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Campylobacter Infections
Updated: Aug 24, 2018
Author: Mahmud H Javid, MBBS; Chief Editor: Michael Stuart Bronze, MD

Overview

Background
Campylobacter infections are among the most common bacterial infections in humans. They produce both diarrheal and
systemic illnesses. In industrialized regions, enteric Campylobacter infections produce an inflammatory, sometimes bloody,
diarrhea or dysentery syndrome.

Campylobacter jejuni (see image below) is usually the most common cause of community-acquired inflammatory enteritis. In
developing regions, the diarrhea may be watery.

Scanning electron microscope image of Campylobacter jejuni, illustrating its corkscrew appearance and bipolar flagella.
Source: Virginia-Maryland Regional College of Veterinary Medicine, Blacksburg, Virginia.

Infections with Campylobacter -like organisms can produce an enterocolitis/proctocolitis syndrome in homosexual males, who
are at increased risk for Helicobacter cinaedi and Helicobacter fennelliae infections. C jejuni infections may also produce serious
bacteremic conditions in individuals with AIDS. Most reported bacteremias have been due to Campylobacter fetus fetus
infection. Campylobacter lari, which is found in healthy seagulls, has also been reported to produce mild recurrent diarrhea in
children. Campylobacter upsaliensis may cause diarrhea or bacteremia, while Campylobacter hyointestinalis, which has
biochemical characteristics similar to those of C fetus, causes occasional bacteremia in immunocompromised individuals.

Campylobacter organisms may also be an important cause of traveler's diarrhea, especially in Thailand and surrounding areas
of Southeast Asia. In a study of American military personnel deployed in Thailand, more than half of those with diarrhea were
found to be infected with Campylobacter species.

These organisms are related to Helicobacter pylori, which was previously known as Campylobacter pylori. No reservoir other
than the human gastric mucosa has been identified for H pylori.

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Pathophysiology
The known routes of Campylobacter transmission include fecal-oral, person-to-person sexual contact, unpasteurized raw milk
and poultry ingestion, and waterborne (ie, through contaminated water supplies). Exposure to sick pets, especially puppies, has
also been associated with Campylobacter outbreaks.

Transmission of Campylobacter organisms to humans usually occurs via infected animals and their food products. Most human
infections result from the consumption of improperly cooked or contaminated foodstuffs. Chickens may account for 50-70% of
human Campylobacter infections. Most colonized animals develop a lifelong carrier state.

The infectious dose is 1000-10,000 bacteria. Campylobacter infection has occurred after ingestion of 500 organisms by a
volunteer; however, a dose of less than 10,000 organisms is not a common cause of illness. Campylobacter species are
sensitive to hydrochloric acid in the stomach, and antacid treatment can reduce the amount of inoculum needed to cause
disease.

Symptoms of Campylobacter infection begin after an incubation period of up to a week. The sites of tissue injury include the
jejunum, the ileum, and can extend to involve the colon and rectum. C jejuni appears to invade and destroy epithelial cells. C
jejuni are attracted to mucus and fucose in bile, and the flagella may be important in both chemotaxis and adherence to
epithelial cells or mucus. Adherence may also involve lipopolysaccharides or other outer membrane components. Such
adherence would promote gut colonization. PEB 1 is a superficial antigen that appears to be a major adhesin and is conserved
among C jejuni strains.

Some strains of C jejuni produce a heat-labile, choleralike enterotoxin, which is important in the watery diarrhea observed in
infections. Infection with the organism produces diffuse, bloody, edematous, and exudative enteritis. The inflammatory infiltrate
consists of neutrophils, mononuclear cells, and eosinophils. Crypt abscesses develop in the epithelial glands, and ulceration of
the mucosal epithelium occurs.

