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 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A review of the literature reveals only one case of neonatal Escherichia coli pericarditis. This is a case report of Escherichia coli pericarditis occurring in a two day old infant. The infant initially presented with lethargy and jaundice but this rapidly progressed into shock. Despite vigorous resuscitative efforts, the infant succumbed and at autopsy 30 cc of purulent fluid were obtained. Cultures of the admission blood and post-mortem pericardial effusion grew Escherichia coli. The clinical diagnosis of pericarditis is often difficult because of vague, nonspecific symptoms and signs. The symptoms are usually those of sepsis plus those of impaired circulation due to mechanical embarrassment by accumulating pericardial effusion. It is difficult to differentiate pericarditis with effusion from myocarditis and pericardial effusion secondary to congestive heart failure. The use of pericardiocentesis as a diagnostic tool and echocardiography are the most helpful techniques presently available for diagnosis. Management consists of vigorous supportive efforts, antibiotics, and drainage of the pericardial effusion. Because of the very high mortality associated with this disorder, a high index of suspicion with a vigorous diagnostic and therapeutic approach to the patient is indicated.
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PMID:Neonatal E. coli pericarditis. 37 Mar 57

Twenty-six young pigs were infected with encephalomyocarditis virus, observed clinically, studied at intervals by noninvasive and invasive methods to assess cardiac function and eventually examined pathologically. All infected animals appeared ill, usually manifesting diminished appetite, lethargy and fever. Spontaneous mortality occurred either 1 to 4 or 20 to 21 days after infection. Electrocardiographic abnormalities, seen in the majority of animals, comprised ST-T wave changes, conduction disturbances or ventricular ectopic rhythm. The majority of animals manifested echocardiographic evidence of left ventricular dilation and decreased systolic function, which improved with time in some animals. Hemodynamic studies revealed elevation of biventricular filling pressures in 3 of 10 animals; as a group, infected animals manifested significantly elevated right ventricular filling pressures. In selected animals, the feasibility of gallium scans as well as left ventriculography and coronary angiography was demonstrated. At autopsy, heart weight/body weight ratio was significantly elevated in infected animals. The heart of all but two animals showed active myocarditis associated with fibrosis and focal calcification in the later stages. In general, the cardiovascular manifestations were parallel with those seen in acute and subacute myocarditis in humans. It is concluded that encephalomyocarditis infection in the pig is a large animal model of viral myocarditis suitable for assessing alterations in the structure and function of the cardiovascular system and the effects of interventions.
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PMID:An experimental model of acute and subacute viral myocarditis in the pig. 131

The earliest written report of selenium poisoning is thought to be the description by Marco Polo of a necrotic hoof disease of horses that occurred in China in 13. century. However recognition of Se as toxic principle come in the early 1930s. Severity of Se poisoning depends on chemical forms of the element, species of animals and routes of administration. The soluble Se salts (Na2SeO3 and Na2SeO4) appear to be among the more toxic compounds; the Se inherent in grains and selenoamino acids (selenomethionine and selenocystine) appear to have relative moderate toxicity; the poorly soluble forms (e.g., elemental Se, Na2Se, SeS2 and diphenyl selenide) are among the least toxic of the Se compounds. In general, toxicity of Se compounds are substantially less when they are administered orally than when they are given parenterally. Rosenfeld and Beath described three clinical types of Se intoxication: acute selenosis, subacute selenosis (i.e., blind staggers type), and chronic selenosis (i.e., alkali disease type). Acute poisoning occurs when high Se content plants are consumed in large quantities within short period. Accidental acute poisoning occurs as consequence of errors in formulation of a Se supplemented diet. The most characteristic sign of acute selenosis is garlic breath due to the pulmonary excretion of volatile Se metabolites. Other signs include lethargy, excessive salivation, vomiting, dyspnea, muscle tremors and respiratory distress. Pathological findings are: congestion of the liver and kidney, fatty degeneration and focal necrosis of the liver, endocarditis and myocarditis. Subacute selenosis ("blind staggers") occurs as a consequence of exposure to large doses of Se over a longer period of time and manifests with neurological signs (e.g., blindness, ataxia, disorientation) and respiratory distress. This form of selenosis is most frequently observed in grazing animals that have consumed Se-accumulated plants. Chronic selenosis ("alkali disease") comes about when animals consume moderate levels of Se (more than 5 mg/kg and less than 40 mg/kg) for period of weeks or months. The usual clinical signs of chronic selenosis in horses, cattle and swine are: loss of hair (horses and cattle lose long hair from the mane and tails), emaciation, hoof lesions and lameness. In advanced cases liver cirrhosis, atrophy of the heart and anemia occur. In swine symmetrical poliomyclomalacia of cervical and lumbal/sacral spinal cord segment has been seen. Sheep seen to be more tolerant and get milder form of the disease. They lose appetite and have reduced gain. In growing chicks reduced gain and feed intake, rough feathers, and characteristics of nervousness has been observed. Reduced egg production, embryonic deformations and reduced hatchability has been observed in hens.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Selenium toxicity in domestic animals]. 134 Apr 80

