Chapter 15 Microorganisms and Human Disease

Seven Virulence Factors Maintain a reservoir Leave reservoir and enter host Adhere to surface of host Invade the body of the host Evade the body’s defenses Multiply within the body Leave the body and return to reservoir

1. Maintain a reservoir Human reservoirs Animal reservoirs sick individuals healthy carriers incubatory carriers not yet developed symptoms chronic carriers Animal reservoirs zoonosis human disease from animal reservoir Environmental reservoirs soil water

2. Enter a host Portals of entry body surfaces conjunctiva nose mouth skin urethra vagina placenta Figure 15.2

Measurements of infection Infectious dose ID50 number of cells required to cause infection in 50% of subjects Lethal dose LD50 number of cells required to cause death in 50% of the subjects Figure 15.3

Modes of transmission Respiratory droplets Fomites Direct contact most common method of transmission spread rapidly Fomites inanimate object Direct contact sexually transmitted diseases kissing, saliva vertical transmission prenatal--across placenta perinatal--during or shortly after birth

Modes of transmission Fecal-Oral route Arthropod Airborne Parenteral direct body contact indirect food water fomite vector Arthropod mechanical vectors biological vectors Airborne suspended in air survive drying Parenteral direct entrance blood vessel tissue below the skin mucous membranes arthropod vectors needles or sharp objects

3. Adherence to body surface Overcome defense mechanisms adhesins bind to receptors tissue trophism Figure 15.6

4. Invade the body Penetration into cells survive phagocytosis induce endocytosis intracellular pathogens Figure 15.7

Invade the body Penetration into tissues beyond entering the cell survival mechanisms rich environment move into blood or lymphatic circulation Figure 15.7

5. Evade Body’s Defenses Phagocytosis Capsules Surface proteins process where foreign substances are eaten by specialized cells Capsules mucoid cover essential for pathogenicity in certain strains Surface proteins interfere with contact between cell and phagocyte

Evade Body’s Defenses Immune system Obtaining iron antigenic variation mutations which change surface antigens IgA proteases enzymes which break down antibodies Serum resistance blocks the complement system a normal defense mechanism to lyse bacteria Obtaining iron tissue has all nutrients except unbound iron siderophores iron-binding proteins secreted by pathogen

6. Multiplication and Pathogenesis Growth leads to pathogenesis Toxins exotoxins endotoxins toxic proteins Damage by host response Viral pathogenesis

Exotoxins Secreted proteins B subunit attaches to cell component two subunits A: active B: binding B subunit attaches to cell component A subunit alters component Figure 15.10

Exotoxins cholera enterotoxin E. coli enterotoxin Tetanus neurotoxin stimulates intestinal cells to secrete fluid E. coli enterotoxin similar to cholera Tetanus neurotoxin rigid contraction of skeletal muscles Botulinum flaccid (limp) muscle paralysis Diphtheria cytotoxin kills cells in throat Pertussis toxin disrupts cellular regulation

Endotoxins Lipopolysaccharide (LPS) Lipid A component of Gram-negative outer membrane Lipid A toxic portion only released when cell lysed activates complement stimulates cytokines

Other mechanisms Toxic proteins Damage by Host response damage cells extracellular enzymes lyse cells spread infection interfere with blood clotting break down tissues Damage by Host response Inflammatory response

Viral pathogenesis Lysis of host cell Persistent infection virus remains inside producing new virions Latent infection virus remains but no new viruses activation at later time Oncogenic transforms the cells Figure 15.12

7. Leave the body Portal of exit same as portal of entry different respiratory sexually transmitted parenteral different gastrointestinal