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PHARM/MHD EXAM - 3 > L2 MHD: Strep/Entero > Flashcards

L2 MHD: Strep/Entero Flashcards

1
Q

Staphylococci Vs. Streptococci

  1. Catalase Test?
  2. Cocci formation?
  3. What type of media does it grow in?
  4. Optimal growth temp?
  5. Optimal growth atmosphere?
A

Staphylococci:

  • Catalase +
  • Cocci in clusters (grape like clusters)
  • Grows in minimal media
  • Grows best at 35-37 C (both Staph and Strep)
  • Prefers aerobic atmosphere

Streptococci:

  • Catalase negative
  • Cocci in pairs/chains
  • Requires complex media
  • Grows best at 35-37 C
  • Prefers anaerobic or CO2 atm
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2
Q

Streptococci are named after their ____________ properties. This is known as what type of grouping?

A
  • Named for their serologic properties

- Lancefield groupings- Streptococci A-H, K-M, O-V

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3
Q

What are the hemolytic properties of Streptococcus alpha, beta, and gamma?

A
  • Alpha: incomplete hemolysis
  • Beta: complete hemolysis
  • Gamma: no hemolysis
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4
Q

What are the 6 important species of streptococcus?

A
  • Streptococcus pyogenes (Group A)
  • Streptococcus agalactiae (Group B)
  • Other Beta hemolytic streptococci
  • Viridans group streptococci (green- alpha)
  • Nutritionally Deficient streptococci
  • Streptococcus pneumoniae
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5
Q

What 3 infections do group A streptococcus pyogenes cause? How do they present?

A
  1. ACUTE PHARYNGITIS
    - usually 5-15 year old with fever, sore throat, headache, and swollen lymph nodes- 5% asymptomatic carriers.
    - Self-limiting- will go away without antibiotics; early treatment WITH antibiotics (penicillin) can prevent rheumatoid fever later on
    - Reoccurs due to lack of a type specific Ab to M protein
  2. IMPETIGO
    - 2-5 year old child with localized skin disease, pustules with yellow crust
    - Associated with trauma/insect bites (impetigo- insect)
    - appears on face or extremities
  3. ERYSIPELAS
    - Spreading erythema with well demarcated edge on the face
    - Fever & lymphadenopathy
    - Lesions on face often with accompanying streptococcal pharyngitis
    - Historically- the face was most affected- today we see it most often in the legs- looks like a severe burn
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6
Q
  • Scarlet Fever is a complication of what streptococcus pyogene infection?
  • What toxin causes it?
  • Describe the rash it causes, specifically what happens when pressure is applied, and what part of the body is spared from rash.
  • What are the characteristic symptoms?
A

Complication of streptococcal pharyngitis

-Caused by erythrogenic exotoxin

Presents:

  • Tiny red bumps on chest abdomen; fine, red and rough textured blanches upon pressure
  • Rash appears 12-48 hours after fever, spreads from chest to armpit, spares the face; rash fades 3-4 days after onset and desquamation (peeling) of skin begins

Characteristics:

  • STRAWBERRY bright red tongue
  • Fever
  • Sore throat
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7
Q

Necrotizing Fascititis is caused by what group of streptococci?

Where does this infection occur? What does it destroy?

Mortality exceeds what percent?

What is a key symptom of necrotizing fasciitis?

A
  • Group A Streptococcus Pyogenes
  • Infection occurs deep in subcutaneous tissues, and spreads along the fascial plane, eventually goes on to destroy muscle & fat
  • Mortality exceeds 50%- requires immediate surgery to remove debris- cannot be treated with antibiotics
  • Key symptom: pain is disproportionate to how it looks- a small cut could have 10/10 pain
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8
Q

Toxic Shock Like Syndrome is caused by what toxin?

  • What does it cause?
  • How can you tell patients a patient with staph toxic shock from one with streptococcal toxic shock?
A
  • SPE Toxin- Streptococcus Pyrogen Exotoxin
  • Causes multi system organ failure (heart, respiratory tract, kidney)
  • Cultures from patients with TSLS will be positive for Group A Strep
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9
Q

Puerperal Sepsis is often seen in women following __________ or __________.

