The main toxic component of streptococcus is. Streptococci, classification

  • The date: 03.03.2020

Streptococcus is a genus of coccal (spherical) Gram-positive bacteria belonging to the type Firmicutes and Lactobacillales(lactic acid bacteria). Cell division in these bacteria occurs along one axis. Therefore, they grow in chains or pairs, hence the name: from the Greek "streptos", that is, easily bent or twisted like a chain (twisted chain).

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In this they differ from staphylococci, which divide along several axes and form clusters of cells similar to grape brushes. Most streptococci are oxidase- and catalase-negative, and many are facultative anaerobes.

In 1984, many organisms that were previously considered streptococci were isolated in the genus Enterococcus and Lactococcus. More than 50 species are currently recognized in this genus.

Classification and pathogenesis of streptococci

In addition to streptococcal pharyngitis (sore throat), certain types of streptococci are responsible for many cases of conjunctivitis, meningitis, endocarditis, bacterial pneumonia, erysipelas, and necrotizing fasciitis ("flesh-eating" bacterial infections). However, many streptococcal species are not pathogenic but form part of the symbiotic microbiome of the human mouth, gut, skin, and upper respiratory tract. In addition, streptococci are a necessary ingredient in the production of Emmental cheese ("Swiss").

Classification Streptococcus carried out on the basis of their hemolytic characteristics - alpha-hemolytic and beta-hemolytic.

For medicine, the most important are the group of alpha-hemolytic organisms S. pneumoniae and Streptococcus viridans, and beta-hemolytic streptococci from Lancefield groups A and B.

Alpha hemolytic

Alpha hemolytic species cause the oxidation of iron in the hemoglobin molecules in red blood cells, which gives it greenish color on blood agar. Beta-hemolytic species cause complete rupture of red blood cells. On blood agar, this appears as wide areas without blood cells surrounding bacterial colonies. Gamma hemolytic species do not cause hemolysis.

pneumococci

S. pneumoniae(sometimes called pneumococcus) is the leading cause of bacterial pneumonia and sometimes the etiology of otitis media, meningitis, sinusitis, and peritonitis. Inflammation is considered to be the main cause of how pneumococci cause disease, so it is taken into account, as a rule, in the diagnoses associated with them.

viridans

Streptococci viridans are a large group of symbiotic bacteria that are either α-hemolytic, giving a green color on blood agar plates (hence their name "virindans", i.e. "green" from the Latin "vĭrĭdis"), or non-hemolytic. They do not possess Lancefield antigens.

Medically important streptococci

Beta hemolytic

Beta-hemolytic streptococci are characterized by Lancefield serotyping, which is described as the presence of specific carbohydrates on the bacterial cell walls. The 20 described serotypes are divided into Lancefield groups with letters of the Latin alphabet from A to V (except I and J) in the name.

Group A

S. pyogenes, also known as group A (GAS), are the causative agents of a wide range of streptococcal infections. These infections can be non-invasive or invasive. In general, non-invasive infections are more common and less severe. The most common infections include impetigo and streptococcal pharyngitis (sore throat). Scarlet fever is also a non-invasive infection, but has been less common in recent years.

Invasive infections caused by group A β-hemolytic streptococcus are less common but more severe. This occurs when the microorganism is able to infect areas where it is not normally found, such as in the blood and organs. Potential illnesses include streptococcal toxic shock syndrome, pneumonia, necrotizing fasciitis and bacteremia.

GAS infections can cause additional complications, namely acute rheumatic fever and acute glomerulonephritis. Rheumatism, a disease that affects the joints, heart valves, and kidneys, is the result of an untreated streptococcal GAS infection not caused by the bacterium itself. Rheumatism is caused by antibodies made by the immune system to fight infection that cross-react with other proteins in the body. This "cross-reaction" essentially causes the body to attack itself and result in damage. Globally, GAS infections are estimated to cause over 500,000 deaths each year, which is why it is one of the leading pathogens in the world. Group A streptococcal infections are usually diagnosed with a rapid strep or culture test.

Group B

S. agalactiae or group B streptococci, GBS, cause pneumonia and meningitis in neonates and the elderly, with rare systemic bacteremia. They can also colonize the intestines and the female reproductive tract, increasing the risk of premature rupture of membranes during pregnancy and transmission of pathogens to the newborn. According to the recommendations of the American College of Obstetricians and Gynecologists, the American Academy of Pediatrics and the US Centers for Disease Control and Prevention, all pregnant women at 35-37 weeks of gestation should be tested for GBS infections. Women who test positive should be treated with antibiotics at the time of delivery, which will usually prevent transmission of the virus to the baby.

The United Kingdom decided to adopt a risk factor based protocol rather than a culture based protocol as in the US. According to current recommendations, if one or more of the following risk factors are present, then women should be treated with antibiotics at birth:

  • Birth before term<37 недель)
  • Prolonged membrane rupture (>18 hours)
  • Intrapartum fever (>38° C)
  • Previously affected infant with GBS infection
  • GBS - bacteriuria during pregnancy

The result of this protocol was the treatment of 15-20% of pregnancies, as well as the prevention of 65-70% of cases of early onset GBS sepsis.

Group C

This group includes S. equi, causing suffocation in horses, and S. zooepidemicus. S. equi is a clonal descendant or biovariant of ancestors S. zooepidemicus, which is the cause of infection in some mammalian species, including the large cattle and horses. Besides, S. dysgalactiae belongs to group C, it is a β-hemolytic streptococcus, which is a potential cause of pharyngitis and other purulent infections, similar to group A streptococci.

Group D (enterococci)

Many group D streptococci have been reclassified and moved to the genus Enterococcus(including E. faecium, E. faecalis, E. avium and E. durans). For example, Streptococcus faecalis is now Enterococcus faecalis.

Other non-enterococcal group D strains include Streptococcus equinus and Streptococcus bovis.

Non-hemolytic streptococci rarely cause disease. However, beta-hemolytic streptococcus and Listeria monocytogenes(actually a gram-positive bacillus) should not be confused with non-hemolytic streptococci.

Group F

In 1934, Long and Bliss described organisms in group F as being among the "tiniest hemolytic streptococci". In addition, they are known as Streptococcus anginosus(according to the Lancefield classification system) or as members of a group S. milleri(according to the European system).

Group G

Usually (not exclusively) these streptococci are beta-hemolytic. S. canis considered an example of GGS organisms typically found in animals, but potentially causing infection in people.

Group H

These streptococci are the causative agents of infection in medium-sized dogs. In rare cases, they cause illness in humans if they do not come into direct contact with the animal's mouth. One of the most common ways it is transmitted is through human-to-animal contact and mouth-to-mouth contact. However, a dog can lick a person's hand and the infection can also spread.

Video about streptococcus

Molecular taxonomy and phylogenetics

The division of streptococci into six groups is based on their 16S rDNA sequences:. S. mitis, S. anginosus, S. mutans, S. bovis, S. pyogenes and S. salivarius. The 16S groups were confirmed by whole genome sequencing. Important pathogens S. pneumoniae and S. pyogenes belong to groups S. mitis and S. pyogenes, respectively. But the causative agent of caries, Streptococcus mutans, is the main one for the streptococcal group.

Genomics

The genome sequences of hundreds of species have been determined. Most streptococcal genomes are 1.8 to 2.3 Mb in size and are responsible for 1700-2300 proteins. The table below lists some important genomes. 4 types indicated in the table ( S. pyogenes, S. agalactiae, S. pneumoniae and S. mutans) have an average pairwise protein sequence identity of approximately 70%.

Property

S. agalactiae

S. mutans

S. pyogenes

S. pneumoniae

base pairs

Open reading frames


Streptococcus is one of those pathogenic microbes that are normally found in the microflora of any person. The bacterium lives on the mucous membrane of the nose and pharynx, in the respiratory tract, large intestine and genitourinary organs, and for the time being does not cause any harm to its host. Streptococcal infections occur only in conditions of weakened immunity, hypothermia, or when a large number of an unfamiliar strain of pathogens enters the body at once.

Not all varieties of streptococci are dangerous to human health, moreover, in this group there are even microbes that are beneficial. The very fact of bacterial carriage should not become a cause for alarm, because it is almost impossible to avoid it, just as it is impossible to completely eradicate streptococcus from your body. And strong immunity and observance of elementary rules of personal hygiene give every reason to expect that the disease will bypass you.

However, everyone is concerned about what to do if you or your loved ones do get sick: what medications to take, and what complications to worry about. Today we will tell you absolutely everything about streptococcus and the diseases that it causes, as well as methods for diagnosing and treating streptococcal infections.

What is streptococcus?

Scientifically, streptococcus is a member of the Streptococcaceae family, a spherical or ovoid asporogenic Gram-positive facultative anaerobic bacterium. Let's understand these complex terms and "translate" them into simple human language: streptococci have the shape of a regular or slightly elongated ball, do not form spores, do not have flagella, are not able to move, but they can live in conditions of complete absence of oxygen.

If you look at streptococci through a microscope, you can see that they never occur alone - only in pairs or in the form of regular chains. In nature, these bacteria are very widespread: they are found in the soil, and on the surface of plants, and on the body of animals and humans. Streptococci are very resistant to heat and freezing, and even lying in roadside dust, they retain the ability to reproduce for years. However, they are easily defeated with penicillin antibiotics, macrolides or sulfonamides.

