Causative organisms vary between primary and secondary IPA. Most often a single organism is responsible; however, secondary cases with a gastrointestinal or urinary source may be polymicrobial. In primary IPA, the most common organism identified is S. aureus. In secondary IPA with a gastrointestinal or urinary source, Escherichia coli is most commonly implicated. Bacteroides, M. tuberculosis, Streptococcus viridans, Enterococcus faecalis, and Peptostreptococcus have also been isolated from IPA. Patients with HIV/AIDS most commonly present with a primary IPA due to M. tuberculosis; S. aureus is the second most common organism in this population. HIV patients with secondary IPA most often have a genitourinary source or lumbar spondylodiscitis. M. tuberculosis is generally associated with secondary IPA with a skeletal, genitourinary, or gastrointestinal source. Primary IPA from this organism may be secondary to hematologic spread from a respiratory focus.

Epidemiology

While IPA is certainly a rare condition, its true incidence is unknown. The earliest definitive worldwide series by Ricci et al. in 1986 suggested a rate of three cases annually worldwide, although underreporting certainly confounds these data. More recent studies suggest higher incidence, although most institutions still only see a few cases per year. Improved imaging modalities may have led to more accurate diagnosis and increased reported incidence. Increasing prevalence of immunocompromised patients such as transplant recipients and HIV/AIDS patients may also partially explain increased incidence.

Classically, the etiology of IPA has varied widely dependent on location. Ricci et al. showed that the vast majority (99.5%) of IPA cases in Asia and Africa were primary in nature while the majority (81.3%) of cases in Europe were secondary and most commonly attributed to Crohn’s disease. In the United States, 61% of cases were primary, but more recent studies have shown that secondary cases are more common with the current incidence of primary cases reported between 7% and 45%. IPA may occur at any age, although the median age at presentation has been reported to range from 45 to 58.

A 2011 series reported by Alonso et al. evaluated admissions to the Johns Hopkins Hospital over a period of 15 years and identified 61 cases of IPA. They demonstrated an increase in the incidence of IPA from 0.5 cases per 10 000 admissions (1993–2004) to 6.5 cases per 10 000 admissions (2005–2007). Eighty percent of cases were secondary with the contiguous source most commonly identified in the skeletal system (48%) or an intra-abdominal organ (23%). Interestingly, the causative organism in this population was noted to be MRSA in 25% of all cases and 37% of those cases with a definitive microbiologic diagnosis. Risk factors included intravenous drug use in 21% of patients, neoplasm in 18%, diabetes mellitus in 15%, and HIV in 15%. Only 11% of patients had inflammatory bowel disease and 10% had suffered traumatic injury during the preceding 30 days.

A 2009 series by Navarro Lopez et al. evaluated admissions to 11 different hospitals in Spain over a period of 15 years and identified 124 cases of IPA. Primary IPA was diagnosed in 21.8% of patients and secondary IPA in 78.2% of patients. The most common source was the skeletal system (50.5%), gastrointestinal tract (24.7%), and urinary tract (17.5%). Risk factors included diabetes mellitus in 18.5% of patients, chronic liver disease in 16.1% of patients, neoplasm in 11.3% of patients and HIV in 6.3% of patients.

Diagnosis

A focused history and physical exam is critical in the diagnosis of IPA. History should specifically assess for risk factors including immunosupression, history of inflammatory bowel disease, intravenous drug use, or recent infection. Symptoms including fever, night sweats, and weight loss should be queried. Full laboratory evaluation including complete blood count, comprehensive metabolic panel, C-reactive protein, and erythrocyte sedimentation rate may help confirm an inflammatory process. Many patients will demonstrate a leukocytosis and some may demonstrate elevated blood urea nitrogen and creatinine or electrolyte disturbances. Blood cultures should be obtained prior to antibiotic administration and are often positive in patients with IPA. Both blood cultures and abscess aspirate may be used to diagnose the causative organism, although direct abscess aspirate is higher yield with greater specificity.

The classic triad of IPA is back/flank pain, fever, and limp (or flexion deformity). These findings may only be seen in 10% to 30% of cases, as most patients will present with nonspecific features including fever or malaise. Symptoms may also include abdominal or flank pain and signs may include a mass in the back, flank, or groin. Patients who are debilitated or immunocompromised may have few or no signs and symptoms. Active contraction and passive extension of the iliopsoas may be painful for patients, and thus the patient tends to relax the muscle by flexion of the thigh and externally rotating the hip. A psoas sign (pain with attempted hip extension) may be seen. Table 73.2 shows signs and symptoms of IPA.

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