This document discusses acute intestinal infections in children. It describes the most common bacterial and viral causes, including Salmonella, Shigella, E. coli, rotavirus and enterovirus. It then focuses on two specific infections - Shigellosis and Salmonellosis. For Shigellosis, it covers the etiology, epidemiology, pathogenesis, clinical manifestations including symptoms for different severities, classifications of clinical forms, and potential complications. For Salmonellosis, it similarly discusses the etiology, epidemiology, pathogenesis and clinical manifestations such as different clinical forms including the most common gastrointestinal form.

1. Acute intestinal infections in
children

2. Acute intestinal infections
are diseases caused by Gram-negative bacteria (Shigella,
Salmonella, Escherichia, Yersinia, and others), coccal flora
(staphylococcus, streptococcus) and viruses (rotavirus, enterovirus).
The etiological structure of acute intestinal infections varies in
different age periods. During the first year of life enteropathogenic
Escherichia, Staphylococcus, Salmonella, rotavirus are the most
important. Shigella, Escherichia eteroinvasive and enterotoxic are
less common for this age. According to the WHO data the etiological
diagnosis in children with diarrheal disease is identified in 68%
cases, among them bacterial agents - in 48% cases, viruses - in
20%. More than one pathogen is found in 20% of patients.

3. The smaller is the child, the less is possibility to find out the
pathogens–in children under 1 year old-it is in 30-40% of cases.
According to WHO data, rotavirus is more likely, then -
enteropathogenic Escherichia, Salmonella, much less - Shigella. In
this age the opportunistic (conditionally pathogenic) agents are
selected very often. In the older age groups / after 2-3 years /
Shigella, Salmonella, Escherichia enteroinvasive are more spread,
rotaviruses, enteroviruses and a large number of opportunistic
pathogens remain and play the important part. Common signs of
acute intestinal infections, regardless of the etiology are the
diarrheal syndrome and more or less severe intoxication. Diarrheal
syndrome itself is a danger to the organism because it causes
dehydration as a result of water-salt loss with vomiting and
diarrhea.

4.  Diarrhea is the result of membrane or intracavitary / parietal/
digestion and absorption disorders/ malabsorption /. At intestinal
infection first the inflammatory process takes place in the bowels ,
and therefore malabsorption syndrome developes. At functional
disorders / disturbances of quantitative and qualitative nutrition,
regimen disorders and so on / on the contrary – malabsorption
syndrome developes first, later intestinal bacterial flora joins,
mostly conditionally pathogenic. Thus, the development of
diarrheal syndrome may be caused by:
 - increased secretion of electrolytes and fluid into the cavity of the
intestine;
 - absorption oppression;
 - increased motility;
 - mixed causes.

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6.  The division of acute intestinal infections by the type of
stool into invasive and secretory diarrhea has certain
practical value in the initial treatment. Later two groups of
intestinal infections will be considered, taking into account
the features of the pathogenesis and morphological
changes in cells of the intestinal mucosa.
 The gastrointestinal tract damage in children manifests
with the following symptoms:
 gastritis / frequent vomiting, pain in the epigastric zone /;
 enteritis / frequent watery stools, green or yellow without
mucus and blood, mild pain around the navel, bloating /;

7.  enterocolitis / stools of
mixed character , liquid,
usually green, with mucus,
spasmodic pain is possible /
 colitis / feces are liquid, not
very bulky, with mucus and
streaks of blood, spasmodic
pain in the colon zone /
 distal colitis / liquid stools,
painful, small portions, may
consist of pure blood and
mucus, tenesmus /.

8. Shigellosis (Dysenteria)
 Shigellosis –is a disease that belongs to a group of
intestinal infections with an predominant damage of the
colon mucosa, especially its distal part.
 Etiology.Pathogens belong to the genus Shigella. All of this
group are gram-negative bacteria, have no capsule and
flagella, grow well on ordinary nutrient media,
morphologically do not differ. Only microbe species
Grigoriev-Shiga Shigella produces exotoxin, all others -
endotoxin.

9. Epidemiology. Source of infection at acute shigellosis are
patients, much less - bacillicarriers. Sick with mild and subclinical
forms of shigellosis have the largest epidemiological importance,
because they are usually not treated, do not seek help from medical
institutions and are not isolated. Bacillicarriers are of limited value,
because this process is transient. The mechanism of transmission is
fecal-oral. Transfer factors are contaminated hands, food, water,
flies. Immunity at shigellosis is type-specific to certain types of
pathogen, that’s why repeated disease is possible.

