Overview of Colisepticemia

The disease is caused by specific invasive serotypes of E coli that possess virulence factors enabling them to cross mucosal surfaces, overcome the bactericidal plasma factors, and produce bacteremia and septicemia. The main determinant of the disease is deficiency of circulating immunoglobulins as the result of a failure in passive transfer of colostral immunoglobulin.

Colisepticemia is seen during the first weeks of life, with the highest incidence in animals 2–5 days old. Bacteremia and septicemia in calves and lambs are most commonly associated with E coli and to a lesser extent Salmonella spp. Approximately 30% of diarrheic calves with severe systemic clinical signs were found to be bacteremic or septicemic, with E coli the most commonly isolated pathogen from blood cultures.

It is assumed that the primary source of the infection is the feces of infected animals, including the healthy dams and neonates, and diarrheic newborn animals, which act as multipliers of the organisms. Invasion occurs primarily through the nasal and oropharyngeal mucosa but can also occur across the intestine or via the umbilicus and umbilical veins. Septicemic strains of E coli produce endotoxin, which results in shock and rapid death. 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.

In the peracute and acute disease, the clinical course is short (3–8 hr), and signs are related to development of septic shock. Fever is not prominent, and the rectal temperature may even be subnormal. Listlessness and an early loss of interest in sucking are followed by depression, poor response to external stimuli, collapse, recumbency, cold extremities, and coma. Tachycardia, a weak pulse, and prolonged capillary refill time are seen. The feces are loose and mucoid, but severe diarrhea is not seen in uncomplicated cases. Tremor, hyperesthesia, opisthotonos, and convulsions are seen occasionally, but stupor and coma are more common. Mortality approaches 100%. With a more prolonged clinical course, the infection may localize. Polyarthritis, ophthalmitis, omphalophlebitis, and meningitis may occur within the first week of the initial bacteremic phase.

No single laboratory parameter is considered reliable for early diagnosis of septicemia. A moderate but significant leukocytosis and neutrophilia are seen early, but leukopenia is more common in severe and advanced cases. A left shift of neutrophils and signs of toxicity of neutrophils as well as hypoglycemia are common findings. Because failure of transfer of passive immunity is the single most important predisposing factor, subnormal serum IgG and total protein concentrations are common. Subnormal platelet counts are the result of a consumptive coagulopathy. In cases of arthritis, the joint fluid has an increased inflammatory cell count and protein concentration. With meningitis, 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 can be differentiated by culture. As with colisepticemia, the primary determinant of these infections is a failure of passive transfer of colostral 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 blood or tissues.

Treatment requires aggressive antimicrobial, fluid, and anti-inflammatory therapy. Although blood cultures are recommended to retrospectively confirm the diagnosis, antimicrobial therapy must be initiated immediately in any animal suspected of being septic. 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. Administration IV of large volumes of balanced electrolyte solutions over several hours is essential to correct hypovolemia and assure adequate peripheral tissue perfusion; fluids should include glucose to correct hypoglycemia. The beneficial effect of NSAIDs has been attributed to their anti-inflammatory, antipyretic, and analgesic properties. Glucocorticoids have also been proposed to treat septicemia, although their benefits for treatment of sepsis are less well established.

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 of 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 in selection of colostrum with adequate immunoglobulin concentration. Although the circulating concentration of immunoglobulin required to protect against colisepticemia is low, high concentrations are desirable to decrease susceptibility to other neonatal infectious diseases.

When natural colostrum is not available for a newborn calf, commercial colostrum substitutes containing 25 g of 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 of 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.