General characteristics of rickettsia and rickettsioses. General characteristics of pathogenic rickettsiae Animal rickettsioses

2. ANIMAL DISEASES, CAUSED BY RICKETSIA(RICKETSIOSES)

2.1. GENERAL CHARACTERISTICS OF RICKETSIA AND RICKETSIOSES

According to modern taxonomy and nomenclature of bacteria, the order Rickettsiales includes three families: Rickettsiaceae, Bartonellaceae and Anaplasmataceae. The order was named after the American microbiologist X. Ricketts (1871-1910).

Based on the morphology of pathogens, adaptability to existence in the cells of arthropods and mammals, as well as some other characteristics, the family Rickettsiaceae is divided into three tribes, of which Rickettsiae itself includes three genera: Rickettsia, Rochalimea and Coxiella.

Most representatives of the genus Rickettsia live in obligate intracellular associations with eukaryotic hosts (vertebrates or arthropods). Some types of rickettsia cause diseases in humans (typhoid fever, Rocky Mountain spotted fever, tsugamushi fever, etc.) or other vertebrates (rickettsial keratoconjunctivitis) and invertebrates. According to the morphology of rickettsia, they are pleomorphic microorganisms of coccoid (0.3...0.4 µm), rod-shaped (up to 2.5 µm), bacillary or filamentous forms. Often form diplo forms. They have a three-layer cell wall, which is typical for gram-negative bacteria. As a rule, they are motionless. They are stained with basic aniline dyes, according to Romanovsky-Giemsa and others. They reproduce by binary fission in the cytoplasm or simultaneously in the cytoplasm and nucleus of certain cells of vertebrates and arthropods. Grows well in chicken embryo cell culture and in some mammalian cell lines. Aerobes form hemolysin and produce toxic substances similar to bacterial toxins that are not released into the environment. Optimal temperature for growth 32...35°C.

Rickettsia are weakly resistant in the external environment and die quickly at high temperatures and under the influence of conventional disinfectants. They are resistant to low temperatures (they retain virulence for a long time in a lyophilized state at -20...-70 °C). They are resistant to sulfonamide drugs and sensitive to tetracycline antibiotics.

Coxiella are similar to representatives of the genus Rickettsia, but unlike them, they reproduce in vacuoles (phagolysosomes) of host cells, and not in the cytoplasm or nucleus. The genus includes one species, Coxiella burnetii, which causes Q fever in humans and animals. C. burnetii are polymorphic short rods (0.2...0.4x0.4...1 µm), gram-negative, without capsules, immobile. They reproduce only in vacuoles (phagolysosomes) of host cells. Cultivated in the yolk sac of a chicken embryo, they are resistant to heating up to 65 ° C and the action of chemicals.

The tribe Erlichiae includes three genera: Erlichiae, Cowdria and Neorickettsia.

The genus Cowdria includes one species - C. raminantium, the causative agent of cowdriosis (hydropericarditis) in ruminants. Morphologically, coudria are pleomorphic coccoid or ellipsoidal (0.2...0.5 µm), less often rod-shaped cells (0.2...0.3x0.4...0.5 µm), gram-negative, immobile. They are localized in the vacuoles of the cytoplasm of ruminant vascular endothelial cells, where specific compact colonies are formed. According to Giemsa they are dyed dark blue and accept other aniline dyes well. They do not grow on artificial nutrient media. They are transmitted by ixodid ticks of the genus Amblyomma. Sensitive to sulfa drugs and tetracycline.

Caused by rickettsiae, they are increasingly being diagnosed in humans of different ages, infection mainly occurs through transmission after infection. One of the reasons for the increase in statistical indicators is the popularity of tourism, however, you can also become infected at home, because carriers of pathogens love to live in gardens, on wet grassy lawns, and in sheds.

Clinical prognosis of the disease is favorable provided timely diagnosis and treatment.

Rickettsial diseases are transmissible febrile diseases caused by rickettsiae.

Rickettsia can live in the body of rodents or cattle, and the most common carriers of infection are head lice, body lice, and ticks. These pathogenic microorganisms enter the human body through the skin.

Tick-borne rickettsiosis is caused by pathogens that are in salivary glands ticks. The survival rate of rickettsiae in environmental conditions is very low, but they can survive at low temperatures or desiccation.

There are several types of rickettsiosis (you can learn more about them below), but they are all united by similar characteristics (clinical, immunological, pathogenetic, etc.).

Penetrating into the human body, rickettsia cause inflammation of the lymph nodes and also enter the blood, leading to rickettsia and toxemia.

Types and groups of disease

Rickettsial diseases are divided into 2 groups:

• anthroponotic (pathogens are carried by body lice and head lice, the source of the disease is a person infected with rickettsia);
• zoonotic (transmitted by tick bites, the source of infection is rodents and small cattle).

The term “rickettsiosis” refers to 6 groups of diseases caused by rickettsia:

• (epidemic and endemic);
• a group of tick-borne fevers (Rocky Mountain spotted fever, tick-borne typhus of North Asia, Marseilles or Mediterranean fever);
• Tsutsugamushi fever;
• Q fever;
• paroxysmal rickettsiosis (tick-borne paroxysmal rickettsiosis and trench fever);
• rickettsioses of animals.

Each type of this disease has its own pathogen.

Depending on the symptoms, human rickettsioses are divided into groups:

• typhus group (epidemic typhus, Tsutsugamushi fever);
• group of spotted fevers (Rocky Mountain spotted fever, Marseilles fever, smallpox rickettsiosis, tick-borne typhus of North Asia);
• other rickettsial diseases, including Q fever.

Signs of typhus

Routes of human infection

There are several ways of infection with rickettsiosis pathogens:

• transmissible - transmission through the saliva of a blood-sucking insect (most common for tick-borne rickettsiosis);
• contact - through interaction with objects “contaminated” with rickettsia;
• blood transfusion - during blood transfusion;
• aspiration – entry of pathogens into the mucous membranes of the respiratory tract;
• transplacental – infection of the fetus from the mother;
• nutritional – with food or liquid contaminated with waste products of a sick animal.

Aspiration is the least common method of transmission.

Symptoms of tick-borne rickettsioses

At the first stages, tick-borne rickettsiosis most often has nonspecific symptoms; over time, more striking symptoms appear:

• fever (body temperature can reach 40 degrees);
• muscle pain;
• severe headaches;
• pain in the joints;
• body aches, general weakness;
• decreased appetite;
• nausea and vomiting;
• cardiac dysfunction (tachycardia or bradycardia);
• pain in the intestinal area;
• pain in the area of ​​the lymph nodes.

These symptoms are typical for rickettsioses transmitted by tick bites; individual signs depend on the type of disease. Let us consider the manifestations of the most common types of rickettsial diseases in Russia.

Manifestations of certain types of disease

Signs of tick-borne rickettsiosis (tick-borne typhus):

• bright pink rashes on the skin;
• severe headaches;
• weakness in the body;
• increase in body temperature.

Symptoms of Marseilles fever:

• hyperthermia of the mucous membrane of the oropharynx, sore throat;
• gray coating on the tongue;
• at the site of the bite - tissue necrosis, formation of a black or Brown;
• swollen lymph nodes;
• rash (appears 2-3 days after the bite), gradually affecting the entire body;
• The rashes are first spotty, then macular-popular, and can take on the appearance of red pimples.
• After the rash subsides, pigment spots remain on the skin.

Smallpox rickettsiosis (pathogens are transmitted by the bites of gamasid ticks) makes itself felt by a number of signs.

• Infiltrate. A non-itching red infiltrate of the skin from 5 to 20 mm at the site of the bite, which after a few days turns into a vesicle, it breaks through and becomes covered with a black scab.
• Rash. Papulo-vesicular rash over the entire body except the soles and palms (as in smallpox).
• Scarring. After the rash disappears, shallow scars remain, which smooth out after at least 3 weeks.
• Relapse. Repeated erythematous (manifested by redness and swelling) or maculopapular rash 2-3 days after the bite, later it turns into blisters. The secondary rash does not leave scars.
• Fever. Appears repeatedly (recurs).

Because of the vesicular rash, this type of rickettsiosis is sometimes called vesicular. Smallpox rickettsiosis is easily confused with chickenpox, but when infected with rickettsia, the blisters are deeper and denser, and the rash affects the entire body at once.

Rocky Mountain spotted fever is one of the most dangerous species rickettsial diseases, since without treatment it can lead to death. Its symptoms are:

• chills followed by fever;
• nosebleeds;
• convulsions;
• deterioration of vision and hearing;
• disturbance of consciousness

The listed types of rickettsioses can occur in mild, moderate or severe form.

Diagnostics

If tick-borne rickettsiosis is suspected, contact an infectious disease specialist.

Diagnosis of the disease begins with an analysis of the primary affect on the human body (local inflammatory reaction to the bite) and the symptoms of rickettsiosis, which allows us to draw preliminary conclusions about the type of disease.

• collection of epidemiological anamnesis;
• serological methods (RIF, ELISA, RIGA and RSK) are used to isolate rickettsia from the patient’s blood;
• linked immunosorbent assay;
• Weill-Felix agglutination reaction;
• general blood test (if infected, there is a decrease in the concentration of leukocytes and lymphocytes in the blood and an increase in ESR);
• laboratory tests of urine, cerebrospinal fluid;
• Allergy skin tests help with differential diagnosis.

During diagnosis, the similarity of the course of rickettsiosis with the following diseases is taken into account:

• flu;
• smallpox;
• measles;
• hemorrhagic fevers;
• enterovirus infection;
• severe allergies;
• meningococcal infection.

Treatment of the disease

Treatment of rickettsial infections is carried out conservatively. Antibiotics of the tetracycline group are prescribed:

• tetracycline (1.2 -2 grams per day, divided into 4 doses),

• doxycycline (100-200 grams per day in a single dose).

Levomycetin and fluoroquinolones are also often prescribed.

The drugs depend on the type of rickettsiosis. The course of treatment is established based on the febrile period + 2-3 days after stabilization of the patient’s condition and normalization of body temperature.

Treatment with drugs is complex, therefore, in addition to antibiotics, anti-inflammatory drugs and drugs for detoxification and desensitization therapy are prescribed.

Tick-borne rickettsiosis in severe form requires treatment with corticosteroid hormonal agents.

In addition to the above-mentioned methods of therapy, there is symptomatic treatment, for example, skin treatment (removal of dead areas of skin, scabs), which is required by smallpox rickettsiosis or intravenous administration of electrolyte solutions for prolonged fever.

All employees of a medical institution are required to wear protective suits and follow safety rules during medical procedures to avoid the spread of infection.

Mild forms of the disease can be treated at home, following the prescription of a specialist.

Preventive measures

Prevention of rickettsiosis is carried out in three directions:

• individual human safety;
• veterinary measures;
• agrotechnical methods.

Personal protective measures:

• avoiding contact with rodents;
• protection against ticks (special suits, thick clothing, tick repellents, Pavlovsky nets, inspection of human skin after walks in nature);
• compliance with personal hygiene rules;
• compliance with sanitary standards.

Note! If a tick is found on the skin, you must immediately remove it and submit it for laboratory testing to the sanitary-epidemiological service.

Veterinary and agrotechnical methods are aimed at combating rodents, ticks and protecting food and water from contamination by animal waste products.

General characteristics of pathogenic rickettsiae

Rickettsia are named after the American microbiologist Howard Taylor Ricketts, who discovered the causative agent of one of the rickettsial diseases, Rocky Mountain spotted fever, in 1909 and died while researching it (1910).

Rickettsia is a fairly large group, represented by pathogenic and non-pathogenic species. There are significantly fewer pathogenic species. In nature, rickettsiae live primarily in the bodies of insects (lice, fleas, ticks), as well as rodents, wild and farm animals.

Taxonomy

Currently, rickettsiae are classified according to Bergey's Guide to Bacteria (1984; 1994) as follows:

Kingdom Procariotae

Division Gracilicutes

Section 9. Rickettsii et Chlamydii. Rickettsia and chlamydia.