Cytotoxin production has been reported in Campylobacter strains from patients with bloody diarrhea. In a small number of
cases, the infection is associated with hemolytic-uremic syndrome and thrombotic thrombocytopenic purpura through a poorly
understood mechanism. Endothelial cell injury, mediated by endotoxins or immune complexes, is followed by intravascular
coagulation and thrombotic microangiopathy in the glomerulus and the gastrointestinal mucosa.

Campylobacter species also produce the bacterial toxin cytolethal distending toxin (CDT), which produces a cell block at the G2
stage preceding mitosis. CDT inhibits cellular and humoral immunity via destruction of immune response cells and necrosis of
epithelial-type cells and fibroblasts involved in the repair of lesions. This leads to slow healing and results in disease symptoms.
[1]

In patients with HIV infection, Campylobacter infections may be more common, may cause prolonged or recurrent diarrhea, and
may be more commonly associated with bacteremia and antibiotic resistance.

C fetus is covered with a surface S-layer protein that functions like a capsule and disrupts c3b binding to the organisms,
resulting in both serum and phagocytosis resistance.

C jejuni infections also show recurrence in children and adults with immunoglobulin deficiencies. Acute C jejuni infection confers
short-term immunity. Patients develop specific immunoglobulin G (IgG), immunoglobulin M (IgM), and immunoglobulin A (IgA)
antibodies in serum; IgA antibodies also develop in intestinal secretions. The severity and persistence of C jejuni infections in
individuals with AIDS and hypogammaglobulinemia indicates that both cell-mediated and humoral immunity are important in
preventing and terminating infection.

The oral cavity contains numerous Campylobacter species, such as Campylobacter concisus, that have been associated with a
subtype of inflammatory bowel disease.[2, 3]

Epidemiology
Frequency

United States

An estimated 2 million cases of Campylobacter enteritis occur annually, accounting for 5-7% of cases of gastroenteritis.
Campylobacter organisms have a large animal reservoir, with up to 100% of poultry, including chickens, turkeys, and waterfowl
having asymptomatic intestinal infections. The major reservoirs of C fetus are cattle and sheep. Nonetheless, the incidence of

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Campylobacter infections has been declining. Changes in the incidence of culture-confirmed Campylobacter infections have
been monitored by the Foodborne Diseases Active Surveillance Network (FoodNet) since 1996. In 2010, Campylobacter
incidence showed a 27% decrease compared with 1996-1998. In 2010, the incidence was 13.6 cases per 100,000 population,
and this did not change significantly compared with 2006-2008.[4]

International

C jejuni infections are extremely common worldwide, although exact figures are not available, particularly in low- and middle-
income countries. In high-income countries, the incidence has been estimated to be 4.4-9.3 per 1000 population.[5] New
Zealand reported the highest national campylobacteriosis rate, which peaked in May 2006 at 400 per 100,000 population.[6]

Mortality/Morbidity

Campylobacter infections are usually self-limited and rarely cause mortality. Exact figures are unavailable, but occasional deaths
have been attributed to Campylobacter infections, typically in elderly or immunocompromised persons and secondary to volume
depletion in young, previously healthy individuals.

Race

Campylobacter infections have no clear racial predilection.

Sex

Campylobacter organisms are isolated more frequently from males than females. Homosexual men appear to be at increased
risk for infection with atypical Campylobacter species such as Helicobacter cinaedi and Helicobacter fennelliae.

Age

Campylobacter infections can occur in all age groups.

Studies show a peak incidence in children younger than 1 year and in persons aged 15-29 years. The age-specific attack rate is
highest in young children. In the United States, the highest incidence of Campylobacter infection in 2010 was in children
younger than 5 years and was 24.4 cases per 100,000 population,[4] However, the rate of fecal cultures positive for
Campylobacter species is greatest in adults and older children.

Asymptomatic Campylobacter infection is uncommon in adults.

In developing countries, Campylobacter infection is very common in the first 5 years of life. Asymptomatic infection is also more
common. In Bangladesh, up to 39% of all children younger than 2 years have asymptomatic infection.

For additional information on pediatric Campylobacter infections, see Campylobacter Infections.

