eMedicine Specialties > Infectious Diseases > Bacterial Infections

Pseudotuberculosis (Yersinia)

Asim A Jani, MD, MPH, FACP, Clinician-Educator and Epidemiologist, Consultant and Senior Physician, Florida Department of Health; Assistant Professor, University of Central Florida College of Medicine
Paul Chen, Public Health Intern, American Public Health Association

Updated: Sep 8, 2008

Introduction

Background

Yersinia pseudotuberculosis is the least common of the 3 main Yersinia species that cause infections in humans. Y pseudotuberculosis primarily causes zoonotic infection in various hosts, including domestic and sylvatic animals and birds, but has been associated with food-borne infection in humans. A few outbreaks of Y pseudotuberculosis infections in humans have been reported. In 2006, Y pseudotuberculosis was implicated in a large point-source outbreak of gastroenteritis attributed to the ingestion of raw grated carrots contaminated during the early phase of the production process. This was supported by epidemiologic, clinical, laboratory, and environmental data.¹

Y pseudotuberculosis infection in humans usually leads to a gastroenteritis (diarrheal component uncharacteristic) characterized by a self-limited mesenteric lymphadenitis that mimics appendicitis. Y pseudotuberculosis invades mammalian cells and survives intracellularly; the primary virulence factor is a plasmid-encoded protein that causes increased invasiveness. Postinfectious complications include erythema nodosum and reactive arthritis. Thus, a major triad for Y pseudotuberculosis infection includes fever, abdominal pain, and rash. In rare cases, it has been associated with septic complications (often in immunocompromised patients with chronic liver diseases).

The bacillus was first described in 1889 and was later renamed twice before the current name, Y pseudotuberculosis, was established in the 1960s. From the late 1920s to the mid 1960s, the organism was identified as Pasteurella pseudotuberculosis and then Shigella pseudotuberculosis. A Russian researcher named Znamenskiy demonstrated that Y pseudotuberculosis was, in fact, a causative agent for clinical illness through self-inoculation.

Because Y pseudotuberculosis infection has zoonotic forms, the animal reservoirs for such transmission include many mammalian and avian hosts, such as dogs, cats, horses, cattle, rabbits, deer, rodents, and birds (eg, geese, turkey, ducks, canaries, cockatoos). An example of occupational exposure to Y pseudotuberculosis related to animal reservoirs involves butchers working in abattoirs slaughtering swine.²

The genus Yersinia also contains the important species Yersinia enterocolitica and Yersinia pestis. Genomic characterization studies using hybridization techniques suggest that the selective loss of certain genes over time allowed interspecies and intraspecies diversity involving Y pseudotuberculosis and Y pestis, the organism that causes plague.

Pathophysiology

Y pseudotuberculosis infections in humans are primarily acquired through the gastrointestinal tract after consumption of contaminated food products. Characteristic of yersinial infections, an inoculum of 10⁹ organisms is often needed to induce infection. Although Y pseudotuberculosis infections generally do not cause diarrheal symptoms, they can cause a range of morbidities, including forms of mesenteric lymphadenitis, granulomatous disease, and dissemination with sepsis. Recent evidence has suggested that Y pseudotuberculosis may also disseminate from sites of bacterial replication within the intestinal tract and not necessarily from regional lymph nodes.³

Because Y pseudotuberculosis does not produce iron-binding compounds, patients with iron-overload states such as hemochromatosis, venous congestion, hemolytic anemia, and cirrhosis are at risk for sepsis.

In 1959, an epidemic that occurred on the Pacific coast of Russia was termed Far East scarlet-like fever (FESLF). Y pseudotuberculosis strains associated with FESLF were recently genetically sequenced, showing mobile gene pools that contain unique plasmids, the expression of which could result in scarlatinoid fever. Interestingly, virulence factors such as the Y pseudotuberculosis –derived mitogen (YPM)—a superantigen—are likely related to the atypical scarlet fever syndromes reported more recently, such as Izumi fever in Japan. YPM includes at least 3 superantigens—YPMa, YPMb, and YPMc—all of which have pathogenetic relevance and differ from other bacterial superantigens.

Although, as of 2007, no single infectious etiology has been shown to cause Kawasaki disease, the condition appears to be more prevalent among populations exposed to Y pseudotuberculosis infection. Kawasaki disease is found mostly in Japan (170,000 cases over 40 y); however, outbreaks of Kawasaki disease have been reported in Korea, the United States, Finland, and other non-Asian countries. Kawasaki disease and Y pseudotuberculosis infection have similar age, sexual, and temporal predilections (higher incidence in the winter months).⁴ Clinical comparisons of patients with Kawasaki disease with and without laboratory evidence of Y pseudotuberculosis infection has suggested that Y pseudotuberculosis infection may be associated with the development of coronary artery lesions and a poor treatment outcome in patients with Kawasaki disease.⁵

The incubation period of Y pseudotuberculosis infection varies from 5-10 days. Fecal excretion of the organism can occur several weeks after illness but often does not result in secondary person-to-person transmission or clinical relapses. A latent duration of 2-20 days has been reported in sporadic outbreaks, with peak incidence rates at 4 days after ingestion.

Frequency

United States

No specific pattern of Y pseudotuberculosis infection in the United States has been reported. Most Yersinia -related outbreaks in the United States and abroad have been associated with Y enterocolitica rather than Y pseudotuberculosis. In 1976, an outbreak of Y enterocolitica infection in children in Oneida, New York, was caused by contaminated chocolate milk. This was the first food-borne Yersinia -related outbreak reported in the United States, with both of the above Yersinia species being studied. Drinking from well water, mountain streams, and soil is associated with infection. Epidemics of Y pseudotuberculosis infection are uncommon, unlike the increased frequency of outbreaks associated with Y enterocolitica.

International

The distribution of Y pseudotuberculosis infection is worldwide. Most cases occur in winter, probably because of the increased seasonal incidence of infection among animals. The increased prevalence in winter may also be due to the enhanced growth characteristics in cold temperatures. Although many cases of Y pseudotuberculosis infection have been reported in Europe, large-scale outbreaks in the Aomori region of Japan were noted in the early 1990s. Fewer than 30 cases of associated septicemia have been reported in the literature.⁶

In November 1998, 4 laboratory-confirmed cases of Y pseudotuberculosis infection were reported to the British Columbia Centre for Disease Control Society (BCCDCS).⁷ Through a follow-up case-control study evaluating risk factors in a multivariate analysis, possibly contaminated homogenized milk was implicated in the outbreak. In 1991, children consuming untreated drinking water in Okayama, Japan, were exposed to Y pseudotuberculosis, leading to clinical disease.⁸ Isolation of Y pseudotuberculosis in well water has also been reported (in Czechoslovakia).

