Congenital cutaneous histiocytosis in a piglet.

A 2-week-old crossbred male piglet with numerous congenital, variably sized macules, plaques, and papules distributed all over the body was submitted for necropsy. Significant gross and histological lesions were restricted to the skin. On light microscopic examination, these cutaneous lesions corresponded to dermal and/or subcutaneous masses composed of spindle-shaped to round cells that multifocally contained hemosiderin; epidermotropism was not observed. Immunohistochemically, the neoplastic cells were strongly positive for CD204; moderately positive for CD163, lysozyme, and vimentin; and negative for Mac 387, α-1-antitrypsin, S-100 protein and E-cadherin; frozen tissues were not available for CD1a and CD11c. Transmission electron microscopic examination of sections from formalin-fixed tissues did not reveal Birbeck's granules. The clinical, morphological, and immunohistochemical results were consistent with a congenital cutaneous histiocytosis of non-Langerhans cell origin. The condition most resembled juvenile xanthogranuloma in humans, a generally skin-limited non-Langerhans histiocytic disorder that can be congenital. Cutaneous and/or systemic histiocytic disorders are well characterized in dogs and have been described in cats, and a case with some similarities to ours has been reported in a neonatal piglet, but this is to our knowledge the first immunohistochemically supported report of histiocytosis in the pig and congenital histiocytosis in animals.

Hypertrophy and hyperplasia of abdominal adipose tissues in women.

OBJECTIVE: To examine the expression of selected transcription factors involved in adipogenesis and genes related to lipid metabolism in abdominal subcutaneous and omental fat tissue. RESEARCH DESIGN AND METHODS: We obtained subcutaneous and omental adipose tissue samples from 40 women undergoing abdominal hysterectomies (age: 47+/-5 years; BMI 27.9+/-5.3 kg/m(2)). We measured isolated adipocyte size and metabolism, and detailed measures of body fat accumulation and body fat distribution were obtained (dual-energy X-ray absorptiometry and computed tomography, respectively). RESULTS: Adipocyte size of both subcutaneous and omental fat were increased with higher body fat mass values, with similar regression slopes in each compartment. In contrast, with higher body fat mass values, fat accumulation was progressively higher in the subcutaneous than in the visceral fat compartment, suggesting hyperplasia in the subcutaneous fat compartment. Messenger RNA levels of CEBPalpha, PPARgamma2, SREBP1c and genes related to lipid metabolism (LPL, FABP4, DGAT1, DGAT2, PLIN and HSL) were significantly higher in subcutaneous than in omental fat tissue (P< or =0.001 for all). Only subcutaneous expression of these genes tracked with obesity levels as reflected by significant positive associations between subcutaneous fat CEBPalpha, SREBP1c and DGAT2 expression and total body fat mass (r=0.37, r=0.41, r=0.57, respectively, P< or =0,05), fat percentage (r=0.40, r=0.39, r=058, respectively, P< or =0,05) and subcutaneous adipose tissue area (r=0.36, r=0.38, r=0.58, respectively, P< or =0,05). Omental adipose tissue expression levels of these genes were not significantly related to adiposity measures. CONCLUSIONS: These results show that in obese women, hyperplasia is predominant in the subcutaneous fat depot, whereas fat cell hypertrophy is observed both in the omental and subcutaneous compartments.

Unique responses to mitochondrial complex I inhibition in tuberoinfundibular dopamine neurons may impart resistance to toxic insult.

Tuberoinfundibular dopamine (TIDA) neurons are spared in Parkinson's disease (PD), a disorder that causes degeneration of midbrain nigrostriatal dopamine (NSDA) and mesolimbic dopamine (MLDA) neurons. This pattern of susceptibility has been demonstrated in acute complex I inhibitor-induced models of PD, and extrinsic factors such as toxin distribution, bioactivation, entry into the cell and sequestration into vesicles are postulated to underlie the resistance of TIDA neurons. In the present experiments, direct exposure to rotenone or 1-methyl-4-phenylpyridinium (MPP+) had no effect on mediobasal hypothalamic TIDA neurons, but significantly increased the percentage of apoptag immunoreactive neurons in midbrain primary NSDA and MLDA cultures. In vivo 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) exposure caused an initial decrease (by 4 h) in dopamine (DA) in brain regions containing axon terminals of TIDA (median eminence [ME]), NSDA (striatum [ST]) and MLDA (nucleus accumbens [NA]) neurons. By 16 h after MPTP treatment, DA concentrations in ME returned to control levels, while ST and NA DA levels remained low up to 32 h after treatment with MPTP. When mice and rats were chronically treated with MPTP and rotenone, respectively, the same pattern of susceptibility emerged. TIDA neurons were unaffected while NSDA neurons suffered loss of cell bodies and axon terminal DA. These experiments demonstrate that the resistance of hypothalamic TIDA neurons is not likely to be due to extrinsic factors, and that further examination of the intrinsic properties of these neurons may elucidate mechanisms that can be translated into neuroprotective strategies in PD.

