Changes

Jump to navigation Jump to search
No change in size ,  14:50, 19 August 2010
Line 32: Line 32:     
[[Image:Fasciola  hepatica    adult.jpg|thumb|right|150px|''Fasciola hepatica'' adults from a  horse -    Castellà Veterinary Parasitology Universitat Autònoma de  Barcelona]]
 
[[Image:Fasciola  hepatica    adult.jpg|thumb|right|150px|''Fasciola hepatica'' adults from a  horse -    Castellà Veterinary Parasitology Universitat Autònoma de  Barcelona]]
In sheep, fasciolosis may present as acute, chronic, or infrequently sub-acute manifestations. Acute fasciolosis usually occurs between September and December and is caused by large numbers of immature ''[[Fasciola hepatica]]'' migrating through the liver parenchyma and causing massive damage. It arises within around two to six weeks of ingestion of metacercariae. If sheep are not exposed to at-risk pasture until later in the year, acute fasciolosis may occur as late as the following Feburary. Hepatic damage caused by migration of fluke larvae gives clinical signs including lethargy, pallor, dyspnoea and death in both young and adult animals. Handling of sheep may cause liver rupture and sudden death, and sudden death may also occur due to Black's disease (''Clostridium novyi'' type B) or bacillary haemoglobinuria (''Clostridium novyi'' type D) in unvaccinated sheep. This is a result of necrosis caused by larval migration within the liver: anaerobis conditions are created, enabling multiplication of clostridial organisms and thus toxin production.  
+
In sheep, fasciolosis may present as acute, chronic, or infrequently sub-acute manifestations. Acute fasciolosis usually occurs between September and December and is caused by large numbers of immature ''[[Fasciola hepatica]]'' migrating through the liver parenchyma and causing massive damage. It arises within around two to six weeks of ingestion of metacercariae. If sheep are not exposed to at-risk pasture until later in the year, acute fasciolosis may occur as late as the following Feburary. Hepatic damage caused by migration of fluke larvae gives clinical signs including lethargy, pallor, dyspnoea and death in both young and adult animals. Handling of sheep may cause liver rupture and sudden death, and sudden death may also occur due to Black's disease (''Clostridium novyi'' type B) or bacillary haemoglobinuria (''Clostridium novyi'' type D) in unvaccinated sheep. This is a result of necrosis caused by larval migration within the liver: anaerobic conditions are created, enabling multiplication of clostridial organisms and thus toxin production.  
    
Chronic fasciolosis in sheep is caused by adult flukes in the bile ducts and is usually seen in February and March, 4-5 months after ingestion of metacercariae. However, cases may present in early summer if snails become infected during the winter. Progressive weight loss over weeks to months results in poor body condition, and anorexia is often seen. As adult flukes feed on blood and are capable of consuming 0.5ml each per day, anaemia and pallor frequently occur in chronic fasciolosis. Initially, this regenerative anaemia is normochromic, but becomes hypochromic as iron reserves are depleted. Hypoalbuminaemia may also result from whole blood loss, and from reduced hepatic production. This gives a reduced plasma oncotic pressure, leading to ascites and/or submandibular oedema in advanced cases.
 
Chronic fasciolosis in sheep is caused by adult flukes in the bile ducts and is usually seen in February and March, 4-5 months after ingestion of metacercariae. However, cases may present in early summer if snails become infected during the winter. Progressive weight loss over weeks to months results in poor body condition, and anorexia is often seen. As adult flukes feed on blood and are capable of consuming 0.5ml each per day, anaemia and pallor frequently occur in chronic fasciolosis. Initially, this regenerative anaemia is normochromic, but becomes hypochromic as iron reserves are depleted. Hypoalbuminaemia may also result from whole blood loss, and from reduced hepatic production. This gives a reduced plasma oncotic pressure, leading to ascites and/or submandibular oedema in advanced cases.
6,502

edits

Navigation menu