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Biomedical subjects

C B Panosian

Publications and source records attributed to C B Panosian.

16 recordsLinked to original sources
PubMed2001

Soft tissue echinococcosis: a report of two cases and review of the literature.

Echinococcosis (hydatid cyst disease) is a zoonotic infection caused by the parasitic tapeworm Echinococcus. The larval stage of this parasite can implant in many organs of the body, most commonly the liver, and create internal budding cystic masses. Echinococcal cysts also can implant in soft tissues; however, a review of the literature revealed no published case with the patient initially presenting with a soft tissue mass. Two such cases are reported in the current study. Physicians who evaluate soft tissue masses, particularly in patients from Echinococcus-endemic areas, need to include echinococcosis in their differential diagnoses. The current treatment of choice for soft tissue echinococcosis is wide resection combined with perioperative medical therapy.

Adult↗
PubMed1995

Human antiprotozoal therapy: past, present, and future.

Human protozoal infections are ubiquitous and occur worldwide. In many cases, antiprotozoal agents currently in use predate the modern antibiotic era. Despite the relative lag in development of new antiprotozoal agents, the 1990s have witnessed an increasing level of interest in these infections, inspired by international travel and immigration, a growing awareness of antiprotozoal drug resistance, and the significance of acute and recrudescent protozoal infections in immunosuppressed hosts. This review summarizes for nonclinician readers the past, present, and future therapies for common human protozoal infections, as well as pharmacologic mechanisms of action and resistance and common toxicities associated with these agents.

Antiprotozoal Agents↗
PubMed1995

Uncomplicated cat-scratch disease: findings at CT, MR imaging, and radiography.

PURPOSE: To describe the epidemiologic, clinical, and imaging features of cat-scratch disease (CSD) to facilitate prompt recognition and noninvasive diagnosis of this condition. MATERIALS AND METHODS: Eight otherwise healthy patients with pet cats presented with the subacute onset of epitrochlear, axillary, or groin masses. All underwent cross-sectional imaging with computed tomography (CT) (n = 1) or magnetic resonance (MR) imaging (n = 7). Five patients underwent radiography of the elbow. RESULTS: In all patients, MR imaging and CT showed a poorly defined soft-tissue mass with extensive surrounding edema in an efferent lymphatic distribution. Radiography revealed only soft-tissue edema in two patients and an ill-defined soft-tissue mass with soft-tissue edema in three patients. Six patients underwent biopsy; the findings of all pathologic specimens supported the diagnosis of CSD. No patients underwent serologic evaluation. All patients were asymptomatic within 4 weeks of beginning antibiotic therapy. CONCLUSION: CSD should be considered in all patients with upper extremity or head and neck adenopathy and a history of cat exposure. Although generally not required for diagnosis, cross-sectional imaging will reveal a mass with surrounding edema in an area of lymphatic drainage.

Adolescent↗
PubMed1995

Imported echinococcosis in southern California.

A retrospective chart review conducted at two teaching hospitals in Los Angeles County identified 28 patients with infection due to Echinococcus granulosus diagnosed by positive echinococcal serology and/or tissue biopsy between January 1981 and December 1990. Of these patients, 25 (89%) were foreign born and 19 (68%) were immigrants from the Middle East or central Asia. Only 12 of 22 immigrants questioned about epidemiologic risk factors described a history of rural residence or direct exposure to dogs in their native country. Single cysts of liver, lung, and soft tissue were present in six of 28 patients; multiple cysts in the 22 remaining patients were exclusively hepatic in 13 patients, exclusively pulmonary in two patients, and involved mixed sites including liver, lung, abdomen, central nervous system, and bone in seven patients. Natives of middle eastern countries currently constitute a major risk group for imported infection due to E. granulosus in the United States. Since their epidemiologic risk factors may be absent and clinical presentations varied, a high index of suspicion for echinococcosis is warranted in this population based solely on the presence of a cystic mass in liver, lung, or another organ site.

Adult↗
PubMed1992

Peritonitis caused by Mycobacterium kansasii in a patient undergoing continuous ambulatory peritoneal dialysis.

Mycobacterium kansasii was isolated from the peritoneal fluid, peritoneal biopsy, and the Tenckhoff catheter of a 62-year-old woman undergoing continuous ambulatory peritoneal dialysis (CAPD) who presented with the clinical picture of peritonitis. To the best of our knowledge, this is the first case of CAPD-associated peritonitis caused by M kansasii. Routine susceptibility tests using standard concentrations of isoniazid indicated isoniazid resistance; however, the organism was inhibited in vitro by a higher concentration of this drug. The patient responded to combination therapy with isoniazid and rifampin, as well as removal of the catheter. This report emphasizes the importance of mycobacterial cultures, in certain circumstances, in patients with CAPD-associated peritonitis and the utility of quantitative in vitro susceptibility testing.

Drug Therapy, Combination↗
PubMed1988

Parasitic diarrhea.

This article reviews the biology, epidemiology, and clinical management of amebiasis, giardiasis, and cryptosporidiosis as well as the less common intestinal protozoa, Dientamoeba fragilis, Isospora belli, Balantidium coli, and Blastocystis hominis.

Diarrhea↗
PubMed1985

Antigen recognition by effector T cells in antileishmanial defense.

