Summary Differentiation between infectious and noninfectious disease and rapid initiation of accurate treatment are essential in managing diseases in the neonatal and young foal. Identification of useful inflammatory markers for these purposes is, therefore, of great importance. The aim of this study was to compare the responses of the acute phase protein serum amyloid A (SAA) with the responses of fibrinogen and total leucocyte and neutrophil counts in infectious diseases encountered in the young foal, and to assess whether SAA measurements give additional information useful in the management of these diseases. In a prospective study, foals (n = 25) showing clinical signs indicative of infectious disease were blood sampled on admission and then daily or every second day during hospitalisation. The main presenting signs were neonatal weakness (n = 9), pneumonia (n = 6) and diarrhoea (n = 10). SAA and fibrinogen concentrations on admission were higher in foals with bacterial infections (n = 8) than in foals with nonbacterial or uncertain diagnoses (n = 17). On admission, weak foals with negative blood cultures (n = 3) had normal SAA and fibrinogen concentrations and varying total leucocyte and neutrophil counts. Foals with positive blood cultures (n = 2) had markedly increased SAA, decreased or increased fibrinogen concentration and leuco‐ and neutropenia. Those with ambiguous blood cultures (n = 3) had moderate to markedly increased SAA concentrations and normal fibrinogen concentration, leucocyte and neutrophil counts on admission. All foals with negative or ambiguous blood cultures recovered and had normal or decreasing SAA concentration on discharge. Both foals with a positive blood culture were subjected to euthanasia. One foal born with equine herpesvirus‐1 infection had moderately increased SAA and normal fibrinogen concentration and leuco‐ and neutropenia. Foals with Rhodococcus equi pneumonia had increased concentrations of all parameters on admission. On discharge, recovered foals had normal SAA concentrations, whereas fibrinogen and total white blood cell count and neutrophil counts were still increased. There were no consistent inflammatory changes in the parameters measured in diarrhoeic foals and there was no statistical difference between rotavirus‐positive (n = 4) and ‐negative (n = 6) foals in this respect. The results of this investigation suggest that SAA might be an aid in the differential diagnostic procedure of neonatally weak foals and in foals with diarrhoea as the main presenting clinical sign and that SAA measurements could add information in the monitoring of treatment in Rhodococcus equi pneumonia by responding more rapidly than the markers used to date.
Summary The aim of this study was to investigate the phagocytic and killing capacities as well as expression of CD18 of neutrophils obtained from healthy foals from birth to age 8 months. Blood was taken from 6 Standardbred foals at 7 time‐points between ages 2–56 days and thereafter once a month. For comparison, cells from 16 mature horses were evaluated. Neutrophil phagocytosis of yeast cells was assessed by flow cytometry after opsonisation with mature pooled serum, autologous serum or anti‐yeast IgG. The killing capacity of the neutrophils, as indicated by the oxidative burst, was monitored by chemiluminescence. Serum IgG concentration was measured by radial immunodiffusion. In addition to clinical examination, the amount of serum amyloid A and the total leucocyte count were used as markers for infection. The phagocytic ability was impaired until age 3 weeks, when autologous serum was used as opsonin. Killing capacity was also low initially but, from 3 months onwards, chemiluminescence values were equal to or higher than in mature horses. Serum IgG decreased from 10 g/l at 2 days to 5 g/l at 2 months and then increased gradually to 10 g/l at the end of the study. These findings may in part explain the increased susceptibility to bacterial infections in young horses.
It is not known if pulmonary function and gas exchange during exercise are altered after pyogranulomatous pneumonia caused by Rhodococcus equi infection in the foal. The aim was to evaluate whether pulmonary gas exchange during high intensity exercise was altered in mature Standardbreds with a history of R. equi pneumonia as foals. In 7 foals, R. equi pneumonia was confirmed and treated. At age 3 years, when these horses were subjected to professional training, an inclined treadmill exercise test including 4 speeds was performed. Samples were collected when a steady state in VO2 was obtained. Red cell volume, heart rate, respiratory rate, and systemic and pulmonary mean arterial pressures were measured and cardiac output calculated. Oxygen and carbon dioxide tensions in arterial and mixed venous blood were analysed. The alveolar ventilation and the alveolar-arterial oxygen tension difference were determined. Pulmonary gas exchange was assessed and the ventilation-perfusion distribution, VA/Q, was estimated by the multiple inert gas elimination technique. Ventilation-perfusion mismatch and shunt were determined and diffusion limitation calculated. The gas exchange in Standardbred trotters previously infected with R. equi and successfully treated was not compromised during intense treadmill exercise compared with reference values for healthy, fit Standardbreds. We conclude that adult Standardbreds trotters with diagnosed R. equi pneumonia as foals, can achieve an adequate gas exchange at a workload close to VO2peak.
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