Case reports of squamous cell carcinoma in cows.

The aim was to investigate the frequency of squamous cell carcinoma and the outcome after surgical treatment in cows admitted to the clinic between 2012 and 2018. The study included six cows with squamous cell carcinoma (confirmed in 5 cattle and suspected in 1). All cattle underwent clinical examination and additional testing to confirm the diagnosis. Breed, age, gender, localization of neoplasm and treatment were recorded. In a telephonequ estionnaire owners were asked about survival, culling, integration into the herd after discharge from the clinic, wound healing and neoplasm recurrence. Five ocular squamous cell carcinomas were diagnosed during the study period. Another neoplasm on the dorsolateral thoracic wall of a cow could not be diagnosed with certainty; however, it had characteristics of squamous cell carcinoma. Two cows with ocular squamous cell carcinomawere euthanised.  The prognosis and outcome of squamous cell carcinoma depend on early detection of clinical signs, the presence of metastases and the timing of tumour removal. Surgical removal of a squamous cell carcinoma at or near the eye or at other locations of the body appears to have a good prognosis.

Malnutrition as the cause of recumbency in suckler cows associated with Trypanosoma theileri infection.

BACKGROUND: Recumbent cows are a diagnostic challenge because of a wide range of differential diagnoses, which include trauma, neurological and metabolic disorders, malnutrition and mineral deficiencies. This case report describes recumbent suckler cows that presented as a herd problem. In addition to weakness due to inanition, Cu and Se deficiencies were considered as possible aetiologies of the recumbency. Furthermore, Trypanosoma (T.) theileri, a blood parasite of unknown importance in Germany, was detected in the blood of some cows. CASE PRESENTATION: Three recumbent cows were referred to the Clinic for Ruminants and Swine, Faculty of Veterinary Medicine of the University of Leipzig. They were unable to rise and had low body condition scores and rough hair coats. Haematological and serum biochemical analyses showed neutrophilia, electrolyte imbalances, increased activities of muscle and liver enzymes and decreased concentrations of trace elements, especially Copper (Cu) and Selenium (Se). T. theileri was detected in a routine blood smear from one cow. The cows did not respond to an intensive care protocol, which included intravenous fluids and electrolytes, mineral substitution, non-steroidal anti-inflammatories and antibiotics, and were therefore euthanized or died. Postmortem examination showed cachexia, subcutaneous and scleral oedema and muscular dystrophy, especially in the hind limbs. Follow-up examination of the herd of origin produced similar findings including the detection of T. theileri in a large proportion of the herd. Ration analysis revealed considerable undersupply of several nutrients. CONCLUSIONS: Based on all findings, an aetiological diagnosis of trace mineral and nutrient deficiency with possible involvement of T. theileri was made.

[Effect of different pain management protocols on the health status of German Holstein heifer calves undergoing hot iron disbudding]. / Einfluss der thermischen Enthornung mit unterschiedlichem Schmerzmanagement auf die Gesundheit von Kälbern.

OBJECTIVE: Hot iron disbudding of calves is a stressful and painful procedure. Previous parts of an ongoing comprehensive study on disbudding in dairy calves dealt with various types of pain management and the direct effects of the procedure on physiological, biochemical and behavioral processes. The goal of this study part was to investigate the effects of the disbudding procedure per se, pain management and the age of the calf at the time of disbudding on the health status of the calf. MATERIALS AND METHODS: A total of 337 German Holstein heifer calves were used for this prospective, randomized and triple-blinded study. The calves were disbudded at 4-10 days or at 15-28 days of age. Each calf was randomly assigned to one of 9 treatment groups, which differed with respect to pain management (sedation, local anesthesia, nonsteroidal antiinflammatory drugs, placebo). All but the sham-disbudded calves underwent hot iron disbudding and all calves were monitored clinically before and until 4 weeks after the procedure. The findings were analyzed using valuation scores and a threshold model of the SAS software. RESULTS: Disbudding exhibited adverse effects on respiratory health. Calves undergoing sham disbudding experienced the lowest incidence of respiratory disease and calves that did not receive any anesthesia or pain medication displayed the highest frequency. All treatments showed mitigating effects on the incidence of respiratory tract diseases, however the effects varied with the type of pain management. Fever was less common in calves that were disbudded early in life than calves that underwent disbudding at an older age. CONCLUSION: Disbudding of young calves poses a risk to respiratory health. If breeding of polled offspring is not possible or when farming of horned cattle is not feasible, the risk of respiratory disease induced by disbudding can be minimized by adequate pain management. Disbudding of very young calves is feasible and recommended. CLINICAL RELEVANCE: The present study underlines the importance of optimal pain management during disbudding of dairy calves.

Oxidative stress in sperm affects the epigenetic reprogramming in early embryonic development.

