Arthritis in Animals

Arthritis in Animals

Ajit Kumar Singh¹, V.K. Varun¹, M.V. Jithin¹, Shikhar Yadav², A.K. Gangwar³

1. Assistant professor, Deptt. of VCC, COVAS, SVPUAT, Meerut,
2. M.V.Sc.Scholar, department of VSR, COVAS, SVPUAT, Meerut,

3.Professor and Head, Deptt. of VSR, ANDUAT, Ayodhya.

Arthritis is a nonspecific term denoting inflammation of the joints. All the joint diseases of animals have an inflammatory component to varying degrees. Arthritis of importance include inflammation of hip joint (coxitis), inflammation of stifle joint (gonitis), inflammation of shoulder joint (omarthritis), inflammation of carpal joint (carpitis) etc.

Types of arthritis:

1. Infectious arthritis/ septic arthritis: e.g. joint ill or neonate polyarthritis
2. Traumatic arthritis
3. Degenerative arthritis or osteosrthritis on noninfectitious arthritis or degenerative joint disease (DJD).

Infectious arthritis/ septic arthritis:

• Infectitios arthritis is the inflammation of joint which is caused by microorganisms like bacteria, virus, mycoplasma etc.
• Infectious arthritis with pus in the joint cavity is known as septic arthritis.

Etiology:

• Trauma near the joint leads to periarticular infection which may extend to the joint.
• Systemic infection e.g. joint ill caused by omphalophlebitis.
• Corynebacterium pyogenes, Mycoplasma bovis, Escherichia coli, Staphylococcus sp. and Streptococcus sp. are the common microorganisms responsible for septic arthritis.

Clinical signs:

• Severe lameness with limited motion (due to pain, joint effusions, fibrosis of periarticular tissues and joint ankylosis).
• Swelling of the affected joint (Due to effusion of synovial fluid, inflammation, fibrosis of the synovial membrane and joint capsule and bony enlargements).
• Pain during palpation.
• Pyrexia may be present.
• Joint capsule may rupture with oozing of pus.
• Increase in temperature of the overlying skin of the affected joint which can be accurately measured by thermography.

Pathogenesis:

• After entrance, the microorganism damages cartilage, synovial membrane and fluid.
• Microorganisms are destroyed by neutrophils and their enzymes (elastage, collagenase etc.). At the same time these enzymes also damages the articular cartilage.
• Articular surface is further damaged by free radicals released by neutrophils and damaged tissue.
• Inflammatory mediators decrease proteoglycan production.
• Decreased production and increased degradation of proteoglycans deteriorates the cartilage.
• The presence of fibrin on cartilage and synovial membrane interferes with nutrient and waste product transportation which makes the joint more susceptible to trauma.

Diagnosis:

1. By radiography: Radiographcan be taken in anteroposterior and lateral position.
   • In early stage: Increase in joint space due to synovial effusion and increased soft tissue density around the joint.
   • In middle stage: Narrow joint space due to changes in articular cartilage.
   • In end stage: Increase in joint space due to destruction of subchondral bone. Periarticular new bone formation (osteophytes) and calcification of joint capsule and attached sites of the collateral ligaments.
2. By contrast arthrography:

• Indications: To evaluate the lesions in the articular cartilage, subchondral bone, synovial membrane, thickness of the articular cartilage, joint capsule tear etc.
• Technique: About 10 cc of 25% solution of triiodinated water soluble contrast media is injected in to the joint.

1. Arthroscopy: Arthroscopy is used to make the final diagnosis.
2. Synovial fluid analysis:

• Synovial fluid culture: Normal synovia is sterile. Growth of microorganism indicates septic arthritis.
• Synovial fluid protein: >4 gm/dl
• B.C. count: About 50,000 cells/mm³
• Serofibrinous cloudy synovial fluid.
• Low viscosity of the synovial fluid.
• Mucin precipitate quality is poor.
• Increase in neutrophil count: >75%
• Increased lactate dehydrogenase (LDH) due to damage of articular cartilage.
• Alkaline phosphatase (ALP), Aspartate aminotransferase (AAT) and LDH increased with severity of disease.

1. Ultrasonography: Presence of echogenic (gray) material floating in the joint.
2. Nuclear scintigraphy: Technitium 99 is used for nuclear scintigraphy of joints.
3. CT scan and MRI

Treatment: The following steps should be followed-

1. Treat the primary cause: treat the systemic infections like omphalophlebitis, metritis, endocarditis, mastitis etc.
2. Removal of debris and fluids from the joint cavity (Joint lavage): After sedation, the animal should be restrained in lateral recumbency. Remove the debris and dilute the fluid in the joint with sterile isotonic fluids.
3. Antimicrobial therapy:
   • Antibiotics should be administered after joint lavage because debris in the joint cavity decreases the efficacy of the antibiotics.
   • Specific antibiotic should be used after antimicrobial sensitivity test.
   • Intravenous and intramuscular routes of administration should be preferred.
   • Intraarticular injection and intravenous under tourniquet can be used.
   • Implantation of slow releasing substances (PMMA) with antibiotics.
   • Cephazoline and procaine penicillin are the drug of choice.
4. Arthrodesis: Arthrodesis should only be done when all the treatments are ineffective.
5. Use of NSAIDs.
6. In mycoplasmal arthritis, Oxytetracycline is the drug of choice.
7. Immobilization of the affected joint.
8. Intraarticular injection of polysulfated glycosaminoglycans (PSGAG), hyaluronic acid (HA) and dimethylsulfoxide(DMSO).

References:

https://www.pashudhanpraharee.com/hip-joint-problems-in-dogs/arthritis-in-dog/

1. MSD Vet Manual.
2. GeneralAnimal Surgery and Anesthesiology (2009). A. K. Gangwar. New India Publishing.
3. https://www.msdvetmanual.com/musculoskeletal-system/arthropathies-in-large-animals/arthritis-in-large-animals

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