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Illness in Poults

Research uncovers some interesting questions about the cause(s) of PIPES in U.S. flocks


May 7, 2008
By Brett A. Hopkins MS DVM PhD DACPV CEVA Biomune Company

Topics

Research uncovers some interesting questions about the cause(s) of Poult Immunosuppression Pancreatic Enteritis Syndrome (PIPES) in U.S. flocks

may-2008
CAUSES EXPLORED
Research on a syndrome known as PIPES in poults is being conducted to understand the cause.

Over the years of turkey production producers have observed unexplained illness occurring in their turkeys that has typically been expressed as unthrifty poults with enteritis while they are in the brood barns. The affected flocks never fully recover and they are more susceptible to environmental stresses, hemorrhagic enteritis virus (HEV) vaccination, E. coli and other organisms normally found in a turkey barn.

Names such as summer enteritis, late summer enteritis, eight-12-week syndrome, poult enteritis, two-week enteritis, three-to-five-week syndrome, turkey runting and stunting, noisy poults syndrome, and flushing syndrome have been assigned to the various conditions producers have seen repeat in their poults growout after growout or season to season. The age and time of year but an unexplained illness has been occurring in commercial market turkeys from the Midwest to the east coast.

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In 2007 a focused investigation of these illnesses in turkeys led to finding similar to identical pathology and clinical disease as well as age at onset, duration, and sequelae at several locations in the U.S. The consistent findings and ancillary information gathered to date supports a syndrome and the name given for this illness is: “Poult Immunosuppression Pancreatic Enteritis Syndrome” (PIPES).

The clinical symptoms and known epidemiology of the syndrome are eerily similar to the Runting and Stunting Syndrome (RSS) in broilers. The syndrome name given for the turkey disease provides a more accurate description of the pathology that also leads to reduced growth (stunting), enteritis and to a lesser degree mortality. One of the etiologic agents of PIPES has been initially identified as an Avian Rota virus type D, which is very similar to identical to the Avian Rota virus isolated from broiler chicken with RSS. At present the virus has been isolated from turkey intestines that were exhibiting pathology consistent with PIPES.

The gross pathology of PIPES consist of severe atrophy and eventually complete ablation of the thymus.  I currently estimate it takes a minimum of four to five days after infection of the thymus for complete ablation to occur. As the atrophy of the thymus progresses it loses its lobular appears and coalesces into a single thin band of tissue that continues to get smaller until it is completely gone. Severe and permanent atrophy of the bursa of Fabricius, atrophy of the spleen and atrophy of the pancreas which may or may not have hyperemia with multifocal white spots.

As the infection progresses the pancreas becomes very pale ending up close to white in color and eventually, if the damage is severe enough, some regions of the pancreas may be as hard as cartilage.  

The characteristics of the enteropathy vary with the stage of infection with the classical lesions initially consisting of edema, thickening of the wall and enlargement of the intestines with thick mucoid creamy to curdled milk consistency ingesta seen more commonly in the duodenum, that progresses to extreme thinning of the intestinal wall to the point of transparency with a lumen filled with clear to mildly tan to caramel colored thin mucous, fluid and occasional small chunks of cellular debris or ingesta.

The duodenum, jejunum, ileum, ceca and colon can all be affected but it is has not been common for the lesions to be seen at the same time through the entire gastrointestinal tract. Typically only one or two sections of intestine are affected at necropsy. The enteropathy will progress down the intestine, starting with the duodenum then moving down to the jejunum and then into the ceca and finally the colon in some cases.

Finding poults with only cecal lesions is common especially in flocks that have progressed to a later phase of infection which is more common in flocks older than 12 days of age.

Many poults from an affected flock have had normal appearing intestines upon examination between 8-24 days of age. This is due to those poults not having the disease or they are examined before the pathology has started or too late after the enteropathy has subsided and the intestines have repaired which is typically seen in poults older than 17 days of age. The highest odds of virus isolation occur when culturing poults between 8-18 days of age that have the intestinal lesions described above. 

Many of the poults appear to have thin pale anemic blood that does not clot normally. In these poults the muscles including the heart, liver, kidney, appear very pale in colour. Most poults do not have purulent air sacculitis, tracheitis, peritonitis, synovitis, pericarditis, etc., but mild sudsy air sac and an occasional Aspergillus nodule have been seen as secondary invaders.  Increased mortality and E. coli infections two to three weeks post splenic origin HEV vaccination are also common.

