Bill J. Johnson

Lung Pathology and Infectious Agents in Fatal Feedlot Pneumonias and Relationship with Mortality, Disease Onset, and Treatments

This study charted 237 fatal cases of bovine respiratory disease (BRD) observed from May 2002 to May 2003 in a single Oklahoma feed yard. Postmortem lung samples were used for agent identification and histopathology. Late in the study, 94 skin samples (ear notches) were tested for Bovine viral diarrhea virus (BVDV) by immunohistochemistry (IHC). Bovine respiratory disease morbidity was 14.7%, and the mortality rate of all causes was 1.3%, with more than half (53.8%) attributed to BRD (0.7% total of all causes). The agents isolated were the following: Mannheimia haemolytica (25.0%), Pasteurella multocida (24.5%), Histophilus somni (10.0%), Arcanobacterium pyogenes (35.0%), Salmonella spp. (0.5%), and Mycoplasma spp. (71.4%). Viruses recovered by cell culture were BVDV-1a noncytopathic (NCP; 2.7%), BVDV-1a cytopathic (CP) vaccine strain (1.8%), BVDV-1b NCP (2.7%), BVDV-2a NCP (3.2%), BVDV-2b CP (0.5%), and Bovine herpesvirus 1 (2.3%). Gel-based polymerase chain reaction (PCR) assays were 4.6% positive for Bovine respiratory syncytial virus and 10.8% positive for Bovine coronavirus. Bovine viral diarrhea virus IHC testing was positive in 5.3% of the animals. The mean values were determined for the treatment data: fatal disease onset (32.65 days), treatment interval (29.15 days), number of antibiotic treatments (2.65), number of different antibiotics (1.89), and day of death (61.81 days). Lesions included the following: 1) duration: acute (21%), subacute (15%), chronic (40.2%), healing (2.8%), normal (18.1%), and autolyzed (2.8%); 2) type of pneumonia: lobar bronchopneumonia (LBP; 27.1 %), LBP with pleuritis (49.1 %), interstitial pneumonia (5.1 %), bronchointerstitial pneumonia (1.4%), septic (0.9%), embolic foci (0.5%), other (2.8%), normal (10.3%), and autolyzed (2.8%); and 3) bronchiolar lesions: bronchiolitis obliterans (39.7%), bronchiolar necrosis (26.6%), bronchiolitis obliterans/bronchiolar necrosis (1.4%), other bronchiolar lesions (6.5%), and bronchiolar lesion negative (25.7%). Statistically significant relationships were present among the agents, lesions, and the animal treatment, disease onset, and mortality data. Clinical illnesses observed in this study were lengthier than those reported 16–20 years ago, based on fatal disease onset, treatment interval, and day of death.

Cumulative racing-speed exercise distance cluster as a risk factor for fatal musculoskeletal injury in Thoroughbred racehorses in California

Abstract Thoroughbred racehorses which suffered a fatal musculoskeletal injury (FMI) while racing or race training at a California racetrack during 9 months of 1991 were studied to determine the importance of intensive, high-speed exercise schedules prior to injury. Seventy-seven horses which sustained an FMI while racing and 45 horses which sustained an FMI while race training were successfully matched by race or timed workout session with one control horse and included in the analyses. Race and timed workout (racing-speed exercise) histories were obtained for the case and control horses. Two-month cumulative, racing-speed cutoff distances were calculated from the control horse sample by two methods. Median racing-speed exercise frequencies and distances of the control horses were used to estimate age-specific (2, 3, 4 and ≥ 5 years), 2-month cumulative, racing-speed distances (Method 1). For the second method, the last race or timed workout for each control horse occurring just prior to, or on the date of injury for the matched case horse was identified. Cumulative racing-speed distances 2 months prior to these exercise events were determined for each control horse and used to estimate median age-specific (2, 3, 4 and ≥ 5 years), 2-month cumulative racing-speed distances (Method 2). The cumulative cutoff distances estimated from both methods were used to classify each matched pair according to the presence or absence of a 2-month cumulative, racing-speed distance which exceeded the age-appropriate cutoff distance (exercise distance cluster) within 6 months prior to injury. Manlel-Haenszel matched-pair odds ratios and 95% confidence limits were calculated separately for the racing and race-training fatal injuries. The relative risk for racing FMI was significantly greater for those horses which ran 2-month, cumulative racing and timed workout distances in excess of the cutoff values determined with Method 1 (relative risk (RR) = 3.0, 95% confidence interval (CI) = 1.2, 7.6) and Method 2 (RR = 7.2, 95% CI = 2.6, 20.6). The relative risk for race-training FMI was significantly greater for those horses which ran 2-month, cumulative racing and timed workout distances in excess of the cutoff values determined with Method 2 (RR = 3.4, 95% CI =1.0, 13.2).

