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E3.MHD > StrepEntero.Lecture 2 > Flashcards

StrepEntero.Lecture 2 Flashcards

1
Q

Staph overview

A
  • catalase POSITIVE
  • cocci in clusters
  • grows in minimal media
    • opaque, off-white
  • grows best 35-37 C
  • prefers aerobic atmosphere
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2
Q

Strep overview

A
  • catalase NEGATIVE
  • cocci in pairs and chains
  • requires complex media
    • grey, clear, translucent
  • grows best 35-37C
  • prefers anaerobic or carbon dioxide atmosphere
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3
Q

Classification of Streptococci

A
  • serologic properties: Lancefield groupings
    • A-H, K-M and O-V
  • hemolytic properties
    • COMPLETE hemolysis (Beta)
    • INCOMPLETE hemolysis (Alpha)
    • NO hemolysis (Gamma)
  • biochemical properties
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4
Q

Streptococcal Infections-Important Species

A
  • streptococcus pyogenes (Group A)
  • streptococcus agalactiae (Group B)
  • other beta hemolytic streptococci
  • Viridans (green) group stretococci
  • nutriotionally deficient streptococci
  • Streptococcus pneumoniae
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5
Q

S. pyogenes Infection-Acute Pharyngitis

A
  • 5-15 yo with fever, sore throat, headacher, swollen lymph nodes
  • 5% asymptomatic carriers
  • transmitted by respiratory droplets
  • self-limiting (goes away sans AB, buttt SECUELE)
  • re-occurs due to lack of type specific AB to M protein (staph has many M proteins, will get strep again but can get other types)
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6
Q

S. pyogenes Infection-Impetigo

A
  • 2-5 yo child with localized skin disease
  • associated with trauma/insect bites
  • pustule with yellow crust
  • appears on face or extremities
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7
Q

S. pyogenes Infection-Erysipelas

A
  • spreading erythema with well demarcated edge on the face
  • fever and lymphadenopathy
  • lesions often on face and often with accompanying streptococcal pharyngitis
  • historically face was most affected, today the legs are affected most often, looks like severe burn
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8
Q

S. pyogenes Infection-Scarlet Fever

A
  • complication of streptococcal pharyngitis
  • caused by erythrogenic exotoxin
  • a rash first appears as tiny red bumps on the chest and abdomen
  • fin, red, and rough-textured blanches upon pressure
  • appears 12-48 hours after fever
  • generally starts on the chest, armpits, and behind the ears
  • spares the face (although some circumoral pallor is characteristic)
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9
Q

S. pyogenes Infection-Scarlet Fever-CHARACTERISTICS

A
  • sore throat
  • fever
  • bright red tongue with a “strawberry” appearance
  • rash begins to fade three to four days after onset and desquamation begins (palms of the hand are peeling)
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10
Q

S. pyogenes Infection-Necrotizing Fasciitis

A
  • strep infection that occurs eep in the subcutaneous tissues
  • spreads along the fascial planes
  • extensive destruction of the muscle and fat
  • “flesh eating” bacteria
  • systemic toxicity, mortality> 50%
  • pain is disproportionate for how it looks like a bruise, but has 10/10 pain
  • have to debris out all the dead tissue in two sessions, need surgery, AB useless
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11
Q

S. pyogenes Infection-Toxic Shock-LIKE Syndrome

A
  • multisystem organ failure (all the vital organs-heart, respiratory tract, kidney)
  • SPE toxins are similar to Staph aureus TSST-1
  • Unlike patients with staph toxic shock, cultures are usually positive for Group A strep
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12
Q

S. pyogenes Infection-Puerperal Sepsis

A
  • can be life threatening infection
  • seen in women following delivery or abortion
  • organisms colonizing genital tract or from OB personnel invade the upper genital tract causing endometritis, lymphangitis bacteremia, necrotizing fasciitis, and EVENTUALLY streptococcal toxic shock syndrome
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13
Q

Post-Streptococcal Sequelae-Rheumatic Fever

A
  • nonsuppurative inflammatory dz occurs 1-5 wks after strep pahryngitis (after UNTREATED strep throat)
  • fever, carditis, subcutaneous nodules, chorea, polyarthritis
  • attacks reoccur in adulthood
  • characteristic cardiac lesions=ASCHOFF bodies and valvular damage leads to possible endocarditis later in life
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14
Q