The affected poults are likely to have malformed feathers especially the primary and secondary wing feathers, they will be  stunted in growth, likely have fecal accumulated below the cloaca (pasty vents), may  appear depressed with increased respiration rate and have an elevated temperature or they may exhibit a normal appearance. Some flocks have been reported to exhibit feed passage or flushing with caking of the litter. A through necropsy of several poults ranging from small, sick, cull-like to large normal appearing poults is recommended to aid in making the correct diagnosis.

The development of the PIPES can be broken down into six phases. The hallmark of phase I is the immunosuppression created by the necrosis and eventual absence of the thymus, atrophy of the spleen and bursal of Fabricius and suspected bone marrow suppression. A notable symptom during phase I is increased vocalization (The affected poults are very noisy. This is the first symptom the growers notice). Phase I appears to begin as early as four days of age with five to eight days of age being very common. The poults appear to be immunocompromised for life following the initial infection and immunosuppression.

One explanation for the lifelong immunosuppression is that once the thymus has been completely destroyed, regeneration is impossible and even poults that survive to older ages through to processing never regain a thymus.

Phase II is the damage to the pancreas consisting of multifocal necrosis and degeneration. The exact onset of phase II has not been confirmed and in some cases may occur simultaneously with phase I or III. The pancreatic damage initially appears to be viral related but it is not clear if a different virus or the virus(s) responsible for the immunosuppression or enteritis is also infecting the pancreas. During the time the pancreas is being damaged the poults continue to vocalize (get noisy), go off feed, may appear chilled, (may huddle in some flocks), and exhibit a fever. Phase II is the beginning of the growth retardation. Phase III consists of intestinal lesions. The immunosuppression that occurs in the first phase of the PIPES appears to be so severe that aggressive changes of the intestinal bacterial and micro flora lead to invasion and replication of pathogenic bacteria (Clostridium spp.) and an intestinal virus(s) (Avian Rota virus). The estimated incubation time starting with Phase I, before observing gross lesions in the intestines, is about four to seven days. The intestinal phase (Phase III) is typically first seen between 8-12 days of age. The vocalization continues through Phase III and the poults begin to look rough (curly, dirty feathers, lethargy, depression, sleepy-eyed with head drooped), pasty vents from diarrhea and flushing becomes common, the house may begin to “smell” different, the poults have a fever, an increased respiratory rate and possibly open mouth breathing is common. It becomes obvious that the uniformity of body size is poor as “sizing” has begun to occur and it appears as though some poults have completely stopped growing. It would be very typical to be able to select poults that appear to be the size of six-nine-day-old poults from a flock that was actually 15 days of age. 

Phase IV
is the onset of secondary infections such as crop mycosis, E. coli, air sacculitis as a result of the immunosuppression and enteritis.


Phase V
is the mortality. Limited mortality is associated PIPES but the severity of the enteritis and secondary invaders can be bad enough to increase mortality. There is typically a rise in mortality in the two to three weeks following HEV vaccination, especially when a splenic origin vaccine has been administered. The quality of the husbandry and other interventions play a big role in the degree of mortality associated with PIPES.


Phase VI
consists of surviving poults that are stunted in body size, do not have a functioning thymus, have atrophy of the bursa of Fabricius and spleen and may have overt or covert secondary infections. Crop mycosis was a very common finding in PIPES flocks beyond 21 days of age and especially in the grow-out barns. Most PIPES flocks resume eating and some may even appear “normal” while others still appear to have an illness and stunting would be very obvious in one to 30 per cent of the flock.

The PIPES birds may survive to be processed but they are generally very “light” in weight (three to 15 lbs. less than average).  It should be made clear that at all ages the normal-sized birds in the flock have an intact normal-sized functioning thymus, bursa of Fabricius and spleen, and appear healthy.

The earliest symptom is increased vocalizations (noisy poults). As the infection progresses over the next week the affected poults decrease feed consumption; become lethargic, sleepy-eyed with head drooped, or depressed; have an increased respiration; and run a fever. Once the intestinal disruption or syndrome phase III begins four to seven days after the initial increased sounds the poults begin to exhibit loose stools, flushing, dirty or pasty vents. The feathers become dirty and may be curly.

Body growth is dramatically slowed or stopped for several days. The feathers and especially the wing feathers continue to grow and the primary wing feathers will extend well beyond the tail and rear of the poult.  The overall feather quality is diminished. The feathers appear rough, some may be curly others are very long. Urates may accumulate at the vent in dehydrated poults. The litter quality may suffer as the poults excrete liquid feces and the feet or foot pads will become “caked” with litter and feces. The uniformity of body size deteriorates rapidly and there will multiple sizes of poults by 14 to 21 days of age. Many of the 21-day-old poults will be the same size as they were at 10 to 12 days of age, as it appears they have stopped growing at the onset of Phase II or III.

