Effects of inactivated parapoxvirus ovis on the cumulative incidence of pneumonia and cytokine secretion in foals on a farm with endemic infections caused by Rhodococcus equi.

The objectives of the present study were to determine if administration of inactivated parapoxvirus ovis (IPPVO) can decrease the cumulative incidence of pneumonia and increase the number of IFN-γ- and IL-4-secreting cells among foals. Fifty-nine foals were randomly assigned to 2 treatment groups (IPPVO or placebo) prior to birth. At 24-48 h of age, foals received 2 ml of either IPPVO or a placebo by intramuscular injection. Injections were repeated 24h and 8 days later. The number of IFN-γ- and IL-4-secreting cells was measured using a validated ELISPOT assay on blood mononuclear cells collected when the foals were 1-14 days old. Foals were monitored daily for clinical signs of pneumonia and biweekly for lung lesions by ultrasonography. The proportion of foals that developed clinical or ultrasonographic evidence of pneumonia was not significantly different between IPPVO (16 of 28) and placebo (14 of 31). IFN-γ- and IL-4-secreting cells were detected in only 22 and 15 foals, respectively. There was a significant effect of treatment with IPPVO on the number of IFN-γ secreting cells in foals 7- to 14-days-old but not in younger foals. There was no significant effect of treatment with IPPVO on the number of IL-4-secreting cells. The odds of detecting IFN-γ (5.1; 95% CI: 1.5-15) and IL-4 (3.5; 95% CI: 1.1-12) were significantly higher in foals 7-14 days than in younger foals regardless of treatment group. There was no significant association between IFN-γ or IL-4 secretion early in life and subsequent development of pneumonia.

Determination of the prevalence of antimicrobial resistance to macrolide antimicrobials or rifampin in Rhodococcus equi isolates and treatment outcome in foals infected with antimicrobial-resistant isolates of R equi.

OBJECTIVE: To determine the prevalence of antimicrobial resistance to macrolide antimicrobials or rifampin in Rhodococcus equi isolates and to describe treatment outcome in foals infected with antimicrobial-resistant isolates of R equi. DESIGN: Cross-sectional study. SAMPLE POPULATION: 38 isolates classified as resistant to macrolide antimicrobials or rifampin received from 9 veterinary diagnostic laboratories between January 1997 and December 2008. PROCEDURES: For each isolate, the minimum inhibitory concentration of macrolide antimicrobials (ie, azithromycin, erythromycin, and clarithromycin) and rifampin was determined by use of a concentration-gradient test. Prevalence of R equi isolates from Florida and Texas resistant to macrolide antimicrobials or rifampin was determined. Outcome of antimicrobial treatment in foals infected with antimicrobial-resistant isolates of R equi was determined. RESULTS: Only 24 of 38 (63.2%) isolates were resistant to >or= 1 antimicrobial. Two isolates were resistant only to rifampin, whereas 22 isolates were resistant to azithromycin, erythromycin, clarithromycin, and rifampin. The overall prevalence of antimicrobial-resistant isolates in submissions received from Florida and Texas was 3.7% (12/328). The survival proportion of foals infected with resistant R equi isolates (2/8 [25.0%]) was significantly less, compared with the survival proportion in foals that received the same antimicrobial treatment from which antimicrobial-susceptible isolates were cultured (55/79 [69.6%]). Odds of nonsurvival for foals infected with resistant R equi isolates were 6.9 (95% confidence interval, 1.3 to 37) times the odds for foals infected with susceptible isolates. CONCLUSIONS AND CLINICAL RELEVANCE: Interpretation of the results emphasized the importance of microbiological culture and antimicrobial susceptibility testing in foals with pneumonia caused by R equi.

Cardiac troponin I in pastured and race-training Thoroughbred horses.

Cardiac troponin I (cTnI), a myocardial polypeptide, is a highly sensitive and specific biomarker of myocardial injury in people and dogs. The structure of cTnI is highly conserved across species, and equine myocardium has high reactivity with human immunoassays. The purpose of this study was to describe cTnI concentrations in normal pastured and race-training Thoroughbred horses. Ten horses on pasture and 10 horses in race training were studied. Horses were considered normal on the basis of physical examination, training performance, electrocardiography (ECG), and echocardiography. Serum cTnI concentrations were determined with a colorimetric immunoassay. The assay has an analytical sensitivity of 0.04 ng/mL. Serum cTnI concentrations in race-training horses were not significantly different from those of pastured horses. When groups were combined, mean cTnI concentration (+/- SD) was 0.047 +/- 0.085 ng/mL. and the median was 0 (range, 0-0.35 ng/mL). The 90th percentile for both groups combined was 0.11 ng/mL. This study establishes a preliminary reference range for serum cTnI in normal Thoroughbred horses.

Pneumonia in a Paso-Fino mare.

