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Ureaplasma infections in pre-term infants: Recent information regarding the role of Ureaplasma species as neonatal pathogens

Article information

Korean J Pediatr. 2010;53(12):989-993
Publication date (electronic) : 2010 December 31
doi : https://doi.org/10.3345/kjp.2010.53.12.989
Department of Pediatrics, School of Medicine, Hallym University, Seoul, Korea.
Corresponding author: Tae-Jung Sung, M.D. Department of Pediatrics, Kangnam Sacred Heart Hospital, Hallym University Medical Center, 948-1 Daerim 1-Dong, Yungdungpo-ku, Seoul 150-950, Korea. Tel: +82.2-829-5142, Fax: +82.2-829-4469, neosung@hallym.or.kr
Received 2010 November 02; Accepted 2010 November 30.


Although numerous clinical observational studies have been conducted over a period of over 30 years, the clinical significance of Ureaplasma infection is still under debate. The Ureaplasma speices. is a commensal in the female genital tract and considered to have of low virulence; however, Ureaplasma colonization has been associated with infertility, stillbirth, preterm delivery, histologic chorioamnionitis, and neonatal morbidities, including congenital pneumonia, meningitis, bronchopulmonary dysplasia, and perinatal death. Recently, Ureaplasma was subdivided into 2 separate species and 14 serovars. Ureaplasma parvum is known as biovar 1 and contains serovars 1, 3, 6, and 14, and Ureaplasma urealyticum (biovar 2) contains the remaining serovars (2, 4, 5, and 7-13). The existence of differences in pathogenicities of these 14 serovars and 2 biovars is controversial. Although macrolides are the only antimicrobial agents currently available for use in neonatal ureaplasmal infections, in the current clinical field, it is difficult to make decisions regarding which antibiotics should be used. Future investigations involving large, multicenter, randomized, controlled studies are needed before proper recommendations can be made for clinical practice.


Ureaplasma species are the most common bacteria detected in urogenital infections, including nongonococcal urethritis in men and multiple obstetrical complications in women1, 2). Since Ureaplasma spp. can be found in vaginal flora in 40% of sexually inactive and 67% sexually active women, it is known as a commensal in the female genital tract3).

Although numerous clinical observational studies were conducted over a period of over 30 years, the clinical significance of these bacteria is still under debate4). These bacteria are considered to be of low virulence; however, Ureaplasma colonization has been associated with infertility5), stillbirth6), preterm delivery7, 8), histologic chorioamnionitis9), and perinatal death in neonates10).

This article summarizes recent information on the role of Ureaplasma infection in diseases in preterm infants and future considerations.

Ureaplasma spp.

1. Classification and characteristics

Ureaplasma spp. is a member of the Mollicutes class, which is comprised of 4 orders, 5 families, 8 genes, and nearly 200 known species, 17 of which are known to use humans as their primary host4). Another well-known member of the Mollicutes class is Mycoplasma spp., in which there are 3 species, Mycoplasma hominis, Mycoplasma genitalium, and Mycoplasma fermentans, which are known to occur in the female urogenital tract. Ureaplasma was first described by Shepard in the 1950s and were detected in the male urethritis11). Recently, Ureaplasma was subdivided into 2 separate species and 14 serovars that have been grouped according to 16S dRNA sequencing results into 2 genetically related biovars3, 4).

U. parvum, known as biovar 1, contains serovars 1, 3, 6, and 14, and U. urealyticum (biovar 2) contains the remaining serovars (2, 4, 5, and 7-13)12). Characteristics of all serovars include lack of cell walls, limited biosynthetic abilities, small genome size, and mucosal association in the human host3). The unique characteristic of Ureaplasma is their ability to hydrolyze urea to generate metabolic energy1, 4). Some debates still occur regarding whether there is a difference in pathogenicity exists among these 14 serovars and 2 biovars.

2. Virulence factors

Ureaplasma can directly activate the first component of complements and attach to host erythrocytes, neutrophils, spermatozoa, and urethral epithelial cells1). This can induce inflammation in humans and produces multiple manifestations of clinical diseases4). Since Ureaplasma spp. metabolizes urea to generate energy, it also produces secretory products such as ammonia, which may induce a local cytotoxic effect.

