Prevention of pustular diseases. Prevention of pustular skin diseases Conversation prevention of pustular skin diseases
For prevention, all skin injuries should be treated with alcohol solutions of iodine or brilliant green. The skin should not be overheated, as sweating promotes the development of pustules. If a skin infection has started, do not wash the affected areas with soap and water; you should wipe them with alcohol to prevent the infection from spreading further.
It is better to treat any pustular rash by a dermatologist - this will more reliably protect you from pustules and prevent complications
- Fungal diseases of the SKIN
Mycosis
Typical skin infections caused by certain pathogens
(fungi) and are often found in certain groups of people
Special microorganisms belonging to a large group of fungi affect the skin and its appendages (hair, nails, etc.). Fungal skin diseases, due to their prevalence and high contagiousness (danger of infection), are devoted to a significant section of dermatology. Although improved hygienic conditions have greatly reduced the development of these diseases, conditions can still be found today, mainly in rural areas, that favor the growth of fungal infections. Let's look at some of the causative agents of these forms of the disease.
What are "mushrooms"?
The plant kingdom consists of higher plants, or green plants, and lower plants, which the great Linnaeus called cryptogams (spore-bearing plants). The reproductive organs of fungi are hidden and not visible upon superficial examination. On the contrary, in higher plants the reproductive organs are formed by flowers. Cryptogams include thallophytes, which, among other things, are divided into mycetes, or fungi (mycophytes). The same group of thallophytes also includes schizomycetes (bacteria), i.e. actual bacteria. Their body consists of more or less branched threads called fungal hyphae. The interweaving of these hyphae forms the mycelium. Not all mycetes are pathogens, and not all pathogens lead to skin diseases. The ones we're talking about are called dermatophytes or dermatomycetes.
For a long time, the most common pathogen among mycetes were trichophytons and especially T. violaceum. Today they seem to be retreating slightly. The causative agent of scab (favus) is found mainly in countries with poor hygienic conditions. In most of the population of poor countries it occurs epidemically, i.e. constantly.
Thus, Tinea tonsurans occurs spontaneously at 13-14 years of age, during puberty, and adults never get sick with it. This is explained by the antifungal effect of fatty acids, which appear during puberty in the secretion of the sebaceous glands of the scalp. Hormones of the sex glands, which are active at this age, can also prevent the development of mycetes.
Microscopy
Microsporia in humans is caused primarily by Microsporon audouinii, in animals - by Microsporon canis or lanosum, which has become very widespread in recent years. It affects almost exclusively children aged 4-10 years and is extremely contagious, since the fungi are transmitted by direct touch or indirectly through combs, towels, etc. For this reason, epidemics often occur in schools and kindergartens. In adults, the lesion occurs not only on the scalp, but also on the cheeks and chin (in persons with a beard). At first, this is a reddish round spot, which is most often ignored, since its true essence can only be revealed by special research. The spot enlarges, the reddish color intensifies, small scabs form on the skin and hair breaks easily. A typical picture of the disease develops: the lesions are large (2-6 cm in diameter), grayish in color and can cover most of the scalp. All hairs break off at a height of 0.5 cm from the base and one visual assessment is enough to make sure that they are diseased. They are surrounded by a fibrous grayish shell, mycelium formed by hyphae. Also added here are spores, which lie like a frame around the hair and, under a microscope, give an accurate idea of the changes taking place. For a better understanding, you should know that hair consists of an outer shaft (visible part) and a root. The root thickens downwards into the hair follicle, which is located in the hair papilla. The hair root is surrounded by a so-called hair follicle in the form of a sac; a shaft grows from the opening of this hair follicle. The fungus infects the hair in the area of this hole, attaches to it and multiplies by longitudinal division of its cells.
Trichophytosis
It is also typical for children. The fungus only affects humans. Infection can occur directly or indirectly through hygiene items (combs, towels, etc.). If the fungus gets on the stratum corneum, it forms threads that cover the entire hair up to the hair follicle. But the damage is more serious than with microsporia, and the hair breaks off at the base of the follicle. There are fewer spots on the skin, diseased hair is mixed with healthy ones.
Modern treatment is based on removing diseased hair using hair removal tongs (the surgical intervention is not easy and is carried out carefully and methodically). It is also recommended to extirpate (pull out) healthy hair around the lesion along a circumference of 1 cm in diameter in order to deprive the fungus of the ability to infect new hair. Iodine and sulfur, which have an antifungal effect, are used locally. The development of griseofulvin, an antibiotic that replaced expensive and complex treatment methods, such as not entirely safe x-ray therapy, is considered a therapeutic “breakthrough.” The duration of such treatment is about 40 days. All suspicious cases should be named to the doctor, and after a successful diagnosis, all sick children should be immediately separated from healthy ones. It is enough to free them from school, leave them at home and not allow them to contact their peers. It is clear that this first step to prevent the spread of the disease depends entirely on parents and educators, who must be nearby, supervise the children and ensure that contact with the doctor is maintained.
Favus (head scab)
Favus, or scab, has been known for a long time. It is caused by a fungus that exclusively affects humans. The disease is especially contagious and primarily affects children and young people. Unlike other fungi, it does not lose its danger with the onset of puberty and also affects adults. These are primarily individuals living in disadvantaged environments and communities.
There are cases of constant occurrence of scab in many generations in ONE family or in people in one village. The disease can be transmitted directly through touch or indirectly through general hygiene items, such as combs, brushes and others. A significant distinguishing feature compared to other types is the poor outcome of this disease, since if left untreated it leads to irreversible hair loss and the formation of scar tissue.
A typical sign of favus is the formation of scales. They are small sulfur-yellow, round convex crusts up to 3 mm high. There is a depression in the center where the hair is located. The scale consists of a compact mass of fungal filaments that the fungus forms around the opening of the follicle after it infects the hair all the way to the root. It increases, but never exceeds 2 cm in diameter. Several of these scales may fuse together and form large, crusty lesions that smell like mouse urine. Favus develops more or less slowly into alopecia (baldness), since the diseased hair is a foreign body, which first leads to inflammation and then to scarring of the scalp.
In addition, the fungus can produce toxic substances that have a destructive effect on the epidermis. The spot is smooth, slightly depressed and completely hairless. Famous personalities such as Julius Caesar suffered from this form of scab. It was said that for this reason he always wore a laurel wreath. Scab developing into alopecia requires decisive treatment. Initially, the patient must be isolated. Then the scales of the crust should be cleaned off, the hair near the lesions should be removed. Regular antifungal ointments or liquids should be used for two months.
Women really enjoy trying on shoes in stores, even if they have no intention of buying them. Not everyone knows that in such a situation you can meet not only a prince in a white suit, but also a much less handsome “gentleman”. Fungus is a very insidious disease! - likes to live in shoes and sandals, patiently waiting for a new owner.
According to statistics, every fifth resident of Russia suffers from a fungal disease, and with age, the likelihood of becoming infected with a fungus increases several times. Shoes are far from the only opportunity to pick up a “companion”, which is then very difficult to get rid of. Infection occurs with equal frequency in public places: showers, baths, gyms and swimming pools.
If you are going to visit (where you will, of course, be asked to wear slippers), put special nylon socks in your purse. This method is also suitable for trying on shoes. The fungus is tenacious and unpretentious, like the last surviving soldier of evolution, but it also has its own preferences - weaknesses, so to speak. He likes warm and humid places with a lot of people, preferably naked. Therefore, when going to the pool or the beach, treat the skin of your feet with antifungal ointment. Try to wear flip-flops. When getting a manicure or pedicure at a salon, make sure your technician has disinfected the tools and that the towel is clean and starched.
The fungus is not a desperate brave man; it attacks when it sees an environment suitable for itself or the absence of the necessary protection. The disease can be caused by tight shoes, in which the foot rubs and becomes sore. It is also very convenient for the fungus to “cling” to a person whose body’s barrier functions are weakened due to taking antibiotics.
One of the signals of a skin fungus (dermatomycosis) is an itchy rash in which areas that are constantly exposed to high humidity itch: the perineum, feet (including between the toes), and sometimes the armpits. Fungi can affect any part of the body, but dry areas are much less itchy.
Some fungi even eat music, or rather, its media - CDs. If you do not treat the fungus, then you will give yourself up to it “to be devoured.” But self-medicating this disease is more expensive for yourself. If you have the slightest suspicion, be sure to contact a specialist. The fact is that there are a lot of types of fungal infections, and only a specialist, necessarily after a laboratory examination of the scraping, can understand what kind of fungus has affected your skin.
Please note that amateur “diagnosticians” can be deceived by ordinary sneakers. If worn frequently, rubber shoes can cause an allergic reaction to overheating. In this case, redness and rash can be removed with baths with herbal decoctions. Therefore, be sure to get tested.
After diagnosis and consultation with a doctor, if a “fungal enemy” has been discovered, it is necessary to develop a treatment strategy. With the consent of the doctor, you can combine medicines with “folk” ones. The most “salty” way to treat fungal diseases of the skin of the feet and nails was invented by halotherapists (from the Greek word “halos” - salt). At night, cleanly washed and dried feet are advised to sprinkle with salt (especially between the toes), bandage, put on socks and go to bed. There is also a “sweet” “grandmother’s” recipe: repeatedly rubbing in the juice of a tangerine slice or peel. You just need to realize that “traditional” medicine offers mostly superficial “technologies”, and they, no matter how tempting their simplicity may be, can give, at best, only a very short-term effect.
One should not think that scientists are sitting with their hands folded, watching how the confrontation between fungal bacteria and humans will end. Every year new tools appear, dissertations are written and conferences of mycologists are held. However, in each individual case it is extremely difficult to assess the effectiveness of a new drug - this disease, unfortunately, knows how to hide well. In the long list of remedies against skin fungus, it is perhaps necessary to highlight “Travogen”. This cream is very convenient to use, as it can be used only once a day. In addition, it effectively counteracts fungus both on the surface of the skin and in the body.
It is necessary to fight the fungus on “all fronts.” First, thoroughly disinfect everything that the fungus may have come into contact with. Start the hunt for harmful bacteria in the bedroom. Underwear, stockings, socks, tights can be “neutralized” by boiling for 15-20 minutes in a 2% soap-soda solution. Then they should be ironed with a hot iron. Then look into the bathroom. Nail scissors are disinfected by immersing them in alcohol and then burning them over a burner flame. The walls and bottom of the bathtub must be treated with a mixture of equal parts of washing powder and bleach or chloramine. In the hallway you will have to do a lot of work with shoes. Wipe the insoles and sides of the shoes with a swab moistened with a solution of formaldehyde (25%) or acetic acid (40%). Place the tampon in the toe of the shoe, and place the shoe itself in a hermetically sealed plastic bag for 24 hours. Do not forget that acetic acid has a rather strong odor, so finally, thoroughly air your shoes on the balcony.
