Tetracycline for Cholera Treatment

What is Cholera

Cholera (Lat. «cholera») is an acute intestinal anthroponotic infection caused by bacteria species Vibrio cholerae; characterized by fecal-oral infection mechanism, small bowel lesion, watery diarrhea, vomiting, rapid body fluid and electrolytes loss accompanied with varying degrees of dehydration up to hematogenic shock and death.

Cholera (http://www.nhs.uk/Conditions/Cholera/Pages/Definition.aspx) usually spreads as epidemy. Endemic regions are located in Africa, Latin America, India (South East Asia).

Causes

There are more than 140 serogroups of Vibrio cholerae; they are divided into:

  • agglutinated by typical cholera O1 serum (V. cholerae O1);
  • not agglutinated by typical cholera O1 serum (V. cholerae non 01).

cholera

«Classical» cholera is caused by cholera vibrios of O1 serogroup (Vibrio cholerae O1). There are two biovars (biotypes) of this serogroup:

  1. classical (Vibrio cholerae biovar cholerae);
  2. El Tor (Vibrio cholerae biovar eltor).

According to morphological, cultural and serologic characteristics they are similar: short curved motile rods with flagellum, gram-negative aerobes, well tingible with aniline dyes, do not form spores and capsules, grow in alkaline environment (pH 7,6-9,2) at 10- 40 ° C. Cholera vibrios El Tor, unlike classical, are able to hemolyze sheep red blood cells (not always).

Each of these biotypes according to O-antigen (somatic) are subdivided into serotypes. Inaba serotype contains C fraction, Ogawa serotype – B fraction and Hikojima serotype – B and C fractions. Cholera vibrios H-antigen (flagellar) is common for all serotypes. Cholera vibrios form cholera toxin (CTX) – protein enterotoxin.

Vibrio cholerae non-01 cause choleriform diarrhea of various severity, which can also be fatal.

Pathogenesis

Infection portal of entry is gastrointestinal tract. Cholera vibrios are often die in stomach due to chlorohydric acid. The disease develops only when they pass through gastric barrier and reach small bowel, where they rapidly multiply and release exotoxin. Experiments with human volunteers showed that large cholera vibrios dose (10″ microbial cells) at some individuals caused disease and after preliminary gastric chlorohydric acid neutralization the disease could be cause after administration of 106 vibrios (i. e. 100 000 times less dose).

Cholera syndrome occurrence is connected to two substances present at vibrio:

  1. protein enterotoxin – choleragen (exotoxin);
  2. neuraminidase.

Choleragen binds with specific enterocytes receptor – ganglioside.

Neuraminidase, degrading acetylneuraminic acid residues, forms specific receptor, enhancing choleragen effect, out of ganglioside. Complex choleragen-specific receptor activates adenylate cyclase, which, together with and by means of prostaglandin stimulatory effect increases cyclic adenosine monophosphate formation (AMP). AMP regulates water and electrolytes secretion from cells into intestinal lumen through ion pump. As a result of this mechanism activation, small bowel mucous membrane begins to secrete a huge amount of isotonic fluid, which can’t be absorbed by large bowel, thus causing isotonic fluid intractable diarrhea.

Severe morphological epithelial cells changes at patients with cholera are not identified (during biopsy). Cholera toxin was determined neither in lymph nor in blood in vessels extending from small bowel. In this regard, there is no evidence that this toxin affects any other organs except small bowel. Secreted by small bowel fluid is characterized with low protein content (about 1g per 1l), contains the following amounts of electrolytes: sodium – 120 ± ± 9 mmol/l, potassium – 19 ± 9, dicarhonate – 47 ± 10, chloride – 95 ± ± 9 mmol/l. Fluid loss reaches 1 liter per hour. This results in plasma volume decrease with circulating blood amount reduction and its thickening. Fluid moves from interstitial to intravascular space which can not compensate persisting fluid protein-free blood constituent loss. Therefore haemodynamic and microcirculatory disorders rapidly occur, leading to dehydration shock and acute nephatony. Evolving on this shock background acidosis is enhanced with alkalis deficiency.

Dicarhonate concentration in faeces is twice higher than in plasma. There observed progressive potassium loss, which concentration in faeces is 3-5 times higher than in plasma. If administer sufficient amount of fluid intravenously, all violations rapidly disappear. Improper treatment or its absence leads to acute nephatony and hypokalemia. The latter can cause intestinal atony, hypotension, arrhythmia, myocardium changes. Excretory kidneys function termination leads to azotemia. Cerebral vessels circulation impairment, acidosis and uremia cause central nervous system and patient’s consciousness disorders (drowsiness, soper, coma).

Symptoms

Cholera incubation period ranges from several hours to 5 days (usually 2-3 days). According to clinical manifestations severity, determined by dehydration degree, there distinguish:

  1. slight;
  2. mild;
  3. moderately severe;
  4. severe;
  5. very severe.

There are distinguished the following dehydration degrees:

  • I degree, when patients lose fluid in volume equal to 1-3% of body weight (slight and mild form);
  • II degree – up to 4-6% fluid loss (moderately severe form);
  • III degree – 7-9% (severe);
  • IV degree of dehydration with more than 9% loss corresponds to very severe cholera form.

Currently I dehydration degree occurs in 50-60% of patients, II degree – in 20-25%, III degree – in 8-10%, IV degree – in 8-10%.

At children under age of 3 years old cholera proceeds most severe. Children suffer from dehydration much stronger. In addition, they have a secondary central nervous system lesion: there are adynamia, clonic seizures, convulsions, consciousness impairment up to coma. It is difficult to determine the initial dehydration degree. Relative plasma density due to relative large extracellular fluid volume can’t be relied on. Therefore, it is advisable to weigh children at their admission to get most reliable determination of their dehydration degree. Cholera clinical picture at children has some specific features: frequent fever, more severe apathism, adynamia, tendency to epileptiform seizures as a result of rapid hypokalemia development. Disease duration ranges from 3 to 10 days, its subsequent manifestations depend on adequate electrolytes substitution treatment. When emergency fluid and electrolyte management, physiological functions normalize quite quickly and fatal cases are rare. The main causes of patients death at inadequate treatment is hematogenic shock, metabolic acidosis and uremia due to acute tubular necrosis.

Treatment

tetracycline

Basic principles of cholera treatment are:

  • restoring circulating blood volume;
  • reducing electrolyte tissues composition;
  • affecting pathogen.

Numerous studies of the past years about cholera vibrios resistance to canadian pharmacy antibiotics showed that it was mostly pronounced towards tetracycline drugs. It was found out that minimal concentration of tetracycline, inhibiting cholera vibrios growth, was 0.6-2.5 g/ml. Similar results were obtained in researches conducted by My Canadian Pharmacy.

Tetracycline is a bacteriostatic antibiotic of tetracyclines group. Disturbs complex formation between soluble RNA and ribosome, resulting in protein synthesis inhibition.tetracycline-pellets

Tetracycline is included in WHO Model List of Essential Medicines – the list of essential medicines for basic health system, compiled by the World Health Organization.

High tetracycline efficiency at cholera treatment is based on its ability to quickly suppress vibrios development. Comparative tests of various tetracycline drugs effectiveness at cholera (chlortetracycline, tetracycline-metaphosphate and chloride tetracycline), prescribed in equal dosages, showed that most rapid stool normalization with least amount of faeces was observed at patients administrating tetracycline-metaphosphate.

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