Microbe-Human Interactions

symbioses

two organisms living in close interaction with each other

symbiotic microbe and human interactions

microbes benefit these interactions, classified by effect of human host

mutualism

symbolic relationship where both organisms benefit

mutualism example

normal microbiota and human host

normal microbiota benefit from

nutrients and favorable stable environment conditions

humans benefit from normal microbiota

products digest enzymes, vitamins, training of host immune responses

microbial antagonism

negative interaction, non symbolic relationship between normal microbiota and pathogens

normal microbiota harm

pathogens

ways normal microbiota harm pathogens

block pathogen access to host cell surfaces, compete for nutrients

commensalism

one organism benefits (microorganism) and the other is unaffected (host)

normal microbiota in low numbers

don’t benefit or harm the host

normal microbiota is abundant in

skin and adjacent membranes, upper respiratory tract, mouth, urethra, vagina, external genitalia, external ear and eye

normal microbiota present in low numbers

lungs, bladder, urine, breast milk, fetus

no microbiota in

brain and bloodstream (sacred places)

during vaginal birth babies get normal microbiota from

birth canal of mother, gets same bacteria as mother and becomes immune to it

during C section, babies get normal microbiota from

doctor gets in vagina of mother and places it on baby

the more the baby is exposed to pathogens or environment

the more immune response they have

parasitism

one organism benefits (microbe) and the other is harmed (human host)

pathogenic microbes

cause diseases that harm microbes

synergism

nonsymbiotic relationship between multiple organisms, beneficial but not required

normal microbiota

trains baby’s immune system

breast milk contains

microbes

formula

has no microbes in it

diseases caused by multiple pathogens

chronic ear infections, dental carries, gingivitis, periodontal disease

parasitism is good for

microbes

chronic diseases

difficult to treat, biofilm still there after treatment

infection

microorganisms are successfully multiplying in a host

infections are not diseases if

no damage is done to the host

Steps of establishing infection

find portal of entry, attach firmly to host, survive host defenses and multiply

disease

any deviation from a state of health

infectious disease

caused by microbes or their products, infections that progress to cause direct or indirect damage to the host tissue or organ

infectious disease transmissible from

another host or the environment

pathogen

microorganism capable of causing damage to a host

communicable diseases

infectious disease transmitted through contact or ingestion of another person/ organism

True pathogen

microorganisms capable of causing disease in a healthy individual (functioning host defenses) under the right circumstances

opportunistic pathogens

microbes cause disease only in hosts that have weak immune systems (therapy, radiation)

normal microbiota cause disease only when

they gain access to tissues/areas where they are not normally found

pathogenicity

measure of a pathogen’s ability to cause disease

virulence

measure of a pathogens ability to cause severe disease (how severe is it) can be mild or life threatening

candida albicans

cant make infections well, low pathogenicity, high virulence

cryptosporidium

high pathogenicity, low virulence

virulence factors

any characteristic of a pathogen that assists it in causing disease

pathogenicity and virulence depend on

virulence factors

bacterial virulence factors

allow adhesion, allow evasion of host defenses, direct damage or indirect damage

adhesion

bacterial structures or molecules for attachment to host cell surfaces (fimbriae, capsules, adhesion proteins)

evasion of host defenses

resist phagocytosis, antigenic variation, intracellular life

resist phagocytosis

engulf and destroy by host cell

capsules

reduce engulfment by phagocytosis

mycolic acid

in mycobacterial cell walls, after engulfment by phagocytes, protects pathogens by destruction by lysosomes

antigenic variation

pathogen spontaneous mutation during multiplication causes changes to its surface molecules (antigens)

pathogens avoid complete destruction by

immune system by staying one step ahead

intracellular life

ability to live within host cells hiding from defenses

bacterial invasion proteins

cause host cells to engulf them

direct damage to host

use of host nutrients, exotoxins and exoenzymes

indirect damage to host

host harms self, endotoxins and superantigens

use of hosts nutrients

directly damages host, (siderophores suck up iron, keep it from RBC)

exoenzymes

secreted carried through body by blood, enzymes- specific chemical reactions, directly damage-symptoms variable, toxic in small amounts

exoenzyme examples

coagulase-forms blood clots surrounding bacteria, and kinase-breaks up the blood clot allowing bacteria into blood to spread

hyaluronidase

breaks down hyaluronic acid that holds cells together

break down enzyme

bacteria flows freely throughout the host

endotoxin

chemicals that cause damage, carried by blood throughout body, proteins bind specific cell disrupting function, toxic in small amounts

endotoxin example

cytotoxin, tissue in back is dying off, lesion in throat,

exotoxins can be

neurotoxins, bind nerve cells and prevents transmission of impulses from nerve cells

Botulism toxin

used for migraines or cosmetics for wrinkles

entertoxins

binds to small interstitial cells, flushes water out of intestines, diarrhea

membrane disrupting exotoxins

lyse cells,

membrane disrupting exotoxin examples

hemolysins- lyse RBC and leukocidins- lyse WBC

endotoxin

bad part of normal cell membrane

Liquid A portion of lipopolysaccharide

in outer membranes of gram negative cell walls, released during cell death

endotoxins can

do indirect damage released from cell walls, return to blood, no immune response, trigger inappropriate host defenses, toxic in large amounts

endotoxin high concentration cause

higher concentration to trigger inappropriate host defenses (high fever, shock or death)

superantigens

secreted proteins carried through blood, no binding, indirect damage to host, toxic in large amounts

spikes

attachment proteins that bind to host cell receptors increase ability to get disease

intracellular life

viruses multiply within host cells where they avoid phagocytosis

antigenetic variation

frequent changes to viral surface proteins by mutation, how it escapes to avoid immune system

damage to host

lysis, steal host resources or membranes