The pathology of natural and experimentally induced Campylobacter jejuni abortion in sheep

We describe here the gross and microscopic lesions in 18 experimentally induced and 120 natural Campylobacter abortions. In natural Campylobacter abortions, gross lesions were reported infrequently; placentitis was recorded in 6% and hepatic lesions in 4% of our field cases. Placentitis was the microscopic lesion identified most consistently in natural abortions (93%) and was often observed in association with abundant bacterial colonies in chorionic villi (54%) and less often with placental vasculitis (13%). In natural abortions, suppurative fetal pneumonia (48%), necrosuppurative hepatitis (16%), and purulent meningitis (7%) were also observed. The better-preserved specimens from experimentally induced abortions were utilized to define placental changes more precisely. Placentitis was identified in all 18 experimentally induced abortions and was observed most consistently in the chorionic villus stroma (100%), often accompanied by suppurative surface exudate (89%). An inflammatory infiltrate was less commonly identified in the cotyledonary hilus (39%) and intercotyledonary placenta (22%). Bacteria were visualized in H&E-stained sections in 89% of placentas from experimentally infected ewes, primarily as well-demarcated bacterial colonies within subtrophoblastic, sinusoidal capillaries (89%), in the cotyledonary villus stroma (89%), and within the cytoplasm of trophoblasts (22%). Transmission electron microscopy and immunohistochemistry confirmed that the vast majority of the well-demarcated bacterial colonies characteristic of Campylobacter abortion were within subtrophoblastic sinusoidal capillaries. The most characteristic microscopic lesions identified in cases of Campylobacter abortion in sheep were placentitis with placental bacterial colonies, placental vasculitis, and fetal pneumonia.

C1q Nephropathy: The Unique Underrecognized Pathological Entity

C1q nephropathy is a rare glomerular disease with characteristic mesangial C1q deposition noted on immunofluorescence microscopy. It is histologically defined and poorly understood. Light microscopic features are heterogeneous and comprise minimal change disease (MCD), focal segmental glomerulosclerosis (FSGS), and proliferative glomerulonephritis. Clinical presentation is also diverse, and ranges from asymptomatic hematuria or proteinuria to frank nephritic or nephrotic syndrome in both children and adults. Hypertension and renal insufficiency at the time of diagnosis are common findings. Optimal treatment is not clear and is usually guided by the underlying light microscopic lesion. Corticosteroids are the mainstay of treatment, with immunosuppressive agents reserved for steroid resistant cases. The presence of nephrotic syndrome and FSGS appear to predict adverse outcomes as opposed to favorable outcomes in those with MCD. Further research is needed to establish C1q nephropathy as a universally recognized distinct clinical entity. In this paper, we discuss the current understanding of pathogenesis, histopathology, clinical features, therapeutic options, and outcomes of C1q nephropathy.

Severe granulomatous gastric lesions following migration of Spiroxys contortus larvae (Nematoda: Spirurida) in European pond turtles, Emys orbicularis

The European pond turtle gradually disappeared from most of its range due to various factors. Hence, conservation measures are of main concern in all European countries where it is still present. A decent methodology for assessing the effect of parasites on the health of wildlife is microscopic lesion description. In 2002–2007, eight Emys orbicularis were brought for necropsy. The presence of gastric nematodes, identified as adults and larval Spiroxys contortus was noticed in all the turtles. A discrete cellular infiltrate with mononuclear cells and eosinophils was noticed in the gastric mucosa. The most prominent lesions were severe granulomas with or without degenerated larval structures. Some of the granulomas presented a central area of coagulation necrosis surrounded by giant cells, epithelioid cells and macrophages. In mature granulomas, the cluster of macrophage cell line and necrosis were surrounded by a fibrous capsule. Vascular cuffs, hyperemia, edema and venous ectasia were also present.

Epicatechin Used in the Treatment of Intestinal Inflammatory Disease: An Analysis by Experimental Models

Background. This study was pathway of (−)-epicatechin (EC) in the prevention and treatment of intestine inflammation in acute and chronic rat models.Methods. Intestine inflammation was induced in rats using TNBS. The morphological, inflammatory, immunohistochemical, and immunoblotting characteristics of colon samples were examined. The effects of EC were evaluated in an acute model at doses of 5, 10, 25, and 50 mg/kg by gavage for 5 days. The chronic colitis model was induced 1st day, and treated for 21 days. For the colitis relapse model, the induction was repeated on 14th.Results. EC10 and EC50 effectively reduced the lesion size, as assessed macroscopically; and confirmed by microscopy for EC10. The glutathione levels were higher in EC10 group but decreased COX-2 expression and increased cell proliferation (PC) were observed, indicating an anti-inflammatory activity and a proliferation-stimulating effect. In the chronic colitis model, EC10 showed lower macroscopic and microscopic lesion scores and increase in glutathione levels. As in the acute model, a decrease in COX-2 expression and an increase in PC in EC10, the chronic model this increase maybe by the pathway EGF expression.Conclusion. These results confirm the activity of EC as an antioxidant that reduces of the lesion and that has the potential to stimulate tissue healing, indicating useful for preventing and treating intestine inflammation.

