Pulmonary TBL Path Flashcards
The definition of pneumonia?
The definition of pneumonia is inflammation of lung.
Infectious pneumonia can be due to?
Bacteria, fungi, viruses or parasites of various kinds.
Non-infectious pneumonia can be due to?
Autoimmunity, toxins, injury or idiopathic causes.
Almost all acute bacterial pneumonias are due to?
Aspiration of saliva containing the pathogen
Term “aspiration pneumonia” is used only for those due to?
Aspiration of gastroesophageal contents or food misrouted from the oropharynx.
“Infiltrate” is the term for a radiologic manifestation of?
Pneumonia or edema or hemorrhage (pus, or water, or blood).
“Consolidation” refers to manifestations of?
Alveoli filled with blood, pus or water on physical examination or radiology, again not specific for pneumonia.
Most types of pneumonia start with?
Acute inflammation, with neutrophilic infiltration.
Most types of acute inflammation go on to a subacute phase with?
Macrophages replacing neutrophils (garbage collectors replacing first responders) starting about day 3 of the pneumonia.
Individual types of pneumonia tend to be either?
Alveolar or interstitial (involving either airspaces or inter-alveolar septa), and necrotizing or non-necrotizing.
Alveolar non-necrotizing acute bacterial pneumonia is commonly due to?
Streptococcus pneumoniae (pneumococcus), but can also be due to Legionella species, Mycoplasma species and many other bacterial species.
Alveolar necrotizing acute bacterial pneumonia is caused by?
Staphylococcus aureus, Pseudomonas aeruginosa, Klebsiella species and other bacterial species.
Definition: Pneumococcal pneumonia
It is lung parenchymal infection by Streptococcus pneumoniae (pneumococcus) (aerotolerant anaerobic Gram-positive diplococcus).
Epidemiology: Pneumococcal pneumonia:
Very common and is community-acquired. Pneumococcal pneumonia is more common in older adults and more common in men, but has no racial predilection. Risk factors for getting it include smoking, chronic obstructive pulmonary disease, preceding viral respiratory infection (especially influenza), alcohol use, crack cocaine use, homelessness, splenectomy (including the “autosplenectomy” of sickle cell disease), defective humeral (B-cell) immunity, multiple myeloma, transplantation, lupus, incarceration, pregnancy, and other conditions.
Pathogenesis: Pneumococcus
Transient normal flora, colonizing the nasopharynx of 50% of individuals at any one time, acquired by aerosol inhalation, attaching to respiratory epithelial cells via platelet activating factor receptor. Secrete pneumolysin, a potent cytotoxin that binds to cholesterol in membranes and forms lethal pores in erythrocytes and leukocytes.
Gross pathology: Pneumococcal lobar pneumonia untreated has 4 phases:
(1) day 1: congestion with exudation of serous and frothy, blood-tinged fluid into alveoli
(2) days 2-3: red hepatization with drier, granular, dark red consolidation resembling liver
(3) days 4-7: grey hepatization with continuing consolidation, but color change to grey
(4) day 8 and following: slimy yellowish exudate, resolution without scarring
Microscopic pathology: Pneumococcal pneumonia is characteristically:
An acute non-necrotizing alveolitis, which stops at lobar septa because is non-necrotizing.
Pneumococcal pneumonia phases:
Phase (1): engorged septal capillaries, with a few erythrocytes, edema fluid and bacteria in alveoli
Phase (2): continuing congestion, extravasation of red cells and numerous neutrophils and abundant fibrin in alveoli, infection spreading through pores of Kohn into adjacent alveoli
Phase (3): degenerating dead cells (neutrophils, erythrocytes, sloughed pneumocytes and bacteria) in the alveoli, fibrin nets extending through pores of Kohn, foamy macrophages replace neutrophils
Pneumococcal pneumonia Symptoms:
Classic (in young people): sudden single severe shaking chill (rigor), followed by sustained high fever and cough productive of blood-tinged “rusty” sputum +/- pleuritic chest pain. Much more common (in heavy drinking heavy smoking older adults): Also common (in elderly): become confused, tired and cold, with no fever or cough.
