This macro-preparation is a liver. The shape is preserved, the weight and dimensions are reduced. The liver is yellow.
These pathological changes could develop as a result of intoxication, allergic or viral liver damage. In the organ, fatty (yellow) dystrophy develops, the morphogenetic mechanism of which is decompensation. Dystrophy spreads from the center to the periphery of the lobules. It is replaced by necrosis and autolytic decay of central hepatocytes. The fatty protein detritus is phagocytosed, while the reticular stroma with dilated vessels is exposed (red dystrophy). Due to the necrosis of hepatocytes, the liver shrinks and shrinks in size.
1) favorable: transition to a chronic form.
2) unfavorable:
a) death from hepatic or renal failure;
b) post-necrotizing cirrhosis of the liver;
c) damage to other organs (kidney, pancreas, myocardium, central nervous system) as a result of intoxication.
Conclusion: these morphological changes indicate fatty degeneration of hepatocytes and their progressive necrosis.
Diagnosis: Toxic liver dystrophy. Stage of yellow dystrophy.
^ 10. Stomach cancer.
This macro-preparation is the stomach. The shape and size of the organ are changed due to the proliferation of whitish-yellow tissue, which has grown into the stomach wall and significantly thickens it (up to 10 cm or more). The relief of the mucosa is not pronounced. In the central part of the growth, depressions, loosening and hanging areas - ulceration are visible.
Description of pathological changes:
These pathological changes could develop as a result of precancerous conditions and precancerous changes (intestinal metaplasia and severe dysplasia).
In the foci of changes in the epithelium, cells malignancy and the development of tumors (or cancer develops de novo). Guided by the macroscopic picture, we can say that this is a cancer with predominantly endophytic infiltrating growth - infiltrative ulcerative cancer (as evidenced by the ulceration of the tumor). Histologically, it can be both adenocarcinoma and undifferentiated cancer. Progression, the tumor invades the wall of the stomach and significantly thickens it.
1) favorable:
a) slow growth of cancer;
b) highly differentiated adenocarcenoma;
c) late metastasis;
2) unfavorable: death from exhaustion, intoxication, matastases; spread of cancer outside the stomach and germination into other organs and tissues, secondary necrotic changes and decay of carcinoma; dysfunction of the stomach.
Conclusion: these morphological changes indicate mutational transformation of epithelial cells with their malignancy and subsequent tumor progression, which, with infiltrating growth, led to the invasion of the stomach wall with ulcerations, which may represent secondary necrotic changes and tumor decay.
Diagnosis: Infiltrative ulcerative gastric cancer.
^ 11. Erosions and acute stomach ulcers.
This macro-preparation is the stomach. The shape and size of the organ have been preserved, the mass has not been changed. The organ is whitish in color. The mucous membrane is strewn with black formations of a dense consistency. Among the numerous small ones, the diameter is 1-5 mm. there are also larger ones with a diameter of 7 mm, as well as conglomerates of 8x1 cm, 3x0.5 cm, consisting of merged formations with a diameter of 5 mm. Near one of them, we see the formation of a triangular shape, the boundaries of which have pronounced differences from the gastric mucosa, since they are formed by connective tissue.
These morphological changes could develop as a result of exogenous and endogenous influences: malnutrition, bad habits and harmful agents, as well as autoinfections, chronic autointoxication, reflux, neuro-endocrine, vascular allergic lesions. Since the lesions are localized in the fundus, we can talk about an autoimmune process with damage to the parietal cells, which led to dystrophic and necrobiotic changes in the epithelium, a violation of its regeneration and atrophy. Probably in this case, chronic atrophic gastritis developed with atrophy of the mucous membrane and its glands. Defects in the mucosa lead to erosion, which is formed after hemorrhage and rejection of dead tissue. The black pigment at the bottom of the erosion is hydrochloric acid hematin. These changes are joined by the restructuring of the epithelium. The formation, the border of which is formed by the mucous membrane and represents the healing of acute gastric ulcer by scarring and epithelialization.
1) favorable:
a) healing of acute ulcers by scarring or epithelialization;
b) inactive chronic gastritis (remission);
c) mild or moderate changes;
d) epithelialization of erosion;
2) unfavorable:
a) the development of chronic peptic ulcer disease;
b) malignancy of epithelial cells;
c) pronounced changes;
d) active pronounced gastritis.
Conclusion: these morphological changes indicate long-term dystrophic and necrobiotic changes in the epithelium of the mucous membrane with impaired regeneration and structural rearrangement of the mucous membrane.
Diagnosis: chronic atrophic gastritis, erosion and acute gastric ulcer.
^ 12. Chronic stomach ulcer.
