Exploring Gram-Unfavourable Rods: Insights into Enteric Tract Microorganisms
Gram-negative rods are a big group of various organisms
(Figures 18–1, 18–2, and 19–1). On this ebook, these micro organism are
subdivided into three clinically related classes, every in a
separate chapter, in accordance with whether or not the organism is said
primarily to the enteric or the respiratory tract or to animal
sources (Desk 18–1). Though this method results in some
overlap, it must be useful as a result of it permits basic ideas
to be emphasised.
Gram-negative rods associated to the enteric tract embrace a big
variety of genera. These genera have due to this fact been divided
into three teams relying on the key anatomic location
of illness, particularly, (1) pathogens each inside and outdoors the
enteric tract, (2) pathogens primarily throughout the enteric tract,
and (3) pathogens exterior the enteric tract (see Desk 18–1).
The frequency with which the organisms associated to the
enteric tract trigger illness in the US is proven in Desk
18–2. Salmonella, Shigella, and Campylobacter are frequent
pathogens within the gastrointestinal tract, whereas Escherichia,
Vibrio, and Yersinia are much less so. Enterotoxigenic strains of Esch-
erichia coli are a typical reason behind diarrhea in creating coun-
tries however are much less widespread in the US. The medically
necessary gram-negative rods that trigger diarrhea are described
in Desk 18–3. Urinary tract infections are brought on primarily by
E. coli; the opposite organisms happen much less generally. The medically
necessary gram-negative rods that trigger urinary tract infec-
tions are described in Desk 18–4.
Further data relating to the scientific features of
infections attributable to the organisms on this chapter is pro-
vided in Half IX entitled Infectious Ailments starting on
web page 589.
The Enterobacteriaceae is a big household of gram-negative rods
discovered primarily within the colon of people and different animals,
many as a part of the conventional flora. These organisms are the
main facultative anaerobes within the giant gut however are current
in comparatively small numbers in contrast with anaerobes resembling
Bacteroides. Though the members of the Enterobacteriaceae
are labeled collectively taxonomically, they trigger quite a lot of dis-
eases with completely different pathogenetic mechanisms. The organisms
and a few of the illnesses they trigger are listed in Desk 18–5.
Options widespread to all members of this heterogeneous fam-
ily are their anatomic location and the next 4 metabolic
processes: (1) they’re all facultative anaerobes; (2) all of them
ferment glucose (fermentation of different sugars varies); (3) none
have cytochrome oxidase (i.e., they’re oxidase-negative); and
(4) they scale back nitrates to nitrites as a part of their energy-
These 4 reactions can be utilized to differentiate the Entero-
bacteriaceae from one other medically vital group of
organisms—the nonfermenting gram-negative rods, probably the most
necessary of which is Pseudomonas aeruginosa.1
Pseudomonas aeruginosa, a big reason behind urinary tract
an infection and sepsis in hospitalized sufferers, doesn’t ferment
glucose or scale back nitrates and is oxidase-positive. In distinction to
the Enterobacteriaceae, it’s a strict aerobe and derives its power
from oxidation, not fermentation.
All members of the Enterobacteriaceae, being gram-negative,
include endotoxin of their cell partitions. As well as, a number of
exotoxins are produced (e.g., E. coli and Vibrio cholerae secrete
exotoxins, known as enterotoxins, that activate adenylate cyclase
throughout the cells of the small gut, inflicting diarrhea) (see
Chapter 7). As well as, E. coli O157 produces Shiga toxin that
causes hemolytic-uremic syndrome.
The antigens of a number of members of the Enterobacteriaceae, espe-
cially Salmonella and Shigella, are necessary; they’re used for
identification functions each within the scientific laboratory and in epi-
demiologic investigations. The three floor antigens are as follows:
(1) The cell wall antigen (also called the somatic, or O,
antigen) is the outer polysaccharide portion of the lipopolysac-
charide (see Determine 2–6). The O antigen, which consists of
repeating oligosaccharides consisting of three or 4 sugars
repeated 15 or 20 occasions, is the premise for the serologic typing of
many enteric rods. The variety of completely different O antigens may be very
giant (e.g., there are roughly 1,500 sorts of Salmonella
and 150 sorts of E. coli).
(2) The H antigen is on the flagellar protein. Solely flagellated
organisms, resembling Escherichia and Salmonella, have H antigens,
whereas the nonmotile ones, resembling Klebsiella and Shigella, do
not. The H antigens of sure Salmonella species are uncommon
as a result of the organisms can reversibly alternate between two sorts
of H antigens known as part 1 and part 2. The organisms could use
this transformation in antigenicity to evade the immune response.
(3) The capsular or Ok polysaccharide antigen is especially
distinguished in closely encapsulated organisms resembling Klebsiella.
The Ok antigen is recognized by the quellung (capsular swelling)
response within the presence of particular antisera and is used to serotype
E. coli and Salmonella typhi for epidemiologic functions. In S. typhi,
the reason for typhoid fever, it’s known as the Vi (or virulence) antigen.
Specimens suspected of containing members of the Enterobac-
teriaceae and associated organisms are normally inoculated onto two
media, a blood agar plate and a selective differential medium
resembling MacConkey’s agar or eosin-methylene blue (EMB) agar.
The differential capability of those latter media relies on lactose
fermentation, which is an important metabolic criterion
used within the identification of those organisms (Desk 18–6). On
these media, the non–lactose fermenters (e.g., Salmonella and
Shigella) kind colorless colonies, whereas the lactose fermen-
ters (e.g., E. coli) kind coloured colonies. On EMB agar, E. coli
colonies have a attribute inexperienced sheen. The selective impact
of the media in suppressing undesirable gram-positive organisms
is exerted by bile salts or bacteriostatic dyes within the agar.
A further set of screening assessments, consisting of triple sugar
iron (TSI) agar and urea agar, is carried out previous to the definitive
identification procedures. The rationale for the usage of these media
and the reactions of a number of necessary organisms are introduced
within the field titled “Agar Media for Enteric Gram-Unfavourable Rods”
and in Desk 18–7. The outcomes of the screening course of are sometimes
enough to determine the genus of an organism; nonetheless, an array
of 20 or extra biochemical assessments is required to determine the species.
One other invaluable piece of knowledge used to determine some
of those organisms is their motility, which depends on the
presence of flagella. Proteus species are very motile and charac-
teristically swarm over the blood agar plate, obscuring the colo-
nies of different organisms. Motility can be an necessary diagnostic
criterion within the differentiation of Enterobacter cloacae, which is
motile, from Ok. pneumoniae, which is nonmotile.
If the outcomes of the screening assessments counsel the presence of a
Salmonella or Shigella pressure, an agglutination check can be utilized
to determine the genus of the organism and to find out whether or not
it’s a member of group A, B, C, or D.
