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Spontaneous diabetes mellitus in young cattle: histologic, immunohistochemical, and electron microscopic studies of the islets of Langerhans.

Pathomorphologic studies were carried out on three cases of bovine diabetes mellitus with clinical signs of polydipsia, polyuria, severe emaciation, glycosuria, persistent hyperglycemia, and decreased glucose tolerance. At necropsy, two animals had atrophy of the pancreas, whereas other visceral organs, including the endocrine organs, showed no significant changes. Microscopically, there was atrophy and reduced numbers of pancreatic islets accompanied by interlobular and interacinar fibrosis and compensatory enlargement of some remaining islets. Lymphocytes were observed commonly around and within atrophic islets and occasionally around and within enlarged islets. Vacuolar degeneration with occasional accumulation of glycogen granules was observed in the beta-cells of these enlarged islets. Immunohistochemical studies of atrophic islets demonstrated complete loss of beta-cells or only a few small beta-cells. There also was a corresponding decrease in the number of cells that stained with anti-glucagon (alpha-cells) or anti-somatostatin (delta-cells) antibodies. The vacuolated cells in the enlarged islets stained strongly with anti-insulin antibody (beta-cells). Ultrastructurally, the majority of cells in the atrophic islets had reduced cytoplasmic volume and few secretory granules, features consistent with alpha-cells. In contrast, enlarged islets that had prominent immunohistochemical staining for insulin (beta-cells) consisted of beta-cells with cytosolic edema, mitochondrial swelling, dilated smooth endoplasmic reticulum, and reduced numbers of or degranulated secretory granules. These pathomorphologic features found in cattle are similar to those found in juvenile-onset insulin-dependent diabetes mellitus in human beings and suggest autoimmune involvement in diabetes.

Animals↗

Nursing disease in mink: clinical and postmortem findings.

One hundred fifty lactating mink on one ranch in southern Ontario were monitored over the lactation period in 1989 for evidence of clinical disease, and serial blood samples were collected for biochemical analysis. Antemortem blood samples were collected and necropsies performed on the 17 females that developed nursing disease and on 17 controls matched to the same stage of lactation and on ten nonlactating controls. Twenty-two additional nursing disease cases were selected from seven ranches in the following year and processed similarly. The clinical signs typically observed in affected females were sudden onset lethargy and anorexia followed by dehydration, ataxia, and a reluctance to move. The major clinical-pathologic findings were a marked increase in serum osmolality and total protein, urea nitrogen, creatinine, phosphorus, glucose, and potassium concentrations and a decrease in sodium and chloride concentration. In addition, the animals were acidotic, there was a reduction in the urine specific gravity, and the hemogram was consistent with a stress response. Emaciation and dehydration were the only pathologic changes consistently present in cases of nursing disease and not in controls. In almost all cases, bacteria were not cultured from the liver, spleen, and mammary gland, but Campylobacter jejuni was cultured from the intestinal contents of 15/17 affected mink and 2/5 controls. Aleutian disease virus antibody was not present in any of the affected mink. Lipid vacuoles in hepatocytes and renal tubular epithelium, hypertrophy of cells in the adrenal cortex, and pulmonary congestion and atelectasis were present in both diseased females and controls, as were various sporadic inflammatory lesions. Nursing disease may result from energy depletion due to lactation. All lactating females are affected by this process; clinical disease reflects the terminal physiologic decompensation of the most susceptible individuals.

Adrenal Cortex↗

Spontaneous diabetes mellitus associated with persistent bovine viral diarrhea (BVD) virus infection in young cattle.

