Vector-borne diseases include more than 200 nosological forms caused by viruses, bacteria, rickettsia, protozoa and helminths. Some of them are transmitted only with the help of blood-sucking carriers (obligate vector-borne diseases, for example typhus, malaria, etc.), some in various ways, including transmissible (for example, tularemia, infection of which occurs through the bites of mosquitoes and ticks, as well as skinning sick animals).
Vectors
Specific and mechanical vectors are involved in the transmission of pathogens of vector-borne diseases.
In the body of mechanical carriers, pathogens do not develop or reproduce. Once on the proboscis, in the intestines or on the surface of the body of a mechanical carrier, the pathogen is transmitted directly (by a bite) or through contamination of wounds, mucous membranes of the host or food products. The most common mechanical carriers are flies of the Muscidae family, which are known as carriers of viruses, bacteria, protozoa, and helminths.
Characteristics of the carrier and mechanism of transmission of the pathogen
Prevention of most vector-borne diseases is carried out by reducing the number of vectors. With the help of these measures, the USSR managed to eliminate such transmissible anthroponoses as louse-borne relapsing fever, mosquito fever, and urban cutaneous leishmaniasis. In case of natural focal vector-borne diseases, measures to reduce the number of the reservoir - wild animals - sources of pathogens (for example, rodents for plague and desert cutaneous leishmaniasis) are often more effective; the use of protective clothing and repellents, in some cases - vaccination (for example, for tularemia, yellow fever); and chemoprophylaxis (for example, for sleeping sickness). Of great importance is carrying out reclamation work and creating zones around populated areas free from wild rodents and carriers of vector-borne diseases.
domestic and wild animals. Occurs when a person develops the territory of the software. Foci of Japanese encephalitis, cutaneous leishmaniasis, tick-borne relapsing fever, etc. can acquire this character.
Synanthropic foci. The circulation of pathogens is associated only with domestic animals. Foci of toxoplasmosis, trichinosis.
2. By the number of owners
Polygostal. The reservoir is several species of animals (gophers, marmots, tarbagans, gerbils in the natural focus of the plague).
3. By the number of carriers
Monovector. Pathogens are transmitted by only one type of vector. It is determined by the species composition of vectors in a specific biocenosis (only one species of ixodid ticks lives in a certain focus of taiga encephalitis).
Polyvector. Pathogens are transmitted by various types of vectors. (For tularemia - carriers: various types of mosquitoes, horse flies, ixodid ticks).
Epidemics
Manifestations of the epidemic process by territory
It is worth noting that diseases are characteristic mainly of wild animals, but urbanization creates conditions for the spread of pathogens of these diseases among synanthropic animals and humans. This is how anthropurgic and then synanthropic foci of diseases arise, which can pose a significant epidemiological danger.
The term pandemic is used to describe an unusually intense epidemic affecting a number of countries.
Vector-borne diseases are infectious diseases transmitted by blood-sucking insects and arthropods. Infection occurs when a person or animal is bitten by an infected insect or tick.
About two hundred official diseases are known that have a vector-borne transmission route. They can be caused by various infectious agents: bacteria and viruses, protozoa and rickettsia *, and even helminths. Some of them are transmitted through the bite of blood-sucking arthropods (malaria, typhus, yellow fever), some of them are transmitted indirectly, when cutting the carcass of an infected animal, in turn, bitten by an insect carrier (plague, tularemia, anthrax). Such diseases are divided into two groups:
Obligately vector-borne diseases are vector-borne diseases that are transmitted only with the participation of a carrier.
Japanese encephalitis;
Typhus (lousy and tick-borne) typhus;
Relapsing (lousy and tick-borne) typhus;
Lyme disease, etc.
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Facultatively vector-borne diseases are vector-borne diseases that spread in various ways, including with the participation of vectors.
Brucellosis;
Tick-borne encephalitis;
Anthrax;
Tularemia, etc.
Vector classification:
Specific carriers ensure the transfer of pathogens from the blood
sick animals or humans into the blood of healthy ones. In organism
specific carriers, the pathogen multiplies or accumulates. In this way, fleas transmit plague, lice - typhus, mosquitoes - Papatachi fever. In the body of some carriers, the pathogen goes through a certain development cycle. Thus, in the body of a mosquito of the genus Anopheles, malaria plasmodium completes the sexual development cycle. Along with this, in the body of ticks, the causative agents of tick-borne encephalitis and some rickettsioses not only multiply and accumulate, but are also transmitted to a new generation through the egg (transovarial). Therefore, the pathogen in the body of a specific carrier can persist (with some exceptions) throughout the life of the carrier;
Nonspecific (mechanical) carriers that perform
mechanical transfer of the causative agent of the disease without its development and reproduction (horseflies, autumn flies and ixodid ticks for the causative agents of tularemia, brucellosis, anthrax).
Transmissible diseases are also divided into two groups depending on the pathogen:
Invasions (pathogens are animals);
Infections (causative agents - viruses, rickettsia and bacteria).
EPIDEMIOLOGICAL CHARACTERISTICS OF INFECTIONS WITH TRANSMISSION MECHANISM. EPIDEMIOLOGICAL CHARACTERISTICS OF INFECTIONS WITH CONTACT TRANSMISSION MECHANISM
In the process of evolution, different microorganisms have adapted to certain conditions of the natural path of transition from one organism to another. To a large extent, it is the characteristics of the pathogen transmission routes that determine the type of epidemic process.
Blood infectious and invasive diseases are caused by pathogens, the primary and main localization of which in the human body is in the blood.
This group of infections includes typhus, relapsing fever, malaria, tick-borne encephalitis, borreliosis, plague, yellow fever, etc.
Once the pathogen of this group of infections has entered the body, it ends up in a closed circulatory system and in natural conditions can be removed from the infected body only with the help of some blood-sucking insect or mite. Infection of another organism usually occurs also through sucking of blood by an arthropod vector. Thus, the circulation of pathogens of blood infections usually involves the host (human, animal) and some kind of blood-sucking vector (Table 1, Fig. 1).
Table 1
TRANSMISSION OF PATHOGEN DURING BLOOD INFECTIONS
The main localization of the pathogen in the human body is in the blood.
To preserve the pathogen as a biological species (II law of epidemiology), its transmission from one individual to another can only be with the help of a carrier, in whose body it is not only preserved, but also goes through a certain cycle of its development.
Transmission mechanism – transmission
The mechanism of transmission of this group of infections- transmissible.
This group includes anthroponoses, in which the source of infection is only humans (typhoid and relapsing fever, malaria), and zoonoses, where the sources of infection can be animals, most often rodents (tularemia, hemorrhagic fevers, tick-borne encephalitis, Lyme disease, etc. ) (Table 2).
table 2
DIVISION OF BLOOD INFECTIONS INTO SUBGROUPS
I anthroponoses – transmission from person to person (typhus, relapsing fever, malaria)
II zoonoses (tularemia, tick-borne encephalitis, borreliosis, hemorrhagic fevers)
III The source of the pathogen can be both humans and animals, most often rodents (plague, hemorrhagic fevers, anthrax)
Infections with different transmission mechanisms (plague, tularemia, hemorrhagic fevers, anthrax)
The causative agents of most diseases in this group have adapted to certain vectors. Thus, transmission of typhus occurs mainly through the body louse, malaria through Anopheles mosquitoes, and tick-borne encephalitis through ticks (Table 3, Fig. 2, 3).
Table 3
CARRIERS OF VOCAL-BORNE INFECTIONS
BLOOD-SUCKING INSECTS
Lice – body lice, head lice, pubic lice – typhus, relapsing fever, Volyn fever
Mosquitoes – Anopheles (females) – malaria, Aedes – yellow fever
Fleas are a plague
TICKS (larva, nymph, mature tick - each stage feeds on its host). Transovarial transmission of the pathogen (not only the carrier, but also natural reservoir, i.e. 1st link of the epidemiological process)
Ixodidae – tick-borne encephalitis, Omsk and Crimean hemorrhagic fevers, Marseilles fever, Q fever, tularemia
Argaceae – tick-borne relapsing fever, Q fever
Gamasaceae – rat typhus
Red calfs - tsutsugamushi
The specificity of the transmission of pathogenic microorganisms determined a number of epidemiological features of blood infections (Table 4).
The first of them is endemicity. Endemicity (natural focality) determines the spread of this disease in certain geographical areas where specific carriers and keepers (reservoirs) of pathogens in nature (warm-blooded animals, rodents) constantly live. The main endemic focus of jungle yellow fever is the tropical forests of West Africa and South America, where monkeys serve as the source of infection. The yellow fever virus is transmitted from monkey to human certain types mosquitoes Aedes, which are not on our territory, so even if a patient with yellow fever comes to us (and it is a quarantine infection!), there should be no spread of infection. Leishmaniasis is spread by mosquitoes and is common in countries with tropical and subtropical climates.
The second characteristic epidemiological feature is seasonality. The rise of diseases occurs in the warm part of the year, when maximum biological activity of carriers and, in some cases, their biological hosts (for example, rodents during plague) is observed.
For diseases transmitted by lice - typhus and relapsing fever - endemicity is not typical, and seasonality is associated with social factors - crowded population, unfavorable sanitary conditions, etc.
Table 4
FEATURES OF THE EPIDEMIC PROCESS
ENDEMICITY (natural focality) - distribution in certain geographical areas where specific carriers and keepers (reservoirs) of pathogens in nature (warm-blooded animals, rodents) constantly live.
SEASONALITY – predominantly summer-autumn – the time of maximum biological activity of vectors
For diseases transmitted by lice, seasonality is associated with social factors.
Under certain conditions, the causative agents of some infectious diseases, which in nature spread among animals mainly through carriers such as plague (fleas), anthrax (burning flies), tularemia (mosquitoes, horseflies, ticks as mechanical vectors), can penetrate the human body and in other ways. The listed diseases can be transmitted to humans in other ways, i.e. have several or multiple transmission mechanisms. Thus, plague is characterized by contact transmission through damaged skin when skinning infected rodents, airborne through contact with a patient with pneumonic plague, and nutritional through consumption of meat from sick animals (camel, tarbagan, etc.). All known transmission mechanisms are possible in the spread of anthrax and tularemia; infection with typhus has been described in laboratory conditions through the mucous membrane of the conjunctiva.
Measures to combat blood infections are determined by their epidemiology (Table 5).
In cases where the source of infection is rodents, they resort to their mass destruction deratization. Vector extermination is also necessary. The most important role here is played by the improvement of the area through reclamation and improvement of vast areas, individual and collective protection of people from blood-sucking insects and ticks (the use of repellents). Preparations for active immunization have been developed (for the prevention of yellow fever and tick-borne encephalitis).
In case of anthroponoses, measures aimed at early and comprehensive hospitalization of patients are very effective (typhus rule of the 4th day, i.e. the patient must be hospitalized, and in the outbreak, sanitary treatment of all contact persons and chamber disinfection of the patient’s bed linen and clothing are carried out, while the louse is not yet capable of transmitting rickettsia it acquires such properties from the 4-5th day after blood sucking on the patient). Specific chemotherapy drugs are widely used when people stay in areas unfavorable for malaria, etc.
Table 5
PREVENTION OF VOCATE-BORNE INFECTIONS
For zoonoses
Deratization
Vector control (disinsection)
Improvement of the area - landscaping, land reclamation
Individual and collective protection against blood-sucking insects and ticks (repellents)
Active immunization
For anthroponoses - early and complete hospitalization of patients
Specific chemotherapy drugs
INFECTIONS WITH A CONTACT MECHANISM OF TRANSMISSION (INFECTIONS OF THE EXTERNAL INTEGRATION according to the classification of L.V. Gromashevsky)
Mechanism of transmission of pathogens contact (wound)
In some diseases, the pathogen is transmitted primarily without the participation of environmental factors (venereal syphilis, gonorrhea during sexual intercourse; in rabies and sodoku through a bite directly with saliva) direct contact. The rabies virus is unstable in the external environment; infection occurs only through direct contact. At the same time, infection under the same venereal diseases possibly through dishes contaminated with the patient’s secretions, other household items indirect contact. With tetanus, gas gangrene, the disease is possible only as a result of the penetration of pathogens from the soil, where they persist for a long time (years, decades), contaminated dressing material into the human body through damaged outer integument; the likelihood of such infection increases with the increase in traumatism (military, domestic, industrial). For most other infectious diseases of the external integument, pathogen transmission factors include household items contaminated with pus, scales and scabs (clothing, underwear, hats, dishes), dressings, and contaminated hands (Table 6).
The spread of infectious diseases of the external integument largely depends on the population's compliance with personal hygiene rules.
Table 6
CONTACT TRANSMISSION MECHANISM
Anthroponoses – transmission from person to person (syphilis, gonorrhea, HIV/AIDS, etc.)
