Intussusception secondary to retroflexion of a proximal jejunal diverticulum, leading to Type 3 vagal indigestion with severe hypochloraemia in an adult Simmental bull (Bos taurus)

Intussusception is a rare but well described cause of intestinal obstruction in several species, including cattle, and is often associated with enteritis, intestinal parasitism or intestinal neoplasia. Clinical signs are non-specific and include anorexia with reduced faecal output.This report describes a four-year-old Simmental bull that presented with anorexia and reduced faecal output, along with severe ruminal bloat and a large, dilated intestinal loop palpated rectally. Serum biochemistry identified severe hypochloraemia, consistent with proximal intestinal obstruction and a poor prognosis. Although supportive and symptomatic treatment was provided, the bull died before a definitive diagnosis could be made.Post-mortem examination identified a segmental intestinal intussusception, within the proximal jejunum, which had resulted in intestinal obstruction. The primary cause of this intussusception was a retroflexed intestinal diverticulum, which formed the intussusceptum.<br/

The involvement of retroviruses in human T cell leukaemias and lymphomas

Human T lymphotropic virus type 1 (HTLV-I) causes adult T cell leukaemia/lymphoma (ATL), a neoplasm of CD4+ T cells. The related virus HTLV-I I has been isolated from cases of CD8+ T cell variant hairy cell leukaemia but has not been definitively associated with neoplasia. Bovine leukaemia virus (BLV), which causes B cell leukaemia and lymphoma in cattle, belongs to the same group of retroviruses. The hypothesis tested in this study was that HTLV-I, HTLV-II or related viruses are associated with T cell leukaemias and lymphomas in the United Kingdom, particularly mycosis fungoides (MF) and Sezary syndrome (SS). A combination of cell and molecular biology techniques was used in an attempt to identify retroviruses in patients with these neoplasms. Lymphocytes were cultivated from blood, skin and lymph nodes of patients with cutaneous lymphoid infiltrates to establish continuous T cell lines that might propagate HTLV-I, HTLV-II or related retroviruses. Techniques for the establishment of cultures included stimulation with mitogens, cytokines, conditioned medium and cocultivation. Cultured cells were examined for evidence of retroviruses by electron microscopy (EM), reverse transcriptase (RT) assay and the polymerase chain reaction (PCR). No retroviruses were isolated from 158 cultures initiated from 18 patients with cutaneous T cell lymphomas (predominantly MF and SS) and three patients with cutaneous B cell lymphomas (CBCLs). Four interleukin 2-dependent CD8

Lymphoid Hyperplasia and Lymphoma in Transgenic Mice Expressing the Small Non-Coding RNA, EBER1 of Epstein-Barr Virus

Non-coding RNAs have critical functions in diverse biological processes, particularly in gene regulation. Viruses, like their host cells, employ such functional RNAs and the human cancer associated Epstein-Barr virus (EBV) is no exception. Nearly all EBV associated tumours express the EBV small, non-coding RNAs (EBERs) 1 and 2, however their role in viral pathogenesis remains largely obscure.To investigate the action of EBER1 in vivo, we produced ten transgenic mouse lines expressing EBER1 in the lymphoid compartment using the mouse immunoglobulin heavy chain intronic enhancer Emicro. Mice of several of these EmicroEBER1 lines developed lymphoid hyperplasia which in some cases proceeded to B cell malignancy. The hallmark of the transgenic phenotype is enlargement of the spleen and mesenteric lymph nodes and in some cases enlargement of the thymus, liver and peripheral lymph nodes. The tumours were found to be of B cell origin and showed clonal IgH rearrangements. In order to explore if EBER1 would cooperate with c-Myc (deregulated in Burkitt's lymphoma) to accelerate lymphomagenesis, a cross-breeding study was undertaken with EmicroEBER1 and EmicroMyc mice. While no significant reduction in latency to lymphoma onset was observed in bi-transgenic mice, c-Myc induction was detected in some EmuEBER1 single transgenic tumours, indicative of a functional cooperation.This study is the first to describe the in vivo expression of a polymerase III, non-coding viral gene and demonstrate its oncogenic potential. The data suggest that EBER1 plays an oncogenic role in EBV associated malignant disease

