Journal of Postgraduate Medicine
 Open access journal indexed with Index Medicus & ISI's SCI  
Users online: 10207  
Home | Subscribe | Feedback | Login 
About Latest Articles Back-Issues Articlesmenu-bullet Search Instructions Online Submission Subscribe Etcetera Contact
 :: Next article
 :: Previous article 
 :: Table of Contents
 ::  Similar in PUBMED
 ::  Search Pubmed for
 ::  Search in Google Scholar for
 ::  [PDF Not available] *
 ::  Citation Manager
 ::  Access Statistics
 ::  Reader Comments
 ::  Email Alert *
 ::  Add to My List *
* Registration required (free) 

  IN THIS Article
 ::  Abstract
 ::  Introduction
 ::  Material and Methods
 ::  Results
 ::  Discussion
 ::  Acknowledgements
 ::  References
 ::  Article Figures
 ::  Article Tables

 Article Access Statistics
    PDF Downloaded0    
    Comments [Add]    

Recommend this journal


Year : 1978  |  Volume : 24  |  Issue : 1  |  Page : 40-49

Infective endocarditis- (a survey of the past 50 years)

Department of Pathology and. Microbiology, Seth G.S. Medical College. Parel, Bombay-400 012., India

Correspondence Address:
Ajita P Mehta
Department of Pathology and. Microbiology, Seth G.S. Medical College. Parel, Bombay-400 012.
Login to access the Email id

Source of Support: None, Conflict of Interest: None

PMID: 731612

Rights and PermissionsRights and Permissions

 :: Abstract 

Autopsy incidence of infective endocarditis during the past 50 years was analysed to review the changes in the clinico-pathologic pattern if any. 185 cases were recorded in a total of 39931 autopsies giving an average incidence of 0.46%. The cases were classified into groups I, II & III depending upon whether the endocarditis super­vened on normal hearts, diseased hearts or followed surgery, re­spectively. The fifty year period could be divided into three phases on incidence. First phase (1927-41) represented pre-antibiotic era in which group I cases predominated and causative organisms in 801" o f cases were virulent cocci such as staphylococci, haemolytic streptococci and pneumococci. In the second phase (1948-66) the general incidence was reduced by 50%. Group II cases predominat­ed and the most common etiologic agent was streptococcus viridans (40%). In the third phase (1967-76) the general incidence has reached again to preantibiotic level with coagulase positive staphy­lococci, Gram negative bacilli and fungi accounting for 90% of cases. Group III contributed significantly in this phase.
The changes in incidence are primarily due to fall and rise in Group I cases. Incidence of rheumatic heart disease with endocar­ditis which mainly forms Group II is declining steadily in post­antibiotic era. There is no shift in the peak age incidence which remains in the 3rd decade. Males with rheumatic heart disease are more prone to infective endocarditis than similarly affected females. There was no change in frequency of involvement of various valves or sites of embolization.

How to cite this article:
Mehta AP, Dave KM, Kinare SG. Infective endocarditis- (a survey of the past 50 years). J Postgrad Med 1978;24:40-9

How to cite this URL:
Mehta AP, Dave KM, Kinare SG. Infective endocarditis- (a survey of the past 50 years). J Postgrad Med [serial online] 1978 [cited 2023 Jun 10];24:40-9. Available from:

 :: Introduction Top

In the one and half century since Bouillaud [1] described it first, infective en­docarditis has retained the interest of clinicians, pathologists and microbiolo­gists alike. Horder, [9] Thayer [20] and Lib­man and Cellar [15] studied extensively and catalogued precisely the natural history of the disease with predictable signs and symptoms as well as the course in pre antibiotic era. Introduction of antibiotics brought about marked reduction in the incidence of the disease though not com­plete disappearance. The interest in the disease however was kept alive not mere­ly because of its persistence in the anti biotic era, but because of the striking change in the clinical picture on account of the emergence of resistant strains. The changed and changing pattern of the disease has been analysed by seve­ral workers in developed coun­tries. [3],[4],[8],[10],[12],[13],[14],[16],[17],[21]

In a developing country like India with higher incidence of infections, as well as rheumatic disease, combined with inade­quate facilities of detection and poor availability of higher antibiotics, the pat­tern of infective endocarditis may not be the same as in the developed countries. [11] Hence it was thought relevant to review the pattern of this disease through last 50 years as reflected in the autopsy data.

