The spleen is the largest lymphoid organ and the largest filter for blood in the body. Spleen parenchyma is divided into two functionally and morphologically distinct compartments (red and white pulp). Red pulp forms the majority of spleen tissue and consists of blood filled splenic sinusoids. White pulp is mainly made of PALS and lymphoid follicles. The PALS consists of a central artery surrounded by a sheath of lymphocyte-rich tissue. Its inner layer mainly consists of T-lymphocytes, while the outer layer shows a more diverse cellular picture, containing T- and B-lymphocytes. Lymphoid follicles of the spleen contain mainly B-lymphocytes. Splenic follicles demonstrate prominent marginal zones; here marginal zone macrophages expressing C-type lectins and a scavenger-receptor binding antigens on pathogens, such as Mycobacterium tuberculosis and Streptococcus pneumoniae, are located [7].

We hypothesize that the white pulp in our patients may be hyperplastic or otherwise changed in its consistency to be able to be seen more clearly in high-frequency sonography. A variety of pathogens can stimulate white pulp and cause reactive lymphoid hyperplasia [8]. Follicular hyperplasia often with marginal zone hyperplasia is seen in autoimmune diseases but also as reactive process in the setting of known lymphoma [8]. Generalized viral infections, especially EBV but also CMV and herpes virus infection can cause reactive lymphoid hyperplasia without germinal center formation in the spleen. In these spleens, expansion of the red pulp with partial loss of the white pulp is the main histological finding [8]. Also HIV infection is known to change the architecture of the spleen. Autopsy studies showed white pulp depletion and also perivascular hyaline fibrosis, possibly as an exaggeration of normal splenic histology, especially in advanced HIV disease stages [9]. This accentuation could lead to better visibility on ultrasound.

A possible explanation of the visible pulp could be concomitant HHV-8 infection, supported by the fact that almost half of the patients had overt opportunistic disease due to HHV-8. HHV-8 is the causal agent of KS but is also pathogenetically related to several lymphoproliferative disorders, including Multicentric Castleman Disease [10]. These diseases were diagnosed frequently, whether the remaining patients were infected sub-clinically with HHV-8 cannot be ascertained. It can nevertheless be speculated that HHV-8, possibly in conjunction with the advanced HIV disease, may cause changes of white pulp in the spleen.

The possibility to visualize the white pulp as a reticulo-nodular pattern has been described previously in pediatric patients using a 13 MHz linear array transducer [11]. A prominent reticulo-nodular pattern similar to the one seen in our patients was seen in 11 of 100 children; the pattern was associated with age and most frequently seen in the older children but not beyond the age of 10 years. The authors did not find an association with sex or BMI of the patients, but suggest that the increasing size of children makes the access for high-frequency sonography less feasible in larger patients. To our knowledge similar findings have not been described in adults.

Ultrasound evaluation of the spleen in patients with HIV and symptoms suggestive of TB in endemic regions is a viable diagnostic adjunct and detection of splenic micro-abscesses is probably sufficient indication to initiate TB treatment [3]. Nevertheless, in recent years a variety of disseminated infections have been shown to cause similar changes in the spleen; clinical, geographical and epidemiological information must therefore be considered in the diagnosis. Disseminated bartonellosis [12] and disseminated MAC infection [13] can cause splenic micro-abscesses in HIV patients. In Southeast Asian patients, melioidosis of the spleen must be considered as a differential diagnosis [14]. In areas where brucellosis is endemic, this disease poses another potential cofounder [15]. Leishmaniasis causes predominantly homogeneous splenomegaly but focal lesions are as well described [16].

The sonographic pattern described in this article adds another potential confounder because the “sponge pattern” may be interpreted as disseminated micro-abscesses in the spleen. Nevertheless, the lesions are smaller than TB micro-abscesses and the branching sponge-like appearance can be differentiated when moving the transducer. About the etiology of the pattern, not described in adult patients, can only be speculated, but it seems associated with advanced HIV infection and possibly with HHV-8 infection. Further studies of the pattern and its possible associated diseases are needed and clinical observations from other sonographers required.