Presentation

History
Campylobacter infections can range from asymptomatic to severe life-threatening colitis with toxic megacolon.

All Campylobacter species associated with enteric illnesses cause identical clinical manifestations.

Gastroenteritis

The symptoms and severity of the gastroenteritis produced can vary.

Patients may have a history of ingestion of inadequately cooked poultry, unpasteurized milk, or untreated water. The incubation
period is 1-7 days and is probably related to the dose of organisms ingested.

A brief prodrome of fever, headache, and myalgias lasting up to 24 hours is followed by crampy abdominal pain, fever as high
as 40°C, and as many as 10 watery, frequently bloody, bowel movements per day. Fever, which develops in more than 90% of
patients, may be low or high grade and can persist for a week.

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Patients with C jejuni infection who report vomiting, bloody diarrhea, or both tend to have a longer illness and require hospital
admission.[7]

Abdominal pain and tenderness may be localized. Pain in the right lower quadrant may mimic acute appendicitis
(pseudoappendicitis).

Tenesmus occurs in approximately 25% of patients.

In some cases, acute abdominal pain is the only symptom, with pain typically in the right lower quadrant. Among the symptoms,
abdominal pain is more likely to result from Campylobacter infection than from Salmonella or Shigella infections.

Differences based on Campylobacter species

In contrast to C jejuni infection, C fetus infection causes diarrheal illness less frequently and is the most commonly identified
species in bacteremia. However, C fetus infection that produces diarrheal illness results in clinical manifestations that are similar
to those of C jejuni infection. C fetus is an opportunistic agent in debilitated hosts, but healthy hosts may also be affected.

Campylobacter bacteremia is common, and C fetus fetus is frequently isolated from the bloodstream, possibly because it resists
the bactericidal activity of serum, while the more common C jejuni does not. Persons who develop Campylobacter bacteremia
are usually older and are more likely to have cellulitis, endovascular infection, or a device-related infection.[8]

Systemic illness with a predilection for vascular sites is characteristic. Meningitis, vascular infections, and abscesses may be
present.

C fetus infection may cause intermittent diarrhea or nonspecific abdominal pain.

Physical
Patients with Campylobacter infection may appear to be ill.

The patient’s abdomen is diffusely tender, frequently in the right or left lower quadrant.

Among symptoms, only abdominal pain is more likely to result from Campylobacter infections than from Salmonella and Shigella
infections.

Causes
Campylobacter organisms are curved or spiral, motile, non–spore-forming, gram-negative rods. Organisms from young cultures
have a vibriolike appearance, but, after 48 hours of incubation, organisms appear coccoid. Campylobacter organisms are motile
by means of unipolar or bipolar flagellae. They are both oxidase- and catalase-positive and microaerophilic, requiring reduced
oxygen (5-10%) and increased carbon dioxide (3-10%). The organisms grow slowly, with 3-4 days required for primary isolation
from stool samples, and even longer from blood.

DDx

Differential Diagnoses
Clostridium Difficile Colitis

Inflammatory Bowel Disease

Salmonella Infection (Salmonellosis)

Shigellosis
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Vascular Surgery for Arteriovenous Malformations

Yersinia Enterocolitica

Workup

Workup

Laboratory Studies
Clinical diagnosis of enteric Campylobacter infection is established by demonstrating the organism via direct examination of
feces or by isolation of the organisms.

Campylobacter organisms multiply more slowly than other enteric bacteria; thus, unusual techniques are used for isolation from
fecal specimens.

These include growth at 42°C, use of antibiotic-containing media, and micropore filtration to keep larger bacilli from
contaminating the culture.

Specific types of selective media are blood-based, antibiotic-containing media such as Skirrow, Butzler, and Campy-BAP.

Micropore filtration is based on filters with pores small enough to prevent the passage of microbes but large enough to allow
passage of organism-free fluid. Filters with a pore diameter of 25 nm to 0.45 µm are usually used in this procedure, which can
also be used to remove microorganisms from water and air for microbiological testing.

