Pathology

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streptococcus pneumoniae,
bordetella pertussis

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potential pathogens

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pneumocystis carinii,
cytomegalovirus

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opportunistic pathogens

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toxoplasma gondii

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active intracellular invasion

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gram negative bacteria

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endocytosis/phagocytosis

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endotoxin

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lipopolysaccharide

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exotoxin

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secreted proteins that may mimic intracellular signaling molecules-complex mechanisms

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polysaccharide

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constitutes capsule

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adhesins

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allow adherence to cell surfaces or extracellular matrix

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pneumonia, endocarditis, pyelonephritis, appendicitis

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acute suppurative inflammation

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acute bacterial pneumonia

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Streptococcus pneumoniae: encpasulated gram positive coccus

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acute bacterial pneumonia

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polysaccharide capsule (many antigenic types)prevents phagocytosis; IgA proteases inactivate mucosal antibodies

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acute bacterial pneumonia

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cell wall - ribitol phosphate teichoic acid and peptidoglycan are proinflammatory factors that induce TNF and IL1

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acute bacterial pneumonia

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colonization/invasion of blood stream (bacteria), or tissue (pneumonia, meningitis) characterized by the recruitment of PMNs at the site of infection by integrin-mediated (CD18) and other processes

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pneumococcus pathogenesis

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Binding of bacteria to alveolar cells
Activation of PAF and the inflammatory cascade,including IL1
Activation of Tissue Factor and coagulation cascade (C5a)
Cell wall fragments are the active bacterial factor
Recruitment of PMN and other cells
Leakage of blood proteins
Consolidation

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normal lung

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spongy, alveoli still full of air

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consolidated lung

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air spaces in lung full of something else

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acute bacterial pneumonia pathologic stages

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Edema – serous exudate
Acute inflammation - recruitment of PMN and platelets, activation of complement and coagulation cascades, polymerization of fibrin
Consolidation (red and gray hepatization)
Resolution - restoration of architecture by macrophage cleanup of inflammatory infiltrates

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endocarditis

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infection of heart valve

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endocarditis

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can be acute (rapidly progressive) or subacute (indolent)

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endocarditis

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caused by long list of bacterial agents

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subacute endocarditis

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most frequently caused by oral strains of Streptococci (viridans strep)

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acute endocarditis

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most frequently caused by Staph. aureus

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staphylococcus aureus

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pyogenic gram positive coccus

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staphylococcus aureus

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multiple virulence factors encoded by genetic "pathogenicity island" and induced coordinately by peptide secreted by bacterium

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staph virulence factors

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fibrinogen, laminin, and fibronectin receptors on bacterial surface allow adhesion to clot and extracellular matrix

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staph virulence factors

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expopolysaccharide bacterial capsule allows attachment to plastic and metal (catheters, prosthetic heart valves.

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staph virulence factors

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locally destructive excreted enzymes--lipase and collagenase, hemolytic and cytolytic toxins

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staph virulence factors

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secreted toxins may produce other syndromes: enterotoxin causes GI effects and is a superantigen that leads to massive stimulation of T cells and release of cytokines, mediating systemic effects

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staph virulence factors

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exfoliative toxin and Toxic shock syndrome TSS1 cause scalded skin syndrome and toxic shock syndrome

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rheumatic, infectious, "marantic" (non-bacterial), autoimmune

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endocarditis types of vegetations

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staph aureus endocarditis

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seeding of bacteria onto fibrin deposited on valve surface leads to local destruction of tissue with massive PMN infiltrate. aortic and mitral valves most commonly affected

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staph aureus endocarditis

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inflammatory lesion may erode into valve ring, cause hemodynamic decompensation and rapid death

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bacterial endocarditis

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valve, vegetation, bacteria, fibrin, inflammatory infiltrate, PMNs

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endocarditis systemic effects

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septic embolization, peripheral emboli, damage to heart, circulating immune complexes, embolism, stroke, bacteremia with metastatic infections

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pyelonephritis

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bacterial infection of the kidney

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pyelonephritis

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frequently associated with anatomic abnormalities of the urinary collecting system

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pyelonephritis

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may become chronic and destroy the kidney

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pyelonephritis

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bacterial pathogens most frequently are members of gram negative rods

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pyelonephritis

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pus, dilated collecting system

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Escherichia coli

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facultative (anaerobic/aerobic), enteric gram negative bacillus

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E. coli pyelonephritis

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adherence to urinary epithelium, colonization of urethra, increased risk of urinary tract infection

