question: how bacteria don’t just fall off of things? (I.e, how something so small clings on to our skins and such and we can’t shake them off”
comment: It’s an issue of scale. Their holding on at a microscopic level.... much like how the hairs on a spiders legs work to allow it to hold on to its silk in its web. They also have shown this is kind of how geckos are able to stay attached to walls that seemingly have no big surface abrasion that allows them to hold on to a vertical wall or on ceilings.
passages: There are several ways bacteria avoid contact with phagocytes. First, they can grow in sites that phagocytes are not capable of traveling to (e.g., the surface of unbroken skin). Second, bacteria can suppress the inflammatory response; without this response to infection phagocytes cannot respond adequately. Third, some species of bacteria can inhibit the ability of phagocytes to travel to the site of infection by interfering with chemotaxis. Fourth, some bacteria can avoid contact with phagocytes by tricking the immune system into "thinking" that the bacteria are "self". "Treponema pallidum"—the bacterium that causes syphilis—hides from phagocytes by coating its surface with fibronectin, which is produced naturally by the body and plays a crucial role in wound healing.
   Seong and Matzinger have suggested that the "patterns" that the immune system recognizes on bacteria are not as different from the alarm signals released by damaged cells as one might have thought. They suggested that, because life evolved in water, the hydrophobic portions of molecules are normally hidden in the internal parts of molecules or other structures (like membranes) and that the sudden exposure of a hydrophobic portion is a sure sign that some injury or damage has occurred. They suggested that these are the most ancient alarm signals, that they are recognized by evolutionarily ancient systems of repair and remodeling, and that the modern immune system piggy-backed on this ancient system. Thus bacteria and other organisms may have very similar alarm systems. They describe these ancient signals as danger-associated molecular patterns, or DAMPs.
   Bacterial growth can be suppressed with bacteriostats, without necessarily killing the bacteria. In a synecological, true-to-nature situation in which more than one bacterial species is present, the growth of microbes is more dynamic and continual.
  
  Liquid is not the only laboratory environment for bacterial growth. Spatially structured environments such as biofilms or agar surfaces present additional complex growth models.
  
  Section::::Environmental conditions.
   Domingue worked with a team that included pre and post-doctoral students and fellows along with faculty colleagues and laboratory assistants. Together they discovered that L-form bacteria are able to form tiny dense bodies within parent cells that already lack cell walls. They noted that the forms, which they called electron dense bodies were so small that they could pass through bacterial filters that normally withheld ordinary bacteria with cell walls.
   Once pathogens attach to host cells, they can cause direct damage as the pathogens use the host cell for nutrients and produce waste products. For example, "Streptococcus mutans", a component of dental plaque, metabolizes dietary sugar and produces acid as a waste product. The acid decalcifies the tooth surface to cause dental caries. However, toxins produced by bacteria cause most of the direct damage to host cells.
  
  Section::::Mechanisms of damage.:Direct.:Toxin production.
   Most fimbria of gram-negative bacteria function as adhesins, but in many cases it is a minor subunit protein at the tip of the fimbriae that is the actual adhesin. In gram-positive bacteria, a protein or polysaccharide surface layer serves as the specific adhesin. To effectively achieve adherence to host surfaces, many bacteria produce multiple adherence factors called adhesins.
   Section::::Types of bacterial cell envelopes.:Bacteria lacking cell wall.
  
