Aetiology

Some common predisposing factors and agents that cause septicaemia are shown in Table 24.1.

Table 24.1 Some common predisposing factors and agents of septicaemia

Pathogenesis and clinical features

Once the blood stream is invaded by microbes, the host responds by activating its defence mechanisms, leading to the production of a cascade of inflammatory cytokines (e.g. interleukin-1, tumour necrosis factor; see Chapter 10). The cytokine release is orchestrated by endotoxins of Gram-negative bacteria, peptidoglycan of Gram-positive bacteria and exotoxins from both these groups. Generally, these cytokines are beneficial in eliminating the organisms, but excessive production may lead to organ dysfunction and circulatory septic shock – the sepsis syndrome.

Some of these patients are said to develop the systemic inflammatory response syndrome (SIRS) depending on their clinical signs; these include hypotension, fever, rigors, oliguria and renal failure. Sometimes the infection may trigger a pathological activation of the coagulation system (disseminated intravascular coagulation (DIC)) and due to the resultant consumption of platelets and clotting factors, severe bleeding disorders.

Diagnosis

Blood should be cultured for a diagnosis of septicaemia. As the number of organisms circulating in the blood may vary from time to time, depending on the disease condition, more than one blood culture may be required; whenever possible, this should be carried out before antibiotic therapy is instituted. Several positive cultures are required to ensure that the culture result is not due to contamination from the venepuncture site. Cultures from sites suspected to be causing the infection are useful (e.g. pus from an abscess) to establish and localize the infective focus.

Treatment

The principles of therapy are:

Definition

Inflammation of the endocardium of the heart valves, and sometimes the endocardium around congenital defects, resulting from an infection.

Microbial aetiology

Bacteria are predominantly involved, although other organisms, such as fungi, rickettsiae and chlamydiae, may occasionally cause endocarditis (Table 24.2). More than 80% of infective endocarditis is caused by streptococci and staphylococci. The position held by the viridans group of organisms in the league table indicates the major role played by the oral commensals in causing this life-threatening disease. It is noteworthy that nearly all patients with viridans endocarditis have a previous heart lesion, and about a quarter give a history of a recent dental procedure as a precipitating factor.

Table 24.2 Causative microorganisms in infective endocarditis

(cumulative data from several sources)

Clinical features

Although two clinical forms of the disease – acute and subacute – have been identified, the line of demarcation between these forms is not often clear. The acute form is a rapidly progressive condition and is caused by bacteria such as Streptococcus pneumoniae, Staphylococcus aureus and Streptococcus pyogenes. The subacute form is more insidious and chronic, and progresses rather slowly. The agents of this form of the disease are less virulent bacteria, such as viridans streptococci, Staphylococcus epidermidis and Enterococcus faecalis.

Signs and symptoms

The classic signs are fever, malaise, loss of weight, anaemia, splinter haemorrhages, petechiae, cardiac murmur, haematuria and splenomegaly.

Diagnosis

Clinical signs supported by positive blood culture are used to make the diagnosis. Repeated culture may be necessary to isolate the causal organism owing to the low-grade bacteraemia. If possible, blood should be collected when the temperature of the patient rises, indicating fever due to bacteraemia. At least 10 ml of blood should be collected prior to antibiotic therapy and cultured under aerobic and anaerobic conditions (see Fig. 6.4). Any agent isolated from two different blood culture sets (on separate occasions) is considered significant. Identification and antibiotic sensitivity tests are then performed on the isolate.

Pathogenesis and epidemiology

Infective endocarditis normally occurs in patients with some pathological condition of the endocardium, although those with apparently normal heart valves may rarely be affected. The predisposing conditions include valve prostheses, septal defects, atheroma of the valve, congenital valve deformities and pre-existing rheumatic fever (Table 24.3). Infective endocarditis is the end result of the sequential interaction of events shown in