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Microbial Mechanisms of Pathogenicity

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1 Microbial Mechanisms of Pathogenicity
Chapter 15 Microbial Mechanisms of Pathogenicity

2 Microbial Mechanisms of Pathogenicity
Pathogenicity The ability to cause disease Virulence The extent of pathogenicity Many properties that determine a microbe’s pathogenicity or virulence are unclear or unknown But, when a microbe overpowers the hosts defenses, disease results! They need to gain entry, adhere, penetrate and cause damage to cause disease.

3 Disease: Pathogens may cause damage to host
Direct damage in the immediate vicinity Grow and multiply and clog cells and passageways Far removed from site of invasion by toxins Toxins spread through blood and lymph By hypersensitivity The host’s reaction may cause the damage

4 Portals of Entry Entry of a Microbe
Need to adhere, penetrate, and then cause damage Gain access via portal of entry and may a have preferred portal of entry - Streptococcus pneumoniae via GI tract? Small pox via vein? Portals of Entry: Mucous membranes Respiratory GI Urogenital conjunctiva Skin Tough so rare - Necator americanus - hookworm Parenteral route Puncture or injection

5 Mucous Membranes: Respiratory
Respiratory Tract microbes inhaled into mouth or nose in droplets of moisture or dust particles Easiest and most frequently traveled portal of entry Common cold Flu Tuberculosis Whooping cough Pneumonia Measles Strep Throat Diphtheria

6 Mucous membranes: G.I. Tract
Salmonellosis Salmonella sp. Shigellosis Shigella sp. Cholera Vibrio cholorea Ulcers Helicobacter pylori Botulism Clostridium botulinum Fecal - Oral Diseases These pathogens enter the G.I. Tract at one end and exit at the other end. Spread by contaminated hands & fingers or contaminated food & water Poor personal hygiene.

7 Mucous Membranes of the Genitourinary System - STD’s
Gonorrhea Neisseria gonorrhoeae Syphilis Treponema pallidum Chlamydia Chlamydia trachomatis HIV Herpes Simplex II

8 Mucous Membranes: Conjunctiva
mucous membranes that cover the eyeball and lines the eyelid Trachoma Chlamydia trachomatis

9 2nd Portal of Entry: Skin
Skin - the largest organ of the body. When unbroken is an effective barrier for most microorganisms. Some microbes can gain entrance thru openings in the skin: hair follicles and sweat glands

10 3rd Portal of Entry: Parenteral
Microorganisms are deposited into the tissues below the skin or mucous membranes Punctures injections bites scratches surgery splitting of skin due to swelling or dryness

11 Preferred Portal of Entry
Just because a pathogen enters your body it does not mean it’s going to cause disease. pathogens - preferred portal of entry Small pox via variolation Streptococcus pneumoniae if inhaled can cause pneumonia if enters the G.I. Tract, no disease Salmonella typhi if enters the G.I. Tract can cause Typhoid Fever if on skin, no disease

12 Numbers of Invading Microbes
ID50: Infectious dose for 50% of the test population LD50: Lethal dose (of a toxin) for 50% of the test population Example: ID50 for Vibrio cholerea cells (100,000,000 cells) ID50 for Inhalation Anthrax - 5,000 to 10,000 spores ????

13 ID50 and LD50 for Bacillus anthracis
Portal of entry ID50 Skin ??? endospores Inhalation 10,000-20,000 endospores Ingestion 250,000-1,000,000 endospores

14 Key traits to a pathogen
The ability to: 1. Adherence To host surfaces and not be washed off 2. Avoid phagocytosis Prevent host defenses from destroying 3. Penetrate Get into host and spread 4. Produce Enzymes Spread, prevent host defenses and cause damage at or near site of infection 5. Produce Toxins Cause damage at distant site

15 Adherence Adhesions/ligands bind to receptors on host cells so won’t get flushed off. Mechanisms to adhere and avoid host defenses: Glycocalyx Streptococcus mutans Dextran (plaque) Waxes Mycobacteria Fimbriae Escherichia coli M protein Streptococcus pyogenes Tapered end w/ hooks Treponema pallidum

16 Capsules Prevent phagocytosis and help with attachment (adherence)
Streptococcus pneumoniae Klebsiella pneumoniae Haemophilus influenzae Bacillus anthracis Streptococcus mutans Yersinia pestis

17 Enzymes to help penetration
Many pathogens secrete enzymes that contribute to their pathogenicity: Increase virulence by use of enzymes And avoid phagocytosis Coagulase Coagulate blood - wall off from host make boil Kinases Digest fibrin clot - allow spreading streptokinase and staphylolinase Hyaluronidase Hydrolyses hyaluronic acid connective tissue Collagenase Hydrolyzes collagen IgA proteases Destroy IgA antibodies Hemolysins lyse RBC’s

18 Hemolysins Alpha Hemolytic Streptococci Beta Hemolytic Streptococci
secrete hemolysins that cause the incomplete lysis or RBC’s Beta Hemolytic Streptococci - secrete hemolysins that cause the complete lysis of RBC’s

19 Leukocidins Enzymes that attack certain types of WBC’s
1. Kills WBC’s which prevents phagocytosis 2. Releases & ruptures lysosomes lysosomes - contain powerful hydrolytic enzymes which then cause more tissue damage

