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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The protozoan parasite Toxoplasma gondii is a serious cause of fetal mortality in sheep and goats. Oocysts, the parasite stage responsible for initiating infection, are produced following a primary infection in cats. A primary infection in pregnant sheep and goats can establish a placental and fetal infection which may result in fetal death and resorption, abortion or stillbirth. Diagnosis is aided by the clinical picture, the presence of characteristic small white necrotic foci in placental cotyledons, the possible presence of a mummified fetus and on fetal serology and histopathology. Development of the polymerase chain reaction (PCR) specific for T. gondii may also provide a valuable diagnostic tool. Measures to control abortion include improved management of farm cats, fodder and water. Vaccination of sheep with the live vaccine is an effective preventive measure and the use of decoquinate in feed may be useful in some situations. Neospora caninum is related to T. gondii and while its asexual life cycle is similar to that of the latter it is currently not known whether it has a similar sexual life cycle in a definitive host. Neospora is an important cause of fetal loss in cattle and parallels that of T. gondii infection in sheep and goats. While it does not appear to cause frequent losses in these latter animals, experimental infection is readily induced in them and if initiated during pregnancy provides a very good model of the bovine infection. Furthermore clinical signs and pathological lesions in sheep and goats are similar to those induced in them by T. gondii, although there are subtle histopathological differences. These changes will aid possible diagnosis as will specific serological tests such as the indirect immunofluorescent antibody test and the enzyme linked immunosorbent assay and the PCR. Sarcocystis, which exists as numerous species, undergoes a coccidian-like life cycle with each having a distinctive definitive (usually carnivore) host which excretes sporocysts into the environment. Clinical sarcocystiosis is much less commonly diagnosed than toxoplasmosis and neither is it normally associated with fetal infection or abortion in either sheep or goats. However, infection is extremely common throughout the world and follows ingestion of food or water contaminated with sporocysts. Clinical signs, when seen, include fever, anaemia, inappetance and weight loss or reduced weight gain. Central nervous signs (hind limb weakness, ataxia, paresis), acute myopathy and death may occur. Diagnosis is difficult as infection is so common and clinical signs absent, mild or non-specific. Serology may be useful in some situations and histopathology/immunohistochemistry is valuable for confirming the cause of death. Control relies on preventing contamination of pasture and water with faeces of dogs, foxes and cats or by controlling access of young susceptible stock to contaminated land. Relatively little is known of the immunity induced by infection with Sarcocystis spp. but research indicates that protective immunity does develop and that cell-mediated mechanisms are probably important. It is likely that sarcocystiosis is underdiagnosed as a problem and that better diagnostic methods are needed to show the true extent of the losses caused. Neosporosis on the other hand would appear not to be so common in sheep and goats. The value of experimental infections in these animals may be to provide a comparative model of the infection in cattle in the same way that our understanding of toxoplasmosis in sheep provides a superior model of human toxoplasmosis.
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PMID:Protozoan infections (Toxoplasma gondii, Neospora caninum and Sarcocystis spp.) in sheep and goats: recent advances. 968 43

Interleukin 6 (IL-6) has antitumor activity comparable to IL-2 in murine models with less toxicity. Because the biological effects of intermittent and continuous infusions may differ, we conducted two concurrent Phase I trials of daily x5, 1-h, and continuous 120-h i.v. infusions to determine the toxicity, biological effects, and maximum tolerated dose of i.v. IL-6. Cohorts of six patients with advanced cancer received escalating doses (1, 3, 10, 30, 100, and 150 microgram/kg/day) of recombinant human IL-6 on days 1-5 and 8-12 of each 28-day course (1-h trial) or on days 1-5 of each 21-day course (120-h trial). Treatment was administered in regular inpatient wards and in outpatient clinics and was withheld in the event of grade 3 toxicity. Sixty-nine patients (1-h trial, n = 40; 120-h trial, n = 29) were enrolled, including 27 with renal cancer and 16 with melanoma. All were ambulatory, and 40 were asymptomatic. Fever (97%), anemia (78%), fatigue (56%), nausea or vomiting (49%), and elevated serum transaminase levels (42%) were the most frequent toxicities. Transient hypotension developed in 23 patients (33%). There were three deaths during the study due to progressive disease and/or infection. There were no objective responses. Dose-related increases in platelet counts and C-reactive protein levels were detected in most patients. Principal dose-limiting toxicities included atrial fibrillation (1 episode in the 1-h trial and 4 episodes in the 120-h trial) and neurological toxicities (3 episodes in the 1-h trial and 4 episodes in the 120-h trial). The neurological toxicities included confusion, slurred speech, blurred vision, proximal leg weakness, paraparesis, and ataxia. These effects were transient and reversed when IL-6 was discontinued. IL-6 can be given by i.v. infusion at biologically active doses with acceptable toxicity. Dose-limiting toxicities consisted mainly of a spectrum of severe but transient neurological toxicities and occasional episodes of atrial fibrillation. The maximum tolerated doses recommended for use with these i.v. schedules in Phase II trials are 100 microgram/kg/day by daily x5 1-h infusion and 30 microgram/kg/day by 120-h infusion. Phase II trials will be performed to determine the antitumor activity of IL-6 and better define its toxicity. Patients in these and other IL-6 studies should be monitored closely for neurological and cardiac effects.
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PMID:Concurrent phase I trials of intravenous interleukin 6 in solid tumor patients: reversible dose-limiting neurological toxicity. 981 35

