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]
Stage II Neurological manifestations and cardiac abnormalities are the hallmark of Stage II of Lyme disease. Nervous system symptoms may manifest while erythema migrans is present but usually begin one to six months after the erythema migrans has faded. Additionally, the following systemic symptoms and signs (in decreasing order of frequency) may be present at the onset of the neurological abnormalities associated with Stage II of the disease: headache, fatigue, fever, myalgia, neck stiffness, nausea, vomiting, arthralgia, photophobia, and arthritis. The neural involvement in Lyme disease commonly takes the form of a triad of neurological complaints comprised of lymphocytic meningitis, cranial, and peripheral neuropathies, and radiculopathies. This triad of complaints is also known as Banwarth's syndrome. Neurological abnormalities are seen in 15 percent of Lyme disease patients and may occur in the absence of Stage I symptoms and signs. Lymphocytic meningitis is the most common neurological abnormality seen in Stage II of the disease and is preceded by erythema migrans in 40 percent of cases, may follow the erythema migrans by two to 10 weeks, or may be the presenting sign of the disease process. Headache is the most common symptom (seen in 50 percent) of the lymphocytic meningitis, with the patient complaining of frontal or occipital headache varying in intensity from mild to disabling. Extraocular eye movements may cause pain to be increased. The patient may also exhibit mild neck stiffness, seen usually on flexion, with Kernig's and Brudzinski's signs rarely seen. Photophobia has been noted in 10 percent of cases, nausea and vomiting in 25 percent, and low grade fever in 30 percent of cases. The symptoms may persist for up to one to two months and then resolve gradually over several weeks. Cerebral symptoms which may accompany the meningitis include somnolence, emotional liability, depression, impaired memory and concentration, behavioral changes, and fatigue. Associated cerebral symptoms are generally mild; however, more severe cerebral symptoms may result from encephalitis associated with the Lyme disease. In cases of encephalitis secondary to Lyme disease, the symptoms develop rapidly over hours to days. Patients may experience severe somnolence, hallucinatory delirium , disorientation, paranoid psychosis, catatonia, confusion, irritability, agitation, coma, as well as all types of seizures. Focal neurological signs in the form of hemiparesis, cerebellar ataxia, chorea, dystonia, athetosis, tremor, or possible Parkinsonia symptoms may accompany cerebral symptoms of encephalitis and may be gradual or sudden in onset. Myelitis is also associated with Lyme disease and is the most frequent severe central nervous system abnormality seen in Stage II of the disease process. The myelitis may take the form of an acute or subacute transverse myelitis which develops over hours to days. The symptoms of myelitis include: bilateral spastic paraparesis, Babinski signs, and loss of superficial reflexes; a sensory level between T4 and T10; and bowel and bladder incontinence or urinary retention. Cranial neuropathies develop in approximately 60 percent of Lyme disease patients and are commonly seen three weeks after the onset of the erythema migrans. Multiple cranial neuropathies are common. The most common cranial nerve involved is the facial nerve (CN VII). Facial nerve involvement accounts for 70-80 percent of all Stage II cranial nerve palsies. Weakness usually begins in the summer months over one to two days and proceeds to bilateral involvement in over one-third of affected patients, with both sides of the face becoming paralyzed within a few days to three weeks of each other. Outcome for this form of facial nerve paralysis is usually favorable with most patients experiencing a complete recovery within a one to two months period. The facial paralysis of Lyme disease is differentiated from that of Bell's palsy by the following three factors: Summer onset Bilateral involvement History of tick bite or erythema migrans The optic nerve (CN II) may be involved in Stage II of Lyme disease due to increased intracranial pressure, inflammation along the meninges of the optic nerve, or by optic neuritis. Recovery is incomplete if antibiotic therapy is delayed. Involvement of the trigeminal nerve (CN V) is in the form of sensory symptoms such as facial paresthesia, numbness, and pain that may resemble trigeminal neuralgia. The corneal reflex is generally unaffected and the patient usually recovers spontaneously within a few weeks to months. Cranial nerves III, IV, and VI involvement may lead to diplopia. Cranial nerve VIII involvement may lead to a hearing loss and vertigo. Permanent hearing losses have been reported, even with antibiotic treatment. There have also been reports of cranial nerve IX, X, XI, and XII, although incidences are extremely low. Radiculopathy is the last portion of the triad of neurological symptoms associated with Lyme disease. Spinal and radicular pain associated with Lyme disease is generally worse at night and resistant to analgesics. The spinal pain has been characterized as having a generalized burning, gnawing or tearing quality that migrates. Once the pain is established it may last for months and eventually subside completely within a six weeks to three months period. Motor symptoms that may be associated with the intense radicular pain may include motor loss to the lower extremities twice as frequently as the upper extremities, diaphragm paralysis, cauda equina syndrome, or abdominal wall paralysis. Sensory losses are less common than motor losses and tend to be dermatomal and located in the lower cervical and in the T8-T12 regions.
