Antibiotics (Properties, Application, Interactions) - M.P. Cherenko 1999

Acute Specific Infection

TETANUS

Tetanus is a serious infectious disease prevalent in many PARTS OF THE world. It has been recognized since ancient times under various names, with early physicians already noting The Link Between wounds and the onset of the disease. Hippocrates, whose son died of tetanus, described its clinical course over 2,430 years ago. It was also observed back then that tetanus occurred much more frequently during wartime, although this phenomenon could not be explained at the time. N.I. Pirogov was the first to suspect the infectious nature of tetanus. Only 18 years later, in 1883, N. Monastyrsky first observed microorganisms under a Microscope in smears taken from a patient's wound, and in 1884, the Italians Carle and Rattone experimentally reproduced the disease. In 1884, Nicolai provided Evidence of the presence of the tetanus causative agent in soil. S. Kitasato (1889) reported obtaining a pure culture of the microbe.

The CAUSATIVE AGENT OF tetanus is the tetanus bacillus (Bac. tetani), which belongs to anaerobic microbes. Nevertheless, from the perspective of biology, pathomorphological changes, or Clinical presentation, it has nothing in common with the anaerobes that cause gas gangrene.

Epidemiology, Etiology, and Pathogenesis. The tetanus bacillus has three characteristic features: it is an anaerobic Organism, forms spores, and produces a toxin.

It is found in soil, and its spores inhabit the digestive tract of sheep, horses, and other domestic animals. The tetanus bacillus has repeatedly been detected on contaminated clothing, linen, Hair, and in decayed Teeth. It enters the external environment through Human and Animal excrement.

The tetanus pathogen is highly resilient. It can withstand heating up to 80 °C for one hour. In a dried state, it can remain viable in the dark for up to 10 years. Tetanus spores do not always perish after boiling for 30—60 minutes. They can persist in the external environment for long periods (years). When spores encounter favorable conditions, they germinate, forming new tetanus bacilli that multiply rapidly.

The tetanus bacillus ranges from 2 to 4 µm in length and 0.3 to 0.6 µm in width. In shape, it resembles a drumstick.

In addition to humans, domestic animals are susceptible to the tetanus bacillus, including horses, sheep, cattle, pigs, dogs, and cats. If the tetanus bacillus penetrates through the granulation tissue of a detached umbilical cord, tetanus in newborns may develop.

The portals of entry for the tetanus bacillus include accidental wounds, mechanical and thermal superficial Skin injuries, frostbite, and Burns. The tetanus bacillus can also enter the body via criminal abortions, surgeries on the Large Intestine, and the removal of foreign bodies.

Tetanus following so-called clean surgeries warrants separate mention. Its cause may be improperly sterilized catgut or insufficiently prepared surgical fields.

Post-injection tetanus arises from poorly sterilized syringes.

Worldwide, more than 160,000 people die from tetanus annually, which exceeds the number of deaths from cholera, smallpox, plague, and rabies combined. According to international statistics, tetanus ranks third among causes of mortality.

During the Great Patriotic War, tetanus occurred in 0.6—0.7 cases per 1,000 wounded personnel, most frequently following shrapnel injuries.

Tetanus remains a major health concern in developing countries. According to WHO data, tetanus does not pose a serious threat in regions with Arctic and temperate climates.

The morbidity and mortality rates of tetanus depend on numerous factors:

1) frequency, severity, and localization of infected wounds; 2) likelihood of their contamination with the tetanus bacillus; 3) toxicity and serovars (serological variants) of the tetanus bacillus; 4) elapsed time from injury to Treatment; 5) quality of surgical wound debridement; 6) immune status and non-specific reactivity of the organism; 7) AGE AND SEX of the wounded individual; 8) soil composition and climatic conditions.

It has been established that associations of the tetanus bacillus with other microorganisms, particularly anaerobes, exert a more potent effect than a pure culture alone.

The presence of a large population of herbivores in an area contributes to soil contamination with excretions containing both spores and tetanus bacilli.

The entry of the bacillus into a wound does not necessarily lead to The Development of tetanus. Sometimes the tetanus bacillus is cultured from a wound in the absence of clinical signs of the disease. For tetanus to develop in the presence of the microbe, appropriate virulence, favorable local conditions, Hypoxia, the presence of hematomas or foreign bodies (crushed wounds with necrotic tissue lacking oxygen access), and reduced bodily resistance are required.

A characteristic feature of tetanus bacilli is that, once inside a wound, they do not spread beyond its boundaries. However, some authors point to the possibility of pathogen dissemination within the body and even pronounced bacteremia.

The incubation period for tetanus ranges from a few days to 3 months, most commonly lasting 10—14 days. Admittedly, the literature describes cases where tetanus developed within just 24 hours or after 3 months. The shorter the incubation period, the more severe the clinical course of the disease.

