It is not uncommon to hear of broiler flocks experiencing up to one percent mortality, for 3 to 5 days, during the first 3 weeks of brooding. Mortality will appear suddenly, in an apparent normal flock, and often only affects one house on a farm and may repeat in the same house. Affected chicks develop nervous symptoms leading to paralysis and sometimes blindness. Affected birds are usually males, in good condition and are often found with breast down and feet and legs extended. Chicks that die show none of the classical lesions for nervous disorders and while survivors frequently exhibit varying degrees of enteritis and rickets it is not felt that these are initiating factors triggering the disease. Liver hemorrhages and necrosis are noted in a small percentage of birds and regressed thymus and bursa are often seen.

Feed analyses usually fail to indicate toxic compounds and seldom will feed from an infected flock reproduce the problem, nor will changing feeds alleviate the symptoms in an affected flock. While bacteria and viruses have been mentioned as causative agents, to date, no one has been able to conclusively demonstrate a direct involvement. Failure of the disease to spread on a farm suggests the condition is not the result of an infectious agent or feed contaminated with a single toxin.

To date the only consistent blood disorder noted is a severe drop in blood glucose levels (from 12 to 150 mg/dl – normal = 225 to 300 mg/dl). The low blood sugar is probably the cause of the nervous symptoms and weakness noted. However, hypoglycemia has not been shown to occur in tests with feed and water removed from chicks for 72 hours, thus suggesting that spiking mortality, as seen in the field, is not due solely to inadequate intake.

It would appear that two types of symptoms are noted with the condition, which has led workers to classify these as Type A or Type B spiking mortality. Type A is thought to be due to the rapid onset of hypoglycemia. Oral administration of sugar will sometimes reduce mortality, however, when sugar is removed from the diet chicks will still die, suggesting that the hypoglycemia condition still persists.

It is thought that a combination of intestinal and liver problems, coupled with secondary factors related to diet, cause the acute hypoglycemic condition and thus Type A spiking mortality. However, either factor alone does not appear to result in a large mortality spike. The initial factors triggering the condition appear to be intestinal and hepatic in nature and if the secondary feed factor(s) is not present, the Type B condition, resulting in poor performance and high chick variability but with no spike in mortality, is noted.

Since there is nothing specific to recommend as to how to avoid spiking mortality, or steps to take in alleviating an outbreak, it is of interest to look at other conditions that appear with young chicks and poults, which may be similar in nature, as their cause appears to be unknown as with spiking mortality they affect only a small percentage of a flock.

Infectious Stunting Syndrome

Infectious Stunting Syndrome, which has also been referred to as the “Malabsorption Syndrome”, “Helicopter Disease” etc., is a condition with some similarities to spiking mortality. In 1981 a stunting syndrome affecting broiler chickens was reported in the UK which resembled a condition described in the Netherlands in 1978. Severe economic losses were reported in the UK in 1981 from the condition. In 1982 at a seminar held in the UK, British, Dutch and American scientists discussed similarities of a stunting condition noted in their three countries. Proventriculitis was rarely seen in Britain but featured prominently in the malabsorption syndrome noted in the USA, while leg disorders were regarded as the most significant feature of the condition in Holland. The pale bird syndrome often reported in the United States was seldom seen in the UK but this may be due to the small proportion of corn used in UK broiler diets.

As reported from the UK the first sign of an infected flock is usually the observation of uneven birds usually between 1 to 2 weeks of age but it could be as early as 4 days of age. Approximately 5 to 20% of the flock appears stunted and mortality increases up to around 2 weeks of age. No characteristic findings are seen but excessive water consumption and diarrhea are often noted. By 3 to 4 weeks of age differences in feathering between normal and stunted birds is quite apparent. Growth of the primaries is delayed and often angled with the stunted birds, thus the description of “Helicopter Chick”. Appetite of the stunted birds is usually maintained and they often have pendulous or extended abdomens, due mainly to the intestines being full of poorly digested food.

The condition is also seen in turkey poults and is similar to that noted for broilers, however, the degree of stunting is usually less but abnormal feathering is usually more pronounced. Skeletal problems are frequently present with poults but rarely seen with broilers. Pathological examination can detect pancreatic changes as early as 8 days of age. The gland is diminished in size and is pale and firm in texture. The bursa of Fabricus and thymus are usually atrophied. Where bones are affected the growth plate lesions are similar to those seen with rickets. Disinfection of buildings appears to help alleviate the problem but does not eradicate it. There is limited evidence to suggest that some breeder flocks, early in their production cycle, can transmit the disease to their chicks, but with later hatches no problems are noted. Viruses and bacteria have not been ruled out as causative agents as the condition can be reproduced by exposing the chicks to material from infected birds.

An interesting observation is the very early onset of age resistance. By 7 days of age it is difficult to reproduce the stunting syndrome and by 14 days it is practically impossible. This could suggest that development of the normal gut bacterial flora plays a major role in protection.

Malabsorption syndrome, as seen in North America, has been shown to be due, in part, to the reduction of pancreatic digestive enzymes resulting in decreased fat and amino acid absorption. Serum levels of vitamins A, D and E have also been reported to be reduced. Reduced carotenoid absorption obviously accounts for the pale bird syndrome. Some workers have reported that immunoglobulin A, which is synthesized in the gut associated lymphoid tissues and serves in protecting against antigens absorbed through the digestive tract, is very low at the time that poults are hatched and increases markedly during the first few weeks of life. Hence, impaired digestion, along with relatively low gut stimulated immunity, may result in the young chick or poult being susceptible to an enteric disorder such as stunting syndrome.

Poult Enteritis

Poult enteritis, an enteric disease of young turkeys between the ages of one and four weeks, has also been referred to as turkey viral enteritis, malabsorption syndrome, stunting syndrome or maldigestion syndrome. Thus, one can readily see the similarity, as well as the confusion that exists when discussing non-specific early disease problems of broilers and turkeys. It is generally concluded that a major cause of malabsorption is immaturity of the gastro-intestinal tract, thus resulting in incomplete nutrient digestion. Enteric disorders associated with invasion of the GI tract by pathogenic organisms or parasites are probably the greatest cause of malabsorption for poults and broilers. Day old poults exposed to malabsorption syndrome causing material will, by 7 days of age, have growth reduced by 60 to 80%. However, exposure to the same material at 9 days will show reduced gain of less than 10%. Again as mentioned previously, a marked resistance to the condition is noted with age. Affected poult intestines are pale, thin-walled and filled with watery gaseous ingesta.

Changes in metabolism are known to occur as a result of an immune response to infection. During an immune response high priority is given to gluconeogensis and acute phase proteins at the expense of these nutrients for growth. Hence, the use of starter diets that contain a variety of protein sources has been suggested as being possibly helpful when used with an antibiotic like virginiamycin, often referred to as a “gut active” antibiotic.

The cause of malabsorption syndrome remains unidentified. However, since the condition can be reproduced by exposing chicks or poults to material from infected birds, this suggests the primary causative agents are viruses with opportunistic bacteria playing a secondary role.

Turkey Knockdown

Another condition seen in turkeys that is to some extent similar to the conditions described above is turkey knockdown. This condition affects the neuromuscular system with the result that the bird is not able to stand. A number of factors are reported to cause “turkey knockdown”, the most common being lumped into two categories:

1. Deficiencies of vitamins E or D, selenium, or a calcium, phosphorus imbalance which may cause the condition, or any nutrient that triggers musculo-skeletal problems.
   
2. Toxicity, high levels of nitrofurazone, ionophores, organic arsenicals, mycotoxins, salt and insecticides may be responsible for producing the condition. Monensin has been implicated on a number of occasions, but no one has yet to prove a direct involvement. Knockdown affects a small percentage of flocks and not a large percentage of birds within a flock. Since no known cause has been reported the signs of specific problems should be used to eliminate possible factors eg. vitamin D and E deficiency, arsenicals, mycotoxins etc.

Starve Outs

Another condition that may shed some light as to possible factors involved in the nonspecific diseases mentioned above is “starve outs”. Starve outs is a common problem that has been suggested to be the result of “out of phase nutrition”. Starting diets are high in carbohydrates. Such diets may not be in tune with the gastrointestinal tract of the newborn poult or chick. Nutrients to the embryo are manipulated by the yolk sac, especially in late developing embryos. After hatching the GI tract of the poult and chick are still designed to absorb lipid from the yolk. After about 2 days it is stated that the intestine is around 50% mature and complete maturity is not attained until around 2 weeks of age. This has led some people to suggest that the starting diet should contain a reasonable level of an easily digested fat source as well as a mix of well balanced readily digestible proteins.

Tipovers

Tipovers is another problem that is often reported with young poults and appears to be more prevalent with poults from a young breeder flock. Such poults, being hatched from smaller eggs, have a lower percentage of yolk than poults from larger, later hatched eggs. Poults from smaller eggs hatch earlier and expend their glucose reserves on emerging from the shell. If they then spend an extended period of time in the hatchery they depend on the catabolism of body fat to meet their energy requirements. This could lead to an excess of ketone bodies being formed which act like toxins in the body and are disposed of, in part, by cellular antioxidants like vitamin E.

Embryo Viability

It has also been reported that the first egg laid in a sequence (clutch) has less viable embryo than the subsequent eggs in a sequence. The rapid rise to peak production of today’s broiler breeders means that the flock is more synchronized, with respect to sexual maturity, than were the flocks of some few years ago. This would mean that not only are there a greater percentage of early eggs from a young flock, but there would also be a greater percentage of first sequence eggs leading up to peak egg production. What affect such pattern of egg production from young flocks would have on some of the non-specific early disease problems noted is open to speculation.

Vitamin E Supplementation

Recent recommendations call for adding additional vitamin E to poult diets as there are increased reports from the field of improved health status of flocks, with such a practice. Sporadic occurrences of encephalomalacia in 3 to 4 week old poults suggests the need for additional vitamin E supplementation in starter diets. Also there are a number of reports indicating enhanced disease resistance where diets have been supplemented with additional vitamin E.

Of interest is the work of researchers at Iowa State University showing that a marked drop in Vitamin E concentration occurs in the liver and plasma of poults, from around 35μg by 5 days of age and remains very low to at least 21 days (Table 1). While subsequent work failed to demonstrate any significant improvement in weight gain or feed:gain ratio, with increased dl alpha tocopherol acetate supplementation from 12 to 100 IU/kg of diet, Dr. Sell suggests that vitamin E depleted poults may be more susceptible to a variety of stresses and more specifically to be less resistant to disease. It has been well documented that dietary supplemental vitamin E enhances immune response in birds.

Another area of concern related to low vitamin E status of poults is that an insufficient level of antioxidant will be present at the cellular level. Vitamin E is the major antioxidant protecting cells against lipid peroxidation, by way of neutralizing free radicals produced. While the vitamin E status of the breeder will influence poult liver vitamin E levels at day of age, this carryover has little influence on liver vitamin E levels at a week of age. This suggests that supplementation of starter diets with vitamin E may be the only way to ensure adequate vitamin E levels in the young poult or chick.

Research, into identifying what factors influence the vitamin E status of the young poults has been unsuccessful. However, from the results of recent work, it would appear that early poult vitamin E status is not related to dietary fat level or source, nor is it related to diet antioxidant levels.

A recent report, Waibel et al (1994), indicates that the form of supplemental vitamin E may be important. Absorption of vitamin E is facilitated by bile and fat soluble nutrients and their incorporation into micelles for transport through the intestinal mucosa. Synthetic dl-α- tocopherol is the common source of supplemental vitamin E, as it is very stable. Natural α- tocopherol is usually not used as a supplement as it is very susceptible to oxidation. However, it does not require hydrolysis for absorption and when presented in a micellar form may bypass the need for bile salts, emulsification and micelle formation. Waibel and coworkers tested a micellized form of d-α-tocopherol in supplemented poults diets. Their results (Table 2) show the marked drop in liver vitamin E level, as reported by the Iowa workers, and while the micellized form of d-α-tocopherol gave slightly higher liver values when added to the diet, as compared to dl-α-tocopherol acetate, a higher level added to the drinking water, resulted in a marked increase in liver vitamin E levels to 26 days of age. Hence, more work is required to evaluate micellized forms of vitamin E and also to investigate whether increased levels in the liver are beneficial in alleviating some of the non-specific diseases referred to earlier.

Iron Intake

A recent article appeared (Omard and Blakely 1993) pointing out that high levels of iron intake lead to liver peroxidatation with the resultant depletion of liver vitamin E levels. What effect high intakes of iron have on the vitamin E status of poult or chick livers could not be found in a literary survey. There are a number of areas in Ontario that do have problems with high levels of iron in water. It would be of interest to take this into account when researching out possible factors triggering some of the non-specific early disease problems.

While the present article has strayed a fair way from the initial intent to look at factors that may be responsible for “Spiking Mortality” in poultry, a number of points or possible factors that should be considered in an attempt to reduce early, non-specific mortality are as follows:

1. Low blood glucose seems to be a common finding in birds suffering from several of the reported disease syndromes. Is this due to chicks hatching early and if so is this due to young early maturing flocks?
   
2. If as suggested the intestine is immature in young birds and thus not ready to handle the high carbohydrate and poorer digested plant protein sources provided in most starter diets, should a readily available source of an unsaturated fat be added to starter diets along with better balanced and more easily digested animal protein sources?
   
3. If age resistance is very specific, as has been shown by not being able to reproduce the malabsorption syndrome in birds beyond 10 days of age – thus suggesting that gut flora may be an important factor – should a probiotic approach or the feeding of a gut flora mixture be investigated?
   
4. Low levels of vitamin E in plasma and liver appear to be a common finding with young poults and chicks:
   • Is this a natural phenomenon?
     
   • Do high vitamin E liver levels help alleviate some of the non-specific disease problems?
     
   • It would appear that supplementing additional vitamin E starter diets would be a positive approach.
     
   • Looking into micellized tocopherol sources should also be pursued

References

Omard, F.O. and B.R. Blakley 1993 Vitamin E is protective against non toxicity and ironinduced hepatic vitamin E depletion in mice. Journal of Nutrition 123: 1649-1655.

Waibel, P.E., L.J. Felice, J.A. Brannon, F. Chen and M. Chen 1994. Vitamin E forms for turkeys. Journal of Applied Poultry Research 3: 261-267.

Turkey poults need added vitamin E. Turkey World; August – September 1993 pp 13-14.

October 2008