Pneumococcal pneumonia Signs:
Low fever (typically 102-103 F), near or low tachycardia (HR 90-110/min), mild tachypnea (RR 20-24/min), pulmonary crackles (“rales”, old term for them), bronchial or tubular breath sounds (100%, in theory), dullness to percussion (50%).
Pneumococcal pneumonia Diagnosis:
Chest x-ray: lobar alveolar consolidation with air bronchograms (rare), segmental or subsegmental alveolar infiltrates without air bronchograms (common). Blood testing: leukocytosis (5% leukopenia [bad prognosis]), bandemia, elevated lactate dehydrogenase (LDH), elevated bilirubin (occasionally, not above 4 mg/dl), blood culture positive in <25%. Gram stain: diagnostic if patient not already treated (pairs of lancet-shaped organisms, flattened at their point of contact and pointed at the other end, with a capsule). Culture: commonly false negative. Urine antigen test: rapid, 70-80% sensitive, 80-100% specific.
Pneumococcal pneumonia Treatment:
Almost any beta-lactam antibiotic.
Pneumococcal pneumonia Prognosis:
Excellent (usually).
Staphylococcus aureus pneumonia. Definition:
Lung parenchymal infection by Staphylococcus aureus.
Staphylococcus aureus pneumonia
Epidemiology:
Common, community- or hospital-acquired (28% of hospital-acquired) [much smaller percent of community-acquired].
Staphylococcus aureus pneumonia
Demographics:
No age, sex or race predilection. Risk factors: S. aureus skin infection, nursing home residence, recent hospitalization, endotracheal intubation for mechanical ventilation.
Staphylococcus aureus pneumonia
Pathogenesis:
Commonly follows viral respiratory infection, especially influenza. Virulence factors include exotoxins (e.g. leukocidins, hemolysins), protein A (binds to TNF receptor 1 and opens path for invasion between epithelial cells) and resistance to many commonly used antibiotics in methicillin-resistant strains.
Staphylococcus aureus pneumonia
Gross pathology:
Heavy plum-colored lungs, which exude bloody fluid on sectioning and develop numerous small abscesses, which enlarge (and in children can be thin-walled “pneumatoceles”). Commonly with pleuritis and empyema.
Staphylococcus aureus pneumonia
Microscopic pathology:
Acute necrotizing bronchitis, bronchiolitis and alveolitis, with abundant neutrophils, fibrin and edema fluid; the edema fluid can condense into hyaline membranes. Hemorrhage usually present and commonly prominent. Abscesses very commonly present and may rapidly enlarge.
Staphylococcus aureus pneumonia
Symptoms:
Cough (commonly productive of purulent sputum only late in the course), dyspnea, fever, chills, confusion.
Staphylococcus aureus pneumonia
Signs:
Fever, tachycardia, hypotension, tachypnea, pulmonary crackles.
Staphylococcus aureus pneumonia
Diagnosis:
Chest x-ray: bronchopneumonic (alveolar) infiltrates +/- abscesses, pleural effusions. Blood testing: leukocytosis. Gram stain: Gram-positive cocci in clusters. Culture: aerobic, not fastidious. Specific diagnosis: not always easy because positive sputum culture can represent only colonization.
Staphylococcus aureus pneumonia
Treatment:
Oxacillin (or another beta-lactam) for methicillin-sensitive; vancomycin (or linezolid) for methicillin-resistant.
Staphylococcus aureus pneumonia
Prognosis:
Up to 50% mortality, even if treated.
IMPORTANT CONCEPT 3: Staph. aureus pneumonia is much worse than?
Pneumococcal pneumonia, probably because it is necrotizing and abscessing.
Legionella pneumonia
Definition:
Lung parenchyma infection by Legionella species (fastidious Gram-negative bacilli)
Legionella pneumonia
Epidemiology:
Relatively common, community- or hospital-acquired (2-9% of community-acquired, similar % of hospital-acquired), 90% L. pneumophila.
