no symptom no testing- no dog to human lyme in fla vaccine?

Issues involving physical examinations and testing. Questions, answers, theories, and evidence.
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no symptom no testing- no dog to human lyme in fla vaccine?

Postby guest » Fri Oct 31, 2003 8:18 pm

AVMA journal
November 1, 2003 (Volume 223, No. 9)
Zoonosis Update
Lyme borreliosis
Curtis L. Fritz, DVM, MPVM, PhD, DACVPM, and Anne M. Kjemtrup, DVM, MPVM, PhD *


   In 1982, the Centers for Disease Control and Prevention (CDC) initiated surveillance for Lyme borreliosis in humans in the United States. In 1991, the Council of State and Territorial Epidemiologists adopted a standardized surveillance case definition and added Lyme borreliosis to the list of nationally notifiable diseases. In 2000, 17,730 cases of Lyme borreliosis were reported nationwide.59

    Risk of infection with B burgdorferi is correlated with the opportunity of being bitten by an infected tick and dependent on the density of vector ticks in an endemic area, the proportion of ticks infected, and the duration and nature of the susceptible host’s activities in that area. Most cases of Lyme borreliosis are believed to be acquired from the bites of nymphal ticks, which are most abundant in the late spring and early summer. In 1 study,65 > 50% of humans reported to have Lyme borreliosis in an endemic county of New York experienced onset of illness in June or July.

Dogs and horses that have ongoing access to densely vegetated areas near their home (peridomestic exposure) or occasional recreational access to these same areas are at equal or greater risk of becoming infected, compared with humans.68

Signs and Symptoms

   Humans—The signs and symptoms of Lyme borreliosis in humans are commonly categorized as early localized, early disseminated, or late disseminated manifestations.69,70 Early localized Lyme borreliosis is synonymous with erythema migrans, which is a red, expanding rash that occurs 1 to 36 days following a bite from an infected tick.71 Erythema migrans appears most often at the site of the tick bite, expands over the course of several days, often clears centrally, and resolves spontaneously without specific treatment. Nonspecific flu-like symptoms such as fever, headache, fatigue, and muscle and joint pain often accompany or follow erythema migrans. As the erythema migrans resolves, spirochetes complete their migration through the skin and enter other organ systems, where they cause symptoms referable to the tissues invaded. Objective manifestations associated with early disseminated Lyme borreliosis include meningitis and cranial nerve deficits (most commonly a unilateral facial nerve palsy)72 and atrioventricular conduction deficits.73 If not treated, the disease will progress in some patients to late disseminated symptoms, characterized by large joint oligoarthritis74 and central nervous dysfunction, commonly encephalopathy and radiculopathies.75

   Dogs—Surveillance studies have detected serologic evidence of exposure to B burgdorferi in a variable but large percentage (25 to 90%) of dogs in endemic areas.76-80 However, not all infected dogs will develop clinical signs of Lyme borreliosis, and younger dogs are more likely to do so than older dogs.81 Furthermore, dogs appear to lack the spectrum of clinical signs reported in humans with Lyme borreliosis, despite occasionally extensive systemic dissemination of spirochetes.82 The clinical manifestations of Lyme borreliosis in dogs have been previously reviewed.83 Briefly, 2 to 5 months after being infected with B burgdorferi, dogs most commonly develop lameness, frequently with accompanying fever and anorexia.81 Arthritis is usually evident and confined to a single joint, most commonly the carpus or tarsus. In dogs experimentally infected by a single inoculation of B burgdorferi, arthritis was self-limited, although recurrent episodes of 3 to 6 days’ duration occurred for up to several weeks.81,84 The potential for progression and persistence of arthritis in naturally or repeatedly exposed dogs is not as well described. A distinctive renal syndrome attributed to B burgdorferi infection in dogs has been described.85,86 Renal manifestations of Lyme borreliosis are histologically characterized by glomerulonephritis, tubular necrosis, and interstitial lymphoplasmacytic inflammation that are associated with a rapidly progressive and frequently fatal glomerular disease. Although B burgdorferi spirochetes have been identified in renal tissue,86 the pathogenesis of B burgdorferi-associated renal disease is not well understood. In some dogs, CNS dysfunction87,88 and heart block secondary to myocarditis89 have been attributed to B burgdorferi infection.

