Strangulating intestinal obstructions in four captive elephants (Elephas maximus and Loxodonta africana).

Three captive-born (5-day-old, 8-day-old, and 4-yr-old) Asian elephants (Elephas maximus) and one captive-born 22-yr-old African elephant (Loxodonta africana) from three private elephant facilities and one zoo in the United States presented with depression, anorexia, and tachycardia as well as gastrointestinal signs of disease including abdominal distention, decreased borborygmi, tenesmus, hematochezia, or diarrhea. All elephants showed some evidence of discomfort including agitation, vocalization, or postural changes. One animal had abnormal rectal findings. Nonmotile bowel loops were seen on transabdominal ultrasound in another case. Duration of signs ranged from 6 to 36 hr. All elephants received analgesics and were given oral or rectal fluids. Other treatments included warm-water enemas or walking. One elephant underwent exploratory celiotomy. Three animals died, and the elephant taken to surgery was euthanized prior to anesthetic recovery. At necropsy, all animals had severe, strangulating intestinal lesions.

Infections caused by pathogenic free-living amebas (Balamuthia mandrillaris and Acanthamoeba sp.) in horses.

This article describes amebic infections in 4 horses: granulomatous amebic encephalitis caused by Balamuthia mandrillaris and Acanthamoeba culbertsoni and systemic infections caused by Acanthamoeba sp. The former infection occurred in 1 of 4 horses spontaneously without any underlying conditions; the latter amebic infection was perhaps "opportunistic" considering the visceral involvement by this protozoan in association with Aspergillus sp. and/or Escherichia coli and Pseudomonas sp. The clinicopathologic findings and demonstration of the amebic organisms using immunohistochemical techniques, culture, polymerase chain reactions, and electron microscopy are presented.

Association between findings on palmarodorsal radiographic images and detection of a fracture in the proximal sesamoid bones of forelimbs obtained from cadavers of racing Thoroughbreds.

OBJECTIVE: To determine the distribution for limbs and bones in horses with fractures of the proximal sesamoid bones and relationships with findings on palmarodorsal radiographic images. SAMPLE POPULATION: Proximal sesamoid bones obtained from both forelimbs of cadavers of 328 racing Thoroughbreds. PROCEDURE: Osteophytes; large vascular channels; and fracture location, orientation, configuration, and margin distinctness were categorized by use of high-detail contact palmarodorsal radiographs. Distributions of findings were determined. Relationships between radiographic findings and fracture characteristics were examined by use of chi2 and logistic regression techniques. RESULTS: Fractures were detected in 136 (41.5%) horses. Biaxial fractures were evident in 109 (80%) horses with a fracture. Osteophytes and large vascular channels were evident in 266 (81%) and 325 (99%) horses, respectively. Medial bones typically had complete transverse or split transverse simple fractures, indistinct fracture margins, > 1 vascular channel that was > 1 mm in width, and osteophytes in abaxial wing and basilar middle or basilar abaxial locations. Lateral bones typically had an oblique fracture and distinct fracture margins. Odds of proximal sesamoid bone fracture were approximately 2 to 5 times higher in bones without radiographic evidence of osteophytes or large vascular channels, respectively. CONCLUSIONS AND CLINICAL RELEVANCE: Biaxial fractures of proximal sesamoid bones were common in cadavers of racing Thoroughbreds. Differences between medial and lateral bones for characteristics associated with fracture may relate to differences in fracture pathogeneses for these bones. Osteophytes and vascular channels were common findings; however, fractures were less likely to occur in bones with these features.

Seasonal meningoencephalitis in Holstein cattle caused by Naegleria fowleri.

Primary amoebic meningoencephalitis is a fulminant infection of the human central nervous system caused by Naegleria fowleri, a free-living amoeba that thrives in artificially or naturally heated water. The infection usually is acquired while bathing or swimming in such waters. The portal of entry is the olfactory neuroepithelium. This report describes fatal meningoencephalitis caused by N. fowleri in Holstein cattle that consumed untreated surface water in an area of California where summer temperatures at times exceed 42 degrees C. In the summers of 1998 and 1999, severe multifocal necrosuppurative hemorrhagic meningoencephalitis was observed in brain samples from nine 10-20-month-old heifers with clinical histories of acute central nervous system disease. Olfactory lobes and cerebella were most severely affected. Lesions were also evident in periventricular and submeningeal neuropil as well as olfactory nerves. Naegleria fowleri was demonstrated by immunohistochemistry in brain and olfactory nerve lesions and was isolated from one brain. Even though cultures of drinking water did not yield N. fowleri, drinking water was the likely source of the amoeba. The disease in cattle closely resembles primary amoebic meningoencephalitis in humans. Naegleria meningoencephalitis should be included among differential diagnoses of central nervous system disease in cattle during the summer season in areas with high ambient temperatures.

