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- mechanism for clearing respiratory secretions
- voluntary or reflex
- afferent receptors provide stimulis, efferent receptors cause event
- A cough is: inspiration, glottic closure, relaxation of diaphragm, muscle contraction of thorax, creating increased intrathoracic pressure, opening of glottis
Causes of cough
- Irritants: smoke, dust, fumes, foreign bodies
- Endogenous stimulants: upper airway secretions, gastric reflux fluids
- Disorders w/ inflammation, constriction, infiltration, or compression of airways
- Stimulation may affect upper respiratory or lower respiratory receptors
- Cough is either acute or chronic: 3weeks
Etiologies of Cough
- Infection: URI, pneumonia, lung abscess
- Granulomatous dz
- Compression from extrinsic masses
- Interstitial lung dz
- Congestive heart failure
- Medications: Angiotensin-converting enzyme inhibitors
Afferent receptors role in mechanisms of dyspnea
- Sense that there is inadequate "air"
- hypoxia, hypercapnia, acidemia
- Bronchospasm or chest tightness
- interstitial edema/vascular receptors
- Exercise and chest wall/skeletal muscle
Efferent receptors role in the mechanisms of dyspnea
- Disorders of ventilation
- Weak or fatigued respiratory muscles
- A mismatch between sense of inadequate and amount of respiratory effort or function to compensate
- Air hunger creates anxiety which also contributes to sensation and severity
Causes of dyspnea: Respiratory
- Inadequate gas exchange: Pneumonia, pulmonary embolis, pulmonary edema, aspiration, interstitial lung disease
- Inadequate airways: COPD, asthma, chest wall alterations as in scoliosis, myasthenia
- Stimulation to breath: pregnancy, metabolic acidosis, acute bronchospasm, pulmonary embolis, high altitude, respiratory stimulants.
Causes of dyspnea: cardiac
- High cardiac output: anemia, left to right shunts, obesity
- Normal cardiac output: exercise, anaerobic metabolism, hypertension, aortic stenosis, hypertrophic cardiomyopathy, pericardial disease
- Low cardiac output: coronary artery disease, nonischemic cardiomyopathies
What are the multiple categories of pneumonia
- Community acquired pneumonia (CAP)
- Healthcare associated pneumonia
- Hospital acquired pneumonia
- Ventilator associated pneumonia
- Immunocompromised patient associated pneumonia
- Subtypes: HIV, Transplant, Neutropenic
Community acquired pneumonia
- Pts have more severe problems
- Long list of pathogens
- Antibiotic resistance is important
- Lab tests are inadequate
- Risk factors are more severe (coexisting illness, physical exam findings, lab abnormalities)
shortness of breath/dyspnea
pleuritic chest pain
symptoms of pneumonia
Confounding symptoms of pneumonia (coexisting dz's alter presentations)
- Influenza A,B,C (orthomyxoviridae)
- Influenza A subtypes
- H1,H2,H3 have hemagglutinins
- N1,N2 have neuraminidase as surface glycoproteins
Spherical, enveloped viruses
Segmented, negative sense, RNA genome
Surface proteins: hemagglutinin, neuraminidase, M2
Host range: _______ A => humans, swine, ducks; _______ B,C => humans
Spread person-person by resp. droplets (virus remains virulent for up to 2 days outside of host)
Biology of influenza viruses
What is antigenic change?
- allows continued circulation of new subtypes by human populations through processes of mutation and recombination.
- Antigenic drift -- point mutations in the gene segment coding for HA or NA.
- Antigenic shift -- marked changes in HA or NA or both due to acquisition of new gene segments.
Strains: H7N2, H7N3 in N. America and Netherlands (other strains in SE Asia and Texas)
H5 strains were confined to Hong Kong
All are _____ strains and resulted from the slaughter of millions of ______.
- Avian influenza
- All are avian and slaughter of chickens
Asian flu (H5N1) also exists, mainly in SE Asia.
Name the strain.
Frist seen 3/09 in Mexico (in US by april)
By August > 1 million cases
In Jan 99.7% of cases were flu A and 99.4% of those were ____.
8% mortality rate
Differentiate between complicated and uncomplicated influenza pathogenesis
- Initially infects resp. tract mucosa
- Uncomplicated = degeneration of epithelial cells (loss of cilia), edema, hyperemia, mononuclear cell infiltration
- Complicated = hemorrhagic airless lungs, loss of ciliated cells, hyaline membrane formation, mononuclear cell infiltration
What causes the constitution symptoms of influenza?
Cytokines -- increased interferon, increased TNF alpha and interleukin 6 in nasal mucosa and blood.
What factors contribute to a bacterial superinfection in a Pt w/ influenza?
- Damaged bronchial epithelium => disrupted mucociliary clearance => increase bacterial colonization.
- Viral nucleoprotein inhibits PMN leukocyte chemotaxis and superoxide production.
