Major gram neg bacterial pathogens Flashcards

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1
Q

Name the gram negative surface antigens

A

H-antigen = flagellum
K-antigen = capsule
Peptidoglycan
O-antigen = outer membrane lipopolysaccharide (LPS)

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2
Q

Both gram neg and gram pos bac have a capsule - what is it’s purpose?

A

Protection and help it stick down to surface

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3
Q

What does PS o-antigen do?

A

Deters complement c567 - Membrane attack precursors (MAC)

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4
Q

Structure of gram neg bac?

A
2 membranes
OM connected to LPS layer
Thin PG layer
Does NOT retain gram stain = pink
Outer layers and released are LPS major antigens
LPS and capsule help immune evasion
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5
Q

Give examples of medically important gram neg bac

A

Neisseria - meningitis and gonorrhoea
Haemophilus influenza - meningitis, pneumonia
Pseudomonas aeruginosa - burn infecs and lung infecs of CF pts
Yersinia pestis - plague
Bordetella - whooping cough
Legionella - legionnaires disease
Treponema pallidum - syphilis

GI:
Salmonella spp - gastroenteritis
Shigella spp - gastroenterits
Virbio cholera - cholera
Helicobacter pylori - stomach ulcers
Campylobacter jejuni - food poisoning
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6
Q

What is neisseria spp?

A

Gram neg diplococci

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7
Q

Name the pathogens of neisseria spp and what do they do?

A

N-meningitidis;

  • Meningitis/meningococcal septicaemia
  • Infec of CSF and meninges
  • Commensal carriage in pharynx/nasopharynx
  • Capsular, serotyping based on polysaccharides

N/gonorrhoeae;

  • Gonorrhoea
  • STI, genital and oral infec
  • Neonatal transfer - eye infecs
  • Lipopolysaccharide capsule often sialylated

Both fastidious - Growth (Heated blood [chocolate}) + CO2

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8
Q

What is meningitis?

A

Inflam of the meninges
Bac replicates in cerebrospinal fluid, produce lots of protein = meninges inflamed = pressure on brain = aching
Also gives rash, leg pain, cold hands and feet, vomiting, confusion

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9
Q

What is N.meningitidis carriage rate? When may the carriage rate increase?

A

10-25% nasopharynx commensal carriage rate

During disease = carriage rate may rise to 90%

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10
Q

What do N.meningitidis’ serogrpoups depend on? Name the 5 serogroups

A

Dependent on polysaccharide capsular antigen
A, B, C, Y, W135 - account for almost all cases worldwide
UK - 90% serogroup B
A, C and W135 comprise others

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11
Q

N.meningitidis pathogenesis - how does it enter the body?

Name 1 virulence factor of it and the most important Ab in protecting against ti

A

Directly to subarachnoid space or through nasopharyngeal mucosa to enter the bloodstream
Mucosal spread - kissing

Protease IgA for serum resistance
Bactericidal antibody against capsule is most important protective factor

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12
Q

N.meningitidis epidemiology?

A

Outbreak in winter
2000 cases and 80 deaths in UK per yr
2/3 of cases occur in 1st 5yrs of life
Peak prevalence = 1st yr of life, 2nd peak = 16-23
Frequent in young adult pop - uni, military

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13
Q

Where is the highest occurrence of meningitis?

A

In a region of sub-saharan Africa - meningitis belt

Infec of up to 10% of pop - mainly serogroup A

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14
Q

How to diagnose meningitis?

A

CSF - many PMNLs, presence of bac - diplococci
Blood culture;
- Sub-culture on chocolate agar
- Sugar fermentation tests - maltose and glucose positive (red to yellow)
- Oxidase positive (purple)

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15
Q

How to treat meningitis?

A

Penicillin, cefotaxime

  • followed by eradicative treatment (rifampicin or ciproflaxacin often with corticosteroids
  • Vaccines available for group A, C, Y and W135
  • 4CMenB vaccine in 2015 for infants and at-risk groups
  • Expensive
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16
Q

What does haemophilus influenzae (gram neg cocco-bacillus) cause? Complications? Survival percentage?

A

Non-invasive disease: otitis media, sinusitis (2-4yrs old)

Cause septicaemia, pneumonia and meningitis

  • Meningitis and pneumonia (4 months to 2 yrs old)
  • Invasion - penetration of submucosa of nasopharynx
  • Complications; epiglottitis, bacteraemia, cellulitis
  • 15-35% survivors with disability
17
Q

H.influenzae pathogenesis?

A

6 capsular types (a-f`)
Some strains non-capsulate (commensals)
- capsular major virulence factor avoidance of c3b binding
- 99% invasive disease caused by type b capsular type

Commensal carriage of type b 5-10% nasopharynx, non-capsular 25-80%

18
Q

H.influenzae epidemiology?

A

Serious systemic disease in children
300,000 deaths per yr in 2008 - mainly in dev countries
Outbreaks in nursery

19
Q

H.influenzae vaccine?

A

Hib vaccine given at 2, 3, 4 months
Cost of vaccine has been reduced
Increasing antibiotic resistance = vaccine needed more

20
Q

How to diagnose presence of H.influenzae?

A

Sputum, throat swabs, blood culture

Chocolate gar 5-10% CO2

21
Q

What does haemophil need for growth?

A
Factor X (haemin) or V (NAD or NADH)
H.influenzae = needs both X and V
H.ducreyi needs X
22
Q

How to diagnose meningitis - H influenzae?

A

Antigen detection/PCR

23
Q

How to treat H.influenzae?

A

Cefotaxime
Non-invasive disease - amoxycillin
Chemoprophylaxis for contacts - rifampicin

24
Q

What causes the plague?

How is it spread?

A

Yersina pestis

Infected flea bites human

25
Q

Yersinia pestis virulence factors?

A

Gram neg so LPS
Contains 3 large virulence plasmids
Encode type III secretion needle for injection of toxins into host cell: suppress immune response, promote bacterial invasion and survival inside host cells
pCPI - plasminogen activator: helps dissemination (spread) in host - degrades complement components C3b and C5a
pMTI - antiphagocytic capsule and TTSS host evasion

26
Q

Mortality rates of the plague?

A

100% for pneumonic plague, 50% for bubonic plague

Killed 25% of european population, 30% in England

27
Q

How was spread of the plague controlled?

A

Quarantine - on who entered, food dropped at perimeter

28
Q

How is the plague treated today?

A

Streptomycin or tetracycline
Formalin-killed vaccine
Some outbreaks in 3rd world

29
Q

Give an example of an opportunistic pathogen

A

Pseudomonas aeruginosa

30
Q

Pseudomonas aeruginosa features?

A

Common environmental isolate and human commensal
Gram neg, motile rod motile, aerobic
Often multiply antibiotic resistant
Major causes of infec after burns
Many extracellular proteases breakdown tissues
Well adapted to warm moisture in a burn wound
Can lead to septicaemia - Ecythma gangrenosum lesions
Major killer of cystic fibrosis pts - who become chromosomally infected

31
Q

What is ESKAPE?

A

Group of most antibiotic resistant pathogens with highest risk in clinical and hospital situations
4/6 = gram neg = biggest worry as increasingly resistant to last drugs of resort - Carbepenam resitant strains = most scary

Enterococcus faecum (gram pos)
Staphylococcus aureus (MRSA) (Gram pos)
Klebsiella pneumoniae (gra neg)
Acinetobacter (gram neg)
Pseudomonas (gram neg)
Enterobacter (gram neg)