Legionella pneumonia
Demographics:
No age, sex or race predilection. Risk factors: smoking, COPD, transplant, not neutropenia, hematological malignancy or HIV infection
Legionella pneumonia
Pathogenesis:
Habitat: water, esp. warm water (25-42 degrees) in water heaters, shower heads, air conditioners, etc. Can hide inside amoebae. Once inhaled or aspirated, attach to respiratory epithelial cells and macrophages by flagellae and pili. After phagocytosis, evade intracellular destruction by inhibiting phagosome-lysosome fusion (two genes involved: dot [defective organelle trafficking] and icm [intracellular multiplication]). Never transmitted person-to-person
Legionella pneumonia
Gross pathology:
Bulging firm rubbery areas of consolidation
Legionella pneumonia
Microscopic pathology:
Acute non-necrotizing alveolitis, with early infiltration by numerous macrophages (unusual in acute pneumonia).
Legionella pneumonia
Symptoms:
Cough (dry or productive of mucoid sputum), high fever, chills, rigors, dyspnea, headache, diarrhea, confusion, myalgia, chest pain. Gastrointestinal symptoms, especially diarrhea, suggests Legionella.
Legionella pneumonia
Signs:
Fever virtually always, relative bradycardia (esp. in elderly), pulmonary crackles. Neurological signs, especially confusion, suggests Legionella
Legionella pneumonia
Diagnosis:
Chest x-ray: initially patchy unilobar bronchopneumonic (alveolar) infiltrate that progresses, + (in 50%) pleural effusion. Blood testing: leukocytosis, thrombocytopenia, hyponatremia, azotemia, liver dysfunction. Hyponatremia (sodium <130 ) suggests Legionella. Other: hematuria, proteinuria. Gram stain usually false negative. Culture requires buffered charcoal yeast extract agar (ideally supplemented with antibiotics and dyes). Urine antigen test for L. pneumophila rapid, sensitive, specific and cheap.
Legionella pneumonia
Treatment:
Newer macrolide antibiotics (especially azithromycin) or respiratory tract quinolones (especially levofloxacin). Prevention of hospital-acquired: copper-silver ionization units in hot water storage tanks.
Legionella pneumonia
Prognosis:
16-30% mortality untreated, if community-acquired, 50% mortality untreated, if hospital-acquired, <5% mortality if treated early and patient is immunocompetent, but 75% can have persistent fatigue and 66% persistent neurological symptoms more than a year later.
IMPORTANT CONCEPT 4: Acute pneumonia with diarrhea, confusion or hyponatremia suggests?
That Legionella may be the cause.
Pseudomonas aeruginosa pneumonia
Definition:
Lung parenchymal infection by Pseudomonas aeruginosa (Gram-negative bacilli)
.
Pseudomonas aeruginosa pneumonia
Epidemiology:
Common, hospital-acquired (18% of hospital-acquired).
Pseudomonas aeruginosa pneumonia
Demographics:
No age, sex or race predilection. Risk factors: intubation, neutropenia.
Pseudomonas aeruginosa pneumonia
Pathogenesis:
Habitat: water, transmitted from water. Once inhaled or aspirated, attach to respiratory epithelial cells; colonization generally precedes infection.
Pseudomonas aeruginosa pneumonia
Virulence factors
Include resistance to many commonly used antibiotics, ability to form a biofilm, many enzymes (particularly elastase) and many exotoxins
Pseudomonas aeruginosa pneumonia
Gross pathology:
Firm red areas of hemorrhagic consolidation +/- yellow areas of consolidation with a rim of hemorrhage (target lesions [not at all specific for Pseudomonas]).
Pseudomonas aeruginosa pneumonia
Microscopic pathology:
Acute necrotizing alveolitis, with groups of long thin, almost filamentous bacilli invading blood vessels from the adventitia (“Pseudomonas vasculitis” [misnomer because is most common with neutropenia and hence no –itis]) with associated hemorrhage and infarction.
Pseudomonas aeruginosa pneumonia
Symptoms:
Cough productive of purulent sputum, dyspnea, fever, chills, confusion.
