Hepatozoon
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- 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
- Hepatozoon canis
- 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 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