Coliforms & Public Well being
Contamination of the general public water provide system by sewage is
detected by the presence of coliforms within the water. In a basic
sense, the time period coliform consists of not solely E. coli but additionally different
inhabitants of the colon resembling Enterobacter and Klebsiella.
Nonetheless, as a result of solely E. coli is completely a big gut
organism, whereas the others are discovered within the surroundings additionally,
it’s used because the indicator of fecal contamination. In water qual-
ity testing, E. coli is recognized by its capability to ferment lactose
with the manufacturing of acid and fuel, its capability to develop at 44.5°C,
and its attribute colony sort on EMB agar. An E. coli colony
rely above 4/dL in municipal ingesting water is indicative of
unacceptable fecal contamination. As a result of E. coli and the enteric
pathogens are killed by chlorination of the ingesting water, there
is never an issue with assembly this customary. Disinfection of
the general public water provide is likely one of the most necessary advances
of public well being within the twentieth century.
The suitable remedy for infections attributable to members
of the Enterobacteriaceae and associated organisms should be indi-
vidually tailor-made to the antibiotic sensitivity of the organism.
PATHOGENS BOTH WITHIN & OUTSIDE THE ENTERIC TRACT
Escherichia coli is the most typical reason behind urinary tract
an infection and gram-negative rod sepsis. It is likely one of the two
necessary causes of neonatal meningitis and is the bacterium
most regularly related to “traveler’s diarrhea,” a watery
diarrhea. Some strains of E. coli trigger bloody diarrhea and
Escherichia coli is a straight gram-negative rod (see Determine 18–1), in
distinction to the curved gram-negative rods of the genera Vibrio,
Campylobacter, and Helicobacter.
Escherichia coli is probably the most considerable facultative anaerobe in
the colon and feces. It’s, nonetheless, significantly outnumbered by the
obligate anaerobes resembling Bacteroides.
Escherichia coli ferments lactose, a property that distin-
guishes it from the 2 main intestinal pathogens, Shigella and
Salmonella. It has three antigens which are used to determine the
organism in epidemiologic investigations: the O, or cell wall,
antigen; the H, or flagellar, antigen; and the Ok, or capsular, anti-
gen. As a result of there are greater than 150 O, 50 H, and 90 Ok antigens,
the assorted mixtures lead to greater than 1,000 antigenic
sorts of E. coli. Particular serotypes are related to sure dis-
eases (e.g., O55 and O111 trigger outbreaks of neonatal diarrhea).
The reservoir of E. coli consists of each people and animals. The
supply of the E. coli that causes urinary tract infections is the
affected person’s personal colonic flora that colonizes the urogenital space.
The supply of the E. coli that causes neonatal meningitis is the
mom’s beginning canal; the an infection is acquired throughout beginning. In
distinction, the E. coli that causes traveler’s diarrhea is acquired
by ingestion of meals or water contaminated with human feces.
Notice that the primary reservoir of enterohemorrhagic E. coli O157
is cattle and the organism is acquired in undercooked beef, for
Escherichia coli has a number of clearly recognized parts
that contribute to its capability to trigger illness: pili, a capsule,
endotoxin, and three exotoxins (enterotoxins), two that trigger
watery diarrhea and one which causes bloody diarrhea and
Intestinal Tract An infection
Step one is the adherence of the organism to the cells of the
jejunum and ileum via pili that protrude from the
bacterial floor. As soon as connected, the micro organism synthesize entero-
toxins (exotoxins that act within the enteric tract), which act on the
cells of the jejunum and ileum to trigger diarrhea. The toxins are
strikingly cell-specific; the cells of the colon are usually not vulnerable,
in all probability as a result of they lack receptors for the toxin. Enterotoxi-
genic strains of E. coli (ETEC) can produce both or each of two
(1) The warmth-labile toxin (LT) acts by stimulating adenylate
cyclase. Each LT and cholera toxin act by catalyzing the addi-
tion of adenosine diphosphate-ribose (a course of known as ADP-
ribosylation) to the G protein that stimulates the cyclase. This
irreversibly prompts the cyclase. The resultant improve in intra-
mobile cyclic adenosine monophosphate (AMP) focus
stimulates cyclic AMP–dependent protein kinase, which phos-
phorylates ion transporters within the membrane. The transporters
export ions, which trigger an outpouring of fluid, potassium, and
chloride from the enterocytes into the lumen of the intestine, result-
ing in watery diarrhea. Notice that cholera toxin has the identical
mode of motion.
(2) The opposite enterotoxin is a low-molecular-weight, heat-
secure toxin (ST), which stimulates guanylate cyclase.
The enterotoxin-producing strains don’t trigger inflamma-
tion, don’t invade the intestinal mucosa, and trigger a watery,
nonbloody diarrhea. Nonetheless, sure strains of E. coli are
enteropathic (enteroinvasive) and trigger illness not by entero-
toxin formation however by invasion of the epithelium of the massive
gut, inflicting bloody diarrhea (dysentery) accompanied by
inflammatory cells (neutrophils) within the stool.
Sure enterohemorrhagic strains of E. coli (i.e., these with
the O157:H7 serotype) (Shiga toxin–producing E. coli [STEC])
additionally trigger bloody diarrhea by producing an exotoxin known as
Shiga toxin, so known as as a result of it is rather much like that produced
by Shigella species. Shiga toxin acts by eradicating an adenine
from the massive (28S) ribosomal RNA, thereby stopping protein
synthesis. Shiga toxin is encoded by temperate (lysogenic) bac-
teriophages. Shiga toxin can be known as verotoxin as a result of it has a
cytopathic impact on Vero (monkey) cells in tradition.
These O157:H7 strains are related to outbreaks of
bloody diarrhea following ingestion of undercooked ham-
burger, usually at fast-food eating places. The micro organism on the sur-
face of the hamburger are killed by the cooking, however these in
the inside, which is undercooked, survive. Additionally, direct contact
with animals (e.g., visits to farms and petting zoos) has resulted
in bloody diarrhea attributable to O157:H7 strains. E. coli O157 has
a low ID50 of roughly 100 organisms.
Some sufferers with bloody diarrhea attributable to O157:H7 strains
even have a life-threatening complication known as hemolytic-uremic
syndrome (HUS), which happens when Shiga toxin enters the
bloodstream. This syndrome consists of hemolytic anemia,
thrombocytopenia, and acute renal failure. The hemolytic ane-
mia and renal failure happen as a result of there are receptors for Shiga
toxin on the floor of the endothelium of small blood vessels
and on the floor of kidney epithelium. Dying of the endothe-
lial cells of small blood vessels ends in a microangiopathic
hemolytic anemia during which the crimson cells passing by the
broken space grow to be grossly distorted (schistocytes) after which
lyse. Thrombocytopenia happens as a result of platelets adhere to the
broken endothelial floor. Dying of the kidney epithelial cells
results in renal failure. Remedy of diarrhea attributable to O157:H7
strains with antibiotics, resembling ciprofloxacin, will increase the danger
of creating HUS by rising the quantity of Shiga toxin
launched by the dying micro organism.
