MSD Manual

Please confirm that you are a health care professional


Sporadic Bovine Encephalomyelitis

(Chlamydial Encephalomyelitis, Buss Disease, Transmissible Serositis)


Andrea S. Lear

, DVM, DACVIM, MS, PhD , University of Tennessee

Last full review/revision Oct 2014 | Content last modified Jul 2020

Sporadic bovine encephalomyelitis (SBE) is reported in various parts of the world. The disease affects cattle and buffalo, resulting in neurologic signs and polyserositis.

Etiology and Epidemiology:

SBE is caused by Chlamydia pecorum biotype 2. 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 mo 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:

The incubation period 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 stiffness and knuckling at the fetlocks. Calves become uncoordinated and stagger, circle, or fall over objects. Head pressing and blindness are not seen. In the terminal stage, calves are frequently recumbent and may develop opisthotonos. The course of the disease is usually 10–14 days.


Lesions are not limited to the brain; vascular damage can be seen in several organs. Serofibrinous peritonitis, pleuritis, and pericarditis are common and are 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.


A tentative diagnosis 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 rabies, infectious bovine rhinotracheitis with encephalitis, listeriosis, thromboembolic encephalomyelitis, polioencephalomalacia, pseudorabies, paramyxovirus encephalomyelitis, and malignant catarrhal fever. 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.


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 wk. If treatment is effective, the fever should drop significantly within 24 hr. No vaccines are available.

Others also read

Also of Interest


View All
Sulfur-induced polioencephalomalacia, steer
Sulfur-induced polioencephalomalacia, steer
Steer with sulfur-induced polioencephalomalacia. The steer is depressed, blind, does not have...