Preet Mohinder Singh

Kiwi (Apteryx spp.) chicks in conservation captive-rearing programmes commonly suffer from coccidiosis, a parasitic disease that can cause significant morbidity and mortality in young birds. Current management combines preventative husbandry with treatment using coccidiocidal drugs. However, evidence suggests a lack of efficacy of toltrazuril, the primary drug used to treat coccidia, and limited information is available on safe and effective therapeutic alternatives for juvenile kiwi. This study evaluated the prophylactic efficacy of orally administered diclazuril (Coxiril 0.5% (5 g/kg) microGranulate premix, Huvepharma) for preventing coccidiosis in kiwi chicks naturally exposed to infection in captive-rearing facilities. Kiwi chicks (n = 6) received in-feed diclazuril at 0.5 mg/kg daily for 30 days, starting on the day of transfer to outdoor pens. An untreated control group (n = 6) was monitored in parallel. Health was monitored via clinical observation and blood biochemical analyses, while drug efficacy was measured using a combination of faecal oocyst counts, plasma concentration of diclazuril, and a molecular assay to assess changes in Eimeria spp. composition. In-feed diclazuril was well tolerated, with no adverse effects observed. Treated birds shed significantly fewer oocysts than control birds (p = 0.021). Changes in coccidia species composition suggested differential susceptibility of some kiwi Eimeria species to diclazuril. Further investigation of the optimal dose and treatment duration is recommended before integration of diclazuril into standard management protocols.

Captive‐reared kiwi ( Apteryx spp.) chicks commonly suffer from coccidiosis, a parasitic disease that can cause morbidity and mortality in young immune‐naive birds. Disease is currently managed in captivity through a combination of preventative husbandry practices and therapeutic treatment with the coccidiocide toltrazuril, for which no safety or pharmacokinetic data is available for kiwi. In this study we attempted to determine the pharmacokinetics of synthetic triazine anticoccidials, toltrazuril and diclazuril, in healthy three‐to‐four‐week‐old North Island brown kiwi ( Apteryx mantelli ) chicks. Birds were given a single oral dose of toltrazuril (25 mg/kg.bw; n = 6) or diclazuril (5 mg/kg.bw; n = 6), and closely monitored for adverse reactions. Serial blood samples were analysed via liquid chromatography‐mass spectrometry (LC–MS) to determine the pharmacokinetics of both drugs, including the active metabolite of toltrazuril, toltrazuril sulphone. Pharmacokinetics were ascertained for both drugs in kiwi chicks. The mean (standard deviation) C _max of diclazuril in plasma was 539.48 ± 169.63 ng/mL with a T _max of 11.33 ± 1.63 h, while the C _max for toltrazuril was 5622.16 ± 1997.52 ng/mL with a T _max of 11.33 ± 1.63 h and C _max of toltrazuril sulphone 3623.01 ± 1085.71 ng/mL with a T _max of 96 ± 26.29 h. Mild changes to some biochemical parameters were observed, most notably elevations in uric acid in some toltrazuril‐treated birds; however no remarkable clinical changes were observed in any chicks dosed with the drugs trialled.

Juvenile kiwi (Apteryx spp.) within captive-rearing programmes commonly suffer from coccidiosis, which primarily affects the intestine but can also impact other organs, such as the kidneys, liver, lung, and spleen (Morgan et al. Avian Pathol 42:137–146 2013). In some immune-compromised birds, disease causes significant morbidity and, occasionally, mortality (Morgan et al. NZVJ 62:315–320 2014); however, understanding of the biology of disease-causing Eimeria species in kiwi is limited. A probe-based qPCR assay targeting a 115-bp fragment of the Eimeria mitochondrial cytochrome c oxidase I (CO1) gene was developed to identify three distinct kiwi Eimeria species: the two species most commonly recovered from faeces, Eimeria kiwii and Eimeria apteryxii, as well as the newly described species, Eimeria koka (Scheltema et al. Syst Parasitol 102:30 2025). The qPCR assay was then applied to retrospectively analyse formalin-fixed paraffin-embedded intestine, kidney, liver, lung, and spleen tissues from ten historic post-mortem cases from kiwi diagnosed with extraintestinal coccidiosis. This novel assay detected infection more often (33/47 tissues) than manual histopathological identification (25/47 tissues). Only one species, E. koka, was detected in extraintestinal tissues with the highest prevalence (9/10) in kidney tissues. In contrast, E. kiwii was reliably detected in 8/9 intestinal tissues but was not detected in the other tissues tested. E. apteryxii was not detected in any of the tissues analysed. These findings suggest that kiwi are infected by at least one intestinal and one renal-specific species, the latter of which is suspected to disseminate under certain conditions to other organs of the body.

Coccidia (Apiconmplexa) are naturally occurring and occasionally detrimental parasites of kiwi (Apteryx spp.), a unique, flightless bird species dependent upon conservation efforts for survival. Using morphological and molecular data, a new coccidia species, Eimeria koka n. sp., isolated from two closely related but geographically isolated kiwi host species, Apteryx rowi Tennyson et al. (rowi) and Apteryx mantelli Bartlett (North Island brown kiwi), is described. Oocysts are oval (20.8 × 15.9 μm) with a mean L/W ratio of 1.3, and a distinctive rough, crenellated brown oocyst wall (mean 1.2 μm), an oocyst residuum, 1–2 polar granules, and no micropyle. Sporocysts are ellipsoidal (11.6 × 6.3 μm) with a Stieda body and sporocyst residuum. Phylogenetic analysis of the cytochrome C oxidase subunit 1 (CO1) placed E. koka n. sp. in a separate clade to other Eimeria species previously identified from kiwi (Coker et al., Syst Parasitol 100(3):269–281, 2023). Comparison of DNA from oocysts with infected tissues from a single juvenile North Island brown kiwi confirmed parasitism of the kidney and lung tissues. This is the first Eimeria species identified from extraintestinal tissues in kiwi. Further molecular studies are recommended to determine the tissue distribution of E. koka n. sp. and other Eimeria species in kiwi.