This macro-preparation is the stomach. The masses and sizes of the organ are normal, the shape is preserved. The organ is light gray in color, the relief is strongly developed. On the lesser curvature of the stomach in the pyloric section, there is a significant depression in the stomach wall 2x3.5 cm. Its limiting surface of the organ is devoid of characteristic folding. The folds converge to the boundaries of the formation. In the area of the pathological process, there are no mucous, submucous and muscular layers of the stomach wall. The bottom is smooth, filled with a serous membrane. The edges are ridge-like raised, dense, have a different configuration: the edge facing the gatekeeper is shallow (due to gastric peristalsis).
Description of pathological changes:
These pathological changes could develop as a result of general and local factors (general: stressful situations, hormonal disorders; medicinal; bad habits that lead to local disorders: hyperplasia of the glandular apparatus, increased activity of the acid-peptic factor, increased motility, an increase in the number of gastrin-producing cells; and a general disorder: excitation of the subcortical centers and the hypothalamic-pituitary region, an increase in the tone of the vagus nerve, an increase and subsequent depletion of the production of ACTH and glucocarticoids). Acting on the gastric mucosa, these violations lead to the formation of a defect in the mucous membrane - erosion. Against the background of non-healing erosion, an acute peptic ulcer develops, which, with continued pathogenic effects, turns into a chronic ulcer, which goes through periods of exacerbation and remission. During the period of remission, the bottom of the ulcer can be covered with a thin layer of epithelium, layering on the scar tissue. But during the period of exacerbation, "healing" is leveled as a result of fibrinoid necrosis (which leads to damage not only directly, but also by fibrinoid changes in the walls of blood vessels and disruption of the trophism of the ulcer tissues).
1) favorable: remission, healing of the ulcer by scarring followed by epithelialization.
2) unfavorable:
a) bleeding;
b) perforation;
c) penetration;
d) malignancy;
e) inflammation and ulcerative cicatricial processes.
Conclusion: these morphological changes indicate a destructive process in the stomach wall, which leads to the formation of a defect in the mucosa, submucosa and muscular membrane - an ulcer.
Diagnosis: Chronic gastric ulcer.
^ 13. Hyalinosis of the spleen capsule. Glazed spleen.
This macro-preparation is the spleen. The masses and sizes of the organ are not increased, the shape is preserved. The color of the capsule is white, it is coarse, and the tuberosity is more pronounced in front. The depressions are more and less large. An area with a diameter of 0.5 cm is noticeable on the anterior surface of the organ of yellow color. Behind and from the side with the capsule, areas of yellowish tissue are soldered.
Descriptions of pathological changes.
These pathological changes could develop as a result of the destruction of fibrous structures and an increase in tissue-vascular permeability (plasmorrhage) in connection with angioneurotic metabolic and immuno-pathological processes. Plasmorrhage - tissue impregnation with plasma proteins, their absorption on fibrous structures, precipitation and formation of hyaline. Hyalinosis can develop as a result of plasma impregnation, fibronoid swelling, inflammation, necrosis, sclerosis. In the spleen capsule, hyalinosis develops as an outcome of sclerosis. The connective tissue swells, loses fibrillarity, its bundles merge into a homogeneous dense, cartilaginous mass, the cells are compressed, atrophy. The tissue becomes dense, whitish, translucent. Along with hyalinosis of connective tissue in the spleen, local hyalinosis of arterioles can be present as a physiological phenomenon. In this case, simple hyaline is formed (due to sweating of unchanged or slightly changed components of blood plasma).
1) favorable:
a) was possible only as a stage in the process during its stabilization and resorption of hyaline masses;
b) unfavorable - the most frequent: violation of the function of an organ, limitation of its functionality.
Conclusion: the data of morphological changes indicate dystrophic processes in the spleen capsule, which led to its hyalinosis.
Diagnosis: Hyalinosis of the spleen capsule.
^ 14. Dysentery colitis.
This macro-preparation is the large intestine. The shape of the organ is preserved, the mass and dimensions are increased due to the thickening of the wall. The mucous membrane is of a dirty gray color, at the apex of the folds and between them, the film overlays of a brown-green color covering the mucous mass are necrotic, ulcerated, in many places freely hanging down into the intestinal lumen (which is narrowed).
Description of pathological changes:
These pathological changes could develop as a result of an acute intestinal disease with a predominant lesion of the large intestine, the cause of which was the penetration, development and reproduction of Shigella bacteria and their species in the epithelium of the mucous membrane. This group of bacteria has a cytoplasmic effect on these cells, which is accompanied by the destruction and desquamation of the latter, the development of desquamative catarrh. Enterotoxin of bacteria has a vaseoneuroparalytic effect, which is associated with paralysis of blood vessels> increased exudation and damage to intramural nerve ganglia, which leads to the progression of processes and the development of fibrinoid inflammation (as a result of increased sweating of fibrinogen from dilated vessels). If in the first stage we find only superficial necrosis and hemorrhage, then in the second stage a fibrinoid film appears at the apex and between the folds. The necrotic masses of the mucosa are permeated with fibrin. Dystrophic and necrotic changes in the nerve plexuses are combined with leukocyte infiltration of the mucosa and submucosa, its edema, hemorrhages. With the further development of the disease in connection with the rejection of fibrin films and necrotic masses, ulcers are formed, which at 3-4 weeks of the disease are filled with granulation tissue, which matures and leads to the regeneration of ulcers.