Tissue- and site-specific gene expression of type 2 17beta-hydroxysteroid dehydrogenase: in situ hybridization and specificenzymatic activity studies in human placental endothelial cells of the arterial system.

Progesterone and estradiol are the most potent human sex steroid hormones of placental origin and are essential to the maintenance of pregnancy, the timing of parturition, the maturation of many fetal organs, and the preparation of the maternal reproductive system. Naturally, regulatory mechanisms must be in place to coordinate the synthesis and inactivation of these two hormones. We have previously shown that the highest levels of type 1 and type 2 17beta-hydroxysteroid dehydrogenase (17betaHSD) messenger ribonucleic acids (mRNAs) occur in the placenta, particularly in the villi. However, in contrast to type 1 17betaHSD mRNA, type 2 17betaHSD mRNA was not detectable in cell cultures of human cytotrophoblasts or syncytiotrophoblasts. Using in situ hybridization, we unequivocally identified endothelial cells as the only cell type expressing the type 2 17betaHSD gene in fetal villi. Moreover, type 2 17betaHSD mRNA was specifically detected in the endothelial cells of the arterial system, and at higher levels in the villi compared with endothelial cells of the cord arteries when the two tissue sections were cohybridized. In fact, both mRNA levels and enzymatic activity are at their highest levels in arterial endothelial cells. In conclusion, the endothelial cells of the villous arterioles are the primary site of type 2 17betaHSD gene expression. This suggests a regulatory role for these cells in the control of progestin, androgen, and estrogen levels during pregnancy, thus opening a whole new way of viewing regionalization and localization of steroidogenesis in the human villi.

Localization of type 1 17beta-hydroxysteroid dehydrogenase mRNA and protein in syncytiotrophoblasts and invasive cytotrophoblasts in the human term villi.

The 17beta-hydroxysteroid dehydrogenases (17beta-HSDs) play a key role in the synthesis of sex steroids. The hallmark of this family of enzymes is the interconversion, through their oxydoreductive reactivity at position C17, of 17-keto- and 17beta-hydroxy-steroids. Because this reaction essentially transforms steroids having low binding activity for the steroid receptor to their more potent 17beta-hydroxysteroids isoforms, it is crucial to the control of the physiological activities of both estrogens and androgens. The human placenta produces large amounts of progesterone and estrogens throughout pregnancy. The placental type 1 17beta-HSD enzyme (E17beta-HSD) catalyzes the reduction of the low activity estrogen, estrone, into the potent estrogen, estradiol. We studied the cell-specific expression of type 1 17beta-HSD in human term placental villous tissue by combining in situ hybridization to localize type 1 17beta-HSD mRNA with immunohistochemistry using an antibody against human placental lactogen, a trophoblast marker. Immunolocalization of E17beta-HSD was also performed. To ascertain whether other steroidogenic enzymes are present in the same cell type, cytochrome P450 cholesterol side-chain cleavage (P450scc), P450 aromatase, and type 1 3beta-hydroxysteroid dehydrogenase (3beta-HSD) were also localized by immunostaining. Our results showed that the syncytium is the major steroidogenic unit of the fetal term villi. In fact, type 1 17beta-HSD mRNA and protein, as well as P450scc, P450 aromatase, and 3beta-HSD immunoreactivities were found in these cells. In addition, our results revealed undoubtedly that extravillous cytotrophoblasts (CTBs), e.g. those from which cell columns of anchoring villous originate, also express the type 1 17beta-HSD gene. However, CTBs lying beneath the syncytial layer, e.g. those from which syncytiotrophoblasts develop, contained barely detectable amounts of type 1 17beta-HSD mRNA as determined by in situ hybridization. These findings, along with those from other laboratories confirm the primordial role of the syncytium in the synthesis of steroids during pregnancy. In addition, our results indicate for the first time that CTBs differentiating along the invasive pathway contain type 1 17beta-HSD mRNA.

Spontaneous glomerulonephritis in swine.

