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Y1 - Microbio Exam 2 > 8_Gram Positives iI > Flashcards

8_Gram Positives iI Flashcards

1
Q

What are the 3 key diseases caused by S. pneumoniae?

A
  • acute bacterial pneumonia
    • part of normal nasopharyngeal flora (5-40%)
    • major causative agent of pneumonia in the aged and immunocompromised patients
    • Sxs: fever, cough with sputum, dull chest
  • otitis media
    • middle ear infection
  • meningitis
    • most common cause of meningitis
    • Sxs: fever, neck pain, headache
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2
Q

What is the Lancefield grouping of S. penumoniae?

A

NONE! It’s a non-Lancefield pathogen

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3
Q

What is the S. pneumoniae vaccine?

(structure and serotypes)

A
  • Pneumovax
  • Structure is a polysaccharide capsule w/ multiple serotypes
    • Capsular serotypes: some strains are more virulence than others
  • Original vaccine was targeted against the 6 most virulent serotypes
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4
Q

multivalent vaccine:

define

A
  • multivalence means it is directed against multiple serotypes;
  • antigenic portion of the polysaccharide from each of the multiple serotypes is attached to a carrier so the vaccine can be directed against multiple serotypes
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5
Q

of the serotypes in the Streptococcus pneumoniae vaccine, which serotype is most virulent?

A

serotype 4 is more virulent than serotype 19A

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6
Q

Is S. pneumoniae competent?

What does this allow it to do?

A
  • S. pneumoniae is naturally competent
  • can take up DNA by transformation and –> incorporate the new DNA by RecA-mediated homologous recombination.
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7
Q

how are more virulent strains of S. pneumoniae able to escape a vaccine?

A
  • Natural competence allows more virulent strains (such as serotype 4) –> to pick up the capsule from less virulent strains (such as serotype 19A).
  • This allows them to escape the vaccine.
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8
Q

Why do we need 13- and 23-valent vaccines to combat the S. penumoniae bacteria?

A
  • Because of natural competence and the ability of more virulent strains to pick up the capsule from less virulent strains
  • Need the 13 and 23 valent vaccines to cover additional serotypes. (Pneumovax13 and Pneumovax23)
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9
Q

S. pneumoniae:

distinguishing features

A
  • Gram-positive, lancet-shaped diplococci
  • Catalase negative
  • Quellung rxn (capsular swelling) – positive
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10
Q

GBS (Group B Streptococcus);

Streptotoccus agalactiae

location, frequency, transmission, sxs

A
  • found in normal vaginal flora: 10-30% of women
  • transmitted
    • birth or by carrier or by contaminated materials
    • newborns are sensitive due to underdeveloped normal flora
  • Sxs may not develop until the infant goes home
  • Therefore, pregnant women are screened and treated w/ Abx prior to birth
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11
Q

Diseases caused by Group B Streptoccocus, and sxs

(Streptococcus agalactiae)

A
  • Neonatal Meningitis
  • sxs: fever, lethargy, poor feeding, seizures
  • can be cultured from CSF after lumbar puncture
  • Neonatal Pneumonia

•cyanosis, tachypnea (rapid respiration), respiratory distress

  • Post-partum Endometritis
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12
Q

Group B Streptococci (S. agalactiae):

distinguishing features

A
  • Gram-positive cocci in short chains
    • Found in CSF
    • Systemic can be found in blood sample
  • CAMP test positive
  • CAMP factor enhances hemolysis caused by S. aureus hemolysins
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13
Q

What is the CAMP Test Positive?

A
  • identify group B βeta-hemolytic streptococci (Streptococcus agalactiae) based on their formation of a substance (CAMP factor) that enlarges the area of hemolysis formed by the β-hemolysin elaborated from Staphylococcus aureus.
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14
Q

Which 2 genera are Group D Enterococci found in?

A

Group D Enterococci is a diverse group containing bacteria from 2 different genera:

  • Enterococcus and
  • Streptococcus
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15
Q

Enterococci:

location, diseases it can cause, and 2 examples

A
  • Location: GI tract normal flora; nosocomial pathogens (aka found in the hospital and are Abx-resistant)
  • Can cause:
    • septicemia
    • UTI
    • endocarditis
  • Ex. E. faecium, and E. faecalis
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16
Q

How are commensal bacteria converted to pathogens?

A

Virulence factors that are acquired from mobile genetic elements (plasmids, transposons, and PAIs- pathogenicity island) –> can convert the commensals to pathogens

17
Q

What can result from antibiotic resistance?

A

Can lead to:

  • multi-drug resistant strains (MDR)
  • vancomycin resistance enterococci (VRE)
18
Q

Enterococci (Group D):

distinguishing factors

A
  • Enterococci
    • Gram-positive cocci that often occur in singles, pairs (diplococci) or short chains
  • Catalase negative
  • PYR positive (Pyrrolidonyl Arylamidase (PYR) test)
  • Grows in bile salts and 6.5% NaCl
19
Q

Corynebacterium diphtheriae:

distinguishing factors

(shape, location, transmission)

A
  • Gram-positive club-shaped rod
  • does not disseminate but forms pseudomembrane in the back of the throat, including:
    • fibrin
    • leukocytes
    • necrotic epithelial cells
    • bacteria
20
Q

Diphtheria toxin

(structure, function, and targets of the)

A
  • Produced by C. Diphtheriae
  • Structure
    • AB toxin
    • B subunit protective factor
    • A subunit is ADP ribosylates Elongation Factor 2 (EF2) of the ribosome, inhibiting protein synthesis and killing the cell
  • Targets
    • heart cells –> arrhythmia, myocarditis
    • nerve cells –> peripheral and cranial palsy
21
Q

