|
|
When & How Does Rheumatic Heart Disease Occur?Incidence
and epidemiology When streptococcal infection is most frequent and intense. Similarly, the geographic distribution, incidence, and severity of rheumatic fever are, in general, a reflection of the frequency and severity of streptococcal pharyngitis. The attack rate of rheumatic fever following exudative streptococcal pharyngitis in epidemics averages approximately 3 percent. When streptococcal pharyngitis is sporadic and mild or due to strains of lesser or no rheumatic potential. The attack rate of rheumatic fever may be very much lower. Strains of group a streptococci that cause epidemics of streptococcal pharyngitis are most likely to be rheumatogenic. Following such infections, the attack rate of rheumatic fever caused by a variety of serotypes shows some, such as type 5, to be over represented and other to be conspicuously absent. In some population, such as in Trinidad, strains responsible for rheumatic fever and acute glomerulonephritis are serotypically distant. Environmental, bacterial, and host factors, which appear to play a role in the development of rheumatic fever, are important primarily because they are related to the incidence and severity of preceding streptococcal infection. Such factor as latitude, altitude, dampness, economic factors, and age all affect the incidence of rheumatic fever because they are related to the incidence of streptococcal infection in general. Crowding is however, the major environmental factor relating to the occurrence of this disease because, regardless of other variables, it promotes interpersonal spread of the most virulent group a streptococcal strains. Such crowding as occurs in military barracks, closed institutions, large families in small quarters, and those massed in the densely populated core of major urban centers is most likely to be associated with an increase in incidence of rheumatic fever. The attack rate of rheumatic fever following streptococcal infections by rheumatogenic strains in patients who have had previous attacks of rheumatic fever is increased to as high as 5 to 50 percent and also related to the virulence of the reactivating infection. Furthermore, the frequency or rheumatic recurrences following streptococcal infection is consistently greater in those with rheumatic heart disease than in those who escaped cardiac injury during prior attacks. The tendency to suffer recurrences of rheumatic fever following streptococcal infection, also influence the development of rheumatic fever. To what extent such variables are genetic or acquired has not been settled. It is common to obtain a family history of rheumatic fever as well as to encounter multiple cases among siblings of a single family. However, the concordance of rheumatic fever in identical twins is approximately 20 percent, suggesting only a limited penetrance of genetic predisposition to rheumatic fever. Although investigations of the distribution of haplotypes in rheumatic hosts have been limited in the scope and number, there have been so far no class 1 and somewhat limited class II HLA-DR associations occurring along racial lines. Particularly in those who have been found to be strikingly over represented in patients with rheumatic heart disease. Their nature and relation to pathogenesis, however, are not yet known. The incidence of rheumatic fever has been decreasing dramatically in countries where housing and economic conditions have been improving steadily. The rate of decrease in rheumatic fever may have been accelerated by the wide use of antimicrobial therapy. In recent years, however, local outbreaks of rheumatic fever have occurred in the United States in two military populations, one at the San Diego naval base. California,
and the other at fort Leonard wood, Missouri. Outbreaks also have occurred among
school children in Utah, Ohio, and Pennsylvania. Middle-class communities with
relatively high standard of living and medical care have been affected.
|
| ||||
|
| |||||
|
Disclaimer
: All the
material contained on this page is been just provided for educational and
informational purposes only and not intended to any type of consultation.
Please consult with your physician or appropriate healthcare personal for
any kind of opinions or recommendations with respect to your symptoms or
medical condition. The author is not responsible to any person or entity
with respect to any kind of damage, loss, or injuries, caused or alleged
to be caused directly or indirectly by the information contained in this
report. Also, the logos, trademarks, and brand names, if any, depicted on
this site are exclusive property of their respective companies.
Copyright -
© 2004 - 2008 - All Rights Reserved. |