Lecture 5 Pathogenesis, Role, Diagnosis, Drugs (E1) Flashcards
Ch 14, 15, 16, 17
Bacterial Virulence
Causes disease:
Attachment
Toxins
Immune escape
Pathogenicity Islands
group of genes typically with coordinated expression that leads to disease (strains of bacteria)
Disease
Combination of bacterial virulence and host response
Innoculum
required number of bacteria to establish infection
Normal Flora
in the right place, no problem
wrong place, opportunistic
Microbial acquisition
Getting the “normal flora”
Birth canal
Food (breast, bottle)
Breathing
Natural succession
-Lactobacilli (mouth, intestines, vagina during reproductive years)
-Coliforms (mouth, intestines)
-Anaerobes (intestines)
Microbial impact
Normal flora
Biological success (their “perspective”)
Microbial antagonism (“good” bacteria compete for space and resources on the host)
Can improve host nutrition (e.g Vit-K, short chain-Fatty Acids)- Metabolism of good bacteria
Immune stimulation/regulation
Also have potential negative impacts (opportunistic infection, immune dysregulation)
Sterile Sites
heart, liver, Kidneys, Bladder, Brain, Spinal Cord, Bones, Ovaries, Testes, Sinuses (upper), Ear (Middle, inner)
Eye (Internal), Muscles, Glands (internal)
Opportunistic infection
Normal flora in the wrong place
Susceptibility
Weaken Host defenses
Old age and extreme youth
Genetic defects in immunity, and acquired defects in immunity (AIDS)
Surgery and organ transplants
Underlying disease: cancer, liver malfunction, diabetes
Chemotherapy/ immunosuppressive drugs
Physical and mental stress
Portals of Entry
Typically where something is non-moving
Skin
Gastrointestinal tract
Respiratory Tract
Urogential Tract
Attachment to the host
Fimbriae
Capsules
Receptors
Hook or by crook
Surviving the Host
Anti-Phagocytic factors
Capsules
Leukocidins
Virulence Factors (Toxins/Exozymes)
Disease (causing damage to host)
Virulence factors (Toxins/Exozymes)
Inflammation by the host
Portals of Exit
Same as portals of entry
Biofilms
Community of bacteria
Quorum sensing- What makes bacteria difficult
Dental plague
Protection from immune system, antibiotics-have trouble getting through
Bacterial Adhesions
Bacterial structures used to attach to host cell
Fimbriae (pili)- typically the tips have an adhesion molecule (sugar molecules on the end, bind to lectins)- host cell specificity
Blood group antigens
Some adhesins bind to cell oligosaccharide receptors
Some adhesins bind to cell proteins
Host receptors
Fibrinogen
Extracellular matrix components
d-Mannose
etc
Invasion
Active avoidance (our immune system) or destruction of barriers (physical, chemical, immune)
Most bacteria cannot penetrate intact skin, however, most skin has micro-abrasions so can be breached
Induce inflammation- host response, breaks its own barriers
Block phagocytosis (even though this is our go to)- Streptococci, Staphylococci
Encourage Phagocytosis- Salmonella, Yersinia (Engulfed, to avoid our immune system, able to survive)
Secretory Systems
Sec
Tat
Type I-VII
Function- getting into your cells
Exoenzyme
Proteases, Lipases, Glycosylases (secreted outside)
Exotoxin
Toxins that knock out a host enzyme
Secreted enzymes or proteins that alter function/kill a host cell (usually knockout key enzymes)
Ex: Tetanus, Clostridium, Diptheriae, Cholera
Type A-B Toxin
Heterodimeric Toxins
A- Action component
B- Receptor binding
Superantigen
T-cell activation (cytokine storms)
release of large quantities of IL-1, IL-2, IL-6, INF-y, TNF-a, Chemokines (release systemically)
Cause life threatening fever, shock, rash, autoimmunity
Staphylococcus toxic shock syndrome
Diptheria toxin (A-B)
Target Cell Receptor- Growth factor receptor precursor
Biological Effects- Inhibition of protein synthesis, cell death
Anthrax toxin (A-B)
Target Cell Receptor- Tumor endothelial marker-8 (TEM-8); capillary morphogenesis protein 2 (CMG2)
Biological Effects- EF + PA: increase in target cell cAMP level, localized edema; LF+PA: death of target cells and experimental animals
Tetanus toxin (A-B)
Target Cell Receptor- Polysialoganglio sides plus 15-kDa glycoprotein (co-receptors)
Biological Effects- Decrease in neurotransmitter release from inhibitory neurons, spastic paralysis