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lecture 8 strep pneumoniae Flashcards

1
Q

Strep pneumoniae

A

NON lancefield pathogen pneumococci

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2
Q

acute bacterial pneumonia

A

part of normal nasal flora, major cause of pneum. fever, cough, dull chest

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3
Q

ottitis media

A

middle ear infection

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4
Q

meningitis

A

most common cause of meningitis, strep pneum. fever, neck pain, headache

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5
Q

Strep pneum vaccine, how many serotypes

A

polysac. capsule with multiple serotypes, original vaccine was against 6 of the most virulent sterotypes

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6
Q

pneumovax

A

capsular polysac vaccine , multiple capsular serotypes available. Original vaccine was most virulent

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7
Q

Strep pneum vaccine

A

multivalent because it is directed against 6 serotypes. The antigenic portion of the polysac from the 6 serotypes is attached to a carrier so the vaccine can direct against multiple serotypes

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8
Q

Which serotype was most virulent

A

serotype 4 is more virulent than 19 A

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9
Q

How does S pneum. take up DNA

A

by transformation. It is naturally competent and can incorporate the new DNA by RecA mediated homologous recomb.

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10
Q

What does competent mean

A

S pneum can take up DNA from the environment and recombine it into the chromosome by homologous recombination

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11
Q

What benefit does natural competence have?

A

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. and obtain new capsule types via transformation.

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12
Q

Serotype switching

A

serotype 4 replaces capsules genes with genes from 19A escaping original vaccine, obtain new capsule

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13
Q

Why did 13 and 23 valent vaccines develop?

A

because of the ability of more virulent strains to pick up the capsule from less virulent strains, these were created to cover additional serotypes.

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14
Q

serotype

A

strain of a microorganism

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15
Q

Features of S Pneumoniae

A

gram positive lancet shaped diplocci, catalase negative , quelling reaction positive ( capsular swelling)

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16
Q

Streptococcus agalactiae

A

normal vaginal flora 10-30% of women, new born sensitive to underdeveloped normal flora. Can lead to :
neonatal meningitis, neonatal pneumonia, post partum endometriosis, pregnant women are screened prior to giving birth and treated with antibiotics

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17
Q

Neonatal mening.

A

fever, lethargy, seizures, can be cultured from CSF, from Strept. agalactiae, Group B, serious condition

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18
Q

neonatal pneumonia

A

cyanosis, tachypnea , resp distress Group B , more severe, from Streptococcus agalactiae

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19
Q

S agalactiae group B streptococci

A

gram positive cocci in short chains(CSF), CAMP test positive, CAMP factors enhance hemolysis caused by S aureus hemolysins/ toxins

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20
Q

Enterococcus faecalis/faecium

A

bacteria containing 2 different genera, enterococcus and streptococcus. Group D enterococci

21
Q

Enterococci

A

Gi tract normal flora, nosocomial pathogens, can cause septicemia, UTI , endocarditis, E faecium and E faecalis

22
Q

What converts commensals to pathogens

A

HorizontalGeneTransfer HGT, virulence factors are acq from mobile genetic elements( plasmids, transposons) which convert commensals to pathogens

23
Q

What is enterococcus faecalis a major reservoir for?

A

antibiotic resistance gene . Antib res. leading to multi drug resistant strains (MDR) and vancomyocin resistance enterococci (VRE) Many strains hard to treat, and require dual antib. treatment( VRE)

24
Q

Enterococci distinguishing features:

A

Group D, gram positive cocci in shingles, pairs or short chains, catalase negative, PYR positive, grows in bile salts and 6.5% NaCl

