Presentation on theme: "Unit 4 Part 2 Lyme Disease Terry Kotrla, MS, MT(ASCP)BB."— Presentation transcript:
Unit 4 Part 2 Lyme Disease Terry Kotrla, MS, MT(ASCP)BB
Introduction Lyme disease was named in 1977 when arthritis was observed in a cluster of children in and around Lyme, CN Conditions suggested that this was an infectious disease probably transmitted by an arthropod Further investigation revealed that Lyme disease is caused by the bacterium
Causative Organism Borrelia burgdorferi Loosely coiled spirochete 8-20 micrometers Isolated from blood, CSF, skin lesions and joint fluid.
Vector Ixodes scapularis ticks are much smaller than common dog and cattle ticks Below adult female, adult male, nymph, and larva on a centimeter scale. Humans acquire disease from bite of nymphal or adult tick.
Vector Tick reservoir is the white footed mouse, white tail deer and dusky footed wood rat. For infection to occur tick must remain attached 24-48 hours. Peek feeding is late spring, early summer and fall.
Lyme Disease Symptoms The Lyme disease bacterium can infect several parts of the body, producing different symptoms at different times. Not all patients with Lyme disease will have all symptoms, and many of the symptoms can occur with other diseases as well.
Three Stages of Disease 1. Localized rash – erythema chronicum migrans 2. Dissemination to multiple organ systems 3. Chronic disseminated stage often with arthritic symptoms
Stage 1 Localized Rash First sign of infection usually a circular rash called erythema migrans or EM. Rash occurs in approximately 70-80% of infected persons. Begins at the site of a tick bite after a delay of 3-30 days. Distinctive feature of the rash is that it gradually expands over a period of several days, reaching up to 12 inches (30 cm) across. Center of the rash may clear as it enlarges, resulting in a bull's-eye appearance. May be warm but is not usually painful. Some patients develop additional EM lesions in other areas of the body after several days. Patients also experience symptoms of fatigue, chills, fever, headache, and muscle and joint aches, and swollen lymph nodes. In some cases, these may be the only symptoms of infection.
Stage 2 Dissemination Untreated, the infection may spread to other parts of the body within a few days to weeks after appearance of rash, producing an array of discrete symptoms. Neurologic Bell’s Palsy-loss of muscle tone on one or both sides of the face. Severe headaches and neck stiffness Musculoskeletal manifestations may include migratory joint, bone and muscle pains. Late disseminated Lyme disease is intermittent swelling and pain of one or a few joints. Cardiac include carditis and arrhythmia. Symptoms usually resolve without treatment.
Stage 3 Chronic Disseminated After several months 60% will develop chronic arthritis, severe joint pain and swelling. 5% of untreated develop neurological symtpoms. Shooting pains, numbness or tingling in the hands or feet. problems with concentration and short term memory.
Prognosis Lyme disease morbidity may be severe, chronic, and disabling. Rarely, if ever, fatal
Diagnosis Diagnosed clinically, confirmed serologically. Often appropriate to treat patients with early disease solely on the basis of objective signs and a known exposure. CDC recommends testing initially with a sensitive test first, ELISA or an IFA test, followed by testing with the more specific Western immunoblot (WB) test to corroborate equivocal or positive results obtained with the first test.
Diagnosis Serological tests are often falsely negative during early weeks. Antibodies to antigens of B. burgdorferi can be detected by IFA, ELISA and Western Blot.
Immune Response IgM antibodies develop against flagellar antigens. Antibody production peaks between 3 and 4th weeks of infection. IgG lags, not detectable until 4 to 6 weeks after erythema migrans.
Serology Patients with early disseminated or late- stage disease usually have strong serological reactivity Antibodies often persist for months or years following successfully treated or untreated infection. Seroreactivity alone cannot be used as a marker of active disease.
Problems with Serology IFA false positive may occur if patient has syphilis, relapsing fever or RA. IFA interpretation highly subjective EIA lacks sensitivity in early disease. EIA false positives with syphilis, other treponemes, IM and autoimmune disease.
Western Blot Must be used if the Lyme IgG/IgM antibody serology is equivocal or positive "Osp" refers to outer surface protein of the bacteria. "kDa" is the abbreviation for "kilodalton," which is used for molecular weight designations. Lyme antibodies of importance are against the following molecular weights of the B. burgdorferi antigens: 23-25 kDa (Osp C); 31 kDa (Osp A); 34 kDa (Osp B); 39 kDa; 41 kDa; and 83-93 kDa 7. 7
Lane 1, monoclonal antibodies defining selected antigens to B. burgdorferi Lane 2, human serum (IgG) reactive with the 10 antigens scored in the currently recommended criteria for blot scoring; lines indicate other calibrating antibodies. Molecular masses are in kilodaltons.
Treatment Single dose doxycycline shortly after tick bite. Lyme disease give doxycycline followed by amoxacillin Neuroborreliosis requires IV antibiotic therapy.