In order for a streptococcal colony to begin to actively develop, it needs a nutrient medium in the form of serum, sweet solution or blood. In laboratories, bacteria are artificially created favorable conditions in order to observe how they multiply, ferment carbohydrates, release acid and toxins. A colony of streptococci forms a translucent or greenish film on the surface of a liquid or solid nutrient material. her research chemical composition and properties allowed scientists to determine the pathogenicity factors of streptococcus and to establish the causes of the development of streptococcal infections in humans.

Causes of Streptococcal Infections


The cause of almost all streptococcal infections is beta-hemolytic streptococcus, since it is it that is capable of destroying red blood cells- erythrocytes. In the process of life, streptococci secrete a number of toxins and poisons that have a detrimental effect on the human body. This explains unpleasant symptoms diseases caused by streptococcus: pain, fever, weakness, nausea.

Streptococcus pathogenicity factors are as follows:

    Streptolysin is the main poison that violates the integrity of blood and heart cells;

    Scarlatinal erythrogenin- a toxin, due to which the capillaries expand, and a skin rash occurs when;

    Leukocidin - an enzyme that destroys immune blood cells - leukocytes, and thereby suppresses our natural defense against infections;

    Necrotoxin and lethal toxin- poisons that cause tissue necrosis;

    Hyaluronidase, amylase, streptokinase and proteinase- enzymes with the help of which streptococci devour healthy tissues and spread throughout the body.

At the site of introduction and growth of a colony of streptococci, a focus of inflammation occurs, which worries a person with severe pain and swelling. As the disease develops, toxins and poisons secreted by bacteria are carried through the bloodstream throughout the body, so streptococcal infections are always accompanied by general malaise, and in severe cases, large-scale intoxication, up to vomiting, dehydration and clouding of consciousness. lymphatic system reacts to the disease by engorgement of the lymph nodes located near the focus of inflammation.

Since the streptococci themselves and their metabolic products are foreign to our body, the immune system reacts to them as a powerful allergen and tries to develop antibodies. The most dangerous consequence of this process is autoimmune disease, when our body ceases to recognize streptococcus-altered tissues and begins to attack them. Examples of formidable complications: glomerulonephritis, (endocarditis,).

Streptococcus groups

Streptococci are divided into three groups according to the type of hemolysis of red blood cells:

    Alpha hemolytic or green - Streptococcus viridans, Streptococcus pneumoniae;

    Beta hemolytic- Streptococcus pyogenes;

    Non-hemolytic- Streptococcus anhaemolyticus.

For medicine, it is streptococci of the second type, beta-hemolytic, that matter:

    Streptococcus pyogenes - the so-called pyogenic streptococci, which cause scarlet fever in adults and children, and give serious complications in the form of glomerulonephritis and endocarditis;

    Streptococcus pneumoniae - pneumococci, which are the main culprits and;

    Streptococcus faecalis and Streptococcus faecies- enterococci, the most tenacious bacteria of this family, causing purulent inflammation in abdominal cavity and heart;

    Streptococcus agalactiae - the bacteria responsible for most streptococcal lesions urinary organs and postnatal inflammation of the uterine endometrium in parturients.

As for the first and third types of streptococci, green and non-hemolytic, they are simply saprophytic bacteria that feed on humans, but almost never cause serious diseases, because they do not have the ability to destroy red blood cells.

To be fair, it is worth mentioning beneficial bacteria from this family - lactic acid streptococcus. With its help, everyone's favorite dairy products are made at dairies: kefir, curdled milk, fermented baked milk, sour cream. The same microbe helps people with lactase deficiency - this is a rare disease, expressed in a deficiency of lactase - an enzyme necessary for the absorption of lactose, that is, milk sugar. Sometimes thermophilic streptococcus is given to infants to prevent severe regurgitation.

Streptococcus in adults


Pharyngitis

The general practitioner at the reception quickly diagnoses pharyngitis using a visual examination of the pharynx: the mucous membrane is edematous, bright red, covered grayish bloom, swollen tonsils, in some places scarlet follicles in the form of a donut are visible. Streptococcal pharyngitis is almost always combined with, moreover, the mucus is transparent and so abundant that it can cause maceration (soaking) of the skin under the nose. The patient is prescribed local antiseptics for the throat in the form of a spray or lozenges, there is no need to take antibiotics inside.

Usually this disease goes away as suddenly as it started, and does not last long - 3-6 days. Victims of pharyngitis are mostly young, or vice versa, elderly people with weakened immune systems who have been in contact with a sick person, used his dishes or a toothbrush. Although pharyngitis is considered a widespread and non-serious disease, it can lead to very unpleasant complications.

The consequences of pharyngitis can be:

Angina

Streptococcal angina (acute) can turn into a real disaster for an adult patient, especially an elderly one, because untimely and poor-quality treatment of this disease often causes terrible complications in the heart, kidneys and joints.

Factors contributing to the development of acute streptococcal tonsillitis:

    Weakening of general and local immunity;

    hypothermia;

    Recent other bacterial or viral infection;

    Negative impact of external factors;

    Prolonged contact with a sick person and his household items.

Angina begins as suddenly as pharyngitis - the night before, it becomes painful for the patient to swallow, and the next morning the throat is completely covered by the infection. Toxins are carried through the bloodstream throughout the body, causing swollen lymph nodes, high fever, chills, weakness, restlessness, and sometimes confusion and even convulsions.

Symptoms of angina:

    severe sore throat;

    Febrile temperature;

    Submandibular lymphadenitis;

    Swelling and redness of the mucous membrane of the pharynx;

    Enlarged tonsils;

    The appearance on the mucous throat of a loose grayish or yellowish coating, and sometimes purulent plugs;

    In young children - dyspeptic disorders (, nausea,);

    In blood tests, severe leukocytosis, C-reactive protein, ESR acceleration.

Streptococcal angina has two types of complications:

    Purulent - otitis, sinusitis, flux;

    Non-purulent - rheumatism, glomerulonephritis, syndrome, myocarditis, endocarditis, pericarditis.

Angina is treated with local antiseptics, but if inflammation cannot be stopped within 3-5 days, and the body is engulfed in total intoxication, antibiotics have to be resorted to to prevent complications.

Streptococcus in children


Streptococci are very dangerous for newborn babies: if intrauterine infection occurs, the child is born with high temperature, subcutaneous bruises, spotting from the mouth, shortness of breath, and sometimes with inflammation of the meninges. In spite of high level development of modern perinatal medicine, it is not always possible to save such children.

All streptococcal infections in children are conditionally divided into two groups:

    Primary - tonsillitis, scarlet fever, otitis media, pharyngitis, laryngitis,;

    Secondary - rheumatoid arthritis, vasculitis, glomerulonephritis, endocarditis, sepsis.

The undisputed leaders in the incidence in children are tonsillitis and scarlet fever. Some parents consider these diseases to be completely different, and some, on the contrary, confuse them with each other. In fact, scarlet fever is a severe form of streptococcal tonsillitis, accompanied by a skin rash.

Scarlet fever

The disease is highly contagious and spreads among children preschool institutions and schools at the speed of wildfire. Scarlet fever usually affects children between the ages of two and ten, and only once, since a strong immunity is formed to the disease. It is important to understand that the cause of scarlet fever is not streptococcus itself, but its erythrogenic toxin, which causes severe poisoning of the body up to clouding of consciousness and a red rash, by which a pediatrician can accurately distinguish scarlet fever from ordinary tonsillitis.

It is customary to distinguish three forms of scarlet fever:

    Light - the disease lasts 3-5 days and is not accompanied by large-scale intoxication;

    Medium - lasts a week, is characterized by severe poisoning of the body and a large area of ​​\u200b\u200brashes;

    Severe - can drag on for several weeks and go into one of pathological forms: toxic or septic. Toxic scarlet fever is manifested by loss of consciousness, dehydration and, and septic - by severe lymphadenitis and necrotic tonsillitis.

Scarlet fever, like all streptococcal infections, has a short incubation period and strikes the child suddenly, and lasts an average of 10 days.

Scarlet fever symptoms:

    General weakness, lethargy, drowsiness;

    nausea, diarrhea, vomiting, dehydration, loss of appetite;

    Characteristic puffy face and unhealthy luster of the conjunctiva;

    Very strong increase and soreness of the submandibular lymph nodes, up to the inability to open the mouth and swallow food;

    Redness of the skin and the appearance of small roseola or papules on them, first on the upper part of the body, and after a few days on the limbs. It looks like goosebumps, and on the cheeks the eruption merges and forms a scarlet crust;

    Paleness of the nasolabial triangle in combination with cherry lips;

    Coating of the tongue with a gray coating, which disappears after three days, starting from the tip, and the whole surface becomes scarlet with protruding papillae. The tongue resembles a raspberry in appearance;

    Pastia's syndrome - the accumulation of a rash in the folds of the skin and a strong court;

    Clouding of consciousness up to fainting, less often - delirium, hallucinations and convulsions.

Painful symptoms increase during the first three days from the onset of the disease, and then gradually subside. The number and severity of the rash decreases, the skin becomes whitish and dry, sometimes in a child on the palms and feet it comes off in whole layers. The body produces antibodies to erythrotoxin, so if children who have had scarlet fever again encounter the pathogen, this only leads to a sore throat.

Scarlet fever is very dangerous for its complications:, inflammation of the heart muscle, chronic lymphadenitis.

The moderate and severe forms of this disease require adequate and timely antibiotic therapy, as well as careful child care and follow-up measures to strengthen his immunity, for example, rest in a sanatorium and a course of multivitamins.