Genus 1 Rickettsia Genus 1 Bartonella Genus 1 Anaplasma

Genus 2 Rochalimaea Genus 2 Grahamella Genus 2 Aegyptianella

Genus 3 Coxiella Genus 3 Haemobartonella

Genus 4 Ehrlichia Genus 4 Eperhytrozoon

Rod 5 Cowdria

Genus 6 Neorickettsia

Genus 7 Wolbachia

Genus 8 Rickettsiella

The following are the main pathogenic genera and species of rickettsia:

Genus 1 Rickettsia

The species R.conjunctivae is the causative agent of rickettsial keratoconjunctivitis in cattle

The species R. prowacheki is the causative agent of epidemic typhus

A total of sixteen species

Genus 3 Coxiella

The species C. burnetii is the causative agent of Q fever (Q-rickettsiosis)

Genus 4 Ehrlichia

The species E. canis is the causative agent of canine ehrlichiosis (Ehrlichiosis (Rickettsia canis) monocytosis)

The species E. phagocytophila is the causative agent of ehrlichiosis in ruminants and omnivores (E. bovis, E. ovis) (ehrlichiosis monocytosis, rickettsial monocytosis)

The species E. egui is the causative agent of equine ehrlichiosis

The species E. senetsee is the causative agent of Poto Valley fever (E. risticii) poppy (Ehrlichiosis colitis, monocytic ehrlichiosis, equine diarrhea syndrome)

Rod 5 Cowdria

The species C. ruminantium is the causative agent of rickettsial hydropericarditis (coudriosis, infectious hydropericarditis, cardiac hydrops of cattle and small ruminants)

Genus 6 Neorikettsia

The species N. helminthoeca is the causative agent of neorickettsiosis (erlichiosis) in dogs

Genus 7 Wolbachia

Species W. melophagi

Species W. persise – pathogens of insect diseases

Species W. pipientis

Genus 2 Grachamella

The species G. peromysci is the causative agent of the disease in rodents

The species G. talpae is the causative agent of the disease in rabbits

Genus 1 Anaplasma

The species A. centrale is the causative agent of anaplasmosis in cattle

Species A. marginale

The species A. ovis is the causative agent of anaplasmosis in sheep and goats

Roses 3 Haemobartonella

Species H. felis - pathogens of diseases in dogs, cats,

Species H. muris of wild rodents

Genus 4 Eperythrozoon

The species E. ovis is the causative agent of eperitrosoonosis in sheep

The species E. suis is the causative agent of porcine eperitrosoonosis

The species E. wenyonii is the causative agent of eperitrosoonosis in cattle

According to the 9th edition (1994) of “Burgee’s Guide to Bacteria” in 2 volumes, rickettsia are also left in group (section) 9 “Rickettsia and chlamydia”, in which the taxonomic category “tribe” is abolished, the remaining taxonomic categories are families, genera and species remained unchanged.

In accordance with the genus, species most pathogenic rickettsia are divided into groups of diseases: diseases caused by ehrlichia - ehrlichiosis, coudria - coudriosis, neorickettsia - neorickettsiosis, anaplasma - anaplasmosis, bartonella - bartonellosis, etc.

Currently, the most relevant pathogens are: Q fever - C. burnetti, rickettsial keratoconjunctivitis - R. сonjunctivae, cattle anaplasmosis - A. centrale, A. marginalae and sheep and goat anaplasmosis A. ovis.

Morphological properties

The structure of rickettsia is similar to that of other bacteria. In rickettsia, the membrane, cytoplasm and granular inclusions are distinguished. The nuclear structure is represented by grains (from 1-2 to 4). DNA and RNA are detected in cells.

Rickettsia are polymorphic.

All the variety of their forms can be reduced to four main morphological types (according to P.F. Zdrodovsky, 1972).

Type a. Coccoid, monogranular rickettsia, size 0.3-1 µm (usually 0.5 µm) in diameter, this is the most pathogenic type, typical for intensive reproduction of the pathogen in cells.

Type B. Rod-shaped, bipolar (dumbbell-shaped), size: width 0.3 microns, length 1-1.5 microns (also identified with the active development of rickettsiosis).

Type s. Bacillary, elongated, usually curved, size: 0.3-1 µm wide, 3-4 µm long (identified in the initial period of the disease, weakly virulent, often granular rods, sometimes they can include 4 grains located in pairs at the poles).

Type d. Filamentous, polygranular rickettsia look like long, intricately bent filaments, size: width 0.3-1 µm, length 10-40 µm or more; (their release is also characteristic of the initial stages of infection - an indicator of early moderate rickettsiosis).

There are also very small forms up to 0.2 microns, passing through bacterial filters and invisible in a conventional light microscope, which are an early stage of intracellular reproduction of the pathogen.

Rickettsia are immobile and do not form spores or capsules.

Rickettsia reproduce like bacteria by simple transverse division. There are 2 types of division:

the usual division of coccoid a - and b - forms with the formation of homogeneous populations;

reproduction by fragmentation of filamentous d-forms with the subsequent formation of populations consisting of cells of a- and b-types.

Tinctorial properties

Rickettsia stains gram-negative.

Coccoid forms of rickettsia are stained red according to Romanovsky-Giemsa and Ziehl-Nielson, rod-shaped and filamentous forms are stained red-blue (red granules, the cytoplasm between them is blue), according to Zdrodovsky - red (Fig. 2, Appendix 2).

The Romanowsky-Giemsa stain is a classic stain for identifying rickettsiae inside and outside cells.

Staining technique according to the Romanovsky-Giemsa method: smear preparations prepared from a microbial culture are air-dried for 24 hours, chemically fixed and placed in Petri dishes on glass rods, smear down. The paint is diluted at the rate of one drop per 1 ml of distilled water (pH 6.8-7.0). The preparations are stained cold (within 4-24 hours) or hot (a paint solution heated to 90 0C is poured under the smear preparations, painted for 20 minutes. After staining, the preparations are washed with water, dried and microscopically examined.

If necessary, colored preparations can be further differentiated with a weak solution of 0.5% citric acid as a result, the color contrast of rickettsia in relation to the general background improves.

The cold method is most often used. In this case, the cytoplasm of rickettsiae is stained violet or blue, and the nuclear granules are stained red.

Staining of rickettsia according to Romanovsky-Giemsa gives good results only if certain requirements are met (reliable fixation of the drug, good quality of paint, required pH of the water, sufficiently long-lasting staining).

The method is of little use for current work, as it requires a long time.

More often in practice, methods of differential staining with fuchsin and methylene blue are used; these are the Zdrodovsky and Macchiavello staining methods. The essence of staining with these methods is that rickettsiae have a known acid resistance. After staining the preparations with fuchsin, they are differentiated with acid and counterstained with methylene blue. As a result, rickettsia retain their magenta color, and the tissue elements are painted in a contrasting blue or light blue color.

Staining technique according to the method of P. F. Zdrodovsky: this method is a lightweight modification of the Ziehl-Neelsen method (ordinary Ziehl carbolic fuchsin - basic fuchsin 1 g, phenol 5 g, alcohol 10 ml, distilled water 100 ml) diluted in a ratio of 10-15 drops per 10 ml of double distilled water or phosphate buffer at pH 7.4. Drug made thin layer, air-dried and fixed over a flame, stained with diluted fuchsin for 5 minutes. Then they are washed with water, quickly (2-3 seconds) differentiated by immersion in a bath of acid (0.5% citric or 0.15% acetic, or 0.01% hydrochloric, etc.), washed with water and finished painting for 10 seconds 0.5 % aqueous solution of methylene blue, washed, dried with filter paper. Rickettsia are stained ruby ​​red, cellular elements - blue (protoplasm) or blue (nucleus).

Staining technique according to the Machiavello method: the dried preparation is fixed with the flame of an alcohol lamp, stained through filter paper with fuchsin (0.25% alkaline solution of basic fuchsin, pH 7.2-7.4) for 4 minutes, washed with water, immersed in a 0.25% solution of lemon juice acid for 1-3 seconds, stained with a 0.5% aqueous solution of methylene blue, washed, dried with filter paper. Rickettsia are colored red on a blue background.

Cultural and biochemical properties

Rickettsia are aerobes, absorb O2 and release CO2, form hemolysins, actively oxidize glutamic acid, releasing carbon dioxide, but are indifferent to glucose, form endotoxins, similar in immunological reactions to bacterial toxins, but being associated with rickettsia, they are not released into the environment.

Toxin formation

Pathogenic rickettsiae produce toxic substances that play an important role in the pathogenesis of rickettsiosis. They are distinguished from bacterial toxins by their inseparability from microbial cells and their extreme instability. Endotoxins are similar in immunological reactions to bacterial toxins, but being associated with rickettsia, they are not released into the environment. At the same time, they are not identical to endotoxins, since they are thermolabile (proteins) and unstable to the action of formaldehyde (when inactivated, they retain their immunogenic properties). All pathogenic species have hemolytic properties.

Sustainability

Survival in liquid media depends on their properties, pH and ToC; they are better preserved in protein media with a neutral or slightly alkaline pH. Thus, Coxiella burnetii persists in milk at 4°C for up to 2 months. When dried, they last longer on various subsirates (lice feces) for up to 1 – 3 years.

In the external environment, the resistance of rickettsia (except C. burnetii) is low. Heating in a humid environment to 50-60 0C ensures the death of rickettsia in 5-30 minutes, at 70 0C - in 1-3 minutes. Burnet's rickettsia (the causative agent of Q fever) can withstand prolonged (30-90 min) heating at 60-63 0C and are completely killed only by boiling. Low temperatures They do not kill, but preserve the rickettsia. Canned at minus 20-70 0C, when frozen they retain viability and virulent properties for a long time.

When rickettsia are exposed to various disinfectants in normal concentrations (3-5% phenol, 2% chloramine, 2% formaldehyde, 10% hydrogen peroxide, 10% sodium hydroxide), their death occurs within 5 minutes, and a 1% bleach solution kills rickettsia in 1 minute.

Rickettsia is sensitive to tetracycline, dibiomycin, syntomycin, chloramphenicol and sulfonamides.

Lyophilization ensures long-term preservation (for years).

Pathogenicity

The pathogenicity of rickettsia is determined by their ability to penetrate cells sensitive to them, where they multiply, and synthesize a toxin, the effect of which is manifested only during the life of microorganisms. The toxin is not secreted like true exotoxins and does not cause intoxication of the body after the death of the pathogen, like endotoxins. It is thermolabile and is destroyed when the microbial suspension is heated to 600C. intravenous administration of a suspension of live rickettsia to white mice causes acute intoxication and death of animals after 2-24 hours.

Rickettsia is characterized by variability, manifested by a decrease and loss of virulence while maintaining immunogenic properties, which is used in the production of live avirulent vaccines.

Differentiation of rickettsia from viruses and prokaryotic microorganisms

Rickettsia are similar to both viruses and bacteria, but there are a number of distinctive features.

Similarities with prokaryotic microorganisms:

Rickettsia have a three-layer cell wall;

dyed with aniline dyes;

are sensitive to tetracycline antibiotics, sulfonamides, and some species (N. hilminthoeca) to a wide range of antibiotics.

Similarities with viruses:

the smallest forms of rickettsia are filterable through bacterial filters;

Rickettsia can only be cultivated in a living cell (REC, CC, laboratory animals);

rickettsiae have tissue tropism;

Rickettsiae are characterized by a lack of strict host specificity.

Rickettsia stimulates the production of interferon.

Comparative characteristics of prokaryotic microorganisms and viruses

Thus, microorganisms of the order Rickettsiales are characterized by:

pleomorphism;

immobility;

gram-negative staining;

pathogenicity for many species of farm animals, humans and arthropods;

low resistance in the external environment (except for C. burnetii);

special sensitivity to tetracycline antibiotics.

The main distinguishing feature from prokaryotic microorganisms and viruses is the presence of arthropods (lice, ticks, fleas) in the development cycle of rickettsia.

The causative agent of Qu-rickettsiosis (Q fever)

The causative agent is Coxiella burnetii.

Q fever (from the English guery - unclear, uncertain, doubtful) is a natural focal zooanthroponotic disease of domestic, commercial and wild mammals and birds, most often asymptomatic, characterized by the development of rhinitis, bronchitis, pneumonia, conjunctivitis, pleurisy, mastitis (in males orchitis), as well as abortion.

The name of the disease comes from the first letter English word Guery fever literally: “questioning fever,” since at the beginning the cause was not clear, that is, “fever of unknown origin.”