Listeria monocytogenes:

distinguishing factors

(structure, location, diseases caused)

A
  • Gram-positice rod
  • Grows intracellularly;
  • Tx by:
    • food borne illness (milk, soft cheeses, butter, and deli meats)
    • spreads into blood stream –> to CNS
  • Can cause:
    • meningitis in fetus if mother ingests it (even if mother is asymptomatic)
    • can cause meningitis is immunosuppressed patientsa and sometimes pregnant women
22
Q

Define and describe the unique mechanism for:

spreading L. monocytogenes between eukaryotic cells

A
  • “Host Cell Actin Polymerization”
  • Process
    • Internalin (surface protein found on L. monoctogenes) allows invasion
    • Listeria lysin O (LLO) allows escape into the cytoplasm,
    • then the bacteria polymerize host actin to move between eukaryotic cells
23
Q

Spirochetes:

distinguishing characteristics

A
  • Gram-negative bacteria
  • too thin to see by light microscopy
  • uses dark-field microscopy is commonly used.
24
Q

Endoflagella:

define

A
  • structure
    • special flagella of the spirochetes;
    • wound around their tiny cork-screw shape;
    • these endoflagella together form what is called an axial filament
  • location
    • sits between outer membrane and peptidoglycan layer
25
Q

what are the 3 genera that are pathogenic for man?

A
  • Treponema (Syphilis)
  • Borrelia (Relapsing fever and Lyme disease)
  • Leptospira (Leptospirosis)
26
Q
  1. Which bacteria causes Syphilis?
  2. How is it transmitted?
  3. Does the outer membrane have LPS?
A
  1. Treponema pallidum
  2. Usually sexually transmitted; causes a chronic illness
  3. The Treponema pallidum does NOT HAVE LPS in its outer membrane
27
Q

sequential stages of:

Syphilus

A
  1. Inoculation by sexual contact
  2. Primary syphilis
    • chancre, which is a sore on the surface of the tongue - infectious
  3. Secondary syphilis
    • rash and mucocutaneous lesions - infectious
  4. Latent syphilis
    • no symptoms; relapses to secondary syphilis
  5. Tertiary syphilis
    • invasion into cardiac or nerve cells (brain)
28
Q

Describe the step:

Primary Syphilis

A
  • long incubation –>
  • to a lesion that starts as a painless papule and forms an ulcer (chancre)
  • contagious throughout entire period
29
Q

Describe the step:

Secondary syphilis

A
  • mucocutaneous lesions and rash
  • very contagious
  • 2-8 wks after primary chancre
  • (the primary and secondary stages may overlap)
30
Q

Describe the step:

Latent Syphilus

A
  • asymptomatic
  • can cycle back to secondary syphilis (relapse) until there are enough antibodies to prevent more relapses
  • relapses becomes less severe with time
31
Q

Describe the step:

Tertiary syphilis

A
  • Affects the nervous and cardiovascular disease, most commonly
  • Due to growth of spirochetes in the brain or heart disease
  • occurs in untreated patients
32
Q

CC: Congenital Syphilis

(effects, and sxs)

A
  • Treponema pallidum passes the placenta to the fetus causing death or skeletal system defects
  • Newborns will have mucosal patches which are infectious
33
Q

What are the laboratory tests for Treponema pallidum?

A
  • Diagnosed by darkfield microscopy, or
  • fluorescent microscopy or by serology (especially in secondary syphilis)
34
Q

Tx and prevention of syphilis

A
  • Treatment: penicillin (usually)
    • alternatives are tetracycline, doxycycline, and azithromycin
  • Prevention:
    • safe sex practices; all whoa re infected and their sexual contacts should be treated
35
Q

Borrelia burgdorferi:

shape, seen with

A
  • large spirochete; (lrgst in size of pathogenic spirochetes)
  • can be seen w/ light microscope
    • stained w/ Gram stain, Giemsa, or Wright stain
36
Q

Which bacteria causes Lyme disease?

How is it transmitted? Sxs

A
  • Borrelia burdorferi causes Lyme disease
  • transmitted by the Deer tick (most common tick-transmitted disease)
  • variety of sxs, affecting multiple body systems
37
Q

describe the lifecycle of the Ixodes tick

A
  • Deer tick (Ixodes scapularis) takes 2 years to mature
  • 1st year - nymphs feeding on small mammals
  • 2nd year - adults and feed on deer.
    • In both cases the tick becomes infected with Borrelia burgdorferi when it feeds on small mammals (esp. white footed mice).
    • Infected nymphs or adults can infect a person but it is usually a nymph (primary route).
38
Q

First stage, Second stage, and Late stage of

Lyme disease

A
  • First stage:
    • nymphs are small ticks; people don’t usually remember being bitten
    • develops bulls-eye rash (erythema migrans) at bite site
    • sxs: fever, headache, myalgia, joint pain
  • Second stage:
    • days - months later; patient develops neurologic or cardiac abnormalities
  • Late stage:
    • arthritis in 2/3 untreated patients
39
Q

Diagnosis and tratment for:

Lyme’s disease

A

Diagnosis

  • usually based on hx and clinical observations
  • Abx titers to B. bergdorferi can be confirmed by immunofluorescent assay or ELISA
  • positive results can be confirmed by Western blot

Treatment

  • Abx should be initiated as soon as possible
  • Doxycycline and amoxicillin for tx

Prevention

  • prevention is focused on preventing tick bites (clothing, insect repellents)
  • check for ticks and remove immediately

Y1 - Microbio Exam 2 (18 decks)

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