  The obligate intracellular bacteria in family Chlamydiaceae are unique in their morphology as they do not contain detectable amounts of peptidoglycans. However, the extracellular forms of these gram-negative bacteria maintain their structural integrity because of a layer of disulfide bind cross-linked layer of cysteine-rich proteins, which is located between cytoplasmic membrane and outer membrane in a manner analogous to peptidoglycan layer in other gram-negative bacteria. In the intracellular forms of the bacterium the disulfide cross linkage is not found, which confers this form more mechanically fragile.
   Motile bacteria are attracted or repelled by certain stimuli in behaviours called taxes: these include chemotaxis, phototaxis, energy taxis, and magnetotaxis. In one peculiar group, the myxobacteria, individual bacteria move together to form waves of cells that then differentiate to form fruiting bodies containing spores. The myxobacteria move only when on solid surfaces, unlike "E. coli", which is motile in liquid or solid media.
   In order for pathogenic bacteria to invade a cell, communication with the host cell is required. The first step for invading bacteria is usually adhesion to host cells. Strong anchoring, a characteristic that determines virulence, prevents the bacteria from being washed away before infection occurs. Bacterial cells can bind to many host cell surface structures such as glycolipids and glycoproteins which serve as attachment receptors. Once attached, the bacteria begin to interact with the host to disrupt its normal functioning and disrupt or rearrange its cytoskeleton. Proteins on the bacteria surface can interact with protein receptors on the host thereby affecting signal transduction within the cell. Alterations to signaling are favorable to bacteria because these alterations provide conditions under which the pathogen can invade. Many pathogens have Type III secretion systems which can directly inject protein toxins into the host cells. These toxins ultimately lead to rearrangement of the cytoskeleton and entry of the bacteria.
   BULLET::::1. In order to understand the process of attachment one must first examine the properties of both the substratum and the cell surface
  
  BULLET::::- Substratum: can be either very hydrophobic (Teflon) or hydrophilic (glass)
  
  BULLET::::- Cell properties: flagella, pili, fimbriae, or glycocalyx may impact rate of microbial attachment
  
  Section::::Biofilm adhesion.:Inhibiting protein adsorption/ biofilm adhesion.
   Bacterial stress response
  
  The bacterial stress response enables bacteria to survive adverse and fluctuating conditions in their immediate surroundings. Various bacterial mechanisms recognize different environmental changes and mount an appropriate response. A bacterial cell can react simultaneously to a wide variety of stresses and the various stress response systems interact with each other by a complex of global regulatory networks.
   Endospores show no detectable metabolism and can survive extreme physical and chemical stresses, such as high levels of UV light, gamma radiation, detergents, disinfectants, heat, freezing, pressure, and desiccation. In this dormant state, these organisms may remain viable for millions of years, and endospores even allow bacteria to survive exposure to the vacuum and radiation in space. Endospore-forming bacteria can also cause disease: for example, anthrax can be contracted by the inhalation of "Bacillus anthracis" endospores, and contamination of deep puncture wounds with "Clostridium tetani" endospores causes tetanus.
  
  Section::::Metabolism.
   In laboratory cultures, natural competence is usually tightly regulated and often triggered by nutritional shortages or adverse conditions. However the specific inducing signals and regulatory machinery are much more variable than the uptake machinery, and little is known about the regulation of competence in the natural environments of these bacteria. Transcription factors have been discovered which regulate competence; an example is sxy (also known as tfoX) which has been found to be regulated in turn by a 5' non-coding RNA element. In bacteria capable of forming spores, conditions inducing sporulation often overlap with those inducing competence. Thus cultures or colonies containing sporulating cells often also contain competent cells. Recent research by Süel "et al." has identified an excitable core module of genes which can explain entry into and exit from competence when cellular noise is taken into account.
   BULLET::::- Adhesion. Many bacteria must first bind to host cell surfaces. Many bacterial and host molecules that are involved in the adhesion of bacteria to host cells have been identified. Often, the host cell receptors for bacteria are essential proteins for other functions. Due to presence of mucous lining and of anti-microbial substances around some host cells, it is difficult for certain pathogens to establish direct contact-adhesion.
   The superficial layers of the skin are naturally acidic (pH 4-4.5) due to lactic acid in sweat and produced by skin bacteria. At this pH mutualistic flora such as "Staphylococci", "Micrococci", "Corynebacterium" and "Propionibacteria" grow but not transient bacteria such as Gram negative bacteria like "Escherichia" and "Pseudomonas" or Gram positive ones such as "Staphylococcus aureus". Another factor affecting the growth of pathological bacteria is that the antimicrobial substances secreted by the skin are enhanced in acidic conditions. In alkaline conditions, bacteria cease to be attached to the skin and are more readily shed. It has been observed that the skin also swells under alkaline conditions and opens up allowing move to the surface.
   The skin supports its own ecosystems of microorganisms, including yeasts and bacteria, which cannot be removed by any amount of cleaning. Estimates place the number of individual bacteria on the surface of one square inch (6.5 square cm) of human skin at 50 million, though this figure varies greatly over the average of human skin. Oily surfaces, such as the face, may contain over 500 million bacteria per square inch (6.5 cm²). Despite these vast quantities, all of the bacteria found on the skin's surface would fit into a volume the size of a pea. In general, the microorganisms keep one another in check and are part of a healthy skin. When the balance is disturbed, there may be an overgrowth and infection, such as when antibiotics kill microbes, resulting in an overgrowth of yeast. The skin is continuous with the inner epithelial lining of the body at the orifices, each of which supports its own complement of microbes.
   Section::::Environmental cues.
  
