Ch15 Tolli

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

PowerPoint® Lecture Slide Presentation prepared by Christine L. Case

Microbiology

B.E Pruitt & Jane J. Stein

AN INTRODUCTIONEIGHTH EDITION

TORTORA • FUNKE • CASE

Chapter 15Microbial Mechanisms of Pathogenicity


Microbial Mechanisms of Pathogenicity

• Pathogenicity The ability to cause disease

• Virulence The extent of pathogenicity


• Mucous membranes – resp. tract, GI tract, conjunctiva, urogenital

• Skin – damaged skin, hair follicles, sebaceous gland/sweat gland ducts

• Parenteral route – direct deposition into tissues – punctures, bites, lacerations, injections, splitting

Portals of Entry


• ID50: Infectious dose for 50% of the test population

• Number of particles required to cause disease

• LD50: Lethal dose (of a toxin) for 50% of the test population

• Potency of a toxin

Numbers of Invading Microbes


Bacillus anthracis

Portal of entry ID50

Skin 10-50 endospores

Inhalation 10,000-20,000 endospores

Ingestion 250,000-1,000,000 endospores


• Adhesions/ligands bind to receptors on host cells

• Glycocalyx Streptococcus mutans• Glucosyltransferase converts glucose to dextran (sticky) to form glycocalyx

• Fimbriae Escherichia coli• Adhesins specific for cells in GI tract

• M protein Streptococcus pyogenes• Cell wall component

• Opa protein Neisseria gonorrhoeae• Outer membrane protein, in addition to fimbriae

• Tapered end Treponema pallidum

Adherence


• Coagulase S. aureus Coagulate blood

• Kinases S. pyogenes, S. aureus Digest fibrin clots• Hyaluronidase Streptococci, Clostridia Hydrolyses hyaluronic

acid (cell junction carbohydrates)

• Collagenase Clostridia Hydrolyzes collagen

• IgA proteases Nieisseria Destroy IgA antibodies

• Siderophores Take iron from host iron-binding proteins

• Antigenic variation Alter surface proteins to evade immune response

Enzymes


Penetration into the Host Cell

Figure 15.2

Invasins –

rearrange actin fibersassociated with host cell membraneSalmonella, E. coli

Causes membrane ‘ruffling” – result of cytoskeletal disruption

Microbe sinks into ruffle and is Ingested by cell.

Actin can be used as propulsion once inside host cell (shigella spp)


Toxins

• Toxin Substances that contribute to pathogenicity

• Toxigenicity Ability to produce a toxin

• Toxemia Presence of toxin the host's blood

• Toxoid Inactivated toxin used in a vaccine

• Antitoxin Antibodies against a specific toxin


Exotoxin – many are enzyme-like

Source Mostly Gram +

Metabolic product By-products of growing cell

Chemistry Protein

Fever? No (mostly…except type 1)

Neutralized by antitoxin Yes (good antigen)

LD50Small


• A-B toxins or type III toxins

Exotoxins

Figure 15.5


• Membrane-disrupting toxins or type II toxins

• (example – Staph. aureus, Streptococci spp.)

• Lyse host’s cells by:

• Making protein channels in the plasma membrane (e.g., leukocidins, hemolysins)

• Disrupting phospholipid bilayer

• Also allow escape from phagosomes into cytoplasm

Exotoxins


• Superantigens or type I toxins

• Cause an intense immune response due to release of cytokines from T-lymphocytes

• Fever, nausea, vomiting, diarrhea, shock, death

Exotoxins


Exotoxins

Exotoxin Lysogenic conversion

• Corynebacterium diphtheriae A-B toxin. Inhibits protein synthesis. +

• Streptococcus pyogenes Membrane-disrupting. Erythrogenic. +

• Clostridium botulinum A-B toxin. Neurotoxin +

• C. tetani A-B toxin. Neurotoxin

• Vibrio cholerae A-B toxin. Enterotoxin +

• Staphylococcus aureus Superantigen. Enterotoxin.


Exotoxins

Figure 15.4a


Endotoxin

Figure 15.4b


Endotoxins

Figure 15.6

(A cytokine)

TNF – tumor necrosis factor – another cytokine secreted by phagocytes– damages capillaries


Endotoxins

Source Gram–

Metabolic product Present in LPS of outer membrane

Chemistry Lipid-polysaccharide

Fever? Yes

Neutralized by antitoxin No (poor antigen)

LD50 Relatively large


Test for endotoxin presence

Endotoxins are heat resistant, may persist on surfaces.

LAL- Limulus Amoebocyte Lysate – presence of minute amounts of endotoxin lyses amoebocytes which release lysate

Lysate then causes coagulation of the media


Cytopathic Effects of Viruses

Table 15.4


• Fungal waste products may cause symptoms

• Chronic infections provoke an allergic response

• Tichothecene toxins inhibit protein synthesis• (headaches, chills, nausea, vomiting, visual disturbances)

• Fusarium, Stachybotris (common molds)

• Proteases – modify host cell membranes• Candida, Trichophyton (cutaneous mycoses)

• Capsule prevents phagocytosis• Cryptococcus – (meningitis)

• Ergot toxin – LSD is a derivative

• Claviceps purpurea - grain

Pathogenic Properties of Fungi


• Aflatoxin - carcinogenic

• Aspergillus

• Mycotoxins

• Neurotoxins: Phalloidin, amanitin

• Amanita – “Death cap mushroom”

Pathogenic Properties of Fungi


• Presence of protozoa and protozoan waste products may cause symptoms

• Plasmodium (malaria)- Invasion and lysis

• Toxoplasma – are phagositized and survive in phagosome of macropahge

• Avoid host defenses by

• Growing in phagocytes

• Antigenic variation

Pathogenic Properties of Protozoa


• Use host tissue for nutrients/incubation

• Presence of parasite interferes with host function

• Parasite's metabolic waste can cause symptoms

• Wuchereria bancrofti roundworm - elephantiasis

• Tapeworms, flukes

Pathogenic Properties of Helminths


• Neurotoxins produced by dinoflagellates

• Saxitoxin

• Paralytic shellfish poisoning

Pathogenic Properties of Algae


• Respiratory tract

• Coughing, sneezing

• Gastrointestinal tract

• Feces, saliva

• Genitourinary tract

• Urine, vaginal secretions

• Skin

• Blood

• Biting arthropods, needles/syringes

Portals of Exit


Mechanisms of Pathogenicity

Figure 15.9

Ch15 Tolli

Health & Medicine

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