Histologic and immunohistochemical studies were carried out on four young cattle with diabetes mellitus associated with persistent bovine viral diarrhea (BVD) virus infection. Clinical findings included persistent hyperglycemia, decreased glucose tolerance, glycosuria, polydipsia, and severe emaciation. Macroscopically, multiple erosions and ulcers in the mucosa of upper and lower alimentary tracts and swollen lymph nodes were commonly observed. Erosions and ulcers in the mucosa of tongue, esophagus, and forestomach were represented histologically by necrosis of squamous epithelium with neutrophilic infiltration. In the small and large intestines, villous atrophy and suppurative cryptitis were often observed, along with diffuse infiltration of lymphocytes and macrophages and fibroplasia in the lamina propria. In the pancreas of all cattle, there was a reduction in the number of islet cells, and most of the residual islet cells had hydropic degeneration and a decreased number of secretory granules. Immunohistochemical examination confirmed that these cells were severely degranulated beta-cells. In addition, many islets containing necrotic islet cells were observed. These islet cells had increased eosinophilia and shrinkage of cytoplasm, as well as pyknotic nuclei. Inflammation of the islets with mild infiltration of lymphocytes was observed in all pancreatic lobes. In addition, bovine IgG-immunoreactive cells were identified immunohistochemically in the affected pancreatic islets. The BVD virus antigen was not identified in the cytoplasm of the islet cells by immunohistochemical study, although it was identified in the epithelial cells of the small intestine. The histologic and immunohistochemical studies demonstrated that the pancreatic lesions in these animals were similar to those caused by acute insulin-dependent diabetes mellitus (IDDM) in human beings.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Glycogen storage disease type Ia in two littermate Maltese puppies.

Glycogen storage disease type Ia (GSD-Ia) (von Gierke's disease) was identified in two 47-day-old littermate Maltese puppies. The puppies were presented for necropsy with a history of failure to thrive, mental depression, and poor body condition. Gross findings included small body size and emaciation (212 and 246 g versus 595 g for normal littermate), severely enlarged pale livers (48 and 61 g), and pale kidneys. Histologically, there was marked diffuse vacuolation of hepatocytes with large amounts of glycogen and small amounts of lipid. Renal tubular epithelium was mildly to moderately vacuolated. Soft tissue mineralization was present in renal tubules and pulmonary alveolar septa. Biochemical analysis showed that levels of glucose-6-phosphatase were markedly reduced in liver (0.3 and 0.4 microM/minute/g tissue versus 4.7 +/- 1.5 microM/minute/g tissue for controls) and kidney (0.45 and 0.4 microM/minute/g tissue versus 4.1 microM/minute/g tissue for controls) and that glycogen content was increased in liver (9.4% and 9.4% versus 1.3% +/- 1.4% for controls). This is the first confirmed report of animals with glycogen storage disease type Ia.

Animals↗

Systemic adenovirus infection associated with high mortality in mule deer (Odocoileus hemionus) in California.

Seventeen counties in northern California experienced epizootics of high mortality in the mule deer (Odocoileus hemionus) population during the latter half of 1993. Thirteen deer submitted to the California Veterinary Diagnostic Laboratory System as part of this natural die-off had systemic adenovirus infection. Pulmonary edema was present in all 13 deer. Erosions, ulceration, and abscessation of the upper alimentary tract occurred in 7/13 deer. Four of 13 deer had hemorrhagic enteritis. All 13 deer had widespread systemic vasculitis with endothelial intranuclear inclusions. Fluorescein isothiocyanate-labeled antibody directed against bovine adenovirus type 5 bound to antigen in endothelial cells. Adenovirus was identified by transmission electron microscopy within the nuclei of endothelial cells in 6/6 deer examined. An adenovirus was isolated from lung homogenates of one deer that were cultured on black-tailed deer pulmonary artery endothelial cells. With the exception of the intranuclear inclusions evident on histologic evaluation, gross and histologic changes were similar to those described for bluetongue virus infection and epizootic hemorrhagic disease virus infection in white-tailed deer. Nine additional deer were emaciated and had pharyngeal abscesses with focal vasculitis, which may represent the chronic affects of previous nonfatal adenovirus infection.

Adenoviridae↗

Histopathologic and ultrastructural alterations of white liver disease in sheep experimentally depleted of cobalt.

