Difference between revisions of "Lawsonia intracellularis"

Revision as of 22:36, 25 August 2008

BACK TO INFECTIOUS AGENTS AND PARASITES BACK TO BACTERIA

Overview

Causes porcine proliferative enteropathy
Grows intracellularly in pircine enterocytes
Excreted in small amounts in faeces of infected pigs

Characteristics

Slender, curved, Gram negative rod
Microaerophilic
Obligate intracellular bacterium
Requires enterocyte tissue culture for growth

Pathogenesis and pathogenicity

Affinity for porcine enterocytes
Causes proliferation of enterocytes
Adenomatous and inflammatory lesions develop in the terminal ilium, caecum and colon
Synergistic relationship between L. intracellularis and intestinal flora including E. coli, Clostridium species and Bacteroides species
Intestinal organisms may produce correct oxygen tension and conditions for colonisation of L. intracellularis
Infection can only take place in presence of intestinal flora

Clinical disease

Proliferative enteropathy occurs in weaned pigs, 6-12 weeks old
Chronic intermittent diarrhoea with reduced growth or acute haemorrhagic enteropathy
Sudden heath in severe infections
Recovery from mild form in most animals without treatment
Post mortem lesions include thickened wall, mucosal necrosis with clotted blood in the lumen of the ilium, caecum and colon
Enlarged mesenteric lymph nodes

Diagnosis

Clinical signs and pathology give a presumptive diagnosis
Organisms demonstrated in faeces or ileal mucosa by immunofluorescence or PCR
Silver impregnation stains or immunostaining or lesions
Culture in enterocyte cell lines

Treatment and control

Antibiotics such as tylosin, tiamulin used prophylactically or therapeutically in feed/water
Zinc bacitracin in feed
Thorough cleaning and disinfection of premises