1) favorable:
a) complete regeneration with minor defects;
b) abortive form;
2) unfavorable:
a) incomplete regeneration with scar formation> narrowing of the intestinal lumen;
b) chronic dysentery;
c) lymphadenitis;
d) follicular, polycular-ulcerative colitis;
e) severe general changes (necrosis of the epitaleal tubules of the kidneys, fatty degeneration of the heart and liver, impaired mineral metabolism). Complications:
a) perforation of the ulcer: peritonitis; paraproctitis;
b) phlegmon;
c) intraintestinal bleeding.
Extraintestinal complications - bronchopneumonia, pilonephritis, serous arthritis, liver abscesses, ameloidosis, intoxication, exhaustion.
Conclusion: these morphological changes indicate colon diphtheria colitis associated with the toxic effects of Shigella.
Diagnosis: Dysentery and colitis. Stage of diphtheria colitis.
^ 15. Typhoid fever.
This macro-preparation is the ileum. The shape of the organ is preserved, the weight and dimensions are normal. The intestine is whitish in color, the mucous membrane is folded, on which formations of 4x2.5 cm and 1x1.5 cm are noticeable, which protrude above the surface of the mucous membrane. Grooves and convolutions are noticeable on them, the surface itself is uneven, loosened. These formations are dirty gray in color. A formation with a diameter of 0.5 cm is noticeable, with a loss of characteristic folding, whitish color, slightly deepened and compacted.
Description of pathological changes:
These pathological changes could develop as a result of infection (parenteral) with typhoid bacillus and their multiplication in the lower part of the small intestine (with the release of endotoxin). By lymphatic tract -> to Peyer's patches -> salitaric follicles -> regional lymph nodes -> blood -> bacteremia and bacteriocholia
-> into the lumen of the intestine -> hyperergic reaction in the follicles, which leads to an increase and swelling of follicles, tortuosity of their surface. This occurs as a result of the proliferation of monocytes, histiocytes, reticulocytes, which extend beyond the follicles into the underlying layers. Monocytes turn into macrophages (typhoid cells) and form clusters - typhoid granulomas. Catarrhal enteritis joins these changes. With further progression of the process, typhoid granulomas necrotize and are surrounded by a zone of demarcation inflammation, sequestration and rejection of necrotic masses leads to the formation of "dirty ulcers" (as a result of soaking with bile), which eventually change their appearance: they are cleared of necrotic masses, the edges are rounded. The proliferation of granulation tissue and its maturation leads to the formation of delicate scars in their place. Lymphoid tissue is restored. Exodus:
1.favorable:
Complete regeneration of lymphoid tissue and healing of ulcers;
2.adverse:
Death as a result of intestinal (bleeding, perforation of ulcers, peritonitis) and extraintestinal complications (pneumonia, osteomyelitis, intramuscular abscesses, sepsis, waxy necrosis of the rectus abdominis muscles);
dystrophic changes in the parenchymal organs, the formation of typhoid granulomas in them.
Conclusion: these morphological changes indicate an acute infectious disease with local changes in the small intestine - ileolitis.
Diagnosis: Ileolith.
^ 16. Gangrene of the small intestine.
This macro-preparation is a small intestine area. Its dimensions and weight have not been changed. The bowel loops are enlarged, the consistency of one part is loose, the second is not changed. The surface is smooth. The serous membrane is dull and dull. Between the loops, a sticky, viscous, stretching liquid in the form of threads. On the section of the intestine, the walls are enlarged, the lumen is narrowed.
Possible causes: impaired blood supply as a result of strongometic necrochodemonia of the mesenteric arteries.
Morphogenesis: ischemia, dystrophy, atrophy, necrosis of an organ in contact with the external environment - gangrene.
1) unfavorable - putrefactive melting, will distill.
Conclusion: indirect vascular necrosis.
Diagnosis: Wet gangrene of the small intestine.
386. Chronic stomach ulcer.
On the lesser curvature of the stomach, a steep ulcer defect is visible up to 1 cm in diameter, the bottom and edges are dense, ridge-like.
