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Microbiology > Neisseria and Bacteriodes > Flashcards

Neisseria and Bacteriodes Flashcards

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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.

A

true

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

A

true

25
Q

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).

A

Neisseria meningitidis

26
Q

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

A

Neisseria meningitidis

27
Q

LOS/endotoxin release from blood-circulating meningococci (which have a high tendency to auto-lyse and thus spread LOS widely) causes shock.

A

Neisseria meningitidis

28
Q

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.

A

true

29
Q

blood spots, bruising, and discoloration of skin from coagulation in small blood vessels

A

Purpura fulminans

30
Q

Purpura fulminans is seen in what bacterial infection?

A

Neisseria meningitidis

31
Q

______ _____ Can progress to disseminated intravascular coagulation: blood clots throughout the circulatory system resulting in blockages and excessive bleeding elsewhere (clotting factors depleted)

A

Purpura fulminans

32
Q

Ø Large capsule
Ø IgA protease
Ø Pili
Ø Shedding of lots of Endotoxin shock

A

Vi rulence Factors of N.meningitidis

33
Q

What is the virulent role of the large capsule in neisseria meningitidis

A

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
Q

What are the two effective vaccinations against capsular polysaccharides?

A

MenACWY Vaccine

MenB vaccine

35
Q

CDC recommended since 2005 Protection from 4 major disease-causing strains: A, C, W135 and Y (serotyping: 12 antigenic groups)

A

MenACWY Vaccine

36
Q

– 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

A

MenB vaccine

37
Q

t/f: Mandatory vaccination for neisseria meningitidis for students living in dorms
in many states, military recruits, and jail inmates

A

true

38
Q

Neisseria meningitidis is gram __

A

negative

39
Q

Virulence factors:

  • pili
  • Ag-variation
  • OPA IgA protease endotoxin/ LOS

Clinical Features:

  • gonorhea pelvic inflammatory disease
  • arthritis

Epidemiology:

  • sexual transmission
  • asymptomatic carrier
A

Neisseria Gonorrhae

40
Q

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
A

Neisseria meningitidis

41
Q

Gram− bacteria of the human colon/oral cavity

  • Strict anaerobes
  • Commensals
  • Opportunistic pathogens
A

Bacteroidales

G-

42
Q
  • most frequently isolated from clinical specimens of abscesses caused by intestinal bacteria
  • most oxygen-resistant Bacteroides
A

Bacteroides fragilis

43
Q

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

A

Virulence Factors of Bacteroidales

44
Q

______ Disease is caused when bacteria are introduced into deep tissues

  • peritonitis - rupture of infected appendix/diverticulum
  • pulmonary abscess - aspiration of oropharyngeal bacteria
A

Bacteroidales

45
Q

T/F: Bacteroides fragilis is one component in these diseases

polymicrobial diseases

A

true

46
Q

start with acute inflammation

progress to formation of localized abscesses

A

biphasic-

47
Q

____ ____ changes as disease progresses

100’s of different species in inoculum few species in abscess

A

bacterial composition

48
Q
  • 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
A

Course of disease for Bacteroidales

49
Q

treat _____ with Surgery and antibiotic combinations (target aerobes and anaerobes)

A

Bacteroidales

Microbiology (46 decks)

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