A 5-year-old Paso-Fino mare was presented for severe respiratory distress. The mare had foaled 2 months prior to presentation. The horse was in poor body condition with a dull hair coat. A mild fever was noted during physical examination and increased bronchovesicular sounds were auscultated. Thoracic radiographs showed an interstitial pattern and an alveolar infiltrate with distinct air bronchograms. Moderate purulent inflammation with increased mucus was observed in tracheal wash fluid, but no infectious agents were identified. A bronchoalveolar lavage (BAL) contained a large amount of mucus and reactive mononuclear phagocytes with variable numbers of intracellular fungal organisms morphologically consistent with Pneumocystis carinii. The mare had undetectable levels of immunoglobulin M (IgM) and decreased IgG levels in the serum. Immunophenotyping revealed decreased expression of major histocompatibility complex (MHC) class II molecules. Moderate to marked hyperplasia of type II epithelial cells was present throughout histologic sections of lung, but the fungal organisms were not observed. A culture system has not been developed for diagnosis of P carinii infection. Instead, diagnosis of P carinii pneumonia is achieved by microscopic identification of characteristic morphologic features of the pathogen. Cytologic examination of BAL fluid is the preferred method used to diagnose human infection with P carinii. In humans, the diagnostic sensitivity of cytology is significantly higher than the sensitivity of histopathologic examination of lung biopsies. The difference in sensitivity between BAL cytology and lung histopathology may also apply to the diagnosis of P carinii pneumonia in horses.

Effect of a single dose of ponazuril on neural infection and clinical disease in Sarcocystis neurona-challenged interferon-gamma knockout mice.

Interferon gamma-knockout mice were challenged with 5000 Sarcocystis neurona sporocysts acquired from a naturally infected opossum. Ponazuril was administered once, by gavage, at day 1, 3, 7, 10, or 14 post-infection (pi). Ponazuril was given at either 20 or 200mg/kg. Mice that survived to day 30 pi were euthanized. Severity of CNS infection was quantified as schizont density in the cerebellum. Unchallenged mice in treatment and non-treatment groups remained free of disease and gained weight throughout the experiment. All challenged mice, regardless of treatment, developed histologic evidence of CNS infection even though clinical signs were prevented in some groups. The greatest treatment benefits were seen in mice given 200mg/kg ponazuril between days 4 and 14 pi. Weight gain over the course of the experiment occurred only in mice that were given 200mg/kg ponazuril on day 7 or 10 pi. With the exception of groups given 200mg/kg ponazuril on day 7 or 14 pi, mice in groups that got sporocysts developed abnormal neurologic signs. No deaths before day 30 pi occurred in mice given ponazuril at 20mg/kg on day 7 pi or 200mg/kg on day 1, 7, 10, or 14 pi. This effect was not significant. Mice given 200mg/kg on day 7 pi had significantly fewer cerebellar schizonts than did those of the control group that was not given ponazuril. These results indicate that single-dose administration of ponazuril for prevention of CNS infection is partially protective when given between days 4 and 14 pi.

West Nile virus encephalomyelitis in horses: 46 cases (2001).

OBJECTIVE: To determine signalment, clinical findings, results of diagnostic testing, outcome, and postmortem findings in horses with West Nile virus (WNV) encephalomyelitis. DESIGN: Retrospective study. ANIMALS: 46 horses with WNV encephalomyelitis. PROCEDURE: Clinical data were extracted from medical records of affected horses. RESULTS: On the basis of clinical signs and results of serologic testing, WNV encephalomyelitis was diagnosed in 46 of 56 horses with CNS signs. Significantly more males than females were affected. Increased rectal temperature, weakness or ataxia, and muscle fasciculations were the most common clinical signs. Paresis was more common than ataxia, although both could be asymmetrical and multifocal. Supportive treatment included anti-inflammatory medications, fluids, antimicrobials, and slinging of recumbent horses. Results of the IgM capture ELISA and the plaque reduction neutralization test provided a diagnosis in 43 horses, and only results of the plaque reduction neutralization test were positive in 3 horses. Mortality rate was 30%, and 71% of recumbent horses were euthanatized. One horse that had received 2 vaccinations for WNV developed the disease and was euthanatized. Follow-up communications with 19 owners revealed that most horses had residual deficits at 1 month after release from the hospital; abnormalities were resolved in all but 2 horses by 12 months after release. CONCLUSIONS AND CLINICAL RELEVANCE: Our findings were similar to those of previous WNV outbreaks in horses but provided additional clinical details from monitored hospitalized horses. Diagnostic testing is essential to diagnosis, treatment is supportive, and recovery rate of discharged ambulatory horses is < 100%.

Eastern equine encephalomyelitis virus infection in a horse from California.

A yearling quarter horse, which was raised in southern California, received routine vaccinations for prevention of infection by Eastern equine encephalomyelitis virus (EEEV). One week later, severe neurologic signs developed, and the horse was humanely destroyed. A vaccine-related encephalomyelitis was later suspected. A final diagnosis of EEEV infection was established on the basis of acute onset of the neurologic signs, histopathologic and serologic testing, and isolation and molecular characterization of EEEV from brain tissue. The vaccine was extensively tested for viral inactivation. Nucleotide sequences from the vaccine and the virus isolated in the affected horse were also compared. In California, arboviral encephalomyelitides are rarely reported, and EEEV infection has not previously been documented. This report describes the occurrence of EEEV infection in the horse and the investigation to determine the source of infection, which was not definitively identified.