Difference between revisions of "Photosensitisation"

Revision as of 13:11, 10 August 2010

Description

Photosensitisation is a condition of the dermis caused by a reaction induced by photodynamic agents (PDAs) exposed to UV light in the skin of animals that have eaten certain plants. Photosenstisation is primarily a condition of sheep, cattle and horses but other species may also be susceptible. Photosensitisation can be divided into two categories; primary and secondary photosensitisation). Primary photosensitisation occurs due to the normal ingestion of growing lush green plants containing PDAs. Secondary (hepatogenous) photosensitisation occurs as a result of liver or bile duct damagem, leading to accumulation of phylloerythrin in the blood, body tissues and skin due to insufficient conjugation and excretion by the liver.

Clinical signs

The condition is characterised by clearly demarcated 'sunburn-like' lesions that are confined to unpigmented or hairless areas of the skin. The nose, lips, ears, muzzle and udder are commonly affected areas. In the acute stages, the affected area(s) becomes erythematous and oedematous with exudation and crust formation. Animals may be pruritic or painful.

- therefore, the disease occurs mostly in those animals consuming large quantities of grass
- the UV light is changed to a longer wavelength which produces the necrosis of the skin
many unknown/poorly understood causes
- feeding rape, kale, lucerne, alfalfa
- mouldy hay
- lush pasture
- corticosteroid induced

hepatogenous photosensitisation
- chlorophyll is metabolised to phylloerythrin
- when the liver or bile ducts are malfunctioning (eg hepatitis or bile duct obstruction) due to severe toxic damage, phylloerythrin escapes into the circulation and settles in the tissues including the skin
- the pigment accumulates causing photosensitisation
hepatotoxic plants
- Senecio jacobea (Ragwort)
- Lantana camara (Lantana)
- Lupinus angustifolius (Lupins)
- Blue-green algae

Microscopically

subepidermal vesicles
- ulcerate
- become secondarily infected

Treatment

remove from sunlight

Protosensitising Agents

Phenothiazine which was used as an anthelmintic
Tetracycline - if one injects bitches with tetracycline when pregnant, puppies are born with brown teeth, which fluoresce under UV light.
Haemosiderin may also produce pinky / brown colour to teeth usually due to damage and haemorrhage into tooth.

