First, we have a paper on the effects of a single opioid (morphine, butorphanol, or tramadol) dose on GI motility in rabbits. Forty-four rabbits were used in the experiment, and were submitted to radiographic barium follow through and abdominal ultrasound exams before and after the opioids’ IM administration. A nasogastric tube was placed on all rabbits for administration of barium. 

The dosages for each group were of: butorphanol 5 mg/kg, morphine 10 mg/kg, and tramadol 10 mg/kg. The results showed that a single dose of morphine and butorphanol can temporarily affect GI transit in healthy rabbits. No signs of altered GI motility were observed after tramadol administration, and normal cecotroph production cycle was preserved in this treatment group.

It is good to note that these single injections of morphine and butorphanol did not induce ileus (GI stasis).

The take home message is: a single butorphanol or morphine injection can reduce GI motility, but a single dose of tramadol seems to not be able to induce such an efect.

Second, we have a pilot study on the topical administration of phenylephrine and rocuronium in bearded dragons (Pogona vitticeps). Birds and reptiles, unlike mammals, have skeletal muscle in their irises, which allows for voluntary pupil dilation/constriction, and makes traditional mydriatic agents (e.g., atropine, tropicamide) ineffective. There have been reports on the use of rocuronium and phenylephrine, alone or in combo, for inducing mydriasis in various birds and reptiles species.

Eight bearded dragons were divided in four groups: rocuronium (20 μl), phenylephrine (20 μl), rocuronium + phenylephrine (10 μl each), or saline control. On the treatment group, each animal received the drug only in one eye, so the other eye served as a control.

Videos were taken of the treated eyes, and examined by a blinded investigator. Constricting ability was detected in both treated and untreated eyes at all timepoints for all eyes, and the maximum pupillary diameter was not found to be significantly different at any time point from baseline for any treatment.

It is important to note that mild to moderate blepharospasm was noted in eyes treated with rocuronium or rocuronium plus phenylephrine, for up to 2 minutes.
The take home messag4e is: topical application of phenylephrine and rocuronium, alone or in combo, is ineffective at producing mydriasis or impairing constricting ability in bearded dragons at doses used here.

Lastly, we have a case report on cerebellar hypoplasia in juvenile African grey parrots (Psittacus erithacus). Two sibling 12-week-old female African grey parrots were presented for progressive whole-body tremors, proprioceptive deficits, and an inability to stand unassisted. A third bird in the clutch (male) exhibited no clinical signs. Their owner had supplemented calcium and hobbled their legs as they thought it was splay leg, with no response to treatment.

Hematologic and biochemical analyses were normal, as were radiographic images of both birds. The owner declined to move forward with a CT, and elected euthanasia. The necropsy showed marked reduction in cerebellar size and poor folia formation. Microscopic review of the cerebellums demonstrated decreased density of the granular layer and thinning of the molecular layer with poorly organized and differentiated Purkinje fibers, consistent with a diagnosis of cerebellar hypoplasia. These findings characterized a cerebellar hypoplasia.

Differentials would include congenital/developmental abnormalities (e.g., familial cerebellar degeneration, cerebellar hypoplasia, hydrocephalus), infectious diseases (e.g., chlamydiosis, cryptococcosis, paramyxovirus, West Nile Virus), inflammatory (e.g., trauma) and non-inflammatory diseases (e.g., heavy metal toxicosis, alkaloid toxicosis, venous stasis due to hobbles placed on the legs), as well as nutritional diseases (e.g., calcium deficiency, nutritional hyperparathyroidism).

Cerebellar hypoplasia is a rare congenital disease of the cerebellum, infrequently reported. Secondary acquired hypoplasia has been attributed to infectious agents, including parvovirus, avian leukosis virus, Chlamydia psittaci, and cryptococcosis. There are no reports in literature describing toxins affecting only cerebellum and sparing rest CNS in birds, so lead and other heavy metal toxicoses are unlikely to be the underlying cause.
The take home message is: this case describes cerebellar hypoplasia in African grey parrots that suggested a developmental etiology, most likely due to a hereditary and/or congenital, possibly sex-linked, origin.