Confirmation of a Campylobacteriosis Outbreak Associated with Chicken Liver Pâté Using PFGE and WGS

Campylobacter jejuni is known to possess a LuxS/ autoinducer-2 (AI-2) mediated system that have been partially characterized over the last decade

To initiate infection the organism must penetrate the gastrointestinal mucus, which it does by using its high motility and spiral shape. The bacteria must then adhere to the gut enterocytes and once adhered can then induce diarrhoea by toxin release.

Campylobacter jejuni isolates (47.5%). Production of β-lactamase was typically associated with resistance to ampicillin, amoxicillin (amoxicilline), penicillin, and ticarcillin.

Here, we analyzed the antimicrobial susceptibilities of 320 C. jejuni and 115 C. coli isolates obtained from feedlot cattle farms in multiple states in the U.S. The results indicate that fluoroquinolone resistance reached to 35.4% in C. jejuni and 74.4% in C. coli, which are significantly higher than those previously reported in the U.S.

The organism is unusual among enteric pathogens in that it expresses a polysaccharide capsule (CPS) that contributes to serum resistance, invasion of intestinal epithelial cells in vitro, and virulence in ferret and Galleria mellonella larvae models of disease (1–3).

the mucus overlying the epithelial cells primarily in the ceca and the small intestine but may also be recovered from elsewhere in the gut and from the spleen and liver

Our data suggest that binding of these surface exposed proteins may play a key role in C. jejuni-host cell interactions and ultimate invasion.

14 cases are diagnosed each year for each 100,000 persons in the population. Many more cases go undiagnosed or unreported, and campylobacteriosis is estimated to affect over 1.3 million persons every year.

The illness typically lasts about one week

Azithromycin and fluoroquinolones (e.g., ciprofloxacin) are commonly used for treatment of these infections, but resistance to fluoroquinolones is common. Antimicrobial susceptibility testing can help guide appropriate therapy

Azithromycin and fluoroquinolones (e.g., ciprofloxacin) are commonly used for treatment of these infections, but resistance to fluoroquinolones is common. Antimicrobial susceptibility testing can help guide appropriate therapy.

What are public health agencies doing to prevent or control campylobacteriosis?

Do not drink unpasteurized milk or untreated surface water.

Surface water and mountain streams can become contaminated from infected feces from cows or wild birds.

Most cases of campylobacteriosis are associated with eating raw or undercooked poultry meat or from cross-contamination of other foods by these items. Outbreaks of Campylobacter have most often been associated with unpasteurized dairy products, contaminated water, poultry, and produce. Animals can also be infected, and some people get infected from contact with the stool of an ill dog or cat.

Almost all persons infected with Campylobacter recover without any specific treatment. Patients should drink extra fluids as long as the diarrhea lasts. Antimicrobial therapy is warranted only for patients with severe disease or those at high risk for severe disease

Campylobacter jejuni grows best at 37°C to 42°C, the approximate body temperature of a bird (41°C to 42°C), and seems to be well adapted to birds, who carry it without becoming ill. These bacteria are fragile. They cannot tolerate drying and can be killed by oxygen. They grow only in places with less oxygen than the amount in the atmosphere. Freezing reduces the number of Campylobacter bacteria on raw meat.

The organism is isolated from infants and young adults more frequently than from persons in other age groups and from males more frequently than females.

The diarrhea may be bloody

Most people who become ill with campylobacteriosis get diarrhea, cramping, abdominal pain, and fever within two to five days after exposure to the organism.

How do people get infected with this germ?

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.

Cytotoxin production has been reported in Campylobacter strains from patients with bloody diarrhea

Infection with the organism produces diffuse, bloody, edematous, and exudative enteritis

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.

Chickens may account for 50-70% of human Campylobacter infections.