In this investigation, 32 cases of naturally occurring glomerulonephritis in swine were studied retrospectively (1973-1993). Almost all affected pigs were crossbred and more than half were growing pigs. Nearly two thirds of the pigs showed gross renal lesions characterized by bilateral kidney enlargement, palor, edema, and/or cortical petechiation. The most commonly encountered extrarenal lesions were serous bodily effusions and gastric ulcers. The renal disease was considered the primary cause of death in 11 pigs. Histologically, the renal lesions in all pigs were characterized by a generalized and global proliferative glomerulonephritis. Mesangioproliferative glomerulonephritis was diagnosed in 2 pigs, whereas the glomerular lesions found in the other pigs (30/32) were characterized by a proliferative and exudative glomerulonephritis frequently associated with crescent formation. In all pigs, there was histologic evidence of proteinuria. A focal necrotizing vasculitis was found in the kidneys of 7 pigs. Although probably of immune origin, the precise etiopathogenesis of the porcine glomerulonephritis described herein after remains unknown.

The evaluation of postmortem ocular fluid analysis as a diagnostic aid in sows.

This study was undertaken to evaluate the diagnostic usefulness of postmortem ocular fluid analysis in estimating the antemortem status of various serochemical constituents. Chemical values of serum and aqueous and vitreous humors were compared following different procedures. A blood sample and the 2 eyes were collected from each of 100 sows at a nearby abattoir. The results obtained from immediate centrifugation of ocular fluids after sampling were compared with those samples in which centrifugation was delayed by 2 hours. Two different postmortem intervals were used for sampling ocular fluids, 2 and 24 hours. Concentrations of urea, calcium, phosphorus, potassium, sodium, and chloride were determined from serum and humors. Delayed centrifugation did not affect chemical values of ocular fluids nor the relationships between serum and humors. Phosphorus and potassium values increased significantly with the postmortem interval in both aqueous and vitreous humors. The relationships between chemical values of ocular fluids and serum were determined using simple linear regression. There was a poor correlation between ocular fluid and serum values for all electrolytes; a significant correlation was found only for urea concentrations in both humors.

Equine proliferative enteropathy: a cause of weight loss, colic, diarrhoea and hypoproteinaemia in foals on three breeding farms in Canada.

Proliferative enteropathy (PE) is a transmissible enteric disease caused by Lawsonia intracellularis. An outbreak of equine PE was diagnosed in foals from 3 breeding farms. Most foals had been weaned prior to the appearance of clinical signs, which included depression, rapid and marked weight loss, subcutaneous oedema, diarrhoea and colic. Poor body condition with a rough haircoat and a potbellied appearance were common findings in affected foals. Respiratory tract infection, dermatitis and intestinal parasitism were also found in some foals. Haematological and plasma biochemical abnormalities included hypoproteinaemia, transient leucocytosis, anaemia and increased serum creatinine kinase concentration. Postmortem diagnosis of PE was confirmed on 4 foals based on the presence of characteristic intracellular bacteria within the apical cytoplasm of proliferating crypt epithelial cells of the intestinal mucosa, using silver stains, and by results of PCR analysis and immunohistochemistry. Antemortem diagnosis of equine PE was based on the clinical signs, hypoproteinaemia and the exclusion of common enteric infections. Faecal PCR analysis was positive for the presence of L. intracellularis in 6 of 18 foals tested while the serum of all 7 foals with PE serologically evaluated had antibodies against L. intracellularis. Most foals were treated with erythromycin estolate alone or combined with rifampin for a minimum of 21 days. Additional symptomatic treatments were administered when indicated. All but one foal treated with erythromycin survived the infection. This study indicates that equine PE should be included in the differential diagnosis of outbreaks of rapid weight loss, diarrhoea, colic and hypoproteinaemia in weanling foals.

A quantitative study of cardiac ventricular mass in dogs.

This study was undertaken to determine the correlations between heart weight, ventricular weight and body weight in adult dogs. A total of 130 dogs was selected for the study after necropsy and histological examination. The body weights (BW) were obtained and a standardized dissection technique was used to obtain the total heart weight (HW), total ventricular mass (VW), right ventricular mass (RvW) and the left ventricular plus the interventricular septum mass (Lv + SW). A strong and significant correlation was found between all variables (BW, HW, VW, Lv + SW and RvW). The following ratios were calculated: HW/BW, RvW/BW, Lv + SW/BW, RvW/VW, Lv + SW/VW, RvW/HW, Lv + SW/HW and Lv + SW/RvW. No sex effect was observed on any ratios. A straight linear relationship was observed between HW and Lv + SW or RvW and between Lv + SW and RvW. The ratios Lv + SW/HW, RvW/HW and Lv + SW/RvW could then be used to predict a normal value of Lv + SW or RvW from a known HW value, or a normal value of Lv + SW from a known RvW value. The relations between BW and HW, Lv + SW or RvW were best described by second order equations. Such equations should be utilized to predict a normal value of HW, Lv + SW or RvW from a known BW value.

