Lecture 3. Acute intestinal infections

 

SHIGELLA

 

Shigelloses (dysenteries) are acute nhuman infectious diseases with enteral infection that is characterized by colitic syndrome and symptoms of general intoxication, nquite often with development of primary neurotoxicosis.

 

Etiology: Shigella, gram negative bacteria, immobile, sized 2-3 mkm, without sporing and incapsulation, product endotoxin, resistant to the nenvironment (in milk, water, food stay for several days, in soil –for several nweeks), stable to the freezing, but sensitive for boiling. By antigen structure nand biochemical properties shigella are devided into 4 subgroups: A, B, C, D:

·         nSh.dysenteriae – belongs to group A

·         nSh. nflexneri – belongs to group B

·         nSh.boydii – belongs to group C

·         nSh.sonnei – belongs to group D

Sh. flexneri and Sh.sonnei are the most often agents for bacterial dysentery nnowadays.

 

Epidemiology:

Source of infection –

•         nContagious npatient

•         nBacillus ncarrier

Shigella is spread through fecal-oral mechanism of ntransmission.

The way of transmission

•         nContact

•         nAlimentary

•         nWatery

Susceptibility: 60-70% especially infants and npreschoolers.

Seasonality is summer-autumn.

 

Pathogenesis:

1.      Entrance Shigella nto gastrointestinal tract.

2.      Destruction of them under the ninfluence of ferments.

3.      Toxemia.

4.      Toxic changes in organs and systems n(especially in CNS).

5.      Local inflammatory process (due to ncolonizing of distal part of the colon).

6.      Diarrhea.

 

Classification

1. Clinical Form

n

Typical

•         nWith ndominance of toxicosis

•         nwith ndominance of local inflammation

•         nmixed n

Atypical

•         nEffaced n

•         nDyspeptic

•         nSubclinical

•         nHypertoxic

2.  Severity (mild, moderate and severe)

n

3. Duration

n

•         nacute n(up to 1.5 mo)

•         nsubacute (up to 3 mo)

•         nchronic n(about 3 mo)

ü  recurrent

ü  constantly recurring

4. Course

n

•         nSmooth

•         nUneve(with complication)

V. Bacterium carrier

 

Clinical criterions (With dominance of toxicosis):

·         nPeriod nof incubation: a few hours to 7 days.

·         nToxicosis is the first sing even may be neurotoxicosis (lose of appetite, nheadache, fatigue, vomiting, hallucinations, unconsciousness, seizure, febrile ntemperature 39-40°C).

·         nColitis nis secondary (abdominal pain, tenesmus, false urge to ndefecate, sigmoid colon is tender, spastic, anus is open in hard cases. Feces nin the form of a spit of mucus and blood (rectal spit), enlargement of number nof defecation).

·         nDehydratioisn’t developed (except infants).

 

With dominance of local inflammation

•         nSudden onset of high-grade fever

•         n abdominal ncramping

•         nabdominal pain,

•         ntenesmus,

•         nand large-volume , mucus, cylindrical epithelial cells diarrhea →

•         nfecal incontinence, and small-volume mucous diarrhea nwith frank blood

 

Peculiarities of nshigellosis in infants:

·         nAcute nbeginning with slow development of signs and symptoms (for 3-5 days).

·         nDistal ncolitis is less common

·         nEnterocolitis is more often with enterocolitic nfeces, hemocolitis is rare.

·         nHepato– and splenomegaly

·         nCrying, nanxiety, red face during defecation is equivalent to tenesmus.

·         nAlways noccurs gaping anus, sphincteritis

·         nDehydratiois more often

·         nProlonged nduration of the disease

 

Criteria of the Shigellosis Severity

Mild form

•         nConsistent nor acute onset of diarrhea

•         n Stool is 5-8 times per day with mucous and nblood

•         nNot npermanent pain in abdominal region.

•         nThe ntemperature is normal

•         nLoss nof appetites

•         nCabe vomiting 

Moderate form

•         nAcute nonset of diarrhea

•         nSymptoms nof toxicosis

•         n The temperature is 38-39°C

•         nAnorexia

•         nCrampy abdominal pain

•         n Stool is 10-15 times per day

•         nPaiduring palpation in left inguinal region

•         nhepatomegaly

Severe form

•         nMultiple nvomiting not only after receiving the food, but also independent, can be with nbile, sometimes – as coffee lees,

•         nexcrements n- more 15 times per day, sometimes – with each diaper, much mucus, there is nblood, sometimes – an intestinal bleeding

•         nGeneral ncondition is sharply worsened,

•         nquite noften – sopor, loss of the consciousness, cramps,

•         nchanges nin all organs and systems,

•         nsevere ntoxicosis, may be dehydration (in infants),

•         nsignificant nweight loss

 

Laboratory tests:

•         nThe white blood cell count is often within reference range, with a high npercentage of bands. Occasionally, leucopenia or leukemic reactions may be ndetected.

•         nIn HUS, anemia and thrombocytopenia occur. n

•         nStool examination Increasing of red blood cells and nleukocytes

•         nStool culture Specimens should be plated lightly nonto Endo-Levin, Ploskirev, McConkey, nxylose-lysine-deoxycholate, or eosin-methylene blue nagars.

•         nSerological test: (AR, PHAR in dynamics with fourfold title nincreasing in 10-14 days) in children elder than 1 year if fecal culture is nnegative.

 

Diagnosis example:

•         nShigellosis (Sh. sonnei), ntypical form (with dominance of toxicosis), severe ndegree, acute duration.

•         nShigellosis (Sh. flexneri), ntypical form (with dominance of local inflammation), moderate degree, constantly recurring duration, complicated by the rectum prolapse

 

Differential diagnosis should be performed with: nsalmonellosis, escherichiosis, acute appendicitis, nbowel invagination, Krohn’s disease, nonspecific nnecrotizing colitis.