Along with disinfection, it is necessary to use complex therapy - tablets, varnishes, liquids and ointments. Remember that the main task is to expel the fungus from the body. The absence of visual symptoms can deceive the patient, and the disease will return at the most inopportune moment. Therefore, during the treatment process, monitor the body’s condition using tests.
Pyogenic cocci - staphylococci and streptococci - play an important role in the occurrence of the disease. A number of endogenous and exogenous factors contribute to the development of the disease. Among exogenous factors It is necessary to note skin trauma, increased sweating, pollution, overheating or hypothermia of the body. Endogenous factors- a violation of carbohydrate metabolism in diabetes mellitus, endocrine disorders, thyroid diseases, insufficient activity of the pituitary gland - adrenal system, weakening of immune mechanisms, vegetative neuroses. Malnutrition also plays a role - protein deficiency, carbohydrate abuse, hypovitaminosis. In children, the development of pyodermatitis is facilitated by insufficient physiological barriers, loose epidermis, and high absorption capacity of the skin. It must be remembered that pustular skin diseases, especially severe forms, can be a manifestation of AIDS.
Classification. Depending on the ethological factor, pyoderma is divided into staphylococcal, streptococcal and mixed, according to the depth of the lesion - superficial and deep, according to the course - acute and chronic.
Staphylococcal pyodermatitis.
The pathological process develops in the deep layers of the skin, mainly in the area of hair follicles, in the sebaceous and sweat glands. The following types of staphylococcal lesions are distinguished: ostiofolliculitis, vulgar sycosis, folliculitis, furuncle, carbuncle, hidradenitis, epidemic pemphigus of newborns.
Ostiofolliculitis . The pustule is located at the mouth of the hair follicle, permeated with hair in the center and surrounded by a narrow, pink border. Localized on the skin of the face, neck, forearms, thighs, legs. Occurs after mechanical irritation of the skin, as a result of sweating, and scabies. Individual elements can grow up to 1 cm (staphylococcal impetigo of Bockhardt). Treatment consists of repeatedly lubricating the lesions with solutions of aniline dyes, followed by the use of antimicrobial ointments.
Folliculitis. As the infection penetrates deep into the follicle, an infiltrate appears around the pustule, dense and slightly painful on palpation. The localization of the lesion is varied. After healing, a pinpoint scar remains.
Treatment. Lubricating the lesions with solutions of aniline dyes and ichthyol.
Furuncle . The process involves not only the connective tissue of the follicle, but also the surrounding tissue, subcutaneous fatty tissue. Severe swelling and hyperemia develop around the pustule, a deeply located inflammatory infiltrate with necrosis in the center, painful on palpation. The general condition of the patient is impaired. In its development, the boil goes through the stage of maturation (dense and painful infiltrate), the stage of resolution (necrosis with rejection of the necrotic core), and the stage of healing - scarring. The development cycle of a boil takes 8 - 10 days. It is necessary to be very attentive to patients with boils localized on the skin of the face and, in particular, located above the corners of the mouth. The danger lies in the development of purulent thrombophlebitis of the facial veins with the possible development of meningitis and sepsis, which can lead to the death of the patient. When they recur or are present in large numbers, they speak of furunculosis.
Treatment. During the maturation stage, it is recommended to apply topical dressings with ichthyol, dry heat, and rubbing the skin around the lesion with alcohol solutions of salicylic or boric acid. After opening the boil, a hypertonic solution, hydrogen peroxide, and Vishnevsky ointment are used. Washing in a bath or shower is contraindicated. Warming compresses should not be used due to the possible spread of infection. Surgical treatment is indicated for abscessing boils. Internal use of antibiotics, vitamins B, C, A, and immunomodulators is indicated. For chronic furunculosis and recurrent boils, it is indicated specific immunotherapy: staphylococcal vaccine, staphylococcal toxoid, antifagin, staphylococcal immunoglobulin, antistaphylococcal plasma, autovaccine.
Carbuncle . The defeat of several hair follicles and the penetration of infection into the lymphatic vessels of the deep layers of the dermis and subcutaneous tissue causes purulent-necrotic inflammation, a painful infiltrate is formed, the skin above which becomes purple-red, and in the center a bluish color. Severe swelling appears around the infiltrate. Subsequently, several holes form in the lesion, from which thick pus mixed with blood and green necrotic masses are released, separated along with the pus. After the necrotic mass is rejected, an ulcer forms, which leaves a scar. The general condition of the patient is impaired.
Treatment. Antibiotics, sulfonamides, hemodez, polyglucin, and stimulant therapy are prescribed. Extensive tissue necrosis, swelling, and increasing intoxication are indications for surgical intervention. A hypertonic solution, Vishnevsky ointment, is applied locally.
Hidradenitis - purulent inflammation of apocrine sweat glands. It is most often localized in the armpits, in the area of the external genitalia, and the perianal region. Children before puberty and old people never get sick with hidradenitis, because their apocrine glands do not function. The disease begins acutely. In the thickness of the skin, painful nodes the size of a pea form, quickly increasing in size and protruding above the level of the skin, which takes on a purplish-red color. The nodes soften and open, releasing a large amount of creamy pus. The process ends with the formation of a scar. With multiple nodes, the resulting abscesses can merge into one cavity. The disease quite often takes on a chronic, relapsing character.
Treatment the same as with furunculosis. In severe cases, radiotherapy is used.
Vesiculopustulosis (periporitis) - staphylococcal disease of newborns appears at the end of the first week of life. The orifices of the eccrine sweat glands are affected. Small pustules appear on the scalp, in the folds of the torso and limbs, surrounded by an inflammatory halo. Against the background of existing single elements, fresh pustules may appear. The general condition of the child is disturbed, the temperature rises. The disease lasts up to 10 days with an uncomplicated course and proper treatment. It is possible for the infection to spread across the surface and deep into the skin with the development of abscesses or phlegmons. Weak children may develop septicopyemia with damage to internal organs and systems, pneumonia, otitis, and anemia. Forecast in uncomplicated forms, favorable.
Pseudofurunculosis (multiple abscesses). Caused by staphylococci, the ducts of the sweat glands are affected, inflammation affects the entire eccrine gland. Children in the neonatal period are more often affected, less often under the age of 1 year. In the area of the back of the head, the back of the neck, limbs, buttocks and torso, nodes the size of a pea to a hazelnut, purple-red in color, appear. The nodes may open with the release of yellow-green purulent discharge. There is no necrotic core. The general condition is disturbed, weakness, fever, diarrhea, and malnutrition appear. The process can be complicated by lymphangitis, lymphadenitis, and septic condition.
Treatment should be aimed at combating the pathogen and increasing the child’s body’s defenses. Good care and balanced nutrition are required. Mandatory prescription of antibiotics, taking into account the sensitivity of staphylococci to them. They use gamma globulin, antistaphylococcal plasma, and vitamin therapy. External treatment involves the use of alcohol solutions of aniline dyes; if necessary, opening of abscesses is indicated.
Exfoliative dermatitis Ritter is the most severe form of staphylococcal lesions in newborns. Pathogenic Staphylococcus aureus is cultured from the lesions and blood of patients. The disease is especially severe when it occurs 2–6 days after birth. The lesion usually begins with hyperemia and maceration of the skin in the navel or around the mouth. Then, flaccid blisters appear on various parts of the skin, exudate accumulates under the epidermis, and its detachment occurs with the formation of erosions. Within a week, the entire skin of the child is affected, manifested by hyperemia with large erosive surfaces. The epidermis peels off in large areas and hangs down in loose pieces and ribbons. The actual skin is bare, bluish-red in color, and bleeding. The clinical picture resembles a second-degree burn. Positive Nikolsky sign. The general condition of the child is very serious, the body temperature reaches 41 0 C, a toxic-septic condition develops, and then sepsis. Complications may develop: pyelonephritis, candidiasis, pneumonia, phlegmon and abscesses, otitis. Possible death. A milder and benign course of the disease is possible in the form of an “abortive” form with lamellar peeling and slight hyperemia of the skin, without erosion.
Staphylococcal syndrome burnt skin (SSSS - Staphylococcal Scalded Skin Syndrome) develops in children under five years of age. It has been established that SSSS is associated with the penetration of staphylococcus into the child’s body, which produces a special toxin that causes detachment of the epidermis under the granular layer. Clinical picture corresponds to Ritter's disease. The face of a sick child takes on a “weeping” expression, and impetiginous crusts accumulate around natural orifices. Epithelization occurs within a week.
To prescribe rational therapy, timely differential diagnosis between toxic epidermal necrolysis Lyell and SSSS. For this purpose, histological examination is used to determine the depth of damage to the epidermis. With Lyell's epidermal necrolysis it reaches the basal layer, and with SSSS it is limited to the granular layer. In addition, a cytological examination of the affected cells is carried out. SSSS is characterized by acantholytic keratinocytes.
Treatment aimed at combating the pathogen, increasing the body's defenses, correcting metabolic disorders and functional disorders. Rational care and nutrition are necessary. For SSSS, semisynthetic penicillins, gammaglobulin, antistaphylococcal plasma, and detoxification therapy are prescribed. Local treatment consists of using alcohol or aqueous solutions of aniline dyes and antibiotic creams.
Epidemic pemphigus of newborns . Newborns get sick in the first 7-10 days of life. The disease is caused by highly toxic Staphylococcus aureus. The source of infection is medical personnel or a mother who is sick or has recently suffered some kind of staphylococcal skin lesion. The disease is highly contagious, which leads to epidemic outbreaks in maternity wards. Clinic. Against the background of hyperemic or apparently unchanged skin of the upper extremities and abdomen, blisters filled with serous contents appear, surrounded by a narrow rim of hyperemia. Rapidly increasing in size, they become flat with a flabby tire, their contents are cloudy. When opened, erosions are formed, along the periphery of which there are fragments of the bladder tire; there may be detachment of the epidermis outside the erosion. In severe cases, there is a high temperature, septicopyemia develops, and death is possible. Differentiate This disease is necessary for syphilitic pemphigus. Epidemiological measures consist of immediately isolating the child from other children, conducting a medical examination of medical personnel for the presence of staphylococcal and other infectious skin diseases, and removing sick personnel from work. It is necessary to disinfect premises and sterilize linen.
Treatment. Antibiotic therapy, vitamins B and C. Solutions of aniline dyes and ointments with antibiotics are applied locally.
Prevention consists of a daily examination of medical personnel for the presence of pustular diseases, removal of patients from work, and a thorough examination for the presence of pustular diseases in women in labor.
Class hour “Hygiene rules. Infectious diseases and their prevention"
Form of conduct: conference in the form of information messages.
Target:
Protect students from a careless attitude towards hygiene rules (focus their attention on personal items);
Warn children about the dangers of hepatitis C;
Talk about the flu and its prevention.