   Other domestic animals—Parasitism by infected Ixodes spp and detection of antibody against B burgdorferi have been reported in cats,96 but the clinical significance of exposure to B burgdorferi among cats is uncertain. In 1 study in a Lyme borreliosis-endemic area,96 high titers to B burgdorferi were detected in cats with joint lameness; however, the proportion of cats with antibodies against B burgdorferi did not differ between cats with lameness only and cats with non-specific febrile illness.

   Serologic evidence of B burgdorferi infection has been detected in large and small domestic ruminants,97,98 but it remains undetermined whether the organism causes clinical disease in these species. Detection of antibody against B burgdorferi in serum or synovial fluid was associated with lameness and joint swelling among cattle in an endemic region.99,100 Attempts to experimentally infect cattle with B burgdorferi suggest they have a low susceptibility.101


   Diagnosis of Lyme borreliosis can be made on the basis of history of exposure to Ixodes ticks in an endemic area, compatible clinical signs, laboratory evidence of infection, consideration and exclusion of other diseases, and, possibly, response to antimicrobial treatment.83,102 Laboratory results alone are not prima facie evidence of infection but must be interpreted with regard to the pretest probability of the disease existing in the patient.103,104 Establishing the prior probability of Lyme borreliosis is particularly important for species such as dogs that lack a pathognomonic sign of infection like the erythema migrans rash in humans.

   Given the fastidious growth requirements of B burgdorferi, attempts to culture spirochetes from blood or other tissues are difficult and most often unrewarding. Thus, most commercially available clinical laboratory tests rely on detection of antibodies in serum. Serologic assays for IgM, IgG, or combined immunoglobulin against B burgdorferi are available through most commercial laboratories. The sensitivity of serologic assays is directly dependent on the kinetics of the immunologic response following infection. In humans, serum concentration of IgM against B burgdorferi increases within 2 to 3 weeks of infection, peaks around 3 to 6 weeks, and then gradually decreases.105 Changes in serum IgG concentration lag that of IgM; IgG concentration begins to increase 4 to 6 weeks after infection, peaks at 6 to 8 weeks or later, and remains high for months to years.6 In most or all dogs, IgG seroconversion occurs prior to onset of clinical signs, usually within 4 to 6 weeks after exposure.81,102

   Enzyme immunoassays (EIAs) and immunofluorescent assays (IFAs) are the most commonly available serologic tests; however, despite their high sensitivity, these tests generally have poor specificity.104 Unstandardized and variable procedures for manufacture and validation of commercial test kits further reduce the reliability of these assays.106,107 In a laboratory proficiency study108 in which seroimmunologic tests for 14 different pathogens were evaluated, assays for B burgdorferi antibody had the poorest correlation between reference and nonreference laboratories. To improve test reliability for human patients, the CDC currently recommends a 2-step serodiagnostic strategy: an initial EIA or IFA, with specimens that yield positive or equivocal results for B burgdorferi further tested by western immunoblotting for IgM or IgG antibody, whichever is appropriate for the patient’s stage of illness.109

   In dogs, the immunoblot band pattern does not merely enhance test reliability but provides indispensable information to differentiate serologic responses induced by natural infection with B burgdorferi from those produced by vaccination.77 Dogs that are vaccinated react most strongly to spirochetal proteins in the 31- to 34-kd range that correspond approximately to the Osp A , whereas naturally infected dogs show minimal reactivity to these proteins.110,111 Dogs and humans that are naturally exposed have a broad immunologic response to numerous B burgdorferi proteins between 15 and 100 kd; the number of immunoblot bands tends to increase with the progression of the disease.102,112-114 Although uniform interpretation criteria for immunoblots have been determined for diagnosis of Lyme borreliosis in humans,109,115 various strategies have been proposed for sera from dogs,102,110,116 but scientific consensus has not been reached.