The duration of the incubation period in tetanus depends on the following factors:

1) local factors (untreated, crushed wounds, presence of foreign bodies, areas of necrosis, soil contamination of the wound, association of the tetanus bacillus with other microorganisms, notably streptococci);

2) general factors (hypothermia, overexertion, anemia, infectious diseases).

Upon entering a wound, the tetanus bacillus begins to produce a potent exotoxin comprising two fractions: tetanospasmin (responsible for Muscle spasms) and tetanolysin (causing hemolysis of erythrocytes).

Tetanospasmin is a neurotoxin that affects the Central Nervous system. There are several views regarding its MECHANISM OF ACTION. Some researchers believe that the toxin travels from the wound along the axial cylinders of peripheral nerves (via the anterior, motor roots) into the Spinal Cord, where it damages the Cells of the anterior horns. Part of the toxin enters the Lymph and Blood, and through them reaches the endings of motor nerves and further into the cells of the anterior horns of the spinal cord and the motor nuclei of the Brainstem. From the excitation foci formed here, the Muscles are reflexively affected, causing a symptom typical of tetanus—their rigidity.

According to other scientists, the toxin penetrates directly into the BLOOD AND LYMPH from the site of injury, and only from there does it affect the motor centers and neuromuscular junctions.

The toxin also damages certain Internal Organs (the myocardium, Liver, Lungs). It affects the higher autonomic centers of the brainstem, leading to tachycardia, hypotension, and pronounced sweating.

Pathomorphological changes. Tetanus does not cause specific tissue changes. Histological examination of the Brain sometimes reveals Swelling and vacuolation of ganglion cells. In the muscles, foci of necrosis, Hemorrhage, and ruptures of muscle fibers are found.

Classification. According to the site of pathogen entry into the body, a distinction is made between wound-related, post-injection, post-burn, and postoperative tetanus, as well as tetanus resulting from frostbite or Electrical injuries. Neonatal tetanus and postpartum tetanus are classified separately.

By its dissemination, it is classified as follows. Generalized tetanus: the ascending form is more common in animals, while the descending form is more frequently observed in humans. In this form, tension in the Muscles of the HEAD and Neck, along with generalized stiffness, appears first. Subsequently, the muscles of the entire trunk and extremities become involved, and generalized clonic seizures occur.

The mixed form is characterized by uniform manifestations of both ascending and descending tetanus.

There is also localized tetanus, which is characterized by restricted muscle involvement localized to the area of the injury (extremities; head — tetanus develops due to the toxin's effect on the Cranial Nerves, occurring in cases of Facial Nerve involvement and manifesting as spasms of the facial muscles, whereas involvement of the IX–XI pairs of cranial nerves impairs taste; trunk, including tetanus of internal organs; combinations of localized sites, such as arm + trunk, arm + head, etc.).

Localized tetanus usually precedes generalized tetanus, but is often not diagnosed in a timely manner.

Based on the clinical course, 4 forms of tetanus are distinguished: fulminant, acute, subacute, and chronic.

According to the severity of the pathological process, very severe, moderate, and mild forms of tetanus are distinguished.

Clinical picture. Generalized tetanus begins with mildly expressed prodromal signs: weakness, irritability, rapid fatigue, headache, sweating, pain, and minor muscle twitching in the wound area.

Following the prodromal period, the first formidable sign of the disease appears—muscle rigidity. In ascending tetanus, it first arises in the muscles near the wound, whereas in descending tetanus, it affects the masticatory muscles (trismus). Because these muscles have no antagonists, they undergo spasmodic contraction first. The patient experiences difficulty opening the Mouth, brief seizures, and pain in the masticatory muscles (a "locked jaw"). These signs progressively and relentlessly worsen.

Patients are troubled by a pulling pain and rigidity in the muscles of the neck, back, and lumbar region. Walking becomes difficult, accompanied by a feeling of heaviness in the back and lower back. Sometimes, abdominal pain and tension in the anterior abdominal wall muscles occur, which can lead to a misdiagnosis of an acute surgical abdominal pathology. The literature describes cases of erroneous surgical interventions on abdominal organs in patients with tetanus.

Tetanus frequently begins with swallowing disorders and a sore throat, providing grounds for referring such patients for a consultation with an otorhinolaryngologist.

Due to the contraction of the facial expression muscles, the patient's face acquires a characteristic appearance—the "sardonic smile" (risus sardonicus).

All these phenomena are accompanied by a sense of fear, Sleep disturbances, general weakness, and sometimes irritability, sweating, and elevated body Temperature.