BACKGROUND: Reactive oxygen species (ROS)-induced oxidative stress is well known to play a major role in male infertility. Sperm are sensitive to ROS damaging effects because as male germ cells form mature sperm they progressively lose the ability to repair DNA damage. However, how oxidative DNA lesions in sperm affect early embryonic development remains elusive. RESULTS: Using cattle as model, we show that fertilization using sperm exposed to oxidative stress caused a major developmental arrest at the time of embryonic genome activation. The levels of DNA damage response did not directly correlate with the degree of developmental defects. The early cellular response for DNA damage, γH2AX, is already present at high levels in zygotes that progress normally in development and did not significantly increase at the paternal genome containing oxidative DNA lesions. Moreover, XRCC1, a factor implicated in the last step of base excision repair (BER) pathway, was recruited to the damaged paternal genome, indicating that the maternal BER machinery can repair these DNA lesions induced in sperm. Remarkably, the paternal genome with oxidative DNA lesions showed an impairment of zygotic active DNA demethylation, a process that previous studies linked to BER. Quantitative immunofluorescence analysis and ultrasensitive LC-MS-based measurements revealed that oxidative DNA lesions in sperm impair active DNA demethylation at paternal pronuclei, without affecting 5-hydroxymethylcytosine (5hmC), a 5-methylcytosine modification that has been implicated in paternal active DNA demethylation in mouse zygotes. Thus, other 5hmC-independent processes are implicated in active DNA demethylation in bovine embryos. The recruitment of XRCC1 to damaged paternal pronuclei indicates that oxidative DNA lesions drive BER to repair DNA at the expense of DNA demethylation. Finally, this study highlighted striking differences in DNA methylation dynamics between bovine and mouse zygotes that will facilitate the understanding of the dynamics of DNA methylation in early development. CONCLUSIONS: The data demonstrate that oxidative stress in sperm has an impact not only on DNA integrity but also on the dynamics of epigenetic reprogramming, which may harm the paternal genetic and epigenetic contribution to the developing embryo and affect embryo development and embryo quality.

Impacts of oxidative stress on bovine sperm function and subsequent in vitro embryo development.

Low levels of reactive oxygen species (ROS) in sperm are essential for various sperm functions such as capacitation, hyperactivation and acrosome reaction. However, increased synthesis of ROS or a disruption of antioxidative status (e.g. in cryopreserved sperm) can induce oxidative stress (OS). Sperm are particularly vulnerable to OS, as their plasma membrane contains large amounts of polyunsaturated fatty acids and they have limited antioxidative capacity (due to low cytoplasmic volume). Oxidative stress disturbs sperm function by damaging sperm proteins, lipids and DNA. Under relatively low OS sperm may retain their fertilizing ability, which might result in transfer of impaired paternal molecules (e.g. damaged DNA) to the fertilized oozyte. Oocytes can repair damaged paternal DNA, but only to a certain extent. Most embryos are either repaired (based on limited DNA damage in blastocysts) or eliminated (based on low percentage of blastocyst formation when sperm with damaged DNA is used for fertilization). However, some blastocysts had increases in both DNA damage and apoptosis, which could have important implications for subsequent development. In several studies, exogenous antioxidants improved quality of sperm exposed to oxidative stress and subsequent embryo development. However, there is still a knowledge gap regarding whether these alterations affect embryonic survival and further development to a live fetus and healthy offspring.

Excess androgens in utero alters fetal testis development.

Prenatal androgenization induces a polycystic ovary syndrome-like phenotype in adult female offspring, which is associated with alterations that can be detected in the fetal ovary, suggesting gestational origins of this condition. We therefore investigated whether increased prenatal androgen exposure also altered testicular development using ovine animal models. Biweekly maternal testosterone propionate (TP; 100 mg) from day 62 to day 70/day 90 of gestation altered male developmental trajectory. In male fetuses serum LH was decreased (P < .01), and testicular STAR, CYP11, and CYP17 abundance were reduced. Coincident with this, basal testicular T synthesis was decreased in vitro (P < .001). Leydig cell distribution was severely perturbed in all testes prenatally exposed to TP (P < .001). To examine the contribution of estrogens, fetuses were injected with TP (20 mg), the potent estrogen agonist, diethylstilbestrol (DES; 20 mg), or vehicle control at day 62 and day 82 and assessed at day 90. The effects of fetal (direct) TP treatment, but not DES, paralleled maternal (indirect) TP exposure, supporting a direct androgen effect. Cessation of maternal androgenization at day 102 returned Leydig cell distribution to normal but increased basal T output, at day 112, demonstrating Leydig cell developmental plasticity. Earlier maternal androgen exposure from day 30 similarly influenced Leydig cell development at day 90 but additionally affected the expression of Sertoli and germ cell markers. We show in this study that increased prenatal androgen exposure alters development and function of Leydig cells at a time when androgen production is paramount for male development. This supports the concept that gestational antecedents associated with polycystic ovary syndrome may have effects on the male fetus.