Preparation
Find interesting material about infectious diseases.
Make a stand “Health is in your hands.”
Copy the leaflets “Drugs and hepatitis are death.”
Invite specialists to discuss these issues: a biology teacher, a school doctor, a district epidemiologist.
Health is more valuable than anything else. Health comes out in pounds and comes in in ounces.
Russian proverb
Teacher: Guys, in their youth, many people take lightly the most precious thing they have received from nature - their health. Unfortunately, at present we can say that due to chronic diseases of parents, their unhealthy lifestyle and deteriorating environmental conditions, many children are already born sick or with a weakened immune system and are exposed to various diseases in the first days of their existence. Therefore, in order not to follow the expression: “what we have we don’t keep, when we lose it we cry,” it is necessary to be armed with special knowledge about the most dangerous infectious diseases that await us at every step. And to know means not to be afraid, it means to be able to actively resist them!
Conversation one - “Tender” killer
This is the name given to hepatitis C, which was discovered only in 1989, because of its “silent” course. In some patients, clinical symptoms appear only after liver cancer has already developed. The number of patients with hepatitis C in Russia increases every year by an average of 100%, and many doctors are already talking about an epidemic of this virus. How can infection be prevented, who is most susceptible to it, what treatment methods exist? We will try to answer these and some other questions today.
What to do to avoid getting infected with the virus? Avoid contact with blood and other infectious materials; Avoid using general hygiene products (toothbrushes, razors), as well as items such as earrings, etc. Always follow the rules of safe sexual intercourse, including the use of condoms.
How do you know if you are infected with the hepatitis C virus?
As a rule, at the initial stage the disease is very mild, so it can only be detected using a biochemical analysis of blood serum. Then a virological study is carried out. If necessary, liver tissue obtained through biopsy may be examined.
How is the hepatitis C virus transmitted?
Since the virus is contained in the blood of infected people, the main route of transmission of the virus is contact with blood and its products (this is possible not only through blood transfusions, but also through the use of unsterile injection needles and other medical instruments). The virus can also be transmitted sexually, in utero, or during childbirth from an infected mother to her child (rarely). Transmission of the virus is possible through the use of shared personal toilet items - toothbrush, razor, scissors.
How quickly can liver cirrhosis develop due to hepatitis C virus infection?
In 25-30% of patients, cirrhosis develops within 15-20 years, which entails a high risk of developing liver cancer. In 65-75% of patients, acute hepatitis C progresses to the chronic stage.
How is the hepatitis C virus different from other viruses?
Unlike viruses B and D, acute hepatitis C can occur with less severe liver damage, and often without any symptoms at all. Some patients have a fever and may experience nausea and abdominal discomfort. Some people develop jaundice. The disappearance of the virus from the blood within 6 months occurs only in 20% of cases. Next, we need to talk about the chronic stage of the disease, which in most cases is also asymptomatic until the later stages, when cirrhosis of the liver and its complications develop.
Is there a vaccine for hepatitis C virus?
No, there is no vaccine today, but there are modern and effective methods of control and they consist of antiviral therapy, which must be carried out under the strict supervision of a doctor.
Conversation two “About ear hygiene”
Those who use a telephone, player, headphones, or stethoscope for a long time need to remember that these devices should be for individual use.
You can get an infection in your ear by talking from a pay phone, especially if you have abrasions or irritations in your ear. You can expect trouble with a weakened immune system, anemia, gout, but most often with diabetes.
In addition, people for whom headphones and a telephone receiver are a working tool can also suffer from ear dermatitis. These are telephone operators and secretaries. Even doctors can suffer due to frequent use of a phonendoscope, and those who wear a hearing aid or player for a long time.
Symptoms of the disease are discharge from the ear canal and pain when pressing on the auricle.
For itching and mild pain, when the purulent process has not yet developed, the ear canal is lubricated with brilliant green. It dries the skin and reduces itching. This should be done with cotton wool, wound in a thin layer on a match, barely touching the walls of the ear. Do not rub in under any circumstances. Improper lubrication may cause increased itching and watery discharge. Then things will get worse. You should not lubricate the sore spot with “ear” sticks, which are now sold everywhere. Their thickness is not suitable for this procedure. Unfortunately, they can move the decomposed skin closer to the eardrum.
For ear dermatitis, you can drop 1% menthol oil into the ear with a pipette or a teaspoon, 4-5 drops 2-3 times a day. At the same time, tilt your ear so that the instilled solution does not flow out of it.
The disease can also be treated with boric alcohol. Soak a loose cotton wick in it and gently insert it into your ear. You need to keep it for 1 or 2 days and not touch it. The cotton wool itself will spread throughout the skin of the ear canal. To prevent the cotton wool from being dry, you can additionally drip boric alcohol onto it. Then you need to introduce a new wick. The first 2-3 times the procedure is best done under medical supervision.
Treatment with boric alcohol is that it destroys the surface layer of the skin, which dries out and comes off in scales. This is how diseased cells disappear.
If you suffer from allergies, it is best to lubricate the ear canal with hormonal ointments, for example, prednisolone or hydrocortisone. It must be administered using a cotton filter. Under the influence of heat, the ointment in the ear will spread on its own. In severe cases, the disease is treated with antibiotics.
During illness, you need to take multivitamins and B vitamins. Patients with diabetes during an exacerbation of dermatitis need to consult an endocrinologist and strictly adhere to the diet.
Ear dermatitis can be prevented by following basic hygiene rules. To avoid damaging the skin of the ear canal, never remove wax with a needle or pin. Rinsing the ear with dirty water can also lead to the development of the disease. This should only be done by a doctor, who will prescribe special drops to soften the wax and remove it under sterile conditions.
Those who use a telephone, headphones, or stethoscope for a long time need to remember that these devices should be for individual use. If a stranger was talking on your phone, wipe the handset with alcohol or cologne.
Conversation three “What is chlamydiasis?”
The disease is caused by bacteria of the chlamydia genus. In nature, there are two types of chlamydia: the first type affects animals and birds and can cause an infectious disease in humans - psittacosis; the second type of chlamydia is called Chlamydia trachomatis. About 15 of its varieties are known, some of them cause trachoma and lymphogranulomatosis venereum. Two of the 15 varieties of chlamydia infect the human genitourinary system, causing urogenital chlamydia.
In terms of their properties, chlamydia occupy an intermediate position between viruses and bacteria. Therefore, chlamydia is still more difficult to diagnose and treat than ordinary bacterial infections. Urogenital chlamydia is a sexually transmitted disease. There is often a combination of chlamydia with other genitourinary infections - trichomoniasis, gardnellosis, ureaplasmosis.
How does chlamydia manifest?
The incubation period for chlamydia is
approximately 1-3 weeks. A person with chlamydia notices a characteristic glassy discharge from the urethra in the morning. There may be itching or discomfort when urinating, sticking of the sponges of the external opening of the urethra. Sometimes the general condition worsens - weakness is noted, body temperature rises slightly. It should be noted that chlamydia often occurs without obvious symptoms or without them at all.
Even without treatment, after some time (about 2 weeks), the symptoms of the disease disappear. In this case, chlamydia becomes chronic; the chlamydial infection is, as it were, “preserved” in the body, waiting for an opportunity to remind itself again.
What complications can chlamydia cause?
The main danger of chlamydia lies precisely in the complications it can cause. After some time, chlamydia “gets” to the prostate gland, to the seminal vesicles, causing chronic prostatitis and vesiculitis. Further, the chronic process spreads to the epididymis, which can lead to an obstructive form of male infertility.
Chlamydia can also get on the bladder wall and cause hemorrhagic cystitis. Chronic inflammation of the urethra caused by chlamydia leads to the development of its narrowing (stricture). In women, chlamydial infection often causes obstruction of the fallopian tubes, ectopic pregnancy, and postpartum or post-abortion endometritis. Pregnancy in a patient with chlamydia often occurs with complications.
In addition to various complications affecting the genital organs, chlamadia can cause damage to other organs. Then this disease will already be called Reiter's disease or syndrome. With Reiter's syndrome, the eyes (chlamydial conjunctivitis), joints (usually ankles, knees and spine), skin, and internal organs (usually hepatitis, but almost any organs can be affected) can be affected.
What is the diagnosis of chlamydia?
Diagnosing chlamydia is more difficult than diagnosing a bacterial infection. The simplest methods have an accuracy of no more than 40%. The most accurate and accessible method for determining chlamydia in urethral discharge today is the immunofluorescence reaction (RIF) using antibodies labeled with a special substance - FITC.
How difficult is it to treat chlamydia?
Due to the characteristics of chlamydia, antibacterial drugs against them are not as effective as against ordinary bacteria, therefore the treatment of chlamydia is more complex and time-consuming. In addition to the course of antibacterial therapy, it necessarily includes immunomodulatory therapy, multivitamin therapy, normalization of lifestyle, diet, and abstinence from sexual activity for the duration of treatment. Treatment must be carried out by both partners. At the end of the course, control tests are carried out. If chlamydia is not detected, then tests are carried out 2 more times after 1 month (in women - before menstruation). Only after this will it be possible to talk about the effectiveness of the therapy.
What are the preventive measures for chlamydia?
Chlamydia is easier to avoid than to cure. Therefore, we will once again present the rules of sexual hygiene that will protect you from various sexually transmitted diseases:
A permanent partner whom you trust;
Avoid casual sex or use a condom. However, remember that a condom is an effective, but not 100% means of protection against sexually transmitted infections;
If you have the slightest suspicion of infection, consult a urologist;
Remember: an old disease is more difficult to treat.
Conversation four: “Let’s talk about the flu”
Influenza is an acute infectious disease with an airborne transmission mechanism, with epidemic and pandemic (global) spread. Belongs to the group of acute respiratory viral infectious diseases (ARVI), caused by an RNA-containing virus and manifested by high but short-term fever, severe intoxication, and damage to the respiratory system.
Influenza has been known since the time of Hippocrates. The disease received the name “influenza” in the 14th century. The first description of influenza dates back to the beginning of the 17th century.
Virus is the causative agent of the disease
The viral nature of influenza was established in 1918. Influenza viruses belong to the orthomyxovirus family. The genetic information is located in the core of the virus and consists of eight chains of ribonucleic acid (RNA), which encodes the composition of eight structural proteins.
Currently, there are three genera of orthomyxoviruses that cause influenza: A, which was first cultivated in 1939; B - in 1940 and C - in 1947. Cells of the immune system form antibodies to the virus proteins (antigens), which inactivate the virus and protect against recurrence of the disease. The surface antigens most important for antibody production are two: hemagglutinin, designated H, and neuraminidase-N. The structure of virus antigens is variable: depending on their composition, serotypes or strains are distinguished within type A.
