ACUTE BOWEL INFECTIONS

Main Statements By prevalence bowel infections (BI) are only yielding to respiratory diseases; in the

structure of children mortality from infectious causes in Ukraine they posses 2-3rd

place. Currently infectious diarrhea is divided into invasive (inflammatory, bloody) and

secretory (non-inflammatory, watery). Main route of transmission is fecal-oral. Degree of dehydration should be carefully determined in all patients with BI.

Majority of patients with BI do not require any special treatment except oral rehydration. Severe dehydration is corrected by parentheral fluid administration.

Antibiotics are prescribed to children with severe forms of invasive diarrhea, at shigellosis, at campylobacteriosis, cholera, amebiasis, as well as to early age children, children with immunodeficiencies or with bacteremia.

In most cases antibiotics are given per os. There are no contraindications to enteral feeding in children with BI. Breast feeding

is continued during the whole period of the disease; the amount of breast milk and frequency is determined by the child himself/herself.

Acute bowel infections (ABI) is a group of diseases of different etiology

(viral, bacterial, fungal, parasitic), which are characterized by fecal-oral way of

transmission and by predominant involvement of gastro-intestinal tract.

ABI possess an important place in structure of infectious morbidity in

children. They only yield to acute respiratory infections by frequency; in the

structure of mortality from infectious diseases in Ukraine ABI possess 2-3 places.

According to WHO classification all diarrheal human diseases are divided

into infectious and non-infectious. Infectious diarrheas are further divided into

invasive (inflammatory, bloody) and secretory (non-inflammatory, watery).

Secretory diarrheas are caused mainly by viruses and some bacteria producing

enterotoxin. The causative agents of secretory diarrheas are first of all rotaviruses,

noraviruses, adenoviruses (serotypes 40 and 41), enteroviruses, astroviruses,

coronaviruses, reoviruses, as well as such bacteria as cholera vibrion,

enteropathogenic and enterotoxigenic Escherichia coli. Besides, secretory diarrhea

can be caused by some protozoa: giardia, cryptosporidia, microsporidia, balantidia,

isospora.

This diarrhea is characterized by hypersecretion of intestinal mucosal cells or

decrease of their ability to absorb, without microbial invasion of intestinal mucosa.

In majority of cases the pathological process is localized in small intestine. The

stool is watery; at coproscopic examination as a rule there are no admixtures of

mucus and blood found, and the number of leucocytes is less than 5 per field.

Invasive diarrhea is caused by shigella, salmonella, enteroinvasive and

enterohemorrhagic escherichia, intestinal yersinia, campylobacter, clostridia,

staphylococcus and some other enterobacteria. Besides bacteria, invasive diarrhea

can be caused by amoeba hystolytica. Pathological processes are mainly localized

in large intestine. Stool contains blood, mucus, leucocytes and bacteria in large

amount.

Pathogenesis of diarrhea at acute bowel infections. Currently the following

mechanisms of development of diarrhea syndrome at acute bowel infections are

described:

1. Osmotic. At majority of viral diarrhea the villous intestinal epithelium is

damaged; on the surface of this epithelium synthesis of disaccharidases occurs

(lactase, maltase, sucrase). Their insufficient synthesis leads to accumulation of

disaccharides in intestinal lumen and increase in osmotic intra-intestinal pressure,

which prevents water absorption. Besides, at viral diarrhea the activity of К-Na-

АТPase is decreased in enterocytes, resulting into decreased sodium and glucose

transportation inside intestinal cells; these chemicals are conductors of water.

Osmotic mechanism of diarrhea predominates at viral ABI.

2. Secretory. Under the influence of enterotoxins, activation of enzyme

adenylate cyclase occurs in enterocyte membrane; this enzyme promotes synthesis

of cyclic nucleotides (cAMP and cGMP) with participation of ATP. Accumulation

of the latter stimulates specific phospholipases which regulate cell membrane

permeability and increase water and electrolyte secretion into intestinal lumen.

Secretory mechanism of diarrhea is seen at ABI caused by enterotoxin-producing

microbes. Classical examples are cholera and enterotoxic escherichiosis.

3. Exudative or inflammatory. At invasion of some microbes into intestinal

wall there develops inflammation which is accompanied by synthesis of

inflammatory mediators (kinins, prostaglandins, histamine, serotonin, cytokines). It

is accompanied by direct damage of cellular membranes, increase of their

permeability, disturbances in bowel mucosa microcirculation and increase of its

motility. Inflammatory mediators can directly activate adenylate cyclase. A large

amount of exudate containing mucus, protein and blood is secreted into intestinal

lumen at invasive infections. This increases volume of intestinal content and

amount of fluid in it.

Exudative mechanism develops in invasive diarrheas.

The most common acute bowel infections in children.

Shigellosis is an acute infectious disease with fecal-oral mechanism of

transmission, caused by bacteria from Shigella genus. This disease is characterized

by intoxication syndrome and predominant involvement of distal parts of large

intestine.

Etiology. Shigellosis (dysentery) belongs to one of the most common forms

of ABI. It is caused by Gram-negative immobile rod. It does not produce spores or

capsules. It belongs to facultative anaerobes. According to biochemical

characteristics and antigenic structure, by International classification Shigella is

divided into 4 groups: S. dysenteriae (group а), S. flexneri (group b), S. boydii

(group с) and S. sonnei (group d).

Pathogenicity of these bacteria is determined by their ability to produce

endotoxin, as well as by their invasiveness. Shigella Grigoriev-Shig produces

exotoxin. Resistance in outer environment depends on type of shigella. In water S.

sonnei preserves its activity till 48 days, S. flexneri till 10-16 days. In food shigella

preserves its activity up to 30 days.

Epidemiology. The source of infection is a sick person or bacterial carrier.

Sick person is contagious since the first day of the disease. Termination of

contagious period can only be detected by laboratory method, that is, by one

negative result of feces culture.

Routes of transmission: for children under 3 years of age it is contact; for

older age children it is water or food.

Mechanism of infection: fecal-oral.

Transmission factors: water, hands, milk and milk products, flies, etc.

Pathogenesis. The key mechanism of dysentery pathogenesis is large

intestine mucosa damage with further absorption of shigella metabolic products

into blood and their action on different organs. Some bacteria are inactivated in

stomach by gastric and intestinal secretions and bile. Passing the barriers of

gastrointestinal tract, shigella reaches distal parts of large intestine. There the

bacteria invade enterocytes, produce cytotoxic factor which destroys the cells, as

well as endotoxins (ShET-1 and ShET-2) which damage mucosa of distal parts of

large intestine. As a result, inflammatory changes, erosions and bleeding ulcers

develop. The bacteria penetrate through M-cells of epithelium to the cells which

surround grouped lymphatic follicles. These toxins can cause development of

severe complications, including hemolytic-uremic syndrome.

Damage of nervous and vessel apparatus plays a big role in toxicosis and

local intestinal changes; it includes nodules of submucosa and muscle layers

plexuses, damage of intestinal innervation which present with spasms, painful

urges to defecate – tenesmus, severe spastic pain in abdomen.

Clinical manifestations. The disease can develop in any age children, but the

most often affected are the children of second-third year of life. Incubational

period at shigellosis lasts from 6-8 hours till 7 days. It is necessary to point out,

that the severity of primary phase depends mainly from amount of ingested

bacteria and way of transmission. So, infection of the child with food and water,

containing large amount of bacteria, as well as endotoxin, is characterized by short

incubational period with acute onset and severe course. Infection with small

amount of shigella by predominantly contact way leads to disease development in

5-7 days, often with mild or moderate course.

