Difference between revisions of "Erysipelas - Pig"
CallumH003 (talk | contribs) m (→Control) |
|||
| (36 intermediate revisions by 3 users not shown) | |||
| Line 1: | Line 1: | ||
| − | + | {{unfinished}} | |
| − | == | + | ==Description== |
| − | An infectious disease caused by [[Erysipelothrix rhusiopathiae| | + | An infectious disease caused by [[Erysipelothrix rhusiopathiae|Erysipelothrix rhusiopathiae]]. The disease is characterised by sudden death, septicaemia, [[Joints Inflammatory - Pathology#Arthritis|arthritis]], [[Endocardiosis|endocarditis]], diamond shaped skin lesions, laminitis and abortion in pregnant sows. |
| + | Carrier pigs act as a reservoir of infection and organisms are excreted in faeces. Infection occurs via ingestion of contaminated food and water, or through skin abrasions. | ||
==Signalment== | ==Signalment== | ||
| Line 8: | Line 9: | ||
==Diagnosis== | ==Diagnosis== | ||
| − | Development of the | + | Development of the typical diamond shaped lesion on the skin is pathognomic for this disease. Erysipelas should be considered in any cases where fever and lameness occur together, or in pregnant sows struggling to farrow in combination with a fever. |
| + | Post mortem diagnosis may be needed for definitive diagnosis, in particular the, [[Liver - Anatomy & Physiology| liver]], [[Spleen - Anatomy & Physiology|spleen]], heart valves, [[The Endocrine Function of the Kidney - Anatomy & Physiology| kidney]], a long bone and synovial tissues should be submitted for bacterial examination. | ||
| + | Slender Gram-positive rods can be seen on microscopy of acute lesions and filamentous forms in chronic lesions and on smears. | ||
| + | High levels of antibiody may be found in joint fluid and so may aid diagnosis. | ||
| + | [[ELISA testing|ELISA]] and Polymerase Chain Reaction tests are also avilable which can be used directly on tissue or following culture. | ||
| − | + | ==Clinical signs== | |
| − | Clinical outcome depends on | + | |
| + | Clinical outcome depends on susceptibility of pigs and virulence of the strain. Pigs are susceptible after maternal antibody has waned (after 3 months) and before protective immunity acquired (3 years). | ||
Changes in diet, extremes of temperature and fatigue are thought to predispose to infection. | Changes in diet, extremes of temperature and fatigue are thought to predispose to infection. | ||
| − | 3 forms of disease occur: Hyperacute | + | 3 forms of disease occur: |
| + | *Hyperacute | ||
| + | *Acute | ||
| + | *Chronic | ||
| − | + | Hyperacute: | |
| + | Sudden death, more common in younger pigs. May be found dull, collapsed or pyrexic with a scarlet tinge to the skin. | ||
| − | + | Acute: | |
| − | + | Anorexia and pyrexia are the two most common clinical signs of the acute form in young pigs. Affected animals still die but normally after a day during which time they become dyspnoic. | |
| + | Older pigs tend to be pyrexic, anorexic and polydypsic. | ||
| + | Pigs show, pink/purple raised areas or extensive diamond-shaped plaques over the skin within 24-48 hours of developing clinical signs. If pregnant sows are infected at this time they may abort. | ||
| − | + | Chronic: | |
| − | The bacteria localises in joints causing destruction of the synovial membrane lining, hyperaemia, villus formation and lymphocyte and plasma cell infiltration resulting in chronic serofibrinous polyarthritis. | + | Affected animals can completely recover, lesions may resolve within a week, or become necrotic and slough. Ear tips may also be lost. |
| − | Initially joints are hot and swollen leading to stiffness, lameness, non-weight bearing on | + | The bacteria localises in joints causing destruction of the synovial membrane lining, hyperaemia, villus formation and lymphocyte and plasma cell infiltration resulting in '''chronic serofibrinous polyarthritis. |
| + | Initially joints are hot and swollen leading to stiffness, lameness, non-weight bearing on affected limbs and eventual ankylosis. | ||