Multiple media types can be used to cultivate C jejuni, although Mueller-Hinton broth and agar best support C jejuni growth. The
optimum atmosphere for C jejuni growth is 85% N2, 10% CO2, and 5% O2.[9]

Campylobacter organisms are oxidase positive with C jejuni hydrolysing hippurate.[10]

Results of stool cultures usually do not remain positive beyond 2 weeks.

Darkfield or phase-contrast microscopy of fecal specimens can also be used to assess for characteristic darting motility within 2
hours of passage.

A Gram stain of stool samples for characteristic curved rods is specific, with a sensitivity of 50-75%.

Fecal leukocytes and erythrocytes are present in 75% of patients with Campylobacter enteritis and can be detected with direct
light microscopic examination using methylene blue or Gram stain.

Peripheral blood leukocytosis may be present.

Dehydration may be clinically evident in patients who are moderately to severely ill.

If infection with C fetus or another atypical species is suspected, incubation at 37°C and use of media without cephalosporins
are required.

Serodiagnosis of C jejuni infections can be improved by using highly specific recombinant antigens in an enzyme-linked
immunoassay (ELISA) technique.[11]

Real-time polymerase chain reaction (PCR) can be used to quickly and accurately detect C jejuni directly in diarrheal stool.[12]

The newer methods such as molecular biology techniques (PCR) and immunoenzymatic methods[13] are more sensitive than
traditional culture methods.[14]

Culture-independent tests, such as rapid tests for detection of antigens in stool specimens, are available.[15, 16, 17] However,
their use as standalone tests has been questioned.[18]

Procedures
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Up to 80% of patients with Campylobacter infection demonstrate evidence of proctocolitis on sigmoidoscopy. However, findings
may be identical to those observed in pseudomembranous colitis or inflammatory bowel disease. Sigmoidoscopic abnormalities
range from focal mucosal edema and hyperemia with patchy petechiae to diffuse or aphthoid ulceration.

Treatment

Medical Care
Replacement of fluids and electrolytes is the mainstay of therapy in patients with Campylobacter infections. Promote rehydration
with oral glucose-electrolyte solutions. Failure to achieve hydration with oral intake may require intravenous fluids.

The use of antibiotics to treat Campylobacter infections is controversial, with studies showing that erythromycin rapidly
eliminated Campylobacter organisms from the stool without affecting the duration of illness. Studies in children with C jejuni
dysentery have shown benefit from early treatment with erythromycin. Antibiotics may be indicated if any of the following occur:

High fever

Bloody diarrhea

Excessive bowel movements (ie, >8 stools per day)

Worsening symptoms

Failure of symptoms to improve

Persistence of symptoms for longer than 1 week

Pregnancy

HIV infection and other immunocompromised states

Avoid antimotility agents because they prolong the duration of symptoms and have been associated with fatalities.

Individuals with hypogammaglobulinemia who have recurrent C jejuni bacteremia may require fresh frozen plasma with
antibiotics.

Patients with severe dysentery or a relapsing course may require hospitalization.

Patients with endovascular C fetus infections require at least 4 weeks of treatment; gentamicin is believed to be the
agent of choice. Treatment with ampicillin or third-generation cephalosporins is an alternative.

Treat C fetus CNS infections for 2-3 weeks with third-generation cephalosporins, ampicillin, or chloramphenicol.

Surgical Care
Suspected toxic megacolon or aneurysms should be evaluated surgically.

Consultations
Toxic megacolon or infected aneurysms:[19] Consult a surgeon.

Endovascular C fetus infections: Consult an infectious disease specialist.

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Activity
Patients with Campylobacter infection may engage in activities as tolerated.

Medication

Medication Summary
Azithromycin therapy would be a primary antibiotic choice for Campylobacter infections, when indicated (see Medical Care),[20]
with a typical regimen of 500 mg/d for 3 days. However, erythromycin is the classic antibiotic of choice. Its resistance remains
low,[21] and it can be used in pregnant women and children.