10.  Pathogenesis. Infection at shigellosis is only oral,the entering
gate is the gastro-intestinal tract. The infectious dose is of great
importance, it influences upon the duration of the incubation
period and severity of the disease. The macroorganism’s status,
local protective functions of the gastrointestinal tract, as well as
the general immunity have influence upon the infectious process
development. Pathogenic microbes that enter the stomach
partially die as a result of the action of proteolytic enzymes and
hydrochloric acid of gastric juice. Those microbes that are left,
get into the small intestine, where they can stay for several days
and then transfer to the colon, where they multiply and collapse
in the big amount, causing inflammation.

11. Only shigella are able to adherence - sticking to the colonocytes
of the colon. Virulent strains of Shigella are capable of intracellular
invasion. Endotoxin is the leading factor that determines the type
of the morphological changes, the specificity and severity of illness.
It affects all parts of the intestinal wall: mucosal cells -
enterocytes, vascular and nervous apparatus. Getting in the blood,
endotoxins have general toxic effect on the vascular system of the
body, central nervous system, autonomic centers. The greatest
morphological changes occur in the final section of the colon. There
are several morphological forms of shigellosis colitis: catarrhal,
fibrinous, diphtheritic, ulcerative.

12. The clinical manifestation
 The incubation period ranges from several hours to 7 days,
usually 2-3 days. The leading symptoms of shigellosis are
changes in the gastrointestinal tract in the form of so-
called diarrheal syndrome / distal colitis/ and intoxication.
The disease begins acutely with increasing temperature up
to 38-39 ° C, which is kept for 2-3 days. At the beginning of
the disease may be single or double vomiting. The child
becomes unquiet, stops eating, complains of headache,
abdominal pain. Stool becomes frequent, liquid with mucus
and blood streaks.

13. In the early hours of the disease feces are of enough volume,
have fecal character, but at the end of the day or the next day feces
disappear completely, stools are miserable and are a clot of mucus
streaked with blood. During this period the children complain of
spasmodic pain during defecation, stretcing pain from the sigmoid
colon and anus. Tenesmus appear, which is a typical sign of
shigellosis. Tenesmus occur as a result of the simultaneous spasm of
the sigmoid and the anus sphincter. If tenesmus are frequent and
because of tension the rectal mucosa prolapse can happen. In the
first three days clinical signs of disease reach maximum strength.
Signs of intoxication appear, skin is pale and dry, in young children -
a moderate decrease of turgor is possible.

14. The pathogen’s type has some
influence on the course of shigellosis,
the presence of typical symptoms, the
severity of the status. Grigoriev-
Shiga shigellosis has the most
difficult course with an expressed
colitis syndrome and neurotoxicosis.
Flexner shigellosis course is typical,
with a clear colitis syndrome, but
easier than the previous form. Sonnei
shigellosis is the easiest with often
nontypical course , which takes the
largest part among other etiological
forms.

15.  Classification of clinical forms of shigellosis is based on signs,
proposed by Koltipin (type, severity, course). By type: typical
and atypical forms. Typical - it's a form with the ever-present
colitis syndrome. Atypical forms include abortive, dyspepsial,
subclinical, hypertoxic. Typical forms of shigellosis are divided
into mild, moderate and severe. This distribution depends on
the presence and severity of signs of intoxication
(hyperthermia, convulsions, unconsciousness, headache,
lethargy) and local changes in the gastrointestinal tract (the
number of stools, pain, tenesmus, prolapse of the rectal
mucosa).

16.  Mild form meets often now. The general status at this form is
little disturbed, the temperature in most cases does not exceed
38 ° C. On the first day vomiting may be, lethargy is small, loss
of appetite. The number of is stools to 5-8 on the day. Stools
have fecal character, liquid, with mucus and greens. Blood and
tenesmus may be absent. Tensed, slightly painful sigmoid
colon, anus weakness are determined by abdominal palpation.
Crampy abdominal pain may appear during defecation.

17. Middle-form is characterized by moderate intoxication. The
temperature in the first day may rise to 39-40 °, vomiting repeats
3-2 times, the number of stools increases to 10-15 on the day.
Colitis syndrome has all the typical symptoms. Feces completely
disappear from the stools, which contain only mucus and blood.
Patients feel crampy abdominal pain, tenesmus. The younger is
the child, the more frequently weakness and open(gaping) anus
may be observed.