Streptococcus in pregnant women


One of the reasons why expectant mothers should be very scrupulous in matters of personal hygiene is streptococcus and staphylococcus aureus, which can easily enter the genital tract with improper wiping, prolonged wearing of underwear, the use of non-sterile intimate hygiene products, touching the genitals with dirty hands and unprotected sexual intercourse. Of course, streptococcus is normally present in the microflora of the vagina, but the body of a pregnant woman is weakened, and natural defense mechanisms may not be enough to contain the infection.

Highest value in the development of pathology of pregnancy have the following streptococci:

    Streptococcus pyogenes causes tonsillitis, pyoderma, cystitis, endometritis, glomerulonephritis, postpartum, as well as intrauterine infection of the fetus with all the ensuing consequences;

    Streptococcus agalactiae can also cause endometritis and inflammatory diseases of the genitourinary organs in the mother, and cause sepsis, pneumonia and neurological disorders in the newborn.

If a dangerous concentration of streptococci is found in a smear in a pregnant woman, local sanitation is carried out using antibacterial suppositories. And with full-blown streptococcal infections, such as tonsillitis, the situation is much worse, since most antibiotics, to which streptococcus is sensitive, are strictly contraindicated during pregnancy. The conclusion is banal: expectant mothers need to carefully protect their health.

Complications and consequences of streptococcus

Streptococcal infections can cause the following complications:

    Purulent otitis media;

    Rheumatoid arthritis;

    Chronic lymphadenitis;

    Inflammation of the heart membranes - endocarditis, myocarditis, pericarditis;

    Concomitant viral and anaerobic infections: SARS,;

    Sexually transmitted infection.

If there are very few streptococci in the smear, and on the contrary, there are a lot of Doderlein sticks, then we are talking about the first option. If there are more streptococci than Doderlein sticks, but the number of leukocytes in the field of view does not exceed 50 pieces, we are talking about the second option, that is, vaginal dysbacteriosis. Well, if there are a lot of leukocytes, then a diagnosis of "bacterial vaginosis" is made, which is specified depending on the type of the main pathogen. It can be not only streptococcus, but also staphylococcus, gerdnerella (gardnerellosis), trichomonas (), candida (), mycoplasma (mycoplasmosis), (), chlamydia () and many other microorganisms.

Thus, the treatment of streptococcus in the vagina, as well as the eradication of any other pathogen, is carried out only if its amount in the smear is disproportionately large and is accompanied by severe leukocytosis. All such sexual infections have very vivid symptoms, and a smear examination is necessary in order to determine the culprit and select the appropriate antibiotic.

Streptococcus treatment


The treatment of streptococcal infections is carried out by the specialist in whose area of ​​​​responsibility the focus of inflammation is located: colds are treated by a therapist, scarlet fever - by a pediatrician, dermatitis and erysipelas - by a dermatologist, urinary infections– gynecologist and urologist, and so on. In most cases, the patient is prescribed antibiotics from the group of semi-synthetic penicillins, but if they are allergic, they resort to macrolides, cephalosporins or lincosamides.

The following antibiotics are used to treat streptococcal infections:

    Benzylpenicillin- injection, 4-6 times a day;

    Phenoxymethylpenicillin- adults 750 mg, and children 375 mg twice a day;

    Amoxicillin (Flemoxin Solutab) and Augmentin (Amoxiclav) - in the same dosage;

    Azithromycin (Sumamed, Azitral) - adults 500 mg once on the first day, then 250 mg every day, for children the dosage is calculated based on 12 mg per kg of weight;

    Cefuroxime - 30 mg injection per kg body weight twice a day, orally 250-500 mg twice a day;

    Ceftazidime (Fortum) - injection once a day, 100 - 150 mg for each kg of weight;

    Ceftriaxone - injection once a day, 20 - 80 mg per kg of weight;

    Cefotaxime - injectable once a day, 50-100 mg per kg of body weight, only in the absence of effect from other antibiotics;

    Cefixime (Supraks) - orally 400 mg once a day;

    Josamycin - orally once a day, 40-50 mg per kg of body weight;

    Midecamycin (Macropen) - orally once a day, 40-50 mg for each kg of weight;

    Clarithromycin - orally once a day, 6-8 mg per kg of body weight;

    Roxithromycin - orally 6-8 mg per kg of body weight;

    Spiramycin (Rovamycin) - orally twice a day, 100 units for each kg of weight;

    Erythromycin - orally four times a day, 50 mg per kg of body weight.

Standard course of treatment streptococcal infection takes 7-10 days. It is very important not to stop taking the drug immediately after feeling better, to avoid skipping and not to change the dosage. All this causes multiple relapses of the disease and significantly increases the risk of complications. In addition to intramuscular, intravenous, or oral antibiotics, topical antibiotics are used in the treatment of streptococcus. antibacterial agents in the form of aerosols, solutions for gargling and sucking tablets. These drugs significantly accelerate recovery and facilitate the course of the disease.

The most effective drugs for the topical treatment of streptococcal infections of the oropharynx are as follows:

    Ingalipt - sulfanilamide antibacterial aerosol for the throat;

    Tonsilgon N - a local immunostimulant and antibiotic of plant origin in the form of drops and dragees;

    Geksoral - antiseptic aerosol and solution for gargling;

    Chlorhexidine is an antiseptic, sold separately as a solution, and is also included in many tablets for sore throats (Anti-Angina, Sebidina, Pharyngosepta);

    Cetylpyridine - antiseptic, contained in Septolete tablets;

    dichlorobenzene alcohol- antiseptic, contained in many aerosols and lozenges (Strepsils, Agisept, Rinza, Lorsept, Suprima-ENT, Astracept, Terasil);

    Iodine - found in aerosols and solutions for gargling (Iodinol, Vokadin, Yoks, Povidone-iodine).

    Lizobakt, Immunal, IRS-19, Imunorix, Imudon- local and general immunostimulants.

If antibiotics were taken orally to treat a streptococcal infection, you will need drugs to recover normal microflora internal organs:

  • Bifidumbacterin;

  • Bifiform.

Treatment of streptococcus in young children is carried out with the addition of antihistamines:

    Claritin;

It would be useful to take prophylactic vitamin C, which strengthens the walls of blood vessels, helps to increase immune status and detoxification of the body. In difficult situations, doctors use a special streptococcal bacteriophage for treatment - this is an artificially created virus that devours streptococci. Before use, the bacteriophage is tested by placing it in a flask with the patient's blood and monitoring its effectiveness. The virus does not cope with all strains, sometimes you have to resort to a combined pyobacteriophage. In any case, this measure is justified only when the infection cannot be stopped with antibiotics, or the patient is allergic to all topical types of antibacterial drugs.

It is very important to comply correct mode during the treatment of streptococcal infections. A serious illness with severe intoxication of the body requires being in bed. It is active movements and work during the period of illness that are the main prerequisites for the development of serious complications in the heart, kidneys and joints. To remove toxins, you need a lot of water - up to three liters daily, as in pure form, and in the form of warm medicinal tea, juices and fruit drinks. Warm compresses on the neck and ears can be placed only if the patient does not have a fever.

With streptococcal angina, it is categorically impossible to try to speed up recovery by peeling off purulent plaque and plugs from the mucous membrane of the throat with a bandage moistened with iodine or lugol. This will lead to the penetration of the pathogen even deeper and aggravate the disease.

In acute tonsillitis and pharyngitis, one should not irritate the throat with too hot, or vice versa, ice food. Rough food is also unacceptable - it injures the inflamed mucous membrane. It is best to eat cereals, mashed soups, yogurts, soft curds. If the patient has no appetite at all, you do not need to stuff him with food, this will only result in nausea and vomiting. Digestion is a process for which our body spends a lot of energy. Therefore, during the treatment of streptococcal infections, when the digestive organs are already working poorly, and the body is poisoned with toxins, fasting with plenty of fluids may be more useful than good nutrition.

Of course, children suffering from streptococcal tonsillitis or scarlet fever need the most careful care. The child is given warm linden or chamomile tea every hour and a half, cool lotions are applied to the inflamed eyes and hot forehead, itchy and flaky skin is lubricated with baby cream. If the baby is able to gargle, you need to do this as often as possible using infusion or. After recovery from a severe form of scarlet fever, small patients are advised to rest in a sanatorium, take prophylactic multivitamins, immunostimulants, pro- and prebiotics.


Education: In 2009 he received a diploma in the specialty "Medicine", in Petrozavodsk state university. After completing an internship at the Murmansk Regional Clinical Hospital, he received a diploma in the specialty "Otorhinolaryngology" (2010)

The textbook consists of seven parts. Part one - "General Microbiology" - contains information about the morphology and physiology of bacteria. Part two is devoted to the genetics of bacteria. In part three - "Microflora of the biosphere" - the microflora environment, its role in the cycle of substances in nature, as well as human microflora and its significance. Part four - "The Doctrine of Infection" - is devoted to the pathogenic properties of microorganisms, their role in the infectious process, and also contains information about antibiotics and their mechanisms of action. Part five - "The Doctrine of Immunity" - contains modern ideas about immunity. The sixth part - "Viruses and the diseases they cause" - provides information about the main biological properties of viruses and the diseases they cause. Part seven - "Private Medical Microbiology" - contains information about the morphology, physiology, pathogenic properties of pathogens of many infectious diseases, as well as modern methods for their diagnosis, specific prevention and therapy.

The textbook is intended for students, graduate students and teachers of higher medical educational institutions, universities, microbiologists of all specialties and practitioners.

