Acute intestinal infections. Dehydration. Principles of rehydration therapy

particular localization of the causative agent GIT
(small or

large intestine, rectum, mesenterium)

the movement of the agent with feces or vomiting mass
penetrate in a susceptible organism in a special ways of transmission (watery, alimentary, contact-household)

various factors of transmission (foodstuff, water, hands, insects, toys, soil)
different localization of the causative agent in the intestine: in lumen of intestine, intestinal epithelium, on the mucous membrane, in lymphatic tissue of intestine

causative agent can constantly be in intestine (cholera, dysentery, some helminthic invasion) or temporarily,

the ability to penetrate from the intestine to the blood and other tissue (ascariasis, amebiasis, strongyloidiasis, trichinosis, echinococcosis)

- in the warm and/or rainy periods
(in

moderate climatic zones is more often registered during
a summer or autumn);
- in countries with low socio-economic level of development;
- among people of risk-groups:
- age - children and the elderly,
- chronic GIT-pathology - patients with
gastritis, duodenitis, peptic ulcer, cholecystitis;
- profession - sanitary workers, plumbers, teachers,
medical personal;
- occupation – fishermen, water-rescuers,
veterinarians, animal trainers

accompanied with abdominal pains.

Diseases with diarrhea syndrome are divided on

3 types:

Type A - proceeding without an inflammation of intestine

Type B - proceeding with an inflammation of intestine

Type C - caused by the short-term penetration of infectious agents through
mucous membrane of intestine without damage

absorption;

-Mucous membrane of intestine is not involved
in the inflammation

(at biopsy of intestine –
morphological changes are insignificant
or not find);

-General symptoms:
fever, malaise, anorexia - are moderate or absent;

-Typical symptoms:
1) pain in mesogastrium;
2) plentiful, watery stool, meteorism;
3) in coprocytogramm – leucocytes are not found;

-This type of diarrhea can be caused by:
- viruses ( Rotavirus, Parvovirus etc.);
- toxicogenic bacteria (V. cholerae, E.coli, S.aureus, B. cereus);
- parasites (Giardia intestinalis, Ascaris lumbricoides, Cestodes,
Ancylostoma duodenale, Strongyloides stercoralis, Trichinella
spiralis, Cryptosporidium parvum and etc.)

of intestinal wall;
- infectious agents are implanted in a mucous

membrane
of the large intestine and damage it;

- General symptoms:
fever, malaise, anorexia - are moderate or severe;

- Typical symptoms (colitis):
- pain in hypogastrium, painful spasms of large intestine, tenesmus;
- in coprocytogramm – leucocytes, admixture of mucus and blood;
- stool is scanty, brown or pink

- This type of diarrhea is caused by:

- bacteria ( Shigellae, Salmonellae, S. V. Parahaemoliticus, Yersinia
enterocolitica, E. coli, Campylobacter jejuni, Clostridium difficile)

- parasites (E. histolytica, Balantidium coli, Schistosomae)

mucous membrane and lymphatic tissue of intestine (usually small intestine)

without damage.

- General symptomes:
fever, chills, headache, malaise, disorded sleep;

- Typical symptomes:
diarrhea or constipation, mesadenitis,
roseola-spot rash, bradycardia,
hepatosplenomegaly,
leukopenia,
- in coprocytogramm: -macrophages



The classical examples - Salmonella typhi, more rare - Yersinia enterocolitica, Campylobacter jejuni, Pseudomonas aeruginosa

of gasric juice;
- nonactive intestinal peristaltics;
- imbalance of intestinal microflora;
-

insufficien level of coproantibodies;

Sometimes diarrhea can develop as nonspecific response of human organism on the severe infection proceeding outside of the intestine (more often - in newborns, but can be in adults, caused by Gram-negative microflora).
The reasons of noninfectious secretory diarrhea:
1. Exogenous: - after some medicine:
purgatives
antacids
of diuretics, antiasthmatic, cholinergic, cardiac, thyroid, antimetabolitic
drugs
prostaglandines
toxins
errors of a diet
- hypersensitivity of the intestine (without structural damage)

in enterocytes)
D. The functional distresses of intestine
E. Colo-enteritis

(ulcerous, ischemia, necrotization, hemorrhage )
F. Pellagra
Metabolic diseases - hyperthyroidism, insufficiency of adrenal
glands and pancreas
H. Allergy, purpura Schonlein- Henoch

losses
during hospitalization

(except for elderly, children, patients with chronic pathology of

the cardiovascular system, alimentary cachexia: 6-8 hours);

