Pollob K. Shil, Nadeeka K. Wawegama, Glenn F. Browning, Amir H. Noormohammadi, and Marc S. Marenda


All members of the class Mollicutes are commonly referred to as mycoplasmas. Each of the major domestic animal species is host to several different species of pathogenic mycoplasmas, which typically cause chronic, endemic disease. Mycoplasmas lack a cell wall and have the smallest cell size (down to approximately 300 nm diameter) and the smallest genomes (down to 580 kb) of all free‐living organisms, a consequence of their reductive evolution from Gram‐positive bacteria with a low genomic G + C mol% content. They have a broad biological distribution as parasites of mammals, birds, reptiles, fish, cephalopods, crustaceans, arthropods, and plants. They are divided into four phylogenetic groups, Pneumoniae, Hominis, Anaeroplasma and Spiroplasma, but exhibit considerable genetic plasticity, with massive horizontal genetic transfer events between species in different phylogenetic groups shaping the evolution of a number of important pathogenic species. This is exemplified by the Mycoides cluster, a group of highly pathogenic species that only infect ruminants but lie within the Spiroplasma group, which is predominantly composed of insect‐transmitted plant pathogens. While the core genomes of the members of this cluster are most closely related to the spiroplasmas, approximately 20% of their genome is most closely related to the genomes of ruminant mycoplasmas in the Hominis group. One member, Mycoplasma mycoides subspecies mycoides, causes contagious bovine pleuropneumonia (CBPP), one of the most important bacterial diseases of domestic animals.

Characteristics of the Organisms

Mycoplasmas are obligate parasites and most survive on moist mucosal surfaces of their vertebrate hosts, although the hemophilic mycoplasmas are exclusively parasites of erythrocytes. They are highly pleomorphic, but do have a cytoskeleton that controls their shape (Balish and Krause 2006). They lack most of the biosynthetic capacity of other bacteria and thus rely on import systems to scavenge complex nutrients from their hosts and have fastidious requirements for growth in vitro. In all mycoplasmas except acholeplasmas, the osmotic stability of the cell is maintained by incorporation of cholesterol into the cell membrane (uniquely among the procaryotes), which must be obtained exogenously. Unlike all other bacteria, the proteins and lipoproteins embedded in the cell membranes of mycoplasmas interact directly with their host, playing a key role in adhesion, acquisition of essential complex nutrients and evasion of the immune response.

As a consequence of the phylogenetic distance between the mycoplasmas and other bacteria, and their unique adaptations to a dedicated parasitic lifestyle, a large proportion of their genes, and particularly genes predicted to encode surface proteins, only have identifiable orthologues within other mycoplasmas, and sometimes only in closely related mycoplasmas.

While the mycoplasmas share some common features, they are nevertheless a diverse group, particularly with respect to their pathogenic potential, which varies widely both between species and among strains within species. Many species are commensals, while a few can cause acute mortality. Assessing the pathogenic role of mycoplasmas can be problematic. Their isolation from mucosal surfaces in disease states does not necessarily indicate etiological significance, because the same species often can be isolated from the same sites in clinically normal animals. Intercurrent factors, including co‐infection with other agents and adverse environmental influences, can play an important role in precipitating disease.

While animal mycoplasmas are generally regarded as extracellular parasites, at least some species have the capacity to invade non‐phagocytic cells.

Pathogenic Species

Mycoplasmas are usually considered to be relatively host specific. Although infection may occur in more than one host species, there is usually a primary host, to which disease is mostly confined. Table 31.1 lists the important pathogenic species of the major domestic animal species. However, a number of these pathogenic species can also cause disease in minor domestic species and in wildlife, and there are pathogenic species that are only found in minor domestic species or in wildlife.

Source of Infection: Ecology, Evolution, and Epidemiology

The distribution of mycoplasmas generally mirrors the distribution of their hosts, and global dissemination of most pathogenic species has occurred as a result of the international trade in livestock. However, some species are restricted nationally or locally as a result of the implementation of disease control policies in domestic livestock.

Infected animals and prolonged carriers are the principal sources of pathogenic mycoplasmas, with the organisms persisting on mucosal surfaces or in sequestrated lesions, and occasionally in unusual body sites such as the ear canals of ruminants.

