Overview of clinical, diagnosis and therapy of borreliosis

The "tick season" is from April to October. People who work in such professions as forest rangers, forestry workers, gardeners or those who often spend their free time in the garden or in the outdoors. In Germany, approx.
10% of the nymphs (less than 2 mm in size) and 15% to 40% of the adult ticks contain borrelia. An infection results in 10% to 20% of all tick bites. The risk of infection is high whenever a tick can suck blood for a long period of time (> 24 hours) and the tick bite takes place in a region where there is a high incidence of borreliosis. Tick bites often go unnoticed especially through the bites of larvae or nymphs.

Borreliosis infections can develop without any symptoms (elimination of pathogens = spontaneous healing) or with symptoms (borreliosis In symptomatic infections, localised skin redness around the bite area (erythema migrans) occurs within 14 to 30 days in approx. 70% - 80% of all cases.

In 30% to 40% of all cases, the borreliosis remains latent until the infection reaches the dissemination stage. A borrelia infection does not leave the victim with any lasting immunity. Reinfections are therefore possible. A prophylactic vaccination is not yet available.

The pathogens in Europe are:

• Borrelia burgdorferi sensu stricto: mainly in arthritis
• Borrelia garinii: often symptoms in the area of the nervous system
• Borrelia afzelii: especially in skin symptoms which appear later

In Europe, the borrelia is transmitted by the genus Ixodes tick (Ixodes ricinus).

Erythema migrans begins to develop with a small red macular rash or papulation 7 to 40 days after the tick bite, which spreads along the edges within days to weeks and is often accompanied with local pruritis and a burning sensation. The edge of the 4 cm to 15 cm large erythema is usually emphasised.

In case the borreliosis is not eliminated spontaneously or continues to persist due to an insufficient antibiotic treatment of the erythema migrans or if no treatment took place, then the pathogen will disseminate into the body from the local point of infection (the bite). No erythema migrans was observed in 10% - 30% of the patients (the information in the literature varies) where the borreliosis disseminated early.

The symptoms usual began approx. 1 to 4 months after the tick bite.

General symptoms:
Influenza-like symptoms, fatigue, myalgia, arthralgia, headache, light fever, lymphoma, neck stiffness, back pain, lack of appetite

Skin symptoms:
Multiple erythema migrans;
borreliosis lymphocytoma (lymphadenosis benigna cutis): After 1 to 2 months after the infection: localised blueish-reddish papules of a soft, elastic consistency; often accompanied by regional lymphoma (often on the ear lobes, nipples, scrotum or nose)

Central nervous system symptoms:
Meningitis, cranial nerve disorders (often facialis paresis), meningoradiculitis (Bannwarth syndrome), acute enzephalomyelitis, cerebellitis, transverse myelitis

Heart symptoms:
Perimyocarditis, prominent, usually as AV block type I. - III.; rarely chronically inflammatory (dilated) cardiomyopathy

Joint symptoms:
Acute roaming arthralgia or volatile swollen joints ("episodic arthritis"), often monoarticular or asymmetric oligoarticular arthritis

Eye symptoms:
Iritis, uveitis, chorioiditis, episcleritis/scleritis, orbitale myositis, papillitis, retrobulbar neuritis

Diagnosis when disseminated borreliosis is suspected

anamnesis (tick bite?) is decisive for the diagnosis Erythema migrans? Risk behaviour?) and the current clinical picture!!

Laboratory diagnostics

1. Serological tests can facilitate creating the diagnosis, however, they do not guarantee anything. The IgG/IgM screening test is usually primarily performed. A positive screening test must be checked for an increased rate of false positive results in the immunoblot. Since 2011, serological proof of protein-specific antibodies can be obtained (analogue to the bands in the immunoblot by applying the Borrelia recomBead Test (Mikrogen).
   In case there is a contradiction between the clinical and serological findings (seronegative, unspecific reactions, questionable animal remains of an earlier infection), then applying cellular methods can be of aid.
2. The lymphocyte transformation test (LTT borrelia) (2)can be helpful especially if the serology is borderline or positive and if the clinical and anamnesis are uncertain (serum scar or active infection?).

It is in principle possible to cultivate proof of the pathogen (skin biopsy, fluid, blood); however, this has not acquired any significance in everyday practice (low sensitivity, high costs). Proof of the pathogen through specific DNA analysis (PCR - borrelia) can be beneficial, especially in joint punctates and biopsies (especially from the affected skin areas) as well as in fluid. Blood and urine are less suitable since false positive as well as false negative results can occur.

Recommended treatment:
At this point, refer to the current recommendations of the expert associations.

Monitoring therapy takes place primarily in the clinic. In case a failure in therapy is suspected or if there is a reinfection, then a lymphocyte transformation test for borrelia (LTT borrelia) is recommended as well as a new examination of a fluid-serum pair in the case of neuroborreliosis.

The symptoms begin approx 4 to 6 months up to several years after the initial infection. It is often difficult to match the polymorphic symptoms to a borrelia infection which took place a longer time ago.

The "acrodermatitis chronica atrophicans" (ACA) is a chronic inflammatory, partially oedematous process, usually found on areas of the skin exposed to the sun (usually the hands) The chronic inflammatory stage is followed by the chronic atrophic stage (parchment-like skin including typical histological findings). Attendant symptoms are hyperaesthesia, muscle weakness, muscle cramps, solitary or multiple fibrous papules, regional or general lymphoma.A chronic eye borreliosis shows symptoms of the corneal stroma clouding, marginal keratitis, episcleritis, ocular myositis, optic nerve atrophy.