A prospective study of sow mortality in breeding herds.

This investigation was conducted to study the incidence and the causes of sow mortality in breeding herds. Data were obtained from 24 swine breeding herds with an average inventory of 3755 sows and served gilts for the total sample. Producers were involved for 12 consecutive months and agreed to submit to the diagnostic laboratory every dead or moribund sow and served gilt. The average herd death rate was 3.3% +/- 0.5 (SEM), but varied considerably among herds, ranging from 0% to 9.2%. A total of 137 sows and mated gilts died during the year, and these females had produced an average of 4.2 litters +/- 0.2 (SEM). The number of deaths was significantly higher during the months of July, August and October. The peripartum period appeared to be when sows were most at risk, with 42% of all deaths occurring during this short period of the reproductive cycle. The three major causes of death were heart failure (31.4%), torsions and accidents of abdominal organs (15.3%) and cystitis-pyelonephritis (8.0%). Other causes included endometritis (6.6%), uterine prolapses (6.6%), pneumonia (3.6%), gastric ulcers (3.6%), downer sow syndrome (2.2%), miscellaneous (8.0%) and unknown (14.6%).

Attaching and effacing and enterotoxigenic Escherichia coli associated with enteric colibacillosis in the dog.

The objective of this study was to describe observations from cases of enteric colibacillosis in the dog. Thirteen cases of canine enteric colibacillosis were diagnosed from routine necropsy submissions to our diagnostic laboratory from 1980 to 1992. In all cases there was a clinical history of gastrointestinal disease associated with histological and bacteriological evidence of either attaching and effacing Escherichia coli (AEEC) or enterotoxigenic Escherichia coli (ETEC) infection. Of these 13 cases of enteric colibacillosis, 12 were associated with AEEC and one with ETEC. Eight of the 12 AEEC isolates were available for study. They were of various serogroups, non-hemolytic, and negative for the genes coding for fimbrial antigens F4, F5, F6, F41 and F165; enterotoxins STap, STb and LT; and verotoxins VT1 and VT2. These eight isolates were EAE-positive (E. coli attaching and effacing) by colony hybridization; six of these were also EAF-positive (EPEC adherence factor), and six were BFP-positive (bundle-forming pilus). The ETEC isolate was negative for the EAE, EAF and BFP determinants and for the fimbrial antigens tested but was positive for the STap and STb genes. Most of the dogs affected with enteric colibacillosis originated from kennels and pet shops and were aged between 1.5 and 3 months. Coinfection with other enteric pathogens was identified in eight of these 13 cases. This study showed that Escherichia coli should be considered of causal significance when investigating diarrheal disease in dogs, particularly in puppies.

Natural infection with an attaching and effacing Escherichia coli in a diarrheic puppy.

Enteric infection with an attaching and effacing Escherichia coli was diagnosed in a puppy with protracted diarrhea. Extensive colonization of the small intestinal mucosa was observed by light and scanning electron microscopy and characteristic lesions of bacterial attachment of the brush border of the enterocytes were demonstrated by transmission electron microscopy. The E. coli strain isolated from the small intestine belonged to serotype O49:H10, did not produce any known E. coli enterotoxin or cytotoxin, was not invasive, and was negative for the known fimbrial colonization factors produced by animal and human enterotoxigenic E. coli. A positive immunoperoxidase reaction was obtained on the bacteria attached to the enterocytes with an anti-E. coli O49 antiserum.

Disseminated tuberculosis caused by Mycobacterium avium in a cat.

A 5-year-old neutered male Siamese cat was examined by a veterinarian because of a recent decrease in appetite and a large lymph node in the left mandibular area. Clinical findings included fever, icterus, leukopenia, and progressive anemia. Despite various treatments, the cat died approximately 3 weeks after initial examination. The main necropsy findings included necrotizing and granulomatous lymphadenitis of the left mandibular lymph node, multifocal necrotizing hepatitis, and interstitial pneumonia. Acid-fast bacilli were detected in lesions of the mandibular lymph node, liver, lung, spleen, and bone marrow. Mycobacterium avium was isolated from the liver. Avian tuberculosis in cats has been reported rarely.

Bilateral epiphysiolysis of the femoral heads in two dogs.

