Domestic ferrets (Mustela putorius furo) have been used in biomedical research to study influenza viruses since the early 20^th century. Ferrets have continued to gain importance for the study of viral respiratory disease due to their disease susceptibility and anatomic similarities to humans. Here we review features of ferret biology and management that should be considered when planning to work with this species, particularly in models of respiratory disease. We specifically discuss biosafety and husbandry, clinical and pathologic assessments, and anesthetic considerations for ferrets with respiratory disease and systemic illness. These considerations are important for animal welfare, fidelity of the model to human disease, and ensuring accuracy and reproducibility of acquired data. Finally, we briefly review the use of ferrets to study respiratory diseases by discussing their respiratory anatomy and 2 frequently studied viral respiratory diseases, influenza and coronavirus disease 2019 (COVID-19).

Roux-en-Y gastric bypass (RYGB) surgery is one of the most commonly performed bariatric procedures for weight loss in humans. However, this procedure is not risk-free, and patients may experience complications that include small bowel obstruction, gastrointestinal bleeding, chronic diarrhea, ulcers, malnutrition, and anemia. In particular, anemia is a recognized long-term complication and can be severe. Rats have been used as a model to study the effects of gastric bypass surgeries. They can experience similar complications as people, but the development of severe anemia has not previously been reported in rats. We observed 2 cases of severe anemia in female Sprague–Dawley rats after RYGB surgery. These cases prompted us to further investigate the frequency and severity of anemia after RYGB in rats. Blood work and necropsies were performed on 9 additional female Sprague–Dawley rats (5 with RYGB, 4 with sham surgery). In these 9 rats, only one had signs of clinical anemia. These 3 anemic rats displayed moderate to severe pallor of the eyes and ears. Necropsy findings in anemic RYGB rats included pale internal organs and eccentric heart enlargement, which led to a significantly higher heart:body weight ratio in RYGB rats as compared with sham controls. Anemic rats had either a macrocytic normochromic anemia, consistent with vitamin B₁₂ or folate deficiency, or microcytic hypochromic anemia, indicative of iron deficiency. Researchers who perform RYGB surgery in rats should be aware of the potential complication of severe anemia. Plans for the diagnosis and management of this complication and the development of criteria for humane endpoints for severe anemia are recommended as a refinement to these studies.

Corynebacterium bovis (Cb), the cause of hyperkeratotic dermatitis in various immunocompromised mouse strains, significantly impacts research outcomes if infected mice are used. Although Cb has been isolated from a variety of species, including mice, rats, cows, and humans, little is known about the differences in the infectivity and clinical disease that are associated with specific Cb isolates. The infectious dose that colonized 50% of the exposed population (ID₅₀ ) and any associated clinical disease was determined in athymic nude mice (Hsd:Athymic Nude-Foxn1 nu ) inoculated with Cb isolates collected from mice (n = 5), rat (n = 1), cow (n = 1), and humans (n = 2) The same parameters were also determined for 2 of the mouse isolates in 2 furred immunocompromised mouse strains (NSG [NOD. Cg-Prkdc^scid Il2rg^tm1Wjl /Sz] and NSG-S [NOD. Cg-Prkdc^scid Il2rgt^m1Wjl Tg(CMV-IL3, CSF2, KITLG)1Eav/MloySzJ]). To determine the ID ₅₀, mice (n= 6/dose; 3 of each sex) were inoculated topically in 10-fold increments ranging from 1 to 10 8 bacteria. Mice were scored daily for 14 days for the severity of clinical signs. On days 7 and 14 after inoculation, buccal and dorsal skin swabs were evaluated by aerobic culture to determine infection status. The mouse isolates yielded lower ID₅₀values (58 to 1000 bacteria) than did the bovine (6460 to 7498 bacteria) and rat (10,000 bacteria) isolates. Human isolates did not colonize mice or cause disease. Mouse isolates produced clinical disease of vary- ing severity in nude mice. Despite significant immunodeficiency, furred NSG and NSG-S mice required a 1000- to 3000-fold higher inoculum for colonization than did athymic nude mice. Once colonized, clinically detectable hyperkeratosis did not develop in the haired strains until 18 to 22 d after inoculation, whereas athymic nude mice that developed clinically detect- able disease showed hyperkeratosis between 6 and 14 d after inoculation. In conclusion, there are significant differences in Cb's ID ₅₀, disease course, and severity of clinical signs between Cb isolates and among immunodeficient mouse strains.

Our goal in this manuscript is to advance the assessment and treatment of monkey species in neuroscience research. We hope to begin a discussion and establish baseline data on how complications are identified and treated. We surveyed the neuroscience research community working with monkeys and compiled responses to questions about investigator demographics, assessment of animal wellbeing, treatment choices, and approaches to mitigate risks associated with CNS procedures and promote monkey health and wellbeing. The majority of the respondents had worked with nonhuman primates (NHP) for over 15 y. Identification of procedure-related complications and efficacy of treatment generally rely on common behavioral indices. Treatments for localized inflammatory responses are generally successful, whereas the treatment success for meningitis or meningoencephalitis, abscesses, and hemorrhagic stroke are less successful. Behavioral signs of pain are treated successfully with NSAIDs and opioids. Our future plans are to collate treatment protocols and develop best practices that can be shared across the neuroscience community to improve treatment success rates and animal welfare and therefore science. Human protocols can be used to develop best practices, assess outcomes, and promote further refinements in treatment practices for monkeys to enhance research outcomes.

The vector-borne protozoal parasite Trypanosoma cruzi causes Chagas disease in humans and animals. This parasite is endemic to the southern United States where outdoor-housed NHP at biomedical facilities are at risk of infection. In addi- tion to the direct morbidity caused by T. cruzi, infected animals are of limited biomedical research use because infections can produce confounding pathophysiologic changes even in animals with no clinical disease. In part due to concerns for direct T. cruzi transmission between animals, infected NHP at some institutions have been culled, removed, or otherwise isolated from uninfected animal populations. However, data that document horizontal or vertical transmission in captive NHP in the United States are not available. To evaluate the potential for inter-animal transmission and to identify environmental factors that affect the distribution of new infections in NHPs, we conducted a retrospective epidemiologic study of a rhesus macaque ( Macaca mulatta ) breeding colony in south Texas. We used archived biologic samples and husbandry records to identify the time and location of macaque seroconversion. These data were used to perform a spatial analysis of how geographic location and animal associations affected the spread of disease and to infer the importance of horizontal or vertical routes of transmission. The majority of T. cruzi infections were spatially clustered, suggesting that environmental factors promoted vector exposure in various areas of the facility. Although we cannot not rule out horizontal transmission, our data suggest that horizontal transmission was not a critical route for spread for the disease. Vertical transmission was not a contributing factor in this colony. In conclusion, our findings suggest that local triatome vectors were the major source of T. cruzi infections in captive macaques in our colony. Therefore, limiting contact with vectors, rather than segregation of infected macaques, is a key strategy for disease prevention at institutions that house macaques outdoors in the southern United States.

Vitiligo affects a significant portion of human and animal populations. The disease causes irregular and multifocal progressive loss of fur, skin, and mucous membrane pigmentation due to the loss or absence of melanocytes. While etiopathogenesis is not completely understood, autoimmunity, environmental, and genetic factors are implicated We present a case report on a 16-y-old female rhesus macaque (Macaca mulatta ) with depigmented areas that are progressively increasing on the skin and coat and are distributed on the head and back. Histopathology revealed alterations compatible with vitiligo characterized by the absence of melanocytes in the epidermis and dermis. The clinical history and complementary exams support this diagnosis.