Pulmonary edema and emphysema in cattle after intraruminal and intravenous administration of 3-methylindole.

Intraruminal and intravenous administration of 3-methylindole (3MI; skatole) caused interstitial pulmonary edema and emphysema in cattle. In 3 adult heifers given the intraruminal dose of 0.2 g of 3 MI per kilogram of body weight, clinical signs of respiratory disease appeared between 6 and 12 hours after dosing, and death due to pulmonary edema and emphysema occurred at 33, 69, and 72 hours. The mean plasma concentration of 3MI became maximal (18.5 mug/ml) at 3 hours and then decreased to low concentrations by 48 hours. In 2 heifers given an intraruminal dose of 0.1 g of 3MI/kg, clinical signs developed, but they did not die during the 96-hour experiment. The mean plasma concentration of 3 MI became maximal (16.8 mug/ml) at 3 hours and decreased to 1.6 and 0.4 mug/ml at 12 and 36 hours, respectively. At necropsy of the heifers, the lung were large, firm, dark red, and heavier than normal. Diffuse pulmonary edema was the predominant change in cattle which died early, and interstitial emphysema was more severe at later stages of the disease. During the early stages, alveoli were overdistended, and a few more ruptured. Most alveolar spaces were filled with proteinaceous residue, but the alveolar septums were smooth and of normal thickness. At later stages, proliferation of alveolar cells was observed, and alveolar septums were thickened. In 3 cows given 0.06 g of 3MI/kg by jugular infusion, clinical signs appeared in all cows, and 1 cow died of pulmonary edema and emphysema 56 hours after the infusion was started. Severe pulmonary lesions seen in all of the cows given a 3MI infusion were similar to those in the cows given an intraruminal dose of 3MI. The mean plasma concentration of 3MI increased to 10.7 mug/ml at 9 hours after starting the infusion and decreased to 0.5 mug/ml at 18 hours. The results indicate that 3MI, a product of ruminal tryptophan fermentation, can cause pulmonary edema and interstitial emphysema in cattle and support the hypothesis that 3MI is the causative agent in tryptophan-induced pulmonary disease.     

Impairment of sympathetic pulmonary vasoconstriction by 3-methylindole in cattle

Sixteen Holstein cattle allotted into 4 groups (4 cattle/group) were each given a single oral dosage of 0.2 g of 3-methylindole (3MI)/kg of body weight. The groups were killed at 12, 24, 48, and 72 hours, respectively, after 3MI administration. Comparison of clinical signs, pathologic pulmonary lesions, and in vitro pulmonary artery responses to pharmacologic stimuli was made between the 4 treated groups and 8 control Holstein cattle of similar age. Clinical signs of pulmonary distress first appeared 8 to 12 hours after 3MI administration. After 20 hours, clinical signs included dyspnea, moderate depression, and a marked expiratory grunt. A partial remission of these clinical signs was seen between 30 and 45 hours after 3MI administration. After remission, the cattle had clinical signs of severe dyspnea and depression and expiratory grunts were more pronounced. Pathologic pulmonary lesions, including heavy rubbery lungs, dilated interlobular septae, and subplural air bullae characteristic of pulmonary edema and interstitial emphysema were observed. The lungs of treated cattle did not collapse when the thorax was incised at necropsy. In vitro pulmonary artery strips contracted dose dependently to norepinephrine (NE). Group I tissues (12 hours after 3MI administration) responded similarly to control samples. Group II tissues (24 hours after 3MI administration) had a significant inhibition (P less than 0.05) in response to NE stimulation as compared with controls.     

