Pediatric Campylobacter Infections
- Author: Jocelyn Y Ang, MD, FAAP, FIDSA; Chief Editor: Russell W Steele, MD more...
The family Campylobacteraceae includes 2 genera: Campylobacter and Arcobacter. The genus Campylobacter includes 18 species and subspecies; 11 of these are considered pathogenic to humans and cause enteric and extraintestinal illnesses. The major pathogens are Campylobacter jejuni and Campylobacter fetus.
The following Campylobacter species and subspecies are pathogenic to humans:
- C jejuni subspecies jejuni
- C jejuni subspecies doylei
- Campylobacter coli
- Campylobacter upsaliensis
- Campylobacter lari
- C fetus subspecies fetus
- Campylobacter hyointestinalis
- Campylobacter concisus
- C jejuni subspecies jejuni
- C upsaliensis
- C lari
- C fetus subspecies fetus
- C concisus
- Campylobacter sputorum
- Campylobacter curvus
- Campylobacter rectus
Campylobacter pylori has been reclassified as Helicobacter pylori and is not addressed in this article (see Helicobacter Pylori Infection).
Campylobacter pathogens are small, curved, motile, microaerophilic, gram-negative rods. They vary in width from 0.2-0.9 mm and vary in length from 0.5-5.0 mm. They exhibit rapid, darting motility in corkscrew fashion using a single flagellum or 2 flagella (monotrichous, amphitrichous). They also possess a lipopolysaccharide endotoxin.
Campylobacteriosis infects humans and animals. The animal reservoir is the gastrointestinal tract of dogs, cats, and other pets that can carry the organism. Transmission of C jejuni to humans occurs by ingestion of contaminated food or water, including unpasteurized milk and undercooked poultry, or by direct contact with fecal material from infected animals or persons. The 2 types of illnesses associated with Campylobacter infections in humans are intestinal infection and extraintestinal infection. The prototype for intestinal infection is C jejuni, and the prototype for extraintestinal infection is C fetus.
Factors responsible for the diseases caused by C jejuni are not well known. Based on clinical illness, researchers have postulated the following mechanisms:
Adherence and production of heat-labile enterotoxins, inducing secretory diarrhea
Invasion and proliferation within the intestinal epithelium, leading to cell damage and inflammatory response
Translocation of the organism into the intestinal mucosa and proliferation in the lamina propria and mesenteric lymph nodes, leading to extraintestinal infections such as meningitis, cholecystitis, urinary tract infection, and mesenteric adenitis
Information on the pathogenesis of Campylobacter infections other than C jejuni is scarce. Bacteremia is more common with C fetus infection. A surface protein in C fetus inhibits the C3b binding responsible for both the serum and phagocytic resistance of the organism, making the organism resistant to the bactericidal effects of human serum. After oral ingestion, C fetus may colonize the intestinal tract, resulting in portal bacteremia. In immunocompetent hosts, the organism is phagocytosed by the reticuloendothelial cells in the liver, preventing further spread. However, in patients that have predisposing factors that might serve as a local site of infection such as a gravid uterus, bacteremia can lead to severe complications. Infants may be affected hematogenously or by ascending infection during amnionitis and premature rupture of membranes.
In the United States, 2 million symptomatic enteric Campylobacter infections are estimated per year (1% of the US population per year). Incidence in the rural population is 5-6 times higher because of increased consumption of raw milk. According to the Foodborne Diseases Active Surveillance Network (FoodNet) of the Centers for Diseases Control and Prevention (CDC), which collects data on the incidence of infection with foodborne pathogens. In 2010, 6,365 cases of laboratory-confirmed Campylobacter infections were reported in the United States with an overall incidence rate of 13.6 cases per 100,000 population; this was not a significant change when compared with the previous 2 years. Among all age groups, the highest incidence occurred among children younger than 5 years; hospitalization occurred in 927 of cases (4.6%), and 8 individuals died. In 2011, the incidence of Campylobacter infections increased by 11% compared with 2006-2008.
In developing and developed countries, continuous increases in the number of C jejuni infections has been seen, with incidence rates as high as 73 cases per 100,000 population reported.
In England and Wales, an increase of laboratory confirmed Campylobacter cases was noted, from 44,544 per year in 2004 to 64,582 per year in 2011 (provisional data 2011). Between 2004 and 2011, a 36% increase of cases occurred among children younter than 10 years, a 25% increase occurred among persons aged 10-45 years, and an 81% increase occurred among those aged 50 years and older.
The vast majority of patients fully recover from C jejuni infection within 5 days (range, 2-10 d), either spontaneously or after appropriate antimicrobial therapy. Infection with C fetus is a concern in immunocompromised patients, pregnant women, and neonates. Previously healthy patients usually recover without complications.
Campylobacter infection has no race predilection.
In England and Wales, incidence was higher in males from birth until age 17 years and in females aged 20-36 years.
Individuals of any age can be infected with C jejuni enteritis. The rate of infection differs between developed and developing countries. In developed countries, the peak attack rates are in infants younger than 1 year; a second, broader peak attack rate occurs in persons aged 20-29 years. In developing countries, symptomatic infection chiefly affects children younger than 5 years and declines with age.[13, 14] This is likely due to the development of protective immunity secondary to a high level of exposure to the organism early in life.
In contrast to the age-specific distribution of Campylobacter enteritis, the highest rate of bacteremia occurs in patients aged 69 years and older. Roughly 30% of isolates are C jejuni, 9% are C coli, and 53% are C fetus.
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