THE CONCEPT OF ENTEROTOKSIGEN AND ENTEROINVAZIV DIARRHEA. nSHIGELLOSIS, SALMONELLOSIS, CHOLERA. FIRST AID.

 

SHIGELLOSIS (DYSENTERY)

 

Shigellosis is general infectious disease of human, caused by bacterium nof genus Shigella.

Shigellosis is characterized by principal damage of mucous membrane of ndistal section of the large intestine. The disease is accompanied by symptoms nof general intoxication, abdominal spastic pain, frequent watery stool with nadmixture of mucus and blood, and tenesmus.

 

Historic reference

The term shigellosis was used by Hippocrates to indicate a conditiocharacterized by frequent passage of stool containing blood and mucus naccompanied by straining and painful defecation.

In 1898 Shiga conclusively demonstrated that a bacterium was present ithe stools of many patients with shigellosis and that agglutinins could be ndemonstrated in the serum of the infected patient. Two years later, Flexner nfound a similar but serological different organism in stool of other patients nwith shigellosis acquired in Philippines.

http://www.cdc.gov/nczved/divisions/dfbmd/diseases/shigellosis/

Etiology

The agents of shigellosis are regarded to genus Shigella, family Enterobacteriacea. nThere are approximately 50 serotypes of Shigella.

According to modern international classification genus of Shigella is ndivided into  four groups: group A (Sh. Dysentery), group B (Sh. nFlexneri), group C (Sh. Bojdii), group D (Sh. Sonnei). Each ngroup is divided into serologic types and subtypes.

All Shigellas are nsimilar morphologically. They are small gram-negative rods, nonmotile and nnonencapsulated. Shigellas are facultative anaerobias. They grow well othe simple nutritive mediums. Shigella contain thermostable somatic nO-antigen, including group and standard antigens.

Depending on character of toxinoformation Shigella are ndivided into two groups. Shigella Grigoriev-Shiga’s are treated to the nfirst group. They produce strong exotoxin, having protein’s origin, and also nendotoxin. All other types of Shigella (Flexneri, Sonnei) are ntreated to the second group, they produce only endotoxin. Endotoxin consists of nproteins and lipopolysaccharide. Protein part of endotoxin and exotoxin have nexpressive neurotropic action. Endotoxins has enterotropic action.

Epidemiology

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The sources of infection are ill patients, persons in period of nreconvalescence and bacteriocarries. The patients with acute shigellosis are nespecially dangerous.

The  patients  with  acute nshigellosis discharge  the  agent  during all  period  of  the  disease, nespecially  during  period  of  expressive  colitic  syndrome. The  persons  nwith  obliterated, light  forms  of  the  disease  are dangerous too. These  npersons  don’t  address  for  medical help  and  don’t  receive  treatment. nBecause, these “atypical” cases  of  acute shigellosis have  predominant nepidemiological  meaning. The  patients  with  chronic shigellosis are  ndangerous  for  other  persons, especially  in  the  period  of  aggravation.

The  mechanism  of  the  transmission  of  the  infection  nis  fecal-oral. The  transmission  of  the  infection  is  realized  through  ncontaminated  food-stuffs  and  water. Infection   of  food-stuffs, water, ndifferent  objects  happens  due  to  direct  contamination  by  infected  nexcrements, through  dirty  hands  and  also  with  participation  of  flies.  nThe  factors  of  transmission  have  leading  meaning  in  epidemiology  of nshigellosis. Depending on  factors  of  transmission  there  are  the  next  nways  of  contamination –  contact, alimentary  and water. Now, the  nalimentary  way  has  more  important  meaning.   Contamination  over  nfood-staffs  may  be  through  contaminated  vegetables  and  berries  with  ninsufficient  processing  before  use. Food-stuffs,  prepared  for  use  have  nthe  most  important  meaning  in  transmission  of  the  infection (milk, milk nproducts, especially, sour cream, meat stuffing  and  other  meat  products, nbread, soft  drinks, fruits, vegetables.

The  susceptibility  of  human  is  nhigh. It  doesn’t  depend  on  sex  or  age. Shigellosis  occurs  as  in  ninfants  as  in  seniors. However, the  morbidity  of  adult  population  is  nlower  than  children  of  early  age.

Shigellosis is  characterized  by  nseasonal  spread  as  the  other  intestinal  infections. It  is  registered  nmore  frequently  in  summer  and  autumn.

 

Pathogenesis

Pathogenesis of shigellosis is complicated. It is studied insufficiently. nIn some cases the agents perish in the upper section of the gastrointestinal ntract under the influence of acidic conditions. In other cases Shigella nmay pass through intestine, and it is excreted into environment without reply nof the macroorganism.

Diverse theories of pathogenesis of shigellosis were pulled out idifferent years. The next theories are known:

1.                      nBacteriemic ntheory. Reproduction of the agent in the blood is the basis of pathogenesis of nshigellosis according to this theory.

2.                      nToxico-infections nShiga’s-Brauer’s theory. Many positions of this theory don’t lose one’s owmeaning in modern ideas about pathogenesis of shigellosis.

3.                      nAllergic ntheory. According to this theory, shigellosis is general allergic infectiodisease.

4.                      nNervous-reflexious ntheory. According to this theory the damage of nervous system has leading nmeaning in pathogenesis of shigellosis.

5.                      nTheory nof intracellular parasitism. According this theory, all features of the  nshigellosis course are connected with parasitism of Shigella in the epithelium nof mucous membrane of distal section of the  large intestine.

In  was  established  by  investigations  of  the  last  nyears  that  secondary  immune  insufficiency  plays  considerable  role  in  npathogenesis  of  shigellosis. At present time it is known that development and ncourse of the different forms of shigellosis is connected with some factors. nThere are functional state of the organism; interaction of the human’s norganism, agent and environment; biological properties of the agent n(toxigenecity, invasiveness, fermentic activity  and other).

Bacteremia of nshort duration may be observed in decreased resistance, in entering of the nlarge doses of the agent. However, bacteremia hasn’t essential meaning ipathogenesis of shigellosis. Bacteremia is marked only in one third of the npatients with Grigoriev’s-Shiga’s shigellosis.

Toxins, which are absorbed from the nintestine, play an important role in pathogenesis of shigellosis. At first, ntoxins influence directly on the mucous membrane of the intestine and nsubstances, disposing under mucous membrane (nervous endings, vessels, nreceptors). Second, toxins are absorbed and influence to different sections of ncentral nervous system. Involvement of small intestine in pathological process nfrom the first days of the disease is explained by toxinemia (violation of its nmotile, absorbing and digestive functions). The evidence of toxinemia is ndelivery of endotoxin into patient’s blood serum from the first days of the ndisease and its delivery into urine.

Exotoxin of Shigella nGrigoriev’s-Shiga’s and protein part of endotoxin possesses significant nneurotoxic action. Neurotoxins influence on the central nervous system and nperipheral gangiums of vegetative nervous system. It is manifested by severe nintoxicative syndrome and violation of all types of the balance of substances.

Lipopolysaccharide npart of endotoxin damages principally mucous membrane of distal section of nlarge intestine, and in a less degree, other sections of gastrointestinal ntract. It possesses cytotoxic action and causes activation of adenylcyclase.

Activation of nadenylatecyclase leads to accumulation of cyclic 3-5 adenosine-monophosphates, nincreased secretion of electrolytes and water. The violation of water – nelectrolytes balance is observed in gastrointeritic variants of acute nshigellosis course. It is necessary to allow for degree of dehydration of the norganism. Dehydration of II-III degree develops in severe course of ngastroenterocolitic and gastroenteritic variant of acute shigellosis. In severe n(hypertoxic) form it may be development of hypovolemic shock and acute renal ninsufficiency.

Shigella toxins cause nsensibilization of the mucous membrane of the intestine, render damaging actioon it with development of inflammatory changes and erosions formation and nulcers in severe course of the disease.

Toxistimulates discharge of biological active substances (histamine, serotonine, nkinines, prostaglandines) into blood, causes violation of microcirculation of nthe blood in the intestine’s wall, increases intensity of inflammatory process nand disorders of functions of the intestine (motorics, absorbtion, secretion).

The violatioof innervation of the intestine, microcirculation, electrolytic balance and ninflammatory changes of mucous membrane are manifested clinically by sharp nspastic pains in the stomach. Spasms of separate sections of the intestine lead nto excretion of scanty stool (“fractional stool”). Spastic shortening of the nmuscles of sigmoid and rectum cause fecal urgency and tenesmus.

Allergic nfactor plays definite role in pathogenesis of shigellosis. Pathological process ndevelops in large intestine after preliminary sensibility. However, it was nshown experimentally, that shigellosis is not typical allergic disease.

However, intracellular parasitism was nnot confirmed due to biopsy of mucous membrane of the intestine in the patients nwith shigellosis. It  is  not  expected, that  phenomenon  of  intracellular  nparasitism  plays  certain  role  in  shigellosis  too.

In shigellosis, the  invasion  of  Shigellas  ninto  epithelial  cells  is  observed  in  large  intestine,  principally in  nrectum. It  is  caused  by  comparatively prolonged  accumulation  of  nintestinal  content, toxins  and  bacteriums  in  the  large  intestine. They  ncreate  favorable  conditions  for  invasion  of  the  agent  into  nepitheliocytes.  It  is  promoted  by  intestinal  dysbacteriosis  too. nIntestinal  dysbacteriosis  develops  inrarely  under  influence  of  nantibioticotherapy. This  therapy  causes  destruction  of  considerable  part  nof symbiotic flora.

The  disease  may have  prolonged  nor  chronic  course  due  to  addition  of  supplementary  factors  of  nchronic  process. The  cases of formation  of  chronic shigellosis  develops ndue to unfavorable  premorbid  state, delay  of  macroorganism  functions  nreplacement, decreased  activity  of  immune  system.

The  recovery  of  the  patients  is  nprolonged  in  presence  of  damages  at  any  portions  of  gastrointestinal  ntract (defects  of  masticatory  apparatus, anomalies  of  intestinal  tube, ngastritis, ulcerous  disease, appendicitis, pancreatitis, hepatitis, ncholecystitis); presence  of  supplementary  diseases (tuberculosis, nbrucellosis, malaria, helminthiases); state  of  endocrine  system, dysbalance  nof  vitamins. The  factors, promoting  to  prolonged  and chronic course of  nthe  disease, are  late  hospitalization  of  the  patients, incorrect  ntreatment, violation  of  alimentary  regime  after  discharge  of  the  npatients  from  the  hospital.

