Photosensitization in Cows (Bovis) | Vetlexicon
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Photosensitization

ISSN 2398-2993


Synonym(s): Allergy Udder Sun burn sunburn Allergic Toxin Facial eczema Spring eczema

Introduction

  • Cause: photodynamic agent causes damage to cell membranes after exposure to UltraViolet (UV) light. 
    • There are four different types of photosensitization, each with different underlying factors:
      • Type I or Primary.
      • Type II or Aberrant pigment metabolism.
      • Type III or Secondary or Hepatogenous.
      • Type IV or Idiopathic.
  • Signs: dermatological signs of erythema, edema and skin sloughing are mainly seen on non-pigmented skin or hairless areas such as the nose and udder. This condition is very painful and irritating.
  • Diagnosis:
    • Clinical signs and history of exposure.
    • Biochemical indicators. In hepatogenous cases increased liver enzymes, such as GGT, GLDH and AST will be seen to varying degrees
  • Treatment:
    • Anti-inflammatory, such as corticosteroid or non-steroidal anti-inflammatory.
    • Bringing affected animals indoors.
    • Supportive care of skin lesions.
    • Antihistamines may be used, but these are not-licenced in many countries.
  • Prognosis: dependant on underlying cause, but generally good for primary photosensitization and poor for hepatogenous and aberrant pigment metabolism.

Geographic incidence

  • All four types can occur worldwide.
  • Facial eczema  and spring eczema , caused by hepatogenous photosensitization, are recognized in Australia and New Zealand.

Age predisposition

  • Type I and IV tend to be seen in animals over a year old.
  • Type II generally presents in the young animal.
  • Type III, such as facial and spring eczema, are frequently seen from weaned calves up to mature animals.

Breed/Species predisposition

  • All breeds are equally susceptible to Type I, Type III and Type IV.
  • Type II is an inherited condition and is most commonly seen in the Limousin Limousin breed, but has also been reported in the Blonde D'Acquataine.

Cost considerations

  • Loss of production.
  • Loss of affected animal, in cases that fail to respond to treatment, especially Type II and Type III.
  • Labor and increased feed costs, due to the need to bring the affected animals indoors.
  • Cost of treatment and supportive care.

Special risks

  • Exposure to sunlight is necessary to activate the photodynamic agents.

Pathogenesis

Etiology

  • Photosensitization occurs when a chemical/photodynamic agent affects the animal.
  • The photodynamic agent may occur due to a defect in the metabolism of red blood cells, may be ingested from plants or an unknown source, or may be secondary to liver damage.
  • Photodynamic agents makes the skin more susceptible to UV light.
  • The photodynamic agents release free radicals and result in damage to the cell membranes.
    • Type I:
      • The photodynamic agent is ingested, injected or absorbed through the skin.
      • Implicated plants include St. John's wort , Buckwheat, Umbelliferae, Rutaceae, Bishop's weed, species of clover , species of alfalfa, Erodium, Polygonum, Brassica Brassica spp.
      • Other implicated substances include: coal tar derivatives, tetracyclines Chlortetracyline Oxytetracycline and some sulphonamides and phentothiazine anthelmintics.
    • Type II:
      • Photosensitizing porphyrin agents are endogenous pigments that arise from inherited or acquired defective enzymes involved in the synthesis of heme.
    • Type III :
      • Phylloerythrin (a porphyrin) accumulates in the plasma due to impaired heptobiliary excretion.
      • Phylloerythrin is derived from the breakdown of chlorophyll by micoorganisms in the GI tract.
      • Phylloerythrin is normally absorbed into the circulation and then effectively excreted by the liver.
      • Failure of excretion results in a build-up in the circulation and when this reaches the skin it can initiate a phototoxic reaction.
      • Phylloerythrin is incriminated in the following conditions: bile duct occlusion, lupinous, facial eczema, numerous plant poisoning (eg Bog asphodol, several Panicum spp etc) and in animals with liver damage associated with various poisonings, such as pyrrolizidine alkaloid, Senecio spp, red and alsike clover, horse and rabbit brush and chronic fascioliasis Fasciolosis.
    • Type IV:
      • Pathogenesis unknown or the photodynamic agent cannot be identified.
      • Seen in animals exposed to water damaged alfalfa hay, mouldy straw and foxtail.
      • Other plants linked with photosensitization include buttercups , winter wheat and alfalfa.

Timecourse

  • Depends on underlying cause but when the photodynamic agents are present in the circulation and the animal is exposed to UV light skin lesions develop rapidly.
  • Time interval between exposure to photodynamic agent in plants can vary from few hours to ten days and depends on type of agent, dose of agent and exposure to sunlight.

Epidemiology

  • Type I depends on the ingestion, injection or absorption of photodynamic agents.
  • Type II inherited or acquired disorder of the metabolism of heme in the body.
  • Type III follows the build up of photodynamic agents in the circulation as a result of liver damage.
  • Type IV follows the build up of photodynamic agents in the circulation but the agent can not be identified.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed Papers

  • Recent references from PubMed and VetMedResource.
  • Schelcher F, Delverdier M, Bezille P, Cabanie P & Espinasse J (1991) Observation on bovine congenital erythrocytic protoporphyria in the blonde d’Aquitaine breed. Vet Rec 129, 403–407 PubMed.

Other sources of information

  • Barrington G M. Overview of Photosensitisation: chapter of Integumentary System. In: MSD Manaul Veterinary Medicine.