Salmonellosis is a group of infectious diseases of humans and animals, the causative agents of which are bacteria of the Enterobacteriaceae family, the genus Salmonella, represented by two species - S. enterica and S. bongori, among which seven subspecies are distinguished.
Salmonella has three main antigens:
· O-somatic (thermostable);
· H-flagellate (heat-labile);
· K-surface (capsule).
In addition, other antigens have been described for some Salmonella serotypes:
Vi-antigen (one of the components of the O-antigen);
· M-antigen (mucous).
Currently, more than 2.5 thousand serological variants of Salmonella are known. Sero- and phage typing of Salmonella is carried out at the National Salmonella Centers, which provide information up to 60 times a year on the isolation of new Salmonella serotypes and their epidemiology. The identification of new salmonella serovars is confirmed by the WHO Reference Center for Salmonella Research (Institut Pasteur, Paris), which recommends the use of the Kaufman-White diagnostic antigenic scheme (2001) for serotyping and epidemiological surveillance of salmonellosis (2001), based on the serological identification of Salmonella taking into account their antigenic structure ( Oh, H, Vi).
Salmonella - gram-negative rods 2–4 × 0.5 μm; they are mobile, grow well on simple nutrient media at temperatures from 6 to 46 ° C (optimum growth 37 ° C). Most Salmonella pathogens are both for humans and for animals and birds, but in epidemiological terms, only a few serotypes are most significant for humans, which cause 85–91% of human salmonellosis on all continents of the world: S. typhimurium, S. enteritidis, S. ranama , S. infantis, S. newport, S. agona, S. derby, S. london, etc.
Currently, salmonellosis is one of the most common zoonoses in developed countries with a general tendency to increase the incidence. Especially it concerns major cities with a centralized food supply system.
Outbreaks of salmonellosis, caused by antibiotic-resistant Salmonella strains and characterized by high mortality, are regularly recorded in hospitals, especially in maternity, pediatric, psychiatric and geriatric wards. This type of salmonellosis has acquired features
hospital infection with contact and household transmission of the pathogen.
The main pathogenic factors of Salmonella are cholera-like enterotoxin and LPS-endotoxin. Some strains have the ability to invade the colon epithelium (S. enteritidis).
The clinical manifestations of the disease caused by various serotypes of Salmonella do not differ significantly from each other, therefore, at present, only the clinical form of the disease and the serotype of the isolated Salmonella are indicated in the diagnosis, which has epidemiological significance.
Typhoid fever is considered separately from other salmonellosis due to the strict specificity of its pathogen in relation to the host (anthroponosis) and the presence of clinical features of the course.
Salmonellosis
Salmonellosis is an acute zoonotic infectious disease with a fecal-oral mechanism of transmission of the pathogen, characterized by a predominant lesion of the gastrointestinal tract, the development of intoxication and dehydration.
ICD codes -10
A02. Other salmonella infections.
A02.0. Salmonella enteritis.
A02.1. Salmonella septicemia.
A02.2. Localized salmonella infection.
A02.8. Another specified salmonella infection.
A02.9. Salmonella infection, unspecified.
Salmonellosis causes
Salmonella are gram-negative bacilli of the genus Salmonella of the family Enterobacteriaceae.
There are two types of Salmonella - S. enterica and S. bongori, which are not pathogenic to humans. There are 2324 serovars divided by the set of somatic O-antigens into 46 serogroups. In addition to the somatic thermostable O-antigen, salmonella have a flagellated thermolabile H-antigen. Many strains have a Vi surface antigen. The main pathogenic factors are cholera-like enterotoxin and lipopolysaccharide endotoxin. Some S. enteritidis strains are capable of invading the epithelium of the colon. Salmonella persists for a long time in the environment: in water - up to 5 months, in soil - up to 18 months, in meat - up to 6 months, in bird carcasses - more than a year, on eggshells - up to 24 days. They tolerate low temperatures well, at 100 ° C they die instantly.
Epidemiology of salmonellosis
The reservoir and source of the causative agent of infection are sick animals: cattle and small ruminants, pigs, horses, poultry. They have an acute disease or in the form of a bacterial carrier. A person (sick or carrier) can also be a source of S. typhimurium. The transmission mechanism is fecal-oral. The main route of transmission is food, through animal products. Meat infection occurs endogenously during the life of the animal, as well as exogenously during transportation, processing, storage. IN last years there was a significant increase in the incidence (S. enteritidis) associated with the spread of the pathogen through poultry and eggs. Waterway transmission mainly plays a role in the infection of animals. By contact-household (through hands and instruments), as a rule, the pathogen is transmitted in medical institutions. The greatest risk of contracting salmonellosis is in children of the first year of life and people with immunodeficiency. The airborne pathway plays a large role in the spread of infection among wild birds. There is a high incidence of salmonellosis in large cities... Cases of the disease are recorded throughout the year, but more often in the summer months due to the worse storage conditions of food.
Sporadic and group morbidity is observed. The susceptibility of people to the pathogen is high. Post-infectious immunity lasts less than a year.
Prevention of salmonellosis
There is no specific prophylaxis.
Non-specific prevention measures
Veterinary and sanitary supervision over the slaughter of livestock and poultry, technology of carcass processing, preparation and storage of meat dishes. Compliance with sanitary and hygienic and anti-epidemic standards at trade and public catering enterprises.