Macrolide resistance in Campylobacter is mainly associated with target modification and active efflux [55–59]. Modification of the ribosomal target, leading to macrolide resistance in Campylobacter, can occur either by enzyme-mediated methylation or by point mutation in the 23S rRNA and/or ribosomal proteins L4 and L22

In addition to the mutations in GyrA, the multidrug efflux pump, CmeABC, also contributes to FQ resistance by reducing the accumulation of the agents in Campylobacter cells

In Campylobacter, the resistance to FQs is mainly mediated by point mutations in the quinolone resistance-determining region (QRDR) of DNA gyrase A (GyrA)

Generally, the prevalence of erythromycin resistance among Campylobacter strains (including both C. jejuni and Campylobacter coli) isolated from humans, broilers and cattle in the USA and Canada has been reported at 10% or lowe

19–47% of Campylobacter strains isolated from humans were resistant to ciprofloxacin [

Alternative drugs include tetracyclines and gentamicin, which are used in cases of systemic infection with Campylobacter [5]. However, Campylobacter is increasingly resistant to the clinically important antibiotics and this rising resistance is a concern for public health.

Cefoperazone is added to inhibit many gram-positive and gram-negative organisms, both aerobic and anaerobic. Vancomycin inhibits gram-positive microorganisms. Amphotericin B is incorporated to inhibit the growth of yeast.

Campy CVA is recommended. The use of cefoperazone-containing media, as opposed to cephalothin-containing media, is recommended for the primary isolation of Campylobacter from fecal samples

C. jejuni continues to be the most common enteric pathogen isolated form patients with diarrhea

In Campylobacter, a recurring theme is synergy between antibiotic efflux and a second mechanism.

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

Medication Summary

On the Trail of Campylobacter

Tables 2 and 3.

Allculturesgrewat43°Candnotat25°C,werecatalaseandoxidasepositive,didnotproduceH2Sontriplesugar-ironmedia,wereresistanttocephalothin,anddidnotgrowaerobically.Previouslyfrozenorlyophilizedculturesw

Symptoms start 2 - 4 days after being exposed to the bacteria. They usually last 1 week, and may include: Cramping abdominal pain Fever Nausea and vomiting Watery diarrhea, sometimes bloody

Laboratory Diagnosis of Bacterial Gastroenteritis

Virulence Factors

In Thailand and Spain, for example, up to 80% of Campylobacter isolates are fluoroquinolone-resistant

Azithromycin prevents bacteria from growing by interfering with their protein synthesis. It binds to the 50S subunit of the bacterial ribosome, thus inhibiting translation of mRNA. Nucleic acid synthesis is not affected.[18]

Most people with campylobacteriosis develop the following symptoms two to five days after being infected (though symptoms can appear as late as one month after infection): diarrhea (often bloody or watery) abdominal pain fever nausea vomiting (sometimes)

bacteria are found naturally in the intestines of poultry, cattle, swine, rodents, wild birds and household pets like cats and dogs. The bacteria have also been found in untreated surface water (caused by fecal matter in the environment) and manure.

Growth will be visible after48 hr. Heavily restreak the growth onto a newMH agar plate and incubate for another 24 to36 hr.

Multiple types of media can be used to cultivate it; however, Mueller Hinton broth and agar support the best C. jejuni growth. Optimum atmosphere for C. jejuni is 85% N2, 10% CO2, and 5% O2.

being able to execute N-linked glycosylation of more than 30 proteins related to colonization, adherence, and invasion. Moreover, the flagellum is not only depicted to facilitate motility but as well secretion of Campylobacter invasive antigens (Cia). The only toxin of C. jejuni, the so-called cytolethal distending toxin (CdtA,B,C), seems to be important for cell cycle control and induction of host cell apoptosis and has been recognized as a major pathogenicity-associated factor. In contrast to other diarrhoea-causing bacteria, no other classical virulence factors have yet been identified in C. jejuni.

The bacteria colonize the small and large intestines, causing inflammatory diarrhea with fever. Stools contain leukocytes and blood. The role of toxins in pathogenesis is unclear.

Many types of media have been used to culture C. jejuni. Mueller-Hinton medium, blood agar, Columbia blood agar, and BBL medium are commonly used. However, Mueller Hinton (MH) has the highest recovery rate and is recommended in this unit

C. jejuni is also able to grow in anaerobic conditions.

Significant loss of viable bacteria occurs when the bacteria are left at room temperature and atmosphere for only 10 min.

it has been connected with bacterial gastroenteritis as well as the neurological disorders Guillen-Barré Syndrome and Fisher Syndrome in humans. It is now one of the leading causes of gastroenteritis in both the developed and developing worlds.

microaerophilic conditions with a temperature range between 37° and 42°C. Multiple types of media can be used to cultivate it; however, Mueller Hinton broth and agar support the best C. jejuni growth. Optimum atmosphere for C. jejuni is 85% N2, 10% CO2, and 5% O2.