Two Shetland Sheepdogs that did not have a history of trauma were referred because of a gradual onset of lameness in the hind limbs. Bilateral slipped capital femoral epiphysis was diagnosed. Separation of the proximal femoral epiphysis that is not associated with trauma is recognized as a distinct clinical syndrome in adolescent human beings and swine, causing a condition called epiphysiolysis. The precise cause of this type of injury is unknown. Histologic lesions observed in the growth plates could have been the result of an abnormally high mechanical load imposed by obesity. It is not known whether cartilaginous lesions observed in the physis of 1 dog represented a preexisting cartilaginous defect (dyschondroplasia) or a late stage of repair after separation of the capital femoral epiphysis.

Cacao bean shell poisoning in a dog.

Cacao bean shells contain potentially toxic quantities of theobromine, a xanthine compound similar in effects to caffeine and theophylline. A dog, which ingested a lethal quantity of garden mulch made from cacao bean shells, developed severe convulsions and died 17 hours later. Analysis of the stomach contents and the ingested cacao bean shells revealed the presence of lethal amounts of theobromine.

Isolation of group eugonic fermenter-4 bacteria from a cat with multifocal suppurative pneumonia.

A pure growth of Group Eugonic Fermenter-4 bacteria (gram-negative) was isolated from the lungs of an 11-year-old male domestic cat that had been ill for 2 days before death. Clinical signs included anorexia, severe dyspnea, and salivation. The lungs contained several firm, slightly raised, yellowish-gray, spherical nodules of various sizes. Purulent exudate was found in the pericardial sac and left pleural cavity. Histologic evaluation revealed multifocal suppurative pneumonia.

Optimizing longevity in sows and boars.

Longevity of sows and boars affects the productivity and economics of the herd. Implement a culling program that is tailored to the specific needs of the producer and the characteristics of the farm. Evaluate the removal policies regularly, estimate the longevity of breeding animals, calculate the nonproductive sow days associated with culling, and determine the major causes of culling and death. Once a longevity problem and its extent have been identified, the underlying problems and predisposing factors can be more easily corrected.

Infectious agents identified in pigs with multifocal interstitial nephritis at slaughter.

One kidney was taken from each of 100 pigs at slaughter; 50 had gross lesions of multifocal interstitial nephritis and 50 had no gross lesions. Forty-nine of the affected kidneys had lesions that were characterised by the presence of either a few randomly distributed or numerous widely disseminated pale foci, 1 to 3 mm in diameter, on the cortical surface (white-dotted kidneys). Microscopically, these focal inflammatory lesions often had a distinct lymphofollicular pattern (follicular nephritis). Lesions of chronic vasculitis were observed in 21 of the affected kidneys. Histologically, the control kidneys had only small and sparse inflammatory foci. Standard bacterial cultures of kidneys of both groups were not significant, and cultures for the isolation of leptospires were all negative. Virological examination of the kidney homogenates by PCR did not reveal any porcine reproductive and respiratory syndrome virus and only a few cases were positive for the porcine circovirus type 1. However, porcine parvovirus (PPV) and porcine circovirus type 2 (PCV-2) were detected in many kidneys of both groups but in a significantly higher proportion of the kidneys with interstitial nephritis. There was a significant association between the lesions and the presence of PPV and PCV-2 with odds ratios of 7.5 (P<0.0001) and 3.4 (P=0.0074), respectively, and the odds ratio increased to 22.7 (P<0.0001) when both viruses were identified in the same kidney. However, a subsample of kidneys taken from both groups were negative by immunohistochemistry for the presence of PPV and PCV-2 antigens.

Hemorrhagic gastroenteritis caused by Escherichia coli in piglets: Clinical, pathological and microbiological findings.

A retrospective study (1980-1989) was conducted to describe the clinical, pathological, and bacteriological findings in 55 cases of hemorrhagic gastroenteritis (HGE) caused by Escherichia coli in piglets. The condition occurred in weaned and suckling piglets and was associated with several serogroups of E. coli. Most of the isolates of E. coli possessed the adhesin F4 (K88) and were hemolytic. Only a few of the isolates of E. coli tested produced verotoxins. Clinical signs and pathological findings noted in these cases were compatible with shock.

Plasma cell pododermatitis in a cat.

Plasma cell pododermatitis, an uncommon disease of unknown etiology, is described in a six year old male domestic short-haired cat. The cat was referred with a history of lameness associated with swelling, softness and ulceration of the foot pads. The history suggested a seasonal occurrence of the condition. The dermis and subcutis of the foot pads were infiltrated by inflammatory cells which were mainly plasma cells. The large number of plasma cells present in the lesions suggests an immunological basis for the condition.