Species dependent gentamicin pharmacokinetics and nephrotoxicity in the young horse.

Gentamicin pharmacokinetics and nephrotoxic potential were evaluated in twelve 2 to 3 month-old horses. Whereas recent evidence in our clinic indicated that young horses may be especially susceptible to gentamicin nephrotoxicity, young rabbits and rats are usually resistant. Gentamicin (4.5 mg/kg) was given by rapid intravenous injection. Serum gentamicin concentrations over a 13-hour period were fitted to an open, two-compartment, pharmacokinetic model. Subsequently, the same horses were divided into groups of 3 horses each. Each group received 0, 2.2, 4.4 or 8.8 mg gentamicin/kg, intramuscularly, every 12 hours for 15 days. Renal function was monitored. Peak and trough gentamicin concentrations were monitored daily. Renal sections were collected for histopathologic and electron microscopic examination. The (mean +/- SD) serum halflife was 194 +/- 37 minutes, total body clearance (ClB) was 1.65 +/- 0.79 mL/min/kg and volume of distribution at steady state (Vd(ss)) was 30.6 +/- 9.4 L/100 kg. Decreased renal function, as detected by elevated serum urea nitrogen or creatinine concentrations, was detected only in the two youngest foals (including animals in both the 4.4 and 8.8 mg/kg dose groups). The trough serum gentamicin concentrations of these 2 horses increased over time. These horses had the lowest ClB and Vd(ss) in the intravenous study. Morphologic changes were seen in kidneys of all treated horses and were similar to those occurring with gentamicin toxicity in other species. Our results support the clinical impression that very young horses may be more susceptible than adult horses, and adults of other species, to gentamicin nephrotoxicity.

Gentamicin toxic nephropathy in horses with disseminated bacterial infection.

Three clinical cases of toxic nephropathy in young horses were ascribed to gentamicin toxicity. Criteria for defining gentamicin-induced nephrotoxicosis were a serum urea nitrogen value greater than the pretreatment value or cylindruria, hematuria, and proteinuria in the absence of pyuria and bacteriuria. Recommended doses of gentamicin had been given in all cases. The nephropathy was reversible in 1 case in which the toxicosis was detected early and was treated by volume diuresis and drug withdrawal.

Agammaglobulinemia in a horse.

Immunologic deficiency was suspected in an 18-month-old Standardbred horse with persistent fever, multifocal bacterial infection, and neutropenia with a large number of immature neutrophils. Serum protein electrophoresis revealed marked depression of the gamma-globulin fraction (0.2 g/100 ml). Immunologic testing and histologic examination of lymphoid tissues identified the immune deficit as agammaglobulinemia. Serum concentrations of immunoglobulin (Ig)G and IgG(T) were initially low and declined with time; IgM and IgA were not detectable. The horse failed to produce antibodies when inoculated with foreign antigens but had a positive cell-mediated skin reaction to intradermal phytolectin injection, and lymphocytes responded normally to in vitro stimulation by mitogens. Histologic examination of lymphoid tissues revealed absence of germinal centers and plasma cells.

Lactic acid concentration in peritoneal fluid of normal and diseased horses.

Peritoneal fluid from each of 15 clinically healthy horses and five horses with acute abdominal disease was evaluated for lactic acid concentration. The normal range was 2-7--13-4 mg/dl. Simultaneous blood and peritoneal fluid samples from healthy horses revealed consistently lower lactic acid concentrations in the peritoneal fluid than in the blood, whereas peritoneal fluid lactic acid levels were consistently greater than blood levels in the diseased horses. The diseased horses had highly significant (P less than 0-005) increases in both blood and peritoneal fluid lactic acid concentrations compared with those in healthy horses.

Epidural melanoma causing posterior paresis in a horse.

An aged gray stallion was examined because of fullminating posterior paresis, bladder paralysis, and perineal anesthesia. Lower motor neuron dysfunction was detected at the lumbosacral level of the spinal cord, and cerebrospinal fluid was yellow. After brief supportive treatment, the horse died. Necropsy revealed a single epidural melanoma at L5-6. The absence of cutaneous melanotic growth, absence of organ involvement, and extensive vertebral remodeling indicated the neoplasm to have been primary and to have been present for an extended period. Neurologic dysfunction was acute and progressive, as a result of spinal cord compression by the neoplasm.