Ammonia Toxicity and pH

Warren, Kenneth S.

doi:10.1038/195047a0

Cited by 222 publications

(109 citation statements)

References 24 publications

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“…These lesions are considered to be related to the cytotoxic effects developing due to chemical irritation of the cells by ammonium ions or free ammonia which passes across the cell membranes (Milne et al 1958;Warren 1962). The pathological changes in the organs might also be related to tissue ischaemia and hypoxia occurring due to generalised venous congestion and marked increase in central venous pressure associated with failing cardiovascular and respiratory functions.…”

Section: Resultsmentioning

confidence: 99%

Studies of Clinico-biochemical and Pathological Changes in the Urea-Induced Acute Rumen Alkalosis in Buffalo Calves

Randhawa¹,

Dhaliwal²,

Gupta³

et al. 1989

Acta Vet. Brno

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Randhawa S. S., P. S. Dhaliwal, P. P. Gupta, A. K. Ahuja, S. S. R a th 0 r : Studies on Clinico-biochemical and Pathological Changes in the Urea-Induced Acute Rumen Alkalosis in Buffalo Calves. Acta vet. Brno, 58, 1989: 225-243. Peracute rumen alkalosis was induced by intraruminal administration of urea @ 1.25 g/kg. b. wt. as a single dose in six healthy male Murrah buffalo calves of about 1 -2 years age. Peracute ammonia toxicity resulted in profuse salivation, ruminal stress, incoordination, recumbency followed by clonic convulsions, frequency of which increased with the progression of the condition, dyspnea, hyperpnea, tachycardia, opisthotonus, pupillary dilatation followed by death of the animals between 60-150 mts. It was observed that a linear relationship exists between death time and body weight of the calf with the same dose rate. Electrocardiographic studies revealed ventricular fibrillation with superimposition of P wave over T wave. The cardiac potentials gave rise to random osci11ations. Studies on liver function tests revealed that ammonia toxicity markedly affects the functional status of the liver as indicated by increase in serum enzymatic activities of arginase, glutamic oxalotransaminase, glutamic pyruvic transaminase, lactate dehydrogenase and glutamate dehydrogenase with increase in the half life of B.S.P. excretion rate which was subsequently confirmed by histopathological observations. Histopathological changes in the digestive system revealed exfoliation of the epithelial lining of the mucous membrane of the rumen, lymphocytic abomasitis, and necrotic enteritis. Other significant histopathological alterations were follicular cholecystitis, meningo-encephalitis, lymphocytic nephritis and cystitis, and alveolar emphysema. Intoxication, ECG, rumen liquor, blood, urineSudden changes in the dietary constituents with consumption of excess amounts of protein-rich concentrates and/or non-protein nitrogenous compounds has resulted in frequent occurrence of rumen alkalosis in ruminants. The disease is characterised by excessive production of ammonia in the rumen which may produce gastrointestinal, hepatic, renal, circulatory and nervous disturbances (Chalupa 1968; Parkins et aI.

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Section: Resultsmentioning

confidence: 99%

Studies of Clinico-biochemical and Pathological Changes in the Urea-Induced Acute Rumen Alkalosis in Buffalo Calves

Randhawa¹,

Dhaliwal²,

Gupta³

et al. 1989

Acta Vet. Brno

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“…The EPA-recommended concentration of dissolved fluoride in drinking water is 4.0 mg/liter, and most surface water has significantly lower concentrations, but there are areas that have high fluoride concentrations (Ͼ1.0 mg/liter), including portions of the southwestern United States (35). Although fluoride was determined to be statistically nonsignificant as a predictor, an inverse univariate relationship between dissolved fluoride concentrations and viral The inverse relationship between dissolved ammonia concentrations and AI virus persistence was not surprising, as ammonia has long been known to be toxic to viruses (36)(37)(38). Singlestranded RNA viruses have been shown to be particularly susceptible to ammonia, as the mechanism of inactivation involves the cleavage of viral RNA in intact particles and single-stranded genomes are more susceptible to this cleavage (39,40).…”

Section: Discussionmentioning

confidence: 99%

Abiotic Factors Affecting the Persistence of Avian Influenza Virus in Surface Waters of Waterfowl Habitats

Keeler

Dalton

Cressler

et al. 2014

Appl Environ Microbiol

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dAvian influenza (AI) virus can remain infectious in water for months, and virus-contaminated surface water is considered to be a source of infection within wild waterfowl populations. Previous work has characterized the effects of pH, salinity, and temperature on viral persistence in water, but most of that work was done with modified distilled water. The objective of this study was to identify the abiotic factors that influence the duration of AI virus persistence in natural surface water. Surface water samples were collected from 38 waterfowl habitats distributed across the United States. Samples were submitted to the U.S. Geological Survey National Water Quality Laboratory for chemical analysis and the University of Georgia for viral reduction time analysis. Samples were filtered with 0.22-m filters, and the durations of persistence of three wild-bird-derived influenza A viruses within each water sample at 10, 17, and 28°C were determined. The effects of the surface water physicochemical factors on the duration of AI viral persistence in laboratory experiments were evaluated by multivariable linear regression with robust standard errors. The duration of AI virus persistence was determined to be longest in filtered surface water with a low temperature (<17°C), a neutral-to-basic pH (7.0 to 8.5), low salinity (<0.5 ppt), and a low ammonia concentration (<0.5 mg/liter). Our results also highlighted potential strain-related variation in the stability of AI virus in surface water. These results bring us closer to being able to predict the duration of AI virus persistence in surface water of waterfowl habitats. Wild birds are considered to be the primordial reservoir for influenza A virus, with species within the orders Anseriformes and Charadriiformes having the largest and most diverse genetic pool of viruses (1, 2). Within these wild bird hosts, replication of avian influenza (AI) virus occurs primarily in the epithelial cells of the intestinal tract, and large amounts of virus are shed in feces (3, 4). The virus contaminates the surrounding aquatic environment, where it remains infectious, facilitating indirect transmission between birds (5-8). Environmental persistence of AI virus has been determined to be important for the epidemiology of the virus within wild bird populations and within aquatic habitats, and surface water is considered to be the major site of environmental contamination (9-12).The persistence of AI virus in water has been confirmed through environmental surveillance and laboratory-based investigations (6, 13-16). The temperature, pH, and salinity of the water have been identified as important determinants of the duration of persistence (8,(15)(16)(17)(18)(19). Using modified distilled water as a laboratory model, Brown et al. (16) determined that AI viruses are most stable in water with a neutral-to-basic pH (7.4 to 8.2), low salinity (Ͻ20 ppt), and a low temperature (Ͻ17°C). These general trends are supported by further laboratory investigations using natural surface water samples (8,15,1...

