Blood Gas and Hematological Changes in Experimental Peracute Porcine Pleuropneumonia Anthony L. Kiorpes, Peter S. MacWilliams, Daniel I. Schenkman and Lennart R. Bickstr6m



pleuropneumonie porcine suraigue, la defaillance respiratoire progressive The effect of experimental, peracute, L'effet de la pleuropneumonie n'etait pas une caracteristique de la porcine pleuropneumonia on arterial porcine experimentale suraigue a ete maladie et que le niveau des gaz blood gases, acid base status, the etudie chez neuf porcelets en crois- sanguins et lequilibre acido-basique leukogram, and gross and microscopic sance d'un poids moyen de 10,6 ± 2,0 se maintenaient dans les limites lung structure was studied in nine kg. Les gaz sanguins arteriels, lI'equili- physiologiques. Les resultats histopagrowing pigs (mean weight ± SD bre acido-basique, le leucogramme thologiques, hematologiques et physi10.6 ± 2.0 kg). Pigs were inoculated ainsi que les structures macrosco- ologiques semblent pluot converger intranasally with a virulent serotype 5 piques et microscopiques des pou- vers l'hypothese dune ressemblance isolate of Actinobacillus pleuropneu- mons ont ete mesures. Un isolat entre le pleuropneumonie porcine et le moniae, and all showed signs typical of d'A ctinobacillus pleuropneumoniae choc septique. the disease within four hours. Death de serotype 5 a ete inocule intranasaleoccurred in all pigs from 4.5 to 32 hours ment et tous les porcelets ont demonpostinoculation (mean 14 hours). Gross tre les signes typiques de la maladie en INTRODUCTION and microscopic changes were typical moins de quatre heures. Tous les of porcine pleuropneumonia in all pigs. porcelets sont decedes entre 4,5 et 32 Porcine pleuropneumonia is caused Changes in the leukogram included a heures apres linoculation, la duree by infection of susceptible pigs with rapid decline in total white cells, moyenne de survie etant de 14 heures. the gram negative bacterium Actinosegmented neutrophils, lymphocytes, Les changements morphologiques, bacillus pleuropneumoniae, and it is monocytes, and eosinophils. Pigs tant macroscopiques que microsco- becoming an increasingly important maintained alveolar ventilation piques etaient typiques de la pleurop- respiratory disease to the swine throughout the study as arterial CO2 neumonie porcine, et cela chez tous les industry throughout the world (1). tension was unchanged; however, sujets. Les changements du leuco- The disease is most common in young arterial 02 tension and pH decreased gramme comprenaient une diminu- growing pigs and can present as from (mean ± SD) 95.2 ± 5.7 torr and tion rapide du nombre total des peracute, acute, or chronic inflamma7.463 ± 0.018 at baseline to leucocytes dont les neutrophiles tion of the lung, pleura and pericar62.1 ± 12.3 torr and 7.388 ± 0.045, segmentes, les lymphocytes, les mono- dium (2). The pathogenesis is poorly respectively, within 90 minutes prior to cytes et les eosinophiles. La ventilation understood; however, the acute and death. The data showed that in this alveolaire s'est maintenue jusqu'a la peracute forms of the disease resemble model of peracute porcine pleuro- fin, comme en fait foi la tension en septic shock in which endotoxins and pneumonia, progressive ventilatory CO2 arteriel qui est demeuree stable. protein exotoxins may play major failure was not a feature of the disease, Cependant, la tension en 02 arteriel et roles (3-5). If this is true, then peracute and the blood gas values and acid base le pH sanguin ont diminue respective- porcine pleuropneumonia may share status were maintained within physio- ment (moyenne ± ET) de 95,2 ± 5,7 similar characteristics with acute lung logical ranges. The histopathological torr et 7,463 ± 0,018 au debut de injury and septic shock of humans in hematological and physiological find- l'experience a 62,1 ± 12,3 torr et which mortality results from toxemia, ings were consistent with the hypothesis 7,388 ± 0,045 moins de 90 minutes progressive hypoxemia, metabolic that peracute porcine pleuropneumo- avant la mort. Les resultats semblent acidosis, and acute respiratory and nia resembles septic shock. demontrer que dans ce modele de other major organ system failures (6).

