DIARRHEAL SYNDROME IN

CLINIC OF INFECTIOUS DISEASES.

CHOLERA

Diarrhea - more frequent Diarrhea - more frequent bowel movement and stool bowel movement and stool dilution when during the dilution when during the day singleday single or repeator repeateded emptying emptying of intestineof intestine from from the liquid feces more than the liquid feces more than 300 ml300 ml happened happened

Actuality of Actuality of diarrhea diarrhea High incidence of diarrheal disease, which High incidence of diarrheal disease, which

yield only the spread of ARIyield only the spread of ARI.. The structure of infant mortality exceeds The structure of infant mortality exceeds 30-5030-50 %%.. According to WHO, the world annually According to WHO, the world annually from 68.4 to 275 million diarrheal from 68.4 to 275 million diarrheal diseasesdiseases.. Expanding the palette of micro-organisms Expanding the palette of micro-organisms that cause diarrheathat cause diarrhea.. Increasing the number of persons with Increasing the number of persons with immunodeficiency conditions, immunodeficiency conditions, fromfrom which which diarrhea diarrhea is happened.is happened.Significant Significant increasingincreasing of the population in of the population in different regionsdifferent regions and poor and poor water supply water supply..

Actuality of Actuality of diarrhea diarrhea Diarrhea often occurs in travelers - in Diarrhea often occurs in travelers - in

almost one third of people. almost one third of people.   The spectrum of pathogens as follows:   The spectrum of pathogens as follows: enterotoenterotoxinxin-UGI E. coli 40-60-UGI E. coli 40-60 %, %, enteropatogenenteropatogenicic E. coli 15 E. coli 15 %%,, enteroinvaenteroinvasivesive E. coli 5 E. coli 5 % %

Shigella, Salmonella, CampShigella, Salmonella, Campylobacter, ylobacter, rotavirusrotavirus,, l lambliaamblia, amoeba - 5% , amoeba - 5% unknownunknown etiology - up to 40% of cases. etiology - up to 40% of cases.

According to the According to the WHO classification, all WHO classification, all diarrheal diseases are diarrheal diseases are divided into: divided into:

1. I1. Infectious nfectious 2. 2. NonNoninfectiousinfectious

Types of diarrhea according to mechanism

of development

Secretory OsmoticInflammatory

(invasive)

AgentsAgents of of secretory diarrhea secretory diarrhea V. choleraeV. cholerae ClostridiumClostridium perfringensperfringens ЕЕnterotoxin and nterotoxin and ееnteropathogenicnteropathogenic E. coli E. coli BB. . cereuscereus SS. . aureus aureus occasionallyoccasionally

– – campylobacter,campylobacter, yersiniayersinia, , klebsiellaklebsiella Some simpleSome simplestst - - ccryptosporydiryptosporydiaa, ,

mimiccrosporrosporiididiaa, balantydi, balantydiaa, izospor, izosporeses

Pathogenesis of secretory Pathogenesis of secretory diarrhoeadiarrhoea

Enterotoxins

stimulative depressors

phosphodiasterase

↓ decay cAMP

adenylcyclasehyalinecyclase

↓ absorption of electrolytes

↑ cAMP ↑ c GMP

Activation of protein kinase

secretion of electrolytes

↑ fluid and electrolytes

in the intestine

diarrheastrengthening peristalsis

prostaglan-din

Secretory diarrhoeaSecretory diarrhoea Great loss of fluid, which contains little Great loss of fluid, which contains little

protein, and a large number of K +, Na +, protein, and a large number of K +, Na +, Cl-, HCO3-; Cl-, HCO3-; Loss of K +, can be up to 1 / 3 of its content Loss of K +, can be up to 1 / 3 of its content in the body, which leads to: in the body, which leads to:          - Dysfunction of myocardium;          - Dysfunction of myocardium;          - Damage to kidney tubules;          - Damage to kidney tubules;          - Paresis intestines;          - Paresis intestines;          - Co         - Convultionsnvultions; ; DevelopDevelopment ofment of extracellular isotonic extracellular isotonic dehdehyyddrratiationon, hypovolemia , hypovolemia withwith blood blood coagulation and a violation of coagulation and a violation of microcirculation, tissue hypoxia, metabolic microcirculation, tissue hypoxia, metabolic acidosis and respiratory alkalosis, failure of acidosis and respiratory alkalosis, failure of kidney function, liver infarction, kidney function, liver infarction, trombohemortrombohemorrraagicgic syndrome. syndrome.

