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175 Cards in this Set

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streptococcus pneumoniae,
bordetella pertussis
potential pathogens
pneumocystis carinii,
cytomegalovirus
opportunistic pathogens
toxoplasma gondii
active intracellular invasion
gram negative bacteria
endocytosis/phagocytosis
endotoxin
lipopolysaccharide
exotoxin
secreted proteins that may mimic intracellular signaling molecules-complex mechanisms
polysaccharide
constitutes capsule
adhesins
allow adherence to cell surfaces or extracellular matrix
pneumonia, endocarditis, pyelonephritis, appendicitis
acute suppurative inflammation
acute bacterial pneumonia
Streptococcus pneumoniae: encpasulated gram positive coccus
acute bacterial pneumonia
polysaccharide capsule (many antigenic types)prevents phagocytosis; IgA proteases inactivate mucosal antibodies
acute bacterial pneumonia
cell wall - ribitol phosphate teichoic acid and peptidoglycan are proinflammatory factors that induce TNF and IL1
acute bacterial pneumonia
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
pneumococcus pathogenesis
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
normal lung
spongy, alveoli still full of air
consolidated lung
air spaces in lung full of something else
acute bacterial pneumonia pathologic stages
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
endocarditis
infection of heart valve
endocarditis
can be acute (rapidly progressive) or subacute (indolent)
endocarditis
caused by long list of bacterial agents
subacute endocarditis
most frequently caused by oral strains of Streptococci (viridans strep)
acute endocarditis
most frequently caused by Staph. aureus
staphylococcus aureus
pyogenic gram positive coccus
staphylococcus aureus
multiple virulence factors encoded by genetic "pathogenicity island" and induced coordinately by peptide secreted by bacterium
staph virulence factors
fibrinogen, laminin, and fibronectin receptors on bacterial surface allow adhesion to clot and extracellular matrix
staph virulence factors
expopolysaccharide bacterial capsule allows attachment to plastic and metal (catheters, prosthetic heart valves.
staph virulence factors
locally destructive excreted enzymes--lipase and collagenase, hemolytic and cytolytic toxins
staph virulence factors
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
staph virulence factors
exfoliative toxin and Toxic shock syndrome TSS1 cause scalded skin syndrome and toxic shock syndrome
rheumatic, infectious, "marantic" (non-bacterial), autoimmune
endocarditis types of vegetations
staph aureus endocarditis
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
staph aureus endocarditis
inflammatory lesion may erode into valve ring, cause hemodynamic decompensation and rapid death
bacterial endocarditis
valve, vegetation, bacteria, fibrin, inflammatory infiltrate, PMNs
endocarditis systemic effects
septic embolization, peripheral emboli, damage to heart, circulating immune complexes, embolism, stroke, bacteremia with metastatic infections
pyelonephritis
bacterial infection of the kidney
pyelonephritis
frequently associated with anatomic abnormalities of the urinary collecting system
pyelonephritis
may become chronic and destroy the kidney
pyelonephritis
bacterial pathogens most frequently are members of gram negative rods
pyelonephritis
pus, dilated collecting system
Escherichia coli
facultative (anaerobic/aerobic), enteric gram negative bacillus
E. coli pyelonephritis
adherence to urinary epithelium, colonization of urethra, increased risk of urinary tract infection
E. coli pyelonephritis
ascending urinary tract infection, suppurative inflammation in the interstitium and renal tubules
E. coli pyelonephritis
complications: papillary necrosis, pyonephrosis (pus in the renal pelvis), perinephric abscess
abdominal abscess
various etiologies - intestinal infection with rupture, diverticulitis, G U infections
abdominal abscess
caused by mixed bacterial population
abdominal abscess
peritonitis vs. abscess - role of coagulation of serum proteins in walling off infectious process and providing framework for cellular motility
abdominal abscess
example: blockage of appendix leading to necrosis
appendicitis
combined infection including E. coli and Bacteroides fragilis (anaerobic gram negative bacillus) causing full-thickness necrosis of bowel wall, leads to sersitis (peritoneal inflammation)
appendicitis
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
appendicitis
conditions of abscess - diffusion of antibiotics into center and inactivation of some antibiotics (aminoglycosides) in anaerobic environment
appendicitis
requirement of cell surfaces and extracellular matrix for efficient PMN migration and phagocytosis
appendicitis
cure requires both drainage of abscess and antimicrobial therapy
appendicitis
mucosal ulceration, serosal inflammation, necrosis, full thickness inflammation
salmonella
caused by large genus of bacteria
salmonella
most of the large genus of bacteria that cause this infection have animal reservoirs
salmonella typhi
this salmonella has exclusive human host
typhoid fever
salmonella typi: intracellular gram negative enteric bacillus
salmonella typhi - typhoid fever
introduced to GI tract by fecal contamination of water, food (human reservoir)
salmonella typhi - typhoid fever
invades reticuloendothelial cells, produces endotoxin, Vi antigen (polysaccharide)
salmonella typhi - typhoid fever
infection of small bowel lymphatics with bacteremia, ulceration, bleeding, perforation.