NAME THE SYNDROME
systemic symptoms(3-5 days): fever, malaise, headache, myalgia
respiratory symptoms (2-4 wks): sore throat, cough, nasal dishcarge
Dz more severe in smokers or pts w/ underlying cardiorespiratory dz.
What are these complications associated with?
Viral Pneumonia: mild-- patchy infiltrates on CXR; severe-- influenza syndrome followed by increasing cough, tachyapnea, dyspnea; ARDS, hemoptysis; 50% mortality; pulmonary fibrosis and chronic lung dz survivors.
Secondary bacterial pneumonia: re-appearance of fever, increased resp. symptoms during recovery; commonly caused by strep pneumoniae and staph aureus.
Non-pulmonary complications: Rare CNS syndrome, cardiac (myocarditis, pericarditis), acute myositis.
Explain the lab diagnosis of Influeza
- CPE observed in 3-5 days (in monkey cell lines)
- Virus replication may be detected earlier by hemadsorption w/ pig or chicken erythrocytes; immunoflourescence using type specifc antisera.
- Antigen detection
How do you prevent/treat influenza?
SYMPTOMATIC: antipyretics (avoid aspirin), antitussives, ventilatory support; ANTIVIRALS: early treatment reduces viral replication and duration of symptoms by 1-2 days
Lipid bilayer envelope
Peplomers (spike-like glycoprotein projections)
Single stranded RNA (neg. sense)
Large G glycoprotein => attachment
Protein F => fusion
NO hemagglutinins or neuraminidase (H influenza does have them)
RSV (Respiratory syncytial virus)
2/3 of infants get this infection in the 1st year of life (mostly symptomatic)
Very severe in children <6mo.
Repeat infections are common
Transmission: fomites, large particle aerosols, self-inoculation
Peak incidence in winter (annual epidemics)
Contributes to SIDS
Describe the pathogenesis and clinical manifestations of RSV
- Virus replicates in ciliated epithelial cells
- Bronchiolitis: necrosis of bronchiolar epithelial cells, migration of lymphocytes into affected tissues, mucous plugging occludes smaller airways, air-trapping with overdistention.
- Children: expiratory wheezing, air trapping, nasal flaring, subcostal retractions, cyanosis (fever<50%, apnea in 25-30%).
- Complications include bacterial otitis media, sinusitis, bacterial pneumonia, reactive airway disease.
How do you diagnose and treat RSV
- Clinical presentation
- Lab: antigen detection, cell culture (takes 3-5 days, characterized by syncytial pattern, combo of shell and immunofourescence staining => early detection)
- Treatment: Healthy children >1 yr -- supportive therapy; Children <1 yr -- hospitalization req., iv fluids, O2 therapy; Immunocompromised children -- ventilatory support often needed, antiviral therapy.
Name the syndrome
Almost always symptomatic
Four phase dz
Four corners outbreak
Spread via a single rodent species (humans inhale airborn virus particles)
No person-person spread
Hantavirus Pulmonary syndrome
Name the syndrome based on the following clinical manifestations
1) Prodrome(1-10 days): fever, myalgia, severe back and hip pain, nausea, vomiting, abdominal pain.
2) Pulmonary edema/shock: abrupt onset of cough & dyspnea, O2 desaturation, progression to alveolar flooding is accompanied by centrally located infiltrates (need for intubation), thrombocytopenia, hemoconcentration, increased WBC.
3) Spontaneous diuretic phase: recovery is rapid and Pt's are extubated within 12-24 hrs.
4) Convalescent phase: several weeks to months of weakness and fatigue, recovery is usually complete.
- Hantavirus pulmonary syndrome
- confirmed w/ G1 type-specific antibodies, PCR on peripheral blood mononuclear cells.
What is the treatment for Hantavirus?
- Critical care management: intubation w/ mechanical ventilation, vasopressors rather than fluids to support blood pressure
- Intravenous Ribavirin: placebo-controlled trials are ongoing (efficacy not established)
Name the pathogen
smallest free-living microbes
NO cells wall (tri-layer membrane, stains poorly, insensitive to cell wall synthesis inhibitors)
pleomorphic shapes from coccoid to rods
Transmitted via droplet spread
accounts for 20% of CAP (5-15 yrs old)
- Attaches to cilia and microvilli of cells lining bronchial epithelium
- Intense bronchial and peribronchial inflammatory response w/ desquamation of involved mucosa
- 3-13% if infected Pt's => pneumonia
Name the pathogen based on these clinical manifestations
symptoms similar to tracheobronchitis: cough becomes paroxysmal and productive of mucoid even blood streaked sputum (cough=> retrosternal chest pain)
CXR: unilateral patchy segmental infiltrates, bilateral infiltrates, pleural effusions (25%)
Extrapulmonary manifestations: related to autoantibodies, toxins & host response; deratologic, migratory polyarthritis, CNS conditions, hemolytic anemia, cardiac complications (5%), GI syndromes.
