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Biomedical subjects

F M Collins

Publications and source records attributed to F M Collins.

At least 127 records · Page 7Linked to original sources
PubMed1975

Growth and immunogenicity of photochromogenic strains of mycobacteria in the footpads of normal mice.

Specific pathogen-free CD-1 mice were infected subcutaneously in the footpad with mycobacterium kansasii, three strains of M. marinum, and two strains of M. simiae-habana, and the growth of the organisms in the footpad, the draining popliteal lymph node, and the lung and spleen was followed quantitatively for up to 60 days. The ability of a footpad inoculum of M. marinum to spread to the lungs and spleen correlated with the ability of the organism to survive and multiple at 37 C in vitro cultures. The amount of footpad swelling which developed in the M. kansasii- and M. marinum-infected mice varied depending upon the strain of organism and the size of the original footpad inoculum. Injection of dead M. marinum into the footpad also induced an extensive amount of swelling which varied with the strain used, as well as being dose dependent. M. marinum- and BCG-vaccinated mice were protected against a later footpad challenge with M. marinum or the highly mouse virulent M. tuberculosis strain ERDMAN. The significance of this finding is discussed in relation to cross-protection studies using a variety of mycobacteria in the footpad infection model.

Animals↗
PubMed1975

Growth of Mycobacterium marinum in the footpads of T-cell-depleted mice.

Mycobacterium marinum strains 1218 and 1219 were inoculated into the hind footpads of T-cell-depleted specific pathogen-free C57B1/6 mice, and the growth and survival of the organisms at the site of injection, the draining popliteal lymph node, and the spleen and lung were quantitated for up to 70 days. T-cell depletion largely ablated the normal cell-mediated antituberculous response to the M. marinum population. The mice were able to control the further growth of the inoculum within the footpad only after it had reached 5 to 10 times that present in the normal controls. The high temperature-adapted strain (37 C; strain no. 1218) induced an increasing infection in the liver, spleen, and lungs of the THXB mice, and the infection eventually spread to the opposite footpad and to the tail skin. Strain 1219 gave rise to considerable systemic involvement in the THXB host despite its inability to survive at 37 C, but the size of the splenic and lung populations was considerably lower than in the 1218-infected animals. Both M. marinum infections persisted in the tissues of the T-cell-depleted mice with no indication of a cell-mediated immune response. Footpad swelling in the M. marinum-infected mice was not greatly reduced by T-cell depletion, and, if anything, tended to persist at high levels long after the swelling of the control feet had gone into a decline. On the other hand, incorporation of tritiated thymidine by cells within the infected footpads, the draining lymph node, and the spleen was considerably reduced in the T-cell-depleted host compared with control values. Late in the infection, there was a significant increase in the amount of label taken up by the cells in the footpads of the T-cell-depleted host.

Animals↗
PubMed1975

Immunogenicity of an aerogenic BCG vaccine in T-cell-depleted and normal mice.

Aerogenic infection of adult thymectomized, lethally irradiated, bone marrow-reconstituted (THXB) C57B1 times C3H F1 hybrid mice with 1 to 3,000 viable BCG Montreal was followed by an extended period of logarithmic growth to a maximum population of 5 times 10-6 bacilli by day 35. The infection spread to the liver, spleen, and bone marrow with extensive multiplication in all test organs before the growth curves abruptly entered a stationary phase. Up to 30% of the THXB mice eventually died as a result of the ongoing BCG infection. There was no sign of an antimicrobial immune response in the THXB mice analogous to that seen in the control animals beginning about day 30. The THXB mice developed considerable immediate but no delayed hypersensitivity to PPD. Intravenous challenge of the BCG-vaccinated THXB mice with 105 virulent Mycobacterium tuberculosis Erdman indicated that they were as susceptible to the tuberculous challenge as a group of unvaccinated controls. Visible surface lesions developed on the lung 90 days postinfection in the T-cell-depleted host with a sharp rise in counts to 175 per lobe on day 120 followed by a plateau for the remainder of the study. Control mice developed visible lesions about day 50, with 225 lesions per lobe by day 70 and a sharp decline to undetectable levels by day 90. The histopathology of these changes was examined carefully, together with the rate of cellular proliferation (tritiated thymidine uptake) by lung and spleen cells as the BCG infection progressed in the THXB mice. Peak uptake by both organs was depressed during the early stages of the BCG infection in the T-cell-depleted mice, but later the incorporation rates were significantly elevated above control values as the infection progressed.

Animals↗
PubMed1975

Effect of T-cell depletion on the growth of BCG in the mouse footpad.

The growth of Mycobacterium bovis (BCG Montreal) and M. tuberculosis Erdman was determined in normal and T-cell depleted (THXB) mice when injected subcutaneously into a hind footpad. The bacilli multiplied only to a limited extent within the footpad itself but the infection quickly spread to the draining popliteal lymph node to eventually reach the liver, spleen and lung. The amount of systemic growth seen in the THXB mice was 10-100 times greater than in the normal controls, all of which developed a tuberculin hypersensitivity and an immune response in 14-18 days. T-cell depletion completely inhibited the expression of tuberculin sensitivity by the infected host as well as ablating the antituberculous response against both the vaccinating BCG population and a superinfecting Erdman challenge inoculum. Incorporation studies in the THXB mice indicated a striking reduction in cell division within the draining lymph node but there was an unexpected elevation in the level of incorporation by the lung cells as the BCG infection progressed. The significance of these findings is discussed in relation to the possible use of the BCG footpad model for studies of leprosy immunity.

