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<meta name="robots" content="INDEX,NOFOLLOW,NOARCHIVE,NOIMAGEINDEX" /><meta name="citation_inbook_title" content="Medical Microbiology. 4th edition" /><meta name="citation_title" content="Normal Flora" /><meta name="citation_publisher" content="University of Texas Medical Branch at Galveston" /><meta name="citation_date" content="1996" /><meta name="citation_author" content="Charles Patrick Davis" /><meta name="citation_pmid" content="21413249" /><meta name="citation_fulltext_html_url" content="https://www.ncbi.nlm.nih.gov/books/NBK7617/" /><link rel="schema.DC" href="http://purl.org/DC/elements/1.0/" /><meta name="DC.Title" content="Normal Flora" /><meta name="DC.Type" content="Text" /><meta name="DC.Publisher" content="University of Texas Medical Branch at Galveston" /><meta name="DC.Contributor" content="Charles Patrick Davis" /><meta name="DC.Date" content="1996" /><meta name="DC.Identifier" content="https://www.ncbi.nlm.nih.gov/books/NBK7617/" /><meta name="DC.Language" content="en" /><meta name="description" content="A diverse microbial flora is associated with the skin and mucous membranes of every human being from shortly after birth until death. The human body, which contains about 1013 cells, routinely harbors about 1014 bacteria (Fig. 6-1). This bacterial population constitutes the normal microbial flora . The normal microbial flora is relatively stable, with specific genera populating various body regions during particular periods in an individual's life. Microorganisms of the normal flora may aid the host (by competing for microenvironments more effectively than such pathogens as Salmonella spp or by producing nutrients the host can use), may harm the host (by causing dental caries, abscesses, or other infectious diseases), or may exist as commensals (inhabiting the host for long periods without causing detectable harm or benefit). Even though most elements of the normal microbial flora inhabiting the human skin, nails, eyes, oropharynx, genitalia, and gastrointestinal tract are harmless in healthy individuals, these organisms frequently cause disease in compromised hosts. Viruses and parasites are not considered members of the normal microbial flora by most investigators because they are not commensals and do not aid the host.Figure 6-1Numbers of bacteria that colonize different parts of the bodyNumbers represent the number of organisms per gram of homogenized tissue or fluid or per square centimeter of skin surface." /><meta name="og:title" content="Normal Flora" /><meta name="og:type" content="book" /><meta name="og:description" content="A diverse microbial flora is associated with the skin and mucous membranes of every human being from shortly after birth until death. The human body, which contains about 1013 cells, routinely harbors about 1014 bacteria (Fig. 6-1). This bacterial population constitutes the normal microbial flora . The normal microbial flora is relatively stable, with specific genera populating various body regions during particular periods in an individual's life. Microorganisms of the normal flora may aid the host (by competing for microenvironments more effectively than such pathogens as Salmonella spp or by producing nutrients the host can use), may harm the host (by causing dental caries, abscesses, or other infectious diseases), or may exist as commensals (inhabiting the host for long periods without causing detectable harm or benefit). Even though most elements of the normal microbial flora inhabiting the human skin, nails, eyes, oropharynx, genitalia, and gastrointestinal tract are harmless in healthy individuals, these organisms frequently cause disease in compromised hosts. Viruses and parasites are not considered members of the normal microbial flora by most investigators because they are not commensals and do not aid the host.Figure 6-1Numbers of bacteria that colonize different parts of the bodyNumbers represent the number of organisms per gram of homogenized tissue or fluid or per square centimeter of skin surface." /><meta name="og:url" content="https://www.ncbi.nlm.nih.gov/books/NBK7617/" /><meta name="og:site_name" content="NCBI Bookshelf" /><meta name="og:image" content="https://www.ncbi.nlm.nih.gov/corehtml/pmc/pmcgifs/bookshelf/thumbs/th-mmed-lrg.png" /><meta name="twitter:card" content="summary" /><meta name="twitter:site" content="@ncbibooks" /><meta name="bk-non-canon-loc" content="/books/n/mmed/A500/" /><link rel="canonical" href="https://www.ncbi.nlm.nih.gov/books/NBK7617/" /><link rel="stylesheet" href="/corehtml/pmc/css/figpopup.css" type="text/css" media="screen" /><link rel="stylesheet" href="/corehtml/pmc/css/bookshelf/2.26/css/books.min.css" type="text/css" /><link rel="stylesheet" href="/corehtml/pmc/css/bookshelf/2.26/css/books_print.min.css" type="text/css" media="print" /><style type="text/css">p a.figpopup{display:inline !important} .bk_tt {font-family: monospace} .first-line-outdent .bk_ref {display: inline} .body-content h2, .body-content .h2 {border-bottom: 1px solid #97B0C8} .body-content h2.inline {border-bottom: none} a.page-toc-label , .jig-ncbismoothscroll a {text-decoration:none;border:0 !important} .temp-labeled-list .graphic {display:inline-block !important} .temp-labeled-list img{width:100%}</style><script type="text/javascript" src="/corehtml/pmc/js/jquery.hoverIntent.min.js"> </script><script type="text/javascript" src="/corehtml/pmc/js/common.min.js?