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Biomedical subjects

P Krogh

Publications and source records attributed to P Krogh.

At least 37 records · Page 2Linked to original sources
PubMed1981

Effect on calves of barley naturally contaminated with ochratoxin A and groundnut meal contaminated with low concentrations of aflatoxin B1.

Four groups of six 12-week-old male Friesian calves were fed diets containing 390 to 540 microgram ochratoxin A per kg, 320 to 500 microgram ochratoxin A plus 12 to 13 microgram aflatoxin B1 per kg, 10 to 13 microgram aflatoxin B1 per kg, or a control diet containing neither toxin. At the end of the 87-day experiment there was no evidence of kidney or liver damage in any group of animals as judged by serial plasma and urine enzyme assays, haematological examinations including the assay of blood coagulation factors, gross appearance at autopsy or histopathological assessment at the light microscopic level. Nor was there any significant alteration in serum IgA, IgM, IgG1 and IgG2 levels or in titres to environmental bacterial and viral antigens. Trace amounts of ochratoxin A were detected in kidneys of five out of the 12 calves exposed to this toxin but all 12 kidneys contained residues of the metabolite ochratoxin alpha (less than 5 to 10 microgram/kg). Traces of aflatoxin B1 and M1 were detected in the liver of one of the 12 calves exposed to aflatoxin B1 but nine kidneys contained the metabolite aflatoxin M1 (less than 0.01 to 0.03 microgram/kg). There was no evidence of interaction between the two toxins.

Aflatoxin B1↗
PubMed1979

Tissue distribution of radioactivity from ochratoxin A-14C in rats.

Examination of the distribution of radioactivity in rat tissues during the first 24 hr after administration of ochratoxin A-14C demonstrated maximum accumulation in stomach and kidney. The highest counts were observed in stomach, lung, kidney, thymus, spleen and heart during the first 6 hr after treatment, whereas the brain, liver muscle, duodenum, jejunum, ileum, and cecum exhibited the greatest counts at 18 hr after toxin exposure.

Animals↗
PubMed1979

Ochratoxin A contamination of foodstuffs in an area with Balkan (endemic) nephropathy.

Ochratoxin A is a nephrotoxic fungal metabolite (mycotoxin) occurring in foodstuffs. The compound is causally associated with mycotoxic porcine nephropathy, a disease comparable with a human kidney disease, Balkan (endemic) nephropathy. A survey of 768 samples of foodstuffs (cereals and bread), locally produced in an area of Yugoslavia where Balkan (endemic) nephropathy is prevalent, has revealed that ochratoxin A is constantly present in parts of foodstuffs. The mean frequency of ochratoxin A contamination of cereals in the study period was 8.7 per cent, but a pronounced annual variation was encountered, with frequencies of contamination up to 43 per cent. These contamination frequencies are higher than those reported elsewhere for foodstuffs for human consumption. Thus further evidence is provided to support the hypothesis that ochratoxin A might by a disease determinant of Balkan (endemic) nephropathy.

Adult↗
PubMed1979

Porcine nephropathy induced by long-term ingestion of ochratoxin A.

Nine pigs were fed crystalline ochratoxin A in their feed at a concentration of about 1 mg/kg. Three pigs and their controls were killed after 3 months and 6 pigs and controls were killed after 2 years. A decrease of the ratio TmPAH/CIn, increased urinary glucose excretion and decreased ability to concentrate urine, occurred within a few weeks and aggravated slightly during the 2-year period. Changes in renal structure, characterized by degeneration and atrophy of proximal tubules, interstitial fibrosis and hyalinization of glomeruli, were progressive during time of exposure, but terminal renal failure was not reached. The kidney, liver, muscular and adipose tissue contained 3 to 27 microgram ochratoxin A/kg after 3 months of exposure. No further accumulation of ochratoxin A residue was found after 2 years of exposure.

Animals↗
PubMed1978

Mycotoxicoses of animals.

