Imported: Respiratory System- Pneumonia I,ii,iii By Dugan

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Respiratory System- Pneumonia I,II,III by Dugan

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Respiratory System- Pneumonia I,II,III by Dugan

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Acute Exacerbations of Chronic Bronchitis (AECB) is associated with...

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COPD caused by tobacco. The triad of associated pathogens is H. Influenza, M. catarrhalis, and S. pneumonia

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Bronchiectasis is associateed with...

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cystic fibrosis.

this is characterized by a dilated and thickened airway produced by other disease.

Associated pathogens are Haemophilus influenza and pseudomonas aeruginosa.

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Describe Lobar Pneumonia

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homogeneous involvement of a distinct region of the lung.

infection spreads b/w the alveoli until it is contained by the anatomic barriers.

X-ray: dense areas in lung due to consolidation (fluid and neutrophils)

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Main cause of lobar pneumonia?

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streptococcus pneumoniae. a gram + diplococci

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Describe Bronchopneumonia

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infection originates in the airways and extends to nearby areas of the lung.

x-ray: patchy appearance in more than one area of lung

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Main cause of bronchopneumonia

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gram negatives and staph aureus.

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Describe Interstitial pneumonia

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inflammatory process within the lung interstitium

x-ray: hazy image

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Main cause of interstitial pneumonia

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viral pneumonia (ie influenza) and mycoplasma pneumoniae

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What are lung abcesses and what causes them?

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one or more areas of the lung replaced by cavities. this is caused by TB, fungal infections and anaerobic bacteria.

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Where does Acute pneumonia come from?

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Community Acquired:
-person to person transmission
-animal/environmental exposure
-pneumonia in infant/young child
-pneumonia in immunocompromised

Hospital Acquired:
-nonsocomial

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What do subacute pneumonias cause?

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lung abcess, so these come form tuberculosis, fungal infections, and aspiration pneumonias.

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What's the most common cause of community acquired pneumonia?

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pneumococcal pneumonia. the highest incidences are in the young and the old. occurs most in the winter (when you're indoors), and predisposing factors include sickle cell, hodgekins disease, multiple myeloma, and no spleen.

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Symptoms of pneumococcal (aka streptococus) pneumonia?

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-sudden onset
-fever
-bed-shaking chills
-sharp pleuritic chest pains
-bloody or rust coloured sputum
-LOBAR pneumonia on xray

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Where does streptococcous pneumoniae like to hang out?

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in the mucosal epithelial tissue and tends to colonize the naspharynx

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Characterize streptococcous pneumoniae

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Gram +, lancet shaped, diplococci
polysaccharide capsule (antiphagocytic virulence factor)

culture: growth enhanced by CO2, alpha hemolysis, sensitive to optochin, bile soluble

other: pneumolysin, C substance (leads to inflammation), M substance.

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How do you treat strep pneumo? how do you prevent it?

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tx:
DOC: penicillin

for resistant strains, use erythromycin, cephalosporin, vancomycin

prevention:
pneumovax to prevent invasive diseases and polysaccharide vaccine pneumovax to protect against pneumo pneumonia

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What gram negative pneumonia clinically resembles pneumococcal pneumonia?

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Klebsiella pneumoniae. seen in homeless, alcoholics, bedridden pts.

colonization of URT with gram - organisms due to decrease in fibronectin

"currant jelly" sputum (thick gelatinous)

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What does Haemophilus Influenza require for cultures?

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X and V factor. It's mostly nontypable (since type b is less common since the Hib vaccine). they are very tiny.

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What does pseudomonas aeruginosa look like?

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gram stain negative
thin rods
oxidase positive
lactose non-fermenter
assd with cystic fibrosis, ventilators
necrotizing tissue damage

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Who would you imagine can get staph aereus?

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IV drug users. these are gram positive cocci, coagulase positive. may also get it from ventilator usage or cystic fibrosis pts.

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What is atypical pneumonia? What are the agents of it?

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Atypical pneumonia is an acute, community-acquired pneumonic illness presenting with a different pattern of features dominated by mild to moderate systemic symptoms of more moderate onset.