 

Treatment: see treatment of Ecsherichiosis below

 

Prophylaxis

·         nEpidemiological ncontrol for water and food.

·         nIsolatioand sanation of ill person

·         nReconvalescent may be discharged from hospital after one nnegative feces culture ( taken 2 days after course of antibiotic therapy)

·         nDispensarization of reconvalescent nfor 1-3 months

·         nFeces nculture in contacts, carriers

·         nLooking nafter contacts for 7 days, quarantine

·         nDisinfectioin epidemic focus

 

SALMONELLA INFECTIONS

 

Salmonellosis is an acute ninfectious disease of human and animals, that is caused by the numerous strains nof Salmonella and more frequent courses as gastro-intestinal, rare – as typhoid nand septic forms

 

Etiology: Salmonella, over 2000 strains, nGramm-negative movable bacili, nthat don’t form capsules and spores. Their main antigents are O-H-and Vi, by nO-antigen are devided on groups (A, B, C, D, E, F netc.). Most often salmonella infection are called by:

•         nS. typhimurium n

•         nS. enteritidis n

•         nS. java

•         nS. anatum nand other

Bacteria are stable in the environment (for nmonths and years they live in food, water, soil), hot temperature kill them i1 hour.

 

Epidemiology:

• Source of infection: ill person, carrier, ill animals and birds

• Way of spreading – alimentary or by water; by direct contact, rare air-droplet

• Susceptible organism: children, especially before 2 years old

n

 

Pathogenesis

1.      Massive entering of bacteria to the alimentary canal.

2.      Destruction of salmonella in the upper departments of alimentary canal.

3.      Toxemia → nvomit (as a protective factor).

4.      Entering of other nbacteria into thin intestinum, colon, colonization of epitheliocytes.

5.      Local inflammatory process, dysperistalsis, digestion and suction nimparement, biologically active substance accumulation, which impare absorption of water, electrolytes n(diarrhea, dehydration).

6.      Damage of the intestinal, nlymphatic barriers (septic form of nsalmonellosis).

7.      nBacteriemia.

8.      nForming of septic nfocuses.

 

Classification

1.      Local form

•         nGastrointestinal nform

•         n Bacterium carrying

2.      General form

•         nTyphoid fever – nlike

•         nSepsis

3.      Asymptomatic form

     nII.            nSeverity (mild, moderate and severe)

 III.            nDuration

•         nAcute (up to 1.5 mo)

•         nSubacute (up to 3 mo)

•         nChronic (more than 3 mo)

4. Course

n

•         nSmooth

•         nUneve(with complication)

V. Bacterium carrier

 

Clinical ndiagnostic criterions

Of local ngastro-intestinal forms:

·         nperiod of incubation: hours (for gastritis) – several ndays (in case of spreading by direct contact)

·         nacute beginning from: intoxication (nausea, vomiting, nhigh body temperature, headache);

• abdominal pain;

• diarrhea, usually appears secondary, stools are “muddy” , may be with blood and mucus, abdomen is tender; dehydration is moderate.

n

 

Typhoid form

• acute beginning from high temperature (39-40˚ C) lasting for 1-2 weeks,

• vomiting, hallucinations;

• “Typhoid” tongue;

• hepato-, splenomegaly from the 5-6 day of disease;

• skin rash (roseols) on the trunk;

• diarrhea;

• tenderness in the right inguinal part of abdomen.

n

 

Septic form

·         nIncubation period is long (5-10 days).

• Usually occurs iewborns, infants with predisposal factors (hypotrophy, rickets so on).

• Acute beginning from fever that becomes hectic.

• Septic focus: meningitis, pneumonia, osteomyelitis, pyelonephritis, enterocolitis);

• hepatosplenomegaly;

• hemorrhagic syndrome;

• development of toxic-dystrophic syndrome;

• relapses,

• longitude duration, formatio of carrying;

• high mortality;

• antibiotic resistance, nosocomeal strains of Salmonella;

• contact way of spreading.

n

 

Salmonellosis nFeatures in the newborns

·         nGeneralized nform, high lethality.

·         nThe nmechanism of transmission is contact-domestic (through nursery facilities).

·         nSources nare mothers, hospital personnel.

·         nAgent n- hospital strains of Salmonella.

·         nHigh nresistance to antibiotics

·         nProlonged nlatent period (5-10 days).

·         nGradual nbeginning with growth of clinical symptoms.

·         nSevere nand prolonged intoxication.

·         nProtracted nmotion, transmitter, relapses.

·         nToxic-dystrophic nsyndrome development.

 

 Laboratory ntests

• Complete blood count with differential

n

•         nCultures: Isolation of Salmonella from cultures of nstool, blood, urine, or bone marrow is diagnostic. Specimens should be plated nlightly onto Endo-Lewin, Ploskirev, nMcConkey, xylose-lysine-deoxycholate, nor eosin-methylene blue agars.

• Stool examination: Stool may be hemoccult positive and may be stool positive for fecal polymorphonuclear cells.

• Chemistry: Electrolyte tests may reveal metabolic acidosis or other abnormalities consistent with dehydration.

• Serologic tests: (AR, PHAR in dynamics with fourfold title increasing in 10-14 days) in children elder than 1 year if fecal culture is negative.

n

 

Diagnosis example:

·         nSalmonellosis (S. enteritidis), typical local gastrointestinal form (enterocolitis), moderate degree, acute duration. Complication: isotonic dehydration, 1st degree.

·         nSalmonellosis (S. typhimurium), typical generalized septic form (enterocolitis, meningitis, bilateral pneumonia, left nhumeral bone osteomyelitis), severe degree, subacute nduration. Complication: malnutrition, n2^nd degree.

 

Differential diagnosis should be performed with: functional diarrhea, nshigellosis, escherichiosis, klebsiellosis, ntyphoid fever, and sepsis of different etiology.

 

Treatment: see treatment of Ecsherichiosis below

 

Prophylaxis:

 – nEpidemiological control.