Pseudomonas aeruginosa pneumonia
Signs:
Fever, tachycardia, hypotension, tachypnea, pulmonary crackles.
Pseudomonas aeruginosa pneumonia
Diagnosis:
Chest x-ray: diffusely distributed bilateral bronchopneumonic (alveolar) infiltrates +/- nodular lesions, small abscesses, pleural effusions. Blood testing: leukocytosis (unless neutropenia predisposed to Pseudomonas infection). Gram stain: long thin Gram-negative bacilli with pointed ends. Culture: aerobic, with characteristic sweet grape-like odor, green pigment resembling bronze.
Pseudomonas aeruginosa pneumonia
Specific diagnosis:
Difficult because positive sputum culture commonly represents only colonization.
Pseudomonas aeruginosa pneumonia
Treatment:
Combination of an antipseudomonal beta-lactam and antipseudomonal quinolone (or antipseudomonal beta-lactam and an aminoglycoside) [or an antipseudomonal quinolone and an aminoglycoside].
Pseudomonas aeruginosa pneumonia
Prognosis:
Up to 87% mortality, even if treated, but mortality attributable to the pneumonia is as low as 32%.
IMPORTANT CONCEPT 5: Pseudomonas pneumonia is much worse than?
Pneumococcal pneumonia mostly because it hits patients already hospitalized with some other bad disease.
Mycoplasma pneumoniae: Mycoplasma pneumonia.
Definition:
Lower respiratory tract infection by Mycoplasma pneumoniae
Mycoplasma pneumoniae: Mycoplasma pneumonia.
Epidemiology:
Common, community-acquired, more common in fall and winter. 1% of Americans get Mycoplasma pneumoniae infection per year, usually children and young adults, but 95% get only upper respiratory tract infection and 5% pneumonia. Mycoplasma pneumoniae is one of the most common causes of “atypical pneumonia” (as opposed to typical pneumonia, which is more severe), also called “walking pneumonia”. 20% of pneumonia in middle school and high school students and 50% of pneumonia in college students, 25% of pneumonia in non-hospitalized patients and 5% of pneumonia requiring hospitalization
Mycoplasma pneumoniae: Mycoplasma pneumonia.
Pathogenesis:
Smallest of free-living organisms, fastidious short or filamentous bacilli lacking a cell wall and invisible on Gram stain. Transmitted person-to-person by infected respiratory droplets during close contact, attach to respiratory epithelial cells by adherence proteins and cause illness that is largely immune-mediated, with an incubation period of 2-3 weeks.
Mycoplasma pneumoniae: Mycoplasma pneumonia.
Gross pathology:
Minimal
Mycoplasma pneumoniae: Mycoplasma pneumonia.
Microscopic pathology:
Lymphoplasmacytic bronchiolitis with mucosal ulceration and fibrinopurulent exudate in the lumen, then lymphoplasmacytic interstitial pneumonitis extending out from the bronchiolitis, associated with alveolar type 2 pneumocyte hyperplasia.
Mycoplasma pneumoniae: Mycoplasma pneumonia.
Symptoms:
Insidious onset of malaise, headache, anorexia, low-grade fever and chills, then (in 75-100%) a persistent incessant intractable dry cough (may get a little productive), +/- sore throat, +/- ear pain.
Mycoplasma pneumoniae: Mycoplasma pneumonia.
Signs:
All plus or minus: wheezing, scattered pulmonary rales, paranasal sinus tenderness, pharyngeal mucosal erythema, tympanic membrane erythema, mild cervical lymphadenopathy, erythematous maculopapular skin rash (that may go on to Stevens-Johnson syndrome).
Mycoplasma pneumoniae: Mycoplasma pneumonia.
Diagnosis:
Chest x-ray: patchy areas of airspace consolidation or reticulonodular infiltrate + (in 20%) pleural effusion, unilateral or bilateral, areas of consolidation more common in lower lobes. Blood testing: cold agglutinins (titer >1:64) in 60% (with hemolysis, usually mild). White blood cell count is normal in 75-90%. Other: may get cardiac arrhythmias and heart failure, may get meningitis or encephalitis.
