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Yersinia Enterocolitica
Updated: Sep 27, 2018
Author: Zartash Zafar Khan, MD, FACP; Chief Editor: Mark R Wallace, MD, FACP, FIDSA

Overview

Practice Essentials
Yersinia enterocolitica (see the image below) is a bacterial species in the family Enterobacteriaceae that most often causes
enterocolitis, acute diarrhea, terminal ileitis, mesenteric lymphadenitis, and pseudoappendicitis but, if it spreads systemically,
can also result in fatal sepsis.[1]

Gram stain of Yersinia enterocolitica.

Signs and symptoms

Symptoms of Y enterocolitica infection typically include the following:

Diarrhea - The most common clinical manifestation of this infection; diarrhea may be bloody in severe cases

Low-grade fever

Abdominal pain - May localize to the right lower quadrant

Vomiting - Present in approximately 15-40% of cases

The patient may also develop erythema nodosum, which manifests as painful, raised red or purple lesions, mainly on the
patient’s legs and trunk. Lesions appear 2-20 days after the onset of fever and abdominal pain and resolve spontaneously in
most cases in about a month.

See Clinical Presentation for more detail.

Diagnosis

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The following tests can be used in the diagnosis of Y enterocolitica infection:

Stool culture - This is the best way to confirm a diagnosis of Y enterocolitica[2, 3] ; the culture result is usually positive
within 2 weeks of onset of disease

Tube agglutination

Enzyme-linked immunosorbent assays

Radioimmunoassays

Imaging studies - Ultrasonography or computed tomography (CT) scanning may be useful in delineating true appendicitis
from pseudoappendicitis

Colonoscopy - Findings may vary and are relatively nonspecific

Joint aspiration in cases of Yersinia- associated reactive arthropathy

See Workup for more detail.

Management

Care in patients with Y enterocolitica infection is primarily supportive, with good nutrition and hydration being mainstays of
treatment.[4]

First-line drugs used against the bacterium include the following agents:

Third-generation cephalosporins

Trimethoprim-sulfamethoxazole (TMP-SMZ)

Tetracyclines

Fluoroquinolones - not approved for use in children under 18 years

Aminoglycosides

See Treatment and Medication for more detail.

Background
Yersinia enterocolitica is a pleomorphic, gram-negative bacillus that belongs to the family Enterobacteriaceae. As a human
pathogen, Y enterocolitica is most frequently associated with enterocolitis, acute diarrhea, terminal ileitis, mesenteric
lymphadenitis, and pseudoappendicitis,[1] with the spectrum of disease ranging from asymptomatic to life-threatening sepsis,
especially in infants. The bacterium was first reported by Mclver and Picke, in 1934.[5] Schleifstein and Coleman provided the
first recognized description of 5 human isolates of Y enterocolitica, in 1939. (See Prognosis and Clinical Presentation.)[6]

In several countries, Y enterocolitica has eclipsed Shigella species and approaches Salmonella and Campylobacter species as
the predominant cause of acute bacterial gastroenteritis. Y enterocolitica most commonly affects young individuals
(approximately 75% of patients with Y enterocolitica infection are aged 5-15 years), but whether this represents an increased
susceptibility or a greater likelihood of developing symptomatic illness is unclear. Most cases of Y enterocolitica infection are
sporadic, but reports have documented large outbreaks centered on a single contaminated source. (See Epidemiology.)

Human yersiniosis is attributed to contaminated pork, milk, water, and tofu consumption, as well as to blood transfusion. Infected
individuals may shed Y enterocolitica in stools for 90 days after the symptom resolution, suggesting that early detection of Y
enterocolitica from diarrheal stool samples is critical in preventing its transmission and an eventual outbreak. (See
Pathophysiology, Etiology, Clinical Presentation, and Workup.)[7, 8]

Classification

Y enterocolitica is classified according to various distinct biochemical and serologic reactions. Based on biochemical
characteristics, 6 biotypes of the bacterium have been described. Biotypes 2, 3, and 4 are most common in humans. The

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serotyping is based on O and H antigens. More than 60 serotypes of Y enterocolitica have been described. The serotypes most
clearly pathogenic to humans include O:3, O:5,27, O:8, O:9, and O:13.

H-antigen typing can be a valuable supplement to O-antigen typing and biochemical characterization in epidemiologic
investigations. Accurate identification of pathogenic strains requires consideration of both the biotype and the serotype because
some strains can contain multiple cross-reacting O antigens.