Ciprofloxacin and tetracycline are alternatives but should be avoided in young children. In addition, the use of fluoroquinolones
in food animals has resulted in fluoroquinolone-resistant Campylobacter strains worldwide.[22, 23] Quinolone resistance of C
jejuni and Campylobacter coli is conferred by the mutation gyrA C-257-T, which can be identified with methods such as multiplex
PCR.[24] A 2008 study from the United Kingdom found fluoroquinolone-resistant Campylobacter species in 22% of poultry and
75% of pig farms.[25] High levels of ciprofloxacin resistance have also been reported in developing countries, with resistance
ranging from 30% to greater than 70%.[26, 27]

Clindamycin is another therapeutic alternative.

Specific antibiotic doses to treat Campylobacter infections have not been fully defined for tetracycline and clindamycin;
therefore, the doses below are empirical.

Antibiotic treatment does not prolong carriage of C jejuni.[28]

CNS infections can be treated with meropenem,[29, 30] ampicillin,[31] or chloramphenicol.[32]

Antibiotics

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

Azithromycin (Zithromax)
Acts by binding to 50S ribosomal subunit of susceptible microorganisms and blocks dissociation of peptidyl tRNA from
ribosomes, causing RNA-dependent protein synthesis to arrest. Nucleic acid synthesis is not affected.

Concentrates in phagocytes and fibroblasts as demonstrated by in vitro incubation techniques. In vivo studies suggest that
concentration in phagocytes may contribute to drug distribution to inflamed tissues.

Treats mild-to-moderate microbial infections.

Plasma concentrations are very low, but tissue concentrations are much higher, giving it value in treating intracellular organisms.
Has a long tissue half-life.

Effective against a wide range of organisms, including the most common gram-positive and gram-negative organisms. Has
additional coverage of so-called atypical infections such as Chlamydia, Mycoplasma, and Legionella species.

Indicated for treatment of patients with mild-to-moderate infections, including acute bronchitic infections that may be observed
with bronchiectasis.
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Erythromycin (E-Mycin, Ery-Tab, E.E.S.)

DOC for Campylobacter infections. Macrolide antibiotic that inhibits bacterial growth by blocking dissociation of peptidyl t-RNA
from ribosomes, causing RNA-dependent protein synthesis to arrest. For C jejuni (not C fetus) infections.

Ciprofloxacin (Cipro)
Synthetic, broad-spectrum antibacterial compounds. Novel mechanism of action, targeting bacterial topoisomerases II and IV,
leads to a sudden cessation of DNA replication. Oral bioavailability is nearly 100%. For C jejuni (not C fetus) infections.

Clindamycin (Cleocin)
Lincosamide for treatment of serious skin and soft tissue staphylococcal infections. Also effective against aerobic and anaerobic
streptococci (except enterococci). Inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes,
causing RNA-dependent protein synthesis to arrest.

Doxycycline (Bio-Tab, Doryx, Vibramycin, Doxy, Vibra-Tabs)

Inhibits protein synthesis and thus bacterial growth by binding to 30S and possibly 50S ribosomal subunits of susceptible
bacteria. For C jejuni (not C fetus) infections.

Levofloxacin (Levaquin)
For pseudomonal infections and infections due to multidrug resistant gram-negative organisms. For C jejuni (not for C fetus)
infections.

Gentamicin (Garamycin, Gentacidin)

Aminoglycoside antibiotic for gram-negative coverage. Used in combination with both an agent against gram-positive organisms
and one that covers anaerobes. Not the DOC. Consider if penicillins or other less toxic drugs are contraindicated, when clinically
indicated, and in mixed infections caused by susceptible staphylococci and gram-negative organisms. Dosing regimens are
numerous; adjust dose based on CrCl and changes in volume of distribution. May be administered IV/IM. For C fetus (not C
jejuni) infections.