Subsequently, tonic seizures encompass all the Muscles of the Trunk. Because the back muscles are stronger than those of the anterior trunk, their contraction causes the patient to arch backward, resting on their heels and the back of the head. This posture is known as opisthotonus (Fig. 78). At this time, the extremities are flexed at the elbow and hip joints.

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Fig. 78. Opisthotonus in a patient with tetanus

Rigidity of the intercostal muscles severely restricts the respiratory Movements of the chest, rendering it largely immobile. When spasmodic contractions involve the Diaphragm, severe respiratory impairment up to asphyxia may occur. Seizures are triggered by the slightest auditory or visual stimuli. A drop of Water falling from a faucet, a ray of sunlight, or the creak of a bed can provoke them. Initially, the seizures are infrequent, but as the disease progresses, they become increasingly frequent and eventually occur spontaneously.

The duration of mild seizures does not exceed 1–2 s with intervals of several hours, while moderate seizures last 2–5 s with intervals of 10–15 min.

The seizures are accompanied by intense pain. Occasionally, they are so violent that they lead to muscle ruptures and bone fractures.

Due to tonic contractions of the perineal muscles, the acts of defecation and urination are disrupted.

In some cases, tonic (characterized by prolonged spasm) and clonic (where muscle spasms alternate with relaxation) seizures may involve the muscles of only a specific part of the body (localized form of tetanus).

Consciousness remains intact during spasms, which makes the patient's condition even more severe. Blood pressure drops, tachycardia and arrhythmias develop, and urine output decreases (oliguria).

The clinical picture of severe generalized tetanus progresses by the 2nd to 3rd week. With a favorable course, all these symptoms gradually subside: the frequency and intensity of spasms decrease, body temperature drops, trismus lessens, and swallowing improves. Muscle spasms disappear in the reverse order of their onset: masticatory and facial muscles, neck, trunk, and limb muscles.

Each clinical form of tetanus has its own distinctive features. For instance, in the fulminant form, symptoms develop rapidly within 12–24 hours. The disease takes a severe course, accompanied by frequent spasms that often pose a risk of life-threatening asphyxia. Body temperature rises to 39–40 °C, and Heart rate accelerates. Death occurs within 1–2 days.

In the acute form, the full spectrum of symptoms develops within 24–48 hours. Spasm attacks recur several times an hour. The patient frequently dies within 4–5 days.

The clinical presentation is slower in the subacute form, where the incubation period lasts 4–6 days. Symptoms are mild, and spasms occur infrequently, only a few times a day. Other symptoms are moderately expressed. The disease more often ends in recovery.

Chronic tetanus is rare and characterized by a milder course. It involves localized muscle damage confined to the area of the wound.

Late and recurrent tetanus are also distinguished. The former may develop several months or even years after the patient sustains an injury. It is triggered by the Activation of a latent infection due to provocative factors such as trauma or surgery, particularly the late removal of a foreign body.

Recurrent tetanus is likewise caused by the activation of a latent infection.

When the classic triad of symptoms (trismus, dysphagia, nuchal rigidity) is present, diagnosing tetanus is straightforward. The presence of only a single component of the triad does not warrant a Diagnosis of tetanus. Trismus may stem from dental pathology, while isolated dysphagia or neck stiffness can result from a neuropsychiatric condition.

At this stage, treatment initiated only after the typical clinical picture has emerged may be considered delayed. It is crucial to establish a diagnosis in the Cytology/cytology/16.html">Early stages of the disease. The primary indicator is enhanced reflex excitability. This can be tested by gently tapping the parotid region with the fingertips, which triggers facial muscle spasms. Lorin and Epstein suggested testing the masticatory reflex by tapping on a Tongue depressor placed on the lower teeth. In tetanus patients lacking overt clinical signs, prolonged spasmodic contractions of the masticatory muscles are observed.

Early signs of tetanus also include a pulling pain and muscle twitching around the wound, excessive sweating disproportionate to body temperature, and back pain.

The diagnosis of tetanus is confirmed by detecting slender bacilli with drumstick-like spores in necrotic tissue samples, as well as by identifying tetanus toxin in cultures using mouse toxin-antitoxin neutralization tests.

The treatment of tetanus aims to eradicate the tetanus pathogen as completely as possible, neutralize circulating blood toxins, maintain a clear airway, suppress striated muscle reflex excitability, and prevent complications.

Therefore, tetanus management should focus on the following areas: 1) specific therapy; 2) anticonvulsant therapy; 3) general supportive care, including correction of protein, water-electrolyte balance, and acid-base status; 4) Surgical treatment; 5) supportive measures.