To restore the balance of electrolytes, it is necessary to determine the volume of the lost liquid (V);
To do this, you need to know the body weight (m) and the degree of dehydration in percent (%)

To weigh the patient (body mass - m);

Regarding the existing clinical symptoms (see table) to determine the degree of dehydration (according to WHO classification) (%);

the formula:

m × %
V=
100%
5. To determine the method of introduction of fluid: oral or parenteral:
- oral: 1-st and 2-nd degree of dehydration without vomiting
V×1,5
1,5 - a constanta characterizes the ratio between volume of fluid introduced in intestine and absorbed into the blood

Oral solutions: rehydron, glucosolan, citroglucosolan;

- oral – 2/3

of V×1,5;
- parenteral – 1/3 of V (i/v);

Parenteral (1-st and 2-nd degree with vomiting more then 3 t/d or 3-d degree of dehydration) - V;


6. Choice of infusion solutions depends on the level
of potassium (K+) in the blood of the patient:
…….. ≤ 2 ≤ 3 ≤ 3,5-5,5 mmol/l (normal
level of K+)
Qartasol Trisol Disol

1-st degree – 60-80 drops/min (usual);
2-nd degree

– 100-120 drops/min;
3-d degree – by stream;

8. To stop i/v rehydration is possible, if there:
- no vomiting,

- constant, and normal pulse and blood pressure,

- daily diuresis exceeds the daily stool volume
in 1,5 times

described by a preferred lesion of small intestine and development

of severe intoxication and diarrhea in the clinic.

ETIOLOGY:

- Family Enterobacteriaceae, genus Salmonella
Includes 1 species, 7 subspecieses, 2300 serotypes
Gram (-) motile rods without spors
Has 4 antigenes: O – somatic antigene (lipopolysaccharid )
H- a flagellar antigene
K – a capsula antigene – facilitates infiltration
salmonella inside of enterocytes
Vi – virulence antigene

(activation a cAMP)
- cytotoxin - destroys the membrane of the cell,
disrupting the synthesis of proteins
- hyaluronidasum, neuraminidase,
R-plasmide (resistance)
Releases: - endotoxin - (lipopolysaccharid the complex
cellular of a wall) causes a set of toxic
symptoms
Grows well on usual mediums
Stable in environment: - in water – 5 months
- in milk – 300 days
- at 18-24 dg C – 80 days
Sensitive: - usual concentrations of desinfectants inactivate
in 30 min
- at boiling perish immediatly

antigene, promoting the infiltration
R-plasmide – resistance to a/b
Presence of aggressive

enzymes
Ability to cause a bacteriemia, sepsis
Ability to reproduce in many bodies
Ability to cause disbiosis
Ability to derivate L-of the form
Presence of toxins

- patient with manifested form of the disease
- carriers (especially chronic)

Mechanism of transmission – fecal-oral
Routs of transmission – alimentary, watery, contact
Factors of transmission – foodstuffs (meat, lactic products, eggs, fish)
- contaminated water
- dust (at processing skins animal)
- contact with subjects of environment

-Risk groups – children till 2-5 years
- old people
- patient with chronic GIT-pathology
- immunocompromised patient

- Seasonal prevalence – summer-autumn

destruction with excretion endo- and exotoxin –
toxemia
3.

Entering in small intestine, infiltration through
enterocytes, colony, reproduction, accumulation
4. Activation of cAMP, appearance of a secretory diarrhea
The destruction all S. at this stage causes only localized
form with subsequent recovery
5. Bacteriemia at gastrointestinal form is short-term, at
incompetence of immunity S. can penetrate into a blood,
causing hematosepses

material – feces, vomitive masses, gastric

lavage (localized form)
- blood, urine, bile, liquor (generalized form)
medium – cholic broth, selenitic nutrition, bismuth-zinci sulfas
2. Serological test: - IHA test
- CF test
- ELISA
3. Immunofluorescence
4. Detection of antigenes S. in coprofiltrates (express-diagnosis)

NONSPESIFIC INVESTIGATION:

1. CBC- neutrophilia, eosinipenia, shift to the left, acceleration ESR
2. Urinalysis – signs of a set of symptoms “toxic kidney”

the patient of risk-groups and at generalized form :

- quinolones (ciprofloxacin 0,5g×2t/d; ofloxacin 0,4×2t/d)
- chloramphenicol 0,5×4t/d
- cephalosporins of 3-rd generation
- ampicillinum, amoxicillin,amikacinum