Agents Agents of of osmotic diarrheaosmotic diarrhea Viruses: Viruses: rotarota-, aden-, -, aden-, aastro-, crown-, stro-, crown-,

reo-, kalitsy-reo-, kalitsy-, , NorfolkNorfolk & & Breda virus Breda viruseses and others. and others. The simplest: lyambliThe simplest: lyambliaa, , ccooxxydiydiaa. .

AlsoAlso appear appear afterafter enteringentering of excessive of excessive amounts of osmotic active substances amounts of osmotic active substances that are not absorbed in the intestine that are not absorbed in the intestine (sulfate magnesite, lactulose, sorbitol, (sulfate magnesite, lactulose, sorbitol, etc.), or in the formation etc.), or in the formation of them of them due to due to significant malabsorption, as well as significant malabsorption, as well as bacteria overgrowth. bacteria overgrowth.

Pathogenesis of osmoticPathogenesis of osmoticdiarrhoeadiarrhoea

Enterotropic viruses

damage of epithelial cells of small bowel

↑ sucrose

↑ мaltose

↓ activity К+/Nа+-АТphase

↑ lactose

↓ lactase

↓ maltase

↓ sucrase ↓ transportation of Na,

glucose to enterocytes

↑ osmotic pressure in intestine

↓ absorption of fluids in intestine

diarrhea

Agents Agents of of invasive diarrhinvasive diarrhooeaea Bacteria: Shigella, Salmonella, and Bacteria: Shigella, Salmonella, and

enteroinvaenteroinvasivesive enteroh enterohaaemoraemoragic gic escherichiaescherichia, intestinal yers, intestinal yersiniainia, , ccampylobacter, ampylobacter, cclostrydilostrydiaa, , staphylococci and some other staphylococci and some other enterobaenterobaccteriteriaa, , The simplest: lambliThe simplest: lambliaa, amoeba , amoeba histolhistolyytiticca. a.

Pathogenesis of invasivePathogenesis of invasivediarrhoeadiarrhoea

Agent

Invasion of intestinal wall

Inflammation

↑ histamin

↑ pg ↑serotonin

↑ kinin

Damage of membranes

Violation of microcirculation

Increased peristalsis

↑cytokinin

↑ Adenocycla

se

Exudates with mucous and blood

Diarrhea

Secretory diarrhea. Secretory diarrhea. Clinical manifestations Clinical manifestations

Acute bAcute beginingegining fromfrom the imperative the imperative ((orderorder) call for a bowel movement; ) call for a bowel movement; liquid stool, watery, liquid stool, watery, abundantabundant (0,5-1 (0,5-1 litersliters for defecation for defecation), without ), without pathological impurities often turbidly pathological impurities often turbidly with floating white flakes, like rice-with floating white flakes, like rice-water, have a weak smell of fresh fish water, have a weak smell of fresh fish or friction potatoes; or friction potatoes;

Secretory diarrhea. Secretory diarrhea. Clinical manifestationsClinical manifestations

abdominal pain is not typical, may be slightly abdominal pain is not typical, may be slightly unpleasant aching sensation around the unpleasant aching sensation around the navel, which intensifies during defecation; navel, which intensifies during defecation; abundant vomiting, repeated, often abundant vomiting, repeated, often suddenly, without nausea, like a fountain; suddenly, without nausea, like a fountain; initially contains the remains of food initially contains the remains of food, , thethenn - - like rice broth; like rice broth; body temperature is often normal or body temperature is often normal or subfebrsubfebriil, l, in in significant dehydration - significant dehydration - subnormal; subnormal; diarrhea and vomiting diarrhea and vomiting lead lead to dehydration, to dehydration, which can reach the III-IV degree. which can reach the III-IV degree.

