“Slobbers” in laboratory guinea‐pigs as a form of chronic fluorosis

Abstract

DURING 1964 and early 1965 deaths often reaching epidemic proportions occurred in at least nine major guinea-pig breeding units in New South Wales and Canberra. The outstanding sympton in the great percentage of cases was marked fluid loss from the mouth.Outbreaks of a syndrome referred to in the past as " slobbers " have been reported in the guinea-pig from time to time, but the aetiology of the condition leading to this symptom has never been conclusively determined. Pirtle and McKee (1951) recorded an epidemic of unknown origin in the guinea-pig, in which a marked wetness around the chin, neck and ventral abdomen was the outstanding symptom. The authors attributed this dampness to constant nausea accompanied by frequent vomiting. Autopsy revealed only severe depletion of body fat, some meningeal congestion and secondary lung consolidation; no reference was made to the presence or absence of buccal lesions. Histopathological examination demonstrated degenerative changes in the neurones of the hippocampal gyms as the only constant suggestive finding. The authors made no mention of the constitution of the diet.Paterson (1957) observed " slobbers" together with dental overgrowth in postparturient female guinea-pigs fed on Parke's diet 18 and kale but deprived of hay, and inferred that the absence of an unidentified factor in the latter supplement was responsible. The histopathology of the affected teeth was difficult to interpret, but was considered to be one of acute rickets complicated by changes of typical Scurvy.The results of Galloway, Glover and Fox (1964) confiict with Paterson's .observations, as they found that hay deprivation for 36 wk produced no signs of ill health. Profuse salivation has been described in the symptomatology of experimental folic acid deficiency (Reid, Martin and Bnggs, 1956).The syndrome observed in the current Australian epidemic was not unlike those previously described and we therefore studied its epidemiology and pathogenesis. MATERIALS AND METHODSSixty affected guinea-pigs obtained from many of the breeding units and laboratories reporting the disease outbreak were submitted to a complete necropsy. Material from 20 of these was prepared for histological examination. Soft tissues were fixed in formalin, and paraffin sections were stained with haematoxylin and eosin. Bones and teeth were fixed in 5 per cent. formaldehyde-saline followed by preliminary decalcification in picroformalin-formic acid solution and final demineralisation in '' Decal " (Omega). After neutralisation the tissues were J. PAM. BACT.-VOL. 94 (1967) 95 96 G. C . HARD AND F. F. V. ATKINSON double-embedded by a celloidin-paraffin technique. Sections were cut in a sagittal or longitudinal plane at 6 p and stained with haematoxylin and wsin or toluidine blue. For gross examination of the skeletal tissue, the carcasses of at least 30 affected animals were macerated by simmering them in water. RESULTS Clinical signs and gross pathologyThe disease was first recorded in newly weaned animals, housed in wire cages. Later,...