What Happens If You Eat Raw Chicken Health Risks Explained

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Consuming raw chicken exposes individuals to a spectrum of immediate and long-term health hazards driven by bacterial, viral, and parasitic pathogens. Pathogens such as Salmonella, Campylobacter, and E. coli thrive in undercooked poultry, exploiting the human digestive system through rapid colonization and toxin production. Beyond acute gastrointestinal distress—including fever, dehydration, and neurological symptoms—the risks extend to chronic autoimmune disorders and systemic infections, underscoring the critical need for proper food handling and cooking practices.

The biological mechanisms behind foodborne illnesses from raw chicken involve complex interactions between pathogens and the human immune system, often leading to severe complications if untreated. Symptoms may manifest within hours, progressing from mild nausea to life-threatening conditions, while long-term exposure can trigger persistent health issues. This analysis examines the microbiological, clinical, and cultural dimensions of raw chicken consumption, supported by epidemiological data and case studies.

what happens if u eat raw chicken

Immediate Health Risks and Symptoms of Consuming Raw Chicken

Raw chicken is a common reservoir for pathogenic bacteria, including Salmonella, Campylobacter, and Escherichia coli (E. coli), which can cause severe gastrointestinal infections when ingested. These microorganisms exploit the human digestive system’s vulnerability, particularly in the small intestine, where they adhere to epithelial cells, disrupt mucosal integrity, and trigger inflammatory responses. The onset of symptoms typically occurs within 6–72 hours, with progression depending on bacterial strain, host immunity, and inoculum size. Severe cases may lead to systemic complications, including sepsis, organ failure, or neurological deficits, necessitating urgent medical intervention.

The biological mechanisms underlying these infections involve adhesion, invasion, and toxin production. Bacteria such as Salmonella enterica and Campylobacter jejuni secrete virulence factors that impair intestinal barrier function, while E. coli strains (e.g., enterotoxigenic or enterohemorrhagic) release enterotoxins that induce fluid secretion and tissue damage. Once ingested, these pathogens multiply exponentially in the gut, overwhelming local immune defenses and triggering systemic cytokine release, which can escalate to life-threatening conditions.

Pathogen-Specific Mechanisms and Symptom Progression

The clinical manifestations of raw chicken-associated infections vary by pathogen but share core features of acute gastroenteritis. Below is a structured comparison of key symptoms, onset timelines, and systemic risks associated with Salmonella, Campylobacter, and E. coli.
Critical Note: Symptom severity correlates with bacterial load, host age (children and elderly are high-risk), and pre-existing conditions (e.g., HIV/AIDS, diabetes).
Bacterial Multiplication and Immune Evasion:
  • Salmonella invades intestinal epithelial cells via Type III secretion systems (T3SS), disrupting tight junctions and inducing apoptosis.
  • Campylobacter adheres to the gut lining using flagellar motility and cadherin-like proteins, triggering an inflammatory cascade.
  • E. coli (e.g., O157:H7) produces Shiga toxins, which inhibit host protein synthesis and damage endothelial cells, increasing vascular permeability.

    • Timeline of Symptom Onset:

  • 6–24 hours: Initial nausea, abdominal cramps, and watery diarrhea (non-bloody in Salmonella; bloody in Campylobacter and E. coli).
  • 24–48 hours: Fever spikes (38–40°C), chills, and systemic malaise due to lipopolysaccharide (LPS)-induced endotoxemia.
  • 48–72 hours: Dehydration markers (tachycardia, hypotension, oliguria) and post-infectious complications (e.g., Guillain-Barré syndrome in Campylobacter; hemolytic-uremic syndrome in E. coli).

    • Structured Comparison of Pathogen-Associated Symptoms

    The following table summarizes distinguishing features of infections caused by common raw chicken pathogens, including symptom duration, fever patterns, and neurological sequelae.
    Pathogen Primary Symptoms Fever Duration Diarrhea Type Neurological Effects Systemic Risks Incubation Period
    Salmonella enterica Nausea, vomiting, abdominal cramps, headache 1–3 days (spiking) Watery to mucoid (rarely bloody) Meningitis (rare), reactive arthritis Sepsis, bacteremia (5–10% of cases) 6–72 hours
    Campylobacter jejuni Severe cramps, bloody diarrhea, fever, malaise 3–5 days (relapsing) Bloody (50% of cases) Guillain-Barré syndrome (1:1,000 cases), Miller Fisher syndrome Septic arthritis, endocarditis 2–5 days
    E. coli (STEC/O157:H7) Watery diarrhea progressing to bloody, minimal fever 1–2 days (low-grade or absent) Bloody (90% of cases) Hemolytic-uremic syndrome (HUS, 5–10% of cases), seizures Acute kidney injury, thrombotic microangiopathy 3–4 days
    Key Differentiator: Campylobacter and E. coli O157:H7 are more likely to cause bloody diarrhea, while Salmonella typically presents with watery stools and prolonged fever.

