Summary of Lecture 20. Microbe: human interactions on and within the body are normal . Human body is a good habitat for suitable bacteria (nutrients, temperature, pH, etc.) Normal microbe flora is important for general well-being (e.g. vitamin synthesis ).
Entry of the pathogen into the host. Colonisation and growth. Toxins.
to pathogensMicroorganisms and Pathogenesis
to skin or mucosa
Production of virulence factors
toxin effects are local
further growth at original
site and distant sites
TISSUE DAMAGE, DISEASE
Brock: Figure 28.12
Brock: Figure 28.13
capsule (bright green) – note
how capsule extends about 1m
From actual cell (cell is about
0.5 m diameter)
Bacillus anthracis colonies
can be mucoid (slimy) in
Escherichia coli EM showing type P fimbriae. Cell is 0.5 m wide
Brock: Figure 28.15
Pili are longer than fimbriae.
There are less pili found on the surface of the cell.
Both structures bind to host cell surface glycoproteins: leads to adherence to animal cells.
Invasion: Penetration of the microorganism into the host cell (through the epithelium) and subsequently inflicting damage.
Broken skin or mucosal surfaces can be points of entry for pathogens. Once growth is established at these sites, colonisation and invasion begin.
May also spread throughout the host via the circulatory or lymphatic systems.
Impetigo - http://www.healthhype.com/staph-skin-infections.html
Scrumpox - http://www.sciencedaily.com/releases/2008/09/080928210041.htm
Scanning EM of the spiral-shaped bacteria of the genus Leptospira – causative agents of leptospirosis. – Janice Carr (CDC –Image no:138)
Lyme disease infection; (a) deer tick attached to skin, (b) circular rash associated with lyme disease (Madigan et al., 2009. Brock Biology of Microorganisms. pp.1012.
Tetanus is a disease caused by exotoxin produced by Clostridium tetani.
Bacteria stay in localized wound but toxin spreads through the body.
Growth of bacterium in large enough numbers to inhibit cell function.
Streptococcus pneumoniae produces no toxin but grows in large numbers in the lung.
Polysaccharide capsule of the pathogenic strains prevent phagocytosis.
Host responses lead to pneumonia.Toxicity and Invasiveness
(inv and prg
Type 1 fimbriae
(inhibits host cell
calcium influx into
Vi capsule antigen;
Inhibits complement binding
(inhibits phagocyte killing)
H antigen (adherence; inhibits
Brock: Figure 28.17
Special secretion machinery often used
Specific targets usually distant from the site of infection.
Generally no fever
Toxic lipopolysaccharides that are part of the gram negative bacterial cell wall.
Released when bacteria lyse (burst open)
Large bacterial numbers needed for toxic effect.
Fever, diarrhoeaBacterial toxins
ADP ribosylation of EF-2
Protein synthesis stops
Normal protein synthesis
Blocks protein synthesis by ADP ribosylation of EF-2.
Brock Figure 28.20
from the central
Glycine (G) release from inhibitory interneurons
stops acetylcholine (A) release and allows
relaxation of muscle
Tetanus toxin binds to inhibitory interneurons,
preventing release of glycine (G) and relaxation
Brock: Figure 28.22
from the central
Botulinum toxin, , blocks release of A,
Acetylcholine (A) induces contraction
of muscle fibers
Brock: Figure 28.21
A soldier dying from tetanus.
Painting by Charles Bell in the Royal College of Surgeons, Edinburgh.
Large gram negative rod
with terminal endospores
(looks like drumsticks)