Presentation on the topic of prevention of intestinal infections. Viral intestinal infections

OKI is a big group
infectious
gastrointestinal diseases,
combined by availability
general syndrome - diarrhea.

OKI is a collective concept,
uniting more than 30 nosological
forms This includes intestinal infections,
called:
viruses (enterovirus, rotavirus
infection)
bacteria (salmonellosis, dysentery,
cholera, escherichiosis)
bacterial toxins (staphylococcal)

The causative agents of ACI are resistant to
external environment, can last for a long time
preserved on hands, dishes,
toys, household items, soil,
water contaminated with feces.
Some are able to reproduce
in products at low T. They die
during boiling, processing
disinfectants.

Epidemiology.
The source of infection is the patient and the carrier.
Patients with lungs that are worn out are especially dangerous.
and asymptomatic forms. In children's
teams are often sources of infection
there are catering workers. Risk
OCI diseases increase in summer, so
as in the warm season germs are easy
reproduce in the external environment. Especially
it is dangerous to get them on food products,
since the pathogens in them are not only
persist for a long time, but also reproduce,
without changing either the appearance or
no taste, no smell.

Transmission mechanism:
fecal-oral
Transmission routes:
Contact and household
Nutritional
Susceptibility is high, especially in children
younger, premature,
artificial feeding.
Immunity is type-specific, unstable,
high risk of recurrent illnesses

Periods of illness:
incubation - from several hours to 7
days
peak period
convalescence period
Their duration depends on the clinic and severity
diseases

OCI is characterized by 2 groups of symptoms:
intoxication - various variants of toxicosis, increased
T. In younger children it is usually combined with exicosis -
dehydration due to vomiting and diarrhea.
dyspeptic syndromes:
- Gastritis - rare in isolated form. Vomiting and
epigastric pain. More typical for food
toxic infections.
- Enterita. Enteritic stool is frequent, liquid, copious,
splashing, with particles of undigested food, fetid,
sour, irritates the skin, causing diaper rash even with
careful care. Elders complain of abdominal pain, children
At an early age they kick their legs and cry. Stomach is bloated
(flatulence), rumbling along the intestines. Chair in dynamics
loses stool character, becomes watery with
a small amount of mucus and white lumps. Such a chair
may be due to rotavirus and staphylococcal infections,
Escherichiosis, salmonellosis.

- Colitis. The stool is scanty and may consist of greenish-brown
cloudy mucus mixed with pus, sometimes blood (rectal
spit). The child often asks to go to the potty, but bowel movements
doesn't always happen. Such false painful urges
(tenesmus) are characteristic of dysentery. In children 1 year old
anxiety attacks appear in life, the child “kits”
legs, pushes with redness of the face, but the chair does not
stands out. There is pliability or gaping of the anus.
The abdomen is usually retracted. On palpation, rumbling in the right
ileum region and along the colon. In the left
the iliac region is palpated and spasmodic
painful sigmoid colon. This type of chair is typical for
dysentery, maybe with salmonellosis, escherichiosis,
staphylococcal infection.
- Enterocolitis. Sum of symptoms of colitis and enteritis
- Gastroenteritis. Often found in young children.
- Gastroenterocolitis. Occurs at any age.

Mild form – no intoxication syndrome,
T subfebrile or normal, stool 4-6 times per
day. In children of the first year of life there are rare
regurgitation, body weight does not decrease.
Moderate form - symptoms from the first days
intoxication: T 38-39, loss of appetite, lethargy,
vomiting, often repeated, pallor, marbling
skin, acrocyanosis. In children of the first year it is flat
weight curve Stool 8-10 times a day
Severe form – hyperthermia (39 and above),
repeated vomiting, stool 10-15 times or more often,
hemocolitis. The stool loses its fecal character -
"rectal spit" or copious watery without
feces Toxicosis develops, toxicosis with
exsicosis, neurotoxicosis, disseminated intravascular coagulation syndrome with
disorders of the central nervous system, cardiovascular system, water-electrolyte metabolism, acid-base balance, hemostasis

Laboratory diagnostics.
Scatology. With colitis syndrome - mucus,
leukocytes, erythrocytes. With enteritis, undigested food components.
Bacteriological research. Taken
stool culture (lumps of mucus and pus, but not
blood), vomit, rinsing water
stomach, food products. Sowing
carried out before prescribing antimicrobial
drugs. Preliminary answer - h/w 48
hours, final - 3 days.

Treatment complex:
adequate care
therapeutic nutrition
etiotropic therapy
pathogenetic and
symptomatic therapy

Care
adequate hygienic conditions (good
aeration, optimal air temperature in the room)
bed rest during the first days of illness
individual care (preferably maternal care)

Medical nutrition
Feed according to appetite. In case of mild form - age-specific diet with
a decrease in daily volume by 15-20%, for children over one year old - food with
mechanical sparing (table 4 wiped) and additionally
fermented milk mixtures 2 times a day. If appetite decreases, feed
as often as possible. The normal amount of nutrition is restored in 3-4 days.
For moderate and severe cases - a decrease in volume by 30-50% and
increasing the frequency of feedings up to 5-8 times a day with recovery
volume for 5-7 days. Optimally - breast milk. The rest have adapted usual or fermented milk mixtures. As
complementary foods - 5-10% rice and buckwheat porridge with water and puree soup. Puree from
sweet baked apples. It is not recommended to introduce new ones into the menu
foods that the child has not received before.
For children over one year old - pureed food (boiled rice, pureed soups
vegetables) with limited fat. From 3-4 days - well-cooked steam
fish or meat (table 4 pureed). For 2-3 weeks, exclude foods
enhancing intestinal motility and fermentation (whole milk,
rye bread, raw vegetables, peas, beans, beets, cucumbers, cabbage
cabbage, grapes, sour fruits and berries). Fatty,
smoked, fried, hot seasonings and spices.

Etiotropic therapy:
antibiotics and chemotherapy drugs.
Course duration is 5-7 days. At
ineffectiveness within 3 days - change the drug.
Specific bacteriophages These are viruses
pathogenic microbes. Highly selective. Available
dysenteric, salmonella, staphylococcal,
coliproteus, klebsiella and combined
bacteriophage Prescribed per os and rectally in 1-2
hours before meals for a course of 5-7 days. Cannot be combined with
biological products. Do not prescribe during periods of severe
intoxication.

Enterosorbents. Children, especially 1 year olds, have better
smecta. Possibly along with an antibiotic. Prescribe with
1 o'clock. Course 5-7 days. Can't give with others
medications - a break of at least 2 hours. It's better to give in
compote, jelly, water. Can be used
enterodez, enterosgel, polyphepan, cholestyramine,
activated carbon, etc. These drugs
neutralize and remove bacteria from the intestines,
viruses, undigested sugars, strengthen barrier
properties of the intestinal wall, normalize motility,
reduce the loss of water and electrolytes.
Pathogenetic and symptomatic therapy
Oral rehydration

Antidiarrheal drugs. Ca preparations can be used
bismuth, astringents (tannacomp), etc. Should not be used
loperamide (Imodium) as it reduces motility
intestines and creates the risk of dynamic obstruction
k-ka.
Immunotherapy. They use CHBD for children, from orphanages, from
neurological departments, with a protracted course,
long-term bacterial excretion. Apply:
Non-specific protective agents: pentoxyl,
methyluracil, sodium nucleinate, prodigiosan, lysozyme,
yeast extract "Favorite"
Specific immunomodulators:
a) immunoglobulins for enteral administration - complex
immunoglobulin preparations CIP (full set of IG and
high titer of specific antibodies against Escherichia, Shigella,
salmonella, Pseudomonas aeruginosa, rotaviruses), kipferon,
anti-rotavirus IGB)
B) targeted lactoglobulins prepared from
colostrum of cows immunized with different antigens
(escherichiosis, shigellosis, salmonella,
Klebsiella, Proteus, rotavirus). .

Enzyme therapy is aimed at correcting secondary disorders
digestion against the background of OCI (digestion and absorption disorders).
Begins as the transition to physiological nutrition occurs in the repair stage
during or immediately after meals for a course of 2-4 weeks under the control of a coprogram.
A) With a predominant violation of fat digestion (neutral
fat in the coprogram) pancreatic enzymes are used
(pancreatin, creon, pancitrate, prolipase, ultraza, etc.).
b) In case of impaired digestion of plant fiber, starch,
muscle fibers, multicomponent preparations are used (festal,
panzinorm).
C) with decreased gastric secretion and persistent anorexia - abomin,
pepsin.
Antiallergic drugs for various allergic manifestations
Correction of dysbacteriosis under the control of laboratory examination,
which is indicated for patients receiving many antibiotics and long-term
persistence of dyspeptic disorders (unstable stool, decreased
appetite and weight, abdominal pain, flatulence). In the presence of
Decompensated BD of 2-3 degrees is corrected. For her
use:

A) eubiotics - preparations containing living, specially processed
representatives of normal intestinal microflora, which should
take root in the intestines. These include monopreparations containing:
- bifidobacteria (bifidumbacterin, biovestin)
- lactobacilli (lactobacterin, acylact, linex)
- combined preparations containing, in addition to living microorganisms
various additives in the form of sorbents (Bifidum-Forte, Probifor), vitamins
(nutralin-B), immunoprotectorol (atsipol, bifacid, bifiliz, kipacid),
active additives necessary for the life of microbes in the form
vitamins, microelements, amino acids, growth factors (euphlorin B, euphlorin
L, bifiform).
- probiotics - preparations containing metabolites of microorganisms
(disaccharides, organic acids) and other stimulants of flora reproduction
(para-aminobenzoic acid - pamba, amben; hilak-forte, frodo)
- prebiotics - natural oligosaccharides and synthetic disaccharides
(lactulose - drug duphalac), inulin. They do not split in a thin form, but in
the colon serve as a substrate for the growth of normal microflora,
stimulate mucin secretion, immunoprotective effect, normalize
motor skills. There are many oligosaccharides in breast milk, onions, garlic, oats,
Jerusalem artichoke. Adapted mixtures enriched with them appeared (Lemolak,
Omneo, etc.).
Prescribed during the repair period against the background of an adequate diet and enzymes for 30-40
minutes before meals, no more than 2-3 weeks

Antiemetic therapy. Children entering the 1st 2 days are required to
rinse the stomach with 2% sodium bicarbonate solution or clean boiled water
room T to clean wash water (especially with food
toxic infections), after which start oral rehydration within 1-2 hours.
For infrequent but persistent vomiting (of central origin) - antiemetics
(cerucal, motilium, pipolfen, 0.25% novocaine, debridate).
Antipyretics - at T above 38.5C, children at risk for
the occurrence of seizures (encephalopathy, episyndrome, febrile seizures in
anamnesis). First, physical cooling methods, then antipyretic methods
(paracetamol, Calpol, Tylenol, Nurofen).
Painkillers only after excluding surgical pathology.
Antispasmodics (no-spa, buscopan, papaverine, alginatol suppositories), during
convalescence - dicetel.
Vitamin therapy - in the period of convalescence for recovery
permeability of cell membranes, increasing their biopotential,
stimulation of normal microflora (unicap, centrum, supradin, polivit,
alvitil, etc.) 10-14 days
Physiotherapy - for prolonged bacterial excretion outside the island. period - e/f
humizol on the stomach 10 times.

Prevention
allocate for the patient separate dishes, towels, care items that
disinfect after use
pour disinfectant patient's excretory solution
carry out wet cleaning of the room and toilet with disinfectant. means 2-3 times a day
Maintain personal hygiene: wash your hands with soap as often as possible, lathering them
2-3 times, especially after using the toilet and before preparing and eating food.
Change towels and underwear daily.
do not use water from unauthorized sources for domestic purposes
water sources and do not swim in them. Transparent and pleasant-tasting water from
spring can be dangerous. There are 35 sources of unauthorized
water supply, in 2004, 35% of samples were unsatisfactory in terms of
sanitary and chemical indicators and 45% - according to microbiological ones.
Be sure to boil water for drinking, including from tap water and bottled water
Use only good quality water for drinking, washing hands and dishes.
use only high-quality food products
do not purchase food products, especially dairy products, from unauthorized
places of trade, spontaneous markets, from hands, trays
All types of livestock products must be subject to veterinary
examination

store perishable foods in the refrigerator, observing expiration dates
store ready-to-eat foods separately from raw foods
It is necessary to carry out heat treatment of dairy products (cottage cheese, milk,
cream)
Choose fruits for your child that are not damaged, and that the berries are not crushed. At home
thoroughly wash the fruits with running water, pour boiling water over them, apples, pears,
Remove the skin of the peaches.
protect food products from flies. Trash cans and bins should be
be closed with lids and emptied systematically. In summer on the windows
it is necessary to stretch the mesh and use sticky paper to kill flies,
disinfectants.
observe the rules of personal hygiene in public catering areas and
concentration of people
use baby food only in sterile packaging
Keep yard latrines closed, promptly clean and disinfect
at least once every 5 days
inform the population about ways of infection
if the child becomes ill (nausea, vomiting, loose stools, T) immediately call
doctor and do not give antibiotics yourself
when going on vacation with children, take rehydron, paracetamol,
enterosorbent, suprastin
It is planned to develop a multicomponent enteral vaccine against
OKI..

DYSENTERY
The causative agent is Shigella.
The source of infection is the patient
With feces the patient excretes a large amount of
number of bacteria. If they fail to comply
hygiene germs from his dirty hands can
get on surrounding objects, food, water.
Older children are more likely to get sick when they become infected
through unwashed hands, food at a street kiosk,
swimming in ponds. 1 year old children get sick
less often, since there is no place for them to become infected.

Classification

Type
Forms
gravity
Flow
Typical
Atypical:
hypertoxic
dyspeptic
Lightweight
Medium-heavy
Heavy
Abortive
Acute
Subacute
Lingering
Chronic

Clinic.
Acute onset
Intoxication, fever for 1-3 days, in severe cases
neurotoxicosis is possible.
Abdominal pain (usually left iliac region)
Very frequent (10-20 or more times a day) colitis stools with
an abundance of mucus, sometimes mixed with blood and pus).
The only OKI that can be diagnosed before
culture for hemocolitis syndrome. But others can give it too
diseases.
Tenesmus or its equivalent (crying with urge,
facial skin redness)
Anal gaping
Spasmodic Sigma
In the coprogram there are leukocytes, mucus, red blood cells
Sowing Shigella

SALMONELLOSIS
Epidemiology
Sources of infection
animals (cattle, pigs, rodents,
poultry, etc.)
sick person and bacteria excretor
Routes of infection:
nutritional (through meat, dairy products)
fecal-oral - for young children,
especially the 1st year of life.
nosocomial infection. Possibly with
medical procedures (endoscopy),
by contact. Almost always in 1 year old children
life, caused only by S. Typhimurium.

Classification

Type
Forms
gravity
Flow
Localized forms:
Gastrointestinal
Bacterial carriage
Generalized forms:
Septic
Typhoid-like
Lightweight
Medium-heavy
Heavy
Acute
Lingering
Chronic
Flu-like

Clinic
acute onset
intoxication, fever 5-7 days; during hospitalization
infection, prolonged fever of the wrong type.
In mild cases, T may not be present.
diarrhea is usually preceded by vomiting
enterocolitis syndrome - loose, watery stools,
greenish-brown color in the form of swamp mud or
frog eggs, sometimes streaked with blood, maybe
foamy with an unpleasant odor, not too frequent, but
abundant
in hospital infections predominates
gastrointestinal form, gradual onset, more
frequent involvement of not only the small intestine, but also the large intestine,
frequent presence of blood in feces.
In severe forms, neurotoxicosis, toxicosis with
exicosis, septic syndrome
Often occurs in an erased form
In the coprogram there is mucus, leukocytes
Sowing Salmonella from stool, blood, urine

Escherichiosis (COLI-INFECTION)
acute onset
intoxication, long-term wave-like
fever 1-2 weeks
enterocolitis syndrome - profuse frequent
loose, watery stools without tenesmus, with
mixed with green or yellow-orange.
Sometimes streaked with blood.
seeding of enteropathogenic Escherichia coli
the coprogram is not changed, or mucus,
single leukocytes

STAPHYLOCOCCAL INFECTION
May be in the form:
food poisoning - acute onset through
several hours after infection, abdominal pain,
repeated vomiting, loose, frequent stools.
In severe cases, increasing T to high numbers,
intoxication, convulsions.
Recovery within 5-7 days.
Staphylococcal enterocolitis - in young children
age at consumption of infected
milk.
Most often mild or moderate form.
Slight increase in T, frequent watery liquid
stool with mucus. Sometimes streaked with blood.
Complications are typical: otitis media, pneumonia.
Vomiting is rare.

ROTAVIRUS INFECTION
Happens more often in the spring.
Infection through dirty hands, vegetables, fruits,
unpackaged food, unboiled water
Increased T to 39, vomiting, diarrhea. Chair
watery with a yellow tint up to 20 times per
day. There may be a skin rash. Maybe
preceded by runny nose and other symptoms
ARVI.
Prevention:
Personal hygiene Viral intestinal
infections

Acute intestinal infections – group
infectious diseases with
fecal-oral mechanism
infections caused by pathogenic
and opportunistic bacteria,
viruses and protozoa.

Acute intestinal infections (AI)
represent one of the most serious
health problems, current
for all countries of the globe
According to WHO data, every year in the world
register up to 1-1.2 billion diarrheal cases
diseases
~5 million children die annually from
intestinal infections and their complications

In Russia, the incidence of acute intestinal infections is stable
ranks second after ARVI in
infectious pathology
According to Rospotrebnadzor in the Russian
Federations in recent years:
- the incidence of acute intestinal infections was on average
about 280.0 per 100 thousand population,
- incidence of ARVI
from 11000.0 to 13000.0 per 100 thousand population.