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-{{OpenPagesTop}}
+<big><center>[[Infectious agents and parasites|'''BACK TO INFECTIOUS AGENTS AND PARASITES''']]</center></big>
-Also known as: '''''Porcine Adenomatosis Complex — Porcine Intestinal Adenomatosis — Porcine Proliferative Enteropathy '''''
+<big><center>[[Bacteria|'''BACK TO BACTERIA''']]</center></big>
-== Introduction  ==
-[[Image:porcine intestinal adenomatosis campylobacter.jpg|thumb|right|150px|Campylobacter mucosalis in intracellular porcine intestinal adenomatosis (Courtesy of Bristol BioMed Image Archive)]]
-Porcine adenomatosis complex is a disease caused by the obligatory intracellular organism '''''Lawsonia intracellularis''''', a spirochete that does not grow well in the laboratory except in enterocyte tissue culture. It is a slender, curved, microaerophilic, gram negative rod.
-It is only seen in pigs, worldwide, including the United Kingdom. It is characterised by proliferative changes in the epithelium of the small and large intestinal mucosa and is excreted in small amounts in faeces of infected pigs.
+===Overview===
-==Signalment==
+*Causes [[Intestines Proliferative Enteritis - Pathology#Porcine Adenomatosis Complex|porcine proliferative enteropathy]]
+*Grows intracellularly in pircine enterocytes
+*Excreted in small amounts in faeces of infected pigs
-It is a disease that can affect pigs of all ages, but most severe clinical signs tend to appear in weanlings and growers. The infection is transmitted orally.
-==Pathogenesis==
+===Characteristics===
-The bacterium has an affinity for porcine enterocytes. There may be synergistic relationship between ''L. intracellularis'' and intestinal flora including [[Escherichia coli|''E. coli'']], [[:Category:Clostridium species|''Clostridium'' species]] and ''[[Bacteroides]]'' species. The intestinal organisms may produce correct oxygen tension and conditions for colonisation by ''L. intracellularis''. Infection can only take place in presence of intestinal flora.
+*Slender, curved, Gram negative rod
+*Microaerophilic
+*Obligate intracellular bacterium
+*Requires enterocyte tissue culture for growth
-The disease appears in four different presentations:
-'''Intestinal adenomatosis - '''The basic hyperplastic and metaplastic changes are seen in the epithelium, which causes chronic weight loss and diarrhoea.
+===Pathogenesis and pathogenicity===
-'''Necrotic enteritis''' - Predominately affects the colon and terminal ileum and parts of the hyperplastic mucosa develop erosions and ulcerations which then become colonised by ''Fusiformis'' baceria.
+*Affinity for porcine enterocytes
+*Causes proliferation of enterocytes
+*Adenomatous and inflammatory lesions develop in the terminal ilium, caecum and colon
+*Synergistic relationship between ''L. intracellularis'' and intestinal flora including ''E. coli'', ''Clostridium'' species and ''Bacteroides'' species
+*Intestinal organisms may produce correct oxygen tension and conditions for colonisation of ''L. intracellularis''
+*Infection can only take place in presence of intestinal flora
-'''Terminal ileitis - '''Characterised by marked hypertrophic thickening of the muscular portion of the wall of the terminal ileum and there is associated thickening of the mucosa due to hypertrophy and secondary granulomatous inflammation, which is caused by a degree of obstruction to the passage of ingesta along the bowel caused by the mucosal hypertrophy. Its appearance is very similar to [[Johne's Disease|Johnes disease]] with lots of mononuclear cells and a chronic granulomatous type of inflammation.
-'''Proliferative haemorrhagic syndrome - '''The bowel shows proliferation but with ulceration and copious haemorrhage into the bowel lumen. Animals are often found dead. The pathogenesis is unclear but may involve a type of hypersensitivity reaction or secondary infection of some type.
+===Clinical disease===
-== Clinical Signs  ==
+*Proliferative enteropathy occurs in weaned pigs, 6-12 weeks old
+*Chronic intermittent diarrhoea with reduced growth or acute haemorrhagic enteropathy
+*Sudden heath in severe infections
+*Recovery from mild form in most animals without treatment
+*Post mortem lesions include thickened wall, mucosal necrosis with clotted blood in the lumen of the ilium, caecum and colon
+*Enlarged mesenteric lymph nodes
-Clinical signs are variable and can range from anything from poor weight gain to diarrhoea, weight loss, cachexia and death and appears usually in weaned pigs from age 3-4 weeks to adulthood.
-It is seen often as a problem in closed, low infection herds and can lead to a decrease in production of up to 8%. It is not seen in pigs with lots of other pathogens in guts.
+===Diagnosis===
-== Diagnosis  ==
+*Clinical signs and pathology give a presumptive diagnosis
+*Organisms demonstrated in faeces or ileal mucosa by immunofluorescence or PCR
+*Silver impregnation stains or immunostaining or lesions
+*Culture in enterocyte cell lines
-Clinical signs of a failure to thrive and history of a closed herd plus signalment of pigs is indicative. On post mortem examination, the terminal [[Small Intestine Overview - Anatomy & Physiology|small intestine]] and [[Colon - Anatomy & Physiology|colon]] are affected by proliferation of the mucosal epithelium. Signs will include thickened mucosal epithelium, polypoid-like nodules several millimetres in diameter. There may also be undifferentiated epithelium replacing goblet cells. Its appearance is almost neoplastic.
-Histologically it will appear similar to a virus induced proliferation. Organisms seen in the apical part of epithelial cells lining glands of terminal [[Ileum - Anatomy & Physiology|ileum]], [[Colon - Anatomy & Physiology|colon]] and [[Caecum - Anatomy & Physiology|caecum]].
+===Treatment and control===
-The organism from faeces or ileal mucosa can be stained by silver staining by the use of antibody in immunofluorescence or PCR or cultured in enterocyte cell lines.
+*Antibiotics such as tylosin, tiamulin used prophylactically or therapeutically in feed/water
+*Zinc bacitracin in feed
-== Treatment and Control  ==
+*Thorough cleaning and disinfection of premises
-Individually affected animals may be treated with tetracyclines parenterally. These animals must be isolated. In affected groups the same treatment can be given via the drinking water.
-Any new genetic material into the herd should be by A.I. or embryo transfer only so as to reduce risk of introduction of the disease into the herd.
-Vaccination as a control measure is now readily available and will reduce clinical signs of the disease and improve performance. Vaccine is given orally from 3 weeks of age and provides protection for up to 17 weeks. This is excellent for finishing stock, but boosters will need to be given for stock kept on as breeding herd if this is farm protocol.
-== References  ==
-Cowart, R.P. and Casteel, S.W. (2001) '''An Outline of Swine diseases: a handbook '''''Wiley-Blackwell ''
-Jackson, G.G. and Cockcroft, P.D. (2007) '''Handbook of Pig Medicine '''''Saunders Elsevier ''
-Straw, B.E. and Taylor, D.J. (2006)''' Disease of Swine '''''Wiley-Blackwell ''
-Taylor, D.J. (2006) '''Pig Diseases '''(Eighth edition) ''St Edmunsdbury Press''
-{{review}}
-{{OpenPages}}
-[[Category:Enteritis,_Proliferative]] [[Category:Intestinal_Diseases_-_Pig]] [[Category:Enteritis,_Bacterial]] [[Category:Expert_Review - Farm Animal]]
-[[Category:Spirochaetaceae]][[Category:Gram_negative_bacteria]][[Category:Rods]][[Category:Pig Bacteria]]

Difference between revisions of "Lawsonia intracellularis"

Revision as of 22:36, 25 August 2008

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Overview

Characteristics

Pathogenesis and pathogenicity

Clinical disease

Diagnosis

Treatment and control

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