Respiratory Bacteria Flashcards
Bordetella Pertussis
Morphology:
_Small Gram Negative Coccobacilli
Resemble H. influenzae
Diagnosis (Steps):
1) Isolation: Nasopharyngeal Secretions or Swabs
2) Culture: Charcoal Media
(Enriched Media)
_Or can use Bordet Gengou medium that contains penicillin.
3) Immunofluorescence Stain:
Faintly Staining Gram Negative Rods
(Throat swabs unsuitable b/c the cilia to which the microbe attaches are not located there.)
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Epidemiology:
1) Human-to-Human Transmission:
Via Air Droplet nuclei
2) Highly Contagious
_Infects 90%
_Rapid Secondary Spread @ Family, Schools, Hospitals
3) Adults:
_Mild Disease
= Major Source of Outbreaks in Highly Susceptible Patients
(e.g. Infants)
4) Infants:
_Most Severe Form of Disease
_70% Fatal if younger than 1 yr.
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Pathogenesis:
1) Inhale air droplets
2) Adheres to and Rapidly Multiplies @ Ciliated Epithelial Cells Lining the @ Trachea and Bronchi
3) Release Toxins that Irritate Cells, Causing Coughing:
=> Pertussis Toxin and Adenylate Cyclase:
_Together, Kill Effector Immune Cells
(Neutrophils, Macrophages, Lymphocytes)
Pertussis Toxin is absorbed into bloodstream and spread throughout body.
=> Tracheal Cytotoxin:
_Kills Ciliated Epithelial Cells
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Clinical Findings:
(6-Week Disease, each stage lasting 1-2 Weeks.)
– Incubation Period:
1-2 Weeks
(I) Catarrhal Stage: (Indistinguishable from Common URIs) 1) Mild Cough 2) Sneezing 3) Nasal Congestion 4) Rhinorrhea (Runny Nose) _Highly Infectious, But Not Very Ill! _Most Infectious During this Phase
(II) Paroxysmal Stage:
1) Paroxysms of Intense Coughing,
These Episodes are Followed by
2) Whoop Upon Inspiration
(Due to Narrowed glottis)
(Toddlers and Older Infants)
3) Rapid Exhaustion
(Infants Under 6 months)
(Due to apneic episodes/ hypoxemia)
4) Vomiting
5) Cyanosis
6) Convulsions
_Pneumonia can develop.
_Encephalitis: Rare; Potentially Fatal Complication of.
III) Convalescent Phase:
1) Cough becomes less frequent.
2) Chronic cough
3) No longer contagious.
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Treatment:
1) Erythromycin:
_During Catarrhal Stage
_Ineffective during Paroxysmal phase b/c Toxin is causing the disease at that point.
2) Supportive
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Prevention: 1) DTaP Vaccines: (Diphtheria and Tetanus toxids, and Acellular Pertussis) _Primary Immunization @ 1st year of Life (@ 2, 4, and 6 months) _Booster Shots (@ 15-18 months; 4-6 yrs)
2) Tdap Booster:
_Tetanus toxoid with Lower Doses of Diphtheria and Pertussis.
_@ Every 10 Years
Haemophilus influenzae
Morphology:
1) Small, Gram Negative Pleomorphic
_Short, Coccobacilli @ Acute infections,
_Sometimes in Pairs or Short Chains.
Diagnosis:
= Culture
1) Chocolate Agar Medium,
=> *Requires X Factor (Heme) and V Factor (NAD+)
(Released upon Heating of the Blood; causing change agar to chocolate color)
2) *No Hemolysis on Blood Agar
3) Young Cultures (6-18 hrs) are Encapsulated.
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Epidemiology:
1) Human to Human Transmission:
_Via Respiratory Droplets
2) Normal Flora @ Nasopharynx in 20-80% of healthy ppl
_Most of theses are Non-encapsulated strains.
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Pathogenesis:
1) Adheres to Epithelial Cells via Pili and Outer Membrane Proteins (OMP).
2) Invades between cells via Disruption of Cell-Cell Adhesion Molecules.
3) Capsule Allows Evasion of Phagocytosis by Neutrophils (PMNs)
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Clinical:
INVASIVE Disease:
=> Encapsulated Strains,
Mostly Type B (Hib).
1) Epiglottitis
or
2) Cellulitis
3) Blood Invasion:
=> Occurs in All Hib Ds.
=> Meningitis
Recall that Most Bacteria that cause Meningitis are Encapsulated.
LOCALIZED Disease:
=> Non-Encapsulated Strain from Nasopharynx are Trapped in @ Middle Ear, @ Paranasal Sinuses or @ Compromised Bronchi.
1) Community-Acquired Pneumonia (CAP)
2) Otitis Media
3) Conjunctivitis
4) Sinusitis
5) Bronchitis
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Treatment:
1) 3rd Generation Cephalosporins
_e.g. IV Cefotaxime.
