Granulomatous Hepatitis Associated With Cat Scratch Disease

Lenoir, Allen A.; Storch, Gregory A.; DeSchryver-Kecskemeti, K; Shackelford, Gary D.; Wear, Douglas J.; Rothbaum, Robert; Rosenblum, Jerry L.

doi:10.1016/s0140-6736(88)91952-6

Cited by 90 publications

(41 citation statements)

References 11 publications

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“…In that series, systemic manifestations included myalgias, splenomegaly, hepatic abscesses, neuroretinitis, pleurisy, arthralgias or arthritis, mediasti nal adenopathy or abdominal adenopathy. The occur rence of hepatosplenomegaly and hepatic granulomas and microabscesses has also been confirmed by others [4,5,II,12]. In the series and case reports of cat scratch disease in the literature, urinary findings are either re ported as normal or are not specifically mentioned [2][3][4][5][6][11][12][13][14][15].…”

Section: Discussionmentioning

confidence: 70%

“…The vast majority of cases, which are thought to number as many as 2,000 annually in the United States, have disease limited to lymphadenitis with mild constitutional symptoms [1], Less than 15% of cases have been associated with more serious systemic mani festations, including central nervous system disease (en cephalitis, myelitis or radiculitis), osteomyelitis, splen omegaly, necrotizing hepatic lesions, pneumonia and urethritis [1,[3][4][5]. Rare hematologic complications in clude eosinophilia and thrombocytopenic purpura [6].…”

Section: Introductionmentioning

confidence: 99%

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Cat Scratch Disease and Glomerulonephritis

D’Agati¹,

McEachrane²,

Dicker³

et al. 1990

Nephron

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Cat scratch disease is a generally benign, self-limited disease characterized by fever and regional lymphadenitis. Systemic complications are rare and most frequently affect the central nervous system, bone, liver or spleen. We report the first case of glomerulonephritis associated with cat scratch disease which resolved spontaneously concurrent with the resolution of lymphadenitis and constitutional symptoms. Immunopathologic and ultrastructural studies suggest a form of immune-mediated postinfectious glomerulonephritis.

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Section: Discussionmentioning

confidence: 70%

Section: Introductionmentioning

confidence: 99%

Cat Scratch Disease and Glomerulonephritis

D’Agati¹,

McEachrane²,

Dicker³

et al. 1990

Nephron

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“…are at highest risk for developing BAP and suggested than BAP be considered an AIDS-defining opportunistic infection. Also, B. henselae has been shown to induce granuloma formation in experimentally infected animals (9, 22) and in lymph nodes, spleens, and livers of human patients suffering from CSD (8,12,13,27), indicating the induction of CMI in immunocompetent hosts. In addition, in the era prior to detection of B. henselae and its recognition as the main causative agent of CSD, the induction of a delayed-type hypersensitivity reaction, a hallmark of CMI, was used to diagnose CSD clinically (14).…”

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confidence: 99%

Bartonella henselae-Specific Cell-Mediated Immune Responses Display a Predominantly Th1 Phenotype in Experimentally Infected C57BL/6 Mice

et al. 2001

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Immune responses of the immunocompetent host to Bartonella henselae infection were investigated in the murine infection model using C57BL/6 mice. Following intraperitoneal infection with human-derived B. henselae strain Berlin-1, viable bacteria could be recovered from livers and spleens during the first week postinfection, while Bartonella DNA remained detectable by PCR in the liver for up to 12 weeks after infection. are at highest risk for developing BAP and suggested than BAP be considered an AIDS-defining opportunistic infection. Also, B. henselae has been shown to induce granuloma formation in experimentally infected animals (9, 22) and in lymph nodes, spleens, and livers of human patients suffering from CSD (8,12,13,27), indicating the induction of CMI in immunocompetent hosts. In addition, in the era prior to detection of B. henselae and its recognition as the main causative agent of CSD, the induction of a delayed-type hypersensitivity reaction, a hallmark of CMI, was used to diagnose CSD clinically (14). Cats are considered the natural host of B. henselae and source of infection for humans. There are few reports on experimental infection of cats with B. henselae; however, the course of disease in cats differs from that in humans, and the results for clinical manifestations and histopathological findings are conflicting (7,9,11,21,23), possibly as a result of using different B. henselae strains and/or different mechanisms of inoculation. In addition, characterization of the induced immune responses has been difficult because of limitations of immunological tools in feline models. In contrast, murine infection models have been shown to be often advantageous for immunological studies (16). In the present study, we used a murine model of B. henselae infection established in our laboratory (22) to investigate the immune responses induced in the immunocompetent host. Following intraperitoneal (i.p.) infection of C57BL/6 mice with B. henselae, the cellular and humoral immune responses were analyzed at multiple time points until 20 weeks postinfection (p.i.). Proliferative responses were studied in vitro by means of a splenocyte proliferation assay. The roles of different T-cell subsets were investigated by administration of monoclonal antibodies (MAbs) to CD4 and CD8 T cells in proliferation assays. In cytokine release studies, Th cells involved in CMI against B. henselae were further characterized. Humoral immune responses were studied by enzyme-linked immunoassay (ELISA) for Bartonellaspecific immunoglobulin G (IgG) antibodies, and the IgG isotypes were determined. In addition, development and alter-* Corresponding author. Present address: Hygiene-Institut, University of Heidelberg, Im Neuenheimer Feld 324,

