Bronchopneumonia
Gross: Note multiple, focal (perilobular), yellowish areas of pneumonic consolidation filled with purulent exudate. At autopsy, edema fluid could be expressed from the less affected intervening areas.
Bronchopneumonia
Low power: Pink, homogeneous, intraalveolar edema; hemorrhage and fibrin; a blue area in a bronchus composed of neutrophils.
Bronchopneumonia
High power: The blue area under high power. The bronchus is filled with desquamated epithelial cells, debris and neutrophils (pus). This is an example of purulent bronchiolitis which impairs aeration of distal alveoli until exudation is expectorated.
Bronchopneumonia
High power: Pus. The neutrophils are recognized by segmented nuclei. Dead neutrophils are indicated by nuclear pyknosis and karyorrhexis. The occasional large, pale cells are macrophages.
Bronchopneumonia
Areas similar to this are seen in your histology slides. The arterioles and capillaries are congested, alveoli are filled with fluid and neutrophils are also present.
Bronchopneumonia
First stage of pneumonia: Edema. High power: Pulmonary edema. Congestion of arterioles and capillaries. Desquamated alveolar lining the cells in alveoli. Neutrophils are scanty.
Bronchopneumonia
Second stage of pneumonia: Red hepatization. This stage is referred to as red hepatization in lobar pneumonia because the consolidated lobe of the lung has the consistency of liver. The alveoli contain red cells and fibrin.
Bronchopneumonia
Higher power: Red hepatization in which there is deposition of fibrin in the center of the alveoli. There is congestion and there are some neutrophils.
Bronchopneumonia
Higher power: same area.
Bronchopneumonia
Third stage of pneumonia: Gray hepatization. Low power: Alveoli are filled with fibrin and neutrophils. The congestion of vessels is receding.
Bronchopneumonia
High power: Showing fibrin and leukocytes.
Bronchopneumonia
High power: Shows the loss of alveolar lining cells, fibrin and neutrophils. Neutrophils are seen leaving the capillary. On gross examination, this area is yellowish in color like pus and bulges over the surface of surrounding tissue.
Bronchopneumonia
Fourth stage of pneumonia: Area of lysis. Shows disintegrated neutrophils, some edema and a predominance of macrophages. Proteolytic enzymes have lysed the fibrin. Neutrophils are seen in alveolar walls and macrophages have removed the cellular debris.
Bronchopneumonia
High power: macrophages.
Lobar pneumonia
Gross: Note the diffuse pneumonic infiltration of the entire middle lobe (gray hepatization stage) with fibrinous exudate involving the pleura and interlobar fissures.
Lobar pneumonia
Low power microscopic: The alveoli show a uniform infiltration of neutrophils. The pleura shows anthracosis and chronic fibrosis perhaps related to a previous episode of pneumonia. Note that all alveoli show the same stage of pneumonic infiltration and compare this with bronchopneumonia.
Bacterial Endocarditis
Gross view: Mitral valve opened to show row of vegetations on the margins of cusps.
Bacterial Endocarditis
Low power: Vegetation on endocardial surface. The lesion consists mainly of fibrin.
Bacterial Endocarditis
A view of vegetations on a valve cusp. Note how friable they appear. They have a tendency to break off and produce "septic" emboli which in turn produce "septic" infarcts in various organs.
Bacterial Endocarditis
Deeper in the section clumps of bacteria are seen.
Bacterial Endocarditis
Under the vegetation, granulation tissue is seen. Healing produces scarring which deforms the valve and causes stenosis and/or incompetence.
Acute Cholecystitis
Gross: Acute cholecystitis.
Acute Cholecystitis
Lower power : Note ulceration of surface mucosa. The underlying wall is edematous and hemorrhagic. The inflammatory reaction is transmural, leading to separation of muscle layers and a serosal exudate. This can progress to perforation and peritonitis.
Acute Cholecystitis
Details of mucosal surface showing submucosal necrosis with fibrin and leukocytes.
Acute Cholecystitis
Another detailed view of mucosal surface showing submucosal necrosis with fibrin and leukocytes.
Acute Cholecystitis
Another detailed view of mucosal surface showing submucosal necrosis with fibrin and leukocytes.
Acute Appendicitis
Gross: Appendicitis.
Acute Appendicitis
Normal appendix: Note the appearance and relationship of mucosa, lymphoid follicle, muscularis and serosa.
Acute Appendicitis
Shows follicular center surrounded by lymphocytes and externally the muscularis and serosa.
Acute Appendicitis
Acute appendicitis: Observe necrosis of the mucosa. At this magnification the diffuse neutrophilic infiltration of the muscularis is just recognizable.
Acute Appendicitis
Detail of ulcerated necrotic mucosa infiltrated by purulent exudate.
Acute Appendicitis
An early stage of acute appendicitis characterized by capillary dilatation and margination of leukocytes.
Acute Appendicitis
Fibrosis of appendix: Note the replacement of mucosa and lymphoid tissue by fibrous tissue which contains neuro-muscular tangles.
Acute Appendicitis
Shows the dense fibrosis scar inside muscle coat.
