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Biomedical subjects

R C Weiss

Publications and source records attributed to R C Weiss.

At least 37 records · Page 2Linked to original sources

Increased plasma levels of leukotriene B4 and prostaglandin E2 in cats experimentally inoculated with feline infectious peritonitis virus.

Specific-pathogen-free kittens experimentally infected with feline infectious peritonitis virus (FIPV) subsequently demonstrated increased plasma levels of the arachidonic acid metabolites, leukotriene (LT) B4 and prostaglandin (PG) E2. Significant increases (P less than 0.025) in LTB4 plasma levels occurred in all (5/5) FIPV-inoculated kittens on postchallenge-exposure days (PCD) 7 and 14 vs PCD 0. Significant increases (P less than 0.05) in PGE2 plasma levels occurred in 80% (4/5) of FIPV-infected kittens on PCD 7 and 14. Maximal mean plasma levels of LTB4 and PGE2 occurred on PCD 7 (502.5 +/- 45.6 pg/ml and 1108.0 +/- 247.9 pg/ml, respectively). A positive correlation was found between LTB4 plasma levels and body temperature (r = 0.609, P less than 0.01). Mean survival time in FIPV-inoculated kittens was 19.4 +/- 3.2 days. Gross lesions, including peritoneal or pleural effusions (or both) and connective tissue edema, indicated an increased vascular permeability in the FIPV-infected kittens. Histologically, lesions were characterized by vasculitis or perivasculitis, vasodilatation, perivascular edema, and fibrinonecrotizing and pyogranulomatous inflammation. Immunofluorescent studies of tissues from FIPV-infected kittens demonstrated foci of polymorphonuclear leukocytes and FIPV-positive macrophages oriented around dilated blood vessels. Seemingly, arachidonic acid metabolites, including LTB4 or PGE2 released from macrophages, neutrophils or other cells, may be involved in the pathogenesis of FIP vascular and inflammatory lesions and in some of the clinical disease manifestations.

Animals↗

Delayed-type hypersensitivity skin responses associated with feline infectious peritonitis in two cats.

Two cats previously challenge-exposed and seropositive to feline infectious peritonitis virus (FIPV) were evaluated for delayed-type hypersensitivity (DTH) skin responses to intradermal FIPV. Before testing, cat 1 (FIP-resistant) had survived a severe experimental FIPV challenge-exposure and had remained asymptomatic, whereas cat 2 (FIP-susceptible) developed acute fulminant FIP after a considerably smaller virus challenge-exposure. Cat 1 developed a focal thickened plaque at the FIPV-injected skin site at 48 hours after injection. Histological examinations of serial punch biopsies from virus-inoculated skin revealed perivascular and diffuse dermal infiltrations of macrophages, lymphocytes and polymorphonuclear leucocytes which were maximal at 48 to 72 hours after injection. In contrast, cat 2 did not react grossly and showed only very mild dermal infiltrates at 72 hours after injection. The present findings of strong DTH responses to FIPV in a resistant cat and minimal responses in a cat with acute fulminant FIP suggest that certain in vivo cellular immune reactions may be associated with disease resistance.

Animals↗

Inhibition of feline infectious peritonitis virus replication by recombinant human leukocyte (alpha) interferon and feline fibroblastic (beta) interferon.

Replication of feline infectious peritonitis virus (FIPV) in feline cell cultures was inhibited after incubation of cells with either human recombinant leukocyte (alpha) interferon (IFN) or feline fibroblastic (beta) IFN for 18 to 24 hours before viral challenge exposure. Compared with virus control cultures, FIPV yields were reduced by ranges of 0.1 to 2.7 log10 or 2 to 5.2 log10 TCID50 in cultures treated with human alpha- or feline beta-IFN, respectively; yield reductions were IFN dose dependent. Sensitivity to the antiviral activities of IFN varied with cell type; feline embryo cells had greater FIPV yield reductions than did similarly treated feline kidney or feline lung cells. Comparison of the virus growth curves in IFN-treated and virus control cultures indicated marked reduction in intracellular and extracellular FIPV in IFN-treated cultures. Compared with virus control cultures, intracellular and extracellular infectivity in IFN-treated cultures was delayed in onset by 12 and 30 hours, respectively, and FIPV titers subsequently were reduced by 3 to 3.5 and 5 log10 TCID50, respectively. Frequently, immunofluorescent and electron microscopy of IFN-treated cells or cell culture fluids did not reveal virus; however, even in cultures without viral cytopathic changes, small amounts of virus occasionally persisted in cells.

Animals↗

Antibody-mediated enhancement of disease in feline infectious peritonitis: comparisons with dengue hemorrhagic fever.