A

Seen in women following delivery or abortion

It is a pyogene infection (group A)

Organisms colonizing genital tract or from obstetrical personnel invade the upper genital tract causing endometritis, lymphangitis, bacteremia, necrotizing fasciitis, and streptococcal toxic shock syndrome

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10
Q
  • What are the two post-streptococcal sequelae?

- What type of infection causes them?

A

Rheumatic Fever (caused by pharyngitis)

Acute Glomerulonephritis (caused by any of the group A streptococcal pyogene infections)

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11
Q
  • How long after strep pharyngitis does Rheumatic Fever occur?
  • What are the symptoms?
  • Reoccurrence can happen until when?
  • What are the characteristic lesions called?
A
  • Nonsuppurative inflammatory disease starts 1-5 weeks after strep pharyngitis
  • Fever, carditis, subcutaneous nodules, chorea, polyarthritis
JONES
j - joints --> polyarthritis
O - endocarditis
N - Nodules
E - Erythema Marginata
S - Sydenham Chorea
  • Attacks reoccur into adulthood
  • Characteristic cardiac lesions = ASCHOFF BODIES and valvular damage leads to possible endocarditis later in life
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12
Q

What are the symptoms of acute glomerulonephritis?

  • When does it occur?
  • What type of hypersensitivity reaction is it?
  • Certain M-types are what?
A
  • Edema, hypertension, hematuria, proteinuria
  • Occurs after skin (impetigo) / respiratory infection (pharyngitis)
  • Type III Hypersensitivity Rxn: Antigen + antibody + C’ deposited in glomeruli seen on kidney biopsy
  • Certain M types (antigens on strep) are “nephritogenic” meaning they cause nephritis
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13
Q

What are the 4 virulence factors of Group A Streptococcus?

List examples of each.

A
  1. Adhere to surface of host cells
  2. Invade epithelial cells
  3. Avoid opsonization and phagocytosis
  4. Produce a variety of toxins and enzymes
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14
Q

S. pyogenes expresses specific enzymes and proteins that facilitate tissue damage and pathogenesis.

List the 7 specific enzymes/proteins.

A
  • Capsular polysaccharide
  • Lipoteichoic acid
  • Hemolysins
  • Streptolysin S (oxygen stable, non-antigenic)
  • Streptolysin O (oxygen labile, ASO antibodies)
  • Streptokinase
  • Hyaluronidase
  • Nucleases
  • C5a peptidase

Streptolysins and streptokinase allow spread of bacteria in tissues

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15
Q

What does SPE stand for?

What are the three distinct heat labile toxins?

What infections are associated with SPEs and what is their mechanism of action?

A

-Streptococcal Pyrogenic Exotoxins

SPEa- TSLS
SPEb- necrotizing fascititis
SPEc- TSLS

  • Associated with Strep Toxic Shock-Like Syndrome & the rash in scarlet fever (erythrogenic exotoxin)
  • SPEs are considered super antigens. Their mechanism of action is to stimulate cytokine response leading to overstimulation of T-cells (cytokine storm). This leads to organ failure.
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16
Q

What protein allows S. pyogenes to adhere to a host before infection?

What aspect of the complement system does this protein affect?

Are the strains without this protein virulent or avirulent?

A

M Protein (>80 serotypes- highly variable); binds epidermal cells and allows bacteria to survive

  • Degrades complement C3b (antibodies to M protein activate complement and kill bacteria)
  • Strains without M protein are avirulent
17
Q

What antibiotics do you use to treat S. pyogenes?

Which is the drug of choice?

What do you give to a penicillin allergic patient?

A
  • Penicilin (best drug to treat strep!)
  • ->no resistance worldwide
  • Ampicillin/Amoxicillin
  • Cephalosporins
  • Erythromycin (macrolide) is given to patient’s with a penicillin allergy
18
Q

What infections are associated with streptococcus agalactiae?

What group of strep does this belong to?

Where in the body is strep agalactiae apart of the normal flora?

How do newborns get GBS?

A

-Neonatal pneumonia, sepsis, meningitis

–Group B (a galactic baby)

  • Part of normal flora in throat, vaginal and GI tract
  • Newborns get GBS during birth if their mothers are carriers
19
Q

-What is the pathogenesis of GBS when it is transferred from mother to newborn?