Etiology of acute intestinal infections

Pathogens of acute intestinal infections
Bacteria:
Salmonella
Campylobacteriosis
Shigella
E.coli
Clostridium
Protozoa:
Lamblia Giardia
Kriptosporidium
Amoeba
Trichinella
Viruses:
70% OKI
Rotavirus
Norovirus
Astrovirus
Adenovirus
Enterovirus
Sapovirus
Coronavirus

Despite the successes achieved in
studying OKI their etiology in 70-80%
cases it remains unclear that
associated with the predominance of viral
intestinal lesions in 50-80% of cases

Etiology of acute intestinal infections in children (in outpatients)

73,6%
9,8%
7,1%
5,1%
0,7% 2,4%
1,0%
0,3%

Etiology of acute intestinal infections in children (in hospital)

Viral-bacterial
3,0%
Bacterial
15,0%
Viral
57,0%
KINE
25,0%

The opinion that viruses cause
gastroenteritis, was suggested in the 40s
years of the twentieth century, but for the first time the virus in
feces was identified
only in 1972 Kapikian after
diarrhea outbreaks

Causative agents of viral gastroenteritis

rotaviruses (6.0–83.0%),
caliciviruses (8.6-45.0%),
adenoviruses (1.9–27.0%),
astroviruses (2.1-7.9%),
toroviruses (6.8%),
coronaviruses (1.6%),
enteroviruses (2.5–32.4%), etc.
List of viral agents that cause intestinal disorders
is constantly growing (it was found that
and pestiviruses,
picobirnaviruses
causing diarrhea in animals,
are causative agents of viral gastroenteritis in humans)

Prevalence of various viral pathogens of acute intestinal infections

5,3%
5,8%
25,7%
6,8%
56,4%
rotaviruses
adenoviruses
toroviruses
mixed
caliciviruses
Tikhomirova O.V. Federal State Institution Research Institute of Children's Infections

Structure of viral gastroenteritis

40%
in children, Tikunova N.V. With
co-authors, 2007
14% in adults, Gracheva N.M.s
co-authors, 2004
Rotaviruses
Caliciviruses
(noroviruses)
Enteroviruses
(Coxsackie, Echo)
Adenoviruses
40 and 41 serotypes
17%, Tikunova N.V. et al., 2007
25%,
Kalashnikova E.A., 2000
5.4%, in children up to 17%
Kozina
G.A., 2010
Astroviruses
2,2%,
Epifanova N.V., 2004
Coronaviruses
0,1%,
Blokhina T.A., 2000

Rotaviruses

Isolated in 1973 by Bishop from the mucosa
duodenum in children with gastroenteritis
The viral particle resembles a wheel with a wide
hub, short spokes and clearly defined
rim, hence the name of the genus (from Latin rota - wheel).

Family Reoviridae - from English respiratory enteric orphan viruses (family of viruses of humans, animals and plants)

Genus Orthoreovirus
Genus Orbivirus
Genus Rotavirus
Genus Coltivirus
Genus Aquareovirus
Genus Cypovirus
Genus Fijivirus
Genus Phytoreovirus
Genus Oryzavirus

Rotavirus
Rotavirus is subdivided
on
7 groups: A, B, C, D,
E, F, G
VP4(P)
Group A rotaviruses –
VP7(G)
cause 90% of cases
diseases in humans
Outer shell proteins
VP4 and VP7 determine
the virus belongs to
serotype P or G
The VP4 and VP7 proteins cause
production
neutralizing antibodies
Parashar U.D., et al. Emerg Infect Dis 1998; 4:561–70.
15

Classification of rotaviruses (according to Beards I.M., 1992; Molyneaux P.J., 1995)

Group (VP6)
A (90.0%) B C D E F G
Subgroups of rotaviruses A
I, II; I+ II, neither I nor II
1. G serotype (VP7)
1,2,3,4,5,6,7,8,9,10,11,12,13,14
2. P serotype (VP4)
1,2,3,4,5,6,7,8,9,10,11

Viral particles have a certain polymorphism,
therefore in copro materials when used
cryoelectron microscopy reveals several species
particles:
mature (“complete”) virions with a core and complete
a set of shells;
empty or “incomplete” virions are single- or double-enveloped, and
also nuclei without shells and tubular formations.

Distribution of rotavirus strains in the world
G1P causes 65%
rotavirus
gastroenteritis in the world1
5 strains of rotavirus –
cause >90% of cases
rotavirus gastroenteritis1
G1P
G2P
G3P
G4P
G9P
Annual ratio
strains
in geographical regions
the world is changing1
Seroprevalence
rotavirus in the world, 1989-2004
100%
Other8%
G9P 3%
G4P 9%
G3P 3%
G2P 12%
90%
80%
70%
60%
50%
40%
G1P 65%
30%
20%
10%
0%
Prevalence
Serotype
prevalence (%)
serotypes (%)
N=16,474
1. Santos N and Hoshino Y. Rev Med Virol 2005; 15:29–56.
18

Physico-chemical properties of rotaviruses

The infectious activity of rotavirus is stable at pH
3.0 - 11,0.
Resistant to environmental factors,
disinfectant solutions, chloroform, ether,
acidic environment, persist for a long time in feces.
When re-frozen, keep
viability for many months, but
die when boiled.
Effective disinfectant – 50-70% alcohol solution
ethanol

Cultural properties of human rotaviruses

Unlike animal rotaviruses, it is bad
cultivated in cell systems, their adaptation
cell culture is extremely complex.
Various amplification methods are used
viral reproduction in cell culture with
using physical and chemical
factors (centrifugation, rocking,
thermal effects, influence of proteolytic
enzymes and dimethyl sulfoxide, etc.).

Variability of rotaviruses

In the human population at the same time
there are a huge number of different options circulating
rotaviruses, which is due to their genetic
plasticity inherent in RNA genomes
viruses.
Social circulation of rotaviruses of various strains and
types creates the basis for the formation of mixed
populations and reassortant strains,
characterized by different combinations of genes.
Rotaviruses have two types of variability:
drift and shift that occur everywhere,
but most often in countries with intensive
epidemic process (Southeast Asia,
Africa and South America).

Epidemiology
Source of infection
Sick
Virus carrier
Mechanism
Fecal-oral
Paths
Water
Food
Contact
Aerogenic
Susceptible organism

Rotavirus infects 95% of children under 5 years of age worldwide
Rotavirus is highly contagious - only
10-100
viruses
necessary
For
infection
Path
distribution:
fecal-oral - contact - household
(airborne droplets allowed)
10 trillion viruses are released in 1
gramme2
CARRIER!
Very stable in the external environment
(especially in drinking water)
Sanitary and hygienic
partially
infections
influence
on
Events
spreading
23

Universal sensitivity

Children in the first 5 years of life most often suffer from RV
gastroenteritis, acting as a “starter”
mechanism" of various manifestations of epidemic
process.
Adults are in second place in terms of incidence
over 60 years old.
Almost everyone gets sick from RV
infection, which is confirmed by the detection
specific anti-rotavirus antibodies –
immunoholobulin G (IgG) in 60-90% of children already at 6 years of age.
Infectious dose (within 10 viral particles).
Up to 10 billion viruses are found in 1 gram of feces.

Every minute of every day
...children are dying all over the world
from rotavirus infection
25

Diarrhea is the second most common cause of death
children 5 years old in the world
Mortality (millions)
4
3
2.0
2
1.8
0.8
1
0.4
0.3
0
Pneumonia
Diarrhea
Malaria
26
Measles
HIV AIDS
Bryce J, et al. Lancet
2005; 365: 1147–52.

Rotavirus gastroenteritis: pathogenesis
Rotavirus penetrates into
duodenal epithelium
guts
Damage
fine villi
intestines
Selection
viral
enterotoxin
*
Reducing area
suction
Loss of water and
electrolytes
27
Nervous activation
intestinal systems
DIARRHEA
NAUSEA
VOMIT

Rotavirus
Isolation of the pathogen lasts up to 21 days
Incubation period ≈ 2 days
Duration of symptoms 2-6 days
Symptoms
Diarrhea is watery, without
blood impurities
Nausea, vomiting
Dehydration
Body temperatures
Pain in the epigastric region
General intoxication
28

Complications
- Severe dehydration
- Secondary
bacterial
infection
Rotavirus gastroenteritis
- cause of hospitalization

Rotavirus gastroenteritis laboratory diagnostics
Enzyme immunoassay methods
(determination of antigen in
stool samples)
PCR (DNA determination
virus in stool samples) serological
(determination of antibodies in
blood, IgM)
Immunochromatographic
strips (for screening –
diagnostics)
30

Diagnosis of RVI

Detection of RV antigen
ELISA method provides
fast, highly sensitive data diagnostics
infections.
PCR (polymerase chain reaction)

ELISA diagnostics of RVI

In children, detection of rotavirus hypertension is possible from the 1st
days of infection to 10-60 days of illness
Antigen
at
adults
determined
V
copromaterial from day 1 of illness to day 7-10
diseases.
Created for
identifying
Ag of rotavirus group A:
in the feces of patients,
contact persons;
in water.

Rice. . Operating principle of the immunochromatographic rapid test. 1 – sample containing the analyte; 2 – conjugate; 3.4 –

immobilized
antibodies (test and control strips); 5 – sample pad; 6 –
conjugate pad; 7 – membrane; 8 – pad for absorption
reagents; 9 – substrate for the membrane; 10 – test strip: positive
result; 11 – control line: reliable test result.

Positive result of the rapid test RIDA Quick Verotoxin / O157 Combi Test format: at the top - test cassette, at the bottom -

test strip.
1 – sample introduction area.
2 – area where the conjugate is located.
3 – reaction zone; from left to right – control strip (C); test
a band indicating the presence of verotoxin in the sample (T2); test
a band indicating the presence of antigens of strain O157 (T1).
4 – reagent absorption area (covered with a film with the name of the test).

