Eastern Equine Encephalitis confirmed in a Goat
*Corresponding author: Dr. Glen Wright, Florida Agriculture and Mechanical University, 4259 Bainbridge Hwy, Florida,Tel :8508758573; E-mail: email@example.com
Case Description: A 3 month-old Boer cross buck kid was confirmed to have died from an infection of Eastern Equine Encephalitis (EEE) in a rural county of North Florida. Caprine Arthritis Encephalitis and Rabies were included in the list of deferential diagnoses as possible causes of neurologic symptoms that could occur in adolescent caprine[1,5]. PCR analysis of fresh brain tissue preformed at Department of Health in Tampa, Florida (via the Bronson Animal Disease Diagnostic Laboratory (BADDL) in Kissimmee, Florida) showed positive for EEE, then positive by virus isolation. The sample was negative for West Nile Virus, and the fluorescent antibody test for Rabies was negative.
Clinical Findings: The kid was observed by farm workers to stagger and have difficulty walking, often knuckling over and falling into lateral recumbency. The death occurred within 20 minutes of discovery of abnormalities.
Treatment and Outcome: Due to the rapid course of the disease, treatment was not attempted.
Clinical Relevance: In the Southern region of the US during the summer months when mosquito populations are near their peak, the list of differential diagnoses in goats with a presentation of neurologic symptoms, should include Eastern Equine Encephalitis as a possible cause.
Keywords: Eastern Equine Encephalitis, small ruminants, Caprine, neurologic
A three-month old Boer cross buck kid was examined at the Florida Agricultural and Mechanical University Research and Extension Center in Quincy, FL. The kid was first observed by the farm manager and the head of the goat program at the facility. The farm manager described the kid as isolating himself from the herd, circling to one side, and pressing its head against the feed bunk. Ataxia was noted and soon the kid became laterally recumbent. The kid died before the veterinary team arrived at the facility. The goal of the veterinary team, if possible, is to identify the cause of death and to rule out infectious problems that may affect the rest of the herd. The carcass was moved to a cool area to preserve degradation and the postmortem was performed within 30 minutes of the time of death. The postmortem began the thorough investigation of the external anatomy of the animal. The body condition score was 7/9 and the preservation of the carcass was excellent. There was no evidence of external parasites or signs of trauma, the nostrils were clean, the eyes were within normal limits, and there was no evidence of diarrhea. A fecal sample was obtained from the colon to assess the parasite load.
The kid was placed in dorsal recumbency and a midline incision was performed from the xiphoid to the pubis to allow examination of the abdomen. The presentation of the abdominal organs was found to be in a normal orientation. There was an abundant amount of omental and pelvic adipose tissue that had been stored. There was no evidence of congestion or hemorrhage in any of the organs of the abdominal cavity. Grossly, the liver, spleen, kidney, bladder, lymph nodes and glands, and the vascular structures all appeared to be normal. The rumen was incised and a sample was collected for possible analysis of toxins however, the ingesta was consistent with the known diet of the entire herd. The diaphragm was incised allowing the lungs to collapse. The rib cage was removed to facilitate examination of the thoracic cavity. The orientation of the thoracic organs was normal, and the thorough examination of the heart, thymus, nerves, esophagus, and vascular structures were all grossly normal. The lungs contained a moderate degree of congestion with several of the major bronchi collecting frothy fluid. The lymph nodes near the base of the lungs were slightly enlarged with no presence of hemorrhage or congestion. The cervical portion of the esophagus and trachea revealed no abnormalities as well as the oral cavity. The CSF sample was collected at the atlanto-occipital joint and the fluid was centrifuged for 5 minutes and the pellet was examined for cellular contents using a diff quick stain. A brief examination of the prepared slide showed an increase in mononuclear type cells and neutrophils. The cerebrospinal fluid (CSF) was submitted for fluid analysis and the brain was removed for histological examination.
The cytological examination of the CSF reveals increased cellularity of the fluid. This mainly consisted of inflammatory cells. The sample was identified an inflammatory process however, no etiological agents were found. Cytopathological evaluation was insufficient to point out the extent and distribution of the inflammation.
47 % macrophages.
14% neutrophils 3% eosinophils.
Increased cellularity of the CSF due to inflammatory cells (a. macrophages, b. lymphocytes, and c. neutrophils)
Image from Joanna Hyland DVM, MS, DACVP
Increased cellularity of the CSF due to inflammatory cells (a. macrophages, b. lymphocytes, and c. neutrophils).
Image from Joanna Hyland DVM, MS, DACVP
The skin of the skull was reflected back to the dorsal portion of the cranial vault was removed with a saw, and the brain along with the anterior portion of the spinal cord was removed. The brain was separated from the medial sulcus and half of the brain was placed in 10% formalin, the other half was kept fresh. All the major organs were sampled and handled in a similar fashion, with half of the organ samples kept fresh so it could be cultured, while the other half was fixed in 10% formalin. The samples were then sent overnight to the BADDL in Kissimmee Florida.