Urinary Tract Infections
Sure O serotypes of E. coli preferentially trigger urinary tract
infections. These uropathic strains are characterised by pili
with adhesin proteins that bind to particular receptors on the
urinary tract epithelium. The binding web site on these receptors
consists of dimers of galactose (Gal-Gal dimers). These pili are
additionally known as P fimbria or pyelonephritis-associated pili (PAP).
Cranberry juice comprises flavonoids that inhibit the binding
of pili to receptors and could also be helpful within the prevention of recur-
lease urinary tract infections. The motility of E. coli could assist its
capability to ascend the urethra into the bladder and ascend the
ureter into the kidney.
Systemic An infection
The opposite two structural parts, the capsule and the
endotoxin, play a extra distinguished position within the pathogenesis
of systemic, slightly than intestinal tract, illness. The capsular
polysaccharide interferes with phagocytosis, thereby enhancing
the organism’s capability to trigger infections in numerous organs. For
instance, E. coli strains that trigger neonatal meningitis normally
have a selected capsular sort known as the K1 antigen. The endo-
toxin of E. coli is the cell wall lipopolysaccharide, which causes
a number of options of gram-negative sepsis resembling fever, hypoten-
sion, and disseminated intravascular coagulation.
Th-17 helper T cells that produce interleukin-17 are an
necessary host protection towards sepsis attributable to enteric bacte-
ria resembling E. coli and Klebsiella. Sufferers contaminated with human
immunodeficiency virus (HIV) expertise a lack of Th-17 cells
and are predisposed to sepsis attributable to E. coli and Klebsiella.
Escherichia coli causes quite a lot of illnesses each inside and
exterior the intestinal tract. The principle scientific findings, the
main pathogenetic elements, and the primary laboratory outcomes are
described in Desk 18–8.
(1) Medical findings throughout the intestinal tract:
Diarrhea attributable to enterotoxigenic E. coli (ETEC) is usu-
ally watery, nonbloody, self-limited, and of quick length (1–3
days). It’s regularly related to journey (traveler’s diarrhea,
An infection with enterohemorrhagic E. coli (EHEC), on the
different hand, ends in a dysentery-like syndrome characterised
by bloody diarrhea, stomach cramping, and fever much like
that attributable to Shigella.
The O157:H7 strains of E. coli (STEC) additionally trigger bloody
diarrhea, which might be difficult by HUS. This syndrome is
characterised by kidney failure, hemolytic anemia, and throm-
bocytopenia. The hemolytic anemia is attributable to exotoxin-
induced capillary injury, which ends up in injury to the crimson
cells as they move by the capillaries. These distorted, frag-
mented crimson cells known as schistocytes might be seen on blood smear
and are attribute of a microangiopathic hemolytic anemia.
In 2011, an outbreak of diarrhea and HUS in Germany was
attributable to a Shiga toxin–producing pressure of E. coli that was
typed as O104:H4, not O157:H7. This means that strains of
E. coli apart from O157:H7 can even trigger HUS.
HUS happens significantly in kids who’ve been handled
with fluoroquinolones or different antibiotics for his or her diarrhea.
Because of this, antibiotics shouldn’t be used to deal with diarrhea
attributable to EHEC.
(2) Medical findings exterior of the intestinal tract:
Escherichia coli is the main reason behind community-acquired
urinary tract infections. These infections happen primarily in
ladies; this discovering is attributed to 3 options that facilitate
ascending an infection into the bladder, particularly, a brief urethra,
the proximity of the urethra to the anus, and colonization of the
vagina by members of the fecal flora. Additionally it is probably the most frequent
reason behind nosocomial (hospital-acquired) urinary tract infec-
tions, which happen equally regularly in each women and men
and are related to the usage of indwelling urinary catheters.
Enterotoxigenic E. coli is the most typical reason behind traveler’s diarrhea, however
different micro organism (e.g., Salmonella, Shigella, Campylobacter, and Vibrio species),
viruses resembling Norwalk virus, and protozoa resembling Giardia and Cryptosporidium
species are additionally concerned.
Urinary tract infections might be restricted to the bladder or prolong
up the amassing system to the kidneys. If solely the bladder is
concerned, the illness is named cystitis, whereas an infection of the
kidney is named pyelonephritis. Essentially the most distinguished symp-
toms of cystitis are ache (dysuria) and frequency of urination;
sufferers are normally afebrile. Pyelonephritis is characterised by
fever, flank ache, and costovertebral angle tenderness; dysuria
and frequency could or could not happen.
Escherichia coli can be a serious trigger, together with the group B
streptococci, of meningitis and sepsis in neonates. Publicity of
the new child to E. coli and group B streptococci happens throughout
beginning because of colonization of the vagina by these organisms
in roughly 25% of pregnant ladies. Escherichia coli is the
organism remoted most regularly from sufferers with hospital-
acquired sepsis, which arises primarily from urinary, biliary, or
peritoneal infections. Peritonitis is normally a blended an infection
attributable to E. coli or different facultative enteric gram-negative rod
plus anaerobic members of the colonic flora resembling Bacteroides
Specimens suspected of containing enteric gram-negative rods,
resembling E. coli, are grown initially on a blood agar plate and on
a differential medium, resembling EMB agar or MacConkey’s agar.
Escherichia coli, which ferments lactose, varieties pink colonies,
whereas lactose-negative organisms are colorless. On EMB
agar, E. coli colonies have a attribute inexperienced sheen. Some
of the necessary options that assist distinguish E. coli from
different lactose-fermenting gram-negative rods are as follows:
(1) it produces indole from tryptophan, (2) it decarboxylates
lysine, (3) it makes use of acetate as its solely supply of carbon, and (4) it
is motile. Escherichia coli O157:H7 doesn’t ferment sorbitol,
which serves as an necessary criterion that distinguishes it
from different strains of E. coli. The isolation of enterotoxigenic
or enteropathogenic E. coli from sufferers with diarrhea is just not a
routine diagnostic process.
Remedy of E. coli infections is determined by the positioning of illness
and the resistance sample of the precise isolate. For instance,
an uncomplicated decrease urinary tract an infection (cystitis) can
be handled utilizing oral trimethoprim-sulfamethoxazole or nitro-
furantoin. Pyelonephritis might be handled with ciprofloxacin or
ceftriaxone. Nonetheless, E. coli sepsis requires remedy with
parenteral antibiotics (e.g., a third-generation cephalosporin,
resembling cefotaxime, with or with out an aminoglycoside, resembling
gentamicin). For the remedy of neonatal meningitis, a combi-
nation of ampicillin and cefotaxime is normally given.