II zoonoses (glanders, foot and mouth disease, rabies, sodoku)
III sapronoses (tetanus)
Infections with different transmission mechanisms (plague, tularemia, anthrax)
ROUTES OF TRANSMISSION
Direct contact – rabies, sodoku, sexually transmitted diseases
Indirect contact (involvement of environmental factors) - soil (tetanus, gas gangrene), household items (contaminated dressings, clothing, hats, dishes), hands
The fight against infectious diseases of the external integument should be aimed primarily at improving the health of everyday life and educating the population in hygienic skills. Prevention wound infections is closely related to the prevention of various types of injuries. For some zoonoses (rabies, sodoku, glanders, anthrax, etc.), along with sanitary and veterinary measures, the destruction of sick animals – sources of infection – is indicated. In order to prevent tetanus, rabies and a number of other infections of this group, specific immunization is successfully used (Table 7).
Table 7
PREVENTION OF INFECTIONS OF EXTERNAL COVERINGS
Sanitary and veterinary measures
Destruction of sick animals (rabies, sodoku, glanders, anthrax)
Improvement of everyday life
Injury prevention
Educating the population in hygiene skills
Active immunization
EPIDEMIOLOGICAL CHARACTERISTICS OF MALARIA
Malaria - an acute protozoal disease of humans, which is caused by malarial plasmodia and is characterized by periodic attacks of fever, enlargement of the liver and spleen and the development of anemia.
Infection occasionally occurs through the transfusion of infected donor blood, surgical interventions, or the use of insufficiently sterilized instruments. Drug addicts can become infected by using unsterile syringes. Intrauterine infection of the fetus is possible.
Susceptibility is high. Children get sick more often.
Prevention. Malaria is classified as a disease for which sanitary protection of the state territory and mandatory registration are provided.
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Contingents of patients who are subject to mandatory examination for malaria · with fever for 5 days or longer · with fever of any duration - having had malaria over the past two years · with fever – returning from the tropics, for 2 years after return, regardless of the primary diagnosis · in the presence of hepatosplenomegaly, anemia of unknown etiology · with an increase in body temperature in the next 3 months. after blood transfusion · in rural areas with a very high likelihood of malaria spreading during the transmission season for any illness with a febrile reaction on the day of presentation |
The possibility of parenteral transmission of plasmodium requires careful sterilization of medical instruments and prohibition of participation in donation by persons who have had malaria.
Great importance is attached to the control of the vector: draining swamps, cleaning water bodies, treating mosquito breeding sites with larvicidal and imagocidal preparations, and using biological methods. In order to protect people from mosquito bites, repellents, mosquito nets, and window nets are used. Animal prevention is of some importance - placing livestock between a populated area and a reservoir or wetland. Insecticidal treatment of vehicles arriving from an endemic focus of malaria is recommended.
Chemoprophylaxis is essential: persons traveling to an endemic area are prescribed delagil (0.5 g) or chloridine (0.025 g) once a week, starting a week before arrival, throughout the entire period of risk of infection and another 6-8 weeks after leaving a disadvantaged area. In foci of tropical malaria, individual chemoprophylaxis is carried out with mefloquine 0.25 g once a week, Lariam 250 mg/week, Fansidar- 1 tablet/week, doxycycline- 1.5 mg/kg/day.
EPIDEMIOLOGICAL CHARACTERISTICS OF TYPHUS
An acute infectious disease caused by Provacek's rickettsia, prone to epidemic spread and characterized by fever, damage to the nervous and cardiovascular systems, the appearance of a specific rash and general intoxication. The disease is transmitted by lice. There are epidemic typhus and sporadic typhus, or Brill's disease.
Epidemiology. The source of typhus is only a sick person, whose blood is infectious throughout the febrile period, as well as in the last two days of incubation and in the first two days of apyrexia. The only carrier of Provacek's rickettsia is the body louse, the epidemiological significance of head and pubic lice insignificant.
When a patient with typhus sucks blood, rickettsiae enter the body of the louse along with the blood, which penetrate the intestinal epithelium, multiply, accumulate, and after 5-6 days the louse becomes infectious. Multiplying rickettsiae rupture epithelial cells and are released into the intestinal lumen. When an infected louse bites a healthy person, as its intestines fill with blood, during the act of defecation, rickettsiae are pushed out along with feces, which end up on the human skin. Since a louse bite is accompanied by itching, a person involuntarily rubs the infectious material into the resulting wounds. There are no rickettsiae in the salivary glands of lice. Once infected with rickettsia, a louse remains infectious for the rest of its life, but does not transmit the infection to its offspring. An infected louse lives shorter than a healthy one (up to 30 days). Rickettsia Provacek can also enter the human body through the conjunctiva of the eyes, where they are introduced by hands contaminated with lice feces, or while cleaning lice-infested clothes of patients. The feces and urine of patients do not contain rickettsiae. The occurrence and spread of typhus is always closely associated with lice, which increases significantly during social upheavals and disasters. In this regard, such names of the disease as “military”, “hunger”, “prison typhus” become clear.
Susceptibility to typhus is universal in all age groups; transport workers, bathhouses, laundries, and disinfectants are at greatest risk of infection. Outbreaks of typhus are usually seasonal: they occur with the onset of cold weather and gradually increase, reaching their maximum in March-April. During the cold season, people are known to gather indoors, contacts between them increase, all this can contribute to the proliferation of lice that spread the infection.
Brill's disease is a type of typhus. It is considered as a distant relapse of an infection that has been latent for a long time. It is characterized by sporadic incidence in the absence of lice and a source of infection. Elderly and older people who have had typhus in the past are affected. The disease is registered mainly in big cities, no seasonality. Clinically, Brill's disease, as a rule, is milder, with a shortened febrile period, roseola rash or no rash at all. Complications are rare.
Prevention. The spread of typhus is associated with lice. Cases of Brill's disease require strict preventive measures and, first of all, control of lice, since patients have rickettsemia. In this regard, systematic examinations for pediculosis of children in preschool institutions and schools and other populations, as well as patients admitted to medical institutions, are necessary. If lice is detected, complete sanitization is carried out. Hair on the head, pubic area and other hairy areas of the skin should be carefully cut off, and the removed hair should be burned. To collect hair on the floor during haircuts, there should be a sheet or paper moistened with solvent. After cutting the patient's hair, it is necessary to wash it well in the bath or under the shower, and after wiping it dry, treat all shaved areas of the skin with insecticidal substances. Linen and clothes are subjected to chamber disinfection. The transport that delivered the patient is subjected to disinsection, the orderlies who accompanied the sick person change their gowns. If at least one lice is detected in the department for typhus, a thorough sanitary treatment is immediately carried out and all linen is changed. The area where the patient was located is disinfected; clothes and bed linen are subjected to chamber disinfestation. All persons who came into contact with the patient undergo sanitary treatment. Health education plays an important role in the prevention of typhus and the fight against lice.
When typhus diseases occur, early identification and isolation of sick people, their sanitary treatment, and isolation of persons suspected of having typhus disease are necessary. Since the louse becomes capable of transmitting the infection only 5 days after infection, carrying out anti-epidemic measures no later than the 5th day from the onset of the disease prevents the spread of infection by these patients.
So-called door-to-door visits in epidemic outbreaks make it possible to early identify febrile patients, including typhus patients. Persons who have had contact with a typhus patient are subject to 25-day medical observation with mandatory daily thermometry. Everyone is subject to mandatory inspection for pediculosis. If it is detected or if there are persons in the outbreak who have suffered febrile conditions over the past 3 months, a serological examination is carried out. If contact persons have a fever, they will be hospitalized. If typhus is suspected, immediately report to the district SES. In the early identification of patients, a large role belongs to local doctors.
Specific prevention – vaccination according to epidemiological indications (chemical typhus vaccine), emergency prevention – antibiotics + butadione
EPIDEMIOLOGICAL CHARACTERISTICS OF PLAGUE
Etiology. The causative agent of plague, Yersinia pestis, belongs to the Enterobacteriaceae family - a gram-negative bacillus of ovoid shape, 1-2 microns long, 0.3-0.7 microns wide. Easily dyed with aniline dyes, more intense- at the poles (bipolar). The microbe is immobile and has a capsule. Does not create a dispute. Facultative aerobic. Ferments glucose, fructose, galactose, xylose, mannitol, arabinose, maltose and glycogen, forming acid without gas. It has a complex antigenic structure, more than 30 antigens, including those identical to other species of Yersinia, Salmonella, and Shigella. Grows well on regular nutrient media at temperatures from 18-34° C and pH 6.9-7.2. Bacterial growth appears on agar plates within 10-12 hours; after 24-48 hours, mature colonies with a raised brown center and a scalloped, colorless edge (“lace scarf”) are formed. In the broth, bacteria form a surface film, from which threadlike formations in the form of stalactites and a flocculent sediment descend.
The virulence of the plague microbe varies widely. Highly virulent strains are highly invasive, form a heat-labile exotoxin (forms A and B) and a “mouse” toxin with extremely high toxicity - there are more than 80 thousand lethal mouse doses per 1 mg of nitrogen of this toxin.
The resistance of bacteria is low, they have a detrimental effect heat, sunlight, drying. Heating up to 60° C kills them in 1 hour, boiling- in 1 min. However, the pathogen is well tolerated low temperatures: at O° C is maintained for 6 months, at 22°C - 4 months From disinfectants solutions of sublimate, carbolic acid, Lysol, chloramine B, and bleach in normal concentrations have a detrimental effect on it.
Epidemiology. The source of plague in nature is about 200 species and subspecies of wild rodents (marmot, gopher, vole, gerbil, hamsters, rats, etc.) and lagomorphs (hare, pika) (Fig. 6-9).
During epizootics, plague can also affect predatory and insectivorous mammals (weasel, ferret, shrew, fox) and domestic animals (camel, cat), which become an additional source of infection. A person with plague carries the potential risk of infecting others.
The specific carrier of plague is fleas (more than 120 species and subspecies of fleas, as well as 9 types of lice and ticks). The main role in the transmission of the pathogen among animals and people is played by the rat flea, the flea of human habitation and the gopher flea, which become infected by the bite of sick animals that are in the period of bacteremia. Intensively multiplying in the stomach and forestomach of the flea, plague bacteria form a gelatinous lump that blocks the lumen of the digestive canal. Leaving the corpse of a rodent, the flea can pass on to a person and infect him, regurgitating part of the plague lump during the bite. Scratching the bite site contributes to infection. Transmission of plague from person to person by flea bite is rare.
A person can become infected through contact with a sick or dead animal - during the slaughter of sick camels, butchering carcasses and disposing of meat.
A person suffering from pneumonic plague poses a particular danger to others, since the infection is easily transmitted by airborne means. In other clinical forms of the disease, contagiousness is weak; transmission factors include household items contaminated with the pus of patients or other infected material.
Human susceptibility to plague is very high, almost 100%. People who are involved in rodent hunting, caring for camels, or consuming camel meat often get sick.
Many plague foci are characterized by inter-epizootic periods lasting several years. There are different hypotheses regarding the method of preserving the pathogen in nature: in saprophytic or L-form; the possibility of the microbe remaining in the corpses of dead animals and soil, various abiotic objects of the environment; the presence of “smoldering” foci, the introduction of the pathogen from afar by sick mammals and birds, and their fleas.
There are three known main plague pandemics that occurred in our era. The first refers to Art. VI. It is described under the name Justinian's. About 100 million people died then. The second pandemic (“Black Death”) occurred in the 14th century. and took more than 50 million lives. The third pandemic began in 1894 and lasted for several years in port cities. According to available data, from 1894 to 1975, 13 million patients were registered in the world. In the following decades, there was a thousand-fold decrease in the incidence of plague.
Now the plague has lost its meaning epidemic disease. Natural foci of plague pose a potential danger to humans. They are found on all continents except Australia, and occupy about 8-9% of the earth's land. Most cases of this infection are recorded in Vietnam, India, and Madagascar. On the territory of the CIS countries there are natural foci of plague in Transbaikalia, Gorny Altai, Central Asia, Trans-Urals, South-Western Caspian region, Transcaucasia - a total of 8 lowland foci (with a total area of over 200 million hectares) and 9 high-mountain areas (about 4 million hectares). Infection in humans is rare.
Prevention. It is necessary to prevent human diseases in natural foci and the importation of plague from abroad. Since plague is a quarantine disease, it is subject to International Sanitary Regulations.
In natural plague foci, systematic observation is carried out to identify epizootics among rodents and diseases of camels. Early detection of the first case in humans is of fundamental importance, which is immediately reported to higher health authorities.
