Microbial interactions Flashcards
Microbiome
The diverse community of microorganisms, including bacteria, viruses, fungi and other microbes, that inhabit a particular environments, such as the human body, plant roots or seawater
Holobiont
A host organism and its associated community of symbiotic microorganisms collectively functioning as a single ecological unit
Human microbiome
Mutualism – where both partners gain = flowers get pollinated, bee gets nectar
Stability of the human microbiota critical to health
Diversity and abundance of the microbiome varies with host but also part of the body
Some parts of the body diversity is restricted – e.g stomach where there is high acid
Small intestine is a harsh environment for microbial life = short transit time, excretion of digestive enzymes and bile
Colon too = conditions anaerobic, enriched with firmicutes and Bacteroidetes, methanogens and archaea present
Microbial diversity in gut varies:
- Colon harbours trillions of bacteria in exchange for nice host environment, digest complex carbohydrates, boost immune system and fend of pathogens
- Oral antibiotics can kill gut microbiome, reduces diversity and functionality, and exposes host to opportunistic pathogens
Many bacteria associated w human gut are strict anaerobes or facultative aerobes – e. coli most abundant facultative aerobe in gut microbiome
Gut microbiome assembled in stepwise manner:
- Quickly displaced and/or outnumbered with the infants own bacteria
- Increases in richness of bacteria as infants move from milk-based diet to an adult diet
- Firmicutes are the first to colonise
- Proteobacteria are often detected soon after, followed by actinobacteria
- Once solid food introduced, Bacteroidetes established and displace most of the bacteria from other groups except for the firmicutes
- By school age composition of gut microbiome is essentially adult-like = dominated by firmicutes and Bacteroidetes
- Firm and bact phyla remain dominant as host ages
- Within firm and bact species richness increases as host ages
- As host ages diversity and stability increases
Gut communities of individuals with obesity, insulin resistance and/or inflammatory bowel conditions are less diverse than those of healthy individual (although correlation does not mean causation)
Alteration in gut microbiome = dysbiosis
Bacteria gain:
- Microbes in gut do not need to make amino acids (supplied by intestinal epithelium)
- Sporulation genes in firmicutes are downregulated = no need for sporulation; microbes live in a protective environment with plenty of food
Humans gain:
- Bacteria in gut breakdown and ferment complex carbohydrates, such as dietary fibre and generate, format and short-chain fatty acids
- Firmicutes produce scfa butyrate which is absorbed by the colonic epithelium = dominant energy source
- Bact produce scfas distributed by bloodstream to peripheral organs (for energy production and precursor of cholesterol, long-chain fatty acids and amino acids)
- Formate broken into co2 and h2
- Methanogenic archaea remove h produced by fermentation carried out by firm and bact (h inhibits microbial fermentation)
- Methanogenic archaea use co2 as last electron acceptor (anaerobic respiration) and produce methane as by product
Human gut includes other low-abundant bacterial phyla = proteobacteria, actinobacteria, and verrucomicrobia
Some bacteria commensal = benefit from being in the GI but do not cause any harm
Some bacteria opportunistic pathogens = SCFAs if not absorbed by colonic epithelium, help drop pH of intestinal lumen to control growth of harmful bacteria
Fecal material transplant FMT
So specialised are microbes in gut that it is possible to use stool from healthy individuals to restore perturbed gut microbiomes
Rumen microbiome
SCFAs are also consumed by other microbes in gut
Interaction where one species feeds off metabolic products of another is called syntrophy = what happens in gut of ruminants
Digestion of plant materials takes place in the rumen – an anaerobic environment filled w liquid
Bacteria, fungi, protozoa degrade cellulose and other plant polymers into sugars. Sugars fermented into volatile fatty acids
Bacteria and fungi in the rumen cooperate by degrading and fermenting the plant-derived polymers to generate essential nutrients for the host
Protists in the rumen are involved in cellulose degradation and predate on bacteria
Archaea produce methane from h and co2
Syntrophic removal of h2 for a greater fermentation rate = more ATP for microbes are produced
Commensalism
Commensal associations, one partner benefits (the commensal) while other is not affected = barnacles on whales, whale unaffected, barnacles find food
Commensal benefits from amino acids, vitamins and growth factors released by other organisms
Often host releases products that are waste products that the commensal organism scavenges
Bacteria in mouth:
1. Bacteria colonise teeth and build multispecies-biofilms on the enamel-dental plaque
- Bacteria recognise molecules in the saliva that coats our teeth
- First colonisers = streptococci and actinomycetes (commensals)
2. Commensal bacteria form a biofilm that feeds on food debris that stick to it = establish mutualistic interactions and feed one another
3. If biofilm is left to grow pathogenic bacteria join biofilm
4. Pathogens grow leading to
5. Cavity formation and gum inflammation
- S. mutans ferments sugar are secretes acids. Excessive sugar allows s. mutans to produce more acid = erodes enamel causing cavities
- P. gingivalis can evade the gum epithelium = inflammation and gum disease
Parasitism
Pathogenic bacteria that cause infectious disease can be considered a type of parasitism = tick gets blood, cat gets skin irritation
Pathogenic bacteria gain while host loses
Challenges infectious agent confronts:
1. Encounter
- Host and affecting agent must meet
- Source may be environment, animals, other humans
2. Entry
- Can occur with or without penetration of hosts tissue]
- Modes of entry include = inhalation, ingestion, insect bites, sexual contact, wound infection, organ transplants
3. Establishment
- Depends on inoculum size, virulence, host defences
- Requires overcoming host defences
- Outcome of interactions between host and pathogen determines whether there will be symptoms of disease
Bacterial toxins
Cause disease by secreting toxins
Vibrio cholerae example:
- Motile gram-negative bacteria that inhabits lakes and rivers
- Most strains rarely cause disease
- Can swim freely or form biofilms on small crustaceans
- Pathogenic strains contain pathogenicity islands = regions that encode, amongst other genes: cholera toxin (ct) and toxin-corregulated-pilus (tcp). Ct coded by part of genome of a filamentous phage
- Transfers pathogenicity islands to others via transformation or transduction
- CTX phages carry pathogenicity island
- Phage inserted into V. cholera genome as a prophage
- V. cholera now has ability to produce CT and TCP
- TCP mediates bacterial aggregation and helps V. cholera colonise intestine lining
- LPS in outer membrane of vibrios determine if they are resitant to phages (CTX phages)
- Cholera toxin induces efflux of water into lumen of intestine
- Continuous activation of adenylate cyclase fills cells w cAMP and chlorine is pumped into lumen. Water follows direction of Cl- gradient
