Q fever

What is Q fever?

Q fever – zoonotic acute rickettsiosis with the development of reticuloendotheliosis, intoxication syndrome, often with atypical pneumonia.

The name “Q-fever” (from the English queri – unclear) was suggested by E. Derrick, who first described the disease in farmers and meat processing plants in Australia (1937). The rickettsial nature of the disease was established by F.M. Burnet and M. Freeman (1939). Regardless of Australian researchers in the United States, X. Cox isolated a filterable agent from the ticks, carriers of the fever of the Rockies, and proved its rickettsial nature (1938). Later, the pathogen was allocated to a separate genus of rickettsia, named after him. In Russia, foci of disease have been known since 1952 and are widespread; in the 60s of the XX century, they were studied by P.F. Zdrodovsky, MP Chumakov, E.N. Bartashevich and others.

Causes of Q fever

The causative agent of Q fever is a small gram-negative, more often rod-shaped bacteria Coxiella burnetii of the genus Coxiella, Rickettsie fungi of the family Rickettsiaceae, also known as Burnet’s rickettsia. Microorganisms are prone to polymorphism and the formation of L-forms. The basic properties are similar to those of other rickettsiae; their main difference is high environmental stability (in wool, cotton, straw, etc.). In milk, it withstands heating up to 90 ° C for 1 hour, in feces of ticks, dry substrates, sterile milk, non-chlorinated water at 4 ° C remains viable for more than a year, and in meat for more than a month. Rickettsia Burnet resistant to the action of ultraviolet radiation, solutions of formalin, phenol and bleach in normal concentrations. High resistance is determined by the ability to form spore-shaped forms. They are characterized by phase variability with the formation of forms similar to the S- and R-forms of bacteria. Freshly isolated bacteria have phase 1 antigens, but after long transfers on chicken embryos they are transformed into phase II. This dissociation is reversible, and after infection of animals a set of antigens is restored. Phase II bacteria are prone to spontaneous agglutination, are agglutinated by normal serum and are detected in CSC. Phase I antigens exhibit greater immunogenicity, and the resulting antibodies react with antigens of both phases. Phase II antigens induce the formation of antibodies that react only with phase II antigens.

The reservoir and source of infection are domestic and wild animals (mostly rodents) and birds. The custodians of rickettsiaus in nature are ticks (ixodid, gamazovye and argasovy), transovarially transmitting infection to offspring. Sick animals secrete the pathogen throughout the course of the disease, especially during calving and lambing. Man represents an epidemic danger extremely rarely.

The transmission mechanism is varied. The pathogen enters the human body through the mucous membranes of the digestive tract, respiratory tract or damaged skin. Often the infection is realized through contaminated milk and dairy products, meat, water. The pathogen can also be transmitted aerogenically (by inhalation of dust from dried excrements and urine of sick animals, treatment of infected hides, cotton, wool), as well as by contact (through hands contaminated with amniotic fluid, abortions of sick animals). At the same time, the leading way of transmission of coxiel is aspiration.

The natural susceptibility of people is high, but in many cases the disease remains asymptomatic. Post-infectious immunity is stressful, although there are cases of repeated illness.

Major epidemiological signs. Q fever has pronounced foci. Allocate anthropurgic (infection from domestic animals and birds) and natural foci. Found that natural foci support infected ticks. Diseases are sporadic or group. The incidence is clearly associated with the profession: hunters, livestock breeders and people engaged in the collection, storage and processing of animal raw materials are much more common. In the natural foci of the disease infection often occurs in spring, summer and autumn.