Pathophysiologic studies of calves given 3-methylindole intraruminally

Intraruminal administration of 0.25 g of 3-methylindole (3MI; skatole/kg of body weight) to seven young calves generally caused mild respiratory signs and lesions, accompanied by only slight changes in cardiopulmonary function. Moderate depression, trembling, and irregular respiratory rate were observed between postadministration hours (PAH) 6 and 12. By PAH 24 at this dosage, abnormal clinical signs were not present. Statistically significant (P less than or equal to 0.05) changes observed in blood gas data from the seven calves were a decrease in aortic oxygen tension at PAH 12, increases in free-flowing venous oxygen tension in the intervals between PAH 6 and 12 and between PAH 6 and 24, and an increase in occluded venous oxygen tension at PAH 24. All calves had increases (although generally not statistically significant) in heart rate, cardiac output, cardiac index, stroke volume, and stroke index after 3MI administration. Mean aortic and pulmonary arterial pressure changes were generally small and variable. At necropsy, the lungs of the calves did not collapse when the thorax was opened. Patchy areas of consolidation (0.5 cm in diameter) were scattered throughout the parenchyma. Pulmonary edema or emphysema was not observed grossly. Microscopically, the alveolar septae were irregularly thickened because of edema, infiltration by polymorphonuclear and mononuclear cells, and vascular congestion. Interstitial lesions were patchy in distribution and severity and corresponded to the areas of consolidation observed grossly. Alveolar epithelial hypertrophy and hyperplasia were present, and an occasional focus of alevoli contained fluid of edema. Degeneration of individual hepatocytes was observed in scattered areas of the liver, especially in the periportal areas. It was concluded that differences in 3MI dosage response may exist between young calves and adult cattle in which calves are more resistant to the pulmonary cytotoxicity of 3MI.     

Reduction of 3-methylindole production and prevention of acute bovine pulmonary edema and emphysema with lasalocid

A study was conducted to determine the dose of lasalocid that would effectively reduce ruminal conversion of tryptophan (TRP) to 3-methylindole (3MI) and prevent the development of acute bovine pulmonary edema and emphysema (ABPE). After adaptation to a maintenance diet for 3 wk, 20 mature beef cows were randomly divided into four groups of five cows each and fed 0, 200, 400 or 600 mg lasalocid X head-1 X d-1 in .5 kg ground barley for the 12-d experimental period. In vitro conversion of TRP to 3MI and indole by ruminal fluid and volatile fatty acid (VFA) concentrations were determined on d 0, 2, 4, 6 and 12. On d 6, an oral dose of .35 g TRP/kg body weight was given to induce ABPE, and ruminal production of 3MI and indole was determined at intervals thereafter. Formation of 3MI was sharply reduced (P less than .01) both in vitro and in vivo by lasalocid treatment at 200 mg X head-1 X d-1. Further suppression of 3MI production occurred as the lasalocid dose was increased (P less than .05). Linear (P less than .0001) and quadratic (P less than .002) components were determined for the relationship between lasalocid dose and 3MI production. Indole formation was variable, but tended to increase (P less than .05) with increasing lasalocid dose. Cows that received no lasalocid developed moderate to severe clinical signs of ABPE and three cows died of acute lung disease. Lasalocid treatment at all levels prevented ABPE. Lasalocid decreased ruminal acetate and butyrate, and increased propionate concentration (P less than .01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Duration of inhibition of 3-methylindole production by monensin

A series of in vitro and in vivo trials was conducted to determine if continuous monensin feeding for up to 56 d would reduce ruminal conversion of L-tryptophan (TRP) to 3-methylindole (3MI). Fourteen mature beef cows were adapted to a maintenance diet for 3 wk. In trial I, the sampling time to optimize 3MI production was determined. Trials II through IV were to determine the duration of efficacy of monensin on reducing 3MI concentrations in vitro and in vivo. During trials II, III and IV one-half of the cows were fed 200 mg monensin X head-1 X d-1 for 21, 36 and 55 d, respectively, while the remaining cows served as controls. All cows were fed the control diet for 21 d between each trial. Volatile fatty acid (VFA) concentrations and in vitro conversion of TRP to 3MI were determined in ruminal fluid samples collected during trials I through IV. On d 28 of trial IV, all cows were given an oral dose of .35 g TRP/kg of body weight to induce acute bovine pulmonary edema and emphysema (ABPE). Ruminal concentrations of 3MI and indole were measured at intervals for 96 h. Results of trial I demonstrated that ruminal fluid collected 15 h postfeeding produced the highest in vitro conversion of TRP to 3MI. Therefore, ruminal fluid samples were collected at that time in trials II, III and IV. In vitro conversion of TRP to 3MI was lower (P less than .01) in samples from monensin-treated cows (12.1%) compared with controls (25.6%). Monensin reduced 3MI production for 55 d, the longest time tested in these experiments.(ABSTRACT TRUNCATED AT 250 WORDS)     

