Suppurative (Polymorphonuclear) Inflammation
This pattern is the reaction to acute tissue damage, described in Chapter 2 , characterized by increased vascular permeability and leukocytic infiltration, predominantly of neutrophils ( Fig.
8-7 ). The neutrophils are attracted to the site of infection by release of chemoattractants from the "pyogenic" bacteria that evoke this response, mostly extracellular Gram-positive cocci
and Gram-negative rods. Massing of neutrophils forms pus. The sizes of exudative lesions vary from tiny microabscesses formed in multiple organs during bacterial sepsis secondary to a
colonized heart valve to diffuse involvement of entire lobes of the lung during pneumonia. How destructive the lesions are depends on their location and the organism involved. For
example, pneumococci usually spare alveolar walls and cause lobar pneumonia that resolves
Figure 8-7Pneumococcal pneumonia. Note the intra-alveolar polymorphonuclear exudate and intact alveolar septa.
Figure 8-8Secondary syphilis in the dermis with perivascular lymphoplasmacytic infiltrate and endothelial proliferation.
Figure 8-9Herpesvirus blister in mucosa. See Figure 8-13 for viral inclusions.
Figure 8-10Schistosoma haematobium infection of the bladder with numerous calcified eggs and extensive scarring.
Figure 8-11Measles giant cells in the lung. Note the glassy eosinophilic intranuclear inclusions.
Figure 8-12High-power view of cells from the blister in Figure 8-9 showing glassy intranuclear herpes simplex inclusion bodies.
Figure 8-13Cytomegalovirus: distinct nuclear and ill-defined cytoplasmic inclusions in the lung.
Figure 8-14Skin lesion of chickenpox (varicella zoster virus) with intraepithelial vesicle.
Figure 8-15Dorsal root ganglion with varicella zoster virus infection. Note the ganglion cell necrosis and associated inflammation. (Courtesy of Dr. James Morris, Radcliffe Infirmary,
Figure 8-16Pathways of transmission of the Epstein-Barr virus. In an individual with normal immune function, infection leads to mononucleosis. In the setting of cellular
immunodeficiency, proliferation of infected B cells is uncontrolled and may cause B-cell neoplasms. One secondary genetic event that collaborates with Epstein-Barr virus (EBV) to cause
B-cell transformation is a balanced 8;14 chromosomal translocation, which is seen in Burkitt lymphoma. EBV has also been implicated in the pathogenesis of nasopharyngeal carcinoma,
Hodgkin disease, and certain other rare non-Hodgkin lymphomas.
Figure 8-17Atypical lymphocytes in infectious mononucleosis.
Figure 8-18The many consequences of staphylococcal infection.
Figure 8-19Staphylococcal abscess of the lung with extensive neutrophilic infiltrate and destruction of the alveoli (contrast with Figure 8-8 ).
Figure 8-20Streptococcal erysipelas.
Figure 8-21Membrane of diphtheria lying within a transverse bronchus (A) and forming a perfect cast (removed from the lung) of the branching respiratory tree (B).
Figure 8-22Mechanism of action of anthrax toxins. (Adapted from Mourez et al: 2001: a year of major advances in anthrax toxin research. Trends Microbiol 10(6):287, 2002.)
Figure 8-23B. anthracis in the subcapsular sinus of a hilar lymph node of a patient who died of inhalational anthrax. (Courtesy of Dr. Lev Grinberg, Department of Pathology, Hospital
40, Ekaterinburg, Russia and Dr. David Walker, UTMB Center for Biodefense and Emerging Infectious Diseases, Galveston, TX.)
Figure 8-24Nocardia asteroides in a Gram-stained sputum sample. Note the beaded, branched Gram-positive organisms and leukocytes. (Courtesy of Dr. Ellen Jo Baron, Stanford
University Medical Center, Stanford, CA.)
Figure 8-25Gonococcal culture showing pili, as seen by scanning microscopy (A), and in clusters, as seen by transmission electron microscopy (B). (Courtesy of Dr. John Swanson, Rocky
Mountain Laboratories, Hamilton, MT.)
Figure 8-26Whooping cough showing a haze of bacilli (arrows) etangled with the cilia of bronchial epithelial cells.