Diagnosis of Oleander Poisoning in Livestock

Since mid- 1989, 37 cases of oleander poisoning in livestock have been diagnosed at the California Veterinary Diagnostic Laboratory System. The most frequent source for oleander exposure was plant clippings. Sudden death was the most common presenting complaint. Other signs reported included diarrhea, pulmonary edema, tachycardia, cardiac arrhythmias, colic, and lethargy. In the past, a presumptive diagnosis of oleander poisoning could be based only on matching clinical signs with evidence of consumption of oleander. A new 2 dimensional Thin-layer chromatography analysis of ingesta for oleandrin and an awareness of lesions in heart muscle have greatly improved the ability to diagnose oleander toxicosis.

Acute Salinomycin Toxicosis of Pigs

Salinomycin is a monovalent carboxylic ionophore that forms lipid-soluble complexes primarily with potassium ions. It was approved as a coccidiostat for chickens by the Federal Drug Administration in 1983. Overdosage or use in nontarget animal species can result in toxicosis. A case of salinomycin toxicosis in pigs is reported here. Three crossbred pigs and a feed sample were submitted for testing to the California Veterinary Diagnostic Laboratory System. These animals were from a group of 150 pigs that were 11-16 weeks old. A total of 25 pigs from the group died within a 24-hour period, and another 20-30 pigs exhibited abnormal behavior during this time. Some pigs were listless, with elevated rectal temperatures preceding death. Other pigs seemed alert but were reluctant to stand. A few had mild through a charcoal (G-60 charcoal : diatomaceous earth [3: 1]) column for cleanup, and spotted on a silica thin-layer chromatography plate. Ionophores were visualized by this method using a p-anisaldehyde reagent. Neither sample contained detectable levels of monensin or narasin. The fine feed contained 720 ppm of salinomycin, and the coarse feed contained 441 ppm of salinomycin. A diagnosis of salinomycin toxicosis was made based on history, clinical signs, lesions, and excessive levels of this ionophore in the feed made with the floor sweepings. Typically, ionophore toxicosis in pigs results in severe myodegeneration. The lesions are more pronounced in skeletal muscle than in cardiac muscle. Clinical signs frequently include myoglobinuria, progressive weakness, and dysmuscle tremors. Clinical signs included ataxia and voiding pnea. 6,8 Concurrent use of the antibiotic tiamulin increases of dark red to brown urine. Twenty-four hours before the the likelihood of toxicosis, presumably by interfering with pigs became ill, the owner fed the pigs from a new load of the metabolism and excretion of salinomycin. Tiamulin feed that contained a considerable amount of floor sweepings was not being fed to the pigs in this case. from a local feedmill that processed mostly poultry feeds. A case of salinomycin toxicosis was reported in Ireland, Typically, the owner mixed the feed obtained from the feedwhere salinomycin is approved for use as a growth promoter mill with some of his own grains and ground alfalfa hay, but in pigs. The approved dose is 60 ppm for pigs up to 4 months this time the owner fed the new load undiluted to both his old and 20-30 ppm for pigs over 4 months old. However, cattle and his pigs. None of the cattle that ingested the feed toxicosis occurred in finishing pigs accidently fed 166 ppm became ill. of salinomycin in the diet, which did not contain tiamulin. At necropsy, the 3 carcasses were in excellent flesh and Clinical signs of toxicosis did not appear until 5 days after well preserved. All 3 had strands of fibrin over the abdominal the introduction of contaminated feed to the ration. The pigs viscera and between liver lobes. No excess fluid was observed developed rear limb trembling, lethargy, reddish-brown urine, in the abdomens. All 3 sets of lungs failed to collapse, had and reluctance to stand or move. The discolored urine conslightly doughy texture, and exuded light yellow, frothy fluid. tinued for at least 5 days after the removal of the contamiThe bladders of all 3 pigs contained a dark reddish brown nated feed, and a severe degenerative myopathy was noted urine. The bladder mucosa was normal. Grossly, no visible in both skeletal and cardiac musculature. lesions were noted in the kidneys, heart, liver, spleen, skeletal In the present case, microscopic evidence of a degenerative muscle, brain, or intestines. Two of the pigs had milk ulcermyopathy was not seen. However, the presence of the pigation in the nonglandular portion of the stomach. mented urine suggests a release of myoglobin from skeletal Histologically, a nephrosis in sections of kidney from all muscles. Several sections of heart were taken, but only 1 3 pigs was characterized by medullary tubules containing representative section of skeletal muscle was taken from each eosinophilic granular pigmented material along with shrunkpig; therefore, a degenerative skeletal myopathy could have en degenerative tubular epithelium. No inflammatory cell been missed. However, the pigs in this report died just less response was present in the kidney. In sections of lung, the than 24 hours after the introduction of the contaminated alveolar walls, interlobular septa, and the adventitia around feed, which may have precluded any morphologic changes arterioles were thickened by a nonstaining edema. The airvisible grossly or with the light microscope. ways and alveoli were free of inflammatory cell infiltrate. No The most striking clinical and postmortem finding was the abnormalities were noted microscopically in sections of mydark red to reddish brown urine noted in many of the affected ocardium, skeletal muscle, liver, brain, or intestines. pigs. Discolored urine not due to hematuria is rare in pigs. The feed sample submitted contained 2 visible types. One Hemoglobinuria in pigs may be seen with copper toxicosis was a very finely ground mixture and the second was more and Leptospira pomona infection. Pigmented urine in the coarse and in clumps. No mold was visible in either type. absence of a hemolytic crisis suggests the presence of myogloThe two types of material in the feed sample were separated binuria. Ionophore toxicosis should be considered in those and submitted individually for ionophore analysis. The feed cases of pigmented nephrosis without evidence of a hemolytic samples were extracted into methanol : water (9:1), passed crisis. References From the California Veterinary Diagnostic Laboratory System, 1. Carson TL: 1986, Toxic chemicals, plants, metals, and mycoPO Box 1770, Davis, CA 95617. toxins. In: Diseases of swine, ed. Dunn HW, 6th ed., p. 688. Iowa Received for publication February 3, 1994. State University Press, Ames, IA.

