Introduction to Parasitology
Parasites and disease
Many parasites have complex life cycles that involve extensive
migrations in their hosts. Others have simple life cycles with little or no
migrations. The propensity of a parasite to cause disease (its pathogenic
potential) is not a simple prediction since it may depend on a number of factors
including the examples listed below.
Factors influencing the pathogenic
potential of a parasite
The migratory pathway in a host
The anatomical site where a
parasite develops if it does not migrate in its host.
The predilection site
The propensity to stimulate
hyperactive immunological responses in the host that may lead to
immunopathological changes such as fibrosis, granulomas, cachexia,
autoimmuine reactions, allergic reactions and splenomegaly.
The potential of the parasite to
transmit other infectious agents. This property is especially relevant to
Despite the complexities of parasite interactions with their
hosts, we can make certain predictions about the pathogenic potential of a
parasite and the likely clinical signs if we know certain details about its
life cycle, its predilection site and its feeding habits.
The following table summarizes the relevant information about Ostertagia
ostertagi, a nematode parasite of cattle found commonly throughout temperate
areas of the world, and Haemonchus contortus a nematode of sheep
found throughout the world in warm temperate and subtropical areas.
influencing the pathogenic potential of parasites
|Site of parasite development
||In close apposition to the abomasal mucosa
||Ingestion of abomasal contents
|Transmission of other infectious agents
With this information, we can make certain assumptions and
predictions about the pathophysiological changes and the clinical signs in these
Ostertagia ostertagi. The
nematode grows and develops in the gastric glands of the abomasum which it
leaves just before it becomes an adult, approximately 17-21 days after
infection. During its time in a gastric gland, the nematode grows about 100
fold. Therefore we can predict that this growth will result
in erosion of the secretory epithelium
and also that swelling of the gland will occur. In heavy infections these erosive
effects can be widespread resulting in heavy losses of secretory cells and
significant reductions in the output of HCL and pepsinogen. These changes are
summarized in the table below.
of Ostertagia ostertagi
|Loss of chief cells
||Reduction in HCl in the abomasum and a rise in the pH of
||Failure to convert pepsinogen to pepsin. Loss of the
bacteriostatic effect of an acid pH
||Protein digestion impaired.
Bacterial accumulation in the g.i. tract
|Loss of peptic cells
||Reduction in secretion of pepsinogen
||Loss of protein digestion
These changes will result in the collection of osmotically
active materials in the intestine (undigested protein and bacteria) and these,
in turn, will promote the transfer of fluid from the extracellular spaces into
the gut lumen and diarrhea (watery feces) will be the outcome of this
process. Diarrhea is, in fact, the primary clinical sign in acute
ostertagiosis and we can make this prediction from a small, but critical,
amount of information about the parasitic phase of the nematode's life cycle.
Haemonchus contortus. In
this example, unlike Ostertagia, the parasite matures on the mucosal surface
of the the abomasum. Therefore its growth and development has little effect on
the mucosa and makes no contribution to its pathogenic potential.
Despite the fact that adult Haemonchus are no more than 1cm long, they are
voracious blood feeders and it is this blood loss that is entirely responsible
for the pathophysiological changes and clinical signs we see in Haemonchosis.
Pathogenesis of Haemonchus
Impact of feeding
|Blood feeding by L4s and adults may remove
0.05ml blood per worm.
||Severe blood loss. A worm burden of 1,000
worms may remove 50ml blood per day from an infected host.
Loss of red cells
= drop in the PCV
Loss of plasma proteins
= hypoproteinemia (hypoalbuminemia)
The magnitude of the red cells losses due to the feeding
habits of this parasite makes it easy to predict that anemia of varying
degrees of severity will be a constant feature of these infections and will
usually be seen clinically as pale mucous membranes and lethargy. The latter
can be explained by the reduced oxygen carrying capacity of the blood due to
the loss of Hemoglobin along with red cells and a resultant reduction in oxygen
perfusion of tissues such as muscles.
Edema is usually seen in live sheep as a gathering of fluid in
the submandibular space, between the mandibles and for this reason is often
called "bottle jaw". At necropsy a Haemonchus-infected sheep would
show a general wetness of the tissues as well as fluid in the peritoneal (ascites)
and thoracic (hydrothorax) cavities. Edema has a more complicated explanation
than anemia and requires an understanding of the forces controlling fluid flow
in tissues at the capillary level.
|The exchange of fluid between blood and the interstitial
spaces, at the capillary level, is controlled by the opposing effect
of two forces, Hydrostatic Pressure (HP) and Plasma Colloid
Osmotic Pressure (COP). HP tends to force fluid out of the capillaries
and COP tends to draw fluid into the capillaries. The balance of these
two forces will determine what occurs. At the arterial end of a
capillary HP is greater than COP and fluid will leave the capillary to
perfuse the interstitial spaces. At the venous end of a capillary, HP
is lower than COP and fluid will
|return to the capillary from the
interstitial spaces. The concentration of albumin in plasma is the
most important contributor to colloid osmotic pressure and is,
therefore, the most important determinant in regulating fluid flow at
the capillary level. A reduction in the level of albumin, because of
blood loss, in Haemonchosis will result in a corresponding reduction
in the COP with a net outflow of fluid from blood, its accumulation in
the interstitial spaces and this is called edema. We know that
Haemonchus is a blood sucking parasite and causes significant blood
loss including plasma proteins. Our knowledge of the physiological
forces governing fluid flow at the capillary level (Starling's
Principles) leads us to predict that edema will be a logical and
likely outcome of Haemonchus infections