 

Pathological anatomy

In shigellosis pathomorphologic changes are revealed, generally, idistal portion of the large intestine (sigmoid, rectum). There are 4 stages of ninflammatory changes:

1.                      nacute ncatarrhal inflammation (Fig.1);

2.                      nfibrinous nnecrotic (Fig.2);

3.                      nulcerous nand follicle-ulcerous (Fig.3, 4);

4.                      nstage nof formation of scars.

 

Fig.1. Acute ncatarrhal proctosigmoiditis

 

Fig.2. Fibrinous-necrotic nproctosigmoiditis

 

Fig.3. nUlcerous colitis

 

Fig.4. nFollicle-ulcerous colitis

 

At present ntime fibrinous-necrotic and ulcerous damages occur rarely. Catarrhic  ninflammatory process is observed more frequently. It is confirmed by data of npathologoanatomic investigations due to biopsy of rectum. Catarrhic  ninflammation is characterized by edema, hyperemia of mucous membrane and submucous nlayer of rectum. Small hemorrhages and erosions are observed in the mucous nmembrane in the part of the patients. In rectoscopy mucous or nmucous-hemorrhagic exudation is revealed on the surface of mucous membrane and nin the intestine.

Imicroscopical investigation disorders of vessels are marked: increased npermeability, local hemorrhages. Edema of strome and basal membrane leads to ndystrophic changes of epithelium, in severe cases – to formation of ulcers and nerosions. Hyperproduction of mucus is typical.

Fibrinous-necrotic nchanges are manifested by dirty, gray and dense coats on mucous of the nintestine. The membranes consist of necrotic tissue, leukocytes and fibrin. nNecrosis may achieve submucous and muscleous and fated submucous layer. nPurulent damages and necrosis lead to formation of ulcers. In shigellosis nulcers are superficial with dense borders.

The nregeneration of epithelium begins on the 2-3 day of the disease in acute phase nof catarrhic inflammation. However, complete anatomical recovery may be on 4-5 nmonth after discharge the patient from the hospital even in mild course of nshigellosis. Regeneration comes slowly in the destructive changes in the nintestine, and disorders of vessels are preserved for a long time. Regeneratiois combined frequently with focuses of inflammatory changes. In chronic nshigellosis the morphological changes are characterized by multiple forms and nflabby duration of inflammatory process.

 

Immunity

In shigellosis postinfectious specific immunity is shaped and ntyped-specific. The investigations of humoral immunity revealed dependence of nthe level of blood serum immunoglobulins of the patients with shigellosis from ngravity of the disease, kind of the agent, and also, from treatment. Antibodies nplay essential role in execution of functions of phagocytes. However, presence nof antibodies caot be used for rendering of diagnosis and for estimate of ncomplete sanation of the organism from the pathogen. In shigellosis humoral nfactors of immunity preserve the meaning only during one year.

Immunological  nexamination  reveales  depression  of  the  tests  T-system  of  immunity  nwith  different  course  of  acute shigellosis, which  is  more  expressive  nin  the  patients  with  severe, moderate and  lingering  course  of  the  ndisease.

Decrease  of  nthe  tests T-system  of  immunity  is  appearance  of  short  duration. It   nwas  mentioned  a considerable  decrease  of  functional  activity  and  nquantity  of  T-lymphocytes  in  the  patients  with  lingering  course  of nshigellosis   and  in  chronic  form  of  the  disease.

Investigations  of  subpopulations  of  T-  and  B-lymphocytes  were  an  nimportant  stage  for  deciphering  of  violation  of  immune  system  ishigellosis. These  data  allow  to  establish  the  most  important  links  of npathogenetic  process. Corrections  of  these  links  may  be the most  nperspective.

Detailed  analysis  of  subpopulations  of  immune  system  had proved  nthe  presence  of  secondary  immune  deficiency  in shigellosis. So, decrease  nof  T-supressors  is  observed  in case of  moderate  and  severe  course  of  nacute shigellosis. In  chronic  form  of  the  disease  the activity  of  nT-supressors increases, but  the  level  of  T-helpers decreases.

However, the  nfactors  of  cell  immunity  must  be  estimated according to  humoral  and  nespecially,  local  immunity. It  is  possible, that  absence  of  the local  nimmune  reaction  is  a  risk factor  of  lingering, chronic  forms  of  the  ndisease  development  and  also  for  postdysenteric  colites.

The  local  nimmune  response  of  lymphoid  tissue  of  intestine  is  promoted  by  nantibodies – forming  cells  of  mucous  membrane-produced   antibodies  of  nclasses  IgA, IgG, IgM. The  class  of  IgA  has  the  leading  role  in  the  nprotection  of  the  organism.

Thus, the nsecondary immune deficiency in patients with different forms of shigellosis is nconnected in general with violation of regulative and effectoric links of nimmune system. The  causes  of  secondary  immune  deficiency  development  is  ninhibitory  influence  of  antigenic-toxic  complexes  of  the  agent  at  nimmune  system in  infectious  diseases.

 It  is  known, that  endotoxinemia  is  one  of  the  mechanisms  of  npathogenesis  of shigellosis. Toxins  of  the  agent  render  depressive  ninfluence  on  hemopoesis, phagocytosis and  cause  the  disorder  of  nmicrocirculation. Correlation  is  marked  between  degree  of  intoxication, nlevel of depression  of  cell  immunity  and  natural  resistance  of  the  norganism.

The  study  nof  different  cells  populations, their  metabolic  activity  allow  to  ndetermine  their  role  in  different   forms of shigellosis. These  ninvestigations  give  a  possibility  of  application  of  basic  regulation  nof cell’s  functions  with use  immunocorrecting  therapy  for  preventation  nof  the  formation  of  lingering, chronic  forms  of  the  disease and npostdysenteric  colites. 

There are the next clinical variants of acute shigellosis:

1.                      ncolitic nvariant;

2.                      ngastroenterocolitic nvariant;

3.                      ngastroenteric nvariant.

Depending on gravity of the course of nthe disease there are mild, moderate and severe course of shigellosis, and  nalso  carriers.

 

Clinical nmanifestations

http://www.nlm.nih.gov/medlineplus/ency/article/000295.htm

Colitic symptomocomplex is typical for shigellosis. nIncubation period lasts from 2 till 5 days, rarely – 7 days.

Mild course. Onset of the disease is acute. The temperate pains nappears in the lower part of the stomach, principally, in the left iliac area. nThese pains precede act of the defecation. Tenesmus are observed in some npatients. Stool is from 3-5 till 10 times a day. It contains mucus, sometimes – nblood. Temperature is normal or subfebrile. Catarrhic  inflammation of mucous nmembrane is observed at rectorhomanoscopy, sometimes erosions and hemorrhages.

Moderate course. Onset of the disease is acute or with short prodromal nperiod. It is characterized by weakness, malaise, discomfort in the stomach. nThen, spasmatic pain appears in the lower part of the stomach, tenesmus. At nfirst, stool has fecal character. Then, mucus and blood appear in stool. Stool nloses fecal character and has appearance of “rectal spit” (excretion of scanty nstool – “fractional stool”), with mucus and blood. Stool is accompanied by nfecal urgency and tenesmus. Stool is from 10-15 times a day.

In patients with medium nserious course of acute shigellosis temperature increases up to 38-39 °C for  2-3  days. Subfebrile  temperature is possible. The patients complain of weakness, nheadache. It may be collapse, dizziness. The skin is pale. Hypotonia,  relative ntachycardia are observed. Tenderness and condensation of sigmoid are revealed. nIn the peripheral blood leukocytosis and temperate neutrophylosis are observed. nIn  coprocystoscopy erythrocytes (more then 30-40 in the field of vision) are revealed. In rectorhomanoscopy diffusive catarrhic inflammation, local nchanges (hemorrhages, erosions ulcers) are revealed. In patients with moderate ncourse of acute shigellosis functional and morphological restoration may be nprolonged – till 2-3 months.

Severe course. Onset of the disease is acute. Temperature is nincreased up to 39 ˚C and higher. The patients complain of headache, harsh nweakness, nausea, something vomiting. Strong abdominal spasmodic pains, nfrequent stool with smaller volume “without account”, with mucus and blood are nmarked.

There are hypotonia, harsh tachycardia, breathlessness, skin cyanosis. nHarsh tenderness at the left iliac area, especially in the area of sigmoid are nmarked during palpation of the stomach. It is possible pasesis of intestine. nThere are expressive leukocytosis neutrophylosis with shift to the left. ESR is naccelerated.

During microscopical examination of stool erythrocytes are marked through nthe field of the vision. In rectorhomanoscopy infusive  catarrhic or fibrinous ninflammation, presence of the local changes (erosions, ulcers) are marked. The nfunctional and morphological restoration of intestine is longer than 3-4 months nin patients after colitic variant of acute shigellosis.

Gastroenterocolitic variant of shigellosis. The principal feature of nthis variant of the acute shigellosis course is acute impetuous onset of the ndisease after short incubation period (6-8 hours). More frequent way of the ntransmission of the infection is alimentary. The factors of transmission are nmilk, milk products and other.

Intoxicative syndrome and symptoms of gastroenteritis are observed in the ninitial period. The manifestations of enterocolitis predominate in the period nof climax.

There are mild, moderate and severe course of gastroenterocolitic variant nof acute shigellosis. During estimate of the disease course gravity it is nnecessary to allow for not only degree of intoxication and damage of ngastrointestinal tract, but also degree of dehydration, because repeated nvomiting and plentiful diarrhea are observed. It may lead to dehydration of nI-II-III degree.

Gastroenteritic variant of shigellosis. The principal feature of nthis variant of the acute shigellosis course is predominance of clinical nsymptoms of gastroenteritis and presence of certain degree dehydratiosymptoms. Nowedays, besides clinically distinct sings of the disease, lingering nand obliterated course of shigellosis is observed. Obliterated course is ncharacterized by insignificant clinical manifestations. The great ratio of the npatients do not apply to physician. Careful bacteriological examination of the npatient with different gastrointestinal disorders of unknown etiology has large nmeaning for correct diagnostics. In these patients catarrhic inflammatory nchanges of mucous membrane of distal portion of rectum is revealed in the nmajority of cases during rectorhomanoscopy.

