Lyme Disease

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Retrieved

2021-01-23

Source

Orphanet

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Genes

CFH, TLR2, FHL1, HPLH1, CXCL13, POLD3, DCN, HLA-DRB1, PLG, HNRNPD, IFNG, EBPL, ELK3, NUP37, UBXN2B, CDK5R1, HSPD1, CCNH, NT5C2, CD8B, TNF, CDK5R2, CDCA5, ATP6V0D1, MLIP, IL6, CXCL8, IL10, PRH1, CPVL

CFH, TLR2, FHL1, HPLH1, CXCL13, POLD3, DCN, HLA-DRB1, PLG, HNRNPD, IFNG, EBPL, ELK3, NUP37, UBXN2B, CDK5R1, HSPD1, CCNH, NT5C2, CD8B, TNF, CDK5R2, CDCA5, ATP6V0D1, MLIP, IL6, CXCL8, IL10, PRH1, CPVL, IL17A, JUN, TLR1, LAMC2, RMRP, RHBDL2, PRH2, MNAT1, IL12A, ANXA1, NRSN1, FCN2, ERVK-19, CD14, UPK3B, AK6, ERVK-9, CSF2, ENO2, EPHA5, KARS1, FN1, VHLL, GCHFR, ABCC11, DCTN3, SENP6, SRRM2, BRD4, RHOBTB2, ERVK-24, PHB2, CD300A, CHP1, ERVK-11, TMED10P1, PPP1R14A, ERVK-25, TMED10, STIP1, PTGES3, IFNL1, SORBS1, IL23R, CAP1, PDLIM7, HACD1, H3P7, H3P17, IL37, R3HCC1L, ERVK-18, LINC01672, SQSTM1, ERVK-7, MAK16, ERVK-8, GOLPH3, SELENOK, RAB22A, FAM20C, PNO1, HLP, ERVK-10, H3P6, NELFCD, TLR8, TLR7, EXOSC1, ERVK-21, RBM45, IL22, NOP53, SGSM3, RBMS3, FOXP3, TGFB1, RNMT, IFNB1, HK1, HLA-A, HMGB1, IFIT3, IFNA1, IFNA13, IGH, FGF1, IL1B, IRF7, KRT10, LNPEP, CD180, MAZ, HIF1A, ENO1, MIP, CD48, CALR, CANX, CD1B, CD28, CD38, CD40, CD68, EEF1A1, CCR7, CRP, MAPK14, CTAA1, DAG1, DYNC1H1, MBL2, MMP1, AOC3, TPT1, ABCC8, TRBV20OR9-2, TFPI, BGN, TLR5, TNFRSF1A, TTN, CXCL11, TUFM, VCAM1, ARHGEF5, YBX3, BLZF1, RRP1, SRI, CCL19, MMP9, MAPK1, MMP13, MPZ, COX1, NFKB1, SERPINB6, PRF1, PTBP1, CCL2, PTGS1, PTGS2, RAB5A, RAD51, RRAS, S100A8, H3P29

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Lyme disease (named after the towns in the USA where the disease was first identified) is a bacterial infection caused by Borrelia burgdorferi.

Epidemiology

Incidence is variable and is estimated at 1-70/20,000 in Europe.

Clinical description

The clinical manifestations can be divided into three stages. Onset of the initial stage occurs between three days and one month after being bitten by an infected tick (generally the patient is aware of the bite) and is marked by erythema migrans, a characteristic cutaneous lesion that appears over time at various sites of the body. The second stage is characterized by dissemination to the central nervous system (resulting in facial paralysis, encephalitis etc.), joints, skin, heart and eye. The third (chronic) stage of the disease is characterized by joint, neurologic and cutaneous manifestations.

Etiology

The disease is transmitted to humans by bites from contaminated ticks (Ixodes) but rodents, birds and lizards are the main hosts.

Diagnostic methods

Diagnosis relies on recognition of the clinical picture during the initial stage of the disease, detection of Borrelia burgdorferi through analysis of cultures, PCR and detection of Borrelia burgdorferi DNA, or through elevations in antibody levels in patients in the second and third stages of the disease.

Prognosis

Treatment revolves around administration of antibiotics (amoxicillin and cyclines); with the treatment being more effective the earlier the antibiotics are administered. Prevention revolves around eradication of the ticks and on individuals taking protective measures against tick bites when visiting at-risk zones.