Pathogenesis of salmonellosis
In the lumen of the small intestine, Salmonella attach to the membranes of enterocytes and reach the lamina propria of the mucous membrane. This leads to degenerative changes in enterocytes and the development of enteritis. In the lamina propria, macrophages absorb salmonella, but phagocytosis is incomplete and generalization of the infection is possible. When bacteria are destroyed, a lipopolysaccharide complex (endotoxin) is released, which plays a major role in the development of intoxication syndrome. In addition, it activates the synthesis of prostanoids (thromboxanes, prostaglandins), which trigger platelet aggregation in small capillaries. Prostaglandins stimulate the secretion of electrolytes and fluid into the intestinal lumen, induce smooth muscle contraction and increase peristalsis. The main role in the development of diarrhea and dehydration is played by enterotoxin, which activates the synthesis of cAMP by adenylate cyclase of enterocytes, thereby increasing the secretion of Na +, Cl– ions and water into the intestinal lumen. The consequence of dehydration and intoxication is a violation of the activity of the cardiovascular system, which is expressed by tachycardia and a decrease in blood pressure.
The clinical picture (symptoms) of salmonellosis
The incubation period is from 6 hours to 3 days (usually 12-24 hours); in case of nosocomial outbreaks it is extended to 3–8 days.
Salmonellosis classification
Gastrointestinal (localized) form:
- gastritic option;
- gastroenteric option;
- gastroenterocolitic variant.
Generalized form:
- typhoid variant;
- septic option.
Bacterial excretion:
- spicy;
- chronic;
- transitory.
The main symptoms and the dynamics of their development
The gastritic variant is characterized by an acute onset, repeated vomiting and epigastric pain. The intoxication syndrome is weak. A short duration of the disease.
The gastroenteric variant is the most common. The disease begins acutely, with symptoms of intoxication: fever, headache, chills, aching muscles, cramping abdominal pain.
Nausea, vomiting, diarrhea join. Stool is fecal at first, but quickly becomes watery, foamy, fetid, sometimes with a greenish tinge and has the appearance of "swamp mud". Pallor of the skin is noted, in more severe cases - cyanosis. Tongue dry, coated with bloom.
The abdomen is distended, painful on palpation in all parts, more in the epigastrium and in the right iliac region, hums at hand. Muffled heart sounds, tachycardia, blood pressure decreased. Decreased urine output. Convulsions are possible.
With the gastroenterocolitic variant, the clinical picture is the same, but already on the 2-3rd day of the disease, the volume of stool decreases. They contain an admixture of mucus, sometimes blood. On palpation of the abdomen, spasm and soreness of the sigmoid colon are noted. Tenesmus is possible.
The generalized form of the disease, as a rule, is preceded by gastrointestinal disorders. With a typhoid-like variant, the temperature curve becomes constant or wavy. Are increasing headache, weakness, insomnia. The skin is pale, by the 6-7th day of the disease, a roseola rash appears on the abdominal skin. A slight bradycardia is observed. Dry scattered rales are heard over the lungs. The stomach is swollen. By the end of the first week of the disease, an increase in the liver and spleen is noted. The duration of the fever is 1-3 weeks. Relapses are rare. In the first days of the disease, the clinical manifestations of septic and typhoid-like variants are similar. In the future, the condition of patients worsens. Fluctuations in body temperature become irregular, with large daily fluctuations, repeated chills and profuse sweating, tachycardia, myalgia. The formation of purulent foci in the lungs, heart, kidneys, liver and other organs is noted. The disease is long-term and can be fatal. After the transferred disease, some of the patients become carriers of bacteria. In acute bacterial excretion, Salmonella shedding ends within 3 months; if it lasts more than 3 months, it is regarded as chronic. With transient bacterial excretion, a single or double sowing of Salmonella from feces is not accompanied by clinical manifestations and the formation of antibodies.
Complications of salmonellosis
Dehydration and ITSH, circulatory disorders in coronary, mesenteric and cerebral vessels, acute renal failure, septic complications.
Mortality and causes of death
Mortality is 0.2–0.6%. One of the above complications could be the cause of death.
Diagnostics of the salmonellosis
Clinical
Characterized by an acute onset with an increase in body temperature, nausea, vomiting, diarrhea, abdominal pain.
Epidemiological
Eating food cooked and stored in violation of sanitary standards, eating raw eggs, group outbreaks. In megalopolises, the identification of group cases of the disease is very difficult if a product contaminated with salmonella is sold through a retail network or public catering enterprises. Differential diagnosis of salmonellosis with IPT presents great difficulties without confirming the diagnosis by laboratory tests.
Specific and non-specific laboratory diagnostics
Bacteriological examination of feces (one or two times), vomit, blood, urine, bile, gastric lavage, residues of suspicious products.
Salmonella antigens can be detected in blood and urine using ELISA and RGA. For retrospective diagnostics, the determination of specific antibodies (RNGA and ELISA) is used. Explore paired sera taken with an interval of 5-7 days. An increase in titers by four times or more is of diagnostic value.
Differential diagnosis
Carry out with infectious and non-infectious diseases (table. 17-3, 17-4).
