Borrelia afzelii is a species of spirochete bacteria belonging to the Borrelia burgdorferi sensu lato complex, which collectively causes Lyme borreliosis (Lyme disease). This bacterium is one of the primary causative agents of Lyme borreliosis in humans, especially outside of North America. Understanding this specific strain is important because the symptoms it causes often differ from those caused by other Borrelia species. The unique characteristics of B. afzelii influence its geographic spread, diagnosis, and necessary treatment protocols.
Geographic Distribution and Primary Vector
The distribution of Borrelia afzelii is concentrated across Eurasia, making it a dominant cause of Lyme borreliosis throughout Europe and Asia. In contrast, the United States sees the majority of Lyme cases caused by Borrelia burgdorferi sensu stricto. This geographical difference explains many of the clinical variations seen between Lyme disease cases on different continents.
The main vector for B. afzelii transmission throughout Europe is the sheep tick, Ixodes ricinus. In temperate regions of Asia, the related species Ixodes persulcatus takes on the role of the primary vector. These hard-bodied ticks acquire the bacteria from small mammal reservoirs, such as rodents, which are particularly effective at maintaining B. afzelii in the environment.
Transmission to humans occurs when an infected tick, often in its tiny nymphal stage, attaches and feeds unnoticed. While the exact duration required for transmission can vary, the risk generally increases the longer the tick remains attached. The prevalence of infected ticks and the density of tick populations are major factors influencing the human risk of infection in specific areas.
Unique Clinical Presentation
Borrelia afzelii demonstrates a strong preference for skin tissue, resulting in a distinct pattern of clinical manifestations. The earliest sign of infection is typically Erythema Migrans (EM), a circular or oval rash that expands outward from the site of the tick bite. This rash usually appears within a week or two of the bite and is generally neither painful nor itchy.
The most specific manifestation of B. afzelii infection is Acrodermatitis Chronica Atrophicans (ACA), a late-stage dermatological complication. ACA develops months or even years after the initial infection, establishing a chronic presence of the bacteria in the skin. It typically begins as an inflammatory phase, presenting as an ill-defined, bluish-red discoloration and swelling, often on the extremities like the hands, feet, or knees.
This inflammatory stage progresses into an atrophic phase, characterized by skin thinning until it resembles wrinkled, “tissue paper”. The affected skin loses its hair and sweat glands, and underlying blood vessels may become prominent. While ACA is strongly associated with B. afzelii, this bacterium can also cause Neuroborreliosis, which affects the nervous system, and musculoskeletal issues.
Diagnostic Challenges
Diagnosing B. afzelii infection relies heavily on serology, which detects the body’s antibody response to the bacteria, but this process presents several challenges. Standard testing involves a two-tiered approach, typically beginning with an Enzyme-Linked Immunosorbent Assay (ELISA) followed by a Western Blot (Immunoblot). Many US-developed tests are centered on antigens from B. burgdorferi sensu stricto, which may not effectively detect antibodies specific to B. afzelii.
Laboratories must utilize assays that incorporate antigens from B. afzelii and other Eurasian strains to prevent false-negative results. Serological tests are often negative in the very early stage of infection, such as when only Erythema Migrans is present, because the immune system has not yet produced sufficient antibodies. Conversely, antibodies can remain detectable for months or years after the infection has been successfully treated.
Polymerase Chain Reaction (PCR) is a direct detection method that finds the bacterial DNA, but its utility depends on the sample source. PCR is highly sensitive when performed on tissue from skin lesions like ACA or EM, where the bacteria are concentrated. However, its sensitivity is significantly lower when testing blood or cerebrospinal fluid (CSF), making it less reliable for diagnosing disseminated or neurological infection.
Standard Treatment Regimens
Treatment for Borrelia afzelii infection involves the use of specific antibiotics, with the choice and duration depending on the stage and severity of the disease. For early localized disease, such as a solitary Erythema Migrans rash, the first-line oral antibiotic is typically Doxycycline. Alternatives for those who cannot take Doxycycline, including young children and pregnant women, include Amoxicillin or certain macrolides like Azithromycin.
Treatment duration for early, localized infection is usually around 14 to 21 days. More advanced or late-stage manifestations, such as Acrodermatitis Chronica Atrophicans or Neuroborreliosis, require longer courses of antibiotics, often lasting 28 days or more. Disseminated disease or severe neurological involvement may necessitate intravenous antibiotics, such as Ceftriaxone, to ensure sufficient concentration reaches the affected tissues.
A common, temporary occurrence during the first 24 hours of antibiotic treatment for spirochete infections is the Jarisch-Herxheimer reaction (JHR). This reaction is an acute inflammatory response characterized by symptoms like fever, chills, headache, and an exacerbation of existing skin lesions. JHR is caused by the release of bacterial components and associated inflammatory cytokines as the spirochetes are rapidly killed by the medication.