    Flowchart: Pathway from Ingestion to Systemic Infection

    The progression from raw chicken ingestion to systemic infection involves bacterial colonization, toxin-mediated damage, and immune dysregulation. Below is a textual representation of the critical stages, which can be visualized as a flowchart with the following nodes:

    1. Ingestion of Contaminated Raw Chicken

  • Pathogens (Salmonella, Campylobacter, E. coli) survive gastric acidity via acid tolerance responses (ATR) and flagellar motility.
  • Bacterial load determines infection likelihood (e.g., ≥10^5 CFU/g triggers illness).

    • 2. Adhesion and Invasion of Intestinal Epithelium

  • Salmonella: Uses SPI-1 T3SS to inject effector proteins (e.g., SopE) that rearrange host actin, promoting internalization.
  • Campylobacter: Binds to glycosaminoglycans via CadF and penetrates via flagellar-driven penetration.
  • E. coli: Adheres via intimin and injects Tir to form pedestals, disrupting tight junctions.

    • 3. Toxin Production and Mucosal Damage

  • Salmonella: SipA/SopB induce cytoskeletal rearrangements, increasing permeability.
  • Campylobacter: Cdt toxin (cytolethal distending toxin) arrests host cells in G2/M phase, triggering apoptosis.
  • E. coli: Shiga toxin cleaves 28S rRNA, halting protein synthesis in endothelial cells.

    • 4. Immune System Activation and Cytokine Storm

  • Innate response: Macrophages and dendritic cells release TNF-α, IL-1β, and IL-6, causing systemic inflammation.
  • Adaptive response: CD4+ T-cells secrete IFN-γ, exacerbating tissue damage in Campylobacter infections.
  • Gut permeability increase: Zonulin upregulation (via Salmonella effectors) allows bacterial translocation to mesenteric lymph nodes.

    • 5. Systemic Spread and Complications

  • Localized infection: Limited to gastrointestinal tract (mild-moderate cases).
  • Systemic infection: Bacteria or toxins enter bloodstream, leading to:
  • Sepsis (e.g., Salmonella bacteremia).
  • Organ-specific damage (e.g., E. coli HUS-induced renal failure).
  • Neurological sequelae (e.g., Campylobacter-triggered autoimmune responses).
    • Critical Pathway: The transition from localized gastroenteritis to sepsis occurs when bacterial translocation exceeds immune clearance capacity, typically in immunocompromised hosts or high-inoculum exposures.

    what happens if u eat raw chicken - Ilustrasi 2

    Long-Term Health Consequences of Chronic Exposure to Raw Chicken Pathogens

    Chronic consumption of raw or undercooked chicken introduces persistent risks from bacterial, parasitic, and viral pathogens, with cumulative effects extending beyond acute gastrointestinal distress. Repeated exposure to Campylobacter jejuni, Salmonella enterica, and other zoonotic agents may trigger autoimmune dysregulation, inflammatory bowel disease (IBD), and neurological disorders. Epidemiological studies correlate long-term poultry-related pathogen exposure with elevated risks of reactive arthritis, Guillain-Barré syndrome (GBS), and autoimmune hepatitis, underscoring the need for public health interventions targeting food safety practices.
    Key Mechanism: Autoimmune responses in Campylobacter jejuni infections arise from molecular mimicry, where bacterial lipopolysaccharides (LPS) or flagellin proteins cross-react with host tissues, particularly in the gastrointestinal and nervous systems.

