Floppy Kid Syndrome
prepared by: Pam Meier
Floppy kid syndrome, by definition, is an acute onset of profound weakness / tetraparesis associated with metabolic acidosis in which no specific organ systems are abnormally involved. Gastrointestinal and respiratory clinical signs, such as diarrhea, dehydration, or dyspnea, which commonly preclude metabolic acidosis, are not observed. Careful case definition is essential to avoid attributing this syndrome to one of the several conditions of neonatal goat kids that present with nonspecific signs of depression and weakness.
First documented in 1987, floppy kid syndrome is becoming more recognized throughout the United States due to the increasing popularity of goat husbandry. Similar cases have been observed in neonatal calves and a llama cria. Presently, the etiology is unknown and further research into the pathogenesis of this condition is necessary. Treatment with intravenous fluids and supportive care often leads to a dramatic improvement. However, spontaneous recovery can occur suggesting that this syndrome is a transient insult.
The causative agent for this syndrome has not been determined.
Despite the lack of corresponding clinical signs on presentation, gastrointestinal disease is strongly suspected to be the cause for this syndrome since it is the most common cause of neonatal ruminant metabolic acidosis.
It is highly recommended to submit early untreated cases for necropsy in order to aid in the determination of the etiological agent.
Affected kids are normal at birth.
Development of sudden profound muscle weakness (ataxia, flaccid tetraparesis, or tetraparalysis) is apparent at 3 to 10 days of age.
Kids are often reluctant to suckle but can swallow.
Depression is a common finding.
Marked paradoxical metabolic acidosis is present with no detected, repeatable abnormalities in specific organ systems with the exception of mild renal changes in some cases.
Other biochemical findings include an increase in anion gap, decrease in bicarbonate, normal to increased chloride, and occasional hypokalemia.
No gastrointestinal or respiratory dysfunctions are apparent (i.e. diarrhea, dehydration, or dyspnea).
Diagnosis is made based on supportive clinical and laboratory findings.
Blood chemistry is necessary to assess the severity of the base deficit and electrolyte imbalances.
Affected kids are under 2 weeks of age.
Any disease that can lead to a profoundly weak or acidotic kid can be mistaken for this syndrome.
Examples include white muscle disease, abomasal bloat, colibacillosis, septicemia, or enterotoxemia.
Similar disease has been noted in calves and a llama cria.
The llama cria presented in a similar fashion to the kids, without gastrointestinal or respiratory clinical signs.
Acidotic calves were found to suffer from dehydration, diarrhea, and slow, deep respirations which are not observed in goats.
Additionally, the calves demonstrated an increase in blood lactate leading to an overall increase in anions in the plasma that was not consistent with the blood chemistry of the kids.
Early detection and correction of base deficit as well as essential supportive care are critical.
Less severe cases can be treated with oral bicarbonate by owners at the onset of clinical signs.
Kids may need to be fed milk by a stomach tube due to their reluctance to suckle.
More severe cases need to be treated with isotonic intravenous 1.3% sodium bicarbonate solution.
Dramatic clinical improvement is noted after administration of intravenous fluids.
There appears to be no association found between the treatment with a variety of antibiotics or vitamin / mineral supplements and clinical response.
Furthermore, spontaneous recovery without treatment can occur in severely affected cases.
This observation questions the effectiveness of the above-mentioned treatment.
Relapses and prolonged recovery of neuromuscular function (up to 4 to 6 weeks) have been reported.
Herd morbidity have been reported from 10% to less than 50%.
Case mortality rates have been documented as high as 30 to 50%.
There appears to be no correlation between the prevalence of the disease and management risk factors.
Affected kids were found with dam reared, pasteurized hand reared, as well as unpasteurized hand reared herds.
All breeds and dam parities were represented.
Cases tend to occur late in the kidding season.
Rowe JD, East NE. Floppy Kid Syndrome. Western Veterinary Conference, Small Ruminants for the Mixed Animal Practitioner 1998; 986: 135 - 6.
Shepard G, Petrie L, Naylor JM. Metabolic acidosis without dehydration in a llama cria. Can Vet J 1993; 34: 425-6.
Smith M. Goat Medicine. Philadelphia: Lea and Febiger, 1994: 551 - 3.
Tremblay RM, Butler DG, Allen JW, Hoffman AM. Metabolic acidosis without dehydration in seven goat kids. Can Vet J 1991; 32: 308 - 310.
For More Information on this topic or to suggest other topics Contact:
Cleon V. Kimberling, D.V.M.
Colorado State University VTH
Fort Collins, CO 80523
***Information - Service of
GoatConnection.com - Khimaira***
Top of Page