salmonellosis

1. Theme: Food poisoning
Toxic food-borne infections are acute transitory diseases, caused by conditionally pathogenic
bacteria. These bacteria are capable to produce exotoxin (in food-stuffs). The disease is
accompanied with symptoms of the damage of the upper parts of the gastrointestinal tract
(gastritis, gastroenteritis) and by violation of the water-electrolyte balance.
Etiology : Many types of the conditionally pathogenic bacteria may be agents of the toxic food-
borne infections and produce exotoxin out of the human organism on the different food-stuffs.
Enterotoxins (thermoliable and thermostable) increase the secretion of the fluids and salts into
the stomach and intestine. Cytotoxins damage the membranes of the epithelial cells and violate
the protein synthetic processes. The agents, producing enterotoxins are Clostridium perfringeus,
Proteus vulgaris, Proteus mirabilis, Bacillus cereus. These enterotoxins are also formed by
agents from the families of Klebsiella, Enterobacter, Citrobacter, Serrafia, Pseudomonas,
Aeromonas, Edwarsiella. The majority of these enterotoxins are thermoliable.
Epidemiology: Pathogenic organisms of the toxic food infections are widely spread in the
nature. They may be everywhere: in the fecal matters of human and animals; in the soil; in the
water; in air and on the different subjects. The way of the spread of the infection is alimentary.
The factors of the transmission of the disease are solid products (sausages, eggs, meat and fish
canned food) and liquid products (soup, milk, juices, compotes, jellies, lemonade, beer,
cocktails). They are the nutritive mediums for bacteria. The susceptibility to this group of
diseases is very high, sometimes till 90- 100 %. The typical sign of the toxic food-borne
infections is not only group but explosive character of illness due to all participants of the
outbreak become ill during a short period (over a few hours). The toxic food-borne infections are
registered during the whole year, but especially in summer.
Pathogenesis: In toxic food infections exotoxin is contained in food, besides bacteria. Due to
this the incubation period is very short. Time of the of clinical manifestations development after
influence of toxins to the mucous membrane is from 30 minutes till 2-6 hours. Pathogenesis and
clinical manifestations of the disease depend on the type and dose of exotoxin, and also from
other toxical substances of microbial origin, containing in the food-stuff. Enterotoxins
(thermoliable and thermostable) are connected with the epithelial cells of stomach and intestine
and act to the fermental system of the epitheliocytes, but don’t cause morphological changes in
these organs. Enterotoxin activates ferments adenylcyclase and guanylcyclase, increasing
formation of the biological active substances (cyclic adenosinemonophosphates and cyclic
guanidinmonophosphates) in the cells of the mucous membranes. All these changes lead to the
increase rate of secretion of water and salts into the stomach and intestine and to the
development of diarrhea and vomiting.
Clinical manifestation: The incubation period is from 30 minutes to 24 hours (generally 2-6
hours). In the majority of the cases of the disease there is no fever and just considerable
inflammatory changes of the mucous membrane of the stomach and intestine. In toxic food-
borne infections there is combination of the signs of the damage of the gastrointestinal tract
(gastritis, gastroenteritis or gastroenterocolitis) and signs of the general intoxication and
dehydration.The beginning of the disease is an acute. At first the nausea occurs. Frequently the
replated, agonizing and unrestrained vomiting occurs. Almost at the same time with vomiting the
diarrhea starts. Stool is watery from 1 to 10-15 times a day. However the disease may be with
spasmatic pains in the stomach, with the raise of the body temperature up to 38-39 °C. The raise
of the body temperature takes place at the early hours of the disease and through 12-24 hours the
temperature is reduced to normal. During objective examination of the patients the pale skin,
sometimes cyanosis, cold extremities are observed. The tongue is coated. Stomach is soft and
painful in the epigastrium during palpation. There is bradycardia (during hyperthermia –

2. tachycardia). The arterial pressure decrease. In some cases collapse of short duration develops.
Due to repeated vomiting and plenty diarrhea the signs of dehydration develop. It may be
possible of the appearance of the muscle’s cramps of extremities, decrease of the diuresis and
reduced turgor of the skin. In hemogram leukocytosis, neutrophylosis and temperate accelerate
ESR are noted. The duration of the disease in majority of the cases is 1-3 days.
