Over the past 2 months there has been an unusual spike in cases presenting in the field with high fevers (T 104-105) and general malaise. These cases have been sporadic, isolated episodes under a variety of farm managements. To date we have not documented any incidents where other horses on the same premises have subsequently also developed fevers. Horses that have had blood work run early on have been leukopenic with several having total WBC's under 4000. Other clinical signs have been variable. Some horses have been mildly colicky; others have been minimally affected when fevers were controlled. To date 6 of these cases have been admitted to isolation and treated at BREC. Three cases were initially diagnosed on admission as colitis: WBC's were under 3000 and ultrasound detected fluid contents in the large intestine. Only one horse actually broke with watery diarrhea. This horse received IV fluids, Biosponge and flunixin for fevers. The horse was never toxic, never stopped eating and was clinically normal after 3 days of treatment. A PCR panel on feces was negative for Salmonella, Clostridium, Lawsonia and PHF. An additional 3 horses were all negative for the same battery of tests; 2 horses were also negative for tick-borne disease. Several of the horses were hemoconcentrated on admission and received initial IV fluids; otherwise treatment consisted solely of NSAIDs as needed to control fevers (and Gastrogard). One horse received standard doses of flunixin and oxytetracycline for 3 days prior to admission and sustained renal failure. This horse had additional testing for Lepto which was negative. Our ambulatory service has treated at least another 6 cases in the field and Dr. Sage has fielded a number of calls of similar cases treated by other practices. WBC's when available were low or low normal. Two were tested for anaplasmosis and were negative. Several of these horses were treated with oxytetracycline without apparent response.
Certainly it is unlikely that all of these horses had the same disease. The cases have been widely scattered and did not appear to be contagious. Most did not have exposure factors such as recent attendance at horse gatherings or new horses on the premises. All horses to date (except for the renal failure case) treated at BREC or by BREC ambulatory doctors responded without antibiotics and made a full recovery. We would be very interested in hearing if anyone had similar cases and any positive diagnostic tests.
Complex suspensory disease
At the recent ACVS symposium, Dr. Ross (UPenn) presented a nice summary of suspensory disease with involvement of adjacent bone. I'll focus just on the proximal and mid-metatarsus, but most of the entities discussed could also occur in front. This was a "clinical" talk, i.e. no statistics, but served as an excellent reminder that many horses that block to the proximal metatarsus may have something other than desmitis. A quick word about blocking: there are 2 papers out confirming that placement 1'' deep, axial to MT4, 15mm distal to the TMT joint aiming proximally, consistently blocks the lateral plantar nerve and its deep branch that becomes the plantar metacarpal nerves. This block must be preceded by a low plantar block in order to confirm a diagnosis of proximal metatarsal disease. The cases he reviewed had radiographs and ultrasound plus scintigraphy or MRI. "Complex" suspensory disease was characterized by bone disease with or without suspensory lesions or suspensory desmitis that had additional soft tissue lesions (adhesions). Proximally the bone lesions were comprised of plantar cortex avulsion or incomplete longitudinal fractures and osteitis (remodeling associated with the origin of the suspensory). Additionally there are several papers in the literature describing proximal plantar exostoses that are usually located near the junction of MT2-3 or MT3-4 (diagnosed with CT or MR). Suffice to say that all of these conditions are often not detected on good quality radiographs or ultrasound evaluations. This is consistent with the paper from NCSU comparing radiographs, ultrasound and MR in 25 cases of lameness blocked to the proximal metatarsus. Six of 25 cases had desmitis only, 7/25 had a combination of desmitis and boney lesions, 8 had bone lesions only (4 of which were in the tarsus) and in 4 no lesion could be identified on MR. Additionally while ultrasound identified most of the desmitis that was confirmed by MR, there were a large number of false positives, i.e. lesions "seen" that were not present on MR. The complicating soft tissue lesions that Ross discussed were primarily adhesions of a splint exostosis to the adjacent suspensory and, again, these were often quite subtle and could affect origin or mid-body.
The relevance of Ross's talk was highlighted last month in a case at BREC. The horse blocked to proximal metatarsus, US showed some enlargement on cross-section and radiographs revealed some subtle remodeling of MT3 (sclerosis and lysis). The MR lesion was confined entirely to the bone-ligament interface. This information was critical in sorting through the treatment options and we suggest that many horses blocking to the proximal MT would benefit from MR evaluation whenever it is financially feasible (and certainly when insured).
