Neonatal septicemia is the most important non-diarrheal disease of calves. It is a systemic disease associated with microorganisms
and/or their toxins in the blood. It is frequently accompanied by disseminated infection and is almost always predisposal
by failure of passive transfer (FPT) of colostral antibodies. Because FPT is so important in the pathogenesis of neonatal
septicemia, and the prevention of FPT usually results in the prevention of neonatal septicemia. I will begin with a review
of colostrum and FPT.
Most of us know a lot about colostrum, passive transfer and failure passive transfer. Unfortunately some of what we "know"
may have been proven to be untrue or at least remains still unproven.
To achieve good passive transfer, it is necessary to have high quality colostrum. What is high quality colostrum and how can
it be identified? Not the presence of edema, the size or shape(in beef cattle) of the udder, color of colostrum nor the CMT
score is associated with the lgG concentration. The viscosity of colostrum was predictive of the quality of colostrum in an
interesting way. Colostrum with very high and very low viscosity contained more lgG than colostrum with moderate viscosity.
Some studies suggest that cows that produce more colostrum produce poor colostrum, but other studies refute that. Mastitis
in beef cattle and firmness of the udder of dairy cattle were associated with FPT and colostrum with low lgG concentration.
Colostrum from dairy cattle in general has lower lgG concentration than that from beef cattle. It is recommended that dairy
calves receive 3-4 L within the first 4 hours of life while 1 L is often sufficient for beef calves.
How should colostrum be administered? Although studies have shown that calves that suckle absorb slightly more IgG than calves
that are intubated, most experts agree that adequate passive transfer is achieved in a greater percentage of dairy calves
if they are intubated with a standard adequate quantity of colostrum instead of being allowed to suckle the cow or a bottle.
Immunoglobulin molecules are able to pass through the gut mucosa because enterocytes are capable of pinocytosis during the
first day of life. The absorption of lgG decreases gradually so that by 24 hours, almost no absorption occurs. If a calf receives
nothing by mouth before its first colostrum feeding, the closure of the gut to absorption is delayed, but complete closure
is achieved by 36 about hours.
What is the relationship between FPT, mortality and morbidity? FPT increase the risk of mortality in beef and dairy calves
about 3-5 times during the preweaning period. In a large study of dairy calves where overall mortality was 5%, 75% of calves
with FPT survived. In a study of beef cattle where overall mortality was 3.2%, 91% of calves with FPT survive, and 80 % never
got sick. Performance in the feedlot later in life was found to be negatively associated with FPT in one study, but not another.
Therefore, while we all recognize that FPT is a serious risk factor for disease in neonatal calves, it is not a death sentence.
When it comes to passive transfer of colostral antibody, is more better? Not really. In dairy calves at least, there appears
to be a threshold for serum lgG concentration above which there is not an improvement in preweaning survival. There seems
to be little advantage of a total serum protein > 5m5g of lgG/dL.
Septicemia can occur when a pathogenic organism is able to overwhelm the immune system of a host. While the organism may be
present in the environment and may even cause a transient bacteremia in calves with adequate passive transfer, the bacteria
usually cause serious disease only in calves with FPT. Occasionally outbreaks of septicemia occur, but typically the disease
is caused by an environmental opportunist. The intestine is the most common site of entry into the circulatory system of the
calf. Oral and respiratory mucosal may also be sites of entry. The umbilicus, once thought to be the major site of entry,
is probably of secondary importance. Once in circulation, the bacteria may in fact joints, physes, the liver, kidney, bones
or the meninges.
The clinical signs of septicemia are referable to the systemic and local efforts of the bacteria and toxins. Both gram positive
and gram negative bacteria can initiate an inflammatory cascade that ends in fever or hypothermia, depression, hypotensive
shock and cardiac or respiratory failure. Signs referable to local infection include hypopyon, blindness, sceral injection,
lameness, convulsion, or coma. Diarrhea is often associated with septicemia in dairy cattle, but most septicemic beef calves
are not diarrheic.
The etiology could conceivably be any bacterium, but E. coli is the most frequent isolate. Salmonella sp are also important
in dairy cattle. In the author's hospital, Actinobacillas pyogenes is the second most frequent isolate in beef calves. Diagnosis
in the field is usually based on clinical signs like septic arthritis, hypopyon convulsions and a history that the calf was
"fine yesterday". Physical examination and post-mortem findings in some of these calves demonstrate that the disease process
is greater than 24 hours in duration. Having seen several calves develop septicemia in the hospital under close observation,
I realize that the early signs are subtle and nonspecific. Many producers miss the early signs. Any calf under 2 weeks of
age with unexplained fever, depression or inappetence should be considered possibly septicemic. Those with the previous signs
plus omphalitis, swollen joints, hypopyon or neurologic signs should be considered highly likely to be septicemic. Several
scoring systems to help identify septic calves have been developed. Some employ only clinical signs while others include laboratory
Evidence of FPT, abnormal neutrophil count, immature neutrophils in circulation or hyperfibringenemia are also supportive
of the diagnosis. Of course culture of the organism from the blood is the definitive diagnostic test, but it is seldom performed
due to cost and delay in obtaining results.