Mycoplasma pneumoniae: Mycoplasma pneumonia.
Specific diagnosis:
Difficult and rare: serology (ideally requires acute and then convalescent titer 2-3 weeks later with a four-fold rise), PCR on throat specimen (sensitivity 92% and specificity 98% in one study, but sensitivity 48% in first 21 days of symptoms and 29% after that in another study).
Mycoplasma pneumoniae: Mycoplasma pneumonia.
Treatment:
Azithromycin or levofloxacin (or doxycycline) [or erythromycin] {or moxifloxacin}
Prognosis: vast majority recover without sequelae.
IMPORTANT CONCEPT 6: Mycoplasma pneumonia is the prototype?
Atypical pneumonia and walking pneumonia because it is not that bad.
Tuberculosis: Mycobacterium tuberculosis
Definition:
Mycobacterium tuberculosis infection
Tuberculosis: Mycobacterium tuberculosis
Epidemiology:
Uncommon, incidence in the US in 2010 was 3.6/100,000, 10% associated with HIV infection (especially among injection drug users, the homeless, prisoners and alcoholics), seasonal (peak in the spring and trough in the fall), more common in the elderly, more common in men, 83% in racial and ethnic minority groups (especially foreign-born [incidence 25.8/100,000 in Asians, 9.3/100,000 in blacks, 8.4/100,000 in Hispanics, 1.1/100,000 in whites]).
Tuberculosis: Mycobacterium tuberculosis
Pathogenesis:
Contagious, spread by the productive cough of heavily infected patients, four outcomes after inhalation (1) immediate clearance (2) primary disease (3) latent disease (4) reactivation disease.
Tuberculosis: Mycobacterium tuberculosis
Gross pathology:
Caseating granulomas (first one in primary infection usually 1 to 1.5 cm, grey-white, with central necrosis resembling cheese, called Ghon focus, if combined with hilar lymph nodal involvement [common], called Ghon complex), sometimes partly acute necrotizing pneumonia, sometimes with empyema, sometimes large cavitary lesions, rarely diffusely disseminated small foci of infection resembling millet seeds (miliary disease).
Tuberculosis: Mycobacterium tuberculosis
Microscopic pathology:
Necrotizing granulomas with epithelioid histiocytes, multinucleated giant cells (commonly Langhans type [with nuclei arranged in a peripheral semicircle or ring]), a collar of surrounding lymphocytes and very few organisms (dark red beaded bacilli on acid-fast stain), sometimes neutrophilic necrotizing pneumonia (usually with some mixture of granulomatous inflammation), necrosis with minimal inflammation with miliary disease.
Tuberculosis: Mycobacterium tuberculosis
Symptoms:
Insidious onset of anorexia, fatigue, weight loss, chills, fever, night sweats and a mild cough productive of mucopurulent sputum +/- mild hemoptysis, but may be asymptomatic or masked by concomitant chronic bronchitis
Tuberculosis: Mycobacterium tuberculosis
Signs:
Usually none, but may have post-tussive pulmonary rales or tubular breath sounds over a large lesion or amphoric (distant hollow) breath sounds over a cavity
Tuberculosis: Mycobacterium tuberculosis
Diagnosis:
Chest x-ray shows patchy or nodular infiltrate in apical- or subapical posterior areas of upper lobes or superior segment of a lower lobe in early chronic tuberculosis (most suggestive of TB if bilateral or cavitary), or small, nodular, sharply defined lesions (granulomas, increased density with caseation) or scarring, atelectasis, mass lesions or large cavities. Pneumonia associated with hilar adenopathy should always suggest primary tuberculosis.
Tuberculosis: Mycobacterium tuberculosis
Diagnosis: Besides CXR.
Usually not too difficult and made by radiology and sputum acid-fast stain and culture. Positive sputum smear indicates infectivity. Bronchoalveolar lavage or transbronchial biopsy can yield the diagnosis. Culture takes 4-8 weeks; positive requires PCR confirmation. Nucleic acid amplification tests for sputum (trade names Gen-Probe MTD and E-MTD and Amplicor) can be performed in remote sites and yield confirmation of the diagnosis in 2-7 hours and are being hotly researched.
