Perinatal infections with feline panleukopenia virus (FPV) have long been known to be associated with cerebellar hypoplasia in kittens due to productive infection of dividing neuroblasts. FPV, like other parvoviruses, requires dividing cells to replicate which explains the usual tropism of the virus for the digestive tract, lymphoid tissues and bone marrow in older animals. In this study, the necropsy and histopathological analyses of a series of 28 cats which died from parvovirus infection in 2013 were performed. Infections were confirmed by real time PCR and immunohistochemistry in several organs. Strikingly, while none of these cats showed cerebellar atrophy or cerebellar positive immunostaining, some of them, including one adult, showed a bright positive immunostaining for viral antigens in cerebral neurons (diencephalon). Furthermore, infected neurons were negative by immunostaining for p27Kip1, a cell cycle regulatory protein, while neighboring, uninfected, neurons were positive, suggesting a possible re-entry of infected neurons into the mitotic cycle. Next-Generation Sequencing and PCR analyses showed that the virus infecting cat brains was FPV and presented a unique substitution in NS1 protein sequence. Given the role played by this protein in the control of cell cycle and apoptosis in other parvoviral species, it is tempting to hypothesize that a cause-to-effect between this NS1 mutation and the capacity of this FPV strain to infect neurons in adult cats might exist. This study provides the first evidence of infection of cerebral neurons by feline panleukopenia virus in cats, including an adult. A possible re-entry into the cell cycle by infected neurons has been observed. A mutation in the NS1 protein sequence of the FPV strain involved could be related to its unusual cellular tropism. Further research is needed to clarify this point.

Canine angiostrongylosis, a gastropod-borne helminthic infection, is increasingly being described in North America and is now reported in many European countries. In dogs, Angiostrongylus vasorum may cause a wide spectrum of clinical signs. Respiratory distress such as coughing and dyspnoea are the most frequently described manifestations. The aim of the present study was to gain additional information on the distribution, prevalence and risk factors associated with A. vasorum infection in dog from southern Belgium through the combined used of a commercially available in-clinic assay for detection of circulating antigen (Angio Detect™, IDEXX, Westbrook, USA) and coprology in two different canine populations: dogs with clinical signs compatible with angiostrongylosis and asymptomatic dogs or dogs presented for unrelated conditions (control). A total of 979 dogs were enrolled in the study from November 2014 until February 2016. Seven hundred fifty-seven dogs were included in the control group, whereas 222 dogs had clinical signs compatible with angiostrongylosis. Forty-six dogs out of 979 (4.7 %) had A. vasorum circulating antigen. There was a highly significant difference between the two populations (3.6 % (27/747) and 8.6 % (19/222) in control and symptomatic dogs, respectively) (P = 0.00379). First stage larvae (L1) of A. vasorum were found in seven out of 24 serologically positive control dogs and in six out of 17 serologically positive symptomatic dogs. Interestingly, L1 of Crenosoma vulpis were detected by Baermann technique in one control and nine symptomatic dogs, respectively. Out of 17 Angio Detect™ (IDEXX, Westbrook, USA) positive dogs with negative (14) or not performed Baermann test (three), one dog was positive in both in-house ELISAs (Ag and Ab) and one dog was positive for Ag. Statistical analysis was unable to detect any risk factors associated with the direct and/or indirect detection of A. vasorum. This seroepidemiological study demonstrated for the first time a high seroprevalence in Southern Belgium for A. vasorum. The Angio Detect™ was found to be suitable in this context as the collection, preservation and examination of stools were difficult. Nevertheless, discrepancies were observed between the different available tests. Additional research is clearly needed. Also, coproscopy remains a very useful tool in dogs infected for less than nine weeks and for the identification of other canine lung nematodes such as C. vulpis. This study also demonstrates that asymptomatic dogs may shed A. vasorum L1 in their faeces and therefore contribute to the maintenance of A. vasorum life-cycle.

The aim of this study was to identify the pathogens potentially involved in parietal fibrinous peritonitis (PFP). PFP is a complication of laparotomy in cattle, characterized by an accumulation of exudate inside a fibrinous capsule. We have studied 72 cases of PFP in Belgian blue cows, confirmed by a standard diagnostic protocol. Blood was collected to evaluate the presence of antibodies for Mycoplasma bovis(M. bovis), Coxiella burnetii(C. burnetii) and Bovine Herpesvirus 4(BoHV4) by enzyme-linked immunosorbent assays. Peritoneal exudate was obtained from the PFP cavity to perform bacteriological culture, and to identify the DNA of M. bovis, C. burnetii and BoHV4 using real time polymerase chain reaction (qPCR). Bacteriological culture was positive in most peritoneal samples (59/72); Trueperella pyogenes (T. pyogenes) (51/72) and Escherichia coli (E. coli) (20/72) were the most frequently identified. For BoHV4, the majority of cows showed positive serology and qPCR (56/72 and 49/72, respectively). Contrariwise, M. bovis (17/72 and 6/72, respectively) and C. burnetii (15/72 and 6/72, respectively) were less frequently detected (p < 0.0001). Our study proves that PFP can no longer be qualified as a sterile inflammation. Moreover, we herein describe the first identification of BoHV4 and C. burnetii in cows affected by PFP.

