Septicemia caused by Escherichia coli is a common disease of calves, and to a lesser extent lambs, <1 wk old. It may present with signs of acute septicemia or as a chronic bacteremia with localization.
Etiology and Epidemiology
The disease is caused by specific serotypes of E coli that possess virulence factors enabling them to cross mucosal surfaces and produce bacteremia and septicemia. However, the main determinant of the disease is deficiency of circulating immunoglobulins as the result of a failure in passive transfer of colostral immunoglobulin; septicemic disease due to invasion by E coli occurs only in immunoglobulin-deficient calves.
Colisepticemia is seen during the first week of life, most commonly at 2–5 days of age. Chronic disease with localization can be seen up to 2 wk of age. The disease is usually sporadic and is more common in dairy than beef calves.
Transmission and Pathogenesis
Invasion occurs primarily through the nasal and oropharyngeal mucosa but can also occur across the intestine or via the umbilicus and umbilical veins. There is a period of subclinical bacteremia that, with virulent strains, is followed by rapid development of septicemia and death from endotoxemic shock. A more prolonged course, with localization of infection, polyarthritis, meningitis, and less commonly uveitis and nephritis, is seen with less virulent strains. Chronic disease also develops in calves that have acquired marginal levels of circulating immunoglobulin. The organism is excreted in nasal and oral secretions, urine, and feces; excretion begins during the preclinical bacteremic stage. Initial infection can be acquired from a contaminated environment. In groups of calves, transmission is by direct nose-to-nose contact, urinary and respiratory aerosols, or as the result of navel sucking or fecal-oral contact.
Clinical Findings and Diagnosis
In the acute disease, the clinical course is short (3–8 hr), and signs are related to the development of septic shock. Fever is not prominent, and the rectal temperature may be subnormal. Listlessness and an early loss of interest in sucking are followed by depression, poor response to external stimuli, collapse, recumbency, and coma. Tachycardia, poor pulse pressure, and prolonged capillary refill time are seen. The feces are loose and mucoid, but severe diarrhea is not seen in uncomplicated cases. Mortality approaches 100%. With a more prolonged clinical course, the infection may localize. Polyarthritis and meningitis are common; tremor, hyperesthesia, opisthotonos, and convulsions are seen occasionally, but stupor and coma are more common.
A moderate but significant leukocytosis and neutrophilia are seen early, but leukopenia is marked in the terminal stages. The joint fluid contains increased inflammatory cells and protein, and the CSF shows pleocytosis and an increased protein concentration; organisms may be evident on microscopic examination. Less commonly other bacteria, including other Enterobacteriaceae, Streptococcus spp, and Pasteurella spp, produce septicemic disease in young calves. These organisms are more common in sporadic cases than as causes of outbreaks. They produce similar clinical disease, but they can be differentiated by culture. As with colisepticemia, the primary determinant of these infections is a failure of passive transfer of immunoglobulins.
The diagnosis is based on history and clinical findings, demonstration of a severe deficiency of circulating IgG, and ultimately, demonstration of the organism in the blood or tissues. Zinc sulfate or total protein estimation can be used for rapid estimation of IgG (see Calf Immunoglobulin).
Treatment requires aggressive use of antibiotics. Because there is no time for sensitivity testing, the initial choice should be a bactericidal drug that has a high probability of efficacy against gram-negative organisms. Antibacterial therapy should be coupled with aggressive fluid, drug, and other therapy for endotoxic shock. Mortality is high despite aggressive treatment.
Control and Prevention
Calves that acquire adequate concentrations of immunoglobulin from colostrum are resistant to colisepticemia. Therefore, prevention depends primarily on management practices that ensure an adequate and early intake of colostrum. The adequacy of the farm's practice of feeding colostrum should be monitored, and corrective strategies applied as required. In North American Holstein dairy herds, natural sucking does not guarantee adequate concentrations of circulating immunoglobulins, and calves should be fed 2–4 L of first-milking colostrum containing a minimal total mass of 100 g IgG, using a nipple bottle or an esophageal feeder, within 2 hr of birth; this is followed by a second feeding at 12 hr. A cow-side immunoassay test can assist with the selection of colostrum with adequate immunoglobulin concentration. The circulating concentration of immunoglobulin required to protect against colisepticemia is low; however, high concentrations of circulating immunoglobulins are desirable because they decrease susceptibility to other neonatal infectious diseases.
When natural colostrum is not available for a newborn calf, commercial colostrum substitutes containing 25 g IgG will provide sufficient immunoglobulin for protection against colisepticemia if fed early in the absorptive period. Plasma containing at least 4 g and preferably 8 g IgG, administered parenterally, will provide some protection for older calves that have not been fed colostrum and are unable to absorb immunoglobulins from the intestine. Small-volume hyperimmune serum is of benefit only when it contains antibody specific to the particular serotype associated with an outbreak. The risk of early infection should be minimized by hygiene in the calving area and disinfection of the navel at birth. To minimize transmission, calves reared indoors should be in separate pens (without contact) or reared in calf hutches.
Last full review/revision March 2012 by Clive C. Gay, DVM, MVSc, DVSc (Hons), FACVSc, DACIM (Hons)