Children under three years of age develop acute onset of shigellosis.

Temperature is increased till 38—400С. In majority of cases fever continues during

2-5 days, but in 1/5 of cases more than one week.

During the first day toxicosis develops, which involves nervous and cardio-

vascular systems. In 20% of children toxicosis has the form of toxic

encephalopathy with decreased consciousness, seizures, disturbances of

microcirculation, blood coagulation; more seldom exicosis develops.

In all the children under three years of age shigellosis causes gastro-intestinal

function disorders. Stool has more often enterocolitic or colitic character.

Pathological admixtures in stool - mucus, blood and greenish color - are seen in

75% of patients. Blood in stool is more often seen as streaks, rarer as blood spits.

Tenesmas are seldom seen, they are accompanied by child’s restlessness, crying

and facial redness. Vomiting and regurgitations are seldom seen, once or twice per

day. Abdomen is distended in children with shigellosis below three years of age.

The course of shigellosis in first year children is more often prolonged, with

protracted bowel reparation, especially at joining of intercurrent infection.

Neonatal shigellosis develops rather seldom; the symptoms in this case

include mild fever and frequent stool without blood admixtures. However children

of this age group more often develop complications: septicemia, meningitis,

exicosis, intestinal perforation, toxic megacolon.

In children under three years of age the course of shigellosis has some

particularities. The disease onset is gradual, clinical symptoms develop during 3 - 4

days. The stool preserves fecal character, but there are always admixtures of cloud

mucus and greenish color. Blood in stool is seen more seldom that in older age

children, and not in every stool. Majority of children develop abdominal flatulence,

mild sigmoid spasm and equivalents of tenesmus (during defecation child’s face

becomes red, restlessness and crying is seen). Shigellosis presents with clinical

picture of gastroenterocolitis and enterocolitis.

Older children present with more acute disease onset. Fever up to 38 - 400С

continues during 2-4 days. Sometimes vomiting is observed once or twice.

Appetite is decreased, children become flaccid, complain on headache and

abdominal spastic pains. Feces are liquid with admixtures of mucus, green, blood,

sometimes pus. One or two days later the feces become less fecal, similar to rectal

spit. During this period children complain on abdominal pain during defecation.

Tenesmus is typical presentation of the disease. At abdominal palpation spasmodic

and painful sigmoid is seen.

Clinical picture of shigellosis often depends on shigella type. So, at

shigellosis flexneri a large proportion of severe forms is seen, unlike shigellosis

sonnei. Fever is observed in both cases, but it can be present during 6-14 days at

shigellosis flexneri. Toxicosis at shigellosis flexneri is more prolonged. It can

accompany the disease course during 2-3 weeks. At shigellosis flexneri exicosis is

observed more often, while at shigellosis sonnei toxic encephalopathy is seen.

At shigelloses cased by Sh.dуsenteriae, the disease presents with prominent

intoxication and severe intestinal mucosa damage. In majority of cases severe

toxicosis develops; colitic syndrome appears rapidly. Repeated vomiting and

frequent stool lead to severe dehydration.

There are mild, moderate and severe forms of shigellosis by disease severity.

Mild forms of shigellosis present with short-term fever till 38.50С, decreased

appetite, mild malaise, vomiting once or absent, stool up to 5-8 times per day,

liquid fecal stool and small admixture of mucus and green. Blood admixture and

tenesmus are absent or mild. Spastic, hardened and tender sigmoid is palpated, anal

relaxation is seen. Clinical recovery occurs 5-7 days later.

Moderate forms of shigellosis are characterized by presence of moderate

intoxication signs and prominent colitic syndrome. Repeated vomiting is seen,

fever ill 38 - 400С, spastic pains in abdomen and tenesmus. Feces loose fecal

character, become scanty, with large admixtures of cloudy mucus, blood streaks

and green color (hemorrhagic colitis). At palpation tenderness in left iliac area and

anal relaxation are determined. Recovery occurs by the end of the second week.

Severe forms of shigellosis are characterized by development of severe

infectious toxicosis. The disease begins acutely with fever till 39.5 - 400С and

higher, multiple, sometimes continuous vomiting. Hyperthermic syndrome can

often be accompanied by encephalitic and meningeal syndromes with loss of

consciousness, delirium, seizures and hallucinations. General condition of the child

worsens acutely, multiple organ failure develops. Signs of colitic syndrome appear

several hours from disease onset; the stool is frequent, liquid, rapidly loses its

fecal character, becomes mucous-bloody, sometimes with pus admixture, tenesmus

are seen. Signs of infectious toxicosis are accompanied by skin paleness, decreased

arterial pressure and hypothermia.

Atypical forms of shigellosis include dyspeptic, subclinical, low-grade and

hypertoxic forms.

Dyspeptic form is mostly diagnosed in children of the first six months of life.

It is characterized by decreased appetite, not frequent regurgitations and stool

frequency changes. Stool is semi-liquid or liquid with undigested inclusions.

General condition is normal. Diagnosis is based on bacteriologic investigations of

stool.

Стертая from is characterized by gradual onset with short-term mildly liquid

stool and preserved general condition; stool frequency is 1-3 per day. Diagnosis is

confirmed with laboratory investigation.

Subclinical form is diagnosed based on results of serological investigations

(increase of specific antibodies during disease course) and stool culture. Clinical

presentations at this form of the disease are absent.

Hypertoxic form is diagnosed very seldom. From the first hours of the disease

symptoms of toxic encephalopathy and signs of infectious toxic shock develop;

lethal outcome can occur earlier than signs of distal colitis can develop (syndrome

of Ekiri). Seizures are seen, loss of consciousness, repeated multiple vomiting and

cardio-vascular insufficiency (muffled heard tones, cold extremities, tachycardia).

Complications of shigellosis develop in children more often and have more

severe course than at other bowel infections (exception is exicosis). S. dysenteriae

can lead to hemolytic anemia, hemolytic-uremic syndrome (HUS), rectal prolapse,

pseudomembranous colitis, cholestatic hepatitis, conjunctivitis, iridocyclitis,

corneal ulcer, pneumonia, arthritis, which develop 2-5 weeks after disease.

Complications which require urgent surgery are seen more often: appendicitis,

intestinal perforation, bowel obstruction.

Diagnosis. Diagnosis of shigellosis is based on clinical and epidemiological

data. Shigellosis typically presents with acute onset, general intoxication syndrome

and gastro-intestinal involvement. The most typical is colitic syndrome of gastro-

intestinal involvement: spasmodic abdominal pains, tenesmus, imperative urge to

to defecation, sunken abdomen, tenderness to palpation in left ileocecal area,

spastic and tender sigmoid, frequent stool of non-fecal character with admixtures

of cloud mucus, green color and blood.

For definite diagnosis bacteriological and serological methods are used.

Coprological method is auxiliary.

Bacteriological method is the most important. For diagnosis it is necessary to

investigate the stool with pathological admixtures, except blood, before beginning

of antibiotics. Stool is cultured on media of Ploskirev, Levin, etc. Preliminary

result can be obtained on the 2-3rd day, final result on the 4-5th day.

Serological methods of diagnosis (reaction of agglutination and reaction of

passive hemagglutination) are used at negative results of bacteriological stool

investigation. Positive diagnostical titer of shigella sonnei antibodies is 1:100, of

shigella flexneri is 1:200. More reliable is titer increase in dynamics. Specific

antibodies are seen in blood of shigellosis patient on the 3-5 th day of the disease;

their titer increases gradually during 2-3 weeks with further gradual decrease.