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Streptococci belong to the family Streptococcaceae(genus Streptococcus). They were first discovered by T. Billroth in 1874 with erysipelas; L. Pasteur - in 1878 with postpartum sepsis; isolated in pure culture in 1883 by F. Feleisen.

Streptococcus (gr. . streptos- chain and coccus- grain) - gram-positive, cytochrome-negative, catalase-negative cells of spherical or ovoid shape with a diameter of 0.6 - 1.0 microns, grow in the form of chains of various lengths (see color inc., Fig. 92) or in the form of tetracocci; immobile (except for some representatives of serogroup D); the content of G + C in DNA is 32 - 44 mol % (for the family). Dispute does not form. Pathogenic streptococci form a capsule. Streptococci are facultative anaerobes, but there are also strict anaerobes. The temperature optimum is 37 ° C, the optimum pH is 7.2 - 7.6. On conventional nutrient media, pathogenic streptococci either do not grow or grow very poorly. For their cultivation, sugar broth and blood agar containing 5% defibrinated blood are usually used. The medium should not contain reducing sugars, as they inhibit hemolysis. On the broth, the growth is near-wall in the form of a crumbly sediment, the broth is transparent. Streptococci, forming short chains, cause turbidity of the broth. On dense media, serogroup A streptococci form colonies of three types: a) mucoid - large, shiny, resemble a drop of water, but have a viscous consistency. Such colonies form freshly isolated virulent strains having a capsule;

b) rough - larger than mucoid, flat, with an uneven surface and scalloped edges. Such colonies form virulent strains having M antigens;

c) smooth, smaller colonies with smooth edges; form virulent cultures.

Streptococci ferment glucose, maltose, sucrose and some other carbohydrates to form acid without gas (except S. kefir, which forms acid and gas), milk does not coagulate (except S. lactis), do not possess proteolytic properties (except for some enterococci).

Streptococcus classification. The genus Streptococcus includes about 50 species. Among them, 4 pathogens are distinguished ( S. pyogenes, S. pneumoniae, S. agalactiae and S. equi), 5 opportunistic and more than 20 opportunistic species. For convenience, the entire genus is divided into 4 groups using the following features: growth at 10 °C; growth at 45°C; growth on a medium containing 6.5% NaCl; growth on a medium with a pH of 9.6;

growth on a medium containing 40% bile; growth in milk with 0.1% methylene blue; growth after heating at 60 °C for 30 min.

Most pathogenic streptococci belong to the first group (all of these signs are usually negative). Enterococci (serogroup D), which also cause various human diseases, belong to the third group (all of the listed signs are usually positive).

The simplest classification is based on the ratio of streptococci to erythrocytes. Distinguish:

– β-hemolytic streptococci – when growing on blood agar around the colony, there is a clear zone of hemolysis (see color inc., Fig. 93a);

– α-hemolytic streptococci – around the colony greenish coloration and partial hemolysis (greening is due to the conversion of oxyhemoglobin to methemoglobin, see color inc., Fig. 93b);

– ?1-hemolytic streptococci, compared with ?-hemolytic streptococci, form a less pronounced and cloudy hemolysis zone;

- ?- and? 1-streptococci are called S. viridans(green streptococci);

– β-non-hemolytic streptococci do not cause hemolysis on solid nutrient medium.

Serological classification has gained great practical importance. Streptococci have a complex antigenic structure: they have a common antigen for the whole genus and various other antigens. Among them, group-specific polysaccharide antigens localized in the cell wall are of particular importance for classification. According to these antigens, at the suggestion of R. Lansfeld, streptococci are divided into serological groups, denoted by the letters A, B, C, D, F, G, etc. Now 20 serological groups of streptococci are known (from A to V). Streptococci pathogenic for humans belong to group A, to groups B and D, less often to C, F and G. In this regard, the definition group affiliation streptococci is a decisive moment in the diagnosis of the diseases they cause. Group polysaccharide antigens are determined using the appropriate antisera in the precipitation reaction.

In addition to group antigens, type-specific antigens were found in hemolytic streptococci. In group A streptococci, they are proteins M, T and R. The M protein is thermostable in an acidic environment, but is destroyed by trypsin and pepsin. It is detected after hydrochloric acid hydrolysis of streptococci using a precipitation reaction. Protein T is destroyed when heated in an acidic environment, but is resistant to the action of trypsin and pepsin. It is determined using the agglutination reaction. The R antigen is also found in streptococci of serogroups B, C, and D. It is sensitive to pepsin, but not to trypsin, and is destroyed by heating in the presence of acid, but stable by moderate heating in a weak alkaline solution. According to the M antigen, hemolytic streptococci of serogroup A are divided into a large number of serovariants (about 100), their determination is of epidemiological significance. According to the T-protein, serogroup A streptococci are also divided into several dozen serovariants. In group B, 8 serovariants are distinguished.

Streptococci also have cross-reactive antigens that are common to antigens of the cells of the basal layer of the epithelium of the skin and epithelial cells cortical and medullary zones of the thymus, which may be the cause of autoimmune disorders caused by these cocci. In the cell wall of streptococci, an antigen (receptor II) was found, with which their ability, like staphylococci with protein A, is associated, to interact with the Fc fragment of the IgG molecule.

Diseases caused by streptococci divided into 11 classes. The main groups of these diseases are as follows: a) various suppurative processes - abscesses, phlegmon, otitis media, peritonitis, pleurisy, osteomyelitis, etc.;

b) erysipelas- wound infection (inflammation of the lymphatic vessels of the skin and subcutaneous tissue);

c) purulent complications of wounds (especially in wartime) - abscesses, phlegmon, sepsis, etc.;

d) angina - acute and chronic;

e) sepsis: acute sepsis (acute endocarditis); chronic sepsis (chronic endocarditis); postpartum (puerperal) sepsis;

e) rheumatism;

g) pneumonia, meningitis, creeping ulcer of the cornea (pneumococcus);

h) scarlet fever;

i) dental caries - its causative agent is most often S. mutans. The genes of cariogenic streptococci responsible for the synthesis of enzymes that ensure the colonization of the surface of teeth and gums by these streptococci have been isolated and studied.

Although most streptococci pathogenic for humans belong to serogroup A, streptococci of serogroups D and B also play an important role in human pathology. Serogroup D streptococci (enterococci) are recognized as causative agents of wound infections, various purulent surgical diseases, gynecological patients, infect the kidneys, bladder, cause sepsis, endocarditis, pneumonia, food poisoning (proteolytic variants of enterococci). Streptococcus serogroup B ( S. agalactiae) often cause diseases of the newborn - respiratory tract infections, meningitis, septicemia. Epidemiologically, they are associated with the carriage of this type of streptococcus in the mother and staff of maternity hospitals.

Anaerobic streptococci ( Peptostreptococcus), which are found in healthy people as part of the microflora of the respiratory tract, mouth, nasopharynx, intestines and vagina, can also be the culprits of purulent-septic diseases - appendicitis, postpartum sepsis, etc.

The main pathogenicity factors of streptococci.

1. Protein M is the main factor of pathogenicity. M-proteins of streptococcus are fibrillar molecules that form fimbriae on the surface of the cell wall of group A streptococci. M-protein determines adhesive properties, inhibits phagocytosis, determines antigenic type-specificity and has superantigen properties. Antibodies to the M-antigen have protective properties (antibodies to T- and R-proteins do not have such properties). M-like proteins have been found in group C and G streptococci and may be factors in their pathogenicity.

2. Capsule. It consists of hyaluronic acid, similar to that which is part of the tissue, so phagocytes do not recognize encapsulated streptococci as foreign antigens.

3. Erythrogenin - scarlet fever toxin, superantigen, causes TSS. There are three serotypes (A, B, C). In patients with scarlet fever, it causes a bright red rash on the skin and mucous membranes. It has a pyrogenic, allergenic, immunosuppressive and mitogenic effect, destroys platelets.

4. Hemolysin (streptolysin) O destroys erythrocytes, has a cytotoxic, including leukotoxic and cardiotoxic, effect, it is formed by most streptococci of serogroups A, C and G.

5. Hemolysin (streptolysin) S has a hemolytic and cytotoxic effect. Unlike streptolysin O, streptolysin S is a very weak antigen, it is also produced by streptococci of serogroups A, C and G.

6. Streptokinase is an enzyme that converts the preactivator into an activator, and it converts plasminogen into plasmin, the latter hydrolyzes fibrin. Thus, streptokinase, by activating blood fibrinolysin, increases the invasive properties of streptococcus.

7. The factor that inhibits chemotaxis (aminopeptidase) inhibits the mobility of neutrophilic phagocytes.

8. Hyaluronidase is an invasion factor.

9. Clouding factor - hydrolysis of serum lipoproteins.

10. Proteases - destruction of various proteins; possibly associated with tissue toxicity.

11. DNases (A, B, C, D) - DNA hydrolysis.

12. The ability to interact with the Fc fragment of IgG using the II receptor - inhibition of the complement system and phagocyte activity.

13. Pronounced allergenic properties of streptococci, which cause sensitization of the body.

Streptococcus resistance. Streptococci tolerate low temperatures well, are fairly resistant to desiccation, especially in a protein environment (blood, pus, mucus), and remain viable for several months on objects and dust. When heated to a temperature of 56 ° C, they die after 30 minutes, except for group D streptococci, which can withstand heating to 70 ° C for 1 hour. A 3-5% solution of carbolic acid and lysol kills them within 15 minutes.

