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Pulmonology > Cross - Infections > Flashcards

Cross - Infections Flashcards

1
Q

What is pneumonia? When do people get it?

A
  • Lung parenchyma infection
  • Systemic resistance lowered: chronic disease, immuno def, tx w/immuno-suppressants, leukopenia
  • Impaired local defense mechs: loss of cough reflex suppression, injury to mucociliary apparatus (smoking), accumulation of secretions (CF), interference of phagocytic action of alveolar macros (tobacco, alcohol), pulmonary edema
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2
Q

Why the respiratory tract?

A
  • Millions of microorgs (bacteria, viruses, fungi) inhaled daily
  • Evade local defenses via several different mechanisms
    1. Toxins that impair ciliary activity
    2. Capsules or live intracellularly and evade killing
    3. Attach to and enter epi cells through various mechanisms
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3
Q

What is CAP? Characterize it.

A
  • Community-acquired pneumonia: potentially serious, w/considerable morbidity/mortality
  • Rate INC w/INC age and comorbidities
  • Strep pneumo most comm cause of pneum worldwide
  • Etiologic agent usually NOT identified; pts tx empirically
  • Often follows URT viral infection
  • Bacteria invade lung parenchyma -> alveoli filled with inflammatory exudate -> consolidation of the pulm tissue
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4
Q

What is HAP? What are some risk factors?

A
  • Hospital-acquired pneumonia: 48+ hrs post-hosp admission (NOT incubating at admission time)
  • Leading cause of death among hospital-acquired infections (mortality from 20-50%)
  • Highest risk for HAP is in pts on mechanical ventilation
  • Other risk factors: severe underlying illness, immuno-suppression, prolonged AB tx, invasive devices like IV catheters
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5
Q

What is HCAP?

A
  • Healthcare-assoc pneumonia:
    1. Hospitalization of at least 2 days in prior 90, or
    2. Has been receiving IV therapy, chemotherapy or wound care in the last 30 days, or
    3. Patient is resident of nursing home or long term care facility, or
    4. He/she attends hemodialysis clinic or hospital
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6
Q

What are some of the physical exam findings in pneumonia (4)?

A
  • Crackles (rales): scratchy sound via accumulation of fluid/white cells/bacteria in alveolar and interstitial spaces
  • Bronchial breath sounds: dense consolidation of lung parenchyma = transmission of large airway noises to periphery
  • Dullness to percussion: normal, air-filled tissue displaced by fluid (eg. pleural effusion) or infiltrated with white cells and bacteria
  • INC tactile fremitus: consolidation alters transmission of air and sound -> fremitus will become more pronounced
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7
Q

How might you diagnose pneumonia?

A
  • CXR
  • Gram stain/cultures
  • Some orgs have special tests
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8
Q

What are some complications of pneumonia?

A
  • Tissue destruction & necrosis, which can lead to ABSCESS
  • Spread of infection into the pleural cavity causing an EMPYEMA (collection of pus in cavity)
  • Bacteremic dissemination
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9
Q

What is atypical pneumonia? What 3 orgs should you think about?

A
  • Symptoms and CXR atypical when compared with S. pneumo
  • Organism can’t be isolated on routine media
    1. Mycoplasma pneumoniae
    2. Chlamydophila (chlamydia) pneumoniae
    3. Legionella pneumophila
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10
Q

What are some of the staining/detection methods for strep pneumo?

A
  • Gram positive, lancet shaped (oval w/pointed ends) encapsulated diplococcus
  • Alpha hemolysis on blood agar plate -> GREEN RING around colonies
  • Optochin sensitive: distinguishes it from strep viridans
  • Catalase negative: distinguishes from S. aureus (catalase catalyzes decomposition of hydrogen peroxide to water and oxygen)
  • Quellung reaction: type-specific antiserum causes capsules to swell (attached image)
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11
Q

What are the virulence factors of S. pneumo? Is it part of the normal flora?

A
  • Polysaccharide capsule: interferes w/phagocytosis and promotes invasiveness
    1. No virulence without the capsule -> more than 85 antigenically distinct types
  • IgA protease: enhances org’s ability to colonize URT
  • Lipoteichoic acid: activates complement/induces cytokine production
  • 5-50% of the pop colonized w/S pneumo in oropharynx, but not communicable -> healthy people typically resistant to infection
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12
Q

What are the risk factors for S. pneumo?

A
  • Alcohol/drug intoxication (causes cerebral impairment, depressing cough reflex, INC aspiration of secretions)
  • Abnormality of the respiratory tract (viral infection, bronchial obstruction, respiratory tract injury)
  • Abnormal circulatory dynamics (pulmonary congestion, heart failure)
  • Splenectomy
  • Sickle cell disease
  • HIV infection
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13
Q

What are the clinical manifestations of S. pneumo?

A
  • SUDDEN ONSET:
    1. Fever
    2. Shaking chills
    3. Cough productive of rusty sputum
    4. Shortness of breath
    5. Pleuritic pain
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14
Q

How can you diagnose S. pneumo?

A
  • Gram stain and culture (sputum)
  • Blood cultures positive in 15-25%
  • Rapid urinary antigen test
  • CXR will show LOBAR CONSOLIDATION
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15
Q

How can you treat S. pneumo?

A
  • Antibiotics:
    1. Penicillin previously drug of choice, but significant resistance has emerged
    1. Still drug of choice IF susceptible
  • For severe infections: Vancomycin empirically until susceptibilities known
  • Ceftriaxone if susceptible
  • Flouroquinolones (-floxacins) and Azithromycin (macrolide) also options for less severe disease
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16
Q

What are the 2 S. pneumo vaccines?

A
  • High mortality in elderly, immunocompromised, or debilitated
  • Polyvalent (23-type) polysaccharide vax (PPSV23, aka pneumovax) provides 5 yrs protection
    1. Material from 23 pneumo types that have caused 85-90% of disease
    2. Recommended for all people ≥65 years of age and peeps aged 19 - 64 years at INC risk for pneumo and/or serious complications of pneumo infection
  • PCV13 (Prevnar)
    1. Capsular polysaccharides from 13 most common types that cause disease
    2. Recommended for children and infants
  • Since 2012 both vaccines have been recommended sequentially for high risk adults
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17
Q

What other diseases are caused by S. pneumo?

