microbe host

what are the types of symbiosis

mutualism, commensalism, and parasitism

what is mutualism?

where both partners benefit; common in nature; symbiotic partners often gain new abilities → occupy new niches

what are examples of mutualism

• mitochondria evolved from rickettsiae

• chloroplasts evolved from cyanobacteria

• nitrogen fixing bacteria + legumes

• tube worms + chemosynthetic bacteria

what is commensalism?

one partner benefits, the other is unaffected; many normal microbiota relationships fall here

what is parasitism?

one partner benefits at the expense of the other; causes disease

can symbiotic roles shift?

yes (commensal → opportunist → pathogen)

what is endosymbiosis?

when the symbiont lives inside the host

what is the origin of mitochondria according to the endosymbiotic theory?

that mitochondria evolved from rickettsiae-like bacteria

what is the origin of chloroplasts according to the endosymbiotic theory?

that chloroplasts evolved from cyanobacteria

how do mitochondrial and chloroplast genomes compare to their bacterial ancestors?

their genomes are smaller than modern day rickettsiae and cyanobacteria because many genes were transferred to the nuclear genome or lost as the endosymbiont relied on its host

what evidence supports mitochondria and chloroplasts came from bacteria?

binary fission; protein synthesis like bacteria (70S and initiate with fmet); circular chromosomes with no histones; FtsZ proteins for septum formation during division

what is buchnera?

a bacterial endosymbiont of aphids involved in nutrition mutualism

what does buchnera provide for aphids

10 essential amino acids that aphids cannot make on their own?

where are buchnera house?

inside bacteriocytes which are specialized insect cells packed with bacterial endosymbionts

describe the relationship between aphids, bacteriocytes, and buchnera

aphids (organism) → contains bacteriocytes → contains buchnera

how do tube worms survive near hydrothermal vents?

gutless animals dependent on chemosynthetic bacteria

what do these bacteria use as carbon and energy sources?

inorganic carbon and H2S and energy

what is rhizobia?

a nitrogen fixing bacteria that reduced N2 into ammonia (NH3) as a usable form of nitrogen

who can perform nitrogen fixation?

only prokaryotes perform nitrogen fixation

where does symbiotic nitrogen fixation occur?

inside the root nodules as endosymbionts

what does the plant get from rhizobia?

fixed nitrogen to survive in nitrogen poor soils

what does rhizobia get from the plant?

dicarboxylic acids (carbon/energy source)

why is rhizobia-legume symbiosis a good model for studying pathogenesis?

establishing the symbiosis requires infection, invasion, and persistence inside plant cells

what type of symbiosis is a normal microbiota?

mutualistic and commensal

where is normal microbiota found?

gut, skin, mouth, etc.

why are some regions of normal microbiota on the body considered “sterile”?

because the regions are protected by host defenses and are normally inaccessible to microbes (ie: placenta)

what is considered the human microbiome?

all genes and microbes in the body

what are the roles of the human microbiome?

immune system training, metabolism, and modifying drug effectiveness (wallace paper)

what is microbial antagonism? what is this important for?

normal microbiota competing with pathogens for space and nutrients; important in preventing infections like c. diff

what mechanism was the wallace paper explaining/looking for? what had the best outcomes?

the liver inactivates SN-38 by adding the G. SN-38G moves to the intestine where the G is cleaved off which reactivates the gene in the wrong spot and causes side effects; wallace paper was looking for inhibitors for the bacterial enzyme B-glucs that reactivates the SN-38 gene; inhibitor + anti cancer drug (CPT-11) has the best tissue outcomes

what two inhibitors did the wallace paper use?

two inhibitors are CP-11 (inhibits human topoisomerase) and inhibitor of B-glucs

what was used to examine tissue structures in biopsies? what did they stain and what color?

hematoxylin and eosin stains; eosin stains cytoplasm and cell matrix pink; hematoxylin stains nuclei and dna blue/purple

what are opportunistic pathogens?

cause disease only when given the “opportunity”

what can opportunities include for opportunistic pathogens?

immunocompromised host, entry into unusual body site, disturbance of normal microbiota

what is pathogenicity?

ability to cause disease

what is a pathogen?

organism that causes disease

what is a virulence?

severity/intensity of a disease

what do virulence factors help pathogens do?

adhere, invade, evade defense, or damage host

what are the major categories of virulence factors?

adhesion structures, defense evasion factors, toxins, and secretion systems

what are examples of adhesion structures for virulence factors?

adesins, capsules, and pili

what are examples of defense evasion factors for virulence factors?

capsules and hyaluronidase (digests tissue glue and helps them spread)

what are examples of toxins for virulence factors?

endotoxins (LPS; only released when gram negative bacteria die) and exotoxins (powerful, secreted proteins)

what are examples of secretion systems for virulence factors?

type 3 and 4 → inject effectors into host cells

what are pathogenicity islands (aka virulence plasmids)?

clusters of virulence genes that are distinguishable from the rest of the chromosome

how are pathogenicity islands (virulence plasmids) acquired?

by horizontal gene transfer

what are the case studies for key pathogens and their virulence factors?

e. coli o157:h7, tetanus (clostridium tetani), and anthrax (bacillus anthracis)

what does e. coli o157:h57 use? what does it produce? what is it carried by?

uses adhesins to attach to intestinal epithelium; produces shiga-like toxins that damage kidneys → HUS; carried by cattle and infected humans (carriers

what is tetanus (clostridium tetani)? is it invasive?

gram positive, endospore forming, strict anaerobe; non invasive, enters through wounds

what does tetanus produce?

tetanus exotoxins that block inhibitory neurotransmitters, causes spastic paralysis, and one of the more potent toxins

what does c. botulinum cause? (tetanus)

botulism which produces an exotoxin that causes muscle relaxation

what are the virulence factors for anthrax (bacillus anthracis)?

antiphagocytic capsule, anthrax toxin, virulence plasmid (extra: endospores survive long term in soil causing it to be a major environmental reservoir)

what does antiphagocytic capsule do? (virulence factor for anthrax)

inhibits phagocytosis of actively growing bacteria

what does anthrax toxin do? (virulence factor for anthrax)

kills macrophages and causes internal bleeding, septic shock, and death

what does virulence plasmid do? (virulence factor for anthrax)

carries toxin gene