Department of Medical Sciences (Kiorpes, Bickstr6m) and Department of Pathobiological Sciences (MacWilliams, Schenkman), School of Veterinary Medicine, University of Wisconsin-Madison, 2015 Linden Drive West, Madison, Wisconsin 53706. Present address of Dr. A.L. Kiorpes: Hazelton Laboratories America, Inc., 3301 Kinsman Boulevard, Madison, Wisconsin 53704. Supported by the School of Veterinary Medicine, Food Animal Research Funds and the Wisconsin Pork Producers, Inc. Submitted March 8, 1989.


Can J Vet Res 1990; 54: 164-169

Alternatively, we wondered if the severe pneumonia with pleural effusions and adhesions that characterize this disease may cause progressive ventilatory failure with associated hypercapnia and respiratory acidosis leading to death. It was previously demonstrated that in acute, nonfatal porcine pleuropneumonia, pigs developed clinical and pathological signs of the disease, became febrile, developed a neutrophilia with a left shift, but maintained normal blood gases (7). In the present report, gas exchange and ventilatory function were again evaluated in pigs using arterial blood gas measurements in experimentally-induced, peracute pleuropneumonia. Physiological measurements were compared with gross and histopathological changes in the lungs and with changes in the leukogram. Specifically, we tested the hypothesis that mortality from peracute pleuropneumonia results from progressive ventilatory failure. MATERIALS AND METHODS

Nine crossbred pigs, mean weight

(± SD) 10.6 ± 2.0 kg, were studied. All were obtained from a specific pathogen free-derived herd that was determined free from Mycoplasma and Actinobacillus pneumonia by slaughter checks and serology. Pigs were transported in a sanitized truck to the laboratory. All were given thorough physical examinations, and a venous blood sample was obtained from the cranial vena cava for serological testing for complement fixing antibodies to A. pleuropneumoniae. All pigs were clinically normal at the time of the study. Pigs were housed individually in 1. 1 m x 2.5 m concrete dog runs. The gate to each run was made of chain link fence. Nose to nose contact was not possible. An 8 cm high raised platform was provided for each pig for sleeping. Room temperature was maintained at a constant 24° C with a 12 h light-dark cycle. Pigs were fed approximately 0.25 kg of an antibiotic-free, 18% protein, complete growing ration twice daily. Each run was fitted with automatic waterers. Care and housing were in accordance with guidelines equivalent to the "Guide to the Care and Use of

Experimental Animals" of the Canadian Council on Animal Care. All pigs were conditioned to the environment for at least four days prior to experimental infection. Two days prior to inoculation, indwelling, arterial polyvinyl catheters [0.11 cm (inner diameter) x 0.16 cm (outer diameter), Bolab, Inc., Lake Havasu City, Arizona] were placed into the left common carotid artery under general anesthesia using a previously described technique (7). Patent catheters were maintained by daily flushing with heparinized saline (2 units/mL) followed by instillation of approximately 0.7 mL undiluted heparin (1000 units/mL), enough to fill the catheter. Arterial samples for blood gases and complete blood counts (CBC) were obtained from resting pigs while they were restrained in a nylon dog sling (Alice King Chatham Medical Arts, Los Angeles, California). Rectal temperature was monitored during all collections using an electronic thermometer (Model 100, VWR Scientific Inc., San Francisco, California). Blood was obtained anaerobically no less than 20 min after placing pigs in the sling. After a volume of approximately 10 mL had been withdrawn through the catheter into a waste syringe, a blood sample for analysis was taken with a 3 mL syringe containing 0.1 mL heparin. The 3 mL syringe was capped and analyzed within 5 min for arterial partial pressure of oxygen and carbon dioxide (PaO2 and PaCO2) and pH (Model ABL-2, Radiometer Copenhagen, The London Co., Cleveland, Ohio). All blood gas values were corrected to each pig's body temperature at the time of sampling (9). The blood gas analyzer was calibrated using an automatic internal calibration program. Prior to analysis, calibrations for blood gases were checked against calculated values based on local barometric pressure and for pH using commercial standards. Blood for CBC was obtained using a separate 3 mL syringe and transferred immediately to a 2 mL tube containing ethylenediaminetetracetic acid (EDTA, Vacutainer, Becton Dickenson, Inc., Rutherford, New Jersey). Tubes were refrigerated at 40 C and

