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Eperythrozoonosis

This disease affects all age groups. The key clinical signs include anaemia; jaundice; scouring.

Background and history

This is a disease caused by a small ricketsial bacterium called Eperythrozoonosis suis which attaches to the surface of red blood cells and sometimes destroys them. The pig may then become anaemic and the products left after the destruction of the cells may cause jaundice.

Clinical disease is more commonly seen in young growing pigs, however it can also cause reproductive problems in the breeding herd. A sow may carry EPE and yet remain quite healthy. It can cross the placenta resulting in weak pale pigs at birth.

EPE is present in most if not all herds but the mechanisms which allow it to become pathogenic and produce disease in some populations and not in others are unknown. The incidence of disease is low. However, in the past two years a positive diagnosis associated with disease has become more common.

EPE is similar to and should be distinguished from:

  • Actinobacillus pleuropneumonia.
  • Chronic respiratory disease complexed with PRRS and influenza.
  • Glässer's disease – Haemophilus parasuis.
  • Iron/copper anaemia.
  • Leptospirosis – L. icterohaemorrhagiae and L. canicola.
  • Malabsorption and chronic enteritis.
  • Pale piglet syndrome – haemorrhages.
  • Porcine enteropathy (PE, NE, PHE and PIA).

Clinical signs

Sows

  • Affected sows are inappetent with fever 40–42°C (105–107°F) when high numbers of organisms are present in the blood. This clinical picture is often seen after farrowing.
  • Anaemia
  • Increased respiration.
  • Anoestrus.
  • Pale skin
  • No milk – agalactia.
  • Sows become debilitated and pale with jaundice.
  • Poor conception.
  • Repeat matings.
  • Delayed returns to oestrus.
  • Bleeding into tissues.
  • Abortion.
  • Thin.
  • Stillbirths.
  • Pale skin

Piglets

  • In severe cases jaundice may result.
  • Secondary infections tend to occur.
  • More chronic cases result in slow growth and poor-doing pigs.
  • Pale and anaemic pigs.
  • Increased scour (sloppy diarrhoea).
  • Pneumonia.

Weaners and growers

The clinical picture varies:

  • In weaners the acute disease is manifest by primary anaemia.
  • In growers it leads to slow growth and poor-doing pigs.
  • The presence of anaemic and possibly slightly yellow-skinned recently weaned pigs.
  • Pale pigs.
  • Slow or variable growth.
  • Ear necrosis.
  • Enteritis ­– sloppy diarrhoea.
  • Fever.
  • Pneumonia.
  • Poor pigs, wasting, hairy.
  • Pot bellied pigs.

Diagnosis

  • The clinical picture.
  • The identification of the organism in blood smears stained with Wright's stain. Fifty microscopic fields should be examined before a negative diagnosis is arrived at. The presence of EPE in a smear need not necessarily imply disease.
  • Serological tests, including an enzyme-linked immunosorbent assay (ELISA), are still unreliable but are being improved.
  • Evidence of other causes of anaemia (e.g. iron/copper deficiency).
  • Jaundice, particularly in young growing pigs from 7 to 21 days of age.
  • Blood samples should be examined for packed cell volume (PCV) and haemoglobin levels.
    • In normal pigs the mean PCV would be around 35 percent and in clinically affected pigs 24 percent. Haemoglobin levels would normally range from 9 to 14g per 100ml but in anaemic pigs they would be as low as 3 to 7g per 100ml.
  • EPE must be differentiated from similar conditions (listed above).
  • If pale anaemic pigs are evident during sucking or in the immediate post-weaning period and an injection of iron has been given, the possibility of EPE should be considered.

Causes

  • Biting insects.
  • Internal parasites
  • Lice or mange mites.
  • Cannibalism/vice (abnormal behaviour).

Sows – method of spread:

  • Vaccinating sows with the same needle.
  • Tagging gilts.
  • Feeding placenta or farrowing house material.
  • Fighting.
  • Vulval and tail biting, etc.
  • It is also thought that EPE may enter through the mouth to the stomach and intestine and be transferred into the body this way. This is one reason why the practice of feed-back using placenta is not advised.

Piglets – method of spread:

  • Tailing, tooth clipping and iron injections.

Weaners & Growers – method of spread:

  • Fighting.
  • Tail biting and other vices.

Prevention

General techniques

  • Take precautions when vaccinating large numbers. Change needles every 2 to 3 sows and gilts.
  • Wipe the needle between each animal with cotton wool and surgical spirit.
  • Reduce fighting episodes.
  • Take precautions to keep vice at a minimum.
  • Keep stress and immuno-suppression to a minimum.
  • Control mange and lice if they are present.
  • Control biting insects.
  • Tagging gilts - Wash the applicators between animals or hold three pairs in an antiseptic solution and rotate.
  • If the herd is infected with mange it is important to adopt a control programme.

Sows

  • Prevent or control vulval and tail biting etc.
  • Control internal parasites.
  • Wear plastic arm sleeves when attending a farrowing.
  • Do not carry out feed-back using placenta or farrowing liquids.

Piglets

  • Spread occurs during tailing, teething and iron injections – clean tools and replace needles.
  • Control as for sows.

Weaners and growers

  • Prevent fighting at weaning. Reduce mixing.
  • Prevent tail biting and vice.
  • Reduce mixing and use Stresnil to prevent fighting.
  • Prevent spread through vaccination and inoculations between pigs.
  • Control biting insects.
  • Control respiratory diseases.

Treatment

Consider the following and discuss with your veterinarian:

  • The response to treatment is not very good.
  • Inject piglets with oxytetracycline (OTC) at 10mg/kg daily for 4 days or use long-acting preparations, three injections each two days apart.
  • In-feed medicate sows at 800gms/tonne of OTC for 4 weeks and repeat again 4 weeks later.
  • Arsanilic acid in-feed at 85gms/tonne is reported to have an effect but in many countries there is no licensed product in food producing animals. Where it is available it is probably the medicine of choice.
  • The response to other medicines is poor.