Coprology method is used as additional method of laboratory diagnosis of

shigellosis. Stool under the microscope presents with inflammatory changes

(leucocytes up to 30-40 per field, erythrocytes, mucus), as well as signs of

enzymatic intestinal insufficiency (large amount of neutral fat and fatty acids).

At shigellosis CBC shows moderate leukocytosis up to 15*109/l with

prominent neutrophilic bands (sometimes amount of bands is larger than number

of neutrophils), accelerated ESR. Leucopenia ad leukemoid response are also

possible.

Salmonellosis is an acute infectious disease of human and animals caused by

Gram negative bacteria of salmonella genus. This disease has several forms (from

asymptomatic till septicopyemic) but most commonly presents with gastro-

intestinal form.

Etiology. Salmonella are small Gram-negative rods, motile, aerobic (at the

same time facultative anaerobic), which are quire resistant to outer environmental

factors (heating, drying) and can be preserved for a long period (till 9 moths) in

environment. Similar to other representatives of Enterobacteriaceae family, they

contain О- and Н-antigens. Their particularity is high resistance to antibacterial

drugs, and currently to disinfecting solutions as well. There are several types of

salmonellas, however for humans the most important clinically and

epidemiologically are S. enteritidis (S. enterica serotype Enteritidis) and S.

typhimurium (S. enterica serotype Typhimurium).

Epidemiology. Salmonellosis is a wide-spread disease both in the world and

in Ukraine. The sources of infection are sick people, bacterial carriers, swimming

birds, chicken, cattle, pigs and rodents.

Way of infection transmission is fecal-oral.

Routes of transmission are food and contact.

Transmission factors are food products and dirty hands.

Pathogenesis. Clinical presentations of salmonella infection depend of way of

transmission, salmonella serotype, their virulence and number of bacteria (it was

detected that infecting dosage for adults is 106-108 bacteria), reactivity of the host

and child’s age. In majority of cases the entrance route for infection is gastro-

intestinal tract. Passing upper parts of gastro-intestinal tract, salmonella is

replicated in intestine and penetrates enterocytes and macrophages, which leads to

development of inflammation. The latter is the key pathogenetical mechanism in

development of enteritis and enterocolitis. Inflammatory process in intestine causes

damage of its peristalsis, processes of digestion, absorption and accumulation of

osmotically active products in intestinal lumen which prevent water and electrolyte

absorption.

In case of decreased general and local defense mechanisms, salmonella

penetrate cellular and lymphatic barriers and enter blood, which leads to

development of generalized forms of salmonella infection and forming of septic

foci of infection. This course of salmonella infection is seen in newborns and

children below three years of age, in children with inborn and acquired

immunodeficiencies, with decreased gastric acidity (including iatrogenic),

hemolytic anemias, malaria and hypotrophy.

Clinical manifestations. Clinical manifestations of salmonellosis in children

under three years of age are characterized by prominent polymorphism both at the

beginning of the disease and in further course. Even within one outbreak of

salmonellosis caused by the same serovar, different clinical forms are seen.

Incubational period at salmonella is from 8-36 hours at food transmission till

5-7 days at contact transmission.

Very often the clinical picture and disease course depend on child’s age and

its premorbid condition.

In newborns before 10 days of age the disease begins acutely. Its first sign is

decreased appetite or complete refuse of breast feeding. At the first days of the

disease flaccidness, adynamia and skin paleness with grayish tint are seen. From

the first hours of the disease gastro-intestinal involvement is observed. Water stool

contains pieces of mucus and green, which appear in the first portions. Later the

stool becomes less fecal, consisting of cloudy green with watery spot on the diaper

(Picture 61, color plate). The mucus often contain blood admixture. Hemorrhagic

colitis is diagnosed in 60% of newborns. Sometimes the degree of hemorrhagic

colitis can be so prominent that children are hospitalized into surgical departments

with diagnosis of intestinal bleeding.

In 85% of children intoxication and intestinal disturbances increase gradually.

During 2-4 days hemodynamic changes develop, feces become less fecal with

mucus and green. On the 2-3rd day hemocolitis joins.

Clinical particularities of salmonellosis in newborns of the first 10 days of life

are normal body temperature, absence of vomiting and prominent

hepatosplenomegaly syndrome. Typical signs of salmonellosis in this age are

flatulence and rapid development of exicosis.

Children older than 10 days of age present with acute onset of salmonellosis

and fever up to 37.5-390С. Gastrointestinal involvement develops during first hours

of the disease. During the disease course liver and spleen are enlarged. Repeated

vomiting, frequent regurgitations and liquid stool with mucus and green are seen.

Half of the children have protracted, wavy course of the disease.

In 50-60% of cases in children under three years of age septic forms of

salmonellosis can develop. These forms can be both with and without

gastrointestinal involvement.

Septic forms of salmonellosis develop gradually. Body fever and intoxication

increase during 3-7 days, the course has wavy character. All children present with

intoxication symptoms and considerable hemodynamic changes, prominent

hepatolienal syndrome.

In 60-70% of patients with septic forms of salmonellosis extra-intestinal foci

develop (pneumonia, pyelonephritis, otitis, meningitis, osteomyelitis, peritonitis).

Septic foci more often appear on the 3-7th day of the disease.

It is typical for septic form of salmonellosis to have recurrent disease course.

Children under three years of age, except pointed out forms of salmonellosis,

can also present with isolated extra-intestinal forms of the disease. Most often

pyelonephritis, cystitis, recurrent pararectal abscess, osteomyelitis and meningitis

can develop. Rare presentations of salmonellosis in this age group are arthritis,

roseolar rash, myocarditis and abscesses.

Besides severe forms of salmonellosis, children of the first three years of age

can develop mild, low-grade and carriage forms of the disease. Most often these

forms are seen in children with antibiotic course in the history.

The most typical form of salmonellosis is gastro-intestinal which presents

with gastritis, enteritis, gastroenteritis, enterocolitis or gastroenterocolitis.

Children older than three years of age can develop gastric form similar to

food poisoning. The disease begins acutely. After a short incubational period

general malaise, headache, repeated vomiting, fever, intoxication signs, decreased

appetite and possible anorexia develop. At abdomen palpation tenderness in

epigastric area and flatulence are seen. There is no intestinal dysfunction.

Gastroenteric form is seen in older age children and is characterized by

prominent intoxication, fever, repeated vomiting, liquid abundant fetid stool of

brownish-green color with admixtures of mucus and green (“marsh mug”). Several

hours from disease onset spread pains in abdomen appear, rumbling, splashing

sounds along the whole intestine.

Enteric form is characterized by abundant watery stool with admixture of

cloudy mucus and green, together with toxicosis development.

Enterocolitis and gastroenterocolitis forms are diagnosed in fist year old

children. These clinical forms are most often caused by Salmonella typhimurium.

The disease onset is acute with signs of infectious toxicosis, fever up to 38.5 -

390С, which remains during 5-7 days with periodic increases and decreases.

Repeated vomiting is seen 2-4 times per day, which is present 4-5 days. Feces are

abundant, liquid, foamy, with keen unpleasant odor, brownish-green in color

(“marsh mug”), with large amount of mucus and blood streaks. Stool frequency is

12-15 per day. First year of age children can develop anal relaxation and tenesmus.

Length of intestinal dysfunction is from 5-7 days till 2-3 weeks. The abdomen is

distended at palpation; the pain is often localized around umbilicus and along

intestine. Besides GI involvement, general intoxication and CNS involvement

develop, which present with weakness, adynamia, headache, malaise. Liver and

spleen are enlarged. Half of the patients develop dehydration of I-III degree.