Previously reported ureaplasmal virulence factors include IgA protease, urease, phospholipases A and C, and production of hydrogen peroxide13). These factors may allow the organism to evade mucosal immune defenses by degrading IgA and injuring mucosal cells through the local generation of ammonia, membrane phospholipid degradation, prostaglandin synthesis, and membrane peroxidation3). Although phenotypic production of IgA protease and phopholipases was described several years ago, genome examination of multiple serovars has failed to reveal genes encoding these enzymes4).

The multiple-banded antigen (MBA) of Ureaplasma spp. is the predominant antigen recognized during the infection process and may be involved in host inflammatory response stimulation. It undergoes a high rate of variation in vitro and exhibits variable sizes in vitro on invasive isolates, suggesting that antigen size variation may be another mechanism through which the organism evades host defenses3, 4). Ureaplasma serovars have multiple MBA genes, and some contain multiple copies of the same type of MBA gene.

3. Vertical transmission and intrauterine infection

Ureaplasmas can be isolated from endotracheal aspirations in up to 40% of newborn infants within 30 minutes to 24 hours after delivery14, 15), and from maternal and umbilical cord blood at these delivery times16). This provided evidence that vertical Ureaplasma transmission and neonatal infection may occur in newborn infants. Additionally, recovery of Ureaplasma from the chorion increased with the duration of membrane rupture, suggesting an ascending route of infection17). Those born weighing less than 1,000 g are at higher risk of infection when the mother is colonized at up to 90% of the infection rate18). The possible pathogenesis involves fetal exposure to ascending ureaplasmal intrauterine infection, passage through an infected birth canal, hematogenous dissemination through the placenta into umbilical vessels, and colonization of the skin, mucosal membranes, respiratory tract, and dissemination into the blood and central nervous system19, 20).

Intrauterine infection is now believed to be a major cause of preterm birth, particularly in gestations of less than 30 weeks21). Ureaplasma spp. is the most common isolate identified in amniotic fluid. Isolated Ureaplasma spp. from the chorioamnion has been consistently associated with histologic chorioamnionitis, which is inversely related to birth weight22). Several experimental studies with intra-amniotic inoculation of U. parvum showed that it did not stimulate premature labor in mice23) or sheep24), but did stimulate progressive uterine contractions and preterm delivery in rhesus macaques25). The Rhesus macaque experimental result suggests that species differences result in differences in host response or serovar differences in virulence.

Ureaplasma spp. infection in neonatal pathogens

1. Congenital pneumonia in preterm infants

In the mid-1970s, some investigators suggested a potential role for Ureaplasma in neonatal respiratory disease after isolation of these organisms from lungs of stillborn infants with peumonitis26). Evidence that Ureaplasma spp. cause congenital pneumonia includes isolation of bacteria in pure culture from amniotic fluid, affected lungs of neonates less than 14 hours after birth in the midst of an acute inflammatory response, and chorioamnion1, 20). Other evidence includes demonstration of a specific IgM response in the neonate27), radiographic changes indicative of pneumonia in culture-positive infants28), demonstration of the bacteria in lung tissue using immunofluorescence29), and electron microscopy27).

2. Bacteremia and systemic infections

Ureaplasma isolation from cord blood was first described in 196930) and in a recent prospective study it was shown that 23% of infants had a positive cord blood culture for this organism31). Cassell et al.32) reported that 26% of neonates culture-positive for Ureaplasma spp. in the lower respiratory tract were bacteremia with these organisms. Ureaplasma has been isolated from gastric aspirates, blood, cerebrospinal fluid (CSF), lung, and brain tissue, although this organism is most commonly isolated from respiratory secretions3). In 2 recent large prospective cohorts, Ureaplasma was detected in 17% of cord blood cultures and 23.6% of serum or CSF polymerase chain reaction (PCR) samples, with U. parvum as the predominant species detected in serum and CSF10, 31).

3. Meningitis and neonatal brain injury

The largest recent prospective survey of invasive infections analyzed samples from 313 very low-birth-weight (VLBW) infants with suspected sepsis/meningitis or hydrocephalus reported that the risk of severe intraventricular hemorrhage (IVH) (≥grade 3) was 2.5-fold higher in serum PCR-positive than PCR-negative infants after adjustment for gestational age, but there was no association of cranial ultrasound abnormalities with detection of Ureaplasma in CSF10).