| + | Discospondylitis can also occur. | ||
Additionally valvular lesions may develop in the heart causing chronic valvular [[Endocarditis| endocarditis]], vegetative thrombosis of mitral valves and asymptomatic or congestive heart failure sometimes resulting in sudden death following stress. | Additionally valvular lesions may develop in the heart causing chronic valvular [[Endocarditis| endocarditis]], vegetative thrombosis of mitral valves and asymptomatic or congestive heart failure sometimes resulting in sudden death following stress. | ||
| − | + | ==Pathology== | |
| − | + | ===Gross=== | |
| − | + | Hyperacute: | |
| − | + | No specific lesions but congestion of the carcass and change in skin colour. | |
| − | |||
| − | |||
| − | |||
| − | |||
| − | |||
| − | |||
| − | + | Acute form: | |
| − | Skin discolouration | + | Congestion of the carcass, in particular the spleen, lungs are oedematous and petechiae may be found below the kidney, peritoneum and on the heart. Lymph nodes will also be swollen and haemorrhagic. |
| + | Skin discolouration. | ||
| − | + | Chronic form: | |
| − | Necrotic skin lesions may | + | Growths on heart valves may be evident as well as changes in joint architecture. Joint capsules will be thickened in the presence of granulation tissue and in some cases erosion of articular surfaces may have progressed to ankylosis. |
| + | Necrotic skin lesions may be present. | ||
| − | + | ===Histologically=== | |
Vegetative lesions on the heart valves consist of connective and granulation tissue. | Vegetative lesions on the heart valves consist of connective and granulation tissue. | ||
| − | Synovial lesions consist of macrophages and lymphocytes | + | Synovial lesions consist of macrophages and lymphocytes. |
| + | Short gram positive rods may be seen in smears made from blood in the heart. | ||
==Treatment== | ==Treatment== | ||
| − | A 3 day course of | + | A 3 day course of Penicillin or tetracyclines is the treatment of choice and the response is normally rapid. |
Hyperimmune serum is also available however this is an expensive treatment option. | Hyperimmune serum is also available however this is an expensive treatment option. | ||
==Control== | ==Control== | ||
| − | + | Hygience is very important to control eryipelas including good sanitation and regular disinfection of pens. It is advisable to cull chronic cases which will be acting as carrier pigs infecting other animals. Additionally any pigs being treated should be isolated to reduce the spreas of disease. | |
| − | Live attenuated or inactivated | + | Live attenuated or inactivated vaccines are also available. Immunity lasts for months and is normally given to recently weaned pigs or gilts and sows prior to service. |
==Prognosis== | ==Prognosis== | ||
Varies from sudden death to recovery depending on the virulence of the strain and age and immune status of the affected pig. | Varies from sudden death to recovery depending on the virulence of the strain and age and immune status of the affected pig. | ||
| − | |||
| − | |||
| − | |||
| − | |||
| − | |||
==References== | ==References== | ||
Taylor D.J. (2006) '''Pig Diseases. 8th edition''' published by the author. | Taylor D.J. (2006) '''Pig Diseases. 8th edition''' published by the author. | ||
| − | + | [[Category:Pig]][[Category:To_Do_-_Caz]] | |
| − | |||
| − | |||
| − | [[Category: | ||
| − | |||
| − | |||
| − | |||
Revision as of 20:08, 26 July 2010
 |
This article is still under construction. |
Description
An infectious disease caused by Erysipelothrix rhusiopathiae. The disease is characterised by sudden death, septicaemia, arthritis, endocarditis, diamond shaped skin lesions, laminitis and abortion in pregnant sows. Carrier pigs act as a reservoir of infection and organisms are excreted in faeces. Infection occurs via ingestion of contaminated food and water, or through skin abrasions.
