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149 Cards in this Set
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Factors affecting local lung defense mechanisms./predisposition
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Decreased cough reflex
Due to coma, anesthesia, neuromuscular disorders, drugs or chest pain Injury to mucociliary apparatus Impairment of ciliary function or destruction of ciliated epithelium due to cigarette smoke, inhalation of hot or corrosive gases, viral diseases or genetic defects of ciliary function. Interference with phagocytic or bactericidal action of alveolar macrophages due to alcohol, tobacco smoke, anoxia, oxygen intoxication. Accumulation of secretions (cystic fibrosis) Pulmonary congestion and edema. |
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Factors increasing susceptibility to infection
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Chronic disease (CHF, COPD, diabetes)
Immune deficiencies, congenital or acquired. Decreased or absent splenic function (sickle cell disease or post-splenectomy) puts at risk for encapsulated organisms, i.e. pneumococcus.. Treatment with immunosuppressive drugs Leukopenia. Extremes of age. |
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Define
Pneumonia |
any infection of the lung
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patchy consolidation of the lung
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Bronchopneumonia
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consolidation of the entire lobe (or a large portion of it).
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Lobar pneumonia
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any infection of the lung
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Pneumonia
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Pleural fibrinous reaction to underlying inflammation , may resolve or become permanent adhesions
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Pleuritis
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Pleuritis
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Pleural fibrinous reaction to underlying inflammation , may resolve or become permanent adhesions
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(localized within the walls of the alveoli) are frequently caused by viruses or atypical bacteria.
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Interstitial pneumonias
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Interstitial pneumonias
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(localized within the walls of the alveoli) are frequently caused by viruses or atypical bacteria.
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patchy consolidated areas (slightly elevated, dry, granular, gray-red to yellow areas with poorly delineated margins) throughout one lobe or multiple lobes, usually lower lobes.
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bronchopneumonia
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Bronchi, bronchioles and adjacent alveoli filled with neutrophils
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bronchopneumonia
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Classic Morphology/4 stages of Lobar Pneumonia
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1. Congestion –
Gross - Lung is heavy, boggy and red. Histology – Vascular engorgement with intra-alveolar fluid with a few neutrophils and bacteria 2. Red hepatization – Gross – red, firm and airless (resembles liver; hence “hepatization”) Histology – intra-alveolar exudate with neutrophils, red cells and fibrin. 3. Gray hepatization – Gross – grayish brown firm lung Histology – Persistent fibrinopurulent exudate with disappearance of red cells 4. Resolution – Exudate is resolving with debris ingested by macrophages, expectorated or organized by infiltrating fibroblasts. |
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What stage of Lobar Pneumonia ?
Lung is heavy, boggy and red.Vascular engorgement with intra-alveolar fluid with a few neutrophils and bacteria |
Congestion/initial lobar pneumonia stage
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What stage of Lobar Pneumonia ?
red, firm and airless ,intra-alveolar exudate with neutrophils, red cells and fibrin. |
2nd, red hepatization of lobar pneumonia
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What stage of Lobar Pneumonia ?
grayish brown firm lung Persistent fibrinopurulent exudate with disappearance of red cells |
Gray hepatization, 3rd stage of lobar pneumonia
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What stage of Lobar Pneumonia ?
Exudate is resolving with debris ingested by macrophages, expectorated or organized by infiltrating fibroblasts. |
Resolution stage of lobar pneumonia (4)
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Complications of pneumonia
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Abscess formation
Empyema – spread of infection to the pleural cavity with formation of fibrinopurulent exudate Bacteremic dissemination causing endocarditis, meningitis, suppurative arthritis or metastatic abscesses to other sites. |
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Definition os lung abcesses
What organism most likely? |
a local suppurative process characterized by necrosis of lung tissue.
Organisms commonly isolated include S. aureus, gram negative organisms, aerobic and anaerobic streptococci and other anaerobic oral flora (exclusive isolates in 60% of cases) |
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a local suppurative process characterized by necrosis of lung tissue.
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Lung abscess
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causative organisms in lung abscesses
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ASPIRATION (most frequent cause) common in alcoholism, coma, anesthesia, sinusitis, gingivodental sepsis and debilitation with decreased cough reflex.
