Summary The bacterial and fungal flora of 200 normal and 50 infected ears of dogs were studied with the object of isolating and identifying the causative agents. Large numbers of fungi and yeasts were isolated from normal as well as infected ears. It was concluded that Pityrosporum canis may act as a primary pathogen in otitis externa in dogs and can invade the normal healthy skin of the ear canal, whereas Aspergillus niger has no capacity to establish in the normal ear canal. However, it can colonise the ears infected with bacteria and/or fungi. Zusammenfassung Die Bakterien‐ und Pilzflora 200 gesunder und 50 erkrankter Hundeohren wurden durch kulturelle Untersuchun en erfaiβt und die auslösenden Ursachen bestimmt. Zahlreiche Schimmelpilze und Hefen wurden sowohl von gesunden als auch von infizierten Ohren isoliert. Es wird gefolgert, daβ Pityrosporum canis primär pathogen sein kann und durch Besiedlung der gesunden Haut des äuβeren Gehörganges bei Hunden eine Otitis externa hervorrufen kann. Aspergillus niger hingegen besitzt nicht die Eigenschaft, den gesunden Gehörgang zu befallen, sondern dieser Schimmelpilz besiedelt nur durch Bakterien undloder Pilze erkrankte Ohren. Otornycosis in human beings is a well defined clinical entity (CHHANGANI et al. 1958; LAKSHMIPATI and MURTHI 1960; SINHA and MOHADATRA 1961; and SOOD et al. 1966). Fifty‐three different species of fungi have been recorded as aetiological agents of human otornycosis, but their role in otitis externa in dogs is not yet fullyestablished. Otitis externa in dogs is a common condition. Most of the cases have been found to be of bacterial origin (GUSTAFSON 1955; and GRONO 1969), but different fungi have also been implicated in significant proporrions (AINSWORTH 1954; LAPOEVIC and CIRIC 1963; and SMITH 1968). The present paper deals with the survey of fungal flora found in otitis externa in dogs and in clinically normal ears, with the object of isolating and identifying the causative agents.

No abstract

B-cell-deficient mice were prepared by administration of rabbit anti-mouse-,u antiserum to newborn animals within 12 h of birth onwards. Such immunodeficient animals, along with the normal controls, were infected intravenously with Cryptococcus neoformans. There was no difference in the mortality pattern, viable count of cryptococci in different organs, delayed-type hypersensitivity reaction, and antigen level in the sera of control and B-cell-deficient animals. Antibodies were absent in B-cell-deficient animals but were present in low titers in control animals. It is concluded that antibodies are not involved in protection of mice infected with C. neoformans.

No abstract

No abstract