Effect of melengestrol acetate on development of 3-methylindole-induced pulmonary edema and emphysema in sheep.

The involvement of melengestrol acetate (MGA) in susceptibility to developing pulmonary edema and emphysema following oral administration of 3-methylindole (3MI) was investigated using 10 Suffolk ewes receiving 0 or 0.15 mg of MGA daily (n = 5). Blood, urine and ruminal fluid were collected immediately prior to 3MI dosing (0.2 g/kg BW) and 1, 2, 3, 4, 5, 6, 12 and 24 h (blood); 3, 6, 9, 12 and 15 h (urine) and 1, 2, 3 and 12 h (ruminal fluid) afterward. Ewes receiving MGA experienced earlier (P < 0.05) onset of respiratory distress than the control ewes (2.5 vs 4 h), and upon euthanasia at 96 h, their lung weight relative to body weight tended (P < 0.10) to be lower. Ruminal 3MI concentrations did not differ between treatments (P > 0.05). Ewes receiving MGA had higher (P < 0.05) concentrations of 3MI metabolites in plasma prior to dosing than did control ewes, and these values tended to remain higher throughout the sampling period. Immunoreactivity assays indicated more pneumotoxin present in the lungs of MGA-treated ewes than controls. Lung damage was apparently more acute and accelerated in the MGA-treated ewes than in the controls. Urinary 3MI mercapturate concentrations differed (control > MGA-treated, P < 0.05) at 9, 12, and 15 h, but this difference was not apparent when urinary production (as estimated by creatinine concentration) was considered. The implications of these findings for MGA-treated feedlot heifers are currently under investigation.     

Pathophysiologic study of 3-methylindole-induced pulmonary toxicosis in immature cattle

In 5 Friesian calves given 3-methylindole (3-MI) (100 mg/kg once a week for 8 weeks, except calf 4, given a 50 mg/kg dose on weeks 3 to 8), pulmonary function (PF) values and arterial blood gas tensions (PaO2 and PaCO2) were measured 24 hours after dosing was done and were correlated with clinical, biochemical, and pathologic changes. Three of the calves (No. 1, 2, and 3) showed acute respiratory distress syndrome 24 hours after the first 3-MI treatment, with a large increase in respiratory frequency, minute viscous work, and PaCO2 and a large decrease in tidal volume, dynamic lung compliance, and PaCO2. They died 36, 38, and 84 hours after dosing. Pulmonary function changes were compatible with the severe pulmonary edema and alveolar damage observed at necropsy. The 2 other calves, after they were given the 1st dose, showed only subacute respiratory distress syndrome with less severe changes in PF values recorded at 24 hours. Furthermore, they became progressively more tolerant to the 2nd, 3rd, and 4th weekly treatments, and showed base-line PF values after the 5th weekly treatment. Pathologic changes were not observed in lung biopsy material from these 2 animals at 2 and at 12 weeks after the 8th (or last) 3-MI treatment.     

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)     

A case of acute pulmonary edema, splenomegaly, and ascites in guinea fowl

Acute pulmonary edema, splenomegaly, and ascites were observed in a disease outbreak in adult white and pearl guinea fowl. The clinical history and gross and microscopic lesions resembled those described for marble spleen disease of pheasants and avian adenovirus group II splenomegaly of chickens. A small number of intranuclear inclusion bodies were found in liver, spleen, and lung sections of affected guinea fowl. Attempts to isolate virus and serological tests to detect the presence of viral antigens were unsuccessful. Adult female pearl guinea fowl experimentally exposed to pheasant and turkey isolates of type II avian adenoviruses developed gross and microscopic lesions similar to those seen in the field outbreak. The pheasant isolate was the more virulent. Intranuclear inclusion bodies were observed in liver, spleen, and lung sections of pearl guinea fowl inoculated with either of the virus isolates, and direct immunofluorescent examination revealed viral antigen in the spleen and lung.     