_=3.18"> </script><script type="text/javascript" src="/corehtml/pmc/js/large-obj-scrollbars.min.js"> </script><script type="text/javascript">window.name="mainwindow";</script><script type="text/javascript" src="/corehtml/pmc/js/bookshelf/2.26/book-toc.min.js"> </script><script type="text/javascript" src="/corehtml/pmc/js/bookshelf/2.26/books.min.js"> </script><meta name="book-collection" content="NONE" />
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<div class="pre-content"><div><div class="bk_prnt"><p class="small">NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.</p><p>Baron S, editor. Medical Microbiology. 4th edition. Galveston (TX): University of Texas Medical Branch at Galveston; 1996. </p></div><div class="iconblock clearfix whole_rhythm no_top_margin bk_noprnt"><a class="img_link icnblk_img" title="Table of Contents Page" href="/books/n/mmed/"><img class="source-thumb" src="/corehtml/pmc/pmcgifs/bookshelf/thumbs/th-mmed-lrg.png" alt="Cover of Medical Microbiology" height="100px" width="80px" /></a><div class="icnblk_cntnt eight_col"><h2>Medical Microbiology. 4th edition.</h2><a data-jig="ncbitoggler" href="#__NBK7617_dtls__">Show details</a><div style="display:none" class="ui-widget" id="__NBK7617_dtls__"><div>Baron S, editor.</div><div>Galveston (TX): <a href="http://www.utmb.edu/" ref="pagearea=page-banner&amp;targetsite=external&amp;targetcat=link&amp;targettype=publisher">University of Texas Medical Branch at Galveston</a>; 1996.</div></div><div class="half_rhythm"><ul class="inline_list"><li style="margin-right:1em"><a class="bk_cntns" href="/books/n/mmed/">Contents</a></li></ul></div><div class="bk_noprnt"><form method="get" action="/books/n/mmed/" id="bk_srch"><div class="bk_search"><label for="bk_term" class="offscreen_noflow">Search term</label><input type="text" title="Search this book" id="bk_term" name="term" value="" data-jig="ncbiclearbutton" /> <input type="submit" class="jig-ncbibutton" value="Search this book" submit="false" style="padding: 0.1em 0.4em;" /></div></form></div></div><div class="icnblk_cntnt two_col"><div class="pagination bk_noprnt"><a class="active page_link prev" href="/books/n/mmed/A438/" title="Previous page in this title">&lt; Prev</a><a class="active page_link next" href="/books/n/mmed/A537/" title="Next page in this title">Next &gt;</a></div></div></div></div></div>
<div class="main-content lit-style" itemscope="itemscope" itemtype="http://schema.org/CreativeWork"><div class="meta-content fm-sec"><h1 id="_NBK7617_"><span class="label">Chapter 6</span><span class="title" itemprop="name">Normal Flora</span></h1><p class="contrib-group"><span itemprop="author">Charles Patrick Davis</span>.</p></div><div class="jig-ncbiinpagenav body-content whole_rhythm" data-jigconfig="allHeadingLevels: ['h2'],smoothScroll: false" itemprop="text"><div id="mmed_ch6"><h2 id="_mmed_ch6_">General Concepts</h2><div id="A501"><h3>Significance of the Normal Flora</h3><p>The normal flora influences the anatomy, physiology, susceptibility to pathogens,
and morbidity of the host.</p></div><div id="A502"><h3>Skin Flora</h3><p>The varied environment of the skin results in locally dense or sparse
populations, with Gram-positive organisms (e.g., staphylococci, micrococci,
diphtheroids) usually predominating.</p></div><div id="A503"><h3>Oral and Upper Respiratory Tract Flora</h3><p>A varied microbial flora is found in the oral cavity, and streptococcal anaerobes
inhabit the gingival crevice. The pharynx can be a point of entry and initial
colonization for <i>Neisseria</i>, <i>Bordetella</i>,
<i>Corynebacterium</i>, and <i>Streptococcus</i>
spp.</p></div><div id="A504"><h3>Gastrointestinal Tract Flora</h3><p>Organisms in the stomach are usually transient, and their populations are kept
low (10<sup>3</sup> to 10<sup>6</sup>/g of contents) by acidity.
<i>Helicobacter pylori</i> is a potential stomach pathogen that
apparently plays a role in the formation of certain ulcer types. In normal hosts
the duodenal flora is sparse (0 to 10<sup>3</sup>/g of contents). The ileum
contains a moderately mixed flora (10<sup>6</sup> to 10<sup>8</sup>/g of
contents). The flora of the large bowel is dense (10<sup>9</sup> to
10<sup>11</sup>/g of contents) and is composed predominantly of anaerobes.