Early Disseminated Disease - Neurologic and Cardiac Disease Early disseminated disease can occur anywhere from days to months after the initial tick bite with the two most common manifestations being neurologic and cardiac.
Approximately 10 percent of patients with untreated Lyme disease will develop cardiac manifestations which include heart block of any degree or combination of degrees, mild to moderate myopericarditis and rarely chronic cardiomyopathy and persistent heart block.
Neurologic damage also occurs in approximately 10 percent of patients with untreated Lyme disease. Manifestations include cranial nerve palsies, lymphocytic meningitis and radiculoneuritis.
The earliest possible treatment by the family physician can quickly resolve and stifle the progression of both the cardiac and neurologic manifestations of the early-disseminated disease. The absence of treatment leads to the progression and sometimes permanent manifestations of Lyme disease.
Cardiac manifestations of Lyme disease: A review KS Nagi, R Joshi, RK Thakur OBJECTIVE: To describe the clinical features of cardiac manifestations of Lyme disease, the most common vector-borne illness in North America, which occasionally results in cardiac involvement. DATA SOURCES: A review of the English-language clinical literature pertaining to Lyme disease and Lyme carditis indexed in MEDLINE from 1975 to 1995. DATA EXTRACTION: Studies describing diagnosis, clinical features, treatment or outcome were reviewed. DATA SYNTHESIS: Cardiac complications of Lyme disease may occur in up to 8% of patients. Cardiac manifestations occur in the early phase of the illness, at a median of 21 days from the onset of erythema migrans. Manifestations of Lyme carditis include atrioventricular block, myopericarditis, intraventricular conduction disturbances, bundle branch block and congestive heart failure. Temporary cardiac pacing may be required in up to a third of cases and complete recovery occurs in most (greater than 90%) patients. The overall prognosis of Lyme carditis is very good, although recovery may be delayed and late complications such as dilated cardiomyopathy may occur. CONCLUSION: Lyme disease is a tick-borne spirochetal infection caused by Borrelia burgdorferi. Cardiac complications of Lyme disease generally occur in the early phase and include conduction system disturbances, myopericarditis and congestive heart failure. Key Words: Borrelliosis, Carditis, Congestive heart failure, Heart block, Lyme carditis, Myocarditis, Pericarditis, Spirochetal infection, Tick-borne illness
IV. ACTA MED AUSTRIACA: Cardiac manifestations of Lyme borreliosis with special reference to contractile dysfunction. -------------------------------------------------------------------- AUTHORS: Seinost G, Gasser R, Reisinger E, Rigler MY, Fischer L Keplinger A, Dattwyler RJ, Dunn JJ, Klein W ORGANIZATION: Klinischen Abteilung fur Kardiologie, Medizinischen Universitatsklinik Graz, Osterreich. [email protected] REFERENCE: Acta Med Austriaca 1998;25(2):44-50 ABSTRACT:
Borrelia burgdorferi infection (BBI) is suggested to be associated with dilated cardiomyopathy (IDC). Stanek et al. were able to cultivate Borrelia burgdorferi (BB) from myocardial biopsy tissue of a patient with longstanding dilated cardiomyopathy. Here we present a study in which we examined the effect of standard antibiotic treatment on the left ventricular ejection fraction (LV-EF) in patients with dilated cardiomyopathy associated with BBI. In this study we assessed the serum (IgG, IgM ELISA; Western Blot) and the history of 46 IDC-patients with specific respect spect to BBI (mean LV-EF: 30.4 +/- 1.3%; measured by cardiac catheterisation and echocardiography--length-area-volume method). All 46 patients received standard treatment for dilated cardiomyopathy: ACE-inhibitors, digitalis and diuretics. 