Degrees of DehydrationDegrees of Dehydration

I -I - fluid loss 1-3 fluid loss 1-3 %; %; IIII - - 4-6 4-6 %; %;

III - III - 7-97-9 %; %; IV - IV - 1010 % of body weight % of body weight and moreand more

DEHDEHYYDRATDRATIONALIONAL SHOCK SHOCK Develops Develops with bacterial diarrhea, the clinical with bacterial diarrhea, the clinical

syndrome syndrome ofof gastroenteritis, gastroenteritis, caused by:caused by:

cholera; cholera; salmonellsalmonellosisosis ( (ggastrointestastrointestinalinal form); form); esesccherherichiosis ichiosis caused caused by by EEnterotoxicnterotoxic and and EEnteropathogenic species;nteropathogenic species; food poisoningfood poisoning caused by caused by semipathogenic semipathogenic floraflora; ; staphylococcal toxicosis; staphylococcal toxicosis; intestinal yersintestinal yersiinioniosissis. .

PPathogenesis of hathogenesis of hyypovolemic povolemic shockshock

Gastroenterocolitis

Vomit,diarrhea

Polyorgan insufficiency

Disorders of systemic haemodynamics

Loss of isotonic fluids, electrolytes and alkali

Decrease of Blood vol

Metabolic acidosis

Hypoxia Electrolytic violations

Deficit ofmackroergs

Polysat lipids

Dehydrational Dehydrational shock shock Diarrhea (watery Diarrhea (watery or or rice-water stool), without rice-water stool), without

abdominal pain without fever abdominal pain without fever Fountain vomiting without nausea Fountain vomiting without nausea Thirst Thirst Dehydration Dehydration Forensic cyanosis. Wrinkled skin, gray and cold Forensic cyanosis. Wrinkled skin, gray and cold to the touch, a sharp decline in tissue elasticity to the touch, a sharp decline in tissue elasticity and turgor pressure, "washerwoman handsand turgor pressure, "washerwoman hands””, , symptom of glasses symptom of glasses Voice hoarse, often aphonia Voice hoarse, often aphonia Generalized convulsions Generalized convulsions Body temperature decreased Body temperature decreased Pulse filamentary 100-120 and> for 1 min. Pulse filamentary 100-120 and> for 1 min. AT <80 and 50 mm Hg. AT <80 and 50 mm Hg. Heart tones very weak activity often Heart tones very weak activity often arrhythmic, Hyperventilation arrhythmic, Hyperventilation Anuria Anuria

Dehydrational shockDehydrational shock

Cholera, IV degree of dehydration. Skin easily taken in the fold, which is not elastic

Dehydrational face of the patient

A child with IV degree dehydration

Suffering from cholera, dehydration IV degree

Dehydrational shockDehydrational shock Laboratory testLaboratory test

Thickening of blood - Thickening of blood - pseudoerythrocytosispseudoerythrocytosis leukocytosis, increased hematocrit (0.55 l / l leukocytosis, increased hematocrit (0.55 l / l and more), blood viscosity, relative density and more), blood viscosity, relative density plasma (1030 and older), protein, globulin plasma (1030 and older), protein, globulin Renal impairment - creatinine level in blood Renal impairment - creatinine level in blood higher higher than 150 micromole / l than 150 micromole / l A significant deficiency of electrolytes - (K +, A significant deficiency of electrolytes - (K +, Na +, Cl-, HCO3-) Na +, Cl-, HCO3-) Uncompensated metabolic acidosis and Uncompensated metabolic acidosis and respiratory hrespiratory hYYpopoccapnia - (capillary blood pH apnia - (capillary blood pH 7,1-7,3 and often lower - rate 7,36-7,44, lack of 7,1-7,3 and often lower - rate 7,36-7,44, lack of buffer bases reaches 10-20 mmol / l - in normal buffer bases reaches 10-20 mmol / l - in normal 0,5 ± 2, 50,5 ± 2, 5))

Osmotic diarrhea Osmotic diarrhea Acute beginingAcute begining, more often - with vomiting and watery , more often - with vomiting and watery

diarrhea; diarrhea; moderate general signs of intoxication; moderate general signs of intoxication; emptying abundant, watery, yellow or yellow-greenish emptying abundant, watery, yellow or yellow-greenish color, frothy, with a sharp odor, color, frothy, with a sharp odor, undigestedundigested remnants of remnants of food (stearrhea, kreatoreya, amiloreya) without mucfood (stearrhea, kreatoreya, amiloreya) without mucoous us and blood; and blood; short-term increase in body temperature; short-term increase in body temperature; possible rhinitis, swelling of the tongue, mucous possible rhinitis, swelling of the tongue, mucous membrane hyperemia fauces and its granularity membrane hyperemia fauces and its granularity weak pain in epigastric and weak pain in epigastric and periumbilical periumbilical areas, gross areas, gross burburogmi burburogmi at palpationat palpation in caecum in caecum ; ; blood count at the beginning without changes later - blood count at the beginning without changes later - with relative leukopenia and limfotsytozom with relative leukopenia and limfotsytozom monotsytozom; monotsytozom; inin    coprogramcoprogram undigestedundigested food, starch grains, unaltered food, starch grains, unaltered muscle fibersmuscle fibers. .

