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

  1. The migratory pathway in a host

  2. The anatomical site where a parasite develops if it does not migrate in its host.

  3. Feeding habits

  4. The predilection site

  5. 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.

  6. The potential of the parasite to transmit other infectious agents. This property is especially relevant to the arthropods.

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.

Factors influencing the pathogenic potential of parasites Ostertagia ostertagi Haemonchus contortus
Migratory pathway

None

None

Site of parasite development Gastric glands In close apposition to the abomasal mucosa 
Predilection site Abomasum Abomasum
Feeding habits Ingestion of abomasal contents Blood feeder
Immunopathological changes None None
Transmission of other infectious agents None None

With this information, we can make certain assumptions and predictions about the pathophysiological changes and the clinical signs in these infections.

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.

Pathogenesis of Ostertagia ostertagi
Morphological changes Biochemical changes Physiological consequences Results
Loss of chief cells Reduction in HCl in the abomasum and a rise in the pH of abomasal contents 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 contortus

Feeding habits

Impact of feeding

Biochemical changes

Physiological consequences

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

Anemia

Loss of plasma proteins 
= hypoproteinemia (hypoalbuminemia)

Edema

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

 

   

 

Parasites and Parasitic Diseases of Domestic Animals
Dr. Colin Johnstone (principal author)
Copyright 1998 University of Pennsylvania
This page was last modified on January 24, 2000