    Autoimmune and Neurological Complications from Campylobacter jejuni

    Campylobacter jejuni is the leading bacterial trigger for Guillain-Barré syndrome (GBS), with a well-documented association in post-infection autoimmune reactions. A 2019 meta-analysis in The Lancet Neurology estimated that 30–40% of GBS cases follow C. jejuni gastroenteritis, with flagellin proteins (e.g., CjaA) inducing cross-reactive antibodies against peripheral nerve gangliosides (GM1, GD1a). Neurological sequelae may persist as chronic inflammatory demyelinating polyneuropathy (CIDP), requiring long-term immunosuppressive therapy.

    Autoimmune hepatitis has also been linked to C. jejuni exposure, with case reports in Hepatology documenting elevated liver enzymes and anti-smooth muscle antibodies (ASMA) post-infection. A 2017 study in Gastroenterology identified mimicry between bacterial heat-shock proteins (Hsp60) and human liver antigens, contributing to chronic hepatitis in susceptible individuals.

    Chronic Inflammatory Bowel Disease (IBD) and Reactive Arthritis

    Persistent Salmonella or Campylobacter infections disrupt intestinal barrier integrity, increasing IBD risk. A 2020 cohort study in Gut found that individuals with prior poultry-associated foodborne illness had a 2.3-fold higher risk of developing Crohn’s disease within 5 years, attributed to dysbiosis and Th17 immune activation. Reactive arthritis (ReA), characterized by joint inflammation post-enteric infection, affects 1–4% of Campylobacter-infected patients, with HLA-B27 positivity as a predisposing factor.

    Case Study: Progression from Acute Food Poisoning to Chronic Fatigue Syndrome (CFS)

    Patient Case (Anonymized):
    A 34-year-old male presented with severe diarrhea and fever 48 hours after consuming raw chicken at a social gathering. Initial diagnosis confirmed Campylobacter jejuni infection via stool culture. Despite antibiotic treatment, he developed persistent fatigue, cognitive dysfunction, and orthostatic intolerance 6 weeks later. Laboratory tests ruled out Lyme disease and Epstein-Barr virus but revealed elevated anti-GM1 antibodies and mild B-cell lymphocytosis. Over 18 months, his symptoms evolved into chronic fatigue syndrome (CFS), with functional MRI showing reduced hippocampal volume—a marker of neuroinflammation. Follow-up serology detected cross-reactive antibodies to neuronal antigens, suggesting post-infectious autoimmune dysfunction.

    Comparative Risk Analysis: Raw vs. Properly Cooked Poultry

    The following table contrasts long-term health risks associated with raw chicken consumption versus properly cooked poultry, incorporating epidemiological and mechanistic data:
    Risk Factor Raw/Undercooked Chicken Properly Cooked Poultry (74°C/165°F) Epidemiological Evidence
    Autoimmune Trigger Risk High (molecular mimicry in C. jejuni, Salmonella) Minimal (pathogen inactivation) Meta-analysis (Lancet Neurology, 2019): 30–40% of GBS cases post-C. jejuni infection.
    Inflammatory Bowel Disease (IBD) Risk Elevated (2.3× higher Crohn’s risk; Gut, 2020) Baseline population risk Cohort study: Prior foodborne illness linked to dysbiosis and Th17 activation.
    Colorectal Cancer Risk Increased (Salmonella typhimurium promotes inflammation and DNA damage) Reduced (elimination of carcinogenic pathogens) Case-control study (JNCI, 2018): Chronic Salmonella carriers had 1.8× higher colorectal cancer risk.
    Neurological Sequelae (GBS/CIDP) Significant (autoantibody-mediated demyelination) Negligible (pathogen load < infectious threshold) Surveillance data (CDC MMWR, 2021): 90% of GBS cases post-Campylobacter resolved with treatment, but 10% progressed to CIDP.
    Autoimmune Hepatitis Risk Moderate (Hsp60 cross-reactivity; Hepatology, 2017) Rare (pathogen clearance) Case series: 5/20 patients with post-Campylobacter hepatitis developed chronic ASMA positivity.

    Mechanisms of Pathogen-Induced Chronicity

    Three primary pathways contribute to long-term sequelae from raw chicken consumption:
    1. Molecular Mimicry: Bacterial antigens (e.g., C. jejuni flagellin) share homology with host tissues, eliciting autoimmunity.
    2. Persistent Inflammation: Chronic Salmonella or Campylobacter carriage disrupts gut homeostasis, fostering IBD and metabolic dysfunction.
    3. Neuroinvasion: C. jejuni LPS may cross the blood-brain barrier, triggering microglial activation and neurodegenerative changes.
    Critical Insight: The risk of chronic complications scales with frequency of exposure and individual immune susceptibility, particularly in genetically predisposed populations (e.g., HLA-B27 for ReA, HLA-DR3/4 for autoimmune hepatitis).