Pain mitigation strategies for disbudding in goat kids have gained significant attention in recent years because of growing concerns for animal welfare. Disbudding, the removal of horn buds in young goats, is a common practice to enhance safety and manage herd dynamics. However, the procedure will cause pain and distress if not managed effectively. This review covers the array of pain mitigation techniques currently available for disbudding, including the efficacy of these strategies in reducing pain and stress during the disbudding process, with specific attention to the potential toxicity associated with local anesthetics. The current best practice for disbudding on the farm suggests sedation/analgesia with an alpha-2 agonist, the placement of a two-point cornual nerve block, and then an NSAID for postoperative pain. In conclusion, this review offers recommendations for future research directions aimed at enhancing the welfare of young goats subjected to the disbudding procedure. These suggestions hold the promise of fostering significant improvements in the overall well-being of these animals.

Farm animals are routinely subjected to painful husbandry procedures for various purposes. Goat kids are disbudded to improve goat welfare and to ensure safety of other livestock, farm personnel, attending veterinarians and for various other production and managemental procedures. Disbudding is commonly performed on dairy goat farms, in kids under 3 weeks of age. Many scientific studies reported physiological and behavioural changes indicating pain and distress following disbudding, and this can be a significant cause of welfare compromise in goat kids. Recognition and measurement of pain is important to treat and/or manage pain and distress following painful procedures. This review focuses on pain assessment in goat kids following disbudding, using both physiological and behavioural measures. As only a limited information is available on the topic of interest, relevant studies in other young farm animals have also been discussed to compare the status quo in goat kids.

Butorphanol and dexmedetomidine (DXM) can produce analgesia in birds. Intranasal (IN) route of drug administration is easier, and free of risks such as pain and tissue damage compared with intravenous, intramuscular or subcutaneous routes in bird species, including wild birds. Although previous studies have demonstrated the use of IN route for producing sedation, no studies are available on the pharmacokinetics and pharmacodynamics of IN drugs in birds. This study analyzed the pharmacokinetics and sedative–analgesic efficacy of intranasal butorphanol (2 mg/kg), dexmedetomidine (80 µg/kg) and their combination (butorphanol, 2 mg/kg; DXM, 80 µg/kg) in healthy, male, Ross broiler chickens (n = 6/group) aged between 6 and 8 weeks. Maximum plasma concentration (Cmax, p = 0.01), area under the plasma concentration-time curve from time zero to 120 min (AUC_{0 to 120}, p = 0.02) and apparent volume of distribution at steady state (Vss, p = 0.02) of DXM were significantly higher than that of DXM co-administered with butorphanol. The mechanical nociceptive thresholds and the sedation scores of DXM group were significantly higher than the baseline value. Dexmedetomidine (80 µg/kg, IN) was effective in chickens, and the drug absorption was more rapid than that of DXM with butorphanol. However, the duration of action of DXM was short. Lower value of Cmax and nociceptive thresholds showed the nonsignificant efficacy of butorphanol at a dose of 2 mg/kg after IN administration in broiler chickens.

Anaesthetic agents and doses used can significantly impact cerebrocortical responsiveness as assessed by electroencephalography (EEG). The objective of this study was to evaluate the effect of three different halothane concentrations on the EEG of Rock Doves using measures of frequency distribution and burst suppression. Eight healthy Rock Doves (Columba livia) were anaesthetized with halothane in oxygen, their tracheas intubated and their lungs mechanically ventilated. Five minutes of EEG were recorded at three multiples of minimum anaesthetic concentration (MAC), 1× MAC (1.6%), 1.5× MAC (2.4%) and 2× MAC (3.2%), presented in ascending then descending order. Fast Fourier transformation of the raw EEG record gave the median frequency (F₅₀), spectral edge frequency (F₉₅) and the total power (P_tot). Burst suppression, expressed as inactive compared to active EEG (%), was calculated on a representative two-minute section of the raw EEG. Data were analysed using repeated-measures one-way ANOVA with Tukey post hoc correction for comparison of 1×, 1.5× and 2× MAC. Three of eight birds demonstrated negligible (F₅₀, p = 0.04; F₉₅p = 0.02; P_totp < 0.0001) occurred between 1× and 2× MAC. Halothane anaesthesia at MAC multiples of 1×, 1.5× and 2× in the Rock Dove can be considered suitable where cortical responsiveness is desired.

As the introduction of concentrated cattle pour‐on products containing abamectin, there have been veterinary reports of both fatal and non‐fatal poisoning in New Zealand working dogs. Because these products are highly palatable to dogs, a toxic dose is readily ingested. The pharmacokinetic properties of abamectin in dogs are not published in the public domain. This information is important in understanding the processes of absorption and elimination when treating poisoned dogs and is useful in determining an appropriate treatment for poisoned dogs. The pharmacokinetic properties of abamectin administered orally to six healthy dogs (3 male and 3 female) at a dose of 0.2 mg/kg were established. Plasma concentrations of abamectin were determined by high‐performance liquid chromatography (HPLC) coupled with a fluorescence detector. The maximum plasma concentration (C_max) for abamectin was 135.52 ± 38.6 ng/ml at 3.16 ± 0.75 h. The elimination half‐life (T1/2 elim (h)) was 26.51 ± 6.86 h. The area under the curve (AUC 0‐∞) was 3723.50 ± 1213.08 ng h/ml. The mean residence time (MRT) was 38.82 ± 8.93 h. These pharmacokinetic data provide helpful information regarding the treatment of poisoned dogs.