These organisms participate in bile acid conversion and in vitamin K and ammonia
production in the large bowel. They can also cause intestinal abscesses and
peritonitis.</p></div><div id="A505"><h3>Urogenital Flora</h3><p>The vaginal flora changes with the age of the individual, the vaginal pH, and
hormone levels. Transient organisms (e.g., <i>Candida</i> spp.)
frequently cause vaginitis. The distal urethra contains a sparse mixed flora;
these organisms are present in urine specimens (10<sup>4</sup>/ml) unless a
clean-catch, midstream specimen is obtained.</p></div><div id="A506"><h3>Conjunctival Flora</h3><p>The conjunctiva harbors few or no organisms. <i>Haemophilus</i> and
<i>Staphylococcus</i> are among the genera most often
detected.</p></div><div id="A507"><h3>Host Infection</h3><p>Many elements of the normal flora may act as opportunistic pathogens, especially
in hosts rendered susceptible by rheumatic heart disease, immunosuppression,
radiation therapy, chemotherapy, perforated mucous membranes, etc. The flora of
the gingival crevice causes dental caries in about 80 percent of the
population.</p></div></div><div id="A508"><h2 id="_A508_">Introduction</h2><p>A diverse microbial flora is associated with the skin and mucous membranes of every
human being from shortly after birth until death. The human body, which contains
about 10<sup>13</sup> cells, routinely harbors about 10<sup>14</sup> bacteria (<a class="figpopup" href="/books/NBK7617/figure/A509/?report=objectonly" target="object" rid-figpopup="figA509" rid-ob="figobA509">Fig. 6-1</a>). This bacterial population
constitutes the <i>normal microbial flora</i> . The normal microbial flora
is relatively stable, with specific genera populating various body regions during
particular periods in an individual's life. Microorganisms of the normal flora may
aid the host (by competing for microenvironments more effectively than such
pathogens as <i>Salmonella</i> spp or by producing nutrients the host can
use), may harm the host (by causing dental caries, abscesses, or other infectious
diseases), or may exist as commensals (inhabiting the host for long periods without
causing detectable harm or benefit). Even though most elements of the normal
microbial flora inhabiting the human skin, nails, eyes, oropharynx, genitalia, and
gastrointestinal tract are harmless in healthy individuals, these organisms
frequently cause disease in compromised hosts. Viruses and parasites are not
considered members of the normal microbial flora by most investigators because they
are not commensals and do not aid the host.</p><div class="iconblock whole_rhythm clearfix ten_col fig" id="figA509" co-legend-rid="figlgndA509"><a href="/books/NBK7617/figure/A509/?report=objectonly" target="object" title="Figure 6-1" class="img_link icnblk_img figpopup" rid-figpopup="figA509" rid-ob="figobA509"><img class="small-thumb" src="/books/NBK7617/bin/ch6f1.gif" src-large="/books/NBK7617/bin/ch6f1.jpg" alt="Figure 6-1. Numbers of bacteria that colonize different parts of the body." /></a><div class="icnblk_cntnt" id="figlgndA509"><h4 id="A509"><a href="/books/NBK7617/figure/A509/?report=objectonly" target="object" rid-ob="figobA509">Figure 6-1</a></h4><p class="float-caption no_bottom_margin">Numbers of bacteria that colonize different parts of the body. Numbers represent the number of organisms per gram of homogenized tissue
or fluid or per square centimeter of skin surface. </p></div></div></div><div id="A510"><h2 id="_A510_">Significance of the Normal Flora</h2><p>The fact that the normal flora substantially influences the well-being of the host
was not well understood until germ-free animals became available. Germ-free animals
were obtained by cesarean section and maintained in special isolators; this allowed
the investigator to raise them in an environment free from detectable viruses,
bacteria, and other organisms. Two interesting observations were made about animals
raised under germ-free conditions. First, the germ-free animals lived almost twice
as long as their conventionally maintained counterparts, and second, the major
causes of death were different in the two groups. Infection often caused death in
conventional animals, but intestinal atonia frequently killed germ-free animals.
Other investigations showed that germ-free animals have anatomic, physiologic, and
immunologic features not shared with conventional animals. For example, in germ-free
animals, the alimentary lamina propria is underdeveloped, little or no
immunoglobulin is present in sera or secretions, intestinal motility is reduced, and
the intestinal epithelial cell renewal rate is approximately one-half that of normal
animals (4 rather than 2 days).</p><p>Although the foregoing indicates that bacterial flora may be undesirable, studies
with antibiotic treated animals suggest that the flora protects individuals from
pathogens. Investigators have used streptomycin to reduce the normal flora and have
then infected animals with streptomycin-resistant <i>Salmonella</i>.