quantitated within 12 h for total white blood cells using an electronic counter (Model S770, Coulter Electronics, Inc., Elk Grove Village, Illinois). A smear was made at the time of blood collection and later was stained with Wright Giemsa. The differential count of white cells was done using standard techniques. Neutrophils were examined microscopically for morphological evidence of toxic change. Each blood film was assigned a score of 0, 1+, 2+, or 3+, depending on the severity of toxic change and the number of neutrophils affected. Duplicate blood gas and CBC samples were taken over two days during the control period and at 4 h intervals following experimental infection. Pigs showing terminal signs of peracute pleuropneumonia (cyanosis, recumbency, open-mouth breathing) were sampled at more frequent intervals, so that all pigs in the study had a "final" CBC and blood gas sample obtained within 1.5 h, and in several cases, within minutes of death. Experimental challenge was by intranasal inoculation of a 6 h A. pleuropneumoniae brain heart infusion broth culture. Each pig was manually restrained in a head up position, and the broth was instilled

during inspiration using compressed oxygen as a propellant at a flow rate of 30 mL/ s (7). The culture was a previously lyophilized, virulent, serotype 5 isolate from a field case of pleuropneumonia that was thawed, grown on chocolate agar for 22 h, then transferred to the broth (7). Plate colony count, as determined by tenfold dilutions, was 3.4 x 109 CFU/ mL, and the culture was administered to seven pigs in 3 mL per nostril aliquots. Two pigs received 9.7 x 1010 CFU/mL in 2.5 mL per nostril doses. All pigs were returned to their own runs immediately after infection and were allowed access to food and water through the remainder of the

experiment. Pigs were observed between sampling periods from the time of inoculation until death. Immediately after death, pigs were removed from their runs, placed into plastic body bags and held in a cooler at 4°C. Postmortem examination was done on all pigs within 8 h of death, and this included assigning a numerical score


to the gross pathological changes, taking sterile samples for isolation of A. pleuropneumoniae from lung tissues, and collecting representative samples of lung from the least affected and most severely affected areas. These latter tissues were fixed in buffered neutral formalin, processed and mounted into paraffin blocks, cut in 5 ,um sections, mounted onto glass slides, and stained with hematoxylin and eosin for subsequent histopathological examination. The scoring system for macroscopic lung lesions has been described previously and is based on a scale of 0 to 15 with 0 being no gross lesions and 15 being most severe (7). For isolation of bacteria, lung tissue was seared, and a flamed loop was inserted through an incision made with sterile scissors. The loop was streaked onto chocolate and blood agar plates (Gibco, Madison, Wisconsin) and incubated for 48 h at 370 C in 5% CO2. Slide tests for urease and indole (Difco, Detroit, Michigan) were done on suspected A. pleuropneumoniae colonies. Positive identification was based on colony morphology, gram stain, and positive urease and negative indole tests. Three typical broth cultures were made following the same protocol as for the inoculum used here. Each of the cultures was divided into two aliquots: one was serially diluted and plated using standard methods for determining colony counts, and the other was centrifuged at 2000 x g for 20 min. The supernatant was removed from the latter, placed in a plastic vial, and stored at -80° C. The Limulus amoebocyte lysate test (E-toxate, Sigma, St. Louis, Missouri) was used to determine endotoxin concentration in the broth with equipment and reagents rendered pyrogen-free. Pyrogen-free water was used as a negative control and Escherichia coli serotype O55:B5 endotoxin (Sigma) was used as the positive control at concentrations of 100 ng, 10 ng, and 100 pg/mL. Concentration of endotoxin in the broth supernatant was estimated to be < 1 ng/ mL based on time to gel formation (10). Data were checked for normal distribution prior to statistical analysis and were expressed as the mean and standard deviation of the mean for all