In the 1980s, outbreaks of Y pseudotuberculosis infection in Finland and Japan constituted most of the sporadic cases reported in the literature. In 1995, 8 cases of Y pseudotuberculosis infection in a Belgian hospital caused gastrointestinal symptoms .⁹ The organism was isolated with stool analysis and careful isolation techniques involving cold-enriched media.

Mortality/Morbidity

Most Y pseudotuberculosis infections are self-limited with a low case-fatality rate. However, the uncommon sepsis-associated illnesses caused by Y pseudotuberculosis infection in patients with chronic liver disease may carry a mortality rate that exceeds 75%.

Race

Y pseudotuberculosis infections appear to have no specific racial or ethnic predilection.

Sex

Y pseudotuberculosis infections are 3 times more common in men than in women. However, the postinfectious complications of erythema nodosum and arthritis are more common in women.

Age

More than 75% of patients with Y pseudotuberculosis infection are aged 5-15 years.

Clinical

History

Symptoms caused by Y pseudotuberculosis infection include abdominal pain (often right lower quadrant location) and fever. Diarrhea is uncommon. Patients who develop the recently described syndrome of Izumi fever may develop additional systemic symptoms. Late complications of yersinial infection may include reactive arthritis and rheumatologic manifestations.

• Other clinical problems associated with the enteric form of Y pseudotuberculosis infection have included terminal ileitis and intussusception, especially in children. In two thirds of clinical cases, enterocolitis may result and generally lasts 1-3 weeks.
• Izumi fever, a syndrome, has been characterized by scarlatiniform rash, systemic symptoms, and features shared with Kawasaki disease (eg, coronary artery aneurysms). Acute renal failure has been reported, although very rarely.
• Other manifestations of infection may include erythema nodosum, arthralgias, reactive arthritis, and ankylosing spondylitis. Y pseudotuberculosis infection has also been documented to cause lumbar facet joint disease.¹⁰
• Far East scarlatinoid fever was first described in the context of Y pseudotuberculosis infection. A scarlatinoid-appearing rash involving the head and neck, upper and lower extremity erythema, mucous membrane enanthem, and strawberry tongue characterize this syndrome.
• In 1998, a single case report described culture isolation of Y pseudotuberculosis from a prostatic focus in a 55-year-old man. Although no obvious environmental factors were implicated in the clinical syndrome, the patient was treated successfully with a sulfa-based regimen of oral antibiotics.¹¹
• In 2006, Hadou et al reported on an abdominal aortic aneurysm infected by Y pseudotuberculosis in an elderly patient with underlying coronary heart disease.¹²
• As mentioned above, Y pseudotuberculosis infection has been associated with ingestion of contaminated food items, including fresh produce (eg, raw carrots), and has been known to cause gastroenteritis and erythema nodosum. Gastrointestinal illness should prompt an inquiry of food history and other persons who may have also been infected in case of an outbreak to document a potential point-source etiology.
• Although Y pseudotuberculosis is not generally considered an opportunistic pathogen, two recent reports have described fever and altered mental status due to Y pseudotuberculosis infection in immunosuppressed patients infected with HIV. These patients had underlying Y pseudotuberculosis sepsis without the typical gastrointestinal manifestations. Perhaps because of their low CD4 cell counts (<200 cells/µL), the presumed activation of T lymphocytes (particularly CD4) by YPM superantigens may have been blunted in these patients.⁶

Physical

Physical findings caused by Y pseudotuberculosis infection may be grouped into 3 main categories—systemic, enteric, and rheumatologic. The predominant and often self-limited presentation of Y pseudotuberculosis infection is that of a febrile gastroenteritis with right lower quadrant abdominal pain.

• Systemic findings may include fever, skin rash, strawberry tongue, hypotension, and lymphadenopathy.
• Enteric findings include abdominal tenderness with or without rebound indicative of peritoneal involvement. Tenderness may be exquisite over McBurney point.
• Rheumatologic involvement may include joint effusion, tenderness, or decreased range of movement and may be asymmetric in distribution.
• Erythema nodosum lesions (often erythematous indurated tender areas on the anterior surface of the lower extremities) may be found.
• A sporotrichoid pattern (lymphocutaneous spread) of disease has been associated with Y pseudotuberculosis infection.¹³
• Ophthalmic findings such as uveitis and conjunctivitis have also been reported.

Causes

The syndromes associated with Yersinia infections are primarily caused by ingestion or contact with the pathogenic species of Yersinia. The less-common species— Y enterocolitica and Y pseudotuberculosis —have been associated with enteric syndromes. Y pseudotuberculosis has several serotypes (I-VI); the O group, types I and II, are mainly responsible for infection in humans, with type 1 likely responsible for 80% of human disease. Cross-reactivity between bacterial proteins and host antigens plays a role in the development of reactive disease. Iron overload appears to have a significant role in the genesis of the septic variants of the disease.

The following are the major virulence factors associated with Y pseudotuberculosis (specific mechanisms of pathogenicity have not been fully elucidated):

