Lecture 7 mechanisms of infectious diseases

prions

a protein that is folded the wrong way causing other proteins to fold making them fold

prions are

transmissible neurodegenerative diseases (disease spreads and slowly damages the brain)

• slowly pogressive, noninflammatory neuronal degeneration→ loss of coordination (ataxia), dementia and death

loss of coordination

ataxia

prions pathogenesis

conversion of cellular precursor protein (PrPC)→ abnormal folded protein (PrPSC)

modified protein behaves differently- PrPSC is resistant to proteases

accumulate in brain→ aggregation(stick form clumps)→ toxic cells

chlamydiaceae

an obligate intracellular bacterium that scavenges ATP from the host cell.

chlamydiaceae life cycle

infectious form= elementary body

• attaches to and enters host cell

In host, transforms into a larger reticulate body

• Undergoes replication into elementary bodies

• Shed into extracellular environment for another infectious cycle

direct contact

transmitted directly from infected tissue or secretions to exposed, intact mucous membranes (body fluids, genitals, mouth)

• STIs (gonorrhea, syphilis, chlamydia, and genital herpes)

vertical transmission

from mother to child

indirect contact

pathogens are spread from hist to host by fomites=infected objects

inhalation transmission

airborne transmission

• when pathogens travel more than 1 meter via an aerosol= tiny droplets

• Aerosols can occur from various activities like sneezing, coughing, air-conditioning systems, sweeping

sources of infection

another human being- mother to child gestation (pregnancy) (congenital infections)

• inanimate object = fomite

• other animal species = zoonoses

• arthropod bite= vector (insects)

incubation period

pathogen begins active replication without producing recognizable symptoms in host

prodromal stage

initial appearance of symptoms in host

• constitutional symptoms: mild fever, myalgia=muscle aches, headache and fatigue

acute stage (illness)

maximum impact of infectious process corresponding to rapid proliferation and dissemination of pathogen

• causes: tissue damage and inflammation

• symptoms- pronounced and more specific

disease course

• Incubation = no symptoms

• Prodromal = mild symptoms

• Acute = worst symptoms

• Convalescent = recovery and healing

• Resolution

convalescent stage

• repair of damage tissue

• resolution of associated symptoms

exotoxins

• proteins released from bacterial cell (gram positive) during growth that kill host cells

• enzymatically inactive or modify cellular constituents → cell death or dysfunction

• botulism toxin & tetanus toxin

botulism toxin

decreases release of neurotransmitter ACh from cholinergic neurons→ flaccid paralysis

• Muscles can’t contract/move

• flaccid paralysis- weak and floppy muscles

Tetanus toxin

decreases release of neurotransmitter GABA from inhibitory neurons→ spastic paralysis

• muscles can’t relax

• spastic paralysis- tight, stiff muscles

endotoxins

molecules composed of lipid and polysaccharides found in cell wall of gram-negative bacteria

• DO NOT CONTAIN PROTEIN

• Are not actively released from bacterium during growth

• Trigger inflammatory response(host immune reactions) and development of sepsis and septic shock

evasive factors

factors produced by microorganisms to evade host’s immune system

• extracellular polysaccharides (capsules, slime and mucous layers) prevent engulfment and killing of pathogens by host’s phagocytic WBCs (neutrophils and macrophages)

• Encapsulated organisms have antiphagocytic capsules=prevents being evaded by WBC’s

Helicobacter pylori

infectious cause of gastric and gastric ulcers

• produces a urease enzyme on its outer cell wall

• urease converts gastric urea into ammonia

• neutralizes acidic environment of stomach and allowing organism to survive in hostile environment

S. aureus

produces surface protein (protein A) that immobilizes IgG

• produces coagulase= converts soluble human coagulation factors into a solid clot

• envelopes and protects organism from phagocytic host cells and antibodies

H. influenzae and N. gonorrhoeae

secrete enzymes that cleave and inactivate secretary IgA

• neutralizes primary defense of respiratory and genital tracts at site (first line of defense weakened)

invasive factors

produces by infectious agents that facilitate penetration of anatomic barriers and host tissue

enzymes capable of destroying

• cellular membranes (phospolipases)

• connective tissue

• intercellular matrices (hyaluronidase)

• structural protein complexes