Salmonellosis
Salmonellosis– an acute infectious disease of humans and animals with a predominant lesion of the gastrointestinal tract (generalized forms are less commonly observed). The main lesions caused by salmonella are conventionally divided into 3 groups: typhoid fever and paratyphoid fever, gastroenteritis and septicemia. Most commonly, the term salschonemesis is applied to gastroenteritis caused by these bacteria. The frequency is 800 cases: 100,000 population per year. The frequency peak is in July-November. Isolation of Salmonella occurs only in 1-10% of cases. The secondary root cause of bacterial diarrhea is campylobacteriosis. Every year, an average of 55 outbreaks of salmonella infection are recorded, in Russia – 60-80:100,000. The frequency among babies is 130:100,000, among adults – 6:100,000. The frequency is higher in people older than 70 and younger than 20 years. The highest frequency in babies under 1 year old. Etiology. The causative agents are Gram-negative motile bacteria of the Salmonella genus of the Enterobacteriaceae family. The main pathogen is Salmonella enterica, subspecies typhimurium, heidelbergii, enterica, derby. Epidemiology. Diseases are ubiquitous, the natural reservoir of most pathogens is man and all kinds of animals (including reptiles, amphibians, fish and birds). The main routes of transmission are contaminated food and water (contact is less common). Salmonella remain viable in the external environment for a long time: in the water of open reservoirs and drinking water they live 11-120 days, in sea water – 15-27 days, in the soil – 1-9 months, in room dust – 80-547 days, in sausages products – 60-130 days, in frozen meat – 6-13 months, in eggs – up to 13 months, in egg powder – up to 9 months. on frozen vegetables and fruits – 0.5-2.5 months. Salmonella typhimurium is the most resistant, remaining viable on tissues and on paper for up to a year. Clarified 0.3% solution of bleach at 30 minutes of exposure kills salmonella in an hour. Chlorination of wastewater reduces their contamination with salmonella by 6 times. Pathogenesis. Salmonella are not able to independently penetrate into the epithelial cells of the gastrointestinal tract, but enter them through endocytosis. Bacteria are poorly adapted to reproduction in the epithelium and, reaching the basement membrane, penetrate into the lamina propria of the mucous membrane. From here they penetrate into the bloodstream (can be isolated on blood culture), but most Salmonella do not cause clinical manifestations of bacteremia, because rapidly eliminated by phagocytes. The exception is Salmonella typhimurium and Salmonella enterica, which can cause septicemia. The risk of developing bacteremia is significantly increased in individuals with impaired activity of mononuclear phagocytes, for example, in individuals with sickle cell anemia and HIV infection. A significant part of the mechanisms that cause the development of gastroenteritis remains poorly understood. The pathogen penetrates into the lamina propria of the mucous membrane, multiplies there and causes the development of a local inflammatory reaction and the influx of fluid into the lesion. Presumably, the manifestations of the diarrheal syndrome are due to the production of enterotoxins that increase the level of cyclic adenosine monophosphates, activate the synthesis of prostaglandins, or disrupt protein synthesis (similar to Shigella toxins). remains poorly understood. The pathogen penetrates into the lamina propria of the mucous membrane, multiplies there and causes the development of a local inflammatory reaction and the influx of fluid into the lesion. Presumably, the manifestations of the diarrheal syndrome are due to the production of enterotoxins that increase the level of cyclic adenosine monophosphates, activate the synthesis of prostaglandins, or disrupt protein synthesis (similar to Shigella toxins). remains poorly understood. The pathogen penetrates into the lamina propria of the mucous membrane, multiplies there and causes the development of a local inflammatory reaction and the influx of fluid into the lesion. Presumably, the manifestations of the diarrheal syndrome are due to the production of enterotoxins that increase the level of cyclic adenosine monophosphates, activate the synthesis of prostaglandins, or disrupt protein synthesis (similar to Shigella toxins).
Clinical picture and classification
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- Gastrointestinal form. The incubation period varies from 2-6 hours to 2-3 days (approximately 7-24 hours). The onset of the disease is acute: body temperature rises, chills, dyspeptic disorders (repeated repeated vomiting, copious watery loose stools, abdominal pain) are detected. In the initial period of the disease, symptoms of intoxication (weakness, headache, chills, etc.) come to the fore, symptoms of gastrointestinal damage are recorded much less frequently. In the gastrointestinal form of salmonellosis, all parts of the gastrointestinal tract are involved in the pathological process. At the height of the disease, nausea, vomiting, loss of appetite are observed in all patients; in most patients, these manifestations are accompanied by diarrhea. Vomiting during the first day is repeated. The frequency of stool does not exceed 10-15 r / day. Most often, profuse watery stools with an admixture of mucus are noted. A constant symptom is abdominal pain (found in the first hours of the disease) and its soreness on palpation; pains can be spilled or, with severe vomiting, localized in the epigastric and navel areas. With lesions of the colon, pain can take on a cramping character and move to the lower half of the abdomen. In some patients, the pain is cramp-like and associated with the act of defecation. The stool most often remains watery or mushy, but it may contain an admixture of mucus or even blood. On palpation of the abdomen, pain is determined throughout the abdomen, spasm and increased susceptibility of the sigmoid colon, an enlarged rumbling caecum. It is not often that pain is detected on palpation of the epigastric region. The cause of the development of acute functional renal failure may be a violation of the blood circulation of the kidneys along with changes in the water and electrolyte balance. The greatest deviations are noted in the development of infectious-toxic shock. Dehydration, electrolyte imbalance, impaired microcirculation, and hormonal changes lead to the development of acid-base imbalances up to metabolic acidosis. In the peripheral blood, moderate leukocytosis is noted with a sharp shift to the left already in the first hours of the disease with the appearance of young forms, up to myelocytes. Sometimes aneosinophilia and toxic granularity of neutrophils are detected. electrolyte imbalance, impaired microcirculation, and hormonal changes cause the development of acid-base balance disorders up to metabolic acidosis. In the peripheral blood, moderate leukocytosis is noted with a sharp shift to the left already in the first hours of the disease with the appearance of young forms, up to myelocytes. Sometimes aneosinophilia and toxic granularity of neutrophils are detected. electrolyte imbalance, impaired microcirculation, and hormonal changes cause the development of acid-base balance disorders up to metabolic acidosis. In the peripheral blood, moderate leukocytosis is noted with a sharp shift to the left already in the first hours of the disease with the appearance of young forms, up to myelocytes. Sometimes aneosinophilia and toxic granularity of neutrophils are detected.
