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Query: UMLS:C0023380 (lethargy)
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Although used as a condiment and essential supplement since pre-Biblical times, chlorine as a part of the molecule salt has received little research effort by large animal nutritionists. Its low cost and the continued popularity of salt as a condiment and sodium supplement has precluded the appearance of chloride deficiencies. There is great variation in the chloride and sodium content of feedstuffs fed to lactating cows so that some formulations require no supplemental chloride or sodium. Chloride is highly available from feedstuffs, and when dietary chloride is low, the cow can reduce sharply her losses of chloride in urine, feces, skin secretions, and to some degree in milk. Clinical symptoms of chloride deficiency in the lactating cow include pica, lethargy, anorexia, lowered milk yield, constipation, and cardiovascular depression. Metabolic changes are expressed as a severe primary hypochloremia, secondary hypokalemia, and metabolic alkalosis. Requirement for chloride by the lactating cow is about .20%; a working allowance of .25% seems reasonable for cows in positive energy balance. With gradual resolution of the requirements for chloride and more data on chloride in feedstuffs, use of supplemental salt for either sodium or chloride can be reduced greatly.
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PMID:Mineral utilization by the lactating cow--chlorine. 370 Jul 98

Chronic depletion of body chloride developed in a group of infants ingesting a diet consisting almost exclusively of chloride deficient Neo-Mull-Soy. Ten of the 12 infants were on this diet three to five months before loss of appetite, failure to thrive, muscle weakness, and lethargy led to a diagnostic evaluation. The outstanding laboratory features were severe hypokalemic metabolic alkalosis, low urinary chloride concentrations (< 10 mEq/liter), and erythrocyturia. There was marked decrease in weight for age in all 12 infants. Head circumference for age had decreased in five of six and length for age in five of ten infants for whom earlier measurements were available. The biochemical abnormalities reverted to normal following dietary supplementation with either sodium or potassium chloride. Appetite, affect, and muscle strength improved, and weight gain resumed. Head circumference for age has moved toward the percentile level present prior to starting Neo-Mull-Soy in all instances. With one exception, length measurements show a similar pattern. The erythrocyturia has decreased or vanished. Chloride deficiency led to contraction of the extracellular volume and the substitution of poorly reabsorbable anions for readily reabsorbable chloride. These alterations caused development of the negative hydrogen ion and potassium balances which led to the hypokalemic metabolic alkalosis.
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PMID:The dietary chloride deficiency syndrome. 693 41

Chloride deficiency signs were produced in young Holstein calves by a low chloride diet (.063% chlorine) and daily removal of chloride in abomasal contents. General clinical signs included anorexia, weights loss, lethargy, mild polydipsia, and mild polyuria. In latter stages of the deficiency, severe eye defects (scleral injection, sunken eyes, scaliness around eyes) and reduced respiration rate became evident. Feces contained varying amounts of blood and mucus. The chloride imbalance resulted in severe alkalosis and hypochloremia leading to secondary hypokalemia, hyponatremia, and azotemia. All deficient calves died after 24, 28, 38, and 46 days of treatment. Chloride concentrations of plasma in each of the calves just prior to death were similar at 31 to 35 meq/liter, which compares with normal 96 meq/liter. One additional calf made chloride deficient was recovered to normal health in 9 days following a single treatment with salt water and feeding of control diet containing .48% chlorine. Control calves fed a diet with .48% chlorine and which also had their abomasal contents removed daily grew normally and exhibited no deficiency signs. When dietary chloride was adequate, removal of abomasal contents (and chlorine) had no adverse effects on the animals.
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PMID:Chloride deficiency in Holstein calves from a low chloride diet and removal of abomasal contents. 719 42