ANTECEDENT LUNG INFECTION – especially with S. aureus, Klebsiella pneumoniae and type 3 pneumococcus. SEPTIC EMBOLISM – right sided bacterial endocarditis or infected venous thrombi. NEOPLASIA – a cancer obstructing a bronchus (postobstructive pneumonia). Miscellaneous: Direct trauma to lungs, contiguous spread of infection from a neighboring organ, heamtogenous seeding of lung with organism. No known cause : Primary cryptogenic lung abscess. |
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common in alcoholism, coma, anesthesia, sinusitis, gingivodental sepsis and debilitation with decreased cough reflex.
more common on the RIGHT |
aspiration-most common
causative organisms in lung abscesses |
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ANTECEDENT LUNG INFECTION
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especially with S. aureus, Klebsiella pneumoniae and type 3 pneumococcus.
cause of lung abcess |
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– right sided bacterial endocarditis or infected venous thrombi.
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SEPTIC EMBOLISM
causative organisms in lung abscesses |
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a cancer obstructing a bronchus (postobstructive pneumonia). Miscellaneous: Direct trauma to lungs, contiguous spread of infection from a neighboring organ, heamtogenous seeding of lung with organism.
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NEOPLASIA
causative organism in lung abcess |
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Complications of lung abscesses
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Extends into pleural cavity
Hemorrhage Septic emboli with brain abscesses or meningitis Rarely, secondary amyloidosis (type AA seen in many chronic inflammatory conditions) |
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Swollen red mucosa with secretions. Histologically, lymphomoncytic and plasmacytic infiltration of submucosa, excessive mucus production
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Upper respiratory infections- viral
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Vocal cord swelling with increased mucus production, impaired bronchociliary function, increased mucus, inflammatory cells.
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Laryngotracheobronchitis - viral
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plugging of airways with fibrin, cells debris and inflammatory exudate.
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Bronchiolitis-viral
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an acute febrile respiratory disease characterized by patchy inflammatory changes in the lungs, largely confined to the alveolar septa and pulmonary interstitium.
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atypical pneumonia
viral and mycoplasma |
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Most common organism causing primary atypical pneumonia
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Mycoplasma pneumoniae
Other organisms include viruses (influenza type A and B, the respiratory syncitial viruses, human metapneumovirus, adenovirus, rhinovirus and rubeola, and varicella), chlamydia pneumoniae and Coxiella burnetii (Q fever). |
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Causative organisms may cause just an upper respiratory infection.
The organisms attaches to the upper respiratory tract epithelium followed by necrosis of the cells and an inflammatory response. With lower respiratory tract infection, interstitial inflammation occurs. Secondary bacterial infection may occur due to damage and denudation of respiratory epithelium inhibiting mucociliary clearance. |
Pathogenesis of atypical pneumonias
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Pathogenesis of atypical pneumonias
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Causative organisms may cause just an upper respiratory infection.
The organisms attaches to the upper respiratory tract epithelium followed by necrosis of the cells and an inflammatory response. With lower respiratory tract infection, interstitial inflammation occurs. Secondary bacterial infection may occur due to damage and denudation of respiratory epithelium inhibiting mucociliary clearance. |
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patchy lung involvement or lobar, bilateral or unilateral, with affected areas blue-red and congested
alveolar septa are widened with edema and inflammatory cells consisting of lymphocytes, macrophages, plasma cells and sometimes neutrophils in acute cases. Sometimes there is an intra-alveolar proteinaceous material and a cellular exudate. ARDS with hyaline membranes may be a complication. |
Morphology of atypical or interstitial pneumonias
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Morphology of atypical or interstitial pneumonias
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Gross – patchy lung involvement or lobar, bilateral or unilateral, with affected areas blue-red and congested.
Histology- alveolar septa are widened with edema and inflammatory cells consisting of lymphocytes, macrophages, plasma cells and sometimes neutrophils in acute cases. Sometimes there is an intra-alveolar proteinaceous material and a cellular exudate. ARDS with hyaline membranes may be a complication. Some viruses (herpes simplex, varicella, and adenovirus) may have necrosis of bronchial and alveolar epithelium and acute inflammation with viral cytopathic changes with nuclear and/or cytoplasmic inclusions |
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Influenza viruses (orthomyxoviridae family
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Genome composed of eight helices of single-stranded RNA, each encoding a single gene and each bound by a nucleoprotein that determines the type of influenza virus (A, B or C).