18.  At severe shigellosis two clinical types are possible: type A -
with the advantage of intoxication, Type B - with the
advantage of local manifestations of severe intestinal lesions.
In the first case / type A / illness begins suddenly the
temperature raises to 40 ° C and above, there is multiple, and
sometimes incessant vomiting. On the background of
hyperthermia neurotoxicosis occurs with short-term seizures,
meningeal syndrome. Next to this is a violation of the
cardiovascular system - the muffled heart sounds, falling
blood pressure, pale skin, cool extremities. Facial features are
sharpened, tissue turgor and weight decrease. Intestinal
disorders begin in a few hours, but sometimes on the second
day of disease onset.

19.  Stools are frequent, they become liquid, contain large
amounts of mucus and blood, all are accompanied by
tenesmus. The severe form of shigellosis with a predominance
of type B is characterized by lesions of the intestinal tract.
The disease also begins acutely, the temperature rises to 39 °
C. From the onset of the disease stools are very frequent, they
quickly loose fecal character, become miserable, contain only
mucus and blood. Patients complain of spasmodic constant
abdominal pain, frequent tenesmus. There is a paralysis of the
anus sphincter, from anus muddy slime, painted with blood
flows out. The rectal mucosa prolapse may happen. The
abdomen is tense, sigmoid colon is painful to palpation,
spastic.

20. Shigellosis in infants has some features. General typical features of
the disease are present at this age, but colitis syndrome is
manifested more weakly. Stools are quite often enterocolitic,
sometimes - dyspeptic. Mucus in the stools is constant, blood
impurities are present not in every stool. The abdomen is more
often moderately deflated. Instead tenesmus their equivalents
occur: crying, anxiety, facial flushing during defecation, gaping
anus and it’s weakness. Intoxication at an early age is
accompanied by high fever, repeated vomiting, and if there are
frequent enterocolitic stools, it leads to dehydration with
hemodynamic disorders. Shigellosis in children during the first
year is characterized by a slow repair of the mucosa and slow
recovery.
Complications of shigellosis are in the form of colonic mucosa
prolapse, intestinal intussusception. Joining of secondary infection
causes otitis media, pneumonia.

21. SALMONELLOSIS (Salmonellosis)
 Etiology. Salmonellosis is caused by microbes that belong
to genus Salmonella. More than 2000 serological types of
Salmonella are described. Depending on the O-antigen
structure groups of Salmonella are distinguished, which
are denoted by the letters A, B, C, D, E and others, and
depending on the H antigen structure in each group
different serotypes are distinguished (Kauffman-White
classification). Despite the large number of salmonella
serotypes, in 80-90% of cases disease is connected with
10-12 serotypes: S.typhimurium, S.heidelberg, S.anatum,
S.derby, S.panama.

22. Epidemiology. The main source of salmonella infections are
various animals whose meat is used to make food. In addition, in
recent years, especially for young children, the main
epidemiological danger is a sick man and carriers of
salmonellosis. The main way of transmission is alimentary, and
food (meat, dairy, eggs, fish) are an important factor in the
spread of salmonella. In young children the main way of
transmission is contact through contaminated hands of the staff
and mothers, as well as various contaminated things (dishes,
linens, toys, towels, etc.). In recent years the number of cases
among children 1 year of life increased, particularly as a result of
nosocomial infection (departments for infants, the maternity
hospital). The major pathogens are hospital strains of
S.typhimurium. Outbreaks in these cases are very contagious,
widely distributed and marked by severe clinical course.

23.  Pathogenesis. A large number of live agent with oral infection
is rapidly destroyed in the stomach and small intestine, during
this large amount of endotoxin frees. As a result of the heat-
stable endotoxins toxic manifestations of the disease appear. A
certain portion of agents goes to the mesenteric lymph nodes
and enterocytes and further into the blood with bacteremia.
Toxemia causes gastro-intestinal form of the disease with
endotoxic shock manifestations, at toxemia with bacteremia
typhoid form develops, at the prevalence of an infectious
component, bacteremia - septic form (in infants, prematurity).

