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Infection and Immunity > 21 Neisseria - immune system > Flashcards

21 Neisseria - immune system Flashcards

1
Q

what is neisseria like

A

large genus of Gram-negative bacteria

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2
Q

where is neisseria found

A

Natural inhabitants of the mucous membranes of mammals

Several human commensals inhabiting the mucus membranes

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3
Q

human pathogens - neisseria

A

N. meningitidis

N. gonorrhoea

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4
Q

what causes meningococcal diseases

A

Neisseria meningitidis,

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5
Q

what meningococcal diseases can occur

A

meningococcal sepsis

meningitis

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6
Q

what are meningococcal diseases like

A

while normally a harmless commensal, can cause devastating diseases

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7
Q

what is meningococcal sepsis caused by

A

inappropriate immune response

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8
Q

what causes the characteristic of meningococcal diseases - glass cup

A

capillary networks break down and blood not in circulatory system – why glass test occurs
Glass test – rash doesn’t disappear

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9
Q

carriage of meningococcal diseases

A

normally inhabits the nasopharynx

Colonises up to 50% of individuals within a population

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10
Q

transmission of meningococcal diseases

A

Associated with close contact – transmission

Can be coughing, sneezing, kissing

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11
Q

Meningococcal sepsis symptoms

A

High fever
Rash
Arthritis (achy joints)
Coagulopathy (evident as skin lesions but occurs throughout the body)

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12
Q

coagulopathy effect - meningococcal sepsis

A

bacteria will eventually affect the adrenal glands and adrenal insufficiency quickly leads to death

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13
Q

Meningococcal meningitis symptoms

A 
Severe headaches
Photophobia
High fever
Pain and stiffness of the neck, back, and shoulders
nausea
Rash
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14
Q

post infectious sequelae - meningococcal infection

A

Loss of extremities
Liver or kidney failure
Memory loss

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15
Q

what is a gonococcal infection like

A

may be asymptomatic but ultimately this organism is always a pathogen

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16
Q

symptoms of gonococcal disease

A

urethritis (purulent discharge)

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17
Q

where does gonococcal infections infect

A

mucous membranes of the urogenital tract and nasopharynx

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18
Q

what is the major problems with gonococcal diseases

A

antibiotic resistance

More serious for women – can lead to infertility

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19
Q

how is gonococcal diseases spread

A

usually always sexually transmitted disease – but usually is - Infants can get during birth from infected mother

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20
Q

what gonococcal disease can infant get

A

opthalmia neonatorum

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21
Q

Meningococcal pathogenesis

A

Start in oral pharynx and nasopharynx
Associates with mucosal membrane can get between these cells and get into bloodstream
Cross the blood brain barrier - manipulates endothelial cells that make up blood brain barrier
Organisms can get into cerebrospinal fluid

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22
Q

neisseria meningitidis groups

A

Different serogroups if Neisseria meningitidis – depends on which capsule it makes
Serogroup A
Serogroup B, C, W & Y

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23
Q

what is the capsule controlled by

A

Phase-variable antigen (can be turned on/off)

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24
Q

where are Acapsulate isolates of N. meningitidis often found in

A

nasopharynx

25
Q

when are capsulate isolates found

A

found in cases of invasive meningococcal disease

Exceptions include individuals with complement deficiencies

26
Q

what is the problem with serogroup B

A

Serogroup B capsular polysaccharide is identical to molecules found on some neuronal cells
Seen as a self-antigen and is thus hypoimmunogenic

27
Q

how does type IV pilus grow

A

pilE form structure of the pilus – added in the periplasm as added the pilus gets pushed out

28
Q

how does type IV pilus disassemble

A

pilT protein removes subunits – depolymersises pili and pulls it back in

29
Q

what does pilT require

A

PilT-dependent twitching motility

PilT is required for pilus retraction and therefore necessary for motility

30
Q

what is TspB

A

T cell stimulating protein B - potent stimulant of T cells

31
Q

where is TspB

A

outer membrane protein

32
Q

what encodes TspB

A

prophage found in most hyperinvasive isolates

33
Q

TspB function

A

Binds immunoglobulin

Inhibits IgM-mediated activation of the classical complement pathway as binds to Fc not FAB part