Complications:
The toxical food infection may be accompanied by severe complications. Hypovolemic shock
and an acute heart insufficiency, connecting with violations of electrolytic balance
(hypokalemia) are observed.
Diagnosis :The diagnosis of the toxic food-borne infections is made according the results of the
clinical symptoms estimation, epidemiological and laboratory data. The typical signs are the
impetuous development of the disease after short incubation period, presence of symptoms of
gastritis, gastroenteritis or gastroenterocolitis in combination with intoxication, dehydration,
disposition to the vascular dystonia. Materials for bacterial examination are suspicious food
products, vomitory masses, water after irrigation of the stomach, stool of the patient. Serological
methods does not have independent meaning in the diagnostics.
Differential diagnosis : differential diagnosis of toxical food infection is performed with acute
intestinal infections (cholera, acute shigellosis, gastrointestinal form of yersiniosis, rotoviral
gastroenteritis, campylobacteriosis, dyspeptic variants of preicteric period of viral hepatitis and
others), with surgical diseases (acute appendicitis, cholecystopancreatitis, thrombosis of
mysentrical vessels, perforation of ulcers in the stomach and duodenum), with gynecological
diseases (ectopic pregnancy, toxicosis of the pregnancy), with therapeutic diseases (myocardial
infarction, hypertension crisis), with neurological diseases (acute failure of cranial blood
circulation, subarachnoidal hemorrhage), with urological diseases (pyelonephritis, acute renal
failure). During the diagnostics it is necessary to consider the food poisoning, poisoning by
mushrooms, salts of hard metals.
Treatment: It is necessary to wash out a stomach and intestine to release them from microbes
and toxins as soon as possible. For a lavage it is better to use isotonic solution of sodium
chloridum, boiled water or 1-2 % solution of sodium hydrocarbonate. Alternative preparations
are smecta, enterodes and other enterosorbents. Their early indication promotes the fastest
improvement of health state, preserves intoxication, development of the serious form of bacterial
endotoxicosis. In case of development of infection-toxic shock we should immediately infuse in
blood colloid and cristaloid solutions: polyglucin, reopoliglycin, donor albumin, threeisault,
acesault, quartasault, and also glucocorticoides. Etiotropic treatment is indicated only at serious
forms with development of colitic syndrome: antibiotics are indicated in case of development of
sepsis – levomycetin, gentamicin, ampicillin, ofloxacin (or tarivid).
Preventative measures: prophylaxis of the toxical food infection is concluded in prevention of
infection of the food-stuff, of the reproduction of the microorganisms in the food. It is necessary
to keep the food-stuffs and prepared food at the temperature from 2 till 4C. The mechanization
and automatization of the food objects, the elaboration of the new methods of the preserving and
storage of the food-stuff, the freezing at low temperature are conductive to the successful
prophylaxis of the toxical food infection.

3. Theme: Salmonellosis
Salmonellosis is a polyetiological infectious disease caused by various serotypes of bacteria of the
genus Salmonella, characterized by variety of clinical manifestation from asymptomatic carriage
to severe septic forms. In most cases, it proceeds with a predominant lesion organs of digestive
tract (gastroenteritis, colitis).
Etiology : The causative agents of salmonellosis belong to the genus Salmonella, the family of
intestinal Enterobacteriaceae bacteria. Morphologically, salmonalla are sticks with rounded ends
with a size of 1,0-3,0 to 0,2-0,8 microns. Over They for a few expections, mobile, have flagella
over the entire surface of the cell (peritrichi) Spore and capsules do not form, gram negative. They
grow on ordinary nutrient media. Salmonella are capable of producing exotoxins. Among them
are enterotoxins (thermolabile and thermostable) enhancing fluid secretion and salts in the
intestinal lumen, and cytotoxin that violates protein – synthetic processes in mucous cells intestinal
membranes and acting on cytomembranes. When bacteria are destroyed, endotoxin is released,
which causes the development of intoxication syndrome. Salmonella has 3 main antigens: O-
somatic (Thermostable), H-flagellum (thermolabile) and K-surface (capsule).