X-linked sideroblastic anemia and ataxia (XLSA/A) is a recessive disorder characterized by an infantile to early childhood onset of non-progressive cerebellar ataxia and mild anemia with hypochromia and microcytosis. A gene encoding an ATP-binding cassette (ABC) transporter was mapped to Xq13, a region previously shown by linkage analysis to harbor the XLSA/A gene. This gene, ABC7, is an ortholog of the yeast ATM1 gene whose product localizes to the mitochondrial inner membrane and is involved in iron homeostasis. The full-length ABC7 cDNA was cloned and the entire coding region screened for mutations in a kindred in which five male members manifested XLSA/A. An I400M variant was identified in a predicted transmembrane segment of the ABC7 gene in patients with XLSA/A. The mutation was shown to segregate with the disease in the family and was not detected in at least 600 chromosomes of general population controls. Introduction of the corresponding mutation into the Saccharomyces cerevisiae ATM1 gene resulted in a partial loss of function of the yeast Atm1 protein. In addition, the human wild-type ABC7 protein was able to complement ATM1 deletion in yeast. These data indicate that ABC7 is the causal gene of XLSA/A and that XLSA/A is a mitochondrial disease caused by a mutation in the nuclear genome.
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PMID:Mutation of a putative mitochondrial iron transporter gene (ABC7) in X-linked sideroblastic anemia and ataxia (XLSA/A). 1019 63

Immune-mediated hemolytic anemia secondary to bee envenomation developed in 2 dogs. Clinical signs included lethargy, hematuria, ataxia, and seizures; 1 dog died. Clinicopathologic data included nonregenerative anemia, spherocytosis, positive results for Coombs' test, and occult hematuria. Treatment included oral administration of corticosteroids at immunosuppressive dosages and supportive care. The surviving dog initially responded to corticosteroids, but hemolysis recurred as the dosage was tapered. Hemolysis resolved with prolonged administration of corticosteroids. Bee venom contains hyaluronidase, histamines, and hemolysins that cause toxic and hemolytic effects. Envenomation should be considered in any dog with hemolytic anemia in which other causes are ruled out and exposure to bees is known.
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PMID:Bee sting envenomation resulting in secondary immune-mediated hemolytic anemia in two dogs. 1020 Jul 97

An investigation was made of Commiphora myrrha used in traditional medicine for the treatment of various ailments. Twelve 6-mo-old male Nubian goat kids were assigned to 4 groups: undosed controls, C myrrha-dosed at 0.25 g plant resin/kg/d, C myrrha-dosed at 1 g resin/kg/d and C myrrha dosed at 5 g plant resin/kg/d. Results of hepatorenal function tests were correlated with clinical and pathological changes. The use of 1 or 5 g plant resin/kg/d caused grinding of teeth, salivation, soft feces, inappetence, jaundice, dyspnea, ataxia and recumbency. Death occurred between 5 and 16 d. Enterohepatonephrotoxicity was accompanied by anemia, leucopenia, increases in serum ALP activity and concentrations of bilirubin, cholesterol, triglycerides and creatinine, and decreases in total protein and albumin. The oral dose of 0.25 g plant resin/kg/d was not toxic.
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PMID:Toxicity of Commiphora myrrha to goats. 1050 32

Unusual clinical and pathological observations in the field in goats and sheep suffering from Strongyloides papillosus infection prompted experimental work on this parasite. Goats were infected percutaneously with either single or multiple, low or high levels of S. papillosus. Young goats up to 12 months of age were found to be the most susceptible. Some animals, however, showed substantial resistance to infective doses. Clinical signs included transient diarrhoea, misshapen, elongated faecal pellets terminally, dehydration, anorexia, cachexia, gnashing of teeth, foaming at the mouth, anaemia and nervous signs such as ataxia, a wide-based stance, stupor and nystagmus. A 'pushing syndrome' was seen in 22% of the animals. The pathological changes are described and included enteritis, status spongiosus in the brain, hepatosis leading to rupture of the liver, nephrosis, pulmonary oedema, interstitial pneumonia and pneumonia. About 6% of the goats died acutely from fatal hepatic rupture. The development of an acquired immunity was determined. The immunity elicited an allergic skin reaction at the application site of larvae or injection sites of larval metabolites. This immunity, however, could be breached by large doses of larvae. The most profound clinicopathological changes induced by the parasites were an anaemia (most pronounced in the young goats) and hypophosphataemia. Trace element analyses provided evidence of Cu, Mn and possibly Se deficiencies in some goats.
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PMID:Experimental studies with Stronglyloides papillosus in goats. 1063 9

