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The below mentioned article provides a study note on Endocarditis and Septicaemia:- 1. Meaning of Endocarditis and Septicaemia 2. Types of Septicaemia 3. Complications of More Localised Infection 4. Causative Microorganisms of Septicaemia 5. Clinical Types 6. Endocarditis Associated with Intravenous Drug Abuses 7. Pathogenesis 8. Hospital Acquired Native-Valve Endocarditis and Other Details.
Contents:
- Meaning of Endocarditis and Septicaemia
- Types of Septicaemia
- Complications of More Localised Infection
- Causative Microorganisms of Septicaemia
- Clinical Types
- Endocarditis Associated with Intravenous Drug Abuses
- Pathogenesis
- Hospital Acquired Native-Valve Endocarditis
- Laboratory Diagnosis
- Large Volume of Blood and Media
- Antibiotic Sensitivity Test
- Culture Negative Endocarditis
- Other Tests
- Treatment
- Laboratory Monitoring of Therapy
1. Meaning of Endocarditis and Septicaemia:
Septicaemia is a condition in which bacteria circulate and actively multiply in the blood. Pyaemia is primarily septicaemia with metastatic infection.
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Endocarditis is a condition in which bacterial endotoxin circulates in the blood. Blood in the circulation is sterile.
Bacteria may invade the blood:
(a) From an infective focus
(b) By introduction of contaminated material into the circulatory system.
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The microorganisms are cleared from the blood quickly when the immune system of the host is good. When the immune system is not working the microorganisms persist and multiply in the blood, producing signs and symptoms. “Septic shock” is a condition in which hypotension and signs of inadequate perfusion develop.
2. Types of Septicaemia:
Generalized infection-When bacteremia/septicaemia is of greater severity and of longer duration as in brucellosis and enteric fever, there will be generalized infection as basic feature.
3. Complications of More Localised Infection:
When the organisms spread from localised infective focus into the blood stream, the complications (pyelonephritis, cholangitis, pneumonia, peritonitis, osteomyelitis, abscesses of internal organs) may be observed.
4. Causative Microorganisms of Septicaemia:
A. Gram-negative bacilli (60-70%):
1. Salmonella:
(a) S. typhi.
(b) S. paratypi A
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(c) S. paratyphi B
(d) S. paratyphi C
2. Brucella sp.
3. H. influenzae
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4. E. coli
5. Klebsiella pneumonia
6. Proteus mirabilis, Pr. vulgaris.
7. Enterobacter sp.
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8. Bacteroides sp.
B. Gram positive cocci (20-40 %):
1. Staph, aureus
2. Str. pneumonia
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3. Str. pyogenes.
C. Gram-positive bacilli:
In pre-antibiotic era, pneumococci and streptococci were most common causes of septicaemia. Now, Gram-negative enteric bacteria (60-70%) are common causes of septicaemia, staphylococci, pneumococci, streptococci are less (20—40%) frequent causes of septicaemia.
E. coli is often isolated from culture at U.K. About 40% Gram-negative bacilli bacteriaemia is complicated by shock, while 10-15% Gram-positive bacteriaemia is complicated by shock. Shock is mediated by various bacterial products in the blood, in particular Gram-negative endotoxin. Predisposing factors play a great role in septicaemia.
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Infective Endocarditis:
Endocarditis is mostly caused by bacteria, rarely by fungus.
It can be divided into:
(a) Native value-endocarditis,
(b) Endocarditis of prosthetic valve, and
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(c) Endocarditis in drug abuses.
5. Clinical Types:
Clinically and pathologically, endocarditis may be:
(a) Sub-acute
(b) Acute
(c) Postoperative.
The bacteria settle in the previously damaged heart valve. The disease of native valve evolves into two main forms—depending on the type of infecting bacteria. Acute endocarditis is rapidly progressive and fulminating, sub-acute is mild and runs a chronic course.
The correlation between organism and course is not perfect, because infection with Staph, aureus can be associated with sub-acute course and viridans streptococci with an acute course.
A. Sub-acute endocarditis:
When damaged or defective valve cups is infected by an organism of low virulence, large firm vegetation’s comprising of dense fibrin and platelets aggregates with bacteria colonies are formed. Sub-acute endocarditis is more common and comprises of almost 70% cases of bacterial endocarditis. It does not produce metastatic foci and, if untreated, takes more than 6 weeks and even a year to be fatal.
Causative agents:
1. Viridans streptococci (most commonly Str. sanguis, Str. mutans, Str. minor) are responsible for 60-80% cases of sub-acute endocarditis. 2 Other pathogens — Str. faecalis (Syn.Enterococci), Staph, epidermidis, C. burnetti, Str. milleri, Str. bovis.
Fungi, C. albicans, Aspergillus are opportunistic pathogens following antibiotic use and immuno-suppressants.
B. Acute endocarditis:
In this condition, highly virulent pyogenic bacteria (Staph, aureus) affect both normal and abnormal (damaged, defective) valves. The tricuspid valve is more frequently affected. Vegetation’s are large and crumbling. Valve destruction is greater than in sub-acute endocarditis. It is rapidly progressive disease and, if untreated, it is fatal in less than 6 weeks.
Causative Agents:
1. Staph, aureus causes about 25% of native endocarditis. It is also an important cause of hospital acquired endocarditis:
2. Str. pneumoniae is responsible for about 10 percent cases of endocarditis.
3. Other pyogenic cocci, Str. pyogenes and Str. agalactiae (group B) are responsible for 5-6% cases of acute endocarditis.