Features of epidemiology. The source of exogenous streptococcal infection are patients with acute streptococcal diseases (tonsillitis, scarlet fever, pneumonia), as well as convalescents after them. The main method of infection is airborne, in other cases direct contact and very rarely alimentary (milk and other food products).

Features of pathogenesis and clinic. Streptococci are inhabitants of the mucous membranes of the upper respiratory tract, digestive and genitourinary tracts, so the diseases they cause can be endogenous or exogenous in nature, that is, they are caused either by their own cocci or as a result of infection from the outside. Having penetrated through damaged skin, streptococci spread from the local focus through the lymphatic and circulatory systems. Infection by airborne or airborne dust leads to damage to the lymphoid tissue (tonsillitis), regional lymph nodes are involved in the process, from where the pathogen spreads through the lymphatic vessels and hematogenously.

The ability of streptococci to cause various diseases depends on:

a) places of entrance gate (wound infections, puerperal sepsis, erysipelas, etc.; respiratory tract infections - scarlet fever, tonsillitis);

b) the presence of various pathogenicity factors in streptococci;

c) the state of the immune system: in the absence of antitoxic immunity, infection with toxigenic streptococci of serogroup A leads to the development of scarlet fever, and in the presence of antitoxic immunity, tonsillitis occurs;

d) sensitizing properties of streptococci; they largely determine the peculiarity of the pathogenesis of streptococcal diseases and are the main cause of such complications as nephronephritis, arthritis, damage to the cardiovascular system, etc.;

e) pyogenic and septic functions of streptococci;

f) the presence of a large number of serogroup A streptococci serogroup A by M-antigen.

Antimicrobial immunity, which is caused by antibodies to the M protein, is type-specific in nature, and since there are a lot of serovariants for the M-antigen, repeated infections with tonsillitis, erysipelas and other streptococcal diseases are possible. More complex nature has a pathogenesis of chronic infections caused by streptococci: chronic tonsillitis, rheumatism, nephritis. The following circumstances confirm the etiological role of serogroup A streptococci in them:

1) these diseases, as a rule, occur after acute streptococcal infections (tonsillitis, scarlet fever);

2) in such patients, streptococci or their L-forms and antigens in the blood are often found, especially during exacerbations, and, as a rule, hemolytic or green streptococci on the mucous membrane of the pharynx;

3) constant detection of antibodies to various antigens of streptococci. Especially valuable diagnostic value is the detection in patients with rheumatism during an exacerbation in the blood of anti-O-streptolysins and anti-hyaluronidase antibodies in high titers;

4) the development of sensitization to various streptococcal antigens, including the thermostable component of erythrogenin. It is possible that autoantibodies to the connective and renal tissues, respectively, play a role in the development of rheumatism and nephritis;

5) the obvious therapeutic effect of the use of antibiotics against streptococci (penicillin) during rheumatic attacks.

Postinfectious immunity. The main role in its formation is played by antitoxins and type-specific M-antibodies. Antitoxic immunity after scarlet fever has a strong long-term character. Antimicrobial immunity is also strong and long lasting, but its effectiveness is limited by the type specificity of M antibodies.

Laboratory diagnostics. The main method for diagnosing streptococcal diseases is bacteriological. The material for the study is blood, pus, mucus from the throat, plaque from the tonsils, wound discharge. The decisive step in the study of isolated pure culture is the determination of its serogroup. For this purpose, two methods are used.

A. Serological - determination of a group polysaccharide using a precipitation reaction. For this purpose, appropriate group-specific sera are used. If the strain is beta-hemolytic, its polysaccharide antigen is extracted with HCl and tested with antisera from serogroups A, B, C, D, F, and G. If the strain does not cause beta-hemolysis, its antigen is extracted and tested with antisera from groups B and D only. Antisera of groups A, C, F and G often give cross reactions with alpha-hemolytic and non-hemolytic streptococci. Streptococci that do not cause beta hemolysis and do not belong to groups B and D are identified by other physiological tests (Table 20). Group D streptococci have been isolated in independent genus Enterococcus.

B. Grouping method - based on the ability of aminopeptidase (an enzyme produced by streptococci of serogroups A and D) to hydrolyze pyrrolidine-naphthylamide. For this purpose, commercial kits of the necessary reagents are produced for the determination of group A streptococci in blood and broth cultures. However, the specificity of this method is less than 80%. Serotyping of serogroup A streptococci is performed using either precipitation (determine M-serotype) or agglutination (determine T-serotype) reaction for epidemiological purposes only.

From the number serological reactions to detect streptococci of serogroups A, B, C, D, F and G, coagglutination and latex agglutination reactions are used. Determination of the titer of anti-hyaluronidase and anti-O-streptolysin antibodies is used as an auxiliary method for diagnosing rheumatism and for assessing the activity of the rheumatic process.

IFM can also be used to detect streptococcal polysaccharide antigens.

PNEUMOCOCCIS

Special position in the genus Streptococcus takes the form S. pneumoniae which plays a very important role in human pathology. It was discovered by L. Pasteur in 1881. Its role in the etiology of lobar pneumonia was established in 1886 by A. Frenkel and A. Weikselbaum, as a result of which S. pneumoniae called pneumococcus. Its morphology is peculiar: cocci have a shape resembling a candle flame: one

Table 20

Differentiation of some categories of streptococci


Note: + – positive, – negative, (–) – very rare signs, (±) – changeable sign; b aerococci - Aerococcus viridans, is found in approximately 1% of patients suffering from streptococcal diseases (osteomyelitis, subacute endocarditis, urinary tract infections). Separated into an independent species in 1976, not studied enough.

the end of the cell is pointed, the other is flattened; usually arranged in pairs (flat ends facing each other), sometimes in the form of short chains (see color incl., fig. 94b). They do not have flagella, they do not form spores. In humans and animals, as well as on media containing blood or serum, they form a capsule (see color inc., Fig. 94a). Gram-positive, but often Gram-negative in young and old cultures. facultative anaerobes. The temperature optimum for growth is 37 °C, at temperatures below 28 °C and above 42 °C they do not grow. The optimal pH for growth is 7.2 - 7.6. Pneumococci form hydrogen peroxide, but they do not have catalase, so for growth they require the addition of substrates containing this enzyme (blood, serum). On blood agar, small round colonies are surrounded by a green zone formed as a result of the action of the exotoxin hemolysin (pneumolysin). Growth in sugar broth is accompanied by turbidity and a slight precipitation. In addition to the O-somatic antigen, pneumococci have a capsular polysaccharide antigen, which is very diverse: according to the polysaccharide antigen, pneumococci are divided into 83 serovariants, 56 of them are divided into 19 groups, 27 are presented independently. Pneumococci differ from all other streptococci in morphology, antigenic specificity, and also in that they ferment inulin and are highly sensitive to optochin and bile. Under the influence of bile acids in pneumococci, intracellular amidase is activated. It breaks the bond between alanine and peptidoglycan muramic acid, the cell wall is destroyed, and pneumococcal lysis occurs.

The main factor in the pathogenicity of pneumococci is the capsule of a polysaccharide nature. Capsular pneumococci lose their virulence.

Pneumococci are the main causative agents of acute and chronic inflammatory lung diseases, which occupy one of the leading places in morbidity, disability and mortality in the world population.

Pneumococci along with meningococci are the main culprits of meningitis. In addition, they cause creeping corneal ulcers, otitis, endocarditis, peritonitis, septicemia and a number of other diseases.

Post-infectious immunity type-specific, due to the appearance of antibodies against a typical capsular polysaccharide.

Laboratory diagnostics based on isolation and identification S. pneumoniae. The material for the study is sputum and pus. White mice are very sensitive to pneumococci, so a biological sample is often used to isolate pneumococci. In dead mice, pneumococci are found in a smear preparation from the spleen, liver, lymph nodes, and when sowing from these organs and from the blood, a pure culture is isolated. To determine the serotype of pneumococci, an agglutination reaction on glass with typical sera or the “capsule swelling” phenomenon is used (in the presence of homologous serum, the pneumococcal capsule swells sharply).

Specific prophylaxis pneumococcal disease is carried out using vaccines prepared from highly purified capsular polysaccharides of those 12-14 serovariants that most often cause disease (1, 2, 3, 4, 6A, 7, 8, 9, 12, 14, 18C, 19, 25) . Vaccines are highly immunogenic.

MICROBIOLOGY OF SCARLET FINA

Scarlet fever(Late Late . scarlatium- bright red color) - an acute infectious disease that is clinically manifested by tonsillitis, lymphadenitis, small-pointed bright red rash on the skin and mucous membranes, followed by peeling, as well as general intoxication of the body and a tendency to purulent-septic and allergic complications.

The causative agents of scarlet fever are group A beta-hemolytic streptococci, which have the M-antigen and produce erythrogenin. The etiological role in scarlet fever was attributed to various microorganisms - protozoa, anaerobic and other cocci, streptococci, filterable forms of streptococcus, viruses. A decisive contribution to the clarification true reason scarlet fever was made by Russian scientists G. N. Gabrichevsky, I. G. Savchenko and American scientists G. F. Dick and G. H. Dick. I. G. Savchenko back in 1905 - 1906. showed that scarlatinal streptococcus produces a toxin, and the antitoxic serum obtained by it has a good therapeutic effect. Based on the works of I. G. Savchenko, the Dick spouses in 1923 - 1924. showed that:

1) intradermal administration of a small dose of toxin to persons who have not suffered from scarlet fever causes a positive local toxic reaction in the form of redness and swelling (Dick's reaction);

2) in persons who have had scarlet fever, this reaction is negative (the toxin is neutralized by the antitoxin they have);

3) the introduction of large doses of the toxin subcutaneously to persons who have not suffered from scarlet fever causes them symptoms characteristic of scarlet fever.

