Lapis ISSN 2398-2969

Cellulitis

Synonym(s): Deep pyoderma

Contributor(s): Kristina Hunter, Livia Benato

Introduction

  • Cause: acute inflammatory syndrome of the skin. Can be a sequel to suboptimal husbandry or difficulty grooming due to another inciting cause, eg dental disease, obesity. Also reported secondary to respiratory infection.
  • Signs: pain, alopecia, matted fur, purulent exudate, edema, anorexia, ileus, pyrexia, sepsis.
  • Diagnosis: history, clinical signs, bacteriology, cytology, microscopy, histopathology.
  • Treatment: clipping and cleaning of the area, topical and systemic antibiotics, cold compresses, management of predisposing cause (if known), severe cases may require surgical management.
  • Prognosis: guarded to good.
Print off the Owner Factsheet on Cellulitis to give to your clients.

Pathogenesis

Etiology

  • Staphylococcus aureus Staphylococcus aureus is frequently associated with outbreaks of mammary cellulitis Staphylococcosis:
    • Rapid transmission can occur between rabbits where hygiene is suboptimal.
    • Bacterial genotype does not correlate with the development of cellulitis.
    • Outbreaks are more common with seasonal temperature fluctuations – spring and fall outbreaks are common.
    • Up to 20% of animals in a group may be affected.
  • Pasteurella multocida Pasteurella multocida has been implicated in all types of cellulitis Pasteurellosis:
    • P. multocida is carried sub-clinically by many rabbits as a component of respiratory flora.
    • Stressors can lead to immune suppression which enables overgrowth and systemic spread.
    • Frequently associated with respiratory disease, dental and facial abscessation.
  • Bordetella bronchiseptica Bordetella bronchiseptica:

Predisposing factors

  • General factors include:
  • Specific factors include:
    • Head and neck cellulitis:
      • Associated with rabbits kept indoors.
      • May develop after recent respiratory disease.
    • Orbital cellulitis:
      • Brachycephalic facial structure.
      • Recurrent dental disease or abscessation.
    • Mammary cellulitis:
      • Trauma to the affected teat facilitates entry of pathogenic bacteria:
        • Use of rough bedding material causing irritation to cutaneous tissues.
        • Sharp objects in nest box, eg nails.
        • Bites from conspecifics.
        • Injuries during suckling.
      • Poor environmental hygiene.
      • Systemic infection: hematogenous spread of bacteria from other locations is possible, eg metritis, ulcerative pododermatitis, dental disease.
      • Mammary impaction: milk retention due to neonatal death or early weaning can facilitate bacterial colonization.

Pathophysiology

  • Head and neck cellulitis:
    • Hematogenous or local spread from pre-existing respiratory infection or ascending infection through an external wound → superficial pyoderma, rhinitis → failure to resolve infection leads to penetration into deeper subcutaneous tissues → cellulitis → necrosis, sloughing and rupture of cellulitis areas.
  • Orbital cellulitis:
    • Hematogenous or local spread from pre-existing dental infection or ascending infection through an external wound → tooth root abscessation, rhinitis → failure to resolve infection leads to osteomyelitis of the skull and penetration into deeper orbital tissues → retrobulbar abscess with cellulitis → exophthalmos.
  • Mammary cellulitis:
    • Hematogenous spread from pre-existing infection or ascending infection through the teat canal or external wound → suppurative mastitis → failure to resolve infection leads to penetration into deeper subcutaneous tissues → cellulitis and deep abscessation with fistula formation → necrosis, sloughing and rupture of mammary tissue.

Timecourse

  • Cellulitis is an acute syndrome and develops rapidly over 1-2 days.
  • Underlying or inciting pathological processes may be chronic.

Epidemiology

  • Mammary cellulitis:
    • Outbreaks tend to occur sporadically in breeding groups.
    • Risk of infection transmission highest with S. aureus outbreaks: very high risk if cross-fostering is performed and young are transferred from an infected female to a naïve foster rabbit.

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.
  • Viana D, Selva L, Callanan J J et al (2011) Strains of staphylococcus aureus and pathology associated with chronic suppurative mastitis in rabbits. Vet J 190 (3), 403-407 PubMed.
  • Graham J E (2004) Rabbit wound management. Vet Clin North Am Exotic Anim Pract 7 (1), 37-55 PubMed.
  • Tyrrell K L, Citron M, Jenkins J R et al (2002) Periodontal bacteria in rabbit mandibular and maxillary abscesses. J Clin Microbiol 40 (3), 1044-1047 PubMed.
  • Jenkins J R (2001) Skin disorders of the rabbit. Vet Clin North Am Exotic Anim Pract 4 (2), 543-563 PubMed.
  • Miflin J K & Blackall P J (2001) Development of a 23 S rRNA-based PCR assay for the identification of Pasteurella multocida. Lett Appl Microbiol 33, 216–221 PubMed.
  • Dabo S M, Confer A W & Lu Y S (2000) Single primer polymerase chain reaction fingerprinting for Pasteurella multocida isolates from laboratory rabbits. Am J Vet Res 61 (3), 305-309 PubMed.

Other sources of information

  • Anon (2013) Dermatoses of Pet Rodents, Rabbits and Ferrets. In: Muller & Kirk’s Small Animal Dermatology. 7th edn. Elsevier Inc, USA. pp 1415-1458.
  • Hess L (2004) Dermatologic Diseases. In: Ferrets, Rabbits and Rodents Clinical Medicine and Surgery. 2nd Edn. Elsevier Inc, USA. pp 194-202.


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