During 1980 and 1981, we compared antibiotic regimens in 108 adult patients with early Lyme disease. Erythema chronicum migrans and its associated symptoms resolved faster in penicillin- or tetracycline-treated patients than in those given erythromycin (mean duration, 5.4 and 5.7 versus 9.2 days, F = 3.38, p less than 0.05). None of 39 patients given tetracycline developed major late complications (meningoencephalitis, myocarditis, or recurrent attacks of arthritis) compared with 3 of 40 penicillin-treated patients and 4 of 29 given erythromycin (chi square with 2 degrees of freedom = 5.33, p = 0.07). In 1982, all 49 adult patients were given tetracycline; again, none of them developed major complications. However, with all three antibiotic agents nearly half of the patients had minor late symptoms such as headache, musculoskeletal pain, and lethargy. These complications correlated significantly with the initial severity of illness. For patients with early Lyme disease, tetracycline appears to be the most effective drug, then penicillin, and finally erythromycin.
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PMID:Treatment of the early manifestations of Lyme disease. 640 78

A 6-day-old female (Bison bison) was inoculated with 10 million sporocysts of the B1 isolate of Sarcocystis cruzi originally obtained by feeding heart of a naturally infected cow (Bos taurus) to a laboratory-raised coyote. The bison became febrile, lethargic, and anorectic at about 25 days after inoculation of the sporocysts, and was euthanatized 3 days later. There were widespread hemorrhages, hepatitis, myocarditis, nephritis, and enteritis; intravascular meronts were found in the adrenal cortex and lamina propria of the small intestine. Another 7-day-old male bison was inoculated with 100,000 sporocysts of the same B1 isolate of S cruzi. Except for mild fever and transient diarrhea, the bison remained clinically normal. Sarcocysts were found at necropsy on day 76 after inoculation. It was concluded that S cruzi of cattle is transmissible to bison.
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PMID:Sarcocystosis in neonatal bison fed Sarcocystis cruzi sporocysts derived from cattle. 681 77

A 2-phase study was conducted to evaluate the ability of the NEB-1 strain of porcine reproductive and respiratory syndrome virus (PRRSV) to potentiate common bacterial pathogens of swine. In phase I, 25 of 50 4-5-week-old specific-pathogen-free (SPF) pigs were exposed to NEB-1 PRRSV (day 0). Seven days after virus inoculation, 8 groups received 1 of 4 bacterial pathogens: Haemophilus parasuis, Streptococcus suis, Salmonella cholerasuis, and Pasteurella multocida. The ability of NEB-1 PRRSV to produce clinical disease, viremia, neutralizing antibody, gross and microscopic lesions and to potentiate bacterial pathogens was assessed. Response to NEB-1 PRRSV was similar among inoculated pigs; prolonged hyperthermia, lethargy, mild to moderate dyspnea, and cutaneous erythema were consistent clinical signs. No clinical differences were observed in groups after bacterial challenge. Virus was isolated from serum at weekly intervals through the end of the study, and all PRRSV-inoculated pigs had seroconverted by study termination. Two of 5 pigs died in non-PRRSV-inoculated groups challenged with H. parasuis and Streptococcus suis. Mortality in PRRSV-infected pigs was limited to 1 of 5 pigs from the Salmonella cholerasuis-challenged group. Gross lesions were seen in pigs dying after inoculation in H. parasuis- and Streptococcus suis-inoculated groups, in Salmonella cholerasuis- and P. multocida-challenged pigs, and in 1 non-PRRSV-inoculated control pig. Microscopic lesions consisted of mild to moderate proliferative interstitial pneumonia, nonsuppurative myocarditis, lymphoid hyperplasia, and nonsuppurative encephalitis in PRRSV-inoculated pigs. Findings in phase I indicated that NEB-1 PRRSV does not potentiate bacterial disease while inducing consistent clinical signs, viremia, seroconversion, and microscopic lesions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Porcine reproductive and respiratory syndrome: NEB-1 PRRSV infection did not potentiate bacterial pathogens. 757 44