Imipenem and cilastatin (Primaxin)

For treatment of multiple organism infections in which other agents do not have wide-spectrum coverage or are contraindicated
because of potential for toxicity. For C fetus (not C jejuni) infection.

Follow-up

Further Inpatient Care

In some cases, systemic Campylobacter infections are diagnosed retrospectively following empirical antibiotic therapy with
clinical resolution. In such cases, follow-up blood cultures should be obtained, and treatment can be stopped if they are
negative.

Oral erythromycin may not be adequate for systemic C jejuni or C fetus endovascular infections.

Deterrence/Prevention
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Pasteurization of milk and chlorination of drinking water destroy Campylobacter organisms.

Unpasteurized milk and untreated surface water should not be consumed.

Raw milk may not be safe, even if it conforms to routine testing by somatic cell and coliform counts.[33]

Treatment with antibiotics can reduce fecal excretion.

Health care workers with Campylobacter infections should not provide direct patient care or prepare food while they have
diarrhea or are shedding Campylobacter organisms in the stool. However, person-to-person transmission is unusual.

After diarrhea resolves, infective organisms may be present in the stool for up to 3 weeks.

Separate cutting boards should be used for foods of animal origin and other foods. After preparing raw food of animal origin, all
cutting boards and countertops should be carefully cleaned with soap and hot water.[34, 35]

Chicken should be adequately cooked.

When outbreaks occur, community education can be directed at proper food-handling techniques, including thorough cooking of
poultry.

As noted above, handling and consumption of poultry meat is a significant source of illness. One control strategy that has been
suggested is to keep colonized and noncolonized flocks separate.[36]

Fresh chicken can be the dominant source of Campylobacter infection, and replacing this with frozen chicken can reduce
Campylobacter levels.[6]

Complications
Potential complications of Campylobacter infections include the following:

Toxic megacolon

Pseudomembranous colitis

Gastrointestinal hemorrhage

Hemolytic-uremic syndrome

Thrombotic thrombocytopenic purpura

Immunoproliferative small intestinal disease (This is a type of lymphoma that involves mucosa-associated lymphoid
tissue [MALT]. It has been found to be associated with C jejuni infection.[37] )

Reactive arthritis[38, 39]

Bacteremia

Endocarditis

Cholecystitis

Urinary tract infection

Pancreatitis

Stillbirths, septic abortions (C fetus)

Intrauterine growth restriction[40]

Guillain-Barré syndrome (GBS) (GBS may develop secondary to cross-immunoreactivity between human gangliosides
GM1 and GD1a and C jejuni lipopolysaccharides. In one study, up to 25% of patients with GBS had stool cultures
positive for C jejuni. However, because of shortcomings of standard serological methods, the role of C jejuni may have

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been underestimated.[41, 42] In a study using a highly specific ELISA based on recombinant antigens, 80% of 36
patients with acute GBS were found to have serological evidence of preceding C jejuni infection, compared with 3.5% of
controls.[43] In a 2012 study from New Zealand, investigators reported a marked reduction in GBS incidence 3 years
after initiation of an intensive program to prevent food borne campylobacteriosis.[44] Of the over 8,000 C jejuni multilocus
sequence typing sequence types (STs) described, ST-22 has been associated with Guillain-Barré syndrome.[45] )

Meningitis[46, 30, 29]

Infected aortoiliac aneurysms[19]

A sub-group of inflammatory bowel disease[2, 3]

Infected endometrial cysts/tubo-ovarian abscess[47]

Prognosis
Generally, Campylobacter infections carry an excellent prognosis. The disease is almost always self-limited, with or without
specific therapy.

The illness usually lasts less than a week, but some patients develop a longer-relapsing diarrheal illness that lasts several
weeks.

The occasional deaths attributable to C jejuni infection usually occur in elderly or immunocompromised hosts.

Attributable deaths may also occur in young, healthy individuals secondary to volume depletion.

