Report prepared by Drs. Joan Dean Rowe and Nancy E. East

School of Veterinary Medicine

University of California at Davis

Clinical Signs/Case Definition:  A "floppy kid syndrome" case defined as a kid who is normal at birth and develops sudden onset of profound muscular weakness (flaccid paresis or paralysis) or ataxia at 3 to 10 day 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 ( anion gap,  HCO3), normal chloride, with no detected repeatable abnormalities (clinical blood chemistry) in specific organ systems (expect the acidosis and milk renal changes in some cases). Thus the case definition excludes kids with organ system abnormalities which could otherwise explain the acidosis.  The cause of the anion gap in unknown.  Some kids are also hypokalemic.  Affected kids have no sign of diarrhea, respiratory, disease, or other signs referable to a specific  organ system.  Many kids with white muscle disease, abomasal bloat, colibacillosis, septicemia, or exterotoxemia 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 of  Peptobismol 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. Observation of relapses as well as prolonged recovery of neuromuscular function (4-5 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 etiologic agent in 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 agents. 

Diagnosis:   Clinical signs of paresis/paralysis/ataxia in 3-10 day 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 etiologic agents, however these agents have not been definitively proven or excluded as potential causative agents. 

Epidemiologic Notes:   Cases tend to occur most commonly late in the kidding season.  Herd morbidity ranges from 10% to  50%.  Analysis of management factors and treatments 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, and unpasteurized hand reared herds.  All breeds and dam parties were represented. Floppy kid syndrome appears to be unique.  Further exploration of clostridial species, E.Coli and other toxin-producing organisms as well asviruses 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 intriguing and suggests a transient initiating insult.  Careful case definition is needed, however, to avoid attributing floppy kid syndrome to other known causes of neonatal mortality. 

Reference:  Tremblay  RM, Butler DG, Allen JW, Hoffman AM.  Metabolic acidosis without dehydration in seven goat kids. Can Vet J 1991; 32:308-310