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VTPB 911 Pathogen.

Pathogenicity, virulence factors

QuestionAnswer
Leptospira penetrates mm/skin -> leptospiremia (vasc endoth damage, small mucosal hemorrhage, intravasc hemolysis (serovar-dep)) -> localization in kidney/liver/uterus; Ab+complement clears it, but leptospires are protected in renal tubules=carrier state; zoono.
Borrelia reservoir (mice/squirrel)-> deer tick-> host(dog/horse/ppl)->replicate in skin-> bacteremia-> localize in joints; Ag = outer surface proteins; nymph stage infects ppl, adult phase infects dogs
Borrelia: outer surface proteins 1 Osp expressed at a time; B.burgdorferi switches OSP in response to env't (tick midgut - OspA, feeding - move to salivary gland (OspC); in mammal - OspC, VIsE (C6))
Clostridium toxin, endospore, saprophyte; trauma - necrotic tissue (anaer envt) - spore introduced/endogenous - germination to vegetative form - toxins
Clostridium novyi insult to liver tissue by Fasciola hepatica (liver fluke) - necrotic tracts in liver - germination of endospores - vegetative form - exotoxins - localized liver necrosis, enter circulation = generalized tissue damage/necrosis/intravascular hemolysis
Clostridium difficile toxins, adhesins; risk factors = antimicrobial therapy, normal flora shift; exotoxins - death of intestinal epith cells, excessive inflamm rxn
Clostridium botulinum exotoxin (botulism neurotoxin); BoNT absorbed - binds to cholinergic nerves at myoneural synapse - blocks ACh release - flaccid paralysis; no endotoxin (not G-)
clostridium tetani innoculation - reduced O2, spore germination - diffusion of TeNT - intraaxonal transport of TeNT along periph motor nn to CNS - TeNT binds to presynaptic terminal - suppress release of afferent inhibitory messengers - motor neuron hyperact - tonic spasms
Clostridium piliforme hepatic invasion -> spread to other tissues -> ??????????
Bacteroides: virulence factor protease
Dichelobacter: virulence factor fimbriae (vaccine target), protease (confers virulence)
Fusobacterium: virulence factor capsule, leukotoxin (vaccine target)
Prevotella: virulence factor protease
Porphyromonas: virulence factor Gingipains (protease)
contagious footrot (sheep) maceration of wet skin - F. necrophorum (capsule/leukotoxin, inflam/necrosis = interdigital dermatitis) - d. nodosus (mild-interdigital dermatitis, virulent-contagious footrot) - separation of horn from matrix toe to heel - foul-smelling, necrotic exudate
bovine interdigital necrobacillosis (footrot) maceration of wet skin - fusobacterium necrophorum (capsule/leukotoxin, inflammation/necrosis) - prevotella melaninogenica (protease (collagenase)) - necrotizing dermatitis, foul-smelling necrotic exudate
periodontal disease colonization by aerobic cocci - adhesion of aerobic rods, biofilm formation - proliferation of aerobes, establishment of anaer envt, growth of anaer - gingival inflammation, spirochetes
biofilm bacteria attach - communicate - form colony - produce carbohydrate/polysaccharide film - other bacteria join - multiple species enmeshed in protective layer (protected from antimicrobial effects of plasma/serum/Ab's/phagocytes); eventually spread
Mycoplasma cytadhesions (attachment), surface variable lipoprotiens (Vsp) - evade immune attack; enzymes & H2O2/O2- (nutrient aquisition, cell damage); ciliostasis; intimate association/toxic substance/disease
ureaplasma diversum intimate association with host cells, ammonia buildup
haemotrophic mycoplasma adhesins (attachment); cytoskeleton disruption of RBC -> phagocytosis, RBC Ag -> phagocytosis, auto-Ab (IgM?) -> RBC; all lead to anemia
Rickettsia rickettsii infect endothelial cells -> escape phagosome, damage endothelial cells -> phospholipase, reactive O2 intermediates; vasculitis, hemorrhage, edema, thrombosis (clotting)
Ehrlichia infects phagocytes -> inhibits phagosome-lysosome fusion; tick bite -> LN -> circulation; vasculitis; acute & chronic manifestations; morula (embryonic development, intracellular inclusions of rickettsial agents)