Bacillary Dysentery
Gross: Acute bacillary dysentery showing diffuse ulceration of mucosa. The greenish-yellow foci are remnants of partially necrotic mucosa. The mucosa may finally reepithelialize with regeneration of the normal villous pattern. Since the damage is limited to the mucosa, this disease does not result in stricture.
Bacillary Dysentery
Lower power: Small bowel. The glands have almost disappeared and only the basal portions can be recognized. The mucosa is now composed of necrotic tissue covered with a fibrinous pseudomembrane. A true membrane overlies normal tissue. A pseudomembrane consists of necrotic tissue which after removal leaves an ulcerated surface.
Bacillary Dysentery
High power: Pseudomembrane.
Bacillary Dysentery
Shows a remnant of mucosal glands filled with neutrophils and a diffuse neutrophilic infiltration of submucosa.
Bacillary Dysentery
The mucosal surface is repaired by a layer of epithelial cells.
Tuberculosis (Tb) Testis & Epididymus
Gross: Tuberculosis of testis and epididymis.
Tuberculosis (Tb) Testis & Epididymus
Lower power: Tuberculosis of epididymis with the portion of ductus deferens in the center.
Tuberculosis (Tb) Testis & Epididymus
Higher power: For orientation, the slide has a portion of ductus deferens in one corner, venous plexus in the second corner and a dark blue lesion with a central necrotic core separated from the surrounding tissue in the third corner. Between these three structures is a round, pink lesion surrounded by a blue rim of lymphocytes. This is a proliferative tubercle.
Tuberculosis (Tb) Testis & Epididymus
Higher power: This section shows a duct and a giant cell tubercle; a round nodule with a large Langhans giant cell in the center surrounded by fibroblasts; and occasional lymphocytes.
Tuberculosis (Tb) Testis & Epididymus
Higher power: A Langhans giant cell and epithelioid cells.
Tuberculosis (Tb) Testis & Epididymus
The nuclei of Langhans giant cell are situated towards the periphery of the tubercle which is particularly clearly seen in a proliferative tubercle.
Tuberculosis (Tb) Testis & Epididymus
High power: Shows that the fibroblasts in the center of the lesion have the nuclear axis parallel to one another producing a loose, fence-like pattern.
Caseous Tb of lung
Gross view of areas of caseous necrosis.
Caseous Tb of lung
Edge of necrotic area with giant cells.
Caseous Tb of lung
In this slide a stain for "acid fast" bacilli has been used (Ziehl Neelson method). A little search in the areas of caseous necrosis will reveal clusters of bright red rods which represent tubercle bacilli.
Miliary Tb of lung
When a caseous focus ruptures into a blood vessel, rapid vascular spread of infected material occurs. Consequent "seeding" may take place and a large number of tubercles of roughly the same age and size are formed. These are the so-called "miliary" tuberculosis (millet sized granuloma). This can occur in the lungs, liver, spleen, bone marrow, kidney, etc. An important feature is little or no caseation in the granulomas.
Miliary Tb of lung
Another view of miliary Tb.
Fibrocaseous Tb of lung
Lower power: Note large area of caseation surrounded by fibrous tissue.
Fibrocaseous Tb of lung
High power: Shows edema and lymphocytic infiltration.
Fibrocaseous Tb of lung
Part of a fibrotic wall surrounding a tubercle. Note giant cell in one corner.
Fibrocaseous Tb of lung
Langhans giant cell surrounded by epithelioid cells and early fibrosis. During its natural course, the lesions of pulmonary tuberculosis show a marked variation in the tendency to heal or progress. Most favorably the lesions might fibrose and calcify, but still contain viable bacilli. Less favorably, the caseous foci could spread via air passages (tuberculous bronchopneumonia), or lymphatic and blood vessels (miliary tuberculosis). Caseous erosion of a bronchus leads to coughing up of the necrotic material and formation of a cavity. Erosion of blood vessels causes blood-staining of sputum or massive hemoptysis.
Granuloma (Histoplasmosis)
Gross: Lung with walled-off, calcified lesions. On X-ray--coin lesions.
Granuloma (Histoplasmosis)
A walled off granuloma showing a marked similarity to tuberculosis. The specific diagnosis of histoplasmosis would depend on identification of the organisms or more indirectly on a positive serological test.
Varicella
Low power: Epidermis with intraepidermal blisters. The superficial layer is intact. The cystic spaces are in the prickle cell layer.
Varicella
Higher power: A cyst filled with edema fluid. At the base there is a viral inclusion body.
Varicella
High power: Intranuclear inclusion bodies.
Cytomegalovirus of lungs
Low power: Slightly atelectatic lung with no noticeable inflammatory reaction.
Cytomegalovirus of lungs
Higher power: Several large cells one of which is dark pink and contains a viral inclusion body.
Cytomegalovirus of lungs
Neonatal kidney showing viral inclusion bodies filling the cell nuclei.
Molluscum Contagiosum
This viral disease produces 1-2 mm pinhead-sized skin lesions with a central depression. This slide shows the complete lesion of proliferated squamous epithelium filled with eosinophilic inclusion bodies. These are the largest known inclusion bodies, thus they are visible on low power scanning.