 – nIsolation and sanation of ill person and carriers.

 – Reconvalescent may be discharged from hospital after one nnegative feces culture (taken 2 days after stop of antibiotic therapy).

 – Dispensarization of reconvalescents nfor 3 months.

 – Feces nculture in contacts, carriers.

 – Looking nafter contacts for 7 days without quarantine.

 – nDisinfection in epidemic focus.

 

 

ESCHERICHIA COLI

 

Escherichia coli infection is aacute infectious disease mainly of early age children, caused by different npathogenic strains of Escherichia ncoli, and is characterized by localization of pathological process iGastro-intestinal tract with development of toxic and diarrhea syndromes, rarer n- defeat of other organs or generalization of the process up to sepsis or nfailure to thrive development.

 

Etiology: enterotoxigenic, nenteropathogenic, enteroinvasive, nenterohemorrhagic Escherichia Coli. Escherichia ncoli, a facultative anaerobic gram-negative bacillus, is na major component of the normal intestinal flora and ubiquitous in the humaenvironment.

They well grow in ordinary  environments, nave a difficult antigen structure. Microbes contain a nsomatic 0-antigen, flagellate Н-antigen and nsuperficial somatic O-antigen. Distinctions in a 0-antigen devide nbacteria into number of 0-groups (serological groups) Different pathogenic neffects, caused Е. coli, are conditioned by producted enthero-, cyto– and verotoxins, and also by nthe adhesive and invasive activity of bacteria.

Nowadays several categories of Е. coli that cause diarrhea are known: enterotoxigenic, enteropathogenic, nenteroinvasive, enterohemorrhagic, nenteroadgesive (enteroadherrent). n

 

Epidemiology:

·         nSource of ninfection n– ill person or carrier;

·         nWay of spreading – orally – Fecal n(by water, milk, food); by direct contact;

·         nSusceptible organism: children, especially before 2 nyears of old.

 

Pathogenesis:

1.      Invasion of bacteria in GIT

2.      Reproduction of bacteria, selection of toxins

·         nEPE on the enterocytes nsurface

·         nETE on the enterocytes nmicrovilli surface

·         nEIE, EHE in the colon epithelial cells

3.      Local inflammatory process (EPE, EIE), toxemia (EPE, EIE)

4.      Violation of the surface and membrane ndigestion, absorption (EPE, nEIE), hypersecretion, violation nof water, and electrolytes absorption (ETE)

5.      Diarrhea

6.      In severe cases: nbacteremia (sepsis)

 

Clinical features

Enteropathogenic diarrhea is usually nself – limited in older children and adults. Nausea, vomiting, cramps and nvoluminous diarrhea without blood and mucus are common. Diarrhea nlasting 2 weeks or longer in infants.

Enterotoxigenic diarrhea includes nausea, vomiting, cramps and nfrequent watery stools. There no fecal leukocytes in the stool. This syndrome nis usually self – limited and lasts about 5 days.

Enteroinvasive strains are nassociated with a clinical picture comparable to those observed with shigella. Nausea and vomiting frequently accompany nabdominal pain. The diarrhea is less in volume than that seen with ETEC strains nand contains mucus and blood. Fever, headache, and myalgia are common.

Enterohemorrhagic escherichiosis is associated with severe abdominal cramps, nlow – grade fever, grossly bloody stools, nausea and vomiting. This organism nalso has been found in association with hemolytic uremic syndrome (HUS).

5. Enteroadgesive n(enteroadherrent) Е. coli  were primary nselected in 1985. They have not invasive activity, does nnot form cytotoxins and does not have a plasmide adhesive factor. The category of EAEC while is not nrepresented by any serological group.

 

Enteropathogenic E.coli infection criteria

·         nLatent nperiod 5-8 days, iew-born, weakened – 1-2 days.

·         nAccordingly: ngradual or acute illness beginning.

·         nThe nwatery massive yellow-orange feces with the too-bit of mucus the green color nadmixtures sometimes (photo), up to 10-15 times per day.

·         nVomits, nregurgitation from the disease beginning.

·         nGradual ngrowth of symptoms up to 5-7 days.

·         nsubfebril temperature.

·         ntoxicosis with dehydration of 2-3 stage

·         nCredible nacute kidney or adrenal insufficiency, DIC-syndrome, infectious-toxic shock.

 

Enteropathogenic E.coli infection peculiarities iewborns

·         nhospital infection caused by resistant cultures.

·         ninfection generalization with development of sepsis.

·         nFrequent ndamage of brain-membranes, with development of the remaining phenomena

·         nRarely noccurs diarrhea.

·         nHigh nlethality.

 

Enteroinvasive E.coli infection ncriteria

·         nLatent nperiod is 1-3 days.

·         nAcute nbeginning with the severe toxic syndrome, fever (1-3 days), rarer vomits.

·         nDiarrhea nin the 1st day of the disease: feces with the admixtures of mucus and green, nblood 3-5 times per day.

·         nAbdomeis tender by the colon way, infiltrated sigmoid colon, tenesms nare absent.

·         nRapid nrecovery, normalization of feces in 3-5 days.

 

Enteroinvasive E.coli infection npeculiarities in infants

·         nGradual nbeginning.

·         nsevere toxic syndrome increases during 5-7 days.

·         nenteritis, enterocolitic ncharacter of stools.

·         nDehydratiodevelops often.

·         nmoderate or severe disease duration.

·         nThe nfever lasts for 5-7 days, sometimes up to 2 weeks.

·         nNormalizatioof feces delays to 1-2 weeks.

 

Enterotoxigenic E.coli infection ncriteria

·         nLatent nperiod from few hours up to 1-2 days.

·         nAcute nbeginning from the repeated vomiting, watery diarrhea.

·         nIntoxicatiois absent; body temperature is normal or subfebrile.

·         ngrumbling along thin intestine during palpation.

·         nFeces n15-20 time per days, watery without pathological admixtures, of rice-water ncharacter.

