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Vibrios, Campylobacters & Helicobacter

Dan Freeman

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Introduction

  • Vibrios, Campylobacter & Helicobacter are gram-negative rods that are widely distributed in nature.

  • Campylobacter, Helicobacter and Spirillum belong to the group of spiral, motile, Gram-negative, micro-aerophilic bacteria.

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Introduction

  • Vibrio cholerae produces an enterotoxin that causes cholera - a profuse watery diarrhoea that can rapidly lead to dehydration and death.

  • Campylobacter jejuni is a common cause of enteritis in humans.

  • Helicobacter pylori contributes to the pathogenesis of gastritis and peptic ulcers.

  • Spirillum minus causes rat bite fever, known as sodoku in Japan where it is common.

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Vibrio cholerae (Cholera)

The vibrios are among the most common bacteria in surface waters worldwide. They are curved aerobic rods and are motile, possessing a polar flagellum.

Morphology and Identification

V. cholerae is a comma-shaped, curved rod 2-4μm long. They grow well on the selective medium TCBS agar, on which they produce yellow colonies.

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VIBRIO CHOLERAE ON TCBS AGAR

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Antigens and Classification

  • V. cholerae are subdivided into serovars based on their O (lipopolysaccharide) antigens.

  • V. cholerae strains of O group 1 and O group 139 cause classic cholera. Occasionally, non-O1/non-O139 V. cholerae cause cholera-like disease.

  • The V. cholerae serogroup O1 antigen has determinants that make possible further typing; the serotypes are Ogawa, Inaba, and Hikojima. Two biotypes of epidemic V. cholerae have been defined, Classic and El Tor.

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Cholera Enterotoxin

  • Cholera toxin is the sole cause of the clinical disease, inducing enterocytes to increase secretion and loss of electrolytes (mainly Cl ions), resulting in passive water loss.

  • The toxin is heat-labile with a molecular weight (MW) of about 84,000 consisting of subunits A and B.

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Pathogenesis and Clinical picture

  • Infection results from oral ingestion of the pathogen (infective dose ≥108). They are able to colonize the mucosa of the proximal small intestine and secrete the cholera toxin. The pathogen does not invade the mucosa.

  • The incubation period is 1-3 days, depending on the size of the inoculum ingested. There is a sudden onset of nausea and vomiting and profuse diarrhoea with abdominal cramps.

  • Stools contain mucus, epithelial cells and large numbers of vibrios (“rice water” stools). There is rapid loss of fluid and electrolytes (up to 20-30 L/day), which leads to profound dehydration, circulatory collapse and anuria.

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Laboratory Diagnosis

  • Specimens for culture consist of mucus flecks from stools.

  • Smears: Dark-field or phase contrast microscopy may show the rapidly motile vibrios.

  • Culture: Growth is rapid in peptone agar, on blood agar, or on TCBS agar. Typical colonies can be picked in 18 hours.

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Therapy

  • Restoration of the disturbed water and electrolyte balance in the body is the most important measure.

  • Antibiotics (TCNs and cotrimoxazole) can be used, mainly to shorten the period of pathogen secretion.

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Epidemiology, Prevention and Control

  • Six pandemics of cholera occurred between 1817 and 1923 caused most likely by V. cholerae O1 of the classic biotype. Humans are the only source of infection and disease transmission is usually by contact with individuals who are ill, by contact with flies or contaminated water or food.

  • Control requires adequate food and water hygiene and proper disposal of sewage. In case of an outbreak, infected persons must be isolated, infectious excreta and contaminated objects must be disinfected.

  • A vaccine containing killed cells as well as attenuated live vaccine are available, providing protection for about 6months.

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Campylobacters

  • Campylobacters cause both diarrhoeal and systemic diseases and are among the most widespread causes of infection in the world.

Classification

  • Some species previously classified as campylobacters have been reclassified in the genus helicobacter.

  • The genus campylobacter comprises numerous species, among which Campylobacter jejuni, C. coli, C. lari as well as C. fetus have been observed as causative pathogens in human infections.

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Morphology and Culture

  • Campylobacters are gram-negative rods with comma, S or “gull wing” shapes. They are motile, with a single polar flagellum, and do not form spores.

  • Selective media (e.g. Skirrow’s medium) are used for culture, with incubation in an atmosphere with reduced O2 (5%) and added CO2 (10%). The colonies tend to be colourless or grey.

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Pathogenesis and Clinical picture

  • C. jejuni produces an enterotoxin as well as a number of cytotoxins. It causes a form of enterocolitis with watery, sometimes bloody diarrhoea and fever. The incubation period is 2-5 days.

  • C. fetus has been implicated as a pathogen in endocarditis, meningitis, sepsis, peritonitis and salpingitis especially in the elderly or immunocompromised.

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Laboratory Diagnosis

  • Specimens: Diarrhoeal stool is the usual specimen.

  • Microscopy: Gram-stained smears of stool may show the typical “gull wing” shaped rods. Dark-field or phase contrast microscopy may show the typical darting motility of the organisms.

  • Blood Culture: Organisms may occasionally be recovered from blood cultures using selective media, usually from immunocompromised or elderly patients.

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Therapy, Epidemiology �and Control

  • Severe infections are treated with macrolides or quinolones.

  • Campylobacter enteritis resembles other acute bacterial diarrhoeas, particularly shigella dysentery.

  • The source of infection may be food (e.g. milk or undercooked poultry) or contact with infected animals or humans and their excreta.

  • There are no specific preventive measures.

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Helicobacter pylori

  • Helicobacter are spiral-shaped gram-negative rods.

  • H. pylori is associated with antral gastritis, duodenal (peptic) ulcer disease, gastric ulcers, gastric adenocarcinoma.

  • Other Helicobacter species that infect the gastric mucosa exist but are rare.

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Morphology & Identification

  • H. pylori are similar to campylobacters. They are spirally shaped, Gram-negative rods with lophotrichous flagellation and are actively motile.

  • Cultures from stomach biopsies are grown on enriched and selective media under micro-aerobic conditions for 3-4 days.

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Pathogenesis and Clinical picture

  • H. pylori occurs only in humans and is transmitted by the faecal-oral pathway.

  • The pathogen colonizes and infects the stomach mucosa resulting in an acute gastritis, the course of which may or may not involve overt symptoms.

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Laboratory Diagnosis

  • Gastric biopsy specimens can be used for histologic examination or minced in saline and used for culture.

  • Blood is collected for determination of serum antibodies.

  • Stool samples may be collected for H. pylori antigen detection.

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Therapy & Epidemiology

  • Ulcer and/or gastritis patients can be treated successfully with a triple combination therapy with a proton pump blocker (e.g. omeprazole), metronidazole and clarithromycin for 7 days.

  • Transmission is by the faecal-oral route. H. pylori occur worldwide.

  • Generalized contamination of the population begins in childhood and may reach 100% in adults especially in areas with poor hygiene.