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E. coli pyelonephritis

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ascending urinary tract infection, suppurative inflammation in the interstitium and renal tubules

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E. coli pyelonephritis

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complications: papillary necrosis, pyonephrosis (pus in the renal pelvis), perinephric abscess

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abdominal abscess

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various etiologies - intestinal infection with rupture, diverticulitis, G U infections

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abdominal abscess

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caused by mixed bacterial population

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abdominal abscess

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peritonitis vs. abscess - role of coagulation of serum proteins in walling off infectious process and providing framework for cellular motility

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abdominal abscess

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example: blockage of appendix leading to necrosis

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appendicitis

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combined infection including E. coli and Bacteroides fragilis (anaerobic gram negative bacillus) causing full-thickness necrosis of bowel wall, leads to sersitis (peritoneal inflammation)

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appendicitis

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propensity of E. Coli and B. fragilis to form abscess depends on virulence factors of B. fragilis and is promoted by foreign material (vegetable fiber or barium in experimental models

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appendicitis

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conditions of abscess - diffusion of antibiotics into center and inactivation of some antibiotics (aminoglycosides) in anaerobic environment

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appendicitis

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requirement of cell surfaces and extracellular matrix for efficient PMN migration and phagocytosis

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appendicitis

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cure requires both drainage of abscess and antimicrobial therapy

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appendicitis

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mucosal ulceration, serosal inflammation, necrosis, full thickness inflammation

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salmonella

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caused by large genus of bacteria

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salmonella

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most of the large genus of bacteria that cause this infection have animal reservoirs

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salmonella typhi

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this salmonella has exclusive human host

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typhoid fever

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salmonella typi: intracellular gram negative enteric bacillus

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salmonella typhi - typhoid fever

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introduced to GI tract by fecal contamination of water, food (human reservoir)

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salmonella typhi - typhoid fever

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invades reticuloendothelial cells, produces endotoxin, Vi antigen (polysaccharide)

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salmonella typhi - typhoid fever

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infection of small bowel lymphatics with bacteremia, ulceration, bleeding, perforation.

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salmonella typhi

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disseminated infection: osteomyelitis

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salmonella typhi - typhoid fever

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mononuclear (macrophage/lymphocyte) inflammation, necrosis, hemorrhage within Peyer's patches, spleen, liver
mononuclear cells with intracellular bacteria

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salmonella typhi

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infection
dissemination
pathologic lesions

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typhoid fever

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high temp, high pulse, abdominal pain, headache, constipation, rose spots (abdomen), splenomegaly, cough, epistaxis, abnormal mental status, diarrhea, hemorrhage, perforation, hemorrhagic lesions in ileum

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typhoid fever

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mononuclear inflammation in bowel wall - intracellular bacteria

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typhoid fever

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sheets of mononuclear cells and red blood cells in stool

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tuberculosis

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mycobacterium tuberculosis: acid fast, aerobic intracellular bacterium with waxy cell wall

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mycobacterium tuberculosis

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ability to be taken up by macrophages and multiply within non acidified phagosomes

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mycobacterium tuberculosis

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delayed-type hypersensitivity: CD4 cells stimulate TNF-alpha and IFN gamma secretion, lead to macrophage activation and epithelioid granuloma formation. CD8 cells can lyse infected macrophages.

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mycobacterium tuberculosis

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glycolipid "cord factor" induces granulomas

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mycobacterium tuberculosis

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lipoarabinomanan (similar to LPS) inhibits macrophage activation

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mycobacterium tuberculosis

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granulomatous inflammation, caseation necrosis (lymph nodes, vertebral bone), liquefaction, leads to tissue destruction and hemorrhage, fibrosis

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tuberculosis

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most deadly single disease - affecting 1/3 of world's population

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tuberculosis

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mycobacterium tuberculosis--> primary tuberculosis-->
>90%: healing, calcification, dormant organisms, reactivation or reinfection
<10%: progressive primary tuberculosis, greater susceptibility in certain racial groups, children, immunocompromised

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secondary tuberculosis, reinfection/reactivation

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cavitary tuberculosis

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advanced tuberculosis

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cavitary lung disease, intestinal disease, renal

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tuberculosis

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caseous nodule in antracotic lung

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lung granuloma

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lymphocytes, Langhans giant cell, epithelioid cells

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mycobacterium tuberculosis

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peribronchial caseation: route of exit of mycobacteria

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lung abscess and empyema

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mixed aerobic and anerobic bacteria, frequently associated with aspirated upper respiratory flora including staphylococci, streptococci, Bacteroides and Fusobacterium sp.

