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microbial pathogens
margination of leukocytes
Granulocytes
Neutrophils Eosinophils Basophils & Mast cells
Acute inflammation
Mononuclear phagocytes
monocytes and macrophages (histiocytes)
monocyte macrophage
Phagocytic Participates in induction of immune reactions (antigen presentation) Source of proinflammatory cytokines
Lymphocyte Plasma cell
Inflammation definitions
Edema accumulation of extrvascular fluid Effusion accumulation of fluid in a body cavity (e.g. peritoneum or pleura) Transudate edema fluid with low protein content (s.g. <1.015) Exudate edema fluid with high protein content (s.g. >1.015), often with inflammatory cells
Serous exudate exudate lacking g large g number of inflammatory y cells; usually pale yellow Serosanguinous exudate or effusion containing erythrocytes (usually red-tinged) Fibrinous exudate contains large amount of fibrin after coagulation of clotting factors Purulent exudate or effusion contains high inflammatory cell content; often seen with bacterial infections Suppurative inflammation purulent exudate accompanied by significant liquifactive necrosis (pus).
Fibrinous pericarditis
Ulcers
Ulcer
Artery
Gastric Ulcer
Pseudomembranous Inflammation
Pseudomembrane
Depending upon bacterial species, may cause necrosis suppuration (pus) or abscess
exudative with necrosis abscess
With time, ti increasing i i chronic h i i inflammation fl ti b begins i l leading di various degrees of mixed acute and chronic inflammation Examples:
Streptococcus pneumoniae Staphylococcus aureus Pseudomonas aeruginosa Most other bacteria
Exudative Inflammation
vascular permeability, recruitment of leukocytes (esp. neutrophils), pus typically caused by pyogenic, extracellular bacteria usually localized examples:
Exudative Inflammation
group A strep (Streptococcus pyogenes) pharyngitis Staphylococcus aureus furuncle Streptococcus pneumoniae pneumonia and meningitis
Necrotizing Inflammation
exudative inflammation with necrosis (suppuration) host damage may be caused by bacterial virulence factors examples:
Necrotizing pneumonia
Gram stain
Gram stain
Examples:
Mycobacterium tuberculosis (tuberculosis) Rickettsia rickettsii (Rocky Mountain spotted fever) Mycoplasma pneumoniae pneumonitis Chlamydia trachomatis (lymphogranuloma venereum and urogenital infections)
Activated Macrophages
Macrophages can be activated by antigenantigenspecific or by nonnon-specific means. Activation is an operational term indicating an enhanced capacity to do inflammatory battle.
Plasma cell
Causes
Mycobacteria Fungi Parasites Foreign Body Idiopathic
Granuloma formation
A. Recruitment of mixed inflammatory cells, driven by cytokines Enrichment in mononuclear (macrophages, p g , cells ( lymphocytes) organizing into a cluster Fully organized granuloma with fibrosis and disruption of tissue architecture
B.
C.
H&E
H&E
H&E
H&E
Mycobacterium tuberculosis
acid fast
Lepromatous leprosy
H&E
Interstitial Inflammation
nonspecific morphology (chronic nonspecific inflammation) suggestive of viral, mycoplasma mycoplasma, , rickettsial, or spirochetal infections
Rickettsia rickettsii
H&E
Interstitial pneumonitis
Mycoplasma pneumoniae
Influenza A virus
H&E
Interstitial pneumonitis
H&E
Gram stain
Cystic fibrosis Achlorhydria leukocyte adhesion molecule deficiency chronic granulomatous disease complement deficiency, asplenia, susceptibility to encapsulated bacteria hypogammaglobulinemia > defective opsonization HIV, cancer therapy, corticosteroid or immune suppressive therapy diminish effective T lymphocyte responses interferon- receptor deficiencies (recurrent Mycobacteria and Salmonella infections)
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n = 866
Haemophilus influenzae Streptococcus pyogenes Neisseria gonorrhoeae Coxiella burnetii Staphylococcus aureus
Enterococcus faecalis
Mycobacterium tuberculosis Escherichia coli Yersinia pestis Vibrio vulnificus Bacillus anthracis Klebsiella pneumoniae
Pneumocystis jirovecii Saccharomyces cerevisiae Candida albicans Plasmodium falciparum Toxoplasma gondii Brugia malayi Drosophila simulans Homo sapiens Culex pipiens Rattus norvegicus
Homo sapiens
1 10 100 1000 10000
0.1
0 recognized COGs
Influenza virus (V) attached to tracheal cilia (C) and microvilli (M)
Picornavirus binding
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Microbial virulence mechanisms: toxins Bacterial cell walls and microbe-associated molecular patterns (MAMPs)
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Acquisition of exotoxins
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phospholipases
Phagocytosis opsonized pathogens bind to FcR, CR1,3,4, mannose receptors, or fMLP-receptors and must circumvent host degradation in lysosomes Induced endocytosis pathogen binding to host cell surface followed by bacterial initiation of host cell internalization Active invasion does not require participation of host for internalization
Yersinia
inhibition of phagocytosis
Shigella enterocolitis
Shigella enterocolitis
enterocolitis
Shigella enterocolitis
Shigella enterocolitis
Shigella enterocolitis
Pneumococcal meningitis
Pneumococcal meningitis
colonization and systemic invasion
Pneumococcal meningitis
bacteremia / intravascular survival
Phase shift to upregulate antiphagocytic capsule expression enhances survival in blood pneumococci with dense polysaccharide capsules do not adhere well to epithelial surfaces but are antiphagocytic pneumococci with less polysaccharide capsule and more phosphorylcholine and CbpA adhere well but do not resist phagocytosis well
neutrophils in gastric mucosa > Helicobacter pylori abscess with sulfur granules > Actinomycosis (Actinomyces spp.) caseating granulomas > M. tuberculosis granulomas with stellate microabscesses > cat scratch disease (Bartonella henselae) lymphocytic vasculitis > Rocky Mountain spotted fever (Rickettsia rickettsii)
silver stain
H&E
sulfur granule
Gram stain
H&E
actinomycosis
Caseous necrosis in TB
H&E
H&E
lymphocytic vasculitis
Fluorochrome stain
H&E
immunohistochemistry
0 Onset of illness
12 Months
18
24
IgM
IgG
agglutination
Cellular immunity
lymphocyte proliferation IFN production
Protein (Western) immunoblot