Finally, by infecting volunteers with a culture of streptococcus, they were able to reproduce scarlet fever. Currently, the streptococcal etiology of scarlet fever is generally recognized. The peculiarity here lies in the fact that scarlet fever is caused not by any one serotype of streptococci, but by any of the beta-hemolytic streptococci that has the M-antigen and produces erythrogenin. However, in the epidemiology of scarlet fever in different countries, in different regions and at different times, the main role is played by streptococci that have different M-antigen serotypes (1, 2, 4 or another) and produce erythrogenins of different serotypes (A, B, C). It is possible to change these serotypes.

The main factors of pathogenicity of streptococci in scarlet fever are exotoxin (erythrogenin), pyogenic-septic and allergenic properties of streptococcus and its erythrogenin. Erythrogenin consists of two components - a thermolabile protein (actually a toxin) and a thermostable substance with allergenic properties.

Infection with scarlet fever occurs mainly by airborne droplets, however, any wound surfaces can be the entrance gate. The incubation period is 3 - 7, sometimes 11 days. In the pathogenesis of scarlet fever, 3 main points associated with the properties of the pathogen are reflected:

1) the action of scarlatinal toxin, which causes the development of toxicosis - the first period of the disease. It is characterized by damage to the peripheral blood vessels, the appearance of a small-dotted rash of bright red color, as well as fever and general intoxication. The development of immunity is associated with the appearance and accumulation of antitoxin in the blood;

2) the action of the streptococcus itself. It is nonspecific and manifests itself in the development of various purulent-septic processes (otitis, lymphadenitis, nephritis appear on the 2nd - 3rd week of the disease);

3) sensitization of the organism. It is reflected in the form of various complications such as nephronephritis, polyarthritis, cardiovascular diseases, etc. on the 2nd - 3rd week. illness.

In the clinic of scarlet fever, stage I (toxicosis) and stage II are also distinguished, when purulent-inflammatory and allergic complications are observed. In connection with the use of antibiotics (penicillin) for the treatment of scarlet fever, the frequency and severity of complications have decreased significantly.

Post-infectious immunity strong, long-term (repeated diseases are observed in 2-16% of cases), due to antitoxins and immune memory cells. In those who have been ill, the allergic state to the scarlatinal allergen also persists. It is detected by intradermal injection of killed streptococci. In patients who have been ill at the injection site - redness, swelling, soreness (Aristovsky-Fanconi test). To test for the presence of antitoxic immunity in children, the Dick reaction is used. With its help, it was established that passive immunity in children of the 1st year of life is preserved during the first 3-4 months.

The genus Streptococcus includes: Streptococcus pyogenes (hemolytic) and Streptococcus pneumoniae (pneumococcus). Streptococci were first discovered by Billroth (1874), L. Pasteur (1879). They were studied by E. Rosenbach (1884).

Streptococcus pyogenes (hemolytic)

Morphology. Streptococci are cocci that have a spherical shape. The diameter of each coccus is on average 0.6-1 μm, however, they are characterized by polymorphism: there are small and large cocci, strictly spherical and oval. Streptococci are arranged in a chain, which is the result of their division in the same plane. Chain lengths vary. On a dense nutrient medium, the chains are usually short; on liquid ones, they are long. Streptococci are immobile, do not have spores (see Fig. 4). Freshly isolated cultures sometimes form a capsule. On ultrathin sections, a microcapsule is visible, under it there is a three-layer cell wall and a three-layer cytoplasmic membrane. Gram-positive.

cultivation. Streptococci are facultative anaerobes. Grow at a temperature of 37 ° C and pH 7.6-7.8. The optimal media for their cultivation are media containing blood or blood serum. On dense nutrient media, streptococcal colonies are small, flat, cloudy, grayish in color. On blood agar, some varieties of streptococci form hemolysis. β-hemolytic streptococci form a clear zone of hemolysis, α-hemolytic streptococci form a small greenish zone (the result of the transition of hemoglobin to methemoglobin). There are streptococci that do not give hemolysis.

On sugar broth, streptococci grow with the formation of parietal and near-bottom fine-grained sediment, while the broth remains transparent.

Enzymatic properties. Streptococci have saccharolytic properties. They break down glucose, lactose, sucrose, mannitol (not always) and maltose to form acid. Their proteolytic properties are poorly expressed. They coagulate milk, gelatin does not liquefy.

toxin formation. Streptococci form a number of exotoxins: 1) streptolysins - destroy red blood cells (O-streptolysin has a cardiotoxic effect); 2) leukocidin - destroys leukocytes (formed by highly virulent strains); 3) erythrogenic (scarlet fever) toxin - causes the clinical picture of scarlet fever - intoxication, vascular reactions, rash, etc. The synthesis of erythrogenic toxin is determined by the prophage; 4) cytotoxins - have the ability to cause glomerulonephritis.

Streptococci have various antigens. The cytoplasm of the cell contains an antigen of a specific nucleoprotein nature - the same for all streptococci. Protein type antigens are located on the surface of the cell wall. A polysaccharide group antigen was found in the cell wall of streptococci.

According to the composition of the polysaccharide group-specific antigen fraction, all streptococci are divided into groups, denoted by capital Latin letters A, B, C, D, etc. up to S. In addition to groups, streptococci are divided into serological types, which are indicated by Arabic numerals.

Group A includes 70 types. This group includes most streptococci that cause various diseases in humans. Group B includes mainly opportunistic human streptococci. Group C includes streptococci pathogenic to humans and animals. Group D consists of streptococci that are not pathogenic to humans, but this group includes enterococci, which are inhabitants intestinal tract man and animals. Once in other organs, they cause inflammatory processes: cholecystitis, pyelitis, etc. Thus, they can be attributed to conditionally pathogenic microbes.

The belonging of the isolated cultures to one of the serological groups is determined using a precipitation reaction with group sera. To determine serological types, an agglutination reaction with type-specific sera is used.

Streptococci are fairly stable in the environment. At a temperature of 60 ° C, they die after 30 minutes.

In dried pus and sputum, they persist for months. The usual concentrations of disinfectants destroy them in 15-20 minutes. Enterococci are much more resistant, disinfectant solutions kill them only after 50-60 minutes.

Animal susceptibility. Cattle, horses, dogs, and birds are susceptible to pathogenic streptococci. From laboratory animals rabbits and white mice are sensitive. However, streptococci pathogenic for humans are not always pathogenic for experimental animals.

Sources of infection. People (sick and carriers), less often animals or infected products.

Transmission routes. Airborne and airborne dust, sometimes food, contact-household is possible.

Diseases can occur as a result of exogenous infection, as well as endogenously - with the activation of opportunistic streptococci that live on the mucous membranes of the pharynx, nasopharynx, and vagina. A decrease in the body's resistance (cooling, starvation, overwork, etc.) can lead to autoinfections.

Of great importance in the pathogenesis of streptococcal infections is preliminary sensitization - as a result of a previously transferred disease of streptococcal etiology.

When penetrating into the bloodstream, streptococci cause a severe septic process.

Diseases in humans more often cause β-hemolytic streptococci of serological group A. They produce pathogenicity enzymes: hyaluronidase, fibrinolysin (streptokinase), deoxyribonuclease, etc. In addition, a capsule, M-protein, which have antiphagocytic properties, are found in streptococci.

Streptococci cause various acute and chronic infections in humans, both with the formation of pus and non-suppurative, differing in clinical picture and pathogenesis. Suppurative - phlegmon, abscesses, wound infections, non-suppurative - acute infections of the upper respiratory tract, erysipelas, scarlet fever, rheumatism, etc.

Streptococci often cause secondary infections in influenza, measles, whooping cough and other diseases and often complicate wound infections.

Immunity. By nature, immunity is antitoxic and antibacterial. Postinfectious antimicrobial immunity is weak. This is due to the weak immunogenicity of streptococci and large quantity serovars that do not confer cross-immunity. In addition, with streptococcal diseases, an allergization of the body is observed, which explains the tendency to relapse.

Prevention. It comes down to sanitary and hygienic measures, strengthening the overall resistance of the body. Specific prophylaxis has not been developed.

Treatment. Apply antibiotics. More often, penicillin is used, to which streptococci have not acquired resistance, as well as erythromycin and tetracycline.

The value of streptococcus in the etiology of rheumatic heart disease. The pathogenesis of rheumatic heart disease is not well understood. But a number of facts speak in favor of the role of streptococcus in the development of this disease:

1. In patients with rheumatic heart disease, B-hemolytic streptococcus is sown from the pharynx.

2. Rheumatism often occurs after suffering a sore throat, tonsillitis, pharyngitis, sensitizing the body.

3. Antistreptolysin, antistreptohyaluronidase - antibodies to streptococcal enzymes, toxins are found in the blood serum of patients.

4. Indirect confirmation of the role of streptococcus is the successful treatment with penicillin.

AT recent times in the emergence chronic forms rheumatic heart disease attach importance to L-forms of streptococcus.

Prevention of exacerbations of rheumatic heart disease is reduced to the prevention of streptococcal diseases (for example, in spring and autumn, a prophylactic course of penicillin administration is carried out). Treatment is reduced to the use of antibacterial drugs - penicillin.