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lung abscess and empyema

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acute suppurative process with tissue destruction leads to walled-off fibrous cavity with liquefied central cavity

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lung abscess and empyema

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macrophages, lymphocytes, and plasma cells surround areas of continuing bacterial growth; granulation tissue, liquefied cavity, dense chronic inflammation, new vessels and fibrous tissue

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lung abscess and empyema

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resolution by drainage through bronchus or chest wall

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lung abscess and empyema

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scarring and restriction of lung capacity

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empyema (pleural space most commonly affected = pyothorax)

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pus within natural body cavity

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abscess

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collection of pus in a newly formed capsule

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Schistosoma mansoni

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tropical freshwater Trematode bloodfluke

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Schistosoma mansoni

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invasive larva penetrates skin, using protease penetration factors

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Schistosoma mansoni

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adults develop in mesenteric veins, adopt host antigens and cause little inflammation, deposit eggs.
egg antigents elicit eosinophilic infiltrate, granulomas, and dense fibrosis. IL-4, IL-5, IL13
lives in bloodstream

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Schistosoma mansoni

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"pipe stem" fibrosis of liver (scarring), leads to portal hypertension (obstruction of portal venous circulation), leads to ascites (fluid in abdomen) and varices
prominent veins, central vein obliterated so alternate routes
veins most dangerous that follow esophagus--can rupture and cause major GI bleeding

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Schistosoma mansoni

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bladder involvement with hematuria, promotion of squamous cell carcinoma of bladder

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Schistosoma mansoni

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clamdigger's itch

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stages of schistosomes

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miracidium larva, cercaria larva, host snails, adults in mesenteric veins

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schistosomiasis

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acute to chronic
cercariae to schistosomula, to adult worms to eggs

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schistosomiasis

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egg in bowel wall, acute inflammation with eosinophils

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schistosomiasis

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eggs trapped in bowel wall with chronic inflammation

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schistosomiasis

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biopsy bowel mucosa, squeeze between glass slides, eggs have typical ovoid appearance, some with spin sticking out in side, fairly large eggs

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schistosomiasis

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granuloma formation around eggs
balance of cytokines elicited by antigens associated with eggs promote production of collagen and fibrosis

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schistosomiasis

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acute TH1 response with IFNg and TNF
chronic disease supervenes, shift toward TH2 with eosinophils, fibrosis

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schistosomiasis

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granuloma with egg instead of giant cell

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TB and schistosomiasis

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epithelioid cells that started off as macrophages and were changed under influence of cytokines into cells with a lot of pink cytoplasm

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schistosomiasis

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marked fibrosis surrounding granulomas

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schistosomiasis

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Not manifest at this level until beginning of puberty. Can be infected in early childhood but don’t get this until infected for many years.

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cytopathic/cytoproliferative cellular response to infectious agents

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mostly viral diseases, not elicitation of particular pattern of inflammation but of reaction to infection and death of particular subsets of cells within body

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influenza A virus

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orthomyxovirus (RNA), infects animals and humans, capable of genetic recombination, antigenic variation, epidemics

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influenza A virus

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surface hemagglutinin, allows fusion to host cell membranes, neuraminidase allows virus to uncoat

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influenza A virus

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localized necrosis of respiratory epithelium, little inflammatory response, systemic symptoms

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primary viral pneumonia: edema, necrosis of ciliated epithelium, lymphocytic infiltrates in submucosa

secondary bacterial pneumonia: producing pathology of acute suppurative inflammation, S. aureus is a frequent pathogen

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primary viral pneumonia vs. secondary bacterial pneumonia

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influenza A virus

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causes world-wide epidemics when new antigenic type appears (pandemics)

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influenza A virus

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25,000 deaths in US in average year

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influenza A virus

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attaches to respiratory cells and cilia

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influenza pneumonia

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fluffy interstitial infiltrates in lung x-ray

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influenza pneumonia

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lymphocytes in bronchial submucosa, loss of superficial epithelium and fibrin in lumen

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influenza pneumonia

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hyaline membranes

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avian influenza

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high cytokine levels and dysregulation of cytokine balance, leading to lack of control of virus replication and systemic damage

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avian influenza

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begins to resemble pneumococcal pneumonia
inflammation in lower respiratory tract

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avian influenza

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Stain for TNFa, shows lot of production of TNF, high cytokine levels, disregulation, lack of control so get enormous quantities of virus, much more than in other strains. Interferons, IFN-B, not particularly effective in controlling this.