Colitic form. The disease begins acutely with fever. From the first days of the

disease frequent liquid stool and abdominal spastic pains (tenesmus) are seen;

sigmoid is spastic, paresis and anal opening зияние are detected.

Separate and one of the main problems of pediatric infections is nosocomial

form. It is characterized by multiple bacterial resistances to antibiotics, disinfecting

solutions, bacteriophages and ability to preserve activity in environment for a long

period of time.

Nosocomial form of salmonellosis is distinguished by gradual development,

torpid course with repeated bacterial discharge, severe clinical presentations,

prominence and length of intoxication symptoms and gastro-intestinal

involvement.

Asymptomatic course of salmonellosis – bacterial carriage. After

disappearance of clinical symptoms patients can keep excreting salmonella with

feces from several weeks till 1 month. Chronic carriers are people with bacterial

excretion longer than one year. Chronic carriers often have concurrent diseases of

biliary ducts. Asymptomatic course of the infection or bacterial carriage present

the danger for close contacts of the carrier.

Diagnosis. Diagnosis of salmonellosis is based on clinical and

epidemiological data. For salmonellosis it is typical to present with acute onset,

general intoxication and predominant gastrointestinal forms with syndromes of

gastroenterocolitis, enterocolitis and gastroenteritis with repeated vomiting, liquid

stool of dark-green color (“marsh mug”) and hepatosplenomegaly. Development of

generalized forms of salmonellosis is possible – typhoid-like and septic.

Laboratory diagnosis. Bacteriological method is the main: fecal

investigation for bacteria before antibiotic therapy. Materials for investigation,

except feces, can also be vomiting fluid, gastric lavage fluid, blood (during the first

days of the disease), urine (on the second week), food remnants. Material culture is

performed on selective media (Ploskirev) and enrichment media (selenitic

bouillon). Preliminary results can be seen in 2 days, final in 4 days. Coprocytologic

method characterizes inflammation localization in intestine. Patients with

gastroenteritis show fatty acids, neutral fat, muscle bundles. At gastroenterocolitis

and enterocolitis large amount of mucus, leucocytes and erythrocytes are seen.

Serological method detects antibodies in blood serum and their titer increase 4-

times and higher in dynamics by reaction of direct hemagglutination with

salmonella erythrocyte diagnosticum. Diagnostic titer of this method in first year

children is 1:100; in older children it is 1:200.

Alternative to bacteriological and serological methods is determination of

bacteria proteins with PCR method.

Escherichiosis (intestinal coli-infection) is an acute infectious disease caused

by different serological groups of pathogenic Escherichia coli and characterized by

general intoxication and gastro-intestinal involvement.

Etiology. Escherichiae are gram-negative motile rods which are divided into

5 groups by antigenic structure: enteropathogenic (EPE) – О111, О55, О26, О18,

enteroinvasive (EIE) – О15, О25, О28, О115, О151, enterotoxigenic (ETE) – О6,

О7, О78, enterohemorrhagic (EHE) – О157 and enteroaggregative (EAE).

Epidemiology. The source of infection is sick person or bacterial carrier. The

way of transmission is predominantly food or contact. Mechanism of transmission

is fecal-oral. Transmission factors are dirty hands, food and water.

Pathogenesis. Mechanisms of diarrhea development are different at

infections with enteropathogenic, enterotoxigenic and enteroinvasive escherichiae.

Enteropathogenic escherichiae colonize and replicate in intestinal epithelium;

desquamation of small intestine enterocyte villi, extraction of enzymes and

proteins with neurotropic action take place. These changes lead to disturbances in

luminal and parietal digestion, increased water and electrolyte hypersecretion;

diarrheal syndrome develops. Bacteremia is seen very seldom at enteropathogenic

escherichiosis, mainly in first months of age children. At breakage of EPE

endotoxins are released, which are absorbed from intestine. Their influence on

endothelial vessels and nervous centers leads to disturbances of vessel wall

permeability. Intoxication is increased due to absorption of incomplete digestion

products from intestine.

EIE causes changes in large intestine mucosa. It penetrates into epithelial cells

with subsequent epithelium desquamation, catarrhal or catarrhal-ulcerative

inflammation, endotoxin production and its absorption into blood leading to

hemodynamic changes.

ETE adhere and proliferate on surface of microvilli of enterocytes, without

their damage. Enterotoxins (termolabile and termostabile) activate adenylate

cyclase of epithelial cells. It leads to cellular accumulation of cAMP,

prostaglandins, disturbed water and electrolyte secretion into intestinal lumen. This

leads to development of secretory diarrhea and considerable imbalance of water-

electrolyte equilibrium in the body. Decreased amount of circulating blood volume

is accompanied by metabolic acidosis, metabolic disturbances, hypoxemia, which

lead to loss of body weight.

Clinical manifestations.

Escherichiosis caused by enteropathogenic Escherichia coli.

Majority of cases are caused by 4 serotypes: О18, О111, О55, О26. Formula-

fed children of early age are most commonly affected. Depending on ways of

transmission and age of the children, the disease can have three clinical variants.

The first one is cholera-like, most typical for first year of age children. The disease

has gradual onset with enteritis, more seldom gastroenteritis.

Disease onset is accompanied by fever till 37.50С – 380С, intoxication

symptoms and gastro-intestinal signs. Sometimes the disease develops gradually

from watery diarrhea. Body temperature is normal or subfebrile at the first days of

the disease. Later digestive dysfunction increases, regurgitations and vomiting 1-2

times per day appear, appetite decreases. All the clinical symptoms increase

gradually and reach their peak on the 5-7th day of the disease.

Feces at escherichiosis are watery, of bright yellow color. Mucus admixture is

small, mucus is liquid, glassy. Sometimes blood streaks are seen. Vomiting is

persistent, long-term, 1-2 times per day. The abdomen is severely distended, tender

to palpation, but not tense; the child is agitated. Body weight decreases,

dehydration, hypotonia and skin paleness rapidly develop. Depending on degree of

these symptoms escherichiosis can have mild, moderate or severe form. Due to

frequency of severe forms in infants, enteropathogenic escherichiosis posses third

place after yersiniosis and salmonellosis typhimurium. The most severe forms are

caused by EPE О55 and О111. The severity of condition is due not to intoxication

signs, but to prominent water and electrolyte metabolism disturbances and

development of II-III degree of dehydration. In some cases hypovolemic shock

develops: decreased body temperature, cold extremities, acrocyanosis, decreased

consciousness, toxic tachypnea, tachycardia. Oligoanuria can develop.

Newborns and first three months of age children can possibly develop septic

form as one of the severe forms of the disease.

So, “cholera-like” form of EPE in early age children has specific symptoms

and in majority of cases is not difficult for differential diagnosis: watery diarrhea,

persistent not frequent vomiting, moderate fever, dehydration with absence of

prominent signs of toxicosis.

The second variant of the course of EPEC escherichiosis, seen in one third of

patients, is mild enteritis on the background of respiratory disease in early age

children. In these children endogenic way of diarrhea development is possible

during the period of respiratory illnesses.

For children older than one year food route of transmission is typical which

leads to development of the third clinical variant of the disease, food

toxicoinfection (food-borne disease). This syndrome presents with vomiting,

watery diarrhea. The disease has mild or moderate course; the severity is

determined by presence of dehydration.

Escherichiosis caused by enteroinvasive Escherichia coli.

