Experimental infective pneumoconiosis: effect of asbestos dust and Candida albicans infection on the lungs of rhesus monkeys

Our plain-English summary of Experimental infective pneumoconiosis: effect of asbestos dust and Candida albicans infection on the lungs of rhesus monkeys, by S.H. Zaidi, R. Shanker, R.K. Dogra (Environmental Research, 1973).

The study

• Authors: S.H. Zaidi, R. Shanker, R.K. Dogra
• Journal: Environmental Research
• Published: 1973;6(3):274-86
• Cited by: 8 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

The combined effect of Candida albicans, a facultative pathogen in the normal physiological condition in the throat of miners, and amosite dust produces after intratracheal inoculation extensive collagenous fibrosis at 330 days in rhesus monkeys. The lesions produced by amosite dust alone comprise fine reticulin fibrosis around bronchioles and blood vessels and moderate interstitial fibrosis. The C. albicans infection alone caused acute inflammatory reaction in the early stages while at the termination of experiment (330 days) the only evidence of pulmonary candidiasis was a few small fibrotic foci of compactly arranged reticulin fibers.

PubMed has no abstract for this study. This is the authors' abstract, copied from the article.

In plain English

In this animal experiment at the Industrial Toxicology Research Centre in Lucknow, India, the authors studied whether a mild infection with the organism Candida albicans alters lung scarring from asbestos. After two tuberculin-positive animals were discarded, 78 rhesus monkeys were injected into the windpipe with 1 mg of Candida alone, 1 g of Indian amosite asbestos dust alone, or both. Animals were killed and examined at intervals up to 330 days. With Candida alone, early acute inflammation was seen. No live organisms were recovered from 90 days on, and at 330 days a few small scarred spots remained while most lung tissue looked normal. With amosite alone, fibrosis (scarring) around small airways and blood vessels was marked by 330 days. Monkeys given both developed diffuse collagen fibrosis and thick pleural adhesions, which the authors called altogether different from either exposure alone. The authors concluded that extensive fibrosis in the presence of dust is related not only to tuberculosis bacteria but also to infections like Candida. They said the mechanism was unclear and needed further study.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Animal experiment: intratracheal injection of amosite dust, Candida albicans, or both into rhesus monkeys, with animals killed and examined at set intervals up to 330 days (descriptive pathology, no statistical analysis)
• Who was studied: 80 locally obtained rhesus monkeys (Macaca mulatta) with an average body weight of 4 kg, studied at the Industrial Toxicology Research Centre, Lucknow, India. Two tuberculin-positive animals were discarded, and 78 were divided into three groups. Group I had 26 animals; the sizes of the other groups are not clearly legible in the text.
• Exposure: Indian amosite asbestos dust, crushed to pass a 200-mesh sieve and suspended in sterilized saline. Group I received 1 mg Candida albicans alone, Group II received 1 g amosite alone, and Group III received 1 g amosite plus 1 mg Candida albicans, each in 10 ml saline, by intratracheal injection. The doses were chosen after preliminary experiments.
• Main results:
  • Candida alone (Group I): acute inflammatory reaction in the early stages
  • Candida alone (Group I): no live organisms were recovered from the lung from 90 days onwards, but organisms persisted when amosite dust was also present
  • Candida alone (Group I): at 330 days a few isolated fibrotic foci persisted, but most of the lung tissue regained its normal architecture
  • Candida alone (Group I): two animals that died on day 40 and day 172 had small lung abscesses
  • Amosite alone (Group II): by 330 days the lungs showed dense fibrosis of thick collagen fibers around bronchioles and blood vessels and moderate interstitial fibrosis (as described in the Discussion)
  • Amosite alone (Group II): cultures of the lung for Candida were negative at all time points
  • Gross findings: thin adhesions were first seen at 120 days in the amosite-alone group and at 60 days in the combined group
  • Amosite plus Candida (Group III): at 330 days, diffuse fibrosis of collagen and thick reticulin fibers
  • Amosite plus Candida (Group III): live organisms were still recovered at 120 days; counts were negative from 150 days on
  • The authors described the extensive fibrosis in the combined group as altogether different from that seen with amosite alone or Candida alone
• The authors' conclusion: The authors concluded that extensive lung fibrosis in the presence of dust is related not only to tubercle bacilli, as they had reported earlier, but also to other infections like Candida albicans.
• Limitations the authors state:
  • The mechanism behind the extensive fibrosis in the combined group could not be determined from these experiments and needs further investigation
  • It is not clear whether the fibrosis in the Candida-only group came from the live organism or its metabolites, since cultures had turned negative
  • The severity of the amosite lesions may reflect the injection technique, the large dose given, or a species difference
  • How far the organism worsens the fibrosis of asbestosis under real dusty conditions remains to be investigated

Topics

Medical terms in this study, explained in our Lexicon: Pneumoconiosis, Amosite, Fibrosis, Interstitial Fibrosis.

Related studies

• Biochemical studies in infective amosite pneumoconiosis — A.K. Jaiswal (1981)
• Pleural plaques in asbestosis: effect of Candida albicans — K.C. Saxena, L. Srivastava, et al. (1982)
• The relation between lung dust and lung pathology in pneumoconiosis — G. Nagelschmidt (1960)
• Impaired chemotactic responses of bronchoalveolar leukocytes in experimental pneumoconiosis — K. Donaldson, G.M. Brown, et al. (1990)
• Expression of genes coding for growth factors in experimental pneumoconiosis — G.F. Morris, J.Y. Liu, et al. (1996)
• Characterization of the lower respiratory tract inflammation of nonsmoking individuals with interstitial lung disease associated with chronic inhalation of inorganic dusts — W.N. Rom, P.B. Bitterman, et al. (1987)

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