Bovis ISSN 2398-2993

Digital dermatitis

Contributor(s): Louise Cox-O’Shea, Nick Bell, Roger Blowey

Introduction

  • Cause: Treponemes.
  • Signs: lameness (in more severe cases).
  • Diagnosis: history and clinical signs.
  • Treatment: topical antibacterial treatment. Tetracycline or thiamphenicol sprays currently licensed (UK).
  • 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.
Print off the farmer factsheet on Digital dermatitis to give to your clients.

Pathogenesis

Etiology

  • Digital dermatitis (BDD) is caused by a group of spirochaetes called Treponemes, but a huge number of other bacteria are found in BDD lesions as secondary invaders.
  • Treponemes. The three main spirochaetes are:
    • T. medium.
    • T. phagedenis.
    • T. pedis.
  • Commonly found in hair follicles and sebaceous glands associated with lesions, which is thought to be the main point of entry.
  • Damage to the skin surface (caused wet slurry contaminated environments, by prickly/stiff 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 BDD 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). 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.
  • High hydrogen sulphide levels and low oxygen levels appear to predispose to infection.  These conditions are found in most yards, but especially with slatted floors.
  • Not found on healthy skin or in slurry (experimentally the 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 BDD, 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 Footbaths 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: [insert DD scoring and monitoring and DD dynamics image]
  • M0- Healthy skin. smooth interdigital cleft.
  • M1- Early red/ grey lesion <2cm diameter. Acute- pain.
  • M2 Active, red, ulcerated or early granulomatous lesion >2cm. Acute- pain .
  • M3 Healing - covered by scab or film. Early chronic.
  • M4 Later healing. Black proliferative dyskeratotic scab. Late chronic. Treps deep in dermis. Reservoir of infection .
  • 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 BDD vaccine production.
  • Historically it was thought that the causal organism of BDD 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 of infected and uninfected animals in yards and races. These bacteria are assumed to be coming from the skin lesions of infected cows. If this is true of all BDD affected cattle, then this will have an impact on treatment and prevention.
  • Recent discoveries have shown that BDD-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 foot prints 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 dormant 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

This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login

Treatment

This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login

Prevention

This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login

Outcomes

This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login

Further Reading

Publications

Refereed Papers

Other sources of information

  • Losinger W C (2006) Economic impacts of reduced milk production associated with papillomatous digital dermatitis in dairy cows in the USA.
  • National Animal Disease Information Service [online]. NADIS animal health skills - lameness control in dairy herds. Part 5 - Digital Dermatitis- causes, treatment and control.
  • American Society For Microbiology [online]. Evidence of multiple Treponema Phylotypes involved in bovine digital dermatitis as shown by 16S rRNA gene analysis and fluorescene in situ hybridization.
  • Animals [online]. Digital dermatitis in dairy cows: a review of risk factors and potential sources of between - animal variation in susceptibility.


ADDED