Post-Streptococcal Sequelae-Acute Glomerulonephritis

A
  • edema, HTN, hematuria, proteinuria
  • occurs after skin/respiratory infection
  • certain M types are “nephritogenic+; some more than others
  • antigen + Ab + C’ deposited in glomeruli seen on kidney biopsy (Ag-Ab response is complexed with complement. complex will travel through glomeruli and deposit, and cause damage to glomerular tissue)
  • body’s response to organism creates the sequelae
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15
Q

Virulence of Group A Streptococci

A
  • ability of the bacteria to adhere to the surface of the host cells
  • invade into the epithelial cells
  • ovoid opsonization and phagocytosis
  • produce a variety of toxins and enzymes
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16
Q

S. pyogenes virulence factors

A
  • capsular polysaccharide
  • lipoteichoic acid
  • hemolysins
    • Streptolysin S (oxygen stable, non-antigenic)
    • Streptolysin O (oxygen labile, ASO antibodies)
  • Streptokinase——-
  • Hyaluronidase——all cause tissue destruction
  • Nucleases————-
  • C5a peptidase——-
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17
Q

S. pyogenes-Streptococcal pyrogenic EXOtoxins (SPE)

A
  • three distinct heat labile toxins (A,B,C)
  • called “superantigens” that stimulate cytokine response leading to shock and organ failure
  • strep toxic shock-like syndrome
  • responsible for the rash in scarlet fever “erythrogenic exotoxin”
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18
Q

Pathogenesis of S. pyogenes

A

%M proteins (>80 serotypes)
-binds epidermal cells, allows the ever crucial ADHERENCE
-allows bacteria to survive
-strains without M protein are avirulent
-antiphagocytic
%degrades complement C3b
%Ab to M protein activate complement and kill the bacteria
%streptolysins and streptokinase allow spread of bacteria in tissues

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19
Q

Treatment of S. pyogenes

A
  • penicillin/ampicillin/amoxacillin=drug of choice, NO RESISTANCE WORLDWIDE
  • cephalosporins
  • erythromycin (pen allergic pt)
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20
Q

Streptococcus agalactiae (GBS-Group B Strep)

A

Infections:

  • neonatal pneumonia, sepsis, meningitis
  • skin and wound infections in adult diabetic patients
  • endocarditis
  • part of the normal flora in throat, vaginal, and GI tract
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21
Q

Sequelae

A

a condition that is the consequence of a previous disease or injury

22
Q

Group B Streptococcal Infections

A

-**most common!!
-early onset neonatal dz
»first week of life, after delivery, often fatal
»bacteremia, pneumonia, or meningitis
-Late onset neonatal dz
»1 wk-3 months of age (not as deadly)
»bacteremia with meningitis
-pregnant women-UTIs and carrier
-other infections

23
Q

Pathogenesis of GBS

A
  • maternal colonization of vagina or rectum exposes baby at delivery
  • lack of protective maternal antibody
  • sialic acid on polysaccharide capsule inhibits C’ allowing organism to multiply
24
Q

How do you prevent GBS disease?

A

Perform cultures on vaginal/rectal swabs collected at 35-37 weeks gestation

25
Q

Role of the Lab in GBS

A
  • combined vagina/rectal swab improves isolation rates by 40% over vaginal swab alone
  • ALERT PHYSICIAN when cervical or vaginal specimens received
  • use of selective enrichment broth (LIM) will INCREASE GBS isolation by 50% (refined sensitivity-if someone comes in without a history will treat them as POSITIVE)
  • report all GBS in urine regardless of colony count
26
Q

Treatment of S. agalactiae (GBS)

A
  • penicillin/ampicillin=drug of choice; NO RESISTANCE WORLDWIDE
  • add gentamicin to enhance killing (if mom is pen allergic)
  • prophylaxis of culture positive pregnant women during labor with penicillin/ampicillin to prevent neonatal disease; clindamycin for pen allergic
27
Q

Other Beta Hemolytic Strep (C, F, G)

A

Group C

  • associated with veterinary infections
  • pharyngitis in college age patients
  • sepsis