What are the early onset neonatal diseases associated with Group B Strep?

What are the late onset neonatal diseases?

Which have a better prognosis?

How is perinatal GBS disease prevented?

Besides pregnant women being asymptomatic carriers of GBS, what other infections is the bacteria associated with?

A
  • PATHOGENESIS: maternal colonization of vagina or rectum exposes the baby at delivery
  • The baby lacks protective maternal antibody
  • Sialic acid on polysaccharide capsule inhibits C’ allowing organisms to multiply
  • Early onset: Bacteremia, pneumonia, or meningitis ; happens in the first week of life and are often fatal
  • Late onset: neonatal disease, 1-3 months of age; Bacteremia with meningitis- infant has a better chance of surviving this!
  • Prevent perinatal GBS disease by performing vaginal/rectal swab on pregnant woman 35-37 weeks into gestation. Combined vaginal/rectal swab improves isolation rates by 40% over vaginal swab alone
  • ALERT physician when cervical or vaginal specimens are received
  • Use of LIM enrichment broth will increase GBS isolation by 50%
  • If you do not know whether or not the mother is GBS +, treat her as if she was and perform intrapartrum care
  • GBS is also associated with UTIs
  • GBS is the most common type of streptococcus seen in lab
20
Q

What is the preferred antibiotic to treat GBS?

What can be added to enhance killing?

When do you give a pregnant woman who is GBS positive treatment?

What drug is indicated for allergic patients?

A
  • Penicillin/ampicillin = drug of choice
  • ->No resistance worldwide
  • Add gentamycin to enhance killing
  • Prophylaxis (preventative abx therapy) of culture positive pregnant women during labor with penicillin/ampicillin to prevent neonatal disease
  • Clindamycin is used for pen allergic pts
21
Q

Other Beta Hemolytic Strep

Group ____:
Associated with veterinary infections
Pharyngitis in college age patients
Sepsis

Group ____:
Associated with abscesses

Group ____:
Pharyngitis
Sepsis in neonates and elderly

A

Group C (c is for cats and college)
Associated with veterinary infections
Pharyngitis in college age patients
Sepsis

Group F (abscesses are not Fab-scesses)
Associated with abscesses

Group G (g is for grandparent, goo goo ga ga (neonates))
Pharyngitis
Sepsis in neonates and elderly

22
Q

Name 4 lab tests you can do for streptococcus- which one can be done while the patient is still in your office?

A
  1. Antigen test- do right away- throat swab from posterior oropharynx
  2. Culture
  3. Identification
  4. Antibody Detection- see if you have ASO titers (indicates you have had a strep throat infection before). Could be indicative of Rheumatic Fever.
    - ASO
    - Anti-DNAse
23
Q

RADT- Rapid Antigen Detection Test

Is this test sensitive? Specific?

A

Not very sensitive! 69.6% sensitivity
-You can trust a (+) sensitivity test but not a negative one- this needs to be backed up with a culture test for Strep A (verify that the patient does not have Strep)

-Specificity- very good indicator (97.8%); both a positive and negative test can be trusted.

24
Q

Viridans Streptococci

  • What type of hemolytic properties does it have?
  • Where does it normally reside?

-What is it the major cause of?
Important cause of?

It can be an opportunistic pathogen in what type of patient?

A
  • Alpha & gamma hemolytic properties- lacks hemolysins and toxins of beta strep
  • Normally found in upper respiratory tract
  • Major cause of dental caries
  • Important cause of endocarditis

-Opportunistic pathogen causing sepsis in neutropenic (lacks white blood cells) cancer patient

25
Q

What are the 5 Viridans Streptococci Groups?