Molluscum Contagiosum
Higher power: Molluscum lesion
Syphilis of Aorta
Huge aortic aneurysm which has penetrated the chest wall.
Syphilis of Aorta
Destruction of medial elastica leads to mural weakening and aneurysmal dilatation. The aneurysm can rupture, or compress and erode adjacent structures. The aortic cusps may be rolled and the commissaries may widen, which can cause aortic valve incompetence.
Syphilis of Aorta
The "tree barking" effect produced in the intima by the medial scarring.
Syphilis of Aorta
Low power: Showing perivascular cellular infiltration.
Syphilis of Aorta
Similar picture from another area.
Syphilis of Aorta
Higher power: Perivascular "cuffing."
Syphilis of Aorta
Normal aorta elastic stain.
Syphilis of Aorta
Disruption and destruction of elastic tissue in aortitis.
Syphilis of Aorta
Fibrous replacement of elastic tissue.
Candidiasis of Kidney
Low power: Nearly half of this field shows an area of parenchymal necrosis and leukocytic infiltration - an abscess - within which radiating mycelia are seen.
Candidiasis of Kidney
Higher power: A glomerulus is occupied by fungus. Hyphae are indiscriminately growing through normal tissue boundaries. Note the lack of tissue reaction which indicates the patient's diminished response to the organism.
Candidiasis of Kidney
Fungi are seen in the adjacent abscess area.
Candidiasis of Kidney
High power: Shows branching of hyphae.
Candidiasis of Kidney
Blastospores and budding yeast-like forms of Candida. Candidiasis is generally a superficial infection of mucosa. The deep septicemic lesions as seen in this kidney are usually associated with immune deficiency diseases or immunosuppressive therapy.
Chromoblastomycosis of Skin
Severe hyperplasia of skin. Eosinophilic keratin overlying thickened prickle cell layer with elongated papillae. There is diffuse dermal inflammatory infiltration and a micro abscess in one papilla.
Chromoblastomycosis of Skin
High power: Note two intraepithelial abscesses and a subepithelial granuloma containing giant cells. (High power microscopic examination may show thick walled fungi in the abscesses).
Chromoblastomycosis of Skin
Note the brown fungus in the center of the abscess.
Blastomycosis of Lung
Shows diffuse infiltration of lung with abscess resembling confluent pneumonia.
Blastomycosis of Lung
Higher power: Shows histiocytic and a giant cell granuloma. Note one of the giant cells contains a fungus with double contoured cell wall.
Blastomycosis of Lung
Abscess containing mainly neutrophils.
Blastomycosis of Lung
The nuclear structure of this fungus can be seen in the thick wall organisms.
Coccidioidomycosis of Lung
Low power: Shows large areas of necrosis.
Coccidioidomycosis of Lung
Shows two mature sporangia, one of which has just ruptured. Note the neutrophilic reaction.
Coccidioidomycosis of Lung
Immature sporangia. The clear halo is the cell wall. These fungi are often engulfed by giant cells.
Cryptococcosis of Lung
Note the bluish staining fungus surrounded by the red mucin stained capsule. The budding of the fungus is clearly seen. This organism produces granulomata and abscesses in the lungs and other organs particularly the meninges.
Toxoplasmosis of Brain
Brain shows infarct/necrosis. Toxoplasma gondii is a parasite that frequently does not cause tissue damage. Disease results from massive infection or immunodeficiency. Fetal intrauterine infection (particularly of brain) can occur.
Toxoplasmosis of Brain
Higher power: Edge of infarct showing loose fibrillar disarrangement of brain ground substance.
Toxoplasmosis of Brain
Toxoplasma cyst containing toxoplasma organisms.
Toxoplasmosis of Brain
Individual toxoplasma organisms lying free in brain tissue.
Amebic Colitis
Shows the typical undermining ulcer of amebic colitis.
Amebic Colitis
Base of ulcer. Note absence of inflammatory response. Amoeba are in necrotic membrane above the muscle coat.
Amebic Colitis
Note amebae in mucosal glands. Erythrocytes can frequently be seen in Entamoeba histolytica.
Amebic Colitis
Numerous amebae are present.
Pneumocystis Carinii (H&E)
Low power: The alveolar spaces almost universally contain pink proteinaceous exudate.
Pneumocystis Carinii (H&E)
Medium power: In most instances the pink exudate does not quite fill the alveoli, and in some places vacuoles or irregular spaces are seen. This gives the exudate a characteristic "foamy" or "cloudy" appearance.
Pneumocystis Carinii (GMS)
Aggregates of black-stained cysts in the alveolar spaces.
Pulmonary Aspergillosis
Aspergillus species may infect abnormal airways (e.g. old tuberculous of bronchiectatic cavities) and remain non-invasive. In immunocompromised patients, however, this fungus may invade the lung parenchyma, causing a severe, often necrotizing, pneumonia. In this section, taken from the lung of an organ transplant patient, the bronchial lumen is virtually filled by a mass of fungal hyphae.
Pulmonary Aspergillosis
Higher power: Note the hyphae invading the bronchial wall.