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FA C TOR S OF PATOGEN IC ITY AND VIRULENCE

FA C TOR S OF PATOGEN IC ITY AND VIRULENCE. Based upon lectures of doc. Woznicova. P atogeni ci ty a nd virulence. C ontagio s it y - transfer between host s Inva s ivit y entrance to host multiply in host = overrule spreading defence Toxicit y - ability damage the host.

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FA C TOR S OF PATOGEN IC ITY AND VIRULENCE

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  1. FACTORS OF PATOGENICITY AND VIRULENCE Based upon lectures of doc. Woznicova

  2. Patogenicity and virulence Contagiosity-transfer between hosts Invasivity entranceto host multiplyin host =overrule spreadingdefence Toxicity-abilitydamagethe host

  3. Contagiosity Depend on: • transfer type – type of elimination, amountof eliminated microbes, entrance gate • tenacityof microbe– resistanceagainstouterenvironment • minimum infectious dose – amount of microbes beginning an infection • host behaviour

  4. 1. Elimination Due to respiratory secrets,diarrhea stool/otherbiological materials Amountof eliminated microbes: 102 virions/1 infected respiratory epitelium→ 109 virions/ml secret Entrance gate: infection better penetrate through mucous membrane than through skin (tick born encephalitis as laboratory respiratoryinfection)

  5. 2. Tenacity of microbes (stabilityinenvironment) Resistant –bacterial spores(Clostridium tetani), cystsof protozoa(Giardia lamblia),eggs of helmints (Taenia saginata) Vulnerable -directtransmission (sexual transmission – gonococci, treponema), biologic vectors (borrelia), through water (leptospires)

  6. 3. Infectious dose high: V. cholerae salmonela – cca 108 - agens multiplies in vehiculum – salad cream, sauce, yolkin sweets low: shigela 102– dirty handdisease – contaminated objects (door handle - WC etc.) gonococci, M. tuberculosis 101, Coxiella burnetii (Q-fever)

  7. 4. Hostbehaviour Misuse of defence reflexes: cough, sneezing, diarrhea Specific behaviourchange: • Toxoplasma gondii - „inhibits“ reaction of rat, inficated rat loose fear from cats–predator easier kill them • Yersinia pestis - flea (Xenopsylla cheopis) is suckling angry, because Yersinia blocks its digestive tract

  8. Invasivity – Entrance into a host Most often through the mucous membrane If there is previouscolonization= overcoming concurence of commensales Ability to: • adhereto epitelium by the help of various adherence factors • penetratethrough epitelium by the force of barrier factors

  9. Penetration to internal environment – I Direct • Fissure inskin(S. aureus, S. pyogenes, B. anthracis) • Fissure in mucous membrane(T. pallidum, HBV, HIV) • Bite(rabies, P. multocida) • Arthropod sting(borrelia, plasmodia) • With help ofensymes(penetrate factors) lecithinase(C. perfringens) hyaluronidase(S. pyogenes): intercellular cement

  10. Penetration to internal environment – II Forced phagocytosis Change of cellular skeleton with help of invasines Ipa (shigela) internalin (L. monocytogeses)YadA (Y. enterocolitica) Surface undulation (ruffling) of epitelia (salmonela) Unknown mechanism (legionella, chlamydia)

  11. Reproduction in vivo • Intracellular reproductionbetter - nutrients, save before immunity - intracellular parasites(mycobacteria, rickettsia, chlamydia, listeria) • Extracellular reproduction– in plasm exist antibacterial substances (complement, lysozym, antibodies), lessfree Fe - bacteriaform siderofores, hemolysines

  12. Dissemination in organism Local infection(running nose) Systemic infection(grip, meningitis) Generalizate infection(morbilli, abdominal typhus, rarealso local/systemic infection) Way of dissemination: • lymph • blood • per continuitatem • along nerves

  13. Toxicity Direct damageof infectious agens • Cellulardeath-lysisdue to toxins, viruses, immune lymphocytes, apoptosis (HSV, shigella) • Metabolic damage– exotoxins • Mechanic damage(pablanesin diphteria) • Death cause→ septic shock due toendotoxinsG – → lipopolysaccharide G + → teichoic acid + peptidoglycan

  14. Bacterial exotoxins • Penetration factors(DN-ase, elastase, kolagenase) • Cytolysins(lecithinase, sfingomyelinase, hemolysins) • Inhibitorsof proteosynthesis(diphteric toxin) • Pharmacological effective toxins (choleragen, termolab. enterotoxin E. coli, pertussis t.) • Neurotoxins(tetanotoxin, botulotoxin) • Superantigens(staf. enterotoxin+exfoliatin, streptococcus pyrogen toxin)