The stool sample was floated in a commercial flotation solution and the parasite eggs were identified as Haemonchus contortus with occasional coccidia oocysts found. Information from the specimens sent to the lab concluded the following. The culture of the fresh tissues had light growth of various is bacteria consistent with normal flora or contamination during the collection process. There was a moderate growth of enterococcus species that appeared to be nonpathogenic. The culture also grew a beta hemolytic bacillus but anthrax was ruled out. Histopathology of the fixed tissues revealed the following. There was a mild to a moderate expansion of the gastrointestinal lamina by eosinophils, with an increased number of lymphocytes and plasma cells. Crosssections of adult parasites were present in the lumen of the abomasum. With the exception of mild congestion multiple tissues including the kidney, heart, liver, spleen, thymus, and urinary bladder were microscopically within normal limits. Generalized edema of the lungs was identified. Sections of the brain demonstrated a hemorrhagic meningoencephalitis.
As a follow-up, the state veterinarian was notified and the surveillance efforts on the farm were stepped up to monitor other similar cases as well as the mosquito population.
EEE is caused by an arbovirus that has a reservoir in the bird population. Although birds are not typically affected by the virus, as the viremia in birds increases it allows for the transmission of the virus to other species such as horses and man [2,3]. The feeding nature of the female mosquito makes them the ideal vector to spread the virus. Transmission most often occurs when mosquito populations are at high levels and at times of the day when feeding most often occurs. The virus is transmitted when biological vectors, mosquitoes that feed on both birds and mammals, become infected by feeding on birds. This allows the virus to be transmitted to mammals. Once inside the bloodstream it begins to replicate producing inflammation in a number of cells. Initial replication occurs in muscle tissue at the site of the mosquito bite and then progresses in neutrophils and macrophages. If the virus cannot be contained by the immune system, it will infect internal organs like the liver or spleen. This begins the febrile stage of the infection and the virus continues to progress to the nervous tissue of the brain causing areas of necrosis and swelling of the meninges. The mortality rate in animal approaches 100% and represents a difficult and complicated treatment. Vaccination, mosquito control, and the mosquito avoidance are the best defensive measures. EEE has been well documented to infect horses, pigs, birds, bats, reptiles, amphibians, canines, rodents and man .
The incidence of EEE found in goats is poorly documented.
Possible reasons include small herds that may have inadequate records of death losses and/ or the lack of investigation as to the cause of death. Historically, a 15 to 20% death loss  in goat herds is not uncommon which can lead to “The mysterious death syndrome “where the actual cause is never identified. A search of common veterinary databases along with an inquiry to the BADDL animal disease database showed no goat showing positive for EEE. For example, an animal with neurological symptoms and known human exposure would be submitted and tested for rabies and other more likely goat diseases such as CAE, and Listeriosis . This confirmation of EEE in a goat, would suggest that in any situation where a goat death is accompanied by significant neurological signs testing for EEE and WNV should be considered . The poor documentation of the actual number of cases of EEE in goats also creates a challenge as to what measures should be taken for the purpose of surveillance and control. Since the incidence of EEE seems rare, it questions if vaccination would be of benefit to a herd or unlikely that others in the herd would be infected. It also raises the question of if it is more common in goats but just not identified. One conclusion that is important from a zoonotic disease perspective, is the identification of EEE in the farm herd indicates that the viremia in birds is sufficient along with the mosquito population to allow the transfer of the EEE virus from birds to mammals. This puts all of the farm workers, researchers and visitors to the farm at risk of exposure.
Florida serves as a major port of entry for animals, animal products, and tourists from across the world. This intensifies the need for constant vigilance regarding diseases related to human health, animal health, and a major component of food safety.
- Masterson, MA. Neurologic Disease of Goats. Western Veterinary Conference 2012 Large Animal Services, College of Veterinary Medicine, The Ohio State University, Columbus, OH.
- Kahn, CM. Equine Viral Encepahalomyelitis. Merck Veterinary Manual 9th 2010: 1183-1189.
- Romich, JA. Equine Encephalitides. Understanding Zoonotic Diseases.2008:617-626
- National Association of State Public Health Veterinarians Veterinary Infection Control Committee 2008. Compendium of Veterinary Standard Precautions: Zoonotic Disease Prevention in Veterinary Personnel. Appendix A p 27-30.
- Matthews, J. Nervous Diseases. Diseases of the Goat 3rd edition p180-212, 2009.
- Valentine BA, Cebra CK, Taylor GH, Fatal gastrointestinal parasitism in goats: 31 cases (2001–2006) Journal of the American Veterinary Medical Association October 1, 2007,231 (7):1098-1103