108. Chronic stomach and duodenal ulcers.
On the mucous membrane of the stomach and duodenum, 3 ulcerative defects are visible. In the stomach, an elongated ulcer with undermined dense edges and a dense bottom. In the duodenum 2 ulcers of a rounded shape, located opposite each other ("kissing ulcers"), in one of them there is a perforated hole
128. Melena (bleeding into the lumen of the gastrointestinal tract).
The intestinal mucosa is black (pigment hydrochloric acid hematin, methemoglobin, iron sulfide)
149. Saucer-shaped stomach cancer. 184. Skirr of the stomach.
Stomach cancer.
Exo- and endophytic growth.
146. Ulcerative colitis.
On the mucous membrane of the colon, multiple ulcerative defects
of various shapes and sizes.
A. Polypoid cancer.
75b. Myoma of the stomach.
EXPLORE MICROPREPARATIONS:
62a. Chronic stomach ulcer (exacerbation stage).
At the bottom of a chronic ulcer, 4 layers are distinguished:
1) on the surface of the ulcer defect there is a zone of necrosis with leukocytes, 2) beneath it - fibrinoid necrosis, 3) below is a zone of granulation tissue, followed by 4) a zone of sclerosis with lymphoid infiltrates and sclerosed vessels.
90. Acute suppurative appendicitis (phlegmanous-ulcerative).
(see at the same time the drug 151. The appendix is normal)
All layers of the appendix are infiltrated with leukocytes, the mucous membrane is ulcerated. In the submucosa, congested vessels and hemorrhages
177. Chronic appendicitis with regeneration of the mucous membrane.
The wall of the appendix is thickened due to the proliferation in all layers of fibrous connective tissue Newly formed low cubic epithelial cells creep onto the ulcer defect
140. Cholecystitis.
The wall of the gallbladder is thickened due to the proliferation of connective tissue. Against the background of sclerosis, there are infiltrates consisting of leukocytes. The mucous membrane is atrophied
74. Solid stomach cancer.
The parenchyma and stroma in the tumor are evenly developed. The parenchyma is represented by atypical cells that form cells. Anaplastic epithelium proliferates, in places it grows outside the mucous membrane - infiltrating growth
At l and with (pictures):
Testes: choose the correct answers.
433. The causes of acute gastritis are:
1- alcoholism
2- infection
3- ingestion of traumatic substances
434. The following changes are characteristic of atrophic gastritis:
1- pink mucosa, with well-defined folds
2- mucous membrane pale
3- there is a lot of mucus in the stomach
4- focal regeneration of the epithelium
435. The main severe complication of gastric ulcer is:
1- lymphadenitis of regional nodes
2- perforation
3- perigastritis
4- "inflammatory" polyps around the ulcer
436. The most characteristic changes in blood vessels in the bottom of a chronic ulcer are:
1- inflammation and sclerosis of the wall
2- plethora
3- anemia
4- large thin-walled sinusoidal vessels
437. The local factor of importance in the pathogenesis of gastric ulcer and duodenal ulcer includes:
1- infectious
2- violation of trophism
3- toxic
4- decrease in the secretion of gastrin and histamine
5- exogenous
438. The layers of the bottom of a chronic stomach ulcer are:
1- exudate
3- granulation tissue
4- sclerosis
439. An autopsy of the deceased revealed a lot of stomach erosions from burns, covered with hydrochloric acid hematin. Erosion formed:
1- before burn
2- during a burn
440. On the mucous membrane of the stomach, there is a liquid of coffee appearance. When cleansing from it, punctate hemorrhages and defects the size of a pinhead are visible. Specify the name of the process:
1- petechiae
3- acute ulcers
441. An autopsy in the stomach found two round ulcers located on the lesser curvature, the edges are even, the bottom is thin. The ulcers are:
1- sharp
2- chronic
442. The signs of a chronic ulcer are:
1- recurrent bleeding
2- dense sclerosed bottom
3- multiple ulcers
4- one, two ulcers
443. The most common localization of stomach cancer is:
2- large curvature
3- small curvature
444. Cancer grows diffusely all layers of the stomach wall, dense, stomach cavity is reduced. Cancer refers to:
1- differentiated adenocarcinoma
2- mucous cancer
445. A woman has clinically determined solid tumors of the ovary on both sides. It is necessary to investigate the presence of a tumor first of all:
1- in the lungs
2- in the stomach
446. Acute gastritis usually manifests itself in the form of:
1- atrophic
2- hypertrophic
3- purulent
4- superficial
5- with restructuring of the epithelium
447. Chronic atrophic gastritis is characterized by:
1- ulceration
2- hemorrhages
3- fibrinous inflammation
4- enterolization of the mucous membrane
5- plethora and diffuse leukocyte infiltration of its own layer of the mucous membrane
448. Exacerbation of stomach ulcers is characterized by:
1- hyalinosis