Normally, about 10<sup>6</sup> organisms are needed to establish a gastrointestinal
infection, but in streptomycin-treated animals whose flora is altered, fewer than 10
organisms were needed to cause infectious disease. Further studies suggested that
fermentation products (acetic and butyric acids) produced by the normal flora
inhibited <i>Salmonella</i> growth in the gastrointestinal tract. <a class="figpopup" href="/books/NBK7617/figure/A511/?report=objectonly" target="object" rid-figpopup="figA511" rid-ob="figobA511">Figure 6-2</a> shows some of the factors that are
important in the competition between the normal flora and bacterial pathogens.</p><div class="iconblock whole_rhythm clearfix ten_col fig" id="figA511" co-legend-rid="figlgndA511"><a href="/books/NBK7617/figure/A511/?report=objectonly" target="object" title="Figure 6-2" class="img_link icnblk_img figpopup" rid-figpopup="figA511" rid-ob="figobA511"><img class="small-thumb" src="/books/NBK7617/bin/ch6f2.gif" src-large="/books/NBK7617/bin/ch6f2.jpg" alt="Figure 6-2. Mechanisms by which the normal flora competes with invading pathogens." /></a><div class="icnblk_cntnt" id="figlgndA511"><h4 id="A511"><a href="/books/NBK7617/figure/A511/?report=objectonly" target="object" rid-ob="figobA511">Figure 6-2</a></h4><p class="float-caption no_bottom_margin">Mechanisms by which the normal flora competes with invading
pathogens. Compare this schematic with Figure
6-3. </p></div></div><p>The normal flora in humans usually develops in an orderly sequence, or succession,
after birth, leading to the stable populations of bacteria that make up the normal
adult flora. The main factor determining the composition of the normal flora in a
body region is the nature of the local environment, which is determined by pH,
temperature, redox potential, and oxygen, water, and nutrient levels. Other factors
such as peristalsis, saliva, lysozyme secretion, and secretion of immunoglobulins
also play roles in flora control. The local environment is like a concerto in which
one principal instrument usually dominates. For example, an infant begins to contact
organisms as it moves through the birth canal. A Gram-positive population
(bifidobacteria arid lactobacilli) predominates in the gastrointestinal tract early
in life if the infant is breast-fed. This bacterial population is reduced and
displaced somewhat by a Gram-negative flora (Enterobacteriaceae) when the baby is
bottle-fed. The type of liquid diet provided to the infant is the principal
instrument of this flora control; immunoglobulins and, perhaps, other elements in
breast milk may also be important.</p><p>What, then, is the significance of the normal flora? Animal and some human studies
suggest that the flora influences human anatomy, physiology, lifespan, and,
ultimately, cause of death. Although the causal relationship of flora to death and
disease in humans is accepted, of her roles of the human microflora need further
study.</p></div><div id="A512"><h2 id="_A512_">Normal Flora of Skin</h2><p>Skin provides good examples of various microenvironments. Skin regions have been
compared to geographic regions of Earth: the desert of the forearm, the cool woods
of the scalp, and the tropical forest of the armpit. The composition of the dermal
microflora varies from site to site according to the character of the
microenvironment. A different bacterial flora characterizes each of three regions of
skin: (1) axilla, perineum, and toe webs; (2) hand, face and trunk; and (3) upper
arms and legs. Skin sites with partial occlusion (axilla, perineum, and toe webs)
harbor more microorganisms than do less occluded areas (legs, arms, and trunk).
These quantitative differences may relate to increased amount of moisture, higher
body temperature, and greater concentrations of skin surface lipids. The axilla,
perineum, and toe webs are more frequently colonized by Gram-negative bacilli than
are drier areas of the skin.</p><p>The number of bacteria on an individual's skin remains relatively constant; bacterial
survival and the extent of colonization probably depend partly on the exposure of
skin to a particular environment and partly on the innate and species-specific
bactericidal activity in skin. Also, a high degree of specificity is involved in the
adherence of bacteria to epithelial surfaces. Not all bacteria attach to skin;
staphylococci, which are the major element of the nasal flora, possess a distinct
advantage over viridans streptococci in colonizing the nasal mucosa. Conversely,
viridans streptococci are not seen in large numbers on the skin or in the nose but
dominate the oral flora.</p><p>The microbiology literature is inconsistent about the density of bacteria on the
skin; one reason for this is the variety of methods used to collect skin bacteria.
The scrub method yields the highest and most accurate counts for a given skin area.
Most microorganisms live in the superficial layers of the stratum corneum and in the
upper parts of the hair follicles. Some bacteria, however, reside in the deeper
areas of the hair follicles and are beyond the reach of ordinary disinfection
procedures. These bacteria are a reservoir for recolonization after the surface
bacteria are removed.</p><div id="A513"><h3>Staphylococcus epidermidis</h3><p><i>S. epidermidis</i> is a major inhabitant of the skin, and in some
areas it makes up more than 90 percent of the resident aerobic flora.</p></div><div id="A514"><h3>Staphylococcus aureus</h3><p>The nose and perineum are the most common sites for <i>S. aureus</i>
colonization, which is present in 10 percent to more than 40 percent of normal
adults. <i>S. aureus</i> is prevalent (67 percent) on vulvar skin. Its
occurrence in the nasal passages varies with age, being greater in the newborn,
less in adults. <i>S. aureus</i> is extremely common (80 to 100
percent) on the skin of patients with certain dermatologic diseases such as
atopic dermatitis, but the reason for this finding is unclear.</p></div><div id="A515"><h3>Micrococci</h3><p>Micrococci are not as common as staphylococci and diphtheroids; however, they are
frequently present on normal skin. <i>Micrococcus luteus</i>, the
predominant species, usually accounts for 20 to 80 percent of the micrococci
isolated from the skin.</p></div><div id="A516"><h3>Diphtheroids (Coryneforms)</h3><p>The term diphtheroid denotes a wide range of bacteria belonging to the genus
Corynebacterium. Classification of diphtheroids remains unsatisfactory; for
convenience, cutaneous diphtheroids have been categorized into the following
four groups: lipophilic or nonlipophilic diphtheroids; anaerobic diphtheroids;
diphtheroids producing porphyrins (coral red fluorescence when viewed under
ultraviolet light); and those that possess some keratinolytic enzymes and are
associated with trichomycosis axillaris (infection of axillary hair). Lipophilic
diphtheroids are extremely common in the axilla, whereas nonlipophilic strains
are found more commonly on glabrous skin.</p><p>Anaerobic diphtheroids are most common in areas rich in sebaceous glands.