Growth-related changes in the pulmonary function of goats

Growth-related changes in pulmonary function values were investigated in 20 healthy French Alpine goats, aged between 20 and 550 days, weighing 7–55 kg. Pulmonary ventilation, mechanics of breathing and arterial oxyten tension were measured using standardized techniques and methods adapted for goats of different body sizes. The Ppl values and the tI/tTOT ratio showed no significant changes with age and body size. The ventilation values (Vt, Ve, mVI and mVE) increased linearly with growth. There was a significant correlation of age and body weight with dynamic lung compliance (Cdyn), total pulmonary resistance (RL), viscous work of breathing (Wvis tot) and minute viscous work (Wvis min) throughout the age range studied. Cdyn, Wvis tot and Wvis min increased and RL decreased with age and body weight. Arterial blood gases (PaO₂ and PaCO₂) did not show significant changes over the age range studied. Regression equations for each pulmonary function parameter are given with body weight as the independent variable. Data for the mechanics of breathing were compared with those elsewhere for cattle, horses, man and dogs.     

奶山羊急性低血钙症的治疗

奶山羊急性低血钙症主要是发生于泌乳高峰期的高产泌乳母羊 ,多由于在产前和产后机体摄入食物中的钙不能满足大量泌乳的需要 ,而引起的一种代谢性疾病。笔者在近几年临床工作中共诊治 98例 ,死亡 2例 ,治疗率达 98% ,报告如下。1　临诊资料　产后泌乳 40～ 6 0天 2例 ,占 2 % ;6 1～ 1 0 0天 89例 ,占 90 .8% ;1 0 1天以后 7例 ,占7.2 %。产羔 1～ 2胎 3例 ,占 3 .1 % ;3～ 5胎 78例 ,占 79.6 % ;6胎以后 1 7例 ,占 1 7.3 %。日泌乳量在3～ 4kg1 5例 ,占 1 5.3 % ;4.1 kg以上 83例 ,占84.7%。从治疗时间看 ,1～ 2天治愈 77例 ,占78.6 % ;3天…     

Role of goats in epizootiology and epidemiology of Q fever

Numerous data show that the epizootics of Q fever in goats can be particularly related to cases of this disease in humans. The aim of the study was to examine 98 goat serum samples from the farm where abortions, early parturition and parturition of weak goatlings were noted. The microaglutination method was used in this study. Serum dilution 1:8 was defined as a positive titre. The study revealed that 79.6% of serum samples were positive and numerous high titres suggested an acute form of infection. It could be supposed that Q fever was the reason of abortions in the herd. The results obtained point to the necessity of examinations for Q fever in goats, because of the possibility of infection in people who have a contact with these animals. Goats seem to be the animal species especially sensitive to C. burnetii infection. Q fever should be taken into consideration in the differential diagnosis of the goat diseases, when abortions occur.     

Acute pulmonary edema after diazepam-ketamine in a dog

An 8-year-old mixed-breed dog was anesthetized for colonoscopy. Moderate sedation was produced by premedication with glycopyrrolate, acepromazine, and hydromorphone, and anesthesia was induced by IV injection of diazepam and ketamine. Frothy, reddish-colored fluid flowed from the endotracheal tube immediately after endotracheal intubation but ceased after several minutes. Furosemide was injected IV. Anesthesia was maintained by sevoflurane in oxygen. Ventilation and arterial blood pressure were satisfactory, however, after oxygen was administered to maintain normal hemoglobin saturation. Radiography revealed changes consistent with a diagnosis of pulmonary edema. The following day, ventricular premature contractions developed and atrial dissociation, valvular regurgitation, and pulmonary hypertension were diagnosed on echocardiography. The proposed etiology is either profound transient hypotension and/or pulmonary hypertension induced by ketamine. The cardiac abnormalities that were present the following day suggest that myocardial dysfunction after induction of anesthesia was more severe than was apparent as assessed by routine physical examination and monitoring methods.     

Negative-pressure pulmonary edema complicated by acute respiratory distress syndrome in an orangutan (Pongo pygmaeus abelii).

A 22-yr-old, 86-kg, morbidly obese female orangutan (Pongo pygmaeus abelii) was immobilized and transported to the Denver Zoological Gardens hospital for a routine physical examination. Immediately after arriving at the hospital, cyanosis and apparent inadequate ventilatory efforts were noted. Clinically significant hypoxia occurred despite attempts to ventilate the orangutan through face mask, and attempts to place an endotracheal tube began. A large volume of pink-tinged frothy fluid flowed from the trachea when the laryngoscope was inserted into the oropharynx. Severe pulmonary edema due to negative-pressure pulmonary edema, precipitating life-threatening hypoxia was suspected. The orangutan was maintained on a mechanical ventilator using the neuromuscular blocking agent cisatracurium besylate and sedation with periodic doses of isoflurane and midazolam for 48 hr. Positive end-expiratory pressure was used while the orangutan was ventilated mechanically to improve respiratory function. The edema and hypoxia improved, but respiratory arrest ensued 30 min after extubation, when the orangutan was removed from mechanical ventilation. Necropsy and histopathology demonstrated that serious lung injury had led to acute respiratory distress syndrome.     