Clinical recovery comes through 2-3 weeks in the majority of the patients nwith uncomplicated course of all variants of acute shigellosis. Complete nfunctional and morphological restoration of gastrointestinal tract happens i1-2 months and later. Relapses may arise in some part of the patients. The nfactors, promoting to relapses of the disease are the violation of diet, nalcohol use, incorrect therapeutic tactics. The disease may have lingering ncourse. Insufficient reactivity of the organism, sharp decrease of cell nimmunity in acute period of the disease promote to lingering course of nshigellosis.

Lingering course of shigellosis. Shigellosis is estimated as nlingering, if clinical manifestations of the disease are observed over 3-4 nweeks. Declination to lingering course of the disease depends on gravity of the ncourse of shigellosis in acute period. Colitic variant of severe course of nacute shigellosis has prolonged course more frequently than moderate variant. nThe period of functional and morphological restoration of the intestine is over n3 months. In some patients lingering course is manifested only by persistent nbacterioexcretion. Bacterioexcretion is combined with prolonged inflammatory nprocess in rectum.

Bacterioexcretion. dysfunction of intestine is absent nat the period of examination and preceded 3 months in presence of nbacterioexcretion (subclinical bacterioexcretion) or excretion of Shigella nafter clinical recovery (reconvalescent excretion) in this form of infectious nprocess.

 

Diagnosis

The principal methods of diagnostics of shigellosis are bacteriological nand serological methods of investigation.

Excretion of coproculture of Shigella is more reliable method of nconfirmation of diagnosis of shigellosis. It is necessary to take the material nfor bacteriological investigation before beginning of the treatment.

Diagnosis may be confirmed by serological methods. Reaction of indirect nagglutination with standard erythrocytic diagnosticum is used more widely. nDiagnostic titer is 1:200 with increase of titer in 7-10 days.

Treatment

http://emedicine.medscape.com/article/182767-medication

The Complex of treatment nis indicated, which depends on features of disease. In the first days the diet n№4, and diet №2 (till clinical convalescence) are indicated.

At mild current of shigellosis etiotropic agents are not applied, at ndisease of average degree of gravity use basically preparations of nNitrofuranes: Furazolidon, Nifuroxasid 0.1 gr. 4 times per day. Use derivatives nof 8-oxyquinoline – Enteroseptol, Intestopan, among other groups of npreparations – Intetrix, Nalidix acid, Ftalazol. At ambulatory treatment of nshigellosis with moderate stage of gravity Sulfanilamid preparations of prolonged naction are indicated – Phthazin, Sulfadimethoxin.

In case of severe shigellosis current use antibiotics – Ampicillin or a nPolymyxin; when there is no effect – Ciprofloxacin or Ofloxacin in combinatiowith Gentamicin or Cefazolin are prescribed. Duration of course of etiotropic ntreatment at moderate current of shigellosis is 2 – 3 days, at severe case it nlasts  not longer than 4 – 5 days.

Solution of Regidron, in severe cases Quartasol, Lactosol are applying nper os with the purpose of desintoxication and rehydratation. For the nadsorption of bacterial toxins and metabolites from the intestine lumen and for ntheir subsequent removing from the organism Enterodes, coal microspherical nsorbents, Sillard P, Smecta are used. Rectal pollination with Sillard P in a ndose 6 gm (1 – 3 procedures) is effective. There are proved Methyluracil, nPentoxyl, Thymalin as natural factors of nonspecific protection of the organism nlysozyme and stimulators of regeneration. Calcy gluconate, Dimedrol, Suprastin, nTavegil is indicated as pathogenetic treatment.

According to nparameters of coprocytogram use mono or polycomponental fermental preparations. nAt presence of plenty of fat drops in feces Pancreatin, Pancitrat, Pancurmen, nand at detection of cellulose, Amyl, muscular fibers – Pansinorm, Festal, nMezym-forte, Abomin, Vobensim are applied.

There are indicated widely vitamins preparations, these are  ascorbic nacid, nicotinic acid, Thiamin chlorid, Riboflavin,  Pyridoxine  hydrochloride, nCalcy Pangamat, folic acid, Rutin. It is better to use per os the balanced nvitamin complexes – Dekamevit, Glutamevit.

Collibacterin, Bifidumbacterin, Bificol, Lactobacterin, Bactisubtil, nLinex, Hilac forte, α – bacterin, Enterole-250 are indicated for eliminatioof intestinal dysbacteriosis and restoration of the normal biocenosis. Course nof treatment is 2 weeks and longer.

Collectings of herbs and fruits of a bilberry, mint peppery, knot-herb nordinary, camomiles medicinal, herbs of a yarrow, centaury are helpful nordinary. Collecting with the shepherd’s bag ordinary, grasses of St.-Johns nwort are effective at hemocolitis. Fermentative and putrefactive processes nreduces at lingering colitis, that is why collecting of grass of a sage-brush, na horsetail field, grasses of a yarrow ordinary, roots of snakeweed are  napplied.

Broths and juices of herbs, oil of dog rose for microclysters after a ncleansing enema, 0,5 % solution of a colloid silver as medical clysters, ninsufflations of Oxygen are used locally for stimulation of reparative nprocesses in the mucosa of colon.

Prophylaxis

Prophylaxis of shigellosis includes complex of measures, directed to nrevealing of the source of infection, interrupting the ways of transmission, nincreasing     of the organism resistance. Keeping the rules of personal nhygiene and rules of food’s cooking plays the principal role in prophylaxis of nthe disease. Sanitary education of population has an important meaning ishigellosis  prophylaxis too.

 

 

Salmonellosis

Salmonellae are widely dispersed iature, being found in the in the ngastrointestinal tracts of domesticated and wild mammals, reptiles, birds, and ninsects.

May present clinically as ngastroenteritis, enteric fever, a bacteremic syndrome, or focal disease. Aasymptomatic carrier state may also occur.

http://www.cdc.gov/salmonella/

Historic reference

The  term  “Salmonellosis”  unites  na  large  group  of  diseases, caused  by  multiply  serotypes  of  bacteriums  nfrom genus Salmonellae (more than 2000).

Sallmonellae are nnamed for the pathologist Salmon who first isolated S. cholerae suis from nporcine intestine. The nantigenic classification or serotyping of Salmonella used today is the result nof study of antibody interactions with bacterial surface antigens by Kauffmaand White in the 1920s to 1940s. Ames and coworkers in 1973 reported the ndevelopment of the test that uses S.typhimurium auxotrophic mutants to ntest the mutagenic activity of chemical compounds.

Salmonellosis is disease of animals nand humans. It is characterized by essential damage of gastrointestinal tract, nand more rarely by typhus-like or septicopyemic duration.

Etiology

http://www.onlinemedicinetips.com/disease/s/salmonella/Etiology-Of-Salmonella.html

Salmonella are nnon-spore-forming gram negative rods of the family Enterobacteriaceae. nSalmonella are motile by peritrichous flagella. Salmonella strains demonstrate nsufficient differences in biochemical reactions, antigenic structure, host nadaptations, and geographical distribution to be grouped into 10 distinct nsubgroups, which have been variously designated in proposed taxonomic schemes. nVirtually all strains isolated in clinical laboratories and implicated idisease in humans (more than 700 serotypes) (Fig.5).

 

Fig.5. nLactose-negative colonies of salmonella growing on MacConkey agar

 

Like other nenterobacteria, salmonella has somatic (0) antigens, which are nlipopolysaccharide components of the cell wall, and flagella (H)  antigens, nwhich are proteins. There  may  be  detached  some  serological  groups  on  nthe  basic of  the  differences  in  structure  of  O-antigens. Salmonella  npreserve  viability  in  external environment  for  a  long  time: in  water – 11-120 days, in  the  nsea  water – 15-27 days, in  soil – 1-9 months , in  sausage products – 60-130 ndays, in  the  eggs, vegetables  and  fruits  till  2,5 months. The  optimal  ntemperature  for  reproduction is  35-37 °C. There  are  serological  groups A, B, C, D, E  and  other. n

Salmonella can be differentiated from other Enterobacteriaceae non the basis of certain biochemical reactions, including fermentation reactions nwith specific sugars.

Salmonella organisms grow readily on simple media in aerobic or nanaerobic conditions. Cultures of specimens that are normally sterile, such as nblood, joint fluid, or cerebrospinal fluid, can be done on ordinary media such nas blood agar. Excretions or secretions, such as feces or sputum, which have nhigh concentrations of  other microorganisms, are usually grown on selective or ndifferential media, such as bismuth sulfate agar or desoxychlorate  agar, which ncontains inhibitors of growth of non-pathogenic organisms of the normal flora.

Epidemiology

http://www.safe–poultry.com/salmonellaepidemiology.asp

Animals  suffering  from  primary  or  secondary  salmonellosis, water   nswimming  birds and  also  human-sick  or  carries are the  main  sources  of ninfection    in  salmonellosis. Mechanism  of  transmission  of  infection  is  nfecal-oral. The factors  of  the transmission  of  the infection  are  nfood-stuffs  of  animal  origin  and  other  products  which  are polluted  by nexcretions  of  animals  and  humans. The  promotive  factors  are  violation  nof  the  preservation  and  preparing  of  the  food  and  also sanitary.

The  diseases occur  as  separate  sporadic  cases  and  as  outbreaks. nSusceptibility  of  human depends  from  the  premorbidal state  of  the  nmacroorganism and  from  the  quantity  and  variety (serotypes)  of   nSalmonella.

Salmonella are primarily pathogens of lower animals. The nreservoir of infection in animals constitutes the principal source of nnontyphoidal Salmonella organisms that infect man, although infectiomay be transmitted from person to person, Salmonella have been isolated nfrom almost all animals species, including poultry (chickens, turkeys and nducks), cows, pigs, pets (turtles, cats, dogs, mice, guinea pigs and hamsters), nother birds (doves, pigeons, parrots, starlings, sparrows), sheep,  seals, ndonkeys, lizards and snakes.

The most accurate information on sources of humaSalmonellosis is derived from studies of outbreaks. Poultry (chickens, turkeys, nducks) and poultry products (primarily eggs) are the most important sources of nhuman infection and are estimated to be responsible for about one-half of the ncommon – vehicle epidemic. Salmonella in feces of infected hens may contaminate nthe surface of egg shells or penetrate into the interior of the egg through nhairline cracks. In hens with ovarian infection, organism may gain access to nthe yolk. Meat, especially beef and pork, are quite often implicated, naccounting for about 13 % of nthe outbreaks,  and dairy products, including raw and powdered milk account for nabout 4 % of the epidemics.