salmonella typhi
disseminated infection: osteomyelitis
salmonella typhi - typhoid fever
mononuclear (macrophage/lymphocyte) inflammation, necrosis, hemorrhage within Peyer's patches, spleen, liver
mononuclear cells with intracellular bacteria
salmonella typhi
infection
dissemination
pathologic lesions
typhoid fever
high temp, high pulse, abdominal pain, headache, constipation, rose spots (abdomen), splenomegaly, cough, epistaxis, abnormal mental status, diarrhea, hemorrhage, perforation, hemorrhagic lesions in ileum
typhoid fever
mononuclear inflammation in bowel wall - intracellular bacteria
typhoid fever
sheets of mononuclear cells and red blood cells in stool
tuberculosis
mycobacterium tuberculosis: acid fast, aerobic intracellular bacterium with waxy cell wall
mycobacterium tuberculosis
ability to be taken up by macrophages and multiply within non acidified phagosomes
mycobacterium tuberculosis
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.
mycobacterium tuberculosis
glycolipid "cord factor" induces granulomas
mycobacterium tuberculosis
lipoarabinomanan (similar to LPS) inhibits macrophage activation
mycobacterium tuberculosis
granulomatous inflammation, caseation necrosis (lymph nodes, vertebral bone), liquefaction, leads to tissue destruction and hemorrhage, fibrosis
tuberculosis
most deadly single disease - affecting 1/3 of world's population
tuberculosis
mycobacterium tuberculosis--> primary tuberculosis-->
>90%: healing, calcification, dormant organisms, reactivation or reinfection
<10%: progressive primary tuberculosis, greater susceptibility in certain racial groups, children, immunocompromised
secondary tuberculosis, reinfection/reactivation
cavitary tuberculosis
advanced tuberculosis
cavitary lung disease, intestinal disease, renal
tuberculosis
caseous nodule in antracotic lung
lung granuloma
lymphocytes, Langhans giant cell, epithelioid cells
mycobacterium tuberculosis
peribronchial caseation: route of exit of mycobacteria
lung abscess and empyema
mixed aerobic and anerobic bacteria, frequently associated with aspirated upper respiratory flora including staphylococci, streptococci, Bacteroides and Fusobacterium sp.
lung abscess and empyema
acute suppurative process with tissue destruction leads to walled-off fibrous cavity with liquefied central cavity
lung abscess and empyema
macrophages, lymphocytes, and plasma cells surround areas of continuing bacterial growth; granulation tissue, liquefied cavity, dense chronic inflammation, new vessels and fibrous tissue
lung abscess and empyema
resolution by drainage through bronchus or chest wall
lung abscess and empyema
scarring and restriction of lung capacity
empyema (pleural space most commonly affected = pyothorax)
pus within natural body cavity
abscess
collection of pus in a newly formed capsule
Schistosoma mansoni
tropical freshwater Trematode bloodfluke
Schistosoma mansoni
invasive larva penetrates skin, using protease penetration factors
Schistosoma mansoni
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
Schistosoma mansoni
"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
Schistosoma mansoni
bladder involvement with hematuria, promotion of squamous cell carcinoma of bladder
Schistosoma mansoni
clamdigger's itch
stages of schistosomes
miracidium larva, cercaria larva, host snails, adults in mesenteric veins
schistosomiasis
acute to chronic
cercariae to schistosomula, to adult worms to eggs
schistosomiasis
egg in bowel wall, acute inflammation with eosinophils
schistosomiasis
eggs trapped in bowel wall with chronic inflammation
schistosomiasis
biopsy bowel mucosa, squeeze between glass slides, eggs have typical ovoid appearance, some with spin sticking out in side, fairly large eggs
schistosomiasis
granuloma formation around eggs
balance of cytokines elicited by antigens associated with eggs promote production of collagen and fibrosis
schistosomiasis
acute TH1 response with IFNg and TNF
chronic disease supervenes, shift toward TH2 with eosinophils, fibrosis
schistosomiasis
granuloma with egg instead of giant cell
TB and schistosomiasis
epithelioid cells that started off as macrophages and were changed under influence of cytokines into cells with a lot of pink cytoplasm
schistosomiasis
marked fibrosis surrounding granulomas
schistosomiasis
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.