Signalment
Affects pigs of all ages but is most common in pigs kept in poor conditions and also in batches of newly bought gilts. Often occurs during hot humid weather or in particular buildings or fields.
Diagnosis
Development of the typical diamond shaped lesion on the skin is pathognomic for this disease. Erysipelas should be considered in any cases where fever and lameness occur together, or in pregnant sows struggling to farrow in combination with a fever. Post mortem diagnosis may be needed for definitive diagnosis, in particular the, liver, spleen, heart valves, kidney, a long bone and synovial tissues should be submitted for bacterial examination. Slender Gram-positive rods can be seen on microscopy of acute lesions and filamentous forms in chronic lesions and on smears. High levels of antibiody may be found in joint fluid and so may aid diagnosis. ELISA and Polymerase Chain Reaction tests are also avilable which can be used directly on tissue or following culture.
Clinical signs
Clinical outcome depends on susceptibility of pigs and virulence of the strain. Pigs are susceptible after maternal antibody has waned (after 3 months) and before protective immunity acquired (3 years). Changes in diet, extremes of temperature and fatigue are thought to predispose to infection. 3 forms of disease occur:
- Hyperacute
- Acute
- Chronic
Hyperacute: Sudden death, more common in younger pigs. May be found dull, collapsed or pyrexic with a scarlet tinge to the skin.
Acute: Anorexia and pyrexia are the two most common clinical signs of the acute form in young pigs. Affected animals still die but normally after a day during which time they become dyspnoic. Older pigs tend to be pyrexic, anorexic and polydypsic. Pigs show, pink/purple raised areas or extensive diamond-shaped plaques over the skin within 24-48 hours of developing clinical signs. If pregnant sows are infected at this time they may abort.
Chronic: Affected animals can completely recover, lesions may resolve within a week, or become necrotic and slough. Ear tips may also be lost. The bacteria localises in joints causing destruction of the synovial membrane lining, hyperaemia, villus formation and lymphocyte and plasma cell infiltration resulting in chronic serofibrinous polyarthritis. Initially joints are hot and swollen leading to stiffness, lameness, non-weight bearing on affected limbs and eventual ankylosis. Discospondylitis can also occur. Additionally valvular lesions may develop in the heart causing chronic valvular endocarditis, vegetative thrombosis of mitral valves and asymptomatic or congestive heart failure sometimes resulting in sudden death following stress.
Pathology
Gross
Hyperacute: No specific lesions but congestion of the carcass and change in skin colour.
Acute form: Congestion of the carcass, in particular the spleen, lungs are oedematous and petechiae may be found below the kidney, peritoneum and on the heart. Lymph nodes will also be swollen and haemorrhagic. Skin discolouration.
Chronic form: Growths on heart valves may be evident as well as changes in joint architecture. Joint capsules will be thickened in the presence of granulation tissue and in some cases erosion of articular surfaces may have progressed to ankylosis. Necrotic skin lesions may be present.
Histologically
Vegetative lesions on the heart valves consist of connective and granulation tissue. Synovial lesions consist of macrophages and lymphocytes. Short gram positive rods may be seen in smears made from blood in the heart.
Treatment
A 3 day course of Penicillin or tetracyclines is the treatment of choice and the response is normally rapid. Hyperimmune serum is also available however this is an expensive treatment option.
Control
Hygience is very important to control eryipelas including good sanitation and regular disinfection of pens. It is advisable to cull chronic cases which will be acting as carrier pigs infecting other animals. Additionally any pigs being treated should be isolated to reduce the spreas of disease. Live attenuated or inactivated vaccines are also available. Immunity lasts for months and is normally given to recently weaned pigs or gilts and sows prior to service.
Prognosis
Varies from sudden death to recovery depending on the virulence of the strain and age and immune status of the affected pig.
References
Taylor D.J. (2006) Pig Diseases. 8th edition published by the author.