Systemic granulomatous disease in a horse grazing pasture containing vetch (Vicia sp.)

A lo-year-old quarterhorse gelding was presented to theCalifornia Veterinary Diagnostic Laboratory in early Mayfor euthanasia and necropsy. Presenting clinical signs in-cluded weight loss; severe generalized dermatitis; dependentedema in the limbs, preputial sheath, and ventral abdomen;lymphadenomegaly of superficial and palpable lymph nodes;

Comparison of Disease in Calves Dosed Orally with Oak or Commercial Tannic Acid

Commercial tannic acid has been used as a substitute for leaves and acorns in studies of oak toxicosis in some species. The toxicity of a commercial tannic acid given orally to calves was determined, and the clinical signs, laboratory findings, and pyrogallol production were compared with those found in calves dosed orally with oak leaves. The oak-fed calves developed the clinical signs and lesions characteristic of renal failure. Proteinuria developed by 48 hours in 1 calf and by 72 hours in the other calf. Both calves developed hematuria on day 4 and glucosuria on day 5. The blood urea nitrogen and creatinine values increased markedly on day 6. Pyrogallol was detected in the serum only at 3 and 6 hours after the calves began ingesting the oak leaves. Pyrogallol was detected in urine from 1 calf until 60 hours and in the other calf until 48 hours after the beginning of oak intake. The 2 calves that were dosed with tannic acid at the same level as found in the leaves fed to the other calves did not develop clinical signs, abnormal laboratory findings, or pyrogallol production. Calves given high levels of tannic acid at doses of 4.4–5.5 g/kg developed methemoglobinemia rather than renal disease. Therefore, commercial tannic acid given orally cannot be used as a substitute for oak in studies of toxicosis in cattle.

Copper Toxicosis in Two Herds of Beef Calves following Injection with Copper Disodium Edetate

herpesviruses isolated from six sheep and four goats by restriction endonuclease analysis and radioimmunoprecipitation. Am J Vet Res 49:781-785. 16. Whetstone C, Miller J, Bortner D, et al.: 1989, Changes in the restriction endonuclease patterns of four modified-live infectious bovine rhinotracheitis virus (IBRV) vaccines after one passage in host animal. Vaccine 7:527-532. 17. Whetstone CA, Miller JM, Bortner DM, et al.: 1989, Changes in the bovine herpesvirus 1 genome during acute infection, after reactivation from latency, and after superinfection in the host animal. Arch Virol 106:261-279. 18. Whetstone CA, Wheeler JG, Reed DE: 1986, Investigation of possible vaccine-induced epizootics of infectious bovine rhinotracheitis, using restriction endonuclease analysis of viral DNA. Am J Vet Res 47:1789-1795. 19. Wyler R, Engles M, Schwyzer M: 1989, Infectious bovine rhinotracheitislvulvovaginitis (BHV-1). In: Herpesvirus diseases of cattle, horses, and pigs, ed. Wittmann G, pp. 1-72. Kluwer Academic Publ., Norwell, MA.

Fetal protection in heifers vaccinated with a modified-live virus vaccine containing bovine viral diarrhea virus subtypes 1a and 2a and exposed during gestation to cattle persistently infected with bovine viral diarrhea virus subtype 1b.