Identified patients are immediately isolated in specially designated hospitals. Contacts are placed in isolation wards for 6 days; All patients with acute fever are subject to hospitalization in provisional hospitals; they are placed in small isolated groups. In order to early identify patients in a locality where a case of plague has been identified, door-to-door visits are carried out twice a day, and residents’ temperatures are measured.
For active immunization of persons living in enzootic territory and those traveling to a country affected by plague, a dry live vaccine prepared from a strain of the plague microbe EV or Kyzyl-Kum-1 is used. In enzootic areas, vaccination is carried out to the entire population when a patient is identified and selectively- risk groups (hunters, livestock breeders, harvesters, workers of geological and topographic teams). Vaccinations are given subcutaneously and cutaneously. The latter method is less reactogenic, so it is indicated for children aged 2-7 years, women in the first half of pregnancy and lactating women; older people. Revaccination- in a year, and in a difficult epidemiological situation- in six months. Epidemiological effectiveness is achieved when covering 90-95% of the population living in the outbreak. However, vaccination significantly reduces the risk of contracting predominantly bubonic forms of plague and does not protect against the pneumonic form.
Emergency prophylaxis with antibiotics is indicated for persons who have been in contact with sick people, corpses of those killed by the plague, or infected with fleas. For 5 days they are given streptomycin (0.5 g 2 times a day) or tetracycline (0.5 g 4 times a day). In case of a burdened epidemiological history (communication with patients with pneumonic plague), the daily dose of streptomycin is increased by 0.5 g, the intervals between its administrations are reduced to 8 hours.
When plague is detected in a populated area, a quarantine is established. The hospital for patients is maintained under a strict anti-epidemic operating regime. Patients with pneumonic and bubonic plague are placed in separate rooms. All personnel are transferred to barracks status and are subject to immunization and daily thermometry. Depending on the nature of the work and the clinical form of the disease, health workers use anti-plague suits of the 1st and 2nd types.
When carrying out current and final disinfection in an epidemic outbreak, a 5% solution of Lysol or phenol, a 2-3% solution of chloramine, steam and steam-formalin chambers are used. Dishes and linen are boiled in a 2% soda solution for at least 15 minutes. The corpses of the dead are cremated or buried to a depth of 1.5-2 m using dry bleach. Personnel must work in type 1 anti-plague suit. In an epidemic outbreak, it is necessary to carry out sanitary education among the population. The outbreak of plague is considered eliminated after the last patient is discharged from the hospital and subject to all disinfection and deratization measures.
Table 8
ANTI-EPIDEMIC MEASURES
WHEN A PATIENT OR CARRIER IS IDENTIFIED
Immediate isolation of the patient to the hospital and his treatment
Discharge of recovered patients with negative results of 3 studies after treatment
Daily (2 times a day) door-to-door visits of all residents of disadvantaged settlements with thermometry
Identification and hospitalization of persons suspected of OI in a provisional hospital
Identification and isolation of all contacts for 6 days in an isolation ward, emergency antibiotic prophylaxis
Laboratory examination of the population for plague
Disinfection and deratization measures
EPIDEMIOLOGICAL CHARACTERISTICS OF HEPATITIS B, C, D
The term viral hepatitis (VH) combines viral liver diseases, except for hepatitis caused by cytomegaly, herpes, Epstein-Barr and adenoviruses. In this lecture we consider only hepatitis transmitted parenterally.
Etiology. Today there are 7 known causative agents of viral hepatitis. They, in accordance with the WHO recommendation, are designated by the letters A, B, C, D, E, F, G, TT, SEN (Table 9).
Table 9
ETIOLOGY OF VIRAL HEPATITIS
HAV – enterovirus (picornavirus), RNA, inactivated at 100 °C in 5 minutes
HBV – hepadnavirus, DNA; antigens HBsAg HBcAg, HBeAg; inactivated by boiling in 45 minutes, insensitive to ethyl alcohol; persists for a long time - up to six months, in dry plasma - up to 25 years
HCV – flavivirus, RNA; 6 genotypes, >100 subtypes, quasi-variants
HDV (delta) – RNA, defective
HEV – calici-like, RNA
Virus B - the causative agent of hepatitis B (old name serum hepatitis). The remaining pathogens are etiological factors of diseases that were recently called- "VG neither A nor B." All of them belong to different taxonomic groups of viruses; they are united only by hepatotropy. The viruses HB, TTV and SEN are DNA-containing, the rest are RNA.
The causative agent of hepatitis B (HBV) belongs to the hepadnavirus family, is large in size (42 nm), contains DNA and its own DNA polymerase. Main antigens: surface (“Australian”) HBsAg, core (core) HBcAg, additional (infectiousness antigen) HBeAg. Along with complete Dane particles, specific spherical and tubular particles containing HBsAg, smaller than the virus, are detected in the blood serum. They are not capable of causing disease, but have important diagnostic value. From these fragments of the protein shell of the virus, a vaccine against hepatitis B was developed.
HBV is very persistent in the environment. It loses its infectivity when boiled only after 45 minutes, at a temperature of 120 ° C - after 45 minutes, in a dry-heat oven (160 ° C) - after 2 hours, when treated with a 3% solution of bleach. At room temperature The virus persists for six months and in dried plasma for up to 25 years. Not sensitive to the action of ethyl alcohol. Of course, such high resistance complicates the implementation of some anti-epidemic measures.
Hepatitis C virus (HCV) is a flavivirus, has RNA, and has a diameter of 50 nm. HCV is genetically heterogeneous; there are 6 known genotypes of the virus, over 100 subtypes and an infinite number of quasi-variants. A person, as a rule, becomes infected not with one virus, but with a mixture of virions of different types.
The hepatitis D virus (delta) also has RNA, but it is defective and requires the presence of the hepatitis B virus for replication. It is surrounded by a protein coat of HBsAg. The hepatitis G virus has RNA and, like HCV, belongs to the flavivirus family. The “Hepatitis alphabet” cannot be considered exhausted. Recently, there have been reports of the discovery of the TTV and Sen viruses, which may be involved in the etiology of hepatitis. However, in the etiological structure of CH, undeciphered diseases occupy no more than 0.5-1%.
Epidemiology. Viral hepatitis is common throughout the planet. These are typical anthroponotic infections (Table 9).
Table 9
EPIDEMIOLOGY OF VIRAL HEPATITIS
Viral hepatitis B, C, D (parenteral)
Infections of the external integument
Source – patient, virus carrier
Transmission mechanism – contact (wound)
Routes of transmission: parenteral manipulation, sexual intercourse, vertical (mother-fetus)
Seasonality is not typical
According to WHO, 1/6 of the human population is infected with the hepatitis B virus. Hepatitis B is common in all countries. The source of the pathogen is sick people and healthy virus carriers. The infectious period occurs in the last weeks of incubation (up to 2.5 months) and the first 3-4 weeks of the disease. After the 30th day from the onset of the disease, 3/4 of the patients are practically no longer infectious.
There are two categories of carriers: convalescents who have had hepatitis B, and people who have not been sick in the past. In different regions of the Earth, carriage among the population ranges from 0.1 to 33%, common in tropical and subtropical zones, as well as among chronic patients who are often treated in medical institutions. Carriage periods range from several weeks to 20 years, maybe lifelong. Long-term carriage is associated with the formation of chronic hepatitis.
The leading mechanism of transmission is wound, so hepatitis B is common among injection drug addicts, homosexuals and heterosexuals with many sexual partners. Transmission of the pathogen can occur through household means through shaving equipment, tattooing, and in families through sexual contact. In the tropics, blood-sucking arthropods play some role in the spread of the pathogen. A common cause of infection is diagnostic and therapeutic procedures that violate the integrity of the skin and mucous membranes - transfusion of contaminated blood and its preparations, operations, endoscopic examinations and other parenteral interventions. Blood and its preparations are of primary importance. It has been proven that hepatitis with jaundice can be caused by the injection of 1 ml of infectious plasma at a dilution of 1:104, and the subclinical form - 1:107. The virus remains infectious not only in whole blood, but also in plasma, erythrocyte mass, and fibrinogen. The risk of infection through these drugs is maximum. The frequency of blood transfusion increases the risk of infection; the administration of any blood product is associated with a certain risk of infection.
HBV can be found not only in the blood, but also in feces, urine, saliva, and semen if they are mixed with blood.
Transplacental infection of the fetus (“vertical” transmission) occurs relatively rarely. About 10% of children born to HBsAg-positive mothers become infected. But only 5% of them become infected in utero, the remaining 95% - during childbirth, which is confirmed by the relatively late development of hepatitis in children - at 3-4 months. postnatal period. The sexual route of infection is also associated with microtraumas of the skin and mucous membranes.
Susceptibility to hepatitis B is high. Children under one year of age and adults over 30 years of age are most often affected. Occupational risk groups for infection are medical workers (surgical specialists, employees of blood transfusion stations, clinical laboratory assistants, manipulation nurses), whose incidence is 3-5 times higher than the incidence rate of the adult population.
The peculiarity of hepatitis B is that it affects patients in different hospitals relatively frequently. This is a typical iatrogenic infection of our time, one of the most common nosocomial or post-hospital infections.
There is no seasonality or frequency of incidence. There is no protective effect from prophylactic administration of conventional donor γ-globulin.
Hepatitis C is also transmitted parenterally. The main risk of infection is associated with intravenous drug administration and blood transfusions. To groups increased risk infections include hemophilia patients and patients on hemodialysis, and less commonly, perinatal transmission of the virus from an infected mother to a newborn. During sexual intercourse, susceptibility is high. There are about 300 million HCV carriers in the world. Up to 80% of them should be considered sick.
The reservoir of D-infection is predominantly chronic carriers of HBV. Transmission occurs through blood, less commonly through sexual intercourse. More often, antibodies to HDV are found in drug addicts (more than 50%). Natural transmission routes include sexual and perinatal. Southern Europe, certain countries of Africa and the Middle East are considered endemic. In different territories, HDV infection is registered with a frequency of 0.1 to 20-30% of the total number of cases of HBV infection.
Prevention and measures in the outbreak (Table 10). Importance is given early detection and isolation of patients. The initial symptoms of the disease, the presence of anicteric, subclinical and inapparent forms are taken into account as much as possible, attention is paid to patients with chronic liver diseases, and they are examined for markers of CH. All patients with CH are registered in the territorial SES (emergency notification).
Contacts of hepatitis B, C, D, G are monitored for 6 months. Particular attention is paid to clinical, epidemiological and laboratory examination of blood donors, in particular to the identification of VH markers in them. Unfortunately, in practical conditions, only HBsAg and anti-HCV are determined. The following are not allowed to donate: persons who have suffered from CH in the past, regardless of how long the disease has been; having HBsAg and/or anti-HCV in the blood serum; liver diseases, including unknown etiology; contact in the family or in the apartment with a patient with CH during the last 6 months; recipients of donated blood, its products and organs.
Table 10
PREVENTION OF VIRAL HEPATITIS
Parenteral hepatitis (B, C, D)
Use of disposable medical instruments, thorough sterilization of reusable
Clinical, laboratory and epidemiological examination of blood and organ donors
Vaccination against hepatitis B (scheduled - provided for in the Vaccination Calendar for newborns and according to epidemiological indications)
Single and combined vaccines
EngerixTM B (HB), HBVax II (HB), InfanrixTMHepB (diphtheria, tetanus, whooping cough, HB), TwinrixTM (GA+HB, for children and adults)
Vaccine administration schedules
0-1-6 months; 0-1-2-6 months; 0-1-2-12 months; 0-7-21 days and 12 months.
To prevent parenteral infection with hepatitis viruses, it is necessary to make wider use of disposable medical and laboratory instruments, strictly adhere to the rules of complete pre-sterilization treatment and sterilization of medical piercing and cutting instruments, examine medical personnel and pregnant women for infection, and monitor donor blood and its preparations. The promotion of safe sex and moral and ethical standards of life deserves more attention.
A vaccine against hepatitis B has been created, and the high effectiveness of vaccinations has been confirmed. First of all, persons belonging to groups at high risk of hepatitis B infection should be vaccinated. The adult immunization schedule includes 3 vaccinations and a revaccination after 7 years. The vaccine is administered to children in stages: 4 times in the first year of life, then in accordance with the Vaccination Calendar to adolescents, taking into account the increase in incidence among them. Back in 1992, WHO set a goal to include vaccination against hepatitis B in national vaccination programs. This makes it possible to eradicate HBV infection in developed countries at the beginning of the 21st century. But vaccines are expensive and in Ukraine, as in many other countries, vaccination against hepatitis B is carried out in very modest volumes, which cannot significantly affect the incidence rate.