Association of severity of enteric granulomatous inflammation with disseminated Mycobacterium avium subspecies paratuberculosis infection and antemortem test results for paratuberculosis in dairy cows

Disseminated infection (DI) of Mycobacterium avium subspecies paratuberculosis (MAP) in cattle may impair cow health, potentiate spread of disease, and is a potential food-safety risk. The objectives of this study were to determine the association between severity of histologic enteric lesions and the occurrence of DI, clinical signs, and positive fecal culture and serum ELISA results. Bacteriologic fecal culture and serum ELISA were performed on 40 dairy cows from MAP-infected herds. Cows were classified as having DI if MAP was isolated from any of 11 extra-intestinal tissues collected postmortem. A grade of 0-3, corresponding to the severity of histologically evident granulomatous inflammation was determined for sections of ileum, jejunum, mesenteric lymph node, and ileocolic lymph node. An overall intestinal inflammation (OII) grade of 0-3 was assigned to each cow. The proportion of cows with DI increased with tissue-specific lesion grade and OII grade. All cows with grade 3 inflammation in any single tissue had DI, however, some cows with DI had grade 1 inflammation or no lesions. In general, there was a positive association between OII grade and clinical signs, gross enteric lesions, and positive ELISA and fecal culture results. However, 12% of OII grade 0 cows had clinical signs (explained by other conditions recognized with necropsy), and the proportion of positive ELISA results was lower for OII grade 3 cows relative to grade 2 cows. Although MAP dissemination may occur early in the disease process, histopathology of intestinal tissues may be used to detect a substantial proportion of DI cows.     

Acute Atypical Bovine Pneumonia Caused by Ascaris Lumbricoides

A case of acute atypical pneumonia (bovine asthma, pulmonary emphysema, or pulmonary adenomatosis) occurred in a group of cross-bred beef type yearlings in late autumn. Clinical signs included a forced expiratory grunt, excessive salivation, ruminal stasis and, on auscultation over the lungs, pulmonary emphysema and oedema. The cattle had been brought in from a poor summer pasture and housed in a pig pen heavily contaminated with Ascaris lumbricoides eggs as it had contained unwormed feeder pigs all summer.

Fifteen out of seventeen head were affected ten days following housing and all within twenty-four hours. One steer of the group died and at necropsy fourth stage A. lumbricoides larvae were isolated from lungs showing profuse oedema and some emphysema. Histopathological examinations of the lungs showed a diffuse interstitial pneumonia. All remaining animals appeared clinically normal six days following the outbreak.

     

Acute lead poisoning in cows due to feeding of lead contaminated ash residue

In a dairy herd of 21 cows which were on pasture during the day at the end of May 2002, four eight years old cows were suddenly inappetent and showed severe diarrhoea consisting of black discolorate feces. A few days after the onset of the disease, three affected cows exhibited neurological disorders. These cows were admitted to the IInd Medical Clinic of the University for Veterinary Medicine in Vienna. Following clinical signs were observed: circulatory weakness, anorexia, atony of the rumen, diarrhoea and in accordance with acute lead poisoning typical signs of the central nervous system. One cow died and the other two animals were euthanized. Results of blood testing were anaemia, basophil spotting of erythrocytes, increase of liver enzymes and CK, hypocalcaemia, decrease of potassium and phosphate. The cerebrospinal fluid of two cows showed increased CK-, LDH- and AST-values. The lead contents of whole blood samples were between 0.486 and 0.928 mg/kg, of liver samples 13.3 to 114.4 mg/kg, of kidney samples 172.2 to 448 mg/kg and of rumen content 59 mg/kg fresh matter. At necropsy, enteritis, liver fluke disease and severe interstitial and alveolar pulmonary emphysema were found. Pathohistologically typical ischaemic necrosis of neurons predominantly at the tips of the gyri, disseminated petechial hemorrhages and moderate diffuse neovascularisation, but no acid-fast intranucleolar inclusion bodies in the renal tubules were observed. As causative agent of the acute lead poisoning a residue on combustion, taken up by the cows on the pasture, was confirmed. The ash residue was formed by combustion of three tires which contained 450 g heavy weights of 96.5% lead for wheel balance. The lead content of the ash residue was between 2.9 and 28 g/kg dry matter.     