Pathogenic mycoplasmas may be transmitted horizontally by aerosols from the respiratory tract, milk and reproductive tract secretions, or vertically in eggs. Because they lack a cell wall, mycoplasmas are susceptible to desiccation and disinfectants, and do not survive in the environment for long periods, although some species can form biofilms that may provide some protection (McAuliffe et al. 2006). Despite their cellular fragility, transmission over considerable distances via wind or fomites is suspected under intensive animal husbandry conditions. The sources of infection and patterns of transmission can vary between species. For example, directional airborne transmission of Mycoplasma hyopneumoniae in airflows has been demonstrated by following the progression of infection across the pens of a piggery over time (Clavijo et al. 2021), whereas, for Mycoplasma hyorhinis, a longitudinal study has shown that, when there is low prevalence of infection in sows and suckling piglets, transmission occurs mainly by contact between piglets after weaning (Clavijo et al. 2019). Risk factors for transmission, such as levels of excretion and duration of contact, have been explored for some mycoplasmas in wildlife populations, including Mycoplasma ovipneumoniae in bighorn sheep (Manlove et al. 2017), Mycoplasma agassizii in desert tortoises (Aiello et al. 2016), and Mycoplasma gallisepticum in house finches (Adelman et al. 2013, 2015). In the latter example, the relatively recent incursion of M. gallisepticum into wild bird populations in North America has resulted in considerable coevolution of these new hosts and the pathogen (Bonneaud et al. 2018). Despite their reductive evolution, mobile genetic elements, such as phages and integrative and conjugative elements (ICEs), appear to shape the virulence potential of many mycoplasma species (Citti et al. 2020).

Table 31.1 Pathogenic mycoplasmas of domestic animals.

Animal Mycoplasma species Diseases
Cattle Mycoplasma mycoides subsp. mycoides Contagious bovine pleuropneumonia, arthritis in calves

Mycoplasma bovis Pneumonia, mastitis, arthritis, otitis media, surgical wound infections, infertility, abortion, endometritis, salpingitis, vesiculitis

Mycoplasma leachii Polyarthritis, mastitis, abortion, pneumonia

Mycoplasma californicum, Mycoplasma canadense Mastitis

Mycoplasma dispar Pneumonia, mastitis

Mycoplasma alkalescens Arthritis, mastitis, pneumonia, otitis media

Mycoplasma bovoculi Conjunctivitis, keratoconjunctivitis

Mycoplasma bovirhinis Pneumonia, otitis, conjunctivitis, mastitis

Mycoplasma wenyonii Anemia
Sheep and goats Mycoplasma capricolum subsp. capripneumoniae Contagious caprine pleuropneumonia (and a similar disease in sheep)

Mycoplasma agalactiae Contagious agalactia (arthritis, mastitis, conjunctivitis), pneumonia, abortion, granular vulvovaginitis in sheep and goats

Mycoplasma mycoides subsp. capri Contagious agalactia, pneumonia, peritonitis, septicemia in goats; balanitis and vulvitis in sheep

Mycoplasma capricolum subsp. capricolum Contagious agalactia and septicemia in goats

Mycoplasma adleri Arthritis in goats

Mycoplasma putrefaciens Contagious agalactia, abortion, salpingitis, metritis, testicular atrophy in goats

Mycoplasma conjunctivae Keratoconjunctivitis in sheep and goats

Mycoplasma ovipneumoniae Pneumonia, conjunctivitis and mastitis in sheep and goats

Mycoplasma ovis Anemia
Pigs Mycoplasma hyopneumoniae Pneumonia

Mycoplasma hyorhinis Arthritis, polyserositis, otitis media

Mycoplasma hyosynoviae Synovitis, arthritis, pericarditis

Mycoplasma suis Anemia
Poultry Mycoplasma gallisepticum Respiratory disease in chickens and turkeys

Mycoplasma synoviae Respiratory disease and synovitis in chickens and turkeys; eggshell deficits in chickens

Mycoplasma meleagridis Respiratory disease, chondrodystrophy, bursitis, synovitis, embryonic death in turkeys

Mycoplasma iowae Airsacculitis and embryonic death in turkeys
Dogs Mycoplasma cynos Pneumonia, bronchitis, cystitis

Mycoplasma haemocanis Hemolytic anemia
Cats Mycoplasma hemofelis Hemolytic anemia
Multiple species Mycoplasma argininii Pneumonia, vesiculitis, keratoconjunctivitis, mastitis in cattle; pneumonia and keratoconjunctivitis in sheep; arthritis in goats

Mycoplasma bovigenitalium Vulvovaginitis, vesiculitis, epididymitis, abortion, infertility, mastitis, pneumonia, conjunctivitis and arthritis in cattle; pneumonia and conjunctivitis in dogs

Mycoplasma felis Conjunctivitis, rhinitis, ulcerative keratitis, polyarthritis in cats; respiratory disease in horses

Ureaplasma species Urogenital tract disease and pneumonia

Virulence Factors and Pathogenomics

The genetic basis of mycoplasma virulence is multifactorial, and varies between different mycoplasma species, with many characterized virulence factors only found in relatively closely related species.