Table 17-3.Differential diagnosis of salmonellosis, dysentery, cholera
| Clinical signs | Salmonellosis | Dysentery | Cholera |
| Chair | Watery, with an unpleasant odor, often with an admixture of greenery of the color of marsh mud | Lean beskalovy, mixed with mucus and blood - "rectal spit" | Watery, rice-colored, odorless, sometimes with the smell of raw fish |
| Defecation | Painful with colitis | With tenesmus | Painless |
| Abdominal pain | Moderate cramping, epigastric or mesogastric | Strong, with false desires, in the lower abdomen, left iliac region | Not typical |
| Vomiting | Multiple, preceded by diarrhea |
Possible with gastroenterocolitic variant | Multiple watery, later on diarrhea |
| Spasm and soreness of the sigmoid colon | Possible with colitis | Are characteristic | Not marked |
| Dehydration | Moderate | Not typical | Typical, pronounced |
| Body temperature | Increased | Increased | Normal, hypothermia |
| Chills | Typical | Typical | Not typical |
Table 17-4. Differential diagnosis of salmonellosis, acute appendicitis, thrombosis of mesenteric vessels
| Clinical signs | Salmonellosis | Acute appendicitis | Thrombosis of mesenteric vessels |
| Anamnesis | Eating poor quality food, the possibility of group outbreaks | Without features | Ischemic heart disease, atherosclerosis |
| Onset of the disease | Acute, with severe intoxication, clinical picture of acute gastroenteritis | Epigastric pain with movement to the right iliac region | Acute, less often gradual, with abdominal pain |
| The nature of abdominal pain | Moderate cramping, epigastric or diffuse. Disappears before or at the same time as diarrhea stops | Violent persistent, aggravated by coughing. Persists or worsens when diarrhea stops | Sharp, unbearable, persistent or paroxysmal, no specific localization |
| Chair | Liquid, abundant, offensive, with an admixture of greenery, multiple | Liquid feces, without pathological impurities, up to 3-4 times, more often constipation | Liquid, often mixed with blood |
| Seizures, dehydration, chills | During the height of the disease | Absent | Absent |
| Examination of the abdomen | Moderately swollen, hums on palpation, painful epigastric or mesogastric | Soreness in right iliac region with muscle tension. Symptoms of peritoneal irritation are positive | Bloated, diffuse soreness |
| Vomiting | Multiple, in the first hours | Sometimes, at the onset of the disease, 1-2 times | Often, sometimes mixed with blood |
| Leukocytosis | Moderate | Expressed, growing | Expressed, growing |
Indications for consulting other specialists
Consultation with a surgeon is necessary if you suspect appendicitis, mesenteric thrombosis, intestinal obstruction.
A gynecologist's consultation is prescribed for suspected ectopic pregnancy, ovarian apoplexy, salpingo-oophoritis.
Consultation of a cardiologist - to exclude myocardial infarction, hypertensive crisis, correction of therapy with concomitant ischemic heart disease, hypertension.
An example of a diagnosis formulation
A02.0. Salmonellosis. Gastrointestinal form. Gastroenteric option. Moderate course.
Indications for hospitalization
Severe course of the disease, the presence of complications; epidemiological indications.
Salmonellosis treatment
Mode. Diet
Bed rest is prescribed for severe intoxication and loss of fluid. Ward - with moderate and mild course. Diet - table number 4. From the diet exclude foods that irritate the stomach and intestines, dairy products, as well as refractory fats.
Salmonellosis drug therapy
Etiotropic therapy
Moderate and severe localized form of the disease - enterix ♠ two capsules three times a day for 5–6 days; Chlorquinaldol 0.2 g 3 times a day for 3-5 days.
The generalized form is ciprofloxacin 500 mg twice a day; ceftriaxone 2 g once a day intramuscularly or intravenously for 7–14 days. For all forms of bacterial carriage and the decreed category of persons - salmonella bacteriophage, two tablets three times a day or 50 ml twice a day 30 minutes before meals for 5-7 days; sanguirithrin ♠ two tablets 3-4 times a day for 7-14 days.
Pathogenetic agents
Rehydration therapy. Oral (with dehydration of I – II degree and absence of vomiting): glucosolan ♠, citroglucosolan, rehydron ♠. Rehydration is carried out in two stages, the duration of the 1st stage - up to 2 hours, the 2nd - up to 3 days. Volume 30–70 ml / kg, flow rate 0.5–1.5 l / h, temperature 37–40 ° С. Parenteral: chlorosalt ♠, trisol ♠. Rehydration is carried out in two stages, the duration of the 1st stage - up to 3 hours, the 2nd - according to indications (it is possible to switch to oral fluid administration). Volume 55-120 ml / kg, average flow rate 60-120 ml / min.
Detoxification therapy.Only when treating dehydration. Glucose ♠, rheopolyglucin ♠ 200–400 ml intravenously.
Eubiotics and biological products: bactisubtil ♠ one capsule 3–6 times a day 1 hour before meals, linex ♠ two capsules three times a day for 2 weeks; lactobacillus acidophilus + kefir fungi (acipol ♠), one tablet three times a day; bifidobacterium bifidum (bifidumbacterin ♠), five doses three times a day for 1-2 months. Khilak forte ♠ 40-60 drops three times a day for 2-4 weeks.
