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FIM > 17. Haemophilius, Bordetella, Legionella > Flashcards

17. Haemophilius, Bordetella, Legionella Flashcards

1
Q

Haemophilus species and what they cause

A
  1. H. influenzae
    -respiratory tract infection
    -meningitis
    -bloodstream infection
  2. H. ducreyi
    -chancroid (a sexually transmitted infection)
  3. H. aphrophilius (now A. aphrophilus)
    -HACEK endocarditis
    H.influenza and H.aphrophilus colonise the upper respiratory tract
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2
Q

Where is H.influenzae found

A

nasopharynx of healthy adults and children

-capsulated or non-capsulated

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3
Q

Encapsulated H.influenzae type b strains

A
  • severe invasive disease
  • especially in young children in countries that do not include Hib vaccine in the infant schedule
  • hyposplenism/asplenism
  • congenital or acquired immunological deficiencies
  • e.g. depletion of CD4 T-cell in HIV, complement deficiency
  • has a anti-phagocytic polysaccharide capsule: PRP (polyribosylribitol phosphate) that:
    a) makes it resistant to phagocytosis by PMN leukocytes in the absence of specific anti-capsular antibody
    b) reduce the organism’s susceptibility to the bactericidal effect of serum
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4
Q

Non-encapsulated H.influenza

A

mainly associated with respiratory/mucosal infection

  • acute exarcebation of chronic bronchitis
  • otitis media, sinusitis, pneumonia
  • may cause invasive disease
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5
Q

Capsulated H.influenza

A

divided into different strains using antisera against specific capsular polysaccharides

  • 6 type: a-f
  • b: Hib - most commonly associated with systemic disease
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6
Q

Virulence factors of capsulated H.influenzae

A
  • capsule
  • pili/fimbrae
  • outer membrane proteins - adhesion proteins
  • lipooligosaccharide
  • antimicrobial resistance
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7
Q

Pathogenesis of infection with capsulated H.influenzae

A
  1. inhalation of respiratory droplets or direct contact with respiratory secretions
  2. colonization of oropharynx
  3. fimbriae/pili attachments to respiratory epithelial cells
  4. capsule is the critical virulence factor that facilitates invasion and haematogenous dissemination
  5. capsular and lack of anti-PRP antibody complement activation of endotoxin acting on the lipopolysaccharide
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8
Q

Virulence factors of non-capsulated H. influenzae and their biological role

A
  • fimbrae - attachment to pharyngeal cells
  • opacity-associated protein (Aap) - attachment to pharyngeal cell
  • IgA protease - inactivate IgA in the nasopharynx
  • lipooligosaccharide - endotoxin activity when the organism are lysed
  • antimicrobial resistance (esp. beta-lactamase protein)
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9
Q

Pathogenesis of infection with non-capsulated H.influenzae

A
  1. commonly colonise patients with chronic pulmonary disease (e.g. COPD, cystic fibrosis)
  2. ciliated columnar epithelium is damaged by air pollutants, smoking
  3. damaged cilia or reduction in the number of ciliated cells allow collection/pooling of mucus
  4. biofilm formation
  5. predisposes to invasion by bacteria
  6. preceding or coincident viral infection may also precipitate infection
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10
Q

H. influenzae type B may cause

A
  1. respiratory tract infections in early childhood
    - acute epiglottis
    - pneumonia
  2. meningitis
    - untreated -> very high mortality
    - deafness, seizures and intellectual impairment
  3. septicaemia
  4. septic arthritis
  5. cellulitis (closed, spreading)
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11
Q

Non-capsulated H. influenzae may cause

A
  1. recurrent sinusitis
  2. acute/chronic bronchitis
  3. acute and chronic otitis media
  4. community-acquired pneumonia
  5. invasive infection (less common)
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12
Q

Laboratory features of haemophilus species

A
  1. pleomorphic gram negative bacilli/coccobacilli
  2. stain faintly
  3. facultatively anaerobic
    - max growth in 5% CO2
  4. fastidious
    - require either X factor (haemin) or V factor (NAD) or both
    - both found in chocolate agar
    - H.influenzae require both
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13
Q

Laboratory diagnosis of systemic infections such as epiglottis, bloodstream infection, cellulitis and septic arthritis

A
  1. blood culture
  2. joint fluid (septic arthritis)
  3. aspirate from area of cellulitis
  4. swab for culture and antibiotic susceptibility
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14
Q

Laboratory diagnosis of suspected meningitis

A
  1. blood culture and PCR

2. CSF for microscopy, culture and PCR

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15
Q

Antibiotic treatment for haemophilus species

A
  • naturally resistant to penicillin
  • beta-lactamase producers
  • resistant to amoxicillin
    1. In-patient treatment
  • IV co-amoxiclav (respiratory infection)
  • IV cefotaxime/ceftriaxone (BSI, meningitis)
    2. Out-patient treatment
  • oral co-amoxilav
  • macrolide (e.g. clarithromycin)
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16
Q

What does Bordetella pertussis cause

A

whooping cough (pertussis)

17
Q

What is bordetella pertussis

A

pertussis which is a highly contagious infection of the respiratory tract
-may occur at any age, but most severe in infants