    Microbiological Breakdown: Pathogens and Contamination in Raw Chicken

    Raw chicken serves as a reservoir for a diverse array of pathogens, including bacteria, viruses, and parasites, which pose significant risks to human health. These contaminants originate from various sources, including fecal matter, environmental exposure during processing, and cross-contamination in food handling. Understanding the survival rates of these pathogens under different storage conditions is critical for mitigating risks, as improper handling can lead to severe infections. Additionally, cross-contamination in kitchen environments exacerbates exposure, while variations in farming practices—such as free-range versus conventional raising—further influence pathogen prevalence and antibiotic resistance profiles.

    Top 5 Bacterial, Viral, and Parasitic Contaminants in Raw Chicken

    Raw chicken is commonly contaminated with pathogens that vary in virulence, survival rates, and resistance mechanisms. The following five categories represent the most frequently isolated contaminants globally, categorized by pathogen type.
    Note: Survival rates are influenced by temperature, humidity, pH, and microbial competition. Data sourced from the USDA, CDC, EFSA, and WHO reports.
    1. Bacterial Contaminants
      • Salmonella enterica
        • Survival Rates:
          • Room temperature (20–25°C): 2–4 days (viable but declining after 72 hours).
          • Refrigeration (4°C): 4–6 weeks (minimal decline).
          • Freezing (−20°C): Indefinite (no significant reduction).
        • Key Strains: S. Typhimurium, S. Enteritidis (responsible for ~1.2 million infections annually in the U.S.).
        • Transmission: Fecal contamination during slaughter; persists on skin and internal surfaces.
      • Campylobacter jejuni
        • Survival Rates:
          • Room temperature: 2–3 days (rapid decline after exposure to oxygen).
          • Refrigeration: 5–7 days (microaerophilic conditions extend survival).
          • Freezing: Indefinite (but may lose viability upon thawing).
        • Key Strains: C. coli (less common but equally pathogenic).
        • Transmission: Intestinal tract of live birds; contaminates carcass during processing.
      • Clostridium perfringens
        • Survival Rates:
          • Room temperature: Spores survive indefinitely; vegetative cells die in 6–12 hours.
          • Refrigeration: Spores remain viable; outgrowth occurs at >10°C.
          • Freezing: Spores survive; germination upon thawing.
        • Key Strains: Type A (foodborne diarrhea), Type C (necrotic enteritis).
        • Transmission: Soil and fecal contamination; spores resist heat and desiccation.
      • Staphylococcus aureus
        • Survival Rates:
          • Room temperature: 24–48 hours (enterotoxin production at >10°C).
          • Refrigeration: 1–2 weeks (growth inhibited but toxin stable).
          • Freezing: Viable but toxin production halted.
        • Key Strains: Methicillin-resistant S. aureus (MRSA) in conventionally raised poultry.
        • Transmission: Nasal carriage in birds; contaminates skin during processing.
      • Listeria monocytogenes
        • Survival Rates:
          • Room temperature: 7–10 days (growth at >4°C).
          • Refrigeration: Indefinite (psychrotrophic; multiplies slowly).
          • Freezing: Survives but reduced viability upon thawing.
        • Key Strains: Serotypes 1/2a and 4b (high virulence).
        • Transmission: Environmental contamination (slaughterhouses, processing equipment).
    2. Viral Contaminants
      • Astrovirus and Norovirus
        • Survival Rates:
          • Room temperature: 1–2 weeks (stable in moist environments).
          • Refrigeration: Months (resistant to low temperatures).
          • Freezing: Indefinite (inactivated by heating but persists in raw products).
        • Transmission: Fecal-oral route; contaminates carcass during evisceration.
        • Note: Rare in poultry but documented in outbreaks linked to raw chicken handling.
    3. Parasitic Contaminants
      • Toxoplasma gondii
        • Survival Rates:
          • Room temperature: Oocysts survive weeks in moist conditions.
          • Refrigeration: Months (inactivated by freezing at −20°C for 3 days).
        • Transmission: Fecal contamination; tissue cysts in raw meat.
      • Cryptosporidium parvum
        • Survival Rates:
          • Room temperature: Oocysts survive months in water/moisture.
          • Refrigeration: Years (chlorine-resistant).
        • Transmission: Contaminated water during processing; rare in poultry but documented in free-range systems.

