Case. Uvei%s: Systemic and Ocular Approaches to Management. Ocular Health Assessment. Sarcoid Diagnosis. Diagnosis. Sarcoidosis Diagnosis 5/30/15

Transcription

1 Case Uvei%s: Systemic and Ocular Approaches to Management Blair B Lonsberry, MS, OD, MEd., FAAO Diplomate, American Board of Optometry Clinic Director and Professor of Optometry Pacific University College of Optometry blonsberry@pacificu.edu 30 BF presents with eye pain in both eyes for the past several days Severe pain (8/10) Never had eye exam before PMHx: Has chronic bronchi%s Rash on legs Has recently lost weight and has a fever Taking aspirin for pain Ocular Health Assessment Sarcoid Diagnosis VA: 20/30 OD, OS PERRL FTFC EOM s: FROM with eye pain in all quadrants SLE: 3+ injec%on, 3+ cells and trace flare, deposits on endo (see photo) IOP: 18, 18 mmhg DFE: sheathing of posterior pole vasculature, vitreal cells, and white fluffy deposits at ora. Lab Test CBC with differen%al Serum calcium/24 hour calcium Liver func%on tests ACE (angiotensin conver%ng enzyme) Pulmonary x- rays Findings Anemia/thrombocytopenia/leukopenia Hypercalcemia AST/ALT/BUN/Crea%nine elevated in hepa%c disease Elevated in 60% of pa%ents Hilar adenopathy Sarcoidosis Diagnosis CBC count with differential and platelets: leukopenia and/or thrombocytopenia are frequent findings. anemia occurs in 5% of patients. Serum calcium and 24-hour urine calcium levels: Hypercalcemia occurs in sarcoidosis due to increased intestinal absorption of calcium that results from overproduction of a metabolite of vitamin D by pulmonary macrophages. The serum angiotensin-converting enzyme (ACE) level: elevated in 60% of patients; therefore, this test is not sensitive in diagnosing sarcoidosis. Serum ACE levels are helpful in monitoring disease activity and treatment response. ACE is derived from epithelioid cells of the granulomas, therefore, it reflects granuloma load in the patient. Diagnosis Serum chemistries such as: alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase, BUN, and creatinine levels may be elevated with hepatic and renal involvement. Elevated liver function tests suggestive of hepatic dysfunction, elevated erythrocyte sedimentation rate, elevated anti-nuclear antibodies (30%), diabetes insipidus, and renal failure may be noted. 1

2 Diagnosis: Radiographic Diagnosis: Radiographic Radiographic involvement is seen in almost 90% of patients. Chest radiography is used in staging the disease: Stage I disease shows bilateral hilar lymphadenopathy (BHL). Stage II disease shows BHL plus pulmonary infiltrates. Stage III disease shows pulmonary infiltrates without BHL Stage IV disease shows pulmonary fibrosis. CT and MRI scans may be useful in finding granulomas in other organ systems Gallium scangallium 67 has been found to accumulate in active sarcoidal tissue Gallium Scan: Lacrimal/paro%d gland, Hilar glands Stages of Syphilis Syphilis Diagnosis Typical diagnosis is with blood tests using nontreponemal and/or treponemal tests. Nontreponemal test are used initially and include: venereal disease research laboratory (VDRL) The VDRL test checks for an an%body that can be produced in people who have syphilis. This an%body is not produced as a reac%on to the syphilis bacteria specifically, so this test is some%mes not accurate. and rapid plasma reagin (RPR) Syphilis Diagnosis confirmation is required with a treponemal test such as: treponemal pallidum particle agglutination (TPPA) or fluorescent treponemal antibody absorption test (FTA- Abs) The FTA- ABS test checks for an%bodies to the bacteria that cause syphilis and can be used to detect syphilis except during the first 3 to 4 weeks ader exposure to syphilis bacteria.. False positives on the nontreponemal tests can occur with some viral infections such as (varicella and measles), as well as with lymphoma, tuberculosis, malaria, endocarditis, connective tissue disease, pregnancy. Tuberculosis The main problem with tuberculosis diagnosis is the difficulty in culturing this slow-growing organism in the laboratory (it may take 4 to 12 weeks for blood or sputum culture). A complete medical evaluation for TB must include: a medical history, a physical examination, a chest X-ray, microbiological smears, and cultures. It may also include a tuberculin skin test, a serological test. The interpretation of the tuberculin skin test depends upon the person's risk factors for infection and progression to TB disease, such as exposure to other cases of TB or immunosuppression 2