A
  • Meningitis
  • Otitis media
  • Sinusitis
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18
Q

What is S. aureus? Characterize it.

A
  • Gram positive cocci in clusters; part of normal flora
  • Coage and catalase positive
  • Causes many diseases; tons of virulence factors
  • Important cause of post-influenza pneumonia
  • Causes both CAP and HAP/HCAP (one of most common causes of HAP/HCAP)
  • AB resistance common -> must get susceptibilities
  • Complications incl. necrotizing PNA and lung abscess
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19
Q

What does the pneumo caused by S. aureus typically look like?

A
  • Typically causes a brochopneumonia (more diffuse findings on CXR)
    1. Acute inflammatory infiltrates from bronchioles into adjacent alveoli
    2. Patchy distribution usually involving > 1 lobe
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20
Q

What is pseudomonas aeruginosa?

A
  • Aerobic gram-negative bacilli
    1. Does not ferment lactose
    2. Oxidase positive
    3. Produces pyocyanin, giving it blue-green pigment (see attached image)
    4. Grape-like odor on agar plate
    5. Water source
  • One of most common causes of HCAP/HAP/VAP and pneumonia in cystic fibrosis patients
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21
Q

What are the virulence factors for P. aeruginosa? What do they cause?

A
  • Endotoxin: elicits variety of inflam responses, causing fever and shock
  • Exotoxin A: enzyme blocks protein syn by inactivating elongation factor EF-2 by ADP ribosylation, resulting in shutdown of protein synthesis
  • Others: elastase, leucocidin, hemolysins, proteases
    1. Action of virulence factors results in extensive vasculitis with thrombosis and hemorrhage with necrosis
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22
Q

How do you treat P. aeruginosa?

A
  • Highly resistant organism
  • Must get AB susceptibilities and know antibiogram of the institution
  • Antibiotics:
    1. Cefepime (4th generation cephalosporin)
    2. Meropenem or Imipenem (carbapenem)
    3. Ciprofloxacin (flouroquinolone)
    4. Pipericillin/Tazobactam (extended spectrum penicillin)
    5. Gentamicin (aminoglycoside)
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23
Q

What other diseases does P. aeruginosa cause?

A
  • Wound infections in burn victims
  • Sepsis in hospitalized patients
  • External otitis (esp. in diabetics)
  • UTI
  • Hot tub folliculitis (inflammation of hair follicles
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24
Q

What is Klebsiella pneumo?

A
  • Gram (-) bacillus; intestinal flora
  • Ferments lactose, indole (-), incapable of growth at 10o C
  • Capsule is important virulence factor
  • Important cause of pneumo on alcoholics, malnourished
  • One of most freq causes of gram (-) bacterial PNA
  • Produces very mucoid colonies cause by polysaccharide capsules -> red “currant jelly” sputum
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25
Q

What kind of pneumo does Klebsiella cause? What are some complications?

A
  • Both lobar AND bronchopneumonia
  • Complications: abscess and necrotizing pneumo
  • AB resistance is common
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26
Q

What is Haemophilus influenzae?

A
  • Small, gram (-) coccobacillary rod; pleomorphic (can alter shape/size according to the environment)
  • Non-motile, facultative anaerobe
  • Culture on chocolate agar requires factors V (NAD+) and X (hematin) for growth
  • 6 serotypes (encapsulated and non-encapsulated)
    1. Capsule is one of the virulence factors
    2. Most invasive disease capsular type B -> vaccine incorporates capsular polysaccharide b; antibodies against capsule are protective
    3. Disease due to HIB has DEC significantly, while diseases due to nontypeable forms are increasing
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27
Q

What diseases does H. influenzae cause? What is the tx?

A
  • Diseases:
    1. Pneumonia: following viral resp infection in kids, can be severe w/high mortality rate -> pulm consolidation can be lobar OR more diffuse
    2. Otitis media
    3. Epiglottitis
    4. Meningitis
    5. Common bac cause of acute COPD exacerbations
  • Treatment:
    1. Amoxicillin (beta-lactam) for mild infection
    2. Ceftriaxone for more serious infection
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28
Q

What is Moraxella catarrhalis?

A
  • Gram (-) coccobacillary rods
  • 2nd most common cause of acute COPD exacerbations
  • Increasingly recognized as cause of bac pneumo, esp in elderly
  • Also causes sinusitis and otitis media (common cause)
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29
Q

What is Acinetobacter baumanii?

A
  • Gram-negative coccabacillary rods
  • Opportunistic pathogen
  • Commonly found in water and soil, and can be part of normal flora
  • Hospital setting -> many times associated w/respiratory equipment
  • Diseases: VAP/HAP, sepsis, line infections, UTIs
  • Highly resistant to many antibiotics
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30
Q

What is Mycoplasma pneumo? Describe its pathogenesis and clinical manifestations?

A
  • No cell wall, but bac membrane has sterols for stability
  • Classical cause of atypical “walking pneumo” (most common type of atypical PNA)
    1. Most common cause of pneumo in school-aged children; also common in prison and military recruits
  • Pathogenesis: adhesin binds to ciliated epithelial cells and causes reduced ciliary clearance
  • Clinical manifestations: insidious onset of dry cough, headache, low-grade fever, myalgias, sore throat
    1. CXR looks worse than the patient usually
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31
Q

How do you diagnose M. pneumo?

A
  • Serology
  • PCR on respiratory secretions/nasopharynx
  • Cold agglutinins: IgM autoantibodies against type O RBCs that agglutinate the cells at 4 degrees C but not 37 degrees C)
    1. Half of patients with Mycoplasma infection will be positive
  • Will grow on Eaton agar (not done routinely)
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32
Q

How do you treat M. pneumo? What are its extrapulmonary manifestations?