Mycoplasmas produce surface‐exposed proteins, and in some cases complex structures, capable of binding to host tissues or the extracellular matrix. Specific adhesins have only been characterized in a limited number of mycoplasmas, but it is clear that there may be different molecules and structures involved in adhesion in different mycoplasma species.

Terminal Organelle in M. gallisepticum

A distinct tip structure, or terminal organelle, is seen in the poultry pathogen M. gallisepticum. The cell surface proteins GapA and CrmA, which are localized on this tip structure, are required for its formation (Indikova et al. 2014), and for colonization of the respiratory tract (Goh et al. 1998; Papazisi et al. 2003). A similar tip structure is also seen in the phylogenetically related turkey pathogen Mycoplasma iowae. M. gallisepticum also has cytoadhesins that are not part of this tip structure, including PvpA (Boguslavsky et al. 2000) and VlhA (Browning et al. 2011). The chicken apolipoprotein A‐I can act as a receptor for VlhA (Hu et al. 2016). VlhA homologs are also found in the closely related avian pathogen Mycoplasma imitans and the phylogenetically distant avian pathogen Mycoplasma synoviae (Noormohammadi et al. 2000).

Ciliary Adhesin of M. hyopneumoniae

M. hyopneumoniae possesses two paralogous families of specific ciliary adhesins, P97 and P102. A recombinant mutant lacking the P97 ciliary adhesin has been shown to have a reduced capacity to bind purified cilia and cell cultures (Clampitt et al. 2021). In addition to their capacity to bind to cilia, these proteins bind to highly sulfated glycosaminoglycans, fibronectin and plasminogen, and P102 can control plasminogen activation (Seymour et al. 2012). Complete genome analysis of M. hyopneumoniae identified six paralogous genes for P97 and P102 (Minion et al. 2004), but the role of these multiple copies is unclear. In addition to these adhesins, other surface proteins have also been implicated in binding to porcine cells and to heparin (Burnett et al. 2006).

Adhesins of Other Species

The ruminant mycoplasma Mycoplasma bovis causes pneumonia, mastitis, otitis, and arthritis in cattle. It is phylogenetically related to Mycoplasma agalactiae, one of the agents causing contagious agalactia in sheep and goats. M. bovis and M. agalactiae possess homologous families of phase variable cell surface lipoproteins, the Vsps and Vpmas, respectively (Figure 31.1). Both Vsps (Thomas et al. 2003) and Vpmas (Hegde et al. 2018) are involved in cytoadhesion. Adherence of M. bovis to bovine cell cultures is also mediated by the fibronectin‐binding, leucine‐rich repeat lipoproteins P27 (Chen et al. 2018) and MbfN (Adamu et al. 2020). Other adhesins for extracellular matrix proteins have been identified, including the surface‐exposed, plasminogen‐binding fructose‐1,6‐bisphosphate aldolase (FBA; Gao et al. 2018; Huang et al. 2019), the fibronectin‐binding methyltransferase TrmFO (Guo et al. 2017) and the fibronectin‐binding nicotinamide adenine dinucleotide (NADH) oxidase homolog Nox (Zhao et al. 2017). Furthermore, a putative transmembrane protein, Mbov_503 (MBOV_RS02440), binds tight junctions and may contribute to cell invasion (Zhu et al. 2020), demonstrating the wide repertoire of potential adhesins in M. bovis.

In Mycoplasma conjunctivae, a primary cause of infectious keratoconjunctivitis in domestic sheep and goats, as well as wild Caprinae, the 150 kDa protein LppS mediates adherence to lamb synovial cells (Belloy et al. 2003).

Monoclonal antibodies against the lipoproteins Maa1 and Maa2 of the rodent pathogen Mycoplasma arthritidis partially inhibit adherence to rat lung cells. Further studies using transposon mutagenesis of maa1 and maa2, followed by complementation of each with wild‐type alleles, showed that only Maa1 mediated adherence, while Maa2 inhibited adherence (Bird et al. 2008).

The uncultivable hemotropic mycoplasma Mycoplasma suis possesses two surface‐exposed proteins, the 336 aa MSG1, a homolog of glyceraldehyde‐3‐phosphate dehydrogenase (Hoelzle et al. 2007), and a 540 aa homolog of α‐enolase (Schreiner et al. 2012), which can both bind to porcine erythrocytes when expressed as recombinant proteins.