Many cobalt-deficient sheep develop liver lesions known as ovine "white liver" disease, but the etiology of these changes is controversial. It has been suggested that cofactors are required for development of liver damage in cobalt-deficient sheep. In this study, one group of lambs (n = 5) was fed a diet low in cobalt (4.5 micrograms/kg) while a group of control lambs (n = 4) received the same diet after it had been supplemented with cobalt (1000 micrograms/kg). All cobalt-depleted lambs had reduced growth rate, anorexia, lacrimation, and alopecia, and they eventually became emaciated (mean body weight at end of study: 83% of initial body weight). Plasma concentrations of bilirubin and serum activity of glutamate-oxaloacetate transferase were elevated in these animals, while plasma concentrations of vitamin B12 were reduced (less than 220 pmol/L from day 42). Fatty degeneration of the liver associated with reduced concentrations of vitamin B12 (14.5 pmol/g) was seen in these animals at necropsy at 196 days. Microscopic liver lesions included accumulation of lipid droplets and lipofuscin particles in hepatocytes, dissociation and necrosis of hepatocytes, and sparse infiltration by neutrophils, macrophages, and lymphocytes. Ultrastructural hepatocytic alterations included swelling, condensation and proliferation of mitochondria, hypertrophy of smooth endoplasmic reticulum, vesiculation and loss of arrays of rough endoplasmic reticulum, and accumulation of lipid droplets and lipofuscin granules in cytoplasm of hepatocytes. No liver lesions were seen in control lambs. The results of this study indicate that cofactors are not a prerequisite to development of hepatic damage in cobalt-deficient sheep. Reduced activities of the vitamin B12-dependent enzymes, methylmalonyl CoA mutase and methionine synthase, and lipid peroxidation are of likely pathogenetic importance in the development of the lesions.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗

Preliminary findings on the experimental transmission of chronic wasting disease agent of mule deer to cattle.

To determine the transmissibility of chronic wasting disease (CWD) to cattle and to provide information about clinical course, lesions, and suitability of currently used diagnostic procedures for detection of CWD in cattle, 13 calves were inoculated intracerebrally with brain suspension from mule deer naturally affected with CWD. Between 24 and 27 months postinoculation, 3 animals became recumbent and were euthanized. Gross necropsies revealed emaciation in 2 animals and a large pulmonary abscess in the third. Brains were examined for protease-resistant prion protein (PrP(res)) by immunohistochemistry and Western blotting and for scrapie-associated fibrils (SAFs) by negative-stain electron microscopy. Microscopic lesions in the brain were subtle in 2 animals and absent in the third case. However, all 3 animals were positive for PrP(res) by immunohistochemistry and Western blot, and SAFs were detected in 2 of the animals. An uninoculated control animal euthanized during the same period did not have PrP(res) in its brain. These are preliminary observations from a currently in-progress experiment. Three years after the CWD challenge, the 10 remaining inoculated cattle are alive and apparently healthy. These preliminary findings demonstrate that diagnostic techniques currently used for bovine spongiform encephalopathy (BSE) surveillance would also detect CWD in cattle should it occur naturally.

Animals↗

Paratuberculosis in a mandrill (Papio sphinx).

A 2.5-year-old captive female mandrill (Papio sphinx) died following a protracted course of intermittent abdominal bloat, diarrhea, and severe weight loss. Necropsy revealed emaciation and marked gastrointestinal distention with gas and ingesta. Histologic evaluation revealed severe diffuse granulomatous enterocolitis and mesenteric lymphadenitis with massive numbers of 1-2-microm acid-fast bacilli within macrophages. Additionally, there was moderate to severe multifocal myocardial and vascular amyloidosis, moderate multifocal pyogranulomatous interstitial pneumonia with no acid-fast bacteria, and moderate multifocal glossal candidiasis. Samples of feces, ileum, and colon were positive for Mycobacterium avium subsp. paratuberculosis by radiometric culture and a polymerase chain reaction-amplified DNA probe specific for the insertion sequence IS900 of this organism.

Animals↗

Plasma cell myeloma producing IgG, IgM, and IgA immunoglobulins in a cow.