Caliciviruses

Noroviruses were the first viruses
identified as causative agents of acute intestinal infections
(in 1972 by Kapikian)

Classification

Family
Caliciviruses
Noroviruses
Sapoviruses
Pathogenic to humans
Lagovirus
Vesivirus

Sapoviruses were separated into a separate genus in 1997 until 2002 called Sapo-like viruses (SLV) size 35-39 nm (divided into 3

Sapoviruses
highlighted in
separate genus in
1997
until 2002
were called Sapolike viruses (SLV)
size 35-39 nm
(divided by 3
genetic
groups)

Noroviruses

- were the first viruses identified as
pathogens of acute intestinal infections (in 1972 by Kapikian) as a result
immunoelectron microscopy of canned
fecal samples from patients during an acute outbreak
gastroenteritis among primary school children in
November 1968
-Originally named after the area of ​​Norwalk, state
Ohio.
-Cloning and sequencing of the Norwalk virus genome
showed that these viruses have the same genomic
organization as families Caliciviridae.
-The name norovirus (genus Norovirus) has been approved
International Committee on Taxonomy only in 2002
year.

Noroviruses

Noroviruses are divided into two genogroups:
Genogroup I (GI) includes:
Norwalk virus (Hu/NLV/NV/1968/US)
Desert Shield virus
(Hu/NLV/DSV395/1990/SR)
Southampton virus
(Hu/NLV/SHV/1991/UK)
Genogroup II (GII) includes:
Bristol virus,
Lordsdale virus (Hu/NLV/LD/1993/UK),
Toronto virus
Mexico virus (Hu/NLV/MX/1989/MX)
Hawaii virus (Hu/NLV/HV/1971/US)
Snow Mountain virus
(Hu/NLV/SMV/1976/US)

Morphology of noroviruses

- The virion has the shape of an icosahedron with a diameter of 27-40 nm, i.e. V
2 times less than RV, no supercapsid.
- The key characteristic of caliciviruses is the presence of
shell of characteristic recesses - 32 cup-shaped
depressions (hence the name “calyx” - cup in Greek).
- The genome consists of a single-stranded helix + RNA, which
encodes RNA polymerase, helicase, structural proteins
capsid and a small protein whose function is unknown.

Physicochemical properties of noroviruses

The virus is resistant to ether and detergents
More resistant to chlorides than rotavirus
Sensitive to low pH
Inactivated by heating at a temperature of 56°C.
Cultural properties of human noroviruses
Currently, all cultivation attempts
noroviruses were unsuccessful.

The main routes of transmission of norovirus are:

food, i.e. Human
may become infected
for example, by using
unwashed for food
vegetables and fruits;
aquatic when a person
gets infected by drinking
some amount
liquids,
containing a virus;
contact-household, when
the virus enters the body
through unwashed hands,
household items, dishes
etc.

Clinical picture of norovirus infection

Acute onset in 93.2% of cases;
Vomiting – in 84.1% of cases, repeated for 2-3 days;
Diarrhea – in 51.1%, most often mushy stools;
Exicosis – in 37.5% of cases;
Intoxication - in 23.8% of cases, expressed for 1-2 days;
Fever – in 84.1%, 1-2 days;
Abdominal pain – in 43.2% of cases;
Catarrhal phenomena in the nasopharynx - in 71.4% of cases.

Coronaviruses

Genus
Torovirus
Family
Coronaviridae
Genus
Coronavirus

MORPHOLOGY OF CORONAVIRUS (according to Holmes K.V., 2003)

diameter 80 - 240 nm.
3 times more virus
flu
Virions contain a plus chain
polyadenylated RNA 16-30 kb long
infectious
S – receptor protein,
HE – hemagglutinin esterase,
E - small membrane
protein,
M – matrix protein,
RNA+N - nucleocapsid,
RNA in complex with N protein.

Electron microscopic method

Coronavirus found in the feces of a child with acute
gastroenteritis

Classification of coronaviruses

group
1
2
Virus name
Human coronavirus strain 229E (HcoV-229E)
Porcine transmissible gastroenteritis virus
(TGEV)
Porcine respiratory virus (PRCoV)
Canine coronavirus (CcoV)
Feline enteritis virus (FECoV)
Feline infectious peritonitis virus (FIPV)
Rabbit coronavirus (RbCoV)
Human coronavirus strain OC43 (HcoV-OC43)
Mouse hepatitis virus (MHV)
Rat sialodacryoadenitis virus (SDAV-RTCoV)
Hemagglutinating encephalomyelitis virus
pigs (HEV)
Bovine coronavirus (BcoV)
SARS Coronavirus (SARS-CoV)
3
Avian infectious bronchitis viruses (IBV)
Turkey coronavirus (TcoV)
Master
Human
Pigs
Pigs
Dogs
Cats
Cats
Rabbits
Human
Mice
Rats
Pigs
Large
horned
livestock
Human
Chicken
Turkeys

Physico-chemical properties of coronaviruses

Sensitive to physical and
chemical factors.
Due to the content in the viral shell
lipids are sensitive to ether, ethanol, formaldehyde,
propiolactone, chloroform.
Inactivating effect on coronaviruses
has a sharply acidic and sharply alkaline environment (pH< 3,0
and pH > 12.0), UV radiation.
Cultural properties of human coronaviruses
Cultivation of enteric coronaviruses is carried out on
fetal intestinal cell cultures, primary kidney cultures
human embryo and colon tumor cell culture
human (HRT-18).

Epidemiology of coronaviruses

HF circulation has been detected on all continents
Globe;
The seasonality of CV infections is winter-spring (usually
December - March);
The share of COVID-19 in human respiratory pathology
averages 10% (5-19%).
*Every third year there is a tendency towards
formation of peaks of CVI activity;
The transmission mechanism of CVI is aerosol, fecal-oral, contact;
Transmission routes are airborne droplets and airborne dust, the pathogen is released with respiratory
secretions, saliva, urine, feces;
Re-infection with CV is possible, which is associated with
antigenic diversity of viruses even within one
group and short-term immunity to
heterotypic pathogens;

Epidemiology
Source of infection
Sick
Virus carrier
Mechanism
Fecal-oral
Paths
Water
Food
Contact
Susceptible organism
Aerogenic

Susceptibility

incidence of coronavirus and torovirus
infections are most common in young children
age and immunocompromised persons,
suffering from certain disorders
immunity.

Clinical picture of coronavirus infection

Acute onset in 75.0% of cases;
Damage to the gastrointestinal tract – in 89.8%
cases: vomiting is often repeated, not profuse liquid
stool 2-5 days;
Moderate intoxication – in 68.2% of cases;
Fever – about 80.0%;
Abdominal pain – in 18.2% of cases;
Catarrhal phenomena in the nasopharynx about 90.0%
cases.

The role of coronaviruses in human pathology

ARVI (acute rhinitis, nasopharyngitis, tracheitis)
Participation
V
etiology
bronchitis,
pneumonia,
severe ARDS
Combined damage to the respiratory and gastrointestinal tracts
Acute enteritis (in newborns and persons with reduced
immunological reactivity)
Neurological
pathology
(polyradiculitis,
spicy
disseminated
encephalomyelitis with demyelination, multiple
sclerosis, encephalomeningitis)
Otitis, conjunctivitis
Hepatitis, myocarditis
Polyorgan
defeats
(y
immunocompromised persons)

Adenoviruses

The only DNA-containing enteric viruses not
having shells.

Morphology of adenoviruses

-The virion consists of a capsid,
fibrils and cores (core) and
bound proteins.
-The capsid with a diameter of 70-90 nm has
icosahedral shape (cubic type
symmetry), from 12 vertices of which
threads (fibers) come off
varying in length
adenoviruses of different subgroups,
acting as receptors;
-The capsid is made up of 252 capsomeres.
-The virion has antigens:
Antigen A (hexon) - identical
for all blood pressure
(group specific),
Antigen B (penton base),
Antigen C (threads, fibers) –
type-specific.

Family Adenoviridae

Genus Mastadenovirus
Subgroup
Serotype
Tropism
A
12, 18, 31
B1
3, 7, 16, 21, 50
B2
11, 14, 34, 35
C
1, 2, 5, 6
intestinal tract
respiratory
tract
urinary
system
respiratory and
intestinal tract
D
8-10, 13, 15, 17, 19, 20, 22-30, 32,
33, 36-39, 42-49, 51
E
4
F
40, 41
eye tissue, etc.
respiratory
tract
intestinal tract

Physicochemical properties of adenoviruses

Relatively resistant to environmental factors: when
at a temperature of 56°C they die in 30 minutes, at 36°C - after 7
days, 23°C – 14 days.
tolerate low temperatures and drying well,
resistant to changes in pH and organic
solvents (ether, chloroform, etc.).
Cultural properties of human adenoviruses
They do not reproduce on chicken embryos, but they do well
reproduce on primary trypsinized and
continuous cell cultures.

Clinical picture of adenoviral infection

Severe intoxication – about 100.0% of cases;
Fever – 100.0%, 75%>39.0°;
Diarrhea – 80.0%, up to 10-12 times a day;
Vomiting – 40.0%, often repeated;
Abdominal pain – 60.0% of cases;
Exicosis – 40.0% of cases;
Catarrhal phenomena in the nasopharynx - about 100.0%
cases.