values. Because of the decrease in numbers of pigs throughout the study due to mortality and the wide range of time to death between pigs, a paired Student's t-test was applied only to the control and final measurements, which included all pigs. Data at other time periods were expressed as a percent of survival time, and there were no less than four pigs at each of these intermediate time points. Comparisons between control or final values and the intermediate points were by two sample t-test. Statistical significance was set at p < 0.05.


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RESULTS All pigs were confirmed negative for complement fixing A. pleuropneumoniae antibodies prior to experimental inoculation. After inoculation, all pigs showed clinical signs of peracute disease within two to four hours, characterized by depression, anorexia, retching with the appearance of white or blood-tinged foam at the mouth, increased respiratory rate, and occasional coughing. Two pigs showed terminal signs by the 4 h sampling period (lateral recumbency, open mouth breathing, marked depression), and these two along with two others were dead by the 8 h sampling. One more pig died just after the 12 h sampling and four remained alive through 24 h. The time to death ranged from 4.5 to 32 h with a mean survival time of 14 h. Two pigs were hypoxemic by 4 h postchallenge (PaO2 = 55.4 and 66.1 torr), and these were among the earliest to succumb. When related to percent survival time, the blood gas data revealed that all pigs maintained baseline arterial PaO2 values through 60% survival time (Fig. 1). By 80% survival time, however, pigs were hypoxemic. The final arterial P02 for all pigs (mean ± SD), obtained from 2 min to 90 min prior to death, was significantly lower than control values (95.2 ± 5.7 vs 62.1 ± 12.3 torr, p < 0.01). Similarly, there was a trend for arterial pH to fall; although, there was wide variability in this measurement between pigs. Compared with the control, the mean (± SD) final pH arterial was reduced (7.463 ± 0.018 vs 7.388 ± 0.045, p = 0.05).

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Fig. 1. Mean (± SD) arterial 02 tension (PaO2), arterial CO2 tension (PaCO2), and arterial pH values for nine pigs under baseline (control) conditions and after experimental induction of peracute porcine pleuropneumonia. Final samples were taken between 2 and 90 min prior to death. Mean PaO2 values were significantly different from control at 80% survival time and final, and mean final pH values were significantly different from control (p < 0.05).

In contrast, there was no significant difference between control and final PaCO2 values. For three pigs, from which samples were obtained within minutes of death, PaCO2 was within the normal range reported by us and others (7,8). The average rectal temperatures at each postinfection time point did not change significantly from baseline values. The mean total white blood cell count decreased from a baseline of 17,900 + 4.6 to 7,500 ± 2.5/IL at 4 h postinoculation and continued to decline until death (Table I). The disappearance of segmented neutrophils accounted for the majority of the

TABLE 1. Control and fmal mean absolute leukocyte counts (X ± SD x 103/,uL) and toxic neutrophil scores for nine pigs with experimentally induced peracute porcine pleuropneumonia

