Antibody Response to Mycoplasma pneumoniae: Protection of Host and Influence on Outbreaks?

Abstract

In humans of all ages, the cell wall-less and genome-reduced species Mycoplasma pneumoniae can cause infections of the upper and lower respiratory tract. The well-documented occurrence of major peaks in the incidence of community-acquired pneumonia cases reported world-wide, the multifaceted clinical manifestations of infection and the increasing number of resistant strains provide reasons for ongoing interest in the pathogenesis of mycoplasmal disease. The results of recent studies have provided insights into the interaction of the limited virulence factors of the bacterium with its host. In addition, the availability of complete M. pneumoniae genomes from patient isolates and the development of proteomic methods for investigation of mycoplasmas have not only allowed characterization of sequence divergences between strains but have also shown the importance of proteins and protein parts for induction of the immune reaction after infection. This review focuses on selected aspects of the humoral host immune response as a factor that might influence the clinical course of infections, subsequent protection in cases of re-infections and changes of epidemiological pattern of infections. The characterization of antibodies directed to defined antigens and approaches to promote their induction in the respiratory mucosa are also preconditions for the development of a vaccine to protect risk populations from severe disease due to M. pneumoniae.

Positively interacting strains that circulate in a network structured population induce cycling epidemics of Mycoplasma Pneumoniae

“…This simplicity is justified as we focus on the long term behaviour of MP transmission dynamics, and the exposure stage does not influence the overall transmissibility and long-term patterns (Diekmann et al ., 2013; Omori et al ., 2015). Since the many different isolates and strains of MP can be classified into two main types: P1 type 1 and P1 type 2 (Kenri et al ., 2008; Spuesens et al ., 2009; Brown et al ., 2015; Dumke and Jacobs, 2016), our model just considers the transmission dynamics of two strains. Within the SIRS transmission dynamics model, a population of size N is modelled as a network in which every individual randomly contacts a fixed number ( κ ) of other individuals, and is classified into eight compartments (Figure 1), namely those who are susceptible to infection with any strain (S), those who are infected and infectious with strain 1 or 2 (I 1 and I 2 ), those who have recovered from infection with a given strain and are susceptible to infection with the other strain (R 1 and R 2 ), those who are infected and infectious with strain 1 or 2 after recovering from previous infection (J 1 and J 2 ) and those who are immune to infection with both strains (R).…”

“…Multiple strains of MP and their co-circulation were also observed in other countries (e.g., Dumke et al ., 2010; Spuesens et al ., 2009; Martinez et al ., 2010; Zhao et al ., 2015; Brown et al ., 2016). Although there are many different isolates and strains, analysis of repetitive elements distributed in variable size and sequence over the genome of MP strains suggested two main types: P1 type 1 and P1 type 2 (Kenri et al ., 2008; Spuesens et al ., 2009; Brown et al ., 2015; Dumke and Jacobs, 2016).…”

“…The duration of infectiousness is unclear and is commonly estimated to be up to 3 weeks from onset of illness (Clyde, 1993). Immunity occurs post infection, but later re-infection with different subtypes is recognized, suggesting the immunity is not lifelong and no strong cross protection between different subtypes (Foy et al ., 1977; Ito et al ., 2001; Dumke and Jacobs, 2016). The duration of immunity ranges from 2 to 10 years (Lind et al ., 1997; Omori et al ., 2015).…”

Cambiando los paradigmas de la infección por M. pneumoniae en pediatría

“…La infección por M. pneumoniae produce respuesta innata involucrando macró-fagos, mastocitos, neutrófilos y células NK, así como una respuesta adaptativa con anticuerpos tipo IgA, IgM e IgG. 48 Además, hay una adecuada respuesta celular con linfocitos B y T. Al parecer, la respuesta humoral no condiciona protección contra reinfecciones; sin embargo, el efecto neutralizante de los anticuerpos podría ser importante para la contención en la infección aguda, ya que pacientes con deficiencias humorales pueden cursar con cuadros más graves o prolongados, además de tener más riesgo para manifestaciones extrapulmonares, particularmente a nivel neurológico. 10 El papel de los macrófagos parece ser vital en controlar la infección a nivel pulmonar, ya que interviene en la opsonización y depuración del patógeno.…”

Reliability of cold agglutinin test (CAT) for the detection of patients with Mycoplasma pneumoniae pneumonia

“…6 As described previously, IgM specific antibodies may not be elicited in adults with reinfection. 15,16,17 Cold agglutinins being an IgM type antibody, false negative CAT could occur. In addition, CAT is a crude test with subjective result interpretation, resulting in additional false negative results, unlike in the objective readout results obtained using ELISA.…”