(Septicemic Colibacillosis, Septicemic Disease)
Septicemia caused by Escherichia coli is an incidental disease recognized in most mammalian and avian species. E coli strains of intestinal or extraintestinal origin reach the bloodstream, where they cause systemic disease, and from there may invade virtually every organ of the body. It may present with signs of acute septicemia or as a chronic or intermittent bacteremia with localization.
Colisepticemia is caused by pathogenic strains of E coli that possess specific virulence factors that enable them to adhere to and penetrate mucosal surfaces, to effectively compete for iron in the extracellular space, to overcome the bactericidal plasma factors, and to produce bacteremia and septicemia. The single most important determinant of the disease is an immune-compromised host. Severe and debilitating prior disease or failure of transfer of passive immunity are common predisposing factors.
Colisepticemia is most commonly seen during the first weeks of life, with the highest incidence in animals 2–5 days old, but can incidentally also occur in older, immune-compromised individuals. E coli is the most common pathogen isolated in blood from septic patients in most species. 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 colisepticemia 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 peracute and acute colisepticemia, the clinical course is short (3–8 hours), and signs are related to development of septic shock. Fever is not prominent, and the rectal temperature may even be subnormal. Lethargy 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 may become loose and mucoid, and profuse diarrhea may be seen in complicated cases. Tremor, hyperesthesia, opisthotonos, and convulsions are seen occasionally, but stupor and coma are more common. As the disease progresses, signs specifically related to the failure of one or several organs, such as the lung, liver, kidney, or CNS, may become increasingly apparent. Death may occur as a result of either endotoxic shock or multiple organ failure. Mortality approaches 100%.
With the more chronic form of the disease initial signs are less severe and the infection tends to localize to one or a few organ systems. Polyarthritis, omphthalitis, omphalophlebitis, and meningitis may occur within the first week of the initial bacteremic phase.
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. 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.
Bacterial culture of blood obtained aseptically is considered the gold standard to confirm the diagnosis of septicemia by E coli. Although a positive culture result confirms the diagnosis, cases have been reported for which the final diagnosis was made by postmortem examination, including positive culture results from multiple organs, but for which blood cultures obtained from the living patient were negative. Another limitation of the use of blood cultures in acutely sick patients is the lag time of at least two days before results are available.
A tentative diagnosis can be made based on the clinical presentation. Although there is no single blood biochemical or hematologic parameter unambiguously confirming the diagnosis, interpreting a combination of some parameters will be useful to support or refute the suspected diagnosis. Marked leukopenia is common in severe cases in early stage. A degenerative left shift of neutrophils and signs of toxicity of neutrophils as well as pronounced hypoglycemia and sometimes lactatemia develop in the following hours. Increased blood lactate levels are a sign of impaired tissue perfusion and beginning organ function disturbances and are associated with the development of acidemia.
Subnormal total protein concentrations in serum or plasma are the result of increased globulin consumption but are also suggestive of the development of leaky blood vessels. Because failure of transfer of passive immunity is common, subnormal serum IgG and total protein concentrations cannot be solely attributed to sepsis. Subnormal platelet counts are the result of a consumptive coagulopathy.
Treatment for septicemia requires immediate, thorough 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. Hypoglycemia can be challenging to control in cases of acute sepsis due to the massive energy uptake of activated immune cells. It is advisable to monitor the blood glucose concentration, for example by using a handheld glucometer, to adjust the fluid rate to maintain euglycemia.
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. 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 hours of birth; this is followed by a second feeding at 12 hours.
A cow-side immunoassay test or even simply testing colostrum with a brix-refractometer or a colostrometer 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 immunoglobulin to improve 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.