34
Q

what does TspB do

A

Promotes survival in normal human serum

35
Q

what is the matrix composed of that envelopes bacteria aggregates

A

A matrix composed of TspB, IgG and DNA envelopes aggregates of bacteria

36
Q

what makes fHbp

A

Produced by most strains of N. meningitidis (not all strains)

37
Q

what is fHbp

A

OM protein

38
Q

what does fHbp do

A

binds Factor H onto own surface ‘pretend to be host’ so downregulates complement activity

39
Q

what does factor H do

A

regulates the Alternative pathway of the complement system

40
Q

what is fHbp important for

A

survival in human blood, serum and in the presence of antimicrobial peptides

41
Q

Mechanisms that contribute to the resistance ofNeisseria meningitidisagainst complement-mediated killing

A
  • Polysaccharide capsule prevent insertion of MAC
  • Expression of full length LPS is necessary for complement resistance
  • C4BP to PorA - significantly increase the survival of the bacteria in the presence of an active complement system
  • type IV pilus
42
Q

what makes IgA protease

A

Produced by a number of mucosal pathogens

43
Q

what does IgA protease do

A

Cleave IgA1, prominent on mucosal surfaces cuts FAB part from Fc part = ineffective

44
Q

what are the Neisserial IgA proteases virulence-related functions

A

Cleavage of LAMP1 promotes intracellular survival

Acts as a superantigen - massive cytokine release

45
Q

what is IgA protease

A

Gram-negatives belongs to a class of secreted proteins called autotransporters

46
Q

Antigenic variation

A

Expression of antigenically distinct functionally conserved moieties within a clonal population

47
Q

Phase variation

A

Reversible switching between all-or-none (on/off) expressing phase, resulting in variation in the level of expression of one or more molecules between individual cells of a clonal population

48
Q

phase variation examples

A

Streisinger model of slipped strand mispairing

Phase variation mediated by transposons

49
Q

Streisinger model of slipped strand mispairing

A

DNA replication when strands come back together the growing strand can result in addition or removal of one or more repeat units from the daughter duplexes

Simple repeats, typically mono-, di- or tetranucleotides, are liable to slipped strand mispairing

50
Q

Streisinger model of slipped strand mispairing - repeats occur in promoter region

A

can affect the spacing or turn of elements of the promoter (e.g. -10 and -35 regions) and thus the efficiency of the promoter

51
Q

Streisinger model of slipped strand mispairing - repeats occur in ORF

A

changes in repeat number (where the repeat unit does not contain a whole number of codons) can result in placing the region of the gene downstream of the repeat region in or out of frame

52
Q

Phase variation mediated by transposons

A

Transposons are DNA elements encoding their own excision and insertion at specific sequences within DNA molecules. Insertion within a gene can disrupt it
In most cases transposons do not excise themselves precisely and can not mediate phase variation

53
Q

what can switch off capsule expression

A

Capsule expression can be switched off by transposition

54
Q

how does transposition switch off capsule expression

A

Insertion sequences responsible for loss of capsule expression in carriage isolates by insertion into siaA and siaD genes (which are necessary for capule production)

55
Q

Gene conversion in Neisseria meningitidis

A

Gene conversion responsible for antigenic variation particularly of the pilus
pilE – pilus Expressed locus
Many pilS loci in genome – S =silent (not expressed) can recombine with pilE = new variants
Type IV pilus can take up DNA and can then recombine it

56
Q

how is meningococcal immune evasion is triggered

A

high temperature

57
Q

what are the 3 independent RNA thermosensors in 5’ region of genes involved in immune evasion

A

Capsule biosynthesis
Factor H-binding protein
LOS sialylation

58
Q

what does gonococcal infection elicit

A

TGF-β-mediated suppression of Th1 and Th2 responses (cell-mediated responses and antibody reponses)

59
Q

what do gonococcal lack

A

No capsular polysaccharide or fHb – don’t normally see disseminated gonococcal disease is rare

Infection and Immunity (29 decks)

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