Pulmonary Hypertension and Cardiac lnsuff iciency in Three Cows with Primary Lung Disease

Increased pulmonary arterial pressures as a result of pulmonary disease are described in two cows with chronic pneumonia and one cow with acute pneumonia. Based on clinical signs of congestive right heart failure, increased pulmonary arterial pressure, and right ventricular hypertrophy, cor pulmonale was diagnosed in one cow. Two cows had increased pulmonary arterial pressure and signs of right heart insufficiency, but right ventricular hypertrophy was not identified. Two of the cows had ventral edema and exercise intolerance. All cows had jugular venous distention and increased right atrial and pulmonary arterial pressures. Peripheral arterial PaO2 was decreased in two cows, and not measured in the third cow. Although an uncommon cause of congestive heart failure in cattle at low altitudes, pulmonary hypertension should be considered in cattle with clinical right heart failure.     

Role of mixed-function oxidase in 3-methylindole-induced acute pulmonary edema in goats

The relationship between the pulmonary toxicity of 3- methylindole (3MI, skatole) and the mixed-function oxidase (MFO) system was investigated. Nine goats assigned to three groups were given a jugular infusion of [14C]3MI (0.02 to 0.03 g of 3MI/kg of body weight containing 0.5 muCi/kg of body weight) for 1.5 hours to induce acute pulmonary edema. Two groups of three goats each were treated with phenobarbital (PB) or piperonyl butoxide (BT) prior to 3MI infusion to induce or to inhibit the MFO system. Three goats were used as 3MI controls. During a 72-hour test period, blood was collected for determination of plasma 3MI concentration and radioactivity. Urine was collected and was fractionated by column chromatography. The severity of pulmonary lesions was evaluated by gross and microscopic examination. Pretreatment with BT prevented the onset of acute pulmonary edema. Goats pretreated with PB had more severe lung lesions than did 3MI controls. Plasma of goats pretreated with BT had a longer half-life (2.1 hours) of radioactivity, whereas plasma of goats pretreated with PB had a shorter half-life (1.0 hour) when compared with plasma of 3MI control goats (1.5 hours) given the same dosage of [14C]3MI (P less than 0.025). The plasma half-life of 3MI was longer (P less than 0.025) in BT-pretreated goats (0.45 hour) than that in PB-pretreated goats (0.26 hour). At 72 hours, 70% to 98% of the infused radioactivity had been excreted in the urine. The pattern of urinary metabolites of 3MI was altered in BT-pretreated goats compared with patterns in control and PB-pretreated goats. Results indicate that the MFO system is one of the pathways involved in the metabolism of 3MI and that pulmonary toxicosis results from metabolism of 3MI by this enzyme system.     

Radiographic findings in 16 dogs infected with Angiostrongylus vasorum

Thoracic radiographs of 16 dogs infected naturally with Angiostrongylus vasorum showed signs of bronchial thickening, an interstitial pattern and a multifocal and/or peripheral alveolar pattern. In dogs treated with fenbendazole, follow-up radiographs showed that the alveolar pattern had resolved and a mild, hazy interstitial pattern had developed. In contrast with dogs with heartworm (Dirofilaria immitis), no pulmonary vascular lesions were identified.     

