Haemorrhagic enteritis (HE) is an acute infectious disease of turkeys causing a gastrointestinal disorder. It is characterized by haemorrhagic droppings and lesions, which name the disease. This illness is widespread and economically significant in turkey production.

ETIOLOGY

This illness is caused by a type II adenovirus named haemorrhagic enteritis virus (HEV). It affects young turkeys from 4 to 12 weeks of age, although it is more common in turkeys of 7 to 9 weeks old.

Turkeys younger than 4 weeks old are resistant to the disease because of the presence of maternal antibodies against the virus, although they may also get infected if there is a strong environmental challenge and low maternal antibodies are present.

Recent publications revealed that genes affecting virulence were ORF1, E3 and fib. Complete genome sequencing performed in isolates from USA revealed 11 different HEVs because of a mutation in ORF1. Some strains produce no clinical signs nor mortality, while virulent strains cause a clinical disease and variable mortality.

Turkeys are the natural host of HEV, although its presence has also been observed in other gallinaceous birds such as chicken, peafowl and quail. A unique feature of HEV compared to other adenoviruses is the absence of vertical transmission.

TRANSMISSION

Transmission of the virus takes place, mainly, through the feco-oral route. The virus may enter to the farm through equipment or staff contaminated with infected faeces. Infected animals shed a large amount of virus in faeces that fasten the spread through the flock.

It is a highly resistant virus, as it lacks an envelope, and it remains infective for a long time at low temperatures. It is also able to survive under moist conditions, like a wet litter.

PATHOGENESIS

HEV is absorbed in the intestine, replicates in the lymphoid cells of the intestinal tract and, through blood circulation, it reaches the bursa and spleen, where there is a primary replication, and then it is widely distributed in the body.

Target cells of HEV are lymphocytes, especially B lymphocytes. Virus replication leads to a great inflammatory response. Finally, this virus has immunosuppressive effects on humoral and cellular response, causing impaired phagocytosis and antibody production.

Inflammatory mediators in the intestine are initiators of diapedesis in the gut, which leads to intestinal haemorrhage. The damage in the gut walls allows, together with immunosuppression, the infection by opportunistic pathogens, exacerbating the effect on productivity and mortality of the virus.

CLINICAL SIGNS AND LESIONS

Virulent strains of HEV may cause depression, pallor and bloody droppings, followed by death. The clinical course may last for 7 to 10 days. Morbidity usually reaches 100%, and acute mortality can range from 1 to 60%, depending on the protection of the flock, with an average of 10-15%.

Birds that survive the disease suffer from transient immunosuppression, which may lead to secondary bacterial infections at 10-14 days after the exposure to the virus. Therefore, a second wave of mortality might appear and last for 2-3 additional weeks. Mortality due to secondary pathogens, such as E. coli, Clostridium perfringens, Mycoplasma and Eimeria, may overlap the first week and, in less virulent strains, may dominate the clinical picture.

Affected birds will produce low antibody titres after vaccination, as seen in Newcastle disease (ND) vaccination.

Lesions observed in HEV infected birds may include gross congestion and intraluminal haemorrhage in the duodenum, that may be extended distally in severe cases. Splenomegaly and marbled spleen may also appear.

Lesions caused by secondary disorders are commonly associated with respiratory and septicemic lesions, including fibrinopurulent pneumonia, airsacculitis, pericarditis and peritonitis.

DIFFERENTIAL DIAGNOSIS

Diseases causing similar splenic and gastrointestinal lesions to HEV should be considered, including colibacillosis, pasteurellosis, salmonellosis, ersyipelas and other viral diseases like avian influenza and ND.

DIAGNOSIS

Presumptive diagnosis of the disease should be on the clinical signs and necropsy lesions. Definitive diagnosis is based on the identification of viral antibodies or antigens in the laboratory.

Samples of intestinal content and spleen should be used for this purpose. Diagnostic techniques available include:

• Culture of samples in B-cell line of turkey origin.
• Oral or intravenous inoculation of the sample to 6 weeks-old turkeys to assess mortality and splenomegaly.
• Agar gel precipitation, facing sample against anti-HEV sera.
• PCR, which is more sensitive than agar gel immunodiffusion in mild lesions.
• Immunofluorescence of the affected tissue.
• Avirulent and virulent strains of HEV cannot be distinguished by serology.