A
  • Treatment:
    1. Macrolide (e.g., azithromycin), doxycycline, or floroquinolone (e.g., levofloxacin)
  • Extrapulmonary manifestations:
    1. Hemolysis (rupture/destruction of RBC’s)
    2. Rash
    3. CNS involvement (encephalitis most common)
    4. Cardiac involvement (rhythm disturbances, CHF, myocarditis, conduction abnormalities)
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33
Q

What is Chlamydia pneumo?

A
  • Obligate IC organism
  • 2nd most common cause of atypical pneumo
  • Clinically very similar to Mycoplasma pneumo (affects older adults)
  • No good diagnostic test
  • Treatment: doxycycline (tetracycline AB)
    1. Tetracycline AB’s are protein syn INH, inhibiting the binding of aminoacyl-tRNA to the mRNA-ribosome complex -> bind to the 30S ribosomal subunit in the mRNA translation complex
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34
Q

What is Legionella pneumo? What is its pathogenesis?

A
  • Gram negative rod; facultative intracellular
  • Pathogenesis:
    1. Avoid phagolysosome fusion and replicate within alveolar macrophages -> DEC clearance
    2. Has many other virulence factors, most important probably endotoxin
  • Aerosol transmission from environmental source habitat (air conditioning systems etc.)
  • Older population, smokers, alcoholics and those with comorbidities are affected
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35
Q

What are the clinical features of L. pneumo?

A
  • Legionnaire’s disease: severe pneumonia with unique symptoms
    1. Dry cough
    2. Fever
    3. Diarrhea
    4. Confusion
  • Pontiac fever: mild flu-like syndrome
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36
Q

What are the diagnostic features of L. pneumo?

A
  • CXR can show consolidation, diffuse interstitial infiltrates, pleural effusions, etc.
  • Gram stain will show macros and neutros, but no orgs; must use silver stain
  • Grows on charcoal yeast extract culture with iron and cysteine
  • Labs will show hyponatremia
  • Urine antigen used for diagnosis clinically
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37
Q

What is the treatment for L. pneumo?

A
  • Macrolide (azithromycin) OR
  • Flouroquinolone (levofloxacin)
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38
Q

What is aspiration pneumo?

A
  • Caused by aspiration of gastric contents
  • Debilitated or unconscious pts, or those w/repeated vomiting
  • Resultant pneumo is bac from GI flora & chemical due to gastric acid irritation
  • Can be severe
  • Not everyone who aspirates gets pneumo
  • Frequent cause of pneumonia in alcoholics
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39
Q

What kind of pneumonia do viruses cause? What else do they cause?

A
  • Atypical pneumonia: patchy inflammatory lung changes, largely confined to alveolar septa and pulm interstitium
    1. Absence of physical findings of consolidation
    2. Only moderate elevation of WBC count
    3. Path: alveolar walls infiltrated with mononuclear cells (lymphs, some plasma cells)
  • Nearly all viruses that cause pneumonia can cause URTIs (“common colds”) as well
    1. 40-60% of “colds” can be linked to specific viruses.
    2. Risk factors for extension of infection: extremes of age, malnutrition, alcoholism, underlying debilitating illnesses
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40
Q

What are the general mechs of viral pneumo?

A
  • Viruses have tropisms allowing for attachment to resp epithelium
  • Viral replication causes cell death and inflammation
  • Resulting damage and impairment of local defenses (mucociliary clearance) can predispose to bacterial superinfections
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41
Q

What is the epi of influenza?

A
  • Most common cause of respiratory tract infections that results in physician visits and hospitalizations in the U.S.
  • 35-50 million cases in the U.S. annually and 36,000 deaths each year
    1. Mortality highest in elderly and children under 2 years old (different in 2009 H1N1)
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42
Q

Describe the family and structure of influenza.

A
  • Orthomyxovirus family
    1. Helical, enveloped single stranded, negative-sense linear RNA virus consisting of 8 segments
  • Structure -> envelope contains 3 proteins:
    1. Hemagglutinin binds to cell surface receptor and promotes viral entry -> 3 major subtypes (H1-H3)
    2. Neuraminidase cleaves neuraminic acid to release progeny virus from infected cell; degrades protective layer of mucus in resp tract (2 major subtypes: N1, N2)
    3. M2 ion channel essential for virus infectivity
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43
Q

What are the differences between influenza A and B?

A
  • Influenza A: major cause of epidemics (community) and pandemics (worldwide)
    1. Capable of infecting animals
    2. Classified by subtypes -> single subtype predominates throughout the world at any given time
  • Influenza B: causes sporadic outbreaks every year
    1. Can be serious, but only infects humans
    2. Not classified by subtypes
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44
Q

What is the difference between antigenic drift and shift?

A
  • Antigenic drift: spontaneous mutations in viral genome as it replicates (causes epidemics)
    1. New viral strains are different enough to elude (in part) anti-influenza Ab’s produced in pop in response to prior exposures to other flu strains
  • Antigenic shift: occur when HA and NA genes replaced via reassortment w/animal flu viruses
    1. Creates an antigenically “new” virus that has the potential to cause pandemics
    2. All individuals are susceptible
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45
Q

What is an epidemic? Pandemic?

A
  • Pandemic: spread through human populations across a large region (globally); for instance multiple continents, or even worldwide
  • Epidemic: widespread occurrence of an infectious disease in a community at a particular time
  • NOTE: influenza causes both epidemics and pandemics
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46
Q

What are the transmission and pathogenesis of influenza?

A
  • Transmission: airborne respiratory droplets
  • Pathogenesis: virus is inhaled
    1. Neuraminidase degrades protective mucus layer and virus gains access to cells
    2. Necrosis of superficial layers of the respiratory epi
    3. Cytokines released -> characteristic MYALGIAS
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47
Q

What are the clinical manifestations of influenza?

A
  • 24-48 hour incubation period
  • Sudden onset:
    1. Fevers (can be high)/chills
    2. Myalgias
    3. Sore throat
    4. Dry cough
    5. Headache
    6. Vomiting/diarrhea rare (except in children)
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48
Q

What is Reye’s syndrome?