Final Control Cell type 17.9 ± 4.6 5.8 ± 2.7a Total white cells Segmented neutrophils 8.9 ± 4.3 0.3 ± 0.3b 0.2 ± 0.1 1.2 ± 1.2 Immature neutrophils 7.7 ± 2.5 3.5 ± l.5b Lymphocytes 0.7 ± 0.3 0.3 ± 0.3b Monocytes 0.3 ± 0.3 Oc Eosinophils 0 0.1 ±0.1 Basophils 3+ 0 Toxic neutrophilsc aDifferent from control, paired t-test, p < 0.001 bDifferent from control, paired t-test, p < 0.05 cDegree of severity ranges from 0 (normal) to 3+ (most severe)

reduction, but absolute numbers of lymphocytes, monocytes, eosinophils, and basophils also decreased (Table I). The absolute numbers of immature neutrophils increased sixfold from 200 ± 100/,uL at baseline to a final mean value of 1200 ± 1200/,uL; however, this difference was not statistically significant. All pigs developed severe toxic changes in neutrophils between 60 and 100% survival time. These neutrophils were characterized by foamy, basophilic cytoplasm with an occasional Doihle body. Actinobacillus pleuropneumoniae was recovered in pure culture from the lungs of six of nine pigs and in mixed culture with Staphylococcus or Pseudomonas spp. in three of nine. Gross lung lesions were typical of naturally occurring cases of pleuropneumonia (1 1) except for their distribution, which in this study was more cranial than caudal. Overall severity was 10.2 ± 4.1 on a scale of 0 to 15, and the percentage of total lung parenchyma affected in these pigs ranged from 25 to 65. The degree of pleuritis ranged from moderate hemorrhagic pleural effusion to severe fibrinohemorrhagic effusion with massive pleural adhesions. Pericarditis ranged from serous effusion with normal epicardium to marked effusion with fibrin on the pericardial and epicardial surfaces. There was no difference between the right and left lungs and chest walls with regard to extent or distribution of lesions. Microscopic examination of sections from severely affected areas of lung (Fig. 2) contained large irregular areas of coagulative necrosis with hemorrhage and fibrin-filled alveolar spaces

Fig. 2. Experimental porcine pleuropneumonia: severely affected lung, including pleura, interlobular septum and portion of necrotic lobule. Bar = 100 ,um.

and marginating bands of inflamma- bronchi and bronchioles contained tory cells. Many inflammatory cells fibrin, blood, and inflammatory cells, were poorly preserved; nuclei were and there was mild mucosal necrosis. In round or elongated with indistinct most of the sections from macroscopimargins or were pyknotic with eosino- cally normal areas of lung, there was philic and granular cytoplasm. Inter- appreciable inflammation present. In lobar septa and pleura were widened by many of these, there were scattered foci fibrin, edema, hemorrhage, and inflam- of necrotic alveolar parenchyma (Fig. matory cells, and contained numerous 3), some adjacent to bronchi and others bacterial colonies. Lumina of many randomly distributed. Pyknotic nuclei

Fig. 3. Experimental porcine pleuropneumonia: moderately affected lung with foci of exudation and necrosis. Bar = 250 ,um.


maintained the outlines of the necrotic septa. Alveolar spaces in these areas were filled with fibrin and erythrocytes. Fibrin, hemorrhage, and.inflammatory cells were also seen within some airways and along the pleura in some areas. DISCUSSION In the present experimental model of peracute porcine pleuropneumonia, expected clinical signs were observed in all pigs including anorexia, tachypnea, coughing, retching and salivation (2,12). At death, all pigs showed varying degrees of epistaxis. In contrast to what was documented previously in a less severe model of infection (7), pigs in this study did not become febrile. The reasons for this result are unclear. Pigs were the same age and were held under identical environmental conditions as those studied previously. If this disease was caused in part by endotoxemia, then fever would be expected as has been demonstrated (12). Alternatively, if these pigs were in shock, as suggested by the marked depression, lateral recumbency, and cool extremities, then the absence of a rise in rectal temperatures may have reflected decreased splanchnic blood flow (13). Since these pigs were not monitored continuously, a transient fever spike could have been missed. Anal flaccidity or diarrhea was not present. Gross examination of the chest of each pig confirmed pleuritis, pericarditis, and pneumonic lesions typical of porcine pleuropneumonia. In contrast to the usual dorsal caudal distribution, lesions in all pigs were predominantly cranial. Our inoculation technique produced a spray rather than a true aerosol, and it is likely that the major portion of the inoculum was distributed to the more cranial portions of lung. It is unlikely that this difference affected the course of the disease. Histopathological changes were typical of pleuropneumonia, as seen in naturally occurring (2,11) and experimental disease cases (13). Inflammatory cells with elongated nuclei are characteristic of this disease as are vascular changes, parenchymal fibrin accumulation, hemorrhage and necrosis. The coagulative necrosis observed appeared to be primarily associated with capillary damage rather than large 168

