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At least 145 records · Page 8Linked to original sources
PubMed1995

Laboratory evaluation of bait base for the control of Indian field mouse, Mus booduga (Gray).

Species specific bait evaluation is important for the successful control of rodent populations through rodenticides. Experiments were conducted on the bait preference of Indian field mouse, M. booduga. Results reveal that rice normal grain, rice cracked grain, rice +4% coconut oil and millet +2% coconut oil may be used as effective poison carriers for the Indian field mouse. Additives like oil, sugar and salt did not improve the palatability of bait materials.

Animals↗
PubMedDate not supplied

Thallium loading in owls and other birds of prey in Denmark.

Due to previous findings of increased concentrations of the rodenticid, thallium, in free-living Danish carnivores, thallium analysis has been carried out on material from 77 owls and birds of prey. Thallium was found in 2/3 of the birds and in 10% the concentration was so high that the load of thallium may have caused the death of the birds. The load of thallium in birds of prey was lower than concentrations found in carnivores, probably because poisoning caused by direct intake of thallium baits placed for rodent control does not seem to occur among birds of prey. From the investigation of this limited number of birds, it is not possible to tell if thallium did have any influence on the maintenance of a healthy population of birds of prey, but the large number of thallium loaded birds also justify the restrictions in the sue of thallium which were given from the 1st of July, 1975.

Animals↗
PubMed1996

Emerging & re-emerging bacterial pathogens in India.

In spite of major successes against infectious diseases in the 20th century, new infectious diseases have emerged and old ones re-emerged in recent decades in different parts of the world. A brief survey of emerging and re-emerging bacterial diseases of public health importance in India is presented in this paper. Plague re-appeared in two outbreaks in Maharashtra and Gujarat in 1994, indicating a breakdown of the public health measures that had prevented its occurrence for several decades. Leptospirosis appears to be on the increase in Kerala, Tamilnadu and the Andamans during the last 2 decades, probably due to increased farming and inadequate rodent control. It is suggested that melioidosis due to the soil organism Burkholderia pseudomallei may be prevalent in many parts of India, but is under-diagnosed and under-reported. Since 1991, a completely new choleragenic Vibrio cholerae, designated 0139 has emerged in southern India and spread to other parts of India and to neighbouring countries, setting in motion the 8th cholera pandemic. Animal anthrax is very common in many parts of India, but human anthrax is recognised in only certain limited locations. In the Chittoor and North Arcot districts, its prevalence had increased in recent years. Since 1990, a multi-drug resistant variety of typhoid fever had been prevalent in many parts of India, caused by Salmonella typhi resistant to chloramphenicol, ampicillin and trimethoprim-sulphamethoxazole. Nosocomial methicillin-resistant Staphylococcus aureus infection seems to be widely prevalent in hospitals in many regions in India, and its prevalence seems to be on the rise. These pathogens pose new threats to public health, and call for appropriate responses. Microbiological expertise and epidemiological surveillance are deficient in the health care and public health systems in India; therefore even infections and diseases that have been under control elsewhere remain prevalent in the country, but are also under-diagnosed and under-reported. Without improving microbiological expertise and application as well as epidemiological skills and practices, emerging and re-emerging diseases may not be recognised, identified or intercepted in their early stages.

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PubMed1998

[Epidemiology and epizootiology of plague: the major role of the surveillance of reservoir populations of wild rodents in the control of permanent foci].

Plague is a bacterial infection, due to Yersinia pestis. It is essentially a zoonosis of rodents, communicable from rodent to rodent and from rodent to man by flea bite. From the first human case, acquired from rodents, interhuman transmission occurs by means of flea bite (bubonic plague) or is airborne (primary pulmonary plague). Long term implantation of plague amongst wild rodents populations after the third pandemic (1894 to present), created inveterate foci in all continents, except Europe. Those wild rodents settlements in arid biotopes, preserved from human activities, represent the main reservoir of plague. Their determination is mandatory for the surveillance of epizootics and the prevention of epidemics.

Animals↗
PubMedDate not supplied

Perturbation of rodent hepatocyte growth control by nongenotoxic hepatocarcinogens: mechanisms and lack of relevance for human health (review).

During the development of new industrial and pharmaceutical chemicals, it is necessary to determine whether they are potential carcinogens. However, there are no short-term tests available for nongenotoxic carcinogens that do not damage DNA yet cause tumours in rodent bioassays. The peroxisome proliferators (PPs) constitute a diverse class of nongenotoxic carcinogens that include chemicals of therapeutic, industrial and environmental importance such as hypolipidaemic fibrate drugs, clingwrap/medical tubing plasticizers and certain pesticides and solvents. PPs induce DNA synthesis and suppress apoptosis in rat and mouse hepatocytes, leading to tumour formation. In addition to altering hepatocyte growth and survival, PPs cause peroxisome proliferation and the induction of enzymes of the beta-oxidation pathway. PPs mediate their biological responses in rodents via activation of the nuclear hormone receptor PPARalpha (peroxisome proliferator activated receptor alpha) which regulates expression of the genes associated with response to PPs. The mechanisms through which normally quiescent hepatocytes are recruited into the cell cycle currently remain obscure. However, it is probable that expression of hepatic cytokines by hepatic macrophages (Kupffer cells) may be involved. In common with other classes of nongenotoxic carcinogen, there are remarkable species differences in response to PPs; humans respond to the fibrate hypolipidaemic PPs via a reduction in serum cholesterol but appear refractory to the adverse effects of PPs such as hepatic peroxisome proliferation, DNA synthesis and tumour formation. The molecular basis of the observed species differences in response to PPs is unclear at present, but recent data support a quantitative hypothesis wherein PPARalpha expression levels are sufficient in humans to mediate hypolipidaemia, but too low for transcriptional regulation of the full battery of genes associated with the adverse effects seen in rodents such as peroxisome proliferation, liver enlargement and tumours. A more detailed understanding of the mechanisms through which these chemicals cause tumours in rodents and how humans may differ will assist in extrapolation of rodent data to human risk assessment.

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