EQUINE INFECTIOUS ANAEMIA

EQUINE INFECTIOUS ANAEMIA

Equine infectious anaemia (EIA) is a viral infectious disease that causes anaemia and is associated with recurrent periods of fever. Commonly known as “Swamp Fever” or “Horse Malaria”, EIA is caused by a virus in horses that can lead to destruction of platelets, red blood cells, and inflammation in many of the organs in the horse’s body. The virus invades the white blood cells (monocytes and macrophages) and causes a lifelong infection within the spleen, liver, and other tissues. The virus is spread from horse to horse by biting, blood sucking flies such as the horsefly and deerfly. The virus can also be passed from dam to foal through the placenta, through natural breeding as a venereal disease, and by any transfer of blood from an infected horse to an uninfected such as the use of dirty needles or other equipment. The clinical signs in a horse vary and may be an acute form of the disease or a more chronic form. The acute form can be seen as a sudden high fever, lethargy, anemia, and low blood platelets. The chronic form presents as an intermittent fever, weight loss, edema in the legs and lower abdomen, and anemia. Initially the horse’s immune system may be able to stop the virus and the horse will go through periods of no symptoms but can still spread the virus. These animals serve as inapparent carriers. The horse will then have reoccurring episodes that can lead to chronic debilitation. There is no treatment or vaccination for this virus. Control of the disease is through testing of horses to identify carriers of the virus. The Coggins test was developed in 1970 and is used as the standard diagnostic test to detect antibodies in the blood against the virus. This testing is part of a Federal and State program to control this disease. The Coggins test is commonly required when moving horses within and among States. The test requires a blood sample to be taken by an accredited veterinarian and the proper paperwork submitted to a licensed laboratory that performs the test. It is recommended to have your horse tested yearly starting at 6 months of age. Any horses that are tested positive must be either euthanized or quarantined a safe distance from other horses.

Equine infectious anaemia occurs in horses, mules and donkeys, and is transmitted by bloodsucking insects. The foetus can also become infected in pregnant animals. The equine infectious anaemia virus (EIAV) is a lentivirus and belongs to the same family as the maedi-visna virus in sheep and HIV (cause of the disease AIDS) in humans. Once a horse has become infected, the animal may remain infectious for other horses for life. Humans cannot be infected with the EIA virus (EIAV).

Equine infectious anaemia is a notifiable animal disease.

Synonyms

• Swamp Fever, Equine malarial fever

Definition

• Acute infectious disease equine characterised by high fever, anaemia, progressive weakness and debility and jaundice, oedema and haemorrhages as main gross lesions

Etiology

• Lentivirus
• Virus shares serological reactivity with human AIDS lentivirus
• Virus persists in blood through out the life

Incidence

• First recorded in India in 1987 in a equine stud farm at Bangalore
• Seropositive horses in Haryana and Maharashtra

Transmission

• Mechanically by biting insects like mosquitoes, Tabanus sp. , Stomaxys sp.
• Iatrogenic transmission by transfer of minute amounts of blood from infected horses to normal horses through unsterile hypodermic needles, tattoo needles, etc.
• Not spread by contact
• Disease is more prevalent in swampy areas (insect breeding)

Pathogenesis

• Virus localises in various organs like spleen, liver, kidney and lymphnodes
• Virus is detected in greater quantities in severe attacks
• It disappears from tissues in periods between attacks
• Although there is persistent viraemia, throughout the horse life the virus level is low except during periods of clinical activity, so it is at this time the animal is highly infective
• Virus enters and infects macrophages causes destruction of macrophages and release of virus , production of antibodies, to antigenic components; formation of antigen-antibody complexes which induce fever , glomerulitis and complement depletion
• Specific complexes causes hemolysis and phagocytosis by activating reticulo-endothelial system
• Pathological processes subside as virus neutralising antibodies prevent multiplication in macrophages and horses become permanently asymptomatic
• Life-long viral persistence is due to viral induced defect of the macrophages
• EIA virus tries to avoid host’s immune response by undergoing rapid variation in antigenicity
• Erythrocytes of infected horses are coated with antiviral antibodies and complement causes increased osmotic fragility and erythrophagocytosis – Anaemia

Clinical and hematological diagnosis ———-

The terms, acute, subacute, chronic and relapsing types have been used to classify EIA cases. These types have been correlated with clinical and pathological observations. The acute and subacute types have sevet·e clinical symptoms and are often followed by death while the chronic type is identified by the occurrence of intermittent febrile attacks in a sut·viving case of the disease and with mild clinical symptoms.