The lipid bilayer envelope has a hemagglutinin and neuraminidase determining the subtype (H1 to H3; N1 or N2). Antibodies to hemagglutinin and neuraminidase is protective. Immune response to influenza infection. Cytotoxic T cells kill virus-infected cells An intracellular anti-influenza protein (Mx1) is induced in macrophages by interferons (alpha and beta) |
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The major cause of pandemic and epidemic influenza infections.
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Influenza virus type A
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Mutation of the hemagglutinin and neuraminidase in Influenza A
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Antigenic drift-
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Influenza A viruses infect what?....
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humans, pigs, horses and birds.
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Antigenic drift-
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Mutation of the hemagglutinin and neuraminidase in Influenza A
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Recombination of RNA segments with those of animal viruses
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Antigenic shift
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Antigenic shift
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Recombination of RNA segments with those of animal viruses
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What subtype of influenza A dominates in the world at any given time.
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A single subtype of influenza A dominates in the world at any given time.
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interstitial edema and inflammatory infiltrates, diffuse alveolar damage with hyaline membranes, intra-alveolar edema and/or hemorrhage, capillary and small vessel thromboses.
Later stages show organizing diffuse alveolar damage, fibrosis, epithelial regeneration and squamous metaplasia. Secondary bacterial pneumonias. |
influenza
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Opportunistic pneumonias
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Opportunistic infections rarely cause disease in normal hosts.
Immunosuppressed patients. AIDS Cancer patients Transplant patients and other patients on immunosuppressive drugs, i.e. autoimmune diseases. Primary immunodefiencies. |
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HIV associated lung infections
CD4+ >200 |
Bacterial and tuberculosis
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HIV associated lung infections
CD4+ <200 |
Pneumocystis pneumonia (most common opportunistic infection in HIV)
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HIV associated lung infections
CD4+<50 |
Cytomegalovirus (CMV)
Mycobacterium avium complex |
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HIV associated lung infections
general |
Infectious organism associated with CD4+ counts.
CD4+ >200 Bacterial and tuberculosis CD4+<200 Pneumocystis pneumonia (most common opportunistic infection in HIV) CD4+<50 Cytomegalovirus (CMV) Mycobacterium avium complex Lower bacterial respiratory infections caused by the usual bacterial pathogens is common (streptococcus pneumoniae is most common), severe and more likely to be associated with bacteremia. Lung infiltrates may be caused by malignancies such as Kaposi sarcoma, pulmonary non-Hodgkin lymphoma and primary lung cancer occur with increased frequency in HIV/AIDS. |
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Chronic lung infections caused by
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Cause chronic infections (granulomatous reactions) in immunocompetent persons
Fungal infections – Histoplasmosis Blastomycosis Coccidiodomycosis All three are (1) thermally dimorphic (cold = mold; heat=yeast)(2) have geographic predilictions Tuberculosis |
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Fungal infections –
c'teristics |
Histoplasmosis
Blastomycosis Coccidiodomycosis All three are (1) thermally dimorphic (cold = mold; heat=yeast)(2) have geographic predilictions |
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Thermally Dimorphic
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grow as hyphae (mold or mycelia) that produce spores at environmental temperatures but grow as yeasts (spherules or ellipses) at body temperature in the lungs
fungi infections |
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the most common endemic fungal infection in humans
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Histoplasmosis – the most common endemic fungal infection in humans –caused by histoplasma capsulatum
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Histoplasmosis Infection occurs ...and found...
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after inhaling spores in bat or bird droppings
Locations – Ohio and Mississippi river valleys and in the Caribbean |
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found in Ohio and Mississippi river valleys and in the Caribbean
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Histoplasmosis
caused by histoplasma capsulatum |
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Clinical picture and morphologic lesions resemble tuberculosis.
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Histoplasmosis
caused by histoplasma capsulatum |
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Infection occurs after inhaling spores in bat or bird droppings
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Histoplasmosis
caused by histoplasma capsulatum |
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Histoplasmosis
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– the most common endemic fungal infection in humans –caused by histoplasma capsulatum
Infection occurs after inhaling spores in bat or bird droppings Locations – Ohio and Mississippi river valleys and in the Caribbean Clinical picture and morphologic lesions resemble tuberculosis. |
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Pathogenesis of histoplasmosis
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an intracellular parasite of macrophages. Spores transform into yeast in the macrophage
Despite fusion with lysosomes, multiplication continues within phagosome. As host immunity develops, yeast growth ceases in 1-2 weeks after exposure Cytokines activate the fungistatic activity of macrophages against intracellular yeasts. As cell-mediated response matures (T cell mediated Type IV hypersensitivity) delayed-type hypersensitivity to histoplasmal antigens occurs 3 to 6 weeks after exposure. Over weeks to month, the inflammatory response produces calcified fibrinous granulomas with caseous necrosis. |
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an intracellular parasite of macrophages. Spores transform into yeast in the macrophage
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Histoplasmosis
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Despite fusion with lysosomes, multiplication continues within phagosome. As host immunity develops, yeast growth ceases in 1-2 weeks after exposure
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Histoplasmosis
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Over weeks to month, the inflammatory response produces calcified fibrinous granulomas with caseous necrosis.