Association of bovine respiratory syncytial virus with atypical interstitial pneumonia in feedlot cattle

Thirty-three cattle with fatal respiratory tract disease were examined for gross and histologic lesions and for the presence of viral and bacterial agents in the lungs. Fifteen cattle had lesions characteristic of atypical interstitial pneumonia (AIP), and 18 had other respiratory tract diseases, including infectious bovine rhinotracheitis, shipping fever pneumonia, bronchopneumonia, pulmonary abscess, and edema of the trachea. Gross necropsy findings in the cattle with AIP were uncollapsed and emphysematous lungs; histopathologic findings included interstitial edema, thickening of alveolar walls, hyaline membrane formation, and hyperplasia of type-II pneumonocytes. The infective agents found in the lungs of the 33 cattle included bovine respiratory syncytial virus, bovine herpesvirus type 1, Pasteurella sp, mycoplasmas, and Corynebacterium pyogenes. Bovine respiratory syncytial virus was detected by use of immunofluorescence and immunoperoxidase on lung tissue sections; bovine herpesvirus type 1 was detected by these techniques and by isolation of the virus. Bovine respiratory syncytial virus was significantly (P = 0.01) associated with lesions of AIP (11 of 15), compared with those of other respiratory tract diseases (5 of 18).     

Ascaris suum Infection in Calves III. Pathology

Gross changes in the lungs of Ascaris suum- infected calves consisted of atelectasis and hemorrhagic foci, edema and emphysema, frequently with bullae. Prominent microscopic lung lesions were edema and emphysema of the interlobular septa with large numbers of eosinophils within and around lymphatics, peribronchiolar lymphoid nodules and parasitic granulomas. Many of the microscopic features were consistent with those found in atypical interstitial pneumonia. Changes in the alveoli were atelectasis, the exudation of plasma proteins, mononuclear cells and eosinophils, and alveolar wall thickening. Lesions found later included fibrosis and fetalization of the alveolar walls. Plasma cells and neutrophils were not common. Challenge with Toxocara canis after sensitization with A. suum resulted in the lungs developing a few areas of atelectasis. Migration of T. canis to lungs of calves is slower than A. suum. A. suum larvae were always found in bronchi, bronchioles and alveoli of calves that died. Lesions were observed in the liver but not the kidney of A. suum infected calves; both lung and liver lesions tended to resolve with time.     

Proton nuclear magnetic resonance spectroscopy based investigation on propylene glycol toxicosis in a Holstein cow

Background

It is unknown which metabolites are responsible for propylene glycol (PG)-induced toxicosis, and a better understanding of the underlying mechanisms explaining incidences of abnormal behaviour of dairy cows fed PG is therefore needed.

Methods

The study included three cows of which one developed PG toxicosis. In order to investigate how the metabolism of PG differed in the cow developing toxicosis, proton nuclear magnetic resonance (NMR) spectroscopy was applied on ruminal fluids and blood plasma samples obtained before and after feeding with PG.

Results

PG toxicosis was characterized by dyspnea and ruminal atony upon intake of concentrate containing PG. The oxygen saturation of arterial blood haemoglobin and the oxygen pressure in arterial blood decreased along with the appearance of the clinical symptoms. NMR revealed differences in plasma and ruminal content of several metabolites between the cow responding abnormally to PG and the two control cows.

Conclusion

It is concluded that PG-toxicosis is likely caused by pulmonary vasoconstriction, but no unusual metabolites directly related to induction of this condition could be detected in the plasma or the ruminal fluid.     