Antibiotic remedy is normally not indicated in E. coli
diarrheal illnesses. Nonetheless, administration of trimethoprim-
sulfamethoxazole or loperamide (Imodium) could shorten the
length of signs. Rehydration is usually all that’s neces-
sary on this self-limited illness. Nonetheless, diarrhea brought on
by E. coli O157 shouldn’t be handled with antimotility medication
as their use will increase the danger of HUS. Giving antibiotics to
sufferers with E. coli O157 diarrhea is controversial as it might
improve the danger of HUS.
Remedy of HUS is usually supportive however dialysis could also be
essential if renal failure happens. If extreme anemia or thrombocy-
topenia happens, transfusions could also be essential. Plasma change
doesn’t alter the course of HUS.
There isn’t a particular prevention for E. coli infections, resembling
energetic or passive immunization. Nonetheless, numerous basic
measures might be taken to forestall sure infections brought on
by E. coli and different organisms. For instance, the incidence of
urinary tract infections might be lowered by the considered use and
immediate withdrawal of catheters and, in recurrent infections,
by extended prophylaxis with urinary antiseptic medication (e.g.,
nitrofurantoin or trimethoprim-sulfamethoxazole). Using
cranberry juice to forestall recurrent urinary tract infections
seems to be based mostly on the flexibility of flavonoids within the juice to
inhibit the binding of the pili of the uropathic strains of E. coli to
the bladder epithelium slightly than to acidification of the urine,
which was the earlier rationalization.
Some instances of sepsis might be prevented by immediate removing of
or switching the positioning of intravenous traces. Traveler’s diarrhea can
generally be prevented by the prophylactic use of doxycycline,
ciprofloxacin, trimethoprim-sulfamethoxazole, or Pepto-Bismol.
Ingestion of raw meals and unpurified water must be
prevented whereas touring in sure international locations.
Salmonella species trigger enterocolitis, enteric fevers resembling
typhoid fever, and septicemia with metastatic infections such
as osteomyelitis. They’re one of the widespread causes of
bacterial enterocolitis in the US.
Salmonellae are gram-negative rods that don’t ferment
lactose however do produce H2S—options which are used of their
laboratory identification. Their antigens—cell wall O, flagellar
H, and capsular Vi (virulence)—are necessary for taxonomic
and epidemiologic functions. The O antigens, that are the
outer polysaccharides of the cell wall, are used to subdivide
the salmonellae into teams A–I. There are two types of the
H antigens, phases 1 and a couple of. Solely one of many two H proteins is
synthesized at anyone time, relying on which gene sequence
is within the appropriate alignment for transcription into mRNA. The Vi
antigens (capsular polysaccharides) are antiphagocytic and are
an necessary virulence issue for S. typhi, the agent of typhoid
fever. The Vi antigens are additionally used for the serotyping of S. typhi
within the scientific laboratory.
There are three strategies for naming the salmonellae. Ewing
divides the genus into three species: S. typhi, Salmonella chol-
eraesuis, and Salmonella enteritidis. On this scheme there’s one
serotype in every of the primary two species and 1,500 serotypes in
the third. Kaufman and White assign completely different species names
to every serotype; there are roughly 1,500 completely different species, usu-
ally named for town during which they have been remoted. Salmonella
dublin in accordance with Kaufman and White could be S. enteritidis
serotype dublin in accordance with Ewing. The third method to
naming the salmonellae relies on relatedness decided by
DNA hybridization evaluation. On this scheme, S. typhi is just not a
distinct species however is classed as Salmonella enterica serotype
(or serovar) typhi. All three of those naming techniques are in cur-
Clinically, the Salmonella species are sometimes considered in two
distinct classes, particularly, the typhoidal species (i.e., people who
trigger typhoid fever) and the nontyphoidal species (i.e., these
that trigger diarrhea [enterocolitis] and metastatic infections,
resembling osteomyelitis). The typhoidal species are S. typhi and
S. paratyphi. The nontyphoidal species are the numerous serotypes
of S. enterica. Of the serotypes, S. enterica serotype choleraesuis
is the species most frequently concerned in metastatic infections.
Pathogenesis & Epidemiology
The three sorts of Salmonella infections (enterocolitis, enteric
fevers, and septicemia) have completely different pathogenic options.
(1) Enterocolitis is characterised by an invasion of the epi-
thelial and subepithelial tissue of the small and huge intestines.
Strains that don’t invade don’t trigger illness. The organisms
penetrate each by and between the mucosal cells into
the lamina propria, with ensuing irritation and diarrhea.
Neutrophils restrict the an infection to the intestine and the adjoining mes-
enteric lymph nodes; bacteremia is rare in enterocolitis.
In distinction to Shigella enterocolitis, during which the infectious
dose may be very small (on the order of 100 organisms), the dose of
Salmonella required is far greater, at the least 100,000 organisms.
Numerous properties of salmonellae and shigellae are in contrast in
Desk 18–9. Gastric acid is a crucial host protection; gastrec-
tomy or use of antacids lowers the infectious dose considerably.
(2) In typhoid and different enteric fevers, an infection begins in
the small gut, however few gastrointestinal signs happen.
The organisms enter, multiply within the mononuclear phagocytes
of Peyer’s patches, after which unfold to the phagocytes of the liver,
gallbladder, and spleen. This results in bacteremia, which is
related to the onset of fever and different signs, in all probability
attributable to endotoxin. Survival and development of the organism
inside phagosomes in phagocytic cells are a hanging function of
this illness, as is the predilection for invasion of the gallbladder,
which may end up in institution of the service state and excre-
tion of the micro organism within the feces for lengthy durations.
(3) Septicemia accounts for less than about 5−10% of Salmonella
infections and happens in one in all two settings: a affected person with an
underlying continual illness, resembling sickle cell anemia or can-
cer, or a toddler with enterocolitis. The septic course is extra
indolent than that seen with many different gram-negative rods.
Bacteremia ends in the seeding of many organs, with osteo-
myelitis, pneumonia, and meningitis as the most typical
sequelae. Osteomyelitis in a toddler with sickle cell anemia is an
necessary instance of such a salmonella an infection. Previ-
ously broken tissues, resembling infarcts and aneurysms, espe-
cially aortic aneurysms, are probably the most frequent websites of metastatic
abscesses. Salmonella are additionally an necessary reason behind vascular
The epidemiology of Salmonella infections is said to the
ingestion of meals and water contaminated by human and animal
wastes. Salmonella typhi, the reason for typhoid fever, is transmit-
ted solely by people, however all different species have a big
animal in addition to human reservoir. Human sources are both
individuals who briefly excrete the organism throughout or shortly
after an assault of enterocolitis or continual carriers who excrete the
organism for years. Essentially the most frequent animal supply is poultry
and eggs, however meat merchandise which are inadequately cooked have
been implicated as properly. Canines and different pets, together with turtles,
snakes, lizards, and iguanas, are extra sources.
