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A new gene defect in Fleckvieh calves leads to a syndrome with partial phenotype overlap with bovine hereditary zinc deficiency. A mutation in a gene encoding phospholipase D4 (PLD4), an endosomal exonuclease, causes the disorder. In mice, PLD4 activity indirectly regulates the Toll-like receptor 9 (TLR9) pathway via degradation of microbial DNA. PLD4 absence thus results in visceral macrophage activation comparable to human macrophage activation syndrome. In this study, disease progression and the role of macrophages in affected calves were monitored clinically, clinicopathologically, and histologically over time. Breeding data identified 73 risk matings of heterozygous carriers resulting in 54 potentially PLD4 -deficient calves born on farms. PLD4 status was examined via 5′-exonuclease assay, detecting 6 calves carrying the defect. These were purchased and monitored daily until final necropsy. The calves developed progressive skin lesions starting with small scaling areas terminating in severe crusting dermatitis, especially in areas with mechanical exposure. Histological and immunohistochemical analyses indicated that macrophages with cytoplasmic vacuolation increased considerably in skin sections obtained weekly during the disease course. Macrophage increase correlated with increased dermal lesion severity. Macrophage activation was confirmed by prominent phagocytic activity in the superficial dermis using electron microscopy. Dermal mRNA abundance of CCL2 and CCL3 measured by quantitative polymerase chain reaction verified macrophage activation. Further increase in mRNA of downstream molecule MyD88 and cytokine IL12b connected bovine PLD4 deficiency to increased TLR9 pathway activation. In contrast to human macrophage activation syndrome, the main feature of bovine PLD4 deficiency was local disease in organs with contact to microbial DNA (skin, intestine, lungs). [ABSTRACT FROM AUTHOR]

To the Editor: Mycobacterium celatum belongs to the group called 'mycobacteria other than tuberculosis'; it is characterized by slow growth and a slender, rod-shaped form (0.25-0.5 x 0.5-13.0 urn). The [...]

The first continental European association for veterinary pathologists was founded in 1951 as the Arbeitsgemeinschaft der Veterinärpathologen (AG-Vetpath), bringing together veterinary pathologists from Germany, several European countries, and the United States. Yearly meetings were held in conjunction with the Deutsche Gesellschaft für Pathologie (DGP). Although the majority of DGP members were human pathologists, veterinary pathologists had been using the DGP as a forum for scientific exchange since the early 20th century. Renamed in 1969 as the Europäische Arbeitsgemeinschaft für Veterinärpathologen, and in 1974 as the Europäische Gesellschaft für Veterinärpathologie, the AG-Vetpath finally received its present name, the European Society for Veterinary Pathology (ESVP) in 1994. In parallel, national organizations for veterinary pathologists in European countries have also evolved over the years, the earliest being in Germany with the Fachgruppe Allgemeine Pathologie und pathologische Anatomie of the Deutsche Veterinärmedizinische Gesellschaft (DVG). AG-Vetpath represents the parent organization for further specialty organizations like the Gesellschaft für Toxikologische Pathologie (GTP) or the Arbeitskreis Diagnostische Veterinärpathologie (AKDV). Even the European College of Veterinary Pathologists (ECVP) was founded by members of ESVP. [ABSTRACT FROM AUTHOR]

The objective of the present study was to assess safety and immune responses in gilts after intradermal application of Porcilis® PRRS in two different application sites under field conditions. Forty-four gilts were allocated to one of three groups: Gilts of group 1 (n = 10) served as non-vaccinated controls, gilts of group 2 (n = 17) were vaccinated intradermally in the neck and gilts of group 3 (n = 17) received an intradermal vaccination in the perianal region. Clinical observations, local injection site reactions and histopathologic examination of the injection site were used for safety assessments. Frequency and degree of clinical signs were not significantly different between all three groups. Minor local reactions for both vaccination groups were observed; however, at 6, 7, 8, 9 and 15 days post-vaccination (dpv), the mean injection site reaction score was significantly lower in pigs vaccinated in the perianal region. In histopathologic examination, an extended inflammatory dimension was observed more frequently in pigs vaccinated in the neck. Blood samples were analyzed to quantify the post-vaccination humoral (ELISA and virus neutralization test) and cellular (IFN-γ ELISPOT) immune responses. PRRSV-specific antibodies were present in the serum of all vaccinated animals from 14 dpv onwards, whereas all control pigs remained negative throughout the study. Neutralizing antibody titers were significantly higher in pigs vaccinated in the perianal region at 28 dpv. At 14, 21 and 28 dpv, PRRSV-specific IFN-γ secreting cells were significantly increased in both vaccination groups compared to non-vaccinated gilts. Analysis of mean numbers of PRRSV-specific IFN-γ secreting cells did not result in statistically significant differences between both vaccination groups. The results of this study indicate that the perianal region is a safe alternative application site for intradermal vaccination of gilts with Porcilis PRRS. Furthermore, the intradermal application of Porcilis PRRS induced humoral and cellular immune responses independent of the administration site. [ABSTRACT FROM AUTHOR]