The initial lesions in the thymus consist of multifocal to coalescing necrosis of lymphocytes with infiltration of heterophils in more advanced lesions. In many poults with clinical PIPES lesions the thymus is completely gone, thus preventing histologic examinations.

Spleen: moderate to severe diffuse depletion of lymphocytes and white pulp cells were the most common finding and infiltration with RBCs was common. Bursa of Fabricius: moderate to severe lymphocyte depletion and reduction of the number and size of follicles, fimbrae atrophy and fibrosis.

Pancreas: Multifocal to coalescing interstitial necrosis of exocrine cells, and occasional basophilic cytoplasmic inclusion bodies have been seen in some sections.

Crop: Common to find multifocal infiltrations with Candida albicans. Intestines: It was very common to find many poults in a flock with normal intestines; however typical PIPES poults had severe atrophy and fusion of villi, to the point of only having viable crypt cells, RBC congestion or hemorrhage, epithelial necrosis, severe architectural disorganization and some lymphocyte infiltration in the lamia propria.

The intestines that had edema of the intestinal wall and thick mucoid or thin watery intestinal contents had classic severe viral enteropathy histologically with an overgrowth of gram positive bacterial rods typical of Clostridium spp.
 
There does not appear to be any association with breed or sex. Housing and rearing practices may influence the severity of the disease but not the onset of the PIPES. Some companies have reported a seasonal onset (summer or late summer earlier fall) but PIPES can most likely be found year round with seasonal peaks.
 
Poult Immunosuppression Pancreatic Enteritis Syndrome has been recognized in most turkey growing regions from Texas and to the eastern shores of the U.S. The PIPES does not appear to have been recognized yet west of Texas in the U.S. Onset always occurs in the brood barns with observation of typical clinical signs between eight and 12 days of age. Many brood barns are split into two sections by a wire or chain-linked fence that separates the birds into two flocks in a single barn. This fence obviously would not stop the horizontal spread of a virus but the PIPES has not been shown to pass from one flock or half house to the other or to other barns on the same farm.

The initial investigations have led to a suspicion that there may be a link to certain young (<10 weeks in lay) breeder flocks and susceptible poults/flocks, suggesting a role of vertical transmission or an important role of protective maternal antibodies.  At this time it is speculated that the PIPES occurs as a result of either or both, a passive vertical transfer of the infective immunosuppressive virus or the lack of passive transfer of protective maternal antibodies to their progeny. This initial assumption is based on the observation that the PIPES does not appear to spread from one half of the brood barn to the other. One side of the brood barn may be severely or moderately affected by PIPES and the other side or half may have normal poults. The only difference is the breeder flock source or sources.

When affected birds are mixed with normal birds during routine housing changes, the infection does not appear to spread. Horizontal transmission may play some role as infected poults shed virus in the house and it is picked up by susceptible flock mates but having susceptible flock mates is the key. Poults from other breeder flock sources housed in the same brood barn do not appear to be susceptible. There also may be an age of susceptibility of one to 14 days of age or maybe even up to 28 days of age in a rare case. The majority of all affected flocks start to show symptoms before 20 days of age and most start around seven to 14 days of age. When an affected flock has been co-mingled with another flock after four weeks of age there has not been any indication of the spread of the infection. Interestingly though the Avian Rota virus will easily spread from pen to pen on research facilities.

 The cause of and exact age of onset of the immunosuppression has not been determined to date and this aspect of the PIPES has piqued my interest and ranks as the highest priority of the investigation. The enteritis has been duplicated in turkey poults at one day of age in challenge studies using the Avian Rota virus isolated from PIPES turkey poults and the Avian Rota virus isolated form broiler chickens with RSS symptoms. Interestingly there was much less immunosuppression in the poults from these challenges, which provides for the assumption that a second or third virus may be synergistically involved in the PIPES to initiate the immunosuppression. 

What is causing the immunosuppression? Are multiple viruses involved, i.e., is there a single immunosuppressive virus and a second or third pancreatic and intestinal virus? Or is there only a single virus that is replicating in the intestine, pancreas and the lymphoid organs, creating immunosuppression?

Does the initial infection start in the thymus, causing immunosuppression, then move into the pancreas and intestines or does initial immunosuppression open the door for an intestinal virus to invade and create clinical symptoms? What is the role of vertical or horizontal transmission and does the presence of or lack of maternal antibodies play a part in the prevention or onset of the PIPES?

This research was presented at the 2008 Midwest Poultry Federation Conference in St. Paul, Minn.


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