·         nDevelopment nof severe dehydration

·         nDuration of the ndisease is not more than 5-10 days.

 

Enterohemorrhagic Е. coli  infection criteria

• Latent period is 1-7 days, rarer 9-10 days.
• A disease has moderate or severe course.
• Acute beginning.
• Crampy pain in epigastrium or in all abdomenm.
• Development of secretory diarrhea in the first days.
• Future signs of hemocolitis with frequent defecation, in severe cases up to 20-30 times per day.
• Absence of febrile fever.
• Complications:
• hemolytic-uremic syndrome at 2-7%, at the end of the first – beginning of the second week of disease
• acute kidney insufficiency,
• hemolytic anaemia,
• thrombocytopenia,
• Cramps and other neurological disorders (up to blindness).
• Laboratory features – in fecal test dissociation between large number of erythrocytes and less amount of leucocytes.
• Letality is  1-2%. In HUS – 5-10%.

n

 

Enteroadgesive (enteroadherrent) escherichiosis is not good studied

 

Laboratory test

– The examination of the stool n(koprogram): inflammatory changes, intestinal enzymopathy

– A culture of the stools

– Serologic reaction (IHAR idynamics with fourfold title increasing in 10-14 days) in children elder than 1 nyear if fecal culture is negative.

 

 

Differential ndiagnosis should be performed namong acute non infection diarrheas, salmonellosis, shigellosis, staphylococcal ndiarrhea, viral diarrhea, and cholera.

Diagnosis example:

E.coli infection (caused by Enterotoxigenic strain), typical form, severe degree.

Complication: hypertonic ndehydration, 3^rd degree.

 

Treatment

Therapy of an acute intestinal ninfection for children has 4 constituents: diet, rehydration therapy, nantibacterial therapy and auxiliary therapy (enerosorption, nprobiotics).

Dehydration: Dehydration means the body does not have enough nfluids to function at an optimal level. Dehydration can be caused by fluid loss n(through vomiting, diarrhea or excessive urination), inadequate intake, or a ncombination of both. The most common cause of dehydration in infants and nchildren is acute gastroenteritis, nwith its associated vomiting and diarrhea.

 

 

1. Rehydration therapy

Timely and adequate rehydratiotherapy is a near-term and most essential link in treatment of an acute nintestinal infection, both secretory and invasive. Early application of nadequate rehydration therapy is the main condition of rapid and successful treatment. nRehydration therapy is done according the severity of child’s dehydration

 

Oral rehydration (by mouth)

 

Oral rehydration is most effective, nwhen is performed from the first hours of the disease. Oral rehydration must be nthe first aid at home when the disease begins. It doesn’t have any ncontraindications.

In accordance with recommendations nof WHO optimum composition of solutions for oral rehydration is:

sodium – 60 mmol/l;

potassium – 20 mmol/l;

bicarbonates – 10 mmol/l; n

glucose – 110 mmol/l; n

osmolarity is – 250 mosmol/l. n

Content of sodium and potassium isolutions for oral rehydration must correspond their naverage losses at an acute intestinal infection. The concentration of glucose nin them must help water resorption not only in aintestine but also in kidneys. Because high osmolarity nit is not recommended to give fruit juices, sweet drinks (Coca-cola, and others like nthat) during the oral rehydration.

The method of oral rehydration have nto start immediately, because dehydration begins after the first liquid, watery nemptying, yet long before appearance of clinical signs of dehydration. Valuable nrehydration therapy is performed in 2 stages.

The 1^st stage is rehydration therapy which is ncarried out during 4-6 hours for proceeding of the lost liquid volume. During the mild dehydration – 30-50 ml/kg, at moderate degree – n60-100 ml/kg. 

A calculation of oral rehydratiosolutions volume

n

Body weight in kg	An amount of solution for 4-6 hours (ml)
	mild dehydration	moderate dehydration
5	250	400
10	500	800
15	750	1 200
20	1 000	1 600
25	1 250	2 000

Speed of liquid introduction through a mouth is 5 ml/kg/hour.

Criteria of the 1^st stage nefficiency: (are nestimated in 4-6 hours)

·         ndisappearance nof thirst,

·         nimprovement nof the tissues turgor,

·         nmoistening nof mucus membranes,

·         nincrease nof diuresis,

·         ndisappearance of microcirculation violation signs.

Choice of subsequent tactic:

1.      if signs of dehydration have ndisappeared – continue the 2^nd stage of rehydration therapy.

2.      the signs of dehydration have ndiminished, but still are present – it is needed to continue to give solutiothrough a mouth during the following 4-6 hours in a previous volume.

3.      the signs of dehydration have increased n– parenteral rehydration should be start.

The 2^nd stage is supporting therapy, which is done depend the losses of liquid, which nproceed, with vomit and emptying.

Method of the 2^nd stage:

Supporting oral rehydration means nthat to the child for every following 6 hours is entered so many rehydration solution, as he has lost during previous 6 hours.

Oriented volume of solution for nsupporting rehydration for children before 2 yrs is n50-100 ml, children elder than 2 yrs – 100-200 ml or n10 ml/kg of solution after every emptying. On this stage oral rehydratiosolution is possible to alternate with fruit or vegetable sugar free decoctions,  or tea, especially ngreen. At vomit rehydration therapy is continued after 10-minute pauses. In the nhospital in case the child refuse to drink or at npresence of vomit tube rehydration should be done. Nasogastric tube rehydratiocan be done continuously with a help of the system for intravenous infusion, nwith maximal speed 10 ml/min.

 

Parenteral rehydration

 

At acute intestinal infections, nwhich are accompanied by the 3^rd stage of dehydration, with multiple nvomits, anorexia, waiver of drink, oral rehydration is combined with the nparenteral rehydration.

Solutions for parenteral nrehydration:

·         nRinger’s nlactat,

·         nRinger’s nacetate,

·         nIsotonic nglucose solution,

·         nIsotonic nsodium chloride solution.

