Haematological Immunological Conditions

Basset Hound thrombopathia

This condition is seen only in Bassets. Clinical signs include prolonged haemorrhage, particularly at surgery and oestrus. Aural haematomas and petechiae are also seen. The platelets demonstrate defective aggregation and retention. The underlying cause is unknown.

Blood groups

Canine blood groups are classified according to the dog erythrocyte antigen (DEA). There are six main groups, DEA 1.1, 1.2, 3, 4, 5 and 7. DEA 1.1 and 1.2 are alleles so it is not possible to be positive for both. Since there are no naturally-occurring autoantibodies to these two groups, an initial blood transfusion doesn’t usually cause an acute transfusion reaction. However, if the donor and recipient are incompatible, an immune response will be mounted after the first transfusion, so subsequent incompatible transfusions are likely to cause a reaction. DEA 1.1 is inherited as an autosomal dominant. A DEA 1.1 negative female bred with a DEA 1.1 positive male may therefore have DEA 1.1 postive pups, and this can lead to neonatal isoerythrolysis.

Feline blood groups are classified into A, B and AB. A is dominant over B, but the inheritance of the rare AB blood group is determined by a different gene. There are high levels of naturally-occurring antibodies against the other groups, so there are no universal donors, and cross-matching or typing is vital before transfusing.

C3 complement deficiency

The complement system is important in neutrophil function and in fighting bacterial infection. There are two pathways, however, so a defect in one does not always lead to immunodeficiency.

Canine leucocyte adhesion deficiency

An inherited defect in the ability of neutrophils to bind to endothelial cells causes severe and recurrent bacterial infections. A molecular diagnostic test is available to diagnose this condition.

Chediak-Higashi syndrome

In this condition, abnormal lysosomes and neutrophil granules lead to neutrophil dysfunction. Platelet function is also impaired, leading to bleeding. See also under Ocular conditions.

Combined B- and T-cell immunodeficiency

This condition causes severe bacterial infections in young dogs once maternal immunity wanes, from 8-16 weeks of age.

Cyclic haematopoiesis

In this condition, neutrophil numbers decrease every 12 days. There may also be cyclic decreases in platelet, monocyte and reticulocyte numbers.

Factor VII deficiency

This condition leads to a mild clotting disorder. Prothrombin time (PT) is usually prolonged, but activated partial thromboplastin time (APTT) is usually normal, as is consistent with a disorder of the extrinisic pathway.

Factor X deficiency

Factor X is part of the common pathway, so PT and APTT are both prolonged. A specific factor X assay is used to confirm the diagnosis. The severity of bleeding is variable, and some affected dogs may survive into adulthood.

Factor XI deficiency

Heterozygotes for this condition have about 25-50% of the normal activity of factor XI and are asymptomatic. Homozygotes have about 10% activity and suffer from severe and often lethal bleeding.

Glanzmann’s thrombasthenia

This condition affects platelets, leading to decreased platelet retention and absent platelet aggregation. This causes severe mucosal bleeding. Platelet count is usually normal or possibly slightly decreased. The buccal mucosal bleeding time is increased and clot retraction is abnormal. It is inherited as an autosomal recessive trait.

Haemolytic uraemic syndrome

This condition involves hyperaggregability of platelets, leading to platelet thrombi and tissue ischaemia. Clinical signs include neurological symptoms, renal failure, microangiopathic haemolytic anaemia, thrombocytopaenia and pyrexia.

Haemophilia A

This deficiency of factor VIII can cause moderate to severe bleeding. APTT is prolonged, but PT is normal. Many cases may arise from new mutations. The condition is inherited as a sex-linked recessive.

Haemophilia B

Also known as Christmas disease, this clotting deficiency is caused by a deficiency in factor IX. This is a sex-linked condition, but because the size of the gene for factor IX is smaller than for factor VIII, spontaneous mutations are less common for haemophilia B than haemophilia A. APTT is prolonged, but PT is normal.

Hereditary porphyria

This condition leads to anaemia in Siamese cats, but is also seen in non-anaemic domestic short hairs. Affected animals have a defect in haem synthesis. There may also be photosensitisation and red cell haemolysis.

Hereditary stomatocytosis

This condition may lead to a mild anaemia but is usually clinically insignificant.

Immune-mediated haemolytic anaemia

Mild to severe anaemia, chronic or acute, can be seen with this condition. Haematology shows anaemia (with a regenerative response if the anaemia is not too acute) and spherocytosis. Although many cases respond well to treatment, the potential for serious complications means the prognosis for this condition is guarded.

Immune-mediated thrombocytopaenia

This is a common disorder, characterised by immune-mediated destruction of platelets. Epistaxis, haematochezia and mucosal haemorrhage are often seen.