Cross – infection with spread by person – to – person is nresponsible for virtually all the outbreaks ieonatal nerseries  and ipediatric wards and is important in many outbreaks among hospitalized adults.

The stage is set for cross-infectiowhen Salmonella are introduced into the hospital by admission, or for example, na patient with acute enterocolitis or as asymptomatic carrier with other  nmedical problem or by the introduction of a contaminated common- course nvehicle. Hospital personnel then may carry infection on hands or clothing from npatient to patient; in some cases fomites (dust, delivery room, furniture), may nbe implicated in transmission. Hospital personnel who are excreting Salmonella nin stools may also occasionally transmit infection to patient.

Pathogenesis

The development of disease nafter ingestion of Salmonella is influenced by the number and virulence of the norganisms and by multiple host factors.

A large number of Salmonella  nmust be swallowed in most instances to produce disease in healthy human being. nHowever, in the event of infection with unusually virulent organisms or ipatients with reduced resistance, symptomatic infection may result from nextremely small inocula. Ingested organisms pass from the mouth to the stomach. nIn the stomach  Salmonella are exposed to gastric acid and low PH, which nreduce the number of viable organisms. Most  Salmonella are perished nrapidly at 2,0 PH, which is readily achieved in the normal stomach. Viable nbacilli that survive then pass into the small intestine, where the organisms nmay be further reduced iumber or eliminated entirely. The antimicrobial  nactivity observed in the small bowel is related at least in part to the normal nmicrobial flora of the intestine, which elaborate short-chain fatty acids and nperhaps other substances capable of killing or inhibiting growth of Salmonella. nStudies in animals have shown that the increased susceptibility to Salmonella ninfection produced by administration of antibiotics rapidly reverts to normal nwith reestablishment of the normal intestinal flora.

Salmonella that survive the nantibacterial mechanisms in the stomach and upper small bowel may multiply ithe small intestine. Multiplication of Salmonella in the intestinal ntract may be asymptomatic, associated only with transient excretion of organism nin stools, or symptomatic, associated with clinical manifestations of either nenterocolitis (acute gastroenteritis) enteric fever or bacteremia.

Blood stream invasion, nwhich occurs with variable frequency, may lead to localization of infection and nsuppuration at almost any site.

Local factors in the stomach and nupper intestinal tract are important determinants of the disease. Factors that nneutralize the low PH of the stomach or decrease the time the pathogen is nexposed to stomach acid diminish local bactericidal action and increase the nprobability that an infections inoculums will reach the small intestine. The nimportance of gastric acidity as a defense mechanism is emphasized by the nincreased incidence of severe Salmonella enterocolitis in persons with nachlorhydria, prior gastroectomy, gastroenterostomy, or vagotomy, conditions nthat reduce acidity or cause faster gastric emptying time.

The oral administration of buffering ncompounds also increases susceptibility to intestinal infection. It has beesuggested that ingestion  of organisms in food allows for longer exposure to ngastric acid, thereby necessitating the presence of a relatively larger ninoculums to produce disease, whereas water or other liquids, which have a nfast  gastric transit time, may be less heavily contaminated and still cause ndisease.

The small intestine provides other nprotective mechanisms through motility and normal flora. Alteration of the intestinal nflora by antibiotics markedly reduces the size of the inoculums required to nproduce   Salmonella infection in animals and humans and prolongs the nconvalescent carrier state. Prior antimicrobial   therapy also enhances the npossibility of  infection with antibiotic – resistant Salmonella strains.

Age is an important determinant of  ndisease produced by Salmonella. Salmonella enterocolitis occurs with nhighest incidence in children less than 5 years old; newborns and infants less none year of age are especially susceptible. The influence of age on incidence nmay reflect immaturity of humoral and cellular immune mechanisms, diminished nantibacterial action of the normal intestinal flora, a high frequently of fecal n– oral contamination, or other factors. In some instances, increasing nresistance with age is related to immunity consequent to previous exposure to nthe organism, even though disease has not been produced.

Patient with impaired ncellular and humoral immune mechanisms are at increased risk for development of nSalmonellosis. Impairments of host defenses caused by malnutrition, malignancy, ninfection with  human immunodeficiency virus or therapeutic measures such as ncorticosteroid or immunosuppressive therapy also predispose to infection and ndisease.

Salmonella causing enterocolitis are nthought to produce diarrhea by a true infection with mucosal  invasion and npossibly by elaboration of an enterotoxin that acts on upper intestinal ntransport. Salmonella invasion of intestinal mucosa may lead to local nproduction of inflammatory exudates of mediators that stimulate electrolyte nsecretion and smooth muscle contraction (Fig.6).

Fig.6. Flask-shaped ulcer nwith necrosis of epithelium and extrusion of necrotic tissue, fibrin and mucus

There  are  two types of ntoxins: exotoxins and endotoxins. Exotoxins are the toxic products of bacteria nwhich are actively secreted into environment. Endotoxins are toxic substances nwhich are liberated only during the lysis of microbial cells. The principal nfactor responsible for development of this disease is endotoxical complex of nSalmonella, but we should remember that these bacteria produce even exotoxins. nExotoxins and endotoxins have toxical properties.

Stages of salmonellosis development:

1.                      nColonizatio(setting) of pathogenic organism in the place of the inculcation.

2.                      nInvasioand reproduction.

3.                      nDeath nof the pathogenic bacteria and endotoxins liberation.

Infectious process may stop at the nstage of colonization due to unknown reasons. Invasion may be limited by nnearest tissues. In majority cases it leads to development of gastrointestinal nforms of Salmonellosis. For development of the first stage of pathogenesis of nSalmonellosis the factors violating structural and functional state of ngastrointestinal tract play important role (dysbacteriosis, hypovitaminosis and nother). These conditions may promote to development of the disease even due to nsmall quantity of bacteria in food-stuffs.

In salmonellosis the nprincipal pathologoanatomical changes develop in the place of inoculation of nthe agent in the small intestine. Data about changes of small intestine igastrointestinal forms of Salmonellosis may be received only as a result of its nbiopsy. But biopsy is not used in practice. Investigation of material during nbiopsy testifies dystrophical changes of epithelium, infiltration of nepithelium  of mucous membrane by macrophages. Increased quantity of ninterepithelial leukocytes, polymorphonuclear leukocytes and macrophages is nmarked.

Principal  changes develop in lamina npropria of mucous membrane of small intestine in Salmonellosis. These changes nare accompanied by hyperemia, hemorrhages, edema and intensification of cell ninfiltration. At the same time  the  changes of the different parts of ngastrointestinal tract develop. There is an acute inflammatory process, ndystrophic changes of epithelium, edema, hyperemia and cell infiltration istomach. There are dystrophy, erosions, hyperemia, edema in mucous of large nintestine. Changes in all parts of gastrointestinal tract are transient. They nare exposed to reverse development in clinical recovery of the patients.

In half of the patients with nSalmonellosis nonsharp violations of liver are marked. These changes are nconsidered as compensatory mechanism.

In connection with sufficient nefficiency of modern methods of treatment the fatal outcomes are rare. nDystrophic  changes of parenchymatous organs were revealed in autopsy of ndeceaseds from gastrointestinal forms of Salmonellosis. These changes were ndirect cause of death. Inrarely, edema of the lungs and brain, hyperplasia of nspleen and mesenteric lymph nodes may develop.

Clinical  manifestations

http://www.bettermedicine.com/article/salmonella-infections

In connection with nconsiderable variability of clinical duration of Salmonellosis there are nmultitude classifications of this disease. The next classification is more ncomfortable for practice use:

1)                     nLocalized n(gastrointestinal) forms of Salmonellosis:

a)          nGastritic nvariant;

b)         nGastroenteritic nvariant;

c)          n Gastroenterocolitic nvariant.

2)                     nGeneralized nforms:

a)          nTyphus-like nform;

b)         nSeptic nform (septicopyemia).

3)                     nCarrier nstate:

a)          nAcute ncarriers;

b)         nChronic ncarriers;

c)          nTransitory ncarriers.

Clinical symptoms of nSalmonellosis are studied sufficiently completely.  Gastrointestinal forms of nSalmonellosis are observed in most of cases of the disease. According data of ndifferent authors they occur from 79 to 85 %.

Incubation period is from n4-6 hours up to some days. Onset of the disease is an acute. Prodromal period nis not typical or very short. Weakness, malaise, and slight chill characterize nit. Then temperature increases to subfebrile in moderate and severe forms naccordingly.

After ingestion of  ncontaminated food or water, illness begins in many patients with nausea and nvomiting; these symptoms usually resolve within a few hours. Myalgia and nheadache are common. The cardinal manifestation is diarrhea, which may vary nfrom a few loose stools to fulminate diarrhea. In most cases, stools are loose, nof moderate volume,  without blood, swamp-like and bed smell (Fig.7).

Fig.7. Stool in case of salmonellosis

In exceptional cases, the nstools may be watery and of great volume (“cholera-like”), or, in other ninstances, of small volume and associated with tenesmus and gross blood n(“shigellosis-like”). Temperature elevations to 38-39 °C are common, as are nchills; both appear in the majority of patients in whom  definitive diagnosis nis established. Abdominal cramps occur in about two-thirds of the patient and nare often localized to the periumbilical region or lower abdominal quadrants. nBowel sounds are increased and abdominal tenderness is present. At microscopic nexamination, stool show a moderate number of polymorphonuclear leukocytes and, noccasionally, red blood cells. Cross blood  is unusual but may be seen isevere cases. Peripheral leukocyte count is usually normal, although nneuthrophilia with  a shift to younger forms may be present.

The duration of fever is nless than 2 days in the majority of cases. Diarrhea usually persists less tha7 days, although, rarely, gastrointestinal symptoms may last for several weeks. nProlonged fever and diarrhea suggest a complication or a different diagnosis.

Localization of pain ithe right lower quadrant of the abdomen in patients with enterocolitis may lead nto a diagnosis of acute appendicitis. At surgery, such patients may have normal nappendices or occasionally acute appendicitis rarely with perforation.

Clinic of Salmonellosis is ncharacterized by symptoms of damage of cardiovascular system. The basis of nthese violations is water-electrolytes loss and change of reological properties nof the blood.

Changes in organs of nrespiratory systems are not typical for uncomplicated cases of gastrointestinal nforms. But sometimes breathlessness may be observed.

