[2] The Panel noted that Professor Eisen also expressed reservations about the underlying myocardial disease and also said in the same report of 16 March 2009, "Carditis caused by Lyme disease is a rare entity but it is clear that it causes myocarditis rather than hypertrophic cardiomyopathy".
[3] The Panel also noted that Professor Eisen opined that "Mr Jury did have Lyme disease with characteristic skin involvement". He added "I do not believe that the cardiomyopathy was related to Lyme disease because ... the characteristic inflammatory mycoarditis was absent, no Borrelia organisms were seen in the endomyocardial biopsy [performed in June 1997 and which showed no significant increase in inflammatory infiltration in the interstitium], and the report also opined that PCR of the endomyocardial biopsy for Lyme disease was negative and the plaintiff was seronegative on Elisa and Western Blot for antibodies to Lyme disease prior to immunosuppression".
[4] The Panel considered this statement in the context of the documented findings of various studies, about which the Panel informed itself, confirming that 10% of persons suffering from Lyme Disease are seronegative and only 25% or less of Lyme affected persons remember a tick bite or the initial rash of erythema migrans from the tick bite.
[5] The Panel also noted the opinion of Dr Brian Wood, Consultant Cardiologist who attended the plaintiff at the time of his stroke and identified the plaintiff's cardiomegaly, and who stated in his letter dated 9 April 1996, that the echocardiography performed at the Mornington Peninsula Hospital showed a "hypertrophic myopathic process" and the "Cardiac biopsy did not show any infiltrative or inflammatory process ... ".
[6] The Panel noted that all the referral documents contain ample evidence confirming the diagnosis of late stage Lyme disease of the skin with histological and clinical evidence for the diagnosis based on the development of acrodermatitis atrophica chronica and anetodermia, and other essential indicators of the epidemiological circumstances for making the diagnosis of dermatological Borreliosis, but the same examiners express significant reservations about the plaintiff's cardiac involvement in the disease process.
[7] The Panel also considered the relationship between the plaintiff's condition of hypertrophic cardiomyopathy and his subsequent cardiac transplant and whether or not his cardiac condition resulted from chronic Borreliosis affecting the plaintiff's heart muscle.
[8] The Panel noted, as previously indicated, that some emphasis was placed by some medico-legal reporters on the absence of signs of inflammatory disease in the extirpated heart's myocardial tissues, and focussed only on the hypertrophy of the plaintiff's myocardium. The Panel also noted that there is some conjecture, by the medico-legal examiners in their reports, that signs of an inflammatory process would be expected in any infective or inflammatory disease, and that no such signs were evident in any of the histological studies of the plaintiff's heart, apart from hypertrophy. By implication, the medico-legal examiners surmise that the hypertrophic cardiomyopathy possibly did not result from an infective process in the tissues of the heart caused by Borrellia spirochaetes, because no spirochaetes were discovered by histological examination and PCR and Elisa studies of tissues taken from the extirpated heart were inconclusive. The Panel considered all of these opinions and considered that it is acceptable that in Lyme Disease, organisms may not be identified and any identifiable changes in the heart may be considered analogous to post viral cardiomyopathy where myocarditis may be seen initially but not in the advanced phases of viral disease of the myocardium.
[9] The Panel has made extensive enquiry and informed itself of rare cases of dilated cardiomyopathy, in Europe, based upon the isolation of B.burgdorferi from heart tissue and upon serological study of patients with cardiomyopathy. It has been postulated that the inability to detect B.burggdorferi in more persons with chronic heart disease could be due to infection in the remote (rather than recent) past (consistent with the history in this case). In this hypothesis, cardiomyopathy results from residual scarring and fibrosis as opposed to continued active infection. The Panel is aware that this process has yet to be confirmed in the experimental animal model.
[10] The Panel considers that evidence for the existence of Lyme associated cardiomyopathy in the US is less compelling. The association between Lyme disease and cardiomyopathy is not certain for the vast majority of persons in whom the diagnosis of Lyme carditis was based on laboratory tests other than culture. Autopsy findings in unique cases have been reported to reveal an enlarged heart with biventricular hypertrophy and an organizing fibrinous pericarditis.
[11] The Panel is aware that there have been reported cases of concentric hypertrophic myocardiopathy diagnosed by echocardiography in some cases of Lyme carditis, one with a 12 year history of evolving Lyme disease.
[12] The Panel concluded, after very careful consideration of all aspects of the claimed injury, that there is evidence that cardiac abnormalities, in addition to conduction defects and rhythm disorders, including hypertrophic cardiomyopathy can occur, though rarely, as a late complication of infection of the heart with Borrelia burgdorferi.
[13] The Panel reviewed the epidemiology of Lyme Disease in Europe and noted that acrodermatitis atrophica chronica was a well established dermatological entity prior to the recognition of dermal disease caused by spirochaetal infection by the Borrelia organism. It occurred chiefly in older persons under the title of "diffuse idiopathic atrophy of the skin", and was encountered in middle, eastern and northern sections of Europe. It was considered, even then, that due to its limited geographic distribution, and the beneficial effect of antibiotics, that a vector borne infection was a provable cause of the skin condition. The incidence of acrodermatitis atrophica chronica and its geographical distribution matches the distribution of Lyme disease in endemic areas of tick borne disease in Europe.
[14] The Panel considered all these factors, and concluded that the plaintiff has suffered from Lyme disease with its initial manifestations as a stroke resulting from cerebral thromboembolism arising from a left mural thrombus secondary to hypertrophic cardiomyopathy.
[15] The Panel considers that hypertrophic cardiomyopathy can result, though infrequently, from chronic myocardial infection due to late stage Lyme Disease, and notes that a small number of cases of histologically proven Lyme related cardiomyopathy has been reported.
[16] The Panel carefully considered the possible alternative causes of hypertrophic cardiomyopathy and identified no other risk factor, including hypertension, viral myocarditis, ischaemic heart disease, metabolic disorder or congenital factor, or any personal or family history of heart disease. The Panel considered that there is no reason to search for comorbid conditions of any other nature to explain the evolution of hypertrophic cardiomyopathy in this case, when there is documented evidence of late stage Lyme disease resulting in hypertrophic cardiomyopathy.
[17] The Panel considered the known clinical features of Lyme Disease, its causation, the circumstances of actual exposure to the risk of infection in an endemic area, and the known natural history of chronic infection due to Borrelia sp. The Panel considers that there is satisfactory histological evidence of myocardial infection by the Borrelia organism in the plaintiff's case.
[18] The Panel therefore concluded that the plaintiff's employment affected the plaintiff such that he contracted Lyme disease as a result of a tick bite whilst in Germany in the course of his employment and has suffered consequential medical conditions.