Increased presence of T lymphocytes in central nervous system of EPM affected horses.

Equine protozoal myeloencephalitis (EPM), caused by Sarcocystis neurona infection in the central nervous system (CNS), affects up to 1% of all horses during their lifetimes. Neither the protective immune response nor the immunopathology associated with the disease is well understood. To begin to clarify the pathogenesis of the disease, immunohistochemical staining for B and T lymphocytes was performed on spinal cord sections obtained from 17 horses, all of which were all positive for S. neurona based on immunohistochemical staining. Fifteen of the 17 horses included in the study were killed due to neurologic dysfunction; 2 of the 17 horses were killed because of fractures. All 17 horses had histologic changes consistent with S. neurona infection. A significantly greater number of T cells were seen in sections from S. neurona-infected versus control horses. Because this was a small descriptive study, we were not able to determine the mechanisms of enhanced T-cell recruitment in the sections from the S. neurona-infected horses.

Comparison of a serum indirect fluorescent antibody test with two Western blot tests for the diagnosis of equine protozoal myeloencephalitis.

A serum indirect fluorescent antibody test (IFAT) was compared with a Western blot (WB) and a modified Western blot (mWB) for diagnosis of equine protozoal myeloencephalitis (EPM). Using receiver-operating characteristic (ROC) analysis, the area under the curve of the IFAT was greater than the areaunder the curves of the WB and the mWB (P = 0.025 and P = 0.044, respectively). There was no statistically significant difference between the areas under the curves of the WBs (P > 0.05). On the basis of an arbitrarily chosen cut-off titer for a positive test result of 1:80 for the IFAT and interpreting weak positive WB results as positive test results, the sensitivities and 95% confidence intervals (CI) of all 3 tests were identical and equal to 88.9% (51.8-99.7%). The specificities and 95% CIs of the IFAT, WB, and mWB test were 100% (91-100%), 87.2% (72.6-95.7%), and 69.2% (52.4-83%), respectively. The overall accuracy of the IFAT was shown to be better than that of the WBs and, therefore, the test has potential for use in the diagnosis of EPM caused by Sarcocystis neurona.

The occurrence of avian influenza A subtype H6N2 in commercial layer flocks in Southern California (2000-02): clinicopathologic findings.

Between February 2000 and February 2002, the California Animal Health and Food Safety Laboratory System diagnosed 26 cases of low-pathogenic H6N2 avian influenza from 12 commercial egg-laying farms. The most common gross and histologic lesions observed in infected chickens were fibrinous yolk peritonitis, salpingitis, oophoritis, and nephritis. Edema of the mesentery of the oviduct and pale, swollen kidneys were also observed. Mortality in infected flocks ranged from 0.25% to 3%, and egg production dropped 7% to 40%.

Evaluation and comparison of an indirect fluorescent antibody test for detection of antibodies to Sarcocystis neurona, using serum and cerebrospinal fluid of naturally and experimentally infected, and vaccinated horses.

The objectives of this study were to evaluate the accuracy of the indirect fluorescent antibody test (IFAT) using serum and cerebrospinal fluid (CSF) of horses naturally and experimentally infected with Sarcocystis neurona, to assess the correlation between serum and CSF titers, and to determine the effect of S. neurona vaccination on the diagnosis of infection. Using receiver-operating characteristic analysis, the areas under the curve for the IFAT were 0.97 (serum) and 0.99 (CSF). Sensitivity and specificity were 83.3 and 96.9% (serum, cutoff 80) and 100 and 99% (CSF, cutoff 5), respectively. Titer-specific likelihood ratios (LRs) ranged from 0.03 to 187.8 for titers between <10 and 640. Median time to conversion was 22-26 days postinfection (DPI) (serum) and 30 DPI (CSF). The correlation between serum and CSF titers was moderately strong (r = 0.6) at 30 DPI. Percentage of vaccinated antibody-positive horses ranged from 0 to 95% between 0 and 112 days after the second vaccination. Thus, the IFAT was reliable and accurate using serum and CSF. Use of LRs potentially improves clinical decision making. Correlation between serum and CSF titers affects the joint accuracy of the IFAT; therefore, the ratio of serum to CSF titers has potential diagnostic value. The S. neurona vaccine could possibly interfere with equine protozoal myeloencephalitis diagnosis.

Qualitative evaluation of selective tests for detection of Neospora hughesi antibodies in serum and cerebrospinal fluid of experimentally infected horses.