A role for Ureaplasma in neonatal brain injury is supported by recent studies in experimental animal models23). In the murine intrauterine U. parvum infection model, the brains of fetal and newborn mice showed evidence of microglial activation, deleted myelination, and disturbed neuronal development. Future studies are needed to provide additional information regarding mechanisms of Ureaplasma-mediated brain injury.

4. Role of Ureaplasma infection in lung injury and inflammation

Some investigators found that Ureaplasma isolated from lower respiratory tract colonization is associated with peripheral blood leukocytosis, particularly the neutrophil component29, 33). Crouse et al.28) evaluated chest radiographs of 44 preterm infants with Ureaplasma colonization the lower respiratory tract in comparison with those who were culture-negative. They found that pneumonia was twice as common in the Ureaplasma-positive group and early radiographic emphysematous changes within 2 weeks of birth were significantly more common in the Ureaplasma-positive group. In a recent cohort study of infants less than 33 weeks gestation, Ureaplasma spp. were detected during the first week of life in tracheal aspirates or nasopharyngeal aspirates in 35% of infants10). These findings suggest an in utero onset of inflammatory responses and lung injury3).

Ureaplasma infection in neonate promotes a proinflammatory cytokine cascade in the lower respiratory tract; this infection is associated with an increase in tumor necrosis factors (TNF)-α, interleukin (IL)-1β, and IL-820) and blocks expression of the regulatory cytokines IL-6 and/or IL-104). Viscardi et al.33) examined pathological specimens from Ureaplasma-infected infants and reported that Transforming growth factor (TGF)-β1 expression increased in infants with pneumonia compared with control specimens. Li and coworkers34) demonstrated that human macrophages exposed to the Ureaplasma antigen produce TNF-α and IL-6, and Ureaplasma-exposed macrophages release vascular endothelial growth factor and intracellular adhesion molecule-1.

Animal models, such as mouse and primate models, have contributed substantially to the understanding of how the inflammatory potential of ureaplasmal infection induces a deregulated, proinflammatory, interstitial pneumonitis leading to a profibrotic state35, 36).

5. Association of Ureaplasma infection with development of bronchopulmonary dysplasia

The classic definition of bronchopulmonary dysplasia (BPD), a supplemental oxygen requirement at 28 days of age, has been criticized since widespread antenatal corticosteroid treatment, postnatal exogenous surfactant therapy, and gentler ventilator strategies in VLBW infants, a "new" BPD, emerged. Recently, Bancalari et al.37) defined BPD as an oxygen requirement and the presence of radiographic abnormalities at 36 weeks postmenstrual age.

Since BPD etiology is multifactorial and complex, the relationship of Ureaplasma respiratory tract colonization with the development of BPD has been debated. In 1988, 3 independent groups published results of cohort studies linking BPD development with airway colonization with Ureaplasma18, 32, 38). A meta-analysis of 17 clinical studies published before 1995 supported a significant association between Ureaplasma respiratory tract colonization and BPD development. Another recent meta-analysis conducted by Schelonka et al.39), who analyzed 36 cohort studies published between 1988 and 2004 involving approximately 3000 preterm infants, showed a significant association between Ureaplasma respiratory colonization and BPD development whether it was defined as oxygen dependence at 28 days (P<0.001) or at 36 weeks postmenstrual age (P<0.001). Other studies support the Ureaplasma respiratory colonization-BPD association, particularly in the subset of Ureaplasma-colonized infants exposed to chorioamnionitis and leukocytosis at birth3).

Castro-Alcaraz et al.40) observed that persistent, but not transient, Ureaplasma respiratory complications are significantly higher in colonized infants. Mortality due to respiratory complications is significantly higher in colonized infants and the risk of a combined outcome measure of BPD or death due to lung disease was 4.2-fold higher in colonized Ureaplasma rather than in noncolonized VLBW infants14, 32).

Infants with BPD have elevated proinflammatory cytokines such as IL-1, IL-6, and IL-8, with IL-8 acting as a potent neutrophil chemoattractant and, as a result, theses infants have elevated neutrophils in the lungs20). Perinatal Ureaplasma infection may promote the inflammatory cascade in the lung and impair alveolar development directly or in conjunction with oxidant and ventilator-induced lung injury3, 20). Hence, postnatal application of high oxygen concentrations and mechanical ventilation and duration of exposure may potentiate the effect of Ureaplasma-associated injury to the lungs.