 :: Material and Methods Top

Data was collected from the autopsies performed in the Department of Pathology of the King Edward VII Memorial Hospital during the years 1927 to 1976. The number of autopsies constituted, on an average 37% of deaths but after 1962 the number always exceeded 40%. The information about the causative organisms was based on microbiological studies carried out at autopsy as well as on their de­tection in paraffin sections.

 :: Results Top


Infective endocarditis was found in 185 cases out of 39931 autopsies carried out during the period 1927 to 1976. The per­centage varied over the years from 0% to 1.8% giving an average of 0.46%. The graphic representation of yearly incidence as percentage of autopsied cases shows rather irregular distribution with sudden high peaks, [Figure 1]. However, the overall distribution if studied closely showed persistent decline after 1947 with complete absence of cases during 1951-54. There was irregular rise between 1955­-1966. From 1967 onwards the rise is per­sistent and uniform. These periods can be considered as representing three pha­ses of the disease. In further analysis therefore, the data is compared taking these phases into consideration. The first phase (1927-47) corresponds to the pre­antibiotic era in our country as antibiotics became freely available after 1947. In the 3rd phase (1967-76), apart from antibio­tics there was one more modifying factor viz. increase in the number of cardiovas­cular operations, particularly the open heart. The overall incidence of infective endocarditis in the pre-antibiotic period was 0.58% of autopsies. It showed more than 50% reduction in the second phase being 0.26%. The incidence again rose to 0.55% in the last decade. To separate out the significance of important contri­butary factors the cases were grouped in three categories.

Group I: Endocarditis supervening on normal hearts-78 cases (42%).

Group II: Endocarditis supervening on diseased hearts-66 cases(35.8%).

Group III: Endocarditis following cardiac surgery-41 cases (22%).

The change in the pattern of relative incidence of three groups through various phases is depicted in [Figure 2].

Group I which reflects the sepsis in general, was predominating the preanti­biotic era. It showed marked reduction in the second phase but assumed its posi­tion again in the last decade. The emer­gence of group III in the last decade cor­responded with the increase in open heart surgery. Out of 41 cases, endocarditis was a complication of open heart surgery in 37. In 34 of these, endocarditis super­vened on replaced prosthetic valves. Group II cases predominated in post-anti­biotic era but showed marked decline after 1967. This however, is not true in absolute terms. If absolute incidence in autopsies is considered, the group II cases showed a steady decline after 1947. Group II cases formed 0.24% of autopsies in the first phase, 0.20% in the second phase and 0.12% in the last phase.

Group II was further analysed to find out the incidence of predisposing heart disease in various periods. Rheumatic heart disease formed the bulk of these cases. Rest of the cases comprised of con­genital heart disease. Syphilitic heart disease was a rare predisposing cause and only one case each was noted in the first and second periods. The incidence of rheumatic heart disease in this group was 87.5%, 85.6%, and 63.6% respective­ly in the three phases. Thus the inci­dence of rheumatic heart disease showed distinct relative decrease only in the last decade with corresponding rise in con­genital heart disease.

Age and Sex distribution

Nearly 75% of cases belonged to 2nd, 3rd and the 4th decades with peak inci­dence in the 3rd decade [Table 1]. This pattern of incidence is not essentially changed over the years and is seen typi­cally in group II cases. Group I cases showed higher incidence in the 4th de­cade in pre-antibiotic era. In the last decade also number of cases are seen in the 5th, 6th and 7th decades though the peak is in the 3rd decade. Group III cases show higher incidence in the 2nd decade but this is a highly selective group and does not compare with naturally occurr­ing disease.

There is overall male predominance in sex distribution. There is marked dif­ference in sex distribution in various groups in different periods. Group II shows the highest ratio in each period ranging from 7:1 to 3: 1, while group I shows higher ratio in the pre-antibiotic era mainly. It is difficult to interprete these results as various extraneous fac­tors influence the sex ratio. These will be discussed later.