@@ Line 1: / Line 1: @@
+{{unfinished}}
-==Introduction==
-Photosensitisation is an abnormal reaction of the skin to sunlight due to the presence of a photodynamic agent in the dermis. It is
-primarily a condition of sheep, cattle and horses but other species may also be susceptible.
-The condition can be divided into two categories; primary and secondary. '''Primary photosensitisation''' occurs due to the ingestion of lush green plants containing photodynamic agents, such as St John's Wort or clover. '''Secondary (hepatogenous) photosensitisation''' is the most commmon type of photosensitivity seen in animals and occurs due to liver or bile duct damage, most often as a result of ingestion of hepatotoxic plants such as ''Senecio jacobea'' ([[Ragwort Toxicity|ragwort]]), ''Lantana camara'' (Lantana), ''Lupinus angustifolius'' (Lupins) and [[Blue-Green Algae Toxicity|Blue-green algae]]. The normal conjugation and excretion of phylloerythrin (a breakdown product of chlorophyll) is prevented leading to its accumulation in the blood and body tissues. In the skin this leads to the absorption and release of UV light, resulting in a phototoxic reaction.
+==Description==
+Photosensitisation is a condition of the dermis caused by a reaction induced by photodynamic agents (PDAs) exposed to UV light in the skin of animals that have eaten certain plants. Photosenstisation is primarily a condition of sheep, cattle and horses but other species may also be susceptible.
+Photosensitisation can be divided into two categories; primary and secondary photosensitisation). Primary photosensitisation occurs due to the normal ingestion of growing lush green plants containing PDAs. Secondary (hepatogenous) photosensitisation occurs as a result of liver or bile duct damagem, leading to accumulation of phylloerythrin in the blood, body tissues and skin due to insufficient conjugation and excretion by the liver.
 ==Clinical signs==
-[[Image:Cow-_photosensitivity.jpg‎|right|thumb|200px|<small><center>Photosensitisation in a Friesian cow (Image sourced from Wikimedia Commons))</center></small>]]
+The condition is characterised by clearly demarcated 'sunburn-like' lesions that are confined to unpigmented or hairless areas of the skin. The nose, lips, ears, muzzle and udder are commonly affected areas. In the acute stages, the affected area(s) becomes erythematous and oedematous with exudation and crust formation. Animals may be pruritic or painful.
-The condition is characterised by clearly demarcated 'sunburn-like' lesions that are confined to unpigmented or hairless areas of the skin. The nose, lips, ears, muzzle and udder are commonly affected areas. In the acute stages, the affected area(s) becomes erythematous and oedematous with exudation and crust formation. Animals may be pruritic or painful. Other clinical signs may include swollen lips or muzzle, tachypnoea, tachycardia, diarrhoea and salivation.
-If the photosensitisation is secondary (hepatogenous), [[icterus]] may be present. Other signs may include those consistent with [[Hepatic Encephalopathy|hepatic encephalopathy]] such as head-pressing, circling, and behavioural changes.
-==Diagnosis==
-The history and clinical signs of affected animals are important in order to differentiate whether the condition is primary or secondary. In the case of primary photosensitisation there is often a history of exposure to plants containing photodynamic agents. Alternatively, there may be a history of administration of drugs such as phenothiazines, sulphonamides or tetracyclines or exposure to mycotoxins such as blue-green algae. Signs of liver disease are usually absent.
-In animals affected by secondary photosensitisation the classic skin lesions of the condition are often generalised rather than localised, and are accompanied by the signs of liver disease listed above. Serum biochemistry often reveals increased liver enzymes (ALP, GGT, SDH and ALT) but bilirubin and bile acid concentrations are usually normal. Ultrasonography may provide additional diagnostic information.
+**therefore, the disease occurs mostly in those animals consuming large quantities of grass
+**the UV light is changed to a longer wavelength which produces the necrosis of the skin
+*many unknown/poorly understood causes
+**feeding rape, kale, lucerne, alfalfa
+**mouldy hay
+**lush pasture
+**corticosteroid induced
-Definitive diagnosis may be obtained by liver biopsy. In the case of pyrollizidine alkaloid toxicity, histological evaluation may reveal megalocytosis, biliary hyperplasia and fibrosis.
-==Treatment==
-Affected animals should be removed from pasture suspected to contain the photodynamic agent. Any drugs or medications currently received by the animal should be stopped. Affected animals should only be allowed access to grazing at night.
-Anti-inflammatory drugs such as flunixin meglumine and topical steroid creams may be useful to decrease the severity of cutaneous lesions in the acute stage of the disease. Secondary bacterial infections of cutaneous lesions are common and should be treated with antimicrobials and correct wound management. Lesions generally heal well, and surgical debridement is reserved for only the most severely necrotic lesions.
-If the animal is affected by secondary photosensitisation, supportive treatment should be provided. A low-protein, high-energy diet rich in branched-chain amino acids such as beet pulp is recommended. Intravenous fluid therapy with 5% dextrose may be necessary in hypoglycaemic patients with signs of hepatic encephalopathy.
-==Prognosis==
-In general the prognosis is favourable for primary photosensitisation. Cutaneous lesions usually resolve within 48 hours but occasionally may persist for up to six months. The prognosis is poor for secondary photosensitisation due to hepatic involvement. Severely affected animals with liver failure carry a grave prognosis and are not usually treatable.
-==Prevention==
+*hepatogenous photosensitisation
-Animals should not be grazed on pasture known to contain photodynamic agents and contaminated hay and grain should also be avoided. In the case of farm livestock, less valuable or older animals may be used to 'pre-graze' affected pastures before other animals are introduced.
+**chlorophyll is metabolised to '''phylloerythrin'''
+**when the liver or bile ducts are malfunctioning (eg hepatitis or bile duct obstruction) due to severe toxic damage, '''phylloerythrin''' escapes into the circulation and settles in the tissues including the skin
+**the pigment accumulates causing photosensitisation
+*hepatotoxic plants
+**''Senecio jacobea'' (Ragwort)
+**''Lantana camara'' (Lantana)
+**''Lupinus angustifolius'' (Lupins)
+**Blue-green algae
+===Microscopically===
+*subepidermal vesicles
+**ulcerate
+**become secondarily infected
+===Treatment===
+*remove from sunlight
+===Protosensitising Agents===
+*Phenothiazine which was used as an anthelmintic
+*Tetracycline - if one injects bitches with tetracycline when pregnant, puppies are born with brown [[Oral Cavity - Teeth & Gingiva - Anatomy & Physiology|teeth]], which fluoresce under UV light.
+*Haemosiderin may also produce pinky / brown colour to [[Oral Cavity - Teeth & Gingiva - Anatomy & Physiology|teeth]] usually due to damage and haemorrhage into [[Oral Cavity - Teeth & Gingiva - Anatomy & Physiology|tooth]].
-{{Learning
-|flashcards = [[Liver_Flashcards_-_Pathology|Liver Pathology Flashcards]]
-[[Sheep Medicine Q&A 10]]
-|literature search = [http://www.cabdirect.org/search.html?it=any&q2=photosenzitivity&q1=photosensitivity&calendarInput=yyyy-mm-dd&q4=photosensitization&q3=photosensitisation&occuring1=title&show=all&rowId=1&rowId=2&rowId=3&rowId=4&options1=AND&options2=OR&occuring4=title&options3=OR&options4=OR&occuring3=title&occuring2=title&publishedend=yyyy&la=any&publishedstart=yyyy&fq=sc%3A%22ve%22&y=11&x=55 Photosensitisation publications]
-}}
-==References==
-* Gupta, R. C., (2007) '''Veterinary Toxicology: basic and clinical principles''' ''Academic Press''
-* Haskell, S. R. R., (2008) '''Blackwell's five-minute veterinary consult: ruminant''' ''John Wiley & Sons''
-* Lavoie, J. P., (2009) '''Blackwell's five-minute veterinary consult: equine''' ''John Wiley & Sons''
-* Merck & Co (2008) '''The Merck Veterinary Manual (Eighth Edition)''' ''Merial''
-* Pascoe, R. R., Knottenbelt, D. C. (1999) '''Manual of Equine Dermatology''' ''Elsevier Health Sciences''
-{{review}}
-==Webinars==
-<rss max="10" highlight="none">https://www.thewebinarvet.com/emergency-and-critical-care/webinars/feed</rss>
 [[Category:Liver_-_General_Pathology]]
-[[Category:Expert Review]]
+[[Category:To_Do_-_SophieIgnarski]]
-[[Category:Dermatological Diseases - Cattle]]
-[[Category:Dermatological Diseases - Sheep]]
-[[Category:Dermatological Diseases - Horse]]
-[[Category:Integumentary System - Developmental Pathology]]
-[[Category:Integumentary System - Sunlight Damage]]