HOW-TO SESSION: CLINICAL PATHOLOGY


nia in horses, increases SAA anywhere from 30 to 500 g/mL for 24 to 48 hours after shipping healthy Thoroughbreds 1200 km by road over 26 hours. This increase was abrogated by administration of antimicrobials,24 and shorter-distance shipping (4 h) did not have an effect on SAA concentrations.25 In equine influenza, serum SAA increases during the first 48 h of clinical signs and returns to baseline values in 11 to 22 days barring secondary infections, with maximum values of 450 mg/L during the acute phase.26 In ponies experimentally infected with EHV-1, serum levels peaked at 100 to almost 1000 mg/L in the week after inoculation.5 Various methods have been evaluated to screen


foals for sub-clinical Rhodococcus equi pneumonia including sonographic examination, hematology, and physical examination, but each have been found to be imperfect with regard to either diagnostic ac- curacy or cost effectiveness. Acute phase proteins, especially fibrinogen, have been used as moderately effective screening tools for foals on endemic farms. It would seem that with its greater sensitivity and more labile kinetics, SAA would be a better bio- marker for this disease that often exhibits an ex- tended preclinical latency where detection is often difficult. Two recent studies have investigated SAA as a possible predictor of R. equi pneumonia in at-risk populations. The first of these studies used a large, well-selected population of affected foals and age-matched controls from endemic farms. No pre- dictive value was found in SAA levels in 212 foals 7 to 14 days and 196 foals 21 to 28 days of age, nor at the onset of clinical signs of pneumonia.27 The au- thors conclude that “monitoring concentration of SAA is not useful as a screening test for early detec- tion of R. equi.”27 A subsequent smaller study also assessing weekly screening with SAA to identify pre-clinical R. equi infections found similar results. SAA concentrations did not show an association with the development of sonographic evidence of lung abscessation, and of six foals on an endemic farm diagnosed with R. equi pneumonia, only two demonstrated elevated SAA concentrations and this was around the time that the disease became clini- cally evident.28 These results are surprising given that R. equi generally results in a robust increase in fibrinogen and leukocyte count, which for other in- flammatory diseases tend to be less sensitive than SAA. In conclusion, one must wonder why SAA is not a better aid in early identification of R. equi pneumonia; no completely satisfactory explanation is apparent for these results. Recurrent airways obstruction (“heaves”) is a disease of the small airways characterized by neu- trophilic exudate within the alveoli and bronchi. Although it is not associated with explicit signs of inflammation such as fever or peripheral neutrophilia, SAA has the potential to be more sensitive for subtle alterations. A prospective, observational study used six healthy and six heaves-affected horses challenged with hay and straw to examine a variety of acute-


phase proteins.29 Although haptoglobin concentra- tions were higher in the heaves horses both before and during an exacerbation, the SAA did not reliably in- crease, although there was a small but significant dif- ference between heaves-affected horses and controls on day 7 of exacerbation (15.75 vs 3.22g/mL, respec- tively).29 Nonetheless, probably the main use of SAA in horses with recurrent airways obstruction is distin- guishing them from pneumonia cases, in which the SAA is likely to be much higher.


SAA and Surgery


However much attention is paid to careful tissue handling and correct technique, surgery is an in- flammatory stimulus and this fact is revealed by elevations in SAA after even minor, uncomplicated procedures.4,5,30,31 Therefore, its more useful ap- plication is probably identifying postoperative infec- tions both earlier and with more accuracy than other methods. A study looking at standing castrations, for example, found that all horses had elevations of SAA to the 400–600-mg/L ranges at day 3 postop- eratively, but those that went on to develop infections (as evidenced by fever, swelling, serohem- orrhagic or purulent discharge) still had SAA values in this range at the eighth day whereas horses re- covering without complication were in the 200- mg/L range by this point. The increased SAA values associated with infection were not reliably reflected by increases in rectal temperature, leuko- cyte count, or fibrinogen, suggesting that SAA was a superior marker for infection.31A subsequent study found that perioperative treatment with penicillin reduced the SAA in horses undergoing castration from a mean of 708 to 543 mg/L at day 3 postcastra- tion, and from 515 to 125 mg/L on day 8,32 support- ing the idea that even mild infections result in appreciable differences in SAA concentration. Looking beyond orchidectomy, the effect of minor surgical procedures on SAA shows that levels of 100 to 400 mg/L that peak at approximately day 3 after surgery can be expected in cases uncomplicated by infection. These include tibiotarsal arthroscopy and osteochodrosis fragment removal, laryngo- plasty, and ventriculectomy (peaked at 50–150 mg/L at d 2; normal by d 7)30 carotid exteriorization and flexor tendon division (peaked at 100–400 mg/L at d 2; normal by 7–14 d)5 and a variety of elective pro- cedures including minor airway and orthopedic sur- geries (peaked at 16.4 g/mL at 24 h, 15.5 on d 2).16 SAAwas also significantly lower in elective (defined as noninflamed) vs nonelective (pre-existing inflamma- tory foci) cases16 as well as being able to delineate differing levels of surgical trauma based on the inva- siveness of the procedure.30 In several of these stud- ies16,30 SAA response was found to be a more sensitive indicator of inflammation than a variety of other acute-phase protein or leukocyte responses, and de- creased more quickly in response to resolution than fibrinogen (Fig. 3). This is particularly useful to the practitioner who must decide whether hematologic ev-


AAEP PROCEEDINGS  Vol. 61  2015 133


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