• Yersinia species have several plasmid virulence factors encoded. More specifically, Y pseudotuberculosis has a 70-kd plasmid that encodes for a contact-dependent type III secretion system that delivers virulence factors known as Yersinia outer proteins (Yops). This mode of delivery is crucial for the pathogenicity of Y pseudotuberculosis. The major Yops include the following:
  • YopE enters host mammalian cells through a type III secretion system. It is a RhoGTPase-activating protein (RhoGAP) that targets the RhoGTPase activity of GTP-binding proteins. In various host cells, this RhoGAP catalytic activity of YopE has been shown to play a role in the disruption of actin filament arrangement, promotion of cell rounding, prevention of host cell membrane pores that would result because of entry of type III translocation machinery, and inhibition of phagocytosis. Additionally, YopE (along with YopH and YopJ) plays a role in dampening proinflammatory signals of the host cell by decreasing the production of interleukin-8. In contrast to wild-type Y pseudotuberculosis, A YopE- mutant form of Y pseudotuberculosis given orally to mice lacked the ability to colonize the spleen.
  • YopJ disrupts host cell functioning by binding to the superfamily of protein kinases, thereby blocking key phosphorylation steps. Ultimately, this process decreases the production of cellular interleukin-8 and tumor necrosis factor. YopJ inhibits nuclear factor-kappa B (NF-kB) and mitogen-activated protein kinase (MAPK) signaling pathways and promotes apoptosis in macrophages. YopJ works alongside YopE and YopH in the critical process of depressing proinflammatory signals by the host cell. YopJ is translocated into the host cell through a type III secretion system.
  • YopT is a virulent factor that is not found in all pathogenic strains of Y pseudotuberculosis. YopT is also translocated to the host cell through a type III secretion system. Like YopE, YopT plays a role in disrupting actin filament arrangement (thus also contributing to cell rounding) and preventing phagocytic activity by the host cell. The catalytic activity of YopT has been shown to be that of a cysteine protease.
  • YopH is a virulence factor that shares many of the roles described for YopE. YopH takes part in disrupting actin filament arrangement, decreasing the production of interleukin-8, contributing to cell rounding, and preventing phagocytic activity by the host cell. The tyrosine phosphatase activity of YopH is thought to contribute to the antiphagocytic and actin filament disruption roles. Like many other virulent Yops, YopH is translocated to the host cell by the type III secretion system.
• YopB is a protein that makes up part of the type III secretion system that is required to translocate many virulence factors of Y pseudotuberculosis. YopB is thought to trigger a proinflammatory signal from the host cell when the type III secretion system docks onto the plasma membrane of the host cell.
• YopD is another protein that makes up part of the type III secretion system. It has been shown to be an important component because YopD- mutants cannot accomplish translocation. Additionally, YopD is integral in the formation of pores on the host plasma membrane during the infection process.
• Another virulence factor is the superantigen YPM, an exotoxin. Superantigens are generally bacterial or viral classes of proteins that mediate immune system activation. YPM selectively stimulates T lymphocytes that have V beta–containing gene segments and induce excessive amounts of inflammatory cytokines. These appear to correlate with increased systemic symptoms. This is analogous to the role of superantigens in other diseases, such as Kawasaki disease and even staphylococcal and streptococcal toxic shock syndromes.
• Another group that mediates Y pseudotuberculosis pathogenesis is collectively known as adhesion molecules.
  • These proteins bind onto the host cell and facilitate the internalization of Y pseudotuberculosis into the host. Two major proteins in this group are invasin and yadA. Y pseudotuberculosis strains that have the Inv gene (which encodes invasin) have enhanced invasion properties for epithelial host cells. Invasin of Y pseudotuberculosis binds to integrins on the M cells of Peyer patches. These integrins also bind to collagen and fibronectin.
  • Invasin is also involved in promoting the internalization of bacteria across these eukaryotic M cells. The yadA outer membrane protein binds to laminin, collagen, and fibronectin that are themselves bound to their respective beta-1 integrin receptors on the cell surface. These binding interactions contribute to the processes of bacterial adhesion onto the host cell surface and bacterial internalization into the host cell.
• Another molecular mechanism of pathogenesis is the high pathogenicity island (HPI) of Y pseudotuberculosis. It contains the gene that codes for yersiniabactin, the important siderophore used for iron uptake. HPI is common among the highly pathogenic species of Yersinia. Furthermore, transfer of HPI genes to a biotype 2 strain of Y enterocolitica, which ordinarily displays low pathogenicity, has been shown to increase its virulence level. The significant role that pathogenic islands play in the virulence of a wide variety of infectious bacteria continues to be recognized.
• Another important mechanism of virulence is the Yersinia twin arginine translocation (tat) pathway, which is incorporated into the metabolism of gram-negative bacteria, leading to secreted proteins that are functionally important for motility and acid resistance. In addition, cytotoxic necrotizing factors (CNFs) are associated with Escherichia coli (CNF1) and Y pseudotuberculosis (CNFy) and are approximately 60% genetically homologous. Despite having different cellular receptors, the CNFs can lead to endothelial cell invasion and contribute to pathogenesis.

Differential Diagnoses

Other Problems to Be Considered

The main concern for differential diagnoses relates to the predominant presentation of Y pseudotuberculosis disease—the gastroenteritis and mesenteric lymphadenitis syndromes. However, given the other unusual forms, including the Izumi fever syndrome suggestive of atypical scarlet fever or rheumatologic complications, such as erythema nodosum and/or reactive arthritides, the corresponding differential diagnoses for such presentations would likely vary significantly.

In such cases, refer to the differential diagnosis including, but not necessarily limited to, the following:

• Erythema nodosum
• Juvenile rheumatoid arthritis

Workup

Laboratory Studies

• The laboratory diagnosis of Y pseudotuberculosis infection is a matter of confirming the presence of the organism to support the clinical diagnosis of the associated syndromes.
  • Because this is a bacterial infection and so should not affect sterile fluids, the acquisition by culture from sources such as blood, cerebrospinal fluid (CSF), peritoneal fluid, synovial fluid, or other organ-based biopsy (eg, intestinal tissue, skin) is confirmatory.
  • Aside from diagnostic measures that include serological tests (discussed below), researchers have also developed various polymerase chain reaction (PCR) methods that are sensitive, efficient, and accurate tools for identifying and serotyping Y pseudotuberculosis.
  • Histologic examination of specific tissue, such as mesenteric lymph nodes, may provide both pathologic and microbiologic evidence of the organism.
• Microbiology: Y pseudotuberculosis belongs to the genus Yersinia, which has 2 other pathogenic species that infect humans— Y enterocolitica and Y pestis. Y pseudotuberculosis and Y pestis have a remarkable 97-100% homology. Y pseudotuberculosis is a gram-negative, non–lactose-fermenting coccobacillus that is chemically differentiated from other species (eg, Y enterocolitica) by its fermentation of sorbitol and ornithine decarboxylase activity, among other features. The optimum growth of yersinia occurs on MacConkey medium at 20-35°C. The organism is urease-positive.
  • Bacteriology: Y pseudotuberculosis is both aerobic and facultatively anaerobic; it is a gram-negative coccobacillus that grows slowly on blood and chocolate agar plates, forming small gray and translucent colonies at 24-72 hours. It has a good growth pattern on MacConkey or eosin-methylene blue (EMB) agar plates but is enhanced noticeably at lower temperatures (eg, 4°C cold enrichment in buffered saline) and is motile at temperatures lower than 28°C. Biochemically, it is oxidase-negative, urea-splitting, and catalase-producing, and it does not ferment lactose.
  • Stool: Isolation of organism from stool is difficult given the slow growth pattern and overgrowth of normal fecal flora. However, stool culture yield may be increased with cold enrichment, special culture media (eg, cefsulodin-Irgasan-novobiocin [CIN] agar), or alkali treatment, but these methods are generally not cost-effective.
  • Blood, peritoneal fluid, pharyngeal exudate, and synovial fluid may yield the organism.
• Serology
  • Enzyme-linked immunosorbent assay (ELISA) and agglutination tests may be obtained; the antibodies (against the O antigen) may appear soon after the onset of illness and typically wane over 2-6 months. Paired serum specimens taken 2 weeks apart that indicate a 4-fold rise in agglutinating antibodies support the diagnosis. Hemagglutination reaction tests that detect the pili (fimbriae) of either Y pseudotuberculosis or Y pestis have also been developed. Hemagglutination titers of 1:160 or higher are considered generally significant and indicative of true infection.
  • However, cross-reaction between antibodies against other organisms may obscure the diagnostic picture. These other organisms include other Yersinia, Vibrio, Salmonella, Brucella, and Rickettsia species.
  • Researchers have developed monoclonal antibodies that can identify serogroup-specific protein epitopes of Y pseudotuberculosis strains (grown at specific temperatures) from each of the 6 serogroups of the species. These monoclonal antibodies have been shown to not positively react with other Yersinia, Salmonella, Shigella, Escherichia, and Proteus species. This research has great potential to be developed into a potent serotyping tool for Y pseudotuberculosis.
  • A technique known as sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) has been shown to be a reliable serologic procedure for diagnosis of Y pseudotuberculosis or Y enterocolitica infection .

