Online Textbook Bacteriology is continuously updated and includes information on Staphylococcus, MRSA, Streptococcus, E. coli, anthrax, cholera, tuberculosis, Lyme disease and other bacterial diseases of humans.
Kenneth Todar is the author of the Online Textbook of Bacteriology and an emeritus lecturer at the University of Wisconsin-Madison.Class Biologically Clean isolators, cleanrooms, containment units and decontamination chambers for animal research including germ-free and gnotobiotic.
The Online Textbook of Bacteriology is a general and medical microbiology text and includes discussion of staph, MRSA, strep, Anthrax, E. coli, cholera, tuberculosis, Lyme Disease and other bacterial pathogens.
Kenneth Todar, PhDKenneth Todar's Online Textbook of Bacteriology Home PageOnline Textbook of Bacteriology Table of ContentsInformation about materials for teaching bacteriology.Contact Kenneth Todar.





Web Review of Todar's Online Textbook of Bacteriology. "The Good, the Bad, and the Deadly"

Tag words: bacteriology, bacteria, microbiology, microbe, normal flora, indigenous bacteria, E. coli, Staphylococcus, Streptococcus, Enterococcus, Lactobacillus, Bifidobacterium, corynebacteria, clostridium, neisseria, bacteroides, Haemophilus, biofilm, dental plaque, dental caries, periodontal disease.







Kenneth Todar currently teaches Microbiology 100 at the University of Wisconsin-Madison. His main teaching interest include general microbiology, bacterial diversity, microbial ecology and pathogenic bacteriology.

Bacillus cereus bacteria.Print this Page

The Normal Bacterial Flora of Humans (page 2)

(This chapter has 5 pages)

© Kenneth Todar, PhD

Associations Between Humans and the Normal Flora

E. coli is the best known bacterium that regularly associates itself with humans, being an invariable component of the human intestinal tract.  Even though E. coli is the most studied of all bacteria, and we know the exact location and sequence of 4,288 genes on its chromosome, we do not fully understand its ecological relationship with humans.

In fact, not much is known about the nature of the associations between humans and their normal flora, but they are thought to be dynamic interactions rather than associations of mutual indifference.  Both host and bacteria are thought to derive benefit from each other, and the associations are, for the most part, mutualistic.  The normal flora derive from their host a steady supply of nutrients, a stable environment, and protection and transport. The host obtains from the normal flora certain nutritional and digestive benefits, stimulation of the development and activity of immune system, and protection against colonization and infection by pathogenic microbes.

While most of the activities of the normal flora benefit their host, some of the normal flora are parasitic (live at the expense of their host), and some are pathogenic (capable of producing disease). Diseases that are produced by the normal flora in their host may be called endogenous diseases.  Most endogenous bacterial diseases are opportunistic infections, meaning that the the organism must be given a special opportunity of weakness or let-down in the host defenses in order to infect. An example of an opportunistic infection is chronic bronchitis in smokers wherein normal flora bacteria are able to invade the weakened lung.

Sometimes the relationship between a member of the normal flora an its host cannot be deciphered. Such a relationship where there is no apparent benefit or harm to either organism during their association is referred to as a commensal relationship. Many of the normal flora that are not predominant in their habitat, even though always present in low numbers, are thought of as commensal bacteria. However, if a presumed commensal relationship is studied in detail, parasitic or mutualistic characteristics often emerge.

Tissue specificity

Most members of the normal bacterial flora prefer to colonize certain tissues and not others. This "tissue specificity" is usually due to properties of both the host and the bacterium. Usually, specific bacteria colonize specific tissues by one or another of these mechanisms.

1. Tissue tropism is the bacterial preference or predilection for certain tissues for growth. One explanation for tissue tropism is that the host provides essential nutrients and growth factors for the bacterium, in addition to suitable oxygen, pH, and temperature for growth.


Lactobacillus acidophilus, informally known as "Doderlein's bacillus" colonizes the vagina because glycogen is produced which provides the bacteria with a source of sugar that they ferment to lactic acid.


2. Specific adherence  Most bacteria can colonize a specific tissue or site because they can adhere to that tissue or site in a specific manner that involves complementary chemical interactions between the two surfaces. Specific adherence involves biochemical interactions between bacterial surface components (ligands or adhesins) and host cell molecular receptors. The bacterial components that provide adhesins are molecular parts of their capsules, fimbriae, or cell walls. The receptors on human cells or tissues are usually glycoprotein molecules located on the host cell or tissue surface.
 
Figure 2. Specific adherence involves complementary chemical interactions between the host cell or tissue surface and the bacterial surface. In  the language of medical microbiologist, a bacterial "adhesin" attaches covalently to a host "receptor" so that the bacterium "docks" itself on the host surface. The adhesins of bacterial cells are chemical components of capsules, cell walls, pili or fimbriae. The host receptors are usually glycoproteins located on the cell membrane or tissue surface.

Some examples of adhesins and attachment sites used for specific adherence to human tissues are described in the table below.

Table 2. Examples of bacterial specific adherence to host cells or tissue.

Bacterium Bacterial adhesin Attachment site
Streptococcus pyogenes Cell-bound protein (M-protein) Pharyngeal epithelium
Streptococcus mutans Cell- bound protein (Glycosyl transferase)
Pellicle of tooth
Streptococcus salivarius Lipoteichoic acid Buccal epithelium of tongue
Streptococcus pneumoniae Cell-bound protein (choline-binding protein)
 Mucosal epithelium
Staphylococcus aureus Cell-bound protein Mucosal epithelium
Neisseria gonorrhoeae N-methylphenyl- alanine pili Urethral/cervical epithelium
Enterotoxigenic E. coli Type-1 fimbriae Intestinal epithelium
Uropathogenic E. coli P-pili (pap) Upper urinary tract
Bordetella pertussis Fimbriae ("filamentous hemagglutinin") Respiratory epithelium
Vibrio cholerae N-methylphenylalanine pili Intestinal epithelium
Treponema pallidum Peptide in outer membrane Mucosal epithelium
Mycoplasma Membrane protein Respiratory epithelium 
Chlamydia Unknown Conjunctival or urethral epithelium


3. Biofilm formation
Some of the indigenous bacteria are able to construct biofilms on a tissue surface, or they are able to colonize a biofilm built by another bacterial species.  Many biofilms are a mixture of microbes, although one member is responsible for maintaining the biofilm and may predominate.


Figure 3. Cartoon depicting biofilm formation.  Biofilms usually occur when one bacterial species attaches specifically or non specifically to a surface, and then secretes carbohydrate slime (exopolymer)  that imbeds the bacteria and attracts other microbes to the biofilm for protection or nutritional advantages.

The classic biofilm that involves components of the normal flora of the oral cavity is the formation of dental plaque on the teeth. Plaque is a naturally-constructed biofilm, in which the consortia of bacteria may reach a thickness of 300-500 cells on the surfaces of the teeth. These accumulations subject the teeth and gingival tissues to high concentrations of bacterial metabolites, which result in dental disease.
chapter continued

Previous Page





© Kenneth Todar, Ph.D. All rights reserved. - www.textbookofbacteriology.net


Kenneth Todar, PhD | Home | Table of Contents

Kenneth Todar has taught microbiology to undergraduate students at The University of Texas, University of Alaska and University of Wisconsin since 1969.

© 2020 Kenneth Todar, PhD - Madison, Wisconsin