The value of streptococcus in the etiology of scarlet fever. G. N. Gabrichevsky (1902) was the first to suggest that hemolytic streptococcus is the causative agent of scarlet fever. But since the streptococci isolated in other diseases did not differ from the causative agents of scarlet fever, this opinion was not shared by everyone. It is now established that scarlet fever is caused by group A streptococci that produce erythrogenic toxin.

In those who have been ill, immunity arises - persistent, antitoxic. Its tension is determined by setting the Dick reaction - intradermal injection of erythrogenic toxin. In those who are not sick around the injection site, hyperemia and edema occur, which is characterized as a positive reaction (lack of antitoxin in the blood serum). In those who have been ill, such a reaction is absent, since the antitoxin formed in them neutralizes the erythrogenic toxin.

Prevention. Isolation, hospitalization. Contact, weakened children are given gamma globulin. Specific prophylaxis has not been developed.

Treatment. Use penicillin, tetracycline. In severe cases, antitoxic serum is administered.

The purpose of the study: detection of streptococcus and determination of its serovar.

Research material

1. Mucus from the throat (tonsillitis, scarlet fever).

2. Scraping from the affected area of ​​the skin (erysipelas, streptoderma).

3. Pus (abscess).

4. Urine (nephritis).

5. Blood (suspected sepsis; endocarditis).

Basic research methods

1. Bacteriological.

2. Microscopic.

Research progress

Second day of research

Take the cups out of the thermostat and inspect. In the presence of suspicious colonies, smears are made from a part of them, stained according to Gram and microscopically. If streptococci are found in the smear, part of the remaining colony is subcultured into test tubes on agar with serum to isolate a pure culture and on broth with blood in test tubes. By the end of the day, a 5-6-hour culture from broth or agar is subcultured onto Marten's broth with 0.25% glucose to determine the serological group in the Lensfield precipitation reaction. Test tubes and vials are placed in a thermostat and left until the next day.

Third day of research

The cultures are removed from the oven, the purity of the culture is checked on the agar slant, smears are made, Gram stained and microscoped. In the presence of a pure culture of streptococcus, they are sown on Hiss media (lactose, glucose, maltose, sucrose and mannitol), milk, gelatin, 40% bile and put in a thermostat.

Look through Martin's broth. In the presence of specific growth, a Lensfield precipitation test is performed to determine the serological group.

Setting up the precipitation reaction according to Lensfield. The daily culture grown on Martin's broth is poured into several centrifuge tubes, centrifuged for 10-15 minutes (3000 rpm).

The supernatant liquid is poured into a jar with disinfectant solution, and the sediment is poured with sterile isotonic sodium chloride solution and centrifuged again. To the precipitate collected from all centrifuge tubes, add 0.4 ml of 0.2% hydrochloric acid. Then the tube is placed in a water bath and boiled for 15 minutes, shaking occasionally. After boiling, the resulting suspension is again centrifuged. The antigen is then extracted into the supernatant, which is poured into a clean tube and neutralized with 0.2% sodium hydroxide solution to pH 7.0-7.2. Bromothymol blue (0.01 ml of a 0.04% solution) is added as an indicator. With this reaction, the color changes from straw yellow to blue.

Then, 0.5 ml of antistreptococcal group sera, which are prepared by immunizing rabbits, are poured into 5 precipitation tubes (see Chapter 19). Serum A is introduced into the 1st tube, serum B into the 2nd, serum C into the 3rd, serum D into the 4th, isotonic sodium chloride solution (control) into the 5th. After that, with a Pasteur pipette, the resulting extract (antigen) is carefully layered along the wall into all test tubes.

At positive reaction in a test tube with homologous serum, a thin milky-white ring is formed at the border of the extract with serum (Fig. 38).

Fourth day of research

The results are recorded (Table 25).

Currently, deoxyribonuclease is being determined, as well as antistreptohyaluronidase, antistreptolysin-O.

test questions

1. What are the main methods of laboratory research for the detection of streptococci do you know?

2. What is the Lensfield precipitation reaction for?

3. Why should the antigen be transparent during this reaction? Describe the technique for staging this reaction.

Get antistreptococcal serum A, B, C, D and isotonic sodium chloride solution from the teacher. Set the precipitation reaction, show the results to the teacher and draw.

Nutrient media

agar with blood(see chapter 7).

Serum agar(see chapter 7).

Hiss media(dry).

Meat peptone gelatin (MPG). To 100 ml of MPB add 10-15 g of finely chopped gelatin. Gelatin should swell when slowly heated in a water bath (at a temperature of 40-50 ° C). A 10% solution of sodium carbonate (baking soda) is added to the melted gelatin and the pH is adjusted to 7.0. It is then immediately filtered through a pleated filter. Filtration is slow. To speed up the process, filtration can be done in a hot autoclave. The filtered medium is poured into test tubes of 6-8 ml and sterilized. Sterilization is carried out either fractionally at a temperature of 100 ° C for 3 days in a row, or simultaneously at 110 ° C for 20 minutes in an autoclave. Cooling of the medium is carried out in test tubes placed vertically.

Milk preparation. Fresh milk is brought to a boil, put in a cool place for a day, freed from cream, boiled again. Leave for a day and remove the top layer. Skimmed milk is filtered through a layer of cotton wool, then alkalized with 10% sodium carbonate solution to pH 7.2 and poured into test tubes of 5-6 ml.

Bouillon Martin. An equal amount of peptone Marten (minced meat from pork stomachs exposed to hydrochloric acid) is added to the meat water. The resulting mixture is boiled for 10 minutes, alkalized with 10% sodium hydroxide solution to pH 8.0, 0.5 sodium acetate is added, boiled again and poured into sterile dishes. 0.25% glucose is added to Martin's broth.

Wednesday Kitt - Tarozzi(see chapter 34).

Streptococcus pneumoniae (pneumococcus)

Pneumococci were first described by R. Koch (1871).

Morphology. Pneumococci are diplococci in which the sides of the cells facing each other are flattened and the opposite sides are elongated, so they have a lanceolate shape resembling a candle flame (see Fig. 4). The size of pneumococci is 0.75-0.5 × 0.5-1 μm, they are arranged in pairs. In liquid nutrient media, they often form short chains, resembling streptococci. Prevmococci are non-motile, do not have spores, form a capsule in the body that surrounds both cocci. The capsule contains a heat-resistant substance antiphagin (which protects pneumococcus from phagocytosis and the action of antibodies). When growing on artificial nutrient media, pneumococci lose their capsule. Pneumococci are gram positive. Gram-negative bacteria are found in old cultures.

cultivation. Pneumococci are facultative anaerobes. Grow at a temperature of 36-37 ° C and a pH of 7.2-7.4. They are demanding on media, since they cannot synthesize many amino acids, therefore they grow only on media with the addition of native protein (blood or serum). On agar with serum form small, delicate, fairly transparent colonies. On agar with blood, moist greenish-gray colonies grow, surrounded by a green zone, which is the result of the conversion of hemoglobin to methemoglobin. Pneumococci grow well in broth with the addition of 0.2% glucose and in broth with whey. Growth in liquid media is characterized by diffuse turbidity and dusty sediment at the bottom.

Enzymatic properties. Pneumococci have a fairly pronounced saccharolytic activity. They break down: lactose, glucose, sucrose, maltose, inulin with the formation of acid. Do not ferment mannitol. Their proteolytic properties are poorly expressed: they coagulate milk, do not liquefy gelatin, and do not form indole. Pneumococci dissolve in bile. Cleavage of inulin and dissolution in bile is an important diagnostic feature that distinguishes Streptococcus pneumoniae from Streptococcus pyogenes.

pathogenicity factors. Pneumococci produce hyaluronidase, fibrinolysin, etc.

toxin formation. Pneumococci produce endotoxin, hemolysin, leukocidin. The virulence of pneumococci is also associated with the presence of antiphagin in the capsule.

Antigenic structure and classification. In the cytoplasm of pneumococci there is a protein antigen common to the entire group, and in the capsule there is a polysaccharide antigen. According to the polysaccharide antigen, all pneumococci are divided into 84 serovars. Serovars I, II, III are the most common pathogens for humans.

Environmental resistance. Pneumococci belong to the group of unstable microorganisms. A temperature of 60 ° C destroys them in 3-5 minutes. They are quite resistant to low temperatures and drying. In dried sputum, they remain viable for up to 2 months. On a nutrient medium, they remain no more than 5-6 days. Therefore, when cultivating, it is necessary to do reseeding every 2-3 days. Conventional solutions of disinfectants: 3% phenol, sublimate at a dilution of 1:1000 destroy them in a few minutes.

Pneumococci are especially sensitive to optochin, which kills them at a dilution of 1:100,000.

Animal susceptibility. Humans are the natural host of pneumococci. However, pneumococci can cause illness in calves, lambs, piglets, dogs, and monkeys. Of the experimental animals, white mice are highly sensitive to pneumococcus.

Sources of infection. A sick person and a bacteriocarrier.

Transmission routes. Airborne, may be airborne.

entrance gate. The mucous membrane of the upper respiratory tract, eyes and ear.

Diseases in humans. Pneumococci can cause purulent-inflammatory diseases of different localization. Specific for pneumococci are:

1) lobar pneumonia;

2) creeping ulcer of the cornea;

Most common illness is croupous pneumonia, which captures one, less often two or three lobes of the lung. The disease is acute, accompanied by high fever, cough. It usually ends critically.

Immunity. After the illness, unstable immunity remains, since pneumonia is characterized by relapses.