Metabolism

Y enterocolitica is non–lactose-fermenting, glucose-fermenting, and oxidase-negative facultative anaerobe that is motile at 25°C
and nonmotile at 37°C. Most, but not all, Y enterocolitica isolates reduce nitrates. The presence of bile salts in the medium
prevents the organism from fermenting lactose. Colonies of Y enterocolitica do not produce hydrogen sulfide in triple sugar iron
medium, but the organism is urease positive.

Patient education

Educate patients and individuals at risk for infection about appropriate hygiene methods and signs or symptoms of infection.
Encourage public awareness of outbreaks, modes of transmission, and ways to prevent transmission.

Pathophysiology
As with other members of the genus Yersinia, Y enterocolitica is an invasive organism that appears to cause disease by tissue
destruction. Researchers have elucidated several potential pathogenic properties, including chromosomally mediated effects
(eg, attachment to tissue culture, production of enterotoxin) and plasmid-mediated mechanisms (eg, production of Vw antigens,
calcium dependency for growth, autoagglutination).

Invasion and colonization

Invasion of human epithelial cells and penetration of the mucosa occurs in the ileum, followed by multiplication in Peyer patches.
A 103-kd protein, known as invasin and determined by the INV gene, mediates bacterial invasion. The best-defined pathway is
through the action of invasin.[9]

As a foodborne pathogen, Y enterocolitica can efficiently colonize and induce disease in the small intestine. Following ingestion,
the bacteria colonize the lumen and invade the epithelial lining of the small intestine, resulting in the colonization of the
underlying lymphoid tissues known as Peyer patches. A direct lymphatic link between the Peyer patches and mesenteric lymph
nodes may result in bacterial dissemination to these sites, resulting in mesenteric lymphadenitis or systemic infection.

Dissemination to extraintestinal sites, such as the spleen, is hypothesized to occur via 2 main mechanisms: (1) colonization of
the Peyer patches, which can then be used as a staging ground for spread into the blood and/or lymph, ultimately resulting in
the appearance of bacteria in other tissues, and (2) bypass of the Peyer patches, with Y enterocolitica going straight to systemic
colonization. The possibilities of additional avenues for dissemination have yet to be excluded.

Y enterocolitica colonization of the intestinal lymphoid tissues requires transmigration of the bacteria from the intestinal lumen
across an epithelial tissue barrier. Antigen-sampling intestinal epithelial cells known as M cells are thought to be critical for this
transmigratory process. The epithelium overlying the Peyer patches has a high concentration of M cells (although these cells
have also been identified throughout the non–Peyer patch areas of the small intestine).

Y enterocolitica and the related pathogen Y pseudotuberculosis produce at least 3 invasion proteins, Ail, YadA, and the
aforementioned invasin, which could potentially promote adherence to and invasion of M cells. Invasin, the principle invasion
factor of Y enterocolitica and Y pseudotuberculosis, binds to ß1 -chain integrin receptors with high affinity, promoting
internalization. These receptors are found at high levels on the luminal side of M cells but not on the luminal side of enterocytes.
[10]

Enterotoxicity

The enterotoxin produced by Y enterocolitica is similar to that produced by the heat-stable Escherichia coli; however, it likely
plays a minor role in causing disease, as diarrheal syndromes have been observed in the absence of enterotoxin production. In
addition, the toxin does not appear to be produced at temperatures higher than 30°C. The plasmid-mediated outer membrane
antigens are associated with bacterial resistance to opsonization and neutrophil phagocytosis.

Iron and pathogenicity

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One unique property of Y enterocolitica is its inability to chelate iron, which is an essential growth factor for most bacteria and is
obtained through the production of chelators known as siderophores. Y enterocolitica does not produce siderophores but can
utilize siderophores produced by other bacteria (eg, desferrioxamine E produced by Streptomyces pilosus).

Iron overload substantially increases the pathogenicity of Y enterocolitica, perhaps through attenuation of the bactericidal
activity of the serum. Researchers observe differences in the iron requirements of different serotypes of the organism; such
differences may explain, in part, the varying degrees of virulence among serotypes.

Complications

After an incubation period of 4-7 days, infection may result in mucosal ulceration (usually in the terminal ileum and rarely in the
ascending colon), necrotic lesions in Peyer patches, and mesenteric lymph node enlargement. See the image below.

Yersinia enterocolitis in a 45-year-old white woman who presented with chronic diarrhea.