All Campylobacter species are inherently resistant to vancomycin, rifampin, and trimethoprim.

Erythromycin has once again come to be considered the optimal drug for treatment of Campylobacter infections. Despite decades of use, the rate of resistance of Campylobacter to erythromycin remains quite low. Other advantages of erythromycin include its low cost, safety, ease of administration, and narrow spectrum of activity. Unlike the fluoroquinolones and tetracyclines, erythromycin may be administered safely to children and pregnant women and is less likely than many agents to exert an inhibitory effect on other fecal flora.

However, in the past few years, a rapidly increasing proportion of Campylobacter strains all over the world have been found to be fluoroquinolone-resistant

Maintenance of hydration and electrolyte balance, not antibiotic treatment, is the cornerstone of treatment for Campylobacter

contaminated water, contact with pets (especially birds and cats)

Fecal leukocytes and RBCs are detected in the stools of 75% of infected persons

Clinically, Campylobacter infection is indistinguishable from acute gastrointestinal infections produced by other bacterial pathogens, such as Salmonella, Shigella, and Yersinia species.

They grow best at 42°C. Because most Campylobacter species are resistant to cephalothin (an agent to which most other stool flora are susceptible), the usual method for isolation from stool samples is use of a medium that contains cephalothin.

Campylobacter species are motile by means of unipolar or bipolar flagellae. The organisms grow quite slowly; 72–96 h are required for primary isolation from stool samples

ampylobacter infections were found to cause diarrheal disease >2–7 times as frequently as infections with Salmonella species, Shigella species, or Escherichia coli O157:H7

Obtaining cultures of the organism from stool samples remains the best way to diagnose this infection

nonspore-forming, Gram-negative, microaerophilic, nonfermenting bacterium

The vast majority of cases occur as isolated events, not as part of recognized outbreaks.

he bacteria must then adhere to the gut enterocytes and can then induce diarrhea by toxin release. C. jejuni releases several different toxins, mainly enterotoxin and cytotoxins, which vary from strain to strain and correlate with the severity of the enteritis.

grow optimally at 37 to 42 °C.[5][6][7][8] When exposed to atmospheric oxygen, C. jejuni is able to change into a coccal form

oxidase-positive

C. jejuni is also commonly found in animal feces.

14 cases are diagnosed each year for each 100,000 persons in the population.

characteristic curved rods is specific

Campylobacter organisms are oxidase positive with C jejuni hydrolysing hippurate.

The organism is sensitive to oxygen, drying, freezing, salting, and acid conditions

Temperature range: 30-50°C (86-122°F) Optimum Temperature: 42°C (108°F) pH range: 4.9-9.0 Optimum pH: 6.5-7.5 Oxygen Requirement: 3-5% Carbon Dioxide Requirement: 2-10% Optimum Requirements: 5% Oxygen, 10% Carbon Dioxide, 85% Nitrogen Salt Tolerance: 1.0%

Our results showed that when C. jejuni cells were coincubated with Acanthamoeba polyphaga in acidified phosphate-buffered saline (PBS) or tap water, the bacteria could tolerate pHs far below those in their normal range, even surviving at pH 4 for 20 h and at pH 2 for 5 h. Interestingly, moderately acidic conditions (pH 4 and 5) were shown to trigger C. jejuni motility as well as to increase adhesion/internalization of bacteria into A. polyphaga. Taken together, the results suggest that protozoa may act as protective hosts against harsh conditions and might be a potential risk factor for C. jejuni infections.

fluoroquinolones, macrolides, trimethoprim, beta lactam antibiotics, including penicillin and most cephalosporins, as well as to tetracycline, quinolone and kanamycin

COMMUNICABILITY: Low, person-to-person transmission is unusual

C. jejuni has been associated with post-infection sequelae, most commonly Guillain-Barré syndrome and reactive arthritis

Skirrow’s Campylobacter Medium (contains polymixin B, trimethoprim, vancomycin) ·   Preston Campylobacter Medium (contains polymixin B, rifampicin, trimethoprim) ·   Campy Blood Agar ·   CVA Medium (contains cefoperazone, vancomycin, amphotericin) Selective media for Campylobacter jejuni