Salmonella are relatively resistant to various environmental factors, some of which do not die
when frozen to -48 – 82*C and tolerate drying well. On various objects at room temperature they
last 45 – 90 days, in dry feces of animals – up to 3 -4 years. In water, especially at low pH,
Salmonella survive 40 to 60 days. In dairy and Salmonella meat products are not only stored for
up to 4 months, but also propagated without changing organoleptic properties and appearance of
products.
Epidemiology: the source of infection may be animals and people, and the role of animals in
epidemiology is fundamental. Salmonellosis in animals occurs in the forms of a clinically
expressed disease and bacterial excretion. Being apparently healthy, the latter can excrete
pathogens with urine, feces, milk, nasal mucus, saliva. The largest epidemiological the danger is
infection of cattle, pigs, sheep, horses. A significant place in the epidemiology of salmonellosis is
occupied by birds (often broiler chickens), and especially waterfowl, which serve as a powerful
reservoir of various types of salmonella. Salmonella is found not only in meat and internal organs
of birds, but also in eggs. The mechanism of transmission of pathogens is fecal-oral. The main
route of transmission is food. Salmonella transmission factors are foods. Salmonellosis occurs
throughout the year, but more often – in the summer months, which can be explained by the
deterioration of food storage conditions.
Pathogenesis: Infection portals of entry is the small intestine, where the bacteria multiply causing
intestinal inflamation. In the small intestinal mucosa intensive disctruction of bacteria occurs
accompanied by the release of endotoxin and enterotoxin. Enterotoxin activates adenylate cyclase
of enterocytes leads to an increase in the intracellular concentration of cyclic adenosine
monophosphate, phospholipids, prostaglandins, and other biologically active substances.
This leads to disruption of ion transport of Na and Cl through the membrane of intestinal epithelial
cells with their accumulation in the intestinal lumen. Water comes out of the enterocytes, watery
diarrhea develops. In severe cases of the disease due to loss of fluid and electrolytes a significant
violation of water-salt metabolism, decrease in blood volume, low blood pressure and the
development of hypovolemic shock. Endotoksin has diverse effects on different organs and
systems. Most important of these disorders is infectious - toxic shock.
Clinical manifestation: The incubation period for the food route of infection ranges from 6 hours
to 3 days (usually 12-24 hours). With nosocomial outbreaks, when predominates contact
transmission of infection, the incubation period is extended to 3-8 days.
Clinical classification:

4. 1) Gastrointestinal form:
- Gastritis variant
- Gastroenteritis variant
- Gastroenterocolitis variant
2) Generalized form:
- Typhoid-like variant
- Septicopyemic variant
3) Bacteriocarrier:
- Acute
- Chronic
- Transient
Gastrointestinal form (acute gastritis, acute gastroenteritis or gastroenterocolitis) – one of the
most common forms of salmonellosis (96-98% of cases). It begins acutely body temperature
rises (in severe forms up to 39C and above), general weakness, headache, chills, nausea,
vomiting, pain in the epigastric and umbilical regions appear, and later, stool disorders. Stool is
frequent – up to 10 times a day and can lead to dehydration. The stool usually has a watery and
foamy consistency, contains green mucous clots (greenish stool) and has an unpleasant smell.
Typhoid-like variant of the generalized form. The disease often begins acutely. In some patients,
the first symptoms of the disease may be intestinal disorders in combination with fever and
general intoxication, but after 102 days intestinal disfunctions disappear, and body temperature
remains high, symptoms of general intoxication increase. For most patients with onset and
course of the disease are similar to typhoid and paratyphoid A and B. Sick inhibited, lethargic.
The face is pale, in some patients, a herpetic rash appears on the 2-nd-3rd day, and from the 6-th-
7th day, a roseous rash with localization on the skin the abdomen. Relative bradycardia, lowering
blood pressure, muffling of heart sounds are observed. Scattering dry rales are auscultated over
the lungs. The abdomen is swollen. By the end of the 1 st week of the disease, an increase in the
liver and spleen appears. Duration of fever 1-3 weeks. Relapses are rare
The septic form is the most difficult variant of the generalized form of salmonellosis. The disease
begins acutely; in the first days it has a ityphoid-like course. In the future, the condition of patients
worsens. Body temperature becomes wrong sweeping, repeated chills and profuse sweating. The
disease proceeds like usually difficult, difficult to give antibiotics therapy.
Complications: 1. Specific: toxic shock, dehydration shock, acute renal failure.