Imaging Studies

• In patients with mesenteric lymphadenitis, CT scans and, in some cases, ultrasonography of the abdomen and pelvis may reveal enlarged mesenteric lymph nodes and/or peritoneal findings, including appendiceal inflammation, peri-appendiceal fluid, and/or terminal ileitis.
• In patients with pneumonic or septic presentations, chest radiography may reveal infiltrates indicative of acute pneumonia.

Other Tests

In the unusual presentation of a Kawasaki disease–like variant—Izumi fever—ECG abnormalities may indicate ischemia if coronary artery circulation is compromised by aneurysms. These abnormalities are most likely to develop in children.

Procedures

Exploratory laparotomy is often needed in critically ill patients with prominent mesenteric lymphadenitis. Laparotomy serves both diagnostic and therapeutic purposes and enables actual intestinal and/or appendiceal tissue to be obtained and analyzed for histopathologic and microbiologic examinations.

Histologic Findings

Although the affected appendix may appear normal, involved lymph nodes (mesenteric) typically show epithelioid granulomatous changes, lymphoid hyperplasia, coagulative necrosis, and histiocytic cell hyperplasia. Enteric lesions may be associated with crypt hyperplasia, microabscesses, and villus shortening.

Staging

No staging is warranted in Y pseudotuberculosis infection. The most common forms of Y pseudotuberculosis infection include self-limited gastroenteritis or mesenteric lymphadenitis syndromes. Hosts with underlying diabetes, chronic liver disease (eg, chronic hepatitis), hemochromatosis, or immunosuppression may have sepsis accompanied by systemic disease. However, this is not common.

Treatment

Medical Care

Y pseudotuberculosis infection is often self-limited. However, more toxic presentations, including septic syndromes, severe dehydration, or other obscured diagnostic issues, may warrant hospitalization. General supportive care of such patients is needed.

Surgical Care

Exploratory laparotomy may be warranted in patients with complications such as severe abdominal pain, including acute abdominal presentations, peritoneal findings, or, uncommonly, intussusception. However, this intervention is not common.

Consultations

Consultation with an infectious diseases specialist may be helpful. Gastroenterologists or surgeons may be needed if invasive diagnostic or therapeutic interventions are warranted. For unusual presentations, such as rheumatologic, dermatologic, or ocular complications, the respective consultations may be helpful, primarily for assisting with considering Y pseudotuberculosis infection in the differential diagnoses.

Diet

No special diet is recommended; however, given the enteric nature of the symptoms and associated abdominal pain, diarrhea, fever, and anorexia that accompany such illness, it may be prudent to maintain the patient on a nothing–by-mouth (NPO) status through the diagnostic phase of the disease and to push fluids to prevent dehydration as needed, often intravenously. As the enteric syndromes resolve, the patient’s natural appetite will improve, and, accordingly, it is appropriate to ensure adequate caloric intake.

Activity

Bedrest through the acute illness is recommended. Activity as tolerated can be resumed once the enteric and systemic symptoms resolve.

Medication

In most cases, Y pseudotuberculosis infections do not require therapy with antimicrobials. However, in younger or immunosuppressed patients who are critically ill, beta-lactam antibiotic therapy may be prudent. Antibiotic therapy (initially intravenous) is warranted to treat the septic form of Y pseudotuberculosis infection. Guidance by in vitro testing may be helpful; initial empiric therapy should include an aminopenicillin (eg, ampicillin with or without a beta-lactamase inhibitor) and, ideally, an aminoglycoside.

Ampicillin may shorten the duration of culture positivity in patients infected with the Kawasaki-like variant of Y pseudotuberculosis infection; however, ampicillin probably will not alter the clinical situation. Combination therapy is not essential in most cases. The aminoglycoside streptomycin has been used to treat Yersinia infections, although gentamicin and tobramycin are considered appropriate. Third-generation cephalosporins have also been used. Chloramphenicol may be used in patients with allergies to penicillin or aminoglycoside.

Antimicrobials

Therapy must be comprehensive and cover all likely pathogens in the context of the clinical setting.

Ampicillin (Marcillin, Omnipen)

Broad-spectrum antibiotic that can be administered in IV form for septic presentations. Bactericidal activity against susceptible organisms. Alternative to amoxicillin when unable to take medication PO. Because of the resistance of Y enterocolitica to ampicillin and its greater prevalence, this agent would not be a good choice for empiric therapy in a clinical situation where either organism could be present.

