Difference between revisions of "Photosensitisation"

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{{unfinished}}
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{{cow}}
  
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==Introduction==
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*'sunburn-like' lesions
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Photosensitisation is an abnormal reaction of the skin to sunlight due to the presence of a photodynamic agent in the dermis. It is
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*cattle and sheep
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primarily a condition of sheep, cattle and horses but other species may also be susceptible.
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*sharply confined to the unpigmented areas of the skin
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*occurs as a result of the effect of strong sunlight
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**due to the effect of UV light on a photodynamic agent (PDA) present in the skin, such as is '''phylloerythrin''' derived from chlorophyll
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**therefore, the disease occurs mostly in those animals consuming large quantities of grass
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**the UV light is changed to a longer wavelength which produces the necrosis of the skin
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*many unknown/poorly understood causes
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**feeding rape, kale, lucerne, alfalfa
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**mouldy hay
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**lush pasture
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**corticosteroid induced
  
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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.
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===Primary photosensitisation===
  
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==Clinical signs==
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====Causes====
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[[Image:Cow-_photosensitivity.jpg‎|right|thumb|200px|<small><center>Photosensitisation in a Friesian cow (Image sourced from Wikimedia Commons))</center></small>]]
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*normal ingestion of growing lush green plants containing PDA
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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.
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**plants containing such fluorescent pigments
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***''Hypericum perforatum'' (St John's Wort) - active principle is hypercin
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***''Lolium perenne'' (Perennial Rye Grass) - active principle is perloline
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*drugs
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**phenothiazine
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**thiazides
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**tetracyclines
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**sulphonamides
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*inherited porphyria
  
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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.
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===Secondary photosensitisation===
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*photosensitisation secondary to liver damage
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====Cause====
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*hepatogenous photosensitisation
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**chlorophyll is metabolised to '''phylloerythrin'''
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**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
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**the pigment accumulates causing photosensitisation
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*hepatotoxic plants
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**''Senecio jacobea'' (Ragwort)
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**''Lantana camara'' (Lantana)
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**''Lupinus angustifolius'' (Lupins)
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**Blue-green algae
  
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==Diagnosis==
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===Clinical Signs===
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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.
 
  
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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.
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*localised to lightly pigmented skin areas
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*clear cut demarcation of affected area
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*teats, muzzle, ears
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*skin only
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*skin and liver signs
  
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Definitive diagnosis may be obtained by liver biopsy. In the case of pyrollizidine alkaloid toxicity, histological evaluation may reveal megalocytosis, biliary hyperplasia and fibrosis.
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===Microscopically===
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*subepidermal vesicles
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**ulcerate
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**become secondarily infected
  
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==Treatment==
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===Treatment===
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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.
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*remove from sunlight
  
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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.
 
  
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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.
 
  
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==Prognosis==
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===Protosensitising Agents===
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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.
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*Phenothiazine which was used as an anthelmintic
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*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.  
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*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]].
  
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==Prevention==
 
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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.
 
  
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{{Learning
 
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|flashcards = [[Liver_Flashcards_-_Pathology|Liver Pathology Flashcards]]
 
  
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[[Sheep Medicine Q&A 10]]
 
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|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]
 
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}}
 
  
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==References==
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*'''Primary'''
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* Gupta, R. C., (2007) '''Veterinary Toxicology: basic and clinical principles''' ''Academic Press''
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**Ingestion of photodynamic substance from plants (''Hypericum perforatum'' and ''Fagopyrum sagittatum'' - buckwheat) or fungal contaminants
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* Haskell, S. R. R., (2008) '''Blackwell's five-minute veterinary consult: ruminant''' ''John Wiley & Sons''
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**Induced by drug administration - phenothiazines, tetracyclines, thiazides, sulphonamides
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* Lavoie, J. P., (2009) '''Blackwell's five-minute veterinary consult: equine''' ''John Wiley & Sons''
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*'''Abnormal porphyrin metabolism'''
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* Merck & Co (2008) '''The Merck Veterinary Manual (Eighth Edition)''' ''Merial''
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**Bovine congenital porphyria
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* Pascoe, R. R., Knottenbelt, D. C. (1999) '''Manual of Equine Dermatology''' ''Elsevier Health Sciences''
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**Bovine erythropoeitic protoporphyria
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*'''Hepatogenous'''
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**Impaired excretion of phylloerythrin (chlorophyl metabolism product) due to hepatic disease
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**[[Biliary Tract - Obstruction|Biliary obstruction]]
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**Inherited defects
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**Hepatic injury due to toxic plants or fungal contaminants, chemicals or some infectious agents
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*Grossly:
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**In areas lacking hair or pigment
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**Erythema, oedema -> blisters, exudation, necrosis, sloughing or keratitis
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*Microscopically:
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**Subepidermal vesicles
 +
**Ulceration
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**Secondary infection
  
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{{review}}
 
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==Webinars==
 
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<rss max="10" highlight="none">https://www.thewebinarvet.com/emergency-and-critical-care/webinars/feed</rss>
 
  
  
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[[Category:Teeth_-_Developmental_Pathology]]
 
[[Category:Liver_-_General_Pathology]]
 
[[Category:Liver_-_General_Pathology]]
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[[Category:Expert Review]]
 
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[[Category:Dermatological Diseases - Cattle]]
 
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[[Category:Dermatological Diseases - Sheep]]
 
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[[Category:Dermatological Diseases - Horse]]
 
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[[Category:Integumentary System - Developmental Pathology]]
 
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[[Category:Integumentary System - Sunlight Damage]]
 

Revision as of 12:19, 9 June 2010


 This article is still under construction.


Category:WikiClinical BovineCow
  • 'sunburn-like' lesions
  • cattle and sheep
  • sharply confined to the unpigmented areas of the skin
  • occurs as a result of the effect of strong sunlight
    • due to the effect of UV light on a photodynamic agent (PDA) present in the skin, such as is phylloerythrin derived from chlorophyll
    • 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

Primary photosensitisation

Causes

  • normal ingestion of growing lush green plants containing PDA
    • plants containing such fluorescent pigments
      • Hypericum perforatum (St John's Wort) - active principle is hypercin
      • Lolium perenne (Perennial Rye Grass) - active principle is perloline
  • drugs
    • phenothiazine
    • thiazides
    • tetracyclines
    • sulphonamides
  • inherited porphyria

Secondary photosensitisation

  • photosensitisation secondary to liver damage

Cause

  • 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

Clinical Signs

  • localised to lightly pigmented skin areas
  • clear cut demarcation of affected area
  • teats, muzzle, ears
  • skin only
  • skin and liver signs

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.



  • Primary
    • Ingestion of photodynamic substance from plants (Hypericum perforatum and Fagopyrum sagittatum - buckwheat) or fungal contaminants
    • Induced by drug administration - phenothiazines, tetracyclines, thiazides, sulphonamides
  • Abnormal porphyrin metabolism
    • Bovine congenital porphyria
    • Bovine erythropoeitic protoporphyria
  • Hepatogenous
    • Impaired excretion of phylloerythrin (chlorophyl metabolism product) due to hepatic disease
    • Biliary obstruction
    • Inherited defects
    • Hepatic injury due to toxic plants or fungal contaminants, chemicals or some infectious agents
  • Grossly:
    • In areas lacking hair or pigment
    • Erythema, oedema -> blisters, exudation, necrosis, sloughing or keratitis
  • Microscopically:
    • Subepidermal vesicles
    • Ulceration
    • Secondary infection
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