Neonatal septicemia and meningitis

Etiology

• Neonatal calves are born reliant upon ingestion of an adequate volume of high quality colostrum Colostrum: overview to achieve immune competence.
• Inadequate colostrum supply serves as a major risk factor for the development of neonatal septicemia and associated meningitis. This is particularly so for those calves born to heavily contaminated environments.
• Escherichia coli Escherichia coli have long been incriminated as the principle microbial agent responsible for neonatal septicemia in the bovine and whilst it the most commonly encountered causative agent, other bacteria such as Salmonella spp Salmonella spp will also cause clinical disease.

Predisposing factors

General

• The neonate is born into a highly contaminated, unhygienic environment.
• Failure of passive transfer.
• Omphalophlebitis Omphalophlebitis and omaphaloarteritis. 
• Septic arthritis .

Pathophysiology

• Calves born to heavily contaminated environments are susceptible to disease.
• Entry of pathogenic bacteria may occur in utero, during the calving process or shortly after birth.
• Entry points include the respiratory epithelium, oropharynx, nasopharynx, umbilicus and intestines via the fecal oral route.
• In the first postnatal hours, nonspecific pinocytosis allowing immunoglobulin entry may also allow bacterial entry to the systemic circulation and so this is a common route of infection.
• Older calves 2 or 3 weeks of age may succumb to sepsis or meningitis from a chronic, septic focus such as a joint infection or omphalophlebitis.

Timecourse

• Clinical signs usually commence within 24 hours of pathogen entry.
• The duration of clinical signs is dependent upon the infective load, the degree of passive transfer and time to instigation of therapy.
• Return to clinical normality will normally be a number of days.