Sorbents: hydrolytic lignin (polyphepan ♠), one tablespoon 3-4 times a day for 5-7 days; activated carbon (carbolong ♠), 5-10 g three times a day for 3-15 days; dioctahedral smectite (neosmectin ♠), one powder three times a day for 5–7 days.
Enzyme therapy: pancreatin, one powder three times a day for 2-3 months; mezim forte ♠ one tablet three times a day for 1 month; oraza ♠ one teaspoon three times a day for 2-4 weeks with meals.
Antidiarrheal drugs: calcium gluconate 1-3 g 2-3 times a day, indomethacin 50 mg three times a day every 3 hours for 1-2 days, Kassirsky's powders, one powder three times a day.
Antispasmodics: drotaverine (no-shpa ♠) 0.04 g three times a day, papaverine 0.04 g three times a day.
Additional methods of treatment (surgical, physiotherapy, spa)
Gastric lavage by the probeless method is necessary, if the patient's condition allows.
Approximate terms of incapacity for work with salmonellosis
The duration of hospital stay in the localized form is up to 14 days, in the generalized form - 28-30 days. The discharge is carried out after clinical recovery and a negative result of bacteriological examination of feces, which is carried out 2 days after the end of treatment.
Patients of the decreed group are discharged after two control studies of feces (the first - not earlier than the 3rd day after the end of treatment, the second - after 1–2 days). Patients who do not excrete the pathogen are allowed to work.
Clinical examination
Workers food Industry and catering enterprises are subject to medical examination within 3 months with a monthly single examination of feces. Individuals with salmonella are not allowed to work for 15 days and are given other jobs. During this period, they undergo a 5-fold study of feces and a single study of bile. If bacterial excretion continues for more than 3 months, they are transferred to another job for a period of at least 1 year and examined once every 6 months. After this period, a 5-fold study of feces and a single bile is carried out with an interval of 1-2 days. With negative results, such patients are removed from the register and admitted to the main work; if positive, they are suspended from work.
A note for a patient with salmonellosis
Compliance with the diet for 2-3 months with the exception of spicy food, alcohol, refractory animal fats, milk. After generalized forms, it is necessary to limit physical activity for 6 months.
The causative agents of intralesional salmonellosis are "hospital" strains of Salmonella, most often Salmonella typhimurium. In contrast to the "wild" (natural) strains of the same species, they do not cause death of mice when infected through the mouth, but are more pathogenic for humans, and have multidrug resistance due to the presence of R-plasmids. Hospital strains are also found among S. enteritidis.
Disease in humans.Sick people are the source of infection. The spread of nosocomial salmonella occurs through contact-household, air-dust and food routes.
The manifestations of the disease are varied: asymptomatic carrier of bacteria, mild forms, severe intestinal disorders with intoxication, bacteremia, sometimes with septic complications. The disease is especially difficult in young children.
Laboratory diagnostics.Stool and blood are examined. Isolated pure cultures are identified by morphology, biochemical properties, antigenic structure.
Prevention and Treatment.It is necessary to observe the sanitary and hygienic regime in medical institutions, at public catering establishments; identification of carriers of Salmonella and their sanitation. For the purpose of emergency prevention of nosocomial infection, a polyvalent salmonella bacteriophage is prescribed for children who have been in contact with patients and carriers, as well as mothers.
Antibacterial drugs (chloramphenicol, ampicillin) are used to treat patients with generalized forms of salmonellosis.
Shigella
The causative agents of dysentery (shigellosis) are several types of bacteria, united in the genus Shigella. One of them was first discovered in 1891 by the Russian physician A. Grigoriev and studied during the epidemic in Japan in 1898 by Shiga. Subsequently, other species of Shigella were isolated and described. According to the modern classification, 4 groups belong to the genus Shigella, respectively 4 species. All species, except for S. sonnei, are subdivided into serovars, while S. flexneri is also subdivided into subsovars (Table 8).
In recent decades, dysentery is most often caused by Flexner's and Sonne's shigella, less often Boyd's shigella. S. dysenteriae (Grigorieva-Shiga) does not occur in Russia.
Shigella are short gram-negative rods, they do not form spores and capsules, unlike Salmonella, they do not have flagella.
Optional anaerobes. They grow on simple nutrient media, the optimum temperature is 37 ° C, pH 6.8-7.2. They differ in biochemical properties (Table 5). Glucose is fermented, lactose is not fermented on the first day (Sonne's shigella - in a few days), all species ferment mannit, except for S. dysenteriae.
Antigens.Shigella contain O-antigens, some serovars have K-antigen. Among O-antigens there are specific and group antigens.
Toxin formation.A neurotropic exotoxin is produced by S. dysenteriae, and this species causes the most severe disease. All Shigella contain a thermostable endotoxin.
Stability.S. sonnei are the most stable in the external environment. Boiling kills Shigella immediately, at 60 ° C they die in 10-20 minutes, but there are heat-resistant S. sonnei, which die only at 70 ° C for 10 minutes, that is, they can survive when milk is pasteurized. In water, soil, food, on objects, in dishes, shigella remain viable for one to two weeks. S. sonnei can reproduce in milk. In the intestines of flies and on their paws, Shigella survive for 2-3 days. Flying from sewage and garbage to food, flies can carry pathogens.
At the same time, Shigella is very unstable in fecal samples, as they die under the influence of antagonistic microbes and the acidic reaction of the environment. Therefore, samples taken for research must be inoculated immediately on a nutrient medium.