In severe cases, bowel necrosis may occur, as a result of mesenteric vessel thrombosis.[11] Focal abscesses may occur. In
persons with human leukocyte antigen (HLA)–B27, reactive arthritis is not uncommon, possibly because of the molecular
similarity between HLA-B27 antigen and Yersinia antigens. The pathogenesis of Yersinia -associated erythema nodosum is
unknown.[12, 13]

Etiology
Human clinical Y enterocolitica infections ensue after ingestion of the microorganisms in contaminated food or water or by direct
inoculation through blood transfusion.

Y enterocolitica is potentially transmitted by contaminated unpasteurized milk and milk products, raw pork, tofu, meats, oysters,
and fish.[14, 15] Outbreaks have been associated with raw vegetables; the surface of vegetables can become contaminated
with pathogenic microorganisms through contact with soil, irrigation water, fertilizers, equipment, humans, and animals.

Pasteurized milk and dairy products can also cause outbreaks because Yersinia can proliferate at refrigerated temperatures.[16,
17]

Animal reservoirs of Y enterocolitica include swine (principle reservoir), dogs, cats, cows, sheep, goats, rodents, foxes,
porcupines, and birds.

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Reports of person-to-person spread are conflicting and are generally not observed in large outbreaks. Transmission via blood
products has occurred, however, and infection can be transmitted from mother to newborn infant. Fecal-oral transmission
among humans has not been proven.[18, 19] .

Epidemiology
Occurrence in the United States

Yersiniosis is rare in the absence of a breakdown in food-processing techniques. The Centers for Disease Control and
Prevention (CDC) estimates that 1 culture-confirmed Y enterocolitica infection per 100,000 persons is found annually.[20] The
bacterium has been isolated in 1.4-2.8% of stools of children with diarrhea.

For 2010, the CDC’s Foodborne Diseases Active Surveillance Network (FoodNet), using surveillance data from 10 US sites,
preliminarily identified a total of 19,089 laboratory-confirmed cases of infection caused by bacterial pathogens that are
commonly transmitted through food. The number of cases and incidence per 100,000 population were reported as follows[21] :

Salmonella (8256; 17.6)

Campylobacter (6365; 13.6)

Shigella (1780; 3.8)

Shiga toxin-producing E coli (STEC) non-O157 (451; 1.0)

STEC O157 (442; 0.9)

Vibrio (193; 0.4)

Yersinia (159; 0.3)

Listeria (125; 0.3)

In the United States, Yersinia enterocolitica accounts for approximately 5% of bacterial enteric infections among children
younger than 5 years, according to a 2012 study by Scallan et al. The investigators found this to be a greater incidence than that
for the enterohemorrhagic E coli strain O157 (3%), but a lower incidence than those for nontyphoidal Salmonella (42%),
Campylobacter (28%), and Shigella (21%).[22]

Scallan et al estimated that the 5 pathogens together cause more than 290,000 illnesses annually in children under 5 years.

Y enterocolitica infection is more common in cooler climates, and its prevalence peaks from November to January.[23]

International statistics

Y enterocolitica has been isolated in patients in many countries worldwide, but the infection appears to occur predominantly in
cooler climates, being much more common in northern Europe, Scandinavia, and Japan. Most isolates reported from Canada
and Europe are O:3 and O:9 serotypes.[24] The O:3 serotype is also common in Japan. Isolation of Y enterocolitica in
developing countries is uncommon.[25]

Race- and age-related demographics

Higher incidence of Y enterocolitica infection has been observed among black infants in the United States.[26]

Reports document symptomatic Y enterocolitica infection most commonly in younger age groups. A sample collection from
1988-1991 showed that 77.6% of infections occurred in children aged 12 months and younger, making Y enterocolitica the
second most common cause of bacterial gastrointestinal infection in children.[22, 27, 28]

Clinical manifestations of Y enterocolitica infection exhibit some age-dependent predilections, with reactive arthritis and
erythema nodosum being more common in older patients. Older patients with more debility are more likely to develop
bacteremia than are younger, healthier patients.

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Prognosis
Yersiniosis is usually either self-limited or is responsive to therapy; however, reinfection is possible. Most patients with Y
enterocolitica infection are symptomatic; however, asymptomatic carriage may occur. Death is uncommon, but patients with
significant comorbidities are at risk for Y enterocolitica bacteremia, which carries a case fatality rate of 34-50%.

