Haemophilus and Bordetella Flashcards Preview

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Flashcards in Haemophilus and Bordetella Deck (25):

Whare are similarities betweeen Haemophilus and Bordetella?

How are they transmitted?

What is a common side of infection?

Are vaccines available?

How do you treat them?

Both human restricted, fastidious in culture, require factors X and V in vitro.

Transmitted by respiratory droplets,

mostly-pediatric contagious respiratory infection,

vaccines available,

treat with antibiotics and supportive care


What are the bacterial characteristics of Haemophilus?

Gram(-) pleomorphic – may appear as cocci, rods, mixture on microscopy.


Encapsulated H. influenzae (NOT A VIRUS) exhibit which bacteriologic features?

is typically asymptomatic or pathogenic?

Virulence factors?

Does vaccine exist?

What is the worse complication?

What is the pathogenisis (trasmission, site of infection, dissemination)?

What are the most common disease features?

Gram(-) pleomorphic – may appear as cocci, rods, mixture on microscopy.

Encapsulated H. influenzae (Hib) are more pathogenic than unencapsulated

Capsule, IgA protease, pili, adhesins

covered by vaccination,

cause lethal meningitis.

Transmitted by respiratory droplets,

Bacteremia quickly follows upper respiratory infection and underlies all invasive disease:

meningitis, cellulitis, epiglottitis, septic arthritis


What is different about unencapsulated H. Influenzae from encapsulated?

Virulence factors?

Unencapsulated H. influenzae (NTHi) are less pathogenic but not covered by vaccination.

May be normal flora.

Lack capsule but still have IgA protease, pili, adhesins like Hib.

Cause neonatal and postpartum sepsis,

CF pneumonia,

systemic complications after untreated local mucosal infections, particularly with respiratory or immune predisposition.


Describe B. pertussis

Vaccine coverage?

highly contagious short Gram(-) rod, incidence and mortality increasing because of inadequate vaccine coverage. Acellular vaccine used in US has shorter-lived protection than killed-cell, used abroad.


What is characteristic about B. pertussis?

Filamentous hemagglutinin attaches,

pertussis toxin is an exotoxin that causes ciliary stasis and death of ciliated cells → cough for contagion.

No bacteremia, prognosis good.


What is characteristic of whooping cough? what causes it?

Whooping cough is prolonged (~3mo) even with drug treatment,

B. pertussis

dangerous with underlying conditions,

leukocytosis on bloodwork.

Difficult for


What is the treatment for B. pertussis?

Macrolides prevent the disease from progressing and transmitting but do not spontaneously heal the respiratory lining


culturing of B. pertussis involves what? Source of sample
What growwth medium
How long does cutlure take?
How sensitive is culture?

difficult to culture but can from nasopharyngeal swabs or aspirate on Regan-Lowe or Bordet-Gengou agar during Stage 1 or 2, but grows very slowly, and

may be negative if patient is immunized or already on antibiotics


adults particularly if vaccinated against B. pertussis are most likely to have:

Won't necessarily have:

Primary symptom is extremely prolonged upper respiratory infection with “100-day cough”

“Whoop” may be absent
Leukocytosis may be absent


What are the 3 stages of B. pertussis symptoms?

Stage 1 (2wks): Catarrhal: Nonspecific upper respiratory symptoms: congestion, sneezing, rhinorrea, maximally contagious

Stage 2 (2 wks): Paroxysmal: Intense coughing
Cough has characteristic pattern:
∙ Series of hacking coughs
∙ Copious mucus production
∙ Inspiratory “whoop” as air rushes in past narrowed glottis
∙ CNS anoxia and exhaustion may appear but are not lethal
∙ Infants turn blue, children may turn red and vomit

Stage 3 (2mo): Convalescence: Fatigue and chronic cough


What are the complicating co-morbities for B. pertussis?

prematurity, cardiac, pulmonary, neuromuscular, neurologic disease

In infants, pneumonia and oxygen deprivation complicate
Secondary pneumonia may be lethal

Bacteremia does not result: symptoms are mostly toxigenic

Prognosis is good, complications minimal, if patient >6mo w/o predisposing complications


What bacteria?

Small encapsulated aerobic Gram(-) rod (coccobacillus)
Transmitted by respiratory droplets
Causes whooping cough, primarily in infants

B. pertussis


What do close contacts of an invasive H. influenzae disease get given as prophylactic?