Epidemics and pandemics
Approximately every 20-70 years, due to mutation of virus A, a new pandemic strain (i.e., a strain causing a global epidemic) appears, characterized by its own set of hemagglutinin and neuraminidase. Virus A also affects some animals, such as waterfowl and pigs, which are believed to be the source of the new pandemic strain, which usually appears in rural areas of China. Influenza epizootics (epidemics in animals) have not been described in the specialized literature.
Within 2-3 years, an epidemic serotype arises within this strain, which is a variant of the virus with minor deviations in the structure of surface proteins. It causes major epidemics that engulf entire countries. The first recorded influenza epidemic in history occurred in 1889, followed by the devastating Spanish influenza A (H1N1) pandemic in 1918, which killed more than 20 million people. The next pandemic A (H2N2) was noted in 1957-1958. and claimed the lives of 70 thousand people in the United States.
The last influenza A (H3N2) pandemic took place in 1968-1969, during which 34 thousand people died in the United States. The birthplace of the strain is Hong Kong. Another subtype of the A virus, common in our time, A (H1N1), periodically caused large epidemics, but not on the same scale as in 1918-1919. When Asian influenza A (H2N2) appeared in 1957, the A (H1N1) virus disappeared. The A(H2N2) virus also disappeared when the Hong Kong virus was identified in 1968. In 1977, the A (H1N1) virus reappeared and has since spread along with the A (H3N2) virus.
Every year, between 5 and 15% of people worldwide fall ill with influenza. During epidemics, up to 20-40% of the population is affected.
Source of infection. A patient with influenza, especially before the 4-5th day of illness, a recovering person (up to 2-3 weeks), a healthy virus carrier (the virus is in a defective form) contains seven RNA fragments.
The transmission mechanism is airborne. Droplets of mucus when coughing and sneezing spread over a distance of up to 3-3.5 m. The virus can be transmitted through household items (dishes, towels, door handle, etc.). However, it is unstable in the external environment and is destroyed at room temperature in a few hours, and quickly dies when exposed to ultraviolet rays and when dried.
The affected population is people who lack immunity to this variant of the virus. The incidence among children and adolescents is 4.6 times higher than among adults.
Mechanisms of disease development. The virus penetrates the epithelial cells of the mucous membrane of the upper respiratory tract: the nose, then the larynx, trachea and bronchi. Toxic substances (components of the virus, cell decay products, complexes of bacteria with viruses, biologically active substances - kinins and biogenic amines) enter the blood. Severe intoxication and fever develop; the virus penetrates the central nervous system, lungs, heart and skeletal muscles, where it sharply disrupts blood circulation in microvessels: capillaries dilate, the permeability and fragility of their walls increases, blood flow slows down, hemorrhages and swelling occur. These changes cause the appearance of muscle pain, and sometimes the development of inflammation of the heart muscle. Coronary heart disease, peptic ulcers and other chronic diseases may worsen. With the development of disseminated intravascular coagulation (hyperactivation of the blood coagulation system with subsequent depletion and development of bleeding), the danger of damage to the adrenal glands with symptoms of infectious-toxic shock increases. Recovery from uncomplicated influenza, regardless of treatment, occurs on average within 7-12 days.
Immunity, i.e. immunity to infection, appears after an illness. The production of antiviral antibodies (mainly to hemagglutinin and neuraminidase) ensures the creation of specific immunity to a given type and strain of the virus. In some cases, two waves of the disease are observed: first, a person suffers from a mild form of influenza (due to the presence of antibodies from a previous disease), then a more severe form (due to the lack of immunity to the new strain). In people who have had influenza A, immunity lasts on average for about 2-3 years, influenza B - 3-5 years, influenza C - for life. Immunity can be transmitted from mother to fetus and persist in the newborn until the age of six months.
Post-vaccination immunity is developed after 7-15 days and lasts about 4 months. (maximum up to 2 years).
Clinical picture of the disease. The incubation period lasts from 3-4 hours to 3 days. Clinical manifestations for different types of influenza are the same, with the exception of those for influenza C, which is characterized by a predominantly mild course:
1st day: acute onset in 90-92% - chills, general weakness, fever, redness of the face, temperature rises rapidly and reaches high numbers in 6-12 hours (38.5-40°C), muscle pain and joints, headache (behind the eyes, in the temples and parietal region), patients note rawness and dryness in the nasopharynx, sneezing. In the lungs of 60% of patients, scattered dry rales are heard, dullness of percussion sound and tympanitis are detected due to local plethora and edema, swelling of the interstitial tissue of the lungs, and the development of emphysema. The x-ray may show increased pulmonary pattern and thickening of the bronchi. Heart sounds may be muffled, and the heart rate may not correspond to the height of the fever (relative bradycardia);
2-3 days: high fever remains (possibly decreasing by the end of the second day to normal numbers), severe intoxication remains, in 70-80% catarrhal syndrome develops: serous or serous-mucous, slight nasal discharge, cough appears, accompanied by chest pain. Often associated with: hoarseness, a feeling of tightness in the chest, mild shortness of breath. In most patients, by the end of 2-3 days the cough becomes wet and less frequent. In 20-30% of cases, the flu occurs without a runny nose (“dry catarrh”);
Days 4-7: recovery period. The temperature normalizes (usually by the end of 4 days), intoxication gradually decreases (by the 5th-6th day), catarrhal symptoms persist until the 10th-12th day, post-influenza asthenia, general weakness, and increased fatigue appear.
"Intestinal" flu. With influenza, the gastrointestinal tract is not affected, although there may be complaints from the digestive organs. This is usually incorrectly referred to as gastritis or enteritis, possibly associated with an enterovirus infection or food intoxication accompanied by high fever.
Differential diagnosis of influenza. It is carried out by a doctor with an unclear diagnosis - with acute respiratory diseases of a different etiology (parainfluenza, respiratory syncytial infection, rhinovirus infection, adenoviral infections, acute respiratory infections of mycoplasma etiology), tonsillitis, ornithosis; measles, enterovirus infections, typhoid fever, pneumonia. For this purpose, special examinations may be prescribed.
Early criteria for influenza severity. Be sure to consult your doctor if you experience any of the following symptoms that indicate: about severe influenza:
Unusual complexion (pallor at high temperatures, cyanosis, purplish coloration of the skin);
Sharp immobility, lethargy, rarely - agitation;
Severe diffuse headache, severe dizziness, fainting, insomnia;
Severe tachycardia, irregular pulse, decreased systolic (“upper”) blood pressure (below 90 mm Hg);
Shortness of breath, respiratory arrhythmia, suffocation;
Vomiting in combination with any of the above symptoms;
Nosebleeds;
Body temperature is above 40°C.
Complications of influenza. In most cases, the disease self-destructs within 7-12 days, but sometimes complications develop that can pose a threat to the patient’s life. Complications are divided into two groups: those associated directly with the course of influenza and with the addition of a second bacterial infection.
Group I (1-2 days of illness): hemorrhagic pulmonary edema, meningoencephalitis (serous), infectious-toxic shock. Children with high fever may experience febrile seizures;
Group II complications: pneumonia (most often), otitis media, glomerulonephritis, purulent meningitis and septic conditions. Bacterial complications after the patient feels better: high fever may rise again, cough with sputum, chest pain, etc. They may be delayed for up to 1-2 weeks.
Bed rest for at least 5 days.
Plenty of hot drinks, light dairy and vegetable foods.
Antihistamines (diphenhydramine 0.05 g 2-3 times a day).
Ascorbic acid up to 1.5-3 g/day.
In children with influenza, aspirin is not prescribed, since it is possible to develop a rare specific lesion of the central nervous system - Reye's syndrome, which initially manifests itself as uncontrollable vomiting and deterioration of the general condition, with mortality in 20-40% of cases. In 1984, 204 cases of this disease were described in the United States in influenza and chickenpox.
For the treatment of children, the average single dose of paracetamol (regardless of the dosage form - tablets or rectal suppositories) is 5-10 mg/kg of body weight (daily - approximately 65 mg/kg) every 4-6 hours. Children under 12 years of age should not take paracetamol more often 5 times a day. Paracetamol is generally a safer drug than aspirin, but when used in high doses, drug damage to the liver and kidneys is possible.
Conclusion
Teacher: From our conversation about various infectious diseases, you received qualified answers to many questions. Discussion of these problems showed that any disease is accompanied by suffering, painful stress, general physiological ailments and poses a great danger, especially for children. The main conclusion you should make for yourself is not to get sick! And this means being attentive to preventive measures, supporting the protective functions of your body, i.e. your immunity.
Remember: “A healthy person doesn’t need a doctor!”
Pustular skin diseases (pyoderma) are infectious skin lesions that are caused by the introduction of staphylococci or streptococci.
Less commonly, the cause of pyoderma can be other pathogens - Pseudomonas aeruginosa, Proteus vulgaris, Escherichia coli, pneumococci. Pyoderma is a very common disease.
Etiology. The causative agents of pyoderma are most often staphylococci and streptococci, which belong to the gram-positive microbial flora. The most pathogenic of all types of staphylococci are species such as Staphylococcus aureus (the most pathogenic), epidermal and saprophytic staphylococcus (residents of the normal skin flora).
Staphylococci are facultative anaerobes and colonize the upper layers of the epidermis, mainly in the area of the mouths of hair follicles, sebaceous and sweat glands, i.e. they most often affect the skin appendages.
Streptococci (saprophytic and epidermal) are present on the surface of smooth human skin without connection with skin appendages, most often on the face and in the area of natural folds.
Under conditions of normal homeostasis of the human body, normal sweating and sebum secretion with a slightly acidic pH environment, the resident microflora of the skin surface is a constantly operating “biological brake”, which, thanks to microbial antagonism, prevents the proliferation of pathogenic microflora, displacing it from the microbial population. Systemic immune and endocrine disorders of the macroorganism, changing the chemistry of skin sweat and sebum, can lead to biological changes in the resident flora and the transition of pathogenic strains of staphylococci and streptococci to pathogenic ones, which can also be associated with gram-negative flora.
Pathogenesis. There are exogenous and endogenous factors that contribute to the penetration of pyococci into the skin and the development of pyodermatitis.
Exogenous factors include microtraumas and macrotraumas (scratching, abrasions, cuts, insect bites); maceration of the stratum corneum as a result of increased sweating and exposure to moisture; skin contamination, both domestic (violation of hygiene standards) and professional (lubricating oils, flammable liquids, coarse dust particles of coal, cement, earth, lime); general and local hypothermia and overheating.
All of these exogenous factors disrupt the protective barrier function of the skin and promote the penetration of microflora.
Endogenous factors include:
1) the presence in the body of foci of chronic infection (ENT pathology, odontogenic, urogenital chronic pathology);
2) endocrine diseases (diabetes mellitus, hypercortisolism, hyperandrogenism);
3) chronic intoxication (alcoholism, drug addiction);
4) nutritional disorders (hypovitaminosis, protein deficiency);
5) immunodeficiency states (treatment with glucocorticoid drugs, immunosuppressants, HIV infection, radiation therapy).
