Difference between revisions of "Ascaris suum"
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====Indentification==== | ====Indentification==== | ||
− | ''Ascaris suum'' is a large roundworm of pigs, each worm can grow up to 40cm long. | + | ''Ascaris suum'' is a large roundworm of pigs, each worm can grow up to 40cm long. As with all nematodes the females are considerably larger than the males. |
==== Life-Cycle ==== | ==== Life-Cycle ==== | ||
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The larval stages are migratory, moving through several organ systems before becoming adults. This is the stage of the parasite that is mainly responsible for the clinical signs of ''A. suum'' infection. The larvae hatches from the egg at the L2 stage, from here is migrates from the small intesting to the liver via the hepatic portal vein. Whilst migrating through the liver the larvae create heamorrhagic tracts, these are later repaired with fibrous tissue causing the appearance of '''milk spots'''. From the liver the larvae move to the heart and lungs where they cause the major clinical signs of ''A. suum'' infection. In the heart a high worm burden will seriously reduce the cardiac output and may also cause blockage which can be fatal. The presence of larvae in lungs can lead to diffuse [[Lungs Inflammatory - Pathology#Interstitial pneumonia|interstitial pneumonia]] with haemorrhage, [[Lungs Ventilation - Pathology#Atelectasis (Collapse)|atelectasis]], [[Lungs Circulatory - Pathology#Pulmonary oedema|interlobular oedema]] and [[Lungs Ventilation - Pathology#Emphysema|emphysema]]. The larvae in the lungs will move up towards the treachea which will stimulate the coughing reflex and cause them to be coughed up into the pigs mouth to be reswallowed as adults into the gastrointestinal system.<br/> | The larval stages are migratory, moving through several organ systems before becoming adults. This is the stage of the parasite that is mainly responsible for the clinical signs of ''A. suum'' infection. The larvae hatches from the egg at the L2 stage, from here is migrates from the small intesting to the liver via the hepatic portal vein. Whilst migrating through the liver the larvae create heamorrhagic tracts, these are later repaired with fibrous tissue causing the appearance of '''milk spots'''. From the liver the larvae move to the heart and lungs where they cause the major clinical signs of ''A. suum'' infection. In the heart a high worm burden will seriously reduce the cardiac output and may also cause blockage which can be fatal. The presence of larvae in lungs can lead to diffuse [[Lungs Inflammatory - Pathology#Interstitial pneumonia|interstitial pneumonia]] with haemorrhage, [[Lungs Ventilation - Pathology#Atelectasis (Collapse)|atelectasis]], [[Lungs Circulatory - Pathology#Pulmonary oedema|interlobular oedema]] and [[Lungs Ventilation - Pathology#Emphysema|emphysema]]. The larvae in the lungs will move up towards the treachea which will stimulate the coughing reflex and cause them to be coughed up into the pigs mouth to be reswallowed as adults into the gastrointestinal system.<br/> | ||
'''Adults'''<br/> | '''Adults'''<br/> | ||
− | Adult worms reproduce in the smill intestine of pigs. | + | Adult worms reproduce in the smill intestine of pigs. The females are able to produce up to 200,000 eggs per day for a period of 9 months. |
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+ | ==== Epidemiology ==== | ||
+ | ''A. suum'' is seen globally, however in temperate regions infection normally occurs in the summer months due to the warmer temperatures. Young piglets up to about 6 months old are most susceptible although they begin to develop immunity at about 4 months. Sows carrying adult worms will contaminate the farrowing house rapidly, as female worms can produce 200,000 eggs per day, causing a high incidence of infection in the litter. The highly resistant eggs can survive in the environment for up to 4 years with suitable conditions, this makes control very difficult especially in free range systems. | ||
==== Pathogenesis ==== | ==== Pathogenesis ==== | ||
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*These 'carrier sows' are epidemiologically important as they contaminate the farrowing house with eggs, thereby providing a source of infection for the susceptible piglets. | *These 'carrier sows' are epidemiologically important as they contaminate the farrowing house with eggs, thereby providing a source of infection for the susceptible piglets. | ||
− | === | + | ===In Cows=== |
− | + | Calves housed where infected pigs had previously been housed are susceptible to ''A. suum'' infection which can lead to the development of sever pneumonia. | |
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Revision as of 09:59, 7 July 2010
This article is still under construction. |
Ascaris suum is a member of the Ascarididae family and is the major cause of ascariasis in pigs. Its life cycle, like all ascarids, is not typical of nematodes as the infectious stage is within the egg. Due to the migratory life cycle of the larval stages this parasite can be the cause of post-hepatic jaundice and pneumonia. The nematode may also be a reservoir of Swine influenza. The major detremental effects of A. suum is in the economic loss due to the damage to liver tissue, white spot, and the decreased growth rate of the pigs. Up to 7% of pig liver in the UK is trimmed or condemned at slaughter due to the presence of white spot due to A. suum infection.
