What are the causes of splenic microabscesses, particularly in immunocompromised individuals?

Causes of Splenic Microabscesses

Splenic microabscesses most commonly result from hematogenous seeding in immunocompromised patients, with infectious endocarditis being the classic cause in immunocompetent individuals, while immunosuppressed patients develop microabscesses from disseminated fungal infections, tuberculosis, or bacterial septicemia. 1, 2, 3

Primary Mechanisms of Formation

Hematogenous spread is the dominant pathway for splenic microabscess formation, occurring through:

• Septic emboli from infectious endocarditis - produces characteristic wedge-shaped microabscesses, typically measuring <1.5 cm in diameter 2
• Bacteremic seeding from distant infection sites - urinary tract infections, pneumonia, or other primary foci can seed the spleen hematogenously 4
• Direct extension from contiguous infection - less common but can occur from adjacent abdominal processes 5

High-Risk Populations and Predisposing Conditions

Immunocompromised States (Most Important)

Immunosuppression is the predisposing condition in approximately 64% of splenic abscess cases 3:

• Hematologic malignancies - lymphoproliferative disorders, myeloma, leukemia 6
• HIV/AIDS and other immunodeficiency states 1, 2
• Transplant recipients on immunosuppressive therapy 7
• Diabetes mellitus - increases vulnerability to complications including abscess formation 6
• Chronic corticosteroid use or chemotherapy 2, 3

Infectious Endocarditis

• Accounts for a significant proportion of cases in immunocompetent patients, producing septic emboli that lodge in splenic vasculature 1, 2
• Creates characteristic wedge-shaped infarcts that can progress to microabscesses 2

Splenic Infarction

• Microabscesses can form during the acute phase of pyelonephritis and may coalesce to form larger abscesses 6
• Bland infarcts from any cause (embolic, thrombotic, hematologic disorders) can become secondarily infected 8, 7

Other Predisposing Factors

• Splenic trauma - creates devitalized tissue susceptible to infection 1
• Intravenous drug use - introduces bacteria directly into bloodstream 1
• Functional hyposplenism - sickle cell disease (HbSS, HbSC), thalassemia major, essential thrombocythemia 6

Microbiologic Etiology

Bacterial Pathogens (Most Common)

• Staphylococcus species - most frequently isolated organism 1
• Enterobacteriaceae (including Klebsiella pneumoniae, E. coli) - common in hematogenous spread from urinary or GI sources 5, 4
• Streptococcus species - particularly in endocarditis-related cases 5
• Anaerobes (especially Bacteroides) - frequently involved 1, 5

Mycobacterial Infections

• Mycobacterium tuberculosis - accounts for up to 36% of cases in some series, particularly in immunosuppressed patients 3
• Produces characteristic multifocal microabscesses <1.5 cm 2, 3

Fungal Pathogens (Immunocompromised)

• Candida species - in severely immunosuppressed patients 2
• Other opportunistic fungi in transplant recipients and those with profound neutropenia 2

Clinical Recognition Patterns

Important caveat: Multifocal microabscesses (<1.5 cm diameter) are typically seen in four specific scenarios 2:

1. Infectious endocarditis with septic emboli (3 of 7 multifocal cases) 2
2. Immunosuppressed states (3 of 7 multifocal cases) 2
3. Tuberculosis (1 of 7 multifocal cases) 2
4. Acute pyelonephritis progression 6

Key Diagnostic Considerations

• CT with IV contrast remains the gold standard with 90-95% sensitivity and specificity, showing microabscesses as multiple contrast-enhancing cystic lesions 8
• Blood cultures are positive in only 24-80% of cases, making imaging essential 5
• Persistent fever, recurrent bacteremia, or signs of sepsis should raise suspicion for progression from infarction to abscess 8, 7