After an incubation interval of 12 to 48 hours, enterocolitis
begins with nausea and vomiting after which progresses to
stomach ache and diarrhea, which might fluctuate from gentle to
extreme, with or with out blood. Normally the illness lasts a number of
days, is self-limited, causes nonbloody diarrhea, and doesn’t
require medical care besides within the very younger and really outdated.
HIV-infected people, particularly these with a low CD4
rely, have a a lot better variety of Salmonella infections,
together with extra extreme diarrhea and extra critical metastatic
infections than those that are usually not contaminated with HIV. Salmonella
typhimurium is the most typical species of Salmonella to trigger
enterocolitis in the US, however nearly each species has
In typhoid fever, attributable to S. typhi, and in enteric fever,
attributable to organisms resembling S. paratyphi A, B, and C (S. paratyphi
B and C are also called Salmonella schottmuelleri and
Salmonella hirschfeldii, respectively), the onset of sickness is sluggish,
with fever and constipation slightly than vomiting and diarrhea
predominating. Diarrhea could happen early however normally disap-
pears by the point the fever and bacteremia happen. After the primary
week, because the bacteremia turns into sustained, excessive fever, delir-
ium, tender stomach, and enlarged spleen happen. Rose spots
(i.e., rose-colored macules on the stomach) are related to
typhoid fever however happen solely hardly ever. Leukopenia and anemia are
usually seen. Liver perform assessments are sometimes irregular, indicating
The illness begins to resolve by the third week, however extreme
problems resembling intestinal hemorrhage or perforation can
happen. About 3% of typhoid fever sufferers grow to be continual car-
riers. The service price is greater amongst ladies, particularly these
with earlier gallbladder illness and gallstones.
Septicemia is most frequently attributable to S. choleraesuis. The
signs start with fever however little or no enterocolitis after which
proceed to focal signs related to the affected organ,
regularly bone, lung, or meninges.
In enterocolitis, the organism is most simply remoted from a
stool pattern. Nonetheless, within the enteric fevers, a blood tradition is
the process most definitely to disclose the organism throughout the
first 2 weeks of sickness. Bone marrow cultures are sometimes posi-
tive. Stool cultures might also be optimistic, particularly in continual
carriers in whom the organism is secreted within the bile into the
Salmonellae kind non–lactose-fermenting (colorless) colo-
nies on MacConkey’s or EMB agar. On TSI agar, an alkaline
slant and an acid butt, regularly with each fuel and H2S (black
colour within the butt), are produced. S. typhi is the key exception;
it doesn’t kind fuel and produces solely a small quantity of H2S.
If the organism is urease-negative (Proteus organisms, which
can produce the same response on TSI agar, are urease-positive),
the Salmonella isolate might be recognized and grouped by the slide
agglutination check into serogroup A, B, C, D, or E based mostly on its
O antigen. Definitive serotyping of the O, H, and Vi antigens is
carried out by particular public well being laboratories for epidemio-
Salmonellosis is a notifiable illness, and an investigation
to find out its supply must be undertaken. In sure instances
of enteric fever and sepsis, when the organism is troublesome to
get well, the prognosis might be made serologically by detecting a
rise in antibody titer within the affected person’s serum (Widal check).
Enterocolitis attributable to Salmonella is normally a self-limited
illness that resolves with out remedy. Fluid and electrolyte
alternative could also be required. Antibiotic remedy doesn’t
shorten the sickness or scale back the signs; actually, it might
extend excretion of the organisms, improve the frequency of
the service state, and choose mutants immune to the antibiotic.
Antimicrobial brokers are indicated just for neonates or individuals
with continual illnesses who’re in danger for septicemia and dis-
seminated abscesses. Plasmid-mediated antibiotic resistance is
widespread, and antibiotic sensitivity assessments must be completed. Medication
that retard intestinal motility (i.e., that scale back diarrhea) seem
to extend the length of signs and the fecal excretion of
The remedy of alternative for enteric fevers resembling typhoid
fever and septicemia with metastatic an infection is both ceftriax-
one or ciprofloxacin. Ampicillin or ciprofloxacin must be used
in sufferers who’re continual carriers of S. typhi. Cholecystectomy
could also be essential to abolish the continual service state. Focal
abscesses must be drained surgically when possible.
Salmonella infections are prevented primarily by public well being
and private hygiene measures. Correct sewage remedy, a
chlorinated water provide that’s monitored for contamination
by coliform micro organism, cultures of stool samples from meals han-
dlers to detect carriers, handwashing previous to meals dealing with,
pasteurization of milk, and correct cooking of poultry, eggs, and
meat are all necessary.
Two vaccines can be found, however they confer restricted (50–80%)
safety towards S. typhi. One comprises the Vi capsular poly-
saccharide of S. typhi (given intramuscularly), and the opposite
comprises a stay, attenuated pressure (Ty21a) of S. typhi (given
orally). The 2 vaccines are equally efficient. The vaccine is
advisable for many who will journey or reside in high-risk
areas and for these whose occupation brings them in touch
with the organism. A brand new conjugate vaccine towards typhoid
fever containing the capsular polysaccharide (Vi) antigen cou-
pled to a service protein is protected and immunogenic in younger
kids however is just not obtainable in the US right now.
PATHOGENS PRIMARILY WITHIN THE ENTERIC TRACT
Shigella species trigger enterocolitis. Enterocolitis attributable to
Shigella is commonly known as bacillary dysentery. The time period dysentery
refers to bloody diarrhea.
Shigellae are non–lactose-fermenting, gram-negative rods that
might be distinguished from salmonellae by three standards: they
produce no fuel from the fermentation of glucose, they don’t
produce H2S, and they’re nonmotile. All shigellae have O
antigens (polysaccharide) of their cell partitions, and these antigens
are used to divide the genus into 4 teams: A, B, C, and D.
Pathogenesis & Epidemiology
Shigellae are the simplest pathogens among the many enteric
micro organism. They’ve a really low ID50 (see web page 31). Ingestion
of as few as 100 organisms causes illness, whereas at the least 105
V. cholerae or Salmonella organisms are required to provide
signs. Numerous properties of shigellae and salmonellae are
in contrast in Desk 18–9.
Shigellosis is just a human illness (i.e., there is no such thing as a animal
reservoir). The organism is transmitted by the fecal–oral route.
The 4 Fs—fingers, flies, meals, and feces—are the princi-
pal elements in transmission. Foodborne outbreaks outnumber
waterborne outbreaks by 2 to 1. Outbreaks happen in day care
nurseries and in psychological hospitals, the place fecal–oral transmis-
sion is prone to happen. Youngsters youthful than 10 years account
for roughly half of Shigella-positive stool cultures. There
is not any extended service state with Shigella infections, in contrast to that
seen with S. typhi infections.