A
  • Encephalopathy and liver degeneration
  • Rare, life-threatening complication in children following some viral infections, esp. influenza B and chickenpox
  • Aspirin given to reduce fever in viral infections has been implicated in the pathogenesis of Reye’s syndrome
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49
Q

How would you diagnose and treat influenza?

A
  • Diagnosis:
    1. Clinical
    2. RT-PCR: most sensitive, specific for dx flu infection, yields relatively rapid results, and differentiates b/t flu types and subtypes
    3. Direct fluorescent antibody
    4. Rapid viral antigen test
    5. Viral culture (not usually used)
  • Treatment: Oseltamivir or Zanamivir
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50
Q

What are some of the possible influenza complications?

A
  • Secondary viral or bacterial pneumonia -> those at risk:
    1. Young children/elderly
    2. Those with chronic diseases
    3. Immunosuppressed
    4. Pregnant or up to 2 weeks post-partum
    5. Morbidly obese
    6. Nursing home residents
    7. Native Americans or Alaskan natives
  • Reye’s syndrome: encephalopathy and liver degeneration
    1. Rare, life-threatening seen in children following viral infections (most commonly flu and chicken pox)
    2. Aspirin has been implicated in its cause
51
Q

Is there a vaccine/prophylaxis for influenza?

A
  • Vaccine: trivalent or quadrivalent
    1. Everyone 6 mos or older
    2. Protection lasts 6 mos
  • Prophylaxis: Oseltamivir
52
Q

What are the family and structure of RSV?

A
  • Respiratory syncitial virus
  • Paramyxovirus family: pleomorphic, enveloped, negative-sense single-stranded, linear RNA
  • Surface spikes are fusion proteins that cause respiratory epithelium cells to fuse forming multinucleated giant cells (syncytia)
  • Most important cause of bronchiolitis and pneumonia in infants
53
Q

How does RSV affect infants vs. adults? Who is at risk of RSV pneumonia?

A
  • Infection in infants more severe, often involves lower respiratory tract (PNA) -> clinical manifestations:
    1. Persistent cough, wheezing, fever, tachypnea, hypoxemia
  • In healthy adults, infection is a typical URT infection (lasts 4-5 days then resolves)
  • Others at risk of RSV pneumonia:
    1. Immunocompromised (bone marrow transplant)
    2. Institutionalized elderly
    3. Infants with chronic lung disease
    4. Infants born during RSV season who are less than 6 months of age, particularly who attend daycare
    5. Infants born before 35 weeks gestation
54
Q

How is RSV tranmitted?

A
  • Respiratory droplets
  • Direct contact of contaminated hands with nose or mouth
  • Community outbreaks every winter; hospital outbreaks also occur
55
Q

How would you diagnose RSV?

A
  • RT-PCR on nasal swab or washings
  • Rapid antigen test on nasal swab or washings
56
Q

What is the treatment for RSV?

A
  • Supportive care with hydration, albuterol, and oxygen
  • Inhaled Ribavirin:
    1. Routine use in kids not recommended -> efficacy has not been proven in this population
    2. Safety issues during administration
    3. May be beneficial for certain adults (stem cell transplant patients)
57
Q

How can we prevent RSV?

A
  • Palvizumab (Synagis): MAb against F protein
    1. Prevents PNA caused by RSV in premature infants by neutralizing virus infectivity
58
Q

What is the natural course/prognosis for RSV?

A
  • Natural course/prognosis:
    1. Mortality rate low (2%)
    2. In most previously healthy infants, infection resolves w/o complications
    3. Severely affected patients (premies, <12 weeks of age, those with underlying cardiopulmonary disease or immunodeficiency) at INC risk for complications (apnea, respiratory failure)
  • Sequelae: asthma
59
Q

What is adenovirus? How is it transmitted?

A
  • Non-enveloped, double-stranded, linear DNA virus
  • Adenovirus family
  • Transmission: aerosol droplet, fecal-oral, or direct inoculation
60
Q

What diseases are caused by adenovirus?

A
  • Pneumonia: typically more severe in infants than older kids; can be accompanied by lethargy, diarrhea, vomiting
  • URTI
  • Febrile pharyngitis
  • Conjunctivitis (“pink eye”)
  • Hemorrhagic cystitis
  • Gastroenteritis <2 years old
  • Disseminated infection in immunocompromised (up to 70% mortality)
61
Q

What do you see here?

A

CXR with bilateral interstitial infiltrates

62
Q

What are some of the characteristic symptoms of adenovirus?

A
  • Characteristic symptoms: sore throat, headache, runny nose, fever, cough, red eyes and fatigue, lasts 5-7 days
  • Outbreaks common in military
63
Q

How do you diagnose, treat, and prevent adenovirus?

A
  • Diagnosis: clinical
  • Treatment: supportive
  • Prevention: vaccine
    1. Live oral enteric-coated vaccines against serotypes 4 and 7 have been used for years in military recruits
    2. Safe and effective in the prevention of epidemics of acute respiratory disease in military training camps
64
Q

What are some of the sequelae of adenovirus?

A
  • Bronchiectasis: abnormal widening of the bronchi or their branches, causing a risk of infection
  • Bronchiolitis obliterans: rare and life-threatening form of non-reversible obstructive lung disease -> bronchioles are compressed and narrowed by fibrosis or scar tissue
65
Q

What are the family and structure of parainfluenza virus? How is it transmitted?

A
  • Paramyxoviridae family -> enveloped single stranded, linear non-segmented RNA virus
    1. Contain F (fusion protein) & HN (hemagglutinin, neuraminidase)
  • 4 distinct PIV’s (1-4):
    1. Croup: caused by hPIV1, 2, 3 (only 2-3% of infection progress to croup)
    2. hPIV3: pneumonia and bronchiolitis
    3. hPIV4: mild respiratory illness (common cold)
  • Transmission: respiratory droplets
    1. Initially infect throat mucous membrane; more extensive infections involve larynx and upper trachea
66
Q

What is croup?