- Generalized form
- The typhoid-like variant resembles typhoid fever and paratyphoid fever. Lethargy, enlargement of the liver and spleen, pallor of the skin and injection of the sclera are noted, in the aftermath sometimes subicteric. A roseolous rash may appear on the skin of the chest and abdomen
- The septicopyemic variant is essentially Salmonella sepsis
- Clinical picture in children and the elderly. Typhoid-like and septicopyemic variants in children are recorded more often, the incubation period is traditionally shorter, catarrhal phenomena are more often noted, changes in the cardiovascular system are less pronounced, exanthemas, enlargement of the liver and spleen are more often detected. Severe forms are much more often noted in young children. The disease in babies drags on for longer periods, recovery begins more slowly; more often than in adults, a relapsing course of the disease is noted. In the elderly, intoxication is traditionally more pronounced, repeated vomiting is more often observed, normalization of the stool begins later, changes in the cardiovascular system and an increase in the liver and spleen are more pronounced, bacteriocarrier is more often formed and complications develop.
- Bacteriocarrier is considered as a subclinical form of salmonellosis
- Acute carrier. The period of bacteria isolation varies from 15 days to 3 months. Longer isolation (more than 3 months) is regarded as chronic carriage
- Transient carrier. Characterized by the absence of clinical symptoms of the disease both at the time of the examination and in the previous 3 months. One-two-fold isolation of the pathogen with three consecutive negative results of bacteriological examination of feces and urine, negative results of serological examination in dynamics.
Diagnosis
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- bacteriological research. Materials for research: feces, vomit, gastric lavage, blood, urine. They also examine the remnants of food consumed by the sick, the original products and semi-finished products used for its preparation; daily samples of prepared food, animal feed, swabs from various equipment and other items suspected as a pathogen transmission factor. The optimal period for bacteriological studies in gastrointestinal forms of salmonellosis of the disease is the first days; with generalized forms – at the end of the second or beginning of the 30% week. The number of positive results increases significantly with the increase in the frequency of examination. Positive results are most likely to be obtained with a stool test.
- RPHA with a cysteine test, which allows differential determination of AT titers of the IgG class.
Differential Diagnosis
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- Viral gastroenteritis
- Other bacterial gastroenteritis (dysentery, cholera, etc.)
- Sepsis (meningococcal, staphylococcal)
- Appendicitis
- Cholecystitis
- Intestinal perforation.
Treatment:
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- The sparing diet
- First of all, the stomach is washed with a solution of sodium bicarbonate or a weak solution of potassium permanganate
- Rehydration therapy
- Salt solutions (for example, Regidron) inside
- With infectious-toxic shock, IV degree dehydration, III degree dehydration with unstable hemodynamics, indomitable vomiting, fluid loss with vomiting and diarrhea above 1 l / h; oligoanuria, diabetes mellitus and impaired glucose absorption – saline solutions (for example, Disol, Trisol) in / in
- For detoxification (with non-cardinal dehydration or after its elimination), along with salt solutions, synthetic colloidal solutions can be prescribed.
- Antibiotic therapy is not indicated for uncomplicated forms
- For children of the first year of life, elderly patients, with immunosuppressive conditions, with generalized infection – orally for 3-7 days (with immunosuppressive conditions, with generalized infection – longer) ampicillin 500 mg every 4-6 hours (children of the first year of life -50-100 mg / kg / day in 3 doses) amoxicillin 0.5-1 g 3 r / day (for children of the first year of life – 20 mg / kg / day in 3 doses), ciprofloxacin 500 mg orally after 12 hours (for adults)
- In case of bacteriocarrier in some cases (for example, in people working in food blocks, medical personnel), ciprofloxacin 500 mg orally after 12 hours for a month (until a negative result of bacteriological examination) can be prescribed.
Complications
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- dehydration shock
- Infectious-toxic shock.
Prevention. It is necessary to comply with hygienic requirements in the production, transportation and storage of food products. Avoid contact with animal feces, keep cages, bedding, etc. clean. Thorough hand washing.