cytopathic/cytoproliferative cellular response to infectious agents
mostly viral diseases, not elicitation of particular pattern of inflammation but of reaction to infection and death of particular subsets of cells within body
influenza A virus
orthomyxovirus (RNA), infects animals and humans, capable of genetic recombination, antigenic variation, epidemics
influenza A virus
surface hemagglutinin, allows fusion to host cell membranes, neuraminidase allows virus to uncoat
influenza A virus
localized necrosis of respiratory epithelium, little inflammatory response, systemic symptoms
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
primary viral pneumonia vs. secondary bacterial pneumonia
influenza A virus
causes world-wide epidemics when new antigenic type appears (pandemics)
influenza A virus
25,000 deaths in US in average year
influenza A virus
attaches to respiratory cells and cilia
influenza pneumonia
fluffy interstitial infiltrates in lung x-ray
influenza pneumonia
lymphocytes in bronchial submucosa, loss of superficial epithelium and fibrin in lumen
influenza pneumonia
hyaline membranes
avian influenza
high cytokine levels and dysregulation of cytokine balance, leading to lack of control of virus replication and systemic damage
avian influenza
begins to resemble pneumococcal pneumonia
inflammation in lower respiratory tract
avian influenza
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.
influenza A virus
lesions in large airways, lung shows lymphocytic nodules and interstitial pneumonitis, lymphocytes in small nodules in larger/medium airways
1918 influenza A virus
severe alveolar damage, down into deep airways in see bronchiolitis. huge amount of IL-6-systemic manifestations
measles (rubeola) pneumonia
morbillivirus: paramyxovirus (RNA), one strain without antigenic variation
measles (rubeola) pneumonia
hemagglutinin binds to many cell types by CD46, a complement regulatory protein
measles (rubeola) pneumonia
virus multiplies within epithelial and mononuclear cells. viral growth controlled by T cell response. Antibody protects against infection (not disease)
measles (rubeola) pneumonia
suppression of cell-mediated immunity (including by malnutrition) increases severity of disease. typical rash requires cell mediated immune response
measles (rubeola) pneumonia
peribronchiolar and interstitial lymphocytic and mononuclear infiltrate. lymphoid hyperplasia. multinucleate syncytial cells (Warthin-Finkeldey giant cells) in lung, lymph nodes
measles (rubeola) pneumonia
rash, including involvement of conjunctiva and oral mucosa. requires cell-mediated immunity
measles (rubeola) pneumonia
Koplik spots on oral mucosa
measles (rubeola) pneumonia
systemic disease, lung gets inflamed, interstitial inflammation
lymphocytes, giant cell (multiple epithelial cells fuse)
cytomegalovirus
DNA herpesvirus
cytomegalic inclusion disease
opportunistic disease - seen in immunosuppressed, AIDS, congenital infections
cytomegalic inclusion disease
infection of epithelial and endothelial cells - organs most involved are lungs, liver, kidney, GI tract, CNS including retina
cytomegalic inclusion disease
cytopathic effect - large intranuclear inclusion within enlarged cells
cytomegalic inclusion disease
pneumonia, focal necrosis in many organs, ulceration of intestine
amebic dysentery - entamoeba histolytica
protozoan with infectious cyst, invasive trophozoite, motile, infectious by mouth
amebic dysentery - entamoeba histolytica
amebic surface lectin allows trophozoite adherence to colonic epithelium, invasion, also confers complement resistance
amebic dysentery - entamoeba histolytica
invasive trophozoites kill PMNs, liquefy tissues, cause "sterile abscess"
amebic dysentery - entamoeba histolytica
colitis with "flask-shaped" ulcers, liver abscess with liquefied necrotic material
amebic dysentery - entamoeba histolytica
extraintestinal disease form: amebic liver abscess filled with cellular debris
pseudomembranous colitis - clostridium difficile
toxin-producing, gram positive, spore-forming anaerobic bacillus