Specific therapy involves the administration of tetanus antitoxin (TAT). The dosage for adults is 100,000–150,000 IU, for children 20,000–80,000 IU, and for newborns 10,000–20,000 IU. Before administering the therapeutic dose, intradermal and subcutaneous skin tests according to Bezredka must be performed. First, 0.1 ml of diluted (1:100) serum is injected intradermally; after 20 minutes, 0.1 ml of undiluted serum is injected subcutaneously. If the result is negative (papule diameter does not exceed 0.9 cm), the remaining warmed serum is administered intramuscularly and intravenously. Half of the dose is given by slow intravenous infusion (diluted in isotonic sodium chloride solution at a 1:10 ratio), and the other half is administered intramuscularly as a single dose.

The antitoxin is administered for 2–3 consecutive days, gradually tapering the dose. The total course dose ranges from 200,000 to 350,000 IU. Today, some clinicians abroad avoid antitoxin administration due to the risk of hypersensitivity and potential allergic reactions, up to and including anaphylactic Shock.

It must be remembered that antitoxin is effective only as a prophylactic measure, as it neutralizes solely the toxin freely circulating in the blood. None of the modern medications affect toxin fixed by neural tissue. Therefore, the antitoxin must be administered within the first 2–3 days.

Specific therapy also includes the intravenous administration of at least 10,000 IU of human tetanus immunoglobulin diluted in isotonic sodium chloride solution.

Literature highlights the favorable therapeutic effect of homologous antitoxin, i.e., blood serum obtained from Donors immunized or hyperimmunized with toxoid. Antitoxin administration should be combined with antibiotic therapy (intramuscular or intravenous) and rectal administration of 1 g of metronidazole suppositories every 8 hours, which eradicates living microorganisms and prevents further toxin production.

An essential component of comprehensive tetanus management is active anticonvulsant therapy. For mild cases with an incubation period exceeding 2 weeks and infrequent spasms, good therapeutic effects are achieved with neuroleptic agents, a 25% magnesium sulfate solution (20–30 ml intramuscularly), and chloral hydrate enemas. Among neuroleptics, chlorpromazine is used for its calming, anticonvulsant, and analgesic properties (4 ml of a 2.5% solution 4–5 times a day intramuscularly).

For moderate tetanus accompanied by frequent, severe spasms and respiratory disorders, large doses of neuroleptics (50 mg of chlorpromazine every 6 hours) and antihistamines (diphenhydramine, suprastin) combined with narcotics or chloral hydrate enemas are indicated.

In severe cases of tetanus with pronounced respiratory compromise threatening asphyxia and frequent painful spasms, muscle relaxants and mechanical ventilation are utilized. The patient is intubated, given muscle relaxants, connected to a ventilator, and maintained under light nitrous oxide anesthesia. If such therapy needs to be prolonged, a tracheostomy is performed. Nondepolarizing muscle relaxants (tubarine, tubocurarine) are used for this purpose. Mechanical ventilation may be required for an extended period (sometimes up to 14 days).

Corrective infusion therapy is administered to manage protein, water-electrolyte balance, and acid-base status.

Surgical treatment for tetanus consists of wide wound debridement (especially in blind puncture wounds), excision of necrotic tissue, removal of foreign bodies (shrapnel, wood splinters, clothing fragments, etc.), ensuring adequate drainage of wound secretions, and local application of Antibiotics. The wound is thoroughly irrigated with hydrogen peroxide and loosely packed. In cases of extensive limb damage with massive tissue crushing, amputation is indicated.

Hyperbaric Oxygenation and antibiotic therapy play a certain role in tetanus treatment. It is important to bear in mind that most bacteroid microorganisms are antibiotic-resistant, and culture results often take several days. In such cases, broad-spectrum antibiotics (chloramphenicol, metronidazole) are indicated.

A tetanus patient requires specialized care. First and foremost, they must be placed in an isolated, darkened, and quiet room to avoid any sensory stimuli. Dedicated intermediate and junior nursing staff should be assigned to care for the patient, working under the supervision of a physician.

Great attention must be paid to the patient's Nutrition (the diet should be high-calorie, rich in Vitamins, and accompanied by a high fluid intake). During spasms, the patient must be fed liquid food using a feeder with a rubber tip or via a nasogastric tube.

In case of urinary retention, catheterization with a soft catheter is indicated; for constipation, cleansing enemas are prescribed. The bedpan must be made of rubber.

Despite The Use of modern treatment Methods for tetanus, mortality from this disease remains quite high. An important role in reducing mortality is played by the proper Organization OF TREATMENT for such patients in specialized intensive care units, where they are delivered by air ambulance accompanied by an anesthesiologist-resuscitated specialist. The notion that tetanus patients are untransportable has been revised today. Under the cover of potentiated barbiturate anesthesia, the majority of patients experience pronounced relaxation without depression of Blood Circulation and Respiration. In such a state and with appropriate accompaniment, the patient can be transported by helicopter, airplane, or ambulance equipped with intensive care apparatus.