3 Tuberculosis Currently, latent infection is diagnosed in a non-immunized person by a tuberculin skin test, which yields a delayed hypersensitivity type response to an extract made from M. tuberculosis. Those immunized for TB or with past-cleared infection will respond with delayed hypersensitivity parallel to those currently in a state of infection, so the test must be used with caution, particularly with regard to persons from countries where TB immunization is common Tuberculosis The newer interferon release assays (IGRAs) overcome many of these problems. IGRAs are in vitro blood tests that are more specific than the skin test. IGRAs detect the release of interferon gamma in response to mycobacterial proteins These are not affected by immunization or environmental mycobacteria, so generate fewer false positive results. Tuberculosis New TB tests have been developed that are fast and accurate. These include polymerase chain reaction assays for the detection of bacterial Another such test, which was approved by the FDA in 1996, is the amplified mycobacterium tuberculosis direct test (MTD, Gen-Probe). This test yields results in 2.5 to 3.5 hours, and it is highly sensitive and specific when used to test smears positive for acid-fast bacilli (AFB). Helpful Mnemonic Mnemonic for acute forms of non- granulomatous uvei%s: BLAIR G B: Behcet s disease L: Lyme disease A: Ankylosing spondili%s I: Irritable bowel syndrome (Crohns) R: Reac%ve arthri%s G: Glaucomatocycli%c crisis Classifica%on of Uvei%s! 4 main ques%ons we need answered! Where is the inflamma%on located?! Is disease acute or chronic?! Granulomatous or non- granulomatous?! Unilateral or bilateral? Classifica%on of Uvei%s Secondary Ques%ons: Demographics of the pa%ent Has this happened before? If so did it respond to treatment? Systemic ques%ons: Lung /breathing problems? Rashes/skin problems? Joint problems or low back pain? Urina%on issues? Diges%ve problems diarrhea? Bloody stools? Cramps? Have you been out of the country recently? Have you been in a wooded area? Ticks? Any other systemic/autoimmune diseases? 3

4 Classifica%on Classifica%on is the key to the proper diagnosis and management of the uvei%c pa%ent Most common classifica%ons Anterior vs. Intermediate vs. Posterior vs. Panuvei%s Acute vs. Chronic/Recurrent Granulomatous vs. Non- granulomatous Infec%ous vs. Autoimmune Anterior Uvei%s Classifica%on Acute, unilateral (or bilateral), non- granulomatous anterior uvei%s Idiopathic, HLA- B27, Herpe%c, Behcet s Chronic, bilateral (or unilateral), non- granulomatous anterior uvei%s JIA, Fuch s Heterochromic, Idiopathic, Herpe%c Chronic, bilateral (or unilateral), granulomatous anterior uvei%s TB, Sarcoid, Syphilis, VKH, Lyme, Wegeners Ocular Manifesta%ons- Uvei%s Ciliary Flush, Cells, Flare Signs/symptoms include: pain, photophobia, blurred vision, ciliary flush, cells/flare, rarely posterior involvement of Uvei%s Treat the disease properly Minimize complica%ons of the disease itself Minimize complica%ons of the treatment 2 main drugs/drops Cycloplegics Topical Cor%costeroids Cycloplegia: used for reduc%on of pain, break/prevent the forma%on of posterior synechiae also func%ons in the reduc%on of inflamma%on 4

5 Cycloplegics Common cycloplegic agents include: cyclopentolate 1-2% %d for mild- to- moderate, homatropine 5% or scopolamine 0.25% or atropine 1% bid- %d for moderate- to- severe inflamma%on most common is the use of Homatropine 5% bid be careful using atropine as there is poten%al for severe systemic side effects Also makes the iris essen%ally immobile Uvei%s: Classical treatment : Pred forte: every 1-2 hours, ensure taper Pred forte: prednisolone acetate formula%on which allows penetra%on through cornea to anterior chamber Newer treatment op%on: Durezol Steroids: necessary for the treatment of ac%ve inflamma%on Most common is the use of prednisolone acetate 1% (e.g. Pred Forte 1%) Phosphate form - > does not penetrate cornea well Steroid medica%on that is felt to have less IOP response and report to not need as long of a taper is loteprednol etabonate (Lotemax) op%ons Durezol: Difluprednate only difluorinated steroid Steroid emulsion BAK free Increased potency so dosing needs to be less than classical treatment with Pred Forte rough recommenda%on is 1/2 dosing of Pred Forte Topical administra%on is most common though periocular injec%ons and systemic meds are useful for posterior uvei%s and difficult cases Dosing is dependent upon severity of the inflamma%on typically you want to hit the uvei%s hard and fast! E.g 1 gq q 2hrs un%l the inflamma%on is gone! If you have a minimal anterior chamber reac%on then steroid may not be necessary at all NOTE: it is crucial to taper your steroid treatment! You will have a rebound inflamma%on if you simply remove your pa%ent from their steroids The taper will be dependent upon how long you have had them on the steroid to get rid of the inflamma%on! Typically, a slow taper is beqer in order to prevent rebound inflamma%on If the pa%ent has been on the steroid for less than a week a faster taper can be considered. 5

