bio 230 unit 3

mutualism

depend on each other

humans and e. coli

symbiotic

one dependent, other may or may not

commensalism

one benefits, other is unaffected

parasitism

one benefits, other harmed

normal microbiota behavior

do not cause disease under normal conditions.

cause disease during suppression of immune system, change in residing environment, location change in body

normal microbiota locations

upper respiratory tract, upper & lower digestive tract, urinary & reproductive system, eyes & skin

endemic

local in population

epidemic

greater than normal frequency for given population

pandemic

greater than normal frequency throughout world

sporadic disease

occurs only occasionally

epidemiology

study of occurrences, distribution, spread of disease in humans

acute disease

symptoms and disease run quickly

chronic disease

slow symptoms develop over long period of time

asymptomatic disease

disease without symptoms

latent disease

appears after being dormant in the body for a long time

communicable disease

transmitted from one host to another

contagious disease

spreads quickly and easily

noncommunicable disease

cannot transfer host to host

systemic infection

widespread throughout the body.

travel by blood or lymph

local infection

limited to a small region of the body

primary infection

initial infection

secondary infection

follow primary.

opportunistic or normal microbiota taking advantage of weakened immune system

stages of acute infectious disease

1. incubation

2. prodromal

3. illness

4. decline

5. convalescent

incubation

exposure/day zero, no signs or symptoms

prodromal

vague, general symptoms or feeling of discomfort

illness

microorganisms multiplying rapidly, specific symptoms are most severe

decline

microorganisms decline in numbers, where secondary infection may occur, decline in symptoms

convalescence

feeling better but microorganisms still present

koch's postulates

1. agent present in every case

2. agent isolated in pure culture

3. agent causes disease in healthy host

4. same agent reisolated from experimental host

exceptions to koch's postulates

1. multiple agents cause disease (pneumonia)

2. agent may not be culturable (hep B, syphilis)

3. may not have experimental healthy host (HIV)

reservoir

where a pathogen can survive and be transmitted.

living: animals, humans (healthy & sick)

nonliving: water, soil

host

organisms supports growth of the pathogen

vector

arthropod capable of transmission

zoonotic

disease transmitted between animals and humans

rabiesvirus

transmitted by animal bite, fatal once symptoms occur.

travels from bite up nervous system to brain.

reservoir typically racoons, bats, dogs.

direct trasmission

direct contact: skin to skin

close contact: within 1 meter

indirect transmission

fomite: touching objects, anything nonliving

vehicle: air, water, food

airborne transmission

droplets travel greater than 1 meter

foodborne transmission

eating contaminated food

waterborne transmission

drinking contaminated water

nosocomial infection

acquired in hospital

1. presence of microorganisms

2. immunosuppressed patients

3. transmission between patients and staff (only preventable)

portals of entry/exit

• skin (wounds)

• mucus membrane (respiratory, eyes, genital, gastrointestinal)

• parenteral (penetration)

adhesion factor

need adhesion to tissue for infection

virulence factors

increases ability to cause an infection

hyaluronidase & coagulase

virulence factor by allowing penetration into deep tissues. coagulase escapes immune response

capsules

virulence factor by resisting phagocytosis

coagulase and kinase

coagulase allows clots to form around bacteria. fibrin allows bacteria to remain undetected until released by kinase production

endotoxins

outer membrane of G- bacteria.

when cell dies, lipopolysaccharides are released as lipid A.

exotoxins

mostly G+, some G-.

metabolic production from a living cell releases protein.

categorized based on body part infected. gene on plasmids.

neurotoxin

exotoxin in brain.

clostridium tetani (tetanus) produce neurotoxins that travel up spinal cord to block signals that allow muscle relaxation leading to spastic paralysis.

clostridium botulinum (botulism) causes flaccid paralysis in nervous system

enterotoxin

exotoxin in gastrointestinal tract.

intoxication of foodborne illness, food inoculated with staphylococcus at room temperature allows for multiplication and production of enterotoxin. after vomiting toxin leaves.

cytotoxin

exotoxin that disrupts the structure of individual cells.