A national, registry-based study of 52,121 patients in Denmark reported estimates for the risk of developing severe,
hospitalization-requiring complications and long-term sequelae up to 1 year after infection with 5 common bacterial
gastrointestinal pathogens. Of the 3922 cases of Y enterocolitica infection reported, 368 required hospitalization.[29]

A report from the CDC stated that in 2010 (preliminary data), of 159 Yersinia infections in the United States, 52 required
hospitalization and 1 resulted in death.[21]

Various manifestations of Y enterocolitica infection have been reported, including the following[30, 31, 32, 33, 34, 35, 36, 37, 38,
39, 40, 41, 42] :

Enterocolitis

Pseudoappendicitis

Mesenteric adenitis

Reactive arthritis - Can last 1-4 months

Erythema nodosum

Septicemia

Pharyngitis

Dermatitis

Myocarditis

Glomerulonephritis

Iron is an essential growth factor for the organism, and iron overload (eg, chronic hemolysis, hereditary hemochromatosis) is
associated with an increased risk of systemic disease. Deferoxamine therapy also increases susceptibility to Y enterocolitica
disease.

Presentation

History and Physical Examination

The usual presentation of Y enterocolitica infection includes diarrhea (the most common clinical manifestation of this infection),
low-grade fever, and abdominal pain lasting 1-3 weeks. Diarrhea may be bloody in severe cases. Vomiting is present in
approximately 15-40% of cases.

The existence of extraintestinal symptoms after a gastrointestinal illness may also indicate the possibility of yersiniosis.

Enterocolitis

Enterocolitis, the most common presentation of Y enterocolitica, occurs primarily in young children, with a mean age of 24
months. The incubation period is 4-6 days, typically with a range of 1-14 days.

Prodromal symptoms of listlessness, anorexia, and headache may be present. Such symptoms are followed by watery, mucoid
diarrhea (78-96%); fever (43-47%); colicky abdominal pain (22-84%); bloody stools (< 10%); and white blood cells (WBCs) in
the stool (25%). The diarrhea generally has a duration of 1 day to 3 weeks.

Most cases are self-limited. However, concomitant bacteremia may occur in 20-30% of infants younger than 3 months.

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Complications of enterocolitis include appendicitis,[41] diffuse ulceration and inflammation of the small intestine and colon,
peritonitis,[43, 44] meningitis, intussusception,[45] and cholangitis.

Mesenteric adenitis, mesenteric ileitis, and acute pseudoappendicitis

These manifestations are characterized by the following symptoms (although nausea, vomiting, diarrhea, and aphthous ulcers of
the mouth can also occur):

Fever

Abdominal pain

Tenderness of the right lower quadrant

Leukocytosis

Pseudoappendicitis syndrome is more common in older children and young adults.[46] Patients with Y enterocolitica infection
often undergo appendectomy; several Scandinavian studies suggested a prevalence rate of 3.8-5.6% for infection with Y
enterocolitica in patients with suspected appendicitis.

Analysis of several common-source outbreaks in the United States found that 10% of 444 patients with symptomatic,
undiagnosed Y enterocolitica infection underwent laparotomy for suspected appendicitis.

Reactive arthritis

This is associated with HLA-B27 (found in approximately 80% of affected patients). Most commonly reported in Scandinavia,
polyarticular arthritis can occur after Y enterocolitica infection. Joint symptoms, which occur in approximately 2% of patients,
typically arise 1-2 weeks after gastrointestinal illness.[13]

The large joints of the lower extremities are involved most commonly, and symptoms usually persist for 1-4 months, although
reports document prolonged syndromes.

Myocarditis and glomerulonephritis

These are other postinfection sequelae associated with the HLA-B27.[47]

Erythema nodosum

This manifests as painful, raised red or purple lesions, mainly on the patient’s legs and trunk. Lesions appear 2-20 days after the
onset of fever and abdominal pain and resolve spontaneously in most cases in about a month. The female-to-male ratio of
erythema nodosum is 2:1, and it is more common in adults than in children.

Septicemia

In this, a bacteremic spread to extraintestinal sites occurs, resulting in critical illness. Y enterocolitica septicemia is reported
most commonly in patients who have predisposing conditions, including alcoholism, diabetes mellitus, or an underlying immune
defect.