  • Which one consists of non-enterococcal group D streptococci?
  • What is the clinical significance of this group?
  • What is isolation of this group from blood associated with?
A
  1. Sanguis Group
  2. Mitis Group
  3. Mutans Group
  4. Salivarius Group
  5. Bovis Group

Dumb pneumonic that might help:
(Mitas Sang to Green Salivating Bovine Mutants)

  • Bovis Group consists of non-enterococcal group D streptococci
  • This group causes bacteremia, meningitis and both native and prosthetic valve endocarditis

ISOLATION OF S. BOVIS OF THE BLOOD IS ASSOCIATED WITH CARCINOMA OF THE COLON

26
Q

Streptococcus Milleri Group

  • What three strains does this include?
  • What morphology do the colonies typically have?
  • May require _____ for isolation - sometimes mistaken for anaerobic streptococci
  • Have a characteristic odor when cultured on agar plates- what is it?
  • Are they usually commensal or pathogenic?
  • Have been isolated from 56-81% of ________ ________ either in pure or mixed culture
A
  • S. anginosus, S. constellatus, S. intermedius
  • Produce pinpoint colonies
  • may require CO2 for isolation
  • Characteristic caramel butterscotch odor
  • Usually commensals isolated from mouth, oropharynx, GI tract and vagina

HOWEVER, they’ve been reported to cause deep-seated pyogenic infections of cardiac, abdominal, skin and CNS tissues

Have been isolated from 56-81% of brain abscesses either in pure or mixed culture
(Pyogenic)

27
Q

What two genera are nutritionally deficient streptococci placed in?

A
  1. Abiotrophia

2. Granulicatella

28
Q

A 7-year-old child presents with a fever, pain in his ankles, knees and wrist, and a new heart murmur. His mother said that he complained of a “sore throat” last month, but the symptoms resolved without taking him to the pediatrician. A rapid screening test for strep throat is negative. His most likely diagnosis is …?

A

Rheumatic fever

29
Q

Streptococcus Pneumoniae -

Where is it found?

Causes MOPS.. what does MOPS stand for?

The most common cause of _______ and community-acquired ________ in adults

What predisposes adults to this condition (aka primary disease state that may lead to secondary infection)

Also causes…?

A

-Located in normal flora of human upper respiratory tract- children are the greatest reservoir for s. pneumoniae

  • Meningitis (adult- usually secondary to one of the former infections)
  • Otitis media (children)
  • Pneumonia
  • Sinusitis (children)

-Most common cause of meningitis and CA-pneumonia in adults

-Predisposing conditions
Alcoholism- patients tend to fall down & aspirate their own secretions
Diabetes mellitus
Chronic lung disease
Chronic renal disease
Certain malignancies

-Also causes osteomyelitis, septic arthritis, endocarditis, peritonitis, cellulitis and brain abscesses.
(bone, joints, heart, peritoneum, skin, brain)

30
Q

S. Pneumoniae Virulence Factors:

  1. ________– damages ciliated cells and activates alternative complement pathway
  2. Neuraminidase
  3. _________ – Binds to receptors for PAF on cells
  4. _________– prevents IgA-mediated binding of pneumococcal cells to mucus
  5. ______________ – activates complement by alternative pathway
    - ->mediates ____________
    - ->Precipitates C-reactive protein (CRP)
  6. ____________ capsule is an important virulence factor (capsular type-specific antibody is protective)

Why isn’t there a universal vaccine against S. pneumoniae?

A
  1. Pneumolysis
  2. Neuraminidase
  3. Phosphorylcholine
  4. sigA protease
  5. Techoic Acid/Peptidoglycan- mediates inflammation
  6. Polysaccharide Capsule

There isn’t a universal vaccine against S. Pneumoniae because there are more than 90 known serotypes, and this variation makes it too hard to eliminate the carrier state of the vaccine

31
Q

Invasive Pneumococcal Disease in children younger than 2 years old

How does this clinically present?
What is it the most common cause of in the US?

A

Clinically presents as bacteremia in children younger than 2 years

  • Most common cause of bacterial meningitis in the U.S.
  • Highest rate of meningitis among children younger than 2 years
32
Q

S. pneumoniae Laboratory Identification - Morphology

Gram-______, ______-shaped cocci (elongated cocci with a slightly pointed outer curvature).

What type of hemolytic properties does s. pneumonia have?

Catalase Positive or negative?

Bile Soluble or Insoluble?

Inhibited by ethylhydrocupreine (Optochin) or resistant to Optochin?

