Feline lymphoplasmacytic rhinitis (FLPCR): Severity of inflammation correlates with reduced mucosal IgA expression.

Feline lymphoplasmacytic rhinitis (FLPCR) is a rare disease with an unclear pathogenesis characterized by lymphoplasmacytic (LPC) inflammation and progressive tissue destruction. Aims were to evaluate specific FLPCR clinical and pathological features to gain insights into disease pathogenesis. Signalment, clinical signs, serology and 47 pin. h biopsies were retrospectively collected from 33 FLPCR and 3 normal cats. Microscopical lesions and immunohistochemistry results utilizing anti-CD3, anti-CD20, anti-FOXP3, anti-feline-IgA, IgG, IgE and anti-FeLV (p27 and gp70), FIV, FCV and, FHV were scored and most were analyzed statistically. The majority of cats were domestic short haired (26/31) with median age of 11 years and a 0.35 F/M ratio. Serology evidenced 3/22 FIV and 1/22 FeLV positive cats. Immunohistochemistry evidenced 1/33 FeLV-p27 positive cats. Common clinical signs were sneezing (19/24 [79 %]), mucous discharge (13/24 [54 %]) and stertor (10/24 [42 %]). In normal tissues, IgAs were expressed in mucin, apical and lateral cell membrane of columnar cells and in periglandular plasma cells. IgGs were expressed in 20-30 % of columnar cells. Number of clinical signs was statistically significantly higher in female cats (p < 0.0001) and was significantly correlated with chronicity (p = 0.004), and IgG scores (p = 0.01). LPC severity scores correlated positively with infiltration of neutrophils (p = 0.015), gland destruction (p = 0.019) and angiogenesis (p = 0.016) and negatively with fibrosis (p < 0.0001). LPC severity scores were also significantly associated to female sex (p = 0.01) and to IgA (p = 0.03), with higher IgA scores associated to lower LPC scores. FLPCR associated to disruption of mucosal defense mechanisms generating cycles of tissue inflammation, tissue damage and repair with progressive loss of function independent from viral infections.

Sarcoptic Mange in Wild Caprinae of the Alps: Could Pathology Help in Filling the Gaps in Knowledge?

Sarcoptic mange represents the most severe disease for wild Caprinae individuals and populations in Europe, raising concerns for both conservation and management of these ungulates. To date, this disease has been investigated in different wild caprine species and under many different perspectives including diagnostics, epidemiology, impact on the host populations, and genetics of both hosts and parasite, with the aim to disentangle the host-Sarcoptes scabiei relationship. Notwithstanding, uncertainty remains and basic questions still need an answer. Among these are the effect of immune responses on mange severity at an individual level, the main drivers in host-parasite interactions for different clinical outcomes, and the role of the immune response in determining the shift from epidemic to endemic cycle. A deeper approach to the pathology of this disease seems therefore advisable, all the more reason considering that immune response to S. scabiei in wild Caprinae, generally classified as a hypersensitivity, remains poorly understood. In this paper, we reviewed the pathological features associated to sarcoptic mange in wildlife, exploring different kinds of hypersensitivity and outcomes, with the objective of highlighting the major drivers in the different responses to this disease at an individual level and proposing some key topics for future research, with a particular attention to Alps-dwelling wild caprines.

Insight into an outbreak of Salmonella Choleraesuis var. Kunzendorf in wild boars.

An unusual mortality of wild boars occurred in Italy from 2012 to 2015 due to Salmonella Choleraesuis infection. In order to confirm the occurrence of an outbreak of S. Choleraesuis in wild boars and to epidemically characterise the unique S. Choleraesuis biovar, a collection of isolates belonging to wild boars was investigated from the phenotypic, molecular and genomic points of view (PFGE and WGS). Moreover, the possibility of transmission to domestic pigs and humans, temporally and geographically close to the wild boar epidemic, was tested by also including in the panel isolates from infected domestic pigs and from one human case of infection. Wild boar isolates displayed a high genetic correlation, thus suggesting they are part of the same outbreak, with a common invasiveness potential. Conversely, no correlation between pig isolates and those from the other sources (wild boars and human) was found. However, the phylogenetic and PFGE analyses suggest a high degree of similarity between the human and the investigated wild boar outbreak isolates, implying the potential for the spread of Salmonella Choleraesuis among these species.

Phenotypic features and phylogenetic background of extraintestinal hemolytic Escherichia coli responsible of mortality in puppies.

A 10-day-old litter of five puppies of Bracco Italiano dog breed showed weakness and diarrhea and, 2 days later, four of them died. At the same time, the bitch showed high hyperthermia (40 °C) and endometritis. The necropsy of a puppy revealed a severe lobar pneumonia accompanied with a bilateral nephrosis. No gross lesions were detected in other organs. Histopathology of the lung revealed severe multifocal fibrino-suppurative necrotizing bronchiolar-alveolitis associated with rod-shaped bacterial aggregates and diffuse interstitial lymphocytic infiltration. The kidney showed severe multifocal necrosis of the tubular epithelium and diffuse severe congestion of the parenchyma. A pure culture of hemolytic Escherichia coli carrying the Cnf-1 gene was identified, from both the puppy organs and bitch's milk. Moreover, phylo-typing assigned them to the phylogroup B2. Two weeks later, fecal samples from the bitch and the survived puppy were collected for a second microbiological analysis, identifying two hemolytic E. coli strains, Cnf positive and Cdt negative and Cnf and Cdt negative, respectively. Some E. coli pathogenic strains may cause enteric or extraintestinal disease. In dogs and cats, strains of extraintestinal pathogenic E. coli (ExPEC) produce specific virulent factors such as hemolysis and cytotoxin necrotizing factors (Cnf). In this episode, we hypothesize that the bitch's milk could be the main source of ExPEC infection causing high puppies mortality. The role of the bitch as a carrier could not be excluded: stressful conditions, such as pregnancy and delivery, would change the host-pathogen dynamics possibly increasing the release of the infectious burden.