Since the 1950’s intramuscular Benzathine Penicillin G (BPG) has been the recommended treatment choice for rheumatic fever (RF). Rheumatic fever is thought to be linked to socioeconomic status, poor nutrition and crowded living condition. Even though RF has declined in New Zealand since the 1970’s, New Zealand rates of rheumatic fever remain high particularly among Pacific Island and NZ Maori communities (New Zealand Health Strategy, 2003). This assignment will look at pre-disposing factors, and why this disease is prevalent in developing countries. The pathophysiology of rheumatic fever; biological action of Benthazine Penicillin G as an effective treatment, and its effect on recurrent rates of rheumatic fever will be discussed. Three studies that support its use will be discussed and analyzed.
Several Studies have shown environmental factors to play a role in spreading the disease ( McNicholas, et al, 2000: steer et al, 2002). Overcrowding enhances transmission as oral or respiratory secretions transmit the organism by direct contact. Some individuals can be carriers even after pharyngitis symptoms are resolved, and continue the cycle of infecting others ( Chin, 2003). Socio-economic status is another factor in the incidence of rheumatic fever where prevalence of rheumatic heart disease increased with decreasing socio-economic status (Steer et al, 2002). Urbanization has also lead to crowded inner city living and higher incidence of rheumatic heart disease. Over crowding seemed to be the predominant factor where there was a high rate of rheumatic heart disease (Steer et al, 2002) regardless of socio-economic factors (McNicholas et al,2000).
Poor nutrition in early childhood was identified in some studies as increasing susceptibility to acute rheumatic fever (Steer et al, 2002). Lack of access to medical care is another factor in perpetuating the disease (Lenon, 2004). According to Steer et al, (2002) suggest that increased access to medical care with the introduction of primary prophylaxis programmes to treat pharyngitis, and prevent rheumatic heart disease sequelae decreases rheumatic fever incidence.
In response to the 1978 World Health Oragnization promotion of disease registered to coordinate prevention of acute rheumatic fever, New Zealand began register based prevention programmes in the mid 1970’s to monitor and manage acute rheumatic fever (ARHF) case in the community. During 1995-2000, the annual rate of notified acute rheumatic fever was 2.8 per 100,000, a 12% increase from 1990-1995. period. While register based programmes may be better for monitoring ad management of acute rheumatic fever rates compared to general practitioners or hospitals, there is a need for uniformity between registers and protection of collected data from health sector restructuring ( Thornley, McNcholas, Baker,& Lennon, 2001).
The Pacific region continues to have higher rates of rheumatic heart disease as seen in New Zealand’s Maori and Pacific Island children. There is a need for well-designed studies and more reliable data to analyzed the trend. NZ Maori and Pacific Island people made up just over 20% of the total NZ population in 1996 and represented 74.6% of people living in crowded homes (McNicholas, Lennon, Crampton, Howden_Chapman, 2000). Baker, Goodyear, & Howden-Chapman () found from the 1998-2002 NZ census that low-incomes families with children, households containing NZ Maori and Pacific Island people and recent migrants were more likely to experience crowding. Auckland leads as the highest affected region for crowding and acute rheumatic fever rates I children up to 14 years old.
In New Zealand during the early 1980’s rheumatic heart disease in the Hamilton district was 6.5 percent in 1000 in Maori and 0.9 per 1000 in non-Maori (Talbot,1984). Baker Chakraborty (1996) found that during the 1970-1995 period, in New Zealand , rheumatic fever admission had declined markedly, and have remained stable since 1984. According to Carapetis, Curries& Mathews(2000) high rates in Pacific populations are due to Streptococcal exposure and treatment rather than differences in their genetic susceptibility. The genetic link remains unclear.
Rheumatic fever is a multi system inflammatory disease that occurs as a delayed sequel to pharyngeal infection by group A beta-hemolytic streptococci (GABHS) or Streptococcus pyogenes. Not all group A strains (GAS) are rheumatogenic. However ” throat strain” can colonize the throat rapidly and stubbornly (Rullan& Leonard, 2001). Streptococccus pyogenes owes its major success as a pathogen to its ability to colonize and rapidly multiply and spread in its host while evading phagocytosis and confusing the immune system (Todar, 2002).
Diagnosis of acute rheumatic fever is by throat swabs and throat cultures and use of the Jones criteria guidelines ( Stollerman, 2003). If a streptococcal throat infection is undetected or not treated adequately, this can progress in susceptible individuals to rheumatic heart disease where the valves of the heart become damaged or scarred resulting in inadequate functioning of the heart (Rush Univresity Medical Center website, 2005).
This inflammatory disease affects the connective tissues of the heart, joints, skin and central nervous system. Children aged 5-15 years and those with frequent streptococcal throat infections are more susceptible to developing rheumatic fever. Symptoms start about one to five weeks after infection with streptococcus bacteria. Symptoms range from joint inflammation, especially the larger ankle and knee joints, and can be migratory; change in neuromuscular movements eg: chorea; anorexia; rash on trunk, limbs; fever; and fatigue (Lennon, 2004).
Streptococcus pyogenes a genus of Group A streptococci usually reside in the respiratory tract (Todar,2002). They are gram-positive cocci, and penicillin G benzathine is effective for this as it prevents with cell wall replication of susceptible in streptococcus pyogenes, causing the cell walls to swell and burst from osmotic pressure, destroy the cell (Skidmore-Roth, 2005). Group A streptococci strain are highly sensitive to the action of penicillin.
Intramuscular Benzathine Penicillin G remains the drug of choice in preventing rheumatic fever and recurrences, due to its proven effectiveness, low cost and narrow antibacterial spectrum (Stollerman,2003). According to Manyemba & Bongani (2003), two or three weekly intramuscular penicillin injections were more effective than four weekly injections, in reducing the recurrence rates of rheumatic fever and associated streptococcal throat infections. Similar studies carried out by Kassem et al., (1996) and Lue et al., (1996) have shown similar results.
Continuous Benzathine Penicillin prophylaxis prevents recurrent attacks, and the risk of rheumatic fever rises by 25-275% with each subsequent recurrence of a streptococcal throat infection. New Zealand prophylaxis recommendation is for 10 years after presenting episode of acute rheumatic fever or until 21 years of age, whichever is longer (Lennon, 2004). The following selected three key studies will be assessing the effectiveness of intramuscular Benzathine Penicillin G, and providing support for its use against rheumatic fever infections and in reducing recurrence rates.