Toxicosis takes place whelocalized forms of Salmonellosis. It is manifested by headache, pain in the nmuscles, mild ataxia, asymetric reflexes. Development of toxic encephalitis is npossible.

Electrolyte and water ndepletion may be severe during illness, leading to hypovolemic shock. The ndisease is more severe in children, in seniors, and in patient with nachlorhydria, gastroectomy, gastroenterostomy, sickle cell anemia, or other nconditions that impair resistance to infection. The frequency of transient nbacteremia  is less than 5 % in adults. It  is increased in children and ipersons with severe preceded diseases. Bacteremia has been shown to occur i8-16 % of infants and children of 3 years age or younger who are hospitalized nwith Salmonella enterocolitis. Salmonella  intestinal infections nhas tendency to be prolonged in children, who continue to excrete agent istool for a longer time than adults after subsidence  of  clinical nmanifestation of infection.

Salmonella enterocolitis may develop nin hospitalized patients. The illness may be a nosocomial infection or it may nresult of activation of pre-existing  asymptomic intestinal infection by nantimicrobial therapy, of surgical diseases  of  abdomen  or  from other  ncauses.

In one-two third of nchildren over 5 years and adults positive cultures are observed during second nor third week from the onset of the disease. In this time majority of the npatients have no symptoms of the disease.

Salmonella can produce an illness ncharacterized by fever and sustained bacteremia without manifestations of nenterocolitis. This syndrome may be caused by any Salmonella serotypes. nThe clinical syndrome of Salmonella bacteremia is characterized by a hectic nfebrile course lasting for days or weeks. The organism is isolated from blood, nbut stool cultures are ofteegative. More than 70 % of cases of generalized nforms of Salmonellosis begin as gastrointestinal form with dyspeptic nmanifestations. Then, in typhus like variant after subsidence of dyspeptic nmanifestations the disease acquires signs of typhus infection. The second nfebrile wave-like or incorrect type continues in most cases during 10-14 days. nThe principal symptoms of the period of climax of the disease are weakness, nadynamia, severe headache, sleeplessness, pains of muscles and joints.

Typical typhus state is nnot characteristic for this variant of Salmonellosis. In majority of the npatients enlarged liver and spleen, distantion of abdomen are observed.

Approximately, in 25 % of nthe patients scanty rose sports are observed. Rash  appears on 4-10 day, nsometimes later. In peripheral blood leukocytosis is observed only in early nperiod of the disease. Then leukopenia is marked, but with neutrophilosis. nSometimes typhus like variant may be without appearances of gastroenteritis. nThe principal symptoms of beginning period in that cases are fever, chill, nheadache, weakness. In the period of climax adynamia, pale skin, injections of nscleras are observed.

There are single rose nspots on the skin of abdomen and chest. In this variant of generalized form of nSalmonellosis relapses may observed, and rarely, complications, which are ntypical for typhus fever. Typhus like variant may be with temperate nmanifestations of intoxication and dyspeptic appearances, with short duratiofever. There is marked catarrh, hyperemia of pharynx, laryngotracheobronchitis nin these patients rarely.

Septic variant n(septicopyemia) is sepsis of Salmonella etiology. The development of sepsis is nevoked by sharp decrease of the immuneprotective strengths of the organism of nthe patient. This variant of generalized of Salmonellosis is characterized by nacyclic development of the disease, prolonged fever, chills, sweating, nhepatosplenomegaly, sometimes development of jaundice, plural purulent nmetastases in different organs and tissues.

Usually, the disease nbegins from manifestations of gastroenteritis. Then typical septicopyemia ndevelops with hectic fever. The signs of influence of intoxication on central nnervous system are marked from the first days of the disease. They are nmanifested by irritation, violations of sleep, motive trouble, sometimes ndelirium. The skin is pale. Rash may appear on the skin (petechias or large nhemorrhages).

The  secondary  purulent  nfocuses  may  be  in  any  organs  and  tissues. Localization  of  infection  nmay  be  in  thyroid, brain membranes, bones, heart, lungs, kidneys, adrenals, npancreas, spleen, liver, pericardium  and soft  tissues.

Meningitis is a rare ncomplication of Salmonella infection and occur almost exclusively in infants, nparticularly neonates. Even epidemics of meningitis have been reported during noutbreaks of Salmonella infection in hospital nurseries. Clinical nmanifestations are the same as those of any bacterial meningitis in this age ngroup. The clinical course is usually long and marked by relapse. Acute nneurologic complications are common and include subdural empyema, cerebral nabscesses, and ventriculitis. Acute or chronic hydrocephalus may occur. nMortality is high, despite appropriate antimicrobial therapy.

Pleuropulmonary disease. nPneumonia or empyema, the predominant types of serious respiratory diseases, noccur usually in elderly patients or in patients with underlying diseases such nas diabetes mellitus, malignancy, cardiovascular disease, or pulmonary disease. nMortality is high.

Arthritis. Salmonella ninfection may be with localization in major vessels, including the thoracic and nabdominal aortas, coronary arteries, peripheral arteries. Atherosclerotic nintrarenal aortic aneurysms are by far the most common vascular sites of nlocalization. The risk of endothelial infection is high in persons over the age nof 50 years who have Salmonella bacteremia.

The mechanism of arterial ninfection is through to be direct implantation at a site of endothelial injury nin the bacteremia patient on to extension from an adjacent inflammatory lesion, nsuch as vertebral osteomyelitis. Mortality is high.

Osteomyelitis and nArthritis. Osteomyelitis can develop iormal bone but especially likely to noccur in patient with sickle – cell hemoglobinopathies, systemic lupus nerythematosus, immunosuppressive therapy, bone surgery or trauma. Salmonella, nnot Staphylococcus, is the most common cause of osteomyelitis in patients with nsickle-cell anemia.

Salmonella may cause a nmetastatic supportive arthritis. Pyogenic arthritis is much less frequent thareactive arthritis.

Splenic Abscess and nHepatic Abscess. Splenic abscess is a rare complication of Salmonella ninfection. Localization occurs after bacteremia in posttraumatic subcapsular nhematomas or splenic cysts. The clinical manifestation is one of left upper  nquadrant tenderness, fever and leukocytosis.

Salmonella liver abscesses nmay occur. Usually, the patients have pre- existing liver disease including namebic abscesses, ecchinococcal  cysts, and hematomas. Association with biliary ntract disease exists in occasional cases.

Urogenital Tract. nSalmonella in stools of carriers or persons with acute illness may gain access nto the urinary tract to produce cystitis or pyelonephritis. Localization of nSalmonella blood  form with abscess formation in kidneys, testicles, or ovaries nis also occasionally reported.

Bacteriocarriering of nSalmonella is developed after disease. There are acute, chronic and transitory ncarriers. Acute and chronic carriers are divided depending on duration of nexcretion of Salmonella. Acute  carrier has the duration of excretion of nSalmonella from 15 days till 3 months after clinical recovery. The persons, nexcreting Salmonella over a year, are chronic carriers. The conditions of ndevelopment of transitory carrier are insignificant dose of the agent and its navirulence.

Complications  and  outcomes

Complications and outcomes nof Salmonellosis, as and multiple clinical forms are exposed to wide noscillations. Even gastrointestinal forms of Salmonellosis with favorable nduration are not finished clinical recovery.

Generalized form of nSalmonellosis, as rule, is accompanied by complications. Exceeding expressioof symptoms of Salmonellosis frequently leads to collapse (1.5-6 % of the ncases). Collapse may develop at the first day of the disease on the altitude of nclinical manifestations before dehydration. Endotoxinemia plays leading role idevelopment of collapse. It is a manifestation of infectious-toxic shock.

Besides expressive hypodynamic ndisorders acute renal insufficiency, edema of brain, edema of lungs and hemorrhagic nsyndromes develop. The development of dysbacteriosis is connected with large ndoses of antibiotics use at any clinical forms of Salmonellosis. Dysbacteriosis nmay be compensated  or latent.

Outcomes of salmonellosis depend opremorbidal state, age, clinical forms, timely diagnostics and treatment.

Diagnosis

Diagnostics of nsalmonellosis is performed on the basis of epidemiological, clinical and nlaboratory data. Bacteriological and serological methods are used  for nconfirmation of salmonellosis. The main materials for bacteriological  ninvestigation  are vomiting masses, water after irrigation of stomach, stool, nblood, urine.

Serological investigations nare used. These are reaction of agglutination (RA) (7-8^th day of the ndisease) and indirect hemagglutination (RIHA). RIHA is more  sensitive. It ngives  positive results on the 5^th day of the disease. Diagnostical ntiter is 1:200. Serological investigation should be done in dynamics of the ndisease.

Rentgenology investigatioshows the increasing of thick intestin (Fig.8).

Fig.8. Tension and swelling of nsigmoid colon

Differential diagnosis

Differential diagnosis of nsalmonellosis is perform with other intestinal diseases – shigellosis, toxic nfood-borne infections, esherichiasis, cholera; with surgical diseases – nappendicitis, pancreatitis, cholecyctitis, thrombosis of mesenterial vessels; ngynecological pathology and with therapeutic pathology (myocardial infarction, nchronic gastritis aggravation, enterocolitis, ulcerous disease), with acute ngastroenteritis of viral origin (enteroviral, rotaviral etiology), poisoning by norganic and inorganic poisons, poisoning by mushrooms.

Generalized forms of salmonellosis is nnecessary to differentiate from sepsis of different etiology, pneumonia, nmalaria, acute pyelonephritis, tuberculosis.

Treatment

http://emedicine.medscape.com/article/228174-treatment

The volume of medical actions depends on the clinical form and a stage of ngravity of disease. At gastrointestinal form immediately wash out stomach and nintestine with boiled water (isotonic solution of Sodium chloridum is the best) nthen give sorbents per os and give a warm drink. For restoration of nhydro-electrolityc balance and normalization of circulatory disorders there nshould be indicated per os Glucosole or Rehydroni. Infusion therapy is nindicated at expressed dehydration – Trisol, Quartasol, Lactasol. At severe nstage of dehydratation one of the specified solutions is infused in vein with nrate 80-120 mL/min, 5-10 L of solution is necessary on course of treatment. If nhypotension and toxicosis are marked Prednisolon and Hidrocortizon, Polyglucin, nReopoliglycin are infused in vein. Pathogenetically 5 % solution of glucose is nindicated with desintoxication purpose and restoration of power balance, a nsolution of sodium hydrocarbonat for acidosis correction, Heparin for nimprovement of reologic properties of blood, preparations of antiallergic actio- calcii chloridi, Dimedrol, Tavegil, Indomethacin are proved at severe ndiarrhea (for downstroke of Prostaglandines synthesis), calcium gluconate. nAntibiotics at gastrointestinal form of salmonellosis are not used.