Astroviruses

Identified for the first time in the feces of children with acute
diarrhea in 1975
RNA-containing, non-enveloped viruses
family Astroviridae (Greek astron - star).
The family includes 2 genera:
Mamastrovirus (Astroviruses
mammals) and
Avastrovirus (Avian Astroviruses).
There are currently 8 known serotypes
AstV, pathogenic for humans (AstV 1–8), from
which are most widespread
first (Oxford strain).
Viral particle with a diameter of 23-33 nm
has a star shape due to 5-6
projections
(vertices), 12 extend from the surface
little ones
spines making the surface
uneven.
type of symmetry – icosahedral.

Clinical picture of astrovirus infection

Astroviruses are more often associated with mild and
short-term diarrhea, mainly in
children under five years of age.
In early childhood, the disease may have
the same course as with rotavirus infection.
The infection is most severe and lasting in
immunocompromised and elderly people.

Diagnosis of viral diarrhea

1.
2.
Diagnosis of viral diarrhea
Methods for detecting virions and viral antigens
electron microscopy,
isolation of rotaviruses in cell culture,
linked immunosorbent assay,
immunochromatography,
solid-like coagglutination reaction,
diffuse precipitation,
latex agglutination,

immunofluorescence,
immunoelectrophoresis,
radioimmunoassay.
Methods for detecting viral RNA
polymerase chain reaction,
electrophoresis of rotavirus RNA in polyacrylamide gel,
point hybridization method.
3. Methods for detecting specific antibodies
solid-phase coagglutination reaction to determine specific
rotavirus IgM,
passive hemagglutination reaction,
complement fixation reaction,
neutralization reaction.

Diagnosis of viral diarrhea

TEM (transmission electron
microscopy) all viruses
Detection of viral particles in feces
ELISA (enzyme-linked immunosorbent assay)

PCR (polymerase chain
reaction)Identification of specific
sections of RNA, DNA (RV, NV, AD, SV,
AstV)
Immunochromatography
Detection of virus antigens (RV, AD)

ELISA (enzyme-linked immunosorbent assay)
Detection of virus antigens (RV, AD)
designed to detect adenovirus type 40 and 41 antigens in
copromaterial of patients for differential diagnosis of acute
intestinal infections

PCR (polymerase chain reaction) Detection of specific regions of RNA, DNA (RV, NV, AD, SV, AstV)

Application of multiplex RT-PCR method for differential diagnosis of intestinal viral infections

About the PCR method
Polymerase chain reaction (eng. - PCR - polymerase chain
reaction) was discovered by Carey B. Mullis in 1983, for which he was
awarded the Nobel Prize.
Polymerase chain reaction (PCR) is a method that
allows you to find in the studied clinical material
a small piece of genetic information (DNA/RNA)
infectious pathogen, multiply it many times and
identify using various modern technologies
(hybridization-fluorescent detection in the mode
"real time" and "endpoint").
Currently, PCR is one of the highly sensitive
methods for diagnosing infectious diseases, which
allows the detection of single viral particles or
bacterial cells.

Advantages of the PCR method:

The ability to detect the pathogen itself, and not antibodies to
him.
It is highly specific because it detects
unique, characteristic.
Only for a given pathogen is a DNA fragment.
Has high sensitivity compared to
known diagnostic methods.
Automated.
Allows for mass research.
It is possible to perform analyzes within 1-3 days.
The method is universal, because from one clinical sample
material can be done.
Tests for the presence of a wide range of pathogens
diseases.

Reagent kit for detection and differentiation
DNA (RNA) of microorganisms
Shigella genus and enteroinvasive T. coli (EIEC),
Salmonella,
thermophilic Campylobacter,
adenoviruses of group F,
rotavirus group A,
norovirus genotype 2,
astroviruses in environmental objects and
clinical material using PCR method
hybridization-fluorescence detection

Cyto-test is a rapid immunochromatographic test for qualitative
determination of rotavirus infection in stool samples.
Sensitivity - 100%
Specificity - 98%
Storage conditions: 2-30 degrees
Shelf life - 2 years from the date of production

Prevention of viral intestinal infections

Nonspecific prevention
- compliance with sanitary and hygienic rules (hand washing,
use only boiled water for drinking),
- purification and chlorination of tap water,
- sufficient heat treatment of food,
-isolation of the patient with provision of personal utensils.
Specific prevention
rotavirus infection
There are two live attenuated oral vaccines.
Applications:
ROTARIX™ (monovalent, based on human strain G1P8)
prevention of rotavirus infection of serotype G1, as well as G2, G3, G4, G9.
Course - 2 doses. The first from 6 weeks. The second one no less than 4 weeks later. Should
complete before 24 weeks of age.
RotaTek® pentavalent (human-bovine: G1, G2, G3, G4 – human,
G6 – bullish). In children from 6 to 32 weeks. Course 3 doses from 6-12 weeks, intervals
between doses from 4 to 10 weeks. The last one is no later than 32 weeks. age.

ENTEROVIRUSES

Family PICORNAVIRIDAE
Enterovirus
polioviruses (causative agents of poliomyelitis) – 3
serotype
- Coxsackie A viruses – 24 serotypes
- Coxsackie B viruses – 6 serotypes
- ECHO viruses – 34 serotypes
- enteroviruses serotypes 68 - 71 Rhinovirus

The structure of the enterovirus virion

A simple virus with a diameter of 22-30 nm
The capsid is built according to the icosahedral type
symmetry
Consists of 60 protomers grouped into 12
pentamers (pentagons)
Each capsomer consists of 4 proteins - VP1, VP2,
VP3, VP4
The outer surface of the capsid is formed
proteins VP1, VP2, VP3
The VP4 protein is located inside the capsid and is closely
associated with genomic RNA

Enterovirus genome

The genome is represented by a linear
unfragmented single-stranded plus RNA
At the 5` end of the genomic RNA is covalently located
associated genomic protein VPg

Enterovirus antigens

Antigenicity is associated with the capsid protein VP1
Enteroviruses contain
group-specific (genus-specific)
antigen common to the genus Enterovirus is capable of
bind complement
Type-specific antigen – individual
for each serotype (serovar), has
hemagglutinating properties. Total
71 serotypes are pathogenic for humans

Epidemiology of enterovirus infections

Sources – patients and practically
healthy virus carriers. Viruses
excreted mainly in feces
The main mechanism of transmission is fecal-oral (very rarely airborne)
Transmission factors – water (unboiled water,
swimming in open water), unwashed
vegetables and fruits, dairy products (not
heat treated)
household items, flies

Pathogenesis of enteroviral infections

Entrance gate – mucous membranes of the nasopharynx
and digestive tract
The incubation period is 2-7 days
Viruses reproduce in epithelial cells
and cells of the lymphoid tissue of the pharyngeal ring and
lymphoid structures of the small intestine
With sufficient body resistance
virus reproduction occurs limitedly, in place
entrance gate, and is asymptomatic or with
affecting only the mucous membranes.
Low body resistance, high
infectious
dose,
high
virulence
pathogen leads to generalization of infection

Pathogenesis (continued)

Viruses enter the bloodstream and
carried by blood to various organs,
causing damage depending on
tissue tropism.
After multiplication in organs, viruses
can again enter the bloodstream, causing
repeated viremia.
Therefore, enterovirus infections
often have a wavy character.
Viremia stops after
appearance of specific antibodies

Target organs for enteroviruses

Coxsackie viruses are cardiotropic and often
affect the heart in the form of myocarditis, as well as
pancreas, causing pancreatitis with
subsequent development of diabetes
ECHO viruses have a high
tropism for lymphoid tissue
Enteroviruses as opposed to polioviruses
affects the meninges, sometimes the brain and
very rarely anterior horns of the spinal cord

Clinical forms of enteroviral infections

Typical forms are
- Herpetic sore throat
- Serous meningitis
- Epidemic myalgia
- Enteroviral exanthema
Rare forms: ARVI, gastroenteritis, lesions
Central nervous system (encephalitis or polio-like form),
damage to individual organs (myocarditis, pancreatitis,
nephritis, hepatitis, orchitis, uveitis, etc.), enterovirus
fever

Polio virus

Polioviruses
belong to the family
Picornaviridae (from pico small and rna containing RNA), to
genus Enterovirus.
There are three
poliovirus serotype
– type 1, type 2 and type 3.
Typical
representative of the family
Enterovirus and families
Picornaviridae is
polio virus strain Mahoney
poliovirus type 1.

The word polio
(Poliomyelitis) translated
into Russian
means inflammation
gray matter of the brain
(Greek Polios - gray,
myelitis - inflammation
spinal cord). The thing is
what is most important
biological
property of polioviruses
is their tropism towards
nervous tissue, they
affect motor
gray matter cells
spinal cord.

Epidemiology of polio

The source of infection is patients and virus carriers who secrete the virus from
feces.
The main mechanism of transmission is fecal-oral (dirty hands,
objects, toys, contaminated products).
The airborne route of infection is not denied, but no
special significance and is realized mainly during
epidemic outbreaks.
Due to high invasiveness and stable immunity
polio has all the signs of a childhood infection:
75-90% of cases of the disease are observed in children under 7 years of age, but also
the incidence in adults is not uncommon.
Outbreaks of polio in countries with temperate climates have a summer-autumn seasonality.
Immunity after illness is stable, almost
lifelong, although three types of polio virus do not predetermine
formation of cross antibodies, but repeated manifest forms
polio is not observed.

