporins (cefotaxime, cefriaxone)
37
Q

S. pneumoniae

diagnostics

A

green on blood agar

lysis by bile acids

sensitive to optochin

Quellung rxn

38
Q
  • Group D*
    1. Enterococci*
  • E. faecalis
  • E. faecium
  • ​2. non-enterococci*
  • S. bovis
  • ​*virulence
A

enterococcal epidemiology

  • component of normal GI flora
  • resistant to chemicals, persist on fomites
  • opportunistic infections, biliary infections, intra-abd abscesses → lead to endocarditis or bacteremia, sepsis
  • inherently resistant to lots of antibiotics!

component of normal GI flora

  • can grow in 40% bile

bacteremia caused by S. bovis is assoc with GI malignancy and colon cancer

39
Q
  • Group D*
    1. Enterococci*
  • E. faecalis
  • E. faecium
  • ​2. non-enterococci*
  • S. bovis
  • ​*most common clinical manifestations
A

biliary tract infections

UTI (esp enterococci)

40
Q
  • Group D*
    1. Enterococci*
  • E. faecalis
  • E. faecium
  • ​2. non-enterococci*
  • S. bovis

treatment

A

ampicillin + gentamycin

resistant to penicillin G

resistance to vancomycin on the rise

  • due to a transposable element
  • resistance very common in E. faecium (less in E. faecalis)
41
Q
  • Group D*
    1. Enterococci*
  • E. faecalis
  • E. faecium
  • ​2. non-enterococci*
  • S. bovis

diagnostics

A

Gram stain:

culture:

  • enterococci grow in both 40% bile (hydrolyze esculin), 6.5% NaCl
  • non-enterococci grow only in bile

enterococci are salt-resistant!

42
Q

Gram- cocci

Neisseria

A

N. gonorhoeae (gonococci)

N. meningitidis (meningococci)

Gram-, kidney shaped diplococci

  • often seen within PMNs

aerobic

sensitive to heat/drying (like pneumococci)

43
Q

N. gonorrhoeae

virulence

A

unencapsulated

heterogeneous cell surface antigens via gene conversion, phase variation mechanisms

antigenically heterogeneous:

  • pili
  • Opa (opacity proteins, formerly known as PII proteins)
  • LOS (endotoxin; like LPS but shorter, more branched side chains)

addtl virulence factors:

  • IgA protease (helps infect mucosa!)
  • proteins like lactoferrin, transferrin that can extract Fe from host Fe proteins
44
Q

N. gonorrhoeae

epidemiology/pathogenesis

clinical manifestations

A

STD attacking mucous membranes : GU, eye, rectum, throat

suppuration, fibrosis

many infected individuals (esp females) asymptomatic

clinical

1. genitourinary tract infections : urethritis, cervicitis → pelvic infl disease, salpingitis (women) → infertility

2. pharyngitis, rectal infections

3. opthalmia neonatorum

  • routine prophylaxis (erythromycin ointment or AgNO3)

4. bacteremia → disseminated infection

  • rare (gonococci multiply poorly in bloodstream)
  • could cause septic arthritis, scattered skin lesions
45
Q

N. gonorrhoeae

diagnosis

A

pus secretion from mucosal surfaces

smears: intracellular Gram- cocci
culture: complex nutritional reqs

  • oxidase+
  • grow better under enhanced CO2 conditions
  • ThayerMartin media (choc agar with antibiotics that suppress normal flora)

nucleic acid amplification

  • primary method for diag
46
Q

N. gonorrhoeae

treatment

A

resistance is a problem: penicillin, tetracycline, quinolones

  • 20-30% of new cases are PPNG, TRNG, QRNG → penicillinase-producing or tetracycline-resistant or quinolone-resistant

current guidelines: IM Ceftriaxone + azithromycin/doxycycline to hit concurrent chlamydia infection

47
Q

N. meningitidis

virulence

A

antigenic capsule (13 serogroups)

  • antigenic capsule is NOT present in N. gonorrhoeae
  • serogroups A, B, C, Y, W-135 cause most; B most common in US
  • pili, LOS, Opa*
  • IgA protease*
  • Fe extraction system*
  • *similar to N. gonorrhoeae*
48
Q

N. meningitidis

epidemiology

A

epidemic waves in closed communities (schools, dorms, barracks), often winter/early spring - young, healthy individs

  • infants 6mo-2yr especially susceptible

carrier rate: 5-10%, mostly in nasopharynx

rapid onset → progression to life-threatening in 12-24hr

vacinne available

49
Q

N. meningitidis

clinical manifestations

A

meningococcemia

  • bacteria rapidly multiply in bloodstream
  • spiking fevers, chills, jt/muscle pain
  • petechial rash

progresses either into…

  1. meningitis
  • purulent CSP
  • infl response in meninges
  • characteristic symptoms: severe headache, stiff neck, light sensitivity, vomiting, AMS/coma
  1. fulminant septicemia/meningococcemia
  • LOS-mediated septic shock
  • freq seen in infants
    • large purplish blotchy hemorrhages
    • DIC
    • adrenal collapse (Waterhouse-Friderichsen syndrome)
50
Q

N. meningitidis

diagnosis

A

Gram stain CSF, blood, skin, or nasopharyngeal samples…

oxidase+

culture for differentiation…

  • N. meningitidis can utilize glucose and maltose
  • N. gonorrhoeae can utilize glucose only

rapid latex agglutination test for antigenic capsule

51
Q

N. meningitidis

vaccine

A

tetravalent conjugate vaccines (MCV4)

  • polysacchs conjugated to diphtheria toxoid
  • contains capsular antigens A, C, Y, W-135

2014: first serogroup B vaccine = TRUMENBA

52
Q

table at end for N. gonorrhoeae and N. meningitidis

A

Microbiology (13 decks)

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