Exploring Gram-Unfavourable Rods: Insights into Enteric Tract Microorganisms

Exploring Gram-Unfavourable Rods: Insights into Enteric Tract Microorganisms

INTRODUCTION

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.

ENTEROBACTERIACEAE &

RELATED ORGANISMS

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-

producing processes.

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.

Pathogenesis

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.

Antigens

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.

Laboratory Prognosis

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.

Antibiotic Remedy

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

Ailments

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

hemolytic-uremic syndrome.

Vital Properties

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).

Pathogenesis

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

instance, hamburgers.

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

hemolytic-uremic syndrome.

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

enterotoxins.

(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.

Hemolytic-Uremic Syndrome

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.

Medical Findings

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,

or “turista”).2

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.

2

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

and Fusobacterium.

Laboratory Prognosis

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

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.

Prevention

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

Ailments

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.

Vital Properties

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-

lease use.

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

graft infections.

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.

Medical Findings

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

been concerned.

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

hepatic involvement.

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.

Laboratory Prognosis

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

intestinal tract.

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-

logic functions.

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).

Remedy

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 organisms.

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.

Prevention

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

Illness

Shigella species trigger enterocolitis. Enterocolitis attributable to

Shigella is commonly known as bacillary dysentery. The time period dysentery

refers to bloody diarrhea.

Vital Properties

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.

Medical Findings

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.

Laboratory Prognosis

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.)

Remedy

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

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

Ailments

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

Desk 18–10.

Vital Properties

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

and Bangladesh.

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

United States.

Medical Findings

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

is 40%.

Laboratory Prognosis

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

media3

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

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

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

of seafood.

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

Ailments

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.

Vital Properties

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

Campylobacter intestinalis4

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

4

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

unpasteurized milk.

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.

Medical Findings

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.

Laboratory Prognosis

If the affected person has diarrhea, a stool specimen is cultured on a

blood agar plate containing antibiotics5

that inhibit most different

fecal flora.

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

nalidixic acid.

Remedy

Erythromycin or ciprofloxacin is used efficiently in C. jejuni

enterocolitis. The remedy of alternative for C. intestinalis bactere-

mia is an aminoglycoside.

Prevention

There isn’t a vaccine or different particular safety measure.

Correct sewage disposal and private hygiene (handwashing)

are necessary.

 

HELICOBACTER

Ailments

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.

Vital Properties

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.

Medical Findings

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

illness happens.

Laboratory Prognosis

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

KLEBSIELLA–ENTEROBACTER–

SERRATIA GROUP

Ailments

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.

Vital Properties

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