Sites of Endocarditis

The lesions in the majority of cases are confined to the valves. Mural endocar­dium was involved only in 10 cases and that too in group I and III [Table 2]. Mitral valve was the commonest site in all the groups. Aortic valve involvement is comparatively more common in group III but in this group the site of involve­ment is directly related to the operative procedure. Multivalvular involvement particularly the combined involvement of mitral and aortic valves is much more common in group II. No significant dif­ference was observed in the sites of in­volvement through various phases but iso­lated involvement of right sided valves was rarely seen in earlier years and 4 out of 5 cases observed in group I occur­red in the last decade. In these cases there was evidence of prolonged intrave­nous administration.

Etiologic Organisms

Information about organisms responsi­ble for endocarditis was available in 124 cases [Table 3].

In nearly 50% of group I cases coagu­lase positive staphylococcus was the etio­logic organism. In group II, on the other hand, streptococcus viridans was respon­sible for nearly 40%; cases. In group III fungus was responsible for 60% of cases. In the pre-antibiotic era, in 21 out of 26 cases the endocarditis was caused by pyo­genie cocci. Gram negative bacilli were responsible for one case only while no fungal endocarditis was noted [Table 3].

In the post-antibiotic era infection with streptococcus viridans and less virulent organisms were as common as virulent or­gardsms. In the last decade though viru­lent cocci were the commonest agents, there is remarkable increase in infections due to gram negative bacilli and fungi. The fungal infection in all but one case followed prosthetic valve involvement.

Embolic Lesions

Embolic lesions in major organs are common in all the three groups [Table 4].

Embolic infarcts septic or aseptic are seen in myocardium in 34% of cases and are important from the point of view of cardiac failure. In group I cases, kidney is the most frequently involved organ while in group II spleen appears to be the most frequent target. Involvement of central nervous system is significantly higher in group I and III cases than in group II cases. Lung involvement is as expected more common in group I pati­ents.

 :: Discussion Top

Introduction of antibiotics and chemo­therapeutic agents in the management of infectious diseases changed dramatically the natural history and prognosis of many infective disease. With emergence of re­sistant strains however, these are returning with a changed clinical profile. This is amply confirmed in case of infective endocarditis by several reported series. [5],[6],[8],[10],[14],[16],[17],[18],[19],[21]

The mortality of infective endocarditis was 100% before the advent of antibio­tics. [8] In developed countries it is now reduced to around 30% [8],[14] There is no data available in India but mortality is not likely to be less than 50%. The study of autopsies alone is likely to give a ra­ther biased data especially if the mortal­ity is not very high, However, in the ab­sence of proper laboratory data particu­larly the micro-biological one, autopsy data becomes more dependable and hence such a study was thought worthwhile. Moreover a ratio of total deaths and the number of autopsies performed is fairly satisfactory and hence the data obtained can be considered representative.

The antibiotics did bring down the total incidence of endocarditis in our series by more than 50% . In the last decade there is again a notable increase and the inci­dence has almost returned to pre-antibio­tic level. The important change noted in the clinical profile in developed countries is the change in age of patients. This change is attributed to the marked de­crease in the incidence of rheumatic heart disease which is a disease of young. [8],[10],[12],[14] In our data there is no significant differ­ence in the age groups over the last 50 years. Most of the cases belong to 2nd, 3rd and the 4th decades and the peak in­cidence is still in the 3rd decade.

Another feature of the changed clinical profile is increasing male preponderance; which is more marked in older age group. [8],[12],[14] In the present series the male preponderance is marked in the pre­antibiotic era. The ratio decreased mar­kedly in the post-antibiotic period but in the last decade there is a rise again. How­ever, it is difficult to draw any definite conclusions from this data. There are several factors which influence the male and female ratio. The ratio of beds avail­able in the hospital for males and females is 2:1. In earlier years due to socio-eco­nomic conditions there was reluctance on the part of females to enter a general hos­pital as well as there was deliberate neg­lect by family in providing medical re­lief. This may account for high ratio ob­served especially in pre-antibiotic era. It is however, noteworthy that male pre­ponderance is seen also in cases of bac­terial endocarditis associated with rheu­matic heart disease. Autopsy data from the same source shows equal incidence of rheumatic heart disease in males and females in the post-antibiotic era, [11] indi­cating increased succeptibility of male rheumatic patients to bacterial endocar­ditis.

