1. Chapter 15 Microorganisms and Human Disease

2. 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

3. 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

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

5. 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

6. 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

7. 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

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

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

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

11. 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

12. 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

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

14. 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

15. 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

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

17. 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

18. 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

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