Both endogenous and exogenous factors ultimately lead to a decrease in humoral and cellular immunity, as a result of which the protective function of the skin decreases. This leads to a change in the quantity and composition of the microbial flora on the surface of the skin towards the predominance of pathogenic species and strains of cocci.
Classification. Pyoderma is classified according to etiological principle. According to this classification, staphylococcal, streptococcal and mixed (streptostaphylococcal) skin lesions are distinguished. Each group includes superficial and deep pyoderma, which can occur acutely or chronically.
Superficial pustular skin lesions include those nosological forms in which the epidermis and upper layer of the dermis are affected.
With deep pyodermatitis, the lesion can involve not only the dermis, but also the hypodermis.
Staphylococcal pyoderma
Staphylococcal pyoderma, occurring acutely:
1) superficial (ostiofolliculitis, superficial folliculitis, staphylococcal bullous impetigo (in children), staphylococcal pemphigoid of newborns);
2) deep (deep folliculitis, furuncle, acute furunculosis, carbuncle, hidradenitis, multiple abscesses of infants).
Staphylococcal pyoderma, occurring chronically:
1) superficial (sycosis vulgar);
2) deep (chronic furunculosis (localized and general), folliculitis decalvans).
Streptococcal pyoderma
Streptococcal pyoderma, occurring acutely:
1) superficial (streptococcal impetigo, diaper rash);
2) deep (streptococcal ecthyma, erysipelas).
Streptococcal pyoderma that occurs chronically - chronic diffuse streptoderma.
Streptostaphylococcal pyoderma
Streptostaphylococcal pyoderma, occurring acutely:
1) superficial (impetigo vulgar);
2) deep (ecthyma vulgar).
Streptostaphylococcal pyoderma, occurring chronically (chronic atypical pyoderma):
1) ulcerative chronic pyoderma and its varieties (chancriform pyoderma);
2) ulcerative-vegetative pyoderma;
3) abscessing chronic pyoderma and its varieties (inverse conglobate acne).
Various pyoderma can occur primarily on previously unchanged skin, and also secondary to existing skin lesions. Most often these are itchy dermatoses (scabies, lice, atopic dermatitis, eczema), predisposing to the development of pustular pathology.
Clinic. Skin rashes with pyoderma are polymorphic. The type of primary elements of the rash depends on the type of pathogen and the depth of skin damage.
Staphylococcal skin lesions are usually associated with pilosebaceous follicles and sweat glands (apocrine and eccrine), and the inflammatory reaction they cause is purulent or purulent-necrotic in nature.
Different nosological forms of pustular skin lesions can be manifested by the same element of the rash. For example, ostiofolliculitis, superficial folliculitis and vulgar sycosis manifest as a follicular abscess, and an inflammatory follicular nodule occurs with folliculitis (superficial and deep), folliculitis decalvans, and sometimes with a small boil.
An inflammatory node is detected at the onset of a boil, carbuncle, or multiple abscesses in infants (pseudofurunculosis).
Streptococcal skin lesions, unlike staphyloderma, do not affect the pilosebaceous follicle and sweat glands. They are characterized by predominantly superficial inflammatory lesions of smooth skin with the release of serous exudate.
The main primary eruptive element in superficial streptoderma is the superficial blister. In those localizations of the skin where the stratum corneum is relatively thin, the streptococcal vesicle looks sluggish and flabby; it is called phlyctena. In those areas where there is hyperkeratosis (palms, soles, periungual areas), streptococcal blisters may have a tense appearance, a fairly dense covering, serous or cloudy contents.
In case of deep streptococcal lesions of the skin, the primary eruptive element may be a deep epidermal pustule with limited necrosis of the underlying area of the dermis (ecthyma) or edematous erythema with clear, rapidly increasing borders (erysipelas).
1. Staphylococcal pyoderma
Ostiofolliculitis
This is an inflammation of the mouth of the hair follicle. It manifests itself as a small (up to 2–3 mm in diameter) cone-shaped or hemispherical abscess containing whitish or yellowish cloudy pus. The pustule is located at the mouth of the hair follicle, permeated with hair in the center and surrounded by a narrow rim of hyperemia. Ostiofolliculitis most often occurs on open areas of the body exposed to friction, shaving, scratching, and exposure to lubricating oils (face, neck, extensor surfaces of the extremities, scalp). The process is superficial, resolution is observed after 2 – 3 days. The pustule dries to a yellowish-brownish crust, the halo of hyperemia disappears, and after the crust is rejected, slight hyperpigmentation may remain.
In unfavorable situations (friction, maceration), ostiofolliculitis can deepen (transform into folliculitis and even a boil), or individual ostiofolliculitis can increase in area and form the so-called staphylococcal impetigo.
Folliculitis
This is a purulent inflammation of the hair follicle affecting its upper part or the entire hair follicle. Depending on the depth of the lesion, folliculitis is distinguished between superficial and deep.
In most cases, superficial folliculitis begins, like ostiofolliculitis, with a small pustule at the mouth of the follicle. The process quickly spreads deep into the follicle, which is clinically manifested by an increase in the zone of hyperemia, the appearance of a painful dense inflammatory papule at the base of the abscess with a diameter of more than 5 - 7 mm. In cases where superficial folliculitis develops without previous ostiofolliculitis, a follicularly located inflammatory papule with a diameter of about 5 mm immediately forms. It has a conical or hemispherical shape, permeated with hair in the center. After 2–3 days, a follicular tense pustule forms around the hair. After 4 - 7 days, the pustule dries to a yellowish crust, after which stagnant hyperemia may remain and pigmentation may persist.
Deep folliculitis is characterized by total damage to the entire hair follicle, accompanied by severe pain, hyperemia, swelling, and infiltration of tissue around the follicle, i.e., an inflammatory node is formed that clinically resembles a boil. It is distinguished from the latter by the absence of a necrotic core in the center of the infiltrate.
Staphylococcal impetigo
This form of the disease occurs mainly in newborns when they are kept unhygienically. Pathogenic staphylococci that have penetrated the skin release a powerful exotoxin - exfoliatin, which destroys the desmosomes of epidermal cells at the level of the granular layer. This leads to the formation of individual blisters filled with yellow pus. This lesion is called epidemic staphylococcal pemphigus of newborns, or staphylococcal pemphigoid. The disease is severe with an increase in body temperature, the development of intoxication syndrome up to septicemia. Children do not breastfeed well, lose weight, and septic complications are possible.
Staphylococcal pemphigoid usually occurs 3 to 5 days after the baby is born, but it can develop during the first month of life. Superficial flaccid blisters (phlycten) appear, ranging in size from a pea to a hazelnut. Their contents are first serous, then serous-purulent. The blisters are surrounded by a mild inflammatory rim and are located on normal skin.
After the bubble ruptures, a weeping erosion remains, surrounded around the periphery by the remains of the tire. Unlike normal impetigo, a crust does not form. The rashes are most often located on the chest, back, and skin folds. There are practically no rashes on the skin of the palms and soles.
The malignant course of staphylococcal pemphigoid leads to universal skin lesions. This condition is called Ritter von Rittershain exfoliative dermatitis, or staphylococcal scalded skin syndrome. The clinical picture of this syndrome is characterized by an acute onset, high body temperature and intoxication, an increase in diffuse erythema of the skin, first around the navel and mouth, then in the skin folds. There is a superficial detachment of the epidermis at the level of the granular layer, fragments of the stratum corneum hang from the affected skin. The clinical picture may resemble toxic epidermal necrolysis (Lyell's syndrome), in which epidermal detachment is observed at the level of the basement membrane.
Without adequate antibacterial and detoxifying treatment, newborn babies may die.
Staphylococcal or vulgar sycosis
This is a chronic superficial skin lesion, manifested by numerous recurrent ostiofolliculitis and superficial folliculitis with subsequent infiltration of the surrounding skin.
The disease, as a rule, is observed in adult men and is localized on the face (the area where the mustache and beard grow), much less often it spreads to the pubis, the edges of the eyelids, eyebrows, scalp, and axillary areas. In the pathogenesis of vulgar sycosis on the face, chronic foci of infection in the head area and repeated traumatization of the skin during wet shaving are important.
The disease begins with small follicular pustules, which recur repeatedly in the same place. Gradually, the process expands due to the involvement of more and more new follicles and the formation of new follicular pustules along the periphery of the lesion. The skin in the affected area becomes bluish and diffusely infiltrated. After opening the pustules, accumulations of purulent crusts of varying thickness are formed, and diffuse weeping occurs in the places where they arise. Hair removal in the affected area is painless and easy. In the root zones of epilated hair, a glassy muff is clearly visible.
Vulgar sycosis occurs over a long period of time, recurring for many years. Subjective sensations are insignificant; patients may feel slight itching, burning, and tightening of the skin at the affected area.
In its natural course, the process resolves on its own within 2 to 3 months, leaving cicatricial baldness in its place.
Folliculitis decalvans, or lupoid sycosis
This is a rare form of staphylococcal lesions of the hair follicle, in which chronic folliculitis without pronounced pustulization and ulceration leads to skin atrophy and persistent baldness. The etiology and pathogenesis are not well understood. The causative agent is Staphylococcus aureus; additional colonization of gram-negative microbial flora in the hair follicles is also possible. This can be caused by altered immunological reactivity of the body against the background of seborrheic status, chronic focal infection, and diabetes mellitus. The microbial factor, apparently, is only one of the pathogenetic links in the development of this disease.
Middle-aged and elderly men are more often affected. The pathological process can be located in the area of the beard and mustache, in the temporal and parietal areas of the scalp.
The disease is characterized by a chronic course. Against the background of congestive erythema, grouped follicular nodules and pustules appear, as well as follicularly located light yellow crusts and grayish scales, which are easily removed by scraping. These elements merge and form a clearly demarcated round or oval infiltrated plaque with a diameter of 2–3 cm, wine-red in color, with a flat, painless infiltrate at the base. Gradually, in its central part the skin turns pale, thins, becomes smooth, devoid of hair and slightly sinks - characteristic central atrophy of the skin develops. Within its boundaries, new follicles do not appear and single hairs or tufts of hair may still remain. The peripheral zone of the lesion, about 1 cm wide, is slightly elevated, more hyperemic, and moderately infiltrated. In this zone there are numerous follicular papules with rare pustules in the center. The lesion slowly progressively increases in area due to the appearance of new folliculitis along the periphery. Sometimes the growth of the lesion prevails at one of its poles, which leads to the formation of an irregular, asymmetrical shape of the lesion. During diascopy of the edge of the lesion, the apple jelly symptom is not detected.