C. Post – Operative Endocarditis:
Following surgery in which prosthetic valve or other intravascular prosthesis is done, postoperative endocarditis develops. Some 5-10 percent cases with prosthetic valves develop this condition due to infection of prosthetic valves.
Causative agents:
1. Staph, epidermidis is the most common cause organism (27-74% cases).
2. Staph, aureus causes 10% cases of prosthetic valve endocarditis.
3. C. albicans (0.5-1.5%).
6. Endocarditis Associated with Intravenous Drug Abuses:
In drug abuses most-infections occur in tricuspid valve.
Causative Agents:
1. Staph, aureus is responsible for 50% cases.
2. Other organisms-(Viridans streptococci, fungi, C. albicans, pseudomonas aeruginosa account for 1-15% cases).
7. Pathogenesis:
Those with pre-existing cardiac diseases are at risk. Predisposing cardiac diseases are:
1. Rheumatic valvular disease (25-30%). Stenosis and incompetence of mitral valve is most common, followed by that of aortic valve.
2. Congenital valve deformities (10-20%) e.g. biscupid arotic valve, septal defects, patent ductus arteriosus, coarctation of the aorta.
3. Intra-cardiac disease (10-12%) replacement of diseased heart valves with prosthetic valve.
4. Degenerative cardiac disease (5%). Calcified aortic stenosis, Syphilitic aortic valve disease.
5. Drug abuse-Drug abusers who take drugs intravenously are at risk of endocarditis.
8. Hospital Acquired Native-Valve Endocarditis:
Intravascular devices (peripheral-venous, central-venous, pulmonary artery, catheterisation) sometimes lead to endocarditis of normal heart valve. Traumatically induced sterile vegetation’s may become infected after bacteriaemia. Staph, aureus (80%) and C. albicans, Aspergillus, Acinetobacter (20%) cause hospital acquired native-valve endocarditis.
9. Laboratory Diagnosis:
Blood culture is the important diagnosis before antimicrobial therapy, blood should be as collected.
Specimen:
Three to six samples of blood, 10 ml each, are to be collected from antecubital vein over 24 hours. Blood sample should be inoculated into a (50-100 ml) of glucose broth medium. One culture should be obtained from each vene puncture using anaerobic and aerobic techniques. Addition of pyridoxal hydrochloride improves the chances of isolating nutritionally deficient variant streptococci.
10. Large Volume of Blood and Media:
Advantages:
(a) Since the number of organisms in the blood may be very few, even one/ml, at least 10 ml of blood is needed.
(b) Large volume of culture medium is also of great necessity to dilute the effect of bactericidal substances present in the patient’s blood.
(c) The bactericidal effect of substances detrimental to the growth of bacteria can be inhibited by certain substances like bile salts.
Cultivation:
Cultures should be incubated at 37°C and observed daily for growth of bacteria (colony) on the medium, then Gram-staining should be done and sub-cultured on blood agar aerobically or anaerobically, for at least 3 weeks before cultures are discarded as negative.
11. Antibiotic Sensitivity Test:
The routine disk diffusion technique with fixed concentration of drug is not adequate for guiding treatment of infective endocarditis. The measurement of the minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC) of the antimicrobial agents should be determined.
It would be helpful to determine adequate dose of the antibiotic to be used to ensure the serum levels that can penetrate the valves and kill the organisms.
12. Culture Negative Endocarditis:
Several reasons are suggested for persistent negative blood culture:
1. Recent antibiotic therapy:
Infective endocarditis are caused by streptococci that are susceptible to a wide range of antibiotics. Some of these cases will recover, while in others the organisms disappear temporarily from the blood. In such cases, repeated blood cultures done after the stoppage of antibiotics may become positive.
2. Infection by fastidious or slow growing organisms:
These organisms will not grow easily on ordinary media. They require special media with adequate period of incubation (e.g. Hemophilus influenza, Bacteroides, Actinobacillus, β-haemolytic streptococci). When these organisms are suspected, repeated blood cultures should be done by using special media.
3. Bacteriaemia is intermittent:
In this situation repeated blood cultures are necessary.
4. Infection with C. burnetti or Chlamydia psittaci:
They will not be isolated by blood culture, the serological tests (CFT) using both phase I and II antigens will give titres above 250.
5. Sometimes laboratory isolates are reported as contaminants, e.g., Staph, epidermidis may be causative agent.
13. Other Tests:
1. Electrocardiograms will show vegetation and valve changes in 75-80% cases of native valve endocarditis.
2. Leucocytosis, elevated ESR are common. Measurement of C-reactive protein in blood is sometimes more reliable than ESR to assess the progress of the disease.
14. Treatment:
Basically, antibiotic treatment is same in any case of endocarditis.
1. Combined Therapy:
Use of two drugs in combination is preferred and should be bactericidal for the pathogen (Table 81.3). Infecting organism may be very sensitive to antibiotics, but the drug cannot reach the organism within the vegetation in adequate concentration where the bacteria are present in large numbers.
Hence antibiotics should be given in high doses where possible and preferably intravenously to eliminate the organisms in vegetation.
2. Prolonged Therapy:
Treatment should be done for a minimum period of 4 weeks. With intravenous antibiotics and for certain organisms 4 to 8 week may be needed.
15. Laboratory Monitoring of Therapy:
While treating a case of endocarditis minimum bactericidal concentration (MBC) of the antibiotic is estimated in European countries, particularly when there is switch over to oral therapy.
Prevention:
(1) Good dental health,
(2) Prophylactic antibiotic cover before dental extraction and other surgical procedure can be useful in the prevention of endocarditis.