   Recently, an EIA test kit became commercially available for in-office diagnosis of Lyme borreliosis in dogs.a This assay uses a synthetic peptide, C6, as the antigen; this peptide is based on the sixth invariable region (IR6) in the VlsE Osp of B burgdorferi.117 The IR6 is greatly conserved among B burgdorferi strains and highly immunogenic in dogs.24 Although this assay shows promise,118,119 field studies that have validated its performance in large numbers of clinically well-characterized dogs have yet to be reported.

   Detection of antibody against B burgdorferi is not definitive evidence of active or incipient Lyme borreliosis nor an indication of the need for treatment.78 Serologically detectable anti-B burgdorferi IgG may persist for months, years, or indefinitely following infection and resolution of clinical disease.79,120 For this reason, although serologic screening of scientifically selected populations may yield useful epidemiologic information, it is generally uninformative for clinically normal individuals (eg, those with a recognized tick bite that have no clinical signs of illness). In highly endemic areas where dogs may be regularly bitten by infected ticks, serologic testing cannot differentiate between dogs with active Lyme borreliosis and those with persistent antibodies from an earlier exposure. One study79 found that the prevalences of serum antibody against B burgdorferi did not differ between healthy dogs (89.6% seropositive) and those with joint or limb disorders compatible with Lyme borreliosis (92.9% seropositive). Serodiagnostic testing should be reserved for dogs with a history and clinical presentation that are highly suggestive of active Lyme borreliosis.


   Although erythema migrans resolves spontaneously in most humans with Lyme borreliosis,121 the potential for symptoms to progress from mild flu-like illness to severe neurologic or arthritic disease underscores the need for prompt recognition and appropriate treatment. Even before the bacterial cause of Lyme borreliosis was confirmed, antimicrobials were observed to improve the outcome during all stages of disease.122 Numerous clinical trials and case series have demonstrated the efficacy of oral administration of doxycycline or amoxicillin for 14 to 21 days for the treatment of eyrthema migrans and other early symptoms.122-127 Uncomplicated arthritis associated with Lyme borreliosis can be successfully treated with oral or IV administration of doxycycline or amoxicillin for 28 days.128 Intravenous administration of ceftriaxone for 14 to 28 days is recommended for patients with any neurologic manifestations.129-131 Response to treatment may be slow and inversely correlated with duration and severity of symptoms.

   As in humans with Lyme borreliosis, antimicrobial treatment in dogs can accelerate clinical resolution and reduce the chance of recrudescent Lyme borreliosis. Following experimental inoculation of dogs with B burgdorferi, spirochetes were repeatedly cultured from skin biopsy specimens prior to treatment; after 30 days of azithromycin (25 mg/kg [11.4 mg/lb], PO, q 24 h), ceftriaxone (25 mg/kg, IV, q 24 h), or doxycycline (10 mg/kg [4.5 mg/lb], PO, q 12 h), examination of biopsy specimens from multiple tissues failed to yield any viable spirochetes.84 In a similar study132 of experimentally infected dogs, administration of immunosuppresive dosages of corticosteroids led to a recurrence of severe lameness in 2 of 2 dogs that had not received antimicrobial treatment but in none of 12 that received antimicrobial treatment.

   Treatment is rarely indicated for dogs with serologic evidence of B burgdorferi exposure in the absence of clinical disease. As stated previously, although the number of seropositive dogs in an endemic area can be high, the proportion of these that will develop clinical signs is low. Serologic status determined at a singular point in time is not predictive of future illness; a study78 of dogs without signs of illness in an endemic area of Connecticut showed that the incidence of signs of Lyme borreliosis over a 20-month observation period did not differ between dogs that were initially seropositive and those that were seronegative. A course of antimicrobials prescribed solely on the basis of arbitrarily timed serologic findings is unlikely to reduce morbidity or to be effective in preventing reexposure in an endemic area.

