**24. Risk factors**

A prerequisite for the development of SPE appears to be a heavily infected source such as long-term indwelling vascular devices, bacterial endocarditis of the right heart valves or peripheral thrombophlebitis (head and neck or pelvic infections) leading to showers of septic emboli to the lung. In the above-mentioned recent Japanese study with 247 SPE patients, fungal emboli were more common than bacterial emboli. Among the fungi, Aspergillus was the most common pathogen (20.8%) encountered preceding Mucor or Candida. Cancer was the most common predisposing factor associated with fungal SPE (63%) – Leukemia (43.2%), followed by adenocarcinoma and lymphoma. The top three infectious sources showering septic emboli were pneumonia, sepsis and infective endocarditis.

Non-Thrombotic Pulmonary Embolism 87

A peculiar subtype is Lemierre's syndrome (postanginal sepsis), a severe illness caused by the anaerobic bacterium, Fusobacterium necrophorum which typically occurs in healthy teenagers and young adults. The infection originates in the throat as tonsillo-pharyngitis, odontogenic infection, mastoiditis or sinusitis and spreads via a septic thrombophlebitis of the tonsillar vein and internal jugular vein. The ensuing bacteremia is complicated by septic emboli to a range of sites such as lung, joints, and bones. Pulmonary involvement in Lemierre's syndrome has been reported in up to 97% with SPE, lung abscesses and empyema (Golpe et al., 1999; Riordan & Wilson, 2004; Sinave et al., 1989). The causative organisms of Lemierre's syndrome include the anaerobic gram-negative Fusobacterium species, and also Eikenella, Porphyromonas, Streptococci and Bacteroides. Recently, methicillin-resistant Staphylococcus aureus has been identified as a new causative agent

The clinical features of SPE are non-specific and patients generally present with a febrile illness, cough, hemoptysis, dyspnea and pleuritic chest pain. Diffuse cavitary lung nodules and infiltrates associated with an active focus of extra-pulmonary infection should clue the

(Riordan & Wilson, 2004).

Fig. 3.

**26. Clinical features** 

Fig. 2. (a & b): Causes of Septic Pulmonary Embolism (Cook et al., 2005; MacMillan et al., 1978)