Tuberculosis: Mycobacterium tuberculosis
Treatment:
In HIV-negative patients without isoniazid-resistant tuberculosis: 4 drugs (isoniazid, rifampin, pyrazinamide and ethambutol) for 2 months, followed by 2 drugs (isoniazid and rifampin) for 4 months.
Tuberculosis: Mycobacterium tuberculosis
Prognosis:
Good (usually).
IMPORTANT CONCEPT 7: .You might be punished for missing the diagnosis of tuberculosis in your patient?
By getting it from your patient.
Histoplasmosis
Definition:
Infection by Histoplasma species fungi (which mimic Mycobacterium tuberculosis [“TB wannabe”])
Histoplasmosis
Epidemiology:
Common (estimated half a million new infections per year in US), 75% asymptomatic, but can be severe with heavy exposure and disseminated with reactivation of latent infection in patients with acquired immunodeficiency syndrome or immunosuppressive therapy for transplantation. Histoplasmosis is hyperendemic in the Mississippi and Ohio river valleys. Histoplasma grows particularly well in soil enriched with chicken or bat feces, so areas around chicken coops and bat caves can be sites of heavy exposure.
Histoplasmosis
Pathogenesis:
Inhalation of airborne spores, whose small size allows them to get to alveoli, where macrophages phagocytose them, but do not kill them unless activated by sensitized T lymphocytes in a cytokine pathway involving tumor necrosis factor and interferon-gamma. Cellular immunity develops after 10-14 days after exposure. Infection becomes latent in old granulomas in the lungs or lymph nodes.
Histoplasmosis
Gross pathology:
Tan nodules, masses or areas of consolidation that develop caseous necrosis, may cavitate, and eventually become white, fibrotic and calcified, may have pulmonary hilar or mediastinal lymphadenopathy or pleural effusion
Histoplasmosis
Microscopic pathology:
Small 2-5 micron oval basophilic yeast forms with narrow-based budding and often in clusters (sometimes within macrophages). Tissue reaction ranges from none (in the most immunocompromised patients) to vigorous necrotizing granulomatous inflammation with lots of epithelioid histiocytes, multinucleated giant cells and surrounding lymphocytes (in the least immune-compromised patients); initial tissue reaction before cellular immunity has developed is neutrophilic.
Histoplasmosis
Symptoms:
Fever, chills, headache, myalgia, anorexia, cough and substernal chest pain (worse with deep inspiration) 2-4 weeks after exposure, concomitant coryza (runny nose) and/or sore throat go against the diagnosis of histoplasmosis, symptoms usually resolve without treatment in several weeks.
Histoplasmosis
Signs:
Fever, (uncommon: pulmonary crackles).
Histoplasmosis
Diagnosis:
Radiology detects histoplasmosis; chest x-ray typically shows nodules or masses (+/- cavitation) or patchy infiltrates, commonly with hilar or mediastinal lymphadenopathy, but may show reticulonodular infiltrates or miliary disease. Calcification is very common, but takes months to develop in children and years in adults. Diagnosis is made by biopsy, culture and antigen test: biopsy can yield definite diagnosis, culture takes up to 6 weeks and may be false negative, antigen can be detected in bronchoalveolar lavage, serum and urine, but can be cross-reaction due to blastomycosis or coccidioidomycosis.
Histoplasmosis
Treatment:
Itraconazole for mild-moderate disease, amphotericin for severe disease.
Histoplasmosis
Prognosis:
7.5% mortality if bad enough to require hospitalization (not too often).
IMPORTANT CONCEPT 8: Histoplasmosis mimics and is prevalent?
Tuberculosis and is prevalent in the Ohio and Mississippi river valleys.
Aspergillus pneumonia
Definition:
Lung parenchymal infection by Aspergillus (must be distinguished from colonization [of a cavity, for instance, producing a non-invasive fungus ball called an aspergilloma] and an allergic disease [allergic bronchopulmonary aspergillosis].