Prevention and Control

   The foundation for preventing Lyme borreliosis in domestic animals and humans is the reduction of the risk of tick bites at the environmental or individual level. Avoiding tick bites prevents not only Lyme borreliosis but also other tick-borne diseases, such as ehrlichiosis and babesiosis, in regions where these pathogens are present. A knowledge of the ecologic requirements for the tick-borne diseases that are present in a given area is critical toward selection and implementation of the most effective integrated prevention strategies.133 In areas where Lyme borreliosis is a peridomestic risk, tick density may be managed locally by targeting animal hosts or by modifying the environment to decrease the availability of tick habitat. Products that kill or repel ticks can reduce the likelihood that ticks will attach to pets. Induced immunity through vaccination may provide additional protection in some highly endemic areas.


   Control of ticks on dogs is facilitated by the availability of collars impregnated with permethrin or amitraz and topical solutions containing fipronil,c permethrin,d or selamectin.e The myriad of recently developed ectoparasiticides and their control efficacy have been reviewed.141 Amitraz-impregnated collars appear to be more effective at interrupting the tick life cycle and longer acting than topical applications of fipronil.142 The appropriate use of amitraz-impregnated collars on dogs can provide effective tick control and thereby prevent infection with B burdorferi.143 Amitraz is also available as a spray or dip for tick control on domestic livestock; its use is contraindicated in horses, pregnant or nursing bitches, and cats. Selamectin is effective in control of brown dog ticks (Rhipicephalus sanguineus) and American dog ticks (Dermacentor variabilis) on dogs and is safe to use on cats. However, in a study144 in Europe, topical application of permethrin was more effective at repelling European Ixodes spp, compared with topical application of selamectin. Topical administration of permethrin products is contraindicated for cats.141

   Ideally, owners should examine their pets after visiting tick-infested areas. Although a thorough inspection may not reveal all ticks, prompt removal of those that are found can prevent most tick-borne diseases because there is often a lag period between the initiation of feeding by the tick and pathogen transmission. Borrelia burgdorferi spirochetes are not efficiently transmitted to the host until 24 to 48 hours after the tick begins to feed.145 Ticks should be removed with fine-pointed forceps by grasping the tick at the mouth-parts as close to the skin as possible and pulling gently, firmly, and perpendicularly away from the skin. A variety of commercial productsf-h are available that can be effective in removal of nymphal and adult ticks when used properly.146 Crushing the tick during the removal procedure does not appear to increase likelihood of transmission of Borrelia spirochetes.145 After the tick’s removal, the bite site should be washed with an antiseptic compound. The efficacy of antimicrobial prophylaxis for dogs after tick bites is unknown. When considering a prophylactic course of antimicrobials for a tick bite, veterinarians should carefully weigh the risk of tick-borne disease versus the risk of an adverse drug reaction.


Zoonosis Update

Lyme borreliosis

Curtis L. Fritz, DVM, MPVM, PhD, DACVPM, and Anne M. Kjemtrup, DVM, MPVM, PhD *

In 1976, public health officials investigated a cluster of suspected juvenile rheumatoid arthritis cases that occurred among residents of Lyme, Connecticut, and neighboring communities.1 More than 50 residents were evaluated for recurrent, usually short-lived (1 to 2 weeks’ duration) attacks of swelling and pain in a few large joints. Clinical, laboratory, and epidemiologic evidence failed to substantiate an immune-mediated pathogenesis. An arthropod-transmitted bacterium was suspected as the etiologic agent, as many patients also had an expanding, red, annular rash that resembled erythema chronicum migrans (a lesion identified in Europe in the early 20th century that was associated with tick bites and was responsive to penicillin).2,3 An infectious cause for the disease was confirmed when spirochetal bacteria isolated from Ixodes dammini (now considered I scapularis) ticks4 and blood, CSF, and other tissues of patients were shown to be identical.5-7 The bacterium was named Borrelia burgdorferi, and the multisystemic symptoms associated with infection were called Lyme disease or Lyme borreliosis (distinguishing it from other forms of borreliosis caused by other Borrelia spp). Subsequently, B burgdorferi was identified in ticks in numerous regions of the United States, and infection was associated with clinical illness in nonhuman animals, including dogs and horses.