This study aimed to describe the inflammation, hydro-electrolyte and acid-base imbalances caused by generalised peritonitis (GP) and parietal fibrinous peritonitis (PFP) after caesarean section. After clinical examination, blood was sampled from 11 cows with PFP, 30 with GP and 14 healthy cows. Serum and plasma refractometry and glutaraldehyde tests were used to evaluate the inflammation level, while hydro-electrolytes and acid-base parameters were assessed using an EPOC^® device. In addition to clinical signs of dehydration (>10%), blood analysis showed a high fibrinogen concentration (PFP: 8.64 ± 8.82 g/L; GP: 7.83 ± 2.45 g/L) and fast glutaraldehyde coagulation (<3 min) indicative of severe inflammation in both diseases compared to the control group (p < 0.05). Moreover, a severe decrease in electrolytes concentration (Na⁺: 126.93 ± 5.79 mmol/L; K⁺: 3.7 ± 1.3 mmol/L; Ca⁺⁺: 0.89 ± 0.12 mmol/L; Cl⁻: 82.38 ± 6.45 mmol/L) and a significant increase in bicarbonate (30.87 ± 8.16 mmol/L), base excess (5.71 ± 7.42 mmol/l), L-lactate (8.1 ± 4.85 mmol/L) and creatinine (3.53 ± 2.30 mg/dL) were observed in cows with GP compared to the control group (p < 0.05). In contrast, few major perturbations were noticed in PFP, where only K⁺ (3.64 ± 0.25 mmol/L) and Ca⁺⁺ (1.06 ± 0.09 mmol/L) were significantly modified (p < 0.05). In conclusion, a high dehydration and severe inflammation are induced by PFP and GP. Nevertheless, GP causes more electrolytes and acid-base disturbances than PFP.

Oak poisoning is a known intoxication in grazing animals, but is slightly described in the literature. This case report describes 7 cattle from 3 different farms admitted to the clinic for ruminants of the University of Liège for suspected acorn poisoning in the autumn of 2022. The clinical signs were, anorexia, apathy with polyuria with low density. Further investigations led to the diagnosis of renal failure (blood urea 162 ± 88 mg/dL; blood creatinine 12 ± 4 mg/L). Supportive treatment, based on infusions (NaCl 0.9%) and electrolyte rebalancing, was administered and renal values were assessed every 24–48 h. Of these animals, 5/7 were euthanized. At necropsy, digestive erosions and ulcerations, oedema and renal hemorrhages, between the pyloric/caliceal cavity and the medulla were observed. Histopathological examination revealed necrosis of the renal tubules. The renal values of the two remaining animals were reduced, their general condition improved, and they were discharged. Acorn poisoning is a serious disease with no specific antidote or characteristic symptoms. Animals are identified as sick too late, when renal failure is already established. Farmers should be made more aware in order to prevent exposure, especially in years when acorns are abundant. Furthermore, there is no antidote for this intoxication.

The aim of this study was to identify the species and antimicrobial susceptibility of bacteria involved in parietal fibrinous peritonitis (PFP). We studied 156 peritoneal fluid samples from cows presenting PFP after caesarean section. Bacteria were cultured in selective media and their antimicrobial susceptibility was tested by disk diffusion assay. Bacteria were isolated in the majority (129/156; 83%) of samples. The majority (82/129; 63%) of positive samples contained one dominant species, while two or more species were cultured in 47/129 (36%) samples. Trueperella pyogenes (T. Pyogenes) (107 strains) was the most identified species, followed by Escherichia coli (E. coli) (38 strains), Proteus mirabilis (P. mirabilis) (6 strains), and Clostridium perfringens (C. perfringens) (6 strains). Several other species were sporadically identified. Antimicrobial susceptibility was tested in 59/185 strains, predominantly E. coli (38 strains) and P. mirabilis (6 strains). Antibiotic resistance, including resistance to molecules of critical importance, was commonly observed; strains were classified as weakly drug resistant (22/59; 37%), multidrug resistant (24/59; 41%), extensively drug resistant (12/59; 20%), or pan-drug resistant (1/59; 2%). In conclusion, extensive antibiotic resistance in the isolated germs might contribute to treatment failure. Ideally, antimicrobial therapy of PFP should be based upon bacterial culture and susceptibility testing.