Recently launched combination vaccine against hepatitis A and B, which has significant advantages over monovalent vaccines. Considering the greatest tendency for HS to become chronic, the creation of a vaccine specifically for the prevention of this disease is of particular importance. But the great antigenic variability of the pathogen (greater than the influenza virus) prevents the practical solution of this difficult problem. The offensive against viral hepatitis continues, and we can look to the future with optimism.
EPIDEMIOLOGICAL CHARACTERISTICS OF TETANUS
Tetanus - an acute infectious disease caused by the toxin of the anaerobic pathogen Clostridium tetani. Characterized by defeat nervous systems s and is manifested by tonic and tetanic convulsions of skeletal muscles, leading to asphyxia.
Interest in tetanus is explained by many reasons, among which the main one is high mortality (from 30 to 70%). According to WHO, about 150-300 thousand people die from tetanus in the world every year, of which up to 80% are newborns. In many developing countries, tetanus causes 20-40% of newborn deaths. The problem of tetanus is especially acute in the countries of Southeast Asia and Central Africa.
Etiology. The causative agent of tetanus is C. tetani, belongs to the Bacillaceae family, has the appearance of relatively large rods with rounded ends and a large number of peritrichally located flagella. The length of tetanus clostridia is 4-8 microns, width is 0.3-0.8 microns. They are gram-positive, obligate anaerobes. They have a group somatic O- and type-specific flagellar H-antigen.
Important properties of the causative agent of tetanus are the ability to form spores, anaerobiosis and toxin formation. The spores are extremely resistant to physical and chemical environmental factors and persist for decades. The vegetative form is not very stable in the environment: at 100 ° C it dies after 5 minutes, at 60-70 ° C - after 20-30 minutes, under the influence of carbolic acid and sublimate in usual dilutions - after 15-20 minutes. The vegetative form of tetanus bacillus produces an exotoxin - tetanotoxin - one of the most powerful biological poisons. The lethal dose for humans is 130 mcg.
Epidemiology. The pathogen saprophytes in the intestines of many species of animals and humans, both in the form of spores and in a vegetative form that produces a toxin. With feces, tetanus bacilli enter the environment and, turning into spores, contaminate it for a long time. The most polluted by C. tetani are chernozems, rich in organic matter, fertile soils in hot and humid climates. Tetanus clostridia can grow in them and produce toxin. Therefore, a number of scientists classify tetanus as a sapronosis.
According to the classification of L.V. Gromashevsky, tetanus is included in the group of infections of the external integument with a wound mechanism of infection. The disease can develop when the pathogen enters the body through damaged skin or mucous membranes. Transmission factors can be any contaminated objects that cause injury, including medical instruments, suture material, etc.
More often, the disease occurs after injuries when the wounds are contaminated with soil. In peacetime, 80-85% of tetanus cases occur in rural areas. Microtraumas of the legs are especially common causes of infection (60-65%). Tetanus can also occur after animal bites. Tetanus is not transmitted directly from a sick person or animal.
An epidemiological feature of tetanus is the zonal distribution of morbidity. In the tropics, the incidence of tetanus is the same throughout the year. In the subtropics and temperate latitudes it is seasonal with the highest rates in the spring-summer-autumn period.
Susceptibility to the disease is high, but thanks to mass immunization, only isolated cases are recorded. In developing countries, due to poor obstetric care and lack of immunization programs, the incidence of tetanus in newborns, children and women is high. In economically developed countries, injection drug addicts are more likely to suffer from tetanus.
Prevention. Nonspecific prevention consists of preventing injuries, observing safety precautions at work, as well as hygiene measures at home. Sanitary education is essential. Surgical treatment of the wound, removal of foreign bodies, and aeration of the wound are required.
Specific prevention of tetanus is carried out routinely and urgently in case of injury. For routine prevention, the following drugs are used: DTP, ADS-M-anatoxin; AC toxoid. Planned prevention is carried out in accordance with the Vaccination Calendar (2006). All persons who do not have contraindications are subject to immunization. Children are vaccinated with DPT at 3 months. three times with an interval of 30 days. The first revaccination is carried out once at 18 months, the second - ADS at 6 years, the next - at 14 and 18 years. Planned revaccinations for adults are carried out with ADS-M toxoid at intervals of 10 years. For emergency prevention of tetanus, the following is used: antitetanus human Ig, obtained from the blood of actively immunized people (preventive dose 250 MO); PSS from the blood of hyperimmunized horses, prophylactic dose – 3000 MO; AC purified toxoid.
Indications for emergency prevention: injuries with damage to the integrity of the skin and mucous membranes; frostbite and burns of II-IV degrees; out-of-hospital abortions; childbirth outside the hospital; gangrene or tissue necrosis of any type, abscesses; animal bites; penetrating damage to the digestive canal.
Emergency prevention begins with primary surgical treatment of the wound. The administration of immune drugs depends on the availability of previous vaccination records. At documentary evidence The full course of routine vaccinations is not administered with immune preparations. If there are 3 vaccinations made more than 2 years ago, 0.5 ml of toxoid is administered, if there are 2 vaccinations made more than 5 years ago - 1 ml of toxoid. Those who are unvaccinated and in the absence of information about vaccinations are given active-passive immunization: 0.5 ml of toxoid, 250 MO of tetanus Ig or 3000 MO of PSS according to Bezredka are administered.
Contraindications for immunoprophylaxis are: increased sensitivity to the appropriate drug; pregnancy (in the first half, the administration of AS and PSS is contraindicated, in the second - PSS. Such persons are administered antitetanus human Ig).
By following the proper timing of tetanus vaccinations, and in the event of an injury, promptly seeking medical attention, the risk of tetanus can be reduced to zero.
EPIDEMIOLOGICAL CHARACTERISTICS OF RABIES
(hydrophobia, hydrophobia, lissa, rabies)
Zoonosis, an acute neuroinfectious disease with a contact mechanism of infection transmission, affecting warm-blooded animals, birds, and humans. One of the most serious illnesses humans, which always leads to death. Around the world, up to 50 thousand people and more than 1 million heads of various animals die annually from rabies.
Etiology. The causative agent of rabies (Neuroryctes rabiei) is a myxovirus from the rhabdovirus family, containing single-stranded RNA. It has a bullet shape and dimensions of 80-180 nm. The resistance of the virus is low: it quickly dies when boiled, when exposed to 2-3% solutions of Lysol or chloramine, or 0.1% solution of sublimate. At the same time, the virus is well preserved at low temperatures, freezing and vacuum drying in a frozen state. It dies in the stomach, so after drinking milk from a rabid animal, vaccinations are not given. The rabies virion contains RNA, proteins, lipids, and carbohydrates. The rabies virus is pathogenic for humans, all types of warm-blooded animals and birds. When the virus multiplies in the cytoplasm of neurons, specific oval inclusions are formed - Babes-Negri bodies (found in 98% of all cases of rabies in dogs). There are two known versions of the rabies virus: street (“wild”) and fixed (“Virus fixe”), obtained by Pasteur through repeated intracerebral passages on rabbits. This virus had the following differences from the street virus: rabbits get rabies when infected with a street virus after 20-30 days of incubation (fixed - exactly after 6-7 days); the infectious dose of a fixed virus for a rabbit is 10-20 times less than for a street virus; at the same time, Babes-Negri bodies do not develop; the fixed virus is low pathogenic, but leads to the formation of high titer antibodies and infects animals only when injected under the dura mater. The loss of pathogenic properties of the passage virus is firmly maintained while its antigenic and immunizing properties remain unchanged. It has antigenic, immunogenic and hemagglutinating properties.
Epidemiology. The main source of rabies is wild animals. There are natural (natural, primary) foci of rabies maintained by wolves and other animals from the canine family (jackals, raccoon dogs), foxes, wild cats, lynx, carnivorous and insectivorous bats, and anthropurgic (artificial, secondary, urban) foci maintained by domestic animals (dogs, cats, etc.). The infection can spread from wild animals to domestic animals, resulting in the formation of an urban outbreak, which is supported by stray dogs and develops independently of the natural outbreak. The role of synanthropic rodents as a source of rabies infection has not been proven.
Until the middle of the 20th century, the main source of the rabies virus in our country and in Europe were wolves; currently the dominant source of hydrophobia for humans is the fox. In countries where there is a lot of livestock, vampires rarely attack people. Cases of human being infected with rabies after being bitten by insectivorous bats have been described.
Most rabies diseases occur in the warm season; children and young people are most often affected.
The manifestation of rabies in different animals has its own characteristics. Thus, in wild animals it occurs predominantly with excitement, with a loss of fear of humans. A large number of bites of dangerous localization (head, face, hands) inflicted on humans, the significant migratory capabilities of wolves, capable of covering distances of 65-150 km at a running speed of 80 km/h, make these animals very dangerous to human life.
In dogs, the incubation period lasts 2-8 weeks, sometimes up to 8 months. In the first days of illness, they are reluctant to respond to the call of their owner and tend to hide in a dark place; periodically the animal becomes enraged, begins to gnaw and swallow stones, pieces of wood, rags, etc. Breathing sharply quickens, pupils dilate, saliva flows from the mouth in abundance, barking becomes hoarse and dull. After 2-3 days, the second period begins, characterized by extreme excitement - the dog ceases to recognize the owner, loses its voice and, breaking out into the street, always runs straight, silently attacking everything that comes across its path. The muzzle is shrouded in thick saliva, which comes out of the mouth in balls, the tail is lowered, the tongue hangs down, any attempt to swallow causes painful spasms. The period of excitement lasts 2-3 days and is replaced by a period of paralysis, during which the animal’s jaw drops, the tongue falls out, the legs are paralyzed and the dog moves, relying only on the front limbs, which is sometimes mistaken for an injury. With the onset of paralysis of the entire body on the 5-6th day of illness, the animal dies. In a state of excitement that lasts 3-4 days, the dog can run up to 50 km or more per day, attacking people, dogs, and pets. In cats, rabies begins with excitement, turning into a state of sharp aggressiveness, the animal attacks people and animals, paralysis occurs suddenly and the cat dies on the 2-4th day of illness. Foxes, unlike other animals, often do not show anger, but become trusting, affectionate, and easily fall into the hands of people.
Transmission of the infection occurs through a bite or salivation of the skin or mucous membranes. Saliva in dogs is contagious already 4-7 days before the clinical picture of the disease develops. With the so-called “silent rabies” of dogs, the period of excitement is short or even absent, and the stage of paralysis begins earlier and lasts longer. Depending on the danger of infection, the following categories of animals carrying bites are distinguished: A – the diagnosis of rabies is confirmed laboratory, B – the diagnosis of rabies is established clinically, C – the diagnosis is unknown, D – the animal is apparently healthy and is quarantined for up to 10 days. There is no reliable data on the transmission of rabies from person to person.
Prevention. Prevention of rabies consists of identifying and destroying animals that are sources of infection and preventing human illness after infection.
In the CIS countries annually more than 440 thousand people. turns to medical institutions for help regarding bites, scratches and salivation by animals. More than 50% of applicants are sent for rabies vaccinations, including 21% for an unconditional course of vaccinations.
First medical aid consists of local treatment of the wound, which should be immediately washed with soap and water, detergent, treated with alcohol, and tincture of iodine. The edges of the wound are not excised; it is not advisable to apply sutures. Local treatment of the wound, carried out in the first hours after a bite or salivation, is very effective. Next, the wound is irrigated with anti-rabies serum and the surrounding tissues are infiltrated, and tetanus is prevented.
Carrying out specific rabies vaccination depends on clarifying the nature of contact with animals, its biological type and clinical status, the presence of rabies in the area, as well as the ability to monitor the animal or conduct a laboratory examination of it. But treatment for seriously injured individuals should not be delayed until laboratory results are available. The long incubation period for rabies makes it possible to develop immunity before the virus penetrates the central nervous system.
Vaccinations are an emergency prevention of rabies bites. If in pre-Pasteur times 30-35% or more of those bitten by obviously rabid animals died from rabies, now in most countries it is 0.2-0.3%.
There are conditional and unconditional courses of rabies vaccinations.
An unconditional course of vaccinations is prescribed to persons who have been bitten, salivated on the skin and mucous membranes by clearly rabid, suspected rabies, wild or unknown animals. The course of vaccination is carried out with rabies vaccine (culture inactivated purified concentrated) according to a special scheme: 0th, 3rd, 7th, 14th, 30th and 90th days intramuscularly (or non-concentrated vaccine- subcutaneously 15-25 injections of 3-5 ml of the drug with a booster dose (additional) on the 10th, 20th and 30th days after the end of the main course of vaccinations, depending on the severity and location of the bite).
The conditional course consists of 2-4 injections of the vaccine to persons who have received multiple bites or injuries in a dangerous location (head, neck, hands) from apparently healthy animals for which a 10-day veterinary observation has been established. If the animal remains healthy, then immunization is stopped; if it dies or disappears, then the administered drugs create the basis for reliable immunity when anti-rabies immunization is resumed.