2- enterolization
3- regeneration
4- lymphoplasmacytic infiltrate
5- necrotic changes
449. The characteristic symptom of Menetrie's disease is:
1- enterolization of the gastric mucosa
2- chlorohydrolenic uremia (gastric tetany)
3- Virchow metastases
4- giant hypertrophic folds of the gastric mucosa
5- nonspecific intestinal granulomatosis
450. Ischemic colitis can be detected:
1- with atherosclerosis
2- with scleroderma
3- with diabetes
4- with rheumatoid arthritis
451. Rectal changes are characteristic:
1- for ulcerative colitis
2- for Crohn's disease
3- for Hirschsprung's disease
452. When ulcerative colitis is malignant, the intestinal mucosa is:
1- smooth
2- polypoid (granular)
3- atrophic
453. Malignancy of adenomatous polyps is more often found:
1- in the basal departments
2- in the superficial departments
3- in the middle departments
454. Familial multiple colon polyposis is found more often:
1- from birth
4- at the end of the first year of life
5- after 3 years
455. The characteristic histological signs of Whipple's disease are revealed:
1- in the lungs
2- in the myocardium
3- in the liver
4- in the kidneys
456. The most characteristic histological sign of Whipple's disease:
1- hemorrhage
3- macrophage infiltrate
4- leukocytosis
457. Cancer is suspected in an emaciated patient. An enlarged, indurated lymph node is felt over the left clavicle. It is necessary to examine first of all:
2- stomach
3- esophagus
458. The appendix is thickened in the distal part, the serous cover is dull, hyperemic, in the lumen there is fecal masses and purulent exudate. Microscopically - diffuse infiltration of the appendix wall by neutrophils, no ulcers. Appendicitis refers to:
1- to simple
2- to destructive
459. The appendix is thickened in the middle segment, the serous membrane is covered with fibrinous films. Histologically, against the background of diffuse infiltration of the entire thickness of the ulcer wall.
Appendicitis refers to:
1- to phlegmonous-ulcerative
2- to gangrenous
3- to simple
460. The appendix is thickened, the serous integument is covered with fibrin, the wall is black throughout, dull. Appendicitis refers to:
1- to catarrhal
2- to gangrenous
3- to phlegmonous
461. Abortive appendicitis is characterized by:
1- inflammation is mild
2- primary changes resolved
3- the site of inflammation is extremely small
462. Thickening of mucus in the lumen of the sclerosed appendix is called:
1- cystic fibrosis
2- mucocele
3- melanosis
463. The characteristic signs of acute appendicitis are:
2- serous exudate in the mucous and muscular membranes
3- hyperemia
4- sclerosis of the wall of the appendix
5- destruction of muscle fibers
464. The characteristic signs of chronic appendicitis are:
1- sclerosis of the vessel walls
2- sclerosis of the wall of the appendix
3- purulent bodies
4- lymphoplasmacytic infiltration
5- granulomas
465. The morphological forms of appendicitis are.
Department of Gracilicutes
Family Enterobacteriaceaea
Genus Salmonella
S.enteritica species
Subspecies (7 main): S. Choleraesuis, S. salamae, S.arizonae, S.diarizonae, S.houtenae, S.bongori, S.indica. They differ in a number of biochemical characteristics.
Salmonella are the main causative agents of foodborne diseases and a kind of diarrhea - salmonellosis.
Morphology and tinctorial properties.
Short Gr - rods with rounded ends, in most cases mobile (peritrichous). They have no spores and capsules.
Cultivation.
Optional anaerobes. Optimum 37⁰, pH 7.2. Not demanding on nutrient media.
For isolation, differential diagnostic media (bismuth - sulfite agar, Endo, Ploskirev, SS agar) and enrichment media (selenite broth, bile broth, Rappoport's medium) are used. S-forms form small transparent colonies (pinkish on Endo's medium, colorless on Ploskirev's medium, black, with a metallic sheen on ICA). On liquid media, S-forms give uniform turbidity, R-forms - sediment.
Biochemical properties.
Glucose is fermented with the formation of acid and gas (exceptions S.typhi, etc.). Form hydrogen sulfide (but there are exceptions). Give a positive reaction with MR. They grow on starved citrate agar (except S.typhi). Do not ferment lactose (but not all). Do not form indole, etc.
Antigenic structure.
There are O-, H- and K-Ar.
· O-Ar (65 different types). According to O-Ag, salmonella is divided into 50 serological groups.
· Two types of H-Ar: 1 phase and 2 phase. More than 80 types of H-Ar 1 phase and 9 H-Ar 2 phases were found. According to H-Ar, serogroups are divided into serotypes.
· K-Ag are presented in various options: Vi-, M-, 5-Ag.
For serological identification of Salmonella, diagnostic adsorbed mono- and polyvalent O- and H-sera are produced containing agglutinins to O- and H-Ar of those Salmonella serotypes that most often cause diseases in humans and animals.