anaplasma marginale enter erythrocytes (vacuole) - replication in RBC - immune-mediated hemolysis - macrophage clearance; antigenic variation
anaplasma phagocytophilum infets neutrophils (inhibits phagosome-lysosome fusion, inhibits respiratory burst, delays apoptosis of neutrophils), vasculitis (thrombosis, thrombocytopenia)
anaplasma platys infects platelets; immune-mediated destruction of platelets; thrombocytopenia (cyclic)
neorickettsia helminthoeca invades intestinal epithelium, hematogenous spread to lymphatic tissues -> hemorrhagic enteritis, lymphatic inflammation, 50-90% case fatality
neorickettsia risticii infects monocytes, inhibits phagosome-lysosome fusion; infects intestinal epithelium (loss of microvilli, increased cAMP = loss of chloride ions/water, watery diarrhea); complicating outcomes - laminitis, toxemia
neorickettsia risticii life cycle megacercaria (adult) in aquatic insect -> bat/bird -> (egg) -> snail -> cercaria (larva/nymph) in aquatic insect -> metacercaria -> infect horse (primarily; but also egg/larvae/nymph stages can infect horse)
coxiella burnetii infects macrophages (alveolar, Kupffer), replicates in phagolysosome (doesn't prevent p-l fusion = doesn't kill macrophage) - hematogenous dissemination - localization in female repro tract or mammary glands; Zoonotic!
chlamydiaceae attachment: elementary bodies (infectious form)- entry into epith cells, inhibit phagosome-lys fusion; replication - reticulate bodies - within phagosome, use host-produced ATP -> inflammation, epith cell death, LPS
chlamydophilia abortus (sheep) EB shed in products of abortion, remain viable for days at low temperature; ingestion of EBs -> infection of tonsils -> blood -> placenta => placentitis; zoonotic! & reportable
dermatophyte (mold) conidium enters stratum corneum -> germ tube develops -> hyphae -> arthroconidia -> hyphae grow within hair shaft, arthroconidia accumulate on hair surface = ectothrix; proteolytic enzymes: keratinase, elastase, collagenase (weaken hair shafts)
dermatophyte (mold): host response intense inflammatory response; activated lymphocytes, macrophages; interferon-gamma released; fungal growth stops or moves to next hair follicle = lesion spread; Ab role is limited
yeast host factors; changes in microclimate of skin, ear canal, etc (high humidity, excessive wax accumulation, antibiotic/glucocorticoid therapy, allergic dermatitis); trauma; immunosuppression; rarely zoonotic
subcutaneous mycoses pyogranulomatous reactions, nodules, ulceration, pus; infections can disseminate
sporothrix enter through break in skin - dimorphic (mycelial form converts to yeast) - nodules ulcerate & discharge pus - spread along lymphatics - limbs swell
Sporothrix - virulence factors virulence factors (growth at 37 degrees C = invasion of deeper tissues; cell wall substances - lipid, melanin, peptide-rhamnomannan, sialic acids; inhibit phagocytosis, protect from ROI); protease I, II - hydrolyze human skin cells in vitro
Histoplasmosis organism (mold form) uptake by macrophages; 37C - conversion to yeast fase, needed for dz; Virul fact: survival within macrophage, melanin, Ca-binding prot, dormancy; yeast multiplies in mac->released; host response: CMI critical, 95% of infec. subclin
Blastomycosis inhalation (deposition of mycelial fragments/microconidia into alveoli; hematogenous, lymphatic spread); convert to yeast form; virulence factors: BAD-1, WI-1, beta-glucan; host response: CMI critical
Coccidioidomycosis infective unit-arthroconidia; inhale arthroconidia, deposit in lung; CO2, 37C - convert to multinucleated spherule -> endospores -> rupture/release endospores -> spherules
Coccidioidomycosis - virulence factors SOWgp - mutants have reduced virulence; spherule size resists phagocytosis; conidial cell wall components - proteolytic enzymes, antiphagocytic properties, etc
Cryptococcus capsule (limited caps in env't w/high salt, sugars; size of yeast favors deposition in lung alveoli; in host, capsule thickens - reduce phag.); phospholipase - membrane disruption (phag); phenoloxidase (protect from neutrophil oxidants); survival in mac
Created by: shelbell8389