From an epidemiological standpoint, tetanus patients are not contagious and pose no danger to others. The patient requires daily laboratory and radiological examinations (for the timely diagnosis of Pulmonary Atelectasis).

Tetanus prophylaxis. Preventive measures for tetanus are divided into non-specific and specific.

Non-specific tetanus prophylaxis consists of timely and thorough surgical debridement of the wound, clearing it of foreign bodies, necrotic tissues, microbes, and blood clots.

Primary surgical wound debridement is supplemented by the administration of antibiotics.

Specific prophylaxis aims to increase Immunity against the tetanus toxin.

Unlike other infectious diseases, specific immunity is not developed after having tetanus. This is evidenced by numerous observations of individuals who contracted tetanus a second time. Apparently, The amount of tetanospasmin capable of causing disease in humans lacks sufficient immunological properties.

Specific tetanus prophylaxis includes active immunization, regardless of whether an injury has occurred, and active-passive immunization in suspected cases of tetanus.

Active immunization is carried out using adsorbed diphtheria-tetanus-pertussis (DTP) and adsorbed diphtheria-tetanus Vaccines for all children under 1 year of age (1st and 2nd injections at 6–8 week intervals, 3rd after 4–6 months), as well as tetanus toxoid for the entire population living in areas with tetanus incidence rates of 1 or more per 100,000 population, all agricultural workers, construction workers, railway transport employees, water supply, sewage, and treatment plant workers, peat mining and logging workers, laboratory personnel working with tetanus cultures, vivarium workers, athletes, and pre-conscripts.

Tetanus toxoid is administered in 0.5 ml doses (2 vaccinations and 2 revaccinations).

Subsequent active-passive immunization in the event of an injury (emergency prophylaxis) depends on the completeness of active immunization. It is performed for all open injuries, burns, frostbite, gangrene and tissue necrosis, animal bites, criminal abortions, non-hospital deliveries, abscesses, penetrating INJURIES OF THE digestive organs, and the removal of foreign bodies.

Active immunization is carried out using tetanus toxoid and human tetanus immunoglobulin, and less frequently, anti-tetanus serum.

The schedule for emergency specific tetanus prophylaxis, depending on conditions and situations, is provided in a special instruction.

The prognosis in tetanus depends on the duration of the incubation period (the shorter it is, the more severe the disease course), the clinical form of the disease, the body's reactivity, timely specific and non-specific prophylaxis, and the completeness of treatment.

ANTHRAX

Anthrax is an acute specific infectious disease caused by the entry of the anthrax bacillus (Bac. anthracis) into the body. Cases of anthrax are observed in all countries of the world. In the past, anthrax was one of the most widespread infectious diseases. Today, it is more commonly found in economically disadvantaged, agrarian countries.

Etiology. The anthrax bacillus was discovered in 1850 by Davaine and Rayer in the blood of deceased animals. Pasteur and Koch established the morphological and biological properties of this microbe. The bacilli form resistant spores.

The source and vectors of the anthrax bacillus are primarily domestic animals, as well as skin, wool, horns, hooves, and animal-derived food products (meat, milk, etc.).

Other animals can also serve as sources of infection, including cats, bears, brown rats, birds, dogs, and white mice. Cases of anthrax bacillus transmission by blood-sucking insects have been described.

Infection most commonly occurs during livestock slaughter, skinning of animals, and cutting up meat from cattle that suffered from anthrax.

The disease is most frequently observed during the warm season.

Depending on the pathways of spore entry into the body, there are various Clinical forms of anthrax: pulmonary (occurring via the inhalation of microbes) and intestinal (resulting from the consumption of contaminated meat or milk). The disease has a very severe course and frequently results in death.

In surgery, the cutaneous form of anthrax is of paramount importance, manifesting as a specific ulcer known as a carbuncle (pustula maligna, carbunculus malignus).

The pathogenesis of anthrax is fundamentally rooted in specific toxemia caused by the anthrax toxin.

Infection occurs when spores come into contact with damaged skin, mucous membranes of the respiratory tract, or the Digestive System. Infection by the bacilli themselves is less common.

The incubation period for anthrax is relatively short, ranging from a few hours to several days.

The pathogenesis of cutaneous anthrax includes several clinical variants: carbuncular, edematous, bullous, and erysipeloid. Due to generalization of the process, any of these forms can lead to anthrax Sepsis.

A focus of coagulation Necrosis of the skin and subcutaneous tissue develops at the site of pathogen entry. The severity of local changes depends on both the virulence of the microbe and the organism's susceptibility to it. In cases of high microbial virulence and high host susceptibility, local changes may be mild or entirely absent, and the disease proceeds as anthrax sepsis.