The course of the process is chronic, lasting for many months and years with periods of incomplete remission and spontaneous exacerbations. The general condition of the patients is not disturbed, subjective sensations are usually absent. When lesions are located on the scalp, patients may experience pain, which is apparently explained by the anatomical features of the skin in this area (proximity of the aponeurosis).
Furuncle
This is an acute purulent-necrotic inflammation of the hair follicle and perifollicular connective tissue. The furuncle refers to the deep form of staphyloderma. The primary eruptive element of a boil is an inflammatory node that forms around a hair follicle infected with staphylococci.
The onset of the disease is associated with the formation of an inflammatory purulent infiltrate around the hair follicle, which in the early stages can be small in size (like folliculitis), but the process quickly covers the entire depth of the hair follicle, the surrounding connective tissue and the adjacent sebaceous gland and is an inflammatory congestive-hyperemic node , rising cone-shaped above the surface of the skin. Soreness increases, tugging, throbbing pain is possible.
When the boil is localized in the face area, especially on the upper lip, there is extensive swelling around the infiltrate. After 3–4 days, a fluctuation begins to be detected in the center of the infiltrate; a purulent fistula is formed around the hair; when opened, a small amount of thick pus is released and a small ulcer is formed. At the bottom of this ulcer a greenish necrotic core is revealed. After another 2 to 3 days, the necrotic rod is rejected with a small amount of blood and pus, after which pain and inflammation are significantly reduced. In place of the rejected necrotic core, a deep crater-shaped ulcer is formed, which, after being cleared of pus and remnants of necrotic masses, is filled with granulations, a retracted scar is gradually formed, the size and depth of which depends on the size of the necrosis in the center of the boil.
A boil can occur in any area of the skin where there are hair follicles. Single boils are usually localized on the forearms, face, back of the neck, lower back, buttocks, and thighs.
Typically, single boils are not accompanied by a disturbance in general well-being and an increase in body temperature. The exception is a facial boil.
Particular attention should be paid to patients whose boil is located in the lip area, on the nose, in the nasolabial triangle and in the area of the external auditory canal. Mimic movements of the face, traumatization of boils during shaving or an attempt to squeeze them out can lead to serious complications (thrombophlebitis of the facial veins).
The process is accompanied by the appearance of diffuse hyperemia of facial tissues, their tension and soreness.
Pain and signs of general intoxication increase: body temperature can reach 40 ° C, patients complain of chills, weakness, and headache. Confusion may occur. The hemogram changes: leukocytosis, accelerated ESR, shift of the leukocyte formula to the left.
The anatomical features of the venous outflow on the face, the presence of anastomoses with the cavernous sinus of the brain can lead to more severe complications - the spread of staphylococcal infection and the development of meningitis, meningoencephalitis, septicopyemia and sepsis with the formation of multiple abscesses in various organs and tissues. Thus, with untimely and irrational treatment of a facial boil, the process can be malignant and lead to death.
Boils of the extremities, especially those located near the joints and easily injured, can be complicated by regional lymphadenitis and lymphangitis. Sometimes acute glomerulonephritis develops.
Furunculosis
This is the presence of multiple boils on the skin or sequential recurrence of boils. There are acute furunculosis, in which many boils are present on the skin at the same time, and chronic furunculosis, when boils (single or multiple) recur sequentially at short intervals over months and even years. According to prevalence, localized (limited) furunculosis and widespread (disseminated) furunculosis are distinguished.
Acute furunculosis develops, as a rule, with short-term exposure to exogenous and, less often, endogenous predisposing factors, while chronic furunculosis develops with the long-term presence of endogenous predisposing factors. These include the presence of foci of chronic infection, diabetes mellitus, unbalanced nutrition, hypovitaminosis, chronic intoxication, hypercortisolism, and immunodeficiency states.
Localized furunculosis (acute and chronic) develops as a result of the introduction of staphylococci into several adjacent follicles. This is facilitated by a number of factors: pronounced virulence of staphylococcus, trauma, skin contamination with lubricating oils, local hypothermia of the skin.
Carbuncle, or carbon
This is a very severe and deep form of staphyloderma, which is a purulent-necrotic inflammation of the deep layers of the dermis and hypodermis, involving many hair follicles in the process. It is most often caused by the most pathogenic Staphylococcus aureus. In the pathogenesis of carbuncle development, the weakening of the body's defenses, diabetes mellitus, and immunosuppressive conditions are of great importance.
More often, the carbuncle is single and develops in places that are most susceptible to clothing friction (the back of the neck, lower back, buttocks, upper and lower extremities).
The disease begins with the formation of an extensive inflammatory node in the deep layers of the dermis and hypodermis. A dense, painful inflammatory nodule is not clearly defined, quickly increases in depth and width and can reach quite large sizes. Within a few days, the infiltrate acquires a purplish-red color and protrudes significantly above the surface of the skin. Perifocal edema and throbbing pain in the area of the node increase.
The general condition of the patient is sharply disturbed: high temperature, chills, and headache are noted. After 5–7 days, a fluctuation appears in the center of the infiltrate, indicating purulent melting. The skin in the center of the infiltrate becomes black due to necrosis. The cavity is opened to the surface by multiple fistulous openings, corresponding to the mouths of the hair follicles, from which thick yellow-greenish pus mixed with blood is released. In the resulting holes, deep-lying greenish necrotic masses are visible.
Melting of the edges of individual fistula tracts leads to the formation of a single extensive ulcer with uneven edges and a necrotic bottom.
During the natural course of the process, necrotic masses can persist for a long time, up to 2–3 weeks, gradually being rejected. This is accompanied by a gradual improvement in the patient’s general condition, a decrease in body temperature to normal, and a significant reduction in local swelling and pain. After rejection, a deep, sometimes extensive ulcer with undermined edges forms, sometimes reaching the fascia and muscles, the bottom of which is gradually filled with granulations, and the defect is scarred within 2 to 3 weeks. A rough, irregularly shaped scar remains.
The most malignant course has a carbuncle of the facial zone, as it can be complicated by thrombophlebitis of the facial veins, thrombosis of the cerebral sinuses, embolism, septicemia, and symptoms of sepsis.
Hidradenitis
This is a purulent inflammation of the apocrine sweat glands. The disease is characteristic of mature people whose apocrine sweat glands are actively functioning. The most common form of localization is hidradenitis in the axillary area. But hidradenitis can also occur in all anatomical locations where apocrine sweat glands are located: the area around the nipples, perianally, on the skin of the scrotum, labia majora, around the navel.
Factors contributing to the introduction of pathogenic staphylococci into the mouths of hair follicles and excretory ducts of the glands are skin trauma, irrational use of antiperspirant deodorants, as well as all pathogenetic factors leading to immunosuppression.
The disease begins with the appearance in the deep layers of the skin of a dense node or several nodes, which are initially determined only by palpation. Gradually their size increases, the skin over them turns red. As the inflammatory reaction increases, the nodes adhere to the skin, it becomes bluish-red in color, and the pain intensifies.
In cases where several nodes are located nearby, a continuous tuberous infiltrate consisting of hemispherical nodes can form. The process can be two-way. Over the course of several days, the nodes undergo central softening due to the development of an abscess and are gradually opened by purulent fistulas with the release of thick yellow-green pus. Gradually, the abscess cavity empties, the severity of inflammation subsides, and the process of scarring begins. At the site of hidradenitis, a retracted scar or scars are formed (depending on the number of fistula tracts).
In the case of timely treatment at the infiltration stage, the process may not abscess, but gradually resolve without a trace.
2. Streptococcal and streptostaphylococcal pyoderma
Impetigo streptococcal
This common superficial form of streptoderma primarily affects children and young women. Skin lesions usually involve exposed areas: the face (around the nose and mouth), parotid areas, and limbs.
The disease becomes more frequent in the warm season. In conditions of close bodily contact, streptococcal infection is easily transmitted from a sick person to a healthy person. Epidemic outbreaks are possible in children's groups.
In the occurrence of streptococcal impetigo, micro- and macrotraumas of the skin and maceration are of great importance.
Pathogenic streptococci that secrete proteolytic enzymes, having penetrated into the affected areas of the skin, lyse the intercellular connections of the surface layers of the epidermis, leading to the formation of the primary eruptive element - phlyctena, which dries out to form a grayish-yellowish crust. A small halo of hyperemia is noticeable around the phlyctena and crusts. Conflicts and crusts quickly increase in size and can merge. The serous exudate of the opened phlyctenas infects the surrounding skin, and the process quickly spreads.
Under favorable conditions, erosions epithelialize, crusts fall off, and in their place remain slight hyperemia, then light pigmentation. No permanent marks are observed. The average duration of development of phlyctena into the crust and completion of epithelization does not exceed a week. However, with constant dissemination and the emergence of more and more fresh conflicts, the process may be delayed. With single rashes of a small area, subjective sensations are insignificant (mild itching). With large affected areas, patients may complain of burning and itching.
Complications of streptococcal impetigo can include lymphangitis and regional lymphadenitis, eczematization (especially in people prone to atopy), and in children - the development of infectious-toxic glomerulonephritis.
There are several types of impetigo: slit-shaped, ring-shaped, vesicular (bullous) and its variety – periungual impetigo.
Infection with streptococcus of the skin of the wings of the nose and under the nose can lead to the development of superficial impetiginous rhinitis, manifested by superficial inflammation of the skin of the wings of the nose and the formation of phlyctenas there, which dry out as confluent crusts.
Angular impetigo, or streptococcal impetigo, affects the corners of the mouth on one or both sides. The primary eruptive element is the superficial phlyctena, which very quickly opens and forms a slit-like erosion surrounded by a narrow rim of macerated stratum corneum of the epidermis. Periodically, in the morning after sleep, the erosion may become covered with a loose yellowish crust, which quickly peels off, again exposing the weeping, slit-like erosion. Palpation of the base of the erosion does not reveal significant infiltration.
Impetigo vulgar or contagious
The disease is caused by pathogenic streptococci, which cause the primary eruptive element - subcorneal lycten. However, staphylococcal flora very quickly joins in, leading to pronounced suppuration and the formation of purulent cavity elements that dry out with honey-yellow or greenish crusts.
Like streptococcal impetigo, vulgar impetigo most often occurs in children on open areas of the body. With close physical contact, especially in children's groups, massive outbreaks of vulgar impetigo are possible.
Streptococcal diaper rash
Streptococcal infection, accompanied by inflammation of the contacting surfaces in the skin folds and characterized by a long course with frequent relapses.
The development of this lesion is initially based on intertriginous dermatitis (diaper rash), which develops as a result of friction of skin surfaces in the fold, maceration of the stratum corneum due to intense sweating, discharge from natural orifices and other reasons, in the absence of proper hygienic skin care (fermentation and decomposition occurs sebum and sweat). These factors lead to the development of an inflammatory reaction in the skin folds and the addition of streptococcal flora, often in association with yeast-like fungi.
