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  3. Universiteit Van Amsterdam (UvA)
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  5. Medische Microbiologie (5052MEMI6Y)

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Samenvatting hoorcolleges Microbiologie - BMW UvA, jaar 3 ()

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Uitgebreide samenvatting (103 blz.) van alle hoorcolleges ter voorbereiding van het theorie tentamen Microbiologie. Omvat alle tentamenstof voor de drie deelonderwerpen: bacteriologie, virologie, en parasitologie. Begrippen en concepten zijn uitgebreid toegelicht en bijbehorende figuren zijn hierbi...

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  • 5 september 2022
  • 103
  • 2021/2022
  • Samenvatting

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Voorbeeld van de inhoud

Summary – lectures

Medische microbiologie
Bacteriologie, parasitologie & virologie




Bonifiya Visuvasam

1

, Lecture 1
Introduction to bacteriology
Microbiome vs. pathogens
• Human-associated microbes → the microbiome: 4 x 1013 microorganisms, 500 – 1000
different species.
• The composition of these microorganisms differs dependent on the body site. This is because
the conditions of the skin for example are very different than the conditions in the gut, for
example amount of oxygen, pH or nutrients (see figure).

Microbiome as a source of health and disease
• Nutrition and metabolism of food
o Breakdown of indigestible polysaccharides
o Production of vitamins B and K, which we cannot produce ourselves
• Maturation and instruction of immune system
• Colonization resistance (‘good bacteria’): protection against invaders = possibly harmful
microorganisms = pathogens. Good bacteria compete with pathogens for nutrients or simply
already occupy the particular spot in the intestine, such that the incoming pathogens cannot
gain foothold!
Thus, simply depleting all microorganisms by for example antibiotics actually has an enormously
negative impact on our health.
• Potential disease-causing bacteria among healthy microbiome → risk of infection →
opportunistic pathogens:
o A second risk of having so many bacteria in and on our body is the presence of
potential pathogens, so called ‘bad bacteria’ = opportunistic pathogens among the
good ones in the healthy microbiome (see figure). Although usually kept in check by
our immune system, occasionally they do cause disease which can present itself in
many different ways.
o Many pathogens typically colonize skin or mucosal surfaces of healthy individuals
without producing symptoms → this is because our body is equipped with very
effective immune defense mechanisms that kills any invading bacterium in seconds-
minutes → hence, acute infections are caused by failure of the immune system to
fulfill its sentinel defense function.
o Potentially ‘bad bacteria’ among the healthy microbiome: Neisseria meningitidis,
streptococcus pneumoniae, staphylococcus aureus, group A streptococcus (see
figure).

Key concepts 1
• Commensalism: presence of microorganisms multiplying in the host without damage and
reaction from the host
• Infection: presence (invasion) of micro-organisms multiply in the host, with damage to and
reaction of the host

Key concepts 2
• Pathogen: microorganism able to cause disease.
• Pathogenicity: ability to produce disease in a host organism (based on host) → ability of
pathogen to cause infection during host-pathogen interactions.
• Virulence: the degree of pathogenicity of the microbe (based on microorganism) → only the
ability of the pathogen to cause infection and evade host defenses.
• Virulence factor: microbial component that contributes to disease-making ability


2

, • Carrier: host that harbors potential pathogen without disease
The relationship between a host and a pathogen is dynamic, since each modifies the activities and
functions of the other. The outcome of such a relationship depends on the virulence of the pathogen
and the relative degree of resistance or susceptibility of the host, due mainly to the effectiveness of
the host defense mechanisms.

