Q fever is a rickettsiosis infection that occurs with a febrile syndrome and lung damage, in particular, with the development of atypical pneumonia. The initial period is characterized by general toxic manifestations; during the peak period, symptoms of tracheitis, bronchitis, and pneumonia dominate. The diagnosis is based on a complex of clinical, epidemiological and laboratory data (IFT, ELISA, PT, bacteriological analysis), intradermal and biological samples, lung radiography. The basis of the treatment is antibiotic therapy; additionally, detoxification, desensitizing, anti-inflammatory therapy, inhalations are carried out.
ICD 10
A78 Q Fever
General information
Q-fever (pneumoricketsiosis, Balkan flu) is an acute, naturally focal tick–borne rickettsiosis characterized by a predominant lesion of the respiratory system. Disease is common in all geographical areas, most widely in Australia and America. Sporadic and group cases of the disease are also recorded in Europe and Asia. Q fever is highly contagious, people of different ages are susceptible to infection. Rural residents working on livestock farms, poultry farms, slaughterhouses are more often infected; engaged in hunting, collecting, storing and processing meat, leather, fur and down. Despite the insignificant proportion in the structure of infectious diseases, the high frequency of severe pneumonia and complications determine the relevance and infectious alertness in relation to this pathology.
Causes
The causative agents of Q fever are obligate intracellular parasites – rickettsia Burnet (Coxiella, Coxiella burnetii). They are small immobile gram-negative bacteria capable of forming filterable and spore-like forms. Burnet’s rickettsias live and reproduce in living, actively metabolizing cells – inside the epithelial cells of the intestinal tract of ticks, in cells of various human organs and systems. The causative agent of Q fever is distinguished by high resistance to environmental factors: outside of a living organism, they remain viable for several months. Coxiellas are resistant to ultraviolet rays, disinfectants (bleach, formalin), elevated and low temperatures, but they die during boiling within one minute.
The natural source of the causative agent of Q fever is more than 40 varieties of ticks (mainly ixodes, as well as gamaz, argass, etc.), infected wild and domestic animals, birds that emit coxiella into the environment throughout the entire period of the disease. Transmission of infection to humans is carried out in various ways: aspiration, alimentary, contact, transmissible. Most often, the causative agent of Q fever penetrates through the mucous membranes of the respiratory tract when inhaling infected dust during the processing of animal skins and wool; through damaged skin when caring for sick animals; through the gastrointestinal tract when eating infected meat, milk, water. Natural foci of Q fever are supported by infected ticks. Infection of people more often occurs in the spring-summer-autumn period.
At the site of penetration of the pathogen into the human body, an inflammatory reaction does not occur. Bacteremia leads to damage to the reticulohistiocytic system, accompanied by severe toxemia, the development of specific dystrophic changes in the cardiovascular and nervous systems, kidneys, and other internal organs. Burnet’s rickettsias have pronounced pneumotropicity, therefore, with Q fever, the greatest changes occur in the respiratory system.
Symptoms
Q fever can occur in acute, subacute and chronic forms. In the dynamic course of the disease, the incubation, initial period, the period of peak and convalescence are distinguished. The incubation period varies from 3 to 30 days (on average 19-20 days).
The disease begins suddenly, with a rapid rise in temperature to 39-40C, chills and sweating, accompanied by severe headache, myalgia and arthralgia, pronounced weakness and insomnia. There is often hyperemia of the face and neck, pharyngeal mucosa, injection of vessels of the sclera and conjunctiva. Sometimes there is a rash of a roseolous or spotty-papular character. Muffled heart tones, bradycardia, moderate arterial hypotension are detected. The initial period of Q fever lasts 7-9 days. After a few days, the temperature decreases, stays at subfebrile values for a short time, until the second wave of fever occurs.
At the height of the disease, signs of respiratory damage begin to dominate – a picture of tracheitis, bronchitis or atypical pneumonia develops. Patients with Q fever are concerned about a feeling of tightness in the chest, a dry cough or with the release of scanty sputum, accompanied by chest pain. With the development of pneumonia, the cough becomes moist with serous-purulent sputum, sometimes with an admixture of blood; shortness of breath appears, dry, rarely moist, small-bubbly wheezes are heard. The course of pneumonia in Q fever is torpid, with slow resolution of clinical and radiological signs.
The stage of convalescence proceeds with a gradual decrease in temperature, improvement in the well-being of patients, disappearance of the main clinical symptoms. There is a long asthenic syndrome, the restoration of working capacity is slow. The subacute form of Q fever has a duration of 1 to 3 months, usually a mild or moderate course with a wave-like slight rise in temperature. The chronic form is characterized by a frequently recurrent, sluggish process lasting from several months to 1 year or more.
Complications of Q fever are observed infrequently. In some cases, pleurisy, lung infarction, endocarditis, meningoencephalitis, pyelonephritis, pancreatitis, hepatitis, orchitis or epididymitis of rickettsia nature, deep vein thrombophlebitis of the extremities, neuritis may develop. The addition of a secondary infection is accompanied by the formation of abscesses.
Diagnostics
The diagnosis of Q fever is based on a complex of clinical and epidemiological data, the results of laboratory and instrumental examination. In the blood of patients with Q fever there is thrombocytopenia, relative lymphocytosis and monocytosis, a moderate increase in ESR; in urine – proteinuria and hematuria. Q fever is confirmed by the isolation of a culture of the pathogen in the blood, urine, sputum, and liquor of patients using bacteriological seeding on tissue media or by biological sampling on guinea pigs and rodents. Pure rickettsia cultures are obtained by introducing the test material into chicken embryos.
Chest X-ray in rickettsiosis pneumonia reveals small focal infiltrates in the lower parts and basal zones, strengthening of the pulmonary pattern, compaction and expansion of the roots of the lungs, an increase in peribronchial lymph nodes. Specific diagnosis of Q fever includes serological methods: PT, IFT, ELISA, intradermal tests with purified pathogen antigen. Diagnostic titers become positive on 10-12 days of the disease and reach a maximum by 3-4 weeks.
Natural foci of Q fever are determined by examining the hemolymph and intestines of ticks, as well as preparations-prints of internal organs of animals for the presence of rickettsia Burnet. It is necessary to carry out differential diagnosis of Q fever with pulmonary tuberculosis, influenza, typhoid fever, acute and subacute brucellosis, leptospirosis, tularemia, pneumonia of various genesis, sepsis.
Treatment and prevention
Treatment of patients with Q fever is carried out in a hospital, but special isolation of patients is not required. Recommended bed rest, diet. Tetracycline antibiotics (biomycin, oxytetracycline) are prescribed as etiotropic therapy, possibly in combination with chloramphenicol. The duration of the course of therapy is 8-10 days; reducing the timing and dose of taking drugs contributes to the development of relapses.
It is advisable to take antihistamines, NSAIDs, multivitamins. According to the indications, detoxification therapy is prescribed; with the development of pathology of the respiratory system, oxygen therapy, inhalations with bronchodilators are carried out. In severe forms of Q fever, corticosteroids (prednisone, dexamethasone) are used.
The prognosis of Q fever is favorable, most cases of the disease end in complete recovery, sometimes prolonged and chronic forms of the disease can develop. Fatal outcomes are extremely rare. Prevention of Q fever includes a complex of anti-epidemic, veterinary and sanitary-hygienic measures. These measures involve carrying out anti-tick treatment of pastures, the destruction of rodents, veterinary supervision of livestock, thorough heat treatment of meat, milk and water. In natural foci, the issues of personal hygiene, immunization of at-risk individuals with a live vaccine are of particular relevance.