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Biomedical subjects

P B Carter

Publications and source records attributed to P B Carter.

At least 37 records · Page 2Linked to original sources
PubMed1979

Requirement for a bacterial flora before mice generate cells capable of mediating the delayed hypersensitivity reaction to sheep red blood cells.

A delayed-type hypersensitivity (DTH) reaction can be elicited by an injection of 10(8) sheep red blood cells (SRBC) into a rear footpad of conventional (CV) mice previously immunized with small doses of SRBC. In contrast, immunization of germ-free (GF) mice with the same doses of SRBC produced no DTH when immunization was by the intravenous (i.v.) route, and only weak reactions when immunization was by the subcutaneous (footpad) route. Varying the immunizing dose of SRBC, or the time at which DTH was elicited, did not produce a state of DTH responsiveness in i.v. immunized GF mice. However, the transfer of lymphocytes from CV mice, immunized 4 to 5 days previously with SRBC, into GF mice, conferred on GF mice the capacity to express DTH. Although DTH was not readily demonstrable in GF mice immunized with SRBC, they nevertheless produced normal levels of hemagglutinating antibody to SRBC. Finally, it was shown that GF mice could generate a normal DTH response to SRBC if they were first monoassociated with a Gram-negative bacterial flora.

Animals↗
PubMed1979

Host responses to infection with Yersinia enterocolitica.

The mechanism of protective systemic immunity to Y. enterocolitica infection in mice was studied. It was determined that active immunization of mice with heat-killed yersiniae would induce a protective immune response against an intravenous challenge. This protective response was proven to be humoral in nature when it was demonstrated that passively transferred serum, but not cells, protected normal recipients against a lethal challenge. It was also shown that the immune serum caused opsonization of the microorganisms resulting in enhanced phagocytosis and killing of yersiniae by reticuloendothelial organs.

Animals↗
PubMed1978

Mouse Peyer's patches contain T cells capable of inducing the graft-versus-host reaction (GVHR).

The potential of cells from the Peyer's patches (PP) of normal adult DBA/2 Tru mice (DBA/2) to induce a graft-versus-host reaction when injected into (C57BL/6 Tru x DBA/2 Tru)F1 hybrid (B6D2F1) mice was studied. The injection of 10(6) to 10(7) DBA/2 PP or spleen cells i.p. into neonatal F1 mice produced a striking splenomegaly. Comparable doses of parental PP or spleen cells injected into a rear footpad of adult F1 mice also induced a marked enlargement of the draining popliteal lymph node. In addition, PP cells were also capable of producing a lethal runting syndrome when injected i.v. into sublethally irradiated adult F1 recipients. In all assays, injection of syngeneic B6D2F1 cells had little or no effect. Treatment of the DBA/2 PP cells with anti-theta serum and complement abolished their capacity to induce splenomegaly in neonatal F1 mice. The graft-versus-host reaction activity of the PP cells could also be eliminated by thymus deprivation of the donor DBA/2 mice. These data are contradictory to previous findings in which it was observed that mouse PP cells were unable to induce graft-versus-host reaction.

Animals↗
PubMed1978

Growth of salmonellae in orally infected germfree mice.

Germfree mice were infected intragastrically, intravenously, or intraperitoneally with 10(3) to 10(9) viable Salmonella typhi Ty2, S. gallinarum 9240, or S. enteritidis 5694. The 50% lethal doses were compared with those for conventionally raised mice. Substantial growth of the salmonellae occurred in the intestinal tract of the germfree mice but, despite the presence of more than 10(9) viable S. typhi or S. gallinarum in the lumen, the liver and spleen cultures remained Salmonella-free, and all of the mice survived the oral challenge. The ileal and cecal Peyer's patches and the mesenteric lymph nodes of these mice contained 10(3) to 10(4) viable salmonellae within 24 h of introduction of the inoculum into the stomach. Despite this local involvement, the infection did not spread systemically even when host resistance was reduced by means of sublethal, whole-body gamma irradiation before oral challenge. Germfree mice infected orally with as few as 10 mouse-virulent S. enteritidis quickly developed severe diarrhea and died within 5 to 8 days as a result of a spreading systemic disease.

Administration, Oral↗
PubMed1977

Assessment of typhoid vaccines by using the intraperitoneal route of challenge.