Icosahedral symmetry
60 subunits
4 polypeptides VP1-VP4

Pathogenesis of polio

The entry point for infection is the mucous membrane
digestive canal.
Primary reproduction of the virus occurs in the lymphoid
tissue, epithelium of the mucous membrane of the pharynx and intestines, which
leads to the release of the virus in the first days of the disease in a very large
quantity and makes the patient especially dangerous to others
precisely during this period.
Next, the infection generalizes - viremia.
If the pathogen is not neutralized by the cells of the system
mononuclear phagocytes, damage to the nervous system occurs
systems.
The virus penetrates the central nervous system in no more than
1% of infected, in others developing non-paralytic
forms of the disease or virus carriage.

Clinical forms of polio

Asymptomatic form – occurs in 90%
infected
The abortive form (minor disease) occurs through
type of ARVI or gastroenteritis
Meningeal form (non-paralytic
polio)
Paralytic form (great disease)
Progressive post-polio myopathy

A man with an atrophied right leg due to polio

Diagnostics

Diagnostics
polio
founded
on
virus isolation from feces, spinal
fluid, nasopharyngeal swabs and blood on the 3-7th
day of illness.
Materials for research - blood and
cerebrospinal fluid.
On days 1–3, neutrophils predominate in the cerebrospinal fluid, with
2 - 4 days they are replaced by lymphocytes. Content
protein is normal or slightly increased. In the early
period
polio
cellular protein
dissociation, by the end of the 2nd week is noted
protein-cell dissociation.

Laboratory diagnostics

To isolate the virus, take a swab of feces and then
pre-cleaning and treating it with antibiotics
infect cell cultures. In case of receiving the GPA and
corresponding passages, the isolated strain is typed
virus in the pH of the GPD using immune sera.
Direct immunofluorescence methods are used
and electron microscopy.
Recently, the use of
diagnostics based on ELISA and monoclonal
antibodies,
PCR,
What
much
increases
sensitivity and reliability of serological
diagnostics

Progress in polio eradication 1988 – 2005

1988
350,000 children
125 countries
2005
2026 people
21 countries
Persistent polio,
despite high coverage
The latest fact of transmission of wild
poliovirus type 2 - 1999

Four countries remain endemic for polio. This
Afghanistan, Pakistan, India and Nigeria.
At the end of 2003 immunization activities in Kano State
against polio were stopped due to unfounded
rumors about the dangers of the polio vaccine.
As a result of the cessation of immunization in Kano State and
suboptimal quality of work to eradicate polio in
other northern states, the disease quickly spread throughout
Nigeria, by mid-September 2004 more than
500 cases of polio.
The infection was imported into more than 20 neighboring countries, including
from which polio had previously been eradicated.
In 2010, the number of polio cases in Nigeria
decreased by 98% compared to the same period in 2009.

Involvement of the country's top management in the program

The main achievement of 2009 in Nigeria is
strengthening political will
Involvement of the country's top management in the program
Kano Governor vaccinates
your daughter
First time in Kano
85% vaccinated
children
Polio Vaccine
Doses
>3 doses
1 -2 doses
0 doses

Coxsackie and ECHO viruses

Enteroviruses are characterized by small
virion size (28 nm - Coxsackie virus, 10-15 nm
- ECHO), cubic symmetry, ability
form crystals inside the affected cells.
Single-stranded RNA, makes up 20-30% of the virion,
capsid naked.
Resistant to ether.
Some types of enteroviruses agglutinate
human erythrocytes of group 0 or chicken erythrocytes.
Based on their antigenic structure, Coxsackie viruses are divided into
two groups: A and B.
Group A contains 26,
and group B - 6 serological types.

Coxsackie A viruses cause in newborn mice
diffuse myositis, Coxsackie B viruses (not all) -
disease with seizures,
ECHO type 9 - paralytic forms.
Other ECHO viruses are non-pathogenic for laboratory
animals.
Viruses
Coxsackie
type
A7
cause
polio-like diseases in monkeys and adults
cotton rats.
Viruses are resistant to known antibiotics
and medications, 70% alcohol, 5% Lysol, in
They are stored frozen for many years.
Inactivated by heating (50°C for 30 min),
drying,
ultraviolet
irradiation.
Sensitive to formalin and hydrochloric acid
acid.

ECHO viruses

In 1951, other viruses similar to
with polioviruses and Coxsackie viruses, but
characterized by the absence of pathogenicity for
monkeys and newborn mice. Because
that the first discovered viruses of this group
were isolated from the human intestine and had
cytopathic effect, but were not associated
with no diseases, they were called orphan viruses or ECHO viruses for short, which
means: E - enteric; C - cytopathogenik; N -
human; O - orphan - orphan.

Currently the ECHO group has 32
serovariant. A significant part of them have
hemagglutinating properties, and all of them
multiply well in monkey cell culture.
Some ECHO virus serotypes (11,18, 19)
are among the most common pathogens
human intestinal dyspepsia.

Pathogenesis

The virus penetrates through the mucous membrane of the pharynx and other
parts of the digestive tract, penetrates into the blood; during events
meningitis, it is isolated from the cerebrospinal fluid.
Tissue changes are found in the affected heart muscles, in
brain. Coxsackie and ECHO viruses cause acute enteroviral infections
infections that are characterized by clinical polymorphism
currents:
- polio-like diseases,
- gastrointestinal disorders,
- general febrile diseases with and without rash.
More often, Coxsackie A viruses cause paralytic forms,
respiratory tract diseases similar to complete myelitis,
pericarditis, Coxsackie B - aseptic myocarditis in children,
febrile diseases.
Enteroviral infections are characterized by the presence of erased and
asymptomatic forms of the disease, as well as intestinal
virus carriage

Laboratory diagnostics

The materials for the study are samples
feces, blood, liquor, brain, organs.
Most cytopathogenic viruses are isolated from
primary tissue cultures of monkeys and humans, and
some - in cultures of transplanted Hep-2 cells,
FL, HLS or Detroit-6. Coxsackie A viruses with difficulty
adapt to tissue culture.
PCR and ELISA are most often used for
diagnosis of enterovirus infection by direct
detection of virus genomic RNA sequences
in clinical samples.

Purpose: presentation in the lecture material of issues of cause-and-effect patterns, factors of occurrence, spread and clinical features of acute intestinal infections in children pursues the main goal of this lecture. Namely: to develop in students knowledge and practical skills in matters of etiology, epidemiology, anti-epidemic measures in hospitals and children's institutions in order to prevent the spread of acute intestinal infections in children.


Lecture plan Demonstration of the medical history of the thematic patient (complaints, medical history, life history, somatic status, laboratory data) with access to a preliminary diagnosis. Relevance and prevalence of acute intestinal infections in children. Additional laboratory diagnostic methods to clarify the etiological structure of the disease. Determination of links in the epidemiological chain (source, transmission mechanism, susceptibility, incidence, seasonality, frequency). Modern classification of OKI. Treatment of OKI.


Patient D., 5 months old, complains of frequent loose, watery stools up to 12 times a day, repeated vomiting, loss of appetite, temperature rise to 38.8 0C, slight weight loss. Weight before illness. From the anamnesis: ill for 2 days. The disease began with an increase in T to 38.50C, regurgitation appeared after feedings. Stools become more frequent up to 9 times a day - watery, orange in color with white lumps. In the following days, vomiting occurred, up to 2-3 times. Stools became more frequent up to 12 times a day, liquid, watery with pathological impurities in the form of mucus.


On examination: the condition is moderate, the skin is pale, somewhat dry, the skin fold straightens out quickly, elasticity and turgor are not reduced. The large fontanelle is unchanged. The mucous membranes of the oral cavity are pink and dry. He drinks liquids willingly. Heart sounds of medium sonority, 144 beats. in 1 min. The limbs are warm, the nail beds are pale pink. Hemodynamics are stable. The tongue is covered with a white coating. The abdomen is moderately swollen, rumbling along the small intestine. Sigma is not spasmodic. There is hyperemia and irritation around the anus. Weight upon admission: 7.450g. Weight loss is


Complete blood count: red blood cells – 4.0 x 1012 /l; hemoglobin – 120 g/l; CP – 0.8 Leukocytes – 12.5 x 109/l; eosinophils – 2; rod-nuclear – 5, segmented – 67; lymphocytes – 21; monocytes – 5; ESR – 11 mm/h. Coprogram: leukocytes – 20 in the field; no red blood cells, mucus - ++; neutral fat - +++, vegetable fiber - ++, soap - ++


Clinical example 2. A 4-year-old child became acutely ill: the temperature rose to 38.5 0C, and there was a single vomiting after eating. A few hours later, abdominal pain appeared and bowel movements became more frequent. The stool was initially copious, liquid, brown in color, but subsequently became scanty with a lot of mucus and streaks of blood. On examination, the skin was pale and the lips were somewhat dry. The tongue is covered with a white coating and is rather dry. Heart sounds are somewhat muffled, 100 beats per minute. In the lungs there are no features. The stomach is not bloated. Sigma is spasmodic, painful on palpation. The anus is pliable. Coprogram: leukocytes - completely in the p/z; erythrocytes - in the p/z; mucus - +++; This is the clinical and laboratory picture in the case patients.