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influenza A virus

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lesions in large airways, lung shows lymphocytic nodules and interstitial pneumonitis, lymphocytes in small nodules in larger/medium airways

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1918 influenza A virus

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severe alveolar damage, down into deep airways in see bronchiolitis. huge amount of IL-6-systemic manifestations

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measles (rubeola) pneumonia

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morbillivirus: paramyxovirus (RNA), one strain without antigenic variation

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measles (rubeola) pneumonia

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hemagglutinin binds to many cell types by CD46, a complement regulatory protein

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measles (rubeola) pneumonia

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virus multiplies within epithelial and mononuclear cells. viral growth controlled by T cell response. Antibody protects against infection (not disease)

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measles (rubeola) pneumonia

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suppression of cell-mediated immunity (including by malnutrition) increases severity of disease. typical rash requires cell mediated immune response

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measles (rubeola) pneumonia

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peribronchiolar and interstitial lymphocytic and mononuclear infiltrate. lymphoid hyperplasia. multinucleate syncytial cells (Warthin-Finkeldey giant cells) in lung, lymph nodes

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measles (rubeola) pneumonia

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rash, including involvement of conjunctiva and oral mucosa. requires cell-mediated immunity

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measles (rubeola) pneumonia

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Koplik spots on oral mucosa

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measles (rubeola) pneumonia

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systemic disease, lung gets inflamed, interstitial inflammation
lymphocytes, giant cell (multiple epithelial cells fuse)

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cytomegalovirus

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DNA herpesvirus

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cytomegalic inclusion disease

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opportunistic disease - seen in immunosuppressed, AIDS, congenital infections

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cytomegalic inclusion disease

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infection of epithelial and endothelial cells - organs most involved are lungs, liver, kidney, GI tract, CNS including retina

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cytomegalic inclusion disease

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cytopathic effect - large intranuclear inclusion within enlarged cells

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cytomegalic inclusion disease

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pneumonia, focal necrosis in many organs, ulceration of intestine

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amebic dysentery - entamoeba histolytica

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protozoan with infectious cyst, invasive trophozoite, motile, infectious by mouth

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amebic dysentery - entamoeba histolytica

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amebic surface lectin allows trophozoite adherence to colonic epithelium, invasion, also confers complement resistance

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amebic dysentery - entamoeba histolytica

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invasive trophozoites kill PMNs, liquefy tissues, cause "sterile abscess"

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amebic dysentery - entamoeba histolytica

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colitis with "flask-shaped" ulcers, liver abscess with liquefied necrotic material

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amebic dysentery - entamoeba histolytica

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extraintestinal disease form: amebic liver abscess filled with cellular debris

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pseudomembranous colitis - clostridium difficile

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toxin-producing, gram positive, spore-forming anaerobic bacillus

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pseudomembranous colitis - clostridium difficile

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widespread in nature, spores stable in environment. colonization of large bowel, after distrubance of normal flora (antibiotics)

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pseudomembranous colitis - clostridium difficile

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production of cytotoxins A and B

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pseudomembranous colitis - clostridium difficile

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diarrhea, pseudomembrane formation (fibrin, inflammatory cells, bacteria and dead cells)

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cryptococcal meningitis - cyrptococcus neoformans

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encapsulated yeast

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cryptococcal meningitis - cyrptococcus neoformans

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found world wide in high nitrogen soils, (ex: aged pigeon droppings). aerosol spread

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cryptococcal meningitis - cyrptococcus neoformans

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common respiratory infection, immunosuppressed tend to disseminate to meninges, bone, skin

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cryptococcal meningitis - cyrptococcus neoformans

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polysaccharide capsule (useful for diagnosis), no toxin, little acute inflammatory response, loose granulomas

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cryptococcal meningitis - cyrptococcus neoformans

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insidious onset, chronic, hydrocephalus

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nature: in mycelia/hyphae, fruiting body, spores
tissue: yeast

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yeast and fungi in nature and tissue

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cryptococcal meningitis - cyrptococcus neoformans

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phagocytosed yeast in lung macrophages

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cryptococcal meningitis - cyrptococcus neoformans

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takes tryptophan and turns it into something resembling melanin. brown

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cryptococcal meningitis - cyrptococcus neoformans

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diagnosed by stain and India ink preparation--stain doesn't get thru polysaccharide capsule very well, so look for capsule in India ink--suspension of C particles

latex agglutination of secreted polysaccharide in CSF or Serum - few cross reactions

culture of yeast forms: yeast with clear area around them. clear area represents polysaccharide capsule. invasive forms in CSF have very large capsule

