The battle with the host over microbial size
Highlights
► Microbial size varies and is a factor in interaction with a host. ► Small microbial size allows for evasion of important host defenses. ► Several host defenses function by increasing effective microbial size. ► Some pathogens are able to evade defenses that target their small size.
Introduction
Members of the microbial world span a great range of shapes and sizes. The selective value of microbial shape has been reviewed elsewhere [1]. Differences in size are used to distinguish species and impact many aspects of microbial physiology and lifestyle. Bacterial cells, for example, range from 0.15 to 700 μm in length. In addition, for single-celled organisms, modulation of cell division or separation may significantly impact their effective size. For microbes residing in a mammalian host, size may be a determining factor in an infectious agent's success or its clearance [2, 3, 4, 5]. Many successful pathogens have evolved strategies to modulate their effective size to accommodate these challenges [6]. The host in turn appears to target the ability of microbes to escape its defenses with their small size. By analyzing bacteria differing only in effective size it is possible to sort out some of the independent contributions of size to pathogenesis. These studies reveal that microbial size is a battleground in the interaction between pathogen and host.
Section snippets
Why microbial size matters
Most microbes are generally small to minimize their cellular volume and grow most efficiently. While prokaryotic species with large or giant cell morphology may be found in nature, these forms are generally not observed within mammalian hosts. However, pathogens that are typically small may form larger individual cells under certain growth conditions (Table 1). When cell division or septation is inhibited, long filamentous forms that may be 10–50 times longer than usual may result. Filamentous
The host fights back
Although microbes may take advantage of their small surface area to evade key defenses such as the complement system, other aspects of the host response appear to circumvent this strategy. For example, the bivalent or multivalent binding of immunoglobulin agglutinates microbial targets to increase their effective size (Table 1). This process is demonstrated by the ‘threading reaction’, which refers to the inhibition of separation of daughter cells by the bridging of bound immunoglobulin during
Evasion of host defenses based on size
If the immune response subverts the small effective size of microbes, are there ways that successful pathogens evade these defense mechanisms? The agglutinating effect of immunoglobulin requires antigen recognition, while diversity and variation of microbial surfaces provide a means of avoiding binding by antibody. Not all classes of immunoglobulin are equivalent in their ability to agglutinate a target. On the mucosal surface, the most abundant antibody class is IgA, which is quadravalent in
Conclusions
In summary, size may have a pronounced impact the interaction of microbes with their host. Successful pathogens may alter their effective size to evade clearance or promote adhesive interactions (Figure 1). The host, in turn, may subvert the plasticity of microbes and their ability use their size as an advantage. Pathogenesis studies that rely on viable counts of organism in culture and do not routinely incorporate the use of microscopy are unlikely to control for the effects of microbial size
References and recommended reading
Papers of particular interest, published within the period of review, have been highlighted as:
• of special interest
•• of outstanding interest
Acknowledgement
This work was supported by the U.S. Public health Service grant numbers AI38446 and AI78538 to JNW.
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