Prevention. It comes down to sanitary and preventive measures. Specific prophylaxis has not been developed.

Treatment. Antibiotics are used - penicillin, tetracycline, etc.

test questions

1. Morphology of pneumococci. Cultivation and enzymatic properties.

2. What factors determine the pathogenicity of pneumococci and what protects pneumococci from phagocytosis?

3. What are the main gates of pneumococcal infection. What diseases are caused by pneumococci?

Microbiological research

The purpose of the study: detection of pneumococcus.

Research material

1. Phlegm (pneumonia).

2. Mucus from the pharynx (tonsillitis).

3. Discharge from the ulcer (creeping ulcer of the cornea).

4. Discharge from the ear (otitis media).

5. Pus (abscess).

6. Pleural punctate (pleurisy).

7. Blood (suspected sepsis).

1 (It is better to take morning sputum (with specific pneumonia, sputum has a rusty color).)

Basic research methods

1. Microscopic.

2. Microbiological.

3. Biological.

Research progress

biological sample. A little (3-5 ml of sputum) is emulsified in a sterile broth, 0.5 ml of this mixture is injected intraperitoneally to a white mouse. After 6-8 hours, the mice show signs of the disease. At this time, pneumococcus can already be detected in the exudate of the abdominal cavity. The exudate is taken with a sterile syringe. Smears are made from it, stained according to Gram and microscoped. To isolate a pure culture, the exudate is inoculated onto agar with serum. If the mouse dies or becomes ill, blood is cultured from the heart on serum agar to isolate a pure culture. Crops are placed in a thermostat.

An accelerated method for determining the type of pneumococcus(reaction of microagglutination). 4 drops of exudate from the abdominal cavity of an infected mouse are applied to a glass slide. Type I agglutinating serum is added to the first drop, type II serum to the second, type III to the third, isotonic sodium chloride solution (control) to the fourth.

Type I and II sera are pre-diluted in a ratio of 1:10, and type III serum - 1:5. All drops are stirred, dried, fixed and stained with diluted magenta. With a positive result in one of the drops, microbial aggregation (agglutination) is noted.


Second day of research

The cultures are removed from the thermostat, examined, and smears are made from suspicious colonies. In the presence of gram-positive lanceolate diplococci in smears, 2-3 colonies are isolated on a slant of agar with serum to obtain a pure culture. Crops are placed in a thermostat. Smears are made from the broth, Gram-stained, and microscoped.

Third day of research

Crops are removed from the thermostat. Check the purity of the culture - make smears, Gram stain and microscope. If there are gram-positive lanceolate diplococci in the isolated culture, the isolated culture is identified by inoculation:

1) sowing on Hiss media (lactose, glucose, sucrose, maltose) in the usual way- an injection on Wednesday;

2) on the medium with inulin;

3) on the medium with optochin;

4) put a sample with bile.

Inulin test. The studied culture is seeded on a nutrient medium containing inulin and litmus tincture, and placed in a thermostat. After 18-24 hours, the crops are removed from the thermostat. In the presence of pneumococci, the medium turns red (streptococci do not change the consistency and color of the medium).

Determination of sensitivity to optochin. The isolated culture is seeded on 10% blood agar containing optochin 1:50,000. Pneumococci, unlike streptococci, do not grow on media containing optochin.

Bile test. 1 ml of the studied broth culture is poured into agglutination tubes. A drop of rabbit bile is added to one of them, the second test tube serves as a control. Both test tubes are placed in a thermostat. After 18-24 hours, lysis of pneumococci occurs, which is expressed in the clearing of a cloudy broth. In the control, the suspension remains cloudy.

A sample with bile can be placed on a dense nutrient medium. To do this, a grain of dry bile is applied to a colony of pneumococci grown in agar and serum plates - the colony dissolves - disappears.

Fourth day of research

The results are recorded (Table 26).

Note. to - the breakdown of carbohydrates with the formation of acid.

Currently, serological research methods (RSK and RIGA) are widely used to determine streptococcal antibodies. Determination of the group and serovar of the isolated culture is carried out using fluorescent antibodies.

Determination of pneumococcal virulence. Daily broth culture of pneumococcus is diluted with 1% peptone water from 10 -2 to 10 -8 , 0.5 ml of each dilution is administered to two white mice. The culture that caused the death of mice at a dilution of 10 -7 is assessed as virulent, at a dilution of 10 -4 -10 -6 it is considered moderately virulent. The culture that did not cause the death of mice is avirulent.

test questions

1. What methods of isolating a pure culture of pneumococci do you know?

2. Which animal is most susceptible to pneumococcus?

3. What reactions are put with the exudate of an infected mouse and for what purpose?

4. From which representatives of pyogenic cocci should pneumococcus be differentiated and by what test?

5. How to determine the virulence of pneumococci?

Exercise

Draw up a sputum examination scheme, indicating its stages by day.

Nutrient media

Serum agar(see chapter 7).

Whey broth(see chapter 7).

agar with blood(see chapter 7).

Hiss media(dry).

Inulin test medium. To 200 ml of distilled water add 10 ml of inactivated bovine serum, 18 ml of litmus tincture and 3 g of inulin. Sterilize with flowing steam at 100°C for 3 consecutive days. Bile broth (see chapter 7).

DOMAIN → Bacteria; TYPE → Firmicutes; CLASS → Vasilli; ORDER → Lactobacillales;

FAMILY → Streptococcaceae; GENUS → Streptococcus; SPECIES → Streptococcus species (up to 50 species)

The main features of the genusStreptococcus:

1. Cells of spherical or oval (lanceolate) shape 0.5-2.0 microns. Arranged in a chain or in pairs.

2. Motionless, no dispute. Some species have a capsule.

3. Gram-positive. Chemoorganotrophs, demanding on nutrient media, facultative anaerobes

4. Ferment sugars to form acid, but this is not a reliable differentiator within the genus

5. Unlike staphylococci, there is no catalase activity and cytochromes.

6. Usually, erythrocytes are lysed. According to hemolytic properties: beta (complete), alpha (partial), gamma (none). Capable of forming L-shapes.

Antigenic structure of the genusStreptococcus:

    Cell wall polysaccharide on the basis of which they are divided into 20 groups, denoted by Latin letters. Pathogenic species belong primarily to the A. group and less often to other groups. There are species without a group antigen.

    Type-specific protein antigens (M, T, R). M-protein is possessed by pathogenic species. In total, there are over 100 serotypes, most of which belong to group A streptococci. The M-protein is located superficially in the form of filamentous formations braiding the cell - fimbriae.

    Capsular streptococci have capsular antigens of various chemical nature and specificity.

    There are cross-reactive antigens

Group A streptococci are part of the nasopharyngeal microflora and are not normally found on the skin. The most pathogenic for humans are hemolytic streptococci of group A, belonging to the species S. pyogenes

Group A streptococci cause infections at any age and are most common in children between 5 and 15 years of age.

Group A pathogenicity factors

1) Capsule (hyaluronic acid) → Antiphagocytic activity

2) M-protein (fimbriae) → Antiphagocytic activity, destroys complement (C3b), superantigen

3) M-like proteins → Bind IgG, IgM, alpha2-macroglobulin

4) F-protein → Microbe attachment to epithelial cells

5) Pyrogenic exotoxins (erythrogenins A, B, C) → Pyrogenic effect, increased HRT, immunosuppressive effect on B-lymphocytes, rash, superantigen

6) Streptolysins: S (oxygen stable) and

O (oxygen sensitive) → Destroy white blood cells, platelets, red blood cells. Stimulate the release of lysosomal enzymes.

7) Hyaluronidase → facilitates invasion by disintegrating connective tissue

8) Streptokinase (fibrinolysin) → Destroys blood clots (thrombi), promotes the spread of microbes in tissues

9) DNase → Demolymerizes extracellular DNA in pus

10) C5a-peptidase → Destroys the C5a component of complement, chemoattractant

The pathogenesis of infections caused byS. pyogenes:

    It most commonly causes a localized infection of the upper respiratory tract or skin, but can infect any organ.

    Most frequent suppurative processes: abscesses, phlegmon, tonsillitis, meningitis, pharyngitis, sinusitis, frontal sinusitis. lymphadenitis, cystitis, pyelitis, etc.

Local inflammation leads to leukocytolysis in the peripheral blood, followed by tissue infiltration with leukocytes and local pus formation.

Non-suppurative processes causedS. pyogenes:

    erysipelas,

    streptoderma,

    impetigo,

    scarlet fever,

    rheumatoid infection (rheumatic fever),

    glomerulonephritis,

    toxic shock,

    sepsis, etc.

Treatment of streptococcal infections:It is carried out primarily with antibiotics: cephalosporins, macrolides, lincosamides

Prevention of streptococcal infections:

    General sanitary and hygienic measures, prevention and treatment of acute local streptococcal infections are important. To prevent relapse (rheumatic fever) - antibiotic prophylaxis.

    An obstacle to the creation of vaccines is a large number of serotypes, which, taking into account the type-specificity of immunity, makes their production hardly realistic. In the future, the synthesis of M-protein polypeptides and the hybridoma route for its production.

    Associated drugs are produced abroad for the immunotherapy of infections caused by opportunistic microbes - from 4 to 19 types. These vaccines include S.pyogenes and S.pneumoniae.

    Immunoprophylaxis of pneumococcal infections - a vaccine from polysaccharides of 12-14 serovariants, which often cause diseases.

    A vaccine against caries is being developed.

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