Lesson 8.
1
Development of Microbial Infection
Lotis M. Balala
College Of Veterinary Medicine, Visayas State University
Learning Outcomes
1. Discuss general pathogenesis of microbial infection.
2. Illustrate pathogenicity cycle.
Overview of bacterial mechanisms for pathogenicity
(A) Upon encountering a human host, a bacterial pathogen may illicit several host
responses and use a variety of mechanisms to evade the host defenses. The bacterial
components that interact with the host include: (1) capsules that act to “frustrate”
phagocytosis and protect the pathogen from macrophage and neutrophil engulfment,
(2) lipopolysaccharide (LPS) and cell wall components which can cause septic shock,
(3) toxins that can serve to damage host cells and aid invasion, and (4) adhesins which
facilitate binding of the pathogen to host surfaces. The degree to which these various
mechanisms play a part in the pathogenesis of an infection depends on the bacterial
species or strain, the site of pathogen entry, the immune status of the host and other
similar factors.
(B) Once adhered to a host surface, a bacterial pathogen may further invade host tissues. Pathogens
may “burrow” further into a tissue by expressing and secreting proteases and glycanases that digest
host extracellular matrix proteins and polysaccharides. In addition, a pathogen may also invade the host
tissue cells and gain access to the intracellular environment. This can be facilitated by the natural
phagocytosis mechanisms of macrophages and neutrophils or by induced uptake where the pathogen
signals the host cell to engulf adhered bacteria. A common strategy for pathogens to induce uptake is
the use of a type III secretion system which injects bacterial signaling proteins into the host cell. Within
the host cell, the pathogen may reside within a phagolysosome (a phagosome which has fused with a
lysosome), a phagosome which has not fused with a lysosome, or within the host cell cytosol.
Entry, spread and release of
blood-borne viruses
(systemic infection)
Transmission to the host
most bacteria that cause disease do so first by attaching or
adhering to host cells, usually epithelial cells
After the bacteria have established a primary site of infection,
they multiply and spread directly through tissues or via the
lymphatic system to the bloodstream.
This infection (bacteremia) can be transient or persistent.
Bacteremia allows bacteria to spread widely in the body and
permits them to reach tissues particularly suitable for their
multiplication.
Commensals
acquired soon after birth and are able to adhere to body suraces
form stable polymicrobial communities that are present throughout
life as ‘normal microflora’ on the skin and in the hollow organs
whose surfaces and cavities are open to the environment
the proportional representation of the several species is controlled
by competition for nutrients and for adhesion sites and by
antibacterial products such as bacteriocins released by some
members of that microbial community
Uses of Commensals
degrade ingested material in the rumen of cattle and sheep, in the caecum
and colon of horses, and in the colon of pigs
microflora of the rumen synthesizes vitamin K and some of the vitamin B
group, as does the microflora of the intestine in non-ruminants
the normal microflora primes the immune system, facilitating a more efficient
host response to challenge by bacterial pathogens
the immune system is stimulated nonspecifically by antigens associated with
some commensals
the most important beneficial effect of the indigenous microflora is to provide
competition for exogenous bacteria attempting to colonize niches in which
they must compete with the resident flora for nutrients and for receptors