Present laboratory tests for human typhoid vaccines use an intraperitoneal route of challenge given 7 days after injection of increasing doses of standard and test vaccines by the same route. In studies reported here, groups of B6D2 mice were vaccinated intraperitoneally with 2 x 10(8) acetone-killed Salmonella typhi Ty2, with the Vi antigen-free variant O-901, or with Yersinia enterocolitica and Serratia marcescens suspensions. Other groups of mice received 200 mug of purified S. typhi or S. marcescens endotoxin, or their corresponding purified lipid A components. All of the vaccinated mice (except for saline- or thioglycolate-injected controls) exhibited increased protection against the lethal intraperitoneal challenge with S. typhi Ty2. Serial quantitative bacterial counts carried out on peritoneal washouts and on homogenates of the draining mediastinal lymph nodes indicated the development of an antibacterial response by the vaccinated host which was not observed in the control animals. Mice receiving purified endotoxin (lipopolysaccharide) exhibited varying degrees of protection, both in terms of increased host survival and the amount of inactivation of the challenge population in vivo. The response seen when the antigenically unrelated S. marcescens lipopolysaccharide was injected was little different from that seen when the acetone-killed S. typhi Ty2 whole-cell vaccine was used. This suggests that nonspecific inactivation of the intraperitoneal challenge contributes substantially to the immune response seen in mice vaccinated intraperitoneally with specific typhoid antigens.

Animals↗
PubMed1977

Serological reactivity of chemical fractions of Mycoplasma bovis.

Crude chemical fractions, homogenates, and whole cells of Mycoplasma bovis were tested for serological reactivity using agar gel diffusion, ring precipitation, indirect hemagglutination, inhibition of growth inhibition (IGI), and complement-fixation (CF) tests. Only the IGI and the CF tests gave sensitive and reproducible serological information. Preliminary studies indicated lipids to be the serologically reactive components of M. bovis.

Antigens, Bacterial↗
PubMed1977

Immunity to Trichinella spiralis. II. Expression of immunity against adult worms.

Thoracic duct lymphocytes or purified T or B cells obtained from specifically immunized (Lewis x DA)F1 hybrid rats can protect normal recipients against an oral challenge infection with T. spiralis. The immune cells increase the rate of expulsion of adult worms from the small intestine. Immune TDL do not affect adult worm fecundity, as they do in other strains of rats, or the penetration and development of newborn larvae in muscle cells. Irradiated F1 rats reconstituted with either immune TDL or class-enriched populations of immune T or immune B cells also expel adult Trichinella more rapidly than do unprotected controls. However, unfractionated TDL and inocula enriched in B cells are more efficient than T cells in promoting worm expulsion. The above finding, taken in conjunction with the tissue disposition of labelled lymphocytes in the tissues of recipient rats, implies that immune T cells have a 'helper' function in promoting the formation of protective B cells.

Animals↗
PubMed1975

Involvement of the upper respiratory tract in orally induced salmonellosis in mice.

The possible involvement of the tissues of the head and neck during the early pathogenesis of orally or intragastrically induced murine salmonellosis was examined. Viable counts of Salmonella in the local lymphoid tissues and draining nodes indicated that the ileal Peyer's patches were primarily involved in the development of a subsequent enteric fever, irrespective of the method of oral challenge. Contamination of drinking water with a high concentration of salmonellae produced infection of the ileal Peyers patches and the eventual development of systemic disease. The cervical lymph nodes were sporadically involved early in the infection, but this involvement soon became general, with large numbers of salmonellae in the cervical nodes by 36 hr. A lower concentration of salmonellae in drinking water led to primary involvement of the ileal Peyers patches; upper respiratory tract involvement was detected much later in the infection. Intragastrically invected mice exhibited the same low-level infection of the cervical lymph nodes as that in mice infected via drinking water. Thus systemic infection apparently results from infection of the ileal Peyers patches; a small percentage of the animals develop a concurrent upper respiratory tract infection that may be responsible for the development of carrier states after enteric infection.

Animals↗
PubMed1975

Pathogenecity of Yersinia enterocolitica for mice.

A laboratory infection of Yersinia enterocolitica in mice which closely resembles the naturally acquired human infection is described Intravenous inoculation of mice with small numbers of Y. enterocolitica gives rise to a systemic, pyogenic infection involving primarily the spleen, liver, and lungs. Massive neutrophil infiltration of these organs occurs early in the infection, eventually leading to large abscesses and pulmonary consolidation. Mice infected intragastrically show neutophil infiltration in the Peyer's patches of the distal ileum less than 24h postinfection. The Peyer's patches are unable to contain the infection which spreads to the mesenteric lymph node, causing large abscesses in the medullary regions. Soon after, the infection becomes systemic with abscesses forming in the liver, spleen, and lungs, and the total peripheral leukocyte count rises dramatically to over 30,000/mm2. A serological response, in the form of agglutinating antibody, begins to appear 2 weeks after infection. Possible causes of death and the usefulness of this infectious disease model are discussed.

Animals↗
PubMed1975

Phagocytosis of Mycoplasma salivarium by human polymorphonuclear leukocytes and monocytes.