-mycoplasma pneumoniae (Eaton's Agent)
-Chlamydia pneumoniae

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Describe mycoplasma pneumonia

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-smallest known bacteria
-LACK CELL WALL
-require cholesterol
-infect mucuous membranes, esp. in respiratory tract

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Speed of onset of mycoplasma pneumoniae?

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slow onset of fever, headache, malaise, nonproductive cough.

most in kids 5-15

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how to diagnose for mycoplasma pneumoniae? treatment?

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cold agglutins, four fold rise in specific antibody titer, culture, gene probes and PCR tests

treat with doxycycline or erythromycin

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Describe Chlamydia pneumoniae

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-obligate intracellular parasite (can't make ATP; parasitic)
-resembles gram neg. bacteria
-2 forms: elementary body (infectious) and reticulate body (noninfectious)

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Describe the pathogenesis of this Chlamydia pneumoniae

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-it attaches to cells and gets phagocytized.
-it avoids lysosomal fusion
-changes from nonreplicating elementary bodies to metabolically active reticulate bodies
-leaves the cell, lysing it on the way out, where it looks for a new cell to infect.

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Chlamydia pneumoniae is the number 1 cause of _____ in the world.

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blindness.



keep in mind that exposure to birds can give you Chlamydia psittaci

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What are the clinical findings of Chlamydia pneumoniae. epidemiology? lab dx? tx?

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findings: cold symptoms
epi: person to person transmission; Ab prevalence 50-75%
Dx: Isolation using McCoy cell line and staining with specific Ab; Ab titers by micro IF
Tx: tetracycline (doxycycline) is DOC

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Ornithosis caused by C. psittaci clinical findings, epi, dx, doc

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clinical: resp. infections, resembles influenza; dry, hacking persistent cough

epi: disease of birds

dx: 4 fold rise in CF Ab titer; isolated in cell culture

DOC: tetracyclines

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Legionelle pneumophila epidemiology

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highest incidence in summer months, not contagious, predisposing factors are smoking and elderly.

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Characteristics of legionella pneumaphila

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-fastidious gram neg. rod filaments in culture
-counterstain with basic fuchsin
-infects amoeba in natural environment.
-in AC cooling towers, humidifiers, water pipes

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legionella pneumaphila virulence factors

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-cytotoxin interferes with oxygen-dependent processes of phagocytosis
-hemolyins and proteolytic enzymes
-endotoxin
-beta-lactamase

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legionella pneumaphila pathogenesis

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encounter- organisms are inhaled from contaminated water source

spread-once in the lung they are engulfed by alveolar macrophages, resist acidification and lysosomal fusion and multiply

damage- produce a localized patchy infiltrate on x-ray which often progresses to bilateral consolidated, multilobar pneumonia

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clinical findings of legionella pneumaphila

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-mild cough and fever to pneumonia, coma and death.
-sx include fever, cough, malaise, chills, dyspnea, productive cough (white cell production/purulent)
-infiltrates the lungs
-predisposing factors: elderly, immunosuppressed, smoking, previous resp. problems.
-pontiac fever (different degrees of infection)

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lab dx of legionella pneumaphila

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smear: use basic fuchsin countertain for safranin; dieterle silver stain; DFA

culture: lung biopsy, pleural fluid, purulent sputum; buffered charcoal yeast extract agar; requires high humidity

URINE ANTIGEN DETECTION (works good)

serology: four-fold increase in Ab titer or single high titer

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Tx and prevention of legionella pneumaphila

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tx:erythromycin and supportive

prevention: eliminate organism from water supply, head up water above 60 degrees, chlorine

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Properties of an effective biological weapon...

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-highly leathal
-easily produced in large amnts
-stable in aerosol
-cummunicable
-no treatment, vaccine

ex anthrax

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Pathogenesis of bacillus anthracis

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most dangerous is by inhalation, engulfed by macrophages, then the macrophages are lysed, and the bacteria goes into the bloodstream

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What is LF? EF?

