Campylobacter jejeuni
last authored: Dec 2012, Jimmy Yan
last reviewed: Jan 2013, Nilesh Chande
Introduction
Campylobacter jejeuni is one of the most common bacterial causes of gastroenteritis in humans in the world (Acheson and Allos, 2001). While the disease is normally self-limiting, it can cause severe symptoms and can be life-threatening, particularly in children, seniors, and people with significant medical conditions. A smaller number of patients can develop infectious in other sites, as well as the auto-immune condition Guillain-Barre Syndrome.
C. jejeuni is normally a food-borne pathogen. It is found in the intestinal tracts of a wide range of animal hosts, most notably poultry, and is usually spread through contaminated, under-cooked food products.
Treatment is normally conservative and focuses on adequate hydration. Antibiotics are used in severe disease, though increasing antibiotic resistance is a serious worldwide concern.
The Case of Fred B.
Fred is a 32 year old man who began to feel unwell several days after he went to a local county fair, in which he visited a petting zoo and ate some barbecued meat. His initial symptoms included general pain in his joints, sweating, and a mild headache. A day later, he felt much worse with a severe colicky pain in the periumbilical area. He developed acute diarrhea, with 20 bowel movements with loose, mucousy, bloody stool.
As his symptoms continued, he became progressively weak. He was brought to the emergency department, where he was found to be pale and unwell, with a temperature of 38.9, heart rate of 106 and a blood pressure of 96/66.
- Q: how should Fred be initially treated?
- Q: how should his condition be investigated and diagnosed?
Epidemiology
C. jejeuni is a leading cause of bacterial gastroenteritis in humans in the world, and over 2 million cases of C. jejeuni are estimated to occur annually in the US (CDC, 2010). While all ages are susceptible to infection, in developed countries, there is a peak at 0 -4 years of age, with a second peak between the ages 15 - 24 years. In temperate areas of the world, laboratory confirmed cases of infection by C. jejeuni follow a seasonal pattern that peaks in the early to mid summer months and slowly declines towards winter.
In developing nations where the disease is endemic, a different pattern is noted, with a high incidence of repeat infections seen in early childhood. This is due to high transmission rates of the disease. As exposure to the disease increases, so does immunity, and the later peak of incidence seen in industrialized nations is not noted within countries where the bacteria is hyper-endemic.
Classification and Characteristics
Camplyobacter jejeuni is a gram-negative, flagellated, helical-shaped, non-spore forming bacteria. It is small and slender (measuring 0.2-0.5 um wide by 0.5-5.0 um long).
It is part of the Camplyobacter genus, along with C. coli, which also causes bacterial gastroenteritis in humans. C. jejeuni, like typical gram-negative bacteria, possesses a cell wall structure with a hydrophobic outer membrane that contains lipopolysaccharide. Antigenic variation of LPS in the cell wall allows for serotyping and serogrouping of C. jejeuni.
C. jejeuni is adapted to colonize mucosal membranes of the gut. The spiral morphology and long polar flagella allows for increased motility that propels the bacterium past mucus linings. Additionally, the bacteria possess fimbraie-like filaments that aid it in attaching to intestinal epithelial cells. These features lead to the direct cell invasion that is the mechanism behind the characteristic inflammatory (Konkel et al, 2001).
Transmission and Infection
As described, C. jejeuni is normally a zoonotic disease, with reservoirs found in both wild and domesticated animals. Poultry are ny far the biggest source, though it can also be found in cattle, pigs, and sheep, as well as infected cats and dogs (CDC, 2010). It is widely shed into water sources, both fresh and saline, in which it can survive readily for extended periods of time.
The bacteria is transmitted through the fecal-oral route through a contaminated water source, by eating raw or undercooked meat products, through other contaminated foods during improper food preparation , or through unpasturized milk.
Human-human spread can occur through fecal-oral spread, as well as unprotected anal intercourse. Dosing experiments have shown that 800 x106 bacteria were needed to produce illness in 50% of the test subjects (Black et al, 1988).
Clinical Manifesations
The general clinical features of C. jejeuni-induced gastroenteritis can be difficult to distinguish from that of other bacteria that cause invasive, inflammatory diarrhea, such as Salmonella typhi, Yersinia enterocolitia, Enterohemmorhagic E coli, or the Shigellae.
Typically, for the adult patient, the incubation period lasts an average of 2-6 days. The disease begins with a prodrome of fever, headaches, myalgia, and dizziness, which may last one or two days (Acheson and Allos, 2001).