Dosing

Adult

500 mg PO q6h
1-2 g IV q4h
Sepsis/meningitis: 150-250 mg/kg/d PO/IV divided q3-4h

Pediatric

<7 days:
<2000 g: 25 mg/kg IV/IM q12h; for meningitis, 50 mg/kg IV/IM q12h
>2000 g: 25 mg/kg IV/IM q8h; for meningitis, 50 mg/kg IV/IM q8h

>7 days:
<1200 g: 25 mg/kg IV/IM q12h; for meningitis, 50 mg/kg IV/IM q12h
1200-2000 g: 25 mg/kg IV/IM q8h; for meningitis, 50 mg/kg IV/IM q8h
>2000 g: 25 mg/kg IV/IM q6h; for meningitis, 50 mg/kg IV/IM q6h

Infants and children: 100-400 mg/kg/d IV/IM divided q4-6h; for meningitis, 200 mg/kg/d IV/IM divided q4-6h; not to exceed 12 g/d

Children: 50-100 mg/kg/d PO divided q6h; not to exceed 2-3 g/d

Interactions

Probenecid and disulfiram elevate ampicillin levels; allopurinol decreases ampicillin effects and has additive effects on ampicillin rash; may decrease effects of oral contraceptives

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Cross-allergenicity with beta-lactam drugs does exist but is unlikely
Patients with concurrent infectious mononucleosis have a higher likelihood of developing a skin rash while taking ampicillin; it is important to differentiate this rash from a true hypersensitivity reaction
Within the first 1-2 weeks of therapy, pediatric patients may have a <10% risk of developing a generalized, erythematous rash; the rash is characterized by a distribution involving knees and elbows—often intensely at pressure sites
Adjust dose in renal failure

Streptomycin sulfate

Especially recommended in combination therapy with broad-spectrum antibiotics (eg, ampicillin, piperacillin) for septic presentations and/or immunosuppressed hosts.
Recommended when less potentially hazardous therapeutic agents are ineffective or contraindicated.

Dosing

Adult

1 g IM qd; daily dosing likely more appropriate than intermittent dosing
2 times/wk dosing: 15 mg/kg/d IM; not to exceed 1 g/d
3 times/wk dosing: 25-30 mg/kg/d IM; not to exceed 1.5 g/d

Pediatric

Not established

Interactions

Nephrotoxicity may be increased with aminoglycosides, cephalosporins, penicillins, amphotericin B, and loop diuretics

Contraindications

Documented hypersensitivity; non–dialysis-dependent renal insufficiency

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Narrow therapeutic index; not intended for long-term therapy; caution in renal failure not on dialysis, myasthenia gravis, hypocalcemia, and conditions that depress neuromuscular transmission

Tobramycin (Nebcin)

Aminoglycoside antibiotic for gram-negative coverage. Used in combination with both an agent against gram-positive organisms and one that covers anaerobes.

Dosing

Adult

Life-threatening infections: 5 mg/kg/d IV q24h, reduce to 3 mg/kg/d as soon as clinically indicated; not to exceed 5 mg/kg/d; adjust dose based on CrCl and changes in volume of distribution

Pediatric

Not established

Interactions

Increases effects of neuromuscular blockers and potentiates effect of extended spectrum penicillins; concurrent administration with amphotericin B, cephalosporins, and loop diuretics increases risk of nephrotoxicity

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in renal impairment, preexisting auditory or vestibular impairment, and in patients with neuromuscular disorders; aminoglycosides are associated with nephrotoxicity and ototoxicity

Gentamicin (Garamycin)

Aminoglycoside antibiotic for gram-negative coverage. Used in combination with both an agent against gram-positive organisms and one that covers anaerobes.

Dosing

Adult

Serious infections and normal renal function: 3 mg/kg/d IV q8h
Loading dose: 1-2.5 mg/kg IV q8h
Maintenance dose: 1-1.5 mg/kg IV q8h

Pediatric

Not established

Interactions

Coadministration with other aminoglycosides, cephalosporins, penicillins, and amphotericin B may increase nephrotoxicity; enhances effects of neuromuscular blocking agents thus prolonged respiratory depression may occur; coadministration with loop diuretics may increase auditory toxicity; possible irreversible hearing loss of varying degrees may occur (monitor regularly)

Contraindications

Documented hypersensitivity; non–dialysis-dependent renal insufficiency

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Narrow therapeutic index (not intended for long-term therapy); caution in renal failure (not on dialysis), myasthenia gravis, hypocalcemia, and conditions that depress neuromuscular transmission; adjust dose in renal impairment

Chloramphenicol (Chloromycetin)

Binds to 50 S bacterial-ribosomal subunits and inhibits bacterial growth by inhibiting protein synthesis. Effective against gram-negative and gram-positive bacteria.

Dosing

Adult

500 mg PO/IV q6h for 10 d; not to exceed 4 g/d

Pediatric

Not established

Interactions

Concurrently with barbiturates, chloramphenicol serum levels may decrease while barbiturate levels may increase causing toxicity; manifestations of hypoglycemia may occur with sulfonylureas; rifampin may reduce serum levels, presumably through hepatic enzyme induction; may increase effects of anticoagulants; may increase serum hydantoin levels, possibly resulting in toxicity; chloramphenicol levels may be increased or decreased

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Use only for indicated infections, or as prophylaxis for bacterial infections; serious and fatal blood dyscrasias (aplastic anemia, hypoplastic anemia, thrombocytopenia, granulocytopenia) can occur; evaluate baseline and perform periodic blood studies approximately every 2 d while in therapy; discontinue upon appearance of reticulocytopenia, leukopenia, thrombocytopenia, anemia, or findings attributable to chloramphenicol; adjust dose in liver or kidney dysfunction; caution in pregnancy at term or during labor because of potential toxic effects on fetus (gray syndrome)

Piperacillin (Pipracil)

Inhibits biosynthesis of cell wall mucopeptides and stage of active multiplication. Has antipseudomonal activity.

Dosing

Adult

Serious infection: 4 g IV q8h; not to exceed 24 g/d

Pediatric

Not established

Interactions

At high concentrations, piperacillin may physically inactivate aminoglycosides; probenecid may increase levels; coadministration with aminoglycosides has synergistic effects

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in renal impairment or history of seizures

Cefotaxime (Claforan)

Third-generation cephalosporin with gram-negative spectrum. Lower efficacy against gram-positive organisms.
For septicemia caused by susceptible organisms. Arrests bacterial cell wall synthesis, which, in turn, inhibits bacterial growth.

Dosing

Adult

Moderate-to-severe infections: 2 g IV q6h
Life-threatening infections: 1-2 g IV/IM q4h

Pediatric

Not established

Interactions

Probenecid may increase levels; coadministration with furosemide and aminoglycosides may increase nephrotoxicity

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in severe renal impairment; associated with severe colitis

Follow-up

Further Inpatient Care

Supportive care for patients with Y pseudotuberculosis sepsis includes general hospital acute-level care (intensive medical/surgical care may be needed, although uncommon unless the patient is severely ill) and intravenous fluids, frequent monitoring, serial examinations, radiographic studies, intravenous antibiotics, and treatment of any complicating host- or disease-related factors.

Inpatient & Outpatient Medications

In outpatient settings or mild inpatient situations, vigilant observation without the use of antibiotics is reasonable. (See Complications, Prognosis.) Y pseudotuberculosis infection is often benign and self-limited.