Acute hemorrhagic diarrhea syndrome (AHDS), formerly named canine hemorrhagic gastroenteritis, is one of the most common causes of acute hemorrhagic diarrhea in dogs, and is characterized by acute onset of diarrhea, vomiting, and hemoconcentration. To date, histologic examinations have been limited to postmortem specimens of only a few dogs with AHDS. Thus, the aim of our study was to describe in detail the distribution, character, and grade of microscopic lesions, and to investigate the etiology of AHDS. Our study comprised 10 dogs with AHDS and 9 control dogs of various breeds, age, and sex. Endoscopic biopsies of the gastrointestinal tract were taken and examined histologically (H&E, Giemsa), immunohistochemically (Clostridium spp., parvovirus), and bacteriologically. The main findings were acute necrotizing and neutrophilic enterocolitis (9 of 10) with histologic detection of clostridia-like, gram-positive bacteria on the necrotic mucosal surface (9 of 10). Clostridium perfringens isolated from the duodenum was identified as type A (5 of 5) by multiplex PCR (5 of 5). In addition, each of the 5 genotyped isolates encoded the pore-forming toxin netF. Clostridium spp. (not C. perfringens) were cultured from duodenal biopsies in 2 of 9 control dogs. These findings suggest that the pore-forming netF toxin is responsible for the necrotizing lesions in the intestines of a significant proportion of dogs with AHDS. Given that the stomach was not involved in the process, the term “acute hemorrhagic diarrhea syndrome” seems more appropriate than the frequently used term “hemorrhagic gastroenteritis.” [ABSTRACT FROM AUTHOR]

Objectives Feline infectious peritonitis (FIP) is an important cause of death in the cat population worldwide. The ante-mortem diagnosis of FIP in clinical cases is still challenging. In cats without effusion, a definitive diagnosis can only be achieved post mortem or with invasive methods. The aim of this study was to evaluate the use of a combined reverse transcriptase nested polymerase chain reaction (RT-nPCR) and sequencing approach in the diagnosis of FIP, detecting mutations at two different nucleotide positions within the spike (S) gene. Methods The study population consisted of 64 cats with confirmed FIP and 63 cats in which FIP was initially suspected due to similar clinical or laboratory signs, but that were definitively diagnosed with another disease. Serum/plasma and/or effusion samples of these cats were examined for feline coronavirus (FCoV) RNA by RT-nPCR and, if positive, PCR products were sequenced for nucleotide transitions within the S gene. Results Specificity of RT-nPCR was 100% in all materials (95% confidence interval [CI] in serum/plasma 83.9–100.0; 95% CI in effusion 93.0–100.0). The specificity of the sequencing step could not be determined as none of the cats of the control group tested positive for FCoV RNA. Sensitivity of the ‘combined RT-nPCR and sequencing approach’ was 6.5% (95% CI 0.8–21.4) in serum/plasma and 65.3% (95% CI 50.4–78.3) in effusion. Conclusions and relevance A positive result is highly indicative of the presence of FIP, but as none of the control cats tested positive by RT-nPCR, it was not possible to confirm that the FCoV mutant described can only be found in cats with FIP. Further studies are necessary to evaluate the usefulness of the sequencing step including FCoV-RNA-positive cats with and without FIP. A negative result cannot be used to exclude the disease, especially when only serum/plasma samples are available. [ABSTRACT FROM AUTHOR]

Borrelia persica, a bacterium transmitted by the soft tick Ornithodoros tholozani, causes tick-borne relapsing fever in humans in the Middle East, Central Asia and the Indian peninsula. Immunocompetent C3H/HeOuJ mice were infected intradermally with B. persica at varying doses: 1 x 106, 1 x 104, 1 x 102 and 4 x 100 spirochetes/mouse. Subsequently, blood samples were collected and screened for the presence of B. persica DNA. Spirochetes were detected in all mice infected with 1 x 106, 1 x 104 and 1 x 102 borrelia by real-time PCR targeting the flaB gene of the bacterium. Spirochetemia developed with a one- to two-day delay when 1 x 104 and 1 x 102 borrelia were inoculated. Mice injected with only four organisms were negative in all tests. No clinical signs were observed when infected mice were compared to negative control animals. Organs (heart, spleen, urinary bladder, tarsal joint, skin and brain) were tested for B. persica-specific DNA and cultured for the detection of viable spirochetes. Compiled data show that the target organs of B. persica infections are the brain and the skin. A newly developed serological two-tiered test system (ELISA and western blot) for the detection of murine IgM, IgG and IgA antibody titers against B. persica showed a vigorous antibody response of the mice during infection. In conclusion, the infection model described here for B. persica is a platform for in vivo studies to decipher the so far unexplored survival strategies of this Borrelia species. [ABSTRACT FROM AUTHOR]

