Definition of Pneumonia (Pneumonitis)
-Inflammation of lung parenchyma (alveoli)
-Illness with symptoms of cough, fever, dyspnea *and* radiographic infiltrates

Acquisition of Pneumonia
-Aspirating it from mouth after vomiting
-Hematogenous spread from another body site
-Spread down resp tract from upper tract flora

Epidemiology of Community Acquired Pneumonia
-4-6 million cases per year in USA
-Median age 55-68
-*Winter peak*
-7th most common cause of death

Predictors of mortality in patient with CAP
-Age >65
-Chronic lung dz
-Need for mechanical ventilation
-RR >30
-Low BP

Why are elderly patients predisposed to pneumonia
-Elderly patients have more of the underlying conditions, and due to length of exposure more apt to develop pulmonary issues

Common causes of community-acquired pneumonia
-Strep pneumo
-Mycoplasma pneumo
-Haemophilus influenzae
-Moraxella catarrhalis
-Chlamydophila pneumo
-Influenza A/B

Sx of Typical Pneumonia
-Productive cough with purulent (yellow/green) or rusty (RBC-tinged) sputum
-Pleuritic pain
-*Lobar pattern of consolidation* on x-ray

Sx of Atypical Pneumonia
-Dry (non-productive) cough
-Interstitial pattern of fibronodular/patchy infiltrates by x-ray

Organisms causing Typical pneumonia vs Atypical pneumonia
-Typical=S. pneumo, H. influenzae, M. catarrhalis (same as otitis media)
-Atypical= M. pneumo, C. pneumo, Legionella, viruses

Lower tract in normal vs COPD lung
-Normally, upper tract has flora and lower tract sterile
-In COPD, upper and lower tract have pathogenic bacteria

Inflammatory processes active in pneumonia (pic)
Inflammatory processes active in pneumonia (pic)

Defenses in Alveolar lining
-*Alveolar macrophages* ingest particles
-*Fibronectin* attaches to both bacteria and PMNs and promotes phagocytosis
-*Surfactant* binds to bacteria, fungi and viruses to opsonize and enhance phagocytosis

X-ray of lung showing right lower
X-ray of lung showing right lower

X-ray of lung showing right middle consolidation, (obscures right heart border)
X-ray of lung showing right middle consolidation, (obscures right heart border)

X-ray of lung showing right upper
X-ray of lung showing right upper

X-ray of lung showing left lower
X-ray of lung showing left lower

X-ray of lung showing left upper consolidation (lingula)
X-ray of lung showing left upper consolidation (lingula)

Dx testing for CAP
-Sputum for gram-stain and culture
-Blood culture- *more specific* because sputum may be mixed
-Urinary antigen for S. pneumoniae+Legionella
-Serology for Mycoplasma and Chlamydophila
-PCR only reliable for Mycoplasma

Strep pneumoniae
-Gram stain
-Catalase negative
-Optochin sensitive
Strep pneumoniae
-Gram stain
-Catalase negative
-Optochin sensitive

a disk vs p disk
-a disk has bacitracin
-p disk has optochin
-Used for dx of strain on plate

Virulence factors of Strep
-*Capsular polysaccharides* inhibit phagocytosis
-Mutants lacking capsule are avirulent
-*Surface adhesin A* attaches to epithelial cells of nasopharynx
-Surface *protein C* binds to complement factor H, inhibits C3 convertase, reducing phagocytosis
-*Pneumolysin* is cytotoxic and activates complement
-*IgA Protease*

Pathogenesis of Strep pneumoniae
-Colonization of nasopharynx precedes pneumonia
-Organisms reach trachea and bronchi by inhalation/aspiration
-Organisms are normally cleared by cough/ciliary escalator
-Clearance can be impaired by allergies, smoking, viral upper resp infection
-Organisms gain access to alveoli and escape phagocytosis via capsule and inhibit complement activation
-Colonization 2-4 weeks in adults, 4 months in children (much longer in children)
-Antibody develops to clear colonization and prevent pneumonia

Pathogenesis of Strep pneumoniae after accessing alveoli
-In alveoli, bacteria proliferate, *activate complement and generate cytokines*
-Cytokines lead to attaction of neutrophils, exudate into alveolar spaces
-Peptidoglycan and lipotechoic acid active alternate pathways of complement
-Cell wall substances also stimulate TLR-2 leading to further production pro-inflam cytokines