24. Salmonella and their toxins act on the nervous system, causing
vasomotors paralysis that leads to disturbances of
thermoregulation and the development of dyspeptic symptoms.
Vomiting and dehydration cause dehydration (exsicosis) with
violation of hemodynamics and water-salt metabolism, hypoxia
and acidosis. Morphological changes are characterized by edema
and hyperemia of the mucous membrane of the stomach, small
and sometimes large intestine, submucosal hemorrhages, blood
circulation disorders, hypersecretion of the glands of the mucous
membrane, degeneration of the surface epithelium.

25.  Hyperplastic solitary follicles
and Peyer's patches,
hyperplasia of mesenteric
lymph nodes can be
identified. Thick diphtheric
deposition on the colon
mucosa may be appear,
which simulates the changes
to the type of shigellosis. At
very acute toxic forms of
illness morphological
changes may be minor and
do not correlate with the
clinical severity of disease.

26. The clinical
manifestati
on.
 The incubation period lasts from 2-3
hours / after alimentary transmission /,
5-7 days / contact way /. Clinical
manifestations of salmonellosis are
characterized by extreme
polymorphism. We distinguish clinical
forms of salmonellosis:
 gastro-intestinal;
 typhoid;
 fever-like;
 septic;
 flu-like;
 subclinical;
 asymptomatic.

27.  Depending on the duration
of illness:
 - acute (up to 1 month.);
 - prolonged (1-3 months).
 Depending on the severity:
 -mild;
 - moderate;
 - severe.

28. Gastrointestinal form
occurs in 90% of patients, manifests in the form of gastritis,
enteritis, colitis, gastroenteritis, enterocolitis, gastroenterocolitis.
Gastritis, gastroenteritis and enteritis occur in children after 3 years.
The onset is acute, often with fever and chills. On the first day the
main symptoms in patients appear - nausea, repeated vomiting,
vomiting is first with food, then it is stained with bile. In the
abdomen there is diffuse pain. Diarrhea appears quickly. Stools are
frequent up to 3-5 times per day, watery, with small amount of
mucus. Tongue is dry and furred. In addition, patients complain of
headache, malaise, lethargy.

29. Sometimes there are signs of neurotoxicosis (hyperthermia,
disorders of consciousness, seizures). The disease duration is 5-7
days, recovery is quick. The recovery period can be extended to 2
- 3 weeks. Gastroenterocolitis, enterocolitis–are the variants of
salmonellosis, which occur most frequently in young children.
Symptoms of the disease begin to appear gradually, intoxication
increases, diarrhea appears .Stools from the first day are with
mucus and even blood and pus, its colour is greenish. Sometimes
there are symptoms of distal colitis: abdominal pain is
spasmodic/ tenesmus /, sigmoid is tense, vomiting is not often.

30. The temperature rises from the first day and lasts 7-10 days.
The liver may be enlarged. Patients complain of expressed
weakness, headache, the skin is pale, tongue is dry, scleras are
subicteric. Sometimes in the early days of disease the dehydration
occurs / toxemia with exsicosis / with violation of the peripheral
circulation, sclerema, exacerbation of facial features. The
phenomena of toxicosis-exsicosis lasts 6-7 days, regardless of
pathogenetic therapy. The average duration of illness is 2-3 weeks.
Prolonged and chronic forms are rare.

31. Typhoid fever-like form of
salmonellosis occurs in 2-3%
of children and clinically may
resemble typhoid or
paratyphoid fever: a fever for
1-2 weeks, the symptoms of
intoxication / headache,
muscle aches and joint pains,
anorexia /, enlarged spleen,
roseolous or erythematous
rash, disorders of
cardiovascular system/
bradycardia or tachycardia /,
gastrointestinal disorders /
abdominal distention, vomiting,
diarrhea /. The disease course
can be very severe.

32.  Septicaemic form of infection occurs in infants and children
during the first months of life. Septicaemic form often
causes local lesions / meningitis, osteomyelitis, otitis
media, subcutaneous abscesses, pyelonephritis, arthritis /.
The disease course is very severe and runs with violation of
all kinds of metabolism, especially water and salt.
 Thus, typical forms of salmonellosis differ from shigellosis
by the predominant lesion of the small intestine /
enteritis /, more frequent signs of toxicosis-exsicosis,
enlarged liver, slow recovery.