However at syndrome  of hemocolitis and lingering diarrhea Furazolidois  indicated in combination with fermental preparations – Festal, Panzynorm, nPancreatin, Mezym forte, Pancitrat, Vobensim. The broths of herbs has nanti-inflammatory, disinfectant and astringent properties, and also properties nraising organism reactivity. They are vitamin preparations, Pentoxyl, nMethyluracil, Thymalin, Enterol-250 also indicated. Bificol, Colibacterin, nBifidumbacterin, Linex is used at intestinal dysbacteriosis.

At generalized form simultaneously with pathogenetic therapy there are  nindicated antibiotics – Levomycetin, Ampicillin, Monomycin, Gentamycini sulfas, nCefazolin (Kefzol), Cefotaxim (Claforan). At the septic form of disease nantibiotics are better to infuse parenteraly.  For sanitation of chronic ncarriers of salmonelas the specified antibiotics use in average therapeutic ndoses in combination with preparations stimulating nonspecific and nimmunological reactivity (Pentoxyl, Methyluracil, Splenin, Thymalin, T- nactivin).

Prophylaxis

The  measures  of  nprophylaxis  are  veterinary-surveillance upon  animals  and  production  of  nmeat  and   dairy industry, laboratory  control  of  food  stuffs.

It is  necessary  to  nreveal  carriers  on  milk  farms,  in foods, children’s and medical establishments. nThe  maintenance  of  the  rules  of  personal  hygiene  and  rules  of  nfood’s  cooking  plays  an  important  role  in  prophylaxis  of Salmonellosis.

Salmonella

See also

·  1984 nRajneeshee bioterror attack

·  Typhoid fever

·  List of nfoodborne illness outbreaks

 

 

http://intranet.tdmu.edu.ua/data/books/And-INF.pdf

Cholera is an acute  anthroponosic infectious  disease  with  fecal-oral  nmechanism  of  transmission. Cholera  is  characterized  by  dehydration  due  nto  loss  of  the  fluid  with  watery  diarrhoea  and  vomiting. Cholera  is  nconcerned  to  the  group  of  the  diseases, which  are  submitted  to n“international  medical-sanitary  roles”.

http://www.cdc.gov/cholera/general/

Historic reference

Illness nand death due to dehydrating diarrhea and vomiting can be recognized in the nwritings of Hippocrates and Galen. The heartland of cholera is India, the Ganges River’s Delta. From there it has spred from time to time to many other countries.

There were 7 pandemic of cholera in the world.

Fives npandemics of appalling magnitude have occurred during the 19th century, nspreading from India through Asia Minor, Egypt and Russia.

In 1816 ncholera broke out with unusual severity and high mortality in the area of the Ganges River’s Delta. Over the next 8 years it spread over much of Asia and the Middle nEast, but did not invade Europe.

The great npandemic is of importance as being the first to invade Europe. It started in India in 1828 and advancing slowly reached Iran in 1829, extending thence by way of Astrakhan to Russia, Sweden, Northern Europe and England. By 1832 it has spread over the whole Europe. In the nsame year 1832, it reached Canada and thence extended to Fort Dearborn, where it infected the soldiers who subsequently carried the disease down the Mississippi valley.

Cholera  was nalso introduced into New York and Boston and spread from there to south and nwest, so that by 1836 cholera was present in most parts of the United States, not disappearing until 1838. It disappeared in Europe in 1839.

The next nEuropean outbreak, or third pandemic, lasted from 1844 to 1864 and was traced nfrom India by the  way of land and sea, that by land following the caravaroute by way of Iran and Russia and that by sea from Indian pilgrims going to nMecca. This pandemic reached the United States in 1848.

The fourth ngreat pandemic invaded Europe by the usual routes and continued from 1865 to 1875. In 1865 it was carried by sea from Bombay to Arabia and Mecca and was then spread by the nreturning pilgrims throughout Egypt, Syria, and the Southern European ports to nthe East coast of Africa.

The fifth npandemic (1883-1896) began in India, reaching Egypt and Europe.

It was during nthis epidemic, in 1883 that Koch working in Egypt discovered the cause of ncholera, vibrio comma (Spirillum cholera). However, as the epidemic in Alexandria soon subsided, he proceeded to India where, after a study of 42 cases of ncholera and 28 autopsies, he gave confirmatory evidence of the etiology of the ndisease.

A very serious noutbreak of cholera originated in 1891 in pilgrims from the delta of the Ganges attending a religious festival. It was spread of  cholera by returning npilgrims and reached Europe in 1892. Almost a million deaths occurred in Russia. It was during this epidemic that cholera appeared with great virulence in Hamburg. In that city within 2 months there were nearly 17 000 cases and over 8 000 deaths. nThis outbreak gave opportunity for those careful studies as to the transmissioof the disease to be later referred to.

It is usual to nrecognize a sixth pandemic  (1900-1926) which began in Aravia   and spread overIndia, China and Philippines. This pandemic continued to cause great mortality nin Europe and from 1908 to 1910, there were reported some 71 000 cases and 26 n000 deaths in Russia.

The seventh npandemic began in 1961. It is caused by a vibrio cholera El-Tor.

In 1905 nGotschlich isolated six peculiar strains of vibrio cholera from the dead bodies nof returned Mecca pilgrims at the quarantine camp of El Tor. These strains, nwhich produced hemolysins, came from typical cases of cholera and agglutinated nin the classical typing serum. However, not until 1961 when the “El Tor” nbiotype produced an epidemic of major proportions in the Philippines was there general agreement that hemolytic vibrio cholera could be responsible nfor severe epidemic human disease.

http://emedicine.medscape.com/article/962643-overview

Etiology

There are two forms of the vibrio cholera: classical biotype, nwhich was discovered by Koch in 1883 and El Tor biotype.

The vibrion is short. It is gram-negative and curved organism which, from nits shape, is often called the comma bacillus (Fig.1). Typically it is small, comma-shaped nrod. It frequently occurs in S-shapes, owing to the attachment of a  pair of norganisms at their ends, and especially in the old and virulent cultures long ntreads showing a somewhat spiral appearance may be seen. The vibrio cholera nis strictly aerobic and grows readily upon ordinary culture media. There  are  nno  spores  and  capsules.

Vibrio cholera has two antigens flagellar (H) antigen and somatic n(O) antigen.

The  somatic (O)  antigens  do  distinguish V. cholera Ogawa, Inaba and nHikojima, which are responsible for epidemics.

  V. cholera produce 3 fractions of toxin. Cholerogen-exotoxiplays the most important role in the development of dehydration. Cholerogen   nconsists  of  two  types  of  toxin: cholerogen A  and  cholerogen B. nCholerogen A  consists  of  peptide A1  and  peptide A2. Peptide  A1  npenetrates  through  the  cells  membrane. Then  it  manifests  the  specific  ntoxication. Peptide A2  connects  peptide A1  with  peptide B. Peptide B  is  nuntoxic, it  connects the  whole  molecule  of  toxin  with  cell  receptors. V. ncholera  survives  in  low  temperature. The  boiling  kills  V. cholera  nduring  one  minute. It  survives  in  sea  water (till  60 days).

Fig.10. Vibrio ncholera

 

 

Vibrio ncholera is npresent in the intestine and in the rice water-like stool during acute stage of ninfection.

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Epidemiology

Cholera  is  nanthroponosic  intestinal  disease  with  tendency  to  pandemic  spread. nReservoir  and  source  of  infection  is  infected  man. Discharge of nvibrions  is  realized with excrement.

The  sources  of  ninfection  may  be  sick  man  with  typical  or  obliterated  form  of  ncholera, reconvalescent  after  cholera  and clinically  healthy  nvibrio-carriers.

The  patients  with  nclinical  picture  of  cholera  are  the  most  intensive  source  of  agents. nThey  discharge  till  10-20 liters  of  detachments  during  first  4-5  days  nof  the  disease  with  great  content  of  vibrions (10⁶-10⁹  vibrions  nin  1  mL).

The  source  of  ninfection  may  be  reconvalescents-vibriocarriers. They  discharge  vibrions  ninto  environment  in  average  during  2-4  weeks.Healthy (transitory) ncarriers  can  discharge  the  agent  periodically  during some  month.

  The  mechanism  of  ntransmission  of  the  infection  is  fecal-oral. It  is  realized  by  water, nalimentary  and  contact  ways. The  leading  way  of  the  transmission  of  nthe  agents  of  cholera  is  water. This  way  may  lead  to  epidemic  ndistribution  of  cholera. Infection  may  happen  due  to  use  of  infected   nwater and  also  after  use  this  water  for  wash  of  vegetables, fruits  nor  bathing.

Food  has  also  been  implicated  nin  some  epidemics. The  cases  of  cholera  were  described  due  to  ninfected  milk use, boiled  rice  and  other  food-stuffs.

It  is  established  that  ninhabitants  of  different  water  reservoirs (fish, crayfishes, mollusks, nfrogs  and  other  hydrobionts)  are  able  to  accumulate  and  preserve  vibrio n El-Tor  for  a  long  time. They  are  temporary   reservoir  of  ninfection  and may  be  factors  of  transmission  of  the  agents.

The  susceptibility  to  ncholera  is  general  and  high. In  endemic  areas  morbidity  is  observed  nmore  frequently  in  children  and  elderly  persons.

http://emedicine.medscape.com/article/962643-overview#a0156

Pathogenesis

Cholera  is  cyclic  infection  with  nessential  fermental  systems  damage  of  the  enterocytes. Vibrions  ncholera enter  the  organism  through  the  mouth  with  water  or  food.  nSome  part  of  vibrions  perishes  under  influence  of  acid  medium  of  nthe  stomach. Another  part  of  vibrions  enters  small  intestine. Intestine  nreproduction  and  destruction  of  vibrions  is  accompanied  with  discharge  nof  large  amount  of  endo-  and  exotoxic  substances. There  is  no  ninflammatory  reactions.

Cholera  is  characterized  by  ndehydration  due  to  loss  of  fluid  and  salts  with  watery  stool  and  nvomiting. Hypersecretory  processes  play  the  leading  role  in  the  nmechanism  of  the  diarrhea origin. These  processes  are  promoted  by  nactivation  of  ferment  adenylcyclase  in  the  epithelial  cells  of  the  nintestine  under  action  of  exotoxin-cholerogen  and  accumulation  of  ncyclic-3-5-adenosinemonophosphates, leading  to  increase  of  secretion  of  nelectrolytes  and  water.