(25% Hib strains are Resistant to Ampicillin)
Prevention:
1) Hib Vaccine to Children
Legionella pneumophila
Morphology:
1) Aerobic Gram Negative Rod (Bacilli)
Isolation:
1) Bronchial Washings
2) Pleural Fluid
3) Lung Biopsy specimens
4) Blood
Diagnosis:
1) Culture: (fastidious)
* *Buffered Charcoal Yeast Agar with alpha-ketoglutarate and iron (BCYE)
=> Antibiotics Can be Added to the Medium to make is Selective for Legionella.
2) Immunofluorescence Stain
3) Gram Stain:
=> **Silver (Fuchsin) as Counterstain!
(Safranin stains it very poorly!!)
(*False Negative on Gram Stain of clinical specimens!! B/c Stains Poorly!)
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Epidemiology:
1) Warm, Moist Environments
2) Inhalation of Aerosols from:
_Contaminated AC
_Shower heads, etc.
3) Affected:
_Highest @ Men over 55
_Immunocompromised / Debilitated
4) Risk Factors: _Smoking _Chronic Bronchitis, Emphysema _Immunosuppressive Treatment _Diabetes Mellitus
5) Note: Most of the organisms are within Phagocytes
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Clinical:
1) Asymptomatic is Common in All Age Groups
2) Pontiac Fever: _Fever _Mild Cough _Malaise _Myalgia _Headache _Short Duration (Influenza-like) (Abrupt onset, 1-2 Days) _Self-Limiting (~ 1 week)
3) Legionnaires' Disease: _*Severe Pneumonia Acute Purulent. (Common Cause of CAP) _High Fever _Chills, Malaise _Non-productive Cough _Hypoxia _Delirium _Diarrhea _Systemic Spread: CNS and GI _Rapidly Progressive
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Treatment:
1) Macrolides (Erythromycin)
2) Quinolones (Ciprofloxacin)
3) Tetracyclines
Klebsiella pneumoniae
Morphology:
1) Gram Negative Rods (Bacilli)
_Encapsulated
Diagnosis:
1) Gram Stain:
2) Culture
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Epidemiology: _Ubiquitous in Nature 1) Reservoir: _Hands of hospital personnel _Normal GI Flora in5% of normal ppl; _Oropharyngeal Carriage (assoc. with endotracheal intubation, impaired host defenses, antimicrobial use)
=> Thus, can be Aspirated, causing infection.
2) Middle-aged and Older Men with Debilitating Diseases:
(e. g. Alcoholics, Diabetes, Chronic bronchopulmonary disease)
3) Nosocomial infections, including invasive devices
_One of Top 10.
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Clinical: 1) Severe Pneumonia: _*Bloody Sputum, Thick **"Currant Jelly" _Destructive, Cavitation. Hemorrhagic, Necrotizing Consolidation of Lung. _High mortality, despite antibiotics.
2) Nosocomial infection
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Treatment:
_ Requires lab test for antibiotic susceptibility.
_Some strains resistant to many hospital antibiotics.
Pseudomonas aeruginosa
Morphology:
1) Gram Negative Rods (Bacilli)
2) Obligate Aerobe
3) Encapsulated (some strains)
4) Motile
Diagnosis: 1) Culture: => **Does NOT Ferment Lactose (Hence, Obligate Aerobe) => Easily Differentiated form the Lactose-Fermenting Bacteria.
_Grows on wide variety of Culture Media.
2) Pigment Production
_Produces pyocyanin (Blue pigment) and pyoverdin (Green pigment)
_These give a Greenish-Blue color on Culture plates and sometimes in Wound infections.
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Treatment:
1) Piperacillin
2) Tobramycin
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Epidemiology:
1) Widespread in Nature
2) Immunocompromised Patients or with Abnormal Host Defenses
_e.g. Biofilm production chronically infects lower respiratory tract in patients with Cystic Fibrosis.
3) Very Common Cause of Nosocomial Infections
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Pathogenesis:
**Opportunistic and Invasive
**Only Pathogenic when Introduced to Areas Devoid of Normal Defenses.
A-B Exotoxin
(B subunit = Binding)
(A subunit = Active)
1) ExoB binds to cell membrane
2) ExoA is released into cell to inhibit Cell Protein Synthesis
(By blocking Elongation Factor)
(Same Mechanism as Diphtheria A toxin)
3) => Resulting in Cell Death
4) Elastase is secreted Extracellularly to damage cells.
5) Enters Bloodstream
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Clinical:
Note:
=> Does not grow on Dry skin, but Flourishes on Moist Skin.
(Mneumonic: BE PSEUDO)
1) Burn-Wound + Sepsis
2) Endocarditis
(IV Drug Abuse)
3) Necrotizing Pneumonia
_Cystic Fibrosis patients
_Ventilator, Tracheal Tube
_Cancer patients
4) Sepsis
_Burn Wound
_Cancer
_Leukemia
5) Malignant Otitis Externa
(Invasive)
_Diabetics
6) Nosocomial UTI
(usually catheter, surgery, etc.)
7) Corneal Infections
(e. g. w/ Contact lens use)
8) Osteomyelitis
_Diabetics
_IV Drug Abusers
_Puncture Wound @ Foot
9) Hot Tub/Swimming Pool Folliculitis
(Susceptible to Chlorine though!)
