MUTATION OF BACTERIAL CAPSULES.
Introduction
Bacterial capsules help bacteria develop resistance against the immune system hence
preventing destruction of the organism, especially through phagocytosis. Genetic mutations which occur
at the surface of the capsule allow formation of various serotypes. This is seen when an individual is
infected with a different bacterial strain, since the immune system does not recognize the strain’s
capsule, the person ends up falling sick. This is why an individual vaccinated against Neisseria
meningitidis type C could easily develop meningococcal disease from N. meningitidis type B.
How the bacteria managed to survive the host’s immune system:
The bacteria observed in the deer earlier was able survive because it had developed a
mechanism that allows it to adapt without being engulfed by means of phagocytosis. Most bacteria
types achieve this by hiding the capsule with a clotting of protein fibrin. For example, the pathogenic
strain of Staphylococcus aureus emits substances which cause the coagulation of fibrin on the bacterial
cell surface. In such a case, the host’s immunological cells are unable to recognize the bacteria upon
contact.
Cause of death of deer:
The deer died because the bacteria became infectious, causing a disease within the host’s body.
The pathogenicity of the bacteria was induced by the genetic mutation of the bacteria’s capsule.
Research conducted on ‘Mutation of fucose synthesis gene of Klebsiella pneumonia effects on capsule
composition and virulence in mice’ shows that mutation in the genetic make-up of the capsule induced
the pathogenicity of the bacterium.
The rising clinical cases of liver abscess (LA) have provided enough proof for the pathogenicity
nature of Klebsiella pneumonia (KP). K. pneumonia has a thick mucoid capsule. The bacterial capsules for
those strains causing KP have been found to contain fucose but lacking in those strains causing urinary
tract infections. The conversion of mannose to fructose is propagated by the products of gmd and wcaG
genes. Induced mutation was performed to the KPL1 strain of KP known to cause high death rate in
mice. This was done through the insertion of an apramycin-resistance gene into the gmd. The result
mutant expressed upstream and downstream of gmd but not the original gmd itself as was determined
by reverse transcriptase polymerase chain reaction. The gmd gene proved to have been disrupted, and
this was confirmed by the DNA mapping. The experiment conducted showed that the mutant decreased
the ability of the bacteria to kill infected mice hence proving decrease in virulence.
In our case above, the bacteria that were initially found in the deer did not cause infection until
in later stages. Mutation of the bacterial capsule as observed induced the pathogenicity of the bacteria
leading to the death of the deer.