Feline meningioma with extensive nasal involvement

Case summary A 9-year-old male neutered domestic longhair cat was presented with a 3 week history of lethargy and pain of unknown origin. A large extra-axial mass was demonstrated on MRI of the head, with cribriform plate destruction, extensive nasal invasion and intracranial expansion, producing a severe mass effect. The mass was isointense on T1-weighted imaging, predominantly hypointense with some hyperintense areas on T2-weighted imaging and fluid attenuation inversion recovery, markedly contrast enhancing, and caused transtentorial and cerebellar herniation. Histopathological evaluation confirmed a transitional (mixed) meningioma. Relevance and novel information To our knowledge this is the first report of a meningioma with extensive nasal involvement in a cat. Based on this case, meningioma should be considered as a differential diagnosis for tumours involving the nasal cavity and frontal lobe with cribriform plate destruction

Paraneoplastic leukocytosis in a dog following liposarcoma resection

A 10-year-old, female, neutered cocker spaniel presented for surgical debulking of an axillary and cranial thoracic wall liposarcoma. Pre-surgical blood analysis demonstrated anaemia (packed cell volume 17%), leukocytosis (white blood cell count 43.95 × 10 9/L) and thrombocytopenia (15 × 10 9/L), with platelet loss secondary to chronic intra-lesional haemorrhage or immune-mediated destruction, and concomitant Staphylococcus pseudintermedius urinary tract infection. A blood transfusion and antibiotics were administered before surgery. Within 48 hours after surgery, an extreme leukocytosis (white blood cell count 170 × 10 9/L), involving a severe left shift neutrophilia (95 × 10 9/L) was observed; this resolved within 10 days. Serum granulocyte-colony stimulating factor levels were similar to controls. The extreme leukocytosis was suspected to be related to a paraneoplastic leukaemoid reaction combined with an expected postoperative mild leukocytosis. Further investigation into the pathophysiology underlying similar cases is required. One month after surgery, all haematological abnormalities had normalised, and metronomic chemotherapy with chlorambucil commenced.</p

Lymphocyte deficiency limits Epstein-Barr virus latent membrane protein 1 induced chronic inflammation and carcinogenic pathology in vivo

Background: The importance of the malignant cell environment to its growth and survival is becoming increasingly apparent, with dynamic cross talk between the neoplastic cell, the leukocyte infiltrate and the stroma. Most cancers are accompanied by leukocyte infiltration which, contrary to an anticipated immuno-protective role, could be contributing to tumour development and cancer progression. Epstein-Barr virus (EBV) associated cancers, including nasopharyngeal carcinoma and Hodgkin's Disease, show a considerable leukocyte infiltration which surrounds the neoplastic cells, raising the questions as to what role these cells play in either restricting or supporting the tumour and what draws the cells into the tumour. In order to begin to address this we have studied a transgenic model of multistage carcinogenesis with epithelial expression of the EBV primary oncoprotein, latent membrane protein 1 (LMP1). LMP1 is expressed particularly in the skin, which develops a hyperplastic pathology soon after birth. Results: The pathology advances with time leading to erosive dermatitis which is inflamed with a mixed infiltrate involving activated CD8+ T-cells, CD4+ T-cells including CD4+/CD25+/FoxP3+ Treg cells, mast cells and neutrophils. Also significant dermal deposition of immunoglobulin-G (IgG) is observed as the pathology advances. Along with NF-kappaB activation, STAT3, a central factor in inflammation regulation, is activated in the transgenic tissue. Several inflammatory factors are subsequently upregulated, notably CD30 and its ligand CD153, also leukocyte trafficking factors including CXCL10, CXCL13, L-selectin and TGF beta 1, and inflammatory cytokines including IL-1 beta, IL-3 and the murine IL-8 analogues CXCL1, CXCL2 and CXCL5-6, amongst others. The crucial role of mature T- and/or B-lymphocytes in the advancing pathology is demonstrated by their elimination, which precludes mast cell infiltration and limits the pathology to an early, benign stage. Conclusions: LMP1 can lead to the activation of several key factors mediating proliferation, angiogenesis and inflammation in vivo. With the initiation of an inflammatory programme, leukocyte recruitment follows which then itself contributes to the progressing pathology in these transgenic mice, with a pivotal role for B-and/or T-cells in the process. The model suggests a basis for the leukocyte infiltrate observed in EBV-associated cancer and its supporting role, as well as potential points for therapeutic intervention