The nematode Eustrongylides ignotus was found in peritoneal lesions of several great blue herons (Ardea herodias) submitted for necropsy from a wildlife rehabilitation center in northern Delaware. Prior to death, signs of disease included ataxia, emaciation, weakness, and anemia. Blood collection was not uniformly performed, but in cases where it was performed, affected birds demonstrated abnormal clinical hematology. Postmortem findings included numerous lesions associated with verminous peritonitis. Significant histologic granulomatous response to the presence of these organisms was noted, particularly in the proventricular specimens. Other organs involved included intestine, spleen, pancreas, and liver.
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PMID:Eustrongylidiasis in eastern great blue herons (Ardea herodias). 1087 26

Human lymphoblastoid cells of normal origin and from genetic instability syndromes, i.e. Fanconi anemia (FA) group C and ataxia telangectasia, were continuously exposed to extremely low frequency magnetic field (ELF-MF). We report that ELF-MF, though not perturbing cell cycle progression, increases the rate of cell death in normal cell lines. In contrast, cell death is not affected in cells from genetic instability syndromes; this reflects a specific failure of the apoptotic response. Reintroduction of complementation group C in FA cells re-established the apoptotic response to ELF-MF. Thus, genes implicated in genetic instability syndromes are relevant in modulating the response of cells to ELF-MF.
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PMID:Normal and cancer-prone human cells respond differently to extremely low frequency magnetic fields. 1116 65

Rocky Mountain spotted fever (RMSF) was diagnosed in 30 dogs examined at North Carolina State University, Veterinary Teaching Hospital between 1984 and 1997. Historical, physical examination, and laboratory abnormalities were reviewed. Diagnostic criteria included a four-fold rise in antibody titer to Rickettsia rickettsii (R. rickettsii) (n=15) or a single R. rickettsii antibody titer of 1:1,024 or greater (n=15; when this initial titer was determined one week or more after the onset of clinical signs). Fifteen (50%) dogs were greater than seven years of age, and 13 (43%) dogs were between two and seven years of age. There was no sex predilection. Only five (17%) dogs had a history of known tick exposure. Presumably due to delayed diagnosis, dogs with antibody titers of 1:1,024 or greater at the time of presentation had a higher incidence of more severe neurological dysfunction (e.g., ataxia, hyperesthesia, vestibular disease, and seizures) and cutaneous lesions (e.g., hyperemia, edema, petechiae, ecchymoses, and necrosis). Laboratory findings included anemia, leukocytosis accompanied by toxic granulation of neutrophils, hypoalbuminemia, and coagulation abnormalities; signs were generally more severe in the 15 dogs with R. rickettsii antibody titers of 1:1,024 or greater at the time of presentation. Twelve (40%) dogs in this study were severely thrombocytopenic (less than 75 x10(3) platelets/microl; reference range, 200 to 450 x 10(3)/microl), without clinical evidence of fulminant disseminated intravascular coagulation. In this study, the survival rate following R. rickettsii infection was 100%.
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PMID:Canine Rocky Mountain Spotted fever: a retrospective study of 30 cases. 1120 76

The loss of genomic stability is accepted as being one of the most important aspects of cancer. The correlation between genomic instability and cancer proneness in cases of known genetic syndromes (e.g. ataxia telengectasia, Fanconi anemia) is well established. This study was conducted to assess genomic instability in 19 patients with sporadic breast cancer. We used the comet assay on the lymphocytes of patients before radiotherapy and/or chemotherapy. The alkaline comet assay (single-cell gel electrophoresis) is a sensitive and rapid method for detecting DNA damage (single strand breaks and alkali-labile sites) in G(0) cells, at a single-cell level. This assay was achieved in vitro without irradiation and after exposure (dose ranging from 50 cGy to 5 Gy). The results show that the patients have higher baseline values than controls. At 2 Gy, the mean tail moment, score and the percentage of DNA in the tail increase for both groups but these values are much higher for patients. Our results show that the lymphocyte DNA of cancer patients is more damaged than that of controls with or without irradiation. Our hypothesis is that this baseline DNA damage reflect a genomic instability in sporadic breast cancer. This instability seems to increase after in vitro irradiation.
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PMID:Genomic instability and breast cancer. 1149 5


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