Group F
-associated with abscesses (brain)

Group G

  • pharyngitis
  • sepsis in neonates and elderly
28
Q

Lab Dx of other beta hemolytic Strep (C, F, G)

A 
-Antigen Test
>>throat swab from posterior oropharynx
-culture
-identification
-antibody dection (to see if theyve ever had strep)
>>ASO
>>Anti-DNase
29
Q

Details of rapid antigen-detection test

A
  • sensitivity only 70%, specificity is good-if it comes up positive definitely have infection, treat accordingly
  • however, if comes up negative, always back up with culture (there will be some that are in fact positive)
30
Q

Viridans Streptococci

A
  • alpha or gamma hemolytic (lacks hemolysins and toxins of beta strep)
  • normal flora of upper respiratory tract (including mouth)
  • major cause of dental caries (cavities)
  • opportunistic pathogen causing sepsis in neutropenic cancer patients
  • **IMPORTANT CAUSE OF ENDOCARDITIS
    • heart defect, valvular disease, transient organisms from mouth flora may travel and stick to damaged valves and cause endocarditis (Often get transient bacteremias from mouth flora throughout the day that we dont know we have-bleeding from flossing teeth or gum diseases)
31
Q

5 groups of Viridans Streptococci

A
  1. Sanguis group
  2. Mitis group
  3. Mutans Group
  4. Salivarius Group
  5. Bovis group
32
Q

Viridans Streptococci-Bovis Group

A

consists of non-enterococcal group D streptococci, includes 3 diff species:

  1. S. bovis I =S. gallolyticus ss. Gallolyticus
    - strains isolated from humans, cattle, and koala bears
  2. S. bovis II.2 =S. gallolyticus ss. Pasteurianus
    - human strains, in spinal fluid=cause of neonatal disease
  3. S. bovis II.1=S. infantarius ss. infantarius
    - human and bovine strains
33
Q

Clinical Significance of Viridans Streptococci-Bovis Group

A
  • S. bovis causes bacteremia, meningitis, and both native- and prosthetic-valve endocarditis
  • isolation of S. bovis from blood is associated with CARCINOMA OF COLON
34
Q

What is associated with CARCINOMA OF COLON?

A

Isolation of S. bovis (viridians streptococci) from blood!!!

35
Q

Streptococcus Milleri Group

A
  • includes: S. anginosus, S. constellatus, S. intermedius
  • produce pinpoint colonies (small colony Streptococcus); takes 2 days to grow
  • may require CO2 for isolation, sometimes mistaken for anaerobic streptococci
  • have characteristic caramel (butterscotch) odor when cultured on agar plates (CATALASE NEGATIVE like strep)
  • usually commensals isolated from mouth, oropharynx, GI tract, and vagina
  • reported to cause deep-seated pyogenic (pus/abscess producing) infections of cardiac, abdominal, skin, and CNS tissues
  • have been isolated from 56-81% of brain abscesses either in pure or mixed cultures
36
Q

Nutritionally Deficient Streptococci

A
  • placed in two seperate genera: Abiotrophia and Granulicatella
  • vitamin B6 deficient, mostly associated with endocarditis
37
Q

Streptococcus pneumoniae

A
  • KIDS especially are the RESERVOIR
  • normal flora of human upper respiratory tract
  • can cause pneumonia, usually lobar type
  • paranasal sinusitis
  • otitis media
  • meningitis which is usually secondary to one of the former infections
  • also causes osteomyelitis, septic arthritis, endocarditis, peritonitis, cellulitis and brain abscesses
  • gram POSITIVE bacteria
  • more than 90 known serotypes
  • polysaccharide capsule is an important virulence factor
  • capsular type-specific antibody is protective
38
Q

Structural Characteristics of S. Pneumoniae: Virulence Factors

A
  • pneumolysin-damages ciliated cells and activates alternative complement pathway
  • neuraminidase
  • phosporylcholine-binds to receptors for PAF on cells
  • *-sIgA protease-prevents IgA-mediated binding of pneumococcal cells to mucus
  • *-teichoic acid/peptidoglycan-activates complement by alternative pathway–>mediates inflammation (precipitates C-reactive protein; CRP)
39
Q