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“…The formation of ammonia by the coral pathogen may potentially contribute to pathogenesis (specifically by causing coral bleaching). Inhibition of photosynthesis by ammonia is well established (Warren, 1961;Cohen et al, 1975;Abeliovich & Azov, 1976). Ammonia acts as an uncoupler of photosynthesis by passing across membranes, thereby destroying the pH gradient across the thylakoid membrane (Smith & Raven, 1979;Velthuys, 1980).…”

Section: Cultural Physiological and Biochemical Characteristicsmentioning

confidence: 98%

Aurantimonas coralicida gen. nov., sp. nov., the causative agent of white plague type II on Caribbean scleractinian corals

Denner

Smith

Busse

et al. 2003

International Journal of Systematic and Evolutionary Microbiology

207

166

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A bacterium previously isolated from a diseased colony of the scleractinian coral Dichocoenia stokesi (common name elliptical star coral) was subjected to a detailed polyphasic taxonomic characterization. The isolate, designated WP1 T , was halophilic and strictly aerobic and formed golden-orange-pigmented colonies after prolonged incubation. Cells of WP1 T were Gram-negative, rod-shaped and showed a characteristic branching rod morphology. Chemotaxonomically, WP1 T was characterized by having Q-10 as the major respiratory lipoquinone and sym-homospermidine as the main component of the cellular polyamine content. The predominant constituent in the cellular fatty acid profile was C 18 : 1 v7c, along with C 19 : 0 cyclo v8c and C 16 : 0 . Other fatty acids present in smaller amounts were C 17 : 0 , C 18 : 0 , C 16 : 1 v7c, C 20 : 1 v7c and C 18 : 1 2-OH. The major polar lipids were phosphatidylethanolamine, phosphatidylglycerol and phosphatidylcholine. Minor amounts of diphosphatidylglycerol, phosphatidylmonomethylethanolamine and phosphatidyldimethylethanolamine were present. The G+C content of the genomic DNA was 66?3 mol%. Phylogenetic analysis of the 16S rRNA gene sequence showed that WP1 T represents a separate subline of descent within the order 'Rhizobiales' of the 'Alphaproteobacteria'. The new line of descent falls within the group of families that includes the Rhizobiaceae, Bartonellaceae, Brucellaceae and 'Phyllobacteriaceae', with no particular relative within this group. The 16S rRNA gene sequence similarity to all established taxa within this group was not higher than 92?0 % (to Mesorhizobium mediterraneum). To accommodate this emerging coral pathogen, the creation of a new genus and species is proposed, Aurantimonas coralicida gen. nov., sp. nov. (type strain WP1 T =CIP 107386 T =DSM 14790 T ). INTRODUCTIONIn 1995, Richardson and co-workers documented a dramatic coral epizootic that occurred on reefs of the northern Florida Keys, which spread rapidly to infect 17 of the 43 species of scleractinian corals present. Mortality rates of up to 38 % of the most susceptible coral species, Dichocoenia stokesi (the elliptical star coral), occurred within periods as short as 10 weeks (Richardson et al., 1998a). The disease was designated white plague type II The GenBank/EMBL/DDBJ accession number for the 16S rRNA gene sequence of Aurantimonas coralicida strain WP1 T is AJ065627.Abbreviations: DPG, diphosphatidylglycerol; PC, phosphatidylcholine; PDE, phosphatidyldimethylethanolamine; PE, phosphatidylethanolamine; PG, phosphatidylglycerol; PME, phosphatidylmonomethylethanolamine. G 2003 IUMS Printed in Great Britain1115 , 1998a). Beyond it, a replication sequence comparison between the re-determined 16S rRNA gene sequence in the study presented here and the originally deposited sequence revealed that there was no significant degree of similarity (~82 %) between the two sequences.In order to exclude any strain confusion, we have followed the history and distribution of strain WP1 T among our different laborato...

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Ammonia Toxicity and pH

Cited by 222 publications

References 24 publications

Studies of Clinico-biochemical and Pathological Changes in the Urea-Induced Acute Rumen Alkalosis in Buffalo Calves

Studies of Clinico-biochemical and Pathological Changes in the Urea-Induced Acute Rumen Alkalosis in Buffalo Calves

Abiotic Factors Affecting the Persistence of Avian Influenza Virus in Surface Waters of Waterfowl Habitats

Aurantimonas coralicida gen. nov., sp. nov., the causative agent of white plague type II on Caribbean scleractinian corals

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