In response to grower complaints of poor performance of Phytoseiulus persimilis, mites from 14 commercial insectaries and research colonies were examined for pathogens. Some were found to have abdominal discolorations, manifested initially as two white stripes along the dorsal sides of the body within the Malpighian tubules. Advanced signs appeared as a large, centrally located, white spot or U-shaped discoloration in the distal opisthosoma within the rectum/anal atrium. White material often accumulated and hardened within the anus and formed a rectal plug that inhibited further excretion. Most affected mites were lethargic. Adults and immatures with abdominal discoloration contained numerous densely packed, birefringent, dumbbell-shaped entities. Though occasionally observed in the colon, they occurred most frequently within the Malpighian tubules and/or rectum and anal atrium. Dumbbells measured 2-4 &mgr;m long and contained prominent concentric rings. When observed by transmission electron microscopy, the entities lacked cellular organelles. Asymptomatic mites contained few or no such entities. Dumbbell-shaped inclusions were observed in P. persimilis from all sources examined. High levels of potassium, low levels of phosphorous and sulfur, and traces of chlorine were detected by energy-dispersive X-ray analysis. Guanine and uric acid, known nitrogenous wastes of arachnids, do not contain these elements. The chemical composition and structure indicate that the dumbbells are crystals. Both asymptomatic mites and those specimens exhibiting abdominal discoloration were examined for pathogens using light and transmission electron microscopy. Microsporidia, virus-like particles, and a rickettsia (genus Wolbachia) were observed in some mites but showed no correlation with white abdominal discoloration or associated crystal formation. Neither were pathogens always detected in symptomatic mites. Although birefringent crystals may be naturally occurring excretory products, the cause of white abdominal signs associated with crystal accumulation in P. persimilis is unknown. These signs indicate overall poor health.
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PMID:Birefringent Crystals and Abdominal Discoloration in the Predatory Mite Phytoseiulus persimilis (Acari: Phytoseiidae) 905 58

Hydrogen peroxide is an oxidising agent that is used in a number of household products, including general-purpose disinfectants, chlorine-free bleaches, fabric stain removers, contact lens disinfectants and hair dyes, and it is a component of some tooth whitening products. In industry, the principal use of hydrogen peroxide is as a bleaching agent in the manufacture of paper and pulp. Hydrogen peroxide has been employed medicinally for wound irrigation and for the sterilisation of ophthalmic and endoscopic instruments. Hydrogen peroxide causes toxicity via three main mechanisms: corrosive damage, oxygen gas formation and lipid peroxidation. Concentrated hydrogen peroxide is caustic and exposure may result in local tissue damage. Ingestion of concentrated (>35%) hydrogen peroxide can also result in the generation of substantial volumes of oxygen. Where the amount of oxygen evolved exceeds its maximum solubility in blood, venous or arterial gas embolism may occur. The mechanism of CNS damage is thought to be arterial gas embolisation with subsequent brain infarction. Rapid generation of oxygen in closed body cavities can also cause mechanical distension and there is potential for the rupture of the hollow viscus secondary to oxygen liberation. In addition, intravascular foaming following absorption can seriously impede right ventricular output and produce complete loss of cardiac output. Hydrogen peroxide can also exert a direct cytotoxic effect via lipid peroxidation. Ingestion of hydrogen peroxide may cause irritation of the gastrointestinal tract with nausea, vomiting, haematemesis and foaming at the mouth; the foam may obstruct the respiratory tract or result in pulmonary aspiration. Painful gastric distension and belching may be caused by the liberation of large volumes of oxygen in the stomach. Blistering of the mucosae and oropharyngeal burns are common following ingestion of concentrated solutions, and laryngospasm and haemorrhagic gastritis have been reported. Sinus tachycardia, lethargy, confusion, coma, convulsions, stridor, sub-epiglottic narrowing, apnoea, cyanosis and cardiorespiratory arrest may ensue within minutes of ingestion. Oxygen gas embolism may produce multiple cerebral infarctions. Although most inhalational exposures cause little more than coughing and transient dyspnoea, inhalation of highly concentrated solutions of hydrogen peroxide can cause severe irritation and inflammation of mucous membranes, with coughing and dyspnoea. Shock, coma and convulsions may ensue and pulmonary oedema may occur up to 24-72 hours post exposure. Severe toxicity has resulted from the use of hydrogen peroxide solutions to irrigate wounds within closed body cavities or under pressure as oxygen gas embolism has resulted. Inflammation, blistering and severe skin damage may follow dermal contact. Ocular exposure to 3% solutions may cause immediate stinging, irritation, lacrimation and blurred vision, but severe injury is unlikely. Exposure to more concentrated hydrogen peroxide solutions (>10%) may result in ulceration or perforation of the cornea. Gut decontamination is not indicated following ingestion, due to the rapid decomposition of hydrogen peroxide by catalase to oxygen and water. If gastric distension is painful, a gastric tube should be passed to release gas. Early aggressive airway management is critical in patients who have ingested concentrated hydrogen peroxide, as respiratory failure and arrest appear to be the proximate cause of death. Endoscopy should be considered if there is persistent vomiting, haematemesis, significant oral burns, severe abdominal pain, dysphagia or stridor. Corticosteroids in high dosage have been recommended if laryngeal and pulmonary oedema supervene, but their value is unproven. Endotracheal intubation, or rarely, tracheostomy may be required for life-threatening laryngeal oedema. Contaminated skin should be washed with copious amounts of water. Skin lesions should be treated as thermal burns; surgery may be required for deep burns. In the case of eye exposure, the affected eye(s) shod eye(s) should be irrigated immediately and thoroughly with water or 0.9% saline for at least 10-15 minutes. Instillation of a local anaesthetic may reduce discomfort and assist more thorough decontamination.
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PMID:Hydrogen peroxide poisoning. 1529 93

