Neisseria and Bacteriodes Flashcards

1
Q

• Gram− diplococci
• Lipooligosaccharide (vs. LPS): lack O antigen extensions
• common oral flora and other mucous membranes
• pathogens: N.gonorrhoeae and N.meningitidis
Host: only humans

A

Neisseria

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2
Q

What are the virulence factors of N. gonorrhoeae

A

phase variation and antigenic variation of pilin genes

vaccination is not possible.

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3
Q

t/f: there is no capsule for N. gonorrhoeae

A

true

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4
Q

ØPilE single chromosomal copy of pilin structural gene

ØStrains contain 10-15 copies of PilE variants lacking promoter and 5 -end of gene called PilS genes

ØPilS genes recombine with PilE creating unlimited antigenic variants of PilE

ØResult is that antigenic structure of pilus protein is constantly changing

A

Pathogenesis of Gonorrhea

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5
Q

In Neisseriae: Slipped Strand Mispairing resulting from presence of multiple identical repeated sequences at 5 -end of gene. Replication errors due to strand misalignment creates reading frame errors. Often, premature stops, but also results in ON/OFF switch.

A

Phase Variation:

on/off switch for surface protein expression

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6
Q

Multiple Opa (Colony Opacity) protein copies scattered across genome; Slipped strand mispairing results in frequent variation in Opa protein expression or complete absence of Opa

A

Phase Variation:

on/off switch for surface protein expression

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7
Q

Ø Phase Variation: on/off switch

Ø E. coli and other Gm- rods simple inversion
of promoter

A

Pathogenesis of Gonorrhea

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8
Q

Pili mediate bacterial attachment to non-ciliated epithelia

A

Virulence Factors of N. gonorrhoeae

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9
Q

bacteria proliferate and shed into secretions;

A

Virulence Factors of N. gonorrhoeae

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10
Q

secreted IgA protease

A

Virulence Factors of N. gonorrhoeae

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11
Q

Serum-resistant virulent strains cause disseminated gonococcal infections:
• Strains lack Opa proteins (colony opacity proteins = outer-membrane proteins)
Neutrophils unable to engulf bacteria lacking Opa proteins.

• Sialic acid on LOS (Lipidoligosaccharide of outer membrane) binds complement
regulatory proteins, prevents complement-based phagocytosis.

A

Virulence Factors of N. gonorrhoeae

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12
Q

What is the virulent function of secreted IgA Protease?

A
Usefulness of cleaving IgA:
Coating of bacteria with IgA
Fab fragments (does not
activate complement and
also blocks binding by other
IgG and IgM)
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13
Q

addition of sialic acid to lipoligosaccharide inhibits complement fixation

A

Virulence Factors of N. gonorrhoeae

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14
Q

Sexual transmission - urogenital infections

A

Gonorrheal Diseases

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15
Q

in men, urethral pus secretion

leukocytes with many gonococci

A

urethritis

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16
Q

in women, frequently some urination

sensitivity but no other symptoms

A

cervicitis

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17
Q

t/f: Gonorrheal Diseases are Frequently (almost) asymptomatic

A

true

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18
Q

o destructive eye infection, acquired during birth
o Application of erythromycin ointment into both
eyes of newborns is mandatory in many states and is considered standard neonatal care

A

Opthalmia Neonatorum

as a result of Gonorrheal Diseases

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19
Q

Initial infection of cervix, fallopian tubes and vaginal wall glands can lead to PID (15-30%):

o gonococci enter abdominal cavity, cause liver disease

o tissue scarring causes fallopian tube abnormalities which lead to ectopic pregnancies and sterility

A

§ Pelvic Inflammatory Disease (PID) in women

as a result of Gonorrheal Diseases

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20
Q

_____ ____ can cause Urethral and testicular tubule scarring, resulting from epididymitis, leads to sterility
and increased urethral infections by other microbes

A

Gonorrheal Diseases

21
Q

without apparent genital infection, ____ ____ ____ causes skin lesions, suppurative arthritis of a major joint, heart valve destruction.

A

Disseminated Gonococcal Infection

22
Q

t/f: Little or no protective immunity (pilin variability!) is observed after recovery from an infection with
N.gonorrhoeae.

23
Q

What are the factors of Neisseria meningitidis that affect intravascualar survival?