Patients with iron overload conditions and those who are undergoing treatment with deferoxamine are also at an increased risk
for septicemia, secondary to the effect of iron on the virulence of the bacteria.[14]

In addition, Y enterocolitica septicemia is usually reported in patients with a hematologic disease, such as thalassemia, sickle
cell disease, or hemochromatosis.[14, 48, 49, 50] Elderly patients and those who are malnourished are also at increased risk of
developing septicemia.

Metastatic infections following Y enterocolitica septicemia include focal abscesses in the liver, kidneys, spleen, and lungs.
Cutaneous manifestations include cellulitis, pyomyositis, pustules, and bullous lesions. Pneumonia, meningitis, panophthalmitis,
endocarditis, infected mycotic aneurysm, and osteomyelitis may also occur.[47]

DDx

Diagnostic Considerations
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Exercise caution in differentiating yersiniosis from inflammatory bowel disease, specifically Crohn disease. Performing stool
cultures and ruling out infectious etiologies prior to initiating immunomodulatory therapy for inflammatory bowel disease should
be a general practice.[4]

Other conditions to be considered in the differential diagnosis of Y enterocolitica infection, in addition to those in the next
section, include the following:

Ascariasis

Cryptosporidiosis

Cyclospora

Cytomegalovirus colitis

E coli infections

Food poisoning

Bacterial gastroenteritis

Viral gastroenteritis

Giardiasis

Intestinal flukes

Irritable bowel syndrome

Ischemic bowel disease

Isosporiasis

Lactose intolerance

Mesenteric lymphadenitis

Microsporidiosis

Shigellosis

Strongyloidiasis

Trichinosis

Typhoid fever

Ulcerative colitis

Vibrio infections

Differential Diagnoses
Amebiasis

Appendicitis

Campylobacter Infections

Clostridium Difficile Colitis

Crohn Disease

Diverticulitis

Inflammatory Bowel Disease

Pseudomembranous Colitis

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Pseudotuberculosis (Yersinia pseudotuberculosis Infection)

Salmonella Infection (Salmonellosis)

Workup

Workup

Approach Considerations
The following tests can be used in the diagnosis of Y enterocolitica infection (see the image below):

Stool culture - This is the best way to confirm a diagnosis of Y enterocolitica[2, 3] ; the culture result is usually positive
within 2 weeks of onset of disease

Tube agglutination

Enzyme-linked immunosorbent assays

Radioimmunoassays

Imaging studies - Ultrasonography or computed tomography (CT) scanning may be useful in delineating true appendicitis
from pseudoappendicitis

Colonoscopy - Findings may vary and are relatively nonspecific

Joint aspiration - Synovial fluid contains 500-60,000 WBCs/µL, with a predominance of polymorphonuclear cell; cultures
are sterile; testing synovial fluid for bacterial antigens may be of some use in difficult cases

Gram stain of Yersinia enterocolitica.

Stool Culture
Stool samples tested for leukocytes usually produce positive results, but Y enterocolitica is difficult to distinguish from other
invasive pathogens. Stool samples from infected patients should be handled carefully to avoid infecting others.

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When Y enterocolitica infection is suspected, instruct the microbiology laboratory to use cefsulodin-Irgasan-novobiocin (CIN)
agar, which is a differential selective medium with increased yield for Y enterocolitica. It requires 18-20 hours of incubation at
25°C to create unique colony morphology, representing 0.5- to 1-mm colonies with a red "bull's-eye" and a clear border. Use of
this media allows differentiation between Y enterocolitica and Y enterocolitica– like isolates.

When using conventional enteric media, MacConkey agar incubated at 25°C for 48 hours produces the best results.[51]

Recovery of organisms from otherwise sterile samples, such as blood, cerebrospinal fluid (CSF), and lymph node tissue, is
usually faster than recovery from stool samples. Isolation of Y enterocolitica from stool is hampered by slow growth and
overgrowth of normal flora.

Serodiagnosis
Serodiagnosis is possible with various methods, including tube agglutination, enzyme-linked immunosorbent assays, and
radioimmunoassays. However, carefully interpret the serotest results for Y enterocolitica infection if a positive stool culture result
is absent. Cross-reactions with other organisms can occur—including with Brucella, Morganella, and Salmonella —and a
background seroprevalence rate among different populations may confound the diagnosis by acting as a false-positive result.

Agglutinin titers typically increase 1-2 weeks after infection and peak at 1:200. However, elevated levels can be found for years
after infection, which also limits the usefulness of serodiagnosis.

