AVIAN/FUR/EXOTIC SPECIES

A flock of 8,000 7-week-old meat turkeys, fed a ration including an anticoccidial ionophore and virginiamycin, were raised in a concrete-floored grower barn on reused litter.  A sudden spike in mortality with 25 dead per day, elevated from 4 per day, caused the producer to submit birds to his poultry vet for postmortem.

At postmortem, pale caseous exudate was identified in the lumen of the small intestine and small raised white to yellow foci dotted the liver capsule but did not appear to extend into the parenchyma (Figures 1A & B).

Mortality was considered to be due to necrotic enteritis (NE) developing secondary to intestinal coccidiosis.  Four days of treatment with water-soluble potassium penicillin was implemented and birds responded, however mortality recurred 5 days after the completion of the antibiotic treatment.  In the experience of one of the authors (LW), it is not unusual to see recurrence of NE in turkeys following treatment.  More birds were submitted for postmortem and samples of small intestine and liver were submitted for histology and fresh liver was provided for bacterial culture.  Moderate numbers of Clostridium perfringens and E. coli were isolated from fresh liver.

Histologically, the intestinal lesions were typical of necrotic enteritis with foci of acute mucosal necrosis and inflammation populated by colonies of rod-shaped bacteria resembling Clostridium perfringens.  In addition, numerous roundworm larvae with characteristic lateral alae were present in the lumen, penetrating into the mucosa, in association with the foci of acute mucosal necrosis and inflammation (Figure 2).  No coccidial organisms were seen.  In the liver, foci of granulomatous inflammation, often near portal triads, contained central cores of caseous exudate and roundworm larvae (Figure 3).

An uncommon cause of necrotic enteritis in a flock of 7-week-old Ontario meat turkeys  

Marina Brash, Margaret Stalker, Lloyd Weber

 

The histologic diagnoses of necrotic enteritis induced by a heavy burden of intestinal Ascaridia dissimilis roundworm larvae and multinodular parasitic hepatitis secondary to roundworm larval migration were surprising, but explained why the necrotic enteritis recurred shortly after the completion of the antibiotic treatment.  Anthelmintic treatment of the previous 2 flocks of turkeys raised in this grower barn had not been carried out, but the roundworm burden had been continually assessed through the routine checking of daily mortality and was negligible.

The life cycle of A. dissimilis was originally thought to be similar to Ascaridia galli, the chicken ascarid with only intra-intestinal stages.  However, hepatic foci in turkey livers emerged as an issue in US processing plants in the late 1980s causing the slowing of processing lines and increased liver condemnations.  From the field, there were reports of high mortality from necrotic enteritis associated with the presence of large numbers of intestinal roundworm larvae and also of reduced market weights at processing.  At that time, turkey ascarid infection studies were carried out and confirmed the ability of A. dissimilis larvae to cause liver lesions.  If poults are challenged from 1 day of age, liver lesions can develop within 7 days with the route of migration via the portal circulation.

Roundworm eggs are extremely resistant to environmental influences, so if turkeys are being raised on reused litter, routine deworming is highly recommended.  With heavy roundworm infections, the maturation of the fourth-stage A. dissimilis into adults can be delayed, so the choice of parasiticide is also important as certain anthelmintics target the adults but are not larvicidal and it is the larvae that are tissue invasive as part of their normal life cycle.   

Caseous exudate (yellow arrow) was identified in the lumen of the small intestine.

Small raised white to yellow foci dotted the liver capsule.

 Focus of small intestinal mucosal necrosis and inflammation containing colonies of bacteria resembling Clostridium perfringens and multiple ascarid larvae. 40X H & E

Hepatic periportal multinodular inflammation with central cores of caseous exudate and roundworm larvae surrounded by macrophages, multinucleated giant cells with an outer layer of plasma cells, lymphocytes and granulocytes. 100X H & E

Figure 1A: Caseous exudate (yellow arrow) was identified in the lumen of the small intestine.

Figure 1B: Small raised white to yellow foci dotted the liver capsule.

Figure 2: Focus of small intestinal mucosal necrosis and inflammation containing colonies of bacteria resembling Clostridium perfringens and multiple ascarid larvae. 40X H & E

Figure 3: Hepatic periportal multinodular inflammation with central cores of caseous exudate and roundworm larvae surrounded by macrophages, multinucleated giant cells with an outer layer of plasma cells, lymphocytes and granulocytes. 100X H & E