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The below mentioned article provides a short note on Camplyobacter and Prophylaxis.
Introduction to Campylobacter:
Campylobacter (Greek, curved rod) is distributed world-wide has now emerged as new recent pathogen causing Campylobacter enteritis in children (acute infantile diarrhoea) and consists of C. jejuni and C. coli. They are urease negative.
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Small, flagellate, Gram-negative curved, coccoid, degenerate bacilli and exhibit the rapid darting type of motility of Vibrio cholera.
They grow best at 42°C under 5-10% CO2 on Skirrow or Butzler blood agar medium or on blood free medium—Charcoal Cefazolin Sodium Desoxycholate Agar (CCDA) medium of Bolton and produce typical grey, flat spreading moist colonies, which form an important identification characteristic of Campylobacter. They produce oxidase, catalase, H2S biochemically. C. jejuni biotype 1 do not produce H2S.
The incubation period of Campylobacter enteritis is 1-13 days. It is an acute self-limiting diarrhoeal disease mostly affecting children. It is a zoonosis (disease transmitted from animal to man through contaminated milk, food or water with cow dung). There is general malaise, headache, backache, aching limbs, dizziness, abdominal pain and seldom vomiting. First report in children in India at Ahmedabad.
Laboratory Diagnosis of Campylobacter:
Rectal swabs should be carried to the laboratory in transport medium, Cary-Blair medium. Rapid bacteriological diagnosis can be made by direct dark ground microscopy by characteristic darting motility and by colony characteristics, isolation of Campylobacter on selective media.
Treatment of Campylobacter:
Erythromycin, furazolidone, tetracycline, gentamicin are used.
Prophylaxis:
Avoidance of contamination of food or drink with cow dung from animals.
Helicobacter pylori (originally Campylobacter pyloridis) is spiral or curved organism. H. pylori on gastric mucosa can be demonstrated by Cresyl violet stain. It can be cultivated on Campylobacter medium in 3-5 days.
It is the major cause of gastritis, peptic ulcer with subsequent development into gastric cancer. The symptoms are abdominal pain, nocturnal awakening, vomiting, the presence or absence of epigastric tenderness.
Laboratory Diagnosis of Prophylaxis:
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During each examination, two biopsy specimens can be obtained from the first part of duodenum. In addition, two biopsy specimens were taken from the antral mucosa. One specimen for rapid urease test and the second for the histological assessment. Children can be considered to be infected with H. pylori if both the rapid urease test is positive and Cresyl violet stain revealed spiral organisms on gastric mucosa.
Treatment of Prophylaxis:
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Famotidine; combination of Colloidal bismuth sub-citrate and metronidazole is effective. The resolution of infection can be confirmed by the negative urease test and absence of H. pylori after treatment.