  Section::::Environmental cues.:Immune response.
   Bacteria are typically found attached to and living in close association with surfaces. During the bacterial lifespan, a bacterium is subjected to frequent shear-forces. In the crudest sense, bacterial adhesins serve as anchors allowing bacteria to overcome these environmental shear forces, thus remaining in their desired environment. However, bacterial adhesins do not serve as a sort of universal bacterial Velcro. Rather, they act as specific surface recognition molecules, allowing the targeting of a particular bacterium to a particular surface such as root tissue in plants, lacrimal duct tissues in mammals, or even tooth enamel.
   Certain genera of gram-positive bacteria, such as "Bacillus", "Clostridium", "Sporohalobacter", "Anaerobacter", and "Heliobacterium", can form highly resistant, dormant structures called "endospores". Endospores develop within the cytoplasm of the cell; generally a single endospore develops in each cell. Each endospore contains a core of DNA and ribosomes surrounded by a cortex layer and protected by a multilayer rigid coat composed of peptidoglycan and a variety of proteins.
   Section::::Nutritional stress.
   Non-professional phagocytes are more limited than professional phagocytes in the type of particles they can take up. This is due to their lack of efficient phagocytic receptors, in particular opsonins—which are antibodies and complement attached to invaders by the immune system. Additionally, most nonprofessional phagocytes do not produce reactive oxygen-containing molecules in response to phagocytosis.
  
  Section::::Pathogen evasion and resistance.
  
  A pathogen is only successful in infecting an organism if it can get past its defenses. Pathogenic bacteria and protozoa have developed a variety of methods to resist attacks by phagocytes, and many actually survive and replicate within phagocytic cells.
   Should these instances of prokaryotic sociality prove to be the rule rather than the exception, it would have serious implications for the way we view prokaryotes in general, and the way we deal with them in medicine. Bacterial biofilms may be 100 times more resistant to antibiotics than free-living unicells and may be nearly impossible to remove from surfaces once they have colonized them. Other aspects of bacterial cooperation—such as bacterial conjugation and quorum-sensing-mediated pathogenicity, present additional challenges to researchers and medical professionals seeking to treat the associated diseases.
  
  Section::::Environment.
   Bacteria exhibit a high degree of “morphological plasticity” that protects them from predation. Bacterial capture by protozoa is affected by size and irregularities in shape of bacteria. Oversized, filamentous, or prosthecate bacteria may be too large to be ingested. On the other hand, other factors such as extremely tiny cells, high-speed motility, tenacious attachment to surfaces, formation of biofilms and multicellular conglomerates may also reduce predation. Several phenotypic features of bacteria are adapted to escape protistan-grazing pressure.
   In presence of oxygen, aerobic bacteria like "Acidithiobacillus thiooxidans", "Thiobacillus thioparus", and "Thiobacillus concretivorus", all three widely present in the environment, are the common corrosion-causing factors resulting in biogenic sulfide corrosion.
   Though the lack of motility might be regarded a disadvantage, some non-motile bacteria possess structures that allow their attachment to eukaryotic cells, like GI mucousal cells.
  