To the children aged before 3 months nis better not to use 0.9% NaCl, so as it has nrelatively plenty of chlorine (154 mmol/l) nand relatively high osmolarity (308 mosmol/l). Monotherapy by glucose nsolution is not effective. Compositioand correlation of solutions depends from the type of dehydration.

To the children of early age it is nnecessary to eliminate solutions, which contain plenty of sodium, chlorine, nglucose (solutions nof Disol, Trisol, Quartasol, Acesol, Laktasol, Chlosol and others like nthat) because of possible hypernatremia and intracellular edema development.

At presence of some ions deficit in blood plasma (sodium, potassium, magnesium, ncalcium) or acid-base balance changes it is need to correct them.

 To perform parenterally nrehydration it is necessary to define:

·         nDay’s nrequirement of liquid and electrolytes.

·         nType nand degree of dehydration.

·         nLevel nof liquid deficit.

·         nCurrent nlosses of liquid.

Principle of volume calculation for nthe infusion therapy:

Day’s volume of liquid in case of ndehydration consists of:

a)      deficit of liquid before the ntreatment (a loss of body weight during the disease),

b)      physiologic liquid’s requirement,

c)      current pathological losses.

a)         nFor the calculation of physiologic nliquid’s requirement it is possible to recommend the method of Holiday Segar that is used nthe most widely in the world

 

 

Determination of physiology nrequirements is in a liquid on the method of Holiday Segar

n

Weight	Day’s necessity
1-10 kg	100 ml/kg
10,1-20 kg	1000 ml + 50 ml/kg on every kilogram over 10 kg
more than 20 kg	1500 ml + 20 ml/kg on every kilogram over 20 kg

 

The calculation of liquid’s deficit depends on the degree of dehydration is ndetermined by the clinical signs or weight lost %:

1% of dehydration = 10 ml/kg

1kg nof weight loss = 1 liter n

Consequently, at a 1^st ndegree of dehydration (5% weight loss) day’s deficit of liquid is 50 ml/kg/day; nat 2^nd degree (10% weight loss) – 100 ml/kg/day.

The expected volume of liquid is entered during a day.

A liquid is entered in peripheral nveins during 4-8 hours, repeating infusion if necessary in 12 hours. According nto it a patient gets intravenously 1/6 of day’s volume during 4 hours, or 1/3 – nduring 8 hours et cetera). A remained volume is entered through a mouth! n

Liquid’s requirement per hour of the ninfusion is more nphysiologic:

New-born:

1-st day of life – 2 ml/kg/hour;

2-nd day of life – 3 ml/kg/hour;

3-rd day of life – 4 ml/kg/hour;

Elder children:

weight up to 10 kg – 4 ml/kg/hour;

weight from 10 to 20 kg – 40 ml/hour + 2 ml for nevery kg over 10 kg; n

weight more than 20 kg – 60 ml/hour + 1 ml oevery kg of weight of body over 20kg

A calculation of salts requirements: n

Special attention should be paid to nthe correction of sodium and potassium deficit, losses of which can be considerable. It is nnecessary to remember, that sodium a nchild will get with crystalloid solutions which are entered in certaicorrelations with glucose depending type and severity of dehydration. If nlaboratory control is not done, potassium nis entered according the physiologic necessity (1-2 mmol/kg/day). nMaximal daily amount must not exceed 3-4 mmol/kg/day. nMedicine, mainly potassium chloride, nis entered intravenously droplet on 5% glucose solution. Nowadays insuliadding to these solutions is not recommended. A concentration of potassium nchloride in prepared solution must not exceed 0.3-0.5% (maximally 6 ml 7.5% KCl on 100 ml of glucose). 1 ml of 7.5% KCl nsolution contains 1 mmol of K⁺. Before nentering potassium it is necessary to restore urination, as anuria or severe noliguria is contra-indication for intravenous potassium infusion. Blood npotassium in plasma as 6.5 mmol/l is threatened for nthe life, in concentration 7 mmol/l nhemodialysis is needed.

Determination of salts deficit is nbased on laboratory information.

Acute intestinal infections ichildren mainly are accompanied by isotonic type of dehydration, that’s why ndetermination of blood electrolytes to all children with diarrhea is not nnecessary. Determination of Na+ and K+ is necessary at 3^rd degree of ndehydration and for children with 2^nd degree of dehydration, iwhich general condition severity does not correspond nthe diarhea severity, anamnes nis complicated, a rapid effect from the rehydration therapy is absent.

A calculation of sodium and npotassium deficit is done by the following formula:

Ion deficit = (normal ION nconcentration – patient’s ION concentration) х  M х К, where

M is weight of the patient

K is a coefficient of intracellular nliquid volume.

K = 0.3 – before 1 year

K = 0.2 – after 1 year and for nadults.

Than it is necessary to define the namount of sodium and potassium in solutions which are entered, volume and ncorrelations of which are already expected. A content of these ions isolutions which are often used, are represented in a table. After the urgent nintravenous rehydration it is necessary to check up the level of sodium and npotassium in plasma.

Content of ions in crystalloid nsolutions

n

Content of the ion in mmol/l Osmolarity
SOLUTION	Na+	K+	Cl-	Ca++	Acetate (bicarbonate)	mosmol/l
Physiological solution	154	–	154	–	–	308
Ringer’s solution	147	4	155	2	–	308
Ringer’s lactat	130	4	109	1,5	28 (bicarbonate)	273
4% NaHCO3	500	–	–	–	500 (bicarbonate)	1000
5% dextrose solution on 0,45% solution of NaCl	77	–	–	–	–	252

 

Taking into account importance of nmagnesium ions for the child’s organism, and also that the magnesium losses go parallell with potassium losses on the first stage of nrehydration therapy a 25% solution of magnesium is rotined nin the dose of 0,5-0,75 mmol/kg (1 ml of solution = 1 nmmol of magnesium).