Non-immune kittens passively immunized with feline serum containing high-titered antibodies reactive with feline infectious peritonitis virus (FIPV) developed a more rapid disease after FIPV challenge than did kittens pretreated with FIPV antibody-negative serum. Antibody-sensitized, FIPV challenged--kittens developed earlier clinical signs (including pyrexia, icterus, and thrombocytopenia) and died more rapidly than did non-sensitized, FIPV-challenged kittens. Mean survival time in sensitized kittens was significantly (P less than 0.05) reduced compared to non-sensitized kittens (mean +/- SEM, 10.0 +/- 0.6 days vs. 28.8 +/- 8.3 days, respectively). Lesions induced included fibrinous peritonitis, disseminated pyogranulomatous inflammation and necrotizing phlebitis and periphlebitis. FIPV antigen, immunoglobulin G, complement (C3) and fibrinogen were demonstrated in lesions by immunofluorescence microscopy. The pathogenesis of dengue hemorrhagic fever (DHF) in persons bears striking resemblance to that of FIP in experimental kittens. In both FIP and DHF, non-neutralizing antibody may promote acute disease by enhancement of virus infection in mononuclear phagocytes or by formation of immune complexes, activation of complement and secondary vascular disturbances.

Animals↗

Pathogenesis of feline infetious peritonitis: pathologic changes and immunofluorescence.

Feline infectious peritonitis (FIP) was experimentally induced in FIP virus (FIPV) antibody-positive and antibody-negative kittens after challenge exposure to live-virus aerosol. Seropositive kittens developed antiviral immunofluorescence and lesions more rapidly after challenge exposure than did seronegative kittens. In seropositive kittens, FIPV antigen was present in macrophages and large mononuclear cells in tracheobronchial lymph nodes, lungs, and trachea on postchallenge-exposure day (PCD) 2; in liver and spleen on PCD 3; in kidneys and omentum on PCD 4; and subsequently in nasal turbinates, thoracic and abdominal lymph nodes, thymus, bone marrow, parotid salivary gland, eyes, and brain. Initial antiviral immunofluorescence on PCD 2 coincided with the onset of viremia and vascular lesions. Systemic lesions characterized by perivascular necrotizing pyogranulomatous inflammation, phlebitis and thrombosis, fibrinous serositis, and generalized lymphoid necrosis developed on PCD 3 and 4. Coronavirus-like particles were observed by electron microscopy in cytoplasmic vacuoles or smooth endoplasmic reticulum of degenerating macrophages in inflammatory lesions. In seronegative kittens, antiviral immunofluorescence in tracheobronchial lymph nodes was first detected on PCD 5, and viremia occurred on PCD 6. Systemic necrotizing lesions, comparable with those observed in seropositive kittens on PCD 3 or 4, did not occur in seronegative kittens until PCD 13 or 16. In both groups of kittens, initial viral infection in regional lymphoreticular tissue was followed by viremia and infection of macrophages in reticuloendothelial organs (liver, spleen, lymph nodes) and perivascular locations. The accelerated onset of infection and lesions indicative of an Arthus-type reaction in challenge-exposed seropositive vs seronegative kittens further supports the immune-mediated pathogenesis of FIP.

Animals↗

Disseminated intravascular coagulation in experimentally induced feline infectious peritonitis.

Disseminated intravascular coagulation was induced in kittens by intraperitoneal inoculation of feline infectious peritonitis virus (FIPV). Kittens seronegative to FIPV survived significantly (P less than 0.05) longer than those seropositive to FIPV. Pyrexia, anemia, icterus, hyperbilirubinemia, and elevated concentrations of liver-specific enzymes were detected in the inoculated cats. Lesions induced included disseminated fibrinonecrotic and pyogranulomatous inflammation, hepatic necrosis, and widespread phlebitis and thrombosis. Localization of FIP viral antigen and immunoglobulin G was demonstrated in foci of heptic necrosis by immunofluorescence miroscopy. Lymphopenia, thrombocytopenia, hyperfibrinogenemia, and increased quantities of fibrin-fibrinogen degradation products were present in cats after the onset of clinical illness. Depression of factor VII, VIII, IX, X, XI, and XII plasma activities and prolongation of prothrombin and partial thromboplastin times also developed in infected cats. The accelerated onset of clinical disease and mortality in seropositive kittens vs seronegative kittens and the association of virus and antibody in multiple foci of hepatic necrosis suggest an immune-mediated component is involved in the pathogenesis of this disease.

Animals↗

Family planning services for adolescents and young adults.

If we are to influence the numerical trends of venereal disease and of unwanted pregnancies in the young, family planning services should be made easily available to them. To encourage the widest possible and most effective use of such services requires that health professionals openly endorse their ready availability. They must foster non-judgmental attitudes, however unorthodox patient life styles may be, and provide the young with opportunities to explore their own sexual behavior. The Youth Clinics of the Department of Community Health Services in Los Angeles are designed to meet both the immediate therapeutic and preventive health needs of our patients. Contraceptive services, abortion counseling and referrals as well as individual, group and community education are the primary pillars of our program. There is an enormous task for all of us who are concerned with adolescents to press for sex education programs, in or out of the school system, that will include adults as well as our children.

Abortion, Induced↗