Hydrogen Peroxide Production

Hydrogen peroxide (H2O2) is the final product of the flavin‐terminated electron transport chain. Production of H2O2 by M. ovipneumoniae affects ciliary movement in ovine tracheal organ cultures and is also responsible for the hemolysis induced by several pathogenic mycoplasmas. Differences in virulence of some strains of M. mycoides subsp. mycoides have been attributed to the amount of hydrogen peroxide they produce. An ATP‐binding cassette (ABC) transport system for glycerol uptake is intact in virulent African strains, but incomplete in less virulent European isolates, and this difference has been proposed to account for differences in production of hydrogen peroxide, as it is a product of the metabolism of glycerol (Figure 31.1; Pilo et al. 2005). While the levels of H2O2 produced in culture media by virulent M. mycoides subsp. mycoides do not affect embryonic calf nasal epithelial cells, the close proximity of mycoplasma cells to host cells may allow the transfer of hydrogen peroxide across the cell membrane, resulting in cytotoxic effects (Bischof et al. 2008). Production of H2O2 by M. bovis has been detected in strains isolated from caseonecrotic lung lesions (Schott et al. 2014). In M. gallisepticum, production of H2O2 is a potential virulence factor in house finches (Perez et al. 2020), but seemingly not in chickens (Szczepanek et al. 2014). M. gallisepticum possesses a homolog of the Ohr (organic hydroperoxide resistance) family protein (MGA_1142), which enables it to detoxify some of the reactive oxygen species found at the site of infection (Jenkins et al. 2008).

Schematic illustration of overview of virulence factors in mycoplasmas and their role in the pathogenesis of the diseases they cause.

Figure 31.1 Overview of virulence factors in mycoplasmas and their role in the pathogenesis of the diseases they cause.

Source: Based in part on Pilo et al. (2005), Arfi et al. (2016) and Mahdizadeh et al. (2021).

Biofilm Production

Biofilms are formed in vitro by M. bovis, M. agalactiae, Mycoplasma pulmonis, M. mycoides subsp. mycoides and M. gallisepticum. They are associated with resistance to desiccation, heat, complement‐mediated lysis, antimicrobials and detergents (McAuliffe et al. 2006; Simmons and Dybvig 2007; McAuliffe et al. 2008; Chen et al. 2012). Biofilm‐like structures have also been observed in vivo, on the surface of endothelial cells of splenectomized pigs experimentally infected with M. suis (Sokoli et al. 2013), but their role in virulence is yet to be clearly defined.


Capsules of mycoplasmas may aid the formation of biofilms, impede host defenses, and improve persistence in the environment. The galactan capsule of M. mycoides subsp. mycoides has a dramatic toxic effect in calves when injected intravenously, and also increases the duration of bacteremia in infected mice and confers survival in serum (Gaurivaud et al. 2014). In M. mycoides subsp. capri, capsule‐defective mutants are less pathogenic in goats (Jores et al. 2019).

Sialidase Activity

Sialidase and hyaluronidase cause apoptosis in alligator pulmonary fibroblast cultures, and together, or with other cofactors, may contribute to the pathogenicity of Mycoplasma alligatoris (Hunt and Brown 2007). Both M. synoviae (Vasconcelos et al. 2005) and M. gallisepticum (Papazisi et al. 2003) express sialidases. Although knockout mutants lacking sialidase activity are less pathogenic in chickens, complementation experiments failed to restore their virulence to wild‐type levels, so the role of this enzyme in virulence is yet to be fully elucidated (May et al. 2012).

Superantigens and Lipoproteins

Superantigens elicit a massive T‐cell response through interaction with the major histocompatibility complex on antigen presenting cells and the T‐cell receptors on T cells. The arthritogenic pathogen of mice and rats, M. arthritidis, produces a superantigen known as MAM. Diacylated lipoproteins, which are major components of mycoplasma cell membranes, have also been identified as potent non‐specific stimulators of immune responses through activation of Toll‐like receptor (TLR) 2 (Hasebe et al. 2007).

Immunoglobulin Binding Protein and Immunoglobulin Protease

M. mycoides subsp. capri strains produce a two‐component cell‐surface system, comprising a mycoplasma immunoglobulin (Ig)‐binding protein (MIB) and an associated Ig protease (MIP), which act sequentially to bind and then cleave the heavy chain of IgG (Figure 31.1; Arfi et al. 2016). The system can also dissociate antibody–antigen complexes (Nottelet et al. 2021). Homologs of these proteins are observed in many pathogenic mycoplasmas, with numerous species having multiple copies of the genes for each component. It is thought that this system may facilitate evasion of humoral immune responses in infected hosts.

