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Kid Care
Floppy Kid Syndrome
By Brad Gillmore
Oct 27, 2002, 11:29pm

Floppy Kid (Goat) Syndrome
3/31/1998
Brad Gillmore
Area Livestock Agent (Livestock)
Colorado State University Cooperative Extension
Golden Plains Area

It appears isolated cases of Floppy Kid Syndrome have shown up in Colorado. However, it may be more widespread than previously known, due to death of kid goats prior to diagnosis. The following summary hopefully will help with diagnosis, treatment and recovery of kid goats in the future.

Background

Kids with this clinical syndrome were first reported in spring of 1987, although there are anecdotal reports of herds with this syndrome several years earlier. It was first recognized in herds on the west coast and in Canada, but more recently been recognized throughout the U.S. With the increase in popularity of Boer and other meat goats, there has been an apparent increase in reports of floppy kid syndrome in states where meat goat numbers are high.

Clinical Signs/Case Definition

A "floppy kid syndrome" case is defined as a kid who is normal at birth and develops sudden onset of profound muscular weakness (flaccid paresis, paralysis or ataxia) at 3 to 10 days of age. Affected kids cannot use their tongues to suckle but can swallow. Clinical signs are similar to those of infant botulism. Affected kids have a marked paradoxical metabolic acidosis with no detected repeatable abnormalities in specific organ systems. Thus, affected kids have no signs of diarrhea, respiratory disease, or other signs referable to a specific organ system. Many kids with white muscle disease, abomasal bloat, colibacillosis, septicemia, or enterotoxemia have been mistakenly described as floppy kids (remember that any profoundly weak or acidotic kid will appear to be floppy or limp).

Treatment

Early detection and correction of base deficit as well as good supportive care are critical. Less severe cases are most commonly treated by owners with oral bicarbonate at the onset of signs. Kids may need to be fed milk by stomach tube. More severely affected kids require blood chemistry to assess severity of base deficit and correction of electrolyte imbalances by intravenous fluids (1 .3% NaHCO3).

Spontaneous recovery (with no treatment) can occur even in very severely affected cases, but case fatality rates as high as 30-50% have been reported. Observations of relapses, as well as prolonged recovery of neuromuscular function (4-6 weeks) have been reported.

In a review of case histories from multiple herds, no association was found between treatment with a variety of antibiotic and vitamin/mineral supplementation treatments and clinical response. Because the causative agent is not known, no preventive or therapeutic treatments (aside from correction of electrolyte imbalance and supportive care) can be specifically recommended. Further, spontaneous recovery in some kids makes comparison of treated and untreated animals important in assessing treatment efficacy.

Diagnosis

Clinical signs of paresis/paralysis/ataxia in 3-10 days old kids and supporting blood chemistry values (paradoxical acidosis) are diagnostic features. Since the cause of the syndrome is unknown, necropsy of affected kids is highly recommended. Submission of early untreated cases for necropsy is recommended in herd outbreak situations. Clostridium botulinum, E. coli, and caprine herpes virus have been proposed as candidate causative agents, however these agents have not been definitively proven or excluded as potential causative agents.

Epidemiological Notes

Cases tend to occur most commonly late in the kidding season. Herd morbidity ranges from 10% to >50%. Analysis of management factors and treatment used failed to demonstrate goat or management risk factors associated with outbreaks in dairy goats. Affected kids were found in dam reared, pasteurized hand reared, unpasteurized hand reared herds. All breeds and dam parities were represented.

Floppy kid syndrome appears to be unique. Further exploration of clostridial species, E. coli, and other toxin-producing organisms as well as viruses is needed. A better understanding of the anion gap may also be of value in determining the cause of the syndrome. The reversibility of this syndrome is also intriguing. Careful case definition is needed, however, to avoid attributing floppy kid syndrome to other known causes of neonatal mortality.

Source: Joan Dean Rowe, DVM, MPVM, PhD & Nancy E. East, DVM, MPVM School of Veterinary Medicine University of California. Davis 95616


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