Campylobacter jejuni (C. jejuni) bacteria, although quite sensitive to environmental conditions, produce significant illness throughout the world primarily because the human body provides ideal conditions for it to thrive. As a foundation for proving this thesis, the prevalence and incidence of C. jejuni, the structure and function of the bacteria, and control and treatment measures are explored. The methodology applied in developing this dissertation consisted of a review of selected literature on C. jejuni. The literature included professional journals, newspapers and newsletters, reports, and reference materials. This dissertation adds to the body of knowledge by furnishing a proposed flow diagram depicting the transmission of C. jejuni to humans, the effects of its transmission, and control and treatment measures.
“Yersinia, listeria, salmonella, campylobacter, shigella, and E. coli sound like evil characters in a sci-fi movie.
They are in fact bacteria commonly found in food,
and they bring the misery of food poisoning…”
The evil sci-fi movie character metaphor used by McNeil (1998) to describe various bacteria that cause gastrointestinal maladies provides a colorful opening to a discussion of one of the listed bacteria—Campylobacter jejuni, or C. jejuni. Following a brief discussion of the prevalence and incidence of C. jejuni, the structure and function of the bacteria and control and treatment measures will be discussed. With this as a foundation, the paradox of C. jejuni, specifically its fragility vis-à-vis the significant illness that it produces, will be explored. Finally, a conclusion will be presented.
According to Swerdlow (1999, citing Kist, 1985), C. jejuni was “first identified as a human diarrheal pathogen in 1973.” Maiden (2002, citing Calva, et al., 1988; Friedman, et al., 2000) writes that C. jejuni “is the most frequently reported cause of acute inflammatory gastroenteritis in industrialized countries.” In developing countries, the problem seems to be similarly prevalent. Obi (2002, citing Tauxe, 1992; Taylor, 1992; Oberhelman and Taylor, 2000) writes that C. jejuni infection “estimates in the general population in developing and developed countries are similar” with approximately 90 cases in 100,000. Watkins (2003) proposes different infection levels with reports of as many as 1,000 in 100,000 in developed countries with even higher rates in developing countries.
C. jejuni is an emerging problem. Neal (2002) claims that in the United Kingdom “laboratory reports of Campylobacter have increased steadily since surveillance began in 1977.” Brown and associates (2004) indicate that reported cases in the United Kingdom grew from 32,636 in 1991 to 56,420 in 2001. In the United States, C. jejuni is “the most frequently diagnosed bacterial cause of human gastroenteritis” (Swerdlow, 1999) affecting almost one percent of the population annually (Nachamkin, 2001). Swerdlow’s claim seems to be validated by the United States Centers for Disease Control and Prevention’s findings shown in Figure 1.
The most vulnerable groups to infection by C. jejuni seem to be younger children and young adults. According to Sheff (2001), C. jejuni “occurs most often in those ages 5 years and younger and those between 15 and 29 years.” Maiden (2002, citing Calva, et al., 1988; Friedman, et al., 2000) writes that C. jejuni is “a major cause of intestinal disease in children [of less than two] years of age in developing countries.” In developed countries, infection rates for children less than five years of age are approximately 300 cases per 100,000 (Obi, 2002, citing Tauxe, 1992) compared to an estimated 40,000 to 60,000 per 100,000 in developing countries (Obi, 2002, citing Oberhelman and Taylor, 2000; Rao, et al., 2001).
Comparison of cases of Campylobacter with other foodborne infections in the United States by month of specimen collection (Centers for Disease Control and Prevention, 1996, cited in Altekruse et al., 1999).
Campybacteriosis, which is the illness caused by C. jejuni, can occur sporadically or in outbreaks. Swerdlow (1999, citing Tauxe, 1992) writes that “most cases of human campybacteriosis are sporadic,” adding that “[o]utbreaks have different epidemiologic characteristics from sporadic infections” and that many cases occur in the spring and autumn seasons. Concerning the incidence of outbreaks, Gillespie and associates (2003) write: “Despite being the commonest bacterial cause of infectious intestinal disease in England and Wales, outbreaks of Campylobacter infection are rarely reported.” Yet, outbreaks have been reported; for instance, the following examples highlight the variety of sources giving rise to outbreaks of C. jejuni infection:
Reported cases of C. jejuni infection may not closely mirror the actual number of cases. The Philippines’ Business Daily (1998) reports that “[m]any experts believe that the incidence of this infection is much higher than reported, because people mistakenly think they have some type of stomach virus” as the symptoms do not appear for several days after ingestion of the bacteria. Gillespie and associates (2003) agree, suggesting that “outbreaks might be more common than was previously suspected, since a high proportion of cases reported other illness in the home or in the community at the same time as their illness.”
McNeil (1998), continuing her vivid description of C. jejuni and certain other bacteria, writes about the structure, function, and effects of these bacteria:
“When these food fiends run riot in the human gut they cause indescribable discomfort, with symptoms including excruciating stomach cramps, vomiting, and chronic diarrhea…The food-borne bacteria are sly opportunists, invisible to the naked eye, yet strangely photogenic when magnified under an electron microscope. They sneak up on their unsuspecting victims, quickly wreaking havoc in their bodies. Equally quickly, usually after several miserable days, the bacteria depart leaving us limp and lifeless, and deeply suspicious of food.”
Figure 2 validates McNeil’s description of C. jejuni and other foodborne bacteria as “strangely photogenic when magnified under an electronic microscope.”
Image of Campylobacter jejuni through electron microscope, showing corkscrew appearance and bipolar flagella. (Virginia-Maryland Regional College of Veterinary Medicine, n.d., cited in Altekruse et al., 1999).