A
  • Aka, laryngotracheobronchitis:
    1. Seal-like, barking cough: caused by inflammation around the larynx, trachea and bronchi
    2. Fever
    3. Rhinorrhea
    4. Sore throat
    5. Stridor can occur: harsh vibrating noise when breathing caused by obstruction/inflam of larynx
  • Steeple sign in attached x-ray image: tapering of trachea
67
Q

How do you diagnose and treat parainfluenza? What is the prognosis?

A
  • Diagnosis: clinical
  • Treatment: supportive
  • Prognosis: good -> most children recover after a few days, but re-infection is common
68
Q

What are the family, route of transmission, and diseases cuased by metapneumovirus?

A
  • Paramyxoviridae family (discovered in 2001)
  • Route of transmission: likely respiratory droplets
  • Causes both URTIs and pneumonia
    1. Now recognized as major cause of more serious LRTI in children and adults
  • Clinically indistinguishable from RSV, and also often mistaken for influenza
69
Q

What is SARS? What is its history?

A
  • Severe acute respiratory syndrome
  • Coronavirus family: enveloped, single stranded (+)-sense RNA virus (genetically distinct from other known CoV’s)
  • Origin not known, but possible reservoirs are: masked palm civet, horseshoe bat
  • History: Nov. 2002 – Feb. 2003 atypical PNA reported in China, spread to Hong Kong, Vietnam, Singapore, Toronto
    1. March 2003 WHO issued global alert -> by July 2003 WHO declared SARS “under control (8,500 infections reported with approximately 800 deaths)
70
Q

What is the clinical presentation of SARS?

A
  • Fever/chills, rigors, headache, malaise, nonproductive cough, dyspnea, hypoxemia
  • Leukopenia and thrombocytopenia are seen
  • CXR: range from normal to diffuse interstitial infiltrates characteristic of ARDS
    1. Bilateral peripheral infiltrates common, usually in middle or lower lung zones
71
Q

What is MERS? Clinical presentation? What is its history?

A
  • Middle eastern respiratory syndrome: thought to be of animal origin, human-to-human transmission
  • Clinical presentation: severe illness with PNA and ARDS, some with AKI; fever, chills/rigors, cough, SOB, hemoptysis, sore throat, myalgias, n/v/d, abdominal pain
  • Sept 2012: novel coronavirus reported in Saudi Arabia after M presented w/severe PNA, ARDS, AKI in June 2012.
    1. Over 830 cases reported -> # of cases INC dramatically Mar/Apr 2014, then declined sharply
    2. Middle East, Europe, SE Asia, U.S. (on return from Arabian peninsula -> 2 cases, Chicago/IN, Orlando)
72
Q

What are the 4 major types of fungal infections?

A
  • Superficial and cutaneous mycoses: common, and limited to skin, hair, nails
  • Subcutaneous: involve skin, subcu tissue, and lymphatics
  • Endemic: caused by dimorphic fungi; can cause serious disease in both health and immunocompromised people
  • Opportunistic: can cause life-threatening disease in immunosuppressed patients
73
Q

What are dimorphic fungi?

A
  • Most common etiologic agents of pulm infection by fungi in healthy hosts; <1 million infections/year in the U.S.
  • Grow as yeast in human tissue and as mold under some laboratory conditions (typically room temperature)
  • Infection from inhalation of spores that have mold forms in soil
  • In lungs, spores differentiate into yeasts or spherules:
    1. Most lung infections self-limited, even asymptomatic, BUT
    2. All can cause pneumonia and disseminate
  • Geographic location IMPORTANT
74
Q

What are the 4 dimorphic fungi we discussed in class?

A
  • Blastomyces dermatitidis
  • Histoplasma capsulatus
  • Coccidioides immitis
  • Paracoccidioides brasiliensis
75
Q

What are the clinical manifestations of Histoplasma? Where is it endemic to?

A
  • Clinical manifestations:
    1. Asymptomatic pulm inf
    2. Resp inf w/fever, chills, cough, chest pain (usually w/intense exposure)
    3. AIDS: severe disseminated disease can devo (pancytopenia due to bone marrow infiltration, mouth/GI ulcers, skin rash w/pustules and/or nodules, mortality up to 10%)
  • Endemic to: MS and OH river valleys (grows in soil, bird droppings)
76
Q

How do you diagnose Histoplasma?

A
  • Tissue biopsy will show oval yeast cells in macrophages (see attached image)
  • Serology
  • Urinary antigen
  • CXR: infiltrates, mediastinal LAD, cavitary lesions
77
Q

What is the treatment for Histoplasma?

A
  • Amphotericin for severe disease
  • Itraconazole otherwise
78
Q

What is erythema nodosum (EN)? When might you see it?

A
  • Manifests as red, tender nodules (“desert bumps”) on extensor surfaces like skin over the tibia and ulna
    1. Delayed (cell-mediated) hypersensitivity response to fungal Ags -> indicator of a good prognosis bc organism will probably be contained (indicates that cell-mediated immunity is active)
  • Not unique to Histo -> seen in other granulomatous diseases like cocci and TB
79
Q

What are the clinical manifestations of Blastomyces? Where is it endemic to?

A
  • Clinical manifestations:
    1. Asymptomatic respiratory illness -> 50% will have cough, chest pain, sputum production, fever/night sweats, which most often resolves spontaneously
    2. Disseminated disease -> ulcerated granulomatous lesions of the skin (70%), bone (33%), GU tract (25%) and CNS (10%) -> seen in both immunocompetent and immunocompromised
  • Endemic to: OH, MS river valley, Missouri and AK river basins (grows in moist soil)
80
Q

How do you diagnose and treat Blastomyces?

A
  • Diagnosis:
    1. CXR: can see anything -> lobar consolidation, multilobar infiltrates, multiple nodules, etc.
    2. Tissue biopsy: thick-walled yeast cells with single broad-based bud (see attached image)
    3. Serology
  • Treatment:
    1. Itraconazole
    2. Amphotericin used for severe disease
81
Q

What do you see here?