vibrio cholerae (cholera) triggers electrolytes to leave cell & water follows causing diarrhea and dehydration.

poly peptide A enters cell, B interacts with surface.

infection

successful invasion of body by microorganisms

intoxcation

ingest toxin.

shorter incubation period, no immune response, no microorganism

cytopathic effect

structural changes in host seen with light microscope

syncytia formation CPE

fusing of cells

inclusion bodies CPE

structure in infected cells, sites of viral assembly

rounding up and lysis CPE

infected cells bunch up and lyse when virus leaves the cell

interferon

protein produced by infected cells to limit spread of infection by blocking biosynthesis

antigenic change

MHC-I receptor peptide is replaced with viral peptide triggering immune response

co-evolution

viruses overtime evolves to infect host, as host evolves to resist virus infection

innate immunity

present since birth, response is always the same.

no memory.

adaptive immunity

acquired over time, built.

stronger response after exposure, memory of pathogen.

mast & basophil cells

granulated, respond to inflammation

neutrophils, eosinophils, macrophages

phagocytes that fight infection and remove pathogens

dendritic cells

trigger adaptive response by collecting info for T and B cells

B cells

produce antibodies

T cells

helper: adaptive response

cytotoxin: kill cells

natural killer cells (NK)

pathogen must be brought to cell,

kill without antigen-antibody interaction

opsonization

coating antigen with antibody to enhance phagocytosis ingestion

phagocytosis

1. chemotaxis

2. adherence

3. ingestion

4. fusion

5. digestion

6. exocytosis

1. chemotaxis

chemical signals attract microorganisms to phagocyte

2. adherence

pattern recognition receptors (PRR) recognize structures on pathogens to trigger ingestion

3. ingestion

pseudopods (plasma membrane extensions) engulf microorganism, bringing it inside the cell.

opsonins make ingestion easier!

4. fusion

lysosome fuses with phagosome containing the pathogen

5. digestion

microbes are killed

6. exocytosis

expel remains

mechanisms of avoiding phagocytosis

coagulase forms fibrin coat around bacteria to avoid adherence.

capsules avoid ingestion.

leishmania avoid digestion by blocking acidification.

TB mycobacteria avoid fusion.

compliment activation pathways

alternative, classical, lectin

classical compliment

antibodies bind to surface of foreign cell for lysis.

C1 binds to antibodies, C3 cleaves to C3A & C3B

C3A

triggers inflammation

C3B

works with other compliment proteins to cleave C5 into C5A & C5B

C5A

triggers inflammation

C5B

joins compliment proteins to "punch holes in the pathogen" to lyse the cell

alternative and lectin pathways

do not use antibodies.

all pathways use C3 and end in either opsonization, inflammation, or cytolysis

inflammation

innate acute response triggered by tissue damage.

damaged cells release inflammatory mediators to trigger increased blood flow and permeability of blood vessels so microorganisms can be taken care of

cytokine storm

maladaptive inflammatory response that activates cytotoxic T cells, damaging tissues and leading to bleeding out. unregulated inflammation.

interferon production

limits the spread of viruses.

innate response.

interferon type I

alpha - viral infections

betta - triggers production of IL-10

IL-10

suppresses adaptive response (T cells)

interferon type II

intracellular pathogens trigger gamma

fever

hypothalamus raises body temp to allow enzymes to work better.

innate response.

bone marrow

all cells start in bone marrow as T cells and B cells.

B cells mature in bone marrow.

thymus

T cells mature in thymus

lymph nodes & spleen

mature T cells and B cells in lymph nodes that wait to be activated

mucosa-associated lymphoid tissue (MALT)

peyer's patches: cells in intestine that produce antibodies

antibody structure

variable region at the end of light chains connected to a constant region heavy chain.

Fc region in constant region of light chains.

Fab region (antigen binding) at end of light chains.

antigen

protein or large polysaccharide that triggers antibody response

epitope

site on antigen where antibody binds. can be multiple per antigen

antibody diversity

DNA segments are rearranged during genetic recombination