Although the name <i>Corynebacterium</i> acnes was originally used to
describe skin anaerobic diphtheroids, these are now classified as
<i>Propionibacterium acnes</i> and as <i>P.
granulosum</i>. <i>P. acnes</i> is seen eight times more
frequently than <i>P. granulosum</i> in acne lesions and is probably
involved in acne pathogenesis. Children younger than 10 years are rarely
colonized with <i>P. acnes</i>. The appearance of this organism on the
skin is probably related to the onset of secretion of sebum (a semi-fluid
substance composed of fatty acids and epithelial debris secreted from sebaceous
glands) at puberty. <i>P. avidum</i>, the third species of cutaneous
anaerobic diphtheroids, is rare in acne lesions and is more often isolated from
the axilla.</p></div><div id="A517"><h3>Streptococci</h3><p>Streptococci, especially &#x003b2;-hemolytic streptococci, are rarely seen on
normal skin. The paucity of &#x003b2;-hemolytic streptococci on the skin is
attributed at least in part to the presence of lipids on the skin, as these
lipids are lethal to streptococci. Other groups of streptococci, such as
&#x003b1;-hemolytic streptococci, exist primarily in the mouth, from where
they may, in rare instances, spread to the skin.</p></div><div id="A518"><h3>Gram-Negative Bacilli</h3><p>Gram-negative bacteria make up a small proportion of the skin flora. In view of
their extraordinary numbers in the gut and in the natural environment, their
scarcity on skin is striking. They are seen in moist intertriginous areas, such
as the toe webs and axilla, and not on dry skin. Desiccation is the major factor
preventing the multiplication of Gram-negative bacteria on intact skin.
<i>Enterobacter</i>, <i>Klebsiella</i>,
<i>Escherichia coli</i>, and <i>Proteus</i> spp. are the
predominant Gram-negative organisms found on the skin.
<i>Acinetobacter</i> spp also occurs on the skin of normal
individuals and, like other Gram-negative bacteria, is more common in the moist
intertriginous areas.</p></div><div id="A519"><h3>Nail Flora</h3><p>The microbiology of a normal nail is generally similar to that of the skin. Dust
particles and other extraneous materials may get trapped under the nail,
depending on what the nail contacts. In addition to resident skin flora, these
dust particles may carry fungi and bacilli. <i>Aspergillus</i>,
<i>Penicillium</i>, <i>Cladosporium</i>, and
<i>Mucor</i> are the major types of fungi found under the
nails.</p></div></div><div id="A520"><h2 id="_A520_">Oral and Upper Respiratory Tract Flora</h2><p>The oral flora is involved in dental caries and periodontal disease, which affect
about 80 percent. of the population in the Western world. The oral flora, its
interactions with the host, and its response to environmental factors are
thoroughly discussed in another Chapter. Anaerobes in the oral flora are
responsible for many of the brain, face, and lung infections that are frequently
manifested by abscess formation.</p><p>The pharynx and trachea contain primarily those bacterial genera found in the
normal oral cavity (for example, &#x003b1;-and &#x003b2;-hemolytic
streptococci); however, anaerobes, staphylococci, neisseriae, diphtheroids, and
others are also present. Potentially pathogenic organisms such as
<i>Haemophilus</i>, mycoplasmas, and pneumococci may also be found
in the pharynx. Anaerobic organisms also are reported frequently. The upper
respiratory tract is so often the site of initial colonization by pathogens
(<i>Neisseria meningitides</i>, <i>C. diphtheriae</i>,
<i>Bordetella pertussis</i>, and many others) and could be
considered the first region of attack for such organisms. In contrast, the lower
respiratory tract (small bronchi and alveoli) is usually sterile, because
particles the size of bacteria do not readily reach it. If bacteria do reach
these regions, they encounter host defense mechanisms, such as alveolar
macrophages, that are not present in the pharynx.</p></div><div id="A521"><h2 id="_A521_">Gastrointestinal Tract Flora</h2><p>The stomach is a relatively hostile environment for bacteria. It contains
bacteria swallowed with the food and those dislodged from the mouth. Acidity
lowers the bacterial count, which is highest (approximately 10<sup>3</sup> to
10<sup>6</sup> organisms/g of contents) after meals and lowest (frequently
undetectable) after digestion. Some <i>Helicobacter</i> species can
colonize the stomach and are associated with type B gastritis and peptic ulcer
disease. Aspirates of duodenal or jejunal fluid contain approximately
10<sup>3</sup> organisms/ml in most individuals. Most of the bacteria
cultured (streptococci, lactobacilli, <i>Bacteroides</i>) are thought
to be transients. Levels of 10<sup>5</sup> to about 10<sup>7</sup> bacteria/ml
in such aspirates usually indicate an abnormality in the digestive system (for
