Campylobacter jejuni

Morphology

Campylobacters are bacteria that are a major cause of diarrhoeal illness in humans and are generally regarded as the most common bacterial cause of gastroenteritis worldwide. In developed and developing countries, they cause more cases of diarrhoea than, for example, foodborne Salmonella bacteria.

In developing countries, Campylobacter infections in children under the age of two years are especially frequent, sometimes resulting in death. In almost all developed countries, the incidence of human campylobacter infections has been steadily increasing for several years. The reasons for this are unknown.

Campylobacter jejuni is in a genus of bacteria that is among the most common causes of bacterial infections in humans worldwide. The name means "curved rod", deriving from the Greek campylos (curved) and baktron (rod). It has been noted that there "is wide diversity in the genus. The species are metabolically and genetically different to the extent that one can question whether one genus is adequate to house all of the species." Of its many species, C. jejuni is considered one of the most important from both a microbiological and public health perspective.

Campylobacters are mainly spiral-shaped, S-shaped or curved, rod-shaped bacteria. There are 16 species and six subspecies assigned to the genus Campylobacter, of which the most frequently reported in human disease are C. jejuni (subspecies jejuni) and C. coli. C. laridis and C. upsaliensis are also regarded as primary pathogens, but are generally reported far less frequently in cases of human disease. Most species prefer a micro-aerobic (containing 3-10% oxygen) atmosphere for growth. A few species tend to favour an anaerobic environment, although they will grow under micro-aerobic conditions also.

One effect of campylobacteriosis is tissue injury in the gut. The sites of tissue injury include the jejunum, the ileum, and the colon. C jejuni appears to achieve this by invading and destroying epithelial cells.

C. jejuni can also cause a latent autoimmune effect on the nerves of the legs, which is usually seen several weeks after a surgical procedure of the abdomen. The effect is known as an acute idiopathic demyelinating polyneuropathy (AIDP), i.e. Guillain–Barré syndrome, in which one sees symptoms of ascending paralysis, dysaesthesias usually below the waist, and, in the later stages, respiratory failure.

Some strains of C jejuni produce a cholera-like enterotoxin, which is important in the watery diarrhea observed in infections. The organism produces diffuse, bloody, edematous, and exudative enteritis. In a small number of cases, the infection may be associated with hemolytic uremic syndrome and thrombotic thrombocytopenic purpura through a poorly understood mechanism.

Studies on the pathogenesis of C. jejuni show that for this organism to cause disease, the susceptibility of the host and the relative virulence of the infecting strain are both important. Infection results from the ingestion of contaminated food or water, and the infective dose can be as low as 800 organisms. To initiate infection, the organism must penetrate the gastrointestinal mucus, which it does using its high motility and spiral shape. The 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. During infection, levels of all immunoglobulin classes rise. Of these, IgA is the most important because it can cross the gut wall. IgA immobilises organisms, causing them to aggregate and activate complement, and also gives short-term immunity against the infecting strain of organism. 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. C jejuni antigens that cross-react with one or more neural structures may be responsible for triggering the Guillain–Barré syndrome.

Pathogenesis

Studies on the pathogenesis of C. jejuni show that for this organism to cause disease, the susceptibility of the host and the relative virulence of the infecting strain are both important. Infection results from the ingestion of contaminated food or water, and the infective dose can be as low as 800 organisms. To initiate infection, the organism must penetrate the gastrointestinal mucus, which it does using its high motility and spiral shape. The 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.

During infection, levels of all immunoglobulin classes rise. Of these, IgA is the most important because it can cross the gut wall. IgA immobilises organisms, causing them to aggregate and activate complement, and also gives short-term immunity against the infecting strain of organism. 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. C jejuni antigens that cross-react with one or more neural structures may be responsible for triggering the Guillain–Barré syndrome

Campylobacter is one of the most common causes of human bacterial gastroenteritis. For instance, an estimated 2 million cases of Campylobacter enteritis occur annually in the U.S., accounting for 5–7% of cases of gastroenteritis. Furthermore, in the United Kingdom during 2000, Campylobacter jejuni was involved in 77.3% in all cases of laboratory confirmed foodborne illness. About 15 of every 100,000 people are diagnosed with campylobacteriosis every year, and with many cases going unreported, up to 0.5% of the general population may unknowingly harbor Campylobacter in their gut.

A large animal reservoir is present as well, with up to 100% of poultry, including chickens, turkeys, and waterfowl, having asymptomatic infections in their intestinal tracts. Infected chicken feces may contain up to 109 bacteria per 25 grams, and due to the installations, the bacteria are rapidly spread to other chickens. This vastly exceeds the infectious dose of 1000–10,000 bacteria for humans.

Symptoms

The prodromal symptoms are fever, headache, and myalgia, which can be severe, lasting as long as 24 hours. After 1–5 days, typically, these are followed by diarrhea (as many as 10 watery, frequently bloody, bowel movements per day) or dysentery, cramps, abdominal pain, and fever as high as 40 °C (104 °F). In most people, the illness lasts for 2–10 days. It is classified as invasive/inflammatory diarrhea, also described as bloody diarrhea or dysentery.

There are other diseases showing similar symptoms. For instance, abdominal pain and tenderness may be very localized, mimicking acute appendicitis. Furthermore, Helicobacter pylori is closely related to Campylobacter and causes peptic ulcer disease.

In patients with HIV, infections may be more frequent, may cause prolonged bouts of dirty brown diarrhea, and may be more commonly associated with bacteremia and antibiotic resistance. In participants of unprotected anal intercourse, campylobacteriosis is more localized to the distal end of the colon and may be termed a proctocolitis. The severity and persistence of infection in patients with AIDS and hypogammaglobulinemia indicates that both cell-mediated and humoral immunity are important in preventing and terminating infection.