Haemophilus, Bordetella, Flashcards
Two main classes of H. I.
Encapsulated (type able)
Non-encapsulated (non-type able) refers to serotype testing
Ecapsulated H.i.
Respiratory tract infections
Bacterial meningitis, mainly in children and elderly
Before vaccine Hib was leading cause of bacterial meningitis
High death and complication rate
Unencapsulated H.i.
Respiratory infections
Ear aches
Disseminated disease in comprimised indv
H.i Capsule
Made from carbohydrates
Type B most important,
Contributes to VIRULENCE (allows to get to meninges)
- antiphagocytic
- prevents complement binding
H.i. Epidemiology
Reservoir in nasopharynx of human only
75% indv carry H.i.
Opportunistic
Hib Disease Course
Acquired through aerosol
Nasopharyngitis and otitis media
- > baceteremia -> meningitis
- > epiglottitis
- > joint infection
- > cellulitis
Hib Pathogenisis
No known exotoxins, (maybe IgA protease)
Adhesins
Endotoxins (LPS)
- initially covered by capsule, camouflage
- bacteria takes host choline and puts on LPS, more camouflage
Hib immunity
Passive immunity in very young
-maternally acquired
Active immunity in the absence of vaccine
- at about 3-4 years
- usually induced by asymptomatic infections
Hib vaccine
Conjugate capsular vaccine
carbohydrates linked to increase effectivity
Recent inc in non Hib Hi infections, vaccinated indv may have reduced protection against other strains?
Hib treatment
Different antibiotics dependent on specific disease
Low mortality if caught early
Steroid use reduces damage to inflammation
Unencapsulated Hi (NTHi) targets
Restricted to resp tract and ear
- nasopharynx
- otitis
NTHi in adults
Usually occurs in pts with underlying respiratory problem
Needs predisposing factors
NTHi virulence
Adhesins
Both intra and extracellular
-keep in mind for treatment
NTHi immunity
No vaccine
Treatment of NTHi
Antibiotics (mainly amoxicillin)
Hard to fight biofilms
H.i diagnosis (growth and metabolism)
Facultative anaerobe
No fermentation pattern
Fragile, easily killed?
Not grow on blood agar
Fastidious, needs lots of growth factors (x and v)
Bordetella Pertussis
Small Gram-negative coccobacillus
Obligate aero be
BP disease course
Transmission aerosol droplets
Stage 1 mild respiratory symptoms
Stage 2 narrowed glottis and cough attacks
-infants have small airways and died of hypoxia
BP Infection Steps
- Introduction via water droplets
- Interactions with ciliated epithelial cells in the trachea and nasopharynx
- Adherence
- Local multiplication (no dissemination)
- Toxin production
- Evasion of host defenses (stops beating cilia)
- Transmission
BP virulence
- Pertussis toxin
- Adenylate cyclase toxin
- Dermonecrotic toxin
- Tracheal cytotoxin
- LPS
Pertussis Toxin
Leads to increased level of cAMP
-> inc insulin, sensitization of histamine,
Dermonectrotic toxin
causes local necrosis and inflammation
Through actin polymerization
Tracheal cytotoxin (TCT)
Peptidoglycan fragment
Kills tracheal epithelial cell
Ciliostasis (reduces clearance)
BP virulence summary
Ciliary stasis
Adhesins
Toxins
BP vaccine
Subunit/component vaccine
More effective than old whole cell vaccine (and less side effects)
DP diagnosis
Classic cough – Isolation of the organism – Lymphocytosis (increased lymphocytes in blood) – History of contacts
Detection
PCR (only for b pertussis)
Treatment of BP
Therapeutic (like oxygen)
Antibiotics
Corynebacterium
Pleomorphic
Gram positive rods (non spore forming)
Aerobes
Corynebacterium diptheriae
Human only host
2-5 day incubation
Local inflammatory response skin or sore throat and fever
Pseudo membrane and bull neck (swollen Lymph nodes)
Diptheria toxin (general)
Cells localized but toxin becomes systemic
Lethal to eukaryotic cells
-Heart, kidney, nervous system most susceptible
Blocks protein synthesis
Diagnosis and treatment of CD
Need special media (forms metachromatic granules)
Detect toxin: PCR (or Elek test)
Antitoxin available from CDC
Antibiotic therapy
Dip immunization
Depends on immunity (ab) to TOXIN
Led to vaccine that uses toxin
Legionella pneumophila
Gram negative rod
Pleomorphic
Leg epidemiology
Grows wherever water found (can live in amoebae)
-can forms biofilms, difficult to remove
Air ventilation system, water towers, etc
Legi symptoms
Atypical pneumonia
-diffuse localization in lung
Legi Disease
Disseminated, systemic disease
Legi pathogenicity
Airborne transmission (not person to person)
Usually presents as “cold”
Summer and early fall (more air conditioning)
Legi targets
Macrophages and alveolar cells
Induces apoptosis
Legi diagnosis
(Fastidious, grown on charcoal yeast)
Direct fluorescent ab test in sputum usual method
Antigens in urine
Legi prevention
Proper water handling
High temp, chlorine, cleanings
Mycoplasma (general)
Infects upper respiratory tract
Smallest bacterium and smallest genome
NO PEPTIDOGLYCAN CELL WALL
->Pleomorphic
Mycoplasma survival strategy
Variable lipoproteins and lipid anchors stabilize
Increases cell membrane rigidity (by incorporating cholesterol)
Mycoplasma epidemiology
“Walking pneumonia”
Possibly up to 50% of summer pneumonias
-frequency varies by year
Outbreaks in close contact groups
Hits adolescents and college kids
Mycoplasma symptoms
Atypical pneumonia
- diffuse throughout lung
- doesn’t respond to Penicilin
Weakness, fever, cough
Mycoplasma Diagnosis
Clinical picture
PCR detection
Cold agglutination test (present in half pts)
Haemophilus influenzae general characteristics
Small, gram-negative, pleomorphic, non-motile