Aspergillus pneumonia
Epidemiology:
Aspergillus is ubiquitous, but invasive Aspergillus pneumonia is uncommon, primarily in patients with severe and prolonged neutropenia, immunosuppressive therapy or high dose corticosteroid therapy.
Aspergillus pneumonia
Pathogenesis:
Inhalation of airborne conidia, whose small size allows them to get to alveoli, where they germinate into hyphae and invade, especially blood vessels
Aspergillus pneumonia
Gross pathology:
Nodules, commonly with surrounding hemorrhage (may resemble a target, “target lesion”) and associated infarction, or patchy tan-red-brown consolidation, commonly without purulence because patient neutropenic, or masses, or peribronchial consolidation, or any combination of these
Aspergillus pneumonia
Microscopic pathology:
Necrosis, hemorrhage and (if patient has neutrophils) acute inflammation with regular septate hyphae, 3-6 microns in width, with dichotomous branching (two equal size branches) at acute angles (classically 45 degrees), progressive branching (the branches branch), frequently in radiating or parallel array.
Aspergillum = fruiting body producing conidia (resembling Roman Catholic holy water sprinkler in action), rarely seen, only in well aerated sites.
Aspergillus pneumonia
Symptoms:
Classic triad (in neutropenic patients): fever, pleuritic chest pain and hemoptysis, but these patients frequently have fever without symptoms localizing to the lungs. May have cough or dyspnea.
Aspergillus pneumonia
Signs:
Fever, tachycardia, tachypnea, pulmonary crackles or rhonchi.
Aspergillus pneumonia
Diagnosis:
Radiology detects Aspergillus pneumonia; chest x-ray is insensitive, but computed tomography typically shows nodules (+/- cavitation) or (second most common) patchy or segmental consolidation, or (third most common) peribronchial infiltrates (+/- tree-in-bud patterns), nodules most commonly small (subcentimeter), with surrounding ground glass infiltrates (halo sign) representing surrounding hemorrhage. Diagnosis is difficult, sought by biopsy, culture and serum test for galactomannan
Aspergillus pneumonia
Treatment:
Voriconazole.
Aspergillus pneumonia
Prognosis:
Poor (only 20% survival in the past, but getting a little better).
IMPORTANT CONCEPT 9: Aspergillus pneumonia needs distinguishing from?
Mere colonization (e.g. aspergilloma) and allergic bronchopulmonary aspergillosis.
Cryptococcal pneumonia
Definition:
Lung parenchymal infection by Cryptococcus species fungi. Important to note that cryptococcal pneumonia is a much less common and much less threatening infection than cryptococcal meningitis, but pneumonia is the second most common type of infection (65-94% of immunocompromised patients with cryptococcal pneumonia have meningitis).
Cryptococcal pneumonia
Epidemiology:
Uncommon, vast majority in patients with acquired immunodeficiency syndrome, prolonged corticosteroid therapy, transplantation, malignancy or sarcoidosis, more common in African Americans, very uncommon in children (even those with acquired immunodeficiency syndrome).
Cryptococcal pneumonia
Pathogenesis:
Inhalation of airborne spores, whose small size allows them to get to alveoli, where they multiply and resist phagocytosis with their large capsule. Cryptococcus grows particularly well in pigeon feces (and less notoriously chicken feces). Infection becomes latent in old granulomas in the lungs or lymph nodes.
Cryptococcal pneumonia
Gross pathology:
Soft, tan-grey nodules or masses (“cryptococcomas”) that may have a slimy cut surface and may cavitate, but are not hemorrhagic or calcified, or consolidation (that may even be lobar), may have pulmonary hilar or mediastinal lymphadenopathy or pleural effusion.
Cryptococcal pneumonia
Microscopic pathology:
Translucent or faintly basophilic yeast forms with narrow-based budding surrounded by a large clear space (yeast forms usually 4-10 microns, but full range is 2-20 microns and they are more variable in size than other pathogenic yeast forms) [clear space can be up to 5 X diameter of the yeast forms]{the more severe the infection, the more budding, and vice-versa}. Tissue reaction ranges from none (in the most immunocompromised patients) to vigorous mixed suppurative and granulomatous inflammation (in the least immunocompromised patients).