Pulmonary lesions induced by 3-methylindole and bovine respiratory syncytial virus in calves

Our objectives were to describe the ultrastructural morphogenesis of pulmonary lesions induced by 3-methylindole in 30- to 45-day-old Holstein calves and to determine whether toxic exposure to 3-methylindole exacerbates pulmonary lesions induced by bovine respiratory syncytial virus. Administration of 3-methylindole (0.25 g/kg) to calves resulted in interstitial edema and ultrastructural swelling of type-I alveolar epithelial cells and nonciliated bronchiolar epithelial cells as early as 4 to 6 hours after intraruminal administration. More severe alveolar edema containing protein was associated with swelling of capillary endothelial cells at 2 days after administration. Proliferation of type-II alveolar epithelial cells was first observed at 2 days after 3-methylindole administration, and marked hyperplasia of type-II epithelial cells and nonciliated bronchiolar epithelial cells was evident by 4 days after administration. Pulmonary cytochrome P-450 monooxygenase concentrations decreased significantly (P less than 0.001) by 12 hours after administration and did not increase significantly again by 8 days after administration. Calves were inoculated with bovine respiratory syncytial virus 3 days after administration of 3-methylindole, and pulmonary lesions were assessed 5 days after viral inoculation. Viral replication was demonstrated by fluorescence microscopy for viral antigen or by transmission electron microscopy in ciliated and nonciliated airway epithelial cells. Viral antigen was identified infrequently in alveolar macrophages and in type-II alveolar epithelial cells. 3-Methylindole exposure in calves did not result in more widespread distribution of viral antigen in alveolar tissue of respiratory syncytial virus-inoculated calves or in significant enhancement of viral pneumonia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Atypical interstitial pneumonia (AIP) in calves and young cattle in Schleswig-Holstein in conjunction with an infection by the bovine respiratory syncytial virus (BRSV)

It is reported on atypical interstitial pneumonia (AIP) in 16 mostly Holstein-Frisian calves and feeders from 13 different farms in Schleswig-Holstein in association with an infection by the respiratory syncytial virus (BRSV). All animals were submitted with identical clinical histories. Macroscopically the lung lesions were characterized by alveolar and interstitial edema and emphysema. Microscopically there was a diffuse interstitial pneumonia with formation of hyaline membranes and multinucleated giant cells. From the investigation material of the 16 animals BRSV was confirmed by direct immunofluorescence with monoclonal antibodies in 4 animals from 4 different farms.     

The pathology of experimental Lasiospermum bipinnatum (Thunb.) Druce (Asteraceae) poisoning in sheep. II. Pulmonary and miscellaneous lesions

Poisoning with the plant Lasiospermum bipinnatum was studied in 9 lambs at various dose levels. Dyspnoea and tachypnoea, which were dose-related, were observed in 4 of the lambs. Gross and microscopic pulmonary lesions were found in all the lambs receiving plant material originating from one source but not in those given plant from another locality. The severity of the lesions appeared to be dose-dependent. Macroscopic lesions included pulmonary and mediastinal emphysema, congestion and oedema. Microscopically Clara cell hypertrophy and hyperplasia, and interstitial pneumonia were the most outstanding findings. It is speculated that the pulmonary lesions were induced by a furanosesquiterpene or tryptophan or a combination of both of these toxins in the dosed plant material. Miscellaneous and inconsistent lesions observed in the experimental animals included widespread haemorrhage (1 lamb), transudations into the body cavities and adrenocortical hyperplasia.     

Hemorrhagic bowel syndrome in dairy cattle: 22 cases (1997-2000)

OBJECTIVE: To determine signalment, history, and clinical, necropsy, and microbiologic findings in dairy cows with hemorrhagic bowel syndrome. DESIGN: Retrospective study. ANIMALS: 22 adult dairy cows from a single farm in Colorado. PROCEDURE: Medical records were reviewed for information on signalment, medical and reproductive history, the owner's chief complaints, results of physical examinations and ancillary diagnostic tests, treatment and response to treatment, results of microbiologic testing, and, if applicable, postmortem findings. RESULTS: Common clinical signs were acute signs of profound depression, decreased milk production, tachycardia, ruminal stasis, abdominal distention, and dark clotted blood in the feces. Rectal examination revealed distended loops of small intestine in 7 of 14 cows. Transabdominal ultrasonography revealed small intestinal ileus and distention in 12 of 12 cows and homogeneous echogenic intraluminal material compatible with intraluminal hemorrhage and clot formation in 4. Seven of 8 cows treated medically died; 9 of 13 cows that underwent surgery died or were euthanatized. Clostridium perfringens was isolated from fecal samples from 17 of 20 cows. The most common morphologic diagnosis at necropsy was severe necrohemorrhagic enteritis or jejunitis with intraluminal hemorrhage or blood clots. The most prominent histologic finding was severe, segmental submucosal hemorrhage and edema of the small intestine. CONCLUSIONS AND CLINICAL RELEVANCE: Results confirm that in adult cattle, hemorrhagic bowel syndrome is a sporadic acute intestinal disorder characterized by intraluminal hemorrhage and obstruction of the small intestine. Clostridium perfringens was consistently isolated from the feces of affected cows. The prognosis for affected cows was grave.     