Majority of the diseases are caused by serotypes: О124, О151, О28, О32,

О144. Clinical presentation of this group of escherichiosis is similar to mild form

of dysentery. Enteroinvasive escherichiosis very seldom presents with severe

forms.

The disease caused by enteroinvasive escherichiosis begins acutely, after

short incubational period from 18-24 hours till 1-3 days. Suddenly fever appears,

chills, headache, abdominal pains, myalgia. Spastic pains in abdomen, watery

stool, mostly with admixtures of mucus and blood from 3-5 times till 10 and more

per day are observed. Fecal character of the stool is seldom lost, tenesmus are

possible. The abdomen is inflated, tender to palpation along spastic sigmoid.

1-2 days later fever subsides, intoxication signs disappear and on the 5-7 th day

of the disease stool consistency normalizes.

Escherichiosis caused by enterotoxigenic Escherichia coli.

In spite of large variety of causative agents of this group, majority of the

diseases are caused by serotypes: О8, О6, О9, О75, О20.

This group escherichiosis is widely distributed among all age children and is

the etiological factor of every third laboratory confirmed enteritis or gastroenteritis.

This group has predominantly summer seasonality (June-August). Incubational

period is from several hours till 2-3 days. Early age children present with cholera-

like variant of diarrhea; older children present with signs of food-borne disease.

At enterotoxigenic escherichiosis the onset is acute. Suddenly watery liquid

diarrhea appears till 10-20 times per day. Acute diarrhea is accompanied by severe

spastic abdominal pains, multiple vomiting. Body temperature is seldom increased.

The disease has benign course, recovery takes place in 1-2 weeks.

Escherichiosis caused by enterohemorrhagic Escherichia coli.

Majority of the diseases are caused by serotypes: О157 Н7, О104.

Enterohemorrhagic escherichiosis most commonly cause severe hemorrhagic

colitis, more seldom – enteritis or subclinical form. In newborns they can cause

necrotic enterocolitis with high mortality.

Enterohemorrhagic strains of escherichia coli can produce Shiga toxin or

verotoxin. These toxins can cause hemocolitis and can lead to acute renal failure.

Incubational period is 3-7 days. For enterohemorrhagic escherichiosis gradual

onset, frequent watery stool and decreased appetite are typical. On the 2-3 rd day

fever till febrile level, prominent intoxication signs and severe spastic abdominal

pains join. Blood appears in feces. EHEC often has moderate and severe course

with development of hemolytic-uremic syndrome (Gasser syndrome): hemolytic

anemia, acute renal failure and thrombocytopenic purpura.

Particularities of clinical picture of escherichiosis caused by

enteroaggregative escherichiae are not studies enough.

Diagnosis. Diagnosis of escherichiosis is based on clinical and

epidemiological data. For escherichiosis it is typical to have acute or gradual onset,

fever, signs of general intoxication. The leading syndrome of the disease is

diarrhea syndrome of enteritis or gastroenteritis with development of toxico-

exicosis of II-III degree.

Laboratory diagnosis of escherichiosis.

Bacteriological method is obligatory and the only one for laboratory

confirmation of diagnosis of “escherichiosis”. Material for investigation is stool,

gastric lavage fluid and vomiting masses. Culture is performed at early terms of the

disease, before etiotropic treatment, on media of Endo, Levin. Other group

escherichia (enterotoxigenic, enteroinvasive, enterohemorrhagic) are identifies by

additional methods of diagnosis:

- for detection of enterotoxigenic strains toxin-producing and adhesion ability

are detected;

- for detection of enteroinvasive strains invasion ability is detected;

- for detection of enterohemorrhagic strains verocytotoxin is detected.

Serological method uses reaction of agglutination and reaction of indirect

hemagglutination for detection of titer increase in dynamics; diagnostic titer is 1:80

- 1:100 and higher.

Rotaviral infection is an acute infectious disease caused by human

rotaviruses. It is an acute bowel infection with fecal-oral mechanism of

transmission which presents with symptoms of gastroenteritis and dehydration.

Etiology. Rotaviruses were described in 1973 by Australian scientists R.

Bishop and G. Barnes at electronic microscopy of ultra-thin films of duodenal

biopsies from children with acute gastroenteritis. Rotaviruses belong to reoviruses

family, Rotaviruses genus. All the rotaviruses are divided into 7 groups according

to presence of type specific antigen; these groups are named by Latin letters from

А to G. The largest group is А, it includes majority of human rotaviruses. Human

infection can also be caused by groups В and С. All the rotaviruses have typical

morphological structure: spherical particles 65 - 75 nm in diameter. According to

modern data, rotaviral virion consists of nucleus surrounded by three protein

membranes (capsid), which make it similar to wheels of a toy car. These

particularities of rotaviral structure dictated its name (from Latin rota - wheel).

Epidemiology. Rotaviruses are widely spread in environment, among people

and animals. Rotaviruses are resistant to physical and chemical factors. It is

considered that rotaviruses are the most common etiological factors of viral ABI.

Rotaviral morbidity is increased during autumn and winter months. Both sporadic

cases and outbreaks of this disease are seen. The source of infection is sick person

or carrier. Carriage is mostly seen among adults, including stuff of children

institutions. Mechanism of transmission is fecal-oral. High contagiosity of the

virus and tropism to small intestine enterocytes are typical. Rotaviral infection

mostly affects children from 3 months till 2 years of life.

Pathogenesis. Morphological structure of rotaviruses, namely their three

protein membranes, provides high resistance of the virus in acid gastric media and

alkaline duodenal bile media. Due to these particularities, rotavirus penetrates

child’s organism through mouth and freely reaches small intestine, where it is

activated by proteolytic enzymes and starts to replicate. Rotaviral reproduction

(their replication) occurs in differentiated enterocytes of duodenal and upper small

intestinal villi.

As it is known, highly differentiated epithelial cells of small intestinal villi

normally produce enzymes disaccharidases (lactase, maltase), which digest

complex carbohydrates. After viral penetration into enterocytes, dystrophic or

more seldom necrotic changes develop there. Cellular shedding into intestinal

lumen takes place. As a result of viral reproduction, villi become edematous,

change their forms, stick together, become exposed. These exposed parts of villi

become covered by immature enterocytes of crypts. Cast-off cells with the virus

and remnants of food are accumulated in upper parts of small intestine and later

move to lower parts of intestinal tract and are excreted with feces.

Loss of epithelial cells and appearance of functionally immature cells cause

development of enzymatic disaccharidase (lactase) insufficiency. It is confirmed

by histochemical investigations and has dominating significance in diarrhea

development. As a result, simple sugars are not absorbed and complex sugars are

accumulated. Entering large intestine, these sugars cause osmotic imbalance,

increased water transportation from body tissues into intestinal lumen and

appearance of diarrhea. Concentration of cyclic adenosine monophosphate (cAMP)

in intestinal tissue at rotaviral infection is not changed, unlike escherichiosis.

Other pathogenetic mechanism of diarrhea development at rotaviral infecting

is damage of water and electrolyte absorption, increase of their reverse transport

into intestinal lumen and their uncontrolled loss during diarrhea. This results into

appearance and increase of dehydration (exicosis of II - III degree) with fatal

consequences for the child. Diarrhea can continue in mean 5-7 days, with stool

frequency 12-15 times per day, which leads to dehydration. It is especially

dangerous for newborns and early age children.

Histological investigation reveals villi atrophy of small intestinal mucosa

(enteropathy), which is reversible in character.

Clinical manifestations. Incubational period is 1-5 days. Majority of the

patients develop acute onset; all the symptoms appear during the first day. The

most pathognomic symptoms at rotaviral infection are presentations of

gastroenteritis or enteritis. The stool is liquid, watery, foamy, lightly colored,

without pathological admixtures or with small amount of mucus, with keen smell.