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LF- Lethal factor. EF- edema factor. these are 2 toxins that bind to the toxin released by a bacteria, creating a doughnut shape. This forms a pore that allows the toxins to enter a cell and cause damage.

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Recognition of anthrax.. the 2 phases..

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Initial phase (1-6 days): mild fever, malaise, myalgia, nonproductive cough, chest/abdo pain

Secondary Phase (rapidly progressive, death w/i 24-36 hrs): fever, acute dyspnea, diaphoresis, cyanosis, stridor, obtundation and nuchal rigidity

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On xray, what do we as physicians have to recognize?

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"prominent influenza-like symptoms with a widened mediastinum"

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What does skin anthrax look like?

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Primary lesion: spore introduced at the site of a cut or abrasion; painless, pruritic papule; center area ulcerates leading to a black eshar

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What does anthrax look like under the 'scope

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-large gram pos. rod
-rapid, aerobic growth
-central and subterminal spores
-nonhemolytic on SBA
-nonmotile
-sensitive to penicillin

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Tx for anthrax

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antibiotics (pre or post exposure)- ciprofloxacin, doxycycline, penicillin

vaccine-0,2,4 wks, and 6,12,18 months; watch for side effects (not very effective vaccine)

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Are we ready for biological attack with bacillus anthracis?

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$5 billion for the mail incidents; not sure of the residual effects from long-lasting spores; vaccine not so good.

we're pretty unprepared for an attack.

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Community Acquired Pneumonia in Childhood: birth to 20 days

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Group B Strep agalactiae (most imp)
Gram neg. enteric bacteria
cytomegalovirus

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Community Acquired Pneumonia in Childhood: 3wks to 2 months

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Chlamydia trachomatis
parainfluenza virus 3 (most common)
streptococcus pneumoniae
bordella pertussis
staph auerus

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Community Acquired Pneumonia in Childhood:2 months to 4 years

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-RSV, para influenza virus, flu, adenovirus, rhinovirus
-strep pneumoniae
-haemophilus influenza
-mycoplasma pneumoniae
-mycobacterium tuberculosis

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Community Acquired Pneumonia in Childhood: 5 to 15 yrs

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-mycoplasma pneumoniae
-chlamydia pneumoniae
-strep pneumoniae
-parainfluenza and influenza
-mycobacterium tuberculosis

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Hospital Acquired Pneumonia (HAP)

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it's pneumonia that occurs within 48 hours after hospital admission

-second most common hospital acquired infection but has highest mortality
-25% of all infections in ICU is HAP
-90% because you're on a ventilator
-over 50% of antibiotics prescribed

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Agents for HAP

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most common core pathogens- nonsevere pneumonia:
-enteric gram neg rods (klebsiella, enterobacter, proeus, escherichia coli)
-haemophilus influenza
-serratia marcescens
-strep pneumoniae
-staph auerus
-anerobes

moderate to severe pneumonia:
-pseudomonas aeruginosa
-acinetobacter

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Agents for aspiration pneumonia

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bacteroides, fusobacterium, peptostreptococcus

-it's a problem for alcoholics.
-lung abscesses tend to develop
-clinical course less acute
-patients breath and sputus may have putrid odor
-necrotizing- destroy lung tissue

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What is Actinomyces Israelii? clinical manifestations, patho, DOC?

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Character: gram + filamentous rod; anaerobic; part of normal flora; found in soil

Clinical: early nonproductive cough, after fever you get productive cough, advanced infection may invade lung parenchyma cavity similar to TB

Path: infection often mixed, chronic, granulomatous inflammation necrosis and fibrosis, "sulfur granules' from infected sites

DOC: penicillin

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Nocardia asteroides characteristics, clinical manifestations, DOC

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character: gram positive branching, filamentous; acid fast by modified Ziehl-Neelson stain; found in soil

clinical: humans inhale it infection usually subacute or chronic abscess; difficult to differentiate clinically from TB or fungal infection

DOC: sulfonamides

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What is empyema?

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caused by an infection that spreads form the lung and leads to an accumulation of pus in the pleural space.

a pleural smear examines a sample of pleural fluid under the microscope to detect organisms.