Sequelae of Strep pneumo infection
-*No inflammation* of interstitium, *no necrosis*and *no abscess* formation
-Pleural effusion possible with spread into pleura
-Respiratory failure (especially in patients with prior pulmonary disease)
-Hypoxemia, cyanosis and labored breathing lead to requirement of mechanical ventilator
-Sepsis with spread to meninges can occur
-Leads to shock with poor perfusion of multiple organs like kidney and brain

Haemophilus influenzae
-Gram negative rod
-*Non-encapsulated* strain are *normal URT flora*
-*Encapsulated Hib cause pneumonia*
-Fastidious organism, require 1) Chocolate agar 2) BA around S. aureus(supplies V) 3)Nutrient agar with X & V

Chocolate Agar
-Blood agar that has been heated to release factors X/V

What are supplements X & V required for haemophilus growth
-X=protoporphyrin (hemin)
-H. influenzae grows without supplements on chocolate agar

Gram-negative diplococci called Moraxella catarrhalis
Gram-negative diplococci called Moraxella catarrhalis

Prevention of Pneumonia
-2 vaccines effective
-Pneumococcal conjugate vaccine (PCV)
-Pneumococcal polysaccharide vaccine (PPV)
-Patients 65+ with risk factors should get PCV and PPV 1 year later
-Children 2-15 need PCV in *4 doses*
-Annual influenza vaccine with surface antigens A/B

Atypical Pneumonia Sx, DDx from typical pneumonia
-*Dry* (non-productive) *cough*, thin *white sputum*
-*Interstitial pattern of fibronodular* or patchy infiltrates by x-ray (less severe than typical), DDx from lobar
-Infiltrates in *mildly ill* outpatient (walking pneumonia)
-Less like to have pleuritic pain/pleural effusion than typical pneumonia
-Viral pneumonias are atypical

Mycoplasma pneumoniae
-Short rod bacterium with no cell wall
-2nd most common cause CAP after Strep pneumoniae
-Spread by respiratory droplets disseminated by cough, *gradual onset, 2-3 weeks*
-Not visible on gram stain of sputum, not culturable
-*IgM Ab is best diagnostic method*
-Cold agglutinins also associated with mycoplasma
-Peak incidence in fall

Interstitial Pattern (*linear* markings, *streaky*, patchy fibronodular) on chest-x indicating Mycoplasma pneumoniae
Interstitial Pattern (*linear* markings, *streaky*, patchy fibronodular) on chest-x indicating Mycoplasma pneumoniae

M.pneumoniae causes interstitial inflammation with thickened septae and clear alveolar spaces, with normal septae and PMN exudate in alveoli, fibronodular pattern, vs strep pneumoniae alveolar infiltration on right

Legionella pneumophila
-Aerobic, small gram-negative bacillus seen with *silver stain*
-*Chlorine resistant* (survives h20 treatment)
-Grows at *high temp*
-Lives *intracellularly in macrophages*
-LPS toxin + flagellin
-Slow growing on charcoal yeast extract agar
-Sx include dry cough and fever, abdominal pain/diarrhea common

Photo of legionella growing in amoeba via Gimenez stain
Photo of legionella growing in amoeba via Gimenez stain

Legionella uptake and growth in a macrophage
Legionella uptake and growth in a macrophage

Acquisition of Legionella
-From aerosols from environment created by water coolers, faucets, showers
-More susceptible in smokers, COPD, elderly and immunocompromised
-*Not* contagious from *person to person*

Chlamydia Pneumonia
-Caused by C. pneumoniae and C. psittaci
-Small gram negative bacterium with truncated LPS, requires ATP from host cells
-Antibodies against are not protective

Life Cycle and Contagiousness of Chlamydia
-Elementary body is aerosol droplet, contagious
-Long incubation period (3 weeks)
-Forms reticulate body in cell, cause sx, inflammation
-Then eventually converts back to elementary body and lyses cell
-No seasonal specificity

Sx of Chlamydophila
-Dry cough, malaise, *no fever*
-*Gradual* onset over several days
-X-ray shows interstitial infiltrate but is non specific
-Can cause pharyngitis, bronchitis, otitis media, sinusitis

Dx of Chlamydophila
-Serology via *microimmunofluorescence*
-Antigen detection
-Tissue culture is possible but cumbersome