DNA Microarray
Advanced experimental techniques for diagnosis of Y enterocolitica infection include polymerase chain reaction (PCR) assay,
immunohistochemical staining, and DNA microarray. Diagnostic DNA microarray for pathogenetic organisms is a comparatively
new technique that is used to identify multiple genes from different kinds of pathogens, allowing it to be used to detect different
species, biotypes, and/or toxins of pathogenic organisms in the same specimens. This is the major advantage over the
conventional PCR assay technique, which is used to identify only 1 gene from a hybridization. DNA microarray is also more
sensitive and accurate than the multiplex PCR.[52]

Colonoscopy
Typically, in patients with Y enterocolitica infection, the cecum contains aphthoid lesions and the terminal ileum has small, round
elevations and ulcers (as seen in the image below). An exudate may be present. The left side of the colon is typically unaffected,
but case reports have described left-sided colitis with serotype O:8.

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Yersinia enterocolitis in a 45-year-old white woman who presented with chronic diarrhea.

Histologic Findings
Histologic findings in Y enterocolitica infection are consistent with acute and chronic inflammation. Yersiniosis does not produce
unique histologic findings. Epithelial cell granulomas with suppuration of the centers of the granulomas (central microabscesses)
have been reported. These granulomas were composed of numerous histiocytes with or without epithelioid cell features, along
with scattered small T-lymphocytes and plasmacytoid monocytes.[53]

Treatment

Approach Considerations
Care in patients with Y enterocolitica infection is primarily supportive, with good nutrition and hydration being mainstays of
treatment.[4]

First-line drugs used against the bacterium include aminoglycosides and trimethoprim-sulfamethoxazole (TMP-SMZ). Other
effective drugs include third-generation cephalosporins, tetracyclines (not recommended in children < 8 y), and fluoroquinolones
(not approved for use in children < 18 y).

In the event of an acute outbreak of Y enterocolitica, attempt to isolate persons who have been in contact with the index patient.

Surgical therapy

Abscesses may require surgical drainage. Surgical exploration may be warranted if appendicitis cannot be safely ruled out.

Laparotomy findings in Y enterocolitica infection usually include mesenteric lymphadenitis and terminal ileitis, with a healthy
appendix.

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Consultations

The diagnosis and management of yersiniosis do not require specific consultations. However, consultation with an infectious
diseases specialist or gastroenterologist may be useful. Consultation with a rheumatologist may be helpful in cases of erythema
nodosum or reactive arthritis.

Antibiotic Therapy
The value of antibiotic therapy in uncomplicated acute diarrhea has not been established. Diarrhea should be managed with
fluid and electrolyte replacement. Avoid antimotility medications, which could lead to bacteremia.

In cases of severe enterocolitis, antibiotics have shown some benefit in terms of shortening the duration of illness. Patient
populations who should be considered for empiric antibiotic therapy include the following:

Elderly patients

Patients with diabetes

Patients with cirrhosis

Immunocompromised patients

Patients with cancer who are receiving chemotherapy

Healthcare and childcare workers who are at an increased risk of person-to-person spread

Antibiotic treatment should be used in patients with bacteremia with extraintestinal manifestations. They should be used in
cases of primary extraintestinal disorders, such as the following:

Cellulitis

Ophthalmitis

Endocarditis

Meningitis

Osteomyelitis

Pneumonia

Focal abscesses

Inpatient Care
Admit patients with Y enterocolitica infection who have evidence of severe dehydration, malnourishment, or septicemia.

Patients with conditions that place them at risk for Y enterocolitica septicemia, including the following, should be monitored
closely and admitted for supportive measures and antibiotic therapy at the first sign of disseminated disease:

Elderly patients

Patients who are immunocompromised

Patients who are chronically ill

Patients with iron overload

Patients with chronic hemolysis

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Patients with alcoholism

Patients with diabetes mellitus

Patients on deferoxamine therapy

Deterrence and Prevention

The following steps can be taken to prevent the spread of Y enterocolitica infection:

Instruct patients and at-risk individuals about appropriate hygiene methods and signs and symptoms of infection

Encourage public awareness of Y enterocolitica outbreaks and modes of transmission

Hand washing and control of environmental cross-contamination are principal measures in reducing the spread of enteric
pathogens in daycare centers, healthcare settings, and pet-care facilities, as well as within households

In blood banks, donors should be asked about any recent symptoms of gastroenteritis

Unwashed raw vegetables, uncooked meats (especially pork), and unpasteurized milk should be avoided[14, 15]

Reservoirs should be eliminated

The contamination of food products should be minimized

Enteric precautions should be instituted in the care of patients who have been hospitalized with infection

Medication

Medication Summary
Treatment of Y enterocolitica infection is usually supportive and directed at maintaining euvolemia. Antibiotics may be used in
some cases. Septicemia carries a high mortality rate and should therefore be treated with antibiotics. Uncomplicated cases Y
enterocolitica diarrhea usually resolve on their own without antibiotic treatment. However, in more severe or complicated
infections, antibiotics may be useful.