pseudomembranous colitis - clostridium difficile
widespread in nature, spores stable in environment. colonization of large bowel, after distrubance of normal flora (antibiotics)
pseudomembranous colitis - clostridium difficile
production of cytotoxins A and B
pseudomembranous colitis - clostridium difficile
diarrhea, pseudomembrane formation (fibrin, inflammatory cells, bacteria and dead cells)
cryptococcal meningitis - cyrptococcus neoformans
encapsulated yeast
cryptococcal meningitis - cyrptococcus neoformans
found world wide in high nitrogen soils, (ex: aged pigeon droppings). aerosol spread
cryptococcal meningitis - cyrptococcus neoformans
common respiratory infection, immunosuppressed tend to disseminate to meninges, bone, skin
cryptococcal meningitis - cyrptococcus neoformans
polysaccharide capsule (useful for diagnosis), no toxin, little acute inflammatory response, loose granulomas
cryptococcal meningitis - cyrptococcus neoformans
insidious onset, chronic, hydrocephalus
nature: in mycelia/hyphae, fruiting body, spores
tissue: yeast
yeast and fungi in nature and tissue
cryptococcal meningitis - cyrptococcus neoformans
phagocytosed yeast in lung macrophages
cryptococcal meningitis - cyrptococcus neoformans
takes tryptophan and turns it into something resembling melanin. brown
cryptococcal meningitis - cyrptococcus neoformans
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
cryptococcal meningitis - cyrptococcus neoformans
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
cryptococcal meningitis - cyrptococcus neoformans
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
cryptococcal meningitis - cyrptococcus neoformans
stain with silver impregnation technique, not much inflammation
cryptococcal meningitis - cyrptococcus neoformans
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
malaria - plasmodium
faciparum is worst
anopheles mosquito
malaria - plasmodium
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
malaria - plasmodium
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
malaria - plasmodium
protozoan infection of 200 million people, killing 1.5 million per year
malaria - plasmodium
binding of infected RBC to endothelium by integrin and thrombospondin receptors. local release of high levels of cytokines may cause acute organ dysfunction
malaria - plasmodium
clinical features: fever, high parasitemia, severe anemia, renal failure, cerebral dysfunction, pulmonary edema, death. cerebral form may evolve very rapidly and be fatal
malaria - plasmodium
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
malaria - plasmodium
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
malaria - plasmodium
challenge for producing vaccine is that have to produce one that's better than natural human immunity
malaria - plasmodium
pigment in spleen and liver, breakdown products of hemoglobin in hepatic Kupffer cells
cerebral malaria
cerebral edema, rapidly progressive, sulci and gyri compressed, edematous brain
not everyone with cerebral form of this disease has edema
cerebral malaria
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
plasmodium falciparum
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
malaria - plasmodium
diagnosed by examining blood films--see ring forms, trophozoites, gametocytes, schizonts, merozoites
malaria - plasmodium
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
malaria - plasmodium
challenge for producing vaccine is that have to produce one that's better than natural human immunity
malaria - plasmodium
pigment in spleen and liver, breakdown products of hemoglobin in hepatic Kupffer cells
cerebral malaria
cerebral edema, rapidly progressive, sulci and gyri compressed, edematous brain
not everyone with cerebral form of this disease has edema
cerebral malaria
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
plasmodium falciparum
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
malaria - plasmodium
diagnosed by examining blood films--see ring forms, trophozoites, gametocytes, schizonts, merozoites