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Nonhemotropic Mycoplasma, Ureaplasma, and L‐Form Bacteria
Joachim Spergser, Dipl.Tzt., Dr. Med. Vet., DECVM

Institute of Microbiology, University of Veterinary Medicine, Vienna, Austria

Etiology commensals, but certain members are proven pathogens
or play an etiologic role as opportunists in miscellaneous
Mycoplasmas (general name for members of the class conditions (Table. 98.1).
Mollicutes) are unusual bacteria representing the small­ Little is known about the virulence factors of canine
est and simplest self‐replicating organisms. They are and feline mycoplasmas so far. However, the availability
distinguished from ordinary bacteria by their complete of the complete genome of two canine Mycoplasma spe­
lack of a cell, resulting in cellular pleomorphism and cies (M. canis, M. cynos) will certainly increase under­
resistance to cell wall‐inhibiting antimicrobials. The standing of their pathogenic properties in the future.
lack of a protective cell wall also makes mycoplasmas Recently, a hemagglutinin that is probably involved in
fragile outside their hosts. Due to their extremely small cytadherence to host cells has been identified and char­
genome size, mycoplasmas possess limited anabolic acterized in M. cynos. Furthermore, a secreted sialidase
and metabolic capabilities and maintain intimate para­ that presumably promotes colonization and tissue inva­
sitic lifestyles, depending on nutrients from their host sion has been proposed as a candidate virulence factor of
cell environment. To keep this parasitic mode of life, M. canis and M. cynos. Its expression in canine myco­
mycoplasmas have developed sophisticated mecha­ plasmas varies significantly among strains which may
nisms to colonize their hosts and resist host defense. A contribute to the variable spectrum of clinical manifesta­
highly dynamic, versatile membrane surface architec­ tions and disease outcomes. Intracellular localization of
ture appears to be crucial for their survival, and for M. canis has also been demonstrated which may contrib­
establishing and maintaining a subtle relationship with ute to chronicity of infection or perturbation of cell func­
their host. Certain mycoplasmas are capable of entry tion and integrity.
into nonphagocytic cells, providing them with the abil­ L‐forms are cell wall‐deficient morphotypes of normal
ity to resist host defenses or antibiotic treatment, which bacteria that resemble mycoplasmas. L‐forms can be
may contribute to chronic infection. generated from many bacterial species by treatment with
Nonhemotropic mycoplasmas usually exhibit a rather lysozyme or by exposure to beta‐lactam antibiotics or
strict host and tissue specificity with predilection for host immune responses. Knowledge of the clinical sig­
mucous membranes of the respiratory and urogenital nificance of L‐form bacteria is fragmentary and their role
tract. Pathogenic mycoplasmas are not considered highly as a cause of disease is still under debate.
virulent and mostly cause mild, slowly progressive,
chronic infections. Host cell damage and the resulting
clinical manifestations appear to be mainly due to host Epidemiology
immune reactions and inflammatory responses rather
than to direct toxic effects of mycoplasma components. Mycoplasmas are common inhabitants of the orophar­
Nonhemotropic mycoplasmas that have been isolated ynx and upper respiratory tract of dogs and cats wherein
from cats and dogs include species within the genera they are thought to be part of the normal bacterial flora.
Mycoplasma, Ureaplasma, and Acholeplasma. Some Mycoplasmas have been isolated from lungs of dogs and
canine and feline mycoplasmas are considered mere cats with pneumonia, are shown to be absent in the lungs

Clinical Small Animal Internal Medicine Volume II, First Edition. Edited by David S. Bruyette.
© 2020 John Wiley & Sons, Inc. Published 2020 by John Wiley & Sons, Inc.
Companion website: www.wiley.com/go/bruyette/clinical