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Digital dermatitis

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Introduction

  • Cause: polymicrobial, with treponemes being the major type of pathogens.
  • Signs: lameness and lesions.
  • Diagnosis: history and clinical signs.
  • Treatment: topical antibacterial treatment (tetracycline or thiamphenicol sprays currently licensed in the UK). Chelated copper gels (Hoofit, Intracare).
  • Prevention: regular disinfectant foot bathing, Antibiotics are needed for treatment of heavy herd infections. Improve foot hygiene.
  • Prognosis: control is the main objective, eradication is unlikely.
  • See also Understanding digital dermatitis video. 
Print off the farmer factsheet on Digital dermatitis to give to your clients.
 

Pathogenesis

Etiology

  • Digital dermatitis (DD) is a polymicrobial infection.  Many hundreds of bacterial species may be found in lesions, but three phylotypes of treponemes are consistently found and are believed to be the primary pathogens:
    • T. medium/vicentii-like.
    • T. phagedenis.
    • T. pedis.
  •  Attempts to replicate digital dermatitis in healthy animals, using purely treponemes have been only partially successful. It is hypothesized that an altered microbiome is required on the skin, in order that treponemes colonize and result in the clinical presentation of digital dermatitis. Moist, macerated skin is particularly susceptible.
  • Treponemes are commonly found in hair follicles and sebaceous glands associated with lesions and it is thought that these may be the main point of entry.
  • Damage to the skin surface (caused by wet slurry contaminated environments, by abrasive bedding, automatic scrapers, etc) make the skin more susceptible to invasion.
  • Damage following the cessation of high concentration formalin foot bathing may also create the entry point for invasion.
  • Wet feet predispose to infection. Experimental infection can be achieved by soaking the foot in a rubber boot filled with water for 10 days, then scraping lesional material or single treponeme isolates onto the macerated skin.
  • The treponemes causing DD do not survive at pH below 5:
    • Bovine skin has a pH of 6-7.5, so there is no acid barrier protection.
    • In order to avoid proliferation and invasion of pathogenic microorganisms, permanent and excessive humidity of the skin must be avoided.
  • DD goes deep into the epidermis and dermis then encysts (encysted DD resembles a coiled ball and may be referred to as "round bodies"). The encysted form is considered the main reason for recrudescence later.
  • Once within the soft tissues, these bacteria release enzymes which cause more skin damage, hemorrhage and pain.
  • The hoof horn may also be affected, eg toe necrosis and the related necrotic hoof lesions Digital dermatitis: bones and lesions.
  • High hydrogen sulfide levels and low oxygen levels appear to predispose to infection.  These conditions are found in most yards, but especially with slatted floors.
  • All three treponemes are not found in high abundance on healthy skin. Some treponemes are found on healthy skin, but usually only one phylotype and in low abundance. 
  • Experimentally, treponemes only remain viable for 3 days in slurry.
  • There also appears to be a genetic predisposition with certain individuals seeming far more likely to suffer DD, whereas others within the same environment may never contract the disease.
  • Treponemes have been found in a variety of skin and hoof horn lesions, including toe necrosis, wall ulcers, severe sole ulcers, teat necrosis, hock ulcers and udder cleft dermatitis (ulcerative mammary dermatitis). 

Predisposing factors

Specific

  • Poor hoof hygiene could be associated with spread of DD lesions.
  • Foot baths Footbathing reduce development of new infections.
  • One theory is the use of formalin and other astringent foot baths may drive DD treponemes deeper into the tissue in existing lesions but there is no published evidence supporting this.

Pathophysiology

  • DD may be scored and monitored using the following system: 
    • M0: healthy skin. smooth interdigital cleft (or latently infected with no clinical signs) .
    • M1: early red/ grey lesion <2 cm diameter. Acute: pain .
    • M2: active, red, ulcerated or early granulomatous lesion >2 cm. Acute: pain .
    • M3: healing - covered by scab .
    • M4: black, proliferative, dyskeratotic lesion. May appear “warty”. Late chronic. Treponemes deep in dermis. The major reservoir of infection in most herds .
  • The dynamics of DD are driven by chronic M4 lesions not by active M2 lesions:
    • Treponemes penetrate deep into the dermis and epidermis.
    • DD has long term consequences.

Timecourse

  • Chronic cases can remain with treponemes deep in the dermis as a reservoir for infection for months and possibly the lifetime of the animal.
  • Eradication from the herd is extremely difficult.