As a separate disease, Q fever was first identified in 1935 by Derrick in Southern Queensland (Australia); the causative agent was identified in 1937 and, at Derrick’s suggestion, named Coxiella burnetii. Independently of Australian researchers in the USA, Cox isolated the filterable agent of tick vectors, proving its rickettsial nature (1938).

Cu-rickettsiosis is widespread, but is more common in Australia.

The economic damage caused by Ku-rickettsiosis is significant. It consists of: the lack of offspring of animals (abortions, the birth of non-viable young animals, infertility); a decrease in milk yield in cows and egg production in poultry and exhaustion.

Cattle, pigs, horses, camels, buffaloes, dogs, chickens, geese and pigeons are most susceptible to Burnet's rickettsia. C. burnetii can spontaneously infect 70 species of mammals, 50 species of birds and more than 50 species of various ticks from the genera Dermacentor, Ambliomma, Yxodes, Rhipiceрhalus, Hyalomma, Haemaphisalis, as well as ten species of lice and fleas.

The source of the infectious agent can be susceptible animals, as well as in natural foci ticks and rodents, which are the reservoir of the pathogen.

Under natural conditions, animals and humans become infected transmissibly through tick bites, aerogenously, alimentarily through food and water, through feed contaminated with excreta of sick animals, animal raw materials (skin, wool, meat, milk, etc.).

Infected animals shed the pathogen in their blood, saliva, urine, feces and milk. The membranes and waters are especially infected, so a person often becomes infected during obstetrics.

When sick and healthy animals are kept together, the pathogen can be transmitted directly. Infected guard dogs that excrete the pathogen in urine and feces pose a particular danger in herds of animals. They often become infected by eating placentas or through tick bites.

Epidemic outbreaks of Q fever in rural areas often coincide with the calving and lambing seasons.

In areas with a warm climate, Ku-rickettsiosis occurs more often and is more severe.

V. Ya. Nikitin and L. D. Timchenko (1994), conducting research on three farms. Stavropol Territory and Belgorod Region were diagnosed with Q fever, which manifested itself as keratoconjunctivitis. In 36% of cows with eye damage, retained placenta, necrotic changes in the amniotic membranes and endometritis were recorded (98-100%).

In sick animals, Burnet's rickettsia was found in uterine secretions in 78% of cases.

Due to the asymptomatic chronic course, mortality in Cu-rickettsiosis is minimal.

Pathogenesis

In Q fever, the pathogenesis has been most fully studied in experimental animals. It has been established that the pathogen, having entered the host’s body by aerogenic, alimentary, contact or transmission routes, causes a state of rickettsia and then multiplies in the tissues and cells of the SMF - histiocytes and macrophages, after the destruction of which generalization of the process and toxinemia is noted. After the generalization stage, due to the pronounced selective ability of the pathogen to tissues, the process is localized and C. burnetii begins to multiply abundantly in the lungs, lymph nodes, udder, testes, and especially often in the pregnant uterus. As a result, micronecrotic foci are formed, which are subsequently replaced by connective tissue. From local foci, the pathogen can again penetrate the bloodstream.

This organotropy leads to abortion, conjunctivitis, bronchopneumonia, mastitis and the release of rickettsia with amniotic fluid, placenta, discharge from the eyes, nose and milk.

During the infection, a delayed-type hypersensitivity reaction develops and complement-fixing antibodies are detected.

The incubation period for Q fever lasts from 3 to 30 days. The disease develops slowly, often latently, with the accumulation of specific antibodies in the blood serum.

On the third day of the incubation period (after experimental infection), the body temperature of cattle rises to 41-41.8 0C and is maintained for 3-5 days. Depression, refusal to feed, serous rhinitis and conjunctivitis, a significant and long-term (up to several months) decrease in milk yield, abortions in pregnant cows, and placentitis are noted. Repeated irregular rises in body temperature are recorded over a period of 3-8 months.

Under natural conditions of infection, the disease in cows is often asymptomatic and is detected only by serological studies and infection of laboratory animals. However, sometimes there are attacks of acute fever, abortions in the second period of pregnancy, and prolonged excretion of rickettsiae in milk, urine, and feces. In addition, bronchopneumonia, damage to the genital organs, mastitis (orchitis in bulls), and conjunctivitis are noted.

Experimental infection in animals is severe: with damage to the spleen and other internal organs, abortions.

Pathoanatomical changes are not specific; in pregnant cows, the lungs, membranes and uterus are affected, foci of fibrinous mastitis, enlargement and hyperemia of the supraglenoid lymph nodes, enlargement of the spleen with striped and pinpoint hemorrhages, swelling of the interlobular connective tissue of the lungs and degenerative changes in the liver and kidneys are observed.

Characteristics of the pathogen

Morphological and tinctorial properties.

Burnet's Rickettsia (Coxiella burnetii) are pleomorphic microorganisms, predominantly coccoid and rod-shaped forms 0.2-0.4 µm wide and 0.4-1 µm long, less often filamentous up to 10-12 µm, arranged singly, in pairs, sometimes in short chains . They form filterable forms and are capable of phase variability. They are found in nature in phase I, and after long passages they turn into phase II. Phase II rickettsiae are prone to spontaneous agglutination and agglutination in normal blood serum and are phagocytosed in the absence of antibodies. Sometimes they form spore-like forms, providing resistance to high temperatures and drying.

Cultural properties.

In laboratory conditions, Coxiella is cultivated in REC, the body of laboratory animals (white mice, guinea pigs, hamsters, rabbits), less often in ixodid ticks, as well as in cell cultures (fibroblasts, L cells and others).

Antigenic structure.

The antigenic structure of Burnett's rickettsia differs from microorganisms of the Rickettsiaceae family; serological crossovers with other rickettsia have not been established. They have two antigens: surface (soluble) polysaccharide, present in phase 1 rickettsiae, and somatic (corpuscular) in phase 2. Both antigens are immunologically active and cause the formation of antibodies in experimentally and naturally infected animals. The diagnostic titer of antibodies to phase 1 antigens appears on days 40-60, and to phase 2 antigens on days 7-10.

In humans, second-phase antigens are used for immunization and as an allergen for intradermal testing.

Sustainability

Burnet's rickettsia are more resistant to environmental factors compared to other rickettsia, both in wet and dry material. Coxiella survive in the dried urine of infected animals for several weeks, in dry feces for up to two years, in dried blood taken from sick animals for 180 days, in the feces of ixodid ticks and dead ticks for many months. In sterile tap water – up to 160 days. In sterile milk, Coxiella remain viable for up to 257 days.

In fresh meat, when stored in a glacier, Coxiella survive for at least 30 days, in salted meat - up to 80 days or more, in butter and cheese at 4 degrees they remain viable for more than a year.

Coxiella survive on wool, depending on storage temperature, from 4 to 16 months. The pathogen is very resistant to ultraviolet irradiation(up to 5 hours) and elevated temperature (an hour's heating to 80-90 degrees does not ensure its death). Boiling kills Coxiella within one minute.

Low temperatures (from –4 to –70 degrees) create particularly favorable conditions for the preservation of rickettsia, and the combination with freeze-drying in a protein medium ensures their “preservation” for many years. At the same time, the virulent properties of Coxiella do not change at all or decrease during storage, but are restored quite quickly under favorable conditions.

Neutralization of Coxiella requires the use of higher concentrations of chemicals and greater exposure than for other rickettsia. Using a 3-5% phenol solution, 3% chloramine solution, 2% bleach solution, the latter causes the death of Coxiella within 2-5 minutes. In veterinary practice, 2% solutions of NaOH and formaldehyde, 3% creolin solution, and bleach solution with 2% active chlorine are used to disinfect premises and livestock care items.

The resistance of Coxiella Burnet to environmental factors determines their persistence when transported with contaminated raw materials of animal and plant origin over any distance, and creates the preconditions for the occurrence of Q fever diseases in areas very remote from enzootic areas.

Laboratory diagnostics Cu-rickettsiosis.

It is carried out in accordance with the “Guidelines for laboratory diagnosis of Q fever”, approved by the Main Veterinary Directorate of the State Agro-Industrial Committee of the USSR on June 3, 1986, No. 432-5.

If the presence of Q fever is suspected in farm animals, as well as when a disease of unknown etiology appears on the farm, with symptoms resembling Q fever, laboratory diagnostics are carried out by examining ticks and rodents.

Material for research.

Objects of laboratory research can be: during the life of the animal - blood taken from the jugular vein (2-1.5 ml), ticks collected from animals on pasture, small animals, rodents (voles, rats), or their fresh corpses, exudate from the uterus and vagina, the placenta of an aborted animal, from dead or killed for diagnostic purposes farm animals, parts of the affected lung, brain, spleen, regional lymph nodes, udder parenchyma, blood.

The material is sent to a specialized laboratory in sealed containers, maintaining the temperature in the containers at +4 0C.

Laboratory diagnosis of Q fever consists of:

detection of specific antibodies in the blood serum of farm animals and rodents in the long-term complement fixation reaction (LDCR) using an antigen from the phase 1 pathogen Q fever (retrospective diagnosis);

detection and identification of the causative agent of this disease in pathological material of rodents and farm animals, as well as from ticks collected in a natural outbreak and from animals, by performing a biological test and microscopy of smears.

Serological diagnosis of Q fever

It is carried out in accordance with the “Guidelines for the serological diagnosis of animal Q fever”, approved by the Main Veterinary Directorate of the USSR Ministry of Agriculture on September 14, 1984, No. 115-6a.

Serodiagnosis is based on RDSC, and RSK, RP, RA, RIF (indirect method) have also been developed.

Microscopic examination of smears for the presence of the causative agent of Q fever

Carry out using staining smears according to the Zdrodovsky method. Air-dried smears are fixed in the usual way on a flame and stained with basic Ziehl fuchsin, diluted with bidistilled water at the rate of 15-18 drops of fuchsin per 10 ml of water. The smears are stained for 5 minutes, then the fuchsin is washed off with water, the preparation is immersed for 2-3 seconds in a 0.5% solution of citric acid and washed with water. Then, for 15-30 seconds, they are stained with a 0.5% aqueous solution of methylene blue and washed again with water, the smear is dried with filter paper and microscopically examined in an immersion system at a magnification of 7 * 90. In this case, rickettsiae look like red rods or cocci on a blue background.

If there is no pathogen in the smears, 3 consecutive passages are carried out in the first passage.

Differentiation of the causative agent of Q fever

When differentiating, chlamydia, brucellosis, pasteurellosis and listeriosis are excluded, which can occur independently and in the form of mixed infections.

The diagnosis of Q fever is considered established when one of the following results is obtained:

Detection of specific antibodies in the blood serum of farm animals and rodents in the reaction of long-term complement fixation using an antigen from the pathogen of phase I Q fever (retrospective diagnosis);

detection and identification of the causative agent of this disease in pathological material of rodents and farm animals, as well as from ticks collected in a natural outbreak and from animals, by performing a biological test and microscopy of smears.

Final diagnosis

The final diagnosis of Q fever is established on the basis of epidemiological, clinical and pathological data, taking into account laboratory tests.

Diagnostic evaluation of research results

If the pathogen is isolated from ticks and rodents or specific antibodies are detected in the blood serum of a guinea pig during a bioassay, the area (region) is considered a natural focus of Q fever, and if the pathogen is isolated from the body of farm animals (the farm), it is considered unfavorable for this disease.

In a natural outbreak and in a dysfunctional farm, measures are carried out in accordance with the “Temporary instructions for the prevention and elimination of Q fever in farm animals.”

Duration of the study.

Duration of research: bioassays on guinea pigs - up to 30 days, on white mice and chicken embryos - up to 13 days.

Immunity has not been studied enough. In infected animals (cows, sheep, etc.). Long-term (over 2 months) carriage of the pathogen was noted. During this period, re- and superinfections are possible, and delayed-type hypersensitivity develops.

After recovery, intense immunity is formed.

Vaccines and serums suitable for use have not yet been developed in veterinary practice. In medicine, immunization with the live M-44 vaccine (proposed by P. F. Zdrodovsky and V. A. Genig, 1960-1968) has a good effect. They immunize both animals and people at risk of infection.

For serological diagnosis, RDSC uses dry antigen from Burnet's phase I rickettsia.