Cryptococcal pneumonia
Symptoms:
Fever (up to 94% of immunocompromised patients), productive cough (up to 71%), dyspnea (up to 50%), headache (41%), hemoptysis, chest pain, malaise, night sweats and weight loss, (less common: skin rash, gastrointestinal complaints).
Cryptococcal pneumonia
Signs:
Fever, tachycardia, tachypnea, (uncommon: pulmonary rales), [rare: upper body edema and plethora due to superior vena cava obstruction].
Cryptococcal pneumonia
Diagnosis:
Chest x-ray or computed tomography typically shows nodules or masses (+/- cavitation) or consolidation, but occasionally interstitial infiltrates.Diagnosis is made by biopsy, culture and antigen test: biopsy can yield definite diagnosis, but pathologist must notice the unstained or faintly stained yeast forms; silver stains show the yeast forms well and mucicarmine stain (or Fontana-Masson stain for capsule-deficient organisms) makes a definitive diagnosis even without culture. Culture48 hours and positive culture yields a diagnosis of infection without biopsy.
Cryptococcal pneumonia
Treatment:
Fluconazole (or voriconazole).
Cryptococcal pneumonia
Prognosis:
Not too bad for the pneumonia unless also have meningitis.
IMPORTANT CONCEPT 10: Serum cryptococcal antigen test can?
Frequently nail a specific diagnosis of cryptococcosis.
Pneumocystis jirovecii pneumonia.
Definition:
Lung parenchymal infection by Pneumocystis jirovecii (fungus long thought to be a protozoan, name changed from Pneumocystis carinii in 2001)
Pneumocystis jirovecii pneumonia.
Epidemiology:
Uncommon opportunistic infection in patients with deficient cell-mediated immunity (AIDS, lymphoma, leukemia, immunosuppression, etc.)
Pneumocystis jirovecii pneumonia.
Pathogenesis:
Basically unknown.
Pneumocystis jirovecii pneumonia.
Gross pathology:
Heavy, diffusely consolidated, tan lungs.
Pneumocystis jirovecii pneumonia.
Microscopic pathology:
Foamy eosinophilic, sparsely cellular, centro-alveolar “honeycomb” exudate +/- lymphoplasmacytic interstitial pneumonia.
Pneumocystis jirovecii pneumonia.
Symptoms:
In AIDS patients: insidious onset of progressive dyspnea (95%), cough (95%, non-productive in 70%) and fever. Other symptoms: fatigue, chills, chest pain and weight loss, but 7% asymptomatic. In patients without HIV infection, Pneumocystis pneumonia typically presents as fulminant respiratory failure associated with fever and dry cough.
Pneumocystis jirovecii pneumonia.
Signs:
In AIDS patients: fever (84%), tachypnea (62%), pulmonary crackles and rhonchi (<50%), but chest examination normal in 50%.
Pneumocystis jirovecii pneumonia.
Diagnosis:
Chest x-ray: diffuse bilateral hazy interstitial infiltrates which become dense alveolar infiltrates (most common), but normal in 25% of AIDS patients. High-resolution computed tomography: patchy or nodular ground-glass attenuation (100% sensitive, 89% specific). Blood tests: elevated lactate dehydrogenase level (90%). Pulmonary function tests: decreased diffusing capacity (most). Specific diagnosis: demonstration of the bug in induced sputum smear, bronchioalveolar lavage, aspirate or biopsy, with (1) immunostains [usual method], (2) cyst stains such as Grocott (Gomori) methenamine silver, or (3) trophozoite stains such as Giemsa stain, but not culture (since Pneumocystis does not grow in culture).
Pneumocystis jirovecii pneumonia.
Treatment:
Trimethoprim-sulfamethoxazole (usually).
Pneumocystis jirovecii pneumonia.
Prognosis:
93% survival in AIDS patients, up from 79% before highly active antiretroviral therapy and prophylaxis.