33. ESHERICHIOSIS (Echerichiosis)
 Echerichiosis are acute intestinal infections that mostly
occur in children of the first year of life. The age
distribution of echerichiosis morbidity depends on the
Escherichia serotype fitures, which caused a disease. In
the 50s due to the work of F. Karffman, who worked out
the serological method for differentiation of Escherichia by
somatic O-antigen, the membrane K-antigen and flagellar
H-antigen, it became possible to distinguish pathogenic
strains of Escherichia from saprophytic nonpathogenic.
Pathogenic strains have factors of aggression: toxins,
hemolysin, colicin, and so on.

34.  All the serotypes of
pathogenic Escherichia are
divided into groups:
a) enteropathogenic / EPEC/;
b) enteroinvasive / EIEC /;
c) enterotoxic/ ETEC /;
d) enterohemorrhagic;
e) enteroadgesive
(enteroadherrent).

35.  Group I /EPEC / contains about 30 serotypes, including
O111, O55, O44, O125, etc. Their antigenic structure is
close to salmonella, they multiply well on the mucous
membrane surface of the small intestine, causing local
inflammation. This group of microbes are pathogens in
infants.
 Group II / EIEC / includes serotypes O124, O151, O144,
and others.They are by the antigenic structure similar to
Shigella, so they can multiply in the intracellular cytoplasm
of enterocytes. They cause the disease in older children
and adults, the disease is clinically similar to shigellosis.

36.  Group III / ETEC / consists of separate serotypes (O1, O6, O8,
O15, O78), which produce a toxin similar to the effect of the
choleric toxin. These pathogens don’t penetrate in the intestinal
cells and do not cause inflammation, they multiply on the surface
of the mucous membrane, causing expressed entry of fluid into
the intestinal lumen.
 Escherichias of the second group have properties close to Shigella,
they are capable of invasion into the enterocytes, mainly in the
mucosal cells of the colon.

37.  At the escherichiosis of II group food way of contamination is
typical, the disease more often occurs in summer and autumn.
Small outbreaks of infection in children's groups are possible.
Often bacteria carriering happens. The incubation period is 2-3
days. The disease onset is acute, body temperature increases,
there are fluid stools with mucus and blood 3-5 times a day.
Children complain of spasmodic abdominal pain. Manifestations
of intoxication are kept for 1-2 days. Tenesmus, as in shigellosis
do not happen. The disease has a favorable course and ends with
recovery in 5-7 days. It is not possible to establish the diagnosis
basing only on clinical signs, laboratory tests are necessary.

38. INTESTINAL YERSINIOSIS
 The causative agent of yersiniosis is gram-negative
bacteria, first isolated from a rabbit in 1953, it is spread
every where. By the O-antigen Y. enterocolitica is divided
into 34 serotypes. Like Y. pseodotuberculosis this microbe
is sensitive to physical and chemical factors, but is well
kept at low temperatures, without losing the ability to
multiply and accumulate.
 The clinical manifestation.The incubation period is from 4-5
to 15 days, the clinical manifestations of the disease are
varied and often are similar with pseudotuberculosis.
Depending on the predominance of some syndrome the
following forms are distinguished:

39. I. gastro-intestinal;
II. pseudoappendicitic;
III. septic;
IV. joint;
V. nodular erythema;
VI. hepatitis.

40. Gastrointestinal form occurs most often in the form of
gastroenteritis, enterocolitis. Disease begins acutely, the
temperature increases to 37,5-39°C, nausea, headache appear.
After 8-12 hours vomiting and diarrhea begin. The half of patients
has repeated and numerous vomiting for several days. Stools are
liquid, abundant, brown-green, foamy, bad smelling, often there
is an admixture of mucus, sometimes streaked with blood. The
number of stools per day, in many cases does not exceed 5-7
times, sometimes up to 10-15 times. Mild forms of the disease
end in recovery in the first week.

41. At more severe course of disease fever is growing, bacteremia
occurs with the development of extraintestinal focuses of infection:
endotoxic shock, myocarditis, hepatitis. During bacteremia exanthem
occurs in the form of maculopapular or punctate rash on the trunk
and extremities with predominant localization around the joints, on
the hands, feet / symptom of "socks" and "gloves" /.
Pseudoappendicitic form unites together an acute appendicitis,
mesenteric adenitis, terminal ileitis. At this form abdominal pain,
which is spasmodic, localized around the umbilicus and the right
ileocecal region is stable. Acute abdomen with signs of irritation of
the peritoneum is possible.