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Histoplasmosis
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Morphology of granulomas in histoplasmosis
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Granuloma formations occur with persistent or nondegradable antigen
Activated macrophages morphologically change into epithelioid cells Aggregates of epithelioid cells (some coalesce into giant cells) are surrounded by a cuff of lymphocytes forming a granuloma May have caseating central necrosis. The granulomas under go fibrosis and concentric calcification. In immunocompromised, NO granulomas, but accumulations of yeast forms in mononuclear phagocytes throughout various organs and tissues. |
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Self-limited (may have calcified granulomas in lungs or other locations)
Chronic, progressive secondary lung disease with fever, cough, night sweats Widely disseminated disease in immunocompromised patients. |
disease course of histoplasmosis
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Blastomycosis
Geographic locations ...found in... |
Blastomyces dermatitidis – hard to isolate, soil-inhabiting, dimorphic fungus
Geographic locations – central and southeastern US and may also occur in Canada, Mexico, Middle East, Africa and India. Common infection in dogs in endemic areas (also seen in horses, cows, cats, bats and lions |
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hard to isolate, soil-inhabiting, dimorphic fungus
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Blastomycosis
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central and southeastern US and may also occur in Canada, Mexico, Middle East, Africa and India
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Blastomycosis
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Common infection in dogs in endemic areas (also seen in horses, cows, cats, bats and lions)
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Blastomycosis
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Infection occurs after inhalation of conidial forms from soil
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Blastomyces dermatitidis
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Thick cell wall gives survival advantage, resistance to phagocytosis.
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Blastomyces dermatitidis
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Yeast express an immune-modulatin virulence fact (BAD-1) on the cell surface
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Blastomyces dermatitidis
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Yeast express an immune-modulatin virulence fact on the cell surface, what is it?
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(BAD-1)
Blastomyces dermatitidis |
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Blastomycosis- infection
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Infection occurs after inhalation of conidial forms from soil
Transform to yeast form in the body Thick cell wall gives survival advantage, resistance to phagocytosis. Yeast express an immune-modulatin virulence fact (BAD-1) on the cell surface Yeast multiply and disseminate. |
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– lungs show suppurative granulomas. Macrophages have a limited ability to ingest and kill it with persistence of the yeast cells leading to continued recruitment of neutrophils.
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Blastomycosis dermatitidis
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5 to 15 um yeast cell
Thick, double-contoured cell wall with multiple nuclei |
Blastomycosis dermatitidis
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BROAD BASED BUDDING
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Blastomycosis dermatitidis
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Asymptomatic in many with some developing varying degrees of pulmonary and systemic symptoms.
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Pulmonary blastomycosis
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– occurs in chronic pulmonary disease and immunocompormised.
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Disseminated blastomycosis
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direct innoculation into skin or occurs from dissemination.
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Cutaneous form
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Marked epithelial hyperplasia (may be mistaken for squamous cell carcinoma)
Intradermal microabscesses Suppurating granulomatous reaction in dermis. Yeast may be seen extracellularly and in multinucleated giant cells. |
Blastomycosis in skin
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Blastomycosis in skin
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Marked epithelial hyperplasia (may be mistaken for squamous cell carcinoma)
Intradermal microabscesses Suppurating granulomatous reaction in dermis. Yeast may be seen extracellularly and in multinucleated giant cells. |
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Coccidioidomycosis
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Endemic to regions of N. and S. America (Western and Southwestern USA)
Infection occurs from inhalation of spores of Coccidioides immitis or posadasii (morphologically identical but genetically different) Isolated from rodent burrows in desert like areas. Most primary infections are asymptomatic. More than 80% or people in endemic areas have a positive skin test. High infectivity rate due to the infective arthroconidia ingested by macrophages blocking fusion of the phagosome and lysosome thereby resisting intracellular killing. |
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Endemic to regions of N. and S. America (Western and Southwestern USA)
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Coccidioidomycosis
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Infection occurs from inhalation of spores of immitis or posadasii (morphologically identical but genetically different)
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Coccidioides immitis or posadasii
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Isolated from rodent burrows in desert like areas.
