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12 Cards in this Set

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Pneumococcal Pneumonia
Streptococcus pneumonia
Diplococcal pneumonia
most common bacterial cause of pneumonia (esp CAP). May be found in the oropharynx of healthy people. Still has an appreciable mortality despite antibiotics.

Clinical picture:
1. Acute onset of a shaking chill
2. May follow an upper respiratory infection
3. Fever, dyspnea, pleuritic chest pain
4. Cough, rusty sputum
5. Leukocytosis
6. Signs of consolidation on exam
7. CXR: lobar consolidation (percussion dullness, bronchial breath sounds, increase tactile/vocal fremitus)
8. Gram stain: gram + lancet shaped diplococci, intracellular

Treatment:
1. Evolving (Current: a macrolide and 3rd generation cephalosporin)
2. Some resistant strains
3. Vaccine is available.

Signs indicating poor outcome:
1. Bacteremia
2. Hematogenous spread (meningitis, endocarditis, arthritis)
3. More than 1 lobe involved
4. Type 3 serotype (more virulent)
5. Very young or very old
Mycoplasma Pneumonia
(Atypical/walking)
Common cause of pneumonia in young otherwise healthy people. Occurs in outbreaks (family, school, military recruits), most commonly in fall and winter. Spread by inhalation of infected aerosol.

Classic clinical picture:
1. Insidious onset
2. Fever, headache, chills, malaise, systemic manifestations
3. Non productive cough
4. No leukocytosis
5. Bullous myringitis
6. Rarely: signs of consolidation; usually patchy rales/crackles
7. Organism: 3 layered membrane not a cell wall thus do not gram stain and do not grow on routine media
8. Diagnosis by serology
9. 33-75% have cold agglutinins
10. CXR: patchy bronchopneumonia

Treatment:
macrolide
tetracycline
Legionella Sp
Organism has presented as an epidemic (1976 Legionnaire’s convention in Philadelphia), sporadically (Cattleman’s Meat Market in Farmington a few years ago), and as a nosocomial infection.
1. contaminated water supply or air conditioning
2. Risk factors: immunosuppression, smoking, COPD, advanced age, male, cardiac disease

Clinical Picture:
1. High fever, recurrent chills, cough
2. GI involvement (diarrhea) common
3. “relative bradycardia” for degree of fever
4. Hyponatremia, hypophosphatemia
5. May have a fulminant systemic course
6. CXR: varied patterns
7. Gram stain doesn’t show it; silver stain or DFA stain
8. Cultured on selective media
9. Serology

Treatment:
Macrolides (rifampin)
Hemophilus Influenza
Occurs in COPD, alcoholics, healthy adults

Sputum: gram – coccobacilli; intracellular
Large amount of sputum production
Klebsiella Pneumoniae
Alcholics, diabetics, debilitated

Bulging fissure on CXR, lobar pneumonia
Sputum: plump gram – rod
“currant jelly”
Staphylococcus Aureus
CAP: IV drug users, those colonized in nasopharnx
Elderly: often follows flu
Nosocomial: IV devices

Sputum: gram + cocci in clusters, easily cultured

Multipe cavitary lesions, destruction, pleural complications
Cocciodiomyocosis
1. Endemic area: SW USA and northern border zone of Mexico, San Joaquin Valley area of California
2. Life Cycle: germinates in the soil as an arthrospore; spores are hardy and are the infectious form for humans; (digging, construction, high winds are associated with epidemics); tissue form of organism is the spherule, which contains endospores.

Immunology:
1. Skin testing: coccidioidin used; produces induration. Value: - to + means new infection; + to - means severe or dissem. disease. Positive 3 days to 3 weeks of illness
2. IgM Serologic testing: by Tube Precipitin or Latex Particle Agglutination: 2-4 weeks of illness
3. IgG Serologic testing: Complement Fixation; becomes + about 8 weeks after infection; results are diagnostic (+ = infected) and prognostic (very high titer = high chance of disseminated disease)
4. Timing of tests is important: window where diagnosis may be missed (see Figure)
5. Culture is dangerous: airborne arthrospores are infectious