Post‐anesthetic pulmonary edema in two horses

Case 1 A two‐year old, 462 kg Standard bred horse was anesthetized for arthroscopy and castration. During anesthesia, hyperemia of the mucosal membranes and urticaria were noticed. During 5 hours of anesthesia subcutaneous edema of the eyelids and neck region developed. In the recovery box, the orotracheal (OT) tube was left in situ and secured in place with tape. Following initial attempts to stand, the horse became highly agitated and signs consistent with pulmonary edema developed subsequently. Arterial hypoxemia (PaO₂: 3.7 kPa [28 mmHg]) and hypocapnia (PaCO₂: 3.1 kPa [23 mmHg]) were confirmed. Oxygen and furosemide were administered. The horse was assisted to standing with a sling. Therapy continued with bilateral intra‐nasal oxygen insufflation. Ancillary medical therapy included flunixin meglumine, penicillin, gentamycin and dimethylsulfoxide. Following 7 hours of treatment the arterial oxygen tensions began to increase towards normal values. Case 2 An 11‐year old, 528 kg Paint horse was anesthetized for surgery of a submandibular mass. The 4‐hour anesthetic period was unremarkable. The OT tube was left in situ for the recovery. During recovery, the horse was slightly agitated and stood after three attempts. Clinical signs consistent with pulmonary edema and arterial hypoxemia (PaO₂: 5 kPa [37.5 mmHg]) subsequently developed following extubation. Respiratory signs resolved with medical therapy, including unilateral nasal oxygen insufflation, furosemide, flunixin meglumine and dimethylsulfoxide. The diagnosis of pulmonary edema in these horses was made by clinical signs and arterial blood‐gas analysis. While pulmonary radiographs were not taken to confirm the diagnosis, the clinical signs following anesthesia support the diagnosis in both cases. The etiology of pulmonary edema was most likely multifactorial.     

Ruminal and plasma concentrations of 3-methylindole associated with tryptophan-induced pulmonary edema and emphysema in cattle.

Five Hereford cows were given an intraruminal dose of L-tryptophan (0.35 g/kg of body weight), and 2 cows were used as controls. Of the 5 treated cows, 3 developed clinical signs of interstitial pul monary edema, and emphysema and severe pulmonary lesions were seen at necropsy after 96 hours. Another cow developed moderate clinical signs and pulmonary lesions, and the remaining cow had few clinical signs and mild pulmonary lesions. The severity of clinical signs in each cow was related to the severity of pulmonary lesions at necropsy. The 3-methylindole (3MI) was present in ruminal fluid and plasma within 6 hours after administration of tryptophan, and the concentrations increased to 3.0 and 9.0 mug/ml within 12 to 24 hours. Severity of pulmonary lesions was related to maximal concentration and duration of 3MI in the plasma. At necropsy, gross lesions were characterized by diffuse, pulmonary edema and interstital emphysema; and the lungs were dark red, firm, and heavier than normal. Predominant microscopic changes included accumulation of proteinaceous residue, hypertrophy and hyperplasia of alveolar lining epithelium, thickening of alveolar septums, and emphysematous thickening of interstitial tissues. These changes were similar to previously reported 3MI-induced pulmonary lesions. The presence of 3MI in ruminal fluid and plasma after administration of tryptophan and the relationship between concentration of 3MI and severity of clinical signs indicate that 3MI is the principal metabolite of ruminal fermentation which leads to the development of acute pulmonary edema and emphysema in cattle given tryptophan.     

Role of catalase in the virulence of Brucella melitensis in pregnant goats

An isogenic katE mutant derived from virulent Brucella melitensis 16M displays hypersensitivity to hydrogen peroxide in disk sensitivity assays but retains the capacity to colonize pregnant goats and induce abortion. These experimental findings indicate that although the sole periplasmic catalase of Brucella melitensis functions as an antioxidant, this enzyme does not play a critical role in virulence in the natural host.