2. Nonspecific: violation of blood circulation in the vessels (coronary, mesenteric, cerebral),
abscess, infectious psychosis, infectious toxic encephalopathy, anemia, pancreatitis, meningitis,
myocarditis, pneumonia, thrombophlebitis, cholecystitis, osteomyelitis, etc.
Diagnosis.: diagnosis of salmonellosis is carried out on the basic of epidemiological, clinical and
laboratory data. The main method for confirming the presence of salmonella is bacteriological
(isolation and identification of the pathogen using nutrient media and biochemical tests). The test
for the presence of salmonella in a person, stool, vomit and gastric lavage, blood urine are taken
Material from the patient should be taken as soon as possible and before treatment. Serological
research methods serve as auxiliary methods: passive hemagglutination reaction (RPHA), if
necessary, with separate determination of IgM and IgG antibodies and molecular genetic
methods (PCR and others).
Differential diagnosis: differential diagnosis of salmonellosis is performed with other intestinal
diseases – shigellosis, toxic food-borne infections, esherichiasis, cholera; with surgical diseases –
appendicitis, pancreatitis, cholecyctitis, thrombosis of mesenterial vessels; gynecological
pathology and with therapeutic pathology (myocardial infarction, chronic gastritis aggravation,

5. enterocolitis, ulcerous disease), with acute gastroenteritis of viral origin (enteroviral, rotaviral
etiology), poisoning by organic and inorganic poisons, poisoning by mushrooms.
Generalized form of salmonellosis is necessary to differentiate from sepsis of different etiology,
pneumonia, malaria, acute pyelonephritis, tuberculosis.
Treatment: At gastrointestinal form immediately wash out stomach and intestine with boiled water
(isotonic solution of sodii chloridum is the best) then give sorbents per os: glucosole or rehydroni.
Infusion therapy is indicated at expressed dehydration
– threesault, quartasault, lactasault. At severe stage of dehydratation one of the specified solutions
is infused in vein with rate 80-120 mL/min, 5-10 L of solution is necessary on course of treatment.
Antibiotics at gastrointestinal form of salmonellosis are not used.
However, at syndrome of hemocolitis and lingering diarrhea antibioticsis indicated in combination
with probiotics preparations – enterol- 250, bificol, colibacterin, bifidumbacterin, linex is used at
intestinal dysbacteriosis.
At generalized form simultaneously with pathogenetic therapy there are indicated antibiotics –
levomycetin, ampicillin, monomycin, gentamycini sulfas, cefazolin (kefzol), cefotaxim (claforan).
At the septic form of disease antibiotics are better to infuse parenteraly. For sanitation of chronic
carriers of salmonelas the specified antibiotics use in average therapeutic doses in combination
with preparations stimulating nonspecific and immunological reactivity (pentoxyl, methyluracil,
splenin, thymalin, T- activin).
Preventative measures: Veterinary and sanitary supervision of slaughter of cattle and poultry,
carcass processing technology, the preparation and storage of meat and fish dishes. Organization
of vaccination of farm animals and birds with salmonella vaccines. After hospitalization, the
patient is monitored for the lesion for a week. Food and enterprises equivalent to them, children
attending childcare facilities, are subjected to a single bacteriological examination. Extract of
convalescents is carried out after complete clinical recovery and a single bacteriological
examination of feces (for food workers – twice) with a negative result. Food workers and children
attending kindergartens are observed for 3 months, with bacteriological examination of feces (1
time per month). Bacterial isolators are not allowed to work in food and equivalent enterprises.
Theme: Shigellosis
Dysentery (Shigellosis) – an infectious disease characterized by general infectious intoxication
syndrome and gastrointestinal tract lesion syndrome, predominantly distal colon.