Clinical Picture:
1. 60% - No Symptoms (only immunologic evidence of infections)
2. Primary Coccidiodomycosis: low grade fever, cough, chest pain, headaches, malaise, joint aches, other constitutional symptoms
a. “Valley Fever” specific subtype, most often in young women: skin lesions, particularly erythema nodosum common.
b. Course: milder than bacterial pneumonia; most recover without therapy in about 8 weeks.
c. Risk factors for dissemination:
i. Age > 50 or < 5 years
ii. Immunosuppression for any reason
iii. “Race” – African Americans, Native Americans, Mexicans, Filipinos have higher risk than Caucasians, Oriental
3. Persistent/Chronic infection: not common; infection lasting > 8 weeks. May require antifungal therapy
4. Disseminated Disease: can affect any organ system; skin most common; worst is meningitis (base of the brain ) (without treatment - fatal. Therapy is antifungals intravenously.
Histoplasmosis
1. Worldwide distribution; endemic areas in the USA are centered around Mississippi, Ohio, Missouri and Tennessee River Valleys
2. Life Cycle: infectious spore is called the microconidia; habitat is soil; dusty conditions increase airborne spores; fowl and bat excrement increase the growth of the fungus (Hx: coops, roosts, bat infested caves, attics, lofts, etc.) Tissue form is characterized by a narrow necked budding yeast.

Immunology:
1. Skin testing: too many people have + reactions; not useful for making diagnosis; skin tests cause false positive serologic tests thus are usually not done
2. Serologic testing: can detect Ab by immunodiffusion; can be helpful diagnostically but not helpful prognostically
3. Difficult to grow in cultures

Clinical Picture:
1. Majority: asymptomatic (or just have a prolonged “cold”) CXR may show calcifications from old infection
2. If symptomatic: nonspecific malaise, headache, fever, nonproductive cough, pain on swallowing. Most recover without treatment.
3. Chronic histoplasmosis: patients with severe underlying lung disease (COPD); if pulmonary status deteriorates may need antifungal therapy.
4. Disseminated Histoplasmosis: rare opportunistic infection. Fatal if untreated. Occurs with decreased cell mediated immunity.
Sites: lung, bone marrow, lymph nodes, GI tract, oropharynx (ulcerations). High dose intravenous antifungals essential.
Blastomyosis
1. Endemic areas not well known; may be similar to Histo. Presumed to grow in soil. Outbreaks reported in south and south-central US and in regions surrounding the Great Lakes
2. Life Cycle: dumbbell shaped spores become airborne from soil. Reproduce in tissue as a broad necked budding yeast

Immunology:
1. Skin testing: not useful; more likely to indicate Histoplasma
2. Serologic testing: not useful. A high titer may suggest illness in someone in whom the infection was not suspected.
3. Culture is definitive; organism is fast growing and easy to culture.

Clinical Picture:
1. Without serology or skin testing, we only presume the majority of infections are asymptomatic or patient recover without therapy.
2. Acute: abrupt onset, high fever, productive cough. Most recover spontaneously in about 4 weeks.
3. Chronic: does require antifungal therapy.
4. Disseminated: lung, ulcerated skin lesions, destructive bony lesions. Males can get prostatitis, epididymitis. Treat with intravenous antifungals.
Aspergillus
Ubiquitous in nature. The type of disease produced in humans is crucially related to the status of that patient.

Immunology:
1. Skin testing: valuable in acute forms of aspergillosis. An immediate (Type I) hypersensitivity reaction.
2. Serology: IgE antibodies can be found in patient with acute manifestations or with fungus balls. IgG Ab may also be seen.


Clinical picture:
1. Hypersensitivity pneumonitis/Extrinsic Allergic Alveolitis: cough, dyspnea, fever and chills within 4 to 6 hours of exposure to spores. Responds to corticosteroids.
2. Allergic Bronchopulmonary Aspergillosis (ABPA): in patients with long standing asthma; manifests as worsening of episodic airflow obstruction, eosinophilia, + skin test, + serology, elevated serum IgE, migratory CXR infiltrates, cough up brown plugs. Treat with steroids.
3. Aspergilloma (fungus ball): colonization of a pre-existing cavity (old TB, etc.). Can cause bleeding due to erosion. May need to remove surgically.
4. Invasive aspergillosis: exclusively seen in the immunocompromised. Immunologic testing not of value. Culture it for diagnosis. May use more than one intravenous antifungal. Very high mortality.
CMV – AIDs post transplant
opportunistic infection

1. Source: donor blood or organ; reactivations of dormant infection in the host/recipient
2. Clinical: fever and interstitial pneumonia (rales or crackles)
3. Diagnosis: viral inclusions in cells, cultures, monoclonal antibodies
4. Treatments: supportive care; immune replacement; antiviral
Pneuocystis Carinii
opportunistic infection

1. In HIV patients, a slowly progressive infections with fever, cough, dyspnea, progressive chest x-ray infiltrates and decreasing oxygenation
2. In children with leukemia: fulminant downhill course
3. Diagnosis: demonstrate organism in secretions or tissue
4. Treatment: trimethoprim-sulfa first line; pentamidine by IV or aerosol in those who don’t tolerate T-S.