Totally different clinical pictures, but same pathogen!
• Staphylococcus aureus, arguably the most prevalent pathogen of humans, may cause up to
one third of all bacterial diseases ranging from boils and pimples to food poisoning, to
septicemia and toxic shock.
• For example, scalded skin syndrome vs. food poisoning: both caused by staphylococcus aureus
→ same pathogen = causative agent, however, two different clinical pictures.
• Staphylococcal scalded skin syndrome = SSSS:
o Caused by staphylococcus aureus.
o Illness characterized by red blistering skin that looks like a burn or scald, hence its
name.
o SSSS occurs mostly in children younger than 5 years, particularly newborn babies.
• Staphylococcus aureus:
o About 15-40% of healthy humans are carriers of Staphylococcus aureus → they have
the bacteria on their skin without any sign of infection or disease = colonization.
o S. aureus can naturally occur in the nasal throat area, ears → colonization.
o S. aureus is an opportunistic pathogen: when it sees a chance it will cause infection.
The bacteria need a kind of “entrance” = port d’entrée to penetrate the skin or
mucosa to enter and cause infection.
• Hence, how can S. aureus cause two different clinical pictures ? → distinct port d’entrée!
o Entry of scalded skin syndrome is through the barrier of the skin or mucous
membranes. However, with food poisoning, you have ingested contaminated food,
thus pathogens enter through gastrointestinal tract membranes! → distinct clinical
pictures.

Course of infection/clinical manifestations
The course of infection is determined by:
• Route of contamination and invasion of the host
• Properties of the microorganism
• Properties of the host

1. Route of contamination and invasion of the host
• Porte d’entrée:
o Skin or mucous membranes: wound infections, STD → can cause SSSS!
o Transcutaneous: via vectors, insects.
o Directly in the bloodstream: IV drug user, tooth extraction.
o Airways: upper/lower respiratory tract → can cause SSSS!
o Gastrointestinal: contaminated food → can cause food poisoning!
• Pathogenicity
1. Invasiveness = ability to invade tissues
o Colonization = first stage of infection: establishment at appropriate porte
d’entrée → pathogens usually colonize host tissues that are in contact with
external environment (urogenital tract, digestive tract, respiratory tract).



3

, o Bypass host defense: tissue adherence mechanisms + ability to overcome or
withstand host defenses at the surface. Invasion follows adhesion and allows
bacteria to evade the humoral immune response and to proliferate in a well-
protected niche.
o Tropism: pathogens also have a preference for certain tissues to invade over
others → types of tropism (see figure):
▪ Cellular tropism (e.g. HIV normally infects macrophages, but not
neurons)
▪ Tissue tropism (e.g. influenza virus normally infects lung tissue but not
brain tissue)
▪ Host tropism (e.g. myxoma virus normally infects rabbits but not
humans)
2. Toxigenesis = ability to produce toxins
o Exotoxins: produced and excreted by bacterial cells → can act on sites other
than site of bacterial growth.
▪ Exotoxins are mostly proteins.
o Endotoxins: cell-associated (bound to surface for example), but may be
released from growing bacterial cells or cells that are lysed as result of
effective host defense or antibiotics.
▪ E.g. LPS.
o Bacterial toxins may be transported by blood and lymph and cause cytotoxic
effects at tissue sites remote from the original point of bacterial invasion or
growth.
o Toxins are major virulence factors → often sufficient to determine the
outcome of the infection.
Thus: pathogenicity of the pathogen is due to the virulence factors of the pathogen, including
adhesins/invasins and toxins.

2. Properties of the microorganism
Virulence factors:
• Adhesins
• Invasins
• Capsule
• Toxins
• Enzymes
• Pili: the presence of pili greatly enhances bacteria's ability to bind to body tissues,
which then increases replication rates and ability to interact with the host organism.

Exfoliative toxins vs. enteroxin in totally different clinical pictures
• Toxins are important for the clinical outcome: scaldes skin syndrome vs. food poisoning.
• SSSS: exfoliative toxins A and B = exotoxins produced by toxigenic strains of S. aureus →
pathogen locally produces exfoliative toxins A and B → toxins bind to a molecule within the
desmosome and break it up so the skin cells become unstuck (see figure) → the bacteria are
from a local infection and thus cause "remote" production of the bacterial toxin via the
bloodstream, the blisters in the skin (see figure).
• Food poisoning: caused by enterotoxin A production by S. aureus: S. aureus enterotoxins (SEs)
→ potent gastrointestinal exotoxins → toxins enter through gaps between intestine epithelial
cells → immune activation → S. aureus does not compete well with indigenous microbiota in
raw foods, thus contamination is mainly associated with improper handling of cooked or
processed foods, followed by storage under conditions which allow growth of S. aureus and
production of the enterotoxin(s). The toxins are resistant to conditions (heat treatment, low

4

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