A number of diseases predispose to the development of diaper rash: obesity, type 2 diabetes mellitus, gout, severe forms of seborrheic dermatitis, hypercortisolism.
Manifestations of streptococcal diaper rash are quite typical: the contacting skin surfaces in the folds (especially in obese people) are hyperemic, swollen, maceration of the stratum corneum and its erosion are noted. Due to the constant impact of friction, the resulting streptococcal lycten instantly opens, leaving behind confluent surface erosions with a border of macerated stratum corneum exfoliated along the edge. The eroded zones become wet, and cracks appear deep in the fold. The edges of the lesions are scalloped. Subjectively, patients complain of burning, itching, and if cracks occur, pain. With regression of diaper rash, persistent pigmentation may remain.
Chronic diffuse streptoderma
This is a chronic diffuse inflammation of the skin of the lower extremities as a result of vascular disorders, prolonged repeated hypothermia or maceration of the skin.
The skin of the legs is usually affected. The first eruptive element is multiple conflicts, which quickly dry out to crusts, under which surface erosions remain on a stagnant-hyperemic base. The lesion is asymmetrical, the contours are clear, the outlines are large scalloped. The surface of the lesion is covered with lamellar and layered crusts or crust-scales of a yellowish-greenish color, when removed, an erosive surface with serous-purulent exudate is revealed.
Due to the peripheral growth of the lesions, their area gradually increases; fresh conflicts may be found at the edges, which merge with the main lesion, dry out with crusts and create scalloped contours of the affected area. The process may be complicated by lymphangitis and lymphadenitis, and eczematization may develop. Without adequate treatment, this form of pyoderma is chronic and can recur. In some cases, chronic diffuse streptoderma develops around infected wounds, purulent fistulas, and trophic ulcers. In such cases, it is usually called paratraumatic streptoderma.
Ecthyma vulgaris, or streptococcal ulcer
This is a deep form of streptoderma.
In addition to streptococci, staphylococci and gram-negative flora (Proteus vulgaris, Escherichia coli and Pseudomonas aeruginosa) may be involved in the development of ecthyma. The development of the disease is facilitated by skin injuries, insufficient skin hygiene, impaired blood supply to the lower extremities, immunodeficiency states, and chronic intoxication.
Ecthyma is most often localized on the skin of the legs, but can occur on the skin of the thighs, buttocks, and lower back. The disease begins with the appearance of a large phlyctena with cloudy (sometimes hemorrhagic) contents or a deep epidermal-dermal pustule. Along the periphery of these elements there is a bright hyperemic border. Rapidly developing necrosis leads to the formation of a deep ulcer covered with a brown crust. The elements are large, with a diameter of 2 cm or more. The crust is deeply immersed in the skin tissue, and a soft infiltrate gradually forms around it.
If the crust is removed, a deep, round ulcer with steep or undermined edges and an uneven necrotic bottom is exposed. Self-regression of ecthyma is slow. Over the course of 2 to 4 weeks, it gradually scars, leaving behind an atrophic scar with surrounding hyperpigmentation. Ecthymas can be multiple, but are always located separately. If no complications arise, the general health of the patients remains satisfactory.
Ecthyma can be complicated by regional lymphadenitis, lymphangitis, and sometimes phlebitis. Glomerulonephritis may develop. With prolonged existence of ecthyma on the legs, transformation into chronic ulcerative pyoderma is possible.
Erysipelas
It is an acute deep streptococcal inflammation of the skin, accompanied by fever and intoxication.
The source of infection can be both bacteria carriers and patients with tonsillitis, chronic rhinitis, tonsillitis, streptoderma, i.e. those diseases caused by streptococci.
The cause of the disease is group A hemolytic streptococcus, which penetrates damaged skin and affects the lymphatic vessels of the skin, leading to acute inflammation. Chronic trauma to the skin, the presence of cracks, and scratching can lead to relapses of erysipelas and persistence of infection in the lymph nodes. Repeated inflammatory processes lead to cicatricial changes in the tissue around the lymphocapillaries, their obliteration and the development of elephantiasis of the limb.
The incubation period of infection ranges from several hours to several days. The disease begins acutely, and some patients experience prodromal phenomena in the form of malaise, chills, and headache. At the site of penetration of the pathogen into the skin, a red, swollen spot appears, which quickly increases in size, acquiring a scalloped character. The boundaries are clear, the skin in the lesion is swollen, tense, shiny, and hot to the touch.
At the site of the lesion, patients are bothered by pain (especially in the marginal zones of the lesion), burning sensations, and distension. This is accompanied by a sharp rise in temperature and other symptoms of intoxication (chills, headache, severe weakness, and in the most severe cases, confusion).
According to the severity of intoxication, mild, moderate and severe forms of erysipelas are distinguished. According to the clinical manifestations in the lesion, the usual form is distinguished (erythema and edema), bullous-hemorrhagic (against the background of erythema, blisters with serous-hemorrhagic contents form), phlegmonous form (suppuration of the subcutaneous fatty tissue) and the most severe - gangrenous form (necrotizing fasciitis), which occurs with gangrene of the subcutaneous tissue, fascia and underlying muscles.
Erysipelas of the face can be complicated by dire consequences, including thrombosis of the sinuses of the brain and the development of sepsis. In all forms of the disease, regional lymph nodes are enlarged and painful.
The main complications of erysipelas include the development of persistent lymphostasis (elephantiasis), the formation of abscesses, phlegmon, phlebitis, and gangrene. Sensitization to streptococcal toxins can provoke the formation of glomerulonephritis, myocarditis, rheumatism, and dermatomyositis.
Due to the high contagiousness of the disease and the possibility of developing severe complications, patients should be hospitalized in a purulent or infectious diseases department for maximum isolation from other patients.
3. Atypical chronic pyoderma
A special group of rare chronic (atypical) pyodermas has been identified from purulent skin diseases. It included ulcerative atypical pyoderma (chronic pyococcal ulcer) and its variety - chancriform pyoderma; chronic abscess pyoderma and its variety – inverse conglobate acne.
All these rare nosological forms of atypical pyoderma have different etiologies and pathogenesis. Monocultures or associations of microorganisms (staphylococci, streptococci, enterococci, Escherichia coli and Pseudomonas aeruginosa, Proteus vulgaris) can be sown from the lesions.
There is no connection between the type of pathogen and the form of pyoderma. The development of these forms of chronic pyoderma is caused not so much by an infectious factor as by an unusual, altered reactivity of the macroorganism, the type and severity of immunodeficiency.
All patients with chronic atypical pyoderma exhibit a variety of immune disorders, as well as a decrease in the body's nonspecific resistance.
In some cases, patients with chronic atypical pyoderma are diagnosed with ulcerative colitis, Crohn's disease, chronic myeloid leukemia, lymphoma, diabetes mellitus, alcoholism and other severe concomitant diseases leading to immunodeficiency.
All forms of chronic atypical pyoderma have common symptoms:
1) presence of immunodeficiency;
2) chronic course;
3) granulomatous structure of the infiltrate in the dermis and hypodermis;
4) resistance to treatment with antibacterial drugs while maintaining the sensitivity of microbial flora isolated from foci to these antibacterial agents;
5) high skin sensitivity to various irritants.
Chronic atypical pyoderma can begin with ordinary pyoderma or with skin injuries secondarily complicated by pyococcal infection. They gradually transform into an ulcerative and ulcerative-vegetative atypical form of pyoderma, clinically resembling skin tuberculosis or deep mycoses.
Diagnosis is based on the clinical picture and the results of microbiological, histological and immunological studies.
There are no standard regimens that could quickly provide a positive clinical effect. Treatment of patients with chronic atypical pyoderma is a difficult task, which often cannot be solved during the first standard treatment.
When immune disorders are detected, they are corrected, after which it is advisable to carry out combined antibacterial therapy for the patient, taking into account the sensitivity of the microbial flora.
However, it should be noted that antibiotic therapy alone does not have a significant effect. It should be combined with short courses of glucocorticosteroids, anti-inflammatory drugs, and sometimes with cytostatics and immune replacement therapy.
For abscessing acne inversus, in addition to antibiotics, treatment is prescribed with isotretinoin at 0.5–1 mg per 1 kg of body weight per day for 12–16 weeks. This treatment has a positive effect, as well as in severe forms of acne. Patients suffering from chronic pyoderma need to undergo repeated courses of well-founded, individually selected therapy.
Principles of therapy for pyoderma. In the treatment of pyoderma, it is necessary to follow the main principles.
1. Influence the cause of pyoderma, i.e. carry out etiotropic (antimicrobial) treatment.
2. Eliminate predisposing factors (pathogenetic therapy): correct carbohydrate metabolism, eliminate vitamin deficiency, sanitize foci of chronic infection, immunostimulating therapy.
3. Prevent the spread of infection to undamaged areas of the skin (temporary prohibition of washing and visiting swimming pools, prohibition of compresses, massage of the skin in the area of pyoderma, treatment of unaffected skin around lesions of pyoderma with antiseptics).
Etiotropic therapy for pyoderma is aimed at suppressing the vital activity of the pyococcal flora that causes a purulent disease of human skin. This therapy can be general (systemic) or external, local (topical).
Indications for general antibacterial therapy:
1) multiple pyoderma, their rapid spread over the skin, lack of effect from external therapy;
2) the appearance of lymphangitis, enlarged and painful lymph nodes;
3) the presence of a general reaction of the body to purulent inflammation: increased body temperature, chills, malaise, weakness;
4) deep uncomplicated and especially complicated facial pyoderma (threat of lymphogenous and hematogenous dissemination of infection up to thrombosis of the venous sinuses of the brain and the development of purulent meningitis).
A relative indication (the issue is resolved in each specific case based on the totality of clinical data) is the presence of even mild forms of pyoderma in weakened patients on the background of immunosuppressive therapy, radiation therapy, HIV-infected patients, patients with exocrine or hematological pathology.
Systemic antibacterial therapy can be carried out with drugs from the group of antibiotics or sulfonamides. It is advisable to select these agents in accordance with the results of a microbiological study of purulent discharge from pyoderma foci (seeding, isolating a pure culture of the pathogen and determining its sensitivity to antibiotics).
Drugs of the penicillin group have the greatest sensitizing activity and cause toxicoderma more often than other antibiotics. It is undesirable to prescribe them to patients who have purulent complications of eczematous rashes or suffer from atopy, since penicillins aggravate the course of the underlying disease (it is better to replace them with macrolides and fluoroquinolones). In patients with psoriasis, penicillin therapy can lead to an exacerbation of the skin process and the development of psoriatic arthritis.
The volume of external therapy for pyoderma is determined by the depth and severity of skin damage. Thus, in case of acute superficial pyoderma, accompanied by the formation of superficial pustules on the skin, they should be opened, followed by immediate treatment with external antiseptics.