TREATMENT AND PREVENTION OF TURKEYS

HE outbreaks can be treated by subcutaneous injection with 0.5-1ml of antiserum from recovered birds. Recording secondary infections, antibiotics may be used and, if possible, election should be based on susceptibility of previous isolations.

The virus is resistant to chloroform, quaternary ammonia and ethyl ether compounds. After an outbreak, organic material should be properly removed and facilities should be cleaned. Disinfection should be made with sodium hypochlorite and phenolic compounds, followed by drying of 7 days at 25°C.

When commercial operations include multiple age groups of turkeys, eradication of the disease is difficult. Vaccination and antiserum are the most viable tools to prevent the infection, together with common biosecurity measures.

Biosecurity measures include pest management, litter complete removal and proper cleaning and disinfection of the facilities between cycles, using the products mentioned above. In addition, visits should be reduced, and all staff should shower and wear clean clothing in the farm.

Vaccination plan of HEV is based on avirulent strains or recombinant vaccines, which can be administered in ovo to embryos of 18-19 days or through the drinking water at 3-6 weeks of age. Field boosts one week after the initial vaccination can be performed. Water quality and supply should be assessed to ensure a proper efficiency of the vaccination. Full protection of vaccination is considered if at least 60% of the flock is serovonverted. Recombinant vaccines may not protect the flock against some field strains. Some vaccination plans may include in ovo vaccination with recombinant vaccines combined with a posterior live vaccine.

Concomitant infections caused by other immunosuppressive virus, added to the stressful condition of the intensive breeding and management practices, may hinder the ability of the immune system to create a proper response to vaccination. The use of natural additives is indicated for these situations.

Natural immunostimulant solutions based on pronutrients, active molecules of plant origin, are able to promote the activity of the innate and adaptative immune system to ensure higher antibody production after vaccination, as seen in the trial below.

EVALUATION OF THE EFFECT OF A NATURAL IMMUNOSTIMULANT
ON VACCINATION TITRES AGAINST HEV

Two groups of 288 turkeys each. One was the control batch (no immunebooster),
while the other received immunostimulant pronutrients in drinking water at 1 ml/l the 5 days
prior and the 5 days after vaccination against HEV.

Antibody titres were evaluated prior to vaccination, and at days 21,
63 and 96 after vaccination.

RESULTS OBTAINED:

PRONUTRIENTS GROUP HAS INITIAL LOWER ANTIBODY TITERS THAN THE CONTROL GROUP BUT SHOWS
A GREATER INCREASE OF THESE TITRES AFTER VACCINATION, WHICH END UP HIGHER THAN THE CONTROL

GREATER INCREASE OF ANTIBODY TITERS THANKS TO IMMUNOSTIMULANT PRONUTRIENTS MEAN THAT
THESE ANIMALS WILL BE MORE PROTECTED AGAINST THE DISEASE.

CONCLUSIONS

Haemorrhagic enteritis (HE) is an acute gastrointestinal disease of turkeys caused by a type II adenovirus. It is a widespread infection affecting young turkeys from 4 to 12 weeks of age.

HE causes high economic impact due to the mortality caused by the virus itself and the secondary bacterial infections related to the immunosuppression caused by HEV.

Nowadays, highly pathogenic outbreaks of the disease are less common thanks to the prevention plans based on vaccination and biosecurity measures stablished. However, when vaccination does not provide a proper immunity, secondary bacterial infections may appear, especially colibacillosis, which may lead to economic losses due to mortality.

Concomitant immunosuppressive infections and stressful conditions may hinder the ability of the immune system to create a proper response to vaccination. The use of natural additives is indicated for these situations.

Natural immunostimulant solutions based on pronutrients, active molecules of plant origin, are able to promote the activity of the immune system to ensure a higher antibody production after vaccination and a proper protection against the disease, as demonstrated in the field trial results described above.

BIBLIOGRAPHY

Dhama, K. et al. (2017). Haemorrhagic enteritis of turkeys – current knowledge. Veterinary Quarterly. http://dx.doi.org/10.1080/01652176.2016.1277281
L. Shivaprasad, H. L. (2014). Overview of Hemorrhagic Enteritis/Marble Spleen Disease in Poultry. Merck Veterinary Manual.