Other Virulence Factors

Cell‐surface degradative enzymes and nutrient transporters also appear to play a role in virulence. The p65 antigen of M. hyopneumoniae is a cell‐surface lipoprotein with lipolytic enzymatic activity and a preference for long‐chain fatty acids. In addition to its probable role in catabolism to supply nutrients, it may play a role in disease by damaging lung surfactant (Schmidt et al. 2004). Oligopeptide transport also appears to be an essential virulence factor (Figure 31.1). M. gallisepticum mutants with transposon insertions in the oligopeptide transporter oppD have reduced virulence in experimentally infected chickens (Tseng et al. 2017). In M. synoviae, comparative genomic analysis of the attenuated strain MS‐H and its virulent parent 86079/7NS has identified a frameshift mutation in the oppF‐1 gene, resulting in expression of a truncated version of the protein (Zhu et al. 2019). In M. gallisepticum, an ABC transporter for glycerol is essential for colonization of the host (Mahdizadeh et al. 2021) (Figure 31.1).

Regulation of Virulence

Mycoplasma genomes lack homologs of many of the known virulence regulators characterized in other bacterial pathogens, although a novel sigma factor has been identified in the human pathogen Mycoplasma genitalium that controls the recombination underlying generation of antigenic variation (Torres‐Puig et al. 2015). As discussed below, considerable phase variable expression of cell surface proteins occurs via variations in the length of polynucleotide repeats or through site‐specific recombination. In chickens experimentally infected with M. gallisepticum there is a distinct temporal change in levels of expression of different members of the vlhA gene family and expression of different members of this gene family appears to be influenced by specific host tissues (Pflaum et al. 2020). Expression of phase variable antigens is also influenced by exposure to specific antibodies against these antigens (Browning et al. 2011). Increased expression of certain virulence genes has been detected in in vitro models of infection (Pritchard and Balish 2015; Cizelj et al. 2016) and in experimentally infected animals (Madsen et al. 2008), but the mechanisms underlying this are yet to be elucidated.

Types of Disease and Pathologic Changes

From a pathogenetic point of view, it is convenient to define two types of mycoplasmal disease: (i) disease resulting from invasive infections characterized by dissemination via the blood; and (ii) disease where infection remains primarily localized. In the latter, mycoplasmemia may occasionally occur, but is not a regular feature of pathogenesis. Lists of diseases within the two categories for different hosts and their etiology is provided in Tables Table 31.2 and 31.3. Where other manifestations of disease are regularly recognized, they are also included in these tables.

Invasive Infections

Invasive mycoplasmas have the capacity to penetrate epithelial barriers and enter the blood stream, although this usually requires, or is exacerbated by, intercurrent factors. Common sequelae following a usually inapparent mycoplasmemia are localization in, and inflammation of, serosal cavities or joints, manifesting as one or a combination of polyserositis, tenosynovitis or arthritis. Sometimes more generalized infection and even acute septicemia may occur. Septicemic diseases are acute and associated with fever, and often death. Infections leading to polyserositis/arthritis tend to become persistent and are accompanied by more chronic inflammatory processes.

Septicemia and Multiple System Diseases

M. mycoides subsp. capri can cause septicemia, principally in young goats. This may occur when host immunity is poor or as a sequela of primary disease at another site (conjunctivitis, pneumonia or mastitis). Clinical, pathological and clinicopathological signs in kids are typical of acute septicemic disease. Mortality is high, with lesions including fibrinopurulent polyarthritis, embolic pneumonia and thromboembolic lesions in various organs, indicating a generalized intravascular coagulation crisis.

Table 31.2 Mycoplasma diseases of animals characterized by invasive blood‐borne infection.

Primary disease Host(s) Species Other manifestations
Septicemia Goats, sheep Mycoplasma mycoides subsp. capria) Polyarthritis, pneumonia, mastitis, conjunctivitis

Mycoplasma capricolum subsp. capricolum Arthritis, mastitis, pneumonia
Polyserositis/arthritis Swine Mycoplasma hyorhinis Pneumonia

Alligators (Alligator mississippiensis) Mycoplasma alligatoris Pneumonia
Tenosynovitis/arthritis Chickens, turkeys Mycoplasma synoviae Airsacculitis

Turkeys Mycoplasma meleagridis Airsacculitis and chondrodystrophy
Arthritis/polyarthritis Cattle Mycoplasma bovis
Mycoplasma leachiib)
Mycoplasma alkalescens
Mastitis, pneumonia

Sheep, goats Mycoplasma agalactiae Mastitis, conjunctivitis, pneumonia

Swine Mycoplasma hyosynoviae

Rats Mycoplasma arthritidis

Crocodiles (Crocodylus niloticus) Mycoplasma crocodyli Pneumonia
Hemolytic anemia Cats, cattle Mycoplasma haemofelis,c) Mycoplasma wenyonii Hyperthermia, lower limb and teat edema, transient milk drop
Meningoencephalitis Dogs M. canis

a) Includes former subspecies M. mycoides subsp. mycoides large colony type and M. mycoides subsp. capri.

b) Formerly Mycoplasma sp. Bovine Group 7.

c) Formerly Haemobartonella felis.