Treatment of Ureaplasma infection in preterm infants

Although it is known that macrolides are the only antimicrobial agents currently available for use in the treatment of neonatal ureaplasmal infections, in the clinical field it is difficult to make decisions regarding which antibiotics should be used. Due to its toxicity, doxycycline is not an alternative unless U. urealyticum is isolated from CSF. Clindamycin has also been used to successfully treat systemic M. homin is infections in infants1). As such, making specific recommendations for treating neonatal ureaplasma infections is difficult because the spectrum of ureaplasmal disease has not been fully described and there are very few clinical studies indicating the in vivo efficacy of antibiotics1). Therefore, not only are choices between limited drug options controversial, but also the actual indications concerning conditions under which treatment should be offered, dosage, and duration of therapy is debated.

Antibiotic therapy is a standard treatment modality for premature rupture of membranes (PROM). However, standard regimens failed to eradicate organisms including Ureaplasma or diminish inflammation in the amniotic cavity with PROM41). In an experimental Ureaplasma intraamniotic infection (IAI) in Rhesus monkeys, azitromycin alone or in combination with dexamethasone and indomethacin prevented fetal lung damage42).

Despite the in vitro susceptibility of Ureaplasma to erythromycin, trials of erythromycin therapy in the first few weeks of life in Ureaplasma-colonized preterm infants have failed to demonstrate efficacy in preventing BPD3). Recently, Walls and colleagues43) demonstrated that azithromycin prophylaxis, but not erythromycin, improved outcomes and reduced inflammation in a murine neonatal Ureaplasma infection model. This finding suggests that azithromycin is effective if administered immediately after birth. However, there have been no published investigations of azithromycin in neonates regarding low birth weight infants. Hence, until appropriate pharmacokinetics and efficacy trials are conducted, a dosing regimen for azithromycin in neonates cannot be recommended41).

Conclusions and future perspectives

Recent clinical and experimental studies have shown significant evidence that Ureaplasma infection may induce inflammatory processes early in utero and, as a result it can cause intrauterine chorioamnionitis, postnatal systemic infection, and lung injury, including BPD. However, more studies are needed to determine the relationship of Ureaplasma virulence factors, host immune factors affecting pathogen susceptibility, and inflammatory variability, and interactions with environmental factors such as oxygen exposure and mechanical ventilation3). Furthermore, a study analyzing antimicrobial therapy of Ureaplasma-colonized infants should be conducted in a large, multicenter, randomized clinical trial to determine whether these antibiotics are effective in reducing BPD rate and improving neonatal outcomes.


