Q fever - Causes and pathogenesis

Causes of Q fever

Cause of Q fever Coxiella burnetii is a small polymorphic gram-negative non-motile microorganism measuring 200-500 nm, capable of forming an L-form. In terms of morphological, tinctorial and cultural properties, C. burnetii is similar to other rickettsiae, but its antigenic activity is unstable. They have phase variability: antigens of the first phase are detected in the RSC during the late convalescence period, and antigens of the second phase are detected in the early period of the disease. C. burnetii is an obligate intracellular parasite that reproduces in the cytoplasm and vacuoles of affected cells (but not in the nucleus) and is capable of forming spores that are resistant in the environment. Coxiella are grown on cell culture, chicken embryos and by infecting laboratory animals (guinea pigs are the most sensitive).

C. burnetii is resistant in the environment and to various physical and chemical influences. They can withstand heating up to 90 C for an hour (they do not die during pasteurization of milk): they remain viable in dry feces of infected ticks for up to one and a half years, in dry feces and urine of infected animals - up to several weeks, in animal hair - up to 9-12 months, in sterile milk - up to 273 days, in sterile water - up to 160 days, in butter (in refrigerated conditions) - up to 41 days. in meat - up to 30 days. They can withstand boiling for 10 minutes or more. C. burnetii is resistant to ultraviolet radiation, the effects of formalin, phenol, chlorine-containing and other disinfectants, and is sensitive to tetracycline antibiotics and chloramphenicol.

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Pathogenesis of Q fever

Q fever is a cyclic benign rickettsial reticuloendotheliosis. Due to the lack of tropism of the pathogen to the vascular endothelium, panvasculitis does not develop, so the disease is not characterized by rash and other symptoms of vascular damage. Unlike other rickettsioses, coxiella multiply mainly in histiocytes and macrophages.

K.M. Loban et al. (2002) describe the pathogenesis of Q fever as a series of successive phases:

• introduction of rickettsia without reaction at the entry point;
• lymphogenous and hematogenous dissemination of rickettsia (primary or “minor” rickettsiaemia) with their introduction into macrophages and histiocytes;
• proliferation of rickettsia in macrophages and histiocytes, release of a large number of pathogens into the blood (repeated or “major” rickettsiemia);
• toxemia with the formation of secondary foci of infection in internal organs;
• allergic restructuring and the formation of intense (with elimination of the pathogen and recovery) or non-intense (with repeated rickettsia and the development of protracted and chronic forms of the process) immunity.

The probability of a protracted, recurrent and chronic course of the disease with the development of endocarditis, interstitial pneumonia and long-term persistence of the pathogen is an important feature of the pathogenesis of Q fever. This may be due to immune defects, such as incomplete phagocytosis of C. burnetii and immune complex pathology with damage to various tissues and organs (heart, liver, joints).

Epidemiology of Q fever

Q fever is a natural focal zoonotic infection. There are two types of foci of the disease: primary natural and secondary agricultural (anthropurgic). In natural foci, the pathogen circulates between carriers (ticks) and their warm-blooded hosts: ticks → warm-blooded animals → ticks.

The reservoir of the pathogen in natural foci is ixodid, partially gamasid and argasid ticks (more than seventy species), in which transphase and transovarial transmission of rickettsia is observed, as well as wild birds (47 species) and wild mammals - carriers of rickettsia (more than eighty species). The existence of a stable natural focus of infection contributes to the infection of various types of domestic animals (cattle and small cattle, horses, camels, dogs, donkeys, mules, poultry, etc.). They release rickettsia into the environment with excrement, sputum, milk, amniotic fluid for a long time (up to two years) and can play the role of an independent reservoir of the pathogen in anthropurgic foci of the disease.

Infection of humans with Q fever in anthropurgic foci occurs in various ways:

• alimentary - when consuming infected milk or dairy products;
• waterborne - when drinking contaminated water:
• airborne dust - when inhaling dust containing dry feces and urine of infected animals or feces of infected ticks;
• contact - through mucous membranes or damaged skin when caring for sick animals, processing raw materials of animal origin.

A transmissible route of infection is possible (during an attack by infected ticks), but it does not have significant epidemiological significance.

A sick person may excrete C. burnetii with sputum, but it is very rarely a source of infection; isolated cases of Q fever are known among contact persons (infants who received milk from a sick mother, obstetricians, pathologists).

People of different ages are susceptible to Q fever, but men involved in agricultural work, animal husbandry, slaughtering, processing animal skins and wool, bird down, etc., are more likely to get sick. As a result of the increasing human influence on nature, natural foci have gone beyond the initially established "old" boundaries and formed anthropurgic foci involving domestic animals. The disease, previously considered a disease of lumberjacks, geologists, hunters, forestry and agricultural workers, has now become a disease of residents of large settlements and cities. The incidence, observed mainly in spring, summer and autumn, is sporadic; group outbreaks occur occasionally; asymptomatic forms of infection are found more often. Repeated diseases are rare; post-infection immunity is persistent.

Sporadic cases and local outbreaks of Q fever are registered on all continents. There are few "blank spots" of Q fever on the geographical map. Mandatory registration of Q fever cases in Ukraine was introduced in 1957. Currently, the incidence is low: about 500-600 cases of the disease are registered annually.

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