A diagnosis of plasma cell myeloma was made in a 6-year-old Holstein cow that showed continuous nosebleed, progressing emaciation, and hyperglobulinemia. Necropsy revealed enlargement of the caudal mesenteric lymph nodes. Lymph nodes and spleen were infiltrated by neoplastic plasma cells. Renal lymph nodes, bone marrow, and kidneys also were affected. Amyloid-like material that was negative for Congo red was present in most of the affected lymph nodes. Congo red-positive amyloid material was noted in spleen, kidneys, liver, and adrenal glands. Neoplastic plasma cells exhibited immunohistochemical reactions for lambda-light chain and 3 classes of heavy chain but not for kappa-light chain. Nonamyloid deposits were labeled with antisera against lambda-light chain and heavy chains. Plasmacytoid cells, which stained positively for IgG, IgM, or IgA, were intermingled in all lesions. Production of 3 types of immunoglobulins may be caused by heavy-chain class switching, constantly occurring in certain proportions.

Animals↗

Surveillance of amyloidosis and other diseases at necropsy in captive trumpeter swans (Cygnus buccinator).

The purpose of this study was to characterize the incidence and diagnostic features of amyloidosis and other diseases found at necropsy in captive trumpeter swans (Cygnus buccinator). A search of Iowa State University's Department of Veterinary Pathology and Veterinary Diagnostic Laboratory databases yielded 31 trumpeter swan (C. buccinator) necropsy cases from captive swans in protected habitats. Eleven of the 31 birds had amyloid deposition most commonly in the spleen (8 of 11), liver (7 of 11), and kidney (6 of 11) and less often in the pancreas (2 of 11) and adrenal gland (2 of 11). Amyloid deposition effaced normal tissue with adjacent necrosis and hemorrhage in severe cases. Amyloidosis was most often diagnosed in February and March. Other disease diagnoses in the trumpeter swans included aspergillosis (5 of 31, 16%); bacterial infection (5 of 31, 16%); lead toxicosis (3 of 31, 10%); gout (2 of 31, 6%); parasitic infection (2 of 31, 6%); vitamin E deficiency (1 of 31, 3%); trauma (1 of 31, 3%); and ventricular foreign body (1 of 31, 3%). Histopathologic, toxicologic, and microbiologic analyses did not define an etiologic diagnosis in the deaths of 9 trumpeter swans. In these cases, necropsy lesions included emaciation (5 of 9), enteritis (1 of 9), pulmonary hemorrhage (1 of 9), and no lesions (3 of 9). The number of trumpeter swan case submissions was greatest in January and February. This study provides a reference for veterinary diagnosticians concerning incidence and diagnostic features of amyloidosis and other diseases in captive trumpeter swans of the midwestern United States.

Amyloidosis↗

Erysipelothrix rhusiopathiae septicemia in a Laughing kookaburra (Dacelo novaeguineae).

Erysipelothrix rhusiopathiae (E. rhusiopathiae) septicemia was demonstrated in a captive Laughing kookaburra (Dacelo novaeguineae). The bird died after a 2-week period of weakness and weight loss. At necropsy, the bird was emaciated and had reddened and wet lungs. Microscopic lesions were limited to hepatic and pulmonary congestion with focal thrombosis. Erysipelothrix rhusiopathiae was isolated by routine bacterial culture from several organs. Further characterization of the isolate by pulsed-field gel electrophoresis indicated that the isolate has a new genotype pattern 3A(III), which is 91.7% homologous to an E. rhusiopathiae that was isolated from a pig in 2001 and 88% homologous to an isolate recovered in 2000 from a turkey with septicemia. This is the first report of E. rhusiopathiae-induced septicemia in a kookaburra.

Animals↗

Canine leishmaniasis caused by Leishmania leishmania infantum in two Labrador retrievers.

Canine leishmaniasis, a generally fatal parasitic disease, was diagnosed in 2 dogs with a medical history of foreign travel, lymphadenopathy, emaciation, anorexia, intermittent fever, and cutaneous lesions. Clinically, hyperproteinemia, proteinuria, azotemia, and glomerulopathy were evident. Isolation of Leishmania species was done using Schneider's Drosophila medium. Syrian hamsters were used for infectivity studies. Clear taxonomic identification was done biochemically by isoenzyme analysis and comparison of zymogram banding patterns with 6 World Health Organization reference strains. Based on the geographic origin of affected dogs, clinicopathologic presentation, visceralization with hepatosplenomegaly in hamsters, and isoenzyme analysis, a diagnosis of Leishmania leishmania infantum was made. This study, representing the first taxonomic identification of an isolate from canine leishmaniasis, demonstrates the zoonotic and epidemiologic implications of this disease.