Animals with severe symptoms of Q fever, reacting positively in the RDSC, as well as without clinical signs, but with an elevated temperature, are treated for two or more days with tetracycline and its derivatives. Chlortetracycline is given orally, oxytetracycline and tetracycline are given intramuscularly at the rate of 25-30 mg/kg of animal weight 2-3 times a day until recovery and for another three days after that. At the same time, symptomatic treatment is carried out.

The causative agent of rickettsial keratoconjunctivitis in cattle

Infectious keratoconjunctivitis, infectious keratitis, infectious eye inflammation.

An acute disease affecting the cornea and conjunctiva of the eye, mainly in cattle.

Rickettsial keratoconjunctivitis was first described by D. Coles (1931) in South Africa and named the causative agent Chlamydozoon conjunctivae.

Later, the pathogen was studied in more detail and assigned to the genus Rickettsia, species R. conjunctivae.

Brief epidemiological data

In 1953-1954. in the former USSR this rickettsiosis was diagnosed (V.P. Panin and L.A. Dorofeev). Large and small cattle, camels, pigs, horses, birds are susceptible to it; among laboratory animals, only rabbits are susceptible; humans are not susceptible. The most sensitive are calves aged 3 months to 1.5 years and lambs older than 15 days of age.

The source of the pathogen is sick animals and rickettsia carriers, which secrete it with conjunctival secretions and mucus from the nose.

The main route of transmission is airborne droplets, contact or with the participation of insects, mechanical carriers (flies, ticks, etc.). The disease is characterized by extremely rapid spread, especially when animals are kept in large groups; it is recorded at all times of the year, but more often in spring and summer; the disease tends to be stationary. The degree of damage to animals is negatively affected by poor living conditions and a lack of vitamin A.

Pathogenesis

rickettsiae penetrate the corneal stroma and end up in the intercellular substance among slightly disorganized collagen fibrils, which leads to the development of stromal keratitis. This is facilitated by endotoxin produced by microorganisms, a delayed-type infectious-allergic reaction (V. A. Ado, 1985, E. A. Kiryanov, 1988).

Main clinical signs

The incubation period for infectious keratoconjunctivitis is from 2 to 12 days. The main symptom of the disease is conjunctivitis, often unilateral. Discharge appears from the diseased eye, the eyelids swell, and a reaction to light occurs (photophobia). There is fine granularity on the surface of the edematous conjunctiva. The inflammation may spread to the cornea, causing keratitis. The cornea becomes cloudy, acquires a yellowish tint, an abscess forms in it, body temperature rises, the animal’s condition is depressed, and appetite is reduced. Then the abscess opens and an ulcer forms - ulcerative necrotizing keratitis; complete perforation of the cornea may be observed. Mucopurulent discharge appears. After 8-10 days, animals usually recover, but the disease can last 20-35 days. After recovery, a scar (thorn) forms in the eye.

Characteristics of the pathogen

Rickettsia conjunctivae are small polymorphic organisms, rod-shaped, ring-shaped, horseshoe-shaped, bean-shaped, but more often coccoid-shaped, size 0.5-3 microns.

Cultural properties

Cultivation is carried out in RKE. 5-6 day old chicken embryos and the yolk sac are infected. In the process of cultivating rickettsia, 4-6 “blind” passages are carried out, using yolk sac membranes washed in sterile saline, ground and suspended. In a positive case, death or developmental lag (compared to control) of infected embryos is noted.

Sustainability

Tolerance to environmental factors and chemicals is not high. In a 0.85% NaCl solution at a temperature of 20-22 degrees, rickettsia retain their virulence for 24 hours.

On sheep wool, the pathogen dies after 96 hours; a 5% solution of collargol inactivates them in 15 minutes.

R. conjunctivae is sensitive to tetracycline antibiotics.

Laboratory diagnostics

Pathological material – scrapings from the conjunctiva of the upper eyelid and the cornea of ​​the affected eyes of sick animals, mucus from the nose, tear fluid on the second – fifth day of the disease. Only fresh material is examined. In case of long-term transportation, the material is frozen at a temperature of –5-10 0C and transported in a thermos with ice.

Laboratory diagnosis of rickettsial keratoconjunctivitis includes:

1. Microscopic method,

2. Isolation of rickettsia culture on RKE,

3. Biological method.

Microscopic method:

1) Light microscopy: smear preparations from pathological material, stained using Romanovsky-Giemsa or Zdrodovsky methods, are microscoped three times with an interval of 1-2 days (for staining technique, see the section “General characteristics of pathogenic rickettsiae”, “Tinctorial properties”).

When stained according to Romanovsky-Giemsa, rickettsia are stained red-violet (purple with red granules), according to Zdrodovsky - red.

Luminescence microscopy: To detect rickettsiae under a luminescent microscope, fluorochrome plating is used. The drug is fixed in methanol for 5 minutes, treated with a solution of acridine orange (1:3,000, pH 3.8), washed with distilled water, dried and viewed under an immersion lens using non-fluorescent immersion oil (filters - SZS-7, Zh-1, BS-8 and KS-18).

Rickettsia fluoresce green and red and are clearly visible on dark background drug.

Isolation of culture on RKE.

Biological method:

To identify and determine the pathogenicity of rickettsia - the causative agents of keratoconjunctivitis - bulls aged 2-5 months or rabbits are infected by introducing material into the eye of the animal. A suspension (1:5) is prepared from the original pathological material or from an embryonic culture. The disease in bulls manifests itself after 7-12 days in the form of keratoconjunctivitis and lasts 8-10 days or longer. In rabbits, the disease manifests itself on 2-4 meshes in 90% of cases. When they are opened, in addition to inflammatory phenomena in the area of ​​the infected eye, focal catarrhal inflammation of the lungs is revealed.

Serological diagnosis of rickettsial keratoconjunctivitis has not been developed.

Rickettsial keratoconjunctivitis must be differentiated from conjunctivitis caused by chlamydia, thelyasia, pasteurella, as well as traumatic injuries.

The diagnosis is made on the basis of epizootic and clinical data and is confirmed by laboratory tests (detection of the pathogen by microscopy of smears).

The duration of laboratory tests is 1.5 months.

Immunity, means of specific prevention and therapy

Animals that have recovered from rickettsial keratoconjunctivitis develop long-term immunity – up to a year.

Specific preventive measures have not been developed.

Sick animals are isolated in a dark room and treated: eye wash with furatsilin solution (1:5000), eye drops (0.5% zinc sulfate solution and 3% boric acid solution), novocaine-chlortetracycline ointment (novocaine 5.0, chlortetracycline - 5.0, petroleum jelly - 30.0), etc., synthomycin emulsion, 5% protargol, corticosteroid ointments with antibiotics, albucid solutions and ointments.

Causative agent of anaplasmosis in cattle and small ruminants

Anaplasmosis is a vector-borne disease of large and small cattle, as well as other domestic and wild animals, occurring acutely or chronically with signs of acute anemia, intermittent fever, disruption of the cardiovascular system, and gastrointestinal tract.

The causative agent of anaplasmosis in cattle is Anaplasma marginale (Theiler, 1910) and A.centrale (Theiler, 1911), in sheep and goats A.ovis (Lestoguard, 1924).

Brief epidemiological data

Moose, reindeer, sheep, goats, zebu, roe deer, antelope and buffalo are susceptible to A. marginale.

A. ovis includes sheep, goats, argali, mouflon, saigas, antelope, roe deer, elk, and deer, which makes it possible to classify anaplasmosis as a natural focal disease. Zebu livestock (young animals) are more susceptible than domestic animals. Pregnant and high-yielding cows are most susceptible to the disease.

Anaplasmas are transmitted transphasically, transovarially and within one mature phase of the tick during intermittent feeding. Mechanical transfer of the pathogen is possible.

Anaplasmas can be transferred from sick animals to healthy animals during blood collection and various operations performed with the same instrument.

Intrauterine infection is possible.

There is a seasonality of anaplasmosis; it is recorded in summer and autumn, rarely in winter. The disease in sheep is recorded from April to October. It is often diagnosed together with babesiosis, theileriosis and eperitrosoonosis. It occurs severely with mixed infestations of helminthiasis, as well as in combination with infectious diseases. In winter, anaplasmosis is diagnosed more often in animals under conditions that reduce resistance: poor-quality feeding, iodine, cobalt or vitamin deficiency.

Anaplasmosis is characterized by stationarity. The incidence is 40-50%. Mortality reaches 40%.

Pathogenesis

The development of the disease process begins with the introduction of anaplasmas into erythrocytes and their release of metabolic products. As a result, the physiological functions of red blood cells and their hematopoiesis are disrupted. At the same time, the activity of the central nervous system changes, and pathology of internal organs occurs. The body responds to the introduction of anaplasmas by mobilizing cellular and humoral mechanisms with the formation of antibodies against the pathogen, which leads to increased erythrophagocytosis. The lifespan of affected red blood cells is on average about 20 days, while healthy red blood cells live about 90-120 days. The number of red blood cells and hemoglobin in seriously ill animals is reduced by 2.5 times. Hypoxemia and hypoxia occur in the body, which leads to even greater disruption of the central nervous system, so some animals develop paresis of the hind limbs and impaired coordination of movement. Weight loss progresses. Due to disruption of the autonomic system, intestinal atony develops. When immunobiological mechanisms are suppressed, the body's resistance decreases, and then the process often ends in death.

Main symptoms and pathological changes

The incubation period is from 10 to 175 days.

In cattle, anaplasmosis occurs acutely and chronically. In the acute course, the body temperature rises to 41, the mucous membranes become pale to the color of porcelain - progressive anemia develops (the number of red blood cells decreases to 1.5-2 million/mm of blood, hemoglobin - 2-4%), sometimes jaundice develops. Cardiovascular activity and breathing are impaired, and a cough often appears. Animals quickly lose weight and intestinal atony develops. There may be abortions.

Microscopy reveals anisacytosis, poikilocytosis and polychromasia.

The chronic course is characterized by less pronounced symptoms and lasts 20-30 days.

In sheep, anaplasmosis occurs acutely, chronically and asymptomatically, with essentially the same symptoms as in cattle. There is a decrease in the quantity and quality of wool, and there may be paresis.

The blood of large and small cattle is pale red and watery. Sick animals lag behind the herd, lie down a lot, and move away from the sun into the shade. Weakness and loss of strength gradually develop, and sometimes death occurs due to coma symptoms.

At autopsy, severe emaciation of the corpses is noted, the mucous membranes are anemic, sometimes with a tinge of yellowness. The skeletal muscles are pale pink, the blood is light and liquid. The cardiac muscle is flabby, and there are striped and spotted hemorrhages under the epicardium. The spleen is enlarged 2-3 times, with hemorrhages. The liver is in most cases enlarged, with blunt thickened edges, icteric and spotty, the gallbladder is filled with thick bile.

In mixed diseases, changes in the corpse correspond to the diseases that caused the death of the animal.

Characteristics of the pathogen

Morphology and tinctorial properties

Gram-negative, stains well according to Romanovsky-Giemsa in a dark red color. You can stain with azure-eosin and the accelerated method according to Shchurenkova.

Sustainability

Anaplasmas are resistant to low temperatures; when frozen to minus 70 0C and minus 196 0C, they persist for years, but quickly die at plus 50 0C.

Laboratory diagnostics

Laboratory diagnostics are carried out in accordance with the “Instructions for combating anaplasmosis in large and small ruminants”, approved on July 31, 1970, Appendix No. 1 (Antonov B.I., 1987).

The material for the study is the blood of a sick animal, as well as blood serum (3-5 ml).

Laboratory diagnostics include:

1. Microscopic method - detection of anaplasmas in blood smears stained according to Romanovsky-Giemsa, azure-eosin or the accelerated method of Shchurenkova;

2. Serological method - RSK.

Anaplasmas are painted dark red, they have a round shape (like dots), and are located along the periphery of red blood cells. Dimensions 0.2-2.2 microns.

The degree of infection of red blood cells varies - from insignificant to 50% or more infected red blood cells. Unlike Jolly bodies, anaplasmas are usually smaller and less intensely colored.

Anaplasma should not be confused with basophilic granularity of erythrocytes, which in most cases is manifested by a multiplicity of various forms of inclusion in one erythrocyte.