    Cross-Contamination in Kitchen Environments: Mechanisms and Visualization

    Cross-contamination occurs when pathogens from raw chicken transfer to other surfaces, utensils, or foods via direct contact, airborne droplets, or improper hygiene. The following step-by-step procedure illustrates common pathways, with visual descriptions of critical transfer points.
    Key Principle: Pathogens spread via three primary vectors:
    1. Direct contact (e.g., cutting board, knife).
    2. Indirect contact (e.g., hands, sponges).
    3. Airborne transmission (e.g., splashing, aerosolization).
    1. Initial Contamination of Raw Chicken
      • A raw chicken carcass is thawed at room temperature for 2 hours, allowing surface pathogens (Salmonella, Campylobacter) to proliferate in moisture.
      • During handling, a droplet of raw chicken juice (containing ~10^6–10^8 CFU/mL of Salmonella) splashes onto the cutting board, creating a 5 cm diameter wet zone.
    2. Transfer to Utensils
      • A chef uses the same knife to slice the chicken and then chops vegetables without washing the blade. The knife’s serrated edge retains pathogens in crevices.
      • Visual: A microscopic cross-section of the knife blade shows Salmonella colonies (red) embedded in grooves, with viable cells persisting for up to 4 hours post-contact.
    3. Surface Spread via Hands
      • The chef touches the contaminated cutting board and then opens a package of lettuce without washing hands. Fingerprints transfer ~10^3–10^4 CFU of Campylobacter to the lettuce.

        • what happens if u eat raw chicken - Ilustrasi 3

        Cultural and Regional Practices Involving Raw or Undercooked Chicken

        The consumption of raw or minimally cooked chicken persists in select culinary traditions worldwide, often balanced by centuries-old food safety adaptations. These practices reflect a convergence of microbial risk management, fermentation science, and cultural identity, where traditional methods—such as fermentation, curing, or rapid cooking techniques—mitigate but do not eliminate pathogen exposure. Industrial and artisanal approaches to preparation further influence safety outcomes, with regulated systems (e.g., high-end restaurants) employing stricter protocols than informal street food vendors. Below, regional traditions, preparation methodologies, and pathogen-related outbreaks are examined, alongside the microbial mechanisms underlying fermentation-based risk reduction.

        Traditional Dishes Featuring Raw or Undercooked Chicken

        In certain cuisines, raw or partially cooked chicken is integrated into dishes through fermentation, marinades, or rapid heat exposure to achieve texture and flavor profiles unattainable with fully cooked meat. These preparations often rely on lactic acid bacteria (LAB) or nitrite curing to suppress pathogens, though residual risks remain. Key examples include:
        • Tartare and Ceasar Salad Variations
          In Western haute cuisine, chicken tartare—ground raw chicken served with raw egg, capers, and herbs—emerges as a luxury dish, though its preparation adheres to strict HACCP (Hazard Analysis Critical Control Point) protocols, including pathogen testing and sourcing from USDA-inspected, frozen (−20°C for ≥7 days) poultry to inactivate Salmonella and Campylobacter. Ceasar salads with raw chicken (e.g., in some European or American gourmet versions) similarly require pasteurized chicken or high-pressure processing (HPP) to ensure safety.
        • Fermented and Cured Poultry
          • Korean Dakgalbi (Chicken Galbi) and Samgyeopsal Fermentation
            While Dakgalbi typically involves grilled chicken, fermented chicken products like kimchi chicken or jeotgal (salted/fermented poultry) leverage lactic acid fermentation (via Lactobacillus strains) to lower pH (<4.6), inhibiting E. coli and Listeria. Studies indicate that 3–5 days of fermentation at 4°C reduces Campylobacter counts by 90–99% through competitive exclusion and organic acid production.
          • Japanese Torisashi (Chicken Sashimi)
            A niche preparation in Japan, torisashi involves sliced raw chicken thigh, often served with wasabi or soy sauce. Safety relies on flash-freezing (−15°C for ≥7 days) and visual inspection for parasites (e.g., Toxoplasma gondii), though outbreaks linked to Salmonella Enteritidis have occurred in unregulated settings.
          • Latin American Carne Cruda (Raw Chicken)
            In regions like Peru and Bolivia, raw chicken is occasionally consumed in ceviche-style dishes, where citrus juices (limón) and antimicrobial peptides (e.g., in ají peppers) may partially neutralize pathogens. However, CDC reports link such practices to salmonellosis outbreaks, particularly in rural areas lacking refrigeration.
        • Street Food and Informal Preparations
          In Southeast Asia and parts of Africa, raw or undercooked chicken appears in dishes like Thai Yum (spicy salads) or Nigerian Suya (spicy grilled skewers), where smoking or brief grilling may not fully eliminate pathogens. A 2018 WHO study on street food safety in Nigeria identified Campylobacter jejuni in 60% of raw chicken samples sold at markets, with children under 5 being the most vulnerable demographic.