Animals↗

Outbreaks of yersiniosis caused by Yersinia pseudotuberculosis in farmed cervids.

Yersiniosis, caused by Yersinia pseudotuberculosis, was diagnosed in 25 deer submitted to the Veterinary Diagnostic Laboratories of the Ontario Ministry of Agriculture and Food from 8 farms in Ontario, Canada, over the 4-year period of January 1990 to December 1993. The organism was cultured, usually in large numbers, from the intestines and, less frequently, mesenteric lymph nodes and/or the spleen of 13 red deer (Cervus elaphus), 6 elk (C. e. canadiensis), 4 fallow deer (Dama dama), and 2 red deer-elk hybrids. Outbreaks occurred almost exclusively in the fall (September-November) and affected recently weaned calves, 4-6 months old. Sudden death usually signalled the start of an outbreak. Outbreaks often occurred during inclement weather; usually a sudden cold snap, with or without rain, after a period of relatively mild fall weather. At necropsy, the animals were usually emaciated and dehydrated, and the perineum and tail were sometimes fecally stained. The small and large intestines were congested and filled with serofibrinous and/or seroanguineous fluid. Mesenteric lymph nodes were edematous and congested. Microabscesses surrounding large bacterial colonies in the lamina propria in the jejunum and ileum were typical lesions seen histologically. Peyer's patches were depleted and sometimes contained microabscesses. Purulent lymphadenitis associated with bacterial colonies was the prominent histologic lesion in mesenteric lymph nodes.

Animals↗

Electroencephalographic correlates of compulsive eating.

Fifty-nine compulsive eaters were interviewed, had a complete waking and sleep EEG tracing, and were offered a trial with phenytoin. Forty-seven patients had an adequate pharmacological intervention. Analyses of the EEGs showed a disproportionately higher percentage of abnormal EEGs and of paroxysmal EEGs in particular among compulsive eaters as contrasted with unselected psychiatric patients and normal controls. Patients with abnormal EEGs responded to phenytoin treatment statistically more frequently than those with normal EEGs--even after conservatively classifying "uncertain" patients as non-responders. Patients with 14 & 6/sec. positive spikes alone showed a phenytoin improvement significantly greater than that seen with either normal EEG subjects or other EEG abnormalities. There are suggestions of a weight by EEG interaction in that the combination of weight deviance (viz: emaciated or obese) plus abnormal EEG seems especially highly predictive of good phenytoin response. The EEG results combined with phenytoin response suggest that neurophysiological etiological hypotheses may have merit for some compulsive eating disorders. Suggestions for additional research are made and the need for controlled replication of these data results is stressed.

Adult↗

Zn, Cu, Cd and Hg binding to metallothioneins in harbour porpoises Phocoena phocoena from the southern North Sea.

BACKGROUND: Harbour porpoises Phocoena phocoena from the southern North Sea are known to display high levels of Zn and Hg in their tissues linked to their nutritional status (emaciation). The question arises regarding a potential role of metallothioneins (MTs) with regard to these high metal levels. In the present study, metallothionein detection and associated Zn, Cd, Cu and Hg concentrations were investigated in the liver and kidney of 14 harbour porpoises collected along the Belgian coast. RESULTS: Metallothioneins seemed to play a key role in essential metal homeostasis, as they were shown to bind 50% of the total hepatic Zn and 36% of the total hepatic Cu concentrations. Renal MTs also participated in Cd detoxification, as they were shown to bind 56% of the total renal Cd. Hg was mainly found in the insoluble fraction of both liver and kidney. Concomitant increases in total Zn concentration and Zn bound to MTs were observed in the liver, whereas Zn concentration bound to high molecular weight proteins remained constant. Cu, Zn and Cd were accumulated preferentially in the MT fraction and their content in this fraction increased with the amount in the hepatocytosol. CONCLUSION: MTs have a key role in Zn and Cu homeostasis in harbour porpoises. We demonstrated that increasing hepatic Zn concentration led to an increase in Zn linked to MTs, suggesting that these small proteins take over the Zn overload linked to the poor body condition of debilitated harbour porpoises.