Disease associated with Mycoplasma capricolum subsp. capricolum in goats and sheep is acute and severe and typically occurs as a generalized infection, which may proceed to fatal septicemia or result in joint localization with a fibrinopurulent polyarthritis.

M. alligatoris has also been identified as the cause of a fatal multisystemic disease, including fibrinous polyserositis, arthritis, and necrotizing pneumonia, in captive American alligators (Alligator mississippiensis; Clippinger et al. 2000; Brown et al. 2001a).

Mycoplasma zalophi has been isolated from several different lesions in California sea lions (Zalophus californianus) undergoing rehabilitation. The most common lesion seen was subdermal abscessation, although intramuscular abscesses, septic arthritis and lymphadenopathy were also seen (Haulena et al. 2006). In Australian fur seals, Mycoplasma phocicerebrale has been isolated from the fetal thymus. Infected fetuses had interstitial pneumonia and inflammatory cardiac lesions, suggesting a role in gestational failure (Lynch et al. 2011).

Polyserositis/Arthritis/Synovitis Syndromes

In pigs, M. hyorhinis colonizes the upper respiratory tract, and Mycoplasma hyosynoviae the tonsils, without apparent signs, although M. hyorhinis is a common secondary opportunistic pathogen in pre‐existing pneumonia. However, in young pigs around weaning age, M. hyorhinis may on occasion cross the epithelial barrier and disseminate to cause acute inflammation in serosal and synovial cavities that subsequently becomes chronic. Affected pigs fail to thrive and may become runts. Serofibrinous pleuritis, pericarditis and peritonitis are present and, in chronic cases, fibrous adhesions are prominent. Affected joints initially contain serosanguineous synovial fluid and the synovial membranes in the chronic stages show non‐suppurative proliferative changes. Virulent strains of M. hyosynoviae cause arthritis in older growing pigs following stresses such as movement or vaccination. Joint lesions are similar to, but milder than, those caused by M. hyorhinis. Heavy breeds are more susceptible.

Table 31.3 Mycoplasma diseases of animals characterized by localized extension of infection.

Primary disease Host(s) Species Other manifestations
Pneumonia Cattle Mycoplasma dispar

Mycoplasma bovis Mastitis, arthritis

Sheep Mycoplasma ovipneumoniae

Swine Mycoplasma hyopneumoniae

Dogs Mycoplasma cynos

Mice, rats Mycoplasma pulmonis Salpingitis, endometritis, placentitis
Pleuropneumonia Cattle CBPP Mycoplasma mycoides subsp. mycoides Arthritis in calves

Goats CCPP Mycoplasma capricolum subsp. capripneumoniae
Pleuritis Horses Mycoplasma felis
Airsacculitis Chickens/turkeys Mycoplasma gallisepticum Tracheitis, sinusitis, conjunctivitis

Mycoplasma synoviae Sinusitis (turkeys)

Turkeys Mycoplasma meleagridis Osteodystrophy
Conjunctivitis Cattle Mycoplasma bovoculi

Sheep, goats Mycoplasma conjunctivae

Cats Mycoplasma felis

Mice Mycoplasma neurolyticum “Rolling disease”

Songbirds and house finches Mycoplasma gallisepticum

Tortoises; Gopherus and Testudo spp. Mycoplasma agassizii Rhinitis
Vulvovaginitis Cattle Ureaplasma diversum Infertility, abortion, pneumonia
Seminal vesiculitis Cattle Mycoplasma bovigenitalium Decreased sperm motility
Mastitis Cattle Mycoplasma bovis Pneumonia, arthritis

M ycoplasma bovigenitalium Vulvovaginitis

Mycoplasma californicum

Mycoplasma canadense

Mycoplasma alkalescens Arthritis

Sheep, goats Mycoplasma agalactiae, Mycoplasma putrefaciens, Mycoplasma capricolum subsp. capricolum and Mycoplasma mycoides subsp. capri Arthritis, septicemia, keratoconjunctivitis

Mycoplasma capricolum subsp. capricolum As for M. agalactiae

Mycoplasma mycoides subsp. capri As for M. agalactiae

Goats Mycoplasma putrefaciens
Erythrodermatitis Freshwater fish (Tinca tinca) Mycoplasma mobile Necrotizing gill lesions
Chondrodystrophy Turkeys Mycoplasma meleagridis, Mycoplasma iowae, Mycoplasma gallisepticum Airsacculitis, tenosynovitis/arthritis
Otitis Cattle Mycoplasma bovis Pneumonia, arthritis