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Coccidioidomycosis
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Most primary infections are asymptomatic.
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coccidiodomycosis
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More than 80% or people in endemic areas have a positive skin test.
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coccidiodomycosis
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High infectivity rate due to the infective arthroconidia ingested by macrophages blocking fusion of the phagosome and lysosome thereby resisting intracellular killing
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coccidiodomycosis
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San Joaquin Valley fever complex
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develops in 10% of infected people with lung lesions, fever, cough, pleuritic pain with erythema nodosum or erythema multiforme
coccidiodomycosis |
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develops in 10% of infected people with lung lesions, fever, cough, pleuritic pain with erythema nodosum or erythema multiforme
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San Joaquin Valley fever complex
coccidiodomycosis |
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Rarely have disseminated disease involving multiple organs which frequently involves the skin and meninges.
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coccidiodomycosis
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– the most common form of panniculitis, an inflammatory reaction in the subcutaneous tissue that may preferentially affect the connective tissue septa separating lobules of fat or the lobules of fat themselves often involving the lower legs with a subacute to chronic course
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Erythema nodosum in coccidiodomycosis
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Granulomatous lesions which may be purely granulomatous, pyogenic (purulent with neutrophils), or mixed.
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coccidiodomycosis
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appear as thick-walled, nonbudding spherules 20 to 60 um in diameter containing endospores
Rupture of the spherule releasing the endospores causes a pyogenic reaction. |
Coccidioides
coccidiodomycosis |
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slender, aerobic bacilli with a unique waxy wall composed of mycolic acid which makes them acid fast (resist decolorization with acidified alcohol once they have been stained with carbolfuchsin)
Weakly gram positive. |
Mycobacterium cause TB
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Pathogenesis of tuberculosis in previously unexposed immunocompetent person
Primary pulmonary TB (0 – 3 weeks |
Primary pulmonary TB (0 – 3 weeks)
M. tuberculosis enters macrophage through endocoytosis mediated by mannose receptors and complement receptors (bind opsonized organisms). Organisms replicate in the cell by blocking phago-lysosome fusion. Bacteria proliferate and disseminate to multiple sites with minimal (mild flu Sxs) to no symptoms Genetic make-up of host may influence course of disease. Polymophisms in the NRAMP1 gene may have progressive TB (NRAMP1 is a transmembrane protein in lysosomes that pumps divalent cations out of the lysosome which limits availability of ions needed by bacteria) |
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Primary pulmonary TB (>3 weeks
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T-helper 1 response activates macrophages to become bactericidal
Mycobacterial antigens enter draining lymph nodes and are displayed to T cells by antigen presenting cells producing IL-12 producing T-helper 1 cells T-helper 1 response mounted that produces IFN – gamma (interferon) which activates macrophages to become bactericidal by: Stimulating the formation of the phagolysosome in infected macrophages Stimulating production of nitric oxide which destroy mycobacterium. T helper 1 cells cause the formation of granulomas from epithelioid histiocytes or activated macrophages (may fuse to form giant cells) and caseous necrosis . The activated macrophages secrete TNF recruiting more monocytes. |
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What is NRAMP 1?
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IS A TRANSMEMBRAINE PROTEIN FOUND IN ENDOSOMES AND LYSOSOMES THAT PUMPS DIVALENT CATIONS (E.G. Fe) out of the lysosome.
NRAMP1 may inhibit microbial growth by limiting availability of ions needed by the bacteria. pulmonary TB by mycobacterium |
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what causes differentiation of T-helper1 cells in TB?
