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ASEPTIC MENINGITIS IN THE NEWBORN:

http://www.aafp.org/afp/990515ap/2761.html

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Clinical Aspects of Lyme Disease: Dermatologic, Cardiac, GI, and Gestational

Harry Goldhagen, MS   Julie Rawlings, MPH   Disclosures

Like syphilis at the turn of the previous century, Lyme disease can be considered the great impersonator. The myriad clinical presentations of this multisystem disease have been part of the diagnostic dilemma, especially for chronic Lyme disease. It is often difficult to determine whether specific symptoms are caused by Borrelia burgdorferi or are unrelated but occurring in a patient with serologic evidence of past infection.

A number of investigators at the 14th Lyme Disease Conference examined less common clinical presentations of Lyme disease, conditions for which B burgdorferi is not one of the usual suspects. These body systems include the gastrointestinal tract, the heart, and the skin (not counting the common dermatologic presentation of erythema migrans [EM]). And one speaker discussed the extremely rare syndrome of congenital Lyme disease.

 

Morphea and Lyme Disease: Are They Related?

Morphea is a rare and untreatable dermatologic condition characterized by thickening and induration of the skin from excess collagen deposition. There are at least 5 forms of the disease: localized, generalized, guttate, linear, and coup de sabre (an indentation that can extend to and damage the underlying muscle and bone). The cause is generally not known, but as with any idiopathic condition, proposed etiologies abound, including radiation damage, autoimmunity, infection, vaccination, trauma, and genetic predisposition. One of the leading infectious disease candidates in the pathogenesis of morphea is B burgdorferi, although this association is a subject of controversy.^[1] A number of European studies have found a correlation, while most US studies, including a frequently cited study from the Mayo Clinic,^[2] have found no evidence of B burgdorferi in morphea lesions.

Andrew G. Franks, Jr, MD,^[3] of New York University School of Medicine (NYU), believes there is a connection between the 2 diseases. For instance, it can be difficult to differentiate between EM and certain morphea lesions, especially if the EM lesion is not the typical bull's-eye with central clearing. The differential diagnosis for EM-like lesions is varied and can include spider bites, herpes simplex or zoster, cellulitis, fungus or tinea, granuloma annulare, drug eruption, erythema multiforme, and subacute lupus erythematosus. In many cases, it can be difficult to culture B burgdorferi from EM lesions.

Part of the disagreement between the US and other studies may be due to differences in B burgdorferi serotypes and strains that cause morphea, according to Dr. Franks. For instance, only the sensu stricto strain is found in the United States, but all 3 pathogenic strains are found in Europe. Two skin diseases -- acrodermatitis (similar in appearance to scleroderma) and lymphocytoma -- have been identified in Europe as linked to B burgdorferi; the former is associated with the B afzelii strain, and the latter with the B garinii strain.

Dr. Franks believes that serologic testing is unreliable in morphea. He said that in published US studies of B burgdorferi antibodies in morphea patients, the investigators did not check whether the subjects received antibiotics recently. Antibiotic treatment can alter the results of serologic testing. Polymerase chain reaction (PCR) testing for B burgdorferi DNA in morphea patients may also be inaccurate in the US. For instance, the PCR tests may have been too specific and missed strains or serotypes more likely to cause morphea-like skin disease. European studies have detected B burgdorferi DNA by PCR in patients with morphea. For instance, a PCR study by Fujiwara and colleagues^[4] tested for afzelii and garinii strains and found evidence of B burgdorferi in non-US cases. US PCR amplification has generally only tested for the sensu stricto strain.

Dr. Franks and colleagues at NYU have recently completed an unpublished study of the association of B burgdorferi, autoimmunity, and morphea. In this study, 82 patients (average age of 27 years; range, 2-61 years) with new-onset morphea were enrolled; 14 were male. The investigators tested for antibody to autoimmune disease and to B burgdorferi by IgG and IgM Western blot (WB), with all bands reported. They used their own criteria for diagnosis of underlying Lyme disease: more than 1 IgG band on WB was taken as a positive result for Lyme. None of the subjects had clinically defined Lyme disease during the trial. For autoimmune serology, any positive test was defined as positive.