Deterrence/Prevention

Food-borne epidemics of Y pseudotuberculosis infection can occur. Contact precautions, especially in the inpatient setting, apply to appropriate barriers (eg, gown, gloves) to exposure to enteric secretions, such as with diarrhea. Avoid ingestion of uncooked meat, contaminated water, or unpasteurized milk. Careful handwashing should follow consumption or handling of chitterlings (pork intestines).

Complications

Postinfectious sequelae may include arthritis and erythema nodosum. Additionally, severe Y pseudotuberculosis infection may be complicated by formation of coronary aneurysms, septic features associated with iron-overload states, and renal involvement with tubulointerstitial nephritis. Intussusception has also been reported in children.

Prognosis

Patient Education

Patients with Y pseudotuberculosis infection (and their families) should be familiar with forms of exposure, routes of infection, variable manifestations of the disease, difficulties in the diagnostic issues, and the potential for associated complications, including sepsis, reactive arthritis, erythema nodosum, and rare events such as cardiac or renal sequelae.

Miscellaneous

Medicolegal Pitfalls

• Y pseudotuberculosis infection is an unusual infection, meaning that its diagnosis may be missed or delayed because of its variable presentation. In addition, because this infection has a wide variety of differential diagnoses based on which features predominate in a given patient (intestinal vs extra-intestinal), documentation and communication with the patient, family, and colleagues should be realistic and comprehensive.
• Patients with sepsis and those with complicated mesenteric adenitis syndromes should be treated promptly, and consultation with infectious diseases specialist and gastroenterologist (adult or pediatric, as indicated) is recommended.
• Because of the uncertainties involved in predicting the extent of disease and/or potential postinfectious sequelae, practitioners may opt for empirical antimicrobial therapy in patients with uncomplicated presentations. However, no significant data have shown that antibiotic therapy directly reduces the likelihood of postinfectious sequelae.

References

1. Jalava K, Hakkinen M, Valkonen M, et al. An outbreak of gastrointestinal illness and erythema nodosum from grated carrots contaminated with Yersinia pseudotuberculosis. J Infect Dis. Nov 1 2006;194(9):1209-16. [Medline].

2. Merilahti-Palo R, Lahesmaa R, Granfors K, et al. Risk of Yersinia infection among butchers. Scand J Infect Dis. 1991;23(1):55-61. [Medline].

3. Barnes PD, Bergman MA, Mecsas J, et al. Yersinia pseudotuberculosis disseminates directly from a replicating bacterial pool in the intestine. J Exp Med. Jun 12 2006;203(6):1591-601. [Medline].

4. Vincent P, Salo E, Skurnik M, et al. Similarities of Kawasaki disease and Yersinia pseudotuberculosis infection epidemiology. Pediatr Infect Dis J. Jul 2007;26(7):629-31. [Medline].

5. Tahara M, Baba K, Waki K, et al. Analysis of Kawasaki disease showing elevated antibody titres of Yersinia pseudotuberculosis. Acta Paediatr. Dec 2006;95(12):1661-4. [Medline].

6. Paglia MG, D'Arezzo S, Festa A, et al. Yersinia pseudotuberculosis septicemia and HIV. Emerg Infect Dis. Jul 2005;11(7):1128-30. [Medline].

7. Nowgesic E, Fyfe M, Hockin J, et al. Outbreak of Yersinia pseudotuberculosis in British Columbia--November 1998. Can Commun Dis Rep. Jun 1 1999;25(11):97-100. [Medline].

8. Sato K, Komazawa M. Yersinia pseudotuberculosis infection in children due to untreated drinking water. Contrib Microbiol Immunol. 1991;12:5-10. [Medline].

9. Van Noyen R, Selderslaghs R, Bogaerts A, et al. Yersinia pseudotuberculosis in stool from patients in a regional Belgian hospital. Contrib Microbiol Immunol. 1995;13:19-24. [Medline].

10. Cormier G, Lucas V, Varin S, et al. Yersinia pseudotuberculosis infection of a lumbar facet joint. Joint Bone Spine. Jan 2007;74(1):110-1. [Medline].

11. Naiel B, Raul R. Chronic prostatitis due to Yersinia pseudotuberculosis. J Clin Microbiol. Mar 1998;36(3):856. [Medline].

12. Hadou T, Elfarra M, Alauzet C, et al. Abdominal aortic aneurysm infected by Yersinia pseudotuberculosis. J Clin Microbiol. Sep 2006;44(9):3457-8. [Medline].

13. Amjad M, Butt T, Hanif MM. Cutaneous infection with Yersinia pseudotuberculosis presenting with sporotrichoid spread. J Coll Physicians Surg Pak. Feb 2007;17(2):120-1. [Medline].

14. Abe J, Onimaru M, Matsumoto S, et al. Clinical role for a superantigen in Yersinia pseudotuberculosis infection. J Clin Invest. Apr 15 1997;99(8):1823-30. [Medline].

15. Abe J, Takeda T. Characterization of a superantigen produced by Yersinia pseudotuberculosis. Prep Biochem Biotechnol. May-Aug 1997;27(2-3):173-208. [Medline].

16. Amromin I, Chapnick EK, Morozov VG. Nonplague yersiniosis: report of four cases and review of the literature. Infect Dis Clin Pract. 2000;9:236-40.

17. Bearden SW, Fetherston JD, Perry RD. Genetic organization of the yersiniabactin biosynthetic region and construction of avirulent mutants in Yersinia pestis. Infect Immun. May 1997;65(5):1659-68. [Medline]. [Full Text].

18. Black DS, Bliska JB. Identification of p130Cas as a substrate of Yersinia YopH (Yop51), a bacterial protein tyrosine phosphatase that translocates into mammalian cells and targets focal adhesions. EMBO J. May 15 1997;16(10):2730-44. [Medline]. [Full Text].

19. Black DS, Bliska JB. The RhoGAP activity of the Yersinia pseudotuberculosis cytotoxin YopE is required for antiphagocytic function and virulence. Mol Microbiol. Aug 2000;37(3):515-27. [Medline]. [Full Text].

20. Bliska JB. Yop effectors of Yersinia spp. and actin rearrangements. Trends Microbiol. May 2000;8(5):205-8. [Medline].

21. Blumenthal B, Hoffmann C, Aktories K, et al. The cytotoxic necrotizing factors from Yersinia pseudotuberculosis and from Escherichia coli bind to different cellular receptors but take the same route to the cytosol. Infect Immun. Jul 2007;75(7):3344-53. [Medline].