Vaccinations are not carried out in case of provoked salivation of intact skin unknown domestic animals in areas staunchly free from rabies, as well as upon contact with a sick person, if there was no obvious drooling of the mucous membranes or damage to the skin.
In combination with the vaccine, anti-rabies γ-globulin is prescribed, which creates passive immunity, at a dose of 0.25-0.5 ml/kg body weight. In case of bites from dangerous localizations by rabid animals, it is recommended to administer 30 ml of γ-globulin to the victim and begin vaccination only a day later. Despite the high therapeutic effectiveness of anti-rabies γ-globulin, it is highly reactogenic and often causes serum sickness and complications from the central nervous system, so its administration should be carried out with all precautions.
For active immunization, a fixed virus is used - the Rabivak-Vnukovo-32 vaccine, produced in the culture of primary young kidney cells Syrian hamsters and inactivated UV radiation. When introducing a culture vaccine general reactions, as a rule, are absent, and local ones are found no more often than in 6% of vaccinated people.
Another cause of complications when using brain vaccines is the occurrence of allergic reactions to proteins of brain tissue, manifested by neuritis, myelitis, encephalomyelitis of the Landry type, and post-vaccination encephalitis. The combined use of cultured vaccine and γ-globulin increases the effectiveness of immunization.
The epizootic situation of rabies in certain areas depends on the prevalence of the disease among representatives of wild fauna, and therefore it is necessary to regulate the number of wild carnivores, large-scale oral vaccination of foxes with live rabies vaccines in the field, and shoot them; carry out preventive immunization of dogs, cats, as well as vaccination of large cattle in the countryside.
The fight against epizootics among domestic animals consists of trapping stray dogs, cats, mandatory registration and vaccination of dogs, regardless of their value; possible vaccination of cats, active and timely identification of foci of rabies among domestic and farm animals, laboratory diagnosis of each case of the disease, establishment of quarantine and other measures in the outbreak of the disease. Dogs must be muzzled or on a leash when outdoors. Any obviously rabid animal is subject to immediate destruction, as is any dog, cat or other animal of little value that has been bitten by a rabid or suspected rabid animal. Establishment of quarantine for imported dogs and cats.
An important place in the prevention of rabies belongs to sanitary and veterinary propaganda, improvement of existing and development of new anti-rabies drugs, development of reliable methods for the rapid diagnosis of rabies in animals that have caused damage.
VOCAL-BORNE DISEASES(lat. transmissio transfer to others) - infectious human diseases, the pathogens of which are transmitted by blood-sucking arthropods.
Group T. b. includes more than 200 nosological forms caused by viruses, bacteria, protozoa and helminths. Depending on the method of transmission of pathogens, E. N. Pavlovsky and V. N. Beklemishev share T. b. into obligate-transmissible and facultative-transmissible.
Causative agents of such obligate-transmissible diseases as yellow fever (see), epidemic typhus (see Epidemic typhus), filariasis (see), leishmaniasis (see), sleeping sickness (see), malaria (see) , are transmitted only with the help of blood-sucking carriers (see). The circulation of the pathogen in the donor-carrier-recipient scheme ensures an indefinitely long existence of T. b. in nature.
Pathogens of facultatively vector-borne diseases are transmitted in various ways, including transmissible. The latter route of transmission may contribute to the maintenance and spread of the disease and the occurrence of outbreaks, but the pathogen can circulate indefinitely and without the help of a vector. For example, the causative agents of tularemia (see) can be transmitted not only by mosquitoes (see Blood-sucking mosquitoes), horse flies (see), ixodid ticks (see), but also through air, water, food products contaminated with the feces of mammals, to- some contain pathogens, as well as through contact - when removing skins from sick animals; The causative agents of the plague are transmitted by fleas, but it is possible to become infected with the plague by skinning sick marmots OR by eating poorly cooked meat from sick camels; the plague is also transmitted from a sick person by airborne droplets.
T.b. It is customary to subdivide also into anthroponoses (see) and zoonoses (see). A small group of anthroponoses includes epidemic typhus and louse-borne relapsing fever (see Relapsing fever), phlebotomy fever (see), malaria, Indian visceral leishmaniasis, Gambian form of sleeping sickness, certain filariases (see). A more representative group of zoonoses includes the plague (see), tick-borne and mosquito encephalitis (see), endemic rickettsioses (see) and others; Most vector-borne zoonoses are natural focal diseases.
Characteristics of the carrier and mechanism of transmission of the pathogen. In the transmission of pathogens T. b. specific and mechanical vectors are involved (see Mechanism of transmission). Specific, or biological, carriers are, as a rule, blood-sucking arthropods. Transmission of pathogens by specific vectors is a complex biol. a phenomenon based on a historically established ancient system of relationships and mutual adaptations of the pathogen, vector and warm-blooded animal. The pathogen in the body of a specific carrier either multiplies and accumulates (for example, viruses - in the body of ticks, mosquitoes and mosquitoes; rickettsia and spirochetes - in the body of lice), or does not multiply, but goes through one of the stages of development, this is typical, for example, for causative agents of wuchereriosis Wuchereria bancrofti and mosquitoes (see Wuchereriosis) and for the causative agent of loiasis Loa loa and horseflies (see Loiasis). The closest relationships arise in cases where the pathogen in the carrier’s body both develops and multiplies; this kind of complex relationship is characteristic of malarial plasmodia and mosquitoes (see Anopheles, Malaria), for trypanosomes and tsetse flies (see Tsetse fly, Trypanosomes), etc. A specific carrier receives the pathogen from a donor host only through blood sucking, and this predetermines the mandatory the presence of pathogens in the blood of a warm-blooded animal.
The causative agents of malaria are unicellular microorganisms belonging to the phylum Protozoa, class Sporozo genus Plsmodium. About 60 species of Plasmodium are known in animals and birds; Human malaria is caused by 4 types of pathogens: Plsmodium flciprum, the causative agent of tropical malaria mlri tropic Plsmodium vivx, the causative agent of three-day vivaxmalaria mlri vivx Plsmodium ovle, the causative agent of three-day malaria mlri ovle and Plsmodium mlrie, the causative agent of four-day malaria mlri qurtn. The causative agents of malaria consist of individual...
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PAGE 32
Ministry of Health of Ukraine
Odessa National Medical University
Department of Infectious Diseases
"Approved"
At the methodological meeting of the department
“___” ______________ in 200__
Protocol ____
Head Department ___________________ K.L. Servetsky
Lecture No. 9. Vector-borne infections
for students
V year medical faculty
Vector-borne infections are a group of diseases, the main condition for the spread of which is the presence of an insect vector. In this case, the person is a carrier of the infection and, in the absence of an insect carrier, does not pose a danger to others.
Currently, vector-borne diseases are becoming increasingly important in human pathology, which is associated with their wide distribution, active migration of the population, and the development of tourism. As a result, the ecological balance in certain regions is disrupted, a person occupies ecological niches that are unusual for him, encounters diseases for which he was not prepared, as a result of which a severe course of diseases is observed, and in some cases a high mortality rate is recorded.
There are 2 groups of vector-borne diseases:
- endemic: either the main source of infection, or the carrier is strictly “tied” to a certain area, where it finds the most favorable conditions for its habitat and reproduction;
- epidemic: the main source of infection is humans, the main (sometimes the only) carrier of infection is the louse.
Taking into account the etiology and characteristics clinical course highlight:
I . Diseases caused by viruses (arboviral diseases).
A. Viral encephalitis.
1. Tick-borne (Central European) encephalitis.
2. Mosquito (Japanese) encephalitis.
B. Hemorrhagic fevers.
1. Yellow fever.
2. Congo-Crimean hemorrhagic fever.
3. Omsk hemorrhagic fever.
4. Hemorrhagic fever Dengue.
B. Systemic fevers.
1. Pappataci fever (phlebotomy, mosquito).
2. Classic dengue fever.
II . Systemic diseases caused by rickettsia (rickettsiosis).
III. Diseases caused by spirochetes.
1. Tick-borne relapsing fever (tick-borne spirochetosis).
2. Louse-borne relapsing fever.
3. Lyme disease.
IV . Diseases caused by protozoa.
1. Malaria.
2. Leishmaniasis.
V. Diseases caused by helminths.
Filariasis.
MALARIA
Malaria (Febris inermittens - lat., Intermittent fever, Malaria - English, Paludisme - French, Febremalariche - Italian, Paludismo - and cn .) - a group of protozoal vector-borne human diseases, the causative agents of which are transmitted by mosquitoes of the genus Anopheles . It is characterized by predominant damage to the reticulohistiocytic system and erythrocytes, manifested by febrile paroxysms, hepatosplenomegaly, and anemia.
The causative agents of malaria consist of separate geographical varieties or strains, differing in morphological properties, degree of pathogenicity, sensitivity to medicines. For example, African strains of Pl. falciparum cause more severe forms of malaria than Indian malaria.
Features of the sporogony process and its duration depend on the type of malarial plasmodia and the ambient temperature. Temperature threshold for completion of sporogony Pl. vivax must be at least + 16 C, for other plasmodia is not lower than + 18 C. The higher the external temperature, the faster sporogony ends.
An infected malaria mosquito, attacking a person, injects sporozoites into the bloodstream along with saliva, which enter the liver through the bloodstream and penetrate into hepatocytes. The duration of stay of sporozoites in the bloodstream does not exceed 30-40 minutes. The stage of tissue (exoerythrocytic) schizogony begins, as a result of which the sporozoites are rounded, the nucleus and protoplasm increase in size and tissue schizonts are formed. As a result of multiple divisions, merozoites are formed from schizonts (up to 10,000 in Pl. vivax and up to 40,000 in Pl. falciparum).
In the population of “northern” strains of Pl. vivax is dominated by bradysporozoites, infection with which leads to the development of the disease after prolonged incubation. Among the “southern” strains, on the contrary, tachysporozoites predominate. For this reason, infection with “southern” strains causes disease after a short incubation period, often followed by the development of late relapses.
As a result of the breakdown of erythrocytes, the merozoites formed in the process of erythrocyte schizogony are released into the blood plasma and the process of erythrocyte schizogony is repeated.
The potential for malaria to spread is determined by the length of the transmission season. When the number of days per year with air temperatures above 15°C is less than 30, the spread of malaria is impossible; if there are from 30 to 90 such days, the possibility is assessed as low, and if there are more than 150, then the possibility of spread is very high (if there are mosquito vectors and a source infections).
The source of infection is a sick person or a gamete carrier. Vectors are various species (about 80) of mosquitoes from the genus Anopheles. A person becomes infected when they are bitten by an infected mosquito, or through a blood transfusion from a person with malaria. Intrauterine infection of the fetus is possible. A mosquito becomes infected from a sick person from the period when mature gamonts appear in the blood. With three- and four-day malaria, this is possible after the second or third attack, with tropical malaria - after the 7-10th day of illness.
Malarial attacks are accompanied by a generalized narrowing of peripheral blood vessels during chills, which during fever is replaced by a sharp dilation. These changes enhance the production of kinins and other substances that increase the permeability of the vascular wall. As a result of sweating of water and proteins into the perivascular space, blood viscosity increases and blood flow slows down. Thromboplastic substances formed during hemolysis enhance hypercoagulation. It is believed that plasmodia produce cytotoxic factors that inhibit cellular respiration and phosphorylation. Against the background of severe microcirculation disorders, disseminated intravascular coagulation develops.
Adrenal insufficiency, disturbances of microcirculation, and cellular respiration can lead to acute renal failure - “shock kidney”. In acute attacks of malaria, due to impaired tissue respiration and changes in adenyl cyclase activity, the development of enteritis is also possible.
During the first attacks of malaria, the spleen and liver enlarge due to acute blood supply and a significant increase in the reaction of the RES to the breakdown products of erythrocytes and Plasmodium toxins. With a large amount of hemomelanin in the liver and spleen, endothelial hyperplasia occurs, and with a long course of the disease, connective tissue grows, which is expressed in the induration of these organs.
Microcirculatory disorders in the lungs manifest themselves as symptoms of bronchitis, and in severe cases of malaria the development of pneumonia may occur. The slowdown and even cessation of blood circulation in the liver lobules leads to dystrophic and necrotic changes in hepatocytes, increased activity of AlAt, AsAt, and disruption of pigment metabolism.
Classification. Depending on the type of pathogen, there are:
Vivax malaria;
Malaria ovale;
Four-day malaria ( quartana);
Tropical malaria ( tropica, falciparum).
Depending on the period of illness:
Primary malaria;
Early relapses of malaria (up to 6 months after the initial attack);
Distant relapses of malaria;
Malaria latency period.
Taking into account the severity of the current:
Lung;
Moderate;
Heavy;
Very severe (malignant) course of malaria.