Neospora hughesi is a newly recognized protozoan pathogen in horses that causes a myeloencephalitis similar to Sarcocystis neurona. There are no validated serologic tests using the gold standard sera that are currently available to detect specific N. hughesi antibodies and, thus, no tests available to detect antemortem exposure or estimate seroprevalence in the horse. The objectives of the present study were to establish a bank of gold standard equine sera through experimental infections with N. hughesi and to assess several serologic tests for the detection of related protozoan antibodies. Seven horses were inoculated with N. hughesi tachyzoites, and 7 horses received uninfected cell culture material. The horses were monitored, and blood and cerebrospinal fluid were collected repeatedly over a 4-mo period. With the sera, 4 different serologic techniques were evaluated. including a whole-parasite lysate enzyme-linked immunosorbent assay (ELISA), a recombinant protein ELISA, a modified direct agglutination test, and an indirect fluorescent antibody test. Qualitative and quantitative evaluation of the results showed that the N. hughesi indirect fluorescent antibody test (IFAT) consistently discriminated between experimentally infected and noninfected horses, using a cutoff of 1:640. Sera from 3 naturally infected horses had titers >1:640. Cerebrospinal fluid in all but I infected horse had very low N. hughesi IFAT titers (<1:160), starting at postinoculation day 30.

Sensitivity and specificity of western blot testing of cerebrospinal fluid and serum for diagnosis of equine protozoal myeloencephalitis in horses with and without neurologic abnormalities.

OBJECTIVE: To determine sensitivity and specificity of western blot testing (WBT) of CSF and serum for diagnosis of equine protozoal myeloencephalitis (EPM) in horses with and without neurologic abnormalities. DESIGN: Prospective investigation. ANIMALS: 65 horses with and 169 horses without neurologic abnormalities. PROCEDURE: CSF and serum from horses submitted for necropsy were tested for Sarcocystis neurona-specific antibody with a WBT. Results of postmortem examination were used as the gold standard against which results of the WBT were compared. RESULTS: Sensitivity of WBT of CSF was 87% for horses with and 88% for horses without neurologic abnormalities. Specificity of WBT of CSF was 44% for horses with and 60% for horses without neurologic abnormalities. Regardless of whether horses did or did not have neurologic abnormalities, sensitivity and specificity of WBT of serum were not significantly different from values for WBT of CSF. Ninety-four horses without EPM had histologic evidence of slight CNS inflammation. CONCLUSIONS AND CLINICAL RELEVANCE: The low specificity of WBT of CSF indicated that it is inappropriate to diagnose EPM on the basis of a positive test result alone because of the possibility of false-positive test results. The high sensitivity, however, means that a negative result is useful in ruling out EPM. There was no advantage in testing CSF versus serum in horses without neurologic abnormalities. Slight CNS inflammation was common in horses with and without S neurona-specific antibodies in the CSF and should not be considered an indication of CNS infection with S neurona.

Fatal musculoskeletal injuries of Quarter Horse racehorses: 314 cases (1990-2007).

OBJECTIVE: To determine major causes of death and the anatomic location of musculoskeletal injuries in Quarter Horse racehorses in California. DESIGN: Retrospective case series. ANIMALS: 314 Quarter Horse racehorses with musculoskeletal injuries that were necropsied through the California Horse Racing Board Postmortem Program from 1990 to 2007. PROCEDURES: Postmortem pathology reports were retrospectively reviewed. Musculoskeletal injuries were categorized by anatomic region and described. The number of Quarter Horse starts and starters for the same period of time were obtained from a commercial database for determination of fatal injury incidence. RESULTS: Musculoskeletal injuries accounted for 314 of the 443 (71 %) Quarter Horse racehorses that died during the 18-year study period. Fatal musculoskeletal injuries occurred at a rate of 2.0 deaths/1,000 race starts and 18.6 deaths/1,000 horses that started a race. Musculoskeletal injuries occurred predominantly during racing (84%) and in the forelimbs (81%). The most common fatal musculoskeletal injuries were metacarpophalangeal and metatarsophalangeal joint (fetlock) support injuries (40%) and carpal (24%), vertebral (10%), and scapular (8%) fractures. Proximal interphalangeal (pastern) joint luxations resulted in death of 3% of horses. Fracture configurations of some bones were consistent with those of Thoroughbred racehorses. Evidence of preexisting stress remodeling of bone was reported for some fractures. CONCLUSIONS AND CLINICAL RELEVANCE: Knowledge of common locations and types of fatal musculoskeletal injuries in racing Quarter Horses may enhance practitioners' ability to detect mild injuries early, rest horses, and help prevent catastrophic injuries.

Isolation and molecular typing of Naegleria fowleri from the brain of a cow that died of primary amebic meningoencephalitis.

Naegleria fowleri causes an acute and rapidly fatal central nervous system infection called primary amebic meningoencephalitis (PAM) in healthy children and young adults. We describe here the identification of N. fowleri isolated from the brain of one of several cows that died of PAM based on sequencing of the internal transcribed spacers, including the 5.8S rRNA genes.