Two avian mycoplasmas are known to cause tenosynovitis. Mycoplasma meleagridis is a specific pathogen of turkeys and colonizes the respiratory tract and joints. M. synoviae infects the respiratory tract of chickens and turkeys, usually as a subclinical infection. Strains vary greatly in virulence and some may have a tropism for synovial tissues, causing clinical signs of tenosynovitis and arthritis. Exudate that is initially clear, then turbid, and later caseous is a prominent feature. Some strains of M. synoviae are reported to induce amyloid arthropathy, with accumulation of orange‐colored exudates within joints, especially during the chronic stages (Landman and Feberwee 2001).

Several mycoplasma species are associated with arthritis and polyarthritis in cattle, particularly in young cattle soon after arrival at a feedlot. With M. bovis, arthritis often follows a primary pneumonia. It also occurs at high incidence in calves suckling cows with M. bovis mastitis. M. agalactiae is invasive and may localize in joints of sheep and goats following a primary mastitis (contagious agalactia).

Polyarthritis and subacute pneumonia caused by Mycoplasma crocodyli has been described in farmed Nile crocodiles (Crocodylus niloticus), and a strong correlation has been seen between arthritis/tenosynovitis in American black vultures (Coragyps atratus) and the isolation of Mycoplasma corogypsi from the joints (Van Wettere et al. 2013).

Hemotropic Infections

The hemotropic mycoplasmas (previously Haemobartonella and Eperythrozoon species) are predominantly epicellular parasites of red cells. A number of species have been described, with each specific for a particular host. Mycoplasma haemofelis in cats, M. ovis in lambs and M. suis in pigs are regularly associated with clinically apparent hemolytic anemia. Anemia is thought to result from increased erythrophagocytosis rather than intravascular hemolysis. Persistently infected animals act as infectious reservoirs and transmission occurs via transfer of infected blood, which for some species is effected by biting arthropods. Vertical transmission may also occur. A novel strain of M. suis has been shown to invade erythrocytes and to cause severe anemia and mortality in pigs (Groebel et al. 2009). Mycoplasma wenyonii has been detected in cattle with anemia, edema of the limbs and/or the udder, and a transient drop in milk production (Nouvel et al. 2019).

Localized Infections

Respiratory Tract

There are two main manifestations of mycoplasmal respiratory disease in mammalian species. In calves, lambs, pigs, dogs, mice and rats, bronchitis, bronchiolitis and pneumonia are a feature of respiratory mycoplasmoses, which are frequently part of a respiratory disease complex (referred to as enzootic pneumonia in food‐producing animals). The second form is pleuropneumonia, with two specific, well‐recognized conditions: CBPP and contagious caprine pleuropneumonia (CCPP). Pleuritis in the horse is occasionally associated with Mycoplasma felis. In avian species mycoplasmal respiratory disease occurs mainly as sinusitis, tracheitis and airsacculitis.

A persistent airway infection is a feature of many mycoplasmal pneumonias (see Table 31.3 for species most commonly involved). Early stages involve direct damage of the ciliated epithelium of the bronchi and bronchioles by the organism, provoking a predominantly neutrophil and mononuclear cellular response. This progresses to a chronic interstitial pneumonia, with lymphocytes, plasma cells and macrophages the predominant cell types involved. A characteristic of most chronic mycoplasmal pneumonias is proliferation of bronchiolar lymphoid tissue (cuffing pneumonia). Bronchiectasis is a feature of the disease caused by M. pulmonis in rats and mice. Mycoplasma cynos in dogs causes a mild bronchointerstitial pneumonia and may contribute to the kennel cough complex. M. bovis is more aggressive than other mycoplasma species associated with pneumonia in calves, and produces lesions that include foci of necrosis. M. hyopneumoniae is of global economic importance as the cause of porcine enzootic pneumonia and as a key component in the porcine respiratory disease complex.

Pneumonic lesions typically occur in ventral parts of the apical and cardiac lobes of the lung, a distribution consistent with gravitational effects on the deposition of infectious aerosols and drainage of inflammatory products. It should be emphasized that pneumonic lesions caused by Mycoplasma species alone are often mild and, in the case of M. ovipneumoniae (non‐progressive pneumonia) in lambs and Mycoplasma dispar in calves, typically subclinical. However, they may predispose to secondary bacterial infections and more severe pneumonic lesions. Complex respiratory diseases with mycoplasmas as a key primary component are common and important and will be described in more detail below.

