Serological investigation of transplacental infection with Neospora hughesi and Sarcocystis neurona in broodmares.

The aim of the present study was to investigate the likelihood of transplacental transmission of Neospora hughesi and Sarcocystis neurona in foals, born from seropositive mares. Three broodmares with persistent N. hughesi infection gave birth to eight healthy foals over a period of 7 years. These foals were seropositive to N. hughesi prior to colostrum ingestion, with titers ranging between 640 and 20,480, measured by indirect fluorescence antibody test (IFAT). Of 174 foals born at another farm to mares with a high seroprevalence to S. neurona, only one (with a pre-colostrum antibody titer of 80) tested seropositive. Transplacental transmission of N. hughesi seems to occur from latently infected mares to their foals, while this route of transmission does not seem to occur commonly for S. neurona.

Endogenous transplacental transmission of Neospora hughesi in naturally infected horses.

Over a 2-yr study period, we investigated possible endogenous transplacental transmission of Neospora hughesi in 74 mare and foal pairs following the diagnosis of neuronal neosporosis in a weanling foal. Presuckle and postsuckle serum of each foal, serum and colostrum of each periparturient mare, and serum of each mare and foal pair, collected at 3-mo intervals thereafter, were tested for N. hughesi using an indirect fluorescent antibody test (IFAT). Furthermore, whole blood and colostrum samples and placentae were tested for the presence of N. hughesi by real-time PCR. The mares' seroprevalence at foaling based on IFAT (titer ≥ 160) was 52 and 6% in 2006 and 2007, respectively. Colostral antibodies against N. hughesi were detected in 96 and 11% of the mares in the 2-yr study. With the exception of 3 foals, all remaining foals were born seronegative to N. hughesi. Passive transfer of colostral antibodies to N. hughesi was documented in 15 foals. Three foals born from 2 different mares had presuckle antibodies at a titer ranging from 2,560 to 20,480. All 3 foals were born healthy. Two foals were born to the same dam that also gave birth to the weanling diagnosed with neuronal neosporosis in 2005. The third foal was born to a second mare with no previous foaling history at the farm. Seroconversion was documented in 10 foals and 9 mares over the 2-yr study. All blood and colostrum samples tested PCR negative for N. hughesi. Only 1 placenta collected in 2007 from the mare with the 2 congenitally infected foals tested PCR positive for N. hughesi. In conclusion, N. hughesi persisted in this population via endogenous transplacental infection.

Association of Stenotrophomonas maltophilia infection with lower airway disease in the horse: a retrospective case series.

Stenotrophomonas maltophilia is being reported with increasing frequency as a human nosocomial pathogen, especially among immuno-compromised patients. To the authors' knowledge, this pathogen has not previously been associated with lower airway disease in the horse. In this paper the clinical findings, laboratory diagnosis and response to treatment of seven cases of respiratory infection with S. maltophilia in horses, presented at three equine referral hospitals in Denmark in 2007, are described. In all cases there was a clinical history of chronic coughing and abundant mucopurulent exudate was observed in the lower trachea on endoscopy. On culture of tracheal aspirate, grey, slow-growing colonies, identified as S. maltophilia by both API 20NE identification and 16s ribosomal DNA sequencing, were identified. All isolates had a similar antibiotic susceptibility pattern characterised by resistance to all penicillins and cephalosporins, and to imipenem, gentamicin, amikacin and rifampicin. Ribotyping and pulsed-field gel electrophoresis of the S. maltophilia isolates from different patients indicated that they were either indistinguishable or closely related. This study indicates that S. maltophilia can be associated with chronic lower airway disease in the horse and provides useful initial insights into the diagnosis, therapy and epidemiology of this novel condition.

Molecular evidence for transplacental transmission of Theileria equi from carrier mares to their apparently healthy foals.

The intra-erythrocytic parasite Theileria equi is one of two tick-transmitted causative agents of equine piroplasmosis. Piroplasms of T. equi can be transmitted across the equine placenta and once a horse is infected, it appears to remain a lifelong carrier, since anti-theilerial drugs suppress but do not eliminate the parasite. Carrier mares may transmit the organism to their offspring and this may result in abortion or neonatal piroplasmosis, but observations by some researchers suggest that foals may be born as carriers yet remain apparently healthy. Using a T. equi-specific oligonucleotide probe, we have determined that transplacental transmission occurs early in equine foetal development and that carrier mares may give birth to healthy carrier foals. Investigation of parasite levels and the effect of maternal colostrum on the newborn suggests that colostral T. equi antibody may act to suppress parasitaemia in the newborn, reducing the incidence of clinical neonatal piroplasmosis.