   Findings of experimental, ecologic, epidemiologic, and clinical research conducted in the last 2 decades have tremendously expanded our scientific understanding of Lyme borreliosis. The genome of the causative spirochete has been sequenced, ecologic dynamics of its maintenance in nature have been described, effective diagnostic and treatment protocols have been established, and vaccines have been developed. However, as coverage by the popular media of this complex disease is often a farrago of fact, fallacy, and opinion, familiarity with the current scientific body of knowledge on Lyme borreliosis is critical to enable practicing veterinarians to appropriately address concerns of their clients and to effectively manage animals with the disease.


   The genus Borrelia is in the order Spirochetae, which contains genera that are pathogenic to humans and other animals, such as Leptospira and Treponema, to which belong the agents of leptospirosis and syphilis, respectively.8 Like other spirochetes, Borrelia spp are spiral shaped, gram-negative, and have an outer sheath encasing endofibrils.9 Unique to Borrelia spp are a singular linear chromosome (with additional linear and circular plasmids) and life cycles that require both arthropod vectors and mammalian hosts.10

   Borrelia spp may be generally grouped into those that cause a relapsing fever-type illness (eg, B hermsii) and those that cause Lyme borreliosis.10 Spirochetes in the relapsing fever group typically utilize soft (ie, argasid) ticks as their vector. Some relapsing fever-type Borrelia spirochetes have recently been recovered from hard (ie, ixodid) ticks,11,12 but the pathogenic potential of these isolates remains unknown. The Lyme borreliosis Borrelia complex is often divided into B burgdorferi sensu stricto (B burgdorferi ss; those Borrelia genetically identical to the type-strain B31, recovered from an I scapularis tick from Long Island, NY13) and B burgdorferi sensu lato (B burgdorferi sl; all other closely related Borrelia). Borrelia burgdorferi ss, B afzelii, and B garinii cause Lyme borreliosis in humans and animals in Europe and Japan.14,15 Only B burgdorferi ss is recognized as a cause of Lyme borreliosis in the United States.16 Recently, B bissettii was recovered from a human patient in Slovenia17; although B bissettii has been identified in ticks in the United States,18 no infection of mammals with this bacterium has been documented.

   A linear chromosome and 21 plasmids comprise the genome of the B burgdorferi B31 type strain.19 The genome codes for over 150 lipoproteins, some of which are key to the spirochete’s ability to transfer dbetween the tick vector and mammalian host. Several lipoproteins that localize to the outer surface of the spirochete (outer surface proteins [Osps]) are important in the transmission of Borrelia spirochetes to a vertebrate host and the host’s subsequent immune response. While in the gut of the tick, the spirochete expresses chiefly Osp A.20 The spirochete switches from Osp A to Osp C expression during a period of accelerated reproduction at the beginning of the tick’s blood meal.20 The variable major protein-like sequence expressed (VlsE) Osp has an invariable region conserved across many species of Borrelia and is highly immunogenic in mice, dogs, and primates.21-24 An understanding of the kinetics of these and other expressed proteins (eg, decorin binding proteins and flagellin) is important for diagnosis (measurement of mammalian antibody response to bacterial proteins) and prevention (identification of potential vaccine candidates) of Lyme borreliosis.