S. pneumoniae-Epidemiology

A
  • commonest cause of community acquired acute bacterial pnuemonia, estimated 500,000 cases annually
  • predisposing conditions:
    • alcoholism (aspirate own secretions)
    • DM
    • chronic lung dz
    • chronic renal dz
    • certain malignancies
40
Q

Invasive Pneumococcal Disease

A
  • bacteremia most common clinical presentation among children younger than 2 years (alway get sputum and blood culture if you suspect it)
  • most common cause of bacterial meningitis in the US
  • highest rate of meningitis among children younger than 2 years
41
Q

What is bacteremia??

A

bacteria in the BLOOD

42
Q

S. pneumoniae-Lab ID, Morphology

A
  • gram POSITIVE, lancet-shaped cocci (elongated cocci with a slightly pointed outer curvature)
  • usually seen as pairs of cocci (DIPLOcocci), but also may occur singly and in short chains
  • on blood agar: ALPHA hemolytic, individual cells: 0.5-1.25 micro-meter in diameter
43
Q

S. pneumoniae-Lab ID, Biochemical Tests

A
  • catalase NEGATIVE
  • bile soluble
  • inhibited by ethylhydrocupreine (Optochin)
  • halo/zone of inhibition=positive sign, presence of strep pneumoniae
44
Q

Recommended Treatments for Pneumococcal Infections

A

-Penicillin if susceptible (have to have low MIC for it to work in CSF because penicillin doesnt cross the BBB very well)
-Cefotaxime or ceftriaxone if susceptible
-alternative agents (if allergic to pen)
»macrolides: erythromycin, clarithromycin, azithromycin
»Fluoroquinolones: Levofloxacin, Moxifloxacin
-breakpoinst differ for meningeal and NON-meningeal isolates
»interpretation of susceptibility
»NON-meningeal
»Meningeal

45
Q

Enterococcus

A
  • formally Group D streptococci
  • enteric bacteria
  • E. faecalis (pertaining to feces)
  • E. faecium (of feces)
  • inherently resistant to many commonly used AB
46
Q

Enterococcus Characteristics

A
  • gram POSITIVE cocci in pairs and short chains
  • alpha, beta, or gamma hemolytic
  • group D antigen pos
  • PYR pos–(L-pyrridonyl-beta-naphthylamide) impregnated discs serve as a substrate for detection of pyrrolidonyl peptidase); if it has the peptidases it will hydrolyze the compound and produce the red color
47
Q

Enterococcal Infections

A
  • urinary tract
  • mixed bacterial wound infections and decubiti (skin ulcer from lying in a position for too long)
  • sepsis, endocarditis
  • rarely causes meningitis
  • second most common nosocomial pathogen
48
Q

Enterococcus: Virulence Factors

A 
-Colonization Factors
>>aggregation substance
>>carbohydrate adhesins
-Secreted Factors
>>cytolysin
>>pheromone
>>gelatinase
49
Q

Enterococcus: Epidemiology

A
  • originates from the patients bowel flora
  • transferred from patient to patient
  • acquired through consumption of contaminated food or water
50
Q

VRE-vancomycin resistant enterococci

A

-Increasing incidence in hospital especially ICU or chemotherapy patients
-most often in E. faecium in US
-Van phenotypes (become resistant if they require any of these genes)
»Van A-plasmid-mediated, hi-level resist
»Van B-chromosomal, ho or low lever resist
»Van C-intrinsic “intermediate” level in E. gallinarum and E. casseliflavus. can differentiate by motility and pigment. both species are motile, T. casseliflavus produces YELLOW COLONIES

51
Q

Treatment of Enterococcal Infections

A
  • INTRINSICALLY RESISTANT TO ALL CEPHALOSPORINS, TRIMETHOPRIM-SULFA, AMINOGLYCOSIDES
  • systemic infections require ampicillin plus aminoglycoside for synergy
  • E. faecalis is susceptible to pen/amp
  • E. faecium is RESISTANT to pen/amp
  • some strains vancomycin resistant (VRE)
  • Linezolid (oxazolidinone: unique class of synthetic antibiotic) effective in treating VRE

E3.MHD (6 decks)

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