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Summary Cases & Lectures minor BMS: Infection and immunity
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Document detailing all cases and lectures of the minor Infection and immunity.
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Cases: Infection and immunityCase 1: Commensal microbes
Keywords:
- commensals, opportunists, strict pathogens
- role of microbiome in opportunistic infections (antibiotic-associated colitis, bacterial
vaginosis, urinary tract infection/pyelonephritis)
- skin microbiome, Staphylococcus epidermidis, Staphylococcus aureus
- respiratory tract microbiome
- eye & ear microbiome
- gastrointestinal tract microbiome (including role of pH, diet, functions of gut microbiota, and
bile acids)
- genitourinary tract microbiome
- intestinal microbial colonization (including impact of birth mode, infant diet, lifestyle)
- intestinal microbial aid in host metabolism (SCFA synthesis, carbohydrates and protein
fermentation, methanogenesis)
- colonization resistance
- intestinal microbiota and disease (metabolic syndrome, cardiovascular disease, cancer)
- prebiotics, probiotics, fecal microbiota transplantation
33.1 Humans are holobionts
Microbiome= refers to all the genes found in one’s microbiota; all the microorganisms that
live in and on an organism
humans cannot live a normal life without their microbial partners → we are holobionts
Holobionts= host and microbes relying on each other and importantly, evolving together.
Adult carries about same number of microbial cells as human somatic cells
Commensal= organisms that are normally found on those parts of the body exposed
to the external environment, e.g. the bacteria in the gut and on the skin (normal
microbiota)
Opportunist pathogens= an organism that can cause an infection in individuals with
abnormal host defences: commensals can be opportunistic pathogens → only infect
the host when immune system is decreased
Pathogen= organisms that cause infections in an individual with normal host defences
33.2 The microbiome develops from birth to adulthood
Development of a stable microbiome
The community of microbiota we host is not static → begins developing at birth, changes as
we age
During infancy, our microbiota are most sensitive to the environment
This early time in our lives appears to be a “win down of opportunity” for the development
of the kinds of microbes that will be beneficial for the maturation of our immune systems
At 3 years we have adopted a more stable community of microbes
, A diverse community is linked to better health. Some factors have a clear negative influence
(antibiotics) or positive impact (breast milk), but it is the complex interaction of many factors
that determines microbial diversity.
Newborns are colonized by microorganisms from immediate environment
➢ Babies born vaginally acquire most of their microorganisms from their mother’s birth
canal
➢ Babies born by caesarean delivery acquire microorganisms from the skin of their
initial caretakers (nurse, doctors, midwives, parents etc.)
➢ Newborn colonization is very important → swabbing the mouths of new-borns with
maternal vaginal secretions after caesarean delivery are underway
Early in life, human milk act as a selective medium for non-pathogenic bacteria
➢ Maternal milk contains < 100 different human milk oligosaccharides (HMO)
(unique for humans)
➢ Cannot be digested by our own digestive enzymes
➢ Bifidobacterial specialized to ferment: HMOs into acetate and lactate →
abundance bifidobacterial goes up
➢ Acetate and lactate are an energy source for the baby and lower intestinal pH
➢ Lower pH prevents colonization by (opportunistic) pathogens
➢ Maternal milk also contains bacteria (incl. bifidobacterial) that can seed the
infant gut
➢ Formula-fed infants have more diverse collection of gut microbiota, including
opportunistic pathogens.
➢ Switching to cow’s milk or solid food (mostly polysaccharide) → result in loss of
bifidobacterial
- proteobacteria, firmicutes, and bacteroidetes—specifically enterobacteria,
enterococci, lactobacilli, clostridia, and Bacteroides spp.—increase and
outcompete bifidobacteria.
, With dysbiosis= lower amount of Bifidobacterium, these bacteria produce acetates
and lactates which prevents pathogens to colonized
With dysbiosis → link to immune development. Immune system needs to learn what
good and bad bacteria are.
❖ Gut microbiota- immune maturation
Immune development starts before birth and it continues after birth
Most important phases is the first 6 months
, Left side: before birth (prenatal)
• Have some developing mesenteric lymph nodes
• Some Peyer’s patches → are immune complexes, they are connected to
the outside by M cells
• M cells
• Cryptopatch → will develop into lymphoid follicle. Get stimulated by
lymphoid tissue inducing cells.
Right side: after birth (postnatal)
• Lot of B & T cells going into lymphoid follicle → they can send out IgA
producing plasma cells
• Mature lymphoid follicle → can release IgA producing plasma cells
• IgA can be released into the lumen and binds to bacteria. IgA can neutralize
pathogens
• Peyer’s patch are only in small intestine
• Mesenteric lymph node are deeper into the tissue → can communicate with
dendritic cells
While adult microbiota is relatively stable over time, it is highly variable from person to
person and at different sites within the same person. each human has a relatively unique
microbiota
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