Animals↗

Case report of 5 siblings: malnutrition? Rickets? DiGeorge syndrome? Developmental delay?

BACKGROUND: Parents of six children are facing a trial on charges of aggravated manslaughter in the care a 5 1/2 month old infant who died suddenly and neglect of their four older children for causing them to be malnourished by feeding them all an exclusively raw foods vegan diet. Both parents declined plea bargains and plan to defend themselves in court. CASE PRESENTATION: The fifth child born to a married couple was breast-fed until 2 1/2 months. Subsequently, the parents fed the baby an exclusively raw foods diet prepared in a blender at home. The four older children, ages 18 months-6 1/2 years also ate an exclusively raw foods vegan diet. None of the four older children had significant previous injuries or serious illnesses. At autopsy, the infant weighed 3180 mg (6.99 pounds) and appeared emaciated. The thymus gland was absent and parathyroid glands were not located. The lungs were "congested." DiGeorge anomaly cannot be ruled out from these findings. Although, the coroner ruled that "malnutrition" was the sole cause of death, malnutrition, according to the World Health Organization definition, cannot be diagnosed in this infant. Compared with standard growth charts, the older children fell 2.1-4.1 standard deviations below the mean for North American children in height and weight. Labs were normal except for a low cholesterol level in all and a low prealbumin in one of three children tested. Therefore, malnutrition cannot be diagnosed in these children. The pediatrician diagnosed rickets in the four-year-old. However, chest x-rays were normal in all and long bone x-rays showed minimal changes in one child--no sign of rickets. The clinical diagnosis of rickets was not confirmed by the Center for Disease Control's criteria. A psychologist diagnosed the 18-month-old as developmentally delayed to the level of a 15-month-old, but this diagnosis is questionable. CONCLUSION: The raw foods vegan diet and possibly inherited small stature from the father's side account for their relatively low heights and weights. Catch-up growth will probably occur on the standard American diet but would have also been expected if they had remained on a vegan diet.

Body Height↗

Disturbances in body image estimation as related to other characteristics and outcome in anorexia nervosa.

Body image distortion in 79 female anorexia nervosa patients were examined on a visual-size estimation apparatus during the emaciated stage of illness. Both they and an age-matched female control group overestimated their body widths, so this overestimation cannot be considered unique to anorexia nervosa. Among anorexia patients the degree of overestimation was associated with less weight gain during treatment, greater denial of illness, and several other pretreatment characteristics indicative of poor outcome.

Animals↗

Anorexia nervosa in 'non-white' populations.

BACKGROUND: Comparisons were made between two groups of anorectic patients, 'non-white' and 'white', on a variety of clinical and social characteristics. METHOD: The study is based on a 34-year long database (1960-93) associated with a national tertiary referral centre. Thirty-six non-white patients meeting DSM-III-R criteria for anorexia nervosa (AN) and five with 'partial syndrome' are compared with a white group comprising 944 patients with full syndrome. RESULTS: The main finding is clinical similarity between the two groups, extending to social class and pathological patterns of family relationship. The non-whites are shorter in stature (P = 0.004) and report earlier menarche (P = 0.004); they are younger at presentation (P < 0.001), somewhat less emaciated, and practice veganism slightly more commonly; they less often acknowledge sensitivity to 'fatness' (P < 0.003). This sensitivity was exposed later whenever treatment involved substantial weight gain. The proportion of non-white cases accepted for assessment has not changed in respect of year of onset (around 6%) for the last 20 years, or year of presentation (around 6-7%) over the last 15 years. There was a tendency for non-white patients to be referred earlier in their illness. CONCLUSIONS: The clinical and background profiles of non-white and white anorectics are generally similar. The numbers arising and presenting have not changed recently. Non-white patients apparently have as ready access as white patients to assessment and treatment by us.

Adolescent↗