Overt symptoms normally include abdominal pain, cramping, and diarrhea. The diarrhea can appear to be loose, watery, mucousy, bloody, or exudative, and patients often report of ten or more bowel movements per day. Nausea commonly occurs. The pain can be crampy or constant, and is often periumbicular with radiation towards the right lower quadrant of the abdomen, mimicking that of appendicitis.
The diarrhea is usually self-limiting after a course of a few days to a week, although about 10% of patients report relapsing symptoms. A smaller number of people may develop chronic infection.
However, in children, seniors, and patients that are immuno-suppressed or otherwise compromised, systemic infection, with bacteremia and sepsis can result. Cholecystitis, pancreatitis, or peritonitis can result from abdominal spread. While rarer, meningitis, osteomyelitis, endocarditis, and septic arthritis can also occur (Acheson and Allos, 2001).
C. jejeuni infection has also been linked to a latent reactive arthritis one to two weeks following gastrointestinal infection. Wrist, ankles, knees, and small joints of the hands are commonly affected, typically with a duration of a week to several months. Reiter syndrome can also occur, with inflammation of the joints, eyes, and urethra.
C. jejeuni has also been found to cause a late onset autoimmune reaction several weeks after initial infection. The effects are an acute, immune-mediated polyneuropathy, also known as Guillian-Barre Syndrome, for which Campylobacter infection is believed to account for approximately 30% of cases (Acheson and Allos, 2001).
Diagnosis
Campylobacter should be suspected in any setting of sudden onset severe abdominal pain with bloody diarrhea.
Gram stain can be done to reveal pathogens, and while the specificity is high, sensitivity is only moderate. As such, diagnosis is normally made by stool culture. A fecal sample is plated on selective media and incubated in a microaerobic gas mixture (5 to 10% oxygen, 10% carbon dioxide). C. jejeuni has a distinguishing spiral appearance under the microscope. Oxidase and catalase positivity is also tested in order to make a diagnosis.
Treatment
Campylobacter jejeuni infections are generally self-limiting, and in most cases maintaining proper hydration and electrolyte balance is adequate therapy. This normally occurs in an outpatient setting with oral rehydration, though patients may be admitted to hospital for IV rehydration if necessary.
Generally, antibiotic therapy is not required; however, they should be administered in severe cases. C. jejeuni is inherently resistant to beta-lactam antibiotics. Drugs of choice for treatment are fluoroquinolones (in particular ciprofloxacin) or macrolide (in particular azithromycin). Erythromycin has been used in the past, and is effective at eliminating the bacteria. Unfortunately, there has been a rise of macrolide and fluoroquinolone resistant cases of C. jejeuni, mediated by widespread use in animals. In the presence of these resistant isolates, clindamycin or tetracycline can be used. Gentamicin can be used in cases where the disease has spread into a systemic infection, but is not useful for infections of the alimentary tract.
Specific dosing strategies can be found in resources such as Medscape.
Anti-diarrheal agents such as loperamide should not be used, as this can lead to gut perforation and death.
Prevention of the disease relies heavily on maintaining proper hygiene during food production and preparation. Meats, particularly poultry, need to be cooked thoroughly, and utensils and preparatory instruments in contact with raw poultry need to be thoroughly cleaned.
Resources and References
Acheson D, Allos BM. 2001. Campylobacter jejuni Infections: Update on Emerging Issues and Trends. Clin. Infect. Dis. 32(8): 1201-1206.
Allos BM. 2012. Microbiology, pathogenesis, and epidemiology of Campylobacter infection. UpToDate.
Black RE et al. 1988. Experimental Campylobacter jejuni infections in humans. J Infect Dis. 157:472-9.
Centers of Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Diseases (2010). Campylobacter.
Gladwin, M, & Trattler, B. 2010. Clinical Microbiology Made Ridiculously Simple. (4th ed.). Miami (FL): Medmaster Inc.
Health Canada, Food and Nutrition: Food-Related Illnesses: Campylobacter Jejuni.
Konkel ME, Monteville MR, Rivera-Amill V, Joens LA. 2001. The pathogenesis of Campylobacter jejuni-mediated enteritis. Curr Issues Intest Microbiol, 2: 55–71.
Smith KE et al. 1999. Quinolone-resistant Campylobacter jejuni infections in Minnesota, 1992-1998. Investigation Team. N Engl J Med. 340(20):1525-32.
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