vessel thrombosis. This was particularly apparent in the small necrotic foci of the less severely affected tissues. These changes were consistent with those associated with bacterial toxins (1 1). The changes in the leukogram were consistent with acute septic inflammatory disease and endotoxemia, which include a precipitous fall in the number of segmented neutrophils, a degenerative left shift, the appearance of toxic neutrophils, and a reduction in the number of mononuclear cells. A similar differential leukocyte pattern has been reported for pigs infused with endotoxin (12). Recovery of A. pleuropneumoniae from the lungs of all pigs and the observation of large numbers of bacteria in microscopic sections suggested that the pathophysiological events following inoculation resulted from infection; however, the possibility that lesions were caused in part by preformed bacterial toxins in the broth culture cannot be discounted. Fenwick et al (12) and Rosendal et al (15) have reported typical pleuropneumonia lesions following endobronchial instillation of endotoxin at concentrations as low as 0.1 ,ug/mL in 10 mL saline. The concentration of endotoxin in our typical broth cultures was 100 times less than this amount. It is possible that the changes reported here resulted not only from establishment of septic foci with the subsequent production and release of toxins in vivo but also from toxins produced in vitro. Inoculation of pigs with broth only following centrifugation of the bacteria has been done in only two pigs. In one pig, no lesions were observed; in the other, a focal, 1 cm lesion, typical of pleuropneumonia, was seen. The supernatant used in these two pigs was not filtered, and bacteria may still have been present. In the present model of peracute pleuropneumonia, pigs did not develop arterial hypoxemia secondary to hypoventilation. Indeed, all pigs maintained arterial PCO2. There was no evidence of acute hypoxemia secondary to the administration of the inoculum as has been shown in calves (16). Hypoxemia developed progressively and independently of PaCO2 values and was similar in that respect to acute lung injury and septic shock in human beings (6,17).

The possible mechanisms for the observed hypoxemia were not investigated here, but include diffusion impairment, right to left shunts, and ventilation-perfusion inequality (18). Diffusion impairment appears possible in those lung lobes most affected by diffuse, severe alveolar hemorrhage, inflammation, and edema. Intrapulmonary shunting and ventilationperfusion mismatch have been demonstrated in human patients with acute respiratory distress syndrome (19) and are suggested to occur in endotoxemic pigs based on increased arterialalveolar 02 gradients (5). Metabolic acidosis occurs frequently in septic shock, and in human patients, it may signal an increased risk of death (13). In the present study, there was a trend toward metabolic acidosis, but in only one pig was pH abnormally low at the final sample (7.137, base excess -13 mEq/ L). This sample, taken during the last two minutes of life, was most likely indicative of peripheral anoxia. All other pigs had normal pH and base excess values at the final sample. One possible explanation for mild acidosis in pigs showing clinical signs of shock is the presence of a confounding mixed metabolic alkalosis. Almost all pigs in this study retched throughout the study, and in prior studies with less severely affected pigs, some were noted to develop mild base excesses of 5 to 7 mEq/ L. This would have tended to blunt any decline in pH secondary to shock until later in the disease. Future studies should include measurement of serum lactate, which might reveal a more severe acidosis than suggested by this data. Death of pigs in this study was not caused by progressive ventilatory failure characterized by increasing PaCO2, decreasing PaO2, and respiratory acidosis. Hypoxemia developed by other mechanisms while alveolar ventilation was maintained. It should be noted that at no time was the arterial hypoxemia severe enough to be lifethreatening, and PaCO2 was maintained within or slightly below the normal range (7). Death resulting from ventilatory fatigue and failure has been demonstrated in an endotoxin dog model by Hussain et al (19). Such ventilatory failure should have resulted in increased PaCO2 values by 80% survival time. A rising PaCO2 could