InvasivInvasivee diar diarrhrheaea BBeginning with acute abdominal pain and eginning with acute abdominal pain and

diarrhea; diarrhea; dominant features of lesions of colon: tenesmus, dominant features of lesions of colon: tenesmus, sensation of incomplete evacuation, sensation of incomplete evacuation, falsefalse call call for for defecationdefecation; ; stool scanty, containing only mucstool scanty, containing only mucoous us with with admixture of admixture of bloodblood (rectal sp (rectal spllit); it); sigma painful, tight; sigma painful, tight; expressed signs of intoxication; expressed signs of intoxication; Sigmoidoscopy: catarrhal, catarrhal-hemorrhagic, Sigmoidoscopy: catarrhal, catarrhal-hemorrhagic, erosive or ulcerative proerosive or ulcerative procctostosigmoigmoididiittisis and and ssphphininccterteriittisis; ; leukocytosis, <eosinophilleukocytosis, <eosinophileses count and ESR ↑; count and ESR ↑; coproscopycoproscopy - remains - remains of undigestedof undigested food food additives and pathological - mucus accumulation additives and pathological - mucus accumulation of leukocytes with a predominance of of leukocytes with a predominance of neutrophils, many red blood cells and epithelial neutrophils, many red blood cells and epithelial cells; cells; Dehydration is not typical. Dehydration is not typical.

Treatment of secretory diarrhea Treatment of secretory diarrhea Rehydration therapy - restoration of Rehydration therapy - restoration of

electrolyte and water homeostasis. electrolyte and water homeostasis.

      - By the time of - the primary and       - By the time of - the primary and compensatcompensatoryory

      - By way of - parenteral and oral      - By way of - parenteral and oral

Solutions for parenteral Solutions for parenteral rehydration rehydration

TrisaultTrisault ( (Philips Philips І)І) QuartasaultQuartasault AcesaultlAcesaultl ChlosaultChlosault LactosaultLactosault DisaultDisault ( (philips-philips- ІІ) – ІІ) – withoutwithout К К++

Solutions for oral rehydration Solutions for oral rehydration therapy (ORStherapy (ORS))

First First generation - generation - oralitoralit (containing 3.5 g (containing 3.5 g sodium chloride, 2.5 g sodium, 1.5 g sodium chloride, 2.5 g sodium, 1.5 g potassium chloride and 20 g of glucose), potassium chloride and 20 g of glucose), gglyulyuccosolanosolan, , gastrolitgastrolit and others. and others. Second generation - Second generation - rehidronrehidron, , citrogcitroglyulyuccosolanosolan and others. - More and others. - More potassium chloride, citrate instead of soda. potassium chloride, citrate instead of soda. Super-ORS (third generation) - ORS-200 Super-ORS (third generation) - ORS-200 (HIPP) - in which glucose-monohydrate (HIPP) - in which glucose-monohydrate replaced it replaced it short chain short chain polymers contained in polymers contained in the broth cereals (rice, corn, sago), carrots, the broth cereals (rice, corn, sago), carrots, reduce the frequency and reduce the frequency and vvolume olume of stool. of stool.

«cholera» bed

Hypovolemic shockIntensive therapy

Hypovolemic shockIntensive therapy

Rehydration is Rehydration is performed performed in the hospital in 2 in the hospital in 2 stages: stages: II(primary) - immediately (primary) - immediately byby the the infusionsinfusions of standard saline of standard saline solutionssolutions 3-4 3-4 IVIV amounting to 10% of body weight amounting to 10% of body weight duringduring 1 1 - - 1,5 h1,5 hourour, the patient is placed on a "cholera" , the patient is placed on a "cholera" bed, carefully consider all the fluid lossbed, carefully consider all the fluid loss

