Summary
The organisms of the pleuropneumonia group, PPO, AGO and PPLO, constitute a uniform class of microbes. They all grow in small colonies, which can easily be overlooked unless inspected microscopically. Their colony form, a dark central portion embedded in the agar medium and lighter peripheral zone, is characteristic. Their morphology is fundamentally simple. Small granular forms, of the size of vaccinia virus, called minimal reproductive units, can initiate the growth of the larger forms. The organisms lack rigid cell walls, but have a flexible outer boundary (‘plasmalemma’). The shape and size of the organisms vary and depend on environmental conditions. Filamentous forms, small globules, disks and, on solid media, large flat forms are observed. Eventually, all these forms produce the minimal reproductive units.
The nutritive requirements of the members of the group are rather exacting. Some grow well on ordinary media, but most of them require an additional factor derived from serum and some other growth factors as well. Suitable media are of paramount importance for the isolation and maintenance of these exacting organisms.
Identification of organisms of the pleuropneumonia group in material from lesions by means of fixed and stained preparations is very difficult and liable to error. In most cases only the established culture on penicillin‐free media can be regarded as positive evidence of the presence of a PPLO in the specimen.
For the identification of species the serological method is most reliable, though some organisms can be distinguished by their special growth characteristics.
Pleuropneumonia organisms are killed by disinfectants, organic gold compounds, streptomycin and aureomycin, but not by sulphonamides and penicillin.
Some varieties of organisms have been found in humid soil, in decaying plant material and in polluted water, and others have been isolated from the organs or body fluids of animals, or from their mucous membranes. Those that are known as causes of animal diseases, though widely varying in their effect on their hosts, show an interesting similarity in their mechanism of infection. Though the diseases produced are often devastating and lethal, infection in the field does not readily follow exposure to the infective agent. However, outbreaks of the disease often occur in animals exposed to stress, and it appears that these events light up inap‐parent infection acquired some time previously; that is to say, the infection becomes manifest when the resistance of the animal is lowered. This has been observed in the great epizootics of bovine pleuropneumonia and agalactia of sheep and goats, where the second factor may be fatigue or, in the case of sheep and goats, parturition and lactation. In laboratory animals also a natural latent infection may become active on application of unspecific substances or of a second infective agent, which may or may not be itself pathogenic for the injected animal.
A new line of research has been opened by experiments on mixed infections. When the n...