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Sem2: MDSA30160: Cardiorespiratory Disease > L15 Haemophiles, Bordetella, Legionella > Flashcards

L15 Haemophiles, Bordetella, Legionella Flashcards

1
Q

Hemophilus microbiological characteristics:

Gram-positive/negative?

Anaerobic/Aerobic?

Culture?

Other?

A
  • small Gram-negative coccobacilli
  • facultative anaerobe
  • Cultured on Chocolate Agar
  • require growth factors to grow on culture media

X factor

  • supplied by heat-stable iron-containing pigments haemin, haemoglobin, haematin
  • concentrated within erythrocytes

V factor

  • supplied by nicotinamide adenine dinucleotide (NAD), nicotinamide adenine dinucleotide phosphate (NADP), or nicotinamide nucleoside (NN)
  • present in erythrocytes, lysis required for release
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2
Q

Haemophilus Influenzae Description?

Unique Characteristics?

Transmission/Colonization?

A

small Gram-negative anaerobic coccobacilli that requires X and V factors for growth on Chocolate Agar

Exhibits satellitism: pinpoint colonies in zone of haemolysis surrounding S. aureus streak

Nontypeable: strains of H. influenzae that lack a capsule are non-reactive with typing antisera raised against each of the six capsules

Spread by inhalation of respiratory droplets or direct contact with secretions, colonizes nasopharynx and conjunctiva

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3
Q

Haemophilus Influenzae Virulence Factors (5)

A
  1. Polysaccharide Capsule: Resistance to phagocytosis and bacteriolysis
  2. Pili: Attachment to epithelial cells
  3. IgA Protease: Inactivates IgA and facilitates evasion of local immune response
  4. Outer Membrane proteins: Attachment
  5. LPS: Aids in invasion
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4
Q

Clinical Manifestations of Haemophilus Influenzae

A

Invasive: Colonization=> penetration of nasopharyngeal mucosa => bloodstream

Non-invasive: Physiological or anatomical abnormality

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5
Q

Treatment of Haemophilus Influenzae?

A

Treatment

Serious Infection: Third-generation cephalosporins (Ceftraxone or Ceftaxime)

Non-Typeable: amoxicillin, amoxicillin-clavulanic acid, fluoroquinolones, newer macrolides (e.g., azithromycin, clarithromycin), and various extended-spectrum cephalosporins.

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6
Q

Prevention of Haemophilus Influenzae?

A

Hib vaccine:

–all infants at 2, 4 and 6 months with a booster dose at 13 months

–unvaccinated aged 1 to 10 years should be given 1 dose

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7
Q

Bordetella microbiological characteristics?

Gram-positive/negative?

Anaerobic/Aerobic?

Culture?

A

Bordetella microbiological characteristics:

  • small gram-negative coccobacilli
  • strictly aerobic
  • fastidious–special media required
  • Bordet-Gengou agar
  • charcoal blood agar, made selective w/ antibiotics (Regan-Lowe media)
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8
Q

Bordetella Pertussis description?

Transmission?

A

spread by droplets, highly contagious

Pre-vaccine era nearly all children infected between the ages of 1 and 5 years.

adults with waning vaccine-induced immunity are increasingly infected

often goes undiagnosed because infection may be atypical.

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9
Q

Bordetella Pertussis Virulence factors (7)

A
  1. Pertussis Toxin (PT)
    1. AB Toxin activates adenyl cyclase => increased cAMP
    2. Promotes lymphocytosis
    3. Hypoglycemia due to islet cell activation
    4. blocks immune effector cells
    5. increased Histamine sensitivity
  2. Pertacin (PRN): outer membrane protein involved in adhesion
  3. Pili
  4. Filamentous Hemagglutinin (Fha): attachment of B Pertusus to cuilliated rtespirator epithelia
  5. Lipooligosachirade
  6. Adenylate Cyclase Toxin: Enters leucocytes interfering w/ their function
  7. Tracheal Cytotoxin: Causes allostasis, inhibits DNA synthesis killing ciliated epithelial cells
  8. Dermonecrotic Toxin: Causes vascular smooth muscle contraction resulting in focal ischemic necrosis
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10
Q

Mechanisms of Bortetella Perusis’s Pertussis Toxin?

A
  1. Pertussis Toxin (PT)
    1. AB Toxin activates adenyl cyclase => increased cAMP
    2. Promotes lymphocytosis
    3. Hypoglycemia due to islet cell activation
    4. blocks immune effector cells
    5. increased Histamine sensitivity
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11
Q

Stages of Bordetella Pertussis Infection?

A

Catarrhal stage (1 –2 weeks)

–profuse rhinorrhoea, malaise, low-grade fever, cough

–indistinguishable from other URTI

Paroxysmal stage (1 –4 weeks)

–cough paroxysm consists of a series of short expiratory bursts,

=> followed by a characteristic inspiratory whoop

=> Vomiting frequently follows whoop

– Miserable and exhausted.