In children with a severe nmalnutrition daily necessity in potassium and magnesium is enlarged (up to 3-4 mmol potassium and 0.4-0.6 mmol nmagnesium).

c) Current pathological losses are determined by weighing of dry and wet ndiapers, determining the amount of the vomit or with a help of calculations:

10 ml/kg/day on every degree of ntemperature over 37.0 ^oC;

20 ml/kg/day  in case of vomit;

20-40 ml/kg/day in case of nintestinal paresis;

25-75 ml/kg/day in case of diarhea;

30 ml/kg/day for nperspiration.

Control of correct rehydratiotherapy is frequency of pulse, frequency of breathing, body weight and diuresis ndynamics.

Rehydration therapy depending the type of ndehydration

It is necessary to take into account nthe type of dehydration to choice solutions and their correlations for the nrehydration therapy. There are 3 types of dehydration: isotonic, hypertonic n(water deficient) and hypotonic  (salt deficient)

 

Main Differential Signs of the Dehydration Types

 

 

At isotonic rehydration (Na 130-150 mmol/l) ndevelops as a result of equal losses of salts and water; it is the most oftetype of dehydration in children with an acute intestinal infection. In the nfirst days (in case of microcirculation maintenance) rehydration is performed nby 5% glucose solution in combination with 0.9% sodium chloride or Ringer’s nlactate solution in correlation (2:1) with parallel correction of electrolytes. n

Next days of rehydration therapy nglucose-saline solutions in a volume which provides the physiology liquid’s nrequirement of organism, remnant volume for the compensation of dehydration, ncurrent pathological losses, correction of plasma electrolytes are performed.

Hypertonic dehydration (Na > 150 mmol/l) ndevelops as a result of liquid losses predominance above salts loses, ninadequate rapid injection of salts with small amount of water.

Rehydration therapy should be done nby a 5% glucose solution in combination with 0.9% sodium chloride solution icorrelation (3:1).

During the rehydration therapy for npatients with hypertonic dehydration it is need to take into account daily nsodium requirements (2-3 mmol/kg). Thus should be ntaken into account sodium in solutions for infusion.

If the level of sodium is 140-150 mmol/l, then amount of sodium should be  decreased 2 times from physiology nnecessities, and at the increase of it more than 150 mmol/l nsolutions which contain sodium are eliminated, except  colloid ones.

It is necessary to investigate a npotassium level and correct it if it is needed.

To prevent cerebral edema control of nplasma osmolarity and body weight is needed. On this nstage a speed of infusion is 15-20 drops per hour.

Hypotonic dehydration (Na < 130 mmol/l) ndevelops as a result of salts losses predominance above liquid loses, excessive ninjection of water with small amount of salts. It developes in case of intestinal infections which are naccompanied by frequent vomit, or during oral rehydration by solutions with nsmall amount of salts.

Rehydration therapy is done by 5% nglucose solution in combination with 0.9% sodium chloride in correlation (1:1). n

If the level of sodium is less than 129 mmol/l it is needed to ncorrect it (calculate it by formula described before). During the ncorrection of sodium hypertyonic solutions are navoided. Their infusion can result in acute intracellular dehydration, first of nall cerebral. Except this, anaphylactic reactions can develop. The correctioof sodium is done by 0.9% NaCl, Ringer’s lactat.

If it is impossible to investigate nblood electrolytes, glucose-saline solutions are infused in correlation 1:1.

By the WHO recommendations (if the nfast rehydration is necessary in case of laboratory control absence) the volume nand speed of 0.9% NaCl, Ringer’s lactat ninfusion on the first rehydration stage should be the following:

 

Speed of infusion during the nrehydration therapy

n

Age of the child	Speed of infusion	Speed of infusion
Before 12 months	30 ml/kg for the first 1 hour	70 ml/kg for the next 5 hours
Elder than 12 months	30 ml/kg for the first 30 minutes	70 ml/kg for the next 2.5 hours

 

The condition of the child is nchecked up each 15-30 minutes to normal pulse filling on a radial artery. If nthe condition of child does not get better, speed of infusion should be nincreased. After that the condition of the child is estimated every hour n(abdominal skin fold, consciousness, possibility to drink).

After all volume is entered the nchild’s condition should be estimated again:

·         nif the signs of severe dehydration still present n– repeat infusion again according the table n6.

·         nif the child’s condition gets better, but there nare signs of moderate dehydration – continue oral rtehyderation naccording the table 2. If a child is nbreast fed, it is recommended to continue feeding; numbers of feeding should be nincreased.

·         nif signs of dehydration are absent, then the nduration of feeding should be increased. At the same time at presence of ndiarrhea for supporting rehydration 50-100 ml of oral rehydratiosolution is given to the children aged before 2 yrs, n100-200 ml to the children elder than 2 yrs or 10 nml/kg  additionally after every emptying n(up to 1/3 expected volume for oral rehydration). Children on the artificial nfeeding are fed by the same chart, by lactose free formulas.

Supervision after children with a nsevere malnutrition and dehydration during the rehydration therapy should be ndone each 30 minutes during the first 2 hours, and then every hour next 4-10 nhours. At signs of hyperhydratation (increase of npulse frequency on 15 per minute, breathing frequency on 5 per minute) nrehydration should be stopped. Than estimate the child’s condition through ahour.

During parenteral rehydration for such nchildren, and also for children with pneumonia, toxic encephalopathy, speed of nliquid infusion must not exceed 15 ml/kg/hour. At these states daily body nweight gain in the first 3 days must not exceed 1-3%.

In case if dehydration is absent and ninfectious toxic shock is developed reanimation measures according the protocol nshould be done.

 

1.      nAntibacterial therapy

 

Antibacterial therapy at invasive ndiarrhea is ngiven to:

1.      Children with severe and moderate nforms of disease.

2.      Children aged before 3 months independent nof the disease severity.

3.      Children with the immune deficiency, nHIV-infected children,  children, that nreceive immune suppressive therapy (chemical, ray), long corticosteroid ntherapy, children with hemolytic anemia,  nhemoglobinopathies independent of age and the ndisease severity.