Some patients can have cloudy-whitish stool like “rice water”. Stool frequency is

from 5 till 20 times per day. It is typical for rotaviral infection to have imperative

urgency of defecation which appears suddenly, is accompanied by increased bowel

rumblings and results into passage of gases and splashing stool. After defecation

patient feels better. Length of diarrhea is 7-10 days.

Vomiting is the leading symptom at rotaviral infection and is seen in 80 % of

cases. It appears more often simultaneously with diarrhea. Vomiting is repeated

but short-term (1-2 days). Early age children develop vomiting from the first hours

of the disease in 100 % of cases with frequency 1-3 times per day, or can be

repeated and continue from 1 till 3 days.

Older age children complain on abdominal pain. The pain is more often

permanent, but can be spastic. However, pain is not obligatory at rotaviral

gastroenteritis in children and is seen in only 1/3 of patients, but its prominence,

spastic character, repeated pattern and length (in part of patients till days from the

beginning of gastro-intestinal disturbances) present some diagnostic meaning.

Early age children often present with flatulence, increased peristalsis and increased

bowel rambling.

Fever is usually not higher than 380С - 390С and it disappears on the 3-4th day

of the disease. The most typical signs of intoxication are flaccidness, adynamia and

headache.

Presence of triad of symptoms: diarrhea, fever and vomiting, allowed H.

Champsaur et.al. (1984 y.) describe DFV – syndrome (diarrhea, febrile, vomit) как

as the most typical presentation of acute rotaviral infection.

One third of patients since 3-4th day of the disease show catarrhal signs of

upper respiratory tract. Respiratory syndrome is characterized by mild hyperemia

and enlarged follicles of posterior pharyngeal wall which are less prominent than at

acute viral respiratory illness and tend to decline rather than increase.

Rapid losses of water and electrolytes at rotaviral infection result in

development of dehydration. Isotonic dehydration of I-II degree is most common.

In some cases, especially in early age children, severe exicosis can develop which

can lead to death.

Rotaviral infection in newborns is often caused by special type of rotavirus

with defect in nucleotide sequence of 4th gene, coding VР-3 protein. VР-3 protein

determines the virulence of the virus. Besides, newborns can have low enzymatic

activity of gastro-intestinal tract caused by protective action of breast milk. It

justifies predominantly mild forms of the disease in newborns with gradual

development of the symptoms.

Unlike newborns, children of the first year of life can develop severe forms of

rotaviral infection. The disease begins acutely; one third of children can develop

the symptoms gradually with its maximal development on the 3-4th day. Severe

forms of rotaviral infection in early age children are accompanied by prominent

symptoms of intoxication (flaccidness, adynamia, anorexia, “marble picture” of the

skin, cyanosis, loss of consciousness, seizures) as well as II-III degree dehydration.

Diagnosis. Diagnosis of rotaviral infection is based on clinical and

epidemiological data. It is typical for rotaviral gastroenteritis to have acute onset

with fever, general intoxication, often with upper respiratory tract catarrhal

symptoms and gastrointestinal involvement with repeated vomiting, flatulence,

abdominal pain, frequent watery diarrhea and absence of inflammatory changes in

CBC and coprocytogram.

Laboratory diagnosis. For confirmation of rotaviral infection virusological,

serological and molecular-diagnostic methods are used. Material for investigation

is stool, vomiting masses and blood serum.

1. Electronic microscopy reveals rotaviruses in feces on the 1 – 4 th day of the

disease.

2. The most common method of rotaviral infection diagnosis is detection of

rotaviral antigen in feces with simple express methods: immunoenzyme analysis

(ELISA), hard phase co-agglutination assay and reaction of latex-agglutination.

These methods allow reveal 103 and 106 rotaviral particles in stool in later terms of

the disease. Final diagnosis of rotaviral infection can only be made with its

laboratory confirmation.

Treatment of acute bowel infections in children.

Diet. Clinical nutrition is a permanent and important component of diarrheal

diseases management on all stages of the disease. Principal important point in sick

children feeding is abandoning of water-and-tea interval, as it was proved that even

at severe forms of diarrhea the digestive function of largest part of intestine is

preserved, whereas starvation intervals slow down the processes of reparation,

decrease intestinal tolerance to food, promote disturbances of digestion and

considerably decrease protective mechanisms of the body.

Breast feeding must continue in spite of diarrhea. It is justified by the fact that

breast milk lactose is well tolerated by children with diarrhea. Besides, breast milk

contains epithelial, transformed and insulin-like growth factors. These factors

promote rapid recovery of intestinal mucosa in children. The regimen of breast

feeding is similar to that before the disease.

Formula fed children in acute phase of gastroenteritis should decrease the

daily volume of meals on 1/2-1/3, at colitis on 1/2-1/4. The frequency of meals can

be increased till 8-10 times per day for infants and till 5-6 per day for older

children, especially with retching. At the same time the most physiological is

considered to be early gradual restoration of feeding. Returning to qualitative and

quantitative contain of food typical for given age is performed in the shortest

possible terms after rehydration and disappearance of dehydration signs. It is

considered that early recovery of normal meals pattern together with oral

rehydration promotes decrease of diarrhea and more rapid intestinal reparation.

Important method influencing the duration of watery diarrhea is exclusion of

disaccharides from food, if possible. In acute phase of viral diarrhea in infants

usual adapted milk formula are recommended to be substituted by for low-lactase

formula. Duration of low-lactase diet is individual and depends on the child’s

condition. Usually it is given for acute period of the disease and is immediately

stopped after appearance of more solid stool.

Children receiving additional food besides milk are recommended to be given

milk-free cereals. It is recommended to suggest pectin-rich food (baked apples,

banana, apple and carrot sauce). The latter are mostly indicated at ABI with colitis

syndrome.

Rehydration therapy. Timely and adequate rehydration therapy is the first-

step and the most important point in ABI management.

Rehydration therapy should be preferably performed orally. This is a highly

effective, simple, accessible and cheap method. It is necessary to underline that

oral rehydration is most effective if started from the first hours of the disease.

There are no contraindications for oral rehydration. Even repeated vomiting does

not preclude oral fluid administration. At performance of oral rehydration it is not

recommended to use fruit juices, sweet and carbonated drinks due to high

concentration of glucose in them, high osmolarity and inadequate concentration of

sodium.

Optimal solution contain for oral rehydration is the following due to

recommendations of WHO specialists:

Sodium – 60-75 mmol/l (2.5 g/l)

Potassium – 20 mmol/l (1.5 g/l)

Bicarbonates (citrate) – 10 mmol/l (2.9 g/l)

Glucose – 75 mmol/l (13.5 g/l)

Solution osmolarity – 230-250 mosm.

Method of oral rehydration performance. If the child with diarrhea does not

show any signs of dehydration, the main goal of rehydration therapy is prophylaxis

of dehydration. With this goal children are given increased amount of fluid from

the very first hours of the disease: children younger than 2 years should be given

50-100 ml after each stool, children from 2 to 10 years should receive 100-200 ml

after each stool; children older than 10 years should be suggested as much fluid as

they want. For dehydration prophylaxis at ABI the following solutions are

recommended:

- glucose-salt solutions for oral rehydration;

- vegetable or rice waters with salt (3g of salt is recommended per 1 liter of

solution);

- chicken bouillon with salt (3g of salt is recommended per 1 liter of solution);

- weak tea without sugar (better green tea);

- boiled dry fruits without sugar.