Figure 8-27Pseudomonas vasculitis in which masses of organisms form a perivascular blue haze.
Figure 8-28The sequence of events in primary pulmonary tuberculosis, commencing with inhalation of virulent M. tuberculosis and culminating with the development of cell-mediated
immunity to the organism. A, Events occurring in the first 3 weeks after exposure. B, events thereafter. The development of resistance to the organism is accompanied by the appearance of
a positive tuberculin test. Cells and bacteria are not drawn to scale. iNOS, inducible nitric oxide synthase; MHC, major histocompatibility complex; MTB, M. tuberculosis; NRAMP1,
natural resistance-associated macrophage protein.
Figure 8-29The natural history and spectrum of tuberculosis. (Adapted from a sketch provided by Dr. R. K. Kumar, The University of New South Wales, School of Pathology, Sydney,
Figure 8-30Primary pulmonary tuberculosis, Ghon complex. The gray-white parenchymal focus is under the pleura in the lower part of the upper lobe. Hilar lymph nodes with caseation
are seen on the left.
Figure 8-31The morphologic spectrum of tuberculosis. A characteristic tubercle at low magnification (A) and in detail (B) illustrates central caseation surrounded by epithelioid and
multinucleated giant cells. This is the usual response seen in patients who have developed cell mediated immunity to the organism. Occasionally, even in immunocompetent individuals,
tubercular granulomas might not show central caseation (C); hence, irrespective of the presence or absence of caseous necrosis, special stains for acid-fast organisms need to be performed
when granulomas are present in histologic section. In immunosuppressed individuals, tuberculosis may not elicit a granulomatous response ("nonreactive tuberculosis"); instead, sheets of
foamy histiocytes are seen, packed with mycobacteria that are demonstrable with acid-fast stains (D). (D, Courtesy of Dr. Dominick Cavuoti, Department of Pathology, University of Texas
Southwestern Medical School, Dallas, TX.)
Figure 8-32Secondary pulmonary tuberculosis. The upper parts of both lungs are riddled with gray-white areas of caseation and multiple areas of softening and cavitation.
Figure 8-33Miliary tuberculosis of the spleen. The cut surface shows numerous gray-white granulomas.
Figure 8-34Mycobacterium avium infection in a patient with AIDS, showing massive infection with acid-fast organisms.
Figure 8-35Leprosy. A, Peripheral nerve. Note the inflammatory cell infiltrates in the endoneural and epineural compartments. B, Cells within the endoneurium contain acid-fast positive
lepra bacilli. (Courtesy of E.P. Richardson, Jr. and U. De Girolami, Harvard Medical School.)
Figure 8-36Lepromatous leprosy. Acid-fast bacilli ("red snappers") within macrophages.
Figure 8-37Treponema pallidum (dark-field microscopy) showing several spirochetes in scrapings from the base of a chancre. (Courtesy of Dr. Paul Southern, Department of Pathology,
University of Texas Southwestern Medical School, Dallas, TX.)
Figure 8-38Protean manifestations of syphilis.
Figure 8-39Syphilitic chancre in the scrotum (see Figure 8-8 for the histopathology of syphilis). (Courtesy of Dr. Richard Johnson, Beth Israel-Deaconess Hospital, Boston, MA.)
Figure 8-40Trichrome stain of liver shows liver gumma (scar), stained blue, which is caused by tertiary syphilis (also known as hepar lobatum). Compare with nodules of alcoholic
cirrhosis ( Chapter 18 ).
Figure 8-41Tiny deer tick (bottom), which transmits Lyme disease and Babesia and Ehrlichia organisms, contrasted with a larger dog tick (top), which is not thought to transmit human
infections. (Courtesy of Dr. F.R. Matuschka, Free University of Berlin, Germany.)
Figure 8-42Clinical stages of Lyme disease.
Figure 8-43Boxcar-shaped Gram-positive Clostridium perfringens in gangrenous tissue.
Figure 8-44Peripheral blood granulocyte (band neutrophil) containing an Ehrlichia inclusion (arrow). (Courtesy of Dr. Stephen Dumler, Johns Hopkins Medical Institutions, Baltimore,
TABLE 8-10-- Rickettsial Diseases and Pathogens
Typhus Group (No Eschar)
Date: 2016-04-22; view: 574