1. Waites KB, Katz B, Schelonka RL. Mycoplasmas and Ureaplasmas as neonatal pathogens. Clin Microbiol Rev 2005;18:757–789. 16223956.
2. Volgmann T, Ohlinger R, Panzig B. Ureaplasma urealyticum-harmless commensal or underestimated enemy of human reproductions? A review. Arch Gynecol Obstet 2005;273:133–139. 16044191.
3. Viscardi RM. Ureaplasma species: Role in diseases of prematurity. Clin Perinatol 2010;37:393–409. 20569814.
4. Waites KB, Schelonka RL, Xiao L, Grigsby PL, Novy M. Congenital and opportunistic infections: Ureaplasma species and Mycoplasma hominis. Semin Fetal Neonatal Med 2009;14:190–199. 19109084.
5. Gupta A, Gupta S, Mittal A, Chandral P, Gill AK. Correlation of mycoplasma with unexplained infertility. Arch Gynecol Obstet 2009;280:981–985. 19322575.
6. Gibbs RS. The origins of stillbirth: infectious diseases. Semin Perinatol 2002;26:75–78. 11876570.
7. Yoon BH, Romero R, Park JS, Chang JW, Kim YA, Kim JC, et al. Microbial invasion of the amniotic cavity with Ureaplasma urealyticum is associated with a robust host response in fetal, amniotic, and maternal compartments. Am J Obstet Gynecol 1998;179:1254–1260. 9822511.
8. Perni SC, Vardhana S, Korneeva I, Tuttle SL, Paraskevas LR, Chasen ST, et al. Mycoplasma hominis and Ureaplasma urealyticum in midtrimester amniotic fluid: association with amniotic fluid cytokine levels and pregnancy outcome. Am J Obstet Gynecol 2004;191:1382–1386. 15507969.
9. Hillier SL, Martius J, Krohn M, Kiviat N, Holmes KK, Eschenabach DA. A case-control study pf chorioamnionic infection and histologic chorioamnionitis in prematurity. N Engl J Med 1988;319:972–978. 3262199.
10. Viscardi RM, Hashmi N, Gross GW, Sun CC, Rodriguez A, Fairchild KD. Incidence of invasive Ureaplasma in VLBW infants: relationship to severe intraventricular hemorrhage. J Perinatol 2008;28:759–765. 18596706.
11. Shepard MC. The recovery of pleuropneumonia-like organisms from Negro men with and without nongonococcal urethritis. Am J Syph Gonorrhea Vener Dis 1954;38:113–124. 13138817.
12. Robertson JA, Stemke GW, Davis JW Jr, Harasawa R, Thirkell D, Kong F, et al. Proposal of Ureaplasma parvum sp. Nov. and emended description of Ureaplasma urealyticum (Shepard et al. 1974). Int J Syst Evol Microbiol 2002;52:587–597. 11931172.
13. Glass JI, Lefkowitz EJ, Glass JS, Heiner CR, Chen EY, Cassell GH. The complete sequence of the mucosal pathogen. Nature 2000;407:757–762. 11048724.
14. Colaizy TT, Kuforiji T, Sklar RS, Pillers DA. PCR methods in clinical investigations of human ureaplasmas: a minireview. Mol Genet Metab 2003;80:389–397. 14654351.
15. Cordero L, Coley BD, Miller RL, Mueller CF. Bacterial and Ureaplasma colonization of the airway: radiologic findings in infants with bronchopulmonary dysplasia. J Perinatol 1997;17:428–433. 9447527.
16. Kelly VN, Garlnad SM, Gilbert GL. Isolation of genital mycoplasmas from the blood of neonate and women with pelvic infection using conventional SPS-free blood culture media. Pathology 1987;19:277–280. 3431914.
17. Kundsin RB, Leviton A, Allred EN, Poulin SA. Ureaplasma Urealyticum infection of the placenta in pregnancies that ended prematurely. Obstet Gynecol 1996;87:122–127. 8532246.
18. Sanchez PJ, Regan JA. Vertical transmission of Ureaplasma urealyticum from mothers to preterm infants. Pediatr Infect Dis J 1990;9:398–401. 2367160.
19. Waites KB, Crouse DT, Philips JB 3rd, Canupp KC, Cassell GH. Ureaplasmal pneumonia and sepsis associated with persistent pulmonary hypertension of the newborn. Pediatrics 1989;83:79–85. 2909979.
20. Schelonka RL, Waites KB. Ureaplasma infection and neonatal lung disease. Semin Perinatol 2007;31:2–9. 17317421.
21. Goldenberg RL, Hauth JC, Andrews WW. Intrauterine infection and preterm delivery. N Engl J Med 2000;342:1500–1507. 10816189.
22. Cassell GH, Waites KB, Watson HL, Crouse DT, Harasawa R. Ureaplasma ureaplyticum intrauterine infection: role in prematurity and disease in newborns. Clin Microbiol Rev 1993;6:69–87. 8457981.
23. Normann E, Lacaze-Masmonteil T, Eaton F, Schwendimann L, Gressens P, Thébaud B. A novel mouse model of Ureaplasma-induced perinatal inflammation: effects on lung and brain injury. Pediatr Res 2009;65:430–436. 19127208.
24. Moss TJ, Nitsos I, Ikegami M, Jobe AH, Newnham JP. experimental intrauterine Ureaplasma infection in sheep. Am J Obstet Gynecol 2005;192:1179–1186. 15846199.