have been missed in some of the pigs in this study; however, in three pigs, the blood gases of which were measured within minutes of death, no increase in PaCO2 was seen. Our findings suggest that despite the presence of severe pneumonia and pleural effusion, mortality in pigs resulted from causes other than progressive ventilatory failure following experimental infection with A. pleuropneumoniae. The possibility of acute respiratory muscle failure can not be discounted, and the work of breathing necessary to maintain ventilation in this disease needs to be critically assessed. The effect of this disease on the function of other organ systems was not investigated in this study and may be important in its pathogenesis. If porcine pleuropneumonia shares common mechanisms with septic shock, then current therapies, now limited mostly to antibiotics, may need revision. New approaches might consider blocking the biological effects of bacterial and host cell toxins (5,21).

ACKNOWLEDGMENTS The authors acknowledge the assistance of Drs. Meg Warner, Kerry Foreman and Leighann Daristotle, technician Teresa Conrad, and veterinary students Jeff Marvig, Peter Ammon, Maura Mansfield, Jean Giles, Mike Boselevac, Paul Polzin and Ellen Ertel.

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12. FENWICK BW, OSBURN BI, OLANDER HJ. Isolation and biological characterization of two lipopolysaccharides and a capsularenriched polysaccharide preparation from Haemophilus pleuropneumoniae. Am J Vet Res 1986; 47: 1433-1441. 13. PETERSDORF RG. Septic shock. In: Wintrobe MM, Thorn GW, Adams RD, Bennet IL, Braunwald E, Isselbacher KJ, Petersdorf RG, eds. Harrison's Principles of Internal Medicine. 6th ed. New York: McGraw-Hill Book Company, 1970: 736740. 14. BERTRAM TA. Quantitative morphology of peracute pulmonary lesions in swine induced by Haemophilus pleuropneumoniae. Vet Pathol 1985; 22: 598-609. 15. ROSENDAL S, MITCHELL WR, WEBER M. Haemophilus pleuropneumoniae: lung lesions induced by sonicated bacteria and sterile culture supernatant. (Abst), Copenhagen: Proc Int Pig Vet Soc Congr 1980; 5: 221. 16. KILLINGSWORTH CR, SLOCOMB RF, ALNORR SA, ROBINSON NE, DERKSEN FJ. Pulmonary dysfunction in neonatal calves after intratracheal inoculation of small volumes of fluid. Am J Vet Res 1987; 48: 1589-1593. 17. RASHKIN MC, BOSKEN C, BAUGHMAN RP. Oxygen delivery in critically ill patients relationship to blood lactate and survival. Chest 1985; 87: 580-584. 18. WEST JB. Pulmonary Pathophysiology. 2nd ed. Baltimore: Williams and Wilkins Co., 1982: 171-177. 19. DANTZKER DR, BROOK CJ, DEMART P. Ventilation-perfusion distributions in the adults respiratory distress syndrome. Am Rev Resp Dis 1979; 120: 1039-1052. 20. HUSSAIN SNA, SIMKUS G, ROUSSOS C. Respiratory muscle fatigue: a cause of ventilatory failure in septic shock. J Appl Physiol 1985; 58: 2033-2040. 21. OLSON NC, BROWN TT Jr, ANDERSON DL. Dexamethasone and indomethacin modify endotoxin-induced respiratory failure in pigs. J Appl Physiol 1985; 58: 274-284.


Blood gas and hematological changes in experimental peracute porcine pleuropneumonia.

The effect of experimental, peracute, porcine pleuropneumonia on arterial blood gases, acid base status, the leukogram, and gross and microscopic lung...
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