Ecology and Transmission

   Borrelia burgdorferi is maintained in nature in a cycle that involves hard ticks of the Ixodes genus as vectors and small mammals or birds as reservoir hosts. Ixodes spp are 3-host ticks that attach to a host and take a blood meal at each life stage (larva, nymph, and adult), then drop off the host to molt in the environment.25 Larval and nymphal stages of Ixodes spp are found in moist, protected areas, such as under leaf litter in humid hardwood forests. The principal hosts of immature Ixodes ticks are small rodents, lizards, and ground-feeding birds. The immature ticks typically require 2 to 4 days of attachm

  Two whole-cell B burgdorferi bacterin vaccines are available for canids.i,j An initial efficacy study147 by 1 of the manufacturers indicated that the vaccine protected laboratory dogs against the development of lameness following syringe-delivered challenge with several different strains of B burgdorferi. Results of a large-scale field study61 indicated that the vaccine was safe and effective at preventing development of Lyme borreliosis in many breeds of dogs. A survey148 of dogs from a single practice in a Lyme borreliosis-endemic area showed a higher prevalence of seroreactivity to the B burgdorferi C6 antigen among unvaccinated dogs (64%), compared with the prevalence among dogs that had received annual vaccination with the whole-cell bacterin (5%). Results of a study149 involving a model of Lyme borreliosis in hamsters indicated that immunity that develops subsequent to administration of the bacterin is specific to B burgdorferi infections (ie, not protective against B afzelii or B garinii) and short-lived (< 1 year). Findings of a similar study150 suggested that immune-mediated arthritis was associated with the B burgdorferi bacterin; however, it remains uncertain whether there is an association between immune-mediated arthritis in dogs and use of this vaccine.

   A recombinant subunit vaccine that contains the highly immunogenic Osp A is the next generation of vaccines available for prevention of Lyme borreliosis in dogs.k Because Osp A is expressed by B burgdorferi primarily in the gut of ticks prior to feeding, immunity against Osp A is thought to function through complement-mediated lysis of B burgdorferi in the tick’s gut soon after the tick begins its blood meal.151 In a study152 involving use of the subunit vaccine in dogs, protection against B burgdorferi transmission by naturally infected I scapularis was demonstrated. A recombinant B burgdorferi vaccine for horses, also based on the Osp A antigen, has been shown to be safe and protective but is not yet commercially available.153

   Recommended schedules for both the bacterin and recombinant vaccines require administration of an initial dose, a booster vaccination 2 to 4 weeks later, and annual revaccination.147,152 The decision to vaccinate against B burgdorferi should be based on an assessment of each dog’s risk of exposure to B burgdorferi, including factors such as the regional endemicity of Lyme borreliosis and the dog’s likelihood of contact with Ixodes spp.154 Vaccination should target at-risk dogs prior to exposure to B burgdorferi, because limited information is available regarding the safety and efficacy of the vaccine after administration to previously exposed dogs.61 Clients who choose to have their dogs vaccinated against B burgdorferi should be cautioned that the vaccine confers no protection against other tick-borne diseases (eg, ehrlichiosis), and therefore acaracides or other measures for reducing tick bites should nonetheless be adopted. These same factors should be considered for vaccination of horses when a commercial product becomes available.

Public Health Considerations

   Recognition of ixodid ticks on pets provides the veterinarian an opportunity to provide a public health service by alerting owners to their own potential exposure to tick-borne diseases. Clients should be assured that dogs with Lyme borreliosis do not serve as a direct or indirect source of infection for humans. Although ticks may rarely acquire B burgdorferi from infected dogs,155 dogs are not efficient maintenance reservoirs of these spirochetes and are only incidental hosts for larval and nymphal Ixodes spp that serve as vectors for Lyme borreliosis. However, pets may incidentally acquire ticks from outside and transport them to the peridomestic environment before the ticks have had an opportunity to attach. Detection of a tick on a client’s pet should motivate a discussion on appropriate acaracide use.

lyme testing or antimicrobial after tick bite not advised

Postby guest » Sun Feb 27, 2005 5:54 pm


Practice Guidelines for the Treatment of Lyme Disease

Gary P. Wormser,1 Robert B. Nadelman,1 Raymond J. Dattwyler,2 David T. Dennis,6 Eugene D. Shapiro,7 Allen C. Steere,9 Thomas J. Rush,5 Daniel W. Rahn,10 Patricia K. Coyle,3 David H. Persing,11 Durland Fish,8 and Benjamin J. Luft4