Pathogenesis during Q fever

In accordance with the mechanisms of infection, the pathogen is introduced into the body through the respiratory tract, gastrointestinal tract or skin. With the subsequent occurrence of bacteremia, rickettsia affect the reticulohistiocytic system with the formation of foci of proliferation of the reticuloendothelium, perivasculitis and necrobiosis of the cells. Severe toxemia accompanies ricketcemia, leading to the formation of foci of infection in internal organs with the development of allergic reactions. When aerogenic infection due to severe pneumotropic rickettsia develops an infiltrative process in the lungs. Depending on the intensity of the immunological reactions in patients, in most cases, rickettsia is eliminated, and full recovery occurs. However, at the same time, the causative agent may be delayed in the body, which causes the development of protracted and chronic forms of the disease.

Symptoms of Q fever

Incubation period. Varies from 3 to 30 days, sometimes it lasts up to 3 months. Acute, subacute and chronic forms of Q fever of varying severity are distinguished. The most common acute form of the disease with lung lesions.

The disease usually begins with a rapid, within 1-2 days, increase in body temperature to 39-40 “C, but the beginning can be gradual.

Starting period. Lasts a few days, noted chills, sweating, severe weakness, headache with a predominant localization in the orbits of the eyes, myalgia and arthralgia, sleep disorders. In severe Q fever, there may be agitation, insomnia, delirium. In the acute onset of the disease, hyperemia of the face and neck, vascular injection of the sclera, conjunctiva and mucosa of the oropharynx, looseness and hypertrophy of the tonsils, enanthema in the soft palate are often noted. In cases of gradual onset of the disease, the skin may be pale. Occasionally (1-4% of cases) rash appears, usually roseolous or spotted-papular. Pathology of the respiratory system during the first days of the disease usually does not develop. Muffled heart sounds, characteristic changes in the pulse are not observed.

The period of height. Main complaints of patients remain. The high temperature lasts on average up to 1 week, but sometimes after that the fever is delayed by subfebrile values ​​for another 7-8 days, after which the second wave of temperature rises. In such cases, the total duration of fever is 2-3 weeks or more; typical temperature curve is uncharacteristic.

Relative bradycardia, muffled heart sounds, moderate arterial hypotension are noted. Only during this period begin to show clinical signs of respiratory organs in the form of bronchitis or tracheitis. However, already at this time, an X-ray examination reveals an increase in pulmonary pattern and small focal cone-shaped infiltrates, localized mainly in the lower sections of the lungs or root zones. The latter sometimes merge with the formation of massive darkening of the lung tissue, but without the formation of cavities. An increase in the peribronchial lymph nodes creates a picture of the expansion, compaction and deformation of the roots of the lungs. With the development of pneumonia in patients, dry cough increases, and then a wet cough with the release of sero-purulent sputum, occasionally with blood. There is shortness of breath, there may be minor pain in the chest, aggravated by lesions of the pleura. Physical data compared with radiographic changes are scarce: they reveal areas of shortening of percussion sound and hard breathing, a small amount of dry or moist finely bubbling wheezing in the lungs. For pneumonia torpid, radiographic changes disappear slowly.

In cases of severe intoxication, nausea and vomiting are possible, appetite is dramatically reduced. As a result of the defeat of the autonomic nervous system, patients sometimes have unstable abdominal pain and flatulence. Externally, the tongue resembles that of typhoid fever: edematous, coated with a dirty gray scurf, with clean edges and a tip, as well as imprints of the teeth at the edges. Characterized by a moderate increase in the liver and spleen.

Period of convalescence. Manifested by a decrease in body temperature within 2-4 days, improvement in the health and condition of patients, the gradual disappearance of the main clinical signs of the disease. This period is usually characterized by physical and mental asthenia.

In addition to acute cyclic Q fever, it can manifest itself in a subacute form lasting from 1 to 3 months or in a chronic form lasting from several months to 1 year or more. In these cases, the disease proceeds against a subfebrile condition with radiological pronounced infiltrative processes in the lungs.

The above description of Q-fever allows the doctor to suspect the disease on the basis of clinical and epidemiological data. At the same time, the manifestations of the disease are very diverse and can be expressed in the form of influenza-like, fallopian tuberculosis, tuberculous, septic and other clinical options. In these cases, setting a clinical diagnosis is difficult without special laboratory diagnostic methods.