25
Corynebacterium diptheriae
gram positive club shaped rod , does not disseminate but forms pseudomembrane in the back of throat* fibrin, leukocytes, necrotic epi cells, bacteria
26
What does C dip produce?
Diptheria toxin : AB toxin, B subunit protective factor, A subunit is ADP ribosylates elongation Factor 2 ( EF2) INHIBITS protein synthesis and kills cell targets
27
What cells can C dip affect?
heart cells causing arrhythmia, myocarditis , nerve cells causing peripheral and cranial palsy
28
What does EF2 do
INHIBITS protein synthesis and kills cell targets. Elongation factor 2(ribosome)
29
Listeria Monocytogenes features:
gram positive rod, grows intracellularly, food borne illness( dairy and deli meats) spreads in blood to CNS, meningitis in fetus if mother ingests, even if mother is ASYMPTOMATIC. Can cause meningitis in immunosuppressed patients.
30
What mechanism does Listeria Monocytogenes have?
unique spreading between eukaryotic cells that uses host cell actin polymerization. Internalin allows invasion, LLO listeria lysin O allows escape into the cytoplasm, and then the bacteria polymerize host actin to move between eukaryotic cells.
31
What are the features of Spirochetes?
gram negative bacteria that are too thin to see by light microscopy so dark field microscopy is used.
32
What is endoflagella
sits between the outer membrane and the peptidogylcan layer, allows for motility, bacteria move in corkscrew fashion
33
What three genera are pathogenic for man?
Treponema (syphillis) Borrelia (relapsing fever and lyme disease) Leptospira (Leptospirosis)
34
What is syphilis caused by?
Treponema pallidum
35
Treponema does not contain what in its outer membrane?
LPS
36
What are the stages of syphilus
inoculation by sexual contact, 1. primary syphilis- canchre infection, 2. secondary syphilis- rash plus mucus lesions-infectious 3. latent syphilis no symptoms-relapses to secondary syph. 4. tertiary invasion into cardiac or nerve cells (brain)
37
What are characteristics of primary syphilus
long incubation period (9-30 days) leading to a lesion that starts as a painless papule and forms an ulcer (chancre) contagious throughout entire period
38
secondary syph
mucocutaneous lesions and rash, contagious , develops 2-8 weeks after primary chancre. May persist for weeks to months
39
latent syphilus
patient is usually asymptomatic, can cycle back to secondary syph (relapse) until there are enough antibodies to prevent relapses. Becomes less severe with time. Patients become resistant to infection
40
Tertiary syphilus
nervous and cardiovascular disease due to growth of the spirochetes in the brain or hear tissues, occurs in untreated patients
41
Congenital syphilus
T pallidum passes the placenta to the fetus causing death or skeletal system defects, acute, extensive invasion of all body organs. New borns will have mucosal patches which are infectious.
42
How is syphilis diagnosed
darkfield microscopy or fluorescent microscopy or by serology-secondary syph
43
How do you treat and prevent syphilis
penicillin is drug of choice, alt are tetracycline, azithromyacin, doxy
44
Borrelia Burgdorferi
large spirochete can be seen with a light microscope, largest in size of the pathogenic spirochetes. INSECTS NEEDED FOR TRANSMISSION
45
What is lyme disease
Borrelia burdorferi causes lyme disease, transmitted by deer ticks , involves multiple body systems
46
How does a tick become infected with Bor burg?
deer tick (ixodes scapularis) takes 2 years to mature. The first year they are nymphs feeding on small mammals. 2nd year they feed on deer. Tick becomes infected with BB when it feeds on small mammals. Normally infected nymphs affect a person. (primary) hidden transfer
47
What are early symptoms/first stage of lyme disease
1st stage: lymph are small ticks, looks like bulls eye rash, erythema migrans, forms at bite site. fever, headache, myalgia, joint pain. 2nd stage: days to months later patient develops neurologic /card. abnor Late stage: arthritis in untreated (both curable)
48
What are diagnosis and treatment of lymes disease?
dx: history and clin. obs. antibody titers to BB can be confirmed by immunoflo. assay or ELISA. Positive results confirmed by Western blot. tx antibiotic, doxy and amoxicilin. Prevention focused on preventing tick bites. 24hrs for tick to inject spirochete

Microbiology (7 decks)

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