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32 Cards in this Set

  • Front
  • Back
Pneumococcal Pneumonia
Causative Agent
– Streptococcus pneumoniae
• Gram-positive
• Diplococci
• Thick polysaccharide capsule
• Capsule responsible for virulence
• 80 different types of
S. pneumoniae based on capsular antigen
Pneumococcal Pneumonia
Symptoms
– Cough
- Fever
– Chest pain
- Sputum production
– Runny nose and upper respiratory congestion precede above symptoms
– Chest pain is aggravated with each breath and by cough
• Resulting pain causes breathing to become shallow and rapid
– Causes skin to become dusky colored due to poor oxygenation
– Symptoms abate in individuals who survive within 7 to 10 days without treatment
Pneumococcal Pneumonia
Pathogenesis
– Infection develops when bacteria are inhaled into alveoli •Bacterial capsule interferes with phagocytosis
– Pneumococci that enter bloodstream are responsible for fatal complications
• Septicemia
• Endocarditis
• Meningitis
– Recovery is usually complete
Pneumococcal Pneumonia
Epidemiology
– 30% of healthy individuals carry encapsulated strain in their throat
• Bacterial rarely reach lung due to mucociliary escalator
• Risk of pneumonia rises when escalator is destroyed
– Underlying disease and age also increase risk of disease
Pneumococcal Pneumonia
Prevention and Treatment
– Prevention is aided by vaccine
• Gives immunity to 23 strains
• Conjugate vaccine against 7 types is available for infants
– Antibiotic treatment is generally successful if given early
• Penicillin and erythromycin
• More strains are becoming antibiotic resistant
Klebsiella Pneumonia
Causative Agent
– Several species of Klebsiella cause pneumonia
– Primary cause Klebsiella pneumoniae
• Gram-negative
• Bacillus
• Encapsulated
Klebsiella Pneumonia
Symptoms
– Most symptoms are undistinguishable from pneumoncoccal pneumonia; they include
• Cough • Fever • Chest pain

– Other symptoms include
• Repeated chills
• Red gelatinous sputum
– 50% to 80% mortality in untreated patients
• These patients tend to die sooner than with other pneumonia
Klebsiella Pneumonia
Pathogenesis
– Organism colonizes mouth and throat
– Carried to the lung with inspired air or mucus
– Survival in the lung is aided by capsule
• Interferes with phagocytosis
– Specifically interfering with complement protein C3b
– Organism causes tissue death
• Leads to formation of lung abscess
– Infection in bloodstream leads to abscess in other tissues
Klebsiella Pneumonia
Epidemiology
– Part of the normal flora of the intestine
– Colonization of mouth and throat is more common in debilitated individuals
• Especially in institutional settings
Klebsiella Pneumonia
Prevention and Treatment
– No specific prevention measures
– Disinfect environment
• Make sure medical equipment is sterile
– Use antimicrobials only when necessary
• Help to control antimicrobial resistance
Mycoplasmal Pneumonia
Symptoms
– Onset is typically gradual
– First symptoms include
• Fever, headache, muscle
pain, fatigue
– Later symptoms are
• Dry cough and
mucoid sputum
Mycoplasmal Pneumonia
Causative Agent
– Mycoplasma pneumoniae • Small
• Deformed bacterial lacking cell wall
• Slow growing
• Aerobic
• Colonies have a distinctive fried egg appearance
Mycoplasmal Pneumonia
Pathogenesis
– Small infecting dose
– Organism attaches to receptors on epithelium
• Attachment interferes with ciliated cell action
• Ciliated cells slough off
– Inflammation initiates thickening of bronchial
and alveolar walls
• Causes difficulty in breathing
Mycoplasmal Pneumonia
Epidemiology
– Bacteria are spread by aerosolized droplets from respiratory secretions
• Survive for long periods in secretions – Aids in transmission
– Accounts for approximately one-fifth of bacterial pneumonias
• Peak incidence in young people
– Natural immunity is not permanent
Mycoplasmal Pneumonia
Prevention and Treatment
– No practical prevention
• Avoid crowding in schools and military facilities
– Particularly dormitories and recruit barracks
– Antibiotic treatment is successful
• Cell wall synthesis inhibitors?
– ineffective
• Antibiotics of choice are tetracycline and erythromycin (What are the targets?)
– Must be given early
– Both are bacteriostatic
» Will only inhibit growth, not kill organism
Whooping Cough
Symptoms
– Runny nose followed by bouts of uncontrollable coughing
• Termed paroxymal coughing – Severe cough can cause rupture of small blood vessels
in the eyes
– Coughing spasm followed by characteristic “whoop”
• Sound made by the forceful inspiration of air
– Vomiting and seizure may occur
Whooping Cough
Causative Agent
– Bordetella pertussis
• Small
• Encapsulated
• Strictly aerobic
• Gram-negative
• Bacillus
• Does not survive long periods outside the host
Whooping Cough
Pathogenesis
– Enters respiratory tract with inspired air and attaches to ciliated cells
– Organism colonizes structures of the upper and lower respiratory tract
– Mucous secretion increases which causes ciliary action to decrease
• Cough reflex is only mechanism for clearing secretions