Etiology : the causative agent of dysentery refers to genus Shigella of the family
Enterobacteriaceae. There are 4 types of Shigella:
1) Group A – Sh.dysenteriae which includes bacteria Sh.dysenteriae 1 – Grigoryeva-Shiga,
Sh.dysenteriae 2 – Schtutzer-Schmitz and Sh.dysenteriae 3-7 Lardj-Saks, serovars 1-12, of
which 2-3 dominate;
2) Group B – Sh.Flexneri with a subspecies Sh.Flexneri 6 – Newcastle, serovars 1-5, each of
them is subdivided into subserovars a and b, as well as serovars 6, X and Y, of which 2a,
1c and 6 dominate;
3) Group C – Sh.boydii, serovars 1-18, of which 4 and 2 dominate;
4) Group D – Sh.Sonnei

6. Morphologically, all Shigella are similar to each other, have the form of sticks wizh size of (0,3 –
0,6)% (1,0 – 3,0) microns with rounded ends. They are motionless, do not form spores and
capsules, gram-negative, grow well on simple nutrient media, but better – on bile-containing
media. Shigella contain thermostable somatic O-antigen. When they are destroyed, endotoxin is
secreted, which is largely associated with the development of intoxication syndrome. Among them
enterotoxins (thermolabile and thermostable), reinforcing secretion of fluid and salts into the
intestinal lumen, and cytotoxin, which damages the epithelial membrane cells. Grigoriev-Shigi
bacteria, in addition, produce a potent neurotoxin.
Epidemiology: the source of infection are patients with acute or chronic dysentery, convalescents
are people with a cubclinical form of the infection process (bacteriostatic). The greatest
epidemiological danger is presented by patients with acute dysentery, secreting in during the hight
of the disease in the environment a huge number of pathogens. Dysentery is an infection with the
fecal-oral mechanism of transmission of pathogens, the implementation of which is carried out by
the food, water and contact-household routes. Shigella transmission factors include food, water,
hands and objects everyday life, flies, soil. The main route of transmission for shigellosis
Grigorieva-Shiga is a contact household, Flexneri – water, Sonnei – food (especially milk).
Dysentery, like other acute intestinal diseases, is characterized by a pronounced autumn-summer
seasonality.
Pathogenesis: Shigella can be in the stomach from several hours to several days (in rare cases).
However, some of them are already disintegrating, releasing endotoxin. Overcoming acid barrier
of the stomach, Shigella enter the intestines. In the small intestine, they attach to enterocytes and
secrete enterotoxic exotoxin, which causes increased secretion of fluid and salts into the intestinal
lumen. Pancreatic enzymes contained in small intestine, temporarily inactivate hemolysin of the
outer shigella membrane, ensuring their invasion into epithelial cells, and this protects the latter.
However, some bacteria penetrates into enterocytes, mainly the ileum, and multiplies in them.
Under the action of hemolysin destroys phagocytic vacuoles and cytopathic changes in enterocytes
develop. Shigella actively move in the cytoplasm and move to neighboring enterocytes, causing
an inflammatory process in the small intestine, which is supported and exacerbated by the action
of Shigella – produced cytotoxic exotoxin, which inhibits protein synthesis. However, the
intracellular spread of the pathogen in the small intestine, as a rule, quickly breaks off due to the
killer action of lymphocytes. Endotoxin is formed in the result of the destruction of Shigella in the
foci of initial invasion in the epithelium of the small intestine, into the blood and causes the
development of intoxication. With a severe and extremely severe course of the disease, bacteremia
can develop. In the colon, invasion of shigella colonocytes occurs somewhat later, but massive.
This leads to a more significant local and resorbtive action of Shigella toxins. Interepithelial
progression of Shigella colonocytes progresses; defects increase epithelial cover; immune
complexes, of which endotoxin is a component, are fixed in the capillaries of the colon mucosa
and, violating microcirculation, increase its damage. Secretion by sensitized eosinophils and mast
cells of toxic substances in combination with circulatory disorders in the submucosa the layer and
cytotoxic effect of leykocytes determine the development of the pathological process from the 2nd
week of the disease. As a result of this, DIC-syndrome develops, including local (in the intestine),
with further development of thrombosis of mesenteric vessels, as well as vessels of the lungs and
brain. Shigella toxins can be fixed by the central nervous system and affect the centers of the
autonomic nervous system. In addition to the direct effect on a number of organs, Shigella
endotoxin contributes to the development of general metabolic disorders. In chronic dysentery, the
leading role is not intoxication, but a progressive violation of the functional state of the GIT, which
determines the clinical picture of the disease.
Clinical manifestation: the incubation period is 1 – 7 (average 2 -3) days, but may reduced to 2
– 12 hours.

7. Clinical classification: 1. Typical forms: colitic, hemocolitic. 2.Atypical forms: erased,
gastroenterocolitis, hypertoxic.