>4x rise in serum antibody
Mycoplasma Pneumoniae (confirmed by serology: complement fixation, ELISA, immunoflourescence techniques or Cold agglutinins)
Name the pathogen
obligate intracellular bacteria
cell wall similar to gram neg. bacteria-LPS (no peptidoglycan)
possess eubacterial ribosomes
synthesize own proteins
small DNA genome
dependent upon host cell for energy (cannot synthesize ATP or reoxidize reduced NADP)
Chlamydia Pneumonia (transmission: resp. secretions)
- Syndromes: severe pharyngitis w/ hoarseness, Sinusitis (5%), Otitis media.
- 3rd or 4th most common cause of CAP (more common in elderly)
- Pharyngitis proceeds pneumonia
- Biphasic illness
- Long interval from onset of symptoms to clinic visit
- Diagnosis: Culture (50-75% sensitive), Serology: MIF (88% sensitive)-- 4x increase in IgM>16, IgG >512, pre-existing antibody --IgG, 8-256.
- alpha hemolytic
- usually grow in pairs
- virulent strains are encapsulated
- susceptible to lysis
- Bile sensitive
- Incidence highest in infants and alder adults (<2 and >60)
Diseases caused by streptococcus pheumoniae
- Otitis media
- Septic arthritis
- Streptococcus pneumoniae (pneumococcus) causes lobar pneumonia
- In this CXR you can see the clear line where the pneumonia is present in one lobe and not in another.
Streptococcus pneumoniae lab diagnosis
- Gram stain: Gram + diplococci (associated w/ PMNs)
- Detection of pneumococcal antigen in urine
- Direct detection of nucleic acid in samples using PCR (no standardized method)
Sterptococci Pneumoniae identification
- 23 valent polysaccharide vaccine: Major serotypes causing dz; not effective for young children and immunocompromised; Recommended for: immunocompetent adults and children >2 and immunocompromised Pt's at risk for serious pneumococcal dz.
- 7-valent pneumococccal conjugate vaccine: serotypes 4,6B,9V,14,18C,19F,23F, coupled w/ non-toxic variant of diphtheria toxin CRM 197; first dose 2-6 months old-- also for Pt's w/ underlying conditions.
Name the pathogen
severe, necrotizing pneumonia
second most common cause of superinfection in influenza
multifocal dz w/ possible abscesses
may have other primary focus of infection
Staphylococcus aureus pneumonia
a) Staphylococcus epidermidis, diptheroids, candida have high or low virulence?
b) Staph aureus, TB, mycoplasma, Strep pneumoniae have high or low virulence?
What type of things can decrease host resistance?
cystic fibrosis, ciliary immotility, tumor, neurologic problems, defects in T or B cells, neutropenia, splenectomy
most common bacterial pneumonia, can be lobar
aggressive baterial pneumonia, can form abscesses
causes bacterial pneumonia in young children in poor countries.
water contaminant, antibiotic resistance, common in CF, also seen in burn Pt's and urinary infections.
aggressive, necrotizing, systemic symptoms, in water systems, hard to culture, test by urine Ag test.
Left = bronchopneumonia
Right = Lobar pneumonia
- L: Bronchopneumonia
- R: Lobar Pneumonia
- Radiographs are key for finding pneumonia (CT and MRI are even better)
- Infiltrates can persist for up to 6 weeks, so recheck the Pt 6 weeks after to make sure there isn't an underlying tumor.
- Bacterial Pneumonia(other side)
- Gram stain(this side)
Intravascular growth causes necrosis and abscess
Abscesses are often seen with
aspiration, anaerobes, staph, klebsiella, septic emboli, obstructing tumor
Neutropenic pneumonia (no neutrophils because Pt lacked them)
Empyema -- infected inflammation
Bronchiectasis -- scarred, irregularly dilated airways, rare except with cystic fibrosis
- Diffuse alveolar damage or acute alveolar injury or
Name the type of pneumonia
cough, fever, but little to no sputum
difficult to culture (cold agglutinin titers)
necrotizing bronchiolitis with fibrinous exudate
like legionella, nonpulmonary symptoms (rash, arthralgia, diarrhea, neurologic)
- Primary TB: peripheral granuloma and hilar lymph node involvement (Gohn complex)
- Secondary TB: Reactivation or reinfection, cavitations and granulomas
- Granulomatous: macrophages, giant cells and lymphocytes; caseous necrosis in center, eventually becomes fibrous scar or cavity when healed.
Secondary TB: nodules and cavities
For TB AFB stains, should you trust a negative culture?
No, false negatives happen all the time.
disseminated tiny (2mm) granulomas all over the place. Occur mainly in immunocompromised Pt's.