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Mycobacterium binding to TLR 2 stimulates antigen-presenting cell to make IL12 which causes differentiation of T-helper1 cells. Mycobacterial antigens draining to nodes also stimulates TH1 Cells
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In TB
Immunity mediated by |
T-helper 1 cells which stimulate macrophages to kill the bacteria
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HYPERSENSITIVITY in TB
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Immune response occurs at the cost of hypersensitivity with accompanying tissue destruction
Delayed Hypersensitivity is the basis of tuberculin skin test |
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What is the the basis of tuberculin skin test
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Delayed Hypersensitivity
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Clinical-pathologic patterns of tuberculosis
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Primary tuberculosis (usually begins in lungs in countries where infected milk eradicated)
Secondary tuberculosis Progressive pulmonary tuberculosis Miliary pulmonary disease Systemic miliary Isolated tuberculosis [appears in any organ or tissue as presenting manifestation; i.e. tubercuous meningitis, adrenal, vertebra (Pott disease)] Lymphadenitis (most frequent presentation of extrapulmonary tuberculosis; called scrofula in the cervical region) Intestinal tuberculosis |
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focal lung consolidation resulting after implantation of inhaled bacilli in the lower part of upper lobes or upper part of lower lobes, usually sub-pleural.
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Ghon focus in primary TB
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Ghon focus
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in primary TB
focal lung consolidation resulting after implantation of inhaled bacilli in the lower part of upper lobes or upper part of lower lobes, usually sub-pleural. |
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Ghon complex
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lymph node involvement combined with lung lesion
fibroses and calcifies (Ranke complex) |
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lymph node involvement combined with lung lesion
fibroses and calcifies (Ranke complex) |
Ghon complex in primary TB
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Occurs in a previously sensitized host usually from re-activation of a latent infection or from exogenous reinfection
Classically involves the apex of the upper lobes of one or both lungs. Cavitary lesions are common. |
Secondary tuberculosis
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Secondary tuberculosis
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Occurs in a previously sensitized host usually from re-activation of a latent infection or from exogenous reinfection
Classically involves the apex of the upper lobes of one or both lungs. Cavitary lesions are common. |
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Histology of tuberculosis
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Granulomas composed of epithelioid histiocytes with giant cells surrounding central caseation.
Fibrous encapsulation with a rim of lymphocytes Eventually, fibrocalcific scar. Tuberculous granulomas may exist without central caseation. Stain granulomas for acid fast organisms. |
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Granulomas composed of epithelioid histiocytes with giant cells surrounding central caseation.
Fibrous encapsulation with a rim of lymphocytes Eventually, fibrocalcific scar. Granulomas may exist without central caseation. Stain granulomas for acid fast organisms. |
Histology of tuberculosis
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Granulomas composed of epithelioid histiocytes with giant cells surrounding central caseation
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Histology of tuberculosis
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Tuberculous granulomas may exist without central caseation.
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Histology of tuberculosis
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Elderly and immunosuppressed
Expanding apical lesion with large caseous center, cavitation, erosion into blood vessels. With adequate Rx, will heal with fibrosis/scarring . If inadequate treatment or poor host defenses, it may spread via the airways, lymphatic channels or hematogenously Pleural involvement may occur. |
Progressive pulmonary tuberculosis
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Expanding apical lesion with large caseous center, cavitation, erosion into blood vessels
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Progressive pulmonary tuberculosis
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Organisms enter lymphatics, then venous blood and returns to lung via circulation
Lungs show multiple scattered tiny foci (few millimeters) of yellow-white consolidation which may expand and coalesce |
Miliary tuberculosis-pulmonary
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Lungs show multiple scattered tiny foci (few millimeters) of yellow-white consolidation which may expand and coalesce
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Miliary tuberculosis-pulmonary
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pulmonary TB
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Pulmonary miliary tb
Organisms enter lymphatics, then venous blood and returns to lung via circulation Lungs show multiple scattered tiny foci (few millimeters) of yellow-white consolidation which may expand and coalesce |
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systemic TB
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miliary tb
Organisms disseminate throughout body via the systemic arterial circulation. Most prominently involved sites are liver, bone marrow, spleen, adrenals, meninges, kidneys, fallopian tubes and epididymis. |
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Organisms disseminate throughout body via the systemic arterial circulation.
Most prominently involved sites are liver, bone marrow, spleen, adrenals, meninges, kidneys, fallopian tubes and epididymis. |
systemic Miliary tuberculosis
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Most prominently involved sites are liver, bone marrow, spleen, adrenals, meninges, kidneys, fallopian tubes and epididymis
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systemic Miliary tuberculosis
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Most prominently involved sites of miliary tb
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liver, bone marrow, spleen, adrenals, meninges, kidneys, fallopian tubes and epididymis.