A

Gram positive, LANCET shaped cocci

Usually seen as pairs of cocci (diplococci), but they may also occur singly and in short chains.

Alpha hemolytic

Catalase Negative

Bile Soluble

Inhibited by ethylhydrocupreine (Optochin)

33
Q

What is the preferred drug to treat s. pneumococcal infections?

What do breakpoints differ for in determining treatment?

A
  • Penicillin if susceptible
  • Cefotaxime or ceftriaxone if susceptible

Alternative agents

  • Macrolides: Erythromycin, Clarithromycin, Azithromycin
  • Fluoroquinolones: Levofloxacin, Moxifloxacin

Breakpoints differ for meningeal and non-meningeal isolates
Interpretation of susceptibility
Non-meningeal 8 R
Meningeal 0.12 = R

34
Q

Enterococcus- group D antigen

  1. E. ______ “pertaining to feces”
  2. E ______ “of feces”

Inherently __________ to may commonly used antibiotic

Gram positive or gram negative?

Hemolytic properties?

Group ____ antigen positive.

PYR positive or negative?

Where do enterococcus typically cause infection?

Is enterococcus a common cause of meningitis?

A

Enteric bacteria

  1. E. faecalis “pertaining to feces”
  2. E faecium “of feces”

Inherently resistant to may commonly used antibiotic

  • Gram positive cocci in pairs and short chains
  • Hemolytic properties: Alpha, beta or gamma hemolytic
  • Group D antigen pos.
  • PYR positive
  • Typically cause infection in urinary tract, mixed bacterial wound infections and decubiti, sepsis, endocarditis
  • RARELY causes meningitis! Second most common nosocomial pathogen

DO U HEART TREES

  1. UTI
  2. Endocarditis
  3. Biliary tract infections
35
Q

How is an enterococcus infection typically acquired?

What are its 2 main virulence factors and what are examples of each?

A

Originates from patient’s bowel flora- normal GI flora. It’s transferred from patient to patient or acquired through consumption of contaminated water or food.

VIRULENCE:

  1. Colonization factors
    - Aggregation Substances
    - Carbohydrate adhesins
  2. Secreted factors
    - Cytolysin
    - Pheromone
    - Gelatinase
36
Q

VRE- what does it stand for?

Increasing incidence where and with what type of patients?

What are the different phenotypes?
VanA:
VanB:
VanC:

A

Vancomycin Resistant Enterococci

  • Increasing incidence in hospital ICUs and with chemotherapy patients
  • Most often in E. faecium in US

Phenotypes:
VanA: plasmid mediated, hi-level resistance
VanB: chromosomal, hi or low level resistance
VanC: intrinsic intermediate level in – intrinsic “Intermediate” level in E. gallinarum and E. casseliflavus. Can differentiate by motility and pigment. Both species are motile, E. casseliflavus produces yellow colonies

37
Q

What is VRE intrinsically resistant to?

Systemic infections require ______ plus aminoglycoside for synergy

  • E. faecalis ________ to pen / amp
  • E. faecium _________to pen / amp

What antibiotic is effective in treating VRE?

A
  • Intrinsically resistant to all cephalosporins, trimethoprim-sulfa, aminoglycosides
  • Systemic infections require ampicillin plus amino glycoside for synergy
  • E. faecalis susceptible to pen / amp
  • E. faecium resistant to pen / amp
-Some strains vancomycin resistant (VRE)
Linezolid (oxazolidinone: unique class of synthetic antibiotic) effective in treating VRE
38
Q

An organism is isolated from the blood of a 65 year-old male patient with a diagnosis of probable bacterial endocarditis. The organism displays streptococcus-like morphology on gram stain and is catalase-negative. On blood agar the colonies appear gamma hemolytic and are PYR positive. Patient was being treated with vancomycin plus an aminoglycoside with no response. This isolate is likely to be:

A

An Enterococcus species

39
Q

Which SPE (A, B or C) is associated with Necrotizing Fasciitis? Which which TSLS?

SPE = -Streptococcal Pyrogenic Exotoxins

A

B = NECROTIZING FASCITIS

A & C =
TSLS

PHARM/MHD EXAM - 3 (21 decks)

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