Shigellae trigger illness nearly completely within the gastroin-
testinal tract. They produce bloody diarrhea (dysentery) by
invading the cells of the mucosa of the distal ileum and colon.
Native irritation accompanied by ulceration happens, however the
organisms hardly ever penetrate by the wall or enter the blood-
stream, in contrast to salmonellae. Though some strains produce an
enterotoxin (known as Shiga toxin), invasion is the essential issue
in pathogenesis. The proof for that is that mutants that fail
to provide enterotoxin however are invasive can nonetheless trigger illness,
whereas noninvasive mutants are nonpathogenic.
Shiga toxins are encoded by lysogenic bacteriophages. Shiga
toxins similar to these produced by Shigella are produced
by enterohemorrhagic E. coli O157:H7 strains that trigger entero-
colitis and HUS.
After an incubation interval of 1 to 4 days, signs start with
fever and stomach cramps, adopted by diarrhea, which can
be watery at first however later comprises blood and mucus. The dis-
ease varies from gentle to extreme relying on two main elements:
the species of Shigella and the age of the affected person, with younger
kids and aged folks being probably the most severely affected.
Shigella dysenteriae, which causes probably the most extreme illness, is
normally seen in the US solely in vacationers returning
from overseas. Shigella sonnei, which causes gentle illness, is iso-
lated from roughly 75% of all people with shigellosis
in the US. The diarrhea regularly resolves in 2 or
3 days; in extreme instances, antibiotics can shorten the course. Serum
agglutinins seem after restoration however are usually not protecting as a result of
the organism doesn’t enter the blood. The position of intestinal IgA
in safety is unsure.
Shigellae kind non–lactose-fermenting (colorless) colonies on
MacConkey’s or EMB agar. On TSI agar, they trigger an alkaline
slant and an acid butt, with no fuel and no H2S. Affirmation of
the organism as Shigella and dedication of its group are completed
by slide agglutination.
One necessary adjunct to laboratory prognosis is a methy-
lene blue stain of a fecal pattern to find out whether or not neutro-
phils are current. If they’re discovered, an invasive organism such
as Shigella, Salmonella, or Campylobacter is concerned slightly
than a toxin-producing organism resembling V. cholerae, E. coli,
or Clostridium perfringens. (Sure viruses additionally trigger diarrhea
with out neutrophils within the stool.)
The principle remedy for shigellosis is fluid and electrolyte
alternative. In gentle instances, no antibiotics are indicated. In
extreme instances, a fluoroquinolone (e.g., ciprofloxacin) is the
drug of alternative, however strains immune to fluoroquinolones have
emerged and antibiotic sensitivity assessments should be carried out.
Trimethoprim-sulfamethoxazole is another option. Anti-
peristaltic medication are contraindicated in shigellosis, as a result of they
extend the fever, diarrhea, and excretion of the organism.
Prevention of shigellosis depends on interruption of fecal–
oral transmission by correct sewage disposal, chlorination of water,
and private hygiene (handwashing by meals handlers). There’s
no vaccine, and prophylactic antibiotics are usually not advisable.
Vibrio cholerae, the key pathogen on this genus, is the trigger
of cholera. Vibrio parahaemolyticus causes diarrhea related
with consuming uncooked or improperly cooked seafood. Vibrio vulnificus
causes cellulitis and sepsis. Vital options of pathogenesis
by V. cholerae, C. jejuni, and Helicobacter pylori are described in
Vibrios are curved, comma-shaped, gram-negative rods (see
Determine 18–2). V. cholerae is split into serogroups accord-
ing to the character of its O cell wall antigen. Members of the O1
and O139 serogroups trigger epidemic illness, whereas non-O1
organisms both trigger sporadic illness or are nonpathogens.
The O1 organisms have two biotypes, known as traditional and El Tor,
and three serotypes, known as Ogawa, Inaba, and Hikojima. (Bio-
sorts are based mostly on variations in biochemical reactions, whereas
serotypes are based mostly on antigenic variations.) These options are
used to characterize isolates in epidemiologic investigations.
Serogroup O139 organisms, which brought on a serious epidemic
in 1992, are recognized by their response to antisera to the O139
polysaccharide antigens (O antigen).
Notice that solely the O1 and O139 organisms trigger cholera
as a result of solely they produce cholera toxin. They produce cholera
toxin as a result of they’re lysogenized by a bacteriophage that car-
ries the gene for the toxin (see beneath). The non-O1 strains can
trigger milder outbreaks of diarrhea however not cholera.
Vibrio parahaemolyticus and V. vulnificus are marine organ-
isms; they stay primarily within the ocean, particularly in heat salt
water. They’re halophilic (i.e., they require a excessive NaCl con-
centration to develop).
1. Vibrio cholerae
Pathogenesis & Epidemiology
Vibrio cholerae is transmitted by fecal contamination of water
and meals, primarily from human sources. Human carriers are
regularly asymptomatic and embrace people who’re both
within the incubation interval or convalescing. The principle animal res-
ervoirs are marine shellfish, resembling shrimp and oysters. Inges-
tion of those with out satisfactory cooking can transmit the illness.
A significant epidemic of cholera, which spanned the Nineteen Sixties and
Seventies, started in Southeast Asia and unfold over three continents
to areas of Africa, Europe, and the remainder of Asia. One other epi-
demic of cholera started in Peru in 1991 and has unfold to many
international locations in Central and South America. The organism iso-
lated most regularly was the El Tor biotype of O1 V. cholerae,
normally of the Ogawa serotype. The elements that predispose to
epidemics are poor sanitation, malnutrition, overcrowding,
and insufficient medical providers. Quarantine measures failed
to forestall the unfold of the illness as a result of there have been many
asymptomatic carriers. In 1992, V. cholerae serogroup O139
emerged and brought on a widespread epidemic of cholera in India
The pathogenesis of cholera depends on colonization of
the small gut by the organism and secretion of enterotoxin.
For colonization to happen, giant numbers of micro organism should be
ingested as a result of the organism is especially delicate to stom-
ach acid. Individuals with little or no abdomen acid, resembling these
taking antacids or those that have had gastrectomy, are a lot
extra vulnerable. Adherence to the cells of the comb border of
the intestine, which is a requirement for colonization, is said to
secretion of the bacterial enzyme mucinase, which dissolves the
protecting glycoprotein coating over the intestinal cells.
After adhering, the organism multiplies and secretes an
enterotoxin known as choleragen (cholera toxin). This exotoxin
can reproduce the signs of cholera even within the absence of
the Vibrio organisms. The mode of motion of cholera toxin is
described within the subsequent paragraph and in Determine 7–3 within the chapter
on bacterial pathogenesis.
