Lecture 5: Microbiology Virulence and Pathogenesis

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Chapter 15

Endotoxin

Part of the outer portion of the cell wall (lipid A) of most gram-negative bacteria; released on destruction of the cell.

Antigenic Variation

Changes in surface antigens that occur in a microbial population.

Extotoxin

A protein toxin released from living, mostly gram-positive bacterial cells.

Adherence

Attachment of a microbe or phagocyte to another's plasma membrane or other surface.

1. Describe the principal portals of entry by pathogens for infection to occur

Many microorganisms can penetrate mucous membrane of the conjunctiva and the respiratory, gastrointestinal, and genitourinary tracts. Cannot penetrate intact skin; can enter hair follicles and sweat ducts. Can gain access to tissues by inoculation through the skin and mucous membranes in bites, injections, and other wounds called parenteral route.

the portals of exit for disease transmission to occur

Respiratory tract: Coughing or sneezing. Gastrointestinal tract: Diarrhea, feces, saliva
Genitourinary tract: STDs, urine
Skin or wound infections: Direct contact, contaminated fomites, insects. Blood-borne diseases: Hypodermic syringes, insects, bleeding. General : surgery, butchering

2. Compare the LD50 to the ID50.

Diseases are compared by using their LD50 and their ID50. Numbers of Invading Microbes: 1) LD50 - corresponds to the potency of a toxin (lethal dose) 2) ID50 - corresponds to the virulence of a microbe (infectious dose).

3. Using examples, explain how microbes adhere to host cells.

Attachment to host tissue. Adhesins or ligands - surface molecules on the pathogen that bind specifically to host cell receptors. Adhesins may be on the glycocalyx, pili, fimbriae, and flagella, or component of capsules or cell walls. Most are glycoproteins or lipoproteins. Some microbes come together in biofilms.

4. Explain how capsules and cell wall components contribute to pathogenicity.

Capsule - glycocalyx material around cell wall
Impairs phagocytosis. Ex. S. pneumoniae, Yersinia pestis. M proteins produced by S. pyogenes - mediates attachment to epithelial cells of host. Waxy lipid of cells wall of M. tuberculosis resists phagocytosis. Opa protein on Fimbriae of N. gonorrhoeae used for attachment - is taken up by cells, multiplies in leukocytes.

5. List several enzymes of pathogens that are virulence factors, and describe their function.

1) Coagulase - clot the blood (Staph and boils) 2) Kinase - break down fibrins, dissolve clots (Streptococcus pyogenes) 3) Hyaluronidase - breaks down polysaccharide that holds cells together (blackening of tissue wounds) Streptococci and clostridia 4) Collagenase - breaks down collagen (Clostridium spp.) - facilitates spread of gas gangrene 5) IgA protease - destroys antibodies - N. gonorrhoeae, N. meningitidis

6. Describe how bacteria use the host cell's cytoskeleton to enter the cell.

Bacteria may produce proteins that alter the actin of the host cell's cytoskeleton allowing bacteria into the cell. Ex: Ruffles induced on an M cell by cytoskeleton remodeling which leads to uptake of pathogen.

7. Describe the function of siderophores.

Bacteria get iron from the host using siderophores. Use host nutrients: Siderophores produced by MOs bind up iron. Free Iron is a limiting nutrient in low quantities in any environment, except for example when an individual is taking supplemental iron and it is circulating in the blood stream.

8. Contrast the nature and effects of exotoxins

Found Mostly in Gram + species: Clostridium, Corynebacterium, Vibrio, Staphylococcus, Streptococcus, Escherichia, Shigella. They Can be classified as neurotoxins, enterotoxins, or cytotoxins
Most are also in one of the following three categories:
1. Superantigens
2. Membrane-disrupting toxins
Ex. Leukocidins, hemolysins
3. A-B toxins

Contrast the nature and effects of endotoxins

From Gram - organisms. Part of the outer membrane of the cell wall. Lipid A - a portion of the LPS. Are lipopoly-saccharides. Cause chills, fever, weakness, aches, shock, and death

9. Compare and contrast neurotoxins, enterotoxins, and cytotoxins.

Neurotoxins (A-B) is an exotoxin that interferes with normal nerve impulse conduction. Enterotoxins (A-B and superantigen) is an exotoxin that causes gastroenteritis, such as those produced by Staphylococcus, Vibrio, and Escherichia. Cytotoxins is a bacterial toxin that kills host cells or alters their functions.

Cytotoxins

Membrane-disrupting toxins or type II toxins. Can Lyse host's cells by: Making protein channels in the plasma membrane. Disrupting the phospholipid bilayer. If they lyse red blood cells they are given the special name of hemolysins.

A-B Toxins

Consists of 2-parts: 1) A subunit - active
Usually an enzyme - responsible for the toxic effects to cells. 2) B subunit - binds to the specific receptors on the cell. Is responsible for the type of cells that the toxin can bind to and affect.

Superantigen Toxins

Type I toxins: They Disrupt T-cell normal function, cause an intense immune response due to massive release of cytokines from host cells. Can cause Fever, nausea, vomiting, diarrhea, shock, organ failure, death.

Membrane-disrupting toxins

Type II toxins: Can Lyse host's cells by: Making protein channels in the plasma membrane. Disrupting the phospholipid bilayer. They are cytotoxins. If they lyse red blood cells they are given the special name of hemolysins.

11. Using examples, describe the role of plasmids and lysogeny in pathogenicity.

Plasmids may carry genes for antibiotic resistant, toxins, capsules, and fimbriae. Lysogenic conversion can result in bacteria with virulence factors, such as toxins or capsules. Ex: Tetanus Neurotoxin or tooth decay.

12. Describe the pathogenesis of viruses

Cause Cell death of host cells - lysis, and induced apoptosis. Induce Inclusion bodies in nucleus or cytoplasm. Cell fusion - creating a syncytium (or giant cell)- avoiding antibodies. Transformation - cause genetic changes - cancer causing genes (oncogenes) may be activated. Inhibit apotosis.

Give examples of cytopathic effects

Cytopathic effects - are visible effects of viral infection . We can see effects with a normal light microscope! Ex: Inclusion body in tissue from a person who died of rabies. Syncytium (giant cell) formed in a cell infected with measles virus. A mass

13. Give an example mechanism of pathogenicity of a eukaryotic microorganism.

Parasites: Mechanisms- bind to host cells specifically, invade the cell, or taken up by cell. Inside the cell, they are more protected from the host's immune system. After viral replication, lyses cell and infects other neighboring cells or disseminates into blood or lymph systems.

14. Describe the virulence of the Marburg virus.

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Virulence

The degree of intensity of pathogenicity of an organism. And includes: Invasiveness - ability to spread to tissues. Infectivity - ability to establish infection. Pathogenic potential - the degree in which the pathogen can cause toxigenicity.

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