Complications. Due to the specific etiotropic therapy at the present time, almost no complications are observed. In severe cases, in some cases, pleurisy, rickettsial endocarditis, meningoencephalitis, pyelonephritis, pancreatitis may develop.

Diagnosis of Q fever

The diagnosis of Q fever solely on the basis of clinical symptoms is extremely difficult due to the polymorphism of clinical manifestations. In case of lung lesions, it is necessary to differentiate the disease primarily with pulmonary tuberculosis, since in some cases, Qil fever infiltrates may be located in the upper lung regions and resemble tuberculosis. In the first days of the disease, pneumonia in Q fever occurs with scanty clinical manifestations (lack of cough, sputum, chest pain, shortness of breath, dull percussion sound and moist rales). However, during this period, significant changes in the lungs can be observed during X-ray examination. In other forms of the disease, it should be distinguished from influenza, typhoid fever and paratyphoid fever, acute and subacute brucellosis, anicteric leptospirosis and sepsis.

Laboratory diagnosis. In the hemogram, many patients show leukopenia with neutropenia, lymphocytic and monocytosis, and a moderate increase in ESR. The basis of specific diagnostics is made by serological methods: RA, RSK, MFA, etc. In practice, RSK is mainly used in paired blood sera; The specificity of this reaction is quite high. AT diagnostic titers (1: 16-1: 32) appear no earlier than the end of the 2nd or 3rd week of illness.

Q fever treatment

As a means of etiotropic therapy, tetracyclines are used (tetracycline 1.2-1.6 g / day, doxycycline 200 mg / day) or levomycetin in a dose of 2 g / day. The most effective parenteral administration of a combination of tetracycline with chloramphenicol is 0.9 and 1.5 g / day, respectively. The duration of the course of treatment determines the clinical effect of the drugs and averages 8-10 days. Shortening the course or reducing the dose of drugs contributes to the occurrence of relapses. Long-lasting radiographic changes in the lungs are not an indication for prolongation of etiotropic therapy. At the same time carry out detoxification therapy, prescribe desensitizing and non-steroidal anti-inflammatory drugs (indomethacin, butadione, ortofen, diclofenac, etc.). In severe prolonged and chronic forms, glucocorticoids are additionally prescribed (prednisolone at 30–60 mg / day, dexamethasone at 4–5 mg / day).

Prevention of Q fever

Epidemiological and epidemiological surveillance
Carry out in the foci of both types; include monitoring the incidence of humans and animals, continuous monitoring of the extent of pathogen circulation, and monitoring compliance with general health regulations.

The basis for the prevention of Q fever – veterinary and sanitary measures. A variety of sources of infection and ways of transmission greatly complicates the organization and conduct of preventive measures. Anti-mite treatment of pastures, protection of livestock farms from the introduction of pathogens into them have a certain value. In Q-dysfunctional farms, it is prohibited to bring animals into and out of the farm, or to consume the meat of involuntarily killed animals. Milk from dysfunctional farms can be consumed only in boiled form. Calving (lamb) of animals suspicious of Q fever is carried out in separate rooms with subsequent destruction of the afterbirth, the stillborn fetus and thorough disinfection of the room and inventory. Only people who have been ill or vaccinated are allowed to care for sick animals. Risk groups (livestock breeders, meat processing plants workers, veterinarians, livestock processing workers, etc.) are subject to active immunization with live vaccine.

Activities in the epidemic focus
The patient is hospitalized, the discharge is carried out after clinical recovery. Current and final disinfection with the use of chlorine-containing agents is carried out in the outbreak. Emergency antibiotic prophylaxis among people who have been at the site of infection is carried out by administering 0.2 g of doxycycline 1 time per day or 0.3 g rifampicin 2 times per day with a course of 10 days.

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