Resistance.
Heating at 70⁰ is maintained for about 30 minutes. Resistance to high t⁰ increases when Salmonella is found in food (meat). Common chemical disinfectants kill salmonella in 10-15 minutes.
Pathogenic factors.
There are adhesion and colonization factors, invasion factors. They have endotoxin, and some serotypes can synthesize two types of exotoxin:
Heat-labile and heat-stable enterotoxins, type LT and ST
Shiga-like cytotoxins
A feature of toxins is intracellular localization and release after the destruction of bacterial cells.
Toxin formation in Salmonella is combined with the presence of 2 factors of skin permeability in them:
Fast-acting - Produced by many Salmonella strains, thermostable
Slow down - thermolabile, causes the effect (rabbit skin tightening) 18-24 hours after administration
Epidemiology.
Only S.typhi and paratyphi A and B cause disease only in humans. The rest of Salmonella is also pathogenic for animals.
The primary source of Salmonella is animals (cattle, pigs, waterfowl, chickens, etc.)
Diseases of animals caused by salmonella are divided into 3 main groups:
Primary salmonellosis. Are caused by certain pathogens and proceed with a characteristic clinic
Secondary salmonellosis. Occur under conditions when the animal's body is sharply weakened as a result of any reason
Enteritis of cattle. It is characterized by a certain clinical picture. However, enteritis is a secondary manifestation, various predisposing circumstances play a primary role.
The most dangerous sources of foodborne diseases are animals suffering from secondary salmonellosis and enteritis of cattle. An important role in the epidemiology of salmonellosis is played by waterfowl, chickens and their eggs.
Infection of a person from a sick person or a carrier of bacteria is possible not only through food, in which Salmonella find good conditions for reproduction, but also through contact and everyday life.
Pathogenesis and clinic.
Salmonellosis can occur with a different clinical picture: in the form of food toxicoinfections, salmonella diarrhea and generalized (typhoid) form. It all depends on the size of the infecting dose, the degree of virulence of the pathogen and the immune status of the organism.
Massive contamination of food with Salmonella causes food poisoning... The main symptoms are associated with the entry of the pathogen into the blood in large quantities, its decay and the release of endotoxin.
At the heart of salmonella diarrhea is colonization of enterocytes by salmonella. After attachment to the glycocalyx of the small intestine, Salmonella are introduced between the villi, attaching to the enterocyte plasmolemma, colonizing it, damaging the microvilli, causing desquamation of enterocytes and moderate inflammation of the mucous membrane. The released enterotoxin causes diarrhea, and the cytotoxin causes cell death. Salmonella multiply on the plasmolemma (not in enterocytes), invasion occurs through the epithelium into the underlying tissues of the mucous membrane, transported through it in macrophages, enter the lymph and blood, causing bacteremia and generalization of the infectious process.
Post-infectious immunity.
Mostly children are ill, post-infectious immunity is type-specific.
Laboratory diagnostics.
The main method is bacteriological. Material for research: feces, vomit, blood, gastric lavage, urine, food (which caused the poisoning).
Bacteriological diagnostics, features:
Selenite, magnesium enrichment medium (especially when examining stool)
To detect Salmonella, samples should be taken from the last, more fluid part of the bowel movement (upper small intestine)
Maintain a ratio of 1: 5 (1 part of bowel movement to 5 parts of medium)
As a differential diagnostic medium, not only Endo is used, but BCA (since S.arizonae and S..diarizonae ferment lactose). On the ICA, colonies become black (some are greenish).
Rappoport medium is used for inoculation of blood.
Use for preliminary identification of O1 colonies of Salmonella phage, to which up to 98% of Salmonella are susceptible
For the final identification of the isolated cultures, polyvalent adsorbed O- and H-sera are first used, and then the corresponding monovalent O- and H-sera
For rapid detection of Salmonella, polyvalent immunofluorescent sera can be used.
To detect antibodies in the blood serum of patients and those who have been ill, RPHA is used with the use of polyvalent erythrocyte diagnostics containing polysaccharide antigens of serogroups A, B, C, D, and E.
Treatment.
With food toxicoinfection - gastric lavage, the use of antibacterial drugs, fortifying agents.
With salmonella diarrhea - restoration of normal water-salt metabolism, antibiotic therapy.
Specific prophylaxis.
Not applicable. Although various vaccines have been proposed for both killed and live (mutant) S. typhimurium strains.
Specific prophylaxis can be used primarily for typhoid fever. A chemical sorbed typhoid monovaccine is used. Vaccination is currently used mainly for epidemic indications.
Foodborne infections are acute intestinal diseases resulting from the consumption of food contaminated with various types of Salmonella (S. heidelberg, S. typhimurium, S. derby, etc.).