A
  • Blastomyces
  • Most commonly a verrucous lesion; can also be ulcerated -> will often show up on the face, but not always
  • Gray to violet colored
82
Q

What are the pathogenesis and clinical manifestations of Coccidioides? Where is it endemic to?

A
  • Endemic to: SW US and Latin America
  • Patho: forms large spherules in lung, filled with endospores -> if spherule wall ruptures, endospores are released and differentiate to form new spherules
  • Clinical manifestations: most infections asymptomatic
    1. Mild, influenza-like illness w/fever and cough (“valley fever”) in 10% -> erythema nodosum seen
    2. Dissemination in 1% (AA, Filipinos, 3rd trimester of pregnancy at INC risk) -> bone, meninges and skin
83
Q

What are the diagnosis and treatment for Coccidioides?

A
  • Diagnosis:
    1. Serology
    2. Spherule with endospores seen microscopically (attached image)
    3. Eosinophilia is common
    4. Skin test reactivity to diagnose exposure
  • Treatment:
    1. Amphotericin for persistent lung lesions or disseminated disease
    2. Fluconazole for meningitis (crosses CSF): long term suppression to prevent recurrence
84
Q

What are the clinical manifestations, diagnosis, and treatment for Paracoccidioides? Where is it endemic to?

A
  • Endemic to: rural Latin America, esp. Brazil
  • Clinical manifestations: mild respiratory infection that can progress to dissemination and devo or oral, nasal, facial nodular, ulcerated lesions (much more extensive than w/blasto) and submandibular lymphadenopathy
  • Diagnosis: 1) tissue biopsy shows yeast cells with multiple buds (see attached image -> pilot wheel configuration), 2) serology
  • Treatment: several months of Itraconazole; Amphotericin for severe disease
85
Q

What is this?

A

Coccidioides

86
Q

What are these lesions characteristic of?

A

Paracoccidioides

87
Q

The common cold can be caused by what 2 families of viruses?

A

Rhinovirus

and

Coronavirus

88
Q

Describe the rhinovirus - characteristics, what does it cause, why does it affect the URT?

How is it transmitted?

What are the clinical manifestations?

Duration of infection?

How do you treat this?

A

• Icosahedral, non-enveloped positive sense single-stranded linear RNA virus.
–Greater than 100 serotypes

•Most common cause of the common cold (accounts for at least 60% of all URTIs)
•More common in fall and winter
•Acid labile – destroyed by stomach acid
•Replicates better at 33°C (rather than 37°)
–Infects the URT and not the LRT

• Clinical manifestations
–Incubation period 2-4 days
–Sneezing, nasal discharge, sore throat, cough and headache x 1 week
–Mild chills otherwise no systemic symptoms

  • Treatment: supportive
  • No vaccine
89
Q

Describe the coronavirus.

A
  • Helical, enveloped, positive sense single-stranded linear RNA
  • Account for 15-20% of URTIs
  • similar manifestations as common cold
    •Outbreaks in winter on a 2-3 year cycle
    •Does not cause LRTIs (except SARS and MERS)
    •Can cause GI illness
90
Q

Describe the pathogenesis of rhinovirus.

A

–Virus binds to ICAM-1 (intercellular adhesion molecule 1) on respiratory epithelial cells

–Major pathogenesis associated with chemical mediators of inflammation (bradykinin, prostaglandins) that cause vasodilation, mucous secretion, stimulation of sneeze and cough reflexes

91
Q

Describe the characteristics of Bordetella pertussis.

pathogenesis

transmission

clinical manifestations

diagnosis

treatment

and prevention of pertussis

A
  • Encapsulated gram negative rod (coccobacillary)
  • Causes whooping cough
  • AB toxin:

B attaches to host cell surface receptor, enabling endocytosis; A (active) component attaches ADP-ribosyl to disrupt host cell proteins

A component binds to GPCR and blocks its signaling. Adenylate cyclase remains active and cAMP accumulates inside the cell, resulting in overactivity, affecting cell function

* Impairs phagocytosis and causes decreased cilia activity.
  • TRANSMISSION:
    –Airborne droplets produced during coughing episodes
    –Highly contagious
  • CLINICAL MANIFESTATIONS:
    –Stages of infection
    •Catarrhal: 2 weeks of mild URT symptoms
    •Paroxysmal: 2-3 months of severe cough
    –Severe coughing fits with “whooping” sounds at the end of coughing fits
    •Convalescent: 1-2 weeks of reduction in coughing
  • DIAGNOSIS:
    –Nasopharyngeal swab (DFA or PCR)
    –Culture
    –CBC with striking lymphocytosis
    • Pertussis toxin causes striking lymphocytosis in the blood. Toxin inhibits signal transduction by chemokine receptors, resulting in failure of lymphocytes to enter lymphoid tissue such as spleen and lymph nodes.
  • TREATMENT:
    –Azithromycin for all individuals with positive lab diagnosis regardless of age or whether they continue to have symptoms
    –Treatment for patients with clinical diagnosis who have had symptoms less than 21 days
    •Maybe also for those with greater than 21 days of symptoms (contact with high-risk persons)
  • PREVENTION:
    –Vaccine (inactivated toxin). DTaP (diphtheria, tetanus, acellular pertussis).
    • Has lost some of its potency since 1997
    • Boosters required for those >19yoa

*

92
Q

Describe Corynebacterium diphtheriae.