20 Enzymes: Necrotizing Factor
“Flesh Eating Bacteria” Necrotizing fasciitis causes death (necrosis) to tissue cells

21 Summary of How Bacterial Pathogens Penetrate Host Defenses
1. Adherence 2. Capsule 3. Enzymes leukocidins Hemolysins Coagulase Kinases Hyaluronidase Collagenase Necrotizing Factor

22 Penetration into the Host Cell
Figure 15.2

23 Toxins Provide properties to spread and cause damage to the host.
Compare endotoxins and exotoxins Endotoxins from inside the cell. Released upon cell lysis. Exotoxins are secreted out of the cell during cell life. 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

24 Exotoxins Mostly seen in Gram (+) Bacteria
Most gene that code for exotoxins are located on plasmids or phages Figure 15.4a

25 Exotoxin Exotoxin Source Mostly Gram + Metabolic product
By-products of growing cell Chemistry Protein Water soluble Fever? No Neutralized by antitoxin Yes LD50 Small - Very potent 1 mg of Clostridium botulinum toxin can kill 1 million guinea pigs

26 Exotoxins - three types
1. Cytotoxins kill cells 2. Neurotoxins interfere with normal nerve impulses 3. Enterotoxins effect cells lining the G.I. Tract Many toxins have A-B subunit toxins or type III toxins A - active Causes change in host B - binding Figure 15.5

27 Exotoxins Superantigens or type I toxins
Cause an intense immune response due to release of cytokines from host cells Fever, nausea, vomiting, diarrhea, shock, death

28 Exotoxins Cholera enterotoxin
Membrane-disrupting toxins or type II toxins Lyse host’s cells by: Making protein channels in the plasma membrane (e.g., leukocidins, hemolysins) Disrupting phospholipid bilayer Cholera enterotoxin Vibrio cholerae Gram (-) comma shaped rods

29 Exotoxins Exotoxin Lysogenic conversion • Corynebacterium diphtheriae
A-B toxin type III. Inhibits protein synthesis. + • Streptococcus pyogenes Membrane-disrupting. Type II Erythrogenic. • Clostridium botulinum A-B toxin. Neurotoxin - flaccid paralysis Botox • C. tetani A-B toxin. Neurotoxin - prevents CNS inhibition - spastic paralysis • Vibrio cholerae A-B toxin. Enterotoxin. Stimulates cAMP to cause severe diarrhea • Staphylococcus aureus Superantigen. Type I. Enterotoxin.

30 Botox Botulism Clostridium botulinum
Gram (+), anaerobic, spore-forming rod, found in soil works at the neuromuscular junction prevents impulse from nerve cell to muscle cell results in muscle paralysis Botulus – latin word for sausage (first known as sausage disease) C. botulinum does not grow in sausage today mainly due to nitrites added. Infant botulism 250 per yr., most associated with honey due to little microbial flora in G.I.

31 Tetanus (Lock Jaw) Clostridium tetani
Gram (+), spore-forming, anaerobic rod neurotoxin acts on nerves, resulting in the inhibition of muscle relaxation Tetanospasmin - “spasms” or “Lock Jaw” 50 cases a yr. in U.S. 1 million per yr. Worldwide 50% in newborns – because they dress severed umbilical cord with soil, clay or cow dung Tetanospasmin inhibits the release of acetylcholine by interfering with activity of cholinesterase (enzyme that normally breaks down acetylcholine)

32 Endotoxin Figure 15.4b

33 Endotoxins Source Gram– Metabolic product
Present in LPS of outer membrane Chemistry Lipid Fever? Yes Neutralized by antitoxin No LD50 Relatively large

34 Endotoxins - part of the Gram (-) Bacterial cell wall
LPS (Lipopolysaccharides) O Antigen Lipid A Heat Stable (exotoxins are typically heat liable) Lipid A - Toxin portion of the LPS responsible for Fever that is associated with many Gram (-) Bacterial infections Gram (-) cells are “digested” endotoxins are released - fever Antibiotics E. coli (0157:H7) enterotoxin causes a hemolytic inflammation of the intestines results in bloody diarrhea

35 Endotoxins Figure 15.6

36 Non bacteria pathogens
Viruses Protozoa Fungi Algae Helminths

37 Cytopathic Effects of Viruses
Table 15.4

38 Pathogenic Properties of Fungi
Fungal waste products may cause symptoms Chronic infections provoke an allergic response Tichothecene toxins inhibit protein synthesis Fusarium Proteases Candida, Trichophyton Capsule prevents phagocytosis Cryptococcus Ergot toxin Claviceps

39 Pathogenic Properties of Fungi
Aflatoxin Aspergillus on peanuts? Mycotoxins Neurotoxins: Phalloidin, amanitin Amanita “death angel” - Liver damage

40 Pathogenic Properties of Protozoa
Presence of protozoa Protozoan waste products may cause symptoms Avoid host defenses by Growing in phagocytes Antigenic variation

41 Pathogenic Properties of Helminths
Use host tissue Presence of parasite interferes with host function Parasite's metabolic waste can cause symptoms Death can cause excessive immune reaction leading to more symptoms

42 Pathogenic Properties of Algae
Neurotoxins produced by dinoflagellates Saxitoxin Paralytic shellfish poisoning

43 Portals of Exit Respiratory tract Coughing, sneezing
Gastrointestinal tract Feces, saliva Genitourinary tract Urine, vaginal secretions Skin Blood Biting arthropods, needles/syringes

44 Mechanisms of Pathogenicity
Figure 15.9

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