NONSPESIFIC THEAPY
Detoxication PO or IV (lavage stomach and intestine; enterosorbents, plentiful drink
Rehydration PO or IV
Metabolites, angioprotectors
Ferment drugs
Biologic preparations
At TIS - glucocorticosteroids

of a feces in 2 days after ending
treatment

Decree group

2 negative bacteriological testes with the subsequent observation
3 month with monthly
bacteriological testing

transmission, saproantroponosis, characterized by functional disorder of enterocytes, development of

dehydration and demineralization, clinically manifested by severe diarrhea-syndrome.
It is the typical disease with a diarrhea of Type A.
Etiology
Vibrio cholerae is presented in 2 species:
- Vibrio cholerae biovar cholerae;
- Vibrio cholerae biovar El-Tor;
The new strain Bengal O139, causes diarrhea of people, but not agglutinate with 01 group antiserum (it is resistant to streptomycin and co-trimoxazole), now it belongs to the 3rd biotype.

of length and 0.2 – 0.4 microns);
mobile, have flagella (the

most mobile between pathogenic infectious agents);
has no spores and capsules;
facultative aerobes, gallophile;
grows on the simple alkaline media with pH of 7.8-8.0;
Feature:
thermostable endotoxin;
thermolabile exotoxin – cholerogen – provides a development of
dehydration;
factors of aggression:- neuraminidase, lipase, protease;
H-antigen, O-antigen (serogroup O1 is divided into:
-Inaba, - Ogava,- Higoshima);
Resistance:
high in water, humid environment (a few months), in food stuffs (2-5 days);
Sensitivity: - to the dryness, ultraviolet irradiation;
- disinfection, high temperature, boiling;
- antibiotics – tetracycline, ampicillin, chloramphenicol.

- they are easily colouring by all aniline stains.
-

well grow on the simple medium (1 % of peptonic water)

Stability in the external environment – survival rate:
- in sea water - 10 - 60 days (Eltor)
- on subjects of use - 3 - 7 days
- in fresh water - 7 - 18 days
- in milk - 7 - 14 days
- on vegetables - 1 - 10 days
- in a fish and sea products - 2 - 14 days
- in the freezer - 21 days

form);
- patients with

clinically manifested form (especially in the first 4-5 d);
- patients with obliterated form,
- convalescents (within 2-4 weeks).
In the first days of the disease the patient discharges about more then 1 million of vibrios.
Mechanism of transsmition:
fecal-oral realized by:- watery way – is leading (drinking, bathing),
- alimentary (milk, rice),
- contact
Susceptibility: general and high, depends on the:
- season (active drinking, bathing, flies),
- age (elderly and children),
- persons with GIT-pathology ( hypoacid gastritis, anemia and
helminthiasis),
Immunity: resistant, specific, antitoxic

Morbidity: high (due to fast distribution) - 1 - 3 %.

mortality from cholera has decreased significantly;
But prognosis is always serious

at the dehydration of III-IV degree.
Recently, the mortality rate decreased from 6% to 1%.

- adds mobility to vibrioes;

- the mucinase - dilutes slime

on a surface of enterocytes, facilitating fixation of
exotoxin on receptors (Gm1-ganglioside);

hyaluronidase and neuraminidase – facilitate infiltration of exotoxin in
enterocytes;

- other toxic components (hemolysins for eltor etc.)

of Vibrio cholerae in the intestine, reproduction in an alkaline

environment and destruction, the release and accumulation of toxins, including cholerogen;
Increased secretion of isotonic fluid:
a) cholerogen activates the cAMF on membranes of enterocytes,
increases a permeability of enterocyte membranes for sodium and
water;
b) blocks the sodium pump and reduces of resorption of
isotonic fluid;
Dehydration (in a severe form);
Haemoconcentration, slowing blood flow,
hypoxemia, hypoxia;
Metabolic acidosis with the accumulation
of toxic products;
Extrarenal urinary disorders up to anuria
in severe cases or extrarenal coma.

the basal layer of the mucosa and the endothelium of

blood vessels,

- structure of enterocytes is not violated,

- signs of functional hyperactivity – (enteritis ) are not developed;

At the autopsy:
severe dehydration of all tissues, ischemia of mucosa in stomach, small intestine and colon, it is swollen, with small hemorrhages,

in all parenchymatous organs expressed dystrophic changes

to 5 days)
2. Prodrome is not typical, but sometimes may

be:
- feeling of anxiety, weakness,
- rumbling in abdomen, pain in chewing and
calf muscles,
- sweating, dizziness, cold extremities.