For treatment purposes, they classified the patients into 4 groups, depending on whether they were positive by WB and/or autoimmune serology. Generally, patients with positive WB received 6 weeks of doxycycline (or an alternative antibiotic), and those with negative WB were given 3 weeks of doxycycline, with an optional additional 3 weeks if improvement was seen during the first 3 weeks.

Of the 61 patients who completed the study, 34 had clinical improvement. The WB-positive, autoimmune serology-negative group was the most likely to respond to antibiotic therapy. The Lyme WB converted to negative in many treated patients.

Dr. Franks and colleagues believe that all patients with morphea are candidates for a therapeutic antibiotic trial, regardless of serologic test results. IgM and IgG WB may be helpful in the diagnosis, but current Lyme tests are unreliable in such patients. Because the risks are minimal with antibiotics, he believes it is worth trying this approach, especially since there is no effective treatment for morphea at the present time.

The NYU group will be conducting a second trial, making use of a recombinant, nested PCR B burgdorferi assay. They are looking for patients to enroll in this and future studies. If you have any new, untreated morphea patients in your practice, call 917-816-2714 to receive a consent form and instructions for obtaining a 4-mm punch biopsy for PCR.

 

Lyme Disease and the Heart

Cardiac manifestations of Lyme disease are relatively uncommon and difficult to diagnose. According to Kornelia Keszler, MD,^[5] of Yale University School of Medicine, the most readily recognized feature of cardiac involvement has been various degrees of heart block on ECG, which usually responds to antibiotic therapy.

Typical complaints of Lyme disease patients with cardiac involvement are chest pain, mild to moderate exertional dyspnea, and palpitations. (However, these symptoms also may be due to neuropsychiatric problems and musculoskeletal infection, so testing is important.) To evaluate such patients, cardiac testing should include thallium stress electrocardiography (ECG) and coronary angiography.

What does cardiac infection look like, and where are the organisms localized? Stanek and colleagues^[6] found thickening of the walls of small endomysial vessels and infiltration by mononuclear cells. In murine studies, Pachner and colleagues^[7] found 3 predominant locations for B burgdorferi in the heart. In mice infected for less than a month, spirochetes could be found mostly around blood vessels. By contrast, for longer infection periods, B burgdorferi could also be seen in cardiac myocytes, often surrounded by clear areas. B burgdorferi were also commonly found among collagen fibers.

Based on her series of cases and a review of the literature, Dr. Keszler drew the following conclusions. Thallium imaging typically reveals diffuse and patchy uptake of isotope in the myocardium, probably indicating involvement of the small vessels of the heart. Patients generally experience decreased exertional tolerance, as exhibited by a rapid increase in heart rate, but there is no ECG evidence of ischemia to account for the decreased tolerance. A variety of arrhythmias are seen, both ventricular and supraventricular, and are more common than heart block. At this time, it is not known whether treatment of Lyme disease will alter the thallium imaging. However, one study has found that cardiac abnormalities do not persist in patients treated for Lyme disease.^[8]

 

Lyme Disease and the GI Tract

Lyme disease generally does not affect the GI tract alone, according to Martin D. Fried, MD,^[9] of the Jersey Shore Medical Center, Neptune, New Jersey. Rather, GI disease is typically only one component of a systemic disease. Patients with Lyme disease can present with a variety of GI symptoms, including abdominal pain, chronic diarrhea, acid reflux, or blood in the stool. Children may develop encopresis -- the loss of bowel training -- which may indicate a neurologic effect of the spirochete.

Evaluation of patients suspected of having Lyme disease includes the ever-important history, physical examination, CBC, liver function tests, and endoscopic examination. The Lyme WB is generally not helpful, but PCR testing of biopsy specimens for B burgdorferi OspA can be useful. Silver staining of biopsy specimens can reveal spirochetes. For those who test positive by PCR, RNA polymerase testing of the biopsy sample can indicate whether the spirochetes are actively multiplying.

The differential diagnosis includes the majority of gastrointestinal diseases, such as pancreatitis, stool infections, peptic ulcer, Crohn's disease, and inflammatory bowel disease. Skin tags are an indication that the patient has Crohn's rather than a complication of Lyme disease. Crohn's patients have a malabsorption syndrome and are therefore generally underweight. By contrast, those with GI Lyme disease often also have fatigue or arthritis, and the inactivity may make them overweight.