6 NSAIDs: do not play an important role in the treatment of an acute uvei%s may be used in the treatment of a chronic uvei%s such as in a JRA pa%ent who is using NSAIDs for the treatment of systemic pain. : Addi%onal Therapies Immunosuppressive agents (cytotoxic) reserved for sight- threatening uvei%s that have not responded to conven%onal treatment e.g. cyclophosphamide An%metabolites (e.g. methotrexate) have been found useful in JRA related iridocycli%s and scleromalacia Cyclosporin has a very specific effect on the immune system and has been found useful in posterior and intermediate uvei%s Follow- up Every 1-7 days in acute phase depending upon severity and every 1-6 months when stable. On each f/u visit the AC reac%on and IOP should be evaluated DFE should be performed for flare- ups, when VA affected, or every 3-6 months. Follow Up If AC reac%on improving, then steroid drops can be slowly tapered. cycloplegia can also be tapered as the AC reac%on improves. slow taper recommended for chronic granulomatous uvei%s. Rules For Managing Uvei%s 1. Remember the classifica%ons. 2. Determine if there is corneal involvement & check IOP. 3. Determine the severity. 4. Is this a chronic problem? 5. Treat strongly. Case 23 WM Eye pain OD Severe, started 2 days ago Photophobia and redness POHx: Had similar problem and was given drops and felt beqer PMHx: Told to get back into shape and to reduce stress Meds: Ibuprofen for lower back pain 6

7 Assessment VA: 20/20-, 20/20+ Entrance skills unremarkable SLE: OD: 2+ injec%on, 2+ cell, Mild flare, Fine deposits IOP: 18, 14 mm HG DFE: unremarkable HLA- B27 CONDITIONS Ankylosing Spondyli%s Ankylosing spondyli%s is a type of arthri%s that affects the spine: symptoms include pain and s%ffness from the neck down to the lower back. The vertebrae may grow or fuse together, resul%ng in a rigid spine. these changes may be mild or severe, and may lead to a stooped- over posture. Ankylosing Spondyli%s Ankylosing spondyli%s affects about 0.1% to 0.5% of the adult popula%on. Although it can occur at any age, spondyli%s most oden affects men in their 20s and 30s. It is less common and generally milder in women and most common in Na%ve Americans. Early diagnosis and treatment helps control pain and s%ffness and may reduce or prevent significant deformity. Ankylosing Spondyli%s Ankylosing Spondyli%s Physical Exam: The overall points taken into account when making an AS diagnosis are: Onset is usually under 35 years of age. Pain persists for more than 3 months (i.e. it is chronic). The back pain and s%ffness worsen with immobility, especially at night and early morning. The back pain and s%ffness tend to ease with physical ac%vity and exercise. Posi%ve response to NSAIDs (nonsteroidal an%- inflammatory drugs). X- rays: The hallmark of AS is involvement of the sacroiliac (SI) joint show erosion typical of sacroilii%s (inflamma%on of the sacroiliac joints). can take 7 to 10 years of disease progression for the changes in the SI joints to be serious enough to show up in conven%onal x- rays. Pre- Surgery Post- Surgery 7