22. Brubaker RR. The V antigen of yersiniae: an overview. Contrib Microbiol Immunol. 1991;12:127-33. [Medline].

23. Butler T. Yersinia species, including plague. In: Mandell GL, Bennett JE, Dolin R, eds. Mandell, Douglas and Bennett's Principles and Practice of Infectious Diseases. 4^th ed. NY: Churchill Livingstone; 1999:2406-2414.

24. Center for Food Safety & Applied Nutrition. Yersinia enterocolitica. In: Foodborne Pathogenic Microorganisms and Natural Toxins Handbook [Center for Food Safety & Applied Nutrician Web site]. 1991:Available at: http://vm.cfsan.fda.gov/~mow/chap5.html. [Full Text].

25. Chart H, Cheasty T. The serodiagnosis of human infections with Yersinia enterocolitica and Yersinia pseudotuberculosis. FEMS Immunol Med Microbiol. Aug 2006;47(3):391-7. [Medline].

26. Cornelis GR. Molecular and cell biology aspects of plague. Proc Natl Acad Sci U S A. Aug 1 2000;97(16):8778-83. [Medline].

27. Cornelis GR, Boland A, Boyd AP, et al. The virulence plasmid of Yersinia, an antihost genome. Microbiol Mol Biol Rev. Dec 1998;62(4):1315-52. [Medline]. [Full Text].

28. de Almeida AM, Guiyoule A, Guilvout I, Iteman I, Baranton G, Carniel E. Chromosomal irp2 gene in Yersinia: distribution, expression, deletion and impact on virulence. Microb Pathog. Jan 1993;14(1):9-21. [Medline]. [Full Text].

29. Donadini R, Fields BA. Yersinia pseudotuberculosis superantigens. Chem Immunol Allergy. 2007;93:77-91. [Medline].

30. Eppinger M, Rosovitz MJ, Fricke WF, et al. The complete genome sequence of Yersinia pseudotuberculosis IP31758, the causative agent of Far East scarlet-like fever. PLoS Genet. Aug 2007;3(8):e142. [Medline].

31. Feodorova VA, Samelija JG, Devdariani ZL. Heat-stable serogroup-specific proteins of Yersinia pseudotuberculosis. J Med Microbiol. May 2003;52(Pt 5):389-95. [Medline]. [Full Text].

32. Fällman M, Persson C, Wolf-Watz H. Yersinia proteins that target host cell signaling pathways. J Clin Invest. Mar 15 1997;99(6):1153-7. [Medline].

33. Gaston JS, Cox C, Granfors K. Clinical and experimental evidence for persistent Yersinia infection in reactive arthritis. Arthritis Rheum. Oct 1999;42(10):2239-42. [Medline].

34. Gomez HF, Cleary TG. Chapter 188. In: Yersinia pseudotuberculosis. Oski's Pediatrics: Principles and Practice; 1999.

35. Heesemann J, Gaede K. Mechanisms involved in the pathogenesis of Yersinia infections. Rheumatol Int. 1989;9(3-5):213-7. [Medline].

36. Heise T, Dersch P. Identification of a domain in Yersinia virulence factor YadA that is crucial for extracellular matrix-specific cell adhesion and uptake. Proc Natl Acad Sci U S A. Feb 28 2006;103(9):3375-80. [Medline]. [Full Text].

37. Hinnebusch BJ. Bubonic plague: a molecular genetic case history of the emergence of an infectious disease. J Mol Med. Sep 1997;75(9):645-52. [Medline].

38. Hubbert WT, Petenyi CW, Glasgow LA, et al. Yersinia pseudotuberculosis infection in the United States. Speticema, appendicitis, and mesenteric lymphadenitis. Am J Trop Med Hyg. Sep 1971;20(5):679-84. [Medline].

39. Iriarte M, Cornelis GR. YopT, a new Yersinia Yop effector protein, affects the cytoskeleton of host cells. Mol Microbiol. Aug 1998;29(3):915-29. [Medline]. [Full Text].

40. Juris SJ, Shao F, Dixon JE. Yersinia effectors target mammalian signalling pathways. Cell Microbiol. Apr 2002;4(4):201-11. [Medline]. [Full Text].

41. Kageyama T, Ogasawara A, Fukuhara R, et al. Yersinia pseudotuberculosis infection in breeding monkeys: detection and analysis of strain diversity by PCR. J Med Primatol. Jun 2002;31(3):129-35. [Medline]. [Full Text].

42. Kim W, Song MO, Song W, et al. Comparison of 16S rDNA analysis and rep-PCR genomic fingerprinting for molecular identification of Yersinia pseudotuberculosis. Antonie Van Leeuwenhoek. 2003;83(2):125-33. [Medline].

43. Koo JW, Cho CR, Cha SJ, et al. Intussusception associated with Yersinia pseudotuberculosis infection. Acta Paediatr. Oct 1996;85(10):1253-5. [Medline].

44. Lavander M, Ericsson SK, Broms JE, et al. Twin arginine translocation in Yersinia. Adv Exp Med Biol. 2007;603:258-67. [Medline].

45. Lesic B, Carniel E. Horizontal transfer of the high-pathogenicity island of Yersinia pseudotuberculosis. J Bacteriol. May 2005;187(10):3352-8. [Medline]. [Full Text].

46. Marra A, Isberg RR. Invasin-dependent and invasin-independent pathways for translocation of Yersinia pseudotuberculosis across the Peyer's patch intestinal epithelium. Infect Immun. Aug 1997;65(8):3412-21. [Medline]. [Full Text].

47. Mecsas JJ, Strauss EJ. Molecular mechanisms of bacterial virulence: type III secretion and pathogenicity islands. Emerg Infect Dis. Oct-Dec 1996;2(4):270-88. [Medline]. [Full Text].

48. Nagel G, Lahrz A, Dersch P. Environmental control of invasin expression in Yersinia pseudotuberculosis is mediated by regulation of RovA, a transcriptional activator of the SlyA/Hor family. Mol Microbiol. Sep 2001;41(6):1249-69. [Medline]. [Full Text].

49. Naktin J, Beavis KG. Yersinia enterocolitica and Yersinia pseudotuberculosis. Clin Lab Med. Sep 1999;19(3):523-36, vi. [Medline].

50. Neyt C, Cornelis GR. Insertion of a Yop translocation pore into the macrophage plasma membrane by Yersinia enterocolitica: requirement for translocators YopB and YopD, but not LcrG. Mol Microbiol. Sep 1999;33(5):971-81. [Medline]. [Full Text].

51. Orth K, Palmer LE, Bao ZQ, et al. Inhibition of the mitogen-activated protein kinase kinase superfamily by a Yersinia effector. Science. Sep 17 1999;285(5435):1920-3. [Medline].