        Industrial vs. Artisanal Preparation: Hygiene Protocols and Risk Mitigation

        The safety of raw chicken consumption varies significantly between industrialized (high-end restaurants, processed foods) and artisanal/street food settings, with the former relying on standardized pathogen reduction and the latter on empirical risk management. Key distinctions include:
        • Industrial/Commercial Preparations
          Regulatory frameworks (e.g., EU Regulation 853/2004, USDA FSIS guidelines) mandate:
          • Pathogen testing for Salmonella and Campylobacter (≤10 CFU/g in raw poultry).
          • Flash-freezing or high-pressure processing (HPP) to inactivate vegetative cells.
          • Use of approved antimicrobials (e.g., lactic acid, organic acids) in marinades.
          • HACCP certification for restaurants serving raw poultry.
          Example: French Poulet Tartare in Michelin-starred restaurants uses vacuum-packed, irradiated chicken (approved in the EU for pathogen reduction) alongside raw egg pasteurization to prevent Salmonella Typhi.
        • Artisanal and Street Food Methods
          Hygiene relies on traditional knowledge rather than scientific validation, with variable efficacy:
          • Fermentation and Curing
            In Korea, kimchi chicken undergoes 10–14 days of fermentation at 10–15°C, where Lactobacillus plantarum produces lactic and acetic acids, reducing E. coli by 95% (Kim et al., 2017). However, cross-contamination during handling remains a critical risk.
          • Smoking and Drying
            In African suya preparation, wood smoke contains phenolic compounds with antimicrobial properties, but incomplete drying (aH >0.85) allows Listeria monocytogenes survival (FAO, 2015).
          • Rapid Cooking Techniques
            Japanese torisashi vendors may blanch chicken in saltwater (3–5 minutes at 80°C) to reduce Campylobacter, but post-cooking contamination during slicing is documented in outbreaks.
        • Critical Gaps in Low-Resource Settings
          A 2020 Lancet study on street food safety in sub-Saharan Africa found that 78% of vendors lacked access to running water for handwashing, and 65% used shared knives between raw and ready-to-eat foods. This contributes to self-limiting outbreaks (e.g., shigellosis) that go unreported.

        Regional Outbreaks Linked to Raw Chicken Consumption

        Historical and documented outbreaks underscore the persistent risks of raw chicken consumption, with children, immunocompromised individuals, and pregnant women bearing the highest burden. Below is a comparative table of notable incidents, pathogens, and governmental responses:

        The consumption of raw chicken poses significant health risks ranging from acute food poisoning to chronic autoimmune and neurological disorders, driven by pathogens like Campylobacter and Salmonella. While cultural practices and fermentation techniques may mitigate some hazards, proper cooking remains the most effective preventive measure. Understanding the biological pathways, contamination sources, and regional adaptations is essential for minimizing exposure and promoting safer food handling practices globally.

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        Region/Country Year Pathogen(s) Affected Population Government Response Key Adaptation Post-Outbreak
        Japan 2015 Salmonella Enteritidis (serotype Typhimurium) 127 cases (Osaka prefecture); 3 hospitalizations
        • Recall of unpasteurized chicken sashimi from 15 vendors.
        • Mandatory pathogen testing for raw poultry in sushi bars.
        		 Introduction of UV-C irradiation for chicken surfaces in high-end restaurants.
        South Korea 2011 Campylobacter jejuni (ST-21 cluster) 456 cases (Seoul); 12% children under 5