example, achlorhydria or malabsorption syndrome). Rapid peristalsis and the
presence of bile may explain in part the paucity of organisms in the upper
gastrointestinal tract. Further along the jejunum and into the ileum, bacterial
populations begin to increase, and at the ileocecal junction they reach levels
of 10<sup>6</sup> to 10<sup>8</sup> organisms/ml, with streptococci,
lactobacilli, <i>Bacteroides</i>, and bifidobacteria
predominating.</p><p>Concentrations of 10<sup>9</sup> to 10<sup>11</sup> bacteria/g of contents are
frequently found in human colon and feces. This flora includes a bewildering
array of bacteria (more than 400 species have been identified); nonetheless, 95
to 99 percent belong to anaerobic genera such as <i>Bacteroides</i>,
<i>Bifidobacterium</i>, <i>Eubacterium</i>,
<i>Peptostreptococcus</i>, and <i>Clostridium</i>. In
this highly anaerobic region of the intestine, these genera proliferate, occupy
most available niches, and produce metabolic waste products such as acetic,
butyric, and lactic acids. The strict anaerobic conditions, physical exclusion
(as is shown in many animal studies), and bacterial waste products are factors
that inhibit the growth of other bacteria in the large bowel.</p><p>Although the normal flora can inhibit pathogens, many of its members can produce
disease in humans. Anaerobes in the intestinal tract are the primary agents of
intra-abdominal abscesses and peritonitis. Bowel perforations produced by
appendicitis, cancer, infarction, surgery, or gunshot wounds almost always seed
the peritoneal cavity and adjacent organs with the normal flora. Anaerobes can
also cause problems within the gastrointestinal lumen. Treatment with
antibiotics may allow certain anaerobic species to become predominant and cause
disease. For example, <i>Clostridium difficile</i>, which can remain
viable in a patient undergoing antimicrobial therapy, may produce
pseudomembranous colitis. Other intestinal pathologic conditions or surgery can
cause bacterial overgrowth in the upper small intestine. Anaerobic bacteria can
then deconjugate bile acids in this region and bind available vitamin
B<sub>12</sub> so that the vitamin and fats are malabsorbed. In these
situations, the patient usually has been compromised in some way; therefore, the
infection caused by the normal intestinal flora is secondary to another
problem.</p><p>More information is available on the animal than the human microflora. Research
on animals has revealed that unusual filamentous microorganisms attach to ileal
epithelial cells and modify host membranes with few or no harmful effects.
Microorganisms have been observed in thick layers on gastrointestinal surfaces
(<a class="figpopup" href="/books/NBK7617/figure/A522/?report=objectonly" target="object" rid-figpopup="figA522" rid-ob="figobA522">Fig. 6-3</a>) and in the crypts of
Lieberkuhn. Other studies indicate that the immune response can be modulated by
the intestinal flora. Studies of the role of the intestinal flora in
biosynthesis of vitamin K and other host-utilizable products, conversion of bile
acids (perhaps to cocarcinogens), and ammonia production (which can play a role
in hepatic coma) show the dual role of the microbial flora in influencing the
health of the host. More basic studies of the human bowel flora are necessary to
define their effect on humans.</p><div class="iconblock whole_rhythm clearfix ten_col fig" id="figA522" co-legend-rid="figlgndA522"><a href="/books/NBK7617/figure/A522/?report=objectonly" target="object" title="Figure 6-3" class="img_link icnblk_img figpopup" rid-figpopup="figA522" rid-ob="figobA522"><img class="small-thumb" src="/books/NBK7617/bin/ch6f3.gif" src-large="/books/NBK7617/bin/ch6f3.jpg" alt="Figure 6-3. (A) Scanning electron micrograph of a cross-section of rat colonic mucosa." /></a><div class="icnblk_cntnt" id="figlgndA522"><h4 id="A522"><a href="/books/NBK7617/figure/A522/?report=objectonly" target="object" rid-ob="figobA522">Figure 6-3</a></h4><p class="float-caption no_bottom_margin">(A) Scanning electron micrograph of a cross-section of rat colonic
mucosa. The bar indicates the thick layer of bacteria between the
mucosal surface and the lumen (L) (X 262,) (B) Higher magnification
of the area indicated by the arrow in Fig. A, showing <a href="/books/NBK7617/figure/A522/?report=objectonly" target="object" rid-ob="figobA522">(more...)</a></p></div></div></div><div id="A523"><h2 id="_A523_">Urogenital Flora</h2><p>The type of bacterial flora found in the vagina depends on the age, pH, and hormonal
levels of the host. <i>Lactobacillus</i> spp. predominate in female
infants (vaginal pH, approximately 5) during the first month of life. Glycogen
secretion seems to cease from about I month of age to puberty. During this time,
diphtheroids, <i>S. epidermidis</i>, streptococci, and <i>E.