Disease in humans.The source of infection is a sick person or a carrier. The transmission mechanism is fecal-oral. Infection occurs through the mouth. The incubation period lasts from 2 to 7 days.
The causative agent enters the epithelial cells of the colon mucosa and multiplies in them. This leads to inflammation (colitis) and ulceration. The main symptoms: fever, lower abdominal pain, vomiting, frequent stools, in severe cases, an admixture of mucus and blood in the stool; a characteristic symptom is tenesmus (false painful desires). The illness lasts 8-10 days. Patients with mild forms of the disease often do not seek qualified help, self-medicating. Untreated dysentery can become chronic.
Immunity.After a disease, immunity is unstable. During the disease, antibodies are formed, the detection of which has diagnostic value.
Laboratory diagnostics.Faeces are the material for bacteriological research. The sample should be taken before starting antibiotic therapy, inoculation should be performed immediately or the sample should be placed in a preservative liquid (30% glycerol and 70% buffer solution) for no more than one day. For sowing, select lumps of mucus. The amount of Shigella in a sample can be very scarce, so inoculation is performed on Ploskirev's elective medium or on enrichment medium - selenite.
The isolated pure culture is identified by morphology, biochemical properties and in the agglutination reaction with adsorbed species sera. Determine the sensitivity to antibiotics. Shigella are among the bacteria that rapidly acquire antibiotic resistance, in most cases associated with R-plasmids. In addition, Shigella antigens are detected in feces using ELISA.
For the purpose of diagnostics, serological reactions are used: agglutination, RIGA. Antibodies appear in the second or third week of the disease.
Medicines.Specific prophylaxis has not been developed. Dysentery bacteriophage is used in the centers of morbidity.
Antibiotic treatment should be carried out taking into account the sensitivity of the pathogens to them. Apply chloramphenicol, tetracycline; effective nitrofuran drugs, polyvalent bacteriophage. For chronic dysentery, vaccine therapy is used with a chemical vaccine given by mouth.
Klebsiella
The genus Klebsiella got its name in honor of the German scientist E. Klebs. Among the representatives of this genus: Klebsiella pneumoniae, Klebsiella ozaenae, Klebsiella rhinoscleromatis.
Morphology, cultural properties.Klebsiella are short, thick sticks. In the preparation, they are located singly, in pairs and in short chains. They do not have flagella, and do not form spores. A characteristic feature of Klebsiella is the formation of capsules both in the body and on nutrient media.
They grow on simple nutrient media, on solid media they form slimy colonies. Their differentiation is carried out according to biochemical characteristics.
Antigens.Klebsiella contain lipopolysaccharide O-antigens and polysaccharide capsular antigens, on the basis of which serotyping is performed. Some antigens are common with Escherichia and Salmonella antigens.
Pathogenicityassociated in Klebsiella with the presence of a capsule that prevents phagocytosis, and endotoxins.
Stability.Klebsiella are stable in the external environment, persist for a long time in water, on objects, in dairy products they can multiply at room temperature and in the refrigerator. They die on boiling and under the action of disinfectants.
Diseases in humans.Klebsiella pneumoniae cause pneumonia (bronchopneumonia), sometimes also sepsis, cystitis, acute intestinal infections; often occur with mixed infections.
Klebsiella ozenes are the causative agents of chronic diseases of the upper respiratory tract with the release of viscous secretions and the formation of crusts that emit a fetid odor. The disease is contagious, transmitted by airborne droplets.
Klebsiella rhinoscleromas cause chronic inflammation of the mucous membranes of the upper respiratory tract, with the formation of nodules (granulomas).
Immunity.Antibodies are formed during the course of illness, but they do not provide immunity. The chronic course of the disease is associated with the development of HRT.
Laboratory diagnostics.Materials under study: for pneumonia - sputum, for ozena - mucus from the pharynx, nose, trachea, with rhinoscleroma - pieces of tissue from granulomas. The study is based on the isolation of pure cultures and identification by morphology, cultural, biochemical properties and determination of the serovar.
An RSK is placed to detect antibodies in the serum of patients.
Medicines.Vaccine prophylaxis has not been developed. For treatment, antibiotics are used (streptomycin, chloramphenicol, neomycin, tetracycline), antimony preparations.
Proteus
Among the bacteria of the genus Proteus, the causative agents of food toxicoinfections and purulent-inflammatory processes can be Proteus vulgaris and Proteus mirabilis.
Morphology, cultural, biochemical properties.Proteus - polymorphic rods, short, long, filamentous, do not form spores and capsules, have flagella located peritrichially. Gram is negative.
Grow well on simple nutrient media. Proteus is characterized by "creeping" growth in the form of a bluish bloom on solid nutrient media, which is formed by swarming H-forms. Strains that have lost their flagella and the ability to swarm, form colonies with smooth edges (O-shapes). When inoculated according to the Shukevich method in condensation water at the bottom of a test tube with slant agar, Proteus quickly covers its entire surface.
Proteins have pronounced proteolytic properties: they liquefy gelatin and curdled whey, curdle milk, break down urea, and form hydrogen sulfide, indole, and ammonia. Many carbohydrates are fermented.
Antigens.Proteins have O-antigens and H-antigens, some of which are common with other enterobacteriaceae.