Indentification
Ascaris suum is a large roundworm of pigs, each worm can grow up to 40cm long. As with all nematodes the females are considerably larger than the males.
Life-Cycle
As with most ascarid species the larvae of Ascaris suum have a migratory life cycle moving through several body organs before becoming mature adults in the small intestine of the pig.
Eggs
Eggs are shed in the feaces of the host and have a thick proteinacious coat that allows them to exist on pasture for extended periods of time, up to 4 years. The proteinacious coat allows this long survival on pasture and also makes the eggs extremely difficult to destroy with common disinfectants.
Larvae
The larval stages are migratory, moving through several organ systems before becoming adults. This is the stage of the parasite that is mainly responsible for the clinical signs of A. suum infection. The larvae hatches from the egg at the L2 stage, from here is migrates from the small intesting to the liver via the hepatic portal vein. Whilst migrating through the liver the larvae create heamorrhagic tracts, these are later repaired with fibrous tissue causing the appearance of milk spots. From the liver the larvae move to the heart and lungs where they cause the major clinical signs of A. suum infection. In the heart a high worm burden will seriously reduce the cardiac output and may also cause blockage which can be fatal. The presence of larvae in lungs can lead to diffuse interstitial pneumonia with haemorrhage, atelectasis, interlobular oedema and emphysema. The larvae in the lungs will move up towards the treachea which will stimulate the coughing reflex and cause them to be coughed up into the pigs mouth to be reswallowed as adults into the gastrointestinal system.
Adults
Adult worms reproduce in the smill intestine of pigs. The females are able to produce up to 200,000 eggs per day for a period of 9 months.
Epidemiology
A. suum is seen globally, however in temperate regions infection normally occurs in the summer months due to the warmer temperatures. Young piglets up to about 6 months old are most susceptible although they begin to develop immunity at about 4 months. Sows carrying adult worms will contaminate the farrowing house rapidly, as female worms can produce 200,000 eggs per day, causing a high incidence of infection in the litter. The highly resistant eggs can survive in the environment for up to 4 years with suitable conditions, this makes control very difficult especially in free range systems.
Pathogenesis
- Large numbers of migrating ascarid larvae can damage the lungs causing respiratory distress and exacerbating other pulmonary infections, as well as providing a portal of entry for pyogenic bacteria.
- Even small numbers of migrating larvae can lead to fibroplastic responses in the liver (chronic interstitial hepatitis - the 'milk-spot' lesion).
- Heavy burdens of adult worms retard growth and may even obstruct intestine and bile duct.
- The 'milk-spot' lestion is the biggest economic loss in the UK attributable to Ascaris - approximately 7% of pig livers are trimmed or condemned at the bacon factory.
Immunity and Milk-Spot
- The relationship is complex as several immune mechanisms are involved:
- initially L4 larvae are killed as they return to the intestine having completed their hepatotracheal migration.
- later, L2 are stopped before they reach the liver.
- Consequently:
- milk-spot can occur in immune baconers if larvae are not killed until after they have passed through the liver.
- milk-spot is less often seen in sows as larvae are killed before they reach the liver in highly immune pigs.
Control of Milk-Spot
- Milk-spot results from ingestion of Ascaris eggs, therefore, milk-spot can only be prevented by decontaminating the environment.
- Ascaris eggs can survive in pig pens for weeks, months or years (depending on the level of hygiene), therefore pigs will still be exposed to eggs after anthelmintic treatment (unless moved to a clean environment).
- Thus, anthelmintic treatments do not 'cure' this condition immediately - a longer term strategy is needed to control this problem.
Immunity
- Pigs do develop immunity, but it takes several months for this to become strongly protective.
- Even so, a small proportion of adults harbour small adult worm burdens.
- These 'carrier sows' are epidemiologically important as they contaminate the farrowing house with eggs, thereby providing a source of infection for the susceptible piglets.
In Cows
Calves housed where infected pigs had previously been housed are susceptible to A. suum infection which can lead to the development of sever pneumonia.