Publisher Summary This chapter explains the Mycoplasma diseases of plants and insects. It discusses the nomenclature and classification of the order Mycoplasmatales. The nonviral nature of the numerous graft-transmissible, arthropod-borne disease agents of plants is established. Electron microscopy reveals the characteristic morphology of the presumptive micro-organisms observed in diseased phloem cells and in various vectors, but absent from healthy phloem or from non-infected vectors. Plants can recover from yellows-type diseases when treated with sulfa drugs that definitely do not affect mycoplasmas, and they sometimes recover when treated solely with fertilizers. The chapter discusses on only specific criteria, accepted by microbiologists, should be used in the determination of the actual etiology of the presumptive mycoplasma diseases. These criteria require the cultivation of the isolated agents on solid media with the production of mycoplasma colonies, the reinoculation of susceptible healthy plants with the cultured mycoplasmas, and the subsequent reproduction of the original disease.

Mycoplasma diseases of plants and insects.

Mice of a Swiss substrain, reared under rigid pathogen-free (PF) conditions, were inoculated intranasally with broth cultures of Mycoplasma pulmonis ranging in dose from 101 to 9 × 109 colony forming units (CFU). A highly reproducible disease resulted with an LD50 of 1.3 × 108 CFU and a PD50 (dose producing pneumonia in 50% of mice) of 3.4 × 105 CFU. The inoculating dose of M pulmonis was found to be the critical determinant of the severity, duration and pathologic character of the respiratory disease produced. PF mice given 104 CFU or less developed a transient illness characterized by low frequencies of rhinitis, otitis media, laryngotracheitis and focal pneumonia. This was proposed as a low dose model. Doses of 105 to 109 CFU resulted in high frequencies of rhinitis, otitis media, laryngotracheitis and pneumonia. Within the first 10 days the pneumonia often was fatal, being characterized by an outpouring of neutrophils and edema fluid into alveolar spaces, pulmonary congestion and hemorrhage and, occasionally, pleuritis. This high dose—acute disease model was shown to be the result of seeding alveoli with large numbers of organisms at the time of intranasal inoculation. In animals surviving doses of 105 to 109 CFU beyond approximately 10 days postinoculation, the larger concentration of organisms was present in bronchi and bronchioles, giving rise to a third model, the high dose—chronic disease model. The predominant lesions were chronic suppurative bronchitis and bronchiolitis, marked peribronchial lymphoid cuffing, variable numbers of neutrophils and macrophages in alveoli, and complications such as bronchiectasis and pulmonary abscesses. Identical lesions were observed in axenic mice infected with M pulmonis. The infection in PF mice is considered a highly useful experimental system, both for comparative study of respiratory mycoplasmosis and for investigations directed toward understanding and eliminating the natural disease this agent causes in conventional mice and rats.

Experimental Mycoplasma pulmonis infection in pathogen-free mice. Models for studying mycoplasmosis of the respiratory tract.

13 – mycoplasma–tissue cell interactions

8 – murine and other small-animal mycoplasmas

WHEN phagocytic cells ingest and kill micro-organisms, a variety of biochemical responses ensue and exercise specific roles in the major phases of the phagocytic process.1 , 2 For example, the incr...

On the interaction between phagocytes and micro-organisms.

Mechanisms of pathogenesis in Mycoplasma infection

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Mechanisms of pathogenesis in Mycoplasma infection