• Fever ——–Although the degree of fever depends upon the severity of disease, the characteristic feve r of this disease is 40 to 41 °C or more and the febrile stage usually continues for 4 or 5 days. In the acute and subacute types, the febrile stage continues for a few days longer. There are typical, recurrent or intermittent febrile periods of about 39°C or more in themore in the chronic type of the disease.

2) Aneniia ——The anemia usually begins at the peak of the febrile stage, becomes quite evident afterchronic type of the disease. the fever crisis, and gradually returns to normal if the fever does not recur. The curve showing the relationship between the fever and anemia is very characteristic of EIA. Severe anemia with a decrease of erythrocyte count to 1 or 1.5 million per mm• of blood sometimes occurs following a single febrile attack. Anemia, however, is not usually seen in the chronic cases which continue to be afebrile.

3.) Appecirance of sideroleukocytes in the circidciting blood

The sideroleukocytes which appear in the circulating blood of EIA cases are mononuclear cells and neutrophils which contain an iron-positive reacting substance such as ferritin and hemosiderin. In EIA, when there is recurrence of fever, anemia occurs at the time of the febril e crisis, and sideroleukocytes appear and increase in number in the circulating blood. The greatest probability of detection of sideroleukocytes is at 1 to 4 days after the fever crisis. The febrile period and during the afebrile stage at 5 to 10 days after the fever crisis are the next period of hi gh probability of detection•>. Sideroleukocytes also appear in the circulating blood of horses affected with trypanosomiasis and piroplasmosis. These diseases, however, can be differentiated from EIA by finding the parasites in the blood smears. In our experience, very few or no sideroleukocytes have been found in the circulating blood of adult horses infectetd with diseases other than EIA, trypanosomiasis and piroplasmosis. In Japan, where neither piroplasmosis nor trypanosomiasis is known to occur, horses in which one or more sideroleukocytes are found per 10,000 leukocytes are legally considered to be positive for EJA•

4) Other changes of the blood and clinicctl signs Although a neutrophilia is observed at the feb1·ile stage, relative lymphocytosis and monocytosis are present after the crisis. The erythrocyte sedimentation ,·ate is also increased. Weakness, loss of appetite, edema and generalized ictel’lls often appear in severe cases. Cardiac weakness is an important clinical sign because of its presence even in those chronic cases with normal temperature.

Clinical signs

Gross lesions

• Acute form
  • Icterus, oedema and haemorrhages of membranes of various organs
  • Oedema on the ventral wall of abdomen, at the base of the heart and perineal fat
  • Petechial or ecchymotic haemorrhages in pleura and peritoneum
  • Heart is enlarged, pale and flabby
  • Haemorrhages on epicardium and pericardium
  • Clear serosanguinous fluid in pericardium
  • Enlarged liver and spleen with haemorrhages sometimes with infarcts
  • Lymph nodes are enlarged
  • Bonemarrow is strikingly red indicating active haemopoeisis
  • Kidneys are oedematous
• Subacute form
  • Anaemia is very prominent than oedema
  • Spleen is enlarged
  • Liver is enlarged , dark brown and hard to incise
  • Muscles are pale
• Chronic form
  • Hypertrophy of spleen and bonemarrow

Microscopical lesions

• Acute form
  • Oedema and haemorrhages on heart
  • Increase in red pulp and infiltration with immature mononuclear cells
  • Infiltration of immature lymphocytes in interstitium of kidneys
  • Immunoglobulins and complements are demonstrated by immunofluorescence in glomeruli of kidneys
  • All organs show reticulo- endothelial hyperplasia
• Subacute form
  • Hyaline degeneration and lymphocytic infiltration of myocardium
  • Congestion of central vein and sinusoids of liver with infiltration of lymphocytes, plasmacells, macrophages laden with haemosiderin
  • Reticulo-endothelial cells form small nodules in sinusoids
  • Hyperplasia of reticulo-endothelial cells  in spleen and lymph nodes
  • Small number of lymphocytes in kidneys
  • Haemorrhages in bone marrow
• Chronic form
  • Myeloid and erythroid elements are in normal proportionindicating that haemopoiesis is activated

Haematological changes – Normocytic and Normochromic anaemia

• Diagnosis
• Clinical signs & lesions
• Isolation and identification of the virus in leucocytic culture
• Agar immunodiffusion test developed by Coggins in 1972 is used to detect antibodiesin serum
• Immunofluorescence test in tissues to demonstrate antigens

DR RAMASWAMY S. MVC

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