-Contracted from fecal aerosol of sick/stressed birds (Parrot)
-Rarely transmits person-person
-Illness like atypical pneumonia
-Much rarer than C. pneumoniae

Bordatella pertussis
-Gram negative coccobacillus causing *tracheitis*
-Aerobic nonfermenting
-Fastidious and delicate (sensitive to cold), requires nicotinamide, grows on Bordet-Gengou agar
-*Highly contagious via respiratory droplets*
-Causes whooping cough

B. pertussis image
B. pertussis image

Virulence factors of B. pertussis
-Filamentous hemagglutinin
-Pertussis toxin=increases intracellular cAMP via ADP-ribosylation of G protein, activating adenyl cyclase
-Adenylate cyclase toxin
-Tracheal toxin

Pathogenesis of Pertussis
-Tracheitis and bronchitis, *accumulation of mucus*, inflammatory cells, *bacteria and dead epithelial cells*
-Intense *coughing against closed vocal cords* (Valsalva maneuver) to expel mucus via buildup of venous pressure
-*Breathing in against thick mucus*
-Valsalva can sometimes cause *hemorrhages in conjunctiva and brain*
-Infection rarely extends to lung to cause pneumonia or to ear to cause otitis media
-Never bacteremia

Cause of Whoop in Pertussis
1) Series of short expiratory coughing bursts working to expel mucus
2) *Inspiratory gasp* with whoop as air passes turbulently through mucus
3) Sometimes vomiting and cyanosis after coughing spells, cough may produce thick mucus plugs
4) Paroxysms may occur up to 30x a day, more at night
-Child seems normal between episodes

Pertussis Vaccine
-Acellular form combined with diphtheria and tetanus
-Contains pertussis toxoid, filamentous hemagglutinin, some with fimbriae
-Advised at 2,4,6,15-18 mo, with booster at age 4-6
-*Give pregnant women before 20th week* to avoid infant pertussis, but only if mother hasn’t had recent booster
-Protects baby for 6 months from passive IgG from mother
-Treat with *erythromycin*

Ventilator-Associated Pneumonia
-Leading cause of death of nosocomial infections in USA
-Mechanical ventilation with endotracheal tube and paralytic drug eliminates cough and ciliary action
-Positive pressure blows microbes into alveoli
-Commonly P. aeruginosa, Actinetobacter, Klebsiella, and S.aureus

Neonatal Pneumonia
-Occurs in 1st month of extrauterine life
-Early onset within 3 days of delivery (Acquisition of microbe from vagina/transplacental passage)
-Late onset occurs >3 days after delivery (Gets microbe from hospital flora or community-acquired)

Microbes involved in early onset neonatal pneumonia
1) Strep. agalactiae
-Carried vaginally asymptomatically in mother
-Prevented by detecting vaginal carriage and giving antibiotic
-Beta hemolysis is a virulence factor as a pore-forming cytolysin
2) HSV-2 venereal disease, transmission prevented via c-section in women with genital blisters

Microbes involved in late onset neonatal pneumonia
1) Staph aureus/Pseudomonas common hospital flora
2) Chlamydia trachomatis (long incubation period)

Non-tuberculous Mycobacteria
-M. avium
-Slow growing, acid-fast
-Differences from M.tuber
1)Soil organisms, aerosolize/get into water
2) Rare compared to tuberculosis
3) Occur *only in immunocompromised*
4) Not transmitted person-person
Dx. MAC via sputum culture or bronchoalveolar lavage

M. avium complex infection with pulmonary nodules and bronchiectasis
M. avium complex infection with pulmonary nodules and bronchiectasis

Disseminated M.avium complex infection in AIDS, with macrophages in lymph nodes as well as spleen, liver, bone marrow and blood, identified by acid-fast stain. Low CD4 count allows MAC to infiltrate many parts of body hematogenously

-Anaerobic Gram-positive *branching* bacilli
-Caused by Actinomyces israela/others
-Facultative or microaeropholic
-*Anaerobic media* =optimal growth
-Usually from *own flora*, not contagious
-Rare due to organisms *susceptibility to penicillin*

Actinomyces staining
Actinomyces staining

Persons predisposed to Actinomycoses
-Poor oral hygiene (lack of brushing, lack of dental checkups)
-Aspiration in alcoholics, seizure patients