8 Ankylosing Spondyli%s HLA- B27 tes%ng: Generally speaking, no more than 2% of people born with this gene will eventually get spondyli%s it is important to note that the HLA- B27 test is not a diagnos%c test for AS the associa%on between AS and HLA- B27 varies in different ethnic and racial groups. over 95% of people in the caucasion popula%on who have AS test HLA- B27 posi%ve. only 50% of African American pa%ents with AS possess HLA- B27 close to 80% among AS pa%ents from Mediterranean countries. Ankylosing Spondyli%s : A common treatment regimen involves: Medica%on (NSAIDs, Methotrexate, An%- TNF), exercise and possibly physical therapy, good posture prac%ces, applying heat/cold to help relax muscles and reduce joint pain. In severe cases surgery may also be an op%on. Psoria%c Arthri%s Psoriasis is a scaly rash that occurs most frequently on the elbows, knees and scalp, but can cover much of the body. It is a chronic, inflammatory disease of the skin, scalp, nails and joints. A normal skin cell matures and falls off the body's surface in 28 to 30 days, but a psoria%c skin cell takes only three to four days to mature and gathers at the surface, thus forming lesions. Psoria%c Arthri%s In 5-10% of those with psoriasis, arthri%s also appears. In most cases the psoriasis will precede the arthri%s, some%mes by many years. When arthri%s symptoms occur with psoriasis, it is called psoria%c arthri%s (PsA). the joints at the end of the fingers are most commonly affected causing inflamma%on and pain, but other joints like the wrists, knees and ankles can also become involved. usually accompanied by symptoms of the fingernails and toes, ranging from small pits in the nails to nearly complete destruc%on and crumbling as seen in reac%ve arthri%s or fungal infec%ons. Psoria%c Arthri%s About 20% of people who develop PsA will eventually have spinal involvement, which is called psoria%c spondyli%s. The inflamma%on in the spine can lead to complete fusion - as in ankylosing spondyli%s - or skip areas where, for example, only the lower back and neck are involved. Those with spinal involvement are most likely to test posi%ve for the HLA- B27 gene%c marker. Up to 40% of people with PsA have a close rela%ve with the disease, and if an iden%cal twin has it, there is a 75% chance that the other twin will have PsA as well. Psoria%c Arthri%s for psoriasis remains suppressive, rather than cura%ve. of ar%cular manifesta%ons generally begins with non- steroidal an%- inflammatory agents (NSAIDs). In pa%ents with aggressive and poten%ally destruc%ve disease, disease- modifying an%- rheuma%c drugs (DMARDs) should be added early on in the course (Methotrexate, TNF- blockers, an%- malarials). 8

9 Reac%ve Arthri%s (also known as Reiter's Syndrome) is a form of arthri%s that can cause inflamma%on and pain in the: joints, the skin, the eyes, the bladder, the genitals and the mucus membranes. Reac%ve arthri%s is thought to occur as a "reac%on" to an infec%on that started elsewhere in the body, generally in the genitourinary or gastrointes%nal tract. Reac%ve Arthri%s Reac%ve Arthri%s Reac%ve arthri%s occurs ader exposure / infec%on caused by certain types of bacteria. These include: Chlamydia, a bacterium contracted during sexually ac%vity, which causes either burning urina%on or watery discharge from the penis or vagina. Bacteria such as Salmonella, Shigella, Yersinia or Campylobacter, which cause dysentery (diarrhea, abdominal pain, vomi%ng, fever). Exposure to these bacteria occurs ader ea%ng spoiled or contaminated food. Not everyone exposed to these bacteria will contract ReA. Those who go on to develop ReA tend to test posi%ve for the HLA- B27 gene%c marker, although other gene%c factors may be involved. Thus, it is an interac%on between an individual's gene%c make- up and the ini%al infec%on that causes Reac%ve Arthri%s. Reac%ve Arthri%s ReA usually develops 2-4 weeks ader the infec%on. A tendency exists for more severe and long- term disease in pa%ents who do test posi%ve for HLA- B27 as well as those who have a family history of the disease. Reac%ve Arthri%s typically follows a limited course, where symptoms subsiding in 3-12 months. However, the condi%on has a tendency to recur. About 15-20% of people with ReA develop a chronic, and some%mes severe, arthri%s or spondyli%s. Reac%ve Arthri%s of reac%ve arthri%s is based on where it has become manifest in the body. For joint inflamma%on, pa%ents are generally ini%ally treated with NSAIDs. prednisone is used in the short- term treatment of inflamma%on in reac%ve arthri%s for the aggressive inflamma%on of chronic joint inflamma%on medica%ons that suppress the immune system such as methotrexate ReA Conjunc%vi%s Enteropathic Arthri%s Eye involvement occurs in about 50% of men with urogenital reac%ve arthri%s and about 75% of men with enteric reac%ve arthri%s. Conjunc%vi%s and uvei%s can include redness of the eyes, eye pain and irrita%on, or blurred vision. Eye involvement typically occurs early in the course of reac%ve arthri%s, and symptoms may come and go includes NSAIDs and/or steroids Enteropathic arthri%s is a form of chronic, inflammatory arthri%s associated with the occurrence of an inflammatory bowel disease (IBD): the two best- known types of which are ulcera%ve coli%s and Crohn's disease. About one in five people with Crohn's or ulcera%ve coli%s will develop enteropathic arthri%s. The most common areas affected by enteropathic arthri%s are inflamma%on of the peripheral (limb) joints, as well as the abdominal pain and possibly bloody diarrhea associated with the IBD component of the disease. In some cases, the en%re spine can become involved as well. 9