Immunodeficiency syndrome of Irish Wolfhounds

Respiratory conditions in related Irish Wolfhounds have been attributed to an underlying immunodeficiency, possibly in cell-mediated immunity or in IgA.

Increased osmotic fragility of erythrocytes

Extreme fragility of the erythrocytes can lead to recurrent and severe anaemia, with splenomegaly and weight loss. Prednisolone and blood transfusions may be helpful.

Lethal acrodermatitis

Clinical signs of this condition include dermato-logical and respiratory problems and stunted growth. Plasma zinc levels are low and tissue T-lymphocytes are depleted.

Methaemoglobin reductase deficiency

This condition causes dark brown mucous membranes and cyanotic blood vessels. Severe methaemoglobinaemia is seen which may be life-threatening. Management is by avoidance of oxidative agents such as onion, drugs and certain food components.

Non-spherocytic haemolytic anaemia

This condition is due to a defect in the calcium pump system. Chronic haemolysis may lead to myelofibrosis.

Neutrophil function defect

Defects in neutrophil function lead to recurrent and/or severe bacterial infections. A pronounced left shift neutrophilia may be present.

Pelger-Huet anomaly

This anomaly involves a decreased segmentation of granulocyte nuclei. There doesn’t seem to be an increased predisposition to infection in these cases.

Phosphofructokinase deficiency

Haemolytic crises and exertional myopathy are seen with this relatively common enzyme deficiency. Exercise intolerance is often seen. A PCR-based DNA test is available for affected dogs and carriers.

Platelet storage-pool deficiency

This condition leads to moderate to severe haemorrhage. Platelet counts are normal, but buccal mucosal bleeding time is prolonged.

Predisposition to tuberculosis

A report has shown five Bassets that developed systemic tuberculosis. It is thought that an immune deficiency, possibly in cell-mediated immunity, was responsible.

Primary idiopathic hyperlipidaemia

This poorly understood familial condition can cause multisystemic signs such as abdominal pain, seizures and pancreatitis.

Pyruvate kinase deficiency

In this condition of erythrocytes, the affected cells lose the ability to retain their normal shape and have a reduced affinity for oxygen and a shortened lifespan.

Selective IgA deficiency

This condition causes different clinical signs in different breeds, including dermatological disease, respiratory disease such as rhinitis, and gastrointestinal disease such as small intestinal bacterial overgrowth and anal furunculosis.

Selective malabsorption of cobalamin (vitamin B12)

See under Gastrointestinal conditions.

Spitz Dog thrombopathia

This condition is similar to Basset Hound thrombopathia. Intermittent mucosal bleeding is seen.

Systemic lupus erythematosus

Diagnosis of this uncommon disease is made on the basis of the presence of at least two signs of autoimmune disease, together with high levels of antinuclear antibodies (ANA) (although 10% of cases are ANA negative). Clinical manifestations include polyarthritis, mucocutaneous lesions, glomerular disease, autoimmune haemolytic anaema, autoimmune thrombocytopaenia and neurological signs.

T-cell dysfunction

This condition of Weimaraners is associated with growth hormone deficiency, thymic aplasia and dysfunction of T-cells.

Tail tip necrosis

This condition has been reported in Birman kittens and is thought to be due to neonatal isoerythrolysis involving cold agglutins.

Thymic aplasia

This congenital condition causes signs of stunted growth, wasting and suppurative pneumonia.

Transient hypogammaglobulinaemia

This condition can lead to a delay in developing active immunity, leading to recurrent respiratory infections. However, most affected puppies are normal by eight months of age.

Undefined immunodeficiency syndrome (susceptibility to Pneumocystis carinii)

A predisposition to respiratory disease caused by this organism is suspected to be caused by an underlying immunodeficiency, but the exact nature of this is not known.

Vaccine-associated vasculitis

Routine vaccinations in Weimaraners occasionally cause an acute systemic vasculitis, with gastrointestinal signs, hypertrophic osteodystrophy and lameness.

Vitamin-K-dependent coagulopathy

Clinical signs of this condition include prolonged bleeding post surgery or trauma. It is thought that an autosomal recessive defect in hepatic vitamin K metabolism leads to reduced levels of factors II, VII, IX and X. Affected animals can be detected by demonstrating a prolonged PT and APTT.

Von Willebrand’s disease

This is the commonest inherited disorder of haemostasis in dogs, and is caused by a deficiency in von Willebrand’s factor (vWF), which is vital for platelet function. There are three recognised types: type I involves a quantitative reduction in vWF, and the severity of the disease varies with breed. Some individuals respond to desmopressin (DDAVP) treatment; type II disease also involves a quantitative reduction in vWF, but the condition is more severe than type I, and there is no response to DDAVP; type III disease is characterised by a complete absence of vWF leading to the most severe clinical disease, again with no response to DDAVP. Genetic tests are also available to identify carriers of the gene to allow appropriate selection of breeding stock.