Choleragen consists of an A (energetic) subunit and a B (bind-
ing) subunit. The B subunit, which is a pentamer composed of 5
equivalent proteins, binds to a ganglioside receptor on the floor
of the enterocyte. The A subunit is inserted into the cytosol,
the place it catalyzes the addition of ADP-ribose to the Gs protein
(Gs is the stimulatory G protein). This locks the Gs protein in
the “on” place, which causes the persistent stimulation of
adenylate cyclase. The ensuing overproduction of cyclic AMP
prompts cyclic AMP–dependent protein kinase, an enzyme
that phosphorylates ion transporters within the cell membrane,
ensuing within the lack of water and ions from the cell. The watery
efflux enters the lumen of the intestine, leading to an enormous watery
diarrhea that comprises neither neutrophils nor crimson blood cells.
Morbidity and dying are on account of dehydration and electrolyte
imbalance. Nonetheless, if remedy is instituted promptly, the
illness runs a self-limited course in as much as 7 days.
The genes for cholera toxin and different virulence elements are
carried on a single-stranded DNA bacteriophage known as CTX.
Lysogenic conversion of non–toxin-producing strains to toxin-
producing ones can happen when the CTX phage transduces
these genes. The pili that connect the organism to the intestine mucosa
are the receptors for the phage.
Non-O1 V. cholerae is an occasional reason behind diarrhea associ-
ated with consuming shellfish obtained from the coastal waters of the
Watery diarrhea in giant volumes is the hallmark of cholera.
There aren’t any crimson blood cells or white blood cells within the stool.
Rice-water stool is the time period usually utilized to the nonbloody
effluent. There isn’t a stomach ache, and subsequent symp-
toms are referable to the marked dehydration. The lack of fluid
and electrolytes results in cardiac and renal failure. Acidosis and
hypokalemia additionally happen because of lack of bicarbonate and
potassium within the stool. The mortality price with out remedy
The method to laboratory prognosis is determined by the state of affairs.
Throughout an epidemic, a scientific judgment is made and there’s
no need for the laboratory. In an space the place the illness is
endemic or for the detection of carriers, quite a lot of selective
that aren’t in widespread use in the US are used
within the laboratory.
For prognosis of sporadic instances on this nation, a tradition of
the diarrhea stool containing V. cholerae will present colorless
colonies on MacConkey’s agar as a result of lactose is fermented
slowly. The organism is oxidase-positive, which distinguishes
it from members of the Enterobacteriaceae. On TSI agar, an
acid slant and an acid butt with out fuel or H2S are seen as a result of
the organism ferments sucrose. A presumptive prognosis of V.
cholerae might be confirmed by agglutination of the organism by
polyvalent O1 or non-O1 antiserum. A retrospective prognosis
might be made serologically by detecting an increase in antibody titer in
acute- and convalescent-phase sera.
Remedy consists of immediate, satisfactory alternative of water
and electrolytes, both orally or intravenously. Glucose is added
to the answer to boost the uptake of water and electrolytes.
Antibiotics resembling tetracycline are usually not essential, however they do
shorten the length of signs and scale back the time of excre-
tion of the organisms.
Prevention is achieved primarily by public well being measures that
guarantee a clear water and meals provide. An oral, stay attenuated
vaccine known as Vaxchora is obtainable in the US for trav-
elers to areas the place cholera attributable to serogroup O1 is endemic.
Different oral vaccines containing killed organisms can be found in
international locations the place cholera epidemics happen.
Using tetracycline for prevention is efficient in shut
contacts however doesn’t forestall the unfold of a serious epidemic.
Immediate detection of carriers is necessary in limiting outbreaks.
2. Vibrio parahaemolyticus
Vibrio parahaemolyticus is a marine organism transmitted by
ingestion of uncooked or undercooked seafood, particularly shell-
fish resembling oysters. It’s a main reason behind diarrhea in Japan,
the place uncooked fish is eaten in giant portions, however is an rare
pathogen in the US, though a number of outbreaks have
occurred aboard cruise ships within the Caribbean. Little is thought
about its pathogenesis, besides that an enterotoxin much like
choleragen is secreted and restricted invasion generally happens.
The scientific image attributable to V. parahaemolyticus varies
from gentle to fairly extreme watery diarrhea, nausea and vomiting,
stomach cramps, and fever. The sickness is self-limited, lasting
about 3 days. Vibrio parahaemolyticus is distinguished from
V. cholerae primarily on the premise of development in NaCl: V. parahae-
molyticus grows in 8% NaCl answer (as befits a marine organ-
ism), whereas V. cholerae doesn’t. No particular remedy is
indicated, as a result of the illness is comparatively gentle and self-limited.
Illness might be prevented by correct refrigeration and cooking
3. Vibrio vulnificus
Vibrio vulnificus can be a marine organism (i.e., it’s present in
heat salt waters such because the Caribbean Sea). It causes extreme
pores and skin and smooth tissue infections (cellulitis), particularly in shellfish
handlers, who usually maintain pores and skin wounds. It will probably additionally trigger a
quickly deadly septicemia in immunocompromised individuals who
have eaten uncooked shellfish containing the organism. Hemorrhagic
bullae within the pores and skin usually happen in sufferers with sepsis attributable to V.
vulnificus. Continual liver illness (e.g., cirrhosis) predisposes to
extreme infections. The advisable remedy is doxycycline.
Campylobacter jejuni is a frequent reason behind enterocolitis, espe-
cially in kids. C. jejuni an infection is a typical antecedent to
Guillain-Barré syndrome. Different Campylobacter species are uncommon
causes of systemic an infection, significantly bacteremia.
Campylobacters are curved, gram-negative rods that seem
both comma- or S-shaped. They’re microaerophilic, grow-
ing greatest in 5% oxygen slightly than within the 20% current within the
environment. Campylobacter jejuni grows properly at 42°C, whereas
doesn’t—an statement that’s use-
ful in microbiologic prognosis.
Pathogenesis & Epidemiology
Home animals resembling cattle, chickens, and canine function
a supply of the organisms for people. Transmission is usu-
ally fecal–oral. Meals and water contaminated with animal
feces are the key sources of human an infection. Meals, resembling
poultry, meat, and unpasteurized milk, are generally concerned.
Puppies with diarrhea are a typical supply for youngsters.
Human-to-human transmission happens however is much less frequent
than animal-to-human transmission. Campylobacter jejuni is a
main reason behind diarrhea in the US; it was recovered
Often known as Campylobacter fetus subsp. fetus.
in 4.6% of sufferers with diarrhea, in contrast with 2.3% and 1%
for Salmonella and Shigella, respectively. Campylobacter jejuni
is the main reason behind diarrhea related to consumption of
Options of pathogenesis by Campylobacter are described in
Desk 18–10. Irritation of the intestinal mucosa usually happens,
accompanied by blood in stools. Systemic infections (e.g., bacte-
remia) happen most frequently in neonates or debilitated adults.