From August 1990 to June 1991, a moderate die-off of 4- to 5-year-old green sea turtles (Chelonia mydas) occurred at Cayman Turtle Farm, Grand Cayman, British West Indies. Clinical signs included lethargy, anorexia, and inability to dive. Many of the ill turtles floated on the surface of their tanks. There was no apparent sex predilection. Complete necropsies, including histopathologic examination of tissues, were performed on eight turtles. Necropsies revealed multiple irregular discrete to patchy 1-10 mm pale gray foci throughout the hearts of four turtles. By light microscopic examination, the most severe and consistent lesions were necrotizing myocarditis, histiocytic to fibrinous splenitis, and hepatic lipidosis and necrosis. A mixed leukocytic infiltrate of acidophils, macrophages, and lymphocytes was present in affected areas of the heart. Other lesions included lymphocytic/plasmacytic interstitial nephritis, subacute interstitial pneumonia, subacute mesenteric vasculitis, chronic/active enteritis of the small intestine, and occasional granulomas associated with spirorchid trematode ova. Chlamydiae could be demonstrated in macrophages in sections of paraffin-embedded heart, liver, and spleen and in myocardial fibers and hepatocytes using a modified Macchiavello's stain. Chlamydial antigen was detected by light microscopic examination in the cytoplasm of myocardial fibers and in occasional hepatocytes using a commercially available genus-specific antichlamydial monoclonal antibody and the avidin biotin peroxidase complex staining method. Electron microscopic examination of the heart of the most severely affected turtle revealed developmental stages of chlamydial organisms. A suspension of heart from this turtle was inoculated into the yolk sacs of chicken embryos.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chlamydiosis in mariculture-reared green sea turtles (Chelonia mydas). 814 Jul 12

The Lelystad virus or one of two US isolates (VR2385, VR2431) of porcine reproductive and respiratory syndrome virus were given intranasally to 25 4-week-old cesarian-derived colostrum-deprived pigs. Pigs from these groups were necropsied at 1, 2, 3, 5, 7, 10, 15, 21, or 28 days postinoculation. The Lelystad virus and VR2431 induced mild transient pyrexia, dyspnea, and tachypnea. VR2385 induced labored and rapid abdominal respiration, pyrexia, lethargy, anorexia, and patchy dermal cyanosis. All three isolates induced multifocal tan-mottled consolidation involving 6.8% (n = 9; SEM = 3.4) of the lung for Lelystad, 9.7% (n = 9, SEM = 2.7) of the lung for VR2431, and 54.2% (n = 9, SEM = 4.4) of the lung for VR2385 at 10 days postinoculation. Characteristic microscopic lung lesions consisted of type 2 pneumocyte hypertrophy and hyperplasia, necrotic debris and increased mixed inflammatory cells in alveolar spaces, and alveolar septal infiltration with mononuclear cells. Lymphadenopathy with follicular hypertrophy, hyperplasia, and necrosis was consistently seen. Similar follicular lesions were also seen in Peyer's patches and tonsils. Lymphohistiocytic myocarditis and encephalitis were reproduced with all three isolates. Clinical respiratory disease and gross and microscopic lung lesion scores were considerably and significantly more severe in the VR2385-inoculated pigs. All three viruses were readily isolated from sera, lungs, and tonsils throughout the 28 days of the study. The lymphoid and respiratory systems have the most remarkable lesions and appear to be the major site of replication of these viruses. This work demonstrated a marked difference in pathogenicity of porcine reproductive and respiratory syndrome isolates.
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PMID:Comparison of the pathogenicity of two US porcine reproductive and respiratory syndrome virus isolates with that of the Lelystad virus. 859