Animals↗
PubMed1975

Relative immunogenicity of streptomycin-susceptible and -resistant strains of BCG. II. Effect of the route of inoculation on growth and immunogenicity.

Normal CD-1 mice were infected intravenously, subcutaneously, or aerogenically with live bacille Calmette Guerin (BCG) Tice or BCG streptomycin resistant (SM-res) and growth of the organisms in the footpad, the draining popliteal lymph node, the blood, lung, liver, and spleen was followed for as long as 50 days. The vaccinated mice were then challenged on day 50 with 10-5 viable Mycobacterium tuberculosis Erdman organisms introduced intravenously or subcutaneously. The growth of the Erdman challenge was followed in the appropriate organs for the next 20 days. Measurement of tuberculin hypersensitivity was carried out by footpad tests. The BCG Tice introduced aerogenically or subcutaniously into normal mice induced degrees of antituberculous resistance equivalent to those seen earlier in intravenously infected mice. The BCG SM-res was still nonimmunogenic when introduced subcutaneously or by the aerogenic route. Suspension of the organisms in sterile mineral oil before their injection into the footpad slowed their rate of inactivation and marginally increased the immune response seen later in the host. Introduction of BCG SM-res into T-cell depleted mice by the 3 inoculation routes was associated with no marked improvement in the survival of this organism in vivo, suggesting that BCG SM-res is inactivated in vivo by a nonimmunologically mediated mechanism.

Aerosols↗
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

The cytokinetics of monocytosis in acute salmonella infection in the rat.

The mechanisms responsible for monocytosis occurring in acute Salmonella infection were studied by means of isotopic labeling and autoradiography. Male (Lewis x BN)F(1) hybrid rats (160-180 g) were pulse-labeled with [(3)H]TdR at varying intervals with respect to the time of i.v. injection of about 10(6) living Salmonella enteritidis. The half time for monocytes in the blood was estimated from the exponential decline in the percentage of labeled monocytes. The average generation time for dividing monocyte precursors in bone marrow was estimated by fitting a regression line to the decline in median grain counts (halving-time = T(G)). After an initial fall, the absolute number of blood monocytes rose to a plateau about 2.5 x normal on day 5, suggesting the reimposition of steady state conditions. The half time of monocytes in the blood of infected rats was shortened to 25 h throughout the infection, compared with 61 h estimated in uninfected rats. T(G) was reduced to 15 h (days 1-3) but later reverted to the preinfection level of 34 h (days 4-8). Another early response to infection was the release of immature monocytes into the blood. These cells, however, were too few to offset the initial monocytopenia. Under these conditions, with little or no division of blood monocytes, the sustained monocytosis (days 4-8) must have been due to enlargement of the dividing precursor pool. Excessive loss of monocytes from the blood thus appears to activate a feedback mechanism. However, a more direct stimulating effect on monocyte production by endotoxin could have contributed substantially to the monocytosis.

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↗
PubMed1974

Effect of Corynebacterium parvum treatment on the growth of Salmonella enteritidis in mice.

The growth of Salmonella enteritidis in mice pretreated with 700 mug of killed Corynebacterium parvum was less than that seen in normal CD-1 mice. In treated mice, there was an early increased inactivation of the blood, liver, and spleen bacterial populations, followed by a prolonged period of slow but continuous bacterial growth. The treated mice failed to develop significant delayed hypersensitivity and did not show the characteristic antibacterial immune response seen in untreated infected animals. Eventually sufficient resistance did develop in most of the treated animals to protect them against the lethal effects of the challenge infection. The peak C. parvum effect was seen when S. enteritidis was injected 7 to 14 days later. Injection of C. parvum 24 h after the bacterial challenge actually potentiated the Salmonella infection. There was no evidence of an increased specific humoral response by the C. parvum-treated mice, suggesting that the slower growth of the S. enteritidis was due to the continued enhanced killing of the bacterial population by the nonspecifically stimulated cells of the reticuloendothelial system, rather than to any specific augmentation of the host immune response.

Animals↗
PubMed1973

Immunogenicity of living and heat-killed Salmonella pullorum vaccines.

Specific pathogen-free CD-1 and C57Bl mice were infected in a hind footpad with 5 x 10(4) viable Salmonella enteritidis cells or 10(7) viable S. pullorum cells. The resulting bacterial growth within the footpad, the draining lymph nodes, and the liver and spleen was followed for 14 days. Mice vaccinated with live S. enteritidis rapidly developed an effective antibacterial resistance to both intravenous and intragastric challenge with S. enteritidis SM(R). The viable inoculum of S. pullorum was rapidly eliminated from the normal mouse tissues and failed to induce a detectable anