Spiking Mortality Syndrome of Chickens
Spiking mortality syndrome of chickens (SMSC) has been classified as such for approximately ten years. During the first experiences with the disease a number of causative agents were implicated, yet the symptoms remained relatively the same.
From approximately 1988 to 1990 the syndrome reached critical epidemic proportions particularly in the Delmarva area of the U.S. Isolated cases were also reported at that time in Georgia, Alabama and Arkansas. In 1990 the problem became so severe that a task force was developed in the Delmarva area in order to bring some definition to the syndrome. Since that time some management changes were made and the incidence of the disease decreased in that area.
Approximately around 1992, the incidence of spiking mortality in chickens took a severe jump in Georgia and to a lesser extent Alabama. Sporadic cases were also still being reported in the Delmarva/North Carolina area. Several possible causes were implicated, but nothing conclusive was identified. Since that time Dr. James Davis of the Georgia Poultry Laboratory, in conjunction with several researchers across the U.S., conducted exhaustive and extensive research and uncovered an emerging virus with other interesting revelations. The conclusions of the Delmarva task force and the research findings of Dr. Davis have helped to reduce the severity of a flock that experiences SMSC. Yet, the syndrome still occurs and no absolute eradication of the problem is in sight.
The general symptom of spiking mortality in broilers is a sudden and unexpected jump in mortality from 8 to 16 days of age. The mortality lasts for three to five days, after which, the mortality patterns return to a relatively normal level.
Affected birds become recumbent, depressed and often go into a star-gazing spasm. Death often occurs within two to six hours after the onset of the symptoms. Characteristically, birds that exhibit clinical symptoms but survive the acute phase, will continue to be unthrifty and stunted for the rest of the grow-out. Dr. Davis has presented research to indicate that surviving birds may weigh as little as one half of the weight of unaffected flock-mates by the end of the grow-out cycle.
The 1990 Delmarva Task Force on SMSC further defined the lesions and symptoms into Type A and Type B. Type A was defined as any house of birds experiencing a daily mortality of >5 birds per 1000 between 8 to 16 days of age. The symptoms must occur for a duration of not more than three days, with birds exhibiting all or a portion of the physical signs and lesions characteristic of the syndrome. Those signs included, huddling of the birds, trembling, blindness, loud chirping, litter eating, ataxia, comatose, birds dead with breast down and feet and legs straight out behind birds. Males are predominantly affected and survivors exhibit great variation in sizes. Lesions described with this syndrome include hemorrhages in the liver with necrosis of liver cells, regressed thymus, regression of the bursa of Fabricius, dehydration with the accumulation of kidney urates, fluid in the crop, fluid in the lower gut and watery contents of the ceca.
Type B spiking was defined as any house of birds exhibiting a significant mortality during the ages of 8 to 16 days of age. The mortality may extend longer than three days but the rate is less than five deaths per 1000 per day. Also the Type B affected birds did not exhibit the symptoms and lesions of the Type A affected birds.
Regardless of the "Type" of spiking mortality, one of the hallmark lesions is hypoglycemia or low blood sugar. Also most cases have been refractive to supplemental medication or feed changes.
A number of causative agents have been implicated in this devastating syndrome.
Mycotoxins or a microtoxin were first implicated. This was based on the evidence of liver lesions and trace-back examinations of affected flocks. Through trace-back investigations, several investigators found that affected farms received feed containing feed ingredients from specific geographic locations in the U.S. Further research at the University of Georgia indicated that the syndrome was indeed feed related. When the feed from affected birds was given to normal birds, the normal birds started exhibiting signs of SMSC.
Feed ingredients have also been investigated. Investigations by the Delmarva Task Force studied the possibility of cocklebur seeds getting into the feed. Nothing was ever substantiated that cocklebur seeds were getting into the feed, and laboratory studies proved inconclusive in reproducing the syndrome.
Management factors were suspected during the early outbreaks of SMSC by many live production managers. Several ideas were put forth such as cold half house brooding, starvation of the birds and starting chicks on old feed. Substantiation of these mismanagement situations are difficult to address. However, it is interesting that as some attention has been given to improving management practices, the incidence of SMSC has declined.
Viruses were suspected during the initial outbreaks of SMSC. The Delmarva Task Force reported on the isolation of an adenovirus from flocks experiencing the syndrome. Additional studies on the effect of an adenovirus have been conducted at the University of Georgia. These experiments have also not been conclusive.
An arenavirus has been consistently isolated, in extensive studies by Dr. James Davis, from the feces of chicks exhibiting SMSC. Dr. Davis’ work has shown that higher numbers of arenavirus particles are found in the feces of broilers, broiler breeders and commercial layers experiencing enteritis. However, the feces of chickens experiencing spiking mortality, have particularly high numbers of virus particles. Since then, Dr. Davis and others have conducted a number of different experiments and have reproduced the syndrome with the arenavirus. However, it appears that it may take more than just a viral infection to incite the syndrome. Dr. Davis’ research indicates that shortly after infection by the virus, a short period of starvation for the chicken is enough to elicit the syndrome. Arenaviruses are known to infect mice, other rodents, birds and men. The virus infects areas of the brain that regulate hormone levels in the body, particularly growth hormone. Mice infected with the arenavirus have been found deficient in growth hormone which results in hypoglycemia and growth depression.
As there have been a number of different causative agents suggested, there have been a number of suggested treatments and preventative measures.
The only successful treatment of SMSC in the face of an outbreak has been the therapeutic use of quinolone antibiotic in the water. Other remedies tried have included, changing feed, vitamin supplementation in the water, and adding sugar to the drinking water. No consistent success have been achieved with these treatments.
A number of management techniques have been employed to reduce the chance of SMSC. Some common-sense measures such as adequate warming of the post-brood chambers, rodent control and darkling beetle control appear to have offered some help.
One technique that has offered the best help in reducing the incidence of the syndrome is a lighting program, which restricts the amount of light the broilers are exposed to. The theory of the lighting program is to increase the amount of darkness the broiler is exposed to as the bird matures. The effect of this is to increase the level of melatonin (a natural hormone released from areas of the brain). Higher levels of melatonin may help to elevate the level of growth hormone and reduce the opportunity for hypoglycemia. Thus far, it appears that the lighting program has been successful both experimentally and in practical usage. However, the lighting program has not proven to be a cure-all. Sporadic outbreaks of SMSC still occur regardless of what management practices have been employed.
By Dr. John Schleifer (Hoechst Roussel Vet, Gillsville, GA)
Published by the Government of Alberta Agriculture and Rural Development