As separate clinical forms describe:
Congenital malaria;
Transfusion malaria;
Malaria in pregnant women;
Mixed malaria.
Clinic. All types of malaria are characterized by a cyclical course, in which the following periods of illness are distinguished:
Incubation period;
Primary attack;
Remission period (fever-free period);
Nearest relapses;
Latent period (absent in tropical malaria);
Distant relapse (repeated attack) is absent in tropical malaria.
Duration incubation perioddepends on the number of sporozoites entering the body, the type of malaria, the condition immune system person. There are 2 stages in its course:
Primary attackprimary attack, primary malaria. The onset of the disease in most cases is acute and sudden. However, a prodrome is possible for several days in the form of weakness, lower back pain, low-grade fever, and chills.
Typical malarial paroxysms go through 3 stages: chills, fever, sweat.
Chills are stunning, sudden, the skin acquires a grayish tint, the lips are cyanotic, shortness of breath and tachycardia may be observed. The temperature in the armpit is normal or slightly elevated, the rectal temperature rises by 2-3°C. The duration of this stage is 2-3 hours.
Fever gives way to chills, the temperature rises quickly, reaching 40-41°C in 10-30 minutes. Patients complain of severe headache, nausea, thirst, and sometimes vomiting. The face is hyperemic, the skin is dry, the eyes are shiny, tachycardia. This stage lasts for vivax - malaria 3-5 hours, with four days up to 4-8 hours, with tropical up to 24-26 hours or more.
Sweat profuse, often profuse, temperature drops critically, sometimes to sub-zero normal numbers. Facial features become sharper, pulse slows, hypotension.
The duration of the entire paroxysm of malaria depends on the type of pathogen and ranges from 6-12 to 24-28 hours. This is followed by a period of apyrexia lasting 48-72 hours (depending on the type of malaria).
From the end of the first week, the liver and spleen enlarge in patients, and the spleen enlarges earlier (tense, sensitive to palpation).
Nearest relapsesoccur as a result of increased erythrocyte schizogony. There may be one or more such relapses; they are separated by periods of apyrexia. The same paroxysms occur as during the initial attack.
Latent period lasts from 6-11 months (with vivax - and ovale - malaria) up to several years (with four-day malaria).
In case of four-day malaria, distant relapses are not preceded by the pre-erythrocytic stage; they arise due to the activation of erythrocyte schizogony. The disease can last for years, accompanied by relapses with typical paroxysms.
Three-day malaria.The pathogen has the ability to cause disease after short (10-21 days) and long (6-13 months) incubation, depending on the type of sporozoite. Three-day malaria is characterized by a long-term benign course. Repeated attacks (distant relapses) occur after a latent period of several months (3-6-14) and even 3-4 years. In some cases, in non-immune individuals, malaria can be severe and fatal.
In non-immune individuals who become ill for the first time, the disease begins with a prodrome - malaise, weakness, headache, aches in the back and limbs. In most cases, typical attacks of malaria are preceded by a 2-3-day increase in body temperature to 38-39 ° C of the wrong type. Subsequently, attacks of malaria are clinically clearly defined, occurring at regular intervals and more often at the same time of day (between 11 a.m. and 3 p.m.). In moderate to severe cases of the disease, during chills the patient experiences severe weakness, a sharp headache, aching pain in large joints and lower back, rapid breathing, and repeated vomiting. Patients complain of tremendous chills. The face is pale. Body temperature quickly reaches 38-40°C. After the chill, the fever begins. The face turns red, the skin of the body becomes hot. Patients complain of headache, thirst, nausea, and tachycardia increases. Blood pressure decreases to 105/50-90/40 mm Hg. Art., dry wheezing is heard above the lungs, indicating the development of bronchitis. Almost all patients experience moderate bloating, loose stool. The duration of chills is from 20 to 60 minutes, heat - from 2 to 4 hours. Then the body temperature decreases and reaches normal numbers after 3-4 hours. During this period, sweating increases. Feverish attacks last from 5 to 8 hours. Enlargement of the liver and spleen can be detected already in the first week of the disease. Anemia develops gradually. In the natural course of the disease in untreated cases, febrile attacks last 4-5 weeks. Early relapses usually occur 6-8 weeks after the end of the initial fever and begin with regularly alternating paroxysms; prodromal phenomena are not typical for them.
Complications from three-day malaria are rare. In underweight individuals with overheating and dehydration, severe malaria can be complicated by endotoxic shock.
Tropical malaria.The incubation period is about 10 days with fluctuations from 8 to 16 days. Tropical malaria in non-immune individuals is characterized by the greatest severity and often acquires a malignant course. Without taking antimalarial drugs, death can occur in the first days of illness. Some people who become ill with malaria for the first time experience prodromal phenomena - general malaise, excessive sweating, loss of appetite, nausea, loose stools, two to three days of increased body temperature to 38°C. In most non-immune individuals, the onset of the disease is sudden and is characterized by moderate chills, high fever, agitation of patients, severe headache, aching muscles and joints. In the first 3-8 days, the fever is of a constant type, then it takes on a stable intermittent character. At the height of the disease, attacks of fever have some characteristics. There is no strict frequency for the onset of fever attacks. They can begin at any time of the day, but most often occur in the first half of the day. A decrease in body temperature is not accompanied by sudden sweating. Feverish attacks last more than a day (about 30 hours), periods of apyrexia are short (less than a day).
During periods of chills and heat, the skin is dry. Characterized by tachycardia and a significant decrease in blood pressure to 90/50-80/40 mm Hg. Art. The respiratory rate increases, a dry cough, dry and moist wheezing appear, indicating the development of bronchitis or bronchopneumonia. Dyspeptic symptoms often develop: anorexia, nausea, vomiting, diffuse epigastric pain, enteritis, enterocolitis. The spleen enlarges from the first days of the disease. On palpation, there is pain in the left hypochondrium, which intensifies with deep inspiration. By the 8-10th day of illness, the spleen is easily palpable, its edge is dense, smooth, and painful. Toxic hepatitis often develops. The content of direct and indirect bilirubin in the blood serum increases, and the activity of aminotransferases increases 2-3 times. Renal dysfunction in the form of mild toxic nephrosonephritis is observed in 1/4 of patients. From the first days of the disease, normocytic anemia is detected. On the 10-14th day of illness, the hemoglobin content usually decreases to 70-90 g/l, and the number of red blood cells - to 2.5-3.5 10 12 /l. Leukopenia with neutropenia, relative lymphocytosis and a nuclear shift towards young forms of neutrophils are noted, reticulocytosis and ESR increase. IN peripheral blood From the first days, plasmodia are detected in the ring stage.
Ovale malaria. Endemic to West African countries. The incubation period is from 11 to 16 days. This form of malaria is characterized by a benign course and frequent spontaneous recovery after a series of attacks of primary malaria. The clinical manifestations of oval malaria are similar to tertian malaria. Distinctive feature- onset of attacks in the evening and at night. The duration of the disease is about 2 years, however, relapses of the disease have been described that occurred after 3-4 years.
Complications. Malignant forms of malaria are of great danger: cerebral (malarial coma), infectious-toxic shock (algic form), severe form of hemoglobinuric fever.
Cerebral form occurs more often in the first 24-43 hours from the onset of the disease, especially in people with underweight. Harbingers of malarial coma are severe headache, severe weakness, apathy or, conversely, anxiety and fussiness. In the precomatous period, patients are inactive, answer questions monosyllabically and reluctantly, quickly become exhausted and again plunge into a soporotic state.
During examination, the patient's head is thrown back. The legs are often in an extension position, the arms are bent at the elbow joints. The patient has severe meningeal symptoms (stiff neck, Kernig's, Brudzinski's symptoms), caused not only by cerebral hypertension, but also by damage to the tonic centers in the frontal region. Hemorrhages in the lining of the brain cannot be ruled out. In some patients, phenomena of hyperkinesis are observed: from clonic muscle spasms of the limbs to general tetanic or epileptiform convulsive seizures. At the beginning of the coma, the pharyngeal reflex disappears, later the corneal and pupillary reflexes.
Upon objective examination: body temperature is 38.5-40.5°C. Heart sounds are muffled, pulse rate corresponds to body temperature, blood pressure is reduced. Breathing is shallow, rapid from 30 to 50 per minute. The liver and spleen are enlarged and dense. The function of the pelvic organs is impaired, resulting in involuntary urination and defecation. In the peripheral blood, half of the patients have an increase in the number of leukocytes to 12-16 10 9 /l with a nuclear shift towards young forms of neutrophils.
For infectious-toxic shock(algic form of malaria) severe weakness and lethargy develop, turning into prostration. The skin is pale gray, cold, covered with sweat. The facial features are pointed, the eyes are sunken with blue circles, the gaze is indifferent. Body temperature is reduced. The distal parts of the limbs are cyanotic. Pulse more than 100 beats/min, low filling. Maximum blood pressure drops below 80 mm Hg. Art. Breathing is shallow, up to 30 per minute. Diuresis less than 500 ml. Sometimes there is diarrhea.
Hemoglobinuric feveroccurs more often after taking quinine or primaquine. Massive intravascular hemolysis can also be caused by other drugs (delagil, sulfonamides). The complication occurs suddenly and is manifested by stunning chills, hyperthermia (up to 40°C or more), aching muscles, joints, severe weakness, vomiting bile, headache, discomfort in the upper abdomen and lower back. The main symptom of hemoglobinuria is the discharge of black urine, which is due to the content of oxyhemoglobin in freshly released urine, and methemoglobin in standing urine. When standing, urine separates into two layers: the upper layer, which has a transparent dark red color, and the lower layer, which is dark brown, cloudy, and contains detritus. In urine sediment, as a rule, clumps of amorphous hemoglobin and single unchanged and leached red blood cells are found. The blood serum becomes dark red, anemia develops, and the hematocrit decreases. The content of free bilirubin increases. In the peripheral blood, neutrophilic leukocytosis with a shift towards younger forms, the number of reticulocytes increases. The most dangerous symptom is acute renal failure. Creatinine and urea levels quickly increase in the blood. The next day, the skin and mucous membranes become jaundiced, possibly hemorrhagic syndrome. In mild cases, hemoglobinuria lasts 3-7 days.
Malaria is diagnosed based on characteristic clinical manifestations: fever, hepatolienal syndrome, anemia (may be absent in the first days of the disease). It is natural to increase the number of reticulocytes as an indicator of the compensatory activity of erythropoiesis. Leukopenia or normocytosis, hypoeosinophilia, neutropenia with a band shift are characteristic. The presence of leukocytosis is a sign of severe, malignant malaria. Involvement of the liver in the pathological process is indicated by an increase in the activity of aminotransferases and alkaline phosphatase.
It is necessary to pay attention to the epidemiological history data: stay in the epidemiological zone for a period of up to 2 years from the onset of the disease.
To confirm the diagnosis, laboratory tests of thick drops and blood smears are performed. Currently, enzyme-linked immunosorbent test systems are also used to detect antigen. If malaria is suspected and immediate laboratory testing is not possible, it is necessary to take smears and “thick” drops of blood and, without waiting for laboratory test results, begin emergency treatment.
In tropical malaria, in the early stages of the disease, only young ring-shaped trophozoites are detected in the blood, because erythrocytes with developing forms of plasmodium are retained in the capillaries of internal organs, where the cycle of erythrocyte schizogony ends.
Different age stages Pl. falciparum appear in the peripheral blood during severe, malignant malaria. Development and maturation of gametocytes Pl. falciparum also occurs in the capillaries of internal organs, and adult gametocytes in the form of crescents appear in the peripheral blood no earlier than 8-11 days from the onset of the disease.
Due to the fact that the clinical symptoms of malaria may not be distinct in areas unfavorable for malaria (or in those arriving from endemic areas up to 2 years before the onset of the disease), any febrile condition should be microscopic studies stained “thick” drop of blood for malarial plasmodia.
Differential diagnosis should be made with typhoid fever, acute respiratory diseases, pneumonia, Q fever, leptospirosis.
Treatment. Antimalarial drugs are divided into 2 groups according to the type of action:
1. Schizotropic drugs:
Gametoshisotropic, acting on erythrocyte schizonts derivatives of 4-aminoquinoline (chloroquine, delagil, hingamine, nivaquin, etc.); quinine, sulfonamides, sulfones, mefloquine, tetracycline;
Histoschisotropic, acting on tissue forms of plasmodium primaquine.
2. Gamototropic drugs effective against sexual forms of plasmodium primaquine.
To treat three- and four-day malaria, a three-day course of treatment with delagil is first carried out: on the first day, 0.5 g of the drug salt is prescribed in 2 doses, on the second and third days, 0.5 g in one dose, then primaquine is prescribed 0.009 g 3 times a day for 14 days.
