Pathogenicity of Candida viswanathii for normal and cortisone-treated mice.

The pathogenicity of Candida viswanathii, PCI 501/1 (CBS 4024), originally isolated from CSF of a fatal case of meningitis in India, is reported. Also, included is a global overview of the occurrence of C. viswanathii in clinical and environmental sources. The investigation was done in normal and cortisone-treated albino mice challenged intravenously with variable doses of 1×10(6), 4×10(6) and 16×10(6) actively growing yeast cells of the fungus. The animals were kept under observation up to 3 weeks when they were sacrificed for a mycological and histopathologic study. As apparent from the data on morbidity and mortality, the species exhibited low virulence for normal mice, whereas it caused significantly higher mortality (P<0.0008) and morbidity (macroscopic lesions) (P<0.0004) in cortisone group. Likewise, there was overall higher recovery of C. viswanathii in culture from the cortisone-treated than in the normal group of mice. These observations are indicative of C. viswanathii being an opportunistic pathogen. It is recognized that a definitive identification of C. viswanathii requires mycological expertise for comprehensive phenotypic characterization or the application of expensive techniques such as Matrix-assisted laser desorption/ionization mass spectrometry (MALDI-TOF MS) and molecular techniques, facilities for which are generally lacking in a vast majority of laboratory diagnostic centers especially in developing countries. Consequently, the prevalence of C. viswanathii in clinical and environmental samples is currently likely to be underestimated.

Pathogenicity of some ordinarily harmless yeasts for cortisone-treated mice.

The pathogenicity for normal and cortisone-treated mice of Candida requinyii, Pichia etchellsii, Candida famata (Torulopsis candida) Trichosporon cutaneum and Sterigmatomyces aphidis, isolated from foodstuffs or clinical material, is reported. The test species proved nonpathogenic to normal mice inoculated intravenously with up to 10(7) cells. There was neither any mortality nor gross or microscopic lesions, and cultures were negative from the visceral organs and brain when these animals were necropsied after 3 weeks of observation. In cortisone-treated mice, on the other hand, the yeasts caused mortalities, the extent of which varied according to the infecting species and the challenge dose. Candida requinyii was the most pathogenic species, causing 100% mortality in 8 days, followed by S. aphidis, C. famata, T. cutaneum and P. etchellsii which killed 75%, 50%, 38% and 25% of the infected animals. Apart from the higher mortalities, C. requinyii and S. aphidis caused more frequent visceral lesions than did either T. cutaneum or C. famata. Involvement of the brain occurred more commonly with C. requinyii and T. cutaneum than with C. famata or S. aphidis. P. etchellsii was the only yeast that failed to incite any gross or microscopic lesions. The study re-emphasizes the pathogenic potential of ordinarily harmless fungi for immunosuppressed hosts.

Aspergillosis in imported penguins.

An outbreak of aspergillosis in imported penguins caused by Aspergillus fumigatus is described. The birds probably acquired the infection from the country of origin or during their transportation. Predisposing circumstances are discussed.

Conditional virulence of a p-aminobenzoic acid-requiring mutant of Aspergillus fumigatus.

The induced auxotrophy for p-aminobenzoic acid (PABA) resulted in a complete loss of virulence of Aspergillus fumigatus for normal as well as cortisone-treated mice. The PABA-requiring mutant of A. fumigatus survived in vivo for 4 to 7 days without causing any infection. However, it showed conditional virulence in animals receiving PABA in very small quantities. Repeated inoculations of the viable spores of the avirulent mutant strain gave favorable results in building immunity against intravenous challenge of the virulent strain. The immunogenicity of the PABA-requiring mutant was comparable with that of a wild strain of the fungus in agar gel double-diffusion tests using clinical and hyperimmune sera and in skin tests on patients with allergic bronchopulmonary aspergillosis.

Mycetoma of the knee due to Nocardia caviae.

Mycetoma of the knee, caused by Nocardia caviae and idangosed by culture and histopathology, occurred in a 20 year old farmer from a rural area of Varanasi District in Uttar Pradesh, India. The isolate was pathogenic to mice and it showed close agreement with the standard description of the species. It is suggested that infection due to this species has a higher prevalence than is currently recognized.

Effect of cortisone administration on experimental nocardiosis.

Effect of cortisone administration on the pathogenicity of Nocardia asteroides, N. caviae, and N. brasiliensis for white mice has been investigated by using the intravenous route of inoculation. The observations indicated that the susceptibility of white mice to nocardiosis was enhanced by cortisone. Test strains of the three species of Nocardia caused a higher and more rapid mortality, as well as more extensive lesions, in the cortisone-treated than in the normal mice. The mean lethal dose (LD(50)) values of N. asteroides and N. caviae for the cortisonetreated group were found to be seven and eight times lower than their respective values for the normal group. N. asteroides and N. caviae were more virulent than N. brasiliensis, the LD(50) of N. brasiliensis for cortisone-treated mice being 30 and 26 times higher than that of the former two species, respectively. N. brasiliensis also differed from the other two species in its inability to infect the brain. In the untreated animals, N. asteroides and N. caviae showed a tendency to form conglomerate growth, in contrast to formation of freely dispersed growth in the lesions of cortisone-treated animals.

Mechanism of excitation of type J receptors.

The type J receptors are stimulated during pulmonary congestion produced by occluding the aorta or left a-v junction which causes the left atrial pressure to rise with consequent rise in pulmonary artery pressure. Such acute congestion can be maintained only for brief periods (1-2 min). Longer lasting congestion leading eventually to pulmonary oedema is produced by injecting alloxan into the right atrium or right ventricle. A marked rise in pulmonary artery pressure follows the injection and after a lag there follows intense excitation of the type J receptors. It was concluded that this excitation was due to a rise in pulmonary capillary pressure and increase in permeability of the capillary membrane. Recent experiments have revealed that a considerable increase in activity can also be produced by injecting plastic microemboli (diameter 50 minus-plus 10 micrometers, i.v.). This increase occurs a few minutes after the rise in pulmonary artery pressure and is not due to a direct action of the microemboli on the endings nor can it be due to increased capillary permeability. Here, there can be no doubt that the increase in activity is a consequence of the rise in pulmonary artery pressure leading to a rise in pulmonary capillary pressure. This causes increase in interstitial volume leading to excitation of the endings. It was postulated that the endings were located in collagen tissue which acts like a sponge. Recently electronmicroscopic evidence has been obtained showing the presence of non-medullated sensory fibres in this collagen tissue but the precise structure of the endings (presumably type J) and their physical relation to the collagen tissue still remains to be established.