A similar scenario can be observed when the protoscoleces of Echinoccocus granulosus
are transplanted directly or within a diffusion chamber into the peritoneal cavity of a mouse.
The end product is a very definite macroscopic capsule surrounding a protoscolex.
However a small percentage of live protoscoleces can survive when the mouse is infected
with a relatively large number of juvenile tapeworms.
The eggs of Schistosoma mansonithat travel via the blood circulation and end up in the
hepatic tissue remain there. A granuloma (see section 7.5) develops round the egg and
eventually eosinophils can be observed in close contact with the egg, which is then destroyed.
However with some helminths the host can react to the presence of a live healthy para-
site and encapsulate it, but the parasite within the host capsule remains alive.
The tetrathyridia of Mesocestoides cortican live free in the peritoneal cavity and can also
invade the liver tissue. The hepatic cells along the migratory path are necrosed and
replaced with cells associated with inflammation. Eventually the tract is filled with col-
lagen and fibrin (scar tissue). Once the tetrathyridium has settled, a host capsule forms
round it. This type of capsule differs from the granuloma that forms round schistosome
eggs. The parasite remains active within a semi-fluid mucilaginous medium. The inner
boundary of the capsule is composed of regular epithelial cells and outside of these are
layers of fibrocytes among deposits of collagen. Outside of this layer are found
eosinophils, lymphocytes, macrophages and mast cells. No host cells can normally be seen
attached to the parasite.
If the same host is infected with both M. cortiand S. mansoniboth tetrathryridia and eggs
can be seen within the liver. However the eggs are surrounded by a typical granuloma
whereas the tetrathyridia stay alive within a host capsule. This is evidence for the fact that
parasites appear to have a great deal of influence in controlling the nature of the host response.
If the eggs of Taenia soliumare accidentally swallowed by man (the wrong host) they
develop into cysticerci and migrate round the body. Often they settle in organs such as
the brain. Once settled, the host reacts with an innate inflammatory response. A fibrous
capsule eventually forms round the cyst which may increase in size with time. The
enlarging ‘cyst’ causes the surrounding brain tissue to become necrotic and impairs
aspects of the functioning of the central nervous system. This condition is known as
neurocysticercosis and one of the symptoms of this infection is very similar to epilepsy.
n 7.4 ORGAN AND SYSTEMIC PATHOLOGY
The spleen is a lymphoid organ that reacts uniformly to all types of infection. Within the
white pulp of the spleen there is a great deal of activity related to an adaptive immune
response. An increase in the amount of white pulp area is probably due to the increased
numbers of lymphocytes (both T and B cells) cloned in response to the infection. The
giant cells found in the red pulp are probably a fusion of individual macrophages and also
increase in number. This may be due to the fact that the infection is producing excess
waste products that need to be detoxified and removed from the system.
The outer capsular layer of the liver, spleen and visceral organs that comes in contact
with the parasites becomes thickened and fibrosed. If there is a heavy infection of loose
parasites within the peritoneal cavity, the fibrin deposits on the surface of the organs cause
the organs to adhere to one another.
The presence of a parasite within the abdominal cavity stimulates a general inflammat-
ory response with an increase in fluid-secreting ascites cells. Hence there is an accumula-
tion of fluid within the peritoneal cavity, a condition referred to as oedema. Parasitised
organs increase in size and often show signs of a colour change or even decolorisation.
Often within the organ the pathology is localised arround the parasite.
PATHOLOGICAL EFFECT OF THE PARASITE UPON THE HOST
Epileptic fits due to
neurocysticercosis is a
not uncommon condition
encountered in areas
such as Mexico, India,
vast regions of Africa
and S. America where
T. soliumis endemic.