Skin lesions in anthrax are caused by specific metabolic products of the bacillus, the so-called "death factor." When there are few anthrax bacilli at the site of entry and the "death factor" they produce is insufficient, skin changes remain minimal and localized. However, if A large number of pathogens are present in the primary lesion, they can enter the bloodstream and settle in secondary localization sites.

The Clinical presentation of cutaneous anthrax depends on its specific variant. The carbuncular form is the most common (99.1%). The localization of the carbuncle depends on occupational factors and the patient's lifestyle. Most frequently affected areas include the Cheeks, eyelids, forehead, neck, hands, and forearms. Anthrax carbuncles never occur on the palms or auricles.

Local changes in an anthrax carbuncle begin with mild itching. Subsequently, a dense, red, itchy spot appears on the skin, resembling an insect bite. The itching gradually intensifies, and a small vesicle forms at the center of the induration, which soon ulcerates and rapidly increases in size.

After the vesicles rupture and the ulcer forms, the itching subsides, but systemic symptoms emerge: fever, headache, insomnia, and loss of appetite. The rise in body temperature parallels the enlargement of the carbuncle. An inflammatory ridge forms around the ulcer, protruding above the skin surface.

At this stage, a soft tissue swelling develops around the ulcer and spreads to adjacent areas. The Base of the ulcer sinks and turns dark purple. A significant amount of serous or serosanguineous fluid discharges from the ulcer. Daughter vesicles form around the main ulcer and eventually coalesce; if they do not merge, they grow large, further enlarging the carbuncle (sometimes up to 10 cm in diameter).

A characteristic feature of the anthrax carbuncle is a necrotic ulcer with profuse serous discharge, a sunken dark center, surrounded by an inflammatory rim and a crown of vesicles. It has a firm base and is surrounded by edematous tissues.

Unlike common bacterial carbuncles, the anthrax carbuncle is painless. It is frequently accompanied by regional lymphadenopathy. The enlarged Lymph Nodes are slightly tender, but not painful.

After some time, exudation from the ulcer decreases, and the necrotic areas dry out. The central part of the carbuncle becomes darker and nodular, and body temperature drops. The carbuncle becomes covered with a scab. The edema gradually resolves. The edges of the scab detach from the skin and begin to protrude above its surface. By the end of the 3rd week, the scab detaches completely, revealing a granulating ulcer with significant purulent discharge—this occurs when the process extends into the subcutaneous tissue. If necrosis is confined to the skin, the scab falls off without granulation, following complete epithelialization of the ulcer. Subsequently, the granulating ulcer scars and epithelializes.

The edematous form of anthrax has a very severe clinical course. Its first sign is mild itching at the site of microbial entry, followed by rapidly progressive edema. Body temperature peaks within 2–3 days and remains elevated until necrosis ceases and scab formation begins. The edema is painless and firm, and it soon becomes covered with tiny vesicles filled with serous fluid and areas of necrosis. On the 3rd or 4th day, the vesicles rupture, releasing a copious amount of serous fluid. By the 8th to 10th day, the vesicles and necrotic areas become covered with a scab.

From the moment the vesicles rupture and skin necrosis begins, the disease follows the same course as the carbuncular form of anthrax. It is characterized by severe systemic manifestations: body temperature reaches 40 °C, accompanied by delirium, cerebral disorders, convulsions, and vomiting. Death may occur on the 3rd or 4th day.

The bullous form of anthrax, like the edematous form, is rare.

The erysipeloid form of anthrax is even rarer.

This variant of cutaneous anthrax is characterized by a mild course and a favorable outcome.

Laboratory Bacteriological examination plays a crucial role in diagnosing anthrax. In the cutaneous form, examiners analyze the contents of vesicles, carbuncles, ulcer discharges, or fallen scabs.

Blood samples for analysis (1 ml) are drawn from a vein, preferably during the febrile period. The blood is inoculated directly onto culture media, and smears are prepared on Glass slides.

Treatment for cutaneous anthrax must be conservative. Active surgical interventions (such as incisions, probing, or curettage) are strictly prohibited. Vesicles are incised only if they become suppurated and form an abscess.

Treatment should begin by ensuring complete rest for the affected area. Specific therapy, along with ANTIBIOTICS AND CHEMOTHERAPEUTIC agents, plays the primary role.

Specific therapy involves administering anti-anthrax serum. For adults with a mild course, 40–50 ml is administered; for moderately severe cases, 50–75 ml; and for severe cases, 75 to 100 ml.

Simultaneously with the anti-anthrax serum, specific anti-anthrax gamma-globulin is administered: 20 ml for mild cases, 30–40 ml for moderate cases, and 60–150 ml for severe and extremely severe cases.

Specific anti-anthrax serum and gamma-globulin are used in combination with antibiotics. The total course dose of penicillin-group drugs is 3,000,000–5,000,000 IU.