In doubtful cases, blood serum in an amount of 3-5 ml is sent to the laboratory to test RSC, which is carried out according to the “Method for testing RSC for the diagnosis of anaplasmosis in cattle and small ruminants.” Approved 09/29/1971

The diagnosis of anaplasmosis is made on the basis of epizootic, clinical, pathological data and laboratory test results.

Anaplasmosis should be differentiated from theileriosis, piroplasmosis, babesiosis, francaiellosis, leptospirosis, and in sheep, additionally from eperitrosoonosis.

The diagnosis of anaplasmosis is considered established in one of the following cases: when the pathogen is detected in blood smears by light microscopy.

With leptospirosis, pronounced yellowness of the mucous membranes and skin, short-term fever, hemorrhagic diathesis, necrosis of the mucous membranes of the skin, hemoglobinuria, which is confirmed by laboratory testing.

Immunity, means of specific prevention and therapy

Cellular immunity plays a leading role in protecting the body from anaplasma. Humoral antibodies are not of great importance in protecting against anaplasma.

For treatment, tetracycline antibiotics are used, which are dissolved in a 1-2% solution of novocaine, for 4-6 days in a row, a dose of 5-10 thousand units / kg of animal body weight.

Sulfonamides are also used, and the introduction of diamidine is indicated.

Necessary pathogenetic therapy: administration of microelements (magnesium sulfate, copper sulfate, cobalt chloride), vitamins (B12), cardiac medications - caffeine, camphor and others.

In the epizootic zone they are fighting against ticks. Animals newly introduced into the farm should be examined using serodiagnostic methods.

The causative agent of porcine epirythrozoonosis

The disease was first described by Doyle in Indiana in 1933 as a “rickettsia-like or anaplasma-like disease in swine” (Doyle, 1932). Splitter and Williamson (1950) described an organism that causes jaundice in pigs --- Eperythrozoon suis and other similar pathogens that cause eperythrozoonosis -- in cattle -- E. wenyonii and in sheep -- E. ovis.

Various types of causative agents of eperitrosoonosis were also identified in these animals in 1977 (Gothe and Kreier), pathogenicity and clinical manifestations were demonstrated only - E. suis (in pigs), E. wenyonii (in cattle), E. ovis (in sheep) and E. coccoides (in mice).

Brief epidemiological data

Epirythrizoonosis is a species-specific disease. It is caused only by Eperythrozoon suis and is observed only in domestic pigs.

Eperitrosoonosis is recorded on all continents. In addition to pigs, rodents and ruminants are also affected. The disease has been registered in England, Germany, Romania, Czech Republic, Slovakia, France, Yugoslavia, Sardinia, Canada, Taiwan, and Poland.

Pigs of all ages are susceptible to the disease. Weaned piglets and piglets within a few days after castration are especially susceptible to the disease. Piglets get sick more often at the age of 1-14 days and up to 3-6 months.

The source of the infectious agent is sick animals.

The pathogen is released into the external environment with body secretions containing blood.

Transmission factors include care items, bedding, floors, feeders, feed contaminated with blood, as well as various instrument during veterinary treatments.

Infection occurs through nutritional, contact, intrauterine and transmissible routes (ticks, mosquitoes, fly flies, lice).

Eperitrosoonosis is characterized by stationarity, which can be explained by the long-term carriage of the pathogen in the body of recovered and clinically healthy animals.

There is no pronounced seasonality, since patients are detected throughout the year, but most cases of the disease occur in the summer. In pigs, the disease is more often observed during the period of mass farrowing.

Clinical signs: anemia, fever, jaundice, necrosis will be observed only in a weakened animal’s body. Stress factors, unsatisfactory living and feeding conditions, chronic generalized infections predispose to the clinical manifestation of the disease.

Epirytrozoonosis complicates the course of accompanying diseases, in turn a number of diseases causing relapses. Interference of epirythrozoons with anaplasmas, babesias and other protozoa has been noted.

The incidence depends on the immune status of the livestock and reaches 30% or more. Mortality rate is less than 1%.

Pathogenesis

Eperitrosoons have tropism for erythrocytes, platelets and leukocytes. The pathogen can be located separately or in a chain on the outer membrane of the erythrocyte, and can also be located inside the erythrocyte.

Free microorganisms were seen only in blood plasma. These misshapen red blood cells are removed and then hemolyzed in the spleen. The acid-base balance in the blood is disturbed and acidosis develops. In acute cases, genirilized hemolytic jaundice may occur.

Epirythrizoonosis causes autoimmune hemolytic anemia associated with cold agglutination. During the interaction of Eperythrozoon suis with the surface (membrane) of an erythrocyte, the structure of the membrane changes, ending with the release of masked antigens or modification of existing antigens - that is, an alien response of the body's immune system.

Once the microorganism adheres to the red blood cell membrane, autoantibodies are produced as part of the defense mechanism and attack the red blood cells, infecting the animal.

The presence of microorganisms in the plasma leads to microagglutination of red blood cells in those parts of the body where the temperature is lower, particularly the ears, tail and limbs. With insufficient blood flow, the ears turn blue, resulting in later ischemia. Clinically, this can manifest itself as necrosis.

Main symptoms and pathological changes

In experimentally infected and diseased pigs, the incubation period lasts on average 7 days (but can be from 2 to 26 days), after the introduction of infected ticks from 8 to 90 days.

Eperitrosoonosis can occur acutely and chronically.

There may be subclinical, genital and latent forms.

The incubation period depends on the virulence of E. suis, the age and state of the body’s immune system, as well as on the dose of infection, living conditions and feeding of the animals. The most characteristic clinical signs of epiritrozoonosis in pigs appear in suckling piglets between birth and the 1st day of life, an increase in body temperature on days 1 - 3 after infection within the range of 40.0 - 41.5 ° C. In sick piglets, the first clinical sign is short-term (1-3 days) fever up to 41.5 ° C, pale skin, apathy, anemia or periodically manifested yellowness. These signs disappear after a few days. Clinical signs may not appear in all piglets in the litter. After a few days, changes appear in the blood. Liver dysfunction - increased bile secretion.

Fattening piglets experience apathy, short-term fever, difficulty breathing (dyspnea), loss of appetite, anemia, and sometimes jaundice. In sick animals, lacrimation, hyperemia, and then pallor of the mucous membranes, sometimes jaundice, periodic diarrhea, constipation, and sometimes clonic seizures. Sick piglets die due to coma, hypothermia and acute anemia.

Clinical signs in the acute course: pallor, fever up to 42°C, jaundice, as well as cyanosis of the extremities, especially in the area of ​​​​the cartilaginous tissue of the ears. These processes lead to the weakening and death of young individuals.

The classic form of jaundice is very rare. Anorexia (diarrhea), apathy, difficulty breathing (shortness of breath) occur depending on the degree of anemia. Pigs' weight gain decreases.

Marbling or bleeding of the ears occurs due to deterioration of blood supply in the microvasculature of the ears. A characteristic feature The so-called cold agglutination in the acute course of the disease is a dark red coloration of the limbs and tips of the ears. This occurs due to microagglutination and thrombocytosis in the capillaries of the bloodstream. In some cases, cyanosis is observed, especially in piglets after veterinary and zootechnical measures - castration, weaning. Also, in suckling, weaned and fattening piglets, anemia is observed in the entire area of ​​the ear, tail and limbs of the legs. Necrosis ears and large areas of ear cartilage may occur as a result of long-term exposure to Eperythrozoon suis or as a result of the acute course of the disease. Necrosis can be not only on the tops of the ears, but also on the sides, in the abdomen. A cured animal (herd) may become ill again as a result of weakened immunity. Reinfection is possible at any time of the year. With reinfections, clinical signs are mild.

The chronic course of the disease is characterized by pallor and some allergic skin reactions in the form of “urticaria”. A characteristic sign is necrosis of the tops of the ears. In the chronic course of the disease in pigs in older fattening groups, lesions are expressed on the ears, on the sides, and on the stomach between the front and hind limbs. In older pigs, changes on the sides are the size of a small plate. Sick piglets often develop concomitant secondary infectious diseases due to a weakened immune system. Some fattening pigs exhibit apathy, loss of appetite, fever of 40.5 - 41.5 °C, difficulty breathing and decreased weight gain.

In sows, clinical signs appear 3 - 4 days after farrowing, and are characterized by anorexia, fever up to 42 ° C and occurs in the chest or genital form for 1 - 3 days. These pigs are characterized by depressed milk production and ejection and abnormal or absent maternal behavior. The onset of clinical signs may also occur in the postpartum period. After several days after infection, pigs experience fever for 1-3 days and loss of appetite, and milk production is inhibited.

With the genital form, pigs experience reproductive problems: irregular cycles, poor fertility, abortion, birth of still or weak (non-viable) piglets. These signs are observed in serologically positive herds. In herds infected with Eperythrozoon suis, 65% of piglets after weaning for 7 days are without visible clinical signs of the disease. Problems with irregular sexual cycles (anestrus) can reach 60% of the pig population.

In the subclinical form, the hemoglobin level is low, the body temperature is low-grade, and young animals are more severely ill. They experience depression, loss of appetite, fever, weakness, shortness of breath, and anemic mucous membranes.

The latent form is not clinically manifested.

Pathoanatomical changes are mostly uncharacteristic and depend on concomitant infections. In piglets, exhaustion, yellowness of the skin, and sometimes dermatitis behind the ears are noted. At autopsy, an enlargement of the spleen, lymph nodes and the wall (lining) of the stomach is observed, and yellowness is observed in the lining blood vessels. Mucous and serous membranes, subcutaneous tissue are icteric. Jaundice may also occur in other organs. The liver is yellow or yellow-brown. Hydrothorax, hydropericarditis and ascites are sometimes observed. Petechiae are possible under the serous membrane of the kidneys and bladder. The contents of the stomach and intestines are yellowish in color.

Histopathologically, an increase in hemosiderin content is found in Kupffer cells of the liver, as well as in the cells of the reticular cellular layer of the stomach.

Characteristics of the pathogen

Morphology and tinctorial properties.

The causative agent of eperitrosoonosis is polymorphic, can have a round, oval, rod-shaped, dumbbell-shaped, ring-shaped form, can occur in the form of a comma and be granular. Size from 0.2 to 2 µm, in clusters from 1.0 to 2.5 µm. In blood preparations they lie individually or in a chain on the outer membrane of the erythrocyte and can be located inside the erythrocyte. In a febrile state, free-lying bacteria can be found.

Laboratory diagnostics.

For laboratory diagnosis, blood serum or whole blood stabilized with heparin or another anticoagulant is needed.

The diagnosis of Eperythrozoon suis is made comprehensively based on epidemiological data, clinical signs, and pathological changes. Laboratory diagnostics are decisive in making a diagnosis. Laboratory diagnostics include:

Microscopic method - preparation of blood smears, staining according to Romanovsky - Giemsa and Zdrodovsky, microscopy to detect eperithrosoons;

Serological method - detection of specific antibodies in blood serum using RSK, ELISA, identification of antigen in ELISA;

Molecular genetic method - polymerase chain reaction(PCR);

Biological method - infection of animals susceptible to eperitrosoonosis;

Hematological studies - leukogram, determination of hemoglobin, red blood cell count, hematocrit and iron levels in the blood.

Histological method - a histological examination of the liver, kidneys and spleen is carried out in order to establish accumulations of hemosiderin.

Microscopic method.

In sick and suspected animals, blood is taken from peripheral vessels (ear, tip of the tail, sometimes the eye sinus), preventing hemolysis of red blood cells. The blood is stabilized with Trilon B, heparin, and sodium citrate. The best results for animals are obtained when testing blood from animals with acute eperitrosoonosis. Blood smears are prepared according to standard methods immediately after blood collection. Slides must be perfectly clean and free of grease. The blood temperature must be 37 °C, otherwise the red blood cells will agglutinate due to cold agglutination, which makes it difficult to detect Eperythrozoon suis in smears. After preparing blood smears, they are dried and fixed chemically: methyl alcohol - 5 minutes, ethyl alcohol - 30 minutes, Nikiforov's liquid (rectified ethyl alcohol 96˚ and ether for anesthesia in a ratio of 1: 1) - 30 minutes.

Smears are stained according to Romanovsky - Giemsa or Zdrodovsky.

Staining technique according to Romanovsky - Giemsa.