II (II (compensatorycompensatory) - replenish lost fluids and ) - replenish lost fluids and electrolytes, which continues electrolytes, which continues After stopping vomiting - combined adeAfter stopping vomiting - combined adequatequate an an IV IV and and peroralperoral standard rehydration salt standard rehydration salt solutionsolution - oralit, rehidron - oralit, rehidron Causal treatment - Causal treatment - doxacyclindoxacyclin

Principles of osmotic diarrhea Principles of osmotic diarrhea therapytherapy

Rehydration Rehydration Enzyme preparations Enzyme preparations Probiotics Probiotics Enterosorbents Enterosorbents IIn children n children ((severesevere)) - antiviral drugs - antiviral drugs (human and recombinant interferons)(human and recombinant interferons)

Principles of Principles of invasiveinvasive diarrhea diarrhea therapy therapy

Etiotropic therapyEtiotropic therapy: :     - Chemotherapeutic drugs     - Chemotherapeutic drugs     - Antibiotics     - Antibiotics DeDessintoxication intoxication Spasmolithics Spasmolithics Probiotics Probiotics ReparantReparantss Local - Local - adsorbentsadsorbents, anesthetics, , anesthetics, reparantreparantss

Cholera Cholera – – is a dangerous is a dangerous intestinal infection, that is intestinal infection, that is caused by caused by Vibrio choleraeVibrio cholerae and characterized by and characterized by destruction of small destruction of small intestine with diarrhea, intestine with diarrhea, vomiting and dehydration vomiting and dehydration of organismof organism

DrawingDrawing of of DeathDeath

bringing the bringing the cholera, in cholera, in LeLe PetitPetit JournalJournal

By 12 By 12 February February 2009, the 2009, the number of number of cases of cases of

infection by infection by cholera in cholera in

sub-Saharan sub-Saharan Africa had Africa had reached reached

128,548 and 128,548 and the number the number of fatalities, of fatalities,

4,053.4,053.

I pandemicI pandemic – 1816-1826: Began in Bengal – 1816-1826: Began in Bengal and then spread across India by 1820.and then spread across India by 1820.

II II – 1829-1851: reached Russia, Hungary – 1829-1851: reached Russia, Hungary and Germany in 1831, London and Paris in and Germany in 1831, London and Paris in 1832.1832.

III III – 1852-1860: mainly affected Russia, with – 1852-1860: mainly affected Russia, with over a million deaths.over a million deaths.

IV IV – 1863-1875: spread mostly in Europe – 1863-1875: spread mostly in Europe and Africa.and Africa.

V V –– 1881-1896: was the last serious 1881-1896: was the last serious European outbreak.European outbreak.

VIVI – 1899-1923: Russia, Ottoman Empire, – 1899-1923: Russia, Ottoman Empire, Phulippines.Phulippines.

VII VII –– began in Indonesia, called El Tor after began in Indonesia, called El Tor after the strain and reached Bangladesh, India, the strain and reached Bangladesh, India, USSR, North Africa.USSR, North Africa.

Recent and ongoing outbreaksRecent and ongoing outbreaks In 2000, some 140,000 cholera cases In 2000, some 140,000 cholera cases

were officially notified to WHO.were officially notified to WHO. August 2007 – The cholera epidemic August 2007 – The cholera epidemic

started in Orissa, India. Has affected started in Orissa, India. Has affected Rayagada, Koraputand Kalahandi Rayagada, Koraputand Kalahandi districts where more than 2,000 districts where more than 2,000 people have been admitted to people have been admitted to hospitals.hospitals.

August 2008 – April 2009: In August 2008 – April 2009: In Zimbabwean cholera outbreak, which Zimbabwean cholera outbreak, which is still continuing, an estimated is still continuing, an estimated 96,591 people have been infected 96,591 people have been infected and 4,201 deaths had been reported. and 4,201 deaths had been reported.

Reasons of dangerReasons of dangerRapid increasing of morbidity

to epidemic and pandemic levels

Quarantine infection Quarantine infection (according to International (according to International convention, 1926)convention, 1926)

High lethalityHigh lethality

EtiologyEtiologyBiovars - Vibrio classical, El-Biovars - Vibrio classical, El-TorTorSerovarsSerovars -- OgavaOgava, , InabaInaba, , Hikojima,Hikojima, Bengal Bengal О-139О-139 Toxic substances - exotoxin Toxic substances - exotoxin ((cholerogencholerogen), ), penetration penetration factorfactor, , endotoxinendotoxinMorphologyMorphology -- gramnegative gramnegative comma-shaped rodcomma-shaped rod, , motile, motile, don’t produce capsules and don’t produce capsules and sporesspores

EpidemiologyEpidemiologySourse of infectionSourse of infection – – sick personsick person,,

reconvalescent and vibrio-reconvalescent and vibrio-

carriercarrier(1:100)(1:100)

Mechanism of transmissionMechanism of transmission – – fecal- fecal-

oraloral

Susceptibility – Susceptibility – highhigh

Seasonal – Seasonal – summer-autumnsummer-autumn

Types of epidemicsTypes of epidemicsWater (most frequent)Water (most frequent)FoodFoodContact - domesticContact - domestic MixedMixed

Features of VII pandemics of Features of VII pandemics of cholera:cholera:

Endemic area – IndonesiaEndemic area – Indonesia Detection of Detection of V. choleraeV. cholerae ( (El-Tor)El-Tor) from from

reservoirs (water) before the reservoirs (water) before the beginning of epidemiabeginning of epidemia

Obliterated and atypical forms more Obliterated and atypical forms more oftenoften

Lethality is lowLethality is low Prolonged careeringProlonged careering

PathogenesisPathogenesis Penetration into the organismPenetration into the organism Adhesion to intestinal wall, multiplication Adhesion to intestinal wall, multiplication

(without destroying of epithelial cells and (without destroying of epithelial cells and inflammation)inflammation)

Exotoxin-cholerogen have activate Exotoxin-cholerogen have activate adenylcyclase adenylcyclase

Increasing production of cyclic-3-5-Increasing production of cyclic-3-5-adenosynemonophosphatesadenosynemonophosphates

Destroying of “natrium pump” Destroying of “natrium pump” Increasing secretion of electrolytes and Increasing secretion of electrolytes and

waterwater Dehydratation, demineralizationDehydratation, demineralization Hypovolemia, hemodynamics disordersHypovolemia, hemodynamics disorders Tissue hypoxia, metabolic acidosis, Tissue hypoxia, metabolic acidosis,

respiratory alcalosisrespiratory alcalosis

Cholera Toxin. Cholera Toxin. The delivery The delivery region (blue) region (blue)

binds binds membrane membrane

carbohydrates carbohydrates to get into cells. to get into cells. The toxic part The toxic part

(red) is activated (red) is activated

inside the cellinside the cell

ClassificationClassification Causative agentsCausative agents: : V. cholerae O1 biovar V. cholerae O1 biovar

cholerae (A00.0), V. cholerae O1 biovar El-cholerae (A00.0), V. cholerae O1 biovar El-Tor (A00.1), unspecified (A00.9)Tor (A00.1), unspecified (A00.9)

Clinical formsClinical forms: : typical and atypical typical and atypical (mildest, gastric, in breast feeding childs (mildest, gastric, in breast feeding childs and in elderly people)and in elderly people)

Degree of severity in typical form:Degree of severity in typical form: mild, moderate, severe, very severemild, moderate, severe, very severe

Degree of dehydration:Degree of dehydration: without without dehydration, with dehydration I, II, III, IV dehydration, with dehydration I, II, III, IV degreesdegrees

Complications:Complications: choleric algid, collapse, choleric algid, collapse, acute kidney insufficiency, pneumonia, acute kidney insufficiency, pneumonia, abscess, phlegmon abscess, phlegmon

Clinic featuresClinic features Incubation periodIncubation period - from some - from some

hours till 5 days (in average 48 hours till 5 days (in average 48 hours)hours)

Acute onsetAcute onset DiarrheaDiarrhea appears suddenly, without appears suddenly, without

pain, often at night or in the pain, often at night or in the morning. Often accompanied by morning. Often accompanied by gurgation in the stomach. After 1-2 gurgation in the stomach. After 1-2 defecation stool become cloudy, defecation stool become cloudy, white, fluid, without smell and “rice-white, fluid, without smell and “rice-water” water”

VomitingVomiting fountain fountain

““Rice-water” character of stool in choleraRice-water” character of stool in cholera

Clinical-epidemiological features of Clinical-epidemiological features of choleracholera