Treatment involves antibiotics, but regular follow-up is important to detect recurrences and lack of response. Dr. Fried has seen B burgdorferi persist in the GI tract despite multiple rounds of antibiotics over many years.

 

Gestational and Congenital Lyme Disease

Any infectious disease contracted during pregnancy has the potential to be transmitted to the fetus. Tessa D. Gardner, MD,^[10] of Washington University School of Medicine, St. Louis, Missouri, who has recently written an extensive chapter on the subject,^[11] discussed the rare conditions of gestational and congenital Lyme disease (borreliosis) and the best approaches (based on limited case reports) to diagnosis and treatment.

How rare are these conditions? According to published figures, 16,000-17,000 cases of Lyme disease are reported each year in the United States. Roughly 8000 cases are in women, and approximately 1200-3400 cases are in women of childbearing age (20-49 years old). Dr. Gardner did some back-of-the envelope estimates to get a sense of how many cases of gestational Lyme disease may be occurring. If you assume that one quarter of the women in the child-bearing age group are pregnant (a gross overestimate, by Dr. Gardner's admission), and that 10% are either untreated or inadequately treated, and that one fifth transmit the organism to the fetus or newborn, this calculates to approximately 40 cases of congenital Lyme disease a year in the United States. It would be unusual for any large city to have more than 1 or 2 cases a year, and it would be extremely rare for any physician to see more than a few cases in a lifetime.

Dr. Gardner has conducted an extensive literature review (through 1998) that turned up 263 cases.^[10] She found that 25% resulted in adverse outcomes: 8% resulted in fetal death and 2% in neonatal death. Fifteen percent of the babies were liveborn but were ill or had an abnormality. The effect of antibiotic therapy was dramatic in these patients: with antibiotics, 85% of neonates were normal, while 15% had an adverse outcome. In striking contrast, without antibiotics, only 33% were normal, while 67% had an adverse outcome. The conclusion: Proper, prompt diagnosis and antibiotic therapy are vital for healthy neonates born with congenital Lyme disease.

However, it can be quite difficult to recognize such a rare disease. The differential diagnosis is extensive and includes sepsis/meningoencephalitis (bacterial or viral), other congenital infectious diseases (eg, syphilis, leptospirosis, relapsing fever, toxoplasmosis), congenital heart or bone disease, inherited or infectious immunodeficiency, sudden infant death syndrome, and more. A history suggestive of Lyme disease in the mother or positive serologic or other tests for B burgdorferi can suggest the diagnosis. Dr. Gardner has provided a list of clues to the various presentations of congenital Lyme disease (Table). One interesting radiologic clue is "celery stalking" -- lucent metaphyseal bands -- on the long bones of the neonate. These are occasionally seen in infants with gestational syphilis or viral infections. In 2 neonates Dr. Gardner has treated, the bands disappeared shortly after treatment.

 

Table. Signs and Symptoms of Congenital Lyme Borreliosis

Stage	Mild Early	Severe Early	Late
Onset	Usually first 2 weeks of life	Usually first week of life	Usually > 2 wks and < 2 yrs of age
Maternal gestational Lyme borreliosis	Usually first or second trimester	Usually first or second trimester	Usually second or third trimester
Signs and symptoms	Mild suspected sepsis or meningoencephalitis   Hyperbilirubinemia   Adenopathy   Rash   Intrauterine growth retardation   Miscellanous anomalies (eg, genitourinary [GU], skeletal, cardiac)	Severe suspected sepsis or meningoencephalitis   Respiratory distress   Perinatal death   Intrauterine growth retardation   Fever   Rash   Adenopathy, hepatosplenomegaly   Hyperbilirubinemia   Miscellaneous anomalies (eg, GU, skeletal, cardiac)	Subacute illness   Developmental delay/meningoencephalitis   Growth retardation/failure to thrive   Prematurity   Fever   Adenopathy   Rash   Hepatosplenomegaly   Miscellaneous anomalies (eg, GU, skeletal, cardiac)
Prematurity?	< 4 weeks	< 5 weeks	--

The prognosis for gestational Lyme disease is good if diagnosed and treated adequately. The prognosis for neonates with early congenital Lyme disease depends on prompt diagnosis, especially in severe early cases. Similarly, the prognosis in late congenital Lyme depends not only on prompt diagnosis and treatment, but also on the extent of irreversible damage present at the time of diagnosis. Long-term follow-up is important for detecting possible recurrence of disease.

