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Health

Q fever: causes and pathogenesis

, medical expert
Last reviewed: 23.04.2024
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Causes of fever

Coke fever cause Coxiella burnetii is a small polymorphic gram-negative immobile microorganism 200-500 nm in size, capable of forming an L-form. According to the morphological, tinctorial and cultural properties of C. Burnetii is similar to other rickettsia, however their antigenic activity is unstable. They have a phase variability: in the DSC in the late convalescence antigens of the first phase are detected, in the early period of the disease - antigens of the second phase. C. Burnetii is an obligate intracellular parasite that multiplies in the cytoplasm and vacuoles of affected cells (but not in the nucleus) and is capable of forming spores that are stable in the environment. The coxiella is grown on cell culture, chick embryos and by infecting laboratory animals (guinea pigs are most sensitive).

C. burnetii are resistant to the environment and to various physical and chemical influences. Heat up to 90 C for an hour (do not die during pasteurization of milk): they remain viable in dry faeces of infected mites for up to 1.5 years, in dry faeces and urine of infected animals - up to several weeks, in animal wool - up to 9-12 months, in sterile milk - up to 273 days, in sterile water - up to 160 days, in oil (under refrigerator conditions) - up to 41 days. In meat - up to 30 days. Continue boiling for 10 minutes or more. C. Burnetii are resistant to ultraviolet radiation, the effects of formalin, phenol, chlorine and other disinfectants, are sensitive to tetracycline antibiotics, chloramphenicol.

trusted-source[1], [2], [3], [4], [5]

Pathogenesis of ku-fever

Ku-fever is a cyclic benign rickettsial reticuloendotheliosis. In connection with the absence of tropism of the causative agent to the vascular endothelium, panvasculitis does not develop, therefore the rash and other symptoms of vascular lesions are not characteristic of the disease. Unlike other rickettsiosis, coxiella reproduce mainly in histiocytes and macrophages.

K.M. Loban et al. (2002) describe the pathogenesis of ku-fever in the form of a series of successive phases:

  • the introduction of rickettsia without reaction at the entrance gate;
  • lymphogenous and hematogenous dissemination of rickettsia (primary or "small" rickettsiaemia) with their introduction into macrophages and histiocytes;
  • reproduction of rickettsia in macrophages and histiocytes, the release of a large number of pathogens into the blood (repeated or "large" rickettsiemia);
  • Toxemia with the formation of secondary foci of infection in internal organs;
  • allergic restructuring and the formation of strained (with elimination of the pathogen and recovery) or relaxed (with repeated rickettsiemia and the development of protracted and chronic forms of the process) immunity.

The likelihood of prolonged, recurrent and chronic course of the disease with the development of endocarditis, interstitial pneumonia and prolonged persistence of the pathogen is an important feature of the pathogenesis of ku-fever. It can be caused by immune defects, such as incomplete phagocytosis of C. Burnetii and immunocomplex pathology with the defeat of various tissues and organs (heart, liver, joints).

Epidemiology of ku-fever

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

The reservoir of the pathogen in natural foci is ixodids, partially gamasaceous and argasid mites (more than seventy species), in which transfacial and transovarial rickettsia transfer are observed, as well as wild birds (47 species) and wild mammals - rickettsia carriers (more than eighty species). The existence of a persistent natural foci of infection contributes to the infection of various types of domestic animals (large and small cattle, horses, camels, dogs, donkeys, mules, poultry, etc.). They prolonged (up to two years) rickettsia into the environment with excrement, sputum, milk, amniotic fluid and can play the role of an independent reservoir of the pathogen in the anthropurgic foci of the disease.

Infection of a person with ku-fever in anthropurgic foci occurs in various ways:

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

It is possible for the transmissible pathway of infection (when attacking infected mites), which has no significant epidemiological significance.

A sick person can secrete S. burnetii with phlegm, but the source of infection is very rare; There are isolated cases of ku-fever among contact persons (infants, mothers who received milk, obstetricians, pathologists).

People of different ages are sensitive to fever fever, but men who engage in agricultural work, livestock, slaughter, processing of animal skins and fur, bird fluff, etc. Are more likely to suffer. As a result of the increasing influence of man on nature, natural foci have gone beyond the originally established " old "borders and formed anthropurgic foci with the participation of domestic animals. The disease, previously considered a disease of loggers, geologists, hunters, forestry and agriculture workers, has now become a disease of residents of large settlements and cities. Morbidity. Observed mainly in spring, summer and autumn, is sporadic in nature; occasional group flashes; more often find asymptomatic forms of infection. Repeated diseases are rare; postinfectious immunity resistant.

Sporadic cases and local outbreaks of fever are recorded on all continents. "White spots" for ku-fever on the geographical map is not much. Mandatory registration of diseases with fever in Ukraine was introduced in 1957. Currently, the incidence is low: about 500-600 cases of the disease are recorded annually.

trusted-source[6], [7], [8], [9]

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