Y enterocolitica is usually susceptible in vitro to aminoglycosides, chloramphenicol, tetracycline, trimethoprim-sulfamethoxazole

(TMP-SMZ), piperacillin, ciprofloxacin, and third-generation cephalosporins. Isolates are often resistant to penicillin, ampicillin,
and first-generation cephalosporins, as the organism often produces beta-lactamase. Clinical failure with cefotaxime has been
reported.[54] Resistance to macrolides and fluoroquinolones is also sporadically reported.[55]

Clinically, Y enterocolitica infection responds well to aminoglycosides, TMP-SMZ, ciprofloxacin, and doxycycline.

Antimotility agents are contraindicated in the treatment of Y enterocolitica infection because of the increased risk of invasion.

Antibiotics, Other

Class Summary
The value of antibiotic therapy in uncomplicated acute colitis and mesenteric adenitis is not established. Antibiotic treatment
may be required in patients with septicemia, with focal extraintestinal manifestations, and in immunocompromised patients with
enterocolitis.

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Ciprofloxacin (Cipro)
The bactericidal agent ciprofloxacin is a second-generation quinolone. It acts by interfering with DNA gyrase, by inhibiting the
relaxation of supercoiled DNA, and by promoting the breakage of double-stranded DNA. Ciprofloxacin is highly active against
gram-negative and gram-positive organisms.

Trimethoprim and sulfamethoxazole (Bactrim, Bactrim DS, Septra DS)

Trimethoprim and sulfamethoxazole (Bactrim, Bactrim DS, Septra DS)

The combination antibiotic TMP-SMZ inhibits bacterial growth by inhibiting the synthesis of dihydrofolic acid. It is not helpful in
cases of uncomplicated gastroenteritis.

Ceftriaxone (Rocephin)
Ceftriaxone is a third-generation cephalosporin with gram-negative activity.

Gentamicin
Gentamicin is an aminoglycoside that is bactericidal for susceptible gram-negative organisms. This agent is not helpful for
uncomplicated gastroenteritis.

Cefotaxime (Claforan)
Cefotaxime is a third-generation cephalosporin with a gram-negative spectrum. It has lower efficacy against gram-positive
organisms. This agent is not helpful for uncomplicated gastroenteritis.

Tetracycline
Tetracycline treats gram-positive and gram-negative organisms, as well as mycoplasmal, chlamydial, and rickettsial infections. It
inhibits bacterial protein synthesis by binding with the 30S and possibly 50S ribosomal subunit(s).

Chloramphenicol
Chloramphenicol binds to 50S bacterial-ribosomal subunits and inhibits bacterial growth by inhibiting protein synthesis. It is
effective against gram-negative and gram-positive bacteria.

Piperacillin and tazobactam sodium (Zosyn)

This drug combination consists of an antipseudomonal penicillin plus a beta-lactamase inhibitor. It inhibits the biosynthesis of
cell wall mucopeptide and is effective during the active multiplication stage.

Carbapenems

Imipenem/cilastatin (Primaxin)
In vitro susceptibility to imipenem has been reported.

Contributor Information and Disclosures

Author
https://emedicine.medscape.com/article/232343-print 14/19
2/25/2019 https://emedicine.medscape.com/article/232343-print
Zartash Zafar Khan, MD, FACP Infectious Disease Consultant

Zartash Zafar Khan, MD, FACP is a member of the following medical societies: American College of Physicians, Infectious
Diseases Society of America, International Society for Infectious Diseases

Disclosure: Nothing to disclose.

Coauthor(s)

Michelle R Salvaggio, MD, FACP Assistant Professor, Department of Internal Medicine, Section of Infectious Diseases,
University of Oklahoma College of Medicine; Medical Director of Infectious Diseases Institute, Director, Clinical Trials Unit,
Director, Ryan White Programs, Department of Medicine, University of Oklahoma Health Sciences Center; Attending Physician,
Infectious Diseases Consultation Service, Infectious Diseases Institute, OU Medical Center

Michelle R Salvaggio, MD, FACP is a member of the following medical societies: American College of Physicians, Infectious
Diseases Society of America

Disclosure: Received honoraria from Merck for speaking and teaching.