Morphology and tinctorial properties. Rods with rounded ends, 1-3 microns long. Most of them, due to the peritrichial flagella, are mobile. According to Gram, they are colored negatively.
Cultural properties. The causative agents of foodborne diseases are facultative anaerobes. The optimum temperature for breeding is 35-37 ° C. They can grow at a pH value of 4.1-9.
On nutrient media, small transparent, bluish colonies are formed with a diameter of 2-4 mm. On Endo medium, they are slightly pinkish, transparent; on Ploskirev's medium - colorless, unclear, look denser. Colonies on bismuth sulfite agar are always black, with a metallic sheen. The culture medium under the colony is colored black.
Antigenic structure. Salmonella - causative agents of foodborne diseases, have three main antigenic complexes: O-somatic, H-flagellate and K-capsule.
Resistance. Salmonella survives for a long time in the environment and in food. They tolerate low temperatures well and for a long time, but at temperatures above 46 ° C they quickly die, and at 100 0 C they instantly die.
Virulence factors. The main factor responsible for the development of the disease is the endotoxin complex. Salmonella's adhesive properties also determine their virulence.
Epidemiology. The main source of infection is livestock and poultry - patients with salmonellosis or asymptomatic carriers. The main route of infection is alimentary, and the factors of transmission of infection are various food products (animal meat, eggs and egg products, milk). Salmonellosis as an "nosocomial" infection is becoming one of the important problems of modern medicine. The source of it in this case is a person, most often sick children. The spread of such salmonellosis occurs in three ways: contact-household, air-dust and food.
Pathogenesis and clinic. Foodborne toxicoinfections are accompanied by significant intoxication, deep lesions of the gastrointestinal tract, as well as bacteremia and the development of toxic-septic conditions. Patients, as a rule, are worried about general weakness, fever, abdominal pain, nausea, vomiting, diarrhea, often with a fetid odor. There are several clinical forms of salmonellosis: gastrointestinal, generalized, bacterial excretion.
Laboratory diagnostics. The most important laboratory methods are bacteriological and serological.
Bacteriological the method of research can be exposed to the feces of patients, vomit, gastric washings, urine, blood, bile.
From serological methods use the reaction of agglutination and indirect hemagglutination.
Treatment. In patients with the gastrointestinal form of the disease, the main method of treatment is pathogenetic therapy, including measures aimed at detoxification and restoration of water-electrolyte balance and hemodynamics. In generalized forms of salmonellosis, along with pathogenetic therapy, it is necessary to use antibacterial agents (chloramphenicol, ampicillin).
Currently, about 1000 species of Salmonella are known, which are grouped into groups A, B, C, D, E, etc.
The cause of the disease is more often Salmonella typhimurium (Bact.enteritidis Breslau), Salmonella enteritidis (Bact.enteritidis Gartneri), Salmonella Heidelberg, Salmonella newport, etc. ... In salted meat (10-15%), salmonella survive up to 3 months, in chicken eggs - up to 3 weeks, in duck eggs - more than a month, they multiply well in milk. When heated to t ° 60 °, bacteria die after 1 hour, and when boiled - instantly.
Epidemiology. The source of infection is large and small ruminants, pigs, poultry (ducks, geese, less often chickens, turkeys) and some rodents. A sick person or a healthy carrier of bacteria can also be a source of infection. In the spread of infection, the infected play a role - meat, sausage, sausages, eggs, milk, etc. Sporadic cases of the disease are usually recorded during the year; outbreaks are more common during the hot season.
Pathogenesis. A true infectious process develops, caused by living microbes. Although they are mildly pathogenic for an adult, salmonella only cause disease if they enter the gastrointestinal tract in very large numbers. This is usually observed with abundant microbes in the food as a result of violation of sanitary and hygienic requirements during its preparation and storage. From the intestine, microbes enter the general circulation through the lymphatic vessels, causing bacteremia. When Salmonella is destroyed in the intestines and blood, endotoxin is released from them, which causes general intoxication of the body with damage to various organs, primarily the neurovascular apparatus.
Clinical presentation (symptoms and signs). The incubation period is from 4-6 hours. up to 2 days. The disease begins acutely, with chills. The temperature often rises to high numbers and lasts for 2-4 days. Appears up to 5-15 times a day; feces offensive, watery, sometimes with mucus and even blood, abdominal pain, more often in the epigastric region. Blood pressure goes down. In the blood: leukocytosis (9000-15000) with neutrophilia. The disease, with proper treatment, lasts 3-6 days.
With a severe course of the disease, all clinical phenomena develop rapidly: indomitable vomiting appears, profuse diarrhea - feces are similar to rice water, as in. Symptoms of severe dehydration are observed. Acute cardiovascular failure (collapse) is possible. Death may come.
