Hepatozoon

• Tick borne disease
• Two species:
  • Hepatozoon canis
    • Usually subclinical disease
  • Hepatozoon americanum
    • SE USA
    • Grossly:
      • Thickened and edematous periskeletal soft tissue and periosteum of the lower legs
      • Multifocal parasitic myositis
    • Histologically:
      • Swelling and hypertrophy of osteoprogenitor cells
      • Hyperplasia of spindle cells
      • Osteoid is produced

• Myositis
  • Develop cysts in skeletal muscle of dogs and cats
  • May be accompanied by pyogranulomatous myositis - macrophages and neutrophils mainly with occasional other cells

[Skeletal lesions of canine hepatozoonosis caused by Hepatozoon americanum. Panciera Rj et al. Vet Path (2000) 37 225-230]

• Hepatozoon americanum
  • SE USA
  • Clinical signs:
    • Fever
    • Weakness
    • Myalgia
    • Bone pain
    • Mature neutrophilic leukocytosis
    • Wasting
    • Poor response to treatment
    • Periosteal new bone formation
  • Much more aggressive and higher mortality rate than the disease in the Old World
  • Gross skeletal lesions:
    • Markedly thickened and edematous periskeletal soft tissue and periosteum of the lower legs ***+/- petechiation
    • Eccentrically or circumferentially arranged plaques of new bone formation deposited on the original cortex
    • Boney plaques look ‘porous’ to compact, often in layers with the spongey areas covered by more compact bone
    • No evidence of endosteal bone formation
    • Periosteoproliferative lesions most prominent in proximal long bones of the limbs (esp. femur and humerus)
    • Metaphyses usually spared
    • Caudal and lateral surfaces of the proximal tibia and fibular and radius and ulnar diaphyses affected
    • Distal diaphyses and metaphyses less severely affected/free from lesions
    • Metacarpals/tarsals mildly affected
    • Lateral surface of scapula affected
    • Axial skeleton less severely affected
    • Often bones of the skull prominently affected – orbits, rostrolateral maxilla and mandible, lateral aspect of zygomatic arch
    • Lateral aspects of vertebral arches and spinous processes sometimes affected
    • Ribs normal
    • Multifocal parasitic myositis
  • Histologically:
    • Earliest change in periosteum -> swelling and hypertrophy of osteoprogenitor cells in the deeper layers of the periosteum
    • Spindle cells become stellate and plumper
      • Become aligned in single or multiple layers
      • Undergo hyperplasia creating a thick and densely cellular zone on the cortical surface
    • Osteoid is produced and osteoblasts become entrapped forming spiccules of trabecular new bone
    • New spicules arranged perpendicular to the cortical surface
    • With time, considerable osteoclastic activity, remodeling occurs firstly adjacent to the older cortex and then extends outwards
    • As the remodeling continues, the spicules become longitudinally arranged
    • Pseudocortices form that can contain bone marrow parenchyma
    • Endothelial hypertrophy prominent in vessels adjacent and within the periosteum
    • Severe edema present in adjacent soft tissue
    • Muscle atrophy and fibrosis often accompanied the edema
    • No evidence of inflammation
    • No parasites in adjacent muscle/soft tissue
  • Lesions develop in young dogs, within 5wks of experimental infection and progress rapidly, looking just like hypertrophic osteopathy
  • No obvious link between site of infection and generalized boney lesions
• Differentials for periosteal new bone formation:
  • Hypertrophic osteopathy
  • Craniomandibular osteopathy
  • Canine panosteitis
  • Hypertrophic osteodystrophy
• Hypertrophic osteoarthropathy
  • V difficult to distinguish from this syndrome
  • Again no inflammation, histologically look identical, but these cases don’t have an abdominal/thoracic mass, and HO usually starts on the metacarpals/tarsals
• ?Pathogenesis
  • Thought to occur secondary to increased blood flow and fluid retention within the limbs, leading to vascular and then periosteal proliferation