Daniel R Bronfin, MD Clinical Professor of Pediatrics, Tulane University School of Medicine; Vice Chairman of Pediatrics,
Ochsner Children's Health Center

Daniel R Bronfin, MD is a member of the following medical societies: American Academy of Pediatrics, American Cleft Palate-
Craniofacial Association

Disclosure: Nothing to disclose.

Chief Editor

Mark R Wallace, MD, FACP, FIDSA Clinical Professor of Medicine, Florida State University College of Medicine; Clinical
Professor of Medicine, University of Central Florida College of Medicine

Mark R Wallace, MD, FACP, FIDSA is a member of the following medical societies: American College of Physicians, American
Medical Association, American Society for Microbiology, Infectious Diseases Society of America, International AIDS Society,
Florida Infectious Diseases Society

Disclosure: Nothing to disclose.

Acknowledgements

Daniel R Bronfin, MD Head, General Academic Pediatrics, Ochsner Children's Health Center

Daniel R Bronfin, MD is a member of the following medical societies: American Academy of Pediatrics and American Cleft
Palate/Craniofacial Association

Disclosure: Nothing to disclose.

Richard B Brown, MD, FACP Chief, Division of Infectious Diseases, Baystate Medical Center; Professor, Department of Internal
Medicine, Tufts University School of Medicine

Richard B Brown, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Chest
Physicians, American College of Physicians, American Medical Association, American Society for Microbiology, Infectious
Diseases Society of America, and Massachusetts Medical Society

Disclosure: Nothing to disclose.

Brooks D Cash, MD, FACP Director of Clinical Research, Assistant Professor of Medicine, Gastroenterology, National Naval
Medical Center

Disclosure: Nothing to disclose.

Joseph Domachowske, MD Professor of Pediatrics, Microbiology and Immunology, Department of Pediatrics, Division of
Infectious Diseases, State University of New York Upstate Medical University

Joseph Domachowske, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of
Pediatrics, American Society for Microbiology, Infectious Diseases Society of America, Pediatric Infectious Diseases Society,
and Phi Beta Kappa

https://emedicine.medscape.com/article/232343-print 15/19
2/25/2019 https://emedicine.medscape.com/article/232343-print
Disclosure: Nothing to disclose.

Thomas E Herchline, MD Professor of Medicine, Wright State University, Boonshoft School of Medicine; Medical Director, Public
Health, Dayton and Montgomery County, Ohio

Thomas E Herchline, MD is a member of the following medical societies: Alpha Omega Alpha, Infectious Diseases Society of
America, and Infectious Diseases Society of Ohio

Disclosure: Nothing to disclose.

Mark H Johnston, MD Associate Professor of Medicine, Uniformed Services University of the Health Sciences; Consulting Staff,
Lancaster Gastroenterology, Inc

Mark H Johnston, MD is a member of the following medical societies: American College of Gastroenterology, American College
of Physicians, American Gastroenterological Association, and Christian Medical & Dental Society

Disclosure: Nothing to disclose.

Leonard R Krilov, MD Chief of Pediatric Infectious Diseases and International Adoption, Vice Chair, Department of Pediatrics,
Professor of Pediatrics, Winthrop University Hospital

Leonard R Krilov, MD is a member of the following medical societies: American Academy of Pediatrics, American Pediatric
Society, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, and Society for Pediatric Research

Disclosure: Medimmune Grant/research funds Cliinical trials; Medimmune Honoraria Speaking and teaching; Medimmune
Consulting fee Consulting

Gregory J Martin, MD Director, Infectious Diseases Clinical Research Program (IDCRP) Associate Professor of Medicine,
Uniformed Services University, Bethesda, MD

Gregory J Martin, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians,
American Society of Tropical Medicine and Hygiene, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Swetha G Pinninti, MD Fellow in Pediatric Infectious Diseases, Department of Pediatrics, University of Alabama at Birmingham
School of Medicine

Swetha G Pinninti, MD is a member of the following medical societies: American Academy of Pediatrics, Infectious Diseases
Society of America, and Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Russell W Steele, MD Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor,
Department of Pediatrics, Tulane University School of Medicine

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of
Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America,
Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, and Southern Medical
Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy;
Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-
Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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