Chapter 15: Mechanisms Of Pathogenicity Flashcards

Question

Representative A-B exotoxins: neurotoxins

Answer 1

-affect nerve impulse transmission -Clostridium tetani: Tetanospasmin -Clostridium botulinum: Botulinum toxin -Gram -(+) rod anaerobic endospore forming

Answer 2

- induce fluid and electrolyte loss from the host cell -Vibrio cholerae: cholera toxin -Enterotoxigenic E.coli and Shigella species

Answer 3

-Signs and symptoms: fever, pseudomembrane (gray) in tonsils, enlarged lymph nodes -Transmission: droplets -Dx: throat culture, toxin detection- PCR test amplify gene -Prevention: vaccine

Answer 4

-Clostridium difficile -Exotoxin B- damage colon -Clostridium perfringens -Gas gangrene -Signs and symptoms: swelling (extremities), tissue necrosis -Endospores germinate and exotoxin is released: causes signs and symptoms -Treatment: amputation, antibiotics, hyperbaric chamber (increase O2 in the blood- to cause death of pathogen) -Reservoir: soil -Transmission: puncture -Dx: endospore stain, anaerobic culture of wound or tissue -Source: gram-(+) and some gram-(-) bacteria (ex. E. coli) -Relation to microbe: By-products of growing cell -Chemistry: proteins; specific modes of action- Pharmacology -Fever: no -Neutralized by antitoxin: Yes- give antibodies to exotoxin -LD50: small -Heat stability: Unstable -Toxicity: large -Botulisms, Tetanus, gas gangrene

Answer 5

-Lipid A (lipopolysaccharide) of gram-(-)’s -Salmonella typhimurium is an example of gram-(-) bacterium that produces endotoxin -Toxins composed of lipids that are part of outer membrane of cell wall -Representative organisms include -Neisseria meningitidis -Meningococcal meningitis -Salmonella typhi -Typhoid fever -Proteus mirabilis, E. coli -UTI -Source: Only Gram-(-) due to cell wall -Relation to microbe: Present in LPS of outer membrane -Pharmacology- fever, shock, general -signs and symptoms -Chemistry: lipid -Fever: yes -Neutralized by antitoxin: no -LD50: relatively large -Heat stability: stable -Toxicity: low reacts with lipopolysaccharide-sensitive cells producing endogenous mediators such as tumour necrosis factor alpha (TNFα). Macrophages are cells mediating the toxic activities of LPS and TNFα is the primary mediator of the lethal action of endotoxin.

Answer 6

1) a macrophage ingests a gram-(-) bacterium 2) the bacterium is degraded in a vacuole, releasing endotoxins that induce the macrophages to produce cytokines IL-1 and TNF-alpha 3) the cytokines (proteins that act as chemical messengers) are released into the bloodstream by the macrophages, through which they travel to the hypothalamus of the brain 4) the cytokines induce the hypothalamus to produce prostaglandins, which rest the body’s “thermostat” to a high temp, producing fever

Answer 7

-Life threatening loss of BP -Shock produced by endotoxins is related to secretion of tumor necrosis factor (TNF) -TNF damages blood capillaries

Answer 8

-Carry genes for R factors (for antibiotics resistance), toxin production, etc. -Virulence factor s. Some virulence factors are toxins that damage or kill animal cells, others help bacteria to attach to and invade animal cells (Fig. 20.20), whereas yet others protect bacteria against retaliation by the immune system.

Answer 9

-A change in the characteristic of the microbe due to a prophage -Can result in bacteria w/ virulence factors, such as toxins or capsules

Answer 10

-Stopping mitosis -Herpes simplex type 1 -Inclusion bodies -Particles of the virus inside the infected cells -CMV and rabies -Syncytium (giant cell) -Cell fusion -RSV and measles -Induction of antigenic changes in the host -Interferon production -Hep B and C

Answer 11

Abnormal dark, spindle-shaped cells, loss of contact inhibition

Answer 12

-Fungal toxins: aflatoxin -Have carcinogenic properties -Aspergillus flavus -Protease modifies host cell membrane -Candida, Trichophyton -Capsules- protection from phagocytosis -Cryptococcus neoformans

Answer 13

-Plasmodium invades RBC’s -Toxoplasma grows in phagocytic vesicle -Adherence (adhesive disks of Giardia) -Some protozoa change their surface antigens (Plasmodium)

Answer 14

-Adherence (hookworm- mouth, tapeworm-scolex) -Use host tissue for their own growth -Presence of parasite interferes w/ host function- Ascaris -Parasite’s metabolic waste

Answer 15

-Respiratory tract -GI tract -Genitourinary tract -Skin -Blood

Answer 16

Many pathogens have a preferred portal of entry that enables them to cause disease. If they enter the host by another portal, disease may not occur. Ex: typhoid fever - if the bacteria Salmonella typhi is swallowed (PPOE) disease can occur, but if the same bacteria is rubbed on the skin there is no reaction

Answer 17

Using a preferred Portal of Exit allows a pathogen to spread through the population by moving from one susceptible host to another. *They tend to be the same portal as entry

Answer 18

*ID(50) stands for Infectious Dose, and is the number of microbes necessary to cause disease in 50% of the test population. *LD(50) stands for Lethal Dose, and is the number of microbes necessary to cause death in 50% of the test population. *The smaller the number of microbes needed to cause disease or death gives you greater chances of becoming infected and/or dying from microbes

Answer 19

Pathogenicity is the ability to cause disease, whereas virulence refers to the degree of pathogenicity (high or low).

Answer 20

Antigenic variation or antigenic alteration refers to the mechanism by which an infectious agent such as a protozoan, bacterium or virus alters the proteins or carbohydrates on its surface and thus avoids a host immune response, making it one of the mechanisms of antigenic escape.

Answer 21

Invasins are a class of bacterial proteins associated with the penetration of pathogens into host cells. Invasins play a role in promoting entry during the initial stage of infection.

Answer 22

Bacterial iron-binding protein

Answer 23

the attachmentt is accomplished via surface molecules on the pathogen called adhesins (glycoproteins or lipoproteins) or ligands that bind specifically to complementary surface receptors

Answer 24

Bacterial toxins are virulence factors that manipulate host cell functions and take over the control of vital processes of living organisms to favor microbial infection

Answer 25

1: Inhibition of macromolecular synthesis 2: Release of lysosome contents 3: Inclusion bodies (site of viral synthesis/assembly) 4: Formation of fused cells (Syncytium) 5: Change in cell function - e.g. when measles virus attaches to CD46 cells they reduce IL-12 production 6: Some viral infected cells produce interferon 7: Viral infections can induce antigenic changes on host cell surface 8: Changes to host chromosomes, oncogenes may be added 9: Cancer causing viruses inhibit "contact inhibition" between host cells thus promoting cancer.