Chryseobacterium (formerly Flavobacterium) indologenes, is a non-fermentative gram-negative bacillus which is widely found in the nature, primarily soil and water. Since it can survive in chlorine-treated municipal water supplies, and can colonize the sink basins and tap waters of the hospitals, this bacterium may be a potential infectious agent. Contamination of the medical devices containing water (respirators, intubation tubes, humidifiers, incubators for newborns, etc.) in hospital settings may lead to serious infections especially in patients with predisposing diseases, newborns and immunocompromized patients. In this report, a case of fatal C.indologenes septicemia developed in a newborn with hydrocephalus has been presented. A two-months old male infant was admitted to our hospital with the complaints of failure to suck and lethargy for five days and head enlargement. He was diagnosed as meningitis based on the clinical and laboratory findings of cerebrospinal fluid (CSF) (protein: 572 mg/dl, glucose 9.5 mg/dl, chlorine: 111 mg/dl, and presence of abundant polymorphonuclear leukocytes), and empirical antibiotic treatment (ampicillin/sulbactam and cefotaxime) had been started. Since the computerized tomography of the brain pointed out hydrocephalus, an external shunt was placed for CSF drainage on the second day of hospitalization. A total of five CSF and two blood cultures collected during the hospitalization period were inoculated into pediatric aerobic CSF and blood culture bottles (BacT/ALERT, BioMerieux, France) and incubated for 24-48 hours. The isolated bacteria from all of the cultures were identified as C.indologenes by conventional methods and BD Phoenix (Becton Dickinson, USA) system. Antibiotic susceptibility tests were performed with microdilution method according to CLSI guidelines. The isolate was found susceptible to ciprofloxacin, levofloxacin and trimethoprim/sulfamethoxazole, while it was resistant to amikacin, gentamicin, tobramycin, piperacillin, cefotaxime, ceftazidime, aztreonam, meropenem, imipenem, tetracycline, and chloramphenicol. The treatment continued with ampicillin/sulbactam and levofloxacin without removing the shunt. However, C.indologenes growth persisted in CSF and blood cultures of the patient. The general condition of the patient deteriorated on the 65. day of the hospitalization and the patient was lost due to cardiopulmonary arrest. Case reports related to isolation of C.indologenes from blood cultures are present in the literature, however, isolation of C.indologenes from central nervous system was reported previously in a single case. In conclusion, C.indologenes should be considered as opportunistic infectious agents especially in the infectious diseases that develop in immunocompromised patients with underlying disease and with foreign device implementation.
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PMID:[Sepsis caused by Chryseobacterium indologenes in a patient with hydrocephalus]. 2209 Mar 5