3. Climex –
1) In typical cases disease begins suddenly, more often at the night or
before morning with acute diarrhea but without abdominal pain and
tenesmus.
2) Stool quickly becomes watery and then resembles a rice water, loses its
odor and becomes the smell of raw fish or grated potatoes.

3) The patient feels:
- discomfort in epigastric and paraumbilical area,
- rumbling around the navel, murmurs in abdomen, feeling of
bloating,
- insuperable desire on defecation;
- after a few hours, sometimes a day, diarrhea accompanied with
repeated vomiting, sometimes a fountain, without nausea.
Vomit quickly becomes watery and resembles rice water.

endogenous character), weakness, thirst,
dryness of the mouth;
5)

The skin becomes bluish, cold and loses its elasticity, turgor;
6) Tongue is dry, abdomen is retracted, painless, possible meteorism
(hypokalemia);
7) Voice becomes hoarse, breathing quickens (tachypnea);
8) Tachycardia and decreased blood pressure;
9) Reduced diuresis, convulsions of some groups of muscles;
10) Consciousness is not changed, patient indifferent, feels fear;
11) Body temperature remains normal;
12) CBC without significant changes;






Severity of the disease is determined by the degree of dehydration,
hemodynamic and metabolic disorders.

Vibrio in the biliary tract, small intestine and penetration of

its toxins in the blood in high concentrations):
- sudden onset and rapid development of dehydration,
- fast development of hypovolemic shock,
- convulsions of all muscle groups,
- symptoms of encephalitis and coma;

Dry cholera (cholera sicca) is very severe (“tragic”) form of the disease
with a malignant course:
- severe weakness,
- rapid development of collapse,
- dyspnea, convulsions,
- cyanosis, coma.
This form of the disease is rare, usually in malnourished patients.

Obliterated cholera is characterized by unclear symptoms and mild
severity (often observed in the case of cholera El-Top).

vomiting, dehydration (isotonic dehydration),
seizures,
Acute onset

of illness with diarrhea and following vomiting
(without nausea, abdominal pain, tenesmus), vomit and feces in the form of rice-water,
3. Subnormal or normal body temperature,
Acrocyanosis (total cyanosis), the symptoms of “cholera face”, “hands
of washerwoman”, cholera folds, “cholera glasses”,
Hoarse voice (aphonia), tachypnea,
Tachycardia, decreased blood pressure (collapse), oligoanuria.

diagnosis of cholera. For bacteriological study using feces and vomit

(10-20 ml) and 1% peptone water;
Serologic method –
- immobilized reaction (RI),
- microagglutination of Vibrio cholera by O-serum
(contrast microscopy) (result in a few minutes),
- reaction of immunofluorescence (results in 2 - 4 hours),
- RIHA, RN, ELISA.
Nonspesific diagnostic

CBC+Ht – relative leukocytosis, shift of formula to the left, increased ESR
and Ht, hemoconcentration;

2) Urinalysis - leukocyturia, proteinuria, microhematuria, admixture

is contraindicated, due to increased disturbance of microcirculation, assisting in

the development of kidney failure;
Diet №4, and in 3-4 days - with a predominance of foods that contain a lot of potassium (e.g. potatoes);
Pro – and eubiotics, sorbents;
Specific therapy:
The principles of antibiotic therapy of cholera:

Administration of antibiotic after obtaining material for bacteriological
examination,
b) Continuity of the drug (including night hours),
c) Parenteral using of a/b till disappearance of vomiting, after that – in oral form,
Determine susceptibility to antibiotics,
Treatment with antibiotics regardless of the degree of dehydration should be at least 5 days.

0.1g × 2t/d PO
- tetracyclinum

0.5g × 3t/d PO
- biseptolum 960 mg × 3-4 t/d PO
- furazolidonum 0.1 – 0.15g × 4t/d PO
- ciprofloxacin 0.5g -1.0g × 2-3t/d PO

quinolones and cephalosporins of 3-rd generation

Rules of discharging from the hospital:

Patients discharged from hospital after receiving negative results of bacteriological examination, which is taking before discharge, 24-36h after the treatment with antibiotics.

- complete convalescence;

+ 3 negative tests of a feces;

+ 1 negative test of bile;

the external environment;

- use only of high-quality WATER;

vaccination forms

antibacterial and antitoxic immunity
(does not influence onspreading of cholera and consequently in the
present the time widly does not be used!);

Persons who were in close contact with cholera patients need in emmediate prevention.
For this purpose, use tetracycline in dose - 0,3g × 3 t/day for 4 days.
The dose for children is reduced in accordance with age.