  15. Case 71 years oldwoman bitted by dog - manywounds penetratingto fasciaon leftleg and lefthand,ambulant revision 48 hrs later: diarrhea, vomitting, pain in wounds. Surgical revision,expansion of hematomas, hospitalization rejected 72 hrs later – pain in LDL, vomitting, vertigo. LDL edema, any secret, shock - intubation http://www.lib.uiowa.edu/hardin/md/pictures22/dermatlas/Necrotizing_Fasciitis_1_030302.jpg

  16. Microbiology • Hemocultures - 2x Streptococcus pyogenes • Sputum and stool – normal flora • Urine- negative • Wound - Streptococcus pyogenes andStaphylococcus aureus (TSST–1 and enterotoxine A producer) • ATB susceptibility: S. pyogenes - penicilin, erytromycin, linkomycin, chloramphenicol, ofloxacin S. aureus - oxacilin, cotrimoxazol, erytromycin, linkomycin, tetracyclin

  17. Case - end http://www.jyi.org/articleimages/463/originals/img0.jpg • Development of hemorrhagic bulls, serousliquid from wounds, punctate from bulls – microscopic streptococcus • Therapy: Penicilin, ciprofloxacin • 12 h after hospitalization -surgical revision-myonecrosis leading to high amputation • 47 hrs after hospitalization - deathbecause of sepsis caused by invasive S. pyogenesstrain complicated with toxic shock syndrome caused by S. aureuswith production oftoxic shock syndrom toxine (TSST-1) and enterotoxine A

  18. Toxicity Damagecaused due to defence reaction a) Damagecause viainflamatory reaction(calor, rubor, tumor, dolor, functio laesa = typic inflamatory signs) edema: encephalitis, epiglottitisinflamatory infiltrate: pneumonia purulence: gonococci caused blenorrhoea neonatorum formation of fibrous tissue

  19. Damage as result defence reaction b) Damagevia specific immune reaction I. type: IgE, anafylaxis -helmintosis II. type: cytotoxicity- hepatitis B III. type: imunocomplexes - poststreptococcal renal inflamation, systemicsepticreaction IV. type: later, cellular - tbc

  20. Ability overrule defence A) Overrule congenital immunity: • 1. resist complement inhibition of complement activation surface protection • 2. resist phagocytosis not letting absorb alive inside phagocyte • 3. Interfere with cytokine function

  21. 1. Resist complement Inhibition of complement activation - capsule (meningococci, pneumococci) - inhibitors of activation (S. pyogenes andP. aeruginosa - ensymes cleaving C3b and C5a) Surface protection (flagellaof salmonela, proteus) Ability withstand C →seroresistence www.britannica.com

  22. 2. Resistance to phagocytosis Not letting absorb - inhibitors ofchemotaxis(bordetela, vaginalanaerobes, pseudomonades) - leukocidinsand lecithinase(staphylococci, streptococci, pseudomonades, clostridia) - capsules production – N. meningitidis, H. influenzae, S. pneumoniae, E. coli, K. pneumoniae

  23. Resistance to phagocytosis – II Aliveinside phagocyte - blocade of phagolysosome(chlamydia, mycobacteria, legionella, toxoplasma) - escape from phagosome(rickettsia, shigella, listeria, leishmania, trypanosoma) - antioxidants production(staphylococci, gonococci, meningococci) - high tenacity(coxiella, ehrlichia) phagocytosis

  24. Ability overrule defence B) Overrule acquired immunity: - get round AB, or imunne lymphocytes - quickly multiply(respiratory viruses, agents causing diarrhea, malaric plasmodia) - bluff immune system 1. hidethemselves 3. changetheir antigens 2. evoke tolerance - *suppress immune reaction

  25. Ability bluff imunne system 1.Hide -in ganglias(HSV, VZV) - on intracellular membranes(HIV, adenovirus) - in inf. reservoirs (M. tbc, echinococcus) - in privileg. places(T. gondii in eye) 2. Evoke tolerance (CMV, rubella, leishmania, cryptococcus) 3. Antigenchanges - mimicry(S. pyogenes, T. pallidum) - camouflage(schistosoma – bloodproteins, staphylococci – protein A) - variation(trypanosoma, borrelia, gonococci, influenza)

  26. B) Overrule acquired immunity - end * Suppress immune reaction invasionto immune system (HIV, measless) intervention to cytokine formation (M. leprae, protozoa) superantigens production(staphylococci, streptococci) protease production (meningococci, gonococci, pneumococci) attachment of Fc-fragment IgG (staf./str., HSV) ? (influenza, HBV, EBV)

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