Acute Rheumatic Fever and Rheumatic Heart Disease

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Introduction:
Acute Rheumatic Fever (ARF) and its successive partner, Rheumatic Heart Disease (RHD), pose a serious issue in paediatric health world wide. Alarmingly New Zealand is one of the biggest contributors and has the highest recorded number of ARF cases internationally (Jaine, Baker, & Venugopal, 2008). This essay will discuss the pathophysiology and epidemiology of ARF and RHD. It will focus on the impact this illness has on Maori and Pacific Island children in particular as ARF is almost exclusive within these ethnic groups (Atatoa-Carr, Bell, & Lennon, 2008; Sopoaga, Buckingham, & Paul, 2010). Additionally, the role that paramedics exhibit in acute cases of ARF will be discussed; with focus being on how paramedics and other health professionals are able to reduce the burden ARF imposes on New Zealand society.

Pathophysiology:
ARF originates from an autoimmune response to a common bacterial infection; group A Streptococcus (GAS) (Jaine, Baker, & Venugopal, 2011). A phenomenon called molecular mimicry occurs, in which antibodies directed towards M proteins found on GAS molecules interact with glycoprotein antigens found in connective tissue of the heart and joints (Porth, & Matfin, 2009). This autoimmune response can continue for weeks after GAS infection is cleared from the body and results in irreversible damage to the connective tissues of the heart. Although the likelihood of developing ARF from untreated GAS infection is relatively low, the incidence of ARF development from recurrent GAS infection is much higher (Porth, & Matfin, 2009). Although the pathogenesis of ARF is not fully understood there is a proven correlation between GAS infection and ARF development (Lennon, 2004). Porth & Maftin (2009) state that the...

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