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cryptococcal meningitis - cyrptococcus neoformans

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gelatinous appearance in meninges, like apple jelly, masses of yeast with very dense polysaccharide capsule that blocks flow of CSF and leads over time to enlargement of ventricles

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cryptococcal meningitis - cyrptococcus neoformans

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capsule stained by mucicarmine b/c recognizes polysaccharides. red=capsule, how to recognize yeast in tissue

not much of prominent inflammatory infiltrate, few cells, much less than other fungal infections

normal immune system: polysaccharide prevents much of signaling eliciting normal response

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cryptococcal meningitis - cyrptococcus neoformans

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stain with silver impregnation technique, not much inflammation

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cryptococcal meningitis - cyrptococcus neoformans

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nodular lesions in skin. can begin to resemble viral molluscum contagiosum

within epithelial area are yeasts with big clear spaces around them, not much of inflammatory response

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malaria - plasmodium

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faciparum is worst
anopheles mosquito

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malaria - plasmodium

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infectious forms (sporozoite) are in anopheles mosquito. bite injects form that infects heptocytes. parasite forms that infect erythrocytes mature in liver, break out and infect RBCs

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malaria - plasmodium

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infected RBCs lyse, release infectious merozoites, attach to and invade new RBCs. periodic fevers correlated with RBC infection and lysis cycle. few gametocytes, infectious for mosquitoes formed eventually

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malaria - plasmodium

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protozoan infection of 200 million people, killing 1.5 million per year

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malaria - plasmodium

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binding of infected RBC to endothelium by integrin and thrombospondin receptors. local release of high levels of cytokines may cause acute organ dysfunction

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malaria - plasmodium

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clinical features: fever, high parasitemia, severe anemia, renal failure, cerebral dysfunction, pulmonary edema, death. cerebral form may evolve very rapidly and be fatal

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malaria - plasmodium

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patterns of morphologic change: congestion, enlargement of spleen and liver with deposition of pigment from hemoglobin digestion. cerebral form of disease may show small vessels clogged with parasitized RBC and have ring hemorrhages. little inflammation is noted

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malaria - plasmodium

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goes on for protracted period before very slowly host mounts humoral and cell-mediated response to control infection, but not enough to prevent further infection. multiple bouts common

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malaria - plasmodium

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challenge for producing vaccine is that have to produce one that's better than natural human immunity

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malaria - plasmodium

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pigment in spleen and liver, breakdown products of hemoglobin in hepatic Kupffer cells

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cerebral malaria

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cerebral edema, rapidly progressive, sulci and gyri compressed, edematous brain
not everyone with cerebral form of this disease has edema

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cerebral malaria

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brown dots of erythrocytes that are parasitized, hemoglobin breaking down causing brown pigment, sticking to endothelial cells and causing clogged areas
elaboration of very high levels of cytokines that affect neurons around vessels
can go rapidly from no symptoms to global neuronal dysfunction and coma
if survive, not always permanent damage
can recover but can also be fatal

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plasmodium falciparum

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fever curve up and down
not as regular a fever pattern
release of merizoite stage correlates with peak of fever
RBC's break down, release things in cell, IL-1 produced, make fever

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malaria - plasmodium

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diagnosed by examining blood films--see ring forms, trophozoites, gametocytes, schizonts, merozoites

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malaria - plasmodium

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goes on for protracted period before very slowly host mounts humoral and cell-mediated response to control infection, but not enough to prevent further infection. multiple bouts common

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malaria - plasmodium

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challenge for producing vaccine is that have to produce one that's better than natural human immunity

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malaria - plasmodium

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pigment in spleen and liver, breakdown products of hemoglobin in hepatic Kupffer cells

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cerebral malaria

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cerebral edema, rapidly progressive, sulci and gyri compressed, edematous brain
not everyone with cerebral form of this disease has edema

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cerebral malaria

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brown dots of erythrocytes that are parasitized, hemoglobin breaking down causing brown pigment, sticking to endothelial cells and causing clogged areas
elaboration of very high levels of cytokines that affect neurons around vessels
can go rapidly from no symptoms to global neuronal dysfunction and coma
if survive, not always permanent damage
can recover but can also be fatal

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plasmodium falciparum

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fever curve up and down
not as regular a fever pattern
release of merizoite stage correlates with peak of fever
RBC's break down, release things in cell, IL-1 produced, make fever

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malaria - plasmodium

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diagnosed by examining blood films--see ring forms, trophozoites, gametocytes, schizonts, merozoites