coli</i> predominate at a higher pH (approximately pH 7). At puberty,
glycogen secretion resumes, the pH drops, and women acquire an adult flora in which
<i>L. acidophilus,</i> corynebacteria, peptostreptococci,
staphylococci, streptococci, and Bacteroides predominate. After menopause, pH again
rises, less glycogen is secreted, and the flora returns to that found in
prepubescent females. Yeasts (<i>Torulopsis</i> and
<i>Candida</i>) are occasionally found in the vagina (10 to 30 percent
of women); these sometimes increase and cause vaginitis.</p><p>In the anterior urethra of humans, <i>S. epidermidis</i>, enterococci, and
diphtheroids are found frequently; <i>E. coli</i>,
<i>Proteus</i>, and <i>Neisseria</i> (nonpathogenic species)
are reported occasionally (10 to 30 percent). Because of the normal flora residing
in the urethra, care must be taken in clinically interpreting urine cultures; urine
samples may contain these organisms at a level of 10<sup>4</sup>/ml if a midstream
(clean-catch) specimen is not obtained.</p></div><div id="A524"><h2 id="_A524_">Conjunctival Flora</h2><p>The conjunctival flora is sparse. Approximately 17 to 49 percent of culture
samples are negative. Lysozyme, secreted in tears, may play a role in
controlling the bacteria by interfering with their cell wall formation. When
positive samples show bacteria, corynebacteria, Neisseriae, and Moraxellae are
cultured. Staphylococci and streptococci are also present, and recent reports
indicate that <i>Haemophilus parainfluenzae</i> is present in 25
percent of conjunctival samples.</p></div><div id="A525"><h2 id="_A525_">Host Infection by Elements of the Normal Flora</h2><p>This chapter has briefly described the normal human flora; however, the
pathogenic mechanisms of various genera or the clinical syndromes in which they
are involved was not discussed. Although such material is presented in other
chapters, note that a breach in mucosal surfaces often results in infection of
the host by members of the normal flora. Caries, periodontal disease, abscesses,
foul-smelling discharges, and endocarditis are hallmarks of infections with
members of the normal human flora (<a class="figpopup" href="/books/NBK7617/figure/A526/?report=objectonly" target="object" rid-figpopup="figA526" rid-ob="figobA526">Fig.
6-4</a>). In addition, impairment of the host (for example, those with
heart failure or leukemia) or host defenses (due to immunosuppression,
chemotherapy, or irradiation) may result in failure of the normal flora to
suppress transient pathogens or may cause members of the normal flora to invade
the host themselves. In either situation, the host may die.</p><div class="iconblock whole_rhythm clearfix ten_col fig" id="figA526" co-legend-rid="figlgndA526"><a href="/books/NBK7617/figure/A526/?report=objectonly" target="object" title="Figure 6-4" class="img_link icnblk_img figpopup" rid-figpopup="figA526" rid-ob="figobA526"><img class="small-thumb" src="/books/NBK7617/bin/ch6f4.gif" src-large="/books/NBK7617/bin/ch6f4.jpg" alt="Figure 6-4. Clinical conditions that may be caused by members of the normal flora." /></a><div class="icnblk_cntnt" id="figlgndA526"><h4 id="A526"><a href="/books/NBK7617/figure/A526/?report=objectonly" target="object" rid-ob="figobA526">Figure 6-4</a></h4><p class="float-caption no_bottom_margin">Clinical conditions that may be caused by members of the normal
flora. </p></div></div></div><div id="A527"><h2 id="_A527_">References</h2><ol><li><div class="bk_ref" id="A528"> Bitton G, Marshall KC: Adsorption of Microorganisms
to Surfaces. John Wiley &#x00026; Sons, New York, 1980 .</div></li><li><div class="bk_ref" id="A529"> Draser BS, Hill MJ: Human Intestinal Flora. Academic
Press, London, 1974. </div></li><li><div class="bk_ref" id="A530">Freter R, Brickner J, Botney M. et al. Survival and implantation of <em>Escherichia coli</em> in
the intestinal tract. <span><span class="ref-journal">Infect Immun. </span>1983;<span class="ref-vol">39</span>:686.</span> [<a href="/pmc/articles/PMC348005/" ref="pagearea=cite-ref&amp;targetsite=entrez&amp;targetcat=link&amp;targettype=pmc">PMC free article<span class="bk_prnt">: PMC348005</span></a>] [<a href="https://pubmed.ncbi.nlm.nih.gov/6339389" ref="pagearea=cite-ref&amp;targetsite=entrez&amp;targetcat=link&amp;targettype=pubmed">PubMed<span class="bk_prnt">: 6339389</span></a>]</div></li><li><div class="bk_ref" id="A531">Hentges DJ, Stein AJ, Casey SW, Que JU. Protective role of intestinal flora against <em>Pseudomonas
aeruginosa</em> in mice: influence of antibiotics on colonization