Some authors prescribe only antibiotics for patients with mild forms of anthrax: benzylpenicillin sodium salt at 500,000–1,000,000 IU intramuscularly 6–8 times a day for 5–7 days, alongside tetracycline or oxytetracycline.

Organic arsenic compounds (such as salvarsan) are used to treat anthrax. It is effective only in combination with other therapeutic agents, primarily anti-anthrax serum. Salvarsan is administered intravenously at 0.6–0.9 g.

Along with specific therapy, antibiotics, and sulfonamides, the comprehensive treatment plan for anthrax must include detoxification therapy: daily intravenous infusions of "Trisol" solution (to restore circulating blood volume and relieve dyspnea, cyanosis, and thirst) supplemented with 400 ml of polyglucukin or reopoliglucukin, as well as corticosteroids.

Anthrax prophylaxis is divided into general and individual measures.

General prophylaxis includes:

1) strict sanitary supervision over the identification, registration, certification, and disinfection of animal burial sites;

2) awareness and preventive work among populations residing in anthrax-risk zones, as well as among individuals engaged in the procurement, storage, transportation, Processing, and distribution of animal raw Materials;

3) scheduled vaccination prophylaxis for individuals at risk of anthrax infection;

4) active detection and treatment of patients;

5) active identification of infected objects and items, followed by their disinfection;

6) health education among the general public.

Individual prophylaxis consists of immunizing people against anthrax. Scheduled vaccinations are administered to:

a) individuals working with live cultures of the anthrax pathogen, infected laboratory animals, or researching materials infected with anthrax agents;

b) veterinary and livestock personnel, as well as other persons involved in pre-slaughter animal maintenance, slaughtering, carcass dressing, and skinning;

c) individuals who store, transport, and perform primary processing of animal-derived raw materials.

A live dry vaccine is used to immunize people against anthrax. Primary immunization (via scarification or subcutaneous injection) is administered twice with a 21-day interval.

In cases of direct human contact with materials containing anthrax bacilli or spores, Participation in the slaughter and dressing of carcasses of animals diagnosed with anthrax, caring for infected animals and participating in their burial, or consuming meat from an infected animal, emergency prophylaxis is indicated. It must be administered as early as possible after infection (no later than 5 days).

For emergency prophylaxis, antibiotics and anti-anthrax gamma-globulin (20–25 ml) are used.

RABIES

Rabies (lyssa, rabies, hydrophobia) is an acute infectious disease caused by a virus that affects the central nervous system. As early as 3000 BC, ancient physicians of the East described a disease resembling rabies. Rabies was also known to the ancient Indians, Slavs, Arabs, and Jews. The Talmud describes 5 symptoms of the disease in dogs: the jaw is open, saliva drips, the ears droop, the tail hangs between the legs, and the voice is hoarse or entirely inaudible. It was recommended to kill such an animal from a distance with an arrow.

By the end of the 18th century, more than 300 works dedicated to rabies had been published worldwide.

The science of rabies was placed on a solid scientific foundation thanks to the research of Louis Pasteur. He discovered the anti-rabies vaccine. On July 6, 1885, Pasteur used this method for the first time to prevent the disease in a human bitten by a rabid dog. Pasteur hypothesized that the causative agent of rabies was a submicroscopic microbe. This hypothesis was later confirmed by Remlinger (1903).

ETIOLOGY AND PATHOGENESIS. Today it is known that the causative agent of rabies is a large virus (100–150 nm in diameter).

Until the 18th century, rabies was known primarily as a disease of wild animals, while domestic animals played no significant role in its spread. It was not until the 19th century that it was recognized that dogs could also contract rabies.

Humans most commonly contract rabies from stray dogs. The virus enters The Human Body when saliva and urine from rabid animals come into contact with broken skin or mucous membranes through bites, licking, or scratches. Animals are contagious even during the incubation period. From the wound, the pathogen spreads to the central nervous system (CNS). The closer the entry site is to the head, the more dangerous it is, with bites to the head and neck posing a particularly high risk.

The virus spreads along the perineural spaces of nerve trunks, as well as via the lymphatic and hematogenous pathways.

In addition to Nervous Tissue, the virus is found in the salivary and lacrimal glands.

Pathomorphological changes. Autopsies typically reveal no major macroscopic tissue changes in rabies. Observations are usually limited to mild cerebral edema and hyperemia, along with small petechial hemorrhages in the Basal Ganglia and around the floor of the Fourth ventricle.