A

Capsule: protects against complement-mediated bacteriolysis and phagocytosis

Acquisition of iron from transferrin

24
Q

t/f: Neisseria meningitidis can cross the blood brain barrier and multiply in the subarachnoid space

25
For ____ ______ Symptoms start like a mild cold, progress to throbbing headache, fever, stiffness in neck and back, nausea and vomiting, deafness and coma. Shock and death (100% if untreated) may occur within 24 hours, but frequently is slower so that effective treatment can be given (<10% death in treated cases).
Neisseria meningitidis
26
Obstruction of release of increased fluid pressure (due to PMN attempts at eradication: pus and clotting) impairs brain, causes paralysis of motor nerves and coma. Loss of blood supply to brain is one of the frequent symptoms just prior to death
Neisseria meningitidis
27
LOS/endotoxin release from blood-circulating meningococci (which have a high tendency to auto-lyse and thus spread LOS widely) causes shock.
Neisseria meningitidis
28
T/F: with Neisseria meningitidis, small local skin hemorrhages are observed: Localized loss of vascular integrity: effect of inflammatory cytokines release induced by endotoxin activation of macrophages. this is contrary to other meningitis-causing infections.
true
29
blood spots, bruising, and discoloration of skin from coagulation in small blood vessels
Purpura fulminans
30
Purpura fulminans is seen in what bacterial infection?
Neisseria meningitidis
31
______ _____ Can progress to disseminated intravascular coagulation: blood clots throughout the circulatory system resulting in blockages and excessive bleeding elsewhere (clotting factors depleted)
Purpura fulminans
32
Ø Large capsule Ø IgA protease Ø Pili Ø Shedding of lots of Endotoxin shock
Vi rulence Factors of N.meningitidis
33
What is the virulent role of the large capsule in neisseria meningitidis
Ø Large capsule leads to disseminated intravascular coagulation (DIC) Some virulent strains have capsules with sialic acid on LOS (like N.gonorrhea): reduces phagocytosis further
34
What are the two effective vaccinations against capsular polysaccharides?
MenACWY Vaccine MenB vaccine
35
CDC recommended since 2005 Protection from 4 major disease-causing strains: A, C, W135 and Y (serotyping: 12 antigenic groups)
MenACWY Vaccine
36
– approved in 2014 & also recommended B capsule poly-sialic acid; Andy Marso’s case involved serogroup B bacteria. European MenB vaccine was used in outbreaks at Princeton and UC Santa Barbara in 2013-2014
MenB vaccine
37
t/f: Mandatory vaccination for neisseria meningitidis for students living in dorms in many states, military recruits, and jail inmates
true
38
Neisseria meningitidis is gram __
negative
39
Virulence factors: - pili - Ag-variation - OPA IgA protease endotoxin/ LOS Clinical Features: - gonorhea pelvic inflammatory disease - arthritis Epidemiology: - sexual transmission - asymptomatic carrier
Neisseria Gonorrhae
40
Virulence factors: - polysaccarhide capsule - entoxin/ LOS - Pili - IgA protease Clinical Features: - meningitis - meningococcemia Prevention: -MenACWY & MenB vaccines Epidemiology: - asymptomatic carrier - aerosol transmission - children/young adult
Neisseria meningitidis
41
Gram− bacteria of the human colon/oral cavity - Strict anaerobes - Commensals - Opportunistic pathogens
Bacteroidales G-
42
- most frequently isolated from clinical specimens of abscesses caused by intestinal bacteria - most oxygen-resistant Bacteroides
Bacteroides fragilis
43
Ø Superoxide dismutase - detoxifies oxygen radicals Ø Catalase - breaks down hydrogen peroxide Allows survival in well oxygenated peritoneal cavity Also helps bacteria resisting killing by phagocytosis Ø Polysaccharide capsule
Virulence Factors of Bacteroidales
44
______ Disease is caused when bacteria are introduced into deep tissues - peritonitis - rupture of infected appendix/diverticulum - pulmonary abscess - aspiration of oropharyngeal bacteria
Bacteroidales
45
T/F: Bacteroides fragilis is one component in these diseases | polymicrobial diseases
true
46
start with acute inflammation | progress to formation of localized abscesses
biphasic-
47
____ ____ changes as disease progresses | 100’s of different species in inoculum few species in abscess
bacterial composition
48
- perforation of intestine/spillage of intestinal fluid - neutrophils mobilized - surviving bacteria resistant to phagocytosis (B. fragilis has a capsule) - oxygen-sensitive bacteria are killed (peritoneal cavity well-oxygenated) - facultative anaerobes grow first (E. coli) - some strict anaerobes survive - site becomes anaerobic - surviving strict anaerobes become predominant
Course of disease for Bacteroidales
49
treat _____ with Surgery and antibiotic combinations (target aerobes and anaerobes)
Bacteroidales