Toxin formation.They do not produce exotoxin, contain lipopolysaccharide endotoxin of the cell wall.
Sustainability and diffusion.Bacteria of the genus Proteus are widespread in the external environment. They are found in soil, water, and in the intestines of humans and animals. They participate in the processes of decay, multiplying in waste containing organic matter.
Diseases in humans.Proteas are opportunistic microbes. They can cause purulent-inflammatory diseases in a person: wound suppuration, otitis media, peritonitis, pyelonephritis, cystitis. When eating foods containing a large amount of these bacteria, foodborne toxicity occurs. P. mirabilis causes pyo-inflammatory diseases of the urinary system. They can result from the introduction of bacteria with urological instruments. In newborns, the ingress of proteus into the umbilical wound leads to a septic process.
Laboratory diagnostics.The investigated materials are, depending on the disease, pus, urine, vomit, food. The method of sowing according to Shukevich is used. isolated pure cultures are identified by their cultural and biochemical properties and by the agglutination reaction.
Medicines.Coli-protein bacteriophage, nalidixic acid, antibiotics are used.
Yersinia
Among bacteria belonging to the genus Yersinia, diseases in humans are caused by Yersinia peslis (the causative agent of the plague), Yersinia pseudotuberculosis, and Yersinia enterocolitica.
Yersinia plague
Yersinia pestis was discovered in 1894 by A. Iersen and S. Kitazato during the plague epidemic in Hong Kong.
Morphology, cultural, biochemical properties.Y. pestis - gram-negative small ovoid rods 1-2 microns in size, motionless. They do not form a dispute, they have a capsule. In smears from pathological material, they stain with methylene blue most intensively at the ends - bipolar (Fig. 31). When breeding on solid nutrient media, they look like elongated sticks.
Optional anaerobes. They grow on simple nutrient media at a temperature of 28 ° C, can grow at lower temperatures (up to + 5 ° C), which can be used to isolate a pure culture. In liquid nutrient media, plague rods form a film on the surface and filaments extending from it, similar to stalactites, and a precipitate in the form of flakes. On a dense nutrient medium, colonies are formed that resemble a "lace scarf" - with a dense center and scalloped edges. Such R-forms of colonies form virulent strains, and S-forms - non-virulent. The characteristic cultural properties of the Yersinia plague are used for identification.
Ferments carbohydrates to form acid. Proteolytic activity is poorly expressed (Table 9).
Antigens.Plague rods contain a somatic thermostable antigen, common with other Yersinia, and also an antigen, common with erythrocytes of people of the O-group. Virulent strains have a capsular heat-labile antigen, which is associated with the immunogenicity of the pathogen.
Pathogenic factors.Plague rods form toxic substances that are contained in the body of the bacteria and in the capsule and have the properties of exo- and endotoxin. Virulence is also due to surface-located substances with antiphagocytic activity, and enzymes: hyaluronidase, fibrinolysin, hemolysins, plasmacoagulase.
Stability.They can persist for a long time in the external environment, tolerate low temperatures well, in frozen corpses, fleas - a year or more, in milk - 3 months. When boiled, they die within 1 minute. Sensitive to disinfectants. Direct sunlight kills them within 2-3 hours.
Diseases in humans.The main reservoir of the Yersinia plague in nature is rodents (ground squirrels, tarbagans, rats, etc.). Plague is a zoonotic disease. The source of infection for humans is animals and humans. Infection from animals occurs in a transmissible way - when bitten by an infected flea, by contact. In this case, the microbe penetrates the skin. From a person with pneumonic plague, the pathogen is transmitted through the air. The clinical form of plague depends on the entrance gate of the infection. The bubonic form develops with the penetration of the pathogen through the skin, followed by damage to the regional lymph nodes, which increase and turn into buboes. From here, pathogens can spread through the lymphatic or blood vessels, cause damage to other lymph nodes, lead to the development of a septic form, secondary pulmonary pneumonia.
When infected through the air, primary pneumonic plague develops. In all forms of plague, the pathological process affects all organs and systems.
Immunity.After a disease, immunity is stable.
Laboratory diagnostics.Plague is a particularly dangerous infection. Everything
researches are carried out in special controlled laboratories, trained personnel.The material for the study is the content of bubo, sputum, blood, feces, pieces of organs of deceased, animal carcasses pure culture and its identification but morphology, cultural, biochemical, antigenic properties, according to sensitivity to the plague bacteriophage According to these signs they are differentiated from other Yersinia species They put a biological sample on guinea pigs RIF is also used In materials from decayed animal corpses, it is possible to detect the plague antigen using precipitation reactions
Preventive and therapeutic drugs.Specific prophylaxis is carried out according to epidemic indications, a live plague vaccine containing the EV strain
From therapeutic agents, streptomycin, tetracyclines are effective Yersinia pseudotuberculosis
Yersmm pseudotuberculosis - the causative agent of pseudotuberculosis - discovered by L Malasse and R Vignal in 1883
Causes diseases characterized by the formation of nodules in the organs that are outwardly similar to tuberculosis. One of the forms of pseudotuberculosis observed in Vladivostok is described as "Far Eastern scarlet fever"
Morphology, cultural, biochemical properties.Gram-negative coccobacteria, do not form spores, have flagella and a capsule Facultative anaerobes, reproduce well on simple nutrient media An important property of pathogens for the epidemiology of the disease is their psychrophilicity Optimum breeding temperature 20-28 ° C, also multiply at 0 - + 4 ° C
Fermented rhamnose, urea (Table 9)
Antigens.Contains O-somatic and H-flagellar antigens Serovars and subsovars are distinguished by O- and H-antigens
Pathogenic factors.Yersinia pseudotuberculosis contains endotoxin, which is released when they die Some serovars produce exotoxins
Stability.Resistant in the external environment Being psychrophiles, they can accumulate in large quantities in stored food long time in fridge
When boiled, they die after a few seconds, are sensitive to disinfectants
Diseases in humans.Rodents are the source of infection. People are infected by the alimentary route. Transmission factors are most often vegetable dishes (salads, vinaigrettes) and dairy products.
