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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 |
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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 |
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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 |
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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 |
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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 |
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Klebsiella Pneumonia
Causative Agent |
– Several species of Klebsiella cause pneumonia
– Primary cause Klebsiella pneumoniae • Gram-negative • Bacillus • Encapsulated |
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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 |
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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 |
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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 |
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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 |
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Mycoplasmal Pneumonia
Symptoms |
– Onset is typically gradual
– First symptoms include • Fever, headache, muscle pain, fatigue – Later symptoms are • Dry cough and mucoid sputum |
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Mycoplasmal Pneumonia
Causative Agent |
– Mycoplasma pneumoniae • Small
• Deformed bacterial lacking cell wall • Slow growing • Aerobic • Colonies have a distinctive fried egg appearance |
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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 |
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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 |
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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 |
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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 |
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Whooping Cough
Causative Agent |
– Bordetella pertussis
• Small • Encapsulated • Strictly aerobic • Gram-negative • Bacillus • Does not survive long periods outside the host |
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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 |
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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 |
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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 |
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Whooping Cough
Treatment |
– Erythromycin is effective at reducing symptoms if given early
– Antibiotic usually eliminates bacteria from respiratory secretions |
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Tuberculosis
Symptoms |
– Chronic illness
– Symptoms include • Slight fever with night sweats • Progressive weight loss • Chronic productive cough – Sputum often blood streaked |
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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 |
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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 |
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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 |
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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 |
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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) |
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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 |
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Legionnaires’ Disease
Causative Agent |
– Legionella pneumophila
• Member of γ- proteobacteria • Gram-negative rod |
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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 |
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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 |
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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 |