For deep pyoderma in the infiltration stage, resolving therapy should be prescribed, aimed at increasing hyperemia in the lesion and thereby promoting either rapid self-resolution of the infiltrate, or rapid abscess formation. For this, ichthyol applications are used on the developing infiltrate, physiotherapeutic effects: UHF, low-energy laser radiation, dry thermal procedures . It should be especially noted that compresses, paraffin or ozokerite applications are undesirable, since these procedures are accompanied by maceration of the skin and can cause aggravation of the purulent process.
If there are signs of an abscess of deep pyoderma, they should be surgically opened, followed by drainage of the purulent cavity using turundas moistened with a hypertonic solution of sodium chloride and antiseptic solutions.
After the appearance of active granulations, it is advisable to apply bandages with ointments containing antiseptics and biostimulants.
When pyoderma occurs subacutely or chronically, the surface of the lesions is covered with purulent crusts; they must be removed by softening with an antiseptic ointment, followed by mechanical action with tampons moistened with a 3% aqueous solution of hydrogen peroxide. After removing the purulent crusts, the lesion is treated with an aqueous or alcoholic antiseptic solution.
Pyoallergides
With long-standing pyococcal skin lesions, peculiar secondary skin lesions - pyoallergides - can occur. Most often they are observed in chronic streptococcal skin diseases (chronic diffuse streptoderma, long-standing impetigo, intertriginous streptoderma), much less often - in staphylococcal, in particular atypical, forms of pyoderma.
Pyoallergides appear suddenly, symmetrically on the skin of the trunk and limbs. They look like bright pink spots of various sizes and shapes, covered in the center with fine-plate scales, or small follicular papules or papulovesicles, papulopustules. A disseminated rash of blisters and blisters that are dense to the touch is often noted on the palms and soles. It is accompanied by itching and often an increase in body temperature up to 38 ° C. In such cases, the general condition of the patient is disturbed (headache, fatigue, weakness). Intensifying over several days, the skin rash can become widespread. After holding out for 7-10 days, the disease begins to regress.
Pyoallergides develop as a result of hematogenous spread of microbes or their decay products coming from the main pyogenic focus, in the presence of a pronounced allergic condition. The immediate cause of the appearance of pyoallergides is often irritating external preparations applied to the main lesions, the administration of immunobiological drugs, intercurrent diseases (influenza, etc.).
Treatment. For high fever and general malaise, antibiotics are indicated; in the absence of general symptoms, intravenous injections of calcium chloride or intramuscular injections of calcium gluconate. Externally - indifferent mash and powder.
The significant incidence of pyodermatitis among the population and the disability they cause dictate the need for extensive preventive measures.
The occurrence of pustular diseases is determined not only by the special properties of their pathogens, but also by the influence of unfavorable external factors, as well as disturbances in the general condition of the body. Therefore, the prevention of pyodermatitis consists of various measures. The main ones are:
1) accurate recording and analysis of the incidence of pyodermatitis, making it possible to establish its true causes;
2) sanitary and hygienic measures aimed at maintaining cleanliness of the skin and eliminating excessive contamination in everyday life and at work;
3) sanitary and technical measures, the purpose of which, by improving and improving the sanitary and technical conditions of production, is to eliminate the harmful factors operating in the work process that contribute to the occurrence of pustular diseases;
4) measures aimed at strengthening the physical condition of people, increasing their resistance to infection;
5) sanitary educational work.
The widest possibilities for carrying out all of these activities are available in relation to the organized part of the population, in particular workers in various branches of industry and agriculture, as well as military personnel. Among sanitary and hygienic measures, the creation of conditions for maintaining personal hygiene is of particular importance.
In enterprises, workers must be provided with washbasins with hot and cold water, sufficient soap, and towels to be able to clean contaminated skin during breaks and at the end of the working day. To fully clean the skin from industrial contaminants (lubricating oils, emulsions, kerosene, etc.), in addition to liquid or dry soap, it is recommended to use special cleaning agents.
To protect the skin from contamination and the irritating effects of chemicals that come into contact with it during work, it is of great importance to provide workers with clothing that matches the specifics of production. Regular washing is necessary, since contaminated overalls, aprons, mittens, shoes, etc. sometimes cause more harm than their absence. It is also important to maintain the sanitary condition of residential (dormitories, barracks) and working (shop, workshop, machine park, etc.) premises and, if possible, ensure normal temperature conditions in them. If it is impossible to comply with the latter (hot shop, field work in the summer, especially in the southern regions), it is necessary to create conditions for washing in the shower after work.
Systematic hypothermia of the body also plays an equally important role as a predisposing factor contributing to the occurrence of pustular diseases (especially furunculosis), and therefore it is important to provide warm clothing to persons working outdoors in cold weather.
Sanitary measures include: monitoring the correct maintenance of production tools, cleaning workplaces from production waste (metal shavings, sawdust, nails, etc.), which helps reduce microtrauma; technical measures aimed at preventing contamination of workers’ skin with chemicals; correct organization of first aid for microtraumas. In work rooms, workshops, workshops, garages, and field camps there should be first aid kits with a 1-2% alcohol solution of brilliant green or other dye, a 2% alcohol solution of iodine, and sterile dressing material. For the treatment of microtraumas, Novikov liquid (Tannini 1.0, Viridus nitentis 0.2, Spiritus aethylici 96% 0.2 ml, ol. Ricini 0.5 ml, Collodii 20.0), bactericidal adhesive plaster, furaplast, 5% iodine solution is recommended in ethylcellosolve.
During sanitary and educational work, as well as during special instructions, workers should be taught self- and mutual assistance.
Medical examination of workers, concern for improving living conditions, monitoring public catering, etc. are of great importance. Widespread promotion of physical methods of health promotion is necessary: physical exercise and sports, daily rubbing of the skin with cool water, and in the summer, sun and air baths, bathing, etc. In the overall complex of preventive measures, sanitary and educational work is of great importance: familiarizing workers with the pathogenesis of diseases and the necessary preventive measures.
Preventive measures should also include early detection of the initial forms of pustular diseases and their timely treatment.
Depending on the specifics of the industry, individual workshops, the characteristics of the activities of state farms, etc., working and living conditions, as well as climatic factors, specific plans for preventive measures, based on an analysis of the incidence of pyodermatitis, must be developed locally and strictly implemented.
FUNGAL DISEASES (DERMATOPHYTIAS)
Fungal skin diseases develop as a result of the introduction of pathogenic microfungi into it. When living outside the human or animal body, fungi can maintain their viability and virulence for several years. This explains the possibility of infection through indirect contact - through various objects contaminated with scales falling from the skin of patients or fragments of hair containing elements of the fungus.
There is no single and generally accepted classification of fungal diseases. More often they use the classification developed in the mycology department of the Central Scientific Research Institute of Dermatovenerology of the USSR Ministry of Health. In accordance with this classification, 4 groups of mycoses are distinguished.
1. Keratomycosis: pityriasis versicolor, etc. According to tradition, along with pityriasis versicolor, a similar disease, erythrasma, was considered, which is caused, as has recently been proven, not by fungi, but by corynebacteria and belongs to pseudomycoses (see “Athlete's foot”).
2. Dermatophytosis: epidermophytosis inguinal (true); mycosis caused by interdigital trichophyton (athlete's foot); mycosis caused by red trichophyton (rubromycosis); trichophytosis; microsporia; favus.
3. Candidiasis.
4. Deep mycoses: chromomycosis, etc. Along with deep mycoses, the textbook discusses actinomycosis, a bacterial disease currently classified as pseudomycosis.
In the diagnosis of most mycoses, microscopic examination of scales, vesicle covers, nail plates, and hair plays a significant role. The causative agent of the fungal disease can be detected after the horny substance clears in a hot solution of caustic alkali.
Treatment. Antifungal drugs are used to treat mycoses. Griseofulvin is prescribed orally. It is believed that this antibiotic does not have a fungicidal, but only a fungistatic effect. Coming from the intestines into the blood, it is adsorbed by the cells of the epidermis and accumulates in the stratum corneum and appendages of the skin, as a result of which they become inaccessible for the introduction of the fungus. This is proven by the fact that after approximately 2-3 weeks from the start of treatment, a healthy fungus-free zone appears in the proximal part of the hair (or nail), while fungal elements remain in the distal part. With further use of griseofulvin, the affected part of the hair (or nail) is gradually “pushed out” by the growing part. That is why it is recommended to shave the growing hair every 7-10 days when treating with grisefulvin.
Griseofulvin is taken in tablets (0.125 each) with meals and washed down with 1 teaspoon of sunflower oil or fish oil. The first control test for fungi is carried out 12-14 days from the start of treatment, subsequent ones - every 3-4 days until negative results, then every 5-7 days. The criteria for cure are clinical recovery and triple negative tests. The daily and course doses of griseofulvin depend on the body weight and age of the patient.
Some patients during treatment with griseofulvin experience headache, abdominal pain, diarrhea, vomiting, slight eosinophilia in the blood, and, as a very rare phenomenon, measles or scarlet fever-like toxicderma, urticaria. Sometimes disorientation develops, so griseofulvin is not recommended for outpatient administration to drivers of all types of transport.
Contraindications: diseases of the liver, kidneys, blood, malignant neoplasms, cerebrovascular accidents, stroke, porphyria (griseofulvin can increase photosensitivity), pregnancy, breastfeeding. Griseofulvin can be replaced with drugs of the imidazole group (ketoconazole, etc.).
Anticandidal antibiotics include amphoglucamine, prescribed 200,000 units (2 tablets), then 500,000 units 2 times a day after meals; mycoheptin - 250,000 units (5 tablets or capsules) 2 times a day; levorin - 500,000 units (1 tablet) 2-3 times a day; nystatin - 2,000,000-3,000,000 units (4-6 tablets) per day. The sodium salts of nystatin and levorin dissolve better in the gastrointestinal tract. The duration of treatment with anticandidal antibiotics is 10-14 days. Locally for mycoses, 2-5% alcohol solutions of iodine, nitrofungin, Castellani liquid, as well as ointments - 5-15% sulfur and tar, Wilkinson's ointment (Picis liquidae, Sulfuris depurati aa 15.0; Calcii carbonatis praecipitati 10.0; Saponis) are used viridis, naphthalani aa 30.0; Aq. destill 4 ml), 5% amikazole, 0.5-1% decamin, 1% esulan, zincundan, undecin, mycoseptin, canesten, etc. The antibiotics mycohepgin also have a selective anticandidal effect , nystatin and levorin, used in the form of ointments and solutions, amphotericin and decamine ointment. For acute inflammatory processes, ointments containing corticosteroids and antifungal agents are recommended: dermozolon, mycozolon, lorinden S. For better penetration of fungicidal drugs into the affected skin, their solutions in dimexide (DMSO) are used.