4.      Children with hemocolitis nindependent of age and the disease severity.

5.      Children with the secondary nbacterial complications in all age groups.

Antibacterial therapy at secretory ndiarrhea is ngiven to:

1.      Children with severe and moderate nforms aged before 6 months.

2.      Children with the immune deficiency, nHIV-infected children, children, that receive immune suppressive therapy n(chemical, ray), long corticosteroid therapy, children with hemolytic anemia, hemoglobinopathies.

3.      Cholera, parasitogenic ndiarrhea independent of age and the disease severity.

4.      Children with the secondary nbacterial complications in all age groups.

Antibacterial therapy is not indicated to:

1.       Children with mild, effaced and nmoderate forms of infections, except for those which are listed above.

2.       Children with bacterial transmitting nof any etiology (transitory, postinfectional).

3.       Children with alimentary ndysfunction, as a result of an acute intestinal infection (intestine dysbiosis, lactase insufficiency, celiac syndrome, nsecondary enzymopathy etc.).

 

Antibacterial therapy if the netiology of an acute intestinal infection is known

 

ROTAVIRUS INFECTION

 

Rotavirus infection is aacute contagious disease of men and animals that is caused by Rotavirus, is npassed by a fecal-oral mechanism, and is characterized by the damage of ngastro-intestinal tract (as gastroenteritis).

 

Etiology:  nan agent is Rotavirus from Rheoviridae.

 

Epidemiology:

·         nthe source of infection is patient or virus carrier;

·         nthe nmechanism of transmission  is fecal-oral n(through the infected water, food, direct contact);

·         nreceptivity is high in case of decreased immunity.

 

Pathogenesis

1. Virus invasion to the thin intestine nepithelial cells (enterocytes).

2. Replication of virus and destruction of nenterocytes.

3. Increased growth of immature cells.

4. Enzyme insufficiency.

5. Violation of digestion and suction, naccumulation of disaccharides.

6. Overabundance of liquid and electrolytes ithe intestine.

7. Diarrhea.

 

Diagnostic criteria

1.      Latent period is 1-4 days.

2.      DVF-syndrome (diarrhea, vomiting, nfever):

ü  diarrhea (gastroenteritis, enterocolitis) during 3-6 days stools are «sprinkling», ncolorless, watery;

ü  Vomits (precedes or appears together nwith diarrhea) during 1-3 days;

ü  Fever (moderate) – 2-4 days.

 

Features of Rotavirus infection inew-born

ü  Often is hospital infection.

ü  Acute beginning with the refuse of nbreast feeding, vomits, diarrhea, development of the dehydration ІІ-ІІІ stage

ü  Possible gradual beginning with growth nof degree of dehydration.

Often is nlethal.

 

Confirmation of diagnosis

ü  Virology by immune-electronic nmicroscopy, IEА, ndiffuses precipitation in a gael.

ü  Serological – NR, CBR, DHAR.

ü  In koprogram n- lymphocytes, impaired enzyme intestinal function.

 

Diagnosis example:

Rota-viral infection typical nform, severe degree.

Complication: hypotonic dehydration, 2^nd ndegree.

A differential diagnosis is performed with ncholera, salmonellosis, enterotoxigenic escherichiosis; acute intestinal infections caused by relative pathogenic nbacteria.

 

Treatment: see treatment of Ecsherichiosis

 

Primary Prophylaxis:

ü  Sanitary disposal of human feces

ü  Protection, purification and boiling nof water

ü  Correct preparing and saving of nfoodstuffs 

ü  Person hygiene

 

Secondary Prophylaxis

Ill Person

ü  nIsolation period –until  the stool culture taken 3 days after stopping ntreatment is negative

ü  nCurrent and terminal disinfection

ü  nMedical supervision for 1-3 mo

Contact nchildren   

Stool nculture

 

For the specific prophylaxis of nrotavirus infection there are two vaccines . Both naccepted oral and contain a weak living virus of 1-4^th types.

 

 

 

YERSINIOSIS

 

Yersiniosis is an acute ninfectious disease caused by Yersinia enterocolitica nis characterized by the symptoms of intoxication, GIT, liver, joints, other norgans and systems defeat.

Etiology: Yersinia enterocolitica, ngram-negative bacillus

 

Epidemiology:

·         nSource of infection– ill human and bacterial carrier n(transmitter), wild and home animals (rats, dogs, foxes, cats and other);

·         nMechanism of transmission – fecally-oral, ncontact-domestic

·         nWay of transmission – alimentary (with infected food, prodacts), contact;

·         nSusceptible organism – all age groups, among children – npreschoolers.

 

Pathogenesis:

1.      Entering the bacilli to gastrointestinal tract. An entrance gate is a thin bowel (terminal ndepartment and appendix)

2.      nEnteral phase: invasion of bacteria in enterocytes, ndevelopment of local inflammation, diarrhea, enterotoxin secretion.

3.      Regional lymphadenitis (regional infection).

4.      Generalization n(bacteriemia, toxemia) in severe cases.

5.      Parenhymatous phase: hematogenous distribution of bacteria with forming of the nsecondary focus (lungs, liver, spleen, bones).

6.      Immunological response, recovering from disease.

7.      May be secondary bacteriemia (exacerbations and nrelapses), because of possible persistansy in lymph nnodes.

 

Diagnostic criteria:

ü  Latent period 3-20 days.

ü  Acute (72.2 %) or gradual (27.8 %) nbeginning.

ü  Polymorphism of clinical picture.

ü  The symptoms of the Gastro-intestinal ntract defeat come forward on a foreground (nausea, stomach-aches, tenderness nand grumbling in the ileocecal area, diarrhea as igastroenteritis, enteritis),

ü  Moderately expressed toxic syndrome, nprolonged fever for 1-2 wks.