There is a simple and accessible method of dehydration degree evaluation, recommended by

WHO:

Condition active, normal feeling Restlessness, agitationSleepiness, spoor, stupor, coma

Sclera Normal moist Slightly dry Dry

Thirst The child drinks normally

Prominent thirst The child drinks not refuses drinking

Skin fold Is straightened quickly (before 1 sec.)

Is straightened slowly (2-10 sec.)

Is straightened very slowly (more than 10 sec.)

Evaluation of water and electrolyte imbalance

No signs of dehydration

Mild dehydration (1-2 degree)

Severe dehydration (2-3 degree)

The amount of required liquid at dehydration is calculated depending on the

degree of dehydration. As a rule, for rehydration of patients with exicosis of I-II

degree oral rehydration is enough without infusion therapy.

Oral rehydration is performed in two stages.

I stage: during the first 4-6 hours elimination of water and electrolyte deficit

is performed. On this stage of rehydration it is necessary to use special solutions

for oral rehydration.

Calculation of fluid volume for oral rehydration at exicosis in children

Body weight (kg)Solution amount during 4-6 hours (ml)1st degree dehydration 2nd degree dehydration

5 250 40010 500 80015 750 120020 1000 160025 1250 2000

If not to calculate precisely the volume of fluid for oral rehydration, it is

possible to give 20 ml/kg of fluid per every hour of rehydration.

After 4-6 hours after beginning of the treatment it is necessary to evaluate

therapy efficacy and to choose one of the following patterns of action:

1) transfer to supportive therapy (II stage) at disappearance or considerable

decrease of dehydration signs;

2) at presence of dehydration signs on the same level the treatment is repeated

during the following 4-6 hours in the same regimen;

3) at increase of dehydration severity parentheral rehydration is performed.

II stage: supportive rehydration performed with consideration of ongoing

water and electrolyte losses with vomiting and diarrhea. Approximate amount of

solution for supportive rehydration is 50-100 ml/kg of body weight or 10 ml/kg

after each stool. At this stage the glucose-electrolyte solutions are interchanged

with salt-free fruit and vegetable waters without sugar. At vomiting rehydration is

reinstituted after 10 minutes break.

Parentheral rehydration. At severe dehydration oral rehydration is combined

with parentheral.

Program of parentheral rehydration should consider:

1. Evaluation of daily requirement of fluid and electrolytes for the child.

2. Determination of the type and degree of dehydration.

3. Evaluation of fluid deficit.

4. Evaluation of ongoing fluid losses.

Principles of infusion therapy volume calculation for rehydration.

Calculation of daily amount of fluid includes the sum of fluid deficit during

the disease, physiological requirements of the child and ongoing pathological

losses. Degree of fluid deficit is determined by clinical signs or by percentage of

body weight loss and equals to: 1 % dehydration = 10 ml/kg, 1 kg of body weight

loss = 1 liter.

Physiological fluid requirements of the child. They can be calculated by

method of Holliday Segar, which is used widely in the world. Determination of

physiological fluid requirements by method of Holliday Segar

Body weight Daily requirement1-10 kg 100 ml/kg 10.1-20 kg 1000 ml + 50 ml/kg per every kg over 10

kgMore 20 kg 1500 ml + 20 ml/kg per every kg over 20

kg

Example of calculation of physiological fluid requirements by method of

Holiday Segar: in a child with body weight of 28 kg the daily fluid physiological

requirement is: (100 ml X 10 kg) + (50 ml X 10 kg) + (20 ml X 8 kg) = 1660

ml/day.

Fluid requirement calculation per length of infusion is more physiological in

comparison to daily calculation, as it can decrease the frequency of complications

at infusion therapy.

Physiological fluid requirements can be calculated with this method by the

following way:

1) Newborns:

1st day of life - 2 ml/kg/hour;

2nd day of life - 3 ml/kg/hour;

3rd day of life - 4 ml/kg/hour;

2) Children with body weight under 10 kg - 4 ml/kg/hour;

3) Children with body weight from 10 till 20 kg - 40 ml/hour + 2 ml per every kg

of body weight;

4) Children with body weight more than 20 kg - 60 ml/hour + 1 ml per every kg

of body weight.

Ongoing pathological losses are determined by weighting dry and used

nappies, diapers, determination of amount of vomiting masses or with the

following calculations:

- 10 ml/kg/day per every degree of fever more than 370С;

- 20 ml/kg/day at vomiting;

- 20-40 ml/kg/day at bowel paresis;

- 25-75 ml/kg/day at diarrhea;

- 30 ml/kg/day for perspiration.

Calculation of electrolyte requirements at dehydration. Special attention at

rehydration should be paid to correction of sodium and potassium deficit which is

considerable in children. It should be remembered that the child receives sodium

with crystalloid solutions which are infused in definite proportions with glucose

depending on type and degree of dehydration. If laboratory control is not

performed, potassium is infused calculated from physiological requirements (1-2

mmol/kg/day). Maximal amount of daily potassium should not be more than 3-4

mmol/kg/day. Potassium preparations, mainly potassium chloride, are injected

intravenously in drop infusions with 5 % glucose solution. Adding of insulin is not

recommended. Potassium chloride concentration in infusion should not be more

than 0.3-0.5 % (maximal 6 ml of 7.5 % potassium chloride per 100 ml of glucose).

7.5 % solution of potassium chloride is more commonly used (1 ml of 7.5 %

potassium chloride contains 1 mmol of potassium). Before infusing potassium, it is

necessary to provide adequate diuresis, as the presence of anuria or prominent

oliguria is the contraindication to potassium infusion. Life threatening blood

plasma level of potassium is 6.5 mmol/l. At its concentration of 7 mmol/l

hemodialysis is required.

Compensation of electrolyte deficits. Determination of salts deficit is based

on laboratory data. Considering the predominantly isotonic type of dehydration at

ABI in children, determination of blood electrolytes in all the children with

diarrhea is not obligatory. It is indicated at severe forms of the disease. Detection

of Na+ and K+ is obligatory at severe dehydration. It is possible to calculate the

deficit of sodium, potassium and other electrolytes on the following formula:

Ion deficit = (ION normal – ION in patient) * М * С,

where М is body weight, С is coefficient of extracellular fluid amount

С = 0.5 in newborns

С = 0.3 in children under 1 year of age

С = 0.25 in children after 1 year of age

С = 0.2 in adults

Further it is necessary to determine and calculate the amount of sodium and

potassium in infused solutions, the volume of ratio of which are already calculated.

After performance of urgent intravenous rehydration it is necessary to check the

level of sodium and potassium in blood plasma.

Considering the importance of magnesium ions for the child, as well as the

fact that magnesium losses correlate with potassium losses, on the first stage of

rehydration it is indicated to infuse 25 % solution of magnesium chloride in dosage

0.5-0.75 mmol/kg (1 ml of solution contains 1 mmol of magnesium). Calculated

amount of fluid should be infused during one day. If access to central vein is

impossible and the fluid is infused into peripheral veins, the infusion should be

done during 4-8 hours, repeating as required in 12 hours. Consequently, the child

receives intravenously the part of the daily amount of fluid calculated for this time

period (1/6 of daily requirement per 4 hours, 1/3 per 8 hours, etc.). The remaining

amount of fluid is given orally. Correct rehydration therapy is controlled by child’s

condition, body weight dynamics and diuresis.

If rapid infusion is necessary (bolus infusion), at absence of laboratory control

of infusion therapy, on the first stage of rehydration the amount of solution (Ringer

lactate or normal saline) for infusion therapy and the speed of infusion should

correspond to WHO recommendations.