Pathology of Clostridium perfringens Type C Enterotoxemia in Horses

Clostridium perfringens type C is an important cause of enteritis and enterocolitis in foals and occasionally in adult horses. The disease is a classic enterotoxemia, and the enteric lesions and systemic effects are caused primarily by beta toxin, 1 of 2 major toxins produced by C. perfringens type C. Until now, only sporadic cases of C. perfringens type C equine enterotoxemia have been reported. We present a comprehensive description of the lesions in 8 confirmed cases of type C enterotoxemia in foals and adult horses. Grossly, multifocal to segmental hemorrhage and thickening of the intestinal wall were most common in the small intestine, although the colon and cecum were also frequently affected. All horses had variable amounts of fluid, often hemorrhagic intestinal contents. The most characteristic microscopic lesion was necrotizing or necrohemorrhagic enteritis, with mucosal and/or submucosal thrombosis. Numerous gram-positive rods were occasionally seen in affected mucosa. A definitive diagnosis of C. perfringens type C enterotoxemia in all 8 cases was based on the clinical history, gross and histologic lesions, and detection of the beta toxin in intestinal contents.

Harlequin Ichthyosis in Two Greater Kudu (Tragelaphus strepsiceros)

Two greater kudu calves (Tragelaphus strepsiceros) born 7 years apart were found with fissures and thickened, scaly, cutaneous plates covering over 80% of their bodies. One was dead at presentation, and the other was euthanized shortly after birth. Both animals shared a common sire. On necropsy, chemosis, ectropion, eclabium, and bilateral valgus deformities of the tarsal joints were observed in one calf, presumed to be secondary to the plates restricting normal fetal development. The principal microscopic lesion was severe lamellar orthokeratosis, with focal mild parakeratosis. Ultrastructural epidermal lesions included the absence of normal lamellar granules, large dilated endoplasmic reticulum, and abnormal retention of organelles and vesicles. Gross, histopathologic, and electron microscopic findings in both kudu calves were consistent with those of harlequin ichthyosis, a rare dermatosis of humans believed to have an autosomal recessive inheritance pattern. The underlying genetic and molecular abnormality and heritability of this condition in this greater kudu herd were not determined.

Gross and Microscopic Lesions in Porcine Fetuses Infected with Porcine Reproductive and Respiratory Syndrome Virus

Diagnosis of porcine reproductive and respiratory syndrome virus (PRRSV)-induced reproductive failure in swine is difficult because of the rapid inactivation of virus in fetuses that have died prior to abortion or farrowing. In this report, we describe gross and microscopic lesions of diagnostic value found in fetuses transplacentally infected with PRRSV during late gestation. Seven sows free of PRRSV-specific antibody and 1 sow (#8) that had been previously infected with PRRSV were oronasally exposed to a PRRSV inoculum at or about 90 days of gestation (DG). One control sow (#9) was oronasally exposed to a sham inoculum at 90 DG. Sows were euthanized 21 days postexposure, and fetuses were tested for virus. Transplacental infection was detected in litters 1–7, and gross lesions of the umbilical cord were observed in some fetuses in 6 of the 7 litters. No transplacental infection or fetal lesions were found in litters 8 and 9. The gross lesions in the umbilical cords ranged from segmental hemorrhagic areas 1–2 cm in length to a full length involvement of the cord, which was grossly distended with frank hemorrhage. All live fetuses that had gross lesions in the umbilical cord were viremic, and histopathologic examination revealed a necrotizing umbilical arteritis with periarterial hemorrhage. This was the most consistent microscopic lesion in fetuses infected with PRRSV. Sows 1–7 had endometritis and myometritis of various degrees, suggesting PRRSV also may induce these lesions. Careful gross and microscopic examination of the umbilical cord may aid in the diagnosis of PRRSV-induced reproductive failure.

Quantitative Analysis of Alveolar Type II Cell Tumors in Mice by Whole Lung Serial and Step Sections

Alveolar type II cell tumors were induced transplacentally by intraperitoneal injection of pregnant C3H/HeNCr MTV– or Swiss Webster mice with N-nitrosoethylurea at a dose of 0.5 mmol/kg and 0.74 mmol/kg. At different time points after birth (1–32 weeks), the entire lungs from 40 of the male offspring were inflated with Bouin's fixative, separated into lobes, and sectioned at 5 μm serially to detect every microscopic lesion. Results were compared with those obtained from examining only every 10th, 20th, or a single mid-level section from the same material. On average, 150 serial sections were prepared per mouse lung. Initially, only purely solid/alveolar or purely tubulopapillary types were observed but with tumor progression, papillary structures developed within solid tumors resulting in mixed neoplasms. Analyzing mouse lungs in step sections of every 10th section (50–60 μm), 5/238 (2%) of the tumors were missed, in step sections of every 20th section (100–120 μm), 16/238 (7%) of the tumors were not detected and usually less than half of the tumors were seen in the single mid-level section. The approximate size of the neoplasms is indicated by the total number of sections per tumor. The dimensions of tumors evaluated with step sections of 10 or 20 were comparable to the size observed with serial sections. It is concluded that the evaluation of mouse lung tumors in steps of approximately 50 μm is basically equivalent to the study of serial sections and appears to be a feasible method to assess the complete incidence, histological type, and size of all proliferative processes throughout the entire lung.