Mycoplasmacial activity was exhibited by human peripheal blood leukocytes in the absence of detectable specific antiserum. After incubation of varying concentrations of Mycoplasma salivarium with leukocytes, changes in colony-forming units (CFU) of this species per millilter occurred. The most noticeable decrease in CFU per milliliter was then the incubation mixtures contained five mycoplasmas per leukocyte. At this ratio, the mycoplasmacial min of incubation. Continued incubation demonstrated a tenfold decrease in CFU per milliliter by 4 h. Electron micrographs of incubated mixtures of human leukocytes and M. salivarium showed this mycoplasma to be phagocytized by monocytes and neutrophils whenever mutual contact or pseudopodial formation occurred. The process was continuous. Numerous phagocytic vacuoles developed which contained multiple ingested microorganisms. After the cytoplasmic granules of the leukocytes fused with the phagocytic vacuole, the phagocytized mycoplasmas became disrupted and unrecognizable.

Adult↗
PubMed1974

The route of enteric infection in normal mice.

This study followed the early pathogenesis of orally induced murine typhoid fever. Intragastrically administered Salmonella enteritidis moves quickly through the normal undisturbed gut so that only a small residuum remains in the cecum and large intestine after the first few hours. Dye injection of the gut wall was used to show that lymph from discrete portions of the gastrointestinal tract drains to separate lymph nodes, probably via the regional Peyer's patches. Plating techniques capable of detecting a single colony-forming unit of S. enteritidis within the different Peyer's patches and draining lymph nodes indicate that, although the cecum and large intestine are exposed to large numbers of Salmonella for longer time periods than the small intestine, the primary site of bacterial penetration involves the distal ileum. This area of the small intestine as well as the cecum are both drained by the distal mesenteric lymph nodes, and were the only nodes which contained detectable numbers of viable Salmonella over the first 24 h of infection. Neither the pyloric nor the proximal mesenteric lymph nodes (which drain the stomach and duodenum) nor the pancreatic and caudal lymph nodes (which drain the transverse and descending colon) contained viable Salmonella. Salmonella were observed to infect the ileal mucosa and its Peyer's patches. With time, this infection progresses to the draining lymph node and ultimately reaches the liver and spleen. Some of the implications of these findings relative to the development of acquired resistance to enteric disease are discussed.

Animals↗
PubMed1974

Growth of typhoid and paratyphoid bacilli in intravenously infected mice.

The in vivo growth of Salmonella paratyphi A, S. paratyphi B, S. paratyphi C, and S. typhi, as well as of an S. typhi-typhimurium hybrid, was studied in three different strains of mice. S. paratyphi A and B and S. typhi demonstrated very little growth potential in any of the intravenously infected mice, even after as many as 20 serial mouse passages. It was noted, however, that small numbers of viable S. paratyphi B and S. typhi persisted in the spleens of infected mice for up to 28 days. Salmonella paratyphi C and the S. typhi-typhimurium hybrid gave rise to progressive systemic infections beginning from very small intravenous inocula. The median lethal doses for the C57B1 strain of mouse were about five organisms. The relevance of these findings with regard to the development of an animal model for studying human typhoid fever vaccines is discussed.

Animals↗
PubMed1974

Experimental Yersinia enterocolitica infection in mice: kinetics of growth.

Infection of several strains of laboratory mice with a virulent strain of Yersinia enterocolitica was followed by performing viable bacterial counts on homogenates of selected tissues at intervals after intragastric, aerogenic, or intravenous infection. It is observed that CD-1 mice are more susceptible to Y. enterocolitica infection than either the C(57)B1/6 or B6D2 strains. Development of an enteric infection is dose dependent; less than 5 x 10(7) organisms by mouth yields sporadic, low levels of systemic infection, with many of the animals showing no apparent infection. Increasing the challenge inoculum by a factor of 10 eliminates the variability among the animals, giving rise to an enteric infection in all of the mice that moves quickly to the mesenteric lymph node. The bacterial population in the lymph node multiplies rapidly, and the infection is disseminated to the spleen, liver, and lungs, ultimately killing most of the animals. Exposure to an aerogenic challenge of less than 1,000 organisms resulted in a fulminating pneumonitis with an invariably fatal outcome. Intravenous challenge with 500 organisms caused a rapidly fatal, systemic infection. The growth of the bacteria in the intravenously infected mouse depends upon the temperature at which the challenge inoculum had been grown in vitro. At temperatures below 26 C, the bacteria are cleared from the blood at a slower rate and are more resistant to intracellular killing, as compared to organisms grown at 37 C. This effect results in the inoculum increasing to greater numbers in the tissues in a shorter period of time.

Administration, Oral↗