ü  Rashes for 6-14 days: maculous or maculous-papulous as nin measles, nodular erythema, in folds, round joints, lateral surfaces of ntrunk, chest;

ü  hyperemia of face, hands and feet n(“hood”, “gloves”,”socks” symptom)

ü  “strawberry” tongue

ü  arthralgias, rarer arthritis,

ü  hepatomegaly, sometimes parenchymal nhepatitis with icterus

ü  mild respirator syndrome n(pharyngitis, rhinitis)

ü  Rarely myocarditis, pericarditis,

ü  Splenomegaly (to 20 %),

ü  Lymphoproliferative syndrome (increase of neck, ninguinal and other lymph nodes) is insignificantly expressed,

ü  Toxic damage of kidneys (at severe ndegree)

 

Classification

Form:

·         ntypical

o   ngastro-interstinal,

o   npseudo appendicitis,

o   nseptic (generalized),

o   nhepatic,

o   nnodular erythema,

o   njoint form

·         natypical n(effaced, subclinical)                

Severity:

·         nmild

·         nmoderate

·         nsevere

Course (duration):   

·    nacute:

ü  smooth

ü  relapsed (not smooth, uneven)

·    chronic

 

Diagnosis example:

·    nYersiniosis, typical joint form, moderate severity, chronic relapsed  nduration

·    nYersiniosis, typical gastro-intestinal form, mild severity, acute duration

 

Yersiniosis peculiarities in infants:

ü  more frequent is gastro-intestinal nthat generalized (septic) form;

ü  high fever, protracted, expressed nintoxication;

ü  dehydration development;

ü  from the first days there is a nnoticeable lymphoproliferative syndrome, nsplenomegaly;

ü  frequent respirator syndrome;

ü  seldom develops hepatitis;

·         narthritis is absent.

 

Laboratory finding 

·         nComplete blood analysis: leucocytosis, neutrophilosis nwith left shift, eosynophylia, ERS is enlarged.

·         nUrinalysis: nslight proteinuria, leucocituria, casts uin small amount in case of toxic damage of kidneys.

·         nBacteriological – Yersinia enterocolitica may be found ifeces, urine, blood, pus, lymph nodes and pharyngeal mucus.

·         nCoprogram: Increasing of red blood sells and leukocytes, nmucus.

·         nSerologically n- increasing of special antibodies 4 times and more in 2-4 wks nin paired sera (IHAR 1:200, AR 1:40 – 1:160).

 

Differential diagnosis with: acute intestinal infections, nby viral hepatitis, scarlatina, measles, enterovirus infection, sepsis, pseudotuberculosis, ntyphoid diseases.

 

ü  nhalf-bed regimen in mild cases,

ü  nbed regimen in nmoderate cases

ü  nstraight bed regimen in severe cases

Diet:

ü  nIcteric (jaundice) form – N 5

ü  nAbdominal (intestinal) form – N 4

ü  nOther forms – N 15

 

1.      Etiological:

·         nin mild cases it’s not used;

·         nin moderate and nsevere cases – by chloramphenicol 10-20 mg/kg 4 times per day orally during 6-9 ndays. If not effective – alternative antibiotics: cefalosporins nof the 3^rd-4^th generation 100-150 mg/kg, aminoglycosides nof the 3^rd generation.

·         nCourse of treatment is 7-10 days.

2.      Pathogenetical:

·   disintoxication oral to all patient and in case of nmild dehydration, or parenteral: Rheosorbilact, 0.9% NaCl, 5% glucose (moderate and severe dehydration);

·   Sorbents: enterosgel 0.5-1 g/kg, polysorb (Silix) 100-200 mg/kg per day in 3 doses for 5-7 days

·   antihistamines: claritin, ncetirizin, suprastin, pipolphen 1-3 mg/kg per day,

·   corticosteroids 1-3 mg/kg with a nshort course (in severe cases, in case of myocarditis),

·   Normalisation of the intestinal flora: linex, bifi-form, nacidophilus 1-2 caps 2-3 times per day not less than 2 wks;

·   antipyretics: nparacethamol 10 mg/kg not more than 5 times per day,

·   NSAIDs icase of arthritis, carditis, nodular erythema (ibuprophen 20 mg/kg per day, aspirin 50-75 mg/kg per day, voltaren 2-3 mg/kg per day, indomethacin 2-3 mg/kg per day n(in average doses).

 

Prophylaxis:

1.      Isolation and ntreatment of ill person, disinfection.

2.      Correct storage of products, nbacteriological control, deratization.

3.      Examination of contact persons from nthe epidemic focus for 3 wks (measuring the ntemperature, skin, throat and feces inspection), 1 bacteriological ninvestigation of feces.

 

 

 

References:

 

1.            nManual nof children’s infectious diseases / O. Ye. Fedortsiv, nI. L. Horishna, I. M. Horishniy. n- TERNOPІL n: UKRMEDKNYHA, 2010. – 382 p. – ISBN 978-966-673-145-9

2.            nManual nof Childhood Infections: The Blue Book (Oxford Specialist Handbooks in Paediatrics) by Mike Sharland, nAndrew Cant and al. Published by  Oxford nUniversity Press Inc., New York, 2011 , p. 881  nISBN: 978-019-957-358-5.

3.            nIllustrated nTextbook of Paediatrics, 4th Edition.  Published by  Lissauer n& Clayden, 2012, p. 552 ISBN: 978-072-343-566-2.

4.            n Nelson Textbook of Pediatrics, 19th nEdition Kliegman, Behrman. Published by Jenson & nStanton, 2011, 2608.  nISBN: n978-080-892-420-3.

5.            nOxford Textbook of Medicine: Infection by David Warrell, nTimothy M. Cox, John Firth and Mili Estee Torok , Published by Wiley-Blackwell, n2012

 

Material has been prepared by Associate Professor I. L. Horishna, MD, PhD

Assistant V. B. Furdela, nMD, PhD