Mycotoxicoses are intoxications caused by ingestions of foodstuffs contaminated with mycotoxins, i.e. toxic secondary metabolites of microscopic filamentous fungi (moulds). By field observations and by experimental testing, toxins or toxic strains of more than 100 species of fungi have been encountered. However, causal associations have so far only been established for a small number of mycotoxicoses in farm animals, and the more important mycotoxicoses are aflatoxicosis, facial eczema, mycotoxic nephropathy, and estrogenic syndrome. A full assessment of the impact of mycotoxins on the health of farm animals can hardly be made at present, because the amount of surveillance data from mycotoxicoses is very limited, due mainly to inadequate diagnostic criteria. A new set of criteria for the diagnosis of mycotoxicosis is proposed, which has been successfully applied in the causative study of mycotoxic porcine nephropathy.

Animal Feed↗
PubMed1977

Balkan (endemic) nephropathy and foodborn ochratoxin A: preliminary results of a survey of foodstuffs.

Ochratoxin A is a nephrotoxic fungal metabolite (mycotoxin) occurring in foodstuffs. The compound is causally associated with mycotoxic porcine nephropathy, a disease comparable with a human kidney disease, Balkan endemic nephropathy. A preliminary survey of home-produced foodstuffs in areas of Yugoslavia revealed that contamination with ochratoxin A is more frequent in an area where Balkan endemic nephropathy is prevalent (endemic area) than in area where this disease is absent. This indicates higher exposure to foodborn ochratoxin A in the endemic area. Thus further evidence is provided supporting the hypothesis that ochratoxin A is a disease determinant of Balkan endemic nephropathyk0

Food Analysis↗
PubMed1977

Mycotoxin tolerances in foodstuffs.

In most countries general legislation on food (and feed) prohibits the sale of products containing poisonous or harmful substances, which would include relevant mycotoxins as well. So far only aflatoxin has been dealt with specifically in legislation. The aflatoxin control may include all foods (and feeds) but is limited in most countries to certain commodities likely to be heavily contaminated, viz. oilseeds and derived products. The aflatoxin tolerances established for foods vary from zero (level set by analytical method) through 30 ppb to 50 ppb. Tolerances for feeds are generally higher.

Aflatoxins↗
PubMed1977

Ochratoxin A residues in tissues of slaughter pigs with nephropathy.

Kidneys showing nephropathy changes were collected from slaughtered pigs at seven slaughterhouses in various districts of Denmark. Levels of ochratoxin A residues greater than 2 microgram/kg were detected in 21 out of 60 kidneys (35%). Ochratoxin A residues in liver, muscular and adipose tissues were calculated on the basis of the kidney concentration. Although the 21 kidneys containing ochratoxin A were condemned, the carcasses passed the meat inspection. Routinely only a small fraction of pigs exhibits nephropathy changes at slaughter, but the results of this study provide indirect evidence for a limited occurrence of ochratoxin A residues in commercial meat.

Animals↗
PubMed1976

Experimental avian nephropathy. Changes of renal function and structure induced by ochratoxin A-contaminated feed.

One-day-old chickens were fed ochratoxin A-contaminated diets at 2 levels: 0.3 and 1 mg ochratoxin A per kg feed, for 341 days. The only observable lesion to develop was a kidney damage comparable with the naturally occurring avian nephropathy. The changes in renal function were characterized by impairment of glomerular and tubular function, indicated by a decreased inulin clearance, TmPAH and decreased urine concentrating capacity. The changes of renal structure included degeneration of the tubular epithelium accompanied by regeneration. At slaughter, the kidneys, liver and muscular tissue of the birds contained residues of ochratoxin A (up to 50 mug per kg). As all the birds would have passed the meat inspection because no macroscopical lesions were present, this represents a possible health problem.

Animal Feed↗
PubMed1976

Experimental porcine nephropathy: changes of renal function and structure perorally induced by crystalline ochratoxin A.

Nine pigs were fed crystalline ochratoxin A in amounts corresponding to a feed level of 1 mg per kg for 3 months. The only observable lesion developed was a kidney damage, identical to the naturally occurring porcine nephropathy. The changes of renal function was characterized by impairment of proximal tubular function, indicated by a decrease of the ratio TmPAH/CIn, of the ability to concentrate urine, and by an increased urinary excretion of glucose. The decrease of the ratio TmPAH/CIn is correlated with time of exposure to ochratoxin A. The changes of renal structure were characterized by degeneration of the proximal tubules, leading to tubular atrophy accompanied by interstitial fibrosis. At the end of the experiment the kidney, liver, adipose and muscular tissue of the slaughtered pigs contained sizable amounts of ochratoxin A residues. As the pigs would have passed the meat inspection this represents a possible health problem. The changes observed in this study are identical to those observed by feeding to pigs grains naturally contaminated with ochratoxin A.