The rarer C fetus infection may also be fatal in debilitated hosts.

Patient Education
Many Campylobacter infections are potentially preventable through education.

Meat and poultry should be cooked well.

Hands should be washed carefully after preparing food.

Parents should be informed that sick pets (eg, puppies, kittens) may harbor human pathogens and must be kept away from
young children.

Untreated surface water and unpasteurized milk should be avoided.

Questions & Answers

Overview

What are Campylobacter infections?

What are the signs and symptoms of Campylobacter infections?

Which infectious agent is related to Campylobacter?

How are Campylobacter infections transmitted?

What is the infectious dose of Campylobacter?

What is the pathogenesis of Campylobacter infections?

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What is the pathophysiology of diarrhea in Campylobacter infections?

What are the characteristics of Campylobacter infections in patients with HIV infection?

What is the pathophysiology of C fetus Campylobacter infections?

What is the pathophysiology of C jejuni Campylobacter infections?

What is the incidence of Campylobacter infections in the US?

What is the global incidence of Campylobacter infections?

What are the risk factors for Campylobacter infection caused mortality?

What are the racial predilections for Campylobacter infections?

How does the incidence of Campylobacter infections vary by sex?

Which age groups are at greatest risk for Campylobacter infections?

Presentation

What is the typical history in patients with Campylobacter infections?

What are the signs and symptoms of Campylobacter infections?

How do the clinical histories vary among different Campylobacter species?

What are the physical findings characteristic of Campylobacter infections?

How are Campylobacter organisms characterized?

DDX

What are the differential diagnoses for Campylobacter Infections?

Workup

How are Campylobacter infections diagnosed?

What is the role of sigmoidoscopy in the diagnosis of Campylobacter infections?

Treatment

What is the initial therapy for Campylobacter infections?

What is the role of antibiotics in the treatment of Campylobacter infections?

What is the role of surgery in the treatment of Campylobacter infections?

When should specialists be consulted in the treatment of Campylobacter infections?

What activity restrictions are needed during the treatment of Campylobacter infections?

Medications

Which antibiotics are used in the treatment of Campylobacter infections?

Which medications in the drug class Antibiotics are used in the treatment of Campylobacter Infections?

Follow-up

What are the limitations of oral erythromycin in the treatment of Campylobacter infections?

How are Campylobacter infections prevented?

What are potential complications of Campylobacter infections?

What is the prognosis of Campylobacter infections?

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What is included in patient education for Campylobacter infections?

Contributor Information and Disclosures

Author

Mahmud H Javid, MBBS Consultant in Infectious Diseases, Shifa International Hospital, Pakistan

Mahmud H Javid, MBBS is a member of the following medical societies: Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Coauthor(s)

Shadab Hussain Ahmed, MD, AAHIVS, FACP, FIDSA Professor of Clinical Medicine, The School of Medicine at Stony Brook
University Medical Center; Adjunct Clinical Associate Professor, Department of Medicine, New York College of Osteopathic
Medicine of New York Institute of Technology; Attending Physician, Department of Medicine, Division of Infectious Diseases,
Director of HIV Prevention Services, Administrative HIV Designee, Nassau University Medical Center

Shadab Hussain Ahmed, MD, AAHIVS, FACP, FIDSA is a member of the following medical societies: American College of
Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Disclosure: Received salary from Medscape for employment. for: Medscape.

Michael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed
Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American
College of Physicians; Fellow, Infectious Diseases Society of America; Fellow of the Royal College of Physicians, London

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American College of
Physicians, American Medical Association, Association of Professors of Medicine, Infectious Diseases Society of America,
Oklahoma State Medical Association, Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.

Chief Editor

Michael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed
Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American
College of Physicians; Fellow, Infectious Diseases Society of America; Fellow of the Royal College of Physicians, London

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American College of
Physicians, American Medical Association, Association of Professors of Medicine, Infectious Diseases Society of America,
Oklahoma State Medical Association, Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.

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