A 33-year-old man presented with right scrotal hardening and swelling, accompanied by inguinal pain and flank soreness, for 3 months. An off and on fever was also noted. Right epididymitis was the initial impression, and oral antibiotics of Cephalexin were prescribed. The symptoms persisted after treatment. An ultrasound examination showed heterogeneous echogenicity of the right testis, suggesting a testicular tumor. A further pelvic computed tomographic scan revealed enlargement of the right testis estimated to be 4.5 x 4.0 cm in dimension, with heterogeneous enhancement, suspected of being a testicular tumor (Fig. ). No abdominal lymphadenopathy was found. Serum tumor markers, including α-fetoprotein, β-human chorionic gonadotropin (β-hCG) and lactate dehydrogenase (LDH), were within normal limits. A right radical orchiectomy was performed under the impression of a testicular tumor.\nOn gross examination, the testis revealed an ill-defined, gray to tan, soft-tumor-like lesion measuring 3.3 x 3.2 x 2.6 cm (Fig. , ). Histologically, the lesion disclosed dense lymphoplasma cell and histiocyte infiltration in the interstitium, as well as spindle cell proliferation (Fig. , , ). There were small foci of foamy histiocyte aggregation and microabscess formation in the lesion (Fig. ). Some of the blood vessels revealed obliterative vasculitis (Fig. ). The seminiferous tubules revealed atrophic change (Fig. ). There was no well-formed granuloma or caseous necrosis in the lesion. The inflammatory process had also partially affected the epididymis and spermatic cord.\nA panel of histochemical stains and immunohistochemical (IHC) stains was performed. IHC staining of CD68 (1:250; Biocare) and CD163 (1:50; Leica) proved a histiocytic nature. The spindle cells were focally positive for smooth muscle actin (1:50; DAKO), but negative for ALK (1:200; NOVO) and CD21 (1:100; Cell Marque), suggesting a myofibroblastic origin. No significant immunoglobulin G4 -positive plasma cell infiltration was seen (IgG4, 1:800; Invitrogen). No microorganisms were demonstrated by acid-fast, periodic acid-Schiff, Grocott-Gomori methenamine-silver stains, or Gram’s stain. IHC with a rabbit polyclonal antibody against Treponema pallidum (dilution 1:100, Biocare Medical, Concord, CA, USA) displayed some spirochetes in the cytoplasm of histiocytes (Fig. ), highly suggestive of syphilitic orchitis.\nPolymerase chain reaction (PCR) testing for the T. pallidum DNA polymerase I gene using paraffin-embedded tissue was done. Positive control was applied using an anal biopsy specimen previously diagnosed as syphilis proved by immunohistochemistry and serology. A semi-nested PCR using the primers of TPmod-F1 (5′-GTGTGCACTGGGCATTACAG-3′), TPmod-F2 (5′-TGAAGCTGACGACCTCATTG-3′), and TP mod-R1 (5′- GTCTGAGCACTTGCACCGTA-3′) targeted a different region of the T. pallidum DNA polymerase I gene (Fig. ) []. Direct sequencing proved positivity for T. pallidum, which confirmed the diagnosis of syphilitic orchitis.\nThe patient underwent further serology tests postoperatively. An anti-human immunodeficient virus (HIV) enzyme-linked immunosorbent assay (ELISA) and Western blot tests were positive. However, serology tests for syphilis, including both Venereal Disease Research Laboratory (VDRL) test and Treponema pallidum particle agglutination (TPPA), demonstrated false-negative results. At that time, the patient had a low CD4 count (72 cells/mm3) and a low CD4/CD8 ratio (0.07).
A 49-year-old man presented with sudden confusion and headache. He was diagnosed HIV-positive (CD4 220 cells/mm3, viral load 3898 copies/ml) with acute kidney injury and CMV viraemia. Computerised tomography (CT) brain imaging was normal. He received once daily lamivudine 300 mg, darunavir 800 mg and ritonavir 100 mg with raltegravir 400 mg b.d. He developed symptomatic hypotension. Testosterone was <0.3 pmol/l with biochemical features of panhypopituitarism with cortisol <25 nmol/l, free thyroxine 4.6 pmol/l, TSH <0.05 IU/l, prolactin <10 mIU/l, LH 1.2 IU/l and FSH <0.5 IU/l. Cerebrospinal fluid (CSF) analysis revealed a raised protein (0.66 g/l) and negative microscopy. MR imaging found evidence of subacute haemorrhage in the pituitary gland, with no evidence of pituitary tumour, suggesting direct haemorrhage into the gland, which is unusual (Fig. ). The working diagnosis was CMV infection of the pituitary gland causing haemorrhage []. His hypopituitarism was treated by appropriate endocrine replacement with hydrocortisone, levothyroxine and testosterone.