Convalescent stage (3 –4 weeks)

–decrease in intensity of cough and frequency of paroxysms

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12
Q

Complications of Bordetella Pertussis

A

Complications

  • secondary bacterial infections such as pneumonia and otitis media.
  • increased intra-thoracic pressures during coughing can result in:

Subconjunctival hemorrhage

Cerebral haemorrhages

Pneumothorax

umbilical and inguinal hernias

rectal prolapse

•convulsions, encephalopathy

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13
Q

Diagnosis of Bordetella Pertussis

A

Culture - sample from nasopharynx

PCR

Serology - later stages of disease, sample 2-8 weeks after cough onset

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14
Q

Management of Bordetella Pertussis

A

Management

Supportive care - Oxygen and hydration

Specific therapy - Erythromycin, clarithromycin or azithromycin

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15
Q

Prevention of Bordetella Pertussis

A

Pertussis vaccine

•Whole-cell pertussis vaccine (wP)

–contain a suspension of killed B. pertussis

•Acellularvaccine (aP)

–purified pertussis antigens (Fha, PT toxoid, pertactin, pili)

–significantly less local and systemic side-effects

Indication for Vaccine:

–all infants at 2, 4 and 6 months with a booster at 4-5 years

–further booster (Tdap w/low dose acellular pertussis) at 11-14 years

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16
Q

Bordetella Pertussis Pathogenesis?

A

Pathogenesis:

B. pertussis Inhalation

=> adheres to ciliated epithelium of trachea and bronchi (tropism)

=>bacilli begin to multiply, producing toxins

=> organisms remain localized on respiratory epithelium and DO NOT INVADE

17
Q

Legionella pneumophila Description:

Gram-positive/negative?

Anaerobic/Aerobic?

Culture?

Other?

A

Legionella pneumophila

•Gram-negative bacilli (unencapsulated- stain poorly with Gram stain)

•strict AEROBE

•does not grow on standard media. Needs buffered charcoal yeast extract (BCYE) supplemented with l-cysteine, α-ketoglutarate and ferric ions.

Other: consists of 15 serogroups, serogroups 1, 4, 6 predominant–serogroup 1 causes 70-90% of cases

18
Q

Epidemiology of Legionella pneumophila

A

aquatic environment

Natural: surface waters of rivers, lakes, streams and thermally polluted waters

Man-Made: cooling towersm hot water tanks, air conditioners, whirlpool spas

Growth aided by:

–co-existing micro-organisms, which provide nutrients

–free-living amoebae, in which Legionella reside and multiply

– Found in BIOFILMS => less susceptible to chlorine

dissemination from environment to host

Aerosolization of water

Aspiration of contaminated water

Direct inoculation (surgical wound infection)

NO PERSON TO PERSON TRANSMISSION

19
Q

Legionnaire’s Disease pathogenesis?

A

L. pneumophila’s ability to grow in macrophages is central to pathogenesis.

intracellular multiplication

=> neutrophils, macrophages, and erythrocytes infiltrate alveoli

=> capillary leakage

=> edema

cell-mediated immunity primary host defense, humoral immunity secondary

20
Q

Clinical Manifestation of Legionnaire’s Disease

A

Extrapulmonary common

1. neurological Headaches, Confusion, Obtundation (slowed level of response), Seizures

2. gastrointestinal, diarrhoea, nausea and vomiting, abdominal pain

Usually unilateral, lower lobe predominance=> progresses to bilateral

pleural effusion (1/3) and cavitations in immunocompromised

progresses despite appropriate antibiotic therapy, may take up to 4 months to resolve

21
Q

Diagnosis of Legionnaire’s Disease

A

Legionnaire’s Stains poorly with Gram Stain

Culture is GOLD STANDARD

  • Special complex needed (Buffered Charcol Yeast Extract)
    • L-cysteine and ferric ions support growth
    • antibiotics prevent overgrowth of other organisms
    • Dyes impart color on legionnella
  • Colonies take 3-5 days to apear
    • GROUND GLASS apperance
    • white, gray, pale blue, purple
22
Q

Treatment of Legionella?

Duration?

A

Effective antibiotics are capable of achieving high intracellular concentrations:

Macrolides (clarithromycin and azithromycin)

Fluroquinolones (Severe disease IV initially, ORAL after good response)

Tetracyclines

Rifampicin

Beta-lactams and aminoglycosides have activity against Legionella in vitro but are not clinically effective

Duration of therapy:

–2 weeks for patients with mild disease

–at least 3 weeks for severe disease or immunocompromised patients

23
Q

When to Suspect Legionnaires?

A
  • Gram stain of respiratory samples w/ many polymorphonuclear leukocytes with few or no organisms
  • hyponatremia (Low blood sodium)
  • pneumonia w/ prominent extrapulmonary manifestations (diarrhoea, confusion)
  • failure to respond to administration of beta-lactams or aminoglycosides

Sem2: MDSA30160: Cardiorespiratory Disease (24 decks)

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