52. Paff JR, Triplett DA, Saari TN, et al. Clinical and laboratory aspects of Yersinia pseudotuberculosis infections, with a report of two cases. Am J Clin Pathol. Jul 1976;66(1):101-10. [Medline].

53. Pelludat C, Hogardt M, Heesemann J. Transfer of the core region genes of the Yersinia enterocolitica WA-C serotype O:8 high-pathogenicity island to Y. enterocolitica MRS40, a strain with low levels of pathogenicity, confers a yersiniabactin biosynthesis phenotype and enhanced mouse virulence. Infect Immun. Apr 2002;70(4):1832-41. [Medline]. [Full Text].

54. Perry RD, Balbo PB, Jones HA, et al. Yersiniabactin from Yersinia pestis: biochemical characterization of the siderophore and its role in iron transport and regulation. Microbiology. May 1999;145 (Pt 5):1181-90. [Medline]. [Full Text].

55. Persson C, Nordfelth R, Andersson K, et al. Localization of the Yersinia PTPase to focal complexes is an important virulence mechanism. Mol Microbiol. Aug 1999;33(4):828-38. [Medline]. [Full Text].

56. Persson C, Nordfelth R, Holmstrom A, et al. Cell-surface-bound Yersinia translocate the protein tyrosine phosphatase YopH by a polarized mechanism into the target cell. Mol Microbiol. Oct 1995;18(1):135-50. [Medline].

57. Revell PA, Miller VL. A chromosomally encoded regulator is required for expression of the Yersinia enterocolitica inv gene and for virulence. Mol Microbiol. Feb 2000;35(3):677-85. [Medline]. [Full Text].

58. Rosqvist R, Bolin I, Wolf-Watz H. Inhibition of phagocytosis in Yersinia pseudotuberculosis: a virulence plasmid-encoded ability involving the Yop2b protein. Infect Immun. Aug 1988;56(8):2139-43. [Medline]. [Full Text].

59. Sanekata T, Yoshikawa N, Otsuki K, et al. Yersinia pseudotuberculosis isolation from cockatoo. J Vet Med Sci. Feb 1991;53(1):121-2. [Medline].

60. Shao F, Merritt PM, Bao Z, et al. A Yersinia effector and a Pseudomonas avirulence protein define a family of cysteine proteases functioning in bacterial pathogenesis. Cell. May 31 2002;109(5):575-88. [Medline].

61. Uchiyama T, Kato H. The pathogenesis of Kawasaki disease and superantigens. Jpn J Infect Dis. Aug 1999;52(4):141-5. [Medline].

62. Usui D, Ishii Y, Akaike H, et al. [Yersinia pseudotuberculosis type 4a infection meeting the diagnostic criteria for Kawasaki disease complicated by disseminated intravascular coagulation]. Kansenshogaku Zasshi. Nov 2005;79(11):895-9. [Medline].

63. Viboud GI, Bliska JB. A bacterial type III secretion system inhibits actin polymerization to prevent pore formation in host cell membranes. EMBO J. Oct 1 2001;20(19):5373-82. [Medline]. [Full Text].

64. Viboud GI, Bliska JB. Yersinia outer proteins: role in modulation of host cell signaling responses and pathogenesis. Annu Rev Microbiol. 2005;59:69-89. [Medline]. [Full Text].

65. Viboud GI, So SS, Ryndak MB, et al. Proinflammatory signalling stimulated by the type III translocation factor YopB is counteracted by multiple effectors in epithelial cells infected with Yersinia pseudotuberculosis. Mol Microbiol. Mar 2003;47(5):1305-15. [Medline]. [Full Text].

66. Wang X, Zhou D, Qin L, et al. Genomic comparison of Yersinia pestis and Yersinia pseudotuberculosis by combination of suppression subtractive hybridization and DNA microarray. Arch Microbiol. Aug 2006;186(2):151-9. [Medline].

Keywords

Yersinia pseudotuberculosis, Y pseudotuberculosis, Y pseudotuberculosis gastroenteritis, Far East scarlet-like fever, FESLF, scarlatinoid fever, scarlet fever, Izumi fever, YPM, YPMa, YPMb, YPMc, Kawasaki disease, Pasteurella pseudotuberculosis, P pseudotuberculosis, Shigella pseudotuberculosis, S pseudotuberculosis, Bacillus pseudotuberculosis, B pseudotuberculosis, Yersinia infections, Yersinia mesenteric adenitis

Contributor Information and Disclosures

Author

Asim A Jani, MD, MPH, FACP, Clinician-Educator and Epidemiologist, Consultant and Senior Physician, Florida Department of Health; Assistant Professor, University of Central Florida College of Medicine
Asim A Jani, MD, MPH, FACP is a member of the following medical societies: American College of Physicians, American Medical Association, American Public Health Association, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Coauthor(s)

Paul Chen, Public Health Intern, American Public Health Association
Disclosure: Nothing to disclose.

Medical Editor

Douglas A Drevets, MD, Assistant Professor, Department of Medicine, Section of Infectious Disease, Oklahoma University Health Sciences Center
Douglas A Drevets, MD is a member of the following medical societies: American Association of Immunologists, American Society for Microbiology, Central Society for Clinical Research, and Christian Medical & Dental Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Joseph F John Jr, MD, FACP, FIDSA, FSHEA, Clinical Professor of Medicine, Molecular Genetics and Microbiology, Medical University of South Carolina; Associate Chief of Staff for Education, Ralph H Johnson Veterans Affairs Medical Center
Disclosure: BioMerieux Honoraria Review panel membership; Cubist Honoraria Review panel membership; Pfizer Honoraria Speaking and teaching; Merck Stock dividends stock holdings

CME Editor

Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Chief Editor

Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

The reader may find the following texts useful:

The Genus Yersinia:  From Genomics to Function
Series: Advances in Experimental Medicine and Biology, Vol. 603
Perry, Robert D.; Fetherston, Jacqueline D. (Eds.)
2007, XXIV, 432 p. 242 illus., 2 in color., Hardcover
ISBN: 978-0-387-72123-1

Yersinia enterocolitica and Yersinia pseudotuberculosis Infections (Enteritis and Other Illnesses) In: Pickering LK, Baker CJ, Long SS, McMillan JA, eds. Red Book: 2006 Report of the Committee on Infectious Diseases. 27th ed. Elk Grove Village, IL: American Academy of Pediatrics; 2006:[732-4]

© 1994- by Medscape.
All Rights Reserved
(http://www.medscape.com/public/copyright)