Radiographic, computed tomographic, and ultrasonographic findings with migrating intrathoracic grass awns in dogs and cats.

The purpose of this study was to describe the clinical, radiographic, and computed tomographic findings in dogs and cats with migrating intrathoracic grass awns. Thirty-five dogs and five cats with visual confirmation of a grass awn following surgery, endoscopy or necropsy, and histology were assessed. The medical records and all diagnostic imaging studies were reviewed retrospectively. Labrador Retrievers or English Pointers < 5 years of age, with a history of coughing and hyperthermia, were the most common presentations. Seventeen animals had an inflammatory leukogram of which 14 had a left shift or toxic neutrophils. Radiographs were performed in 38 animals and computed tomography (CT) in 14. Thoracic radiographs were characterized by focal pulmonary interstitial to alveolar opacities (n = 26) that occurred most commonly in the caudal (n = 19) or accessory lobes (n = 8). Additional findings included pneumothorax (n = 9), pleural effusion (n = 8), and pleural thickening (n = 7). Pulmonary opacities identified on radiographs correlated to areas of pneumonia and foreign body location. CT findings included focal interstitial to alveolar pulmonary opacities (n = 12) most commonly in the right caudal lung lobe (n = 9), pleural thickening (n = 11), mildly enlarged intrathoracic lymph nodes (n = 10), soft tissue tracking (n = 7) with enhancing margins (n = 4), pneumothorax (n = 6), pleural effusion (n = 4), and foreign body visualization (n = 4). Histologic diagnoses included pulmonary and mediastinal granulomas or abscesses, bronchopneumonia, and pleuritis. Migrating intrathoracic grass awns should be considered as a differential diagnosis in coughing, febrile animals with focal interstitial to alveolar pulmonary opacities, pleural effusion, pleural thickening, and/or pneumothorax on radiographs or CT.     

N-acetyl-beta-D-glucosaminidase activity in urine of cows with renal parenchymal lesions

OBJECTIVE: To measure N-acetyl-beta-D-glucosaminidase (NAG) activity in urine of cows with renal diseases and to correlate values for NAG activity with renal lesions. ANIMALS: 8 lactating Holstein cows and a Japanese Shorthorn cow, all of which had renal disease. PROCEDURE: Urine samples were collected, and urinary NAG activity and creatinine concentration were measured. The NAG activity was expressed as units per gram of creatinine (NAG index). Cows were euthanatized, necropsy was performed, and correlations between results for urinary NAG index and histopathologic findings for the kidneys were evaluated. RESULTS: The NAG activity and NAG index in urine samples obtained from cows with interstitial nephritis were high, ranging from 4.2 to 13.6 U/L and 3.5 to 23.0 U/g, respectively. A cow with renal amyloidosis also had high values for urinary NAG activity and NAG index. Histologic examination of the kidneys revealed various kinds of parenchymal lesions. However, urinary NAG index in cows with enzootic bovine leukosis was low. CONCLUSIONS AND CLINICAL RELEVANCE: Cows with renal diseases had high urinary NAG indexes that correlated well with their renal lesions, except for cows with enzootic bovine leukosis. Therefore, measurement of NAG index in urine samples has the potential to provide new perspectives on clinical diagnosis of renal disease in cattle.