For tropical malaria, on the first day the dose of delagil should be 1.5 g 0.5 g 3 times a day. On the second and third days 0.5 g in one dose. Clinical improvement and normalization of body temperature occur within 48 hours, schizonts disappear from the blood after 48-72 hours.
Pathogenetic therapy includes prednisolone, reogluman, reopolyglucin, Labori solution, 5% albumin solution. Oxygen barotherapy is indicated.
Forecast With timely diagnosis and treatment, it is most often favorable. Mortality averages 1% and is caused by malignant forms of malaria.
Prevention Chemotherapy does not prevent human infection, but only stops the clinical manifestations of infection. In foci of malaria, delagil is prescribed 0.5 g once a week, amodiaquine 0.4 g (base) once a week. In areas where chloroquine-resistant tropical malaria is widespread, fansidar 1 tablet per week, mefloquine 0.5 g once a week, fansimer (a combination of mefloquine with fansidar) 1 tablet per week are recommended. A promising drug from sweet wormwood artemisin. Taking medications begins a few days before arrival at the outbreak, continues throughout the stay in it and for another 1 month after leaving the outbreak.
RICKETSIOSES
Rickettsial diseases are widespread diseases. The incidence is especially high during wars and still occurs today. In 1987, WHO held a Consultative Meeting on the diagnosis of rickettsioses, and a test kit for diagnosing rickettsial diseases was compiled. Using indirect immunofluorescence in 37 laboratories different countries Patients with unclear febrile illnesses were examined. In Thailand, El Salvador, Pakistan, Tunisia, Ethiopia, and Iran, typhus was detected, its frequency ranged from 15 to 23%. Rickettsioses from the spotted fever group were detected even more often; in Nepal, positive results were obtained from examination of 21.1% of patients, in Thailand - 25%, in Iran - 27.5% and in Tunisia - 39.1%. In China, 17% of febrile illnesses were caused by the tsutsugamushi pathogen. In the United States, 600-650 cases of Rocky Mountain fever are reported annually.
The term “rickettsia” was proposed in 1916 by the Brazilian scientist Roja Lima to designate the causative agent of Rocky Mountain fever, discovered by the American scientist Ricketts. Microbiologist Prowazek died from typhus. The causative agent of typhus, Ricketsia prowaieki, was named in honor of these scientists. Subsequently, a large number of similar microorganisms were discovered. Most species of rickettsia (over 40) are non-pathogenic; they live in arthropods and do not cause pathology in mammals. Pathogenic rickettsiae belong to the order Rickettsiales, family Rickettsiaceae. The tribe Rickettsieae is divided into three genera: 1 - Rickettsia, 2 - Rochalimea, 3 - Coxiella. The genus Rickettsia includes the causative agents of almost all human rickettsioses. Two species were classified into the genus Rochalimea - the causative agent of Volyn, or trench fever (R. quintana) and the causative agent of tick-borne paroxysmal rickettsiosis (R. rutchkovskyi). In addition, in recent years, a new species of Rochalimeae henselae has been isolated, which causes a peculiar disease in HIV-infected people. Only the causative agent of Q fever (Coxiella burnetti) belongs to the genus Coxiella. In addition to these rickettsia from the tribe Rickettsieae, there were 4 species of rickettsia from the tribe Ehrlicheae, which caused diseases only in some domestic animals and were not important in human pathology. IN Lately Two species of ehrlichia pathogenic to humans have been described (Ehrlichia chaffensis, E. canis), and hundreds of cases of human ehrlichiosis have already been reported.
Rickettsia are microorganisms that occupy an intermediate position between viruses and bacteria. The general properties of rickettsia include their pleomorphism: they can be coccoid (up to 0.1 µm in diameter), short rod-shaped (1 - 1.5 µm), long rod-shaped (3 - 4 µm) and filamentous (10 µm or more). They are immobile, gram-negative, and do not form spores. Rickettsia and bacteria have a similar cell structure: a surface structure in the form of a protein shell, protoplasm and a nuclear substance in the form of chromatin grains. They multiply intracellularly, mainly in the endothelium, and do not grow on artificial nutrient media. Rickettsia is cultivated on chicken embryos or in tissue cultures. Most rickettsiae are sensitive to tetracycline antibiotics.
Human rickettsioses can be divided into three groups:
I. Typhus group.
Epidemic typhus (causative agents prowazekii and R. sapada, the latter circulates in North America);
Brill's disease; Zinsser's disease; distant relapse of epidemic typhus;
Endemic or flea typhus (pathogen R. typhi);
Tsutsugamushi fever (caused by R. tsutsugamushi).
II. Group of spotted fevers.
Spotted fever Rocky Mountains (pathogen Rickettsia rickettsii);
Marseilles fever (caused by R. conorii);
Australian tick-borne rickettsiosis (pathogen: Rickettsia australis);
Tick-borne typhus of North Asia (pathogen: R. sibirica);
Vesicular rickettsiosis (causative agent R. okari).
III. Other rickettsial diseases.
Q fever (caused by Coxiella burnetii);
Volyn fever (pathogen: Rochalimea quintana);
Tick-borne paroxysmal rickettsiosis (pathogen - Rickettsia rutchkovskyi);
Diseases caused by recently discovered Rochalimeae henselae;
Ehrlichiosis (pathogens : Ehrlicheae chaffensis, E. canis).
Currently, Rohalimia (R. quintana, R. hensele) are classified as Bartonella.
EPIDEMIC TYPHUS (TYPHUS EXANTHEMATICUS)
Synonyms: louse-borne typhus, war typhus, famine typhus, European typhus, prison fever, camp fever; epidemic typhus fever, louse-born typhus, jail fever, famine fever, war fever - English, Flecktyphus, Flec-kfieber German; typhus epidemique, typhus exanthematique, typhus historique French; tifus exantematico, dermotypho ucn.
Epidemic typhus is an acute infectious disease characterized by a cyclical course, fever, roseola-petechial exanthema, damage to the nervous and cardiovascular systems, and the possibility of rickettsia remaining in the body of a convalescent for many years.
Etiology. The causative agents of the disease are R. prowazekii, distributed throughout the world, and R. canada, the circulation of which is observed in North America. Provachek's rickettsia is somewhat larger than other rickettsia, gram-negative, has two antigens: a superficially located species-specific (common with Muzer's rickettsia) heat-stable, soluble antigen of lipoid-polysaccharide-protein nature, underneath is a species-specific insoluble heat-labile protein-polysaccharide antigenic complex. Rickettsia Provachek quickly die in a humid environment, but persist for a long time in lice feces and in a dried state. They tolerate low temperatures well and die when heated to 58°C in 30 minutes, and to 100°C in 30 seconds. They die under the influence of commonly used disinfectants (Lysol, phenol, formalin). Highly sensitive to tetracyclines.
Epidemiology. Typhoid fever was first identified as an independent nosological form by Russian doctors Y. Shchirovsky (1811), Y. Govorov (1812) and I. Frank (1885). Detailed distinction between typhoid and typhus (according to clinical symptoms) carried out in England by Murchison (1862) and in Russia by S. P. Botkin (1867). The role of lice in the transmission of typhus was first established by N. F. Gamaleya in 1909. The infectiousness of the blood of patients with typhus was proven by the experience of self-infection by O. O. Mochutkovsky (the blood of a patient with typhus was taken on the 10th day of illness, introduced into the skin incision of the forearm, O. O. Mochutkovsky’s disease occurred on the 18th day after self-infection and was severe). Currently, a high incidence of typhus remains in some developing countries. However, the long-term persistence of rickettsia in those who previously had typhus and the periodic occurrence of relapses in the form of Brill-Zinsser disease does not exclude the possibility of epidemic outbreaks of typhus. This is possible when social conditions deteriorate (increased population migration, head lice, deteriorating nutrition, etc.).
The source of infection is a sick person, starting from the last 2-3 days of the incubation period until the 7-8th day from the moment the body temperature normalizes. After this, although rickettsiae can persist in the body for a long time, the convalescent no longer poses a danger to others. Typhus is transmitted through lice, mainly through body lice, less often through head lice. After feeding on the blood of a patient, the louse becomes infectious after 5-6 days and until the end of life (i.e. 30-40 days). Human infection occurs by rubbing lice feces into skin lesions (in scratches). There are known cases of infection from blood transfusions taken from donors in the last days of the incubation period. Rickettsia circulating in North America (R. capada) is transmitted by ticks.
Pathogenesis. The gateway to infection is minor damage to the skin (usually scratching); within 5-15 minutes, rickettsiae penetrate into the blood. Reproduction of rickettsia occurs intracellularly in the vascular endothelium. This leads to swelling and desquamation of endothelial cells. The cells that enter the bloodstream are destroyed, and the released rickettsiae infect new endothelial cells. The main form of vascular damage is verrucous endocarditis. The process can involve the entire thickness of the vascular wall with segmental or circular necrosis of the vessel wall, which can lead to blockage of the vessel by the resulting thrombus. This is how peculiar typhus granulomas (Popov's nodes) arise. In severe cases of the disease, necrotic changes predominate; in mild cases, proliferative changes predominate. Vascular changes are especially pronounced in the central nervous system, which gave I.V. Davydovsky grounds to believe that typhus is a non-purulent meningoencephalitis. Not only clinical changes in the central nervous system are associated with vascular damage, but also changes in the skin (hyperemia, exanthema), mucous membranes, thromboembolic complications, etc. After typhus, a fairly strong and long-lasting immunity remains. In some convalescents, this is non-sterile immunity, since Provachek's rickettsia can persist in the body of convalescents for decades and, when the body's defenses are weakened, cause distant relapses in the form of Brill's disease.
Symptoms and course.The incubation period ranges from 6 to 21 days (usually 12-14 days). In the clinical symptoms of typhus, there is an initial period - from the first signs until the appearance of the rash (4-5 days) and a peak period - until the body temperature drops to normal (lasts 4-8 days from the moment the rash appears). It should be emphasized that this is a classical trend. When tetracycline antibiotics are prescribed, within 24-48 hours the body temperature normalizes and other clinical manifestations of the disease disappear. Typhus is characterized by acute onset, only some patients in the last 1-2 days of incubation may have prodromal manifestations in the form of general weakness, fatigue, depressed mood, heaviness in the head, in the evening it is possible slight increase body temperature (37.1-37.3°C). However, in most patients, typhus begins acutely with an increase in temperature, which is sometimes accompanied by chills, weakness, severe headache, and loss of appetite. The severity of these symptoms progressively increases, the headache intensifies and becomes unbearable. A peculiar agitation of patients is detected early (insomnia, irritability, verbosity of answers, hyperesthesia, etc.). At severe forms there may be a disturbance of consciousness.
An objective examination reveals an increase in body temperature to 39-40°C; body temperature reaches its maximum level in the first 2-3 days from the onset of the disease. In classic cases (i.e., if the disease is not stopped by the prescription of antibiotics), on the 4th and 8th day, many patients experienced “cuts” in the temperature curve, when for a short time the body temperature decreased to a subfebrile level. The duration of fever in such cases often ranges from 12-14 days. When examining patients, already from the first days of illness, a peculiar hyperemia of the skin of the face, neck, and upper chest is noted. The scleral vessels are injected (“red eyes on a red face”). From the 3rd day of illness, a symptom characteristic of typhus appears - Chiari-Avtsyn spots. This is a kind of conjunctival rash. Elements of the rash up to 1.5 mm in diameter with vague indistinct boundaries are red, pink-red or orange, their number is usually 1-3, but may be more. They are located on the transitional folds of the conjunctiva, most often the lower eyelid, on the mucous membrane of the cartilage of the upper eyelid, and the conjunctivae of the sclera. These elements are sometimes difficult to see due to severe hyperemia of the sclera, but if 1-2 drops of a 0.1% adrenaline solution are dripped into the conjunctival sac, the hyperemia disappears and ChiariAvtsyn spots can be detected in 90% of patients with typhus (Avtsyn adrenaline test ).
An early sign is a characteristic enanthema, described by N.K. Rosenberg in 1920. On the mucous membrane soft palate and the uvula, usually at its base, as well as on the anterior arches, small petechiae (up to 0.5 mm in diameter) can be seen, their number is usually 5-6, and sometimes more. Upon careful examination, Rosenberg's enanthema can be detected in 90% of patients with typhus. It appears 1-2 days before skin rashes. Like Chiari-Avtsyn spots, enanthema persists until the 7-9th day of illness. It should be noted that with the development of thrombohemorrhagic syndrome, similar rashes may appear in other infectious diseases.
With severe intoxication, patients with typhus may experience a peculiar coloration of the skin of the palms and feet, characterized by an orange tint. This is not jaundice of the skin; there is no subictericity of the sclera and mucous membranes (where, as is known, jaundice appears earlier). I. F. Filatov (1946) proved that this color is due to a violation of carotene metabolism (carotene xanthochromia).