25. Novy MJ, Duffy L, Axthelm MK, Sadowsky DW, Witkin SS, Gravett MG, et al. Ureaplasma partum or Mycoplasma hominis as sole pathogens cause chorioamnionitis, preterm delivery, and fetal pneumonia in rhesus macaques. Reprod Sci 2009;16:56–70. 19122105.
26. Tafari N, Ross S, Naeye RL, Judge DM, Marboe C. Mycoplasma T strains and perinatal death. Lancet 1976;1:108–109. 54632.
27. Quinn PA, Gillan JE, Markestad T, St John MA, Daneman A, Lie KI, et al. Intrauterine infection with Ureaplasma urealyticum as a cause of fatal neonatal pneumonia. Pediatr Infect Dis 1985;4:538–543. 3900948.
28. Crouse DT, Odrezin GT, Cutter GR, Reese JM, Hamrick WB, Waites KB, et al. Radiographic changes associated with tracheal isolation of Ureaplasma urealyticum from neonates. Clin Infect Dis 1993;17(Suppl 1):S122–S130. 8399902.
29. Panero A, Pacifico L, Rossi N, Roggini M, Chiesa C. Ureaplasma urealyticum as a cause of pneumonia in preterm infants: analysis of the white cell response. Arch Dis Child Fetal Neonatal Ed 1995;73:F37–F40. 7552594.
30. Klein JO, Buckland D, Finland M. Colonization of newborn infants by mycoplasmas. N Engl J Med 1969;280:1025–1030. 5778411.
31. Goldenberg RL, Andrews WW, Goepfert AR, Faye-Petersen O, Cliver SP, Carlo WA, et al. The Alabama Preterm Birth Study: umbilical cord blood Ureaplasma urealyticum and Mycoplasma homminis cultures in very preterm newborn infants. Am J Obstet Gynecol 2008;198:43.e1–43.e5. 18166302.
32. Cassell GH, Waites KB, Crouse DT, Rudd PT, Canupp KC, Stagno S, et al. Association of Ureaplasma urealyticum infection of the lower respiratory tract with chronic lung disease and death in very-low-birth-weight infants. Lancet 1988;2:240–245. 2899235.
33. Viscardi RM, Manimtim W, He JR, Hasday JD, Sun CC, Joyce B, et al. Disordered pulmonary myofibroblast distribution and elastin expression in preterm infants with Ureaplasma urealyticum pneumonitis. Pediatr Dev Pathol 2006;9:143–151. 16822087.
34. Li YH, Brauner A, Jensen JS, Tullus K. Induction of human macrophage vascular endothelial growth factor and intercellular adhesion molecule-1 by Ureaplasma urealyticum and downregulation by steroids. Biol Neonate 2002;82:22–28. 12119537.
35. Viscardi RM, Atamas SP, Luzina IG, Hasday JD, He JR, Sime PJ, et al. Antenatal ureaplasma urealyticum respiratroty tract infection stimulates proinflammatory, profibrotic responses in the preterm baboon lung. Pediatr Res 2006;60:141–146. 16864693.
36. Viscardi RM, Kaplan J, Lovchik JC, He JR, Hester L, Rao S, et al. Characterization of a murine model of Ureaplasma urealyticum pneumonia. Infect Immun 2002;70:5721–5729. 12228302.
37. Bancalari E, Claure N, Sosenko IR. Bronchopulmonary dysplasia: changes in pathogenesis, epidemiology and definition. Semin Neonatol 2003;8:63–71. 12667831.
38. Wang EE, Frayha H, Watts J, Hammerberg O, Chernesky MA, Mahony JB, et al. Role of Ureaplasma urealyticum and other pathogens in the development of chronic lung disease of prematurity. Pediatr Infect Dis J 1988;7:547–551. 2845345.
39. Schelonka RL, Katz B, waites KB, Benjamin DK. Critical appraisal of the role of Ureaplsma in the development of bronchopulmonary dysplasia with metaanalytic techniques. Pediatr Infect Dis J 2005;24:1033–1039. 16371861.
40. Castro-Alcaraz S, Greenberg EM, Bateman DA, Regan JA. Patterns of colonization with Ureaplsma urealyticum during neonatal intensive care unit hospitalizations of very low birth weight infants and the development of chronic lung disease. Pediatrics 2002;110:e45. 12359818.
41. Viscardi RM, Hasday JD. Role of Ureaplasma species in neonatal chronic lung disease: epidemiologic and experimental evidence. Pediatr Res 2009;65:84R–90R.
42. Novy MJ, Sadowsky DW, Grigsby PL, Sparks KE, Duffy LB, Wautes KB. Maternal azithromycin therapy for Ureaplasma intraamniotic infection prevents advanced fetal lung lesions in rhesus monkey. Paper presented at: 55th SGI. Annual Scientific Meeting 2008 March 26-29; San Diego, CA.
43. Walls SA, Kong L, Leeming HA, Placencia FX, Popek EJ, Weisman LE. Antiniotic prophylaxis improves Ureaplasma-associated lung disease in suckling mice. Pediatr Res 2009;66:197–202. 19390479.

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