Which of the following syndromes do you think are leading in the first and second cases: acute respiratory failure heart failure liver failure renal failure diarrhea syndrome exanthema syndrome intoxication syndrome








Relevance of the problem. In infectious pathology of childhood, acute intestinal infections (AI) play a leading role. In terms of prevalence, they are second only to acute respiratory viral infections (ARVI). Intestinal infections are common everywhere. There is a high incidence of acute intestinal infections in Kazakhstan, including among children. Children account for up to 70% of the total number of patients, and most of them are young children.


According to WHO, every child develops 2-4 acute intestinal infections per year. AEIs are characterized not only by high morbidity, but also by high mortality. Those who died from acute intestinal infections account for more than half of the children who died from infectious diseases. In the structure of infant mortality, ACIs occupy one of the first places. Every 4th child on Earth dies from diarrhea.


In % of cases, the death of children from acute respiratory infections could have been prevented. All this is unacceptable, since OKIs relate to sufficiently studied problems. Only in recent years and decades has the etiological role of many bacteria and viruses in acute intestinal infections been established, the clinical manifestations of relatively “new” intestinal infections have been studied, new approaches to treatment have been proposed that limit the use of antibiotics and propose replacing them with newer, more physiological drugs (complex immunoglobulin preparations , biological products).


Preventing the spread of acute intestinal infections is not only a medical, but also a national task, and the participation in this work of all persons involved in childhood problems will improve the conditions of the social environment and serve as the key to success in the fight against intestinal diseases. Acute intestinal infections in children are characterized not only by high morbidity, but also by high mortality. Those who died from acute intestinal infections account for more than half of the children who died from infectious diseases. In the structure of infant mortality, ACIs occupy one of the first places.








The causative agents of intestinal infections belong to various taxonomic groups. Bacteria (Shigella, Salmonella, diarrheagenic Escherichia, Yersinia, Campylobacter, Staphylococcus, Klebsiella, etc.) act as etiological agents; viruses (rota-, adeno-, entero-, astro-, corona-, toro-, caliciviruses, etc.); protozoa (giardia, cryptosporidium, etc.).


What is the epidemiological chain of intestinal infections? Source of infection, mechanism of transmission and susceptible organism. Intestinal infections have a number of epidemiological patterns: widespread distribution, high contagiousness, fecal-oral mechanism of infection, tendency to develop epidemic outbreaks.






In secretory intestinal infections (enterotoxigenic and enteropathogenic escherichiosis, cholera), the occurrence of diarrhea syndrome is associated with activation of adenylate cyclase of cell membranes, followed by increased secretory activity of the small intestinal epithelium and impaired reabsorption of water and electrolytes.


Osmotic diarrhea caused by rota-, adeno-, astroviruses, etc.; develop due to dysfunction of the enzymatic systems of enterocytes that break down carbohydrates. However, it should be noted that it is rarely possible to classify nosological forms accompanied by diarrhea syndrome depending on one mechanism of diarrhea; More often than not, several pathogenetic mechanisms are important.


Intestinal infections are clinically manifested by the following syndromes: intoxication (acute infectious toxicosis), dehydration (dehydration, exicosis), fever and gastrointestinal (gastritis, enteritis, gastroenteritis, enterocolitis, gastroenterocolitis, colitis)


Gastritis syndrome is characterized by nausea, repeated vomiting, pain and a feeling of heaviness in the epigastric region. Enteritis syndrome is manifested by frequent, profuse, loose, watery stools, flatulence, and abdominal pain, mainly in the umbilical region. Gastroenteritis syndrome is characterized by a combination of signs of gastritis and enteritis.


Enterocolitis syndrome is characterized by frequent, profuse loose stools mixed with mucus, sometimes blood, abdominal pain, pain on palpation and rumbling along the colon. Gastroenterocolitis syndrome is a combination of signs of gastritis and enterocolitis. Distal colitis syndrome – retracted “scaphoid” abdomen, cramping abdominal pain with predominant localization in the left iliac region, spasmodic painful rumbling sigmoid colon, compliance of the anal sphincter, tenesmus; change in the frequency and nature of stool (frequent, scanty with mucus, blood - such as “rectal spitting”).

Slide 1

Intestinal infection The presentation was made by the teacher of the Municipal Educational Institution “Secondary School No. 15” in Engels Myadelets M.V.

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-oral cavity – approbation, wetting, neutralization, grinding of food, breakdown of carbohydrates; -esophagus – movement of food into the stomach; -stomach – mechanical processing, food disinfection, breakdown of proteins and partial breakdown of fats; -12 duodenum – breakdown of proteins, fats and carbohydrates under the influence of pancreatic juice and bile; -small intestine – breakdown of proteins and carbohydrates, selective absorption of nutrients into the blood and lymph; -large intestine - absorption of water, formation of feces, digestion of fiber, synthesis of vitamins. Changes that food undergoes in the digestive tract

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Gastrointestinal infections Food poisoning can be caused by various microorganisms, most often salmonella, botulism bacilli, Vibrio cholerae, and dysentery bacillus. salmonella botulism bacilli vibrio cholera dysentery bacilli

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Gastrointestinal infections Once in the body, bacteria secrete poison, which causes acute inflammation of the mucous membrane of the stomach, small and large intestine. The disease begins quite quickly. Already 2-4 hours after eating, the first symptoms are observed: nausea, a feeling of weakness, and later - profuse vomiting, diarrhea. Fever and headache often occur. Children, elderly people and patients with gastrointestinal diseases are especially sensitive to food poisoning. In them, poisoning often occurs in a more severe form.

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Gastrointestinal infections The infection is transmitted through contaminated food products - meat, fish, milk, salads, etc.

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Helminth infestations Infection with helminths occurs through the fecal-oral route through the mouth: -due to direct contact with soil, sand; - through contaminated objects; - through food; - through insects (flies, cockroaches, ants); - through contact with animals (dogs, cats). From person to person, infection can occur with pinworms in children's groups (kindergartens) through toys, as well as through bedding.

Slide 7

Worms can create health problems and aggravate existing disorders, including the implementation of unfavorable hereditary predispositions. The most common syndrome with helminthic infestation is gastrointestinal dysfunction: -unstable stool; -pain syndrome; flatulence; belching, nausea, rapid satiety. One of the most common manifestations of helminthic infestation is allergies. Manifestations of intoxication due to helminthiasis are: loss of appetite, disturbance of night sleep (restlessness, sounds during sleep or frequent awakenings); grinding teeth; irritability, moodiness, aggressiveness; convulsions. Helminths weaken the functioning of the immune system, which can result in frequent respiratory diseases, pustular or fungal lesions of the skin and mucous membranes, and dental caries.

Slide 8

Gastrointestinal infections You can avoid food poisoning and helminthic infestations by following the rules of personal hygiene, the regime and shelf life of food, and food preparation technology.

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1. Wash your hands with soap after using the restroom, contact with animals or the ground. 2. Treating toys with soapy water and cleaning the floor with detergents is mandatory approximately once every 10-14 days. 3. Treat vegetables and fruits with soap before consumption; berries (strawberries, raspberries, etc.) are first filled with clean water, then it is drained and the fruits are washed with running water. 4. Thermal processing of food. These are the conditions that will help you avoid gastrointestinal infections!

Buying pickled mushrooms from grandmothers near the metro, eating expired canned food, going on a trip and simply forgetting to wash our hands and fruits and vegetables before eating, we risk contracting an intestinal infection. At best, this means sitting in the restroom for many hours. At worst, an infectious diseases hospital and even death.


Intestinal infections - what is it? Intestinal infections are a whole group of contagious diseases that primarily damage the digestive tract. There are more than 30 such diseases in total. Of these, the most harmless is so-called food poisoning, and the most dangerous is cholera.


Causes of intestinal infections The causative agents of intestinal infections can be: bacteria (salmonellosis, dysentery, cholera), their toxins (botulism), and viruses (enterovirus). From patients and carriers of infection, microbes are released into the external environment with feces, vomit, and sometimes urine. Almost all pathogens of intestinal infections are extremely tenacious. They are able to exist for a long time in soil, water and even on various objects. For example, on spoons, plates, door handles and furniture. Intestinal microbes are not afraid of the cold, but still prefer to live where it is warm and humid. They multiply especially quickly in dairy products, minced meat, jelly, jelly, and also in water (especially in the summer). Causative agents of intestinal infections enter the body of a healthy person through the mouth: with food, water or through dirty hands.


What's happening? From the mouth, microbes enter the stomach, and then into the intestines, where they begin to multiply intensively. The cause of the disease is the poisons that microorganisms secrete and the damage to the digestive tract that they cause. After microbes enter the body, the disease begins within 6-48 hours. People get intestinal infections more often in the summer. This is due to the fact that in the heat we drink more liquid, which means that the gastric juice that kills harmful microbes is diluted. In addition, in the summer we often drink unboiled water (from springs and from the tap).


Why is it dangerous? All intestinal infections are dangerous because dehydration occurs due to vomiting or diarrhea. The result can be kidney failure and other serious complications. For example, from the nervous system (coma, cerebral edema), heart (cardiogenic shock) and liver.