– B. pertussis produces numerous toxic products
• Pertussis toxin - A-B toxin
– B portion attaches to cell surface
– A portion enters cell and inactivates regulation of cAMP
» Causes increased mucus formation
» Decreases phagocytic killing
Whooping Cough
Epidemiology
– Spreads via infected respiratory droplets
– Most infectious during runny nose period
• Number of organisms decrease with onset of
cough
– Classically disease of infants
• Milder forms are seen in older children and adults
– Often overlooked as a persistent cold
• Fosters transmission
Whooping Cough
Prevention
– Directed at vaccination of infants
• Prevents disease in 70% of individuals
• Pertussis vaccine combined with diphtheria and tetanus toxoids (DPT)
– Injections given at 6 weeks, 4, 6 and 18 months
Whooping Cough
Treatment
– Erythromycin is effective at reducing symptoms if given early
– Antibiotic usually eliminates bacteria from respiratory secretions
Tuberculosis
Symptoms
– Chronic illness
– Symptoms include
• Slight fever with night sweats
• Progressive weight loss
• Chronic productive cough
– Sputum often blood streaked
Tuberculosis
Causative Agent
– Mycobacterium tuberculosis (ALSO NTM)
• Gram-positive cell wall type
• Slender bacillus
• Acid fast due to mycolic
acid in cell wall
• Slow growing
– Generation time 12 hours or more
• Resists most prevention methods of control
Tuberculosis
Pathogenesis
– Usually contracted by inhalation of airborne organisms
– Bacteria are taken up by pulmonary macrophages in the lungs
– Resists destruction within phagocyte
• Organism prevents the fusion of phagosome with lysosomes; allows multiplication in protected vacuole

– Organisms are carried to lymph nodes
– About 2 weeks post infection intense immune reaction occurs
• Macrophages fuse together to make large multinucleated cell
• Macrophages and lymphocytes surround large cell
– This is an effort to wall off infected tissue

– Activated macrophages released into infected tissue
• Causes death of tissue resulting in formation of “cheesy” material
Tuberculosis
Epidemiology
– Estimated 10 million Americans infected
• Rate highest among non- white, elderly poor people
– Small infecting dose
• As little as ten inhaled
organisms

– Factors important in transmission
• Frequency of coughing, adequacy of ventilation, degree of crowding

– Tuberculin test used to detect those infected
• Small amount of tuberculosis antigen is injected under the skin
• Injection site becomes red and firm if infected
• Positive test does not indicate active disease
Tuberculosis
Prevention
– Vaccination for tuberculosis widely used in many parts of the world
• Vaccine known as Bacillus of Calmette and Guérin
– BCG derived from mycobacterium bovis
– Gives partial immunity against tuberculosis
• Vaccine not given in United States because it eliminates use of tuberculin test as diagnostic tool
Tuberculosis
Treatment
– Antibiotic treatment is given in cases of active tuberculosis
• Two or more medications are given together to reduce potential antimicrobial resistance
• Antimicrobials include
– Rifampin and Isoniazid (INH)
» Both target actively growing organisms and
metabolically inactive intracellular organisms

• Therapy is pronged
– Lasting at least 6 months

• MDR, XDR (drug resistant)
Legionnaires’ Disease
Symptoms
– Early symptoms
• Headache
• Muscle ache
• Rapid rise in temperature
• Confusion
• Shaking chills
– Later symptoms
• Dry cough
• Sputum production
• Pleurisy
– One quarter of cases develop alimentary tract symptoms
• Diarrhea, abdominal pain, vomiting
Legionnaires’ Disease
Causative Agent
– Legionella pneumophila
• Member of γ- proteobacteria
• Gram-negative rod
Legionnaires’ Disease
Pathogenesis
– Acquired by breathing aerosolized contaminated water
– Healthy people are quite resistant
– Organisms lodge in or near alveoli and inhibit phagocytosis
– Bacteria releases macrophage invasion potentiator (MIP) which aids entry into macrophage
– Fatal respiratory arrest occurs in 15% of hospitalized cases
Legionnaires’ Disease
Epidemiology
– Organism widespread in natural warm waters
– Relatively resistant to chlorine
– Survives well in water system of buildings
– Person-to-person transmission does not occur
Legionnaires’ Disease
Prevention and Treatment
– Prevention focused on equipment to minimize risk of infectious aerosols

– Adequate disinfection

– Antibiotic treatment is successful
• Treated with high doses of erythromycin
– Rifampin is administered concurrently in some cases
• Bacteria produces β lactamase enzyme
– Makes it resistant to penicillins and cephalosporins