Primary amebic meningoencephalomyelitis caused by Naegleria fowleri in a south-central black rhinoceros (Diceros bicornis minor).

CASE DESCRIPTION A 20-year-old female south-central black rhinoceros (Diceros bicornis minor) was evaluated because of an acute onset of CNS deficits. CLINICAL FINDINGS The rhinoceros had no history of illness. Clinical signs included acute lethargy, ataxia, and decreased appetite. Hematologic abnormalities included leukocytosis with neutrophilia and a profound left shift. Results of serum biochemical analysis revealed hypophosphatemia but no other abnormalities. Results of a quantitative PCR assay for West Nile virus and an assay for anti-Neosporum caninum antibodies in serum were negative; the patient was seropositive for multiple Leptospira serovars. TREATMENT AND OUTCOME Antimicrobials and anti-inflammatory agents were administered, but the condition of the rhinoceros worsened overnight; despite treatment with additional anti-inflammatory and antimicrobial agents, IV fluids, and thiamine, it became obtunded and died of respiratory arrest ≤ 24 hours later. Necropsy revealed severe, diffuse, suppurative, and histiocytic meningo-encephalomyelitis involving the cerebrum, cerebellum, and spinal cord. Amebic trophozoites were observed on histologic examination of affected tissue. Infection with Naegleria fowleri was confirmed by results of immuno-histochemical analysis and a multiplex real-time PCR assay. CLINICAL RELEVANCE Findings suggested that south-central black rhinoceros are susceptible to the free-living ameba N fowleri. Ameba-induced meningoencephalomyelitis should be considered as a differential diagnosis for rhinoceros that have an acute onset of neurologic signs. Diagnosis of N fowleri infection in an animal has a profound public health impact because of potential human exposure from the environment and the high fatality rate in people with N fowleri infection.

Predicting irreparable renal ischemic injury using a real-time marker in the porcine model.

PURPOSE: We determined the maximal renal tolerance of warm ischemia using renal cortical interstitial metabolic changes to identify a potential real-time marker of irreparable renal function. MATERIALS AND METHODS: Using a single kidney model 3 groups of 5 pigs each underwent 120, 150 and 180 minutes of warm ischemia, respectively. Microdialysis samples were collected before, during and after ischemia. Renal function assessments consisting of serum creatinine and GFR measurements were performed before ischemia and on post-ischemia days 1, 5, 9, 14 and 28. Kidneys exposed and not exposed to ischemia were collected for histological study. RESULTS: Interstitial glucose and pyruvate concentrations decreased, while lactate concentrations increased to stable levels during ischemia. Glutamate spiked at 30 minutes of ischemia and subsequently tapered, while glycerol increased throughout warm ischemia time. At post-ischemia day 28 renal function returned to pre-ischemia baseline levels in the group with 120 minutes of ischemia but did not recover to baseline in the 150 and 180-minute ischemic groups. Functional data correlated with histological findings. The 120-minute maximal renal tolerance of warm ischemia correlated with a mean +/- SD glycerol concentration of 167 +/- 24 micromol/l. CONCLUSIONS: Interstitial glycerol is a real-time, renal unit specific, minimally invasive marker of renal function deterioration. Exposure of porcine kidneys to ischemic insults resulting in renal cortical interstitial glycerol concentrations higher than 167 micromol/l is associated with irreparable functional damage in this model.

The effect of alendronate sodium on spinal fusion: a rabbit model.

BACKGROUND CONTEXT: Bisphosphonates affect bone remodeling and increase bone mass through the inhibition of osteoclasts. Their effect on osteoblasts, and the balance between osteoblastic and osteoclastic activity on bone turnover and healing, is not completely understood. Specifically, the effect of bisphosphonates on spinal fusion has yet to be determined. With the increasing use of bisphosphonates in the elderly population, this effect needs to be delineated. PURPOSE: To evaluate the effect of alendronate sodium after an intertransverse process spinal fusion in a rabbit model. STUDY DESIGN/SETTING: Randomized double-blinded in vivo study of the effect of alendronate sodium in a spinal fusion model. METHODS: Fifty New Zealand white rabbits underwent a posterolateral L5-L6 intertransverse process arthrodesis with autogenous iliac crest bone graft. The rabbits were then randomly divided into two groups. Group I received 3 cc of saline placebo per oral gavage, and Group II received 200 micrograms (approximately 0.05 mg/kg/day) of alendronate sodium dissolved in 3 cc of saline per day for 8 weeks. Upon completion, the rabbits were sacrificed and the lumbar spines harvested, radiographed and graded for motion across the fusion site with manual palpation. Two independent pathologists then prepared and sectioned each left and right fusion mass. Three random x10 fields were examined and graded for both the cephalad and caudad ends of each section (516 fields). Fusion quality was graded using an established histological scoring scale (score 0 to 7 based on fibrous and bone content of the fusion mass). RESULTS: Two rabbits died on the day of operation, and 48 rabbits survived the operation. Five additional rabbits died within the first 2 postoperative weeks. Thus, 43 rabbits (21 in Group I, 22 in Group II) completed the 8-week course of treatment. Grading each side separately, 26 of 42 fusion masses (62%) in Group I and 24 of 44 fusion masses (55%) in Group II had radiographic evidence of fusion (p=.76). With gross palpation, 11 of 21 motion segments (52%) in Group I versus 13 of 22 motion segments (59%) in Group II were determined to have a solid fusion (p=.76). Histologically, Group I had a higher median score (6.0; range, 0 to 7 vs. 1.0; range, 0 to 7; p<.0001) and a higher fusion rate (76% vs. 45%; p=.004) than Group II. CONCLUSIONS: Alendronate sodium appears to inhibit or delay bone fusion in a rabbit model. Presumably, this occurs as a result of uncoupling the balanced osteoclastic and osteoblastic activity inherent to bone healing. These findings suggest that a discontinuance of alendronate sodium postoperatively during the acute fusion period may be warranted.