Clinical presentation. The incubation period for rabies ranges from 10 days to 1 year or more, averaging 40 days. The prodromal phase is characterized by fever, general malaise, and headache. Patients are agitated and experience restless sleep. After 1–2 days, the hallmark symptom appears: increased muscle tone accompanied by spastic spasms of the swallowing muscles. These spasms are triggered by the mere mention of water or the act of drinking. Later, air currents or bright light can also provoke spasms. Over time, tonic and clonic spasms develop in other muscle groups. Body temperature rises, and tachycardia ensues. Consciousness becomes clouded, and auditory and visual hallucinations may occur. After 2–3 days, the state of agitation gives way to a paralytic stage: the patient weakens, spasms subside, and death follows. The total duration of the illness is 4–10 days.

The diagnosis of rabies is established based on the Anamnesis and clinical findings. There is currently no rapid serological test available for detecting rabies.

Treatment. No successful therapy for rabies has been developed. Attempts to use various sera, chemotherapeutic agents, and antibiotics have yielded no positive results. Therefore, immediate primary surgical debridement of the wound, along with active and passive immunization, is critically necessary.

Active immunization is performed using the rabies vaccine. If the patient has not been previously immunized, adults and children must receive 6 injections: the first immediately after exposure,

followed by subsequent doses on days 3, 7, 14, 30, and 90. The vaccine is administered intramuscularly in a dose of 1 ml.

Passive immunization is administered to patients with massive bites or those who seek medical help late. Human rabies immunoglobulin is injected at a dose of 0.25 ml per 1 kg of body weight.

Non-specific treatment involves primary surgical wound debridement. Damaged tissues are excised within healthy boundaries, and the wound is left open.

Alongside the aforementioned treatment, symptomatic therapy is administered, including detoxification, cardiac, analgesic, and antihistamine medications, as well as hyperbaric Oxygen therapy.

Rabies Prevention is divided into individual and general measures. Individual prophylaxis is carried out for individuals in high-risk groups due to potential exposure to the rabies virus. These include dog catchers, hunters, staff at rabies diagnostic laboratories, and postal workers in endemic areas. For this purpose, the rabies vaccine is administered according to the following schedule: two subcutaneous injections of 5 ml of the vaccine 10 days apart, followed by annual revaccination.

General prophylaxis involves the elimination of stray and rabid dogs, as well as preventive vaccination of domestic dogs.

The prognosis for untreated rabies is hopeless. All patients, as a rule, die.

WOUND DIPHTHERIA

Diphtheria is an acute infectious disease caused by the Klebs-Löffler bacillus. It affects the mucous membranes of the Pharynx, Tonsils, Nose, Larynx, Trachea, and genitals. From a surgical perspective, wound infection by the diphtheria bacillus (diphtheria vulnerum) is of greater interest.

Etiology and pathogenesis. The diphtheria bacillus is widespread in the environment and is also harbored in the human body. Acting as a saprophyte, it parasitizes the pharynx, intestines, and wound surfaces. The bacillus does not form spores and is rapidly killed by heating to 60 °C.

Wound infection occurs through contact with diphtheria patients (via coughing, sneezing, contaminated utensils, etc.).

The diphtheria bacillus produces a potent toxin that damages The Cardiovascular system and causes paralysis of certain nerves, manifesting as impaired accommodation and paresis of the pharyngeal muscles.

Upon entering a wound, the diphtheria bacillus induces specific inflammation there.

Clinical presentation. In diphtheria, the wound changes dramatically in appearance: gray-yellow fibrinous deposits appear On the surface, firmly adherent to the underlying tissue. Tissue necrosis is observed beneath these fibrinous films. The wound discharges a serous and serosanguineous fluid. The skin surrounding the wound is hyperemic, and the tissues are edematous. Regional lymph nodes are enlarged. If a secondary bacterial infection supervenes, body temperature rises.

Infection of a wound with the diphtheria bacillus is accompanied by a systemic bodily reaction characteristic of diphtheria: paralysis of individual nerves and toxic damage to the myocardium, which can lead to sudden death.

A definitive diagnosis of wound diphtheria can only be established based on the results of bacteriological examination.

The danger of diphtheria wound infection lies in the fact that such wounds heal very poorly, and There is a high risk of microbial invasion into the bloodstream.

Treatment. In diphtheria of wounds, the patient becomes a source of infection and must be isolated. Treatment should be initiated immediately after the diagnosis is established. Antitoxic diphtheria serum is administered subcutaneously, intramuscularly, or intravenously at 20,000 – 40,000 IU (following a preliminary intradermal sensitivity test according to Besredka's method). The wound is covered with dressings moistened with an antiseptic or diphtheria antitoxin.

If the diphtheria bacillus is associated with common microflora, antibiotics are administered for 6–8 days (from 1,000,000 to 10,000,000 IU of benzylpenicillin sodium salt).

Surgical intervention is indicated only in the presence of purulent collections or Phlegmon.

Alongside the aforementioned measures, symptomatic therapy is administered.