Risk of transplacental transmission of Sarcocystis neurona and Neospora hughesi in California horses.

The study objective was to assess the risk of transplacental transmission of Sarcocystis neurona and Neospora hughesi in foals from 4 California farms during 3 foaling seasons. Serum of presuckle foals and serum and colostrum of periparturient mares were tested using indirect fluorescent antibody tests for S. neurona and N. hughesi. Serum antibody titers were < or =10 in 366 presuckle foals tested. There was no serologic or histologic evidence of either parasite in aborted fetuses or placentas examined. Positivity for S. neurona and N. hughesi in mares increased with age. Mares < or =9 yr that originated from Kentucky were 3.8 and 1.4 times more likely to be positive for S. neurona and N. hughesi, respectively, than mares from California. The strength of association between positivity to either parasite and state of birth decreased as age increased. Mares positive for S. neurona and N. hughesi were 2.2 and 1.7 times more likely, respectively, to have a previous abortion than negative mares, adjusted for age and state of birth. The annual mortality rate for mares was 4%. The annual incidence rate of equine protozoal myeloencephalitis was 0.2%. In conclusion, there was no detectable risk of transplacental transmission of S. neurona and N. hughesi. Prevalence of antibodies against both parasites in mares increased with age.

Epidemiological studies of equine herpesvirus 1 (EHV-1) in Thoroughbred foals: a review of studies conducted in the Hunter Valley of New South Wales between 1995 and 1997.

Sero-epidemiological studies conducted between 1995 and 1997 on two large Thoroughbred stud farms in the Hunter Valley of NSW showed clear evidence of EHV-1 infection in foals as young as 30 days of age. Similarly, serological evidence suggested that these foals were infected with EHV-1 from their dams or from other lactating mares in the group, with subsequent foal to foal spread of infection prior to weaning. These studies also provided evidence of EHV-1 infection of foals at and subsequent to weaning, with foal to foal spread of EHV-1 amongst the weanlings. These data indicated that the mare and foal population was a reservoir of EHV-1, from which new cases of infection propagated through the foal population both before and after weaning. The results of these studies support the long standing management practices of separating pregnant mares from other groups of horses to reduce the incidence of EHV-1 abortion. Also, these results have important implications for currently recommended vaccination regimens, as the efficacy of vaccination in already latently infected horses is unknown.

Passive transfer, rate of decay, and protein specificity of antibodies against equine arteritis virus in horses from a Standardbred herd with high seroprevalence.

OBJECTIVE: To determine rate of decay of passively acquired antibodies in Standardbred foals on a farm with a high seroprevalence to equine arteritis virus (EAV) and to determine whether vertical or horizontal transmission of the virus was responsible for infection on the farm. DESIGN: Repeated-measures study. ANIMALS: 46 Standardbred horses (15 brood mares and their foals, 5 stallions, and 11 young horses). PROCEDURE: Serum samples obtained from horses on the farm were evaluated by serum neutralization and western immunoblot analysis to detect EAV-specific antibodies. The half-life of passively acquired antibodies in foals was estimated by use of regression analysis. RESULTS: Most (14/15) of the mares evaluated were seropositive to EAV. After suckling, their foals were also seropositive. Mean biological half-life for passively acquired antibodies in serum samples obtained from foals was 32 days (r2 = 0.61). The foal born to a seronegative dam and all 11 young horses from the farm were seronegative to EAV. At least 2 of 5 stallions on the farm were persistently infected carriers that were shedding virus in their semen. Immunoblot analysis of seropositive serum samples most consistently recognized the M protein of EAV. CLINICAL IMPLICATIONS: Analysis of these data indicated that a modified-live EAV vaccine can be administered to foals after they are 8 months old without risk of interference from maternal antibodies, regardless of serologic status of the foal's dam. Horizontal transmission of EAV via the respiratory tract apparently was uncommon on the farm, indicating that mares primarily were infected by venereal transmission of virus from carrier stallions.