 In  cholera  the  loss of  fluid  with  stool  and  nvomiting  reaches  such a great volume in  a  short  period, practically   not  nmet  during  diarrhea  of  other  etiology. The  general  volume  may  exceed  nin  some  cases  up to  2  times  the  body’s  mass  of  the  patient. The  nloss  of  electrolytes  plays  essential  role  in  pathophysiology  of  ncholera. So, loss of  potassium  may  reach  one  third  its  content  in  the  norganism. It  is  manifested  by  disorder  of  function  of  myocardium, ndamage  of  kidneys  and  also  paresis  of  the  intestine. In  cholera  ndehydration  is  isotonic. Fluid  contains  135 mmole/L Na, 18 mmole/L K, 48 nmmole/L HCO₃  and 100 mmole/L Cl (or 5g NaCl, 4g NaHCO₃  nand 1g KCl in 1  liter  of  defecation’s. An  acute  extracellular  isotonic  ndehydration  develops  in  the  patients  with  cholera. It   is  accompanied  nwith  decreasing  of  the  volume of  circulated  blood  and  nhemoconcentration, leading  to  hemodynamic  disorders  and  violation  of  ntissue  metabolism. Hypovolemia, metabolic  acidosis, hypoxia, nthrombo-hemorrhagic  syndrome  and  acute  renal  failure  develops.

http://emedicine.medscape.com/article/962643-overview#a0104

Pathological anatomy

In  cholera basic tragedy happens in a zone of the jejunal capillaries. nLiquid  get into the intestine from them through the epithelium cells. A venous nreturn  is diminished and as a result of that the heart’s return diminishes ntoo. Blood pressure decreases. The organism reacts with a tachycardia on that n(there is no cholera without tachycardia).

The other ncompulsory sigh is decreased  diuresis. It is explained by increase of the nwater resorbtion by the renal canaliculi. If the loss continues venous flow ndiminishes acutely. Tachycardia caot compensate it already and blood npressure decreases.

The organism nincludes a pressory mechanisms  to preserve  functions  of  the  vital  nimportant  organs (heart, brain, kidneys). A capillary spasm begins. It nimproves for some time blood supply of the heart and brain.  Blood pressure is  nequated but venous return decreases more. As a result of it oxygen transport to nthe organs and tissues and metabolic products transport are violated. PH nbalance of  the  organism changes to acidosis. The  organism reacts oacidosis. It  includes  a new compensatory mechanism. It is dyspnea. nRespiratory alkalosis develops, but it caot cause  neutral PH balance due  nto  violation  of  microcirculations.

A pressory nmechanism is proper for kidneys too. The kidneys capillaries are spasmated. nTissue acidosis develops. Resorbtion  of water and products  of  metabolism is nalterated. That excludes the kidney as organ regulating homeostasis. Renal nfiltration stops entirely under the decrease of blood pressure less than 80 mm. The kidney is sensitive for hypoxia. Hypoxia causes dystrophic changes in the epithelium of nthe sinous canals.

These  changes nare reversible in case of moderate hypoxia (a renovation period is not shorter nthan a week). But if the patient did not get from the hypovolemic shock a nnecrosis of the sinous canals comes (death from anuria – “shock kidney”). In  ncase of prolonged  loss  of  water all  compensatory mechanisms become unable nto keep blood pressure. An original decompensation  comes. It coincides with nthe loss of the liquid equal to 8-12 % of the body’s weight. Then the nunreversable changes become and therapy is uneffective. The volume  of  loss nshouldn’t  be more than 10 %.

In  accordance  with  classification  nWHO  the  patients  with  cholera  may  be  divided  on  three  groups:

1. The  first degree of  dehydration. There  are  the patients which have nloss of  fluid volume equaled to 5 % of body weight.

2. The  second degree of  dehydration. There  are  the  patients which nhave loss of  fluid volume equal to 6-9 % of body weight.

3. The  third degree of  dehydration. nThe patients  which have loss of  fluid volume over 10 % of body weight. That ndehydration is dangerous for life if the reanimation measures are not nentertained.

According  to  classification  of  V. I. Pocrovsky patients  can  be  ndivided  in  four  groups:

1.                      nThe  nfirst  degree  of  dehydration  with  loss  of  fluid  1-3 %  of  body  weight.

2.                      nThe  nsecond  degree  of  dehydration  with  loss  of  fluid  4-6 %  of  body  nweight.

3.                      nThe  nthird  degree  of  dehydration  with  loss  of  fluid  7-9 %  of  body  weight.

4.                      nThe  nfourth  degree  of  dehydration  with  loss  of  fluid  more  then  10 %  of  nbody  weight.

It’s  worth  nto  underline  that  the  clinical  manifestation  of  the third  degree  of  ndehydration  (by  the  WHO  classification)  or  the fourth  degree  (by nclassification  of  V. I. Pocrovsky)  is  hypovolemic  shock.

 

Clinical manifestations

Clinical  manifestations  of  cholera, caused  by  classic  vibrion  nand  vibrion  El-Tor  are  similar.

Incubation  period  is  from  some  hours  till  5  days (in  average  n48  hours). Cholera  may  be  present  in  typical  and  untypical  forms. In  ntypical  course  the  next  forms  of  the  disease  are  differented  in  naccordance  with  the degree  of  dehydration: light,  moderate and  severe  nform. In  untipical  course  obliterated, fulminant  forms  may  be  present.

The onset of the disease is an acute, as rule. In light course of cholera nthe gradual development occurs in the part of the patients. The prodromal nperiod may be 1-1.5 days. The patients mark weariness, ailing, headache, nsometimes subfebrile temperature, heartbeating, sweet.

   A diarrhoea is the first clinical nmanifestation of cholera. It appears suddenly, without the pain, often at night nor in the morning. Diarrhoea is accompanied by gurgation in the stomach. After n1-2 defecation stool has typical shape. It is cloudy, white, fluid, without nsmell and “rice-water”(Fig.2).

In mild course (dehydration of the first degree). The  loss  of  fluid  is  till  3 n%  of  body  weight. Imajority patients stool may be till 10 times in a day, scanty. In one-third of the npatients vomiting may occur 1-2 times. Thirst, light dizziness, weakness ntrouble the patients. Their state is satisfactory. Skin is humid, usual color. nThe mucous of the mouth is dry. There is no hypothermia. Subfebrile temperature nmay be in the part of the patients. There

Fig.11. n“Rice-water” stool in cholera

 

are no changes of the npulse and arterial pressure. An insignificant painfulment occurs due to npalpation of the stomach. The changes of the blood are not typical. There is no nblood’s condensation, change it’s pH and electrolytes.

After corresponding therapy a nvomiting, dizziness, weakness disappear at the first day. The stool become nnormal on the 2-3 day of the treatment.

In moderate course (dehydration of the second degree) the loss of fluid nis 4-6 %. There is considerable weakness, dizziness, and thirst in patients. A nquantity of the defecation is from 10 till 20 times in a day. The stool is nliquid, plentiful. Dehydration appears already after 3-5 defecation at the half nof the patients. A vomiting is annexed early, and it is rice-water-like. The nskin is pale. The moderate cyanosis of lips and extremities may be in the part nof the patients. There is harsh voice. Turgor of the skin decreases. The nfeature of this degree of dehydration is appearance of the cramps without tonic ntension. The pulse is frequent up to 100 per minute. The arterial pressure is ndecreases till 100 mm. May be olyguria.

There are no nchanges of the red blood. Erythrocyte sedimentation rate (ESR) is lightly naccelerated. Leukocytosis, neutrophylosis with the shift of the formula to the nleft, lymphopenia, monocytopenia and uneosinophilia occur in the part of the npatients. Hematocrit is 51-54 %. The relative density of the plasma is n1026-1029. The change of electrolytes is insignificant. Hypokalemia  and nhypochlorinemia are more expressed. Hypotension disappears usually through n20-30 minutes from the onset of rehydration. Turgor is restored through 3-4 nhours. The skin becomes pink. A vomiting continues till a day. Rarely a nvomiting is observed on the second day. The stool becomes facesic through 1-3 ndays, and it becomes normal to 4-5 day. The general loss of the fluid is 5-7 liters in this patients.

Severe course (dehydration of the third degree) occurs more nrarely, approximately in 10 % of the patients. The loss of fluid is 7-9 % of nbody weight. The detachment this degree of dehydration is connected with nnecessity of prevention of development extremly severe course. There are no nsecondary changes of the important system of the organism due to this degree of ndehydration. Because, it may be possible rapid compensation of dehydration and nrestoration of electrolytes. The third degree is characterized by more nintensive clinical manifestations of dehydration and unfirm compensation.

The disease develops impetuously. The stool is watery, abundant from the nfirst hours of the disease. Sometimes the patient cannot count a quantity of ndefecations. In patients sharp weakness, adynamia, severe thirst, cramps of the nmuscles are observed. The state of the patients is serious and very serious.

A cyanosis of lips and extremities is observed. The skin is cold and nshriveled. The turgor decreases. The face is pinched, eyes are deeply sunken ithe orbits. In a third of the patients a symptom of “black eyeglasses” is nobserved (Fig.3). The mucous of the mouth cavity is dry. The lips are dry too. nTongue is dry and covered. A voice becomes hoarse. The cramps are often of long nduration, with tonic character. Cramps are accompanied with pain. The cramps of nthe trunk muscles and diaphragm are not observed. The temperature is 35.7-35.5 nºC. The pulse is 120-130 in a minute, weak. The arterial pressure is low n80/50 mm. Sometimes the breathlessness occurs. Renal failure is manifested by nolyguria, in 25 % – by anuria. There are erythrocytosis, leucocytosis, nneutrophylosis  with the shift of the formula to the left, lymphopenia, nuneosinophilia. The concentration of hemoglobin increases. Protein and nleukocytes are observed  in  urine. Hematocrit is 55-65 L/L in these patients. nThe relative density of plasma is 1030-1035. There is considerable change of nelectrolytes. Hypokalemia, hypochlorinemia are expressive.

Fig.12. nPatient with severe course of cholera

 

Extremly severe course (dehydration of the forth degree) or decompensated ndehydration. It occurs more rarely than the other clinical variants. The loss nof fluid is 10 % of body weight and more.