What are its characteristics, what does it cause?

pathogenesis

transmission

clinical manifestations

diagnosis

treatment

and prevention of diphtheriae

A
  • Gram positive bacillus, pleomorphic, club-shaped, arranged in palisades, beaded appearance.
  • Causes Diphtheria
    • PATHOGENESIS:
      –A-B toxin blocks protein synthesis by inactivating elongation factor 2 (EF-2) by ADP ribosylation, resulting in decreased protein synthesis.
      Toxin also induces formation of a pseudomembrane
      • “Pseudomembrane” refers to abnormal nature of the membrane in contrast to normal anatomic membranes of the body such as tympanic membrane, placental membrane.
        –Composed of necrotic fibrin, leukocytes, erythrocytes, epithelial cells, and organisms
        –Adheres tightly to underlying tissue and bleeds with scraping
        –Toxin induced
        –Can extend and cause mechanical obstruction
  • TRANSMISSION:
    airborne droplets
  • CLINICAL MANIFESTATIONS:
    –Gradual onset of
    –Sore throat that gets progressively worse
    –Malaise/fatigue/low-grade fever
    –Cervical lymphadenopathy (“bull neck”)
    –Cardiac dysfunction (myocarditis) 7-14 days after onset of respiratory symptoms
  • (Myocarditis can be accompanied by heart block, arrhythmias, heart failure. Clinically evident cardiac dysfunction in 10-25%)
    –Neurologic toxicity (local neuropathies and cranial neuropathies – local neuropathies such as paralysis of the soft palate)
    –Mechanical obstruction
  • DIAGNOSIS:
    –Throat swab culture on Loeffler’s medium, tellurite plate (contains a tellurium salt that is reduced to elemental tellurium within the organism; typical gray-black color of tellurium in the colony is diagnostic); and blood agar.
    –If C. diphtheriae is recovered from the culture, either antibody inoculation or antibody-based gel diffusion precipitin test is performed to document toxin production. PCR for presence of toxin gene also used.
    –Smears of throat swab should be stained with gram stain and methylene blue. Methylene blue is excellent for revealing typical metachromatic granules.
  • TREATMENT:
    –Antitoxin administration AND either penicillin or erythromycin
    –Do not wait for diagnosis to be confirmed to treat. If suspected, treat immediately
  • PREVENTION:
    –Vaccine (DTaP, tdap)
93
Q

What is acute otitis media?

What causes it?

Who tends to get this infection?

What are the most common organisms?

How do you treat AOM?

A
  • Acute middle ear infection
  • Usually have antecedent event (eg viral URTI) causing inflammation of nose, Eustachian tube, etc.
  • Tube gets obstructed from inflammation, secretions accumulate and bacteria find their way in (colonizers of URT)
  • WHO: Ear infections are more common in children because their Eustachian tubes are shorter, narrower, and more horizontal than in adults.
  • ORGANISMS:
    –Streptococcus pneumoniae (50%)
    –Haemophilus influenzae (45%)
    –Moraxella catarrhalis (10%)
  • TREATMENT:
    –Amoxicillin 1st line
    • Augmentin for those who have had recent antibiotics or who have history of AOM unresponsive to amoxicillin
    –Patients can be observed for 48-72 hours without immediate antibiotic therapy in certain situations.
    • If worsen or fail to improve, start antibiotics
    • If <2 years old or >2 and appear toxic, need immediate antibiotics
94
Q

What causes acute sinusitis?

Describe the manifestations of this infection.

How do you treat it?

A

•Complication of viral URI

•Patient either improves initially then worsens OR fails to improve after 10 days of illness
–Worsening cough, headache, facial pressure, more nasal congestion, mild fever

•Treatment: Augmentin

95
Q

Describe what epiglottis is.

What organisms cause it?

Who does it usually affect?

What are the clinical manifestations?

Prognosis?

A

• Acute inflammation in the supraglottic region of the oropharynx with inflammation of the epiglottis, vallecula and arytenoids
• Causes
–H. flu (25% of cases) Classically associated with Hib.
–Followed by H. parainfluenzae, S. pneumoniae and Group A strep
•Overall incidence has dropped due to adoption of the vaccine
•Most typical patient affected is an urban male in his 40s.

•Clinical pres: sore throat, odynophagia/dysphagia, muffled voice
•Rapid onset to less fulminant presentation
•Prognosis generally good
–However unrecognized epiglottitis can lead to airway compromise and death and risk of death is still high

[the image shows the ‘thumb sign’]

96
Q

What is Aspergillus fumigatus? What are its clinical features?

A
  • Found worldwide
  • Mold with septate hyphae -> grow on decaying vegetation producing chains of conidia
  • Features of Aspergillus infection:
    1. Fungus ball formed within cavities of the lungs; can produce hemoptysis
    2. Allergic infection of bronchi w/asthmatic symptoms and high IgE titer; causes expectoration of brownish bronchial plugs containing hyphae
    3. Invasive PNA w/hemorrhage, infarction, & necrosis, esp. in those with hematologic malignancies and neutropenia -> common cause of death in these pts
97
Q

Why don’t HIV+ patients get Aspergillus that often?

A
  • Because their lymphos are down, not their neutrophils -> major risk factor is neutropenia
98
Q

How do you diagnose Aspergillus?

A
  • Bio__psy: septate, acute-angle branching hyphae (see the attached image); radiating chains of conidia
99
Q

What is this?

A

Aspergillus: radiating chains of conidia

100
Q

What is this?

A

Aspergillus: septate, acute-angle branching hyphae

101
Q

What does the characteristic Aspergillus CT scan look like?

A
  • Single or multiple nodules with or without cavitation, halo sign (areas of focal hemorrhage around the lesion)
102
Q

What might this be?

A
  • Aspergillus
  • Single or multiple nodules with or without cavitation, halo sign (areas of focal hemorrhage around the lesion)
103
Q

What is the treatment for Aspergillus?

A
  • 1st line treatment: Voriconazole (for invasive pneumonia)
    1. Amphotericin or echinocandins are alternative if patients don’t tolerate Vori
  • Remove the fungus balls (bc can cause hemoptysis)
  • For ABPA: steroids and antifungal agents
104
Q

What is Mucormycosis? Risk factors? Transmission?

A
  • Opportunistic infection caused by bread mold fungi (Mucor, Rhizopus, Cunninghamella, Lichtheimia) belonging to the family Mucormycetes
  • Risk factors for infection: diabetes, neutropenia, iron overload, burns/surgical wounds, corticosteroid use
  • Transmitted by airborne spores, invade tissues of patients with reduced host defenses
    1. Also angioinvasive -> vessels
  • Pretty much a death sentence if it is an invasive infection
105
Q

What are the clinical manifestations of Mucormycosis?

