Borrelia (Lyme Disease) & Leptospira

Here we will learn about infections caused by the non-Treponemal Spirochetes Borrelia and Leptospira, with a focus on Borrelia. Causes relapsing fever and Lyme disease Large, coiled Spirochete bacteria Microaerophilic Difficult to culture due to their complex nutritional needs and long generation times of 18 hours or more. Geimsa and Wright staining are used to visualize Borrelia, and light microscopy is used to identify the bacteria in blood. Multiple flagella, which provide motility. Proteins: – Variable membrane proteins allow the bacteria to adapt to new environments as they move from reservoirs to hosts. – Enable binding to host tissues, and even confer tissue tropism in some strains. – Some proteins provoke host immune responses, which are largely responsible for the damages caused by infection. For example, Borrelia lipoproteins trigger the release of inflammatory cytokines that damage host tissues. The bacteria, themselves, can often evade the host immune system. Antibiotic treatment of Borrelia infections is associated with Jarish-Herxheimer reaction. This reaction tends to exacerbate symptoms, initially, but is not usually fatal (we discuss it in more detail in our tutorial on Treponemal infections). Characterized by recurrent episodes of fever and septicemia, which are the result of bacterial proliferation. Borrelia membrane proteins undergo antigenic variation, which promotes cycling between bacteremia and clearance. Both types of relapsing fever are associated with extreme poverty and crowding. Diagnosed using light microscopy of blood smears; in the image, we can see an example of a Borrelia cell among host blood cells. Treatment includes: tetracycline or erythromycin; for patients with CNS involvement, penicillin is recommended. In response to bacteremia, host antibodies form and begin to clear the bacteria from the blood. Bacteremia recedes, and the host enters the afebrile stage. However, the bacteria are rapidly undergoing antigenic variation. These new variants evade host antibodies and proliferate in the host. Thus, the host enters a new febrile episode. Caused by Borrelia recurrentis Associated with more serious infections and higher mortality than tick-borne relapsing fever. Associated with epidemics, particularly in parts of Africa. Key vector = human body louse (Pediculus humanus) Reservoir = humans Transmission occurs when an infected body louse (or its feces) is crushed into openings in the skin; for example, when scratching or trauma creates abrasions. Characterized by 5 febrile episodes; each episode lasts 3-7 days. Febrile episodes are characterized by fever, chills, and headache, as well as joint and muscle pain, abdominal tenderness, jaundice, epistaxis, and thrombocytopenia. Some patients experience hepatic or cardiac failure, or cerebral hemorrhaging. Endemic in many areas, and is not usually fatal. Associated with several species of Borrelia. Vector = Soft ticks Key reservoirs = soft ticks and small vertebrates, especially rodents. Transmission is the result of infected tick bites. Characterized by 10 or more febrile episodes that last 3-7 days each. Most episodes of tick-borne relapsing fever are mild, and are characterized by fever, chills, and headaches; However, be aware that some species of Borrelia can cause more severe infections. Aka, Lyme borreliosis. Multi-system inflammatory disease Borrelia burdorferi is responsible for Lyme disease in the United States. Other Borrelia species, including Borellia garinii and Borellia afzelii, are responsible for Lyme disease in Europe and Central and Eastern Asia. Diagnosed using serology tests that measure IgM and IgG antibodies. Vectors = Various species of hard ticks, specifically black-legged Ixodes ticks. Transmission occurs during prolonged episodes of tick feeding. Key reservoirs = mice, deer, and pets. Early: Within 3-30 days of infection, localized erythema migrans. A centralized clearing in the lesion is common but not always present. They are characteristically large, red, and flat; the rash gradually expands to several centimeters in diameter. Treatment: Early Lyme disease is treated with doxycycline, amoxicillin, tetracycline, or cefuroxime. Late: Months or even years after untreated infection, late systemic manifestations may appear. These typically include re-appearance and spreading of erythema migrans, severe headache, neck stiffness, and arthritis, particularly of the knees and other large joints. Individuals can experience facial palsy, Lyme carditis, central nervous inflammation, nerve pain, numbness, and tingling. Treatment: Late symptoms are treated with intravenous penicillin or ceftriaxone. Some symptoms vary by the infecting species and geography. – For example, European Lyme disease is associated with acrodermatitis chronica atrophicans, which presents as red-blue bruise-like areas, typically on the extensor surfaces of the extremities. Over time, the tissues become fibrotic. More rarely, European Lyme disease is associated with lymphocytoma, which manifests as a reddish/bluish swelling, often on the earlobe. Spirochetes that reside within the kidneys of small mammals, especially rodents. The animals then shed the bacteria into the environment. Thus, water-sport athletes and industrial workers in contact with contaminated water, soil, or animals are at higher risk of infection. Mild leptospirosis produces flu-like symptoms and conjunctival suffusion. The most severe infections are associated with Weil disease, which is characterized by jaundice, vasculitis, and organ failure, particularly involving the liver and kidneys, which can be fatal. Image Credits: Borrelia (Centers for Disease Control; Public Health Image Library). Erythema migrans (Centers for Disease Control; Public Health Image Library).