18
Q

What is the virulence factors of bordetella pertussis

A
  1. filamentous haemagglutinin adhesin
  2. pertactin
    - outer membrane protein (P69 protein)
  3. fimbriae
  4. capsule
  5. cytotoxin
  6. pertussis toxin
  7. endotoxin (LPS)
19
Q

Pathogenesis of bordetella pertussis

A
  1. inhalation of droplets
  2. attach to respiratory mucosal cells in nasopharynx and trachea:
    - filamentous haemagglutinin adhesin - ciliated cells
    - pertactin (P69 protein) - tracheal cells
    - fimbriae - ciliated cells
  3. capsule to evade the immune system
  4. toxin to damage host cell
    a) cytotoxin
    - paralyes cilia
    - causes paroxysms of coughing
    b) Pertussis toxin
    c) endotoxin
    - causes disruption of host cell
  5. shed in respiratory droplets with coughing or sneezing
20
Q

Stages of whooping cough

A
  1. Catarrhal stage (1-2 weeks)
    -non-specific symptoms: malaise, rhinorrhoea, mild cough
    -most infective stage
  2. Paroxysmal stage (2-4 weeks)
    -paroxysmal cough - severe, vigorous cough that occur during a single expiration following by vigorous inspiration - whooping sound
    -post-tussis vomiting
  3. Convalescent stage (3-4 weeks)
    -gradual reduction in the frequency and severity of the cough
    Total: 3 months
21
Q

Laboratory features of bordetella pertussis

A
  • very small Gram negative cocco-bacillus
  • 3 distinct serotypes: 1-3
  • aerobic
  • capsulated
  • highly infectious - droplet spread
22
Q

Diagnosis of pertussis

A

Microbiological tests

  1. culture (fastidious organism)
    - aspiration of nasopharyngeal secretions or nasopharyngeal swab - special transport medium - rapid transport to laboratory
    - selective and enriched medium
    - charcoal-blood agar, antibiotics to inihibit normal flora (may take up to 10 days to grow)
    - gram-negatve coccobacilli (tiny)
    - lacks sensitivity
    - blood culture are of no benefit because Bordetella do not enter the bloodstream!
  2. serology
    - anti-pertussis IgG detected on samples taken > 2 weeks after onset of symptoms
  3. nucleic acid amplification tests (NAAT) - PCR on pernasal swab or nasopharyngeal aspirate
    - more sensitive than culture and faster
  4. Other supportive lab test
    - increase white cell count with absolute lymphocytosis
23
Q

Treatment of whooping cough

A
  1. primarily supportive
    - fluid administration
  2. erythromycin/clarithromycin
    - if administered in the catarrhal stage, may elimated disease and prevent transmission
24
Q

Which Legionella species is responsible for most infections

A

Legionella pneumophilia serogroup 1

25
Q

Epidemiology of L.pneumophilia

A

colonisation is enhanced by warm temperature (25-42°C), stagnation, scale and sediment
-infection arises following inhalation of aerosols from contaminated water

26
Q

Virulence factors of Legionella pneumophilia

A
  1. pili
    - adherence
  2. outer membrane proteins
    - adherence
  3. flagellae
  4. enzymes
    - protease, phosphatase, lipase, DNAase, RNAse
    - cell damage
  5. LPS
    - endotoxic activity
  6. phagocytosis or invasion?
    - L. pneumophilia is an intracellular pathogen, the bacteria avoid phagolysosome fusion and replicate within alveolar macrophages and epithelial cells in a vacuole
    - virulence proteins secreted into the vacuole enable survival and replication
27
Q

Clinical features of legionnaires’ disease

A
  • male:female 2:1
  • aged 50-60 years
  • pontiac fever: brief flu-like illness
  • cause of community-acquired pneumonia
  • incubation period is 2-10 days
  • abrupt onset of fever, chills, dry cough, headache
  • may get multi-organ disease of GIT, CNS, liver
  • renal involvement result in proteinuria, haematuria and hyponatraemia (due to renal tubular acidosis)
  • higher mortality in patients with severely depressed cell-mediated immunity (transplant recipient) or if treatment is delayed
28
Q

Predisposing factors to severe disease include

A

a) old age
b) cigarette smoking
c) immunosuppression

29
Q

Diagnosis of legionnaires’ disease

A
  1. Culture
    - require specific growth media
    - e.g. buffered charcoal yeast extract (BCYE) agar and antibiotics to which the organism is resistant to inhibit growth of other bacteria
    - sputum/tracheal aspirate/bronchoalveolar lavage
    - colonies appear after 2-3 days incubation
  2. Urinary antigen detection
    - rapid
  3. Serology - antibody detection
    - antibody is detectable about the 8th day of the illness
    - 4 fold increase in the level of antibodies produced between serum taken at acute stage of illness and repeated up to 2 weeks later
  4. Immunofluorescent microscopy
    - difficult to see L.pneumophilia by gram stain
    - high specificity but lack sensitivity
30
Q

Treatment of Legionnaires’ disease

A
  • beta lactam agents are not effective
  • drugs with good intracellular penentration is required
  • respiratory fluroquinolones, e.g. levoflaxacin
  • macrolides, e.g. azithromycin or clarithromycin
  • may combine with rifampicin in the seriously ill

FIM (18 decks)

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