Diseases proceeding by type are noted. In some cases, they may be accompanied by symptoms similar to: there is a prolonged fever (up to 10 days, sometimes more), and increases. In other cases, the clinical picture of the disease is similar to: often kidneys and lungs are affected.
Immunity after the disease is unstable.
Foodborne toxicoinfections of salmonella etiology... According to F. Kaufmann, the genus of Salmonella includes more than 700 types of microorganisms, which are subdivided into groups (A, B, C, D, E, etc.), and within the group - into types. However, only a few types of Salmonella are commonly found in foodborne illness. S. typhi murium (Bact. Enteritidis Breslau), S. enteritidis (Bact. Enteritidis Gartneri) and S. cholerae suis (Bact. Suipestifer) play a major role in the etiology of these diseases.
The main reservoir of Salmonella infection is animals (cattle and small ruminants, pigs, horses), as well as poultry (ducks, geese, chickens). Therefore, foodborne infections caused by salmonella usually occur after eating foods made from beef, pork, horse meat, meat or poultry eggs (most often duck eggs), less often fish or dairy products.
Meat can be infected while the animal is alive or after it dies.
Most foodborne diseases are associated with the consumption of meat for forced slaughter, that is, sick animals. Sometimes, after long heavy hauls of livestock and with poor maintenance of animals, bacteria easily pass from the intestine into the lymph flow and seeding the organs. Posthumously meat becomes infected most often during slaughter and butchering by contamination with intestinal contents or as a result of contact with the carcass of an infected animal, as well as through rodents, flies, etc.
A person (sick or healthy carrier) can also be a source of Salmonella infection. Carriage of Salmonella by persons who have had salmonellosis, with a prescription of several days to 3 years, has been proven. Outbreaks of food toxicoinfection caused by the presence of a bacterium carrier on a food object, which infected food with Salmonella, are described.
Pathogenesis. With food toxicoinfections, it is not the poisoning of bacteria with ready-made endotoxins (food poisoning), as it was thought before, but a genuine infectious process caused by living microbes develops. Although they are mildly pathogenic for an adult, salmonella only cause disease if they enter the gastrointestinal tract in very large numbers. This is usually observed with abundant multiplication of microbes in food as a result of violation of sanitary and hygienic requirements during its preparation and storage. Since the elevated temperature promotes the multiplication of bacteria in meat and other products, the incidence of foodborne diseases usually increases in the warm season. Particularly favorable conditions are created for the growth of bacteria in minced meat, which is a good breeding ground for them. From the intestine, microbes enter the general circulation through the lymphatic vessels, causing bacteremia. When Salmonella is destroyed in the intestines and blood, endotoxin is released from them, which causes general intoxication of the body with damage to various organs, primarily the neurovascular apparatus.
Clinical course. The incubation period ranges from 6 to 36 hours. The disease, as a rule, proceeds according to the type of acute gastroenteritis of varying severity, begins acutely with general malaise, nausea, vomiting, abdominal pain, the temperature rises to 38.5-39.5 °, frequent loose stools appear, sometimes with mucus and even with blood (gastroenterocolitis). The disease lasts 3-6 days.
Sometimes the disease can take a cholera-like form (repeated vomiting, severe diarrhea, cyanosis of the face, limbs, etc.). In cases of severe intoxication, a sharp dehydration of the body occurs, acute vascular insufficiency (collapse) is possible. Typhoid-like and other forms of the disease are much less common.
Treatment. In milder forms of gastritis and gastroenteritis, patients recover without treatment; for more severe ones, urgent medical attention is required. Shows early abundant gastric lavage with weak solutions of potassium permanganate, soda or pure water and the use of saline laxatives. In the absence of a thick probe, the patient is recommended to re-drink 3-5 glasses of these solutions or water, after which they artificially induce vomiting. Prescribe bed rest, heating pads on the stomach, a strict diet. With a large loss of fluid and thickening of the blood, drip intravenous infusions of heated Polosukhin liquid of 300-500 ml and more are performed. In case of collapse, up to 40 mg can be added to the solution. Intravenous physiology, solution, 5% glucose or mixtures thereof, plasma with physiology, solution are also recommended. Effective for collapse is 1% mezaton solution at a dose of 0.3-0.5 ml subcutaneously or 0.1-0.3 ml intravenously, as well as norepinephrine at a dose of 0.5-1 ml intravenously when measuring pressure every 2 minutes. (a solution of norepinephrine is prepared by diluting 4 ml of a 0.2% solution in 1 liter of 5% glucose). The sometimes occurring bradycardia is eliminated by the introduction of 0.5-1 ml of a solution of atropine sulfate in a dilution of 1: 1000. There is a good result from treatment with broad-spectrum antibiotics (tetracycline or terramycin 200,000-300,000 IU per day, streptomycin, chloramphenicol).
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