A
  • Invasive rhinocerebral sinusitis, frontal lobe abscesses
    1. Originates in paranasal sinuses and spreads to orbit, hard palate and brain and carries high mortality rate
    2. Headache, facial pain
  • Pneumonia
  • Cutaneous infection
106
Q

What is this?

A

Mucormycosis: not much hope for th pt on the left (not much you can do)

107
Q

How can you diagnose Mucormycosis?

A
  • Biopsy: nonseptate broad hyphae with frequent right angle branching; spores in a sporangium
108
Q

What is this?

A

Mucormycosis: nonseptate broad hyphae with frequent right angle branching

109
Q

What is this?

A

Mucormycosis: spores in a sporangium

110
Q

What is the treatment for Mucormycosis?

A
  • Treat the underlying disorder plus Amphotericin and surgical removal of necrotic infected tissue
    1. Posaconazole can also be used
111
Q

What is Pneumocystis jiroveci (carinii; PCP)? What does it cause?

A
  • Yeast that can cause:
    1. Most infections asymptomatic; 70% of population has been infected worldwide
    2. IMP cause of immunosuppressed pneumonia (PCP)
    3. Common opportunistic infection, and one of leading causes of death in AIDS patients
  • Reservoir of transmission unknown
  • Cysts in alveoli produce inflammatory response, resulting in frothy exudate that blocks oxygen exchange
    1. Organism does not invade lung tissue.
  • CD4+ T cells recruit monocytes and macrophages which are responsible for clearance of the organism
    1. CD4 count <200 main risk factor
112
Q

What are the clinical manifestations of PCP (incl. CXR findings)?

A
  • Dry cough
  • Dyspnea that is progressive
  • Fever
  • Tachypnea
  • Hypoxemia
  • Most common CXR findings: diffuse, bilateral, interstitial, or alveolar infiltrates (but can be variable)
    1. CXR normal in up to 1/4 of cases
    2. Pneumothorax can also occur
113
Q

How do you diagnose PCP?

A
  • Finding cysts by microscopic exam of lung tissue or fluids obtained by bronchoscopy or lung biopsy
    1. Galactomannan Ag: found in wall of Aspergillus species (suggestive of the diagnosis) -> can be done instead of bronchoscopy for very sick pateints
  • Visualization of cysts by methenamine silver (see attached image -> helmet-like)
    1. Giemsa stain or other stains
  • Flourescent antibody staining
  • PCR on respiratory tract specimens
114
Q

What is the treatment for PCP? Why?

A
  • 1st line: Trimethoprim-sulfamethoxazole (Bactrim)
    1. Other options (2nd line): Clindamycin/Primaquine, Atovaquone, Pentamidine
    2. Prophylaxis for AIDS pts w/CD4 <200: Bactrim, Dapsone, or Atovaquone
  • Doesn’t have ergosterol, so you can’t use normal anti-fungals (used to be classified as a protozoa)
115
Q

What is this?

A

PCP

116
Q

What is Cryptococcus neoformans? What can it cause?

A
  • Yeast present in soil and bird (pigeon) droppings
    1. Oval budding yeast w/wide polysaccharide capsule; forms narrow-based bud
  • Causes meningitis in immunocompromised pts (esp AIDS) and is most common life-threatening disease in AIDS pts
  • Also causes pneumonia in immunosuppressed as well as immunocompetent persons
    1. Vast majority of immunocompetent patients will be asymptomatic or have only mild respiratory symptoms
    2. In immunocompromised pops, symptoms include fever, chest pain, dyspnea, cough, and hemoptysis
117
Q

What is this?

A

Cryptococcus neoformans

118
Q

What do you see here? What might be the causative org?

A
  • Nodules on the left, ground-glass opacities in the middle (more commonly a cause of meningitis than pneumonia)
119
Q

What is Cytomegalovirus?

A
  • DNA-enveloped virus similar in morphology and structure to other Herpes viruses
  • Infection occurs worldwide; > 80% have Ab’s against it
  • Usually asymptomatic except in immunosuppressed
    1. Enters latent state in monocytes; can be reactivated when cell-mediated immunity is decreased
  • In immunosuppressed population (esp. renal, stem cell transplant recipients), pneumonitis commonly develops
    1. AIDS patients: colitis and retinitis (typically NOT pneumonitis)
  • Viral inclusion body characteristic of CMV infection in the histo image on the right
120
Q

What are some of the common CT scan images possible with Cryptococcus?

A

Nodules on the left; ground-glass opacities in the middle (more commonly a cause of meningitis than pneumonia)

121
Q

What do you see here?

A

CMV: characteristic viral inclusion body on the right

122
Q

What is Nocardiosis? What does it cause? Diagnosis? Treatment?

A
  • Caused by the bacterium Nocardia asteroides: aerobes, found in the soil
  • Thin branching filaments, gram (+) -> top right image (can be confused with Actinomyces)
    1. Many isolates are weakly acid-fast (see attached images)
  • In immunocompromised, produce lung infection and may disseminate – have predilection for brain tissue
    1. Can cause pneumonia, lung abscess with cavity formation, lung nodules or empyema
    2. Spreads to brain where it causes brain abscesses (and can cause seizures -> head CT, brain MI)
    3. Occurs in those w/reduced cell-mediated immunity (chronic steroid use is a risk factor)
  • Diagnosis: gram stain/acid-fast stain; culture
  • Treatment: Trimethoprim-sulfamethoxazole (Bactrim)
    1. Sometimes combination therapy is needed
    2. Resistance can occur, so sensitivities should be performed
  • Pneumonia and brain abscess -> think nocardia
  • Can’t do gram stain for most fungi bc it’ll be a (-) test
123
Q

What is this?

A
  • Nocardia
  • Acid-fast stain
  • Can sometimes be confused with actinomyces due to its appearance
124
Q

What is this?

A

Nocardia: gram positive stain

Pulmonology (18 decks)

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