11 (24%) patients showed positive serology and a history of BBI; 9 of these also had a typical history of tick bite and erythema chronicum migrans (ECM) and/or other organ involvement, 2 had no recollection of tick bite or EMC, but showed other BB-associated disorders (neuropathy, oligoarthritis). These 11 patients with BBI received standard antibiotic treatment with intravenous ceftriaxone 2 g bid for 14 days. 6 (55%) recovered completely and showed a normal LV-EF after 6 months, 3 (27%) improved their LV-EF and 2 (18%) did not improve at all. This amounts to 9 (82%) recovery/improvement in the BB-group. The 35 patients who did not show positive serology or a history of BBI did not receive antibiotic treatment. In this group without BBI 12 (26%) showed recovery/improvement following the standard treatment of dilated cardiomyopathy (see above). Our results indicate that BBI could play a decisive role in the development of dilated cardiomyopathy, especially in a geographical region as Graz, where BB is endemic. While aware of the small number of BB-patients in this study, we nevertheless conclude that, in a remarkable number of patients with signs of BBI, dilated cardiomyopathy could be reversed and LV-EF improved upon standard antibiotic treatment.
Lyme disease is caused by the bacterium Borrelia burgdorferi and is transmitted to humans by the bite of infected blacklegged ticks. Typical symptoms include fever, headache, fatigue, and a characteristic skin rash called erythema migrans. If left untreated, infection can spread to joints, the heart, and the nervous system. Lyme disease is diagnosed based on symptoms, physical findings (e.g., rash), and the possibility of exposure to infected ticks; laboratory testing is helpful in the later stages of disease. Most cases of Lyme disease can be treated successfully with a few weeks of antibiotics. Steps to prevent Lyme disease include using insect repellent, removing ticks promptly, landscaping, and integrated pest management. The ticks that transmit Lyme disease can occasionally transmit other tick-borne diseases as well.
further: My late husband nor I were ever tested for Lyme disease until just before he died when I had a positive ELISA test followed by a positive Western Blot. Upon his death there were questions which remained unanswered. The first and foremost was Why our son was following his medical condition? I implored the pathologist to run a DNA tests which showed my husbands DNA to be normal. I asked the pathologist what else can be passed to a child other than DNA and if his DNA was normal could it be an infectious disease? He said that was the only likely factor that might explain common elements. I asked him to run a test for Lyme Disease since our family has been shown to have it and he was never tested.. A test was run on the blood using fluorescent staining to detect the bacteria as the blood was too deteriorated to run the standard Elisa and Western Blot. Serial Dilution showed 1:128
************************************* Is this good enough do you think they will listen now?
-------------------- "Hatred paralyzes life; love releases it. Hatred confuses life; love harmonizes it. Hatred darkens life; love illuminates it." Posts: 1389 | From who knows, who cares, but somewhere over the rainbow | Registered: Mar 2003
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posted
I think you have done a very good job of researching.
My question for you is do you think you could have passed Lyme disease to your son at birth? Not sure how old you said he was?
In my opinion a doctor would be more likely to believe that you gave your son Lyme disease than that your husband did!
I really don't think it is worth arguing over how he contracted Lyme disease if in fact that is his problem. If this was me at this point I would simply be trying to get a diagnosis and treatment and not get sidetracked as to when and how your son got Lyme disease. The truth is that you may never really know the answer to that question.
And be sure the doctor tests and or treats for coinfections.
Good luck with your appt.
WV Hillbilly
Posts: 48 | From Five Mile Creek, WV,USA | Registered: Aug 2005
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