Apply paint diluted with distilled water (pH 7.0 - 7.2) to the fixed smear in a ratio of 3 drops of paint per 2 ml of water, paint for 30 - 45 minutes. Wash with distilled water, air dry and microscope at a total magnification of 900 - 1800 times.

Eperythrozoon suis is colored blue with various shades as polymophic microorganisms on the erythrocyte membrane. Red blood cells are pink.

Painting technique according to Zdrodovsky.

A Ziehl carbol solution pre-dissolved in bidistilled water or phosphate buffer at pH 7.4 is applied to the fixed smear in a ratio of 10 - 15 drops of paint per 10 ml of water or buffer for 5 minutes. Then quickly (1 - 3 seconds) differentiate in 0.5% citric or 0.15% acetic acid by immersing the smear in an acid bath. Wash with water (plentifully) and finish painting with a 0.5% solution of methylene blue for 10 seconds. Wash, air dry and microscope.

Eperitrosoons are painted ruby-red, cellular elements are blue (protoplasm) or blue (nuclei).

In acute cases, rickettsia in the form of grains affects 80 - 100% of red blood cells; for chronic and subclinical – 10 - 30% of red blood cells with single grains; are not detected in latent form.

The detection of microorganisms with characteristic morphology and tinctorial properties is the basis for making a diagnosis of eperitrosoonosis.

Serological method

Includes blood serum testing in RSK and ELISA to detect antibodies. ELISA can be used to identify the pathogen. Serological reactions are carried out in accordance with the instructions for the use of test systems.

Molecular genetic method.

Provides for PCR testing. This method is the most sensitive and specific in identifying Eperythrozoon suis.

Biological method.

It is carried out on piglets 2–4 months of age. Piglets are infected by blood or blood transfusion from a sick animal to a healthy one. Clinical signs of the disease appear after 3 to 4 weeks. A bioassay is considered positive if the clinical picture is characteristic and the pathogen is detected by a microscopic method.

Hematological studies.

Blood taken directly during a fever has a shiny surface and does not settle on the walls of the tube, but agglutinates when room temperature. Microagglutination is a characteristic feature of Eperythrozoon suis. The blood is examined immediately after collection. The temperature of blood and materials should be 37 °C.

Eperythrozoon suis causes hemolytic anemia with characteristic normochromic and chromocytic anemias. Indicators of the disease and its severity are the number of red blood cells in the blood of animals, hemoglobin content and hematocrit. In sick animals, there is a decrease in the number of erythrocytes to 2.6 million/ml and 80% of erythrocytes are affected. Neutrophilic leukocytosis also progresses, the number of platelets decreases, and the blood plasma becomes jaundiced.

There is a decrease in the number of red blood cells in the blood, and a decrease in hemotocrit and hemoglobin values.

Serum bilirubin content and iron binding capacity are examined.

The result of the study is indicated by: the number of erythrocytes from 1 to 2 * 1012/l, hemoglobin 20-40 g/l, often 70-90 g/l, leukocytes 20-50 * 109/l.

The leukogram shows an increase in the number of lymphocytes and monocytes.

In the subclinical form, the number of erythrocytes decreases to 2.4-5 million, leukocytes increases to 8.5 thousand, ESR is accelerated, neutrophilia and eosinophilia are possible. The incidence of red blood cells reaches 90%.

Histological method.

A histological examination of the liver, kidneys and spleen is carried out to identify accumulations of hemosiderin. It is not decisive.

The diagnosis of eperitrosoonosis is considered established in one of the following cases:

When detected by a microscopic method in blood smears of clinically sick animals, eperitrosoons with characteristic morphology and tinctorial properties;

If specific antibodies are detected in RSC, ELISA;

When identifying the pathogen in ELISA or PCR.

Immunity, means of specific prevention and therapy.

Immunity has not been fully studied. It has been established that as a result of illness, the immune response is incomplete and short-lived. During the course of the disease, antibodies of the Ig M class are produced.

No specific means of prevention or therapy have been developed.

Sick animals are given rest and feeding is improved. For fattening pigs with signs of an acute course of the disease, parenteral administration of oxytetracycline is used for treatment at a dose of 20 - 30 mg/kg of live weight. Parenteral oxytetracycline can also be given to pigs in infected (dysfunctional) herds from time to time during stress: regroupings and after veterinary and zootechnical procedures. However, along with parenteral administration, oral treatments, as well as combined treatments, can be carried out. This may reduce the occurrence of anemia.

Healthy and stunted piglets should be given additional iron supplements.

Pigs are also prescribed neoarsphenamine (novarsenol) - 15 - 45 mg per 1 kg of live weight. Azidine and arsenous acid preparations give good results. Symptomatic remedies depending on indications.

The course of treatment is 3–4 weeks.

Q fever (qu-rickettsiosis) is the most common rickettsial disease, often characterized by an asymptomatic course, less often with clinical manifestations.

Clinical signs. Under experimental conditions, the incubation period is 2-3 days, after which a short-term fever (up to 41.8°), depression, loss of appetite, mucous discharge from the nose, dry cough and a sharp decrease in milk yield are noted in sick cattle, and in pregnant cows - abortion or the birth of a non-viable fetus. With natural infection, the disease in cows is often asymptomatic, but in some animals in the second half of pregnancy, inflammation of the udder (mastitis), joints and abortions are observed. Calves may show signs of respiratory and eye damage. Animals rarely die.

Pathological changes. In cows, the liver is enlarged in volume, dotted with multiple dark red lesions 2-5 mm in size, having a mainly round shape and a somewhat sunken, pale-colored center. In the affected lobes of the udder, suprauder and internal inguinal lymph nodes there are dense grayish-yellow nodules (granulomas) the size of a grain of wheat or smaller. Similar but isolated nodules are visible beneath the pulmonary pleura. Endometritis, placentitis and mastitis are also found in aborted cows. In calves, acute catarrh with extensive necrosis, catarrh of the airways, focal pneumonia and the presence of multiple grayish-pale nodules in the lungs and mediastinal lymph nodes are noted.

Pathohistological changes. Numerous granulomas of various stages of formation are detected in the affected organs. Initially, in the focus of inflammation, accumulations of macrophages and neutrophils loaded with rickettsia, erythrocytes and cellular detritus are visible. Then multinucleated cells appear among them, and a zone of epithelioid, lymphoid and connective tissue cells is formed. In the udder, attention is drawn to the peculiar reaction of the cells of the integumentary epithelium of the alveoli. Epithelial cells containing rickettsiae are increased in volume by 3-5 times, divide and have two or more nuclei. Some of the affected cells are exfoliated and, together with macrophages and numerous neutrophils, are located in the lumen of the alveoli. Liver with symptoms of protein and fatty degeneration. In the cytoplasm of hepatocytes, the amount of glycogen is sharply reduced and a yellow-brown pigment is detected. Kupffer cells intensively proliferate, forming nested clusters. The paracortical zones of regional lymph nodes are poor in lymphocytes and infiltrated with histiocytic-macrophage cells containing numerous rickettsiae. In the kidneys, membranous-proliferative glomerulonephritis with granular and vacuolar degeneration of the convoluted tubule epithelium.

With a protracted course of the disease, encapsulated granulomas are found in the organs.

The diagnosis is made on the basis of clinical, epizootological, pathological data and laboratory test results, including microscopic detection, isolation and identification of rickettsia, serological indicators (ROSC) and identification of typical pathohistological changes. Differentiate Q fever from brucellosis, chlamydia and listeriosis.

The term “rickettsiosis” combines 6 groups various diseases: group of typhus (epidemic and endemic typhus), group of tick-borne fevers (Rocky Mountain spotted fever, Marseilles fever, tick-borne typhus of North Asia, etc.), Tsutsugamushi fever and Q fever as separate groups, as well as a group of paroxysmal rickettsioses ( trench fever and tick-borne paroxysmal rickettsiosis) and animal rickettsial diseases.

All rickettsial diseases are divided into anthroponoses (typhus, trench fever), when the source of infection is a sick person or carrier, and zoonoses (all others) with natural focality, in which the source of infection is small rodents, small and cattle, etc.

In anthroponotic diseases, the infection is transmitted through body louse and head louse, and in zoonotic diseases, through sucking arthropods (ticks). The exception is Q fever, the causative agent of which can also be transmitted by contact and nutrition.

Rickettsia are small coccoid or rod-shaped gram-negative microorganisms. There are filterable forms of rickettsiae, which have etiological significance in latent rickettsioses.

Rickettsial diseases occur in all countries of the world, but the incidence in some cases is limited by the natural focus, and in others by sanitary and hygienic conditions and especially the level of lice infestation in the population. Rickettsial infections are rare in children. From this group of diseases in our country, children suffer from tick-borne typhus of North Asia and Mediterranean (Marseilles) fever.

EPIDEMIC (LICE) TYPHUS

Epidemic typhus (A75.0) is an acute infectious disease with fever, intoxication with primary damage to the nervous system and blood vessels; accompanied by the appearance of a roseola-petechial rash on the skin.

Etiology. The causative agent of the disease - Provacek's rickettsia - has the form of small cocci, there are rod-shaped and filamentous forms. The average size of the pathogen ranges from 0.5 to 1 micron. The filamentous forms reach a length of 40 microns, they are larger than other pathogenic rickettsiae. Rickettsia are gram-negative, multiply only in the cytoplasm of cells, and produce a toxin closely associated with the cell body. They contain 2 antigens: general thermostable and thermolabile - species specific. Rickettsia Provaceca have a common antigen with the O-antigens of some variants of Proteus. The pathogen dies at a temperature of 50-60 °C, but can persist for a long time in the external environment in a dried state, especially in dry feces of infected lice, and quickly dies in a humid environment. Among laboratory animals, the most susceptible to Provacek's rickettsia are cotton rats, guinea pigs, white mice and monkeys.

Epidemiology.Source of infection is only a sick person whose blood is contagious for 15-20 days, with last day incubation, throughout the febrile period and for 1-2 days of apyrexia.

Transmission of infection carried out by body lice, less often by head lice. Having sucked on the patient's blood, the louse is able to transmit the infection after 5-6 days, when the intestinal epithelial cells of the louse are filled with rickettsia. Such a louse, while sucking the blood of a healthy person, releases a large number of rickettsiae in the feces, which are then rubbed into the skin while scratching the bite site. The louse remains infectious until its death (up to 45 days), but does not transmit the infection transovarially to its offspring.

Susceptibility to typhus universal and practically independent of age. The exception is children in the first 6 months of life, in whom the disease, even during epidemic outbreaks, is extremely rare due to known isolation, as well as due to passive immunity received transplacentally from the mother if she has had typhus.

After an illness, lifelong immunity is formed. Recurrent diseases are rare, occur only in adults and can be classified as relapses of typhus - Brill-Zinsser disease.

Thus, typhus manifests itself in 2 epidemiological and clinical-immunological variants: tick-borne epidemic typhus; fulminant typhus - Brill's disease.

The emergence and spread of typhus is associated with deteriorating sanitary conditions, poor living conditions, crowding. Currently, typhus as an epidemic disease in our country is rare. Brill-Zinsser disease is reported in isolated cases in adults.

Pathogenesis. Once in the blood, Provacek's rickettsiae penetrate the endothelial cells of blood vessels and multiply in them. Under the influence of endotoxin, endothelial cells swell, die and desquamate. Released rickettsiae penetrate undamaged cells. Thus, widespread acute infectious vasculitis develops. From the sites of primary localization of rickettsia, their toxins in increasing quantities enter the general bloodstream and have a general toxic effect. The local process in the vascular endothelium and the general toxic effect lead to disruption of microcirculation at the level of predominantly small vessels, which is accompanied by a slowdown in blood flow and leads to tissue hypoxia, impaired cell nutrition, and severe metabolic changes.

Pathomorphology. Specific typhus morphological changes can be characterized as generalized endothrombovasculitis. In some cases, blood clots can be located near the wall in limited areas of the lesion (warty endovasculitis), in others they completely fill the lumen of the vessel; this is accompanied by pronounced destructive changes (destructive thrombusculitis). Focal cell proliferation along the vessels with the formation of typhus granulomas is often observed. With the greatest consistency, morphological changes are found in the brain: pons, optic thalamus, cerebellum, hypothalamus, medulla oblongata. As a result, a clinical picture of typhus encephalitis or meningoencephalitis often occurs. Changes in other organs include interstitial myocarditis, granulomatous hepatitis, interstitial nephritis. Interstitial infiltrates are also found in large vessels, endocrine glands, spleen, and bone marrow.