Designations: "+" - the presence of a sign, "-" - the absence of a sign, "±" - a sign of unstable products that have not undergone heat treatment. The waterway of transmission is also important.
Pathogens enter the human body through the mouth. Having overcome the protective barrier of the stomach, they enter the small intestine, resulting in gastroenteritis. The penetration of pathogens into the mesenteric nodes leads to the development of lymphadenitis with signs of irritation of the peritoneum and the formation of an infiltrate (pseudotuberculous appendicitis). With the breakthrough of Yersinia into the blood, generalized forms appear with damage to the joints, with manifestations of scarlet fever.
Immunity.During the course of the disease, antibodies are detected, but they do not have a protective effect.
Laboratory diagnosticsdue to the wide variety of manifestations of the disease, it is critical. The material for bacteriological research is blood, feces and vomit. Cultivation of pathogens and isolation of a pure culture is carried out at the optimum temperature for them. A pure culture is differentiated from other Yersinia by biochemical properties. For serological diagnosis, paired sera taken at the beginning and in the third week of the disease are examined in the agglutination reaction and RNGA.
Medicines.Specific prophylaxis has not been developed. For treatment, chloramphenicol and other antibiotics, nitrofuran preparations are used.
When they talk about the era of great geographical discoveries, his name is remembered last. Although thanks to the efforts of this particular romantic of long voyages and a fanatical crusader warrior, Portugal began the colonial conquest of Africa, and black slaves were first brought to Europe. But the organizer of these trips in his entire life went out to sea only three times and no further than 200 miles. And yet the Portuguese prince Henry deservedly bore the proud nickname "navigator".
Infante Heinrich or Enrique, born in 1394, was the son of King João I of Portugal and Philip of Lancaster, who brought the tradition of British knighthood to the country. Enrique and his brothers were taught the seven knightly virtues - writing poetry, horseback riding, fencing, playing checkers, hunting and swimming, but most of all the young man was interested in the possession of the spear, although he did not neglect the study of natural sciences and theology. Chivalry as a military and religious service determined the entire subsequent life of Henry. At the age of 21, he initiated the capture of the Moors' fortress in northern Africa.
Only 150 miles - this was the length of the first sea voyage, the future mastermind of Portugal's sea conquests.
The king entrusted the Infant Henry with the defense of Ceuta, a new outpost of the Portuguese on the African coast. For this, part of the treasury revenues passed into the full and uncontrolled management of the prince, and after 5 years the prince became the Grand Master of the Order of the Cross.
Now huge power was concentrated in the hands of the navigator: spiritual, military and financial. And Prince Henry disposed of this power in the best way for Portugal. From freed Christian slaves, he learned about caravans that transported gold from the coast of Guinea to Muslim ports across the African desert. Mediterranean Sea... Knowledgeable in geography, the prince decided that Guinea could be reached by sea, then the treasures taken from the infidels could be taken to Lisbon. In addition, bypassing Muslim territories from the south, you can reach Christian Ethiopia and start a profitable trade with it, and then go by sea to India itself.
Scientific curiosity, supported by accurate geographical maps found in Ceuta, was also mingled with the invasive plans of the Infante. And when Henry's brother Prince Pedro brought from Venice the manuscript of the already famous traveler Marco Polo, the Infante firmly decided that the lands lie south of Ceuta.
Prince Henry began organizing sea expeditions to the northwestern shores of Africa. At the insistence of the prince, astronomy and mathematics were included in the program of the University of Lisbon in 1431. In 1438, at Cape St. Vincent in the fortress of Sagres, Prince Henry organized the Villa de Infante observatory and nautical school. Prominent scientists, astronomers, cartographers and navigators from all over Europe were invited there, and the seafaring prince participated in discussions on an equal basis with scientists. The school accepted everyone who was worthy, regardless of class, religious and ethnic differences, which was unusual for Catholic Portugal in the 15th century.
Through the efforts of the prince, the Villa de Infanta nautical school became the first scientific center in European history. The fortress still has a huge 43-meter-high wind rose - a diagram of long-term observations of the direction and strength of the wind. Inspired by the support of the prince, the captains of the Portuguese caravels discovered the island of Madeira in 1418. At the same time, the navigator began to develop new lands and soon the first settlers appeared on Madeira, and wine began to be delivered to the Metropolis - a rare quality even for wine-making Portugal.