42. Yersiniosis hepatitis begins acutely with fever, symptoms of
common infectious toxicosis. At the onset of the disease transient
diarrhea, abdominal pain, skin rash are observed. After 3-5 days
of onset of illness dark urine, acholic feces, jaundice appear,
increased liver becomes painful and dense. Spleen may be
enlarged. Increased levels of bilirubin / direct / are found, level
of ALT and AST increase not very much.

43. Laboratory
diagnosis of acute
intestinal infections
 At shigellosis besides clinical
signs final diagnosis is based
on the data of laboratory
methods. Bacteriological
research method has the
greatest weight. Material /
feces, vomiting, gastric
washings / are put on
selective culture media /
Ploskirev, Levin, etc. /. The
serological method is used if
we get negative results of
bacteriological tests. PHAR,
IHAR, AR are used to detect
specific antibodies. For rapid
diagnosis method of
fluorescent antibodies is
used.

44. Coprological test has an auxiliary value, as well as
sigmoidoscopy. At salmonellosis bacteriological tests of blood, bile,
feces, vomit in the early days of urine for 3-4 weeks is made. This
allows us to confirm the etiology of the disease. If possible, it is
expedient to investigate the remains of food, which were the cause
of infection. Serology / IHAR / is widely used, positive result is
received on 7-8 day and 2-3 week. The diagnostic titer is 1:80 to
1:320. Coprological method and sigmoidoscopy have no diagnostic
value.

45. Diagnosis of esherichiosis is set by both clinical and laboratory data.
The previous value has the selection of pathogenic serotypes of
Escherichia coli from feces. Sowing is done on conventional culture
media / Endo, Levin /. Also immunofluorescence method is used to
detect specific antigens from the stools. Serological tests can be
used (AR and IHAR), but in children of the first year diagnostic titers
are not found.
For the diagnosis of yersiniosis laboratory research are also
important. Bacteriological methods detect Yersinia in feces, urine
and blood. It is desirable to do these tests during the first two weeks
of illness. Serological testing is carried out twice in the dynamics of
the disease. Diagnostic titers are 1:40-1:160 in AR, in IHAR 1:100-
1:200.

46. ROTAVIRUS GASTROENTERITIS
 In recent years, rotavirus is the leading causative agent of
acute intestinal infections in children, especially in the first
years of life.
 Etiology. Rotavirus contains RNA, has several antigenic
types, grows poorly on tissue cultures. It is kept in feces
for a long time and is relatively resistant to disinfectants.
 Epidemiology. Mainly young children, up to 2 years suffer
from this disease. The high susceptibility of infants is due
to immature immune mechanisms, anatomical and
physiological characteristics of the gastrointestinal tract.

47. The clinical manifestation.
 The incubation period is 1-5 days. The onset of the disease is
acute. Vomiting, abdominal pain, diarrhea, fever up to 37,5 ° C-
38, 0 ° C, sometimes up to 39 ° C appear. At first the vomit
contains meal with impurities, and then they become watery
with mucus in the form of floating flakes. There is nausea, loss
of appetite. Stools are watery, abundant, yellow or yellow-
green, foamy, with a bad odor. In some patients, stools are like
at cholera. The older children complain of pain, mostly in the
epigastrium and around the navel, spasmodic abdominal pain
is possible too, stools are abundant.

48.  There is grumbling in the abdomen. In addition to bowel
disorders in some patients there is redness of the oropharynx,
sore throat .
 As a result of severe loss of fluids and electrolytes in infants
dehydration occurs. This is accompanied by weight loss, reduced
tissue turgor, distension of the intestine. Fever, intoxication stay
for 2-3 days. Diarrhea syndrome can last up to 5-6 days. The total
duration of illness is 7-10 days. The prognosis is almost always
favorable. The exception may be cases in infants, when as
consequence of a large dehydration cardiovascular and renal
failure occurs. The diagnosis of rotavirus gastroenteritis should be
based on laboratory studies. Virological study of fecal material has
no diagnostic value, because virus carriering is possible. The only
test is to establish specific seroconversion in relation to rotavirus
in paired serum with an interval of 10-14 days.

49. Toxicosis
and
exsicosis
 dehydration / at AGI are more
frequent at secretory
diarrhea. The criteria of
dehydration is acute weight
loss:
1. I degree - to 5%;
2. II - 10%;
3. III - more than 10%.
 By the type we distinguish
dehydration:
1. isotonic;
2. hypertonic (water
defficiency);
3. hypotonic (salt defficiency).