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“…Among the atypical presentations of CSD, visceral granuloma, especially one without peripheral lymphadenitis, is an important differential diagnosis in the patients with sustained fever of unknown origin [1][2][3][4][5]. It resolves spontaneously in most cases.…”

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confidence: 99%

“…It resolves spontaneously in most cases. Although splenic lesion is occasionally described as "splenic abscess", its histopathological finding is necrotic granuloma with micro-abscess [4,5]. In contrast to peripheral lymphadenitis, it is rare that splenic granuloma caused by B. henselae suppurates and necessitates surgical intervention.…”

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confidence: 99%

Pyogenic splenic abscess in an infant with serological evidence of cat scratch disease

et al. 2006

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AbbreviationsCSD cat scratch disease PCR polymerase chain reaction CT computed tomographyPyogenic splenic abscess is a rare intraperitoneal infection caused by a variety of bacteria, with S. aureus and streptococci most commonly isolated. Splenectomy is indicated when it is resistant to antimicrobial therapy. We report on a pyogenic splenic abscess requiring repeated aspiration in an infant who was serologically diagnosed as having cat scratch disease (CSD). A 7-month-old boy was admitted to a general hospital due to intermittent low-grade fever of 2 weeks' duration, splenomegaly and multiple cystic lesions in the spleen detected by ultrasonography. Despite intravenous administration of cefotaxime on suspicion of splenic abscess, high fever persisted and the intrasplenic lesions expanded. Five days after admission, he was referred to our hospital. There was no history of the presence of a pet. On physical examination, anemia and splenomegaly were noted. There was a strong acute phase response indicated by white blood cell (WBC) count (24,350/μl), C-reactive protein level (117 mg/l) and erythrocyte sedimentation rate (83 mm/h). Microcytic hypochromic anemia [red blood cells (RBCs) 3.88×10 6 /μl, hemoglobin (Hb) 8.2 mg/dl, hematocrit (Ht) 27.9%] was also noted. Chest X-ray showed a small infiltration in the left lower lung field, adjacent to the diaphragm. Abdominal computed tomography revealed an enlarged spleen with multiple cystic lesions, indicating intrasplenic abscesses (Fig. 1a). The patient's immunological parameters, including immunoglobulin levels, IgG subclass levels, lymphocyte subsets, proliferation to phytohemagglutinin, NK activity, and phagocytic and bactericidal activities of neutrophils, were normal. As the cystic lesions continued to enlarge, despite the intravenous administration of panipenem/betamipron and ampicillin, ultrasonography-guided puncture and aspiration were performed on the 10th hospital day. Three abscess lesions yielded a total of 20 ml of odorless yellowish-white pus (Fig. 1b). Cytological and histological examination of the aspirated material showed abscess and necrotic tissue without atypical cells. Neither bacteria nor fungus was identified by microbiological examination [smear, histology including Gram, periodic acid-Schiff (PAS), acid-fast and Warthin-Starry staining, and culture]. After the first aspiration, despite sequential and combined administration of antibiotics including meropenem, clindamycin, doxycycline, tobramycin, rifanpin, azithromycin and clarithromycin, small, low-density areas suppurated to form new abscesses one after another, necessitating a total of six sets (three-to-eight punctures per set) of aspiration (Fig. 1c).

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Granulomatous Hepatitis Associated With Cat Scratch Disease

Cited by 90 publications

References 11 publications

Cat Scratch Disease and Glomerulonephritis

Cat Scratch Disease and Glomerulonephritis

Bartonella henselae-Specific Cell-Mediated Immune Responses Display a Predominantly Th1 Phenotype in Experimentally Infected C57BL/6 Mice

Pyogenic splenic abscess in an infant with serological evidence of cat scratch disease

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