How to recognize? Intestinal infections, like all other infectious diseases, always happen unexpectedly. At the very beginning of the disease, a person feels weak, lethargic, his appetite may deteriorate, he may get a headache, and even have a fever. Very similar to poisoning or even a banal acute respiratory infection. It’s okay, the person thinks, swallows aspirin or activated charcoal and waits for him to feel better. However, it doesn't get any better. On the contrary, new problems appear: nausea and vomiting, cramping abdominal pain, diarrhea. Thirst and chills may bother you.


Treatment of intestinal infections Treatment of intestinal infections is complex and includes: the fight against microbial poisons, the microbes themselves, as well as dehydration of the body. In addition, patients must follow a proper diet and, with the help of special medications, restore normal intestinal microflora.


Prevention To protect yourself from acute intestinal infections, it is enough to follow the following simple rules: drink water and milk only when boiled, wash vegetables and fruits with hot water and soap, follow the rules and shelf life of food products, wash your hands before eating and do not bite your nails.




Typhoid fever is an acute infectious disease caused by bacteria from the genus Salmonella. The pathogen can survive in soil and water for up to 1-5 months. Kills when heated and exposed to conventional disinfectants. The only source of infection spread is a sick person and a bacteria carrier. Typhoid fever bacilli are transmitted directly by dirty hands, flies, and sewage. Outbreaks associated with the consumption of contaminated foods (milk, cold meats, etc.) are dangerous.


Symptoms and course. The disease begins with a gradual increase in temperature to 39 o C, an increase in signs of severe intoxication - headache, weakness, mental retardation. The tongue takes on a rich red color. covered with a gray coating, increased in size, with teeth marks. At the height of the disease, severe mental disorders are observed - “typhoid status” (a state of stupor, apathy, up to a coma). On days 8-10, a rash appears on the skin of the chest and abdomen. When there is intestinal bleeding, the stool turns black.


Treatment. The main antimicrobial drug is chloramphenicol. Prescribe 0.5-0.75 g, 4 times a day for days until normal temperature. Patients must observe strict bed rest for at least 7-10 days. Even with the availability of modern medicines, typhoid fever remains a dangerous disease with a high mortality rate (12-30% in developing countries).


Prevention. Sanitary supervision of food enterprises, water supply, sewerage. Early identification of patients and their isolation. Disinfection of premises, linen, dishes that are boiled after use, control of flies. Dispensary observation of those who have had typhoid fever. Return to list of diseases




Sources of infection. The source of infection is a sick person. Infection with dysentery occurs when personal hygiene rules are not observed. Dysentery is a disease of dirty hands. However, you can get sick by drinking contaminated water or products washed with such water and not sufficiently thermally processed.


What's happening? The incubation period of the disease ranges from several hours to 2-3 days. The causative agent of the disease causes inflammation of the wall of the large intestine. The main symptom of dysentery is not very abundant, partial loose stools with mucus, pus, and blood. In addition, the patient’s general health is disturbed, nausea and vomiting appear, appetite decreases, and headaches occur. As the disease progresses, dehydration may develop.


Treatment Treatment of dysentery is carried out in a hospital. When treating dysentery, two tasks are solved: fighting the microbe that causes the disease (antibiotics are used) and compensating for fluid loss: drinking plenty of fluids and intravenous infusion of special solutions. With good body resistance, the disease is completely cured in 7-10 days, but sometimes it can take on a wave-like character. The immunity of those who have recovered is unstable, and repeated cases of infection are possible. Return to list of diseases




Symptoms and course. The onset of the disease is similar to the flu, often accompanied by diarrhea. Within 2 weeks the disease subsides, leaving weakness, sweating, and fatigue. Later, paralysis and paresis occur in the limbs, often in the legs. Then the movements are somewhat restored, and the muscles partially atrophy. At the first suspicion of polio, the patient should be immediately taken to an infectious diseases hospital, as he poses a danger to others. In addition, the phenomena of paralysis, more or less, always regress. In addition, pneumonia, urinary tract infection, etc. may occur, from which such patients often die.


Treatment. Since there is no specific treatment, prevention with a live vaccine is most important. In 30% of cases, polio ends in residual paralysis with muscle atrophy, in 30% - with milder complications. Complete recovery from the paralytic form without consequences occurs in 30% of cases and in 10% of cases (with damage to the respiratory system) - death. Return to list of diseases


Cholera Cholera is an acute infectious disease that is classified as a particularly dangerous infection. The classic picture of cholera is frequent, up to 10 or more times a day, diarrhea. Fluid loss is colossal, up to 20 liters per day, and each milliliter contains up to a billion vibrios.


Treatment The basis of treatment is replenishing the loss of fluid and microelements, maintaining water-electrolyte and acid-base balances in the body. Antibiotics are only an additional treatment. Thanks to complex therapy, the mortality rate from cholera currently does not exceed 1%. Return to list of diseases


Paratyphoid A and B Paratyphoid A and B are acute infectious diseases that are similar in clinical picture to typhoid fever. The causative agents are mobile bacteria from the genus Salmonella, stable in the external environment. Disinfectants in normal concentrations kill them within a few minutes. The only source of infection in case of paratyphoid A is patients and bacteria excretors, and in case of paratyphoid B it can also be animals (cattle, etc.). The routes of transmission are often fecal-oral, less often contact-household (including fly).


Symptoms Paratyphoid A and B, as a rule, begins gradually with an increase in signs of intoxication (fever, increasing weakness), dyspeptic symptoms (nausea, vomiting, loose stools), catarrhal (cough, runny nose), and ulcerative lesions of the intestinal lymphatic system.


Treatment. Prevention. Treatment should be comprehensive, including care, diet, immune and stimulant medications. Bed rest until 6-7 days of normal temperature, from 7-8 days it is allowed to sit and walk. The food is easily digestible, gentle on the gastrointestinal tract. Prevention comes down to general sanitary measures: improving the quality of water supply, sanitary cleaning of populated areas and sewage systems, fighting flies, etc. Dispensary observation of paratyphoid survivors is carried out for 3 months. Return to list of diseases


Botulism Botulism is a deadly infectious disease. The permanent place of residence of the causative agent of botulism is soil, where they can persist for many years. From the soil the microbe gets onto food products. Without air access (in canned or dense products such as balyk), the causative agent of botulism begins to produce botulinum toxin, the strongest known poison. It is several times stronger than rattlesnake venom. In 95% of cases, the cause of botulism is home-made canned mushrooms, since they are not heat-treated. In the same jar, botulinum toxin accumulates in clusters; infected areas are scattered throughout the contents of the jar. Therefore, not all people who eat canned food from the same can get sick.


Treatment. Prevention. The disease develops very quickly within 2-24 hours. The first symptoms: diarrhea, vomiting, fever, abdominal pain. The first specific manifestations of botulism are impaired visual acuity, double vision, and strabismus. Then comes speech impairment, weakness, dry mouth, difficulty swallowing, voice changes, etc. The temperature is normal or slightly elevated, consciousness is preserved. Treatment of botulism is carried out only in an infectious diseases hospital. First of all, the remains of food poisoned with botulinum toxin are removed from the patient’s intestines (a laxative and gastric lavage are used). The specific treatment for botulism is the urgent administration of anti-botulinum serum, which neutralizes the toxin. Immunity does not develop during botulism, which means you can get sick with this disease more than once. Prevention of botulism consists of careful heat treatment of food, strict adherence to sanitary standards for the preparation, storage and consumption of food. Return to list of diseases


Brucellosis Brucellosis is an infectious disease caused by Brucella - small pathogenic bacteria. A person becomes infected from domestic animals (cows, sheep, goats, pigs) when caring for them or when consuming infected products - milk, poorly aged cheese, poorly cooked or fried meat. The pathogen, penetrating the body through the digestive tract, cracks, scratches and other damage to the skin or mucous membrane, then spreads through the lymphatic tract and blood vessels, which makes any organ accessible to this disease.


Treatment. Prevention. The most effective remedy is antibiotics. In the stage of attenuation of acute inflammatory phenomena, physical therapy and warm paraffin applications to the joints are prescribed. In case of persistent remission - spa treatment, taking into account existing contraindications. Meat can also be eaten after boiling it in small pieces for 3 hours or salting it and keeping it in brine for at least 70 days. Milk from cows and goats in areas where there are cases of disease in large and small livestock can only be consumed after boiling. All dairy products (yogurt, cottage cheese, kefir, cream, butter) should be prepared from pasteurized milk. Brynza, made from sheep's milk, is aged for 70 days. Return to list of diseases


Salmonellosis In some products (milk, meat products), salmonella can not only survive, but also multiply without changing the appearance and taste of the product. Salting and smoking have a very weak effect on them, and freezing even increases the survival time of microorganisms in products. Salmonellosis is transmitted through the eggs of sick birds. Today this is one of the leading ways of spreading this disease. Salmonellosis is an infectious disease transmitted mainly through food. Caused by various microbes of the Salmonella genus.


Treatment. In the treatment of salmonellosis, there are several leading areas: antibiotics to combat salmonella, special solutions to compensate for fluid lost through vomiting and diarrhea, anti-inflammatory drugs - drugs to remove toxins, restoration of normal intestinal microflora. With persistent and competent treatment, salmonellosis can be completely eliminated. Return to list of diseases

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