Mortality,hematology, and histopathology of common snook Centropomus undecimalis (Perciformes: Centropomidae) exposed to acute toxicity of ammonia

This study aimed to evaluate the tolerance of common snook Centropomus undecimalis larvae and juveniles exposed to acute concentrations of un-ionized ammonia for 96 h at 35g L^?1 salinity, after 24 h starvation. For that, 10 larvae (20.85 ± 1.46 mm) of 47 days post hatch (DPH) per experimental unit (1.5 L) were exposed to 0.00 ± 0.00, 0.65 ± 0.04, 1.29 ± 0.09, 2.59 ± 0.18, 3.88 ± 0.27, 5.17 ± 0.34, and 6.47 ± 0.43 mg L^?1 NH₃, in triplicates, at 26.72 ± 0.08°C, dissolved oxygen at 5.72 ± 0.10 mg L^?1 and pH 8.45 ± 0.06. During this period, no mortalities were observed. Another trial was performed with five juveniles (20.35 ± 6.10 g, 13.90 ± 1.75 cm) per experimental unit (60 L) exposed to 0.00 ± 0.00, 2.26 ± 0.07, 2.68 ± 0.11, 3.20 ± 0.13, 3.68 ± 0.17, and 4.27 ± 0.16 mg L^?1 NH₃, in triplicates, at 21.90 ± 0.76°C, dissolved oxygen at 6.27 ± 0.21 mg L^?1 and pH at 8.38 ± 0.04. Fish mortality increased as ammonia concentrations increased at each day, and LC₅₀ 96 h was 3.52 mg L^?1 NH₃. Larvae were less sensitive than juveniles, demonstrating that the environmental toxicity of ammonia to common snook is influenced by age. Sublethal exposition to ammonia caused histological damages in gills of common snook juveniles and variation on glucose levels, hematocrit, and red blood cells number, showing negative effects on fish homeostasis. Moreover, compared to other species, the common snook has great resistance to ammonia.     

Cyclic hematopoiesis in a mixed-breed dog: case report and brief review

An 8-wk-old, male, mixed-breed puppy was adopted from a rescue organization. From the time of adoption, the puppy suffered episodes of illness affecting various organ systems, which resolved with supportive therapy but relapsed once medical therapy was discontinued. Review of the hematologic data revealed cyclic fluctuations in circulating blood cells. Cyclicity was most prominent in neutrophils, with recurrent severe neutropenia. Neutropenic episodes lasted 5–6 d, with regular cycles of 11–14 d between nadir neutrophil counts. Genetic testing determined that the patient was homozygous mutant for the frameshift mutation in the adaptor protein complex 3 β-subunit (AP3B1) gene, originally identified in gray collies with cyclic hematopoiesis (CH). Pedigree information was not available, but the patient’s features were phenotypically distinct from those of collies. We describe here a case of the AP3B1 mutation in a mixed-breed dog that did not resemble a collie, undescribed previously, to our knowledge. Our findings indicate that the AP3B1 mutation and CH are present within the general canine population and are not restricted to collies.