Adipose Tissue↗
PubMed1976

Epidemiology of mycotoxic porcine nephropathy.

Mycotoxic porcine nephropathy is a renal disorder caused by ingestion of feed-borne secondary fungal metabolites, possessing nephrotoxic properties. The disease is present endemically in all areas of Denmark, but unevenly distributed, with frequency varying from 0.6 to 65.9 cases per 10,000 pigs in 1971. Epidemics were encountered in 1963 and 1971, apparently associated with excessive climatic conditions. The highest frequency of the disease is found among pigs from the smaller farms. Ordinarily the same farm delivers cases during only one year. Female pigs contract the disease more frequently than male (castrated) pigs. The epidemiology of mycotoxic porcine nephropathy shows similarities with the epidemiology of endemic Balkan nephropathy.

Animals↗
PubMed1975

Spontaneous toxic nephropathy in poultry associated with ochratoxin A.

At a poultry slaughterhouse 14 birds with macroscopic renal changes were collected, and the kidneys were examined histologically and the muscular tissue was analysed for ochratoxin A residues. Out of 14 birds 5 birds had ochratoxin A residues ranging from 4.3 to 29.2 mug/kg. In 4 of these birds a toxic nephropathy was found characterised by atrophy and degeneration of proximal and distal tubules and interstitial fibrosis. The possibility of birds with ochratoxin A residues being presented for human consumption is discussed.

Animals↗
PubMed1975

[Intoxication in cattle caused by a batch of sugar beet pulp (author's transl)].

During the period from Dec. 7th 1972 to Jan. 8th 1973 76 cattle deaths were reported in 20 herds on the island of Møon and the adjacent south-eastern area of Sealand. The disease was characterized by a sudden onset and a rapid and invariably fatal course. Initially, there was a loss of appetite, depression, excessive salivation and incoordination. These symptoms progressed to paralysis and, in some animals, trmor and convulsions. Death usually ensued less than 2 hours after the first observation of symptoms. Losses in the herds varied from 1 to 12 animals. In herds with multiple incidents the majority of deaths occurred in the 24-hour-period following observation of the first case. Pathology: Gross lesions were few and inconclusive. Histology revealed marked dilatation of cerebral and maningeal blood vessels (arterioles, venoles and capillaries), with perivascular edema and haemorrhage. Adjacent neurons and glia cells showed various degrees of degeneration, apparently secondary to the vascular lesion. In all affected herds sugar beet pulp from one particular sugar mill had been used during the period preceding the outbreak. The syndrome was reproduced by feeding sugar beet pulp from this batch to two heifers. The heifers showed symptoms after 19 and 32 days' feeding, resp. and died after a few hours. Clinical and pathological features were identical with those observed in the spontaneous disease. Thus, it was proved that the particular batch of pulp was responsible for the disease. The investigation did not, however, reveal a toxic factor in this batch. Analyses for lead, arsenic, mercury, nitrite, alkyl phosphates, chlorinated insecticides and Cl. botulinum toxin were negative. Batches of the sugar beet pulp showed pronounced microbial deterioration, the flora being dominated by yeasts and filamentous fungi (moulds). Several species of fungi have been isolated but so fat their possible role in the etiology of the syndrome remains unsettled. The syndrome bears some resemblance to cerebrocortical necrosis (C.C.N.) but differs in several clinical and pathological details. It is tentatively suggested that the beet pulp may have contained one or more toxic substances that interfere with microbial activity in the rumen, resulting in a disturbance of synthesis or absorption of essential metabolites. The clinical, epidemiological and pathological findings are compatible with the hypothesis that the syndrome might be due to fungal toxins. Accordingly, the isolated fungi are now being studied in more detail.

Animal Feed↗