C. jejuni has been described by Sheff (2001) as “comma-shaped, gram-negative rod bacteria” and by Watkins (2003) “a gram-negative, microaerophilic, thermophilic rod.” Regarding genetic structure, Stulberg and associates (2004) write: “The genome sequencing Campylobacter jejuni was finished in 2000 by the Sanger Centre. The findings show the C. jejuni genome to have 1,641,481 base pairs, containing 1,654 protein coding genes. C. jejuni is the most gene-dense bacterium so far to be sequenced, with 94.3% of the genome containing coding genes.”
Stulberg and associates (2004) state that “Campylobacter colonizes the mucosal surfaces of birds and mammals, using their mobility to survive in the mucous flow.” According to Pettipher (1998), C. jejuni “infects the intestinal tract, excreting toxins that destroy the gut mucosa.” Hulupi (2001) writes that “[t]he bacteria release toxic matter and disturb the function of the digestive system.” C. jejuni infection can be introduced to humans through a variety of sources. Sheff (2001) suggests that “consuming contaminated water, unpasteurized milk, or undercooked meat can cause infection” as can “contact with infected humans or pets.” The Philippines’ Business Daily (1998) claims that the presence of C. jejuni in “the intestinal tracts of apparently healthy cattle, turkey, chicken, and sheep…can be spread to all parts of the meat during the slaughtering process.” Swerdlow (1999) writes that infection can be attributed to drinking raw milk; handling raw, or eating undercooked, poultry; drinking untreated water; drinking unpasteurized milk; and handling infected dogs and cats. Fanning (2000), Abramovitz (2002), Ellis (2003) and others suggest many of the same sources of infection. Gillespie and associates (2003) contend that the sources of C. jejuni infection in individual cases and community outbreaks are different. They write that “[i]llness in the home was associated with consuming organic meats, having contact with a pet suffering from diarrhea, or visiting a farm in the [two] weeks before the onset of symptoms” while “[i]llness in the community was associated with the consumption of foods in restaurants or drinking unpasteurized milk.”
C. jejuni is a fragile entity. Swerdlow (1999, citing Ketley, 1997) writes: “Survival of C. jejuni outside the gut is poor, and replication does not occur readily.” Swerdlow (1999, citing Nachamkin, 1995) adds: that “C. jejuni grows best at 37 [degrees] C to 42 [degrees] C (18), the approximate body temperature of the chicken (41 [degrees] C to 42 [degrees] C)”; that “C. jejuni grows best in a low oxygen or microaerophilic environment; and that “[t]he organism is sensitive to freezing, drying, acidic conditions…, and salinity.” Confirming the sensitivity of C. jejuni, Stulberg and associates (2004) write: “Campylobacter grows best in habitats with an oxygen level lower than 5%” and add that “Campylobacter species are sensitive to salinity, freezing, and pH below five. Campylobacter has an optimal growth temperature between 37 and 42° C.”
The first line of defense in fighting C. jejuni is actually an offensive control measure: preventing ingestion of the bacteria. Swerdlow (1999) proposes control measures on the farm and in processing plants. He cites the work of Kapperud (1992) in writing that “control of Campylobacter contamination on the farm may reduce contamination of carcasses, poultry, and red meat products at the retail level.” Swerdlow suggests several farm-based methods for controlling contamination including feeding poultry chlorinated water and vaccinating chicks. During transportation and processing, bacterial counts increase dramatically, according to Swerdlow. As preventive measures, he suggests forced-air chilling, scalding, adding certain chemicals to chiller water in the presence of electrical current, using chlorinated sprays and diligently cleaning working surfaces, applying radiation, and spraying lactic acid on carcasses. During food preparation, Sheff (2001) recommends “eating only thoroughly cooked meat and using a separate cutting board for it” as well as not “drinking unpasteurized milk or untreated water.” Abramovitz (2002) recommends the following food handling steps: cook food to the recommended temperature; separate raw meats, poultry, eggs, and seafood from other foods; clean hands and food preparation surfaces with soap and hot water; and refrigerate foods until they are used.
If preventive control measures fail and infection by C. jejuni occurs, there are treatments available with the primary indicated treatment being to avoid antimicrobial agents while waiting for the symptoms to pass. Obi (2002) states that Campylobacter enteritis, which is an “inflammation of the gastrointestinal tract” (Columbia Encyclopedia, 2005), “is a self-limiting disease, and antimicrobial therapy is not generally recommended.” Swerdlow (1999, citing Blaser, 1990) writes that “[s]upportive measures, particularly fluid and electrolyte replacement, are the principal therapies for most patients.” However, Obi suggests that, in the cases where immune systems are compromised, antimicrobial agents are indicated. Engberg (2001, cited in Obi, 2002) writes that erythromycin and ciproflexin are recommended. One reason for cautiously using antimicrobial agents is the increasing worldwide resistance to these remedies by C. jejuni and other bacteria (Brigid, et al., 2000). Hope for the future may be present in the form of a human vaccine to prevent C. jejuni and other bacterial that produce gastrointestinal illness (Hagan, 2002).
The question posed in the title was: How does such a sensitive organism [as C. jejuni] cause so much disease? A summary of relevant information presented thus far provides a foundation upon which a response to the question can be formulated.
C. jejuni is truly a sensitive organism. A review of the literature revealed that the bacteria’s ability to exist outside of a narrow range of temperature, oxygen, and other conditions is poor. The optimal conditions for growth of C. jejuni include temperatures between 37 and 42 degrees Centigrade and less than five percent oxygen. Ironically, it is just these features that render C. jejuni such a serious problem. With a temperature of approximately 37 degrees Centigrade and a low level of oxygen, the human gastrointestinal system provides ideal conditions for C. jejuni to thrive.
So, in response to the question posed, the sensitive C. jejuni bacteria cause so much disease in humans because humans serve as ideal hosts.
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