The characteristic rash, which gave rise to the name of the disease, appears more often on the 4-6th day (most often it is noticed in the morning of the 5th day of illness). The appearance of a rash indicates the transition from the initial period of the disease to its height. Consists of roseolas (small red spots with a diameter of 3-5 mm with blurred boundaries, not rising above the skin level, roseolas disappear when pressing on the skin or stretching it) and petechiae - small hemorrhages (diameter about 1 mm), they do not disappear when the skin is stretched . There are primary petechiae, which appear against the background of previously unchanged skin, and secondary petechiae, which are located on roseola (when the skin is stretched, the roseola component of the exanthema disappears and only pinpoint hemorrhage remains). The predominance of petechial elements and the appearance of secondary petechiae on most roseolas indicates a severe course of the disease. Exanthema in typhus (as opposed to typhoid fever) is characterized by abundance, the first elements can be seen on the side surfaces of the body, the upper half of the chest, then on the back, buttocks, less rash on the thighs and even less on the legs. It is extremely rare that the rash appears on the face, palms and soles. Roseola quickly and completely disappear from the 8-9th day of illness, and at the site of petechiae (like any hemorrhage) a change in color is noted: first they are bluish-violet, then yellowish-greenish, disappearing within 3-5 days.
Changes in the respiratory system in patients with typhus are usually not detected; there are no inflammatory changes in the upper respiratory tract(redness of the pharyngeal mucosa is not due to inflammation, but to the injection of blood vessels). Some patients experience increased breathing (due to stimulation of the respiratory center). The appearance of pneumonia is a complication. Changes in the circulatory system are observed in most patients: tachycardia, decreased blood pressure, muffled heart sounds, changes in the ECG, and a picture of infectious-toxic shock may develop. Damage to the endothelium causes the development of thrombophlebitis, sometimes blood clots form in the arteries, and during the period of convalescence there is a threat of pulmonary embolism.
In almost all patients, liver enlargement is detected quite early (from the 4-6th day). An enlarged spleen is noted in 50-60% of patients from the 4th day from the onset of the disease. Changes in the central nervous system are characteristic manifestations typhus, which Russian doctors paid attention to a long time ago (“nervous rampant mountain woman”, in the terminology of Ya. Govorov). From the first days of the illness, the appearance of severe headaches, a kind of agitation of patients, which manifests itself in verbosity, insomnia, patients are irritated by light, sounds, touching the skin (hyperesthesia of the sensory organs), there may be attacks of violence, attempts to escape from the hospital, disturbances of consciousness, delirious condition, impaired consciousness, delirium, development of infectious psychoses. In some patients, meningeal symptoms appear from the 7th-8th day of illness. When examining the cerebrospinal fluid, a slight pleocytosis (no more than 100 leukocytes) and a moderate increase in protein content are noted. Damage to the nervous system is associated with the appearance of such signs as hypomia or amymia, smoothness of the nasolabial folds, deviation of the tongue, difficulty in protruding it, dysarthria, impaired swallowing, and nystagmus. In severe forms of typhus, the Govorov-Godelier symptom is detected. It was first described by Y. Govorov in 1812, Godelier described it later (1853). The symptom is that when asked to show his tongue, the patient sticks it out with difficulty, with jerky movements and further than the teeth or lower lip Can't stick out his tongue. This symptom appears before exanthema occurs. Some patients experience general tremor (tremor of the tongue, lips, fingers). At the height of the disease, pathological reflexes and signs of impaired oral automatism are revealed (Marinescu-Radovici reflex, proboscis and distal reflexes).
The duration of the disease (if antibiotics were not used) depended on the severity; in mild forms of typhus, the fever lasted 7-10 days, recovery occurred quite quickly, and, as a rule, there were no complications. In moderate forms, the fever reached high levels (up to 39-40°C) and lasted for 12-14 days, the exanthema was characterized by a predominance of petechial elements. Complications may develop, but the disease, as a rule, ends in recovery. In severe and very severe typhus, high fever (up to 41-42°C), pronounced changes in the central nervous system, tachycardia (up to 140 beats/min or more), and a decrease in blood pressure to 70 mm Hg were observed. Art. and below. The rash is hemorrhagic in nature; along with petechiae, larger hemorrhages and pronounced manifestations of thrombohemorrhagic syndrome (nosebleeds, etc.) may appear. Observed and erased
forms of typhus, but they often remained unrecognized. The above symptoms are characteristic of classical typhus. When antibiotics are prescribed, the disease stops within 1-2 days.
Diagnosis and differential diagnosis.The diagnosis of sporadic cases in the initial period of the disease (before the appearance of a typical exanthema) is very difficult. Serological reactions become positive only from the 7-8th day from the onset of the disease. During epidemic outbreaks, the diagnosis is facilitated by epidemiological data (information about morbidity, the presence of lice, contact with patients with typhus, etc.). When exanthema appears (i.e., from the 4th-6th day of illness), a clinical diagnosis is already possible. The blood picture has some differential diagnostic significance: moderate neutrophilic leukocytosis with a band shift, eosinopenia and lymphopenia, and a moderate increase in ESR are characteristic.
To confirm the diagnosis, various serological reactions. The WeilFelix reaction and agglutination reaction with Proteus OXig retained some significance, especially with an increase in antibody titer during the course of the disease. Most often, RSCs with rickettsial antigen (prepared from Provacek's rickettsiae) are used; the diagnostic titer is considered to be 1:160 or higher, as well as an increase in antibody titer. Other serological reactions are also used (microagglutination reaction, hemagglutination reaction, etc.). A memorandum from the WHO meeting on rickettsial diseases (1993) recommended indirect immunofluorescence as the recommended diagnostic procedure. IN acute phase illness (and convalescence) antibodies are associated with IgM, which is used to distinguish them from antibodies resulting from a previous illness. Antibodies begin to be detected in the blood serum from the 7-8th day from the onset of the disease; the maximum titer is reached after 4-6 weeks. from the onset of the disease, then titers slowly decrease. After suffering from typhus, Provacek's rickettsiae remain in the body of a re-convalescent person for many years, this causes long-term persistence of antibodies (associated with IgG also for many years, although in low titers).
Treatment. The main etiotropic drug currently is antibiotics of the tetracycline group; in case of intolerance, chloramphenicol (chloramphenicol) is also effective. More often, tetracycline is prescribed orally at 20-30 mg/kg or for adults at 0.3-0.4 g 4 times a day. The course of treatment lasts 4-5 days. Less commonly, chloramphenicol is prescribed at a dose of 0.5-0.75 g 4 times a day for 4-5 days. In severe forms, for the first 1-2 days, sodium chloramphenicol succinate can be prescribed intravenously or intramuscularly at 0.5-1 g 2-3 times a day, after normalization of body temperature they switch to oral administration drug. If, against the background of antibiotic therapy, a complication occurs due to the layering of a secondary bacterial infection, then taking into account the etiology of the complication, an appropriate chemotherapy drug is additionally prescribed.
Etiotropic antibiotic therapy has a very rapid effect and therefore many methods of pathogenetic therapy (vaccine therapy developed by Professor P. A. Alisov, long-term oxygen therapy substantiated by V. M. Leonov, etc.) currently have only historical significance. It is mandatory to prescribe a sufficient dose of vitamins, especially ascorbic acid and P-vitamin preparations, which have a vascular strengthening effect. To prevent thromboembolic complications, especially in risk groups (primarily the elderly), it is necessary to prescribe anticoagulants. Their administration is also necessary to prevent the development of thrombohemorrhagic syndrome. The most effective drug for this purpose is heparin, which should be prescribed immediately after the diagnosis of typhus and continued for 3-5 days. It should be borne in mind that tetracyclines to some extent weaken the effect of heparin. Administered intravenously in the first 2 days at 40,000-50,000 units/day. It is better to administer the drug dropwise with a glucose solution or divide the dose into 6 equal parts. From the 3rd day, the dose is reduced to 20,000-30,000 units/day. If an embolism has already occurred, the daily dose on the first day can be increased to 80,000-100,000 units. The drug is administered under the control of the blood coagulation system.
Forecast. Before the introduction of antibiotics, mortality was high. Currently, when treating patients with tetracyclines (or chloramphenicol), the prognosis is favorable even in severe cases of the disease. Fatal outcomes were rare (less than 1%), and no deaths have been observed since the introduction of anticoagulants.
Prevention and measures in the outbreak. For the prevention of typhus great importance has the fight against lice, early diagnosis, isolation and hospitalization of patients with typhus, careful sanitary treatment of patients in the hospital emergency room and disinsection of the patient’s clothes are necessary. For specific prophylaxis, a formalin-inactivated vaccine containing killed Provacek's rickettsia was used. Currently, with the presence of active insecticides, effective methods of etiotropic therapy and low incidence, the importance of antityphoid vaccination has significantly decreased.
BRILL-ZINSSER'S DISEASE (MORBUS BRILU-ZINSSERI)
BrillZinsser disease (synonyms: Brill's disease, recurrent typhus, recurrent typhus; Brills disease. BrillZinsser disease English; Brillische Krankheit German; maladie de Brill, typhus recurrent French) relapse of epidemic typhus appearing many years after primary disease, characterized by more light current, but with clinical manifestations typical of typhus.
Etiology. The causative agent is Provacek's rickettsia, which in its properties is no different from the causative agent of epidemic typhus. The American researcher Brill in New York in 1898 and 1910 first described a disease resembling epidemic typhus. The disease was not associated with contacts with sick people, lice infestation and other epidemiological factors characteristic of typhus. In 1934, Zinsser, based on a study of 538 similar patients, put forward the hypothesis that this disease is a relapse of previously suffered typhus and proposed the name “Brill’s disease.” In 1952, Loeffler and Mooser proposed to call Brill-Zinsser disease, which was included in international classification diseases.
Epidemiology. Brill-Zinsser disease is a relapse, i.e. the disease is a consequence of the activation of rickettsiae that persisted in the body after suffering epidemic typhus. Consequently, in the development of the disease there is no factor of infection (or superinfection) and other epidemiological prerequisites characteristic of epidemic typhus. The incidence of the disease depends on the number of people who have previously had typhus, and is high in areas where there have been epidemic outbreaks of typhus in the past. However, it should be taken into account that in the presence of lice, patients with Brill-Zinsser disease can serve as a source of epidemic infection
typhus.
Pathogenesis. The occurrence of this disease is the transition of a secondary latent form of rickettsiosis to a manifest one. In a latent state, Provachek's rickettsia persist for a long time in the cells of the lymph nodes, liver, and lungs and do not cause any detectable changes clinical methods. The transition from a latent form to a manifest form is often caused by factors that weaken the body - various diseases (ARVI, pneumonia), hypothermia, stress conditions, etc. After the activation of rickettsiae, their release into the blood (usually their number is smaller compared to epidemic typhus), the pathogenesis is as follows the same as with epidemic typhus. Recurrent incidence after Brill-Zinsser disease is very rare. It is relevant to study the role of HIV infection in the occurrence of relapses of typhus (Brill-Zinsser disease). This is especially important for African countries, where the incidence of epidemic typhus is high and HIV infection is widespread.
Symptoms and course.The incubation period from the time of primary infection often amounts to decades. More often than not, 5-7 days pass from the moment of exposure to the factor that provokes the onset of relapse. Clinically, the disease occurs as a mild or moderate form of typhus. The onset is acute, body temperature reaches 38-40°C within 1-2 days, almost all patients have a temperature curve of a constant type (“incisions” are not observed). Without antibiotic therapy, fever persists for 8-10 days. Patients are bothered by severe headache, agitation and signs of hyperesthesia are noted. Facial hyperemia and injection of conjunctival vessels are somewhat less pronounced than with classic typhus. Apparently, this explains the more frequent detection of Chiari-Avtsyn spots without an adrenaline test (in 20%), and in some patients, Rosenberg enanthema is detected from the 3-4th day of illness. The rash is quite abundant, most often roseola-petechial (in 70%), less often only roseola (30%), there may be isolated cases of Brill-Zinsser disease that occur without a rash, but they are rarely detected (they occur easily and usually tests for typhus are not carried out ).
Complications. Isolated cases of thromboembolism have been observed.
Diagnosis and differential diagnosis.Important for diagnosis is an indication of typhus in the past, which is not always documented, so it is necessary to clarify whether during the years of increased incidence of typhus there was a disease that, based on the severity and duration of the fever, could be unrecognized typhus. The differential diagnosis and serological tests used for diagnosis are the same as for typhus.
Treatment, prevention and measures in the outbreakas in epidemic typhus.
The prognosis is favorable.
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