The distinction between acute and subacute endocarditis which was mainly dependent on the clinical duration of the illness is not of much clinical use now as it depends mainly on the causative or­ganism and its succeptibility to antibio­tics. Instead, it is better to classify the cases into those with previously normal heart and those with previously diseased hearts. In the first group, the primary condition is marked bacteriaemia or sep­ticaemia by virulent organisms. In the second group bacteriaemia with less virulent organisms which may have no effect on normal valves affects the diseas­ed valves. Because of known suscepti­bility of this group, endocarditis is gene­rally diagnosed and treated earlier. Moreover, the organisms affecting these hearts are usually susceptible to antibio­tics. In the first group, the clinical diag­nosis is often difficult and majority of cases are diagnosed only at autopsy. [5],[18] This group is the one which was curbed in early post-antibiotic era but is on the increase in recent years. [3],[4],[8],[12],[13],[14] In the present series also this group was domi­nant in the pre-antibiotic era and is domi­nating again in the last decade, thus con­firming the change observed in develop­ed countries. The second group dominat­ed in the early post-antibiotic period mainly due to the decrease in the first group. The absolute figures show that there is a gradual decrease in this group throughout the years though the decrease is not as much as in developed countries, mainly because the rheumatic heart disease is not on wane in this country as yet. The incidence of congenital heart disease and with bacterial endocarditis is significantly increased during the last de­cade chiefly on account of the increased facilities for diagnosis and treatment available for these patients which are at­tracting them to hospital. Post-operative bacterial endocarditis constitutes one of the serious complications of cardiac sur­gery particularly valve surgery. The in­cidence of this complication is rather high and the factors responsible for this are discussed in a separate communication.

The etiologic organisms which play the most crucial role in the course and prog­nosis of endocarditis are showing the same change in the pattern as has been observed by other workers. [4],[6],[8],[10],[12],[13],[14],[16] The increasing role of staphylococci, gram negative bacilli and fungi is clearly seen in the present series.

As far as the site of endocarditis is concerned mitral valve is the site of pre­dilection irrespective of the etiologic agent in the present series. This is in conformity of some of the reported series. [10] Recently however, some work­ers have reported more frequent involve­ment of aortic valve than mitral particu­larly in cases in whom endocarditis supervened on normal valves. [3],[21] The tri­cuspid involvement is rare but is on the increase in the recent years. It is parti­cularly common in drug addicts. In the present series the increase in the tricus­pid involvement in recent years is prob­ably the result of prolonged intravenous therapy. Involvement of mural endocar­dium is seen in virulent infections and is seen in the present series mostly in the last decade.

Embolic lesions which are so charac­teristic of endocarditis are common in all types of endocarditis. Kidney involve­ment is more common in group I cases, while splenic in group II cases. Notable is the involvement of myocardium which is higher than in the reported series. [3],[14] This is particularly common in post-ope­rative endocarditis.

In brief, it can be said that the pattern of endocarditis has changed over last 50 years. The pattern now resembles to that reported from developed countries as far as the general incidence and etiologic or­ganisms are concerned. The decrease in cases of endocarditis associated with rheu­matic heart disease is gradual and is not of the degree reported in developed coun­tries. The increasing incidence of endo­carditis particularly the one supervening on normal hearts in the last decade calls for vigilance.

 :: Acknowledgements Top

We are indebted to the Dean, King Edward VII Memorial Hospital and Seth G. S. Medical College, Bombay, and also to Dr. (Smt.) S. M. Sant, Prof. of Patho­logy and Microbiology, K.E.M. Hospital and Seth G.S. Medical College, for the permission to use the records.

We also thank Dr. A. K. Murthy, Re­sident Pathologist, King Edward Memo­rial Hospital, for the help in collecting the data.