Then, for decades, Henry stubbornly outfitted sea expeditions to the Canary Islands, but the captains could not pass the underwater rocks at Cape Bohador. Sailing ships received holes on the unfortunate cape, where, as it was believed at that time, dragons were found, and they sank.
But in 1434, having rounded it from the side of the open ocean, one of the captains opened the way to West Africa, and Henry received honorary title "navigator".
But why did Heinrich the Navigator never go on long sea expeditions himself?
It was believed that the prince was afraid of pirates or that he considered it offensive for a person of royal blood to be among the sailors, but most likely the prince considered it his main business to analyze the reports of captains, separate truth from fiction and equip new sea \u200b\u200btravel... The romantic of distant wanderings Heinrich the Navigator deliberately closed the sea for himself.
Heinrich the Navigator has never been married. Restrained and gloomy, he considered himself guilty of the death of his younger brother Ferdinand, who was captured by the Moors during their unsuccessful naval expedition to Tangier in 1437.
Heinrich spent his last years in Sagrish, surrounded by the students of his nautical school. Two years before his death, he briefly went to sea for the third time.
Heinrich the Navigator died on November 13, 1460.
His work was continued by the famous Portuguese sailors Bartolomeo Dias, Vasco da Gamma and the greatest of the followers of the Infante - Fernand Magellan. They owe their achievements to the Portuguese Prince Heinrich the Navigator - the man on the coat of arms, which was inscribed: "Talent for good deeds."
HEINRICH THE SEAFARER(1394-1460), correctly Enrique (Dom Enrique o Navigator), Portuguese prince, nicknamed the Navigator. For 40 years, he equipped and sent numerous naval expeditions to explore the Atlantic coast of Africa, creating the prerequisites for the formation of a powerful colonial empire of Portugal. Born March 4, 1394 in Porto. Third son of King Joan I (founder of the Aviz dynasty) and his wife Philip of Lancaster (daughter of John of Gaunt).
In 1415, Prince Henry, together with his father, took part in a military campaign, as a result of which the Moors' fortress of Ceuta, located on the African coast of Gibraltar, was taken. There he learned that caravans laden with gold, following from the valley of the Niger River, crossed the Sahara, but decided that Portugal should look for sea routes to the gold-bearing lands of Guinea. Thus was the beginning (since 1416) of a long and well-organized campaign of sea expeditions. The ships moved along the African continent and returned to Portugal, using a wide belt of tailwinds and coastal currents. One of the results of these expeditions was the discovery of Madeira (1418-1419) and the Azores (1427-1431).
Madeira Island, located 900 km southwest of Portugal, became the first Portuguese colony. Sugarcane and vineyards were cultivated on his lands.
The exploration of Africa itself was fraught with great difficulties, for example, Cape Bohador in the south of the Canary Islands posed a huge danger to navigation. But the southern route to the tropical lands of Africa was finally opened - in 1434 Gilles Ianish rounded the cape.
Henry was strongly influenced by his brother Prince Pedro, the king's second son. In 1418-1428 he visited many of the royal courts of Europe. Later, Pedro arrived in Venice, where he watched with interest the trade of the Venetians with the Eastern countries and where he was presented with a manuscript Books Marco Polo . After reviewing the manuscript, Henry invited the captains of his ships to collect information about the sea route to India, as well as about the African Christian country of Ethiopia. He hoped to reach this land by bypassing Muslim countries from the southeast. Brother Pedro supported him in this.
After the second campaign in Ceuta (1418), Henry established his residence in the Algarve, the southernmost province of Portugal, where the reliable bay of Lagos was located. In 1443, Henry received at his disposal Sagres, the southwestern point of Portugal at Cape San Vicente, or, as it was then called, "Sacred Cape". There, at the expense of the Portuguese spiritual-knightly order of Christ, of which he was the head, the prince founded an observatory and a nautical school. Called Villa do Infante, it became a center of attraction for prominent scientists, cartographers and astronomers of the time.
Henry's life was a chain of personal tragedies. In 1437, together with his younger brother Ferdinand, he participated in an unsuccessful expedition to Tangier; Ferdinand was taken prisoner by the Moors and imprisoned, where he died, since Henry could not ransom him. After that, in 1438, his elder brother, King Duarte, died. The middle brother Pedro became regent, but, having begun a struggle with the pretender to the throne, Alfonso V, he was killed at Alfarrobeira in 1449.
All these events led to the fact that the expeditions were organized by Henry sporadically, and long intervals appeared in their schedule. Nevertheless, in 1444 Henry's captains discovered the Senegal River, two years later they reached the Geba River in Sierra Leone. During the life of Henry, the Portuguese could not advance south of this point. In 1455 and 1456, the Venetian Alvise da Cadamosto, the most famous of Henry's skippers, sailed up the Gambia River in Gambia, and the next year discovered the coast of the Cape Verde Islands. At this time, a mass trade in African slaves began, the center of which was located in Argena, near the Cape of Cabo Blanco. Henry encouraged the slave trade, and considered the act of baptizing slaves as a way to save their souls. The prince's expeditions began to generate income, and in the eyes of the Portuguese nobles and merchants, Henry became a national hero.
Heinrich spent his last years in almost complete seclusion in Sagrish, surrounded only by members of his "university", although in 1458 he accompanied a successful expedition to Tangier and further south to Arquila. Then he returned to Sagrish on the "Sacred Cape", where he died on November 13, 1460.