resistance. <span><span class="ref-journal">Infect Immun. </span>1985;<span class="ref-vol">47</span>:118.</span> [<a href="/pmc/articles/PMC261485/" ref="pagearea=cite-ref&amp;targetsite=entrez&amp;targetcat=link&amp;targettype=pmc">PMC free article<span class="bk_prnt">: PMC261485</span></a>] [<a href="https://pubmed.ncbi.nlm.nih.gov/2856912" ref="pagearea=cite-ref&amp;targetsite=entrez&amp;targetcat=link&amp;targettype=pubmed">PubMed<span class="bk_prnt">: 2856912</span></a>]</div></li><li><div class="bk_ref" id="A532">Herthelius M, Gorbach SL, Mollby R. et al. Elimination of vaginal colonization with <em>Escherichia
coli</em> by administration of indigenous flora. <span><span class="ref-journal">Infect Immun. </span>1989;<span class="ref-vol">57</span>:2447.</span> [<a href="/pmc/articles/PMC313468/" ref="pagearea=cite-ref&amp;targetsite=entrez&amp;targetcat=link&amp;targettype=pmc">PMC free article<span class="bk_prnt">: PMC313468</span></a>] [<a href="https://pubmed.ncbi.nlm.nih.gov/2663724" ref="pagearea=cite-ref&amp;targetsite=entrez&amp;targetcat=link&amp;targettype=pubmed">PubMed<span class="bk_prnt">: 2663724</span></a>]</div></li><li><div class="bk_ref" id="A533"> Maibach H, Aly R: Skin Microbiology: Relevance to
Clinical Infection. Springer-Verlag, New York, 1981 .</div></li><li><div class="bk_ref" id="A534">Marples MJ. Life in the skin. <span><span class="ref-journal">Sci Am. </span>1969;<span class="ref-vol">220</span>:108.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/5761729" ref="pagearea=cite-ref&amp;targetsite=entrez&amp;targetcat=link&amp;targettype=pubmed">PubMed<span class="bk_prnt">: 5761729</span></a>]</div></li><li><div class="bk_ref" id="A535">Savage DC. Microbial ecology of the gastrointestinal tract. <span><span class="ref-journal">Annu Rev Microbiol. </span>1977;<span class="ref-vol">31</span>:107.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/334036" ref="pagearea=cite-ref&amp;targetsite=entrez&amp;targetcat=link&amp;targettype=pubmed">PubMed<span class="bk_prnt">: 334036</span></a>]</div></li><li><div class="bk_ref" id="A536"> Tannock GW: Normal Microflora. Chapman and
Hall,London, UK, 1995 .</div></li></ol></div><div id="bk_toc_contnr"></div></div></div>
<div class="post-content"><div><div class="half_rhythm"><a href="/books/about/copyright/">Copyright</a> © 1996, The University of Texas Medical Branch
at Galveston.</div><div class="small"><span class="label">Bookshelf ID: NBK7617</span><span class="label">PMID: <a href="https://pubmed.ncbi.nlm.nih.gov/21413249" title="PubMed record of this page" ref="pagearea=meta&amp;targetsite=entrez&amp;targetcat=link&amp;targettype=pubmed">21413249</a></span></div><div style="margin-top:2em" class="bk_noprnt"><a class="bk_cntns" href="/books/n/mmed/">Contents</a><div class="pagination bk_noprnt"><a class="active page_link prev" href="/books/n/mmed/A438/" title="Previous page in this title">&lt; Prev</a><a class="active page_link next" href="/books/n/mmed/A537/" title="Next page in this title">Next &gt;</a></div></div></div></div>
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<div xmlns:np="http://ncbi.gov/portal/XSLT/namespace" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance"></div><div class="portlet"><div class="portlet_head"><div class="portlet_title"><h3><span>Views</span></h3></div><a name="Shutter" sid="1" href="#" class="portlet_shutter" title="Show/hide content" remembercollapsed="true" pgsec_name="PDF_download" id="Shutter"></a></div><div class="portlet_content"><ul xmlns:np="http://ncbi.gov/portal/XSLT/namespace" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" class="simple-list"><li><a href="/books/NBK7617/?report=reader">PubReader</a></li><li><a href="/books/NBK7617/?report=printable">Print View</a></li><li><a data-jig="ncbidialog" href="#_ncbi_dlg_citbx_NBK7617" data-jigconfig="width:400,modal:true">Cite this Page</a><div id="_ncbi_dlg_citbx_NBK7617" style="display:none" title="Cite this Page"><div class="bk_tt">Davis CP. Normal Flora. In: Baron S, editor. Medical Microbiology. 4th edition. Galveston (TX): University of Texas Medical Branch at Galveston; 1996. Chapter 6.<span class="bk_cite_avail"></span></div></div></li></ul></div></div><div class="portlet"><div class="portlet_head"><div class="portlet_title"><h3><span>In this Page</span></h3></div><a name="Shutter" sid="1" href="#" class="portlet_shutter" title="Show/hide content" remembercollapsed="true" pgsec_name="page-toc" id="Shutter"></a></div><div class="portlet_content"><ul xmlns:np="http://ncbi.gov/portal/XSLT/namespace" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" class="simple-list"><li><a href="#mmed_ch6" ref="log$=inpage&amp;link_id=inpage">General Concepts</a></li><li><a href="#A508" ref="log$=inpage&amp;link_id=inpage">Introduction</a></li><li><a href="#A510" ref="log$=inpage&amp;link_id=inpage">Significance of the Normal Flora</a></li><li><a href="#A512" ref="log$=inpage&amp;link_id=inpage">Normal Flora of Skin</a></li><li><a href="#A520" ref="log$=inpage&amp;link_id=inpage">Oral and Upper Respiratory Tract Flora</a></li><li><a href="#A521" 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