1Division of Infectious Diseases, Department of Medicine, New York Medical College, Valhalla, 2Division of Allergy, Immunology and Lyme Disease, Department of Medicine, 3Department of Neurology, and 4Department of Medicine, Health Sciences Center, State University of New York at Stony Brook, and 5private practice, Briarcliff Manor, New York; 6Division of Vector-Borne Infectious Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Fort Collins, Colorado; Departments of 7Pediatrics and 8Epidemiology and Public Health, Yale University School of Medicine, New Haven, Connecticut; 9Tufts University School of Medicine, New England Medical Center, Boston, Massachusetts; 10Office of Medical Management, Medical College of Georgia, Augusta; and 11Diagnostics Development, Corixa Corporation, and Infectious Disease Research Institute, Seattle Life Sciences Center, Seattle, Washington

Reprints or correspondence: Dr. Gary P. Wormser, Room 209 SE, Macy Pavilion, Westchester Medical Center, Valhalla, NY 10595.


Executive Summary

Tick bites and prophylaxis. The best currently available method for preventing infection with Borrelia burgdorferi is to avoid vector tick exposure. If exposure to Ixodes scapularis or Ixodes pacificus ticks is unavoidable, measures recommended to reduce the risk of infection include using both protective clothing and tick repellents, checking the entire body for ticks daily, and promptly removing attached ticks, before transmission of B. burgdorferi can occur (A-III [see tables 1 and 2 for recommendation categories, indicated in parentheses throughout this text]).

Table 1. Categories indicating the strength of each recommendation for or against use.
Table 2. Grades indicating the quality of evidence on which recommendations are based.

Routine use of either antimicrobial prophylaxis (E-I) or serological tests (D-III) after a tick bite is not recommended.

lymes C(6) antibody test cannot assess treatment outcome

Postby guest » Mon Feb 28, 2005 7:30 pm

Pre-treatment and post-treatment assessment of the C(6) test in patients with persistent symptoms and a history of Lyme borreliosis. Fleming RV, Marques AR, Klempner MS, Schmid CH, Dally LG, Martin DS, Philipp MT. Eur J Clin Microbiol Infect Dis. 2004 Aug;23(8):615-8.

It was recently reported that antibody to C(6), a peptide that reproduces an invariable region of the VlsE lipoprotein of Borrelia burgdorferi, declined in titer by a factor of four or more in a significant proportion of patients after successful antibiotic treatment of acute localized or disseminated Lyme borreliosis. The present study evaluated the C(6) test as a predictor of therapy outcome in a population of patients with post-treatment Lyme disease syndrome. The serum specimens tested were from patients with well-documented, previously treated Lyme borreliosis who had persistent musculoskeletal or neurocognitive symptoms. All of the patients had participated in a recent double-blind, placebo-controlled antibiotic trial in which serum samples were collected at baseline and 6 months thereafter, $132#e. 3 months following treatment termination. In this patient population no correlation was found between a decline of C(6) antibody titer of any magnitude and treatment or clinical outcome. Antibodies to C(6) persisted in these patients with post-treatment Lyme disease syndrome following treatment, albeit at a markedly lower prevalence and titer than in untreated patients with acute disseminated Lyme disease. The results indicate that C(6) antibody cannot be used to assess treatment outcome or the presence of active infection in this population.

lyme screening

Postby Guest » Sat Sep 17, 2005 9:17 am

My vet recommends the SNAP test to screen asymptomatic dogs for lyme disease (and heartworn and erlichiosis). I have declined this screening for my dogs, arguing that the positive predictive value of these tests in asymptomatic dogs in our geographic area is exceedingly low, and that even a true positive in an asymptomatic dog does not warrant therapy. I have not been able to find good data in dogs to back up my assertion. Is there a source of data for prevalence of lyme in dogs in central Virginia, and for sensitivity and specifity of the C6 ELISA when used in-office?

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