Beginning from diarrhea and Beginning from diarrhea and vomitingvomiting

Development of dehydrationDevelopment of dehydration Accordance with epidemiologic Accordance with epidemiologic

agentsagents Colorless watery stoolColorless watery stool Absence of abdominal pain and Absence of abdominal pain and

tenesmustenesmus Decreasing of body temperature or Decreasing of body temperature or

normalnormal

Cholera Cholera hospital in hospital in

Dhaka Dhaka

DiagnosticsDiagnostics Revealing ofRevealing of causative agent in stoolcausative agent in stool, ,

vomiting massesvomiting massesExpress-methodsExpress-methods ((microscopy of microscopy of ““hanginghanging” ” dropdrop– –

formform,, mobility mobility; ; reaction of immobilization; reaction of immobilization; reaction of agglutinationreaction of agglutination ant choleraeant cholerae О- О-serumserum;; reaction immune fluorescencereaction immune fluorescence))

Inoculation Inoculation to to 1 % 1 % peptonic water with further peptonic water with further reinoculation reinoculation to Ressler mediumto Ressler medium

Determination of antibodies titerDetermination of antibodies titer ((retrospectiveretrospective))

Signs of blood thicken (pachyemia)Signs of blood thicken (pachyemia): : increasing of erythrocyte numberincreasing of erythrocyte number,, leucocytes leucocytes, ,

hemoglobinhemoglobin;;hematocritehematocrite, , relative density of plasmarelative density of plasma;;hypokalemiahypokalemia

TreatmentTreatment Regidration Regidration І (І (primaryprimary)) - - immediately iimmediately i//vv infusion of salt infusion of salt

solutionssolutions ( (Trisol, Acesolum, Lactasol, Quartasol, Trisol, Acesolum, Lactasol, Quartasol, HlosolHlosol)) 10 % 10 % of primary patients weight inof primary patients weight in 1,5-2 1,5-2 hours hours ((under the control of potassium and natrium under the control of potassium and natrium acidic-alkali balance of bloodacidic-alkali balance of blood); );

It is necessary to punct It is necessary to punct 3-4 3-4 vesselsvessels; ; put patient put patient intointo““choleracholera” ” bed for carefully account of sequel bed for carefully account of sequel loss of loss of liquorliquor

ІІ (ІІ (compensatorycompensatory)) – – correction of sequel losscorrection of sequel loss In case of In case of І І andand ІІ ІІ degrees – degrees – adequate per oral adequate per oral

regidration with standart salt solutions regidration with standart salt solutions – о– оralitralit, , regidron regidron ((І – 30 І – 30 mlml//kgkg, ІІ - 60–70 , ІІ - 60–70 mlml//kgkg) –) – inin 1,5 1,5 times higher than loss of liquor with obligatory times higher than loss of liquor with obligatory addition of glucoseaddition of glucose

Antibiotics - Antibiotics - cotrimoxazolecotrimoxazole, , erythromycinerythromycin, , doxycyclinedoxycycline, , chloramphenicolchloramphenicol ( (levomycetin),levomycetin),

furazolidonefurazolidone. . FluoroquinolonesFluoroquinolones such as such as norfloxacinnorfloxacin also may be used, but resistance has been also may be used, but resistance has been reported. reported.

Cholera patient being treated by Cholera patient being treated by medical staff medical staff

Antepidemic measures in case of Antepidemic measures in case of revealing of patient with cholerarevealing of patient with cholera

Immediately isolation of sick person and treatmentImmediately isolation of sick person and treatment;; Discharging of convalescents after clinical Discharging of convalescents after clinical

recovering and negative results of 3 bacteriological recovering and negative results of 3 bacteriological investigationsinvestigations;;

Declaring of quarantine territoryDeclaring of quarantine territory;; Everyday rounds of all citizensEveryday rounds of all citizens;; Revealing and hospitalization of all suspicious Revealing and hospitalization of all suspicious

personspersons;; Revealing and isolation for incubation period Revealing and isolation for incubation period ((in in

case of cholera case of cholera - 5- 5 days days) ) all persons who been in all persons who been in contact with corpse or things of using of dead personcontact with corpse or things of using of dead person;;

Laboratory investigation of populationLaboratory investigation of population;; DisinfectionDisinfection

Thanks For Your Thanks For Your Attention!Attention!