What is the vaccine for H. influenzae made from?

Capsular polysaccharide of type B conjugated to diphtheria toxoid or other carrier protein (Hib)


What treatments are used for H. influenzae meningitis?

Epiglottitis: maintain airway (intubation or tracheostomy), same antibiotics above

Otitis media: amoxicillin

Meningitis: Initial Treatment: ceftriaxone
Meningitis in children >2mo: add Dexamethasone 
May change as results of antimicrobial sensitivity testing come in
Ongoing supportive care likely to be needed after meningitis

Upper-respiratory: amoxicillin+clavulanate or trimethoprim+ sulfamethoxazole

Epiglottitis: maintain airway (intubation or tracheostomy), same antibiotics above

Otitis media: amoxicillin

Cellulitis, Pericarditis, Septic Arthritis:
Surgical drainage in addition to choice of trimethoprim-sulfamethoxazole, cefuroxime axetil, cefixime, clarithromycin, azithromycin, or fluoroquinolones


What would bloodwork show for H. influenzae septic arthritis? Meningitis?

Septic arthritis: Bloodwork shows elevated erythrocyte sedimentation rates and C-reactive protein levels

Meningitis: CSF contains neutrophils, decreased glucose, increased protein, capsular antigen. Also positive gram stain if not yet on antibiotics.


Diagnosis for H. influenzae?

Culture on chocolate (heated-blood) agar with and without factors X and V
Growth only with factors usually suffices for diagnosis
Serotype by quellung reaction (if you give antiserum so specific serotype it makes the capsule baloon)


bacteriology for H. influenza

(gram -/+)?
Spore forminng?
Growth medium?
Major groups?

Small Gram(-) pleomorphic rod (coccobacillus)
Non spore forming
Grows on lab media only with addition of factors X (heme) and V (NAD): extracts of red blood cells for “blood loving” bacteria
Transmitted by respiratory droplet or contact
Encapsulated or unencapsulated are major groups


Hib is what?

What are the features?
Vaccine target?

H. influenza type B

Of all Haemophilus:
High-pathogenicity strains have polysaccharide capsule
Six serotypes (capsule types); type B (Hib) causes the most severe disease (meningitis, pneumonia, septic arthritis)
Hib capsule of polyribosyl ribitol phosphate (PRP) is target of vaccine

Asymptomatic carriage of Hib is rare (


What is NTHi?

Unencapsulated H. influenza strains (NTHi) may cause local mucosal infections, can spread if untreated, not covered by vaccine


What is the function of the capsule in Hib

immune evasion


Pathogenisis of Hib

initial protective virulance factor for Hib?

Evasion? dissemination?

Determinant of severity?

Most serious complications?

Host defenses against Hib?

Duration of disease?

Colonization facilitated by IgA protease: clears IgA from respiratory mucosa

Once established in respiratory system (clears IgA and capsule protects against macrophages), invades bloodstream, causes invasive disease.

Magnitude and duration of bacteremia determine the severity of the illness.
Magnitude and duration of bacteremia determine the severity of the illness.
Magnitude and duration of bacteremia determine the severity of the illness.

Meningitis (usually type B), unvaccinated untreated mortality 90%
50% of survivors have neurological sequelae (deafness, developmental delay)

Host defense by complement and anti-capsule antibody
Vaccination against capsule blocks and reverses infection at early bacteremia stage

Most infections in children 6mo-6yr

(peak 6mo-1yr)

b/c Maternal antibody wanes
Child can’t yet raise strong response, gets disease

Disease may recur until effective memory response ~age5

Rare in patients >6yrs unless immunocompromised


NTHi Pathogenesis

virulance factors?

common complications?

Lacks the capsule needed for high pathogenicity, but still has the pili, attachment proteins, and IgA protease

may cause local mucosal infections, can spread if untreated

Pneumonia w/ biofilm formation in cystic fibrosis patients

septic arthritis after untreated mucosal infection
Neonatal sepsis, maternal sepsis after vaginal delivery if NTHi normal flora


What does Hib cause?

Meningitis, cellulitis, otitis media, sinusitus, epiglotitis, spetic arthritis

also sepsis, pneumonia, pericarditis, osteomyelitis