 In this case the organism cannot compensate the indigence of nwater-electrolytes balance and function of the significant organs. It leads to nhypovolemic shock. The relapsing vomiting is observed. Decompensated ndehydration may develop  through 6-8 hours and even at the first 2-3 hours. The nstate of the patients is serious and very serious. In the last hours diarrhoea nand vomiting may be  absent. It is connected with paresis of the stomach and nintestine muscles, with hypokalemia and metabolic acidosis. At the same time nthere are expressive symptoms of dehydration: cold clammy skin, intensive total ncyanosis.

The color of the hand’s clusters, nouse, aural areas, lips and eyelids is nviolet or black. The face is pinched, eyes deeply sunken in orbits. There is nimpression of the suffering and entreaty about help on the face (facies ncholerica).

The skin is shriveled. The turgor of the skin is decreased (“washwoman’s nhands”). A voice becomes hoarse. The temperature is 34.5 ºC. The ngeneralized tonic muscles cramp are observed, including muscles of the abdomeand back. The agonizing hiccup may be due to clonic spasm of diaphragm. There nis no pulse. The arterial pressure is not determined. The breathing is frequent nand superficial. There is anuria. The condensation of the blood is observed. Iperipheral blood the concentration of hemoglobin increases. Expressive nleucocytosis, neutrophylosis, lymphopenia, uneosinophilia occur. Hematocrit is nhigher than  66 %. The relative density of the plasma is 1036 and more. The nalterations of electrolytes are very expressive: hypokalemia, hypochlorinemia. nHyponatremia is expressed in a smaller degree. Dehydration has isotonic character. nThe deficit bicarbonium (more than 10mmol/l) leads to decompensated metabolic nacidosis and respiratory alkalosis.

   Untreated patients die. The cause of the death is an acute heart’s nfailure (at the first three days of the disease) or renal failure (up to 14-16 nday).

http://www.cdc.gov/cholera/disease.html

Complications

 The next complications may develop in patient with cholera: pneumonia, nsometimes abscesses, phlegmon. The row of complications are connected with nintensive therapy: pyrogenic reactions, phlebitis, thrombophlebitis, nhyperkalemia and other.

 

Diagnosis

The bacteriological research of material from sick man or corpse is the nprincipal method of laboratory diagnostics. The purpose of bacteriological nmethod is detachment of cholera¢s agent and it¢s identification.

The correct ntaking of the material has a great meaning for bacteriological research as the ndelivery of material to the laboratory. A quantity of the material is 0.1-0.2 gm, because the enormous quantity of the agent is contained at stool. It is necessary to take a nbigger quantity of the agent from the patient with light form or carriers. The nsowing is done to the dense or liquid nutritive mediums near patient’s bed. If nthere is no possibility delivering of the material to the laboratory, quickly, nit is necessary adding of conservant, because vibrio cholera begins to nperish already at the first 1-2 hours in usual conditions. An alkaline peptonic nwater is  used for the sowing. The material for the sowing is necessary to take ntill beginning of the treatment. The preliminary answer may be through 12 nhours, the final – through 24 hours.

The serological methods may be also used for diagnostics of cholera. nThere are methods of discovering antibodies to vibrio cholera in blood, nthe methods of detaching antigens of vibrio cholera at stool and other nmaterials. At the last years luminescent-serological method is used. The result nmay be received through 1.5-2 hours.

http://www.bettermedicine.com/article/cholera

Differential diagnosis

Differential diagnostics  of  ncholera  is  performed  with  toxical  food-borne infections, esherichiosis, nrotaviral  gastroenteritis. In  some  untypical cases  of  cholera, especially  nin  obliterated  course  of  the disease it  is  necessary  to  perform  ndifferentiation of  gastrointestinal  form  of  salmonellosis, ngastroenterocolitic  variant  of  acute  shigellosis, poisoning  with  nmashrooms, organic  and  inorganic  chemical  remedies.

 

Treatment

http://www.who.int/mediacentre/factsheets/fs107/en/

Patients needs immediate hospitalization in choleric department. They nrequire emergency treatment which should be started at the pre-admission stage. nIt’s necessary to put them on special bed (Fig.4) and indicate pathogenetic npreparations with the purpose of compensation of liquid and electrolytes loss, nand corrections of metabolic changes. Isotonic polyionic solutions – Trisol, nAcesolum, Lactasol, Quartasol, Hlosol are indicated. Quartasol is more neffective.

Quantity of liquid, which nshould be infused for initial rehydratation (during 1-2 hours), should ncorrespond to stage of the organism dehydratation. At III and IV stages of ndehydratation it makes accordingly 7-9-10 % of body weight and more. Polyionic nsolutions infuse in vein initially-stream introduction, then volumetric rate n70-120 mL/minutes. To infuse liquid with such rate, it is necessary to use nsimultaneously two and more systems for transfusion. Stream introduction of nliquid is replaced by dropwise infusion after normalization of pulse, nrestoration the arterial blood pressure and normalization of body temperature, nhemoconcentration and acidosis.

Fig.13. Special bed for treatment ncholera patient’s

The next infusions of polyionic nsolutions is determined by rate of proceeding loss of water and salts. The ncompensatory rehydratation is provided during several days in severe cases. For ndefinition of its volume it is necessary every 2 hours to determine quantity of nexcrements and vomitive masses to investigate clinical (a pulse rate, the narterial pressure, body temperature) and every 4 – 6 hours laboratory (relative ndensity of blood plasma, haematocrite number, concentration of electrolytes iblood plasma and erythrocytes, PH, concentration of standard Sodii hydrogenii) nparameters.

For preventioof side reactions of polyionic solutions preliminary warm up to 38 – 40 °С, at nthe first hours of treatment infuse Prednisolon 0,5 gr/kg per day. At infusiothere is plenty of solution Trisol the metabolic alkalosis and hyperkalemia cabe developed. In these cases infusion therapy is continued with solution Disol.

It cases of not compensated hypokalemia it is necessary to infuse npreparations of potassium in addition. At a pernicious vomiting, cramps, anaphylactoid nreaction  there should be used Dimedrol or Suprastin with Promedol. As at npatients with severe current of cholera the clotting develops, Cordiamin, ncoffein or epinephrin of hydrochlorid is contrindicated.

In case of I-II stages dehydration (liquid loss up to 6 % of body weight) nand more severe dehydration is managed by intravenous injection of saline nsolutions, at absence of vomiting recommend to apply peroral indication of nGlucosani in tablets or Rehydroni in packages 18,9 gr: the content of 1 package ndissolve in 1 L of boiled water and drink small portions.

Water-salt therapy should be over after appearance of nexcrements of normal character and at prevalence of quantity of urine over nquantity of excrements in the last 6-12 hours.

Panangin or Asparcam during 1 mounth are indicated during early nreconvalescence.

Antibiotics are the additional remedies. They accelerate clinical nconvalescence and prevent the further allocation of choleric vibrions. A npreparation of a choice is Ciprofloxacin: 0,25-0,5 gm 2 times per day, in serious cases enlarge up to 0,75-2 times per day during 5-7 days or nErythromicin, or Laevomycetin. Tetracyclin and Doxycyclin, are effective. nHowever, for the last years the majority of  vibrio, allocated on territory of Ukraine, not sensitive to this antibiotic. For sanitation of vibrio ncarriers use the same antibiotics during 3-5 days.

Complicatioof rehydration

It may be npyrogenic reaction to solutions, hypokalemia, hyperkalemia.

Hypokalemia  nis observed more than 25 % of the patients with III degree of dehydration. The nclinical manifestations are: distention of the stomach, pain in the stomach n(hypokalemitic ileus).

Hyperkalemia ndevelops in 15 % of the patients. The clinical manifestations are: red face and nupper part of the body, cardialgia, typical changes of ECG, bradycardia. Ithis case it is necessary to inject Phillips solution №2. Phillip’s solution № n1 is injected again after signs of hyperkalemia elimination.

Etiotropic  ntherapy  is  performed  with  antibiotics. Antibiotics  cause  shortening  of ndiarrhoea  duration   and  give  possibility  to  decrease  a  quantity  of  nfluid  for  injection.

Doxicycline  nis  prescribed  in  dose 0,1 mg  through  12  hours  at  the  first  day, than  n0,3-0,5 mg  through  6  hours  during  3  days. Tetracycline is  used  for  ntreatment  of  the  patients  with  cholera  in  dose  0,3-0,5 mg  through  6  nhours  during  5  days. It   is  possible  to use  chloramphenicol  in  0,5 mg ndose  through  6  hours  during  5  days.

Prophylaxis

http://www.cdc.gov/cholera/prevention.html

The  measures  of  nprophylaxis   depend  on  epidemic  situation  in  the  country. The  ninformation  of  world  health  organisation  about  cases  of  cholera  in  ndifferent  countries  has  an  important  meaning.

The  incidence  of  ndisease  can  be  diminished  by  sanitary-hygienic  measures, sanitary  ndisposal  of  human  feces, purification  and  protection  of  water  supplies, npasteurization  of  milk  and  milk  products, strict  sanitary  supervision  nof  preparation  and  serring  of  flood  exclusion  of  persons  with  ndiarrhea  from  handling food, organization  of  the  work  about  diseases   nof  gastrointestinal  tract  and  their  examination  on  cholera.

Specific prophylaxis  of  ncholera  is  performed  by  corpuscular  vaccine  and  cholerogen-anatoxin.

Parenterally  inoculated  nkilled  complete  cell  vaccine  has  been  available  for  years, this  nvaccine  stimulates  high  titers  of  serum  vibriocidal  antibodies, but  it  ndoes  not  induce  antibodies  to  toxin. Protection  by  vaccine  has  been  ninduced  for  approximately  1  year, with vaccine  efficacy  approximately  70 n%. Local  gastrointestinal  tract  immunity  against the  organism  and  nagainst  the  toxin  should  provide  a  better, less  reactogenic  immunogen  nusing  recombinant DNA  technology  an “attenuated” V. cholerae  norganism  that  lacks  the  genes  for  production  of  the  A  and  B nsubunits  of  toxin  was  created. A plasmid  containing  the  subunit  gene  nwas  then  constructed  and  inserted. Thus  a  candidate  live  V. cholera  nvaccine  containing  all  the  cell-was  antigens  necessary  for  adherence  nand  the  capacity  to  produce  only  the  subunit  of  toxin  has  been  nengineered.