Volume of infusion therapy and speed of solution infusion

Child’s age Speed of infusion Younger than 12 months, from calculation 100 ml/kg IV during 6 hours

30 ml/kg during the first hour70 ml/kg during the next 5 hours

Older than 12 months, from calculation 100 ml/kg IV during 3 hours

30 ml/kg during the first 30 minutes

70 ml/kg during the next 2.5 hours

Follow-up of the child during rehydration therapy, if rapid rehydration is

required, includes the following: child’s condition is evaluated every 15-30

minutes till complete pulse filling on radial artery. If child’s condition is not

improving, the speed of the infusion is increased. Every hour the child’s condition

is reevaluated by skin fold of abdomen, level of consciousness and ability to drink.

After infusion of the whole amount of fluid, the condition is reevaluated:

- if signs of severe dehydration are still present, repeated infusion on the same

scheme is performed.

- if the condition improves, but signs of moderate dehydration are still

present, oral rehydration with glucose and electrolyte solutions is performed. If the

child is breast-fed, it is recommended to continue feeding.

- if signs of dehydration are absent, breast-fed children receive the same

regimen of feeding as before the disease.

Antibacterial therapy.

Indications for antibiotic prescriptions at ABI:

• severe forms of invasive diarrheas (hemocolitis, neutrophils in coprogram);

• children under 3 months of age;

• children with immunodeficiencies, HIV-infected;

• children on immune suppressive therapy (chemotherapy, radiation therapy),

long-term corticosteroid therapy; children with hemolytic anemia,

hemoglobinopathies, asplenia, chronic intestinal diseases and oncohematological

diseases;

• hemocolitis, shigellosis, campylobacteriosis, cholera, amebiasis (even at

suspicion on these diseases).

Indications for parentheral usage of antibiotics:

• inability of oral use (vomiting, absence of consciousness, etc.);

• patients with severe forms of ABI and immune deficient conditions;

• suspicion on bacteremia (sepsis), extra-intestinal foci of infection;

• children under 3 months of age with high fever.

Antibacterial drugs recommended for ABI therapy in children.

Drug Dose, therapy course

Ceftriaxone (parentheral)50-100 mg/kg * once daily. The course is 3-5 days

Cefixime (per os)Suspension: 8 mg/kg once or twice daily. Capsules: 400 mg * once daily. The course is 5 days

Azythromycin (per os)1st day - 10-12 mg/kg * once daily;2-5th day - 5-6 mg/kg * once daily

Nifuroxazide (per os)

Suspension:Children from 2 to 6 months – 2.5-5 ml (110-220 mg) twice;From 6 months to 6 years – 5 ml (220 mg) * 3 times.Pills: older 6 years – 200 mg * 4 times. The course is 5 days

Co-trimoxazole (per os)

Children from 2 to 5 years – 200 mg sulfamethoxazole/40 mg trimetoprim.Children from 5 to 12 years – 400 mg sulfamethoxazole /80 mg trimetoprim.Children older 12 years – 800 mg sulfamethoxazole /160 mg trimetoprim twice a day. The course is 5 days

Ampicillin (parentheral) 100 mg/kg 4 times a day. The course is 5 days

Additional therapy at ABI is used along with basic therapy (rehydration,

antibacterial). Usage of such groups as probiotics, enteric sorbents and zinc

preparations facilitates more rapid recovery and prevents severe consequences of

the disease.

Prophylaxis. Prophylaxis of bowel infections is first of all propagation of

breast feeding, usage of high-quality food and feeding of the children with only

children food (which is more strictly controlled at production, including cottage

cheese, fruit sauces, juices, etc.).

There are several methods of protection from potentially contaminated by

causative agents of ABI food, infected animals and people. They include first of all

careful hand washing with soap and further careful drying of hands with single-use

or textile towel:

before preparing, serving or taking food

after toilet visit or change of diapers

after work with raw vegetables or meat

after contact with agricultural animals or after visiting the place where

they are contained

after any contact with feces of domestic animals or humans

Food processing:

any person with vomiting or diarrhea should be restrained from

contact with food products

meat, including minced meat, must be carefully prepared and

thermally processed

all the fruits with peels should be carefully washed, peeled off and

further washed under running drinking water before use

all the vegetables must be washed under running drinking water

especially those which will not be thermally processed before use

it is necessary to use separate breadboards for raw meat and cooked

meat or fresh vegetables

Currently there are two types of vaccine against rotavirus in the world:

pentavalent live attenuated vaccine and monovalent live attenuated vaccine.

Vaccination against rotavirus is indicated to all the children from 6 to 24

weeks of life. For complete course of vaccination it is necessary to provide two

dosages of vaccine with minimal interval of 4 weeks in between. Vaccine provides

protection in 73-89% against rotaviral gastroenteritis and in 86-100% against

severe forms of the disease.

Questions for self-control 1. Significance of anatomic and physiological particularities of gastro-intestinal tract in children for development of bowel infections.2. Influence of metabolism particularities on bowel infection course in children.3. Susceptibility to shigellosis, character of specific immunity.4. Classification of salmonellae.5. Characteristics of clinical forms of escherichiosis depending on type of causative agent.6. What types of human adenovirus cause gastroenteritis?7. What are the clinical signs of noroviral infection?8. Epidemiological particularities of coronaviral infection.9. Pathogenesis of diarrhea syndrome at rotaviral infection.10. Principles of treatment of rotaviral infection, indications for hospital admission.

Tests for self-control 1. What is the most frequent route of transmission of shigellosis caused by Sh. sonnei in children older than 3 years of age?А. Water B. Parentheral C. Food D. Transmissible E. Contact 2. What laboratory method of investigation should be used at shigellosis during the first day of the disease for correct etiological diagnosis?А. Coprologic investigation B. Bacteriologic investigation of feces C. Reaction of direct hemagglutination D. Blood culture for sterilityE. Nasopharyngeal mucus culture 3. What sign is not typical for neurotoxicosis?А. Seizures B. Loss of consciousness C. Oliguria D. Focal signs E. Neutrophilic cytosis in CSF 4. What is the antibiotic of choice at ABI with hemocolitis?А. Ceftriaxone B. Penicillin C. Erythromycin D. Amikacin E. Gentamycin5. What clinical form of salmonellosis is predominantly seen in 1st month of age children?А. Gastrointestinal B. Typhoid-like C. Low-grade D. Flu-like E. Septic 6. Which escherichiosis can be accompanied by hemolytic-uremic syndrome?А. Enteropathogenic B Enteroinvasive C. Enteroaggregative

D. Enterohemorrhagic E. Enterotoxigenic 7. Fever at escherichiosis caused by EIEC typically is seen during:А. 1-2 days B. 4-5 daysC. 1 weekD. 2 weeks E. More than 2 weeks 8. What is typical form of coronaviral infection?А. Prominent seasonality B. Affects only children C. Affects only adults D. Combination of rhinitis and pharyngitis E. Development of anemia 9. Which part of gastro-intestinal tract is affected at rotaviral infection?A. Stomach B. Small intestine C. Large intestineD. Distal part of large intestine E. All the questions are correct10. What distinguishes shigellosis from rotaviral gastroenteritis?A. Presence of enteritis B. Presence of hepatolienal syndrome C. Presence of hemocolitis D. Absence respiratory syndrome E. Presence of lymphadenopathy

Test answers

1-C, 2- B, 3-E, 4-А, 5-E, 6- D, 7-А, 8- D, 9-B, 10-С.