Coxiella antibodies

There Coxiella burnetii, commonly called Coxiella, is a gram negative bacterium responsible for Q fever, which is transmitted through ticks and can be transmitted by both domestic and farm animals, as well as wild animals. The diagnosis is made with the dosage of anti-Coxiella antibodies.

The infection in humans occurs through the passage of bacterial spores with the inhalation of small aerosol contaminated droplets with contact with feces, urine and milk of infected animals.

The germ of the Coxiella it is the causative agent responsible for Q fever, which is a disease that manifests itself with muscle pain myalgia headache headache nausea and vomiting fever often above 38 degrees, all often accompanied by skin rash. In the most serious cases, there may be lung colonization, as well as an involvement of the serosa such as endocardium, giving endocarditis even many months or years after contact with Coxiella. Finally, the Coxiellae can nest in the liver parenchyma causing hepatitis. The diagnosis of Q fever occurs with the assay of anti Coxiella antibodies as well as with the isolation of bacterial DNA through molecular diagnosis.

The anti Coxiella antibodies they are considered positive and diagnostic of Coxiella burneti infection when present with an antibody titre greater than 1:80, with a titre increase of two dilutions, as well as in cases of seronegative to seropositive seroconversion.

The most common and less expensive test is the anti-Coxiella antibody assay carried out through a complement fixation reaction (now little used), while the indirect immunofluorescence reaction and ELISA method are currently often used.

The complement fixation reaction technique allows to search for phase II (avirulent) and phase I (virulent) antibodies. The drawbacks are represented by a late positivization (10-15 days from the onset of the disease), by false negatives due to the phenomenon of prozone.

The indirect immunofluorescence reaction and ELISA method: it is currently more reliable and complete, studies IgG, IgM and IgA and, carried out correctly (elimination of the rheumatoid factor, etc.), allows the diagnosis of acute and chronic forms on a blood sample only.

In acute forms, IgM-phase II appears around the 10th day, reaches its maximum (> 400) around the 4th week and disappears around the 4th month.

IgM-phase I appear a little later and have lower titers than IgM phase II.

IgG-phase II appear early after IgM and persist at a high titer for several years. IgG-phase I have a late onset, with much lower titers than the analogous phase II. IgA-phase II is early and inconsistent. There are no IgA-phase I. In the course of endocarditis, very high titers (IF> 800; FC> 200) of IgGphase I and II, presence of IgA-phase I and II, sometimes fluctuating, are detected. IgMs are inconsistent.


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