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most common cause of adrenalin deficiency
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systemic miliary tb
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POTT disease
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vertebral involvement of TB
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Other manifestations of TB
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Isolated disease
TB presenting in another organ Most common are meninges, kidneys, adrenal(used to be important cause of Addision’s), bones, fallopian tubes POTT disease, vertebral involvement Lymphadenitis – Most frequent extrapulmonary presentation, particularly in cervical region (Scrofula) Intestinal tuberculosis – Drinking contaminated milk or swallowing infected sputum. |
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Scrofula
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Lymphadenitis –
Most frequent extrapulmonary presentation, particularly in cervical region (Scrofula) manifestation by TB |
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Drinking contaminated milk or swallowing infected sputum.
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Intestinal tuberculosis
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Mycobacterium avium-intracellulare Complex (MAC)
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Two different species but lumped together since so similar
MAC common in soil, water,dust and domestic animals. Uncommon infection except in people with AIDS and a CD4+ count of <60 |
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Two different species but lumped together since so similar
Common in soil, water,dust and domestic animals. Uncommon infection except in people with AIDS and a CD4+ count of <60 |
Mycobacterium avium-intracellulare Complex (MAC)
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MAC infections
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In severe immune deficiency, MAC infection widely disseminated throughout the mononuclear phagocyte system with enlargement of lymph nodes, liver and spleen.
Lung and GI tract involvement is common Histologic hallmark is abundant acid-fast bacilli within macrophages Minimal to no granuloma formation. |
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In severe immune deficiency, these infection widely disseminated throughout the mononuclear phagocyte system with enlargement of lymph nodes, liver and spleen.
Lung and GI tract involvement is common Histologic hallmark is abundant acid-fast bacilli within macrophages Minimal to no granuloma formation. |
Mycobacterium avium-intracellulare Complex (MAC)
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Histologic hallmark is abundant acid-fast bacilli within macrophages
Minimal to no granuloma formation. |
Mycobacterium avium-intracellulare Complex (MAC)
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Gram stain of sputum from a patient with pneumonia. There are gram-positive cocci in clusters with degenerating neutrophils.
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(Staphylococcus aureus)
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Gram stain of sputum from a patient with pneumonia. Gram-positive, elongated cocci in pairs and short chains and a neutrophil are seen
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(Streptococcus pneumoniae)
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Gram stain of a bronchoalveolar lavage specimen showing gram-negative intracellular rods
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typical of Enterobacteriaceae such as Klebsiella pneumoniae or Escherichia coli
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-- Cowdry Type A droplet like masses of acidophilic material surrounded by clear halos within nuclei, with margination of chromatin on the nuclear membrane and cellular changes
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HSV
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interstitial edema and inflammatory infiltrates, diffuse alveolar damage with hyaline membranes, intra-alveolar edema and/or hemorrhage, capillary and small vessel thromboses.
Later stages show organizing diffuse alveolar damage, fibrosis, epithelial regeneration and squamous metaplasia. |
influenza
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The foamy pink exudate is composed of trophic forms of surfactant phospholipids, cell debris, and host-derived proteins
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Pneumocystis jiroveci in HIV
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Thick, double-contoured cell wall with multiple nuclei
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blastomycosis
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Clinical forms of Blastomycosis
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Pulmonary blastomycosis – Asymptomatic in many with some developing varying degrees of pulmonary and systemic symptoms.
Disseminated blastomycosis – occurs in chronic pulmonary disease and immunocompormised. Cutaneous form – direct innoculation into skin or occurs from dissemination. |
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Marked epithelial hyperplasia (may be mistaken for squamous cell carcinoma)
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Blastomycosis in skin
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Endemic to regions of N. and S. America (Western and Southwestern USA)
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Coccidioidomycosis
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central and southeastern US and may also occur in Canada, Mexico, Middle East, Africa and India.
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Blastomycosis
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Ohio and Mississippi river valleys and in the Caribbean
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Histoplasmosis
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small tan yellow granuloma in a hilar lymph node next to the bronchus.
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ghon complex in TB
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Lungs show multiple scattered tiny foci (few millimeters) of yellow-white consolidation which may expand and coalesce
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Pulmonary
Miliary tuberculosis |
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MAC infection widely disseminated throughout the mononuclear phagocyte system with enlargement of l
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lymph nodes, liver and spleen.
Lung and GI tract involvement is common |
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typical giant cell with round pink intracytoplasmic inclusions in children
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RSV
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most frequent presentation of pulmonary TB
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lymphadenopathy
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