The safety of veterinary vaccines is assessed in clinical trials in Europe. The assessment of the local tissue reaction to vaccination by magnetic resonance imaging (MRI) could reduce the number of animals needed because repeated examinations can be performed in the same animal over time. The present study compared the evaluation of local tissue reactions to vaccination using MRI in live pigs with histopathology of porcine tissue, the current gold standard in regulatory safety testing. Eight piglets each were administered one of two commercial vaccines into marked injection sites. All animals were sedated and scanned repeatedly by MRI using a contrast agent up to day 29 after vaccination. On day 29, the animals were euthanized and underwent a pathological examination. The MRI results were compared with the pathomorphological findings at the injection site by regression analysis. The MR images and the pathological examinations yielded matching results concerning the sizes of the affected tissue volumes or areas. The use of MRI for regulatory safety testing can reduce the number of animals needed to 8 per examination group. The volume of a local reaction and its progression over time can be evaluated and documented. If persistent lesions develop a final pathomorphological examination is needed to identify the kind and local distribution of the reaction. [ABSTRACT FROM AUTHOR]

Morphological lesions in kidneys and brain are all too often considered diagnostic for confirmation of encephalitozoonosis in rabbits. The current study evaluated the diagnostic value of histology versus other etiological tests, including immunohistochemistry and real-time polymerase chain reaction (PCR) for Encephalitozoon cuniculi infection diagnosis. Samples of brain, heart, lungs, intestine, liver, and kidneys from 81 rabbits were examined for morphological lesions attributed to E. cuniculi infection as well as for the presence of spores and E. cuniculi antigen. Of these, 55 rabbits were tested for E. cuniculi DNA. Histological changes consistent with E. cuniculi infection were seen in 33 rabbits (41%, 33/81) representing 87% (33/38) of all rabbits with confirmed E. cuniculi infection. Brains of these rabbits displayed 6 different types of focal lesions corresponding to the stage of infection and specific tissue response. In 5 rabbits that were tested positive, histology was either inconclusive or inconspicuous. Etiological diagnosis was based on histological spore detection in 16% (6/38) of infected rabbits. Immunohistochemistry was more sensitive (42%, 16/38) than histological spore detection, and real-time PCR proved to be the most sensitive of all investigated methods (30/35, 86% of the examined rabbits with E. cuniculi infection). Encephalitozoon cuniculi infection rarely occurs without characteristic kidney and brain lesions. However, the spectrum of brain changes is wider than previously reported. Based on these findings, confirmation of pathogenic E. cuniculi infection should include standard histology of the predilection sites and a specific etiological assay, preferably real-time PCR. [ABSTRACT FROM PUBLISHER]

The article describes a case of cystic echinococcosis due to Echinococcus equinus infection in a horse foaled and raised in southern Germany. Results of X-radiographs of the thorax revealed the presence of tumor-like masses in the caudal lung field of the mare. Necropsy also showed hydatid cysts in the lung containing amber liquid with hydatid sand, which revealed free protoscoleces, intact and ruptured brood capsules, calcareous corpuscles, and debris upon light microscopy.

Maturity onset diabetes of the young (MODY) is a monogenic form of diabetes inherited as an autosomal dominant trait. The second most common cause is GCK-MODY due to heterozygous mutations in the GCK gene which impair the glucokinase function through different mechanisms such as enzymatic activity, protein stability, and increased interaction with its receptor. The enzyme normally acts as a glucose sensor in the pancreatic beta cell and regulates insulin secretion. We report here a three- generation nonobese family diagnosed with diabetes. All affected family members presented with mild hyperglycemia and mostly slightly elevated hemoglobin A1c values. Genetic testing revealed a novel heterozygous T → C exchange in exon 8 of the GCK gene which resulted in a phenylalanine-330 TTC → serine (TCC)/p.Phe330Ser/F330S substitution. [ABSTRACT FROM AUTHOR]