We have observed that T cells (Ly1+2-) from draining lymph nodes of mice that have footpad infections with Leishmania major activate macrophages for antileishmanial effects in vitro in an apparently contact-dependent, noncytotoxic manner. The nature of antigenic specificity in this system was investigated. Whereas lymphocytes sensitized to L. major induced antileishmanial effects in macrophages infected with L. major, lymphocytes sensitized to Listeria monocytogenes were ineffective. When macrophages infected with L. major were primed with listerial antigens, however, the lymphocytes sensitized to Listeria induced antiparasitic effects in an apparently lymphokine-independent manner. Furthermore, lymphocytes sensitized to one Leishmania spp. activated macrophages for in vitro defense against both homologous and heterologous Leishmania spp. These findings suggest that antigen recognition in macrophage activation for antileishmanial defense is critical and is restricted to the initial interaction of effector lymphocytes and macrophages. Recognition of genus-conserved antigens apparently can serve to trigger effector T cells to activate antileishmanial defense in macrophages.

Animals↗
PubMed1984

Treatment of experimental cutaneous leishmaniasis with liposome-intercalated amphotericin B.

The therapeutic efficacy of a liposomal preparation of amphotericin B was evaluated in two murine models of cutaneous leishmaniasis. No significant decrease in tissue parasite density was observed in C57BL/6 mice after systemic treatment instituted seven days after footpad inoculation with Leishmania tropica; in contrast, BALB/c mice showed a modest response.

Amphotericin B↗
PubMed1984

Cell contact-mediated macrophage activation for antileishmanial defense. I. Lymphocyte effector mechanism that is contact dependent and noncytotoxic.

Leishmania are obligate intracellular protozoa in mammalian hosts. They infect and replicate within macrophages. Antileishmanial host defense is largely cell mediated. We conducted studies in vitro to investigate the ability of lymphocytes to activate macrophages for antileishmanial effects. Draining lymph node lymphocytes from C57BL/6 mice with cutaneous Leishmania tropica major infection were co-cultured in suspension with syngeneic, starch-elicited peritoneal macrophages infected in vitro with homologous parasites. In the presence of these effector lymphocytes, parasite replication was inhibited, and in some cases intracellular parasites were destroyed. In contrast, control lymphocytes from complete Freund's adjuvant-treated or Listeria-infected mice exerted no antileishmanial effects. Antileishmanial effects were greatest when Leishmania-sensitized lymphocytes were in direct contact with parasitized macrophages. Effector lymphocytes did not cause detectable damage to infected macrophages. Lymphocytes that induced the most profound antileishmanial effects in vitro were those obtained from mice entering a phase of spontaneous clinical resolution of their infections. We conclude that macrophages can be activated for microbicidal effects by direct contact with appropriately sensitized lymphocytes. This antigen-specific, contact-mediated lymphocyte effector mechanism may be important in host defense against certain intracellular microorganisms such as Leishmania.

Animals↗
PubMed1984

Cell contact-mediated macrophage activation for antileishmanial defense. II. Identification of effector cell phenotype and genetic restriction.

Host defense in cutaneous leishmaniasis, due to Leishmania tropica, is largely--if not exclusively--cell mediated. We observed in vitro that draining lymph node lymphocytes from L. tropica-infected C57BL/6 mice activate L. tropica-infected macrophages to kill the intracellular parasites (leishmanicidal effect). Because direct cell contact between lymphocytes and infected macrophages is required to achieve a maximum leishmanicidal effect, this effect cannot be attributed solely to lymphokines. Furthermore, because effector lymphocytes induced no detectable damage to infected macrophages, the effect also differs from conventional lymphocyte-mediated cytotoxicity. The present study identifies the phenotype of the effector lymphocyte and assesses the genetic restriction of the lymphocyte-macrophage interaction. Nylon wool column-enriched T lymphocytes from infected mice activate macrophages for antileishmanial effects; treatment of lymphocytes with anti-Thy-1.2 antibody plus complement abolishes this capacity. Furthermore, treatment with anti-Lyt-1 antibody plus complement (but not with anti-Lyt-2 plus complement) likewise abolishes the effector capacity of the lymphocytes. Parallel studies reveal that the percentage of Lyt-1+2- cells present in draining lymph nodes increases during the course of infection and reaches a peak with the onset of spontaneous resolution of the infection. Syngeneic, but not allogeneic, combinations of lymphocytes and infected macrophages result in macrophage activation. Furthermore, treatment of cells with appropriate anti-Ia monoclonal antibody abrogates the antileishmanial effects. These results indicate that Lyt-1+2- lymphocytes obtained from mice with spontaneously healing L. tropica infections can exert antileishmanial effects in vitro. This effect is genetically restricted--most likely to the I region of the MHC--and requires direct cell contact. The temporal relationship between the appearance of these effector lymphocytes in mice and the onset of disease resolution argues that they may also exert these antileishmanial effects in vivo.

Animals↗
PubMed1983

Acquired macrophage resistance to in vitro infection with Leishmania.

An important feature of pathogenesis in leishmaniasis is the ability of the intracellular amastigote to gain entry into host mononuclear phagocytes and subsequently replicate. Resident peritoneal macrophages freshly harvested from Leishmania tropica-infected C57B1/6 mice and uninfected controls were therefore compared for their ability to ingest L tropica amastigotes in vitro. Macrophages from infected mice had a strikingly reduced ability to ingest parasites, but they ingested latex beads and IgG-sensitized erythrocytes as well as or more than control macrophages. Preincubation of these macrophages for 24 hr restored the degree of parasite ingestion to control levels. This alteration in macrophage function could be observed as early as two weeks of infection and persisted until spontaneous resolution of the infection occurred at about six weeks. The observations suggest that acquired defense in leishmaniasis may include a specific inhibition of amastigote uptake by host macrophages.

Animals↗