10 Enteropathic Arthri%s The course and severity of enteropathic arthri%s varies from person to person. The disease "flares" - the %mes when the disease is most ac%ve and inflamma%on is occurring - tend to be self- limi%ng, oden subsiding ader 6 weeks, but reoccurrences are common. In some cases the arthri%s may become chronic and destruc%ve. A common treatment regimen for all the spondyloarthropathies (ankylosing spondyli%s, reac%ve arthri%s, psoria%c arthri%s, enteropathic arthri%s, and undifferen%ated spondyloarthropathy) involves medica%on, exercise and possibly physical therapy, good posture prac%ces, and other treatment op%ons such as applying heat/cold to help relax muscles and reduce joint pain. In severe cases of ankylosing spondyli%s, surgery may also be an op%on. Medica%on NSAIDs (nonsteroidal an%- inflammatory drugs) are s%ll the cornerstone of treatment and the first stage of medica%on in trea%ng the pain and s%ffness associated with spondyli%s. However, NSAIDs can cause significant side effects, in par%cular, damage to the gastrointes%nal tract. When NSAIDs are not enough, the next stage of medica%ons, (also known as second line medica%ons), are some%mes called disease modifying an%- rheuma%c drugs (DMARDS). This group of medica%ons include: Sulfasalazine, Methotrexate and Cor%costeroids. Medica%on The most recent and most promising medica%ons for trea%ng ankylosing spondyli%s are the biologics, or TNF Blockers. These drugs have been shown to be highly effec%ve in trea%ng not only the arthri%s of the joints, but also the spinal arthri%s. Included in this group are Enbrel, Remicade, Humira and Simponi References Spondyli%s Associa%on of America hqp:// Juvenile Idiopathic Arthri%s 10

11 Juvenile Rheumatoid Idiopathic Arthri%s (JRA/JIA) Rheumatoid like disease with onset before age 17 Group of arthri%des responsible for significant func%onal loss in children Most common chronic disease with gene%c predisposi%on in children. 2:1 female:male, with peak incidence b/w 2-4 and then Natural History Pathogenesis unknown Immune- mediated ac%vity directed towards Type II collagen RF mediated responses rarely found 1 o involves weight bearing joints of lower extremi%es (knees/ankles) as well as joints of elbows/hands Liqle associated pain/tenderness observed Diagnosis Synovi%s that persists for at least 6 weeks is the essen%al criterion for diagnosis. Hematologic and radiographic studies are beneficial in diagnosis and classifica%on. Fewer than 20% of pa%ents have posi%ve RF Radiographic evalua%on of inflamed joints reveal sod %ssue swelling and peri- ar%cular osteoporosis with possible new bone forma%on. Loss of the car%laginous space with erosions occur ader long dura%on. and Management- Systemic Primary goal is to control pathologic changes in ar%cular %ssues Typically runs self limi%ng course medical therapy needed only when persistent arthri%s warrants Tx. ASA plays significant role in Tx in conjunc%on with exercise. NSAIDs have gained popularity and a few are approved for JIA. Dose dependent on body mass (e.g. indomethacin 1-3mg/kg/day TID) and Management- Systemic An%malarial not used as frequently as in RA efficacy is good but toxicity a concern when used they are limited to a 2 year course at 5-7 mg/kg/day. Use of gold salts common when arthri%s not responding to ASA or NSAIDs. Immunosuppressive reserved for life threatening cases or cases unresponsive to other conserva%ve therapies. Proper DX and TX results in recovery in about 85% cases Ocular Manifesta%ons Classic triad of iridocycli%s, cataract and band keratopathy Overall incidence of iridocycli%s is apprx 20%. Cataract, glaucoma, and band keratopathy are seen in 50% of pa%ents who develop persistent iridocycli%s. 11

