Sporadic bovine encephalomyelitis (SBE) is an infectious neurologic disease caused by Chlamydia pecorum, affecting cattle and buffalo in various parts of the world.
Etiology and Epidemiology of Sporadic Bovine Encephalomyelitis
Sporadic bovine encephalomyelitis is caused by Chlamydia pecorum biotype 2, an obligate intracellular bacteria. Genetically identical C pecorum isolates have been identified from clinical cases in geographically different areas. The C pecorum isolates from clinical cases are distinct from those found in the GI tract of asymptomatic animals. Based on these findings, subclinical intestinal infections in cattle and other animals may not be the source of infection in SBE. The disease is most often seen in calves <6 months old and less commonly in older cattle. Sporadic cases and outbreaks can occur within individual herds. Morbidity rates are most commonly <25% but can reach 50%. The mortality rate can approach 30% and is highest in calves. Many sick animals die if not treated at an early stage.
Clinical Findings of Sporadic Bovine Encephalomyelitis
The incubation period for sporadic bovine encephalomyelitis in experimentally infected calves is 6–30 days. The first sign in natural and experimental cases is fever (104°–107°F [40°–41.7°C]). Appetite remains good for the first 2–3 days despite the fever. Afterward, depression, excess salivation, diarrhea, anorexia, and weight loss occur. Nasal discharge and respiratory disease signs due to pleuritis may be seen. Early neurologic signs include depression, stiffness with knuckling at the fetlocks, decreased tail tone, and incontinence. Calves progressively become uncoordinated and stagger, circle, or fall over objects. Head pressing, blindness, and decreased pupillary light reflexes are not observed. In the terminal stage, calves are frequently recumbent and may develop opisthotonos. The course of the disease is usually 10–14 days.
Lesions of sporadic bovine encephalomyelitis are not limited to the brain; vascular damage can be seen in several organs, particularly the liver and spleen. Polyserositis, appearing as serofibrinous peritonitis, pleuritis, and pericarditis, is common and is especially pronounced in more chronic cases. Microscopic lesions in the brain consist of perivascular cuffs and inflammatory foci in the parenchyma composed primarily of mononuclear cells.
Diagnosis of Sporadic Bovine Encephalomyelitis
Based on clinical signs, bacterial culture, and PCR
A tentative diagnosis of sporadic bovine encephalomyelitis can be based on clinical signs and particularly on the presence of serofibrinous peritonitis in the absence of other causes of peritonitis, such as intestinal volvulus, intussusception, traumatic perforation of the reticulum, perforated abomasal ulcer, or displaced organs.
Differential diagnoses also include:
SBE can be diagnosed by PCR detection of C pecorum DNA in brain tissue, pleural fluid, pericardial fluid, or peritoneal fluid of affected animals. Diagnosis can also be confirmed by culture in either developing chicken embryos or cell cultures, by histologic changes in brain sections, or by evaluation of tissue impression smears after Giemsa or immunofluorescent staining.
Treatment of Sporadic Bovine Encephalomyelitis
Supportive care and antibiotics are the primary treatments
For treatment of sporadic bovine encephalomyelitis, the antibiotics of choice are tetracyclines, oxytetracyclines, and tylosin. For treatment to be effective, it must be given as early as possible in high doses (eg, oxytetracyclines at 10–20 mg/kg/day) and for ≥1 week. If treatment is effective, the fever should drop significantly within 24 hours. No vaccines are available.
Sporadic bovine encephalomyelitis should be considered in calves presenting with a combination of neurologic signs and polyserositis.
Treatment consists of oxytetracycline and supportive care.