Observations on the Ætiology of Psittacosis.

Bedson, S. P.; Western, G.T.; Simpson, Steve

doi:10.1016/s0140-6736(00)87345-6

Cited by 51 publications

(12 citation statements)

References 2 publications

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“…Similar stages in the growth of the related organisms of the psittacosis-lymphogranuloma group were first described for psittacosis virus by Bedson, and his coworkers (Bedson, 1933;Bedson & Bland, 1932,1934Bland & Canti, 1935) and their reports have been amply confirmed by other authors. It was generally believed that the virus remained at least partially infective throughout the growth cycle; though Girardi, Allen & Sigel (1952) concluded that psittacosis virus underwent a noninfective phase.…”

Section: Discussionsupporting

confidence: 66%

A Study by Fluorescence Microscopy of the Replication of Inclusion Blennorrhoea Virus in HeLa Cell Monolayers

Furness

Henderson²,

Csonka

et al. 1962

Journal of General Microbiology

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SUMMARYThe infectious agent of inclusion blennorrhoea was seen by fluorescence microscopy as a particle of deoxyribonucleic acid (DNA) 0.2 p diam.These infectious particles and particles inactivated at 4" and 56" were adsorbed by HeLa cell monolayers. The inactivated particles were visible for at least 6 hr., distributed at random on the cells, while the infectious particles rapidly disappeared. Multiple infections of the cells readily occurred and in cells so infected, a cluster of ribonucleic acid (RNA) particles was first observed at 3 hr. adjacent to the cell nucleus. Since the number of RNA particles, each of which contained a DNA core, was equal to the number of infectious particles adsorbed and since singly infected cells contained only one RNA particle, the infectious unit is almost certainly a single DNA particle. The RNA particle increased in size without dividing and the surrounding cell cytoplasm gradually dissolved to form the inclusion body. DNA particles which were protected from deoxyribonuclease by a layer containing RNA were first observed in the inclusions at 21 hr. and an average of one infective progeny was detected in each infected cell at 22-23 hr. indicating that infectivity was associated with the DNA particles. RNA, DNA and infectious DNA particles reached their maxima between 27-30 hr., 39-42 hr. and 34-38 hr.respectively and decreased thereafter. Infectious DNA particles were released from the inclusions. The total number of DNA particles/inclusion always exceeded the number of infectious DNA particles/inclusion.Glycogen was not detected in the inclusions suggesting that it may not be essential for the formation of virus.

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Section: Discussionsupporting

confidence: 66%

A Study by Fluorescence Microscopy of the Replication of Inclusion Blennorrhoea Virus in HeLa Cell Monolayers

Furness

Henderson²,

Csonka

et al. 1962

Journal of General Microbiology

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“…Bedson, Western & Levy-Simpson , 1930;Findlay, Mackenzie & MacCallum, 1938;Bedson & Gostling, 1954) showed these agents to be obligate intracellular parasites with a complex growth cycle. This involved the development of cytoplasmic inclusions containing relatively large particles (c. 1 p) termed initial bodies, which appeared to multiply by binary fission and give rise to a population of smaller infective particles (c. 0-3 p) termed elementary bodies.…”

Section: Introductionmentioning

confidence: 99%

Fine Structure of Lymphogranuloma Venereum Agent and the Effects of Penicillin and 5-Fluorouracil

Armstrong

Reed

1967

Journal of General Microbiology

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“…The widespread outbreak of psittacosis in man in 1929-30 led to renewed interest in the disease which quickly resulted in the discovery of the facts that the causative agent is not Nocard's bacillus but a filterable virus (1) and that the incidence of laboratory infections is high. Because of these facts it became imperative that further work on the nature of the etiological agent and the mode of spread of the infection be undertaken.…”

mentioning

confidence: 99%

Psittacosis

Rivers

Berry

Sprunt

1931

Journal of Experimental Medicine

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1. The virus of psittacosis is present in the nasal secretions, feces, blood, spleen, and liver of an infected parrot. 2. Parrots are susceptible to intraoral, intranasal, or intramuscular inoculations of the virus. 3. The most constant pathological changes produced by psittacosis in parrots occur in the spleen and liver. The lesions exhibited in the latter organ consist of areas of necrotic liver cells and damage to bile ducts. In no instance, in our experience, were lesions observed in a parrot's lungs comparable to those found in the lungs of men. 4. "Minute bodies" similar to those described by Levinthal and others were found in many, but not in all of the infected birds. 5. Parrots that have recovered from one attack of psittacosis exhibit an active immunity against reinfection.

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Observations on the Ætiology of Psittacosis.

Cited by 51 publications

References 2 publications

A Study by Fluorescence Microscopy of the Replication of Inclusion Blennorrhoea Virus in HeLa Cell Monolayers

A Study by Fluorescence Microscopy of the Replication of Inclusion Blennorrhoea Virus in HeLa Cell Monolayers

Fine Structure of Lymphogranuloma Venereum Agent and the Effects of Penicillin and 5-Fluorouracil

Psittacosis

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