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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
*S. pyogenes; Group A Streptococci* diagnostics
Gram stain: Gram+ cocci in chains catalase- beta-hemolytic bacitracin-sensitive
26
*S. agalactiae; Group B Streptococci* virulence
normal flora of female repro tract leading cause of neonatal sepsis * women are routinely screened and treated for GBS colonization prior to deliver
27
S. agalactiae; Group B Streptococci most common clinical manifestation
neonatal meningitis neonatal pneumonia neonatal sepsis
28
S. agalactiae; Group B Streptococci epidemiology and treatment
penicillin G
29
S. agalactiae; Group B Streptococci diagnostics
* Gram stain: * catalase- * beta-hemolytic * bacitracin-resistant
30
*Viridans group streptococci* virulence
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
Viridans group streptococci most common clinical manifestation
subacute endocarditis dental caries
32
Viridans group streptococci treatment
penicillin G
33
Viridans group streptococci diagnostics
Gram stain: catalase- alpha-hemolytic optochin-resistant
34
* S. pneumoniae* * ​*virulence
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
* S. pneumoniae* * ​*most common clinical manifestations
**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
*S. pneumoniae* treatment
used to be treatable by penicillin → now intermed resistance is common * resistance mediated by PBP * resistant strains sensitive to 3gen cephalosporins (cefotaxime, cefriaxone)
37
*S. pneumoniae* diagnostics
green on blood agar lysis by bile acids sensitive to optochin Quellung rxn
38
* Group D* * 1. Enterococci* * *E. faecalis* * *E. faecium* * ​2. non-enterococci* * *S. bovis* * ​*virulence
**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
* Group D* * 1. Enterococci* * *E. faecalis* * *E. faecium* * ​2. non-enterococci* * *S. bovis* * ​*most common clinical manifestations
biliary tract infections UTI (esp enterococci)
40
* Group D* * 1. Enterococci* * *E. faecalis* * *E. faecium* * ​2. non-enterococci* * *S. bovis* treatment
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
* Group D* * 1. Enterococci* * *E. faecalis* * *E. faecium* * ​2. non-enterococci* * *S. bovis* diagnostics
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
Gram- cocci ## Footnote *Neisseria*
N. gonorhoeae (gonococci) N. meningitidis (meningococci) Gram-, kidney shaped diplococci * often seen within PMNs aerobic sensitive to heat/drying (like pneumococci)
43
N. gonorrhoeae virulence
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
N. gonorrhoeae epidemiology/pathogenesis clinical manifestations
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
N. gonorrhoeae diagnosis
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
N. gonorrhoeae treatment
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
*N. meningitidis* virulence
**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
*N. meningitidis* epidemiology
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
*N. meningitidis* clinical manifestations
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 2. **fulminant septicemia/meningococcemia** * LOS-mediated septic shock * freq seen in infants * **large purplish blotchy hemorrhages** * DIC * adrenal collapse (Waterhouse-Friderichsen syndrome)
50
*N. meningitidis* diagnosis
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
*N. meningitidis* vaccine
tetravalent conjugate vaccines (MCV4) * polysacchs conjugated to diphtheria toxoid * contains capsular antigens A, C, Y, W-135 2014: first serogroup B vaccine = TRUMENBA
52
table at end for N. gonorrhoeae and N. meningitidis

Microbiology (13 decks)

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