 :: References Top

1.Bouillaud, J. P.: New researches on acute articular rheumatism. Haswell, Barrington and Haswell, Philadelphia,1837. Quoted by Friedberg. [7]   Back to cited text no. 1    
2.Bornstein, D. L.: Bacterial endocarditis: `Cardiac and Vascular diseases'. Conn, Hadley J., Jr. and Horwitz, Orville. 1 st Edition, Lea and Febiger, Philadelphia, 1971, p. 830.  Back to cited text no. 2    
3.Buchbinder, N. A. and Roberts, W. C.: Left sided valvular active infective endo­carditis. A study of 45 necropsy patients. Amer. J. Med., 53: 20-25, 1972.  Back to cited text no. 3    
4.Editorial: Infective Endocarditis. Brit. Med. J., 4: 121-122, 1973.  Back to cited text no. 4    
5.Falase, A. V. F., Jaiyessini, A. D., Iyun and Attah, E. B.: Infective Endocardi­tis-Experience in Nigeria. Trop. and Gecgraph. Med., 28: 9-15, 1976.  Back to cited text no. 5    
6.Finland, M. and Barnes, M. W.: Chang­ing etiology of Bacterial Endocarditis in the antibacterial era. Ann. Int. Med., 72: 341-348, 1970.  Back to cited text no. 6    
7.Friedberg, K. C.: Endocarditis and En­docardial Diseases. In `Diseases of Heart' 3rd edition. W. B. Saunders Com­pany, Philadelphia and London. 1966, p. 1019.  Back to cited text no. 7    
8.Hayward, G. W.: Infective endocardi­tis: A changing disease. Brit. Med. J.,2: 706 and 764-766, 1973.  Back to cited text no. 8    
9.Horder, T.: Infective Endocarditis with an analysis of 150 cases and with special reference to the chronic form of the disease. Quart. J. Med., 2: 289, 1909. Quoted by Bornstein.2  Back to cited text no. 9    
10.Hughes, P. and Gauld, W. R.: Bacterial endocarditis. A changing disease. Quart. J. Med., 35: 511-517, 1966.  Back to cited text no. 10    
11.Kinare, S. G.: Chronic rheumatic val­vular heart disease. Ann. Ind. Acad. Med. Sci., 8: 47-51, 1972.  Back to cited text no. 11    
12.Leading article: Bacterial Endocarditis: A changing pattern. Lancet, 1: 605-606,1967.  Back to cited text no. 12    
13.Leading article: Changing face of infec­tive endocarditis: Brit. Med. J . , 2: 385­ 390, 1967.  Back to cited text no. 13    
14.Lerner, P. I. and Weinstein, L.: Infec­tive Endocarditis in the antibiotic era. New Eng. J. Med., 274: 199-205, 259-265, 323-331, 388-393, 1966.  Back to cited text no. 14    
15.Libman, E. and Cellar, H. L.: The etio­logy of subacute bacterial endocarditis. Amer. J. Med. Sci., 140: '517, 1910. Quoted by Bornstein.2  Back to cited text no. 15    
16.Rabinowich, S., Evans, J., Smith, I. M. and January, L. E.: A long term view of bacterial endocarditis: Ann. Int.Mod., 63: 185-198, 1965.  Back to cited text no. 16    
17.Smith, R. H., Radford, D. J., Clark, R. A. and Julian, D. G.: Infective endo­carditis. A survey of cases in S. E. re­gion of Scotland: 1969-72. Thorax. 31: 373-378, 1976.  Back to cited text no. 17    
18.Somers, K., Patel, A. K., Steiner, I., Ar­bela, P. G. and Hutt, M. S. R.: Infec­tive Endocarditis-an African experience. Brit. Heart J., 34: 1107-1112, 1972.  Back to cited text no. 18    
19.Steiner, I., Patel, A. K., Hutt, M. S. RR and Semers, K.: Pathology of Infective Endocarditis-a postmortem evaluation. Brit. Heart. J., 35: 159-164, 1973.  Back to cited text no. 19    
20.Thayer, W. S.: Bacterial or infective endocarditis. Edinborough Med. J., 38: 237-265, 307-334, 1931.  Back to cited text no. 20    
21.Uwaydah, M. M. and Weinberg, A. N.: Bacterial endocarditis-A changing pat­tern. New Eng. J. Med., 273: 1231-1234, 1965.  Back to cited text no. 21    


  [Figure 1], [Figure 2]

  [Table 1], [Table 2], [Table 3], [Table 4]


Print this article  Email this article
Previous article Next article
Online since 12th February '04
© 2004 - Journal of Postgraduate Medicine
Official Publication of the Staff Society of the Seth GS Medical College and KEM Hospital, Mumbai, India
Published by Wolters Kluwer - Medknow