Enterocolitis, brought on primarily by C. jejuni, begins as watery,
foul-smelling diarrhea adopted by bloody stools accompanied
by fever and extreme stomach ache. Systemic infections, most
generally bacteremia, are brought on extra usually by C. intestinalis.
The signs of bacteremia (e.g., fever and malaise) are associ-
ated with no particular bodily findings.
Gastrointestinal an infection with C. jejuni is related to
Guillain-Barré syndrome, the most typical reason behind acute
neuromuscular paralysis. Guillain-Barré syndrome is an auto-
immune illness attributed to the formation of antibodies
towards C. jejuni that cross-react with antigens on neurons
(see Chapter 66). An infection with Campylobacter can be associ-
ated with two different autoimmune illnesses: reactive arthritis and
Reiter syndrome. These are additionally described in Chapter 66.
If the affected person has diarrhea, a stool specimen is cultured on a
blood agar plate containing antibiotics5
that inhibit most different
The plate is incubated at 42°C in a microaerophilic atmo-
sphere containing 5% oxygen and 10% carbon dioxide, which
favors the expansion of C. jejuni. It’s recognized by failure to develop
at 25°C, oxidase positivity, and sensitivity to nalidixic acid.
Not like Shigella and Salmonella, lactose fermentation is just not used
as a distinguishing function. If bacteremia is suspected, a blood
tradition incubated beneath customary temperature and atmospheric
situations will reveal the expansion of the characteristically
comma- or S-shaped, motile, gram-negative rods. Identification
of the organism as C. intestinalis is confirmed by its failure to
develop at 42°C, its capability to develop at 25°C, and its resistance to
Erythromycin or ciprofloxacin is used efficiently in C. jejuni
enterocolitis. The remedy of alternative for C. intestinalis bactere-
mia is an aminoglycoside.
There isn’t a vaccine or different particular safety measure.
Correct sewage disposal and private hygiene (handwashing)
Helicobacter pylori causes gastritis and peptic ulcers. An infection
with H. pylori is a threat issue for gastric carcinoma and is linked
to mucosal-associated lymphoid tissue (MALT) lymphomas.
Helicobacters are curved gram-negative rods comparable in appear-
ance to campylobacters, however as a result of they differ sufficiently in
sure biochemical and flagellar traits, they’re classi-
fied as a separate genus. Particularly, helicobacters are strongly
urease-positive, whereas campylobacters are urease-negative.
Pathogenesis & Epidemiology
Helicobacter pylori attaches to the mucus-secreting cells of the
gastric mucosa. The manufacturing of enormous quantities of ammonia
from urea by the organism’s urease, coupled with an inflam-
matory response, results in injury to the mucosa. Lack of the
protecting mucus coating predisposes to gastritis and peptic
ulcer (see Desk 18–10). The ammonia additionally neutralizes abdomen
acid, permitting the organism to outlive. Epidemiologically, most
sufferers with these illnesses present H. pylori in biopsy specimens
of the gastric epithelium.
The pure habitat of H. pylori is the human abdomen, and
it’s in all probability acquired by ingestion. Nonetheless, it has not been
remoted from stool, meals, water, or animals. Individual-to-person
transmission in all probability happens as a result of there’s clustering of
an infection inside households. The speed of an infection with H. pylori in
creating international locations may be very excessive—a discovering that’s in accord
with the excessive price of gastric carcinoma in these international locations.
MALT lymphomas are B-cell tumors positioned sometimes within the
abdomen, however they happen elsewhere within the gastrointestinal tract
as properly. Helicobacter pylori is commonly discovered within the MALT lesion,
and the continual irritation induced by the organism is
thought to stimulate B-cell proliferation and ultimately a B-cell
lymphoma. Antibiotic remedy directed towards the organism
usually causes the tumor to regress.
Gastritis and peptic ulcer are characterised by recurrent ache
within the higher stomach, regularly accompanied by bleeding
into the gastrointestinal tract. No bacteremia or disseminated
The organism might be seen on Gram-stained smears of biopsy
specimens of the gastric mucosa. It may be cultured on the identical
media as campylobacters. In distinction to C. jejuni, H. pylori is
urease-positive. Urease manufacturing is the premise for a noninvasive
diagnostic check known as the “urea breath” check. On this check, radio-
labeled urea is ingested. If the organism is current, urease will
cleave the ingested urea, radiolabeled CO2 is advanced, and the
radioactivity is detected within the breath.
A check for Helicobacter antigen within the stool can be utilized for
prognosis and for affirmation that remedy has eradicated
the organism. The presence of IgG antibodies within the affected person’s
serum may also be used as proof of an infection.
Remedy & Prevention
The idea that underlies the selection of medicine is to make use of antibiot-
ics to get rid of Helicobacter plus a drug to cut back gastric acidity.
A mixture of two antibiotics is used as a result of resistance,
particularly to metronidazole, has emerged. Remedy of duode-
nal ulcers with antibiotics (e.g., amoxicillin and metronidazole)
and bismuth salts (Pepto-Bismol) ends in a significantly decreased
recurrence price. Tetracycline can be utilized as an alternative of amoxicillin.
There isn’t a vaccine or different particular safety measure.
PATHOGENS OUTSIDE THE ENTERIC TRACT
These organisms are normally opportunistic pathogens that trigger
nosocomial infections, particularly pneumonia and urinary tract
infections. Klebsiella pneumoniae is a crucial respiratory
tract pathogen exterior hospitals as properly.
Klebsiella pneumoniae, Enterobacter cloacae, and Serratia
marcescens are the species most frequently concerned in human infec-
tions. They’re regularly discovered within the giant gut however are
additionally current in soil and water. These organisms have very comparable
properties and are normally distinguished on the premise of a number of
biochemical reactions and motility. Klebsiella pneumoniae has
a really giant polysaccharide capsule, which provides its colonies
a hanging mucoid look. Serratia marcescens produces
red-pigmented colonies (Determine 18–3).
Pathogenesis & Epidemiology
Of the three organisms, Ok. pneumoniae is most definitely to be a
main, nonopportunistic pathogen; this property is said to
its antiphagocytic capsule. Though this organism is a main
pathogen, sufferers with Ok. pneumoniae infections regularly
have predisposing situations resembling superior age, continual
respiratory illness, diabetes, or alcoholism. The organism is
carried within the respiratory tract of about 10% of wholesome folks,
who’re vulnerable to pneumonia if host defenses are lowered.
Enterobacter and Serratia infections are clearly associated
to hospitalization, particularly to invasive procedures resembling