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Biomedical subjects

L Niilo

Publications and source records attributed to L Niilo.

At least 37 records · Page 2Linked to original sources
PubMed1975

Use of the brucellosis card test for screening cattle in Saskatchewan.

One group of 28,714 bovine sera were tested by both the brucellosis tube serum agglutination test and the brucellosis card test. The tube serum agglutination test confirmed 99.8% of the negative brucellosis card test results. The brucellosis card test identified 63% of the tube serum agglutination test reactors. In a second group of 496 sera reacting to either the tube serum agglutination test, complement fixation test, plate serum agglutination test or acid antigen serum agglutination test the brucellosis card test identified 99.1% of the complement fixation test positive sera and 91.3% of the sera reacting to any of the other serological tests. The brucellosis card test showed satisfactory agreement with both the complement fixation test and tube serum agglutination test. It appears to be a useful screening test in operations involving large numbers of animals since under these conditions the reactors can be quickly identified and isolated.

Agglutination Tests↗
PubMed1974

Response of ligated intestinal loops in chickens to the enterotoxin of Clostridium perfringens.

Approximately 45-cm length of jejunoileum of 7-week-old chickens was found to be responsive and suitable for testing the enterotoxin of Clostridium perfringens by the ligated intestinal loop technique. Injections of 20 to 30 mug of enterotoxin per loop caused positive response of fluid accumulation. Chickens were found to be more convenient and economical for this purpose than other laboratory and domestic animals.

Animals↗
PubMed1973

Fluid secretory response of bovine Thiry jejunal fistula to enterotoxin of Clostridium perfringens.

The effect of enterotoxin of Clostridium perfringens type A was studied in Thiry fistula of the bovine jejunum. Accumulation of fluid as a pathological response was demonstrable within 30 min after introduction of enterotoxin into the fistula; the fluid volume increased rapidly within the first 2 hr and reached maximum in 7 hr. The enterotoxin was not destroyed by the jejunal fluid; 52% of it was absorbed in 2 to 3 hr, and all of the enterotoxin was taken up within 8 hr postinoculation. The accumulation of fluid by the fistula after 0.5 to 2 hr of exposure to enterotoxin ceased completely within 5 hr.

Animals↗
PubMed1971

Mechanism of Action of the Enteropathogenic Factor of Clostridium perfringens Type A.

Cell extract of an enteropathogenic strain of Clostridium perfringens type A was administered intravenously to lambs, rabbits, and guinea pigs. Lambs developed transitory diarrhea, lacrimation, salivation, nasal discharge, lassitude, and dyspnea in 1 to 5 hr after inoculation. Large doses of the inoculum caused rapid onset of the clinical signs and subsequent death. Examination of dead animals revealed intensely hyperemic small intestinal mucosa and some congestion in the liver, lungs, spleen, and kidneys. Rabbits showed excessive salivation, frequent defecation, tranquility, and dyspnea, followed by death. Guinea pigs became weak and died in 15 min to 7 hr. Congestion was evident in lungs, liver, spleen, and in the small intestine. In lambs and guinea pigs tested, atropine and epinephrine alleviated the clinical signs. Intradermally injected cell extract caused an immediate increase in capillary permeability and subsequent erythematous reaction without necrosis in the skin of guinea pigs. It is hypothesized that in the enteric infection C. perfringens enteropathogenic factor acts on the small intestine causing increased capillary permeability, vasodilation, and increased intestinal motility.

Journal Article↗
PubMed1970

Experimental winter coccidiosis in sheltered and unsheltered calves.

Hereford calves, seven months old, were inoculated orally with sporulated oocysts of Eimeria bovis and E. zurnii and housed in a heated building together with uninoculated animals. Duplicate groups of similarly treated animals were left unsheltered in cold winter weather. Clinical coccidiosis developed in most of the inoculated calves, sheltered and unsheltered. There was no marked difference in the severity of the infections. The sheltered uninoculated contact animals remained clinically unaffected, but mild coccidiosis developed in the unsheltered controls. The results suggest that cold may increase the host's susceptibility to clinical coccidiosis, but may not increase the severity of the signs once the clinical infection is established.

Animals↗
PubMed1970

The effect of dexamethasone on bovine coccidiosis.

When dexamethasone was administered intramuscularly to Hereford calves at the time of inoculation with Eimeria zurnii and E. bovis, there was no apparent effect on the resulting infection. Medication at the time of appearance of the clinical signs caused sufficient aggravation of the disease to result in the death of the animals. Administration of the drug after subsidence of the clinical signs did not cause a clinical relapse, but resulted in prolonged oocyst discharge in the feces. Treatment of uninoculated normal calves with dexamethasone caused a brief period of increased oocyst discharge without clinical signs.

Animals↗