OBJECTIVE To determine efficacy of a modified-live virus (MLV) vaccine containing bovine viral diarrhea virus (BVDV) 1a and 2a against fetal infection in heifers exposed to cattle persistently infected (PI) with BVDV subtype 1 b. ANIMALS 50 heifers and their fetuses. PROCEDURES Susceptible heifers received a placebo vaccine administered IM or a vaccine containing MLV strains of BVDV1a and BVDV2a administered IM or SC. On day 124 (64 to 89 days of gestation), 50 pregnant heifers (20 vaccinated SC, 20 vaccinated IM, and 10 control heifers) were challenge exposed to 8 PI cattle. On days 207 to 209, fetuses were recovered from heifers and used for testing. RESULTS 2 control heifers aborted following challenge exposure; both fetuses were unavailable for testing. Eleven fetuses (8 control heifers and 1 IM and 2 SC vaccinates) were positive for BVDV via virus isolation (VI) and for BVDV antigen via immunohistochemical analysis in multiple tissues. Two additional fetuses from IM vaccinates were considered exposed to BVDV (one was seropositive for BVDV and the second was positive via VI in fetal tissues). A third fetus in the SC vaccinates was positive for BVDV via VI from serum alone. Vaccination against BVDV provided fetal protection in IM vaccinated (17/20) and SC vaccinated (17/20) heifers, but all control heifers (10/10) were considered infected. CONCLUSIONS AND CLINICAL RELEVANCE 1 dose of a BVDV1a and 2a MLV vaccine administered SC or IM prior to breeding helped protect against fetal infection in pregnant heifers exposed to cattle PI with BVDV1b.

Systemic granulomatous disease in cattle in California associated with grazing hairy vetch (Vicia villosa)

in the state of California, and only 2 cases have been reported, possibly because of lack of recognition of the disease. Vetch is not a major component of range and pasture land in the state of California but is abundant on disturbed soil from coastal areas to the Sierra foothills. It has been grown as a seed crop in northwestern California, and in other parts of California it has been used as a green-manure crop and for hay. In the 1950s and 1960s vetch was planted in the Sierra foothills of California by the Soil Conservation Service for soil erosion control. Vetch has become well established, and with increased awareness and recognition of the disease, reports may increase. Systemic granulomatous disease in horses is most likely multifactorial. There may be multiple etiologies with a common pathogenesis. Consumption of vetch may be 1 etiology associated with SGD in horses, as it is in cattle. The organ distribution, the perivascular nature of the inflammatory infiltrate, and the components of the inflammatory infiltrate of both diseases are similar, except for the lack of a prominent eosinophilic component of the granulomatous inflammation seen in the horse in the present case. Eosinophils have been seen in some horses with SGD (L. W. Woods, personal observation). Many cases of SGD occur without known exposure to vetch pasture. Disease in cattle induced by vetch may be the result of a hypersensitivity to 1 or more plant constituents that are absorbed and combine with host constituents to stimulate the inflammatory response. These plant constituents or immunogens in vetch that induce disease may also be present in other forage or organisms.

Acute bovine viral diarrhea associated with extensive mucosal lesions, high morbidity, and mortality in a commercial feedlot

In 2008, a northwest Texas feedlot underwent an outbreak of Bovine viral diarrhea virus (BVDV) causing high morbidity and mortality involving 2 lots of calves (lots A and B). Severe mucosal surface lesions were observed grossly in the oral cavity, larynx, and esophagus. Mucosal lesions varied from small (1–3 mm) infrequent mucosal ulcerations to large (5 mm to 1 cm) and coalescing ulcerations. Necrotic debris was present in ulcerations of some mortalities with some having plaque-like debris, but other mortalities presented more proliferative lesions. A calf persistently infected with BVDV arrived with one lot and the isolated virus was genotyped as BVDV-1b. Identical BVDV-1b strains were isolated from 2 other mortalities. A BVDV-2a genotype was also isolated in this outbreak. This genotype was identical to all BVDV-2a strains isolated in both lots. Serum samples were collected from exposed and unexposed animals and tested for antibodies for multiple viral pathogens. Seropositivity ranged from zero percent for calicivirus to 100% positive to Pseudocowpox virusx. At the end of the feeding period, the morbidity and mortality for the 2 lots involved was 76.2% and 30.8%, respectively, for lot A, and 49.0% and 5.6%, respectively, for lot B. Differential diagnoses included vesicular stomatitis viruses, Bovine papular stomatitis virus, and Foot-and-mouth disease virus. Based on the present case, acute BVDV should be considered when mucosal lesions are observed grossly.