Epidemiology

  • DD is changing, 3 separate reports from countries reference 'new' lesions:
  • Treponemes modulate gene expression. Treponemes stimulate a protein production which might prevent the degradation of BDD treponemes. This explains high circulating antibody but low immune response. This may be important for DD vaccine production (no effective vaccine has been developed as yet).
  • Historically it was thought that the causal organism of DD was primarily transmitted in slurry. However, as yet we do not know enough about treponemes to know how long they survive within slurry.
  • We now believe transmission is mostly through close (direct) contact in footprints of infected and uninfected animals in yards and races, and also via infected foot trimming equipment. These bacteria are assumed to be coming from the skin lesions of infected cows. If this is true of all DD affected cattle, then this will have an impact on treatment and prevention.
  • Recent discoveries have shown that DD-associated treponeme species have a much greater tolerance of oxygen than previously thought, and are far more likely to be transmitted from cow to cow by direct contact via contaminated footprints in high cow traffic areas.
  • Brief spells of survival away from the cow is possible in slurry, wet bedding, muddy gateways and water-only foot baths. Foot trimming equipment and slurry-contaminated equipment (slurry scrapers) may also allow cross-infection of groups
  • The infected animal represents the main reservoir of infection (bacteria). These may be cows with lesions (infected skin on heels, toe necrosis, wall ulcers and other lesions) or cows with hyperkeratotic infections (M4 lesions) waiting to reactivate.
  • Between farms:
    • The most likely route of spread between farms is from direct cattle movements and shared holding or handling facilities.
    • Other species like sheep may act as reservoirs on certain farms but the significance of this is uncertain, and probably small.
    • All ages of animals on the farm should be considered when looking at infection reservoirs. Animals infected as heifers appear to drive a significant level of infection within the milking herd.

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.
  • Bell N J (2022) Latest concepts relevant to treatment of digital dermatitis in dairy cattle UK-Vet Livestock 27 (2), 54-62 MAGOnline.
  • Kasiora K et al (2021) Evaluation of the use of ketoprofen for the treatment of digital dermatitis in dairy cattle. A randomised, positive controlled clinical trial. Vet Rec 190 (6), e977 PubMed.
  • Bell N J & Vanhoudt A (2020) Treating and controlling digital dermatitis in dairy cattle In Practice 42 (1), 554-567 WileyOnline.
  • Palmer M A & O'Connell N E (2015) Digital dermatitis in dairy cows: a review of risk factors and potential sources of between - animal variation in susceptibilityAnimals (3), 512-535 PubMed.
  • Higginson Cutler J H et al (2013) Randomised clinical trial of tetracycline hydrochloride bandage and paste treatments for resolution of lesions and pain associated with digital dermatitis in dairy cattle. J Dairy Sci 96 (12), 7550-7557 PubMed.
  • Schultz N & Capion N (2013) Efficiency of salicylate acid in the treatment of digital dermatitis in dairy cattle Vet J 198 (2), 518-523 PubMed.
  • Potterton S L et al (2012) A descriptive review of the peer and non-peer reviewed literature on the treatment and prevention of foot lameness in cattle published between 200 and 2011. Vet J 193 (3), 612-616 PubMed.
  • Holzhaueur M et al (2011) Curative effect of topical treatment of digital dermatitis with a gel containing activated copper and zinc chelate. Vet Rec 169 (21), 555 PubMed.
  • Klitgaard K et al (2008) Evidence of multiple Treponema Phylotypes involved in bovine digital dermatitis as shown by 16S rRNA gene analysis and fluorescence in situ hybridization. J Clin Microbiol 46 (9), 3012-3020 PubMed.
  • Laven R A & Logue D N (2006) Treatment strategies for digital dermatitis for the UK. Vet J 171 (1), 79-88 PubMed.
  • Losinger W C (2006) Economic impacts of reduced milk production associated with papillomatous digital dermatitis in dairy cows in the USA. J Dairy Res 73 (2), 244-256 PubMed.
  • Whay H R, Webster A J F & Waterman-Pearson A E (2005) Role of ketoprofen in the modulation of hyperalgesia associated with lameness in dairy cattle. Vet Rec 157 (23), 729-733 PubMed.

Other sources of information

  • National Animal Disease Information Service (online) Lameness Control in Dairy Herds. Part 5 - Digital Dermatitis - Causes, Treatment and Control. In: NADIS Animal Health Skills. Website: www.nadis.org.uk.
  • Veterinary Medicines Directorate (online) Product Details - Intra Hoof-Fit Gel 40 mg/g + 40 mg/g Gel for Dairy Cattle. In: Product Information Database. Website: www.vmd.defra.gov.uk.

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