12 Ciliary Flush, Cells, Flare Ocular Manifesta%ons " Severe vision loss results primarily from cataract forma%on and less frequently from band keratopathy. " Insidious onset of ocular involvement, with the iridocycli%s commonly following the arthri%s symptoms (though occasionally preceding) " Pa%ents are oden asymptoma%c and therefore require ocular evalua%on for detec%on Ocular Manifesta%ons Evidence of chronic iridocycli%s may be presen%ng sign leading to Dx of JIA Posterior segment involvement is not commonly seen Band keratopathy in children <16 is pathognomonic for JIA results from aggressive/chronic ocular inflamma%on (not abnormal calcium metabolism). JIA pa%ents do not present with the dry eye and K sicca manifesta%ons that are so prevalent in RA. and Management- Ocular Systemic medical therapy has minimal effect on ocular inflamma%on Topical steroids and short ac%ng cycloplegics remain primary treatment Decreased VA 2 o to cataract requiring extrac%on Band keratopathy develops in eyes with chronic iridocycli%s and require treatment with chela%ng agents Pa%ents who develop glaucoma need to be treated aggressively What is Lyme disease? Most common tick/insect-borne disease in the U.S. A disease that can cause skin, joint, heart and nervous system problems. Lyme disease can affect people of all ages. Named after the town of Lyme, Connecticut where it was first described in What causes Lyme disease? Caused by a specialized type of bacteria called spirochete. Transmitted by the bite of an infected tick or flea. Other insects that feed on animal blood may be involved. 12

13 Ticks that cause Lyme disease Ticks that cause Lyme disease Black-legged (or deer) tick: Transmits Lyme disease to humans. Found in north-central and northeastern U.S. Lone star tick: Found in Texas and has been know to transmit Lyme disease. Rocky Mountain tick: Can transmit Lyme disease as well as Rocky Mountain spotted fever. Black-legged Tick Rocky Mountain Tick Lone Star Tick Lyme Disease: Signs and Symptoms Two stages of Lyme disease: Stage 1 (Early stage) 3 to 30 days after bite. Flu-like symptoms develop within 7 14 days. Symptoms include fatigue, headache, fever and chills, muscle and joint pain, nausea, vomiting, dizziness and, a non-productive cough. Skin lesion(s) may appear as a small red circular rash around the bite and expand. Secondary skin rashes appear in nearly 80% of individuals with Lyme disease. Lyme Disease Skin Rash Multiple Erythema Migrans (Skin rash) Lyme Disease: Signs and Symptoms Two stages of Lyme disease: Stage II (Late) May occur weeks or months after the onset of Lyme disease. Severe headache and neck pain or stiffness. Arthritis will develop in 60% of patients weeks or months after infection (rarely more than 2 years). Fifteen percent of people infected with Lyme disease develop neurological symptoms, including psychiatric problems. Post- Lyme Disease Syndrome (PTLDS) Approximately 10-20% of pa%ents have symptoms that last months to years ader treatment with an%bio%cs. These symptoms can include muscle and joint pains, cogni%ve difficul%es, sleep disturbances, or fa%gue. The cause of these symptoms is not known, and, according to current research, these symptoms are not due to ongoing infec%on with B. burgdorferi. This condi%on is referred to as Post- treatment Lyme disease syndrome (PTLDS). There is some evidence that PTLDS is caused by an autoimmune response, in which a person's immune system con%nues to respond, doing damage to the body s %ssues, even ader the infec%on has been cleared. Studies have shown that con%nuing an%bio%c therapy is not helpful and can be harmful for persons with PTLDS. 13

14 Diagnosing Lyme Disease CDC currently recommends a two- step process when tes%ng blood for evidence of an%bodies against the Lyme disease bacteria. The first step uses a tes%ng procedure called EIA (enzyme immunoassay) or rarely, an IFA (indirect immunofluorescence assay). If this first step is nega%ve, no further tes%ng of the specimen is recommended. If the first step is posi%ve or indeterminate, the second step should be performed. The second step uses a test called an immunoblot test, commonly, a Western blot test. Results are considered posi%ve only if the EIA/IFA and the immunoblot are both posi%ve. Pa%ents treated with appropriate an%bio%cs in the early stages of Lyme disease usually recover rapidly and completely. An%bio%cs commonly used for oral treatment include doxycycline, amoxicillin, or cefuroxime axe%l. Pa%ents with certain neurological or cardiac forms of illness may require intravenous treatment with drugs such as cedriaxone or penicillin. 14