3.By flow: acute, chronic: recurrent, continuous
4.Bacteriocarrier
A typical form of shigellosis is characterized by an acute onset with symptoms of intoxication
(chills, fever, malaise, headache, decreased appetite), crampin abdominal pain, mainly in the left
iliac region. The stool is fecal at first, gradually the volume of feces decreases, an admixture of
mucus and blood appears, the frequency of bowel movements increases. At the hight of the
disease, bowel movements look like “rectal spitting” (10-20 times a day). Defecation is
accompanied by tenesmus (pulling convulsive pains in the anus), false desires. On palpation of
the abdomen, spasm and soreness of the sigmoid colon are noted. The duration of the course of
sigmoid colon are noted. The duration of the course of uncomplicated shigellosis is 5-7 days.
The gastroenterocolitis form of acute shigellosis resembles foodborne toxicoinfection (nausea,
vomiting, epigastric pain, profuse loose stools), and then symptoms of colitis appear.
The erased current of acute shigellosis is characterized by short-term and unexpressed clinical
symptoms (1-2 times stool disorder, short-term abdominal pain), and the absence of intoxication
symptoms.
Bactericarrier may be reconvalescent after acute shigellosis and subclinical if shigella is isolated
from individuals who do not have clinical manifestations. Chronic shigellosis is recorded when
the pathological process lasts more than 3 months. In a recurring form, periods of exacerbation are
replaced by remission. With a continuous course, the colitic syndrome does not subside.
Complications: septic shock, prolapse of the rectal mucosa, intestinal bleeding, anemia.
Diagnosis. Diagnosis of dysentery is based on results clinical examination of the patient and
anamnestic information. Acute onset of the disease with syndromes of general intoxication (feeling
unwell, general weakness, headache, fever), distal colitis (cramping pains in the lower abdomen,
rapid stools, decreasing in volume and losing fecal character – mucus with streaks blood, false
desires, tenesmus, a feeling of incompleteness of the act of defecation). Of great diagnostic
importance is the examination of feces, in which you can detect an admixture of mucus with
streaks of blood. Laboratory confirmation of dysentery is carried out by bacteriological and
serological methods. The bacteriological method (seeding shugella from feces) with a 3-fold study
provides confirmation of the diagnosis in 40-60% of patients.
1) Complete blood count: leykocytosis, neutrophilia, accelerated ESR
2) Coprological examination: the presence of mucus, white blood cells and red blood cells.
3) Serological examination: RA, CBR (Complement binding reaction), IHT (indirect
hemagglutination test), ELISA
4) Endoscopic examination.
Differential diagnosis: Differential diagnosis is performed with the following diseases –
salmonellosis, toxic food-borne infections, rotaviral gastroenteritis, amebiasis, balantidiasis,
intestinal shistosomiasis, trichocephaliasis, enterobiasis, cancer of large intestine, appendicitis,
ileus, hemorrhoids, diverticulitis, ischemic colitis, Crohn’s disease, non-specific ulcer colitis,
secondary colitis in patients with severe therapeutic pathology, radiation affections and poisonings
with different chemical and biologic substances.
Treatment: Diet №4 (bland, simple foods that are easy to digest and will help absorb some water
from the stool). In case of severe shigellosis course use antibiotics - ampicillin or a polymyxin;
when there is no effect – ciprofloxacin 500- 2 times a day, or ofloxacin in combination with
gentamicin or cefazolin are prescribed. Duration of course of etiotropic treatment at moderate
course of shigellosis is 2 - 3 days, at severe case it lasts not longer than 4 - 5 days. A solution of
regidron, in severe cases quartasault, lactosault are applying per os with the purpose of

8. desintoxication and rehydratation. Normalization of water-electrolyte metabolism (Rehydration):
The start dose of saline solution is 500 ml (Ringer’s solution, Glucose, Reosorbilact, Hemosol).
Preventative measures: Prophylaxis of shigellosis includes complex of measures, directed to
revelate the source of the infection, interrupt the ways of the transmission, increase of the organism
resistance. Keeping the rules of personal hygiene and rules of food’s cooking plays the principal
role in prophylaxis of the disease. Sanitary education of population has an important meaning in
shigellosis prophylaxis too.