50. Isotonic
dehydration
 is characterized by equal
loss of water and
electrolytes level. The
clinical manifestation of this
type of dehydration is:
lethargy, dry skin and
mucous membranes,
decreased skin turgor. The
level of blood electrolytes is
normal, there is blood
concentration. Urine output
is decreased moderately.

51. Hypertonic
type (water
losses)
 of dehydration manifests
with a strong thirst,
agitation. The skin and
mucous membranes are dry.
Turgor and muscle tone are
moderately reduced,
respiration is accelerated,
urine output is decreased
slightly. Electrolyte levels in
the blood are high, blood
concentration is not high.

52. Hypotonic type
 of dehydration occurs in children with prolonged
diarrhea and in case of inappropriately infusion
therapy. At this type of dehydration the child's
status is severe - almost to the development of the
coma, voice is weak, the extremities are cold, the
skin is flabby, pale, with a marble shade, muscle
tone is decreased, heart tones are deaf, urine
output is decreased, blood pressure is low. There
is high blood concentration, a low level of
potassium and sodium. There is a severe syndrome
of decreased potassium level.

53. Treatment of children with acute
enteric infections
 Therapy of acute intestinal infections in children
has four components:
1. diet therapy,
2. rehydration therapy,
3. antibiotic therapy
4. supportive therapy (enterosorbents, probiotics).


54. Rehydration
therapy
 Timely and adequate
rehydration therapy is the
first and most important
element in the treatment of
acute intestinal infections, as
secretory and invasive. Early
use of an adequate
rehydration therapy is
essential for the rapid and
successful treatment.
Rehydration therapy is
conducted according to the
severity of dehydration of the
child

55. Oral rehydration
 While conducting rehydration therapy an advantage to oral
rehydration therapy should be given. Oral rehydration
therapy is highly effective, simple, accessible at home, and
inexpensive method. It should be noted, that oral
rehydration is the most effective when it is performed from
the first hours of the disease. Oral rehydration at acute
intestinal infections must be the first aid at home when the
disease begins. Early administration of oral solution allows
for the majority of children to treat them effectively at
home, reduce the percentage of hospitalized patients, to
prevent development of severe exsicosis. Contraindications
for oral rehydration does not exist.

56. Parenteral
rehydration
 At acute intestinal infections which
which are accompanied by the 3rd
stage of dehydration, with repeated
vomiting, anorexia, refusal to drink,
oral rehydration is combined with
parenteral rehydration. In children
aged before 3 months is better not to
use 0.9% sodium chloride solution,
so as it contains relatively large
amounts of chlorine (154 mmol / l)
and relatively high osmolarity (308
mosmol / l). Monotherapy with a
glucose solution at exsicosis is not
effective. The composition and the
correlation of solutions depends on
the type of dehydration.

57. Antibacteri
al therapy
 Indications for antibiotic therapy
at invasive diarrhea
 1. Children with severe and
moderate forms of disease.
 2. Children aged bebore 3 months.
 3. Children with the immune
defficiency, HIV-infected children,
children that receive immune
suppressive therapy (chemical,
irradiation), long-term
corticosteroid therapy, with
hemolytic anemia,
hemoglobinopathies regardless of
the child's age and disease
severity.

58.  Indications for antibiotic therapy at secretory diarrhea
 1. Children with severe and moderate forms aged before 6
months.
 2. Children with the immune defficiency, HIV-infected
children, children that receive immune suppressive therapy
(chemical, irradiation), long-term corticosteroid therapy,
with hemolytic anemia, hemoglobinopathies regardless of
the child's age and disease severity.
 3. Cholera, diarrhea caused by parasites, regardless of the
child's age and disease severity.
 4. The presence of secondary bacterial complications in all
age groups.

59. Auxiliary therapy
of acute
intestinal
infection
 Probiotics can be used as
independent etiotropic
treatment (in cases when
antibacterial therapy is not
indicated) or as additional
medicine during antibacterial
therapy. Probіtics that contain
lacto-, bifidobacteria and
propinebacteria are used in
the treatment of acute
intestinal infections.
 Enterosorbents the basis for
use in the treatment of
enterosorbents is the fact that
they are able to fix on their
surface hundreds of millions
bacteria.

60. Thank you for your
attention