CBPP and CCCP are caused by M. mycoides subsp. mycoides and M. capricolum subsp. capripneumoniae, respectively. Both diseases are characterized by fibrinonecrotic pneumonia, serofibrinous pleuritis, and accumulations of serosanguinous fluid. Lung lesions may become sequestrated in a fibrous capsule. Organisms may remain viable in these lesions for long periods. Animals with sequestrated lesions may be long‐term carriers. Many cases of CBPP are subclinical and mortality is variable (up to 50% of diseased animals), depending on the susceptibility of the animal and the virulence of the strain involved. Strains isolated in more recent years in Europe are less virulent than classical strains. CCCP is highly contagious and mortality may reach 80%.

M. gallisepticum is one of the primary etiological agents of chronic respiratory disease in poultry. Uncontrolled proliferation of the organism in susceptible birds causes severe inflammation of the mucosa of the sinuses and/or trachea, and infection frequently extends to the lungs and air sacs. Clinical signs may include tracheal rales, nasal discharge and coughing. Gross swelling of the paranasal sinuses and ocular discharge are common in turkeys. Production may be compromised, with reduced feed consumption, egg production and weight gain. A similar respiratory syndrome may be seen in chickens and turkeys infected with M. synoviae, especially when there is concurrent infection with other respiratory pathogens. However, infection with M. synoviae is often subclinical. M. meleagridis infection is confined to turkeys, where it causes mild airsacculitis in poults and has been incriminated in chondrodystrophic conditions. All of the pathogenic avian mycoplasmas can be transmitted horizontally via infectious aerosols or vertically via the egg. M. meleagridis can also be transmitted venereally. Lesions induced by pathogenic avian mycoplasmas are mainly found in the nasal cavity, infraorbital sinuses, trachea and air sacs, and include thickening of the mucosa, hyperplasia and/or metaplasia of the epithelial layer, infiltration and proliferation of lymphocytic cells, and infiltration of other mononuclear inflammatory cells into the lamina propria. Granulomatous changes in the lungs are also common.

Mycoplasma nasistruthionis sp. nov. and Mycoplasma struthionis sp. nov. have been isolated from ostriches (Struthio camelus var. domesticus) with upper respiratory disease (Botes et al. 2005; Spergser et al. 2020), although their role as primary pathogens has not yet been established.


Mycoplasmas have been associated with conjunctivitis in several animal species, either as a primary infection or in conjunction with respiratory disease. M. gallisepticum in chickens and turkeys is a good example of the latter. Conjunctivitis seems to be a feature of outbreaks of disease in house finches and other songbirds in North America caused by M. gallisepticum. In cattle, Mycoplasma bovoculi causes mild conjunctivitis but predisposes to more severe infection with Moraxella bovis. M. conjunctivae causes transient conjunctivitis and keratitis in sheep, goats, ibex and chamois, but the transient disease affects vision and can result in death through misadventure, particularly in wild chamois and ibex living in alpine environments (Giacometti et al. 2002). M. felis is reported as a cause of conjunctivitis in cats, but it may also be isolated from the eyes of clinically normal cats. Mycoplasma neurolyticum also occurs in the conjunctivae of both clinically normal and diseased mice. The organism is of interest in that it appears to be the only mycoplasma known that produces an exotoxin. When inoculated intravenously into mice it elicits a neurological syndrome and rapid death. M. agassizii is widespread in tortoise populations in North America and Europe and is associated with conjunctivitis and chronic upper respiratory tract disease (Brown et al. 2001b).

Reproductive Tract Disease

Reproductive tract disease caused by mycoplasmas is relatively uncommon in animals despite their frequent isolation from this site. In birds, colonization of the oviduct by pathogenic mycoplasmas is important in determining vertical transmission of the organism to progeny, but disease of the reproductive tract of the hen is not a feature of this infection. Some strains of M. synoviae can induce abnormalities of the egg shell around the apex, leading to economic loss in layer farms due to shell cracks and breaks (Feberwee et al. 2009). Mycoplasma anserisalpingitidis has been isolated from the reproductive tracts (oviduct, ovary, phallus and testis) of diseased geese, but its role in disease has not yet been fully established (Volokhov et al. 2020).

Granular vulvovaginitis has been described in cattle (Ureaplasma diversum and Mycoplasma bovigenitalium), sheep (M. capricolum subsp. capricolum and M. mycoides subsp. capri

Only gold members can continue reading. Log In or Register to continue

Stay updated, free articles. Join our Telegram channel

Nov 13, 2022 | Posted by in GENERAL | Comments Off on Mycoplasmas

Full access? Get Clinical Tree

Get Clinical Tree app for offline access