This summer, Dr. Gardner will be starting the North American Gestational and Congenital Lyme Disease Watch to evaluate the relationship of various factors (clinical and laboratory characteristics, antibiotic regimens) to outcomes for gestational Lyme disease, and to evaluate short- and long-term outcomes (infants, stillborns, miscarriages) of pregnancies complicated by Lyme disease and develop clinical and laboratory case definitions of these outcomes. Interested people (physicians and affected women) can enroll on the Internet once the sites are launched in July 2001:

www.LymeInPregnancy.org

www.GestationalLyme.org

www.CongenitalLyme.org

 

References

1. Weide B, Walz T, Garbe C. Is morphoea caused by Borrelia burgdorferi? A review. Br J Dermatol. 2000;142:636-644. Abstract available at: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10792212&dopt=Abstract
2. Hoesly JM, Mertz LE, Winkelmann RK. Localized scleroderma (morphea) and antibody to Borrelia burgdorferi. J Am Acad Dermatol. 1987;17:455-458. Abstract available at: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3308981&dopt=Abstract
3. Franks A. Evidence for Borrelia burgdorferi as an etiologic agent in morphea. Program and abstracts of the 14th International Scientific Conference on Lyme Disease and Other Tick-Borne Disorders; April 21-23, 2001; Hartford, Connecticut.
4. Fujiwara H, Fujiwara K, Hashimoto K, et al. Detection of Borrelia burgdorferi DNA (B garinii or B afzelii) in morphea and lichen sclerosus et atrophicus tissues of German and Japanese but not of US patients. Arch Dermatol. 1997;133:41-44. Abstract available at: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9006371&dopt=Abstract
5. Keszler K. Cardiac manifestations of Lyme disease. Program and abstracts of the 14th International Scientific Conference on Lyme Disease and Other Tick-Borne Disorders; April 21-23, 2001; Hartford, Connecticut.
6. Stanek G, Klein J, Bittner R, Glogar D. Isolation of Borrelia burgdorferi from the myocardium of a patient with longstanding cardiomyopathy. N Engl J Med. 1990;322:249-252.
7. Pachner AR, Basta J, Delaney E, Hulinska D. Localization of Borrelia burgdorferi in murine Lyme borreliosis by electron microscopy. Am J Trop Med Hyg. 1995;52:128-133. Abstract available at: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7872439&dopt=Abstract
8. Sangha O, Phillips CB, Fleischmann KE, et al. Lack of cardiac manifestations among patients with previously treated Lyme disease. Ann Intern Med. 1998;128:346-353. Abstract available at: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9490594&dopt=Abstract
9. Fried M. Gastrointestinal manifestations of Lyme disease. Program and abstracts of the 14th International Scientific Conference on Lyme Disease and Other Tick-Borne Disorders; April 21-23, 2001; Hartford, Connecticut.
10. Gardner T. Lyme disease in pregnancy. Program and abstracts of the 14th International Scientific Conference on Lyme Disease and Other Tick-Borne Disorders; April 21-23, 2001; Hartford, Connecticut.
11. Gardner T. Lyme disease. In: Remington J, Klein JO, eds. Infectious Diseases of the Fetus and Newborn Infant. Philadelphia, Pa: WB Saunders; 2001: 519-641.

Suggested Reading

MacDonald AB. Gestational Lyme borreliosis. Implications for the fetus. Rheum Dis Clin North Am. 1989;15:657-677. Abstract available at: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2685924&dopt=Abstract

Maraspin V, Cimperman J, Lotric-Furlan S, et al. Treatment of erythema migrans in pregnancy. Clin Infect Dis. 1996;22:788-793. Abstract available at: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8722932&dopt=Abstract

 

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