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Background:
Kids with this clinical syndrome were first reported in spring on 1987,
although there are anecdotal reports of herds with this syndrome several
years earlier. First recognized in herds on the west coast and in
Canada (Tremblay et al), it has 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
state where meat goat numbers are high.
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).
PHOTO OF FLOPPY KID ON THE COLORADO STATE WEBSITE.
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 |
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