Neisseria, Bacteroides Flashcards

1
Q

What are the characteristics of Neisseria sp.?

A
  • 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
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2
Q

Is there a vaccine for N. gonorrhoeae?

A

vaccination not possible

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3
Q

What are the virulence factors of N. gonorrhoeae?

A
  • pili
  • antigenic variation adhesions
  • OPA
  • IgA protease
  • endotoxin
  • phase variation
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4
Q

What allows for the antigenic variation in gonorrhea?

A
  • PilE single chromosomal copy of pilin structural gene
  • Strains contain 10-15 copies of PilE variants lacking promoter and 5-end of gene called PilS genes
  • PilS genes recombine with PilE creating unlimited antigenic variants of PilE
  • Result is that antigenic structure of pilus protein is constantly changing
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5
Q

What allows for phase variation for gonorrhea?

A
  • on/off switch for surface protein expression
  • 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.
  • 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
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6
Q

What are the virulence factors for N. gonorrhoeae?

A
  • pili
  • IgA protease
  • endotoxin
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7
Q

What are pili used for?

A
  • mediate bacterial attachment to non-ciliated epithelia
  • bacteria proliferate and shed into secretions
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8
Q

What are IgA proteases used for?

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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9
Q

What does shedding of endotoxins allow for?

A

secretion of pro-inflammatory cytokines

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10
Q

What do Serum-resistant virulent strains of N. gonorrhoeae cause?

A

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
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11
Q

What does gonorrheal disease cause in men?

A

urethritis in men, urethral pus secretion (leukocytes with many gonococci)

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12
Q

What does gonorrheal disease cause in women?

A

cervicitis in women, frequently some urination sensitivity but no other symptoms

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13
Q

What can gonorrheal disease cause in neonatals?

A

Opthalmia Neonatorum
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

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14
Q

What can gonorrheal disease lead to in women if it gets worse?

A

Pelvic Inflammatory Disease (PID) in women
- Initial infection of cervix, fallopian tubes and vaginal wall glands can lead to PID (15-30%):
- gonococci enter abdominal cavity, cause liver disease
- tissue scarring causes fallopian tube abnormalities which lead to ectopic pregnancies and sterility

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15
Q

What can gonorrheal disease lead to in men if it gets worse?

A

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

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16
Q

What can disseminated gonococcal infection (without apparent genital infeciton) cause?

A

causes skin lesions, suppurative arthritis of a major joint, heart valve destruction

17
Q

Once you get gonorrheal disease how suseptible are you to getting it again?

A

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

18
Q

What is a very important fact of neisseria meningitidis that makes it so deadly?

A
  • crosses the blood-brain barrier
19
Q

What are the factors of neisseria meningitidis that affect intrvascular survival?

A
  • capsule
  • acquisition of iron from transferrin
20
Q

What are the symptoms of neisseria meningitidis?

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).
21
Q

What are the reasons for death due to Neisseria meningitidis?

A
  • 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
  • LOS/endotoxin release from blood-circulating meningococci (which have a high tendency to auto-lyse and thus spread LOS widely) causes shock
22
Q

How can you tell a Neisseria meningitidis infection from other types of meningitis?

A

small local skin hemorrhages are observed: Localized loss of vascular integrity: effect of inflammatory cytokines release induced by endotoxin activation of macrophages

23
Q

What is purpura fulminans that occurs in Neisseria meningitids?

A

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

24
Q

What can purpura fulminans progress to in a Neisseria meningitidis infection?

A

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

25
Q

What are the virulence factors of N. meningitidis?

A
  • polysaccharide capsule
  • endotoxin
  • pili
  • IgA protease
26
Q

What are the two effective vaccinations against capsular polysaccharides?

A

MenACWY Vaccine – Protection from 4 major disease-causing strains: A, C, W135 and Y (serotyping: 12 antigenic groups)

MenB vaccine – B capsule poly-sialic acid

27
Q

What are the clinical features of N. gonorrhoeae?

A
  • gonorrhea
  • pelvic inflammatory disease
  • arthiritis
28
Q

What are the clinical features of N. meningitidis?

A
  • meningitis
  • meningococcemia
29
Q

What is the epidemiology of N. gonorrhoeae?

A
  • sexual transmission
  • asymptomatic carrier
30
Q

What is the epidemiology of N. meningitidis?

A
  • asymptomatic carrier
  • aerosol transmission
  • children/young adults
31
Q

What are the virulence factors for bacteroidales?

A
  • superoxide dismutase
  • catalase
  • polysaccharide capsule
32
Q

What are the characteristics of bacteroidales?

A
  • gram -
  • strict anaerobes
  • commensals
  • opportunistic pathogens
33
Q

What is bacteroides fragilis?

A

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

34
Q

What disease is caused by bacteroidales?

A

Disease caused when bacteria are introduced into deep tissues
- peritonitis - rupture of infected appendix/diverticulum
- pulmonary abscess - aspiration of oropharyngeal bacteria

35
Q

What does bacteroides fragilis cause in disease?

A
  • biphasic - start with acute inflammation and progress to formation of localized abscesses
  • bacterial composition changes as disease progresses;100’s of different species in inoculum and few species in abscess
36
Q

What is the course of a bacteroidales disease?

A
  • 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
37
Q

How do you treat bacteroidales?

A

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