The frequency of EMF cases in Uganda has a bimodal peak at age 10 and age 30 [9] . Childhood EMF in this country affects boys and girls equally, while adult EMF affects woman twice as often as men [10] . In Nigeria, some studies have found a two to one male preponderance, while others have not shown any difference between sexes. Majority of cases in India from Kerala state are below the age of 40 years. EMF is not generally observed in children younger than 4 years, although the typical pathology of EMF has recently been described in a 4- month-old infant. EMF appears to be more prevalent in certain ethnic groups. One study in Uganda showed that EMF is more common in individuals with Rwanda/Burundi ethnic origins.

The etio-pathogenesis of EMF remains much of an enigma, with several unvalidated hypothesis ranging from infection, inflammatory and dietary causes as well as eosinophilic toxicity play a role in tropical regions. They include cerium deficiency, magnesium deficiency, cassava, malnutrition, parasitic diseases, viral diseases, autoimmunity, allergy, and ethnicity. The hypotheses postulated to explain the etiology of EMF have not been proven and cannot explain its occurrence worldwide.

Davies himself, who died in 1998 at the age of 83, believed to the end that EMF had a unifying explanation. He thought the clue perhaps lay in the similarity between the heart lesion in EMF and the endocarditis parietalis fibroplastica that Wilhem Loffler and others had described in Europe in the setting of hypereosinophilic syndromes [9] . The eosinophil hypothesis-dominant though still a not well tested-has failed to convince critics who point to other plausible alternatives. In fact, more of the etiologic categories first mentioned by Williams, Ball, and Davies in 1954 have left Table 1 of possible causes given below.

By and large, the endomyocardial fibrosis could be a reaction pattern of the endocardium to a variety of insults [11] . Role of anti-heart antibodies similar to rheumatic process may be involved in the fibrotic process of EMF. The endocardial lesions in EMF are said to evolve in 3 successive stages, namely, necrosis, thrombosis, and fibrosis [12] and these stages have been defined on the basis of postmortem material in Loffler’s endocarditis by Olsen. Davies has described three phases of the disease [13] . The initial phase is an acute carditis phase characterized by febrile illness and in severe cases with heart failure and shock, followed by progress into a

subacute phase and a chronic phase. Most of the patients come to clinical attention in the chronic burnt-out phase. The early part of the disease is rarely clinically recognized in India and the disease come to attention in the late stages and isolated endocardial involvement and intracardiac thrombi are the peculiar features [14] . The climatic restriction of areas where EMF is endemic and the reports of sporadic cases in foreigners after short visits to these areas suggest a role of infectious agents in the pathogenesis of the disease [15] . Increased levels of interleukin-6, endothelial cell activation, and increased fibrinolysis were found in patients with recent-onset EMF, strongly suggesting that inflammation, endothelial injury, and procoagulant changes are major players in the pathogenesis of this condition [16] .

Histology of the heart shows abnormalities in all 3 layers [17] . The most prominent lesion is endocardial thickening, which is due to acellular fibrocollagen tissue deposits under a layer of normal endocardium [18] . While in general, fibrosis in cardiac tissue has been mainly linked to increased level of cytokine, transforming growth factor β₁ [19] , the underlying mechanism of myocardial fibrosis in this entity remain unclear.

Echocardiography is the most valuable tool for the diagnosis of EMF [20] . Mocumbi et al. [14] have described the echocardiographic criteria to diagnose EMF and the criteria described in the literature apply only to the disease in the advanced stages [21] . The presence and location of fibrosis as determined by echocardiography correlate well with autopsy findings. Obliteration of the apex of the involved ventricle is the hallmark of the disease. Ventricular obliteration and cavity retraction are described features of right EMF, clearly depicted on echocardiography. More specifically, EMF is a disease of the inflow tract endocardium, with severe fibrosis extending from the papillary muscles to the apex of the ventricles [22] . Outflow tract is usually preserved. Atrioventricular valves are also usually preserved, but infiltration of the subvalvular apparatus may cause insufficiency. Thickening of the endocardium and infiltration of the myocardium are responsible for partial obliteration of ventricular cavities, resulting in decreased distensibility and diastolic filling. When symptoms of cardiac failure ensue, the prognosis becomes poor.

In this neonate, transthoracic 2 D echocardiographic images showed fibrotic obliteration of the right ventricular apex and its extension into the inflow of the tricuspid valve as shown in Figure 1, with mild tricuspid regurgitation as shown in Figure 2 and Figure 3 and the free RV outflow tract, pulmonary valve and artery as in Figure 4 suggesting the Right ventricular endomyocardial fibrosis

There is a history of febrile illness for one week duration during the 5th month of gestation in the antenatal period of mother of this child and echocardiography of mother revealed normal. The exact etiology of this febrile illness was unknown. Recent studies have demonstrated antibodies against myocardial proteins and a high incidence of cardiotrophic infectious agents like cytomegalovirus, Epstein-Barr virus and Toxoplasma gondii in affected patients suggesting a role of inflammation [23] . A recent study states that the right ventricle was the most affected cavity in EMF and majority of patients were between 5 and 15 years of age group [24] similar to rheumatic fever.

Echocardiographic screening of family members revealed normal even though they are living with same environmental exposure and dietary habits. Some unknown cardiotrophic infectious agents produce inflammatory mediators, cause immune mediated injury to the apical endocardium and inflow portion of the ventricles, result in fibrotic process obliterating the apex and affect the subvalvular apparatus similar to rheumatic process. Thus, future research must focus on identifying the strains of particular organisms responsible for this enigmatic disease worldwide.