Sx of Actinomycosis
1)*Oral*-lumpy jaw (infiltration into salivary glands,) gingivitis
2)*Lung* Pneumonia, Lung abscess or empyema
3)*Constitutional* Fever, cough, shortness of breath, chest pain, may see weight loss over weeks
4) *Abdominal* abscesses, like after ruptured appendicitis
-Forms masses that *mimic cancer*
-*Sulfur granules* (yellow granules in pus, with *clumps of bacteria surrounded by PMN*)

-N. asteroides
-G+ bacilli that are *acid-fast* and have *branching* morphology
-Grows well on *blood agar* with white colonies at 48 hours
-Aerosolizes/gets into water

Spread of Nocardia
-Aerosolizes/gets into water
-*Skin* is important *site of entry*, cellulitis at entry site
-Lung infected by aerosol to develop into pneumonia/lung abscess or empyema in IC host
-Develops *slowly over weeks* contrasted to acute pneumonia(~3weeks)
-Extends into *adjacent tissues*, like chest wall abscess or draining fistula
-Disseminates *hematogenously* to other sites, can cause *brain abscess*

Nocardia image
Nocardia image

Aspergillus fumigatus
-*Monomorphic*, septate and filamentous
-Major recycler of organic material
-*Airborne spores*
-Branching hyphae in body
-Sporulation on sinus surfaces in transplant patients

Aspergillus fumigatus pic
Aspergillus fumigatus pic

Pulmonary Disease caused by Aspergillus
1) Invasive pulmonary aspergillus in IC
2) Free “Ball” growth in old TB cavities
3) Allergic Bronchopulmonary Aspergillosis (grows in lumen of bronchi, asthmatic symptoms)
4) Farmers lung (allergic)

Invasive Pulmonary Aspergillus
-IC patients
-A. fumigatus
-Major problem in *transplant patients*, affects heart and bone marrow
-Spores land on nasal mucosa and colonize surface, leads to sporulation which seeds the lungs
-Causes pneumonia with hematogenous infiltration causing pulmonary hemorrhage, *hemoptysis*

Cryptococcus neoformans
-*Encapsulated* yeast, monomorphic
-Can be found in soil enriched with *pigeon droppings*
-Most common clinical presentation is *meningitis*
-Sputum/biopsy with microscopy and culture

Sx of Meningitis, that is the clinical presentation of Cryptococcus neoformans
-Increasingly severe headache
-Mental confusion
-Fever in IC patients

-Grows on wide variety of plant material including *roses*
-Pulmonary disease in urban homeless alcoholics (inhaled) called *Alcoholic rose garden sleeper’s disease*
-Looks like tuberculosis
-Skin infections which start via puncture from thorns, twigs
-Will not disseminate to lungs from subcutaneous entry

Pneumocystis jirovecii
Pneumocystis jirovecii
-Opportunistic fungi common in AIDS
-Fever, dyspnea, hypoxemia
-Will not occur if CD4 counts can be maintained >200
-Can see interstitial pneumonia, with streaks

Pneumocystis Pneumonia in yeast form via silver stain
Pneumocystis Pneumonia in yeast form via silver stain

Dimorphic fungi
-*Susceptibility in immunocompetent* host, not considered opportunistic
-Exposure via *dusty environment* with airborn dust containing fungal spores
-*Bird/Bat droppings* (Histoplasma)
-*Decaying wood* (Blastomyces)
-*Desert sand, SW US* (Coccidiodes)
-Not contagious person to person, acquired from environment
-In yeast form in body @ 37degrees
-Division via binary fission, exponential growth
-Clinical presentation all 3 resembles TB

Blastomyces dermatitidis
Blastomyces dermatitidis

-Lung inflammation mimicking tuberculosis
-Can be chronic/cavitary

Chest X-ray typical of infection by dimorphic fungi 
1) Histoplasmosis
2) Blastomycosis
3) Coccidiomycosis
-Resembles TB
Chest X-ray typical of infection by dimorphic fungi
1) Histoplasmosis
2) Blastomycosis
3) Coccidiomycosis
-Resembles TB

Sx of Dimorphic fungal infection
-Acute, self-resolving asymptomatic to severe pneumonia
-Cough, fever, malaise
-Problem in AIDS and cancer patients in endemic areas
-Danger during 3rd trimester of pregnancy
-Diagnosis via *culture of sputum*/BAL, serology, *skin test antigens*
-Do not order cultures of coccidiomycosis due to risk of aerosolizing

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