Viral myocarditis is the result of a viral infection that produces myocardial necrosis and triggers an immune response to eliminate the viral agent. Many pathogenic mechanisms may contribute to myocardial cell loss including the following: cytokine production contributing to disease severity; viral persistence, which may produce an autoimmune response to cardiac myosin; and viral invasion of vascular endothelium causing vascular spasm with reperfusion injury. The compensatory response of the myocardium to these mechanisms of cell loss is hypertrophy, which results in fibrosis, scarring, and dilation. The myocardial cell loss and physiological response produces a child with fever, lethargy, symptoms of congestive heart failure, cardiogenic shock, or new onset arrhythmias. The initial presentation may be subtle, but if left untreated will go on to produce severe symptoms. The focus of diagnostic studies is to evaluate cardiac function, identify the viral agent, and eliminate other causes of global cardiac dysfunction. Treatment must provide for support of cardiac function through inotropic and afterload-producing agents while providing rest for the stressed cardiac muscle. The nursing care of children with viral myocarditis must focus on continual assessment of the cardiovascular system while supporting the recovery of myocardial function.
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PMID:Viral myocarditis in children. 885 48

Traditional centrally acting antihypertensives have been associated with a high incidence of adverse effects and are no longer recommended as first-line therapy. The newer imidazoline receptor agonists must overcome this reputation if they are to gain recognition as potential first-line agents for hypertension. Methyldopa, a centrally acting alpha(2)-agonist, is characterized by a number of serious adverse reactions that limit its use. Although unpredictable idiosyncratic or hypersensitivity reactions are uncommon, these include hepatitis, myocarditis, and hemolytic anaemia. Less serious problems such as abnormal liver function tests, positive Coombs test, drug-induced fever, and pancreatitis also occur. Central side effects include drowsiness, fatigue, lethargy, sedation, depression, psychotic reactions, nasal stuffiness, impotence, and exacerbation of Parkinsonism. In hypertensive men, methyldopa is less well tolerated than either captopril or propranolol, and up to 20% of patients discontinue therapy because of adverse effects. Clonidine acts primarily as an alpha(2)-agonist but also acts as an agonist at imidazoline receptors in the rostroventrolateral medulla. It is equipotent to most other antihypertensives but is considerably less well-tolerated in comparative trials. The principal adverse effects of clonidine are drowsiness, sedation, lethargy and dry mouth. Reserpine acts primarily by depleting central catecholamine neurotransmitter stores. It was very extensively used in early hypertension trials, but its central side effects of sedation, nasal stuffiness, and severe depression are now considered so undesirable that the drug is seldom prescribed. The imidazoline (I1) agonists moxonidine and rilmenidine act selectively and have very little central alpha(2)-agonist activity. In comparative studies against placebo and other reference antihypertensives, the only adverse effect consistently associated with these drugs was dry mouth (approximate placebo-corrected incidence 10%). Sedation was not pronounced. Withdrawal syndromes are complex pathophysiologic processes and occur with a variety of antihypertensive drugs. Cessation of therapy with clonidine and, to a lesser extent, methyldopa may result in a severe withdrawal syndrome characterized by restlessness, sweating, anxiety, tremor, palpitations, and headache. There may be a rapid rise in blood pressure, often with a true "rebound" to higher than pretreatment levels. Plasma and urinary catecholamine levels are increased, and fatalities have been reported. It is important to stress that such a syndrome has not been recorded, in animal or human studies, with either moxonidine or rilmenidine.
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PMID:Aspects of tolerability of centrally acting antihypertensive drugs. 887 99


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