The mortality rate for typhus in the 1950s ranged from 1.2 to 1.5% in adolescents, and up to 22.5% in old people. In children, deaths were rare, mainly in the 1st year of life.

Clinical manifestations. The incubation period is about 2 weeks, but can be shortened to 5-7 days or extended to 3 weeks. The disease begins with an increase in body temperature, sometimes there are precursors: weakness, irritability, sleep disturbance, loss of appetite. Simultaneously with the increase in body temperature, headache, dizziness, feeling of heat, weakness, and insomnia appear. All clinical symptoms increase, reaching maximum severity on the 3-6th day of illness. During this period, the face is hyperemic, puffy, the sclera is injected (“red eyes on a red face”). You can often see pinpoint hemorrhages on the mucous membrane of the soft palate; similar rashes also occur on the transitional folds of the conjunctiva (Chiari-Avtsyn symptom). The tongue is coated, dry, there is often a tremor of the tongue and difficulty in protruding it. Tachycardia, muffled heart sounds, arterial hypotension, and rapid breathing are noted. The skin is moist, hot to the touch, the symptoms of pinch and tourniquet are positive. On the 4-5th day of illness, the most characteristic symptom appears - a profuse roseola-petechial rash on the skin. The rash first appears on the sides of the chest, abdomen, and flexor surfaces. upper limbs. A rash on the face, palms and scalp is rare. The rashes are brightly colored for 3-6 days, and then turn pale, roseola disappear, and petechiae become pigmented. At 2-3 weeks from the onset of the disease, the rashes disappear.

At the height of the disease, the spleen is enlarged, and sometimes there is a liver reaction. The stool is usually retained. In severe cases, symptoms of central nervous system damage such as meningitis, encephalitis or meningoencephalitis may appear.

In the peripheral blood, slight leukocytosis, neutrophilia and band shift, plasma cells are detected; ESR is increased.

Body temperature normalizes, symptoms of intoxication disappear by the end of the 2nd week of illness, and complete recovery occurs in the 3rd week and later.

A decrease in temperature means the beginning of the period of convalescence. During the first weeks of normal body temperature, post-infectious asthenia syndrome persists. Appetite and sleep are gradually restored, headaches go away, pulse and blood pressure normalize.

The disease can be complicated by myocarditis, pneumonia, thromboembolism, rupture of cerebral vessels, otitis media, mumps.

Brill's disease manifests itself with all the symptoms inherent in epidemic typhus, but much less pronounced. There is no mortality in Brill's disease, the febrile period is no more than 6-8 days, complications are rare.

Features of typhus in young children. Typhus is very rare in children under 3 years of age. The disease usually begins gradually, with warning signs. Symptoms of intoxication are mild. “Typhosus status” practically does not occur. Facial hyperemia and scleral injection are weak or absent. Skin rashes are often scanty, located on the face and scalp; in a third of patients, there is no rash at all. Enanthema and rashes are rarely found on the transitional folds of the conjunctiva. Damages to the cardiovascular system are rare. The liver is usually not enlarged, stools are frequent. The course of the disease is mild, severe cases are extremely rare. There are no complications.

Diagnostics. The diagnosis is established on the basis of prolonged fever, intoxication, characteristic roseola-petechial rashes, facial hyperemia, injection of conjunctival and scleral vessels, and enlarged spleen. It is important to consider close contact with a typhus patient. In laboratory research, RSK, RNGA, RA and the immunofluorescence method are used. Specific complement-fixing antibodies begin to be detected in the blood from the 5-7th day of illness and reach a maximum at 2-3 weeks of illness.

Differential diagnostics are carried out with typhoid fever, influenza, measles, hemorrhagic fevers, enterovirus infection, meningococcal infection, etc.

Treatment. Tetracycline drugs are prescribed (tetracycline, oletethrin, sigmamycin), as well as chloramphenicol in age-specific doses in 4 doses throughout the febrile period and 2-3 days at normal body temperature. Symptomatic and pathogenetic treatment is widely used. In severe cases, corticosteroid hormones are used. At infectious-toxic shock Intensive therapy is carried out in accordance with the severity of shock.

Prevention aimed at combating pediculosis. All patients with typhus must be hospitalized and strictly isolated. The patient and all persons in contact with him must undergo sanitary treatment. The room where the patient lives is subject to special treatment. The outbreak is monitored for 25 days.

For active prevention, a dry chemical typhus vaccine has been proposed. Children are not actively immunized.

ENDEMIC (FEA, RAT) TYPHUS

Etiology. The causative agents of endemic typhus (A75.2) are rickettsiae, discovered in 1928 by R. Mooser. The morphological properties of Muzer's rickettsia are similar to Provacek's rickettsia. They have a common heat-stable antigen and therefore cross-react with the sera of patients with typhus.

The incidence of rat typhus is sporadic. The disease is characterized by a benign course with acute fever and roseola-papular rash.

The disease occurs in sporadic cases in endemic areas. On the territory of our country, such centers are the basins of the Black and Caspian Seas, the Far East, and Central Asia.

Pathogenesis and pathomorphology similar to those of epidemic typhus. The pathogenesis is based on destructive-proliferative thrombusculitis, most often of arterioles and precapillaries. However, these changes are less pronounced and their manifestations are shorter than with epidemic typhus.

Clinical manifestations. The infection resembles a milder version of epidemic typhus. The incubation period is 5-15 days, with an average of 8 days. The disease begins acutely, with fever, headache, mild chills, and arthralgia. The temperature reaches a maximum on the 4-5th day of illness, remains high for 3-5 days, and then decreases with shortened lysis. Remitting fever with large temperature fluctuations is possible, although more often it is constant, with fluctuations during the period of normalization. The rash usually appears on the 4-5th day of illness at the height of the fever, and is localized on the chest, abdomen, then on the extremities. The face, palms and soles rarely develop a rash. The rash is first predominantly roseola, and then papular, with isolated petechiae and lasts up to 10 days. At the height of the rash, hypotension, a tendency to bradycardia, dizziness, and general weakness are noted. Typhosus status practically does not arise. The liver and spleen are extremely rarely enlarged. In the peripheral blood in the first days of the disease, leukopenia is possible, then leukocytosis with lymphocytosis.

Endemic rat typhus can occur in mild, moderate and severe forms. In children, mild and moderate forms predominate.

The course of the disease is favorable. Complications practically do not occur. Sometimes the development of thrombophlebitis, otitis media, and pneumonia is possible.

The diagnosis is made on the basis of clinical, epidemiological and laboratory data. It is almost impossible to differentiate from mild forms of epidemic typhus based on clinical data. The increase in antibody titer in RSCs with antigen from Muser's rickettsia is of decisive importance. In unclear cases, a bioassay can be carried out to identify the scrotal phenomenon of NeuelMuser during experimental infection of male pigs.

Treatment is the same as for epidemic typhus.

Prevention is aimed at exterminating rats and mice, preventing them from entering homes, isolating food products from rodents. For active immunization, a killed vaccine from Muser's rickettsia has been proposed. The vaccine is not used in children.

TICK-BACK SPOTTED FEVER

The group of tick-borne spotted fevers (A77) includes Rocky Mountain spotted fever, Marseilles fever, Volyn fever, vesicular rickettsiosis, tick-borne typhus of North Asia, etc. In Russia, tick-borne typhus of North Asia is most widespread.

TICK-BORNE NORTH ASIAN RICKETSIOSIS

Tick-borne typhus of North Asia (A77.2), or North Asian tick-borne rickettsiosis, tick-borne rickettsiosis, is an acute infectious disease with a benign course, primary affect, fever and skin rashes.

The disease was first described in our country in 1934 in the Far East by E.I. Mill, then discovered in Western and Eastern Siberia, Mongolia, Kazakhstan, Kyrgyzstan, Turkmenistan, and Armenia.

Etiology. The causative agent of the disease (Rickettsia sibirica) is able to reproduce well in the yolk sacs of chicken embryos and in tissue cultures, not only in the cytoplasm, but also in the nuclei of affected cells. Its antigenic and pathogenic properties are highly variable.

Epidemiology. Tick-borne North Asian rickettsiosis is a natural focal zoonosis. Reservoir of infection are small rodents (gophers, field mice, chipmunks, hamsters, etc.). Transmission of infection transmission from infected rodents to humans is carried out exclusively through ixodid ticks. They transmit rickettsiae transovarially to their offspring up to the 4th generation. The highest incidence is recorded during the activity of ixodid ticks - in spring and summer. Infection of humans occurs not only in the natural habitats of the vector, but sometimes also when ticks are brought into a person’s home by domestic animals, as well as with grass and flowers.

Clinical manifestations. At the site of the tick bite, after 3-5 days, a primary affect occurs in the form of an inflammatory reaction of the skin with lymphadenitis. At the same time, body temperature rises, chills, malaise, headaches and muscle pain appear. Sometimes, before the temperature rises, prodromal phenomena may be observed: chilling, malaise, loss of appetite. The temperature reaches a maximum within 2-3 days, is remitting, and lasts about 5-10 days. At the height of the fever (usually on the 2-3rd day), a profuse polymorphic roseolous-papular rash appears, mainly on the torso and around the joints. In severe cases, the rash occurs throughout the body, including the face and soles of the feet. Sometimes a hemorrhagic component is added.

A typical symptom of tick-borne typhus is primary affect- usually found on exposed parts of the body (head, neck, shoulder girdle). This is a dense painful infiltrate, covered with a brown crust, surrounded by a zone of hyperemia. Often there is necrosis in the center. As a rule, the primary affect is accompanied by regional lymphadenitis.

Tick-borne typhus is accompanied by hypotension, bradycardia, moderate enlargement of the liver and spleen. The patient's face is hyperemic and slightly puffy. Hyperemia of the mucous membranes of the tonsils, soft palate, and arches is constantly noted. Sometimes there is a small enanthema. Moderate neutrophilic leukocytosis and lymphopenia are detected in the blood; ESR is increased.

The course of the disease is benign. Recovery begins on the 7th to 14th day of illness. Sometimes there is an atypical course of the disease - without primary affect, regional lymphadenitis or without rashes.

In children of the first years of life, the disease is rare due to the limited possibility of attack by ixodid ticks. The disease is relatively mild, but severe cases are possible. Lethal outcomes are extremely rare.

Diagnostics in typical cases it does not present any great difficulties. The diagnosis is established on the basis of primary affect, regional lymphadenitis, fever, characteristic rashes and epidemiological data (natural source of infection). To confirm the diagnosis, RSK and RNGA are used. Specific antibodies appear from the 5-6th day from the onset of the disease and reach a maximum at the 3-4th week from the onset of the disease.

Treatment is carried out with tetracycline antibiotics in age-appropriate doses for 7-10 days.

Prevention involves individual and collective protection of children from tick attacks, timely removal of ticks from the body, wiping bite sites with alcohol or iodine solution.

MARSEILLE FEVER

Marseilles (Mediterranean) fever (A77.1) is an acute infectious disease caused by Rickettsia conorii, with primary affect at the site of the tick bite, regional lymphadenitis, fever, maculopapular rash.

Etiology. The causative agent of the disease Rickettsia conorii opened in 1932 Natural reservoir and the carrier of the pathogen are some species of dog ticks, which retain rickettsia for life and transmit them transovarially to their offspring.

Epidemiology. Human infection occurs when ticks bite or crush them, followed by rubbing of rickettsia into damaged skin and mucous membranes. Human-to-human transmission has not been established. On the territory of our country, there are foci of Marseilles fever in the Crimea, on the Black Sea coast of the Caucasus, the Absheron Peninsula and in the coastal regions of Dagestan.

Pathogenesis. At the site of the tick bite, after a few hours, a primary affect appears in the form of an area of ​​inflammation, followed by central necrosis and ulceration. From the primary focus, the pathogen enters the regional lymph nodes through the lymphogenous route, where an inflammatory process often occurs - lymphadenitis. Then the infection generalizes with the penetration of rickettsia into the endothelium of small vessels, which leads to the development of specific vascular granulomatosis (panvasculitis). The severity of vascular changes correlates with the severity of the disease, which is associated with rickettsia and toxemia. A profuse maculopapular rash with necrosis indicates a significant allergic component.

Clinical manifestations. The duration of the incubation period is on average 5-7 days, sometimes up to 18 days. The disease begins acutely, with an increase in body temperature to 38-40 ° C, chills, headache and muscle pain. General lethargy, sleep disturbances, and possible vomiting are noted. The patient's face is moderately hyperemic, the vessels of the sclera and conjunctiva are injected, hyperemia of the mucous membrane of the oropharynx is often noted, and a sore throat is possible. The tongue is covered with a gray coating. Throughout the entire illness, the primary affect remains on the skin, which is an inflammatory dense infiltrate with central necrosis, and then a black or brown scab, surrounded by a zone of hyperemia with a diameter of up to 5-7 mm. The crust disappears after the temperature normalizes, and the ulcer that forms at the site of the scab epithelializes during the period of convalescence (at the 3-4th week of illness). In the zone of primary affect, regional lymphadenitis occurs, while the lymph nodes can be large, up to 5-10 cm in diameter, painful on palpation. If the infection penetrates through the conjunctiva, the primary effect manifests itself in the form of conjunctivitis with chemosis.

A characteristic symptom of Marseilles fever is a rash. It usually appears on the 2-3rd day of illness, first on the torso and then throughout the body, including the face, palms and soles. The rash is initially macular, then becomes maculopapular, sometimes transforming into red, pimple-like formations (“pimply fever”), often with a hemorrhagic component in the center individual elements. The rash lasts throughout the febrile period and fades away gradually. Pigmentation may persist at the site of the rash for 1-3 months.

At the height of clinical manifestations, most patients experience relative bradycardia, dullness of heart sounds, often an enlarged spleen, and less often, a liver. In severe cases, meningism, delirium, tremor of the tongue and hands are possible. Leukopenia with relative lymphocytosis is detected in the blood; ESR is slightly increased. Mild and moderate forms with a favorable course are more often observed. Severe cases are rare. Atypical forms of the disease are possible - without rash, primary affect and regional lymphadenitis.

Forecast favorable for Marseilles fever. Complications are rare, and deaths practically never occur.

Diagnosis established on the basis of primary affect, maculopapular rash, fever, as well as the child’s stay in an endemic focus.

For laboratory confirmation of the diagnosis, RSK, RNGA using whole antigen are performed R. conorii. To isolate rickettsiae from the blood of patients or ticks, the material is injected intraperitoneally into male guinea pigs and when periorchitis develops, the diagnosis is confirmed.

Marseille fever must be differentiated from drug allergies, meningococcal infection, measles and other rickettsioses.

Treatment. As etiotropic therapy, chloramphenicol, tetracycline and its analogues are used in age-specific doses throughout the entire febrile period and another 2-3 days at normal temperature. Antihistamines, anti-inflammatory drugs and other symptomatic drugs are indicated.

Prevention is aimed at combating ticks in endemic foci (treating dogs, doghouses and other places where ticks can reproduce with acaricidal preparations).

TSUTSUGAMUSHI FEVER

Tsutsugamushi fever (A75.3) is an acute rickettsial disease with fever, maculopapular rash and primary affect with lymphadenopathy.

In Russia, the disease occurs in the southern regions of the Primorsky Territory.

A person becomes infected while staying in a natural outbreak.

Clinical manifestations. The disease develops 1-3 weeks after the bite of an infected red tick. By the end of the incubation period, prodromal phenomena are possible: malaise, headache, loss of appetite.

However, more often the disease begins acutely, with fever, chills, and headache. From the 1st day of illness, a primary affect appears at the site of the tick bite. Usually these are closed areas of the body: natural folds of skin, groin, axillary areas, perineum. The primary affect undergoes evolution: first a hyperemic and weakly infiltrated spot is formed, then it quickly turns into a vesicle and finally into an ulcer. Usually a flat ulcer is surrounded by a zone of hyperemia and covered with a brown crust, regional lymphadenitis is determined. Fever reaches a maximum on the 2-3rd day of illness, it is remitting and persists for about 2-3 weeks. The patient's face is slightly hyperemic, the sclera is injected, and there are manifestations of conjunctivitis. On the 3-6th day of illness, a profuse maculopapular rash appears, mostly on the torso and limbs.

With tsutsugamushi fever (and this is how it differs from other rickettsial diseases), exudative inflammation of the serous membranes develops with pericarditis, pleurisy, peritonitis and the accumulation of whitish-yellowish exudate.

Flow The disease is usually benign. The rash disappears after 4-10 days. Ulcer healing occurs in the 2-3rd week of illness. Based on the severity of the course, there are mild, moderate and severe forms of Tsutsugamushi fever.

Diagnosis established on the basis of prolonged fever, the appearance of a primary affect with regional lymphadenitis and the patient’s stay in an endemic focus. To confirm the diagnosis, RSC with pathogen antigens is performed. RA with Proteus OX 19 also retains diagnostic value (the pathogen has a common O-antigen with Proteus OX 19).

Treatment. Levomycetin is prescribed in age-specific doses until body temperature is completely normalized. If necessary, pathogenetic and symptomatic therapy is carried out.

Prevention the same as with others tick-borne rickettsioses. Personal prevention using means to prevent tick attacks is of great importance.

Q FEVER

Q fever (A78), or Central Asian fever, pulmonary typhus is an acute rickettsial disease with fever, frequent defeat Central nervous system and the development of specific pneumonia. The disease is widespread. In Russia it is found mainly in the southern regions.

Unlike other rickettsiae, the causative agent of Q fever Coxiella burneti does not have common antigens with Proteus.

Epidemiology. Under natural conditions, the infection is found in many mammals, birds, and ticks. Warm-blooded animals are temporary carriers of Burnet's rickettsia, and ixodid ticks transmit the pathogen transovarially to their offspring. Domestic animals, which become infected in foci of infection from wild animals and ticks, can also be involved in the circulation process. Infection of a person can occur through the nutritional route by consuming food products from infected animals (milk, eggs, etc.) or by airborne droplets by inhaling dust containing secretions of infected animals (processing skin, wool, fur), or through contact with infected domestic animals. A healthy person cannot become infected from a sick person. Children become infected with Ku-rickettsia mainly through the nutritional route (through milk).

Pathomorphology. In pathological terms, Q fever is an infectious benign reticuloendotheliosis without the development of endovasculitis. Reproduction of rickettsia occurs mainly in the cells of the reticuloendothelial system and, to a lesser extent, in vascular epithelial cells and macrophages. The greatest changes are found in the lungs, cardiovascular system, liver and spleen.

Clinical manifestations very polymorphic. The incubation period is on average 15-20 days. The disease begins acutely, with an increase in body temperature to high values, fatigue, weakness, fever, headache, sweating. From the first days of the disease, hyperemia and puffiness of the face, injection of scleral vessels, hyperemia of the mucous membranes of the tonsils, soft palate, and often enanthema appear. Often at the height of the disease there is tracheitis, tracheobronchitis or bronchitis; the development of focal pneumonia is possible, rarely - pleuropneumonia. The course of pneumonia is torpid. Almost all patients experience headache, insomnia, mental instability, possible hallucinations, pain in the eyeballs and muscle pain. Some patients complain of abdominal pain, they may have upset stools, and in severe cases, the development of serous meningitis and encephalitis.

The leading symptom of Q fever is a prolonged increase in temperature. Typically, fever is constant or remitting, accompanied by sweats and often chills. The duration of fever ranges from several days to 3-4 weeks or more.

The general condition of patients with Q fever remains satisfactory or moderate throughout the entire illness. The severity of damage to individual organs and systems largely depends on the route of infection. In some patients, symptoms of damage to the nervous system predominate, in others - to the respiratory system, and in others - to the gastrointestinal tract. This creates a variety of clinical manifestations of Q fever and makes diagnosis difficult.

There are mild, moderate and severe forms of the disease. In foci of infection in children, erased and subclinical forms are often recorded, diagnosed by serological methods.

The course of the disease can be acute (up to 2-3 weeks), subacute (up to 1.5 months) and chronic (up to 1 year). Relapses are possible.

Diagnostics. Q fever can be suspected in an endemic focus based on a prolonged increase in temperature with sweats, muscle pain, arthralgia, and headaches. Laboratory confirmation is required for definitive diagnosis. Use RN, RSC, allergic skin test. Isolation is of great importance R. burneti from blood, sputum, urine, cerebrospinal fluid. Guinea pigs, white mice or cotton rats are infected with material from patients. Burnet's Rickettsia large quantities accumulate in the liver, spleen and other organs of infected animals.

Treatment is carried out with antibiotics from the group of tetracycline and chloramphenicol in age-specific doses for 7-10 days and symptomatic agents.

Prevention is aimed at exterminating ticks in nature, protecting domestic animals from tick attacks, and strictly observing quarantine for sick animals. Sanitary education among the population is of great importance, especially in endemic areas. It is important to strictly follow the rules of personal prevention when caring for sick pets. Only boiled milk is allowed. For active immunization, a live M-44 vaccine has been proposed, which is administered strictly according to epidemiological indications.

RICKETSIOSISIS-LIKE

Smallpox-like rickettsiosis (A79.1), or rickettsial pox, is caused by R. acari and refers to acute febrile diseases with primary skin lesions in the form of papular-vesicles of the fever rash and the subsequent development of a general infectious syndrome.

This disease was first identified as an independent nosological form in 1946 during an outbreak in New York. Then the causative agent of American “rickettsial smallpox” was discovered in France and Russia.

Etiology. The causative agent of rickettsial pox is a diplococcal form of rickettsia, which belongs to the causative agents of rickettsial diseases of the tick-borne spotted fever group. The natural reservoir of infection in nature is gamasid mites, in which rickettsiae are found at all stages of metamorphism and do not have any harmful effects.

In patients with smallpox-like rickettsiosis, the pathogen is found in the blood throughout the entire febrile period.

Pathogenesis Smallpox-like rickettsiosis is no different from that of other rickettsial diseases. It is based mainly on damage to the vascular system (capillaries, small veins and arteries).

Clinical manifestations. The incubation period is 10-12 days. The disease begins acutely, body temperature rises, chills appear, and headaches occur. In most patients, at the site of the tick bite, a primary affect appears in the form of a dense, non-itching red skin infiltrate with a diameter of 0.5-2 cm, which turns into a papule. After a few days, a blister forms in the center of the papule; it soon bursts and becomes covered with a crust. Due to the nature of the papulovesicular rash, the disease was called smallpox-like rickettsiosis. As with smallpox, with this rickettsiosis there are no rashes on the palms and soles. After the crusts fall off, a delicate scar is formed that lasts 3 weeks or longer. Regional lymph nodes are enlarged, but upon palpation they remain soft and there is no suppuration.

On the 2-3rd day from the onset of the disease, erythematous and maculopapular rashes reappear, which gradually increase in size and turn into blisters. These are secondary rashes, they are smaller than the primary ones and disappear after a week, leaving no scars.

The febrile period with smallpox-like rickettsiosis lasts 5-8 days, the duration of the rash is from 2 to 20 days. The intensity of skin rashes depends on the severity of the disease. With the exception of fever, regional lymphadenitis and skin rashes, with smallpox-like rickettsiosis, other disorders (for example, changes in internal organs) are almost not detected. During the acute period of the disease, leukopenia is observed in the peripheral blood.

Differential diagnosis. Most often, osporicketsiosis in children must be differentiated from chickenpox. With rickettsial smallpox, the blisters are deeper and denser and appear all over the body at once. Differential diagnosis must be made with meningococcemia, Rocky Mountain spotted fever, and typhus.

Confirmation of the clinical diagnosis is the isolation of the pathogen from the blood of patients with its subsequent identification. For this purpose, serological studies are used according to the RSC principle with the Konori rickettsia antigen.

Treatment. Tetracycline antibiotics or chloramphenicol are prescribed in age-specific doses until body temperature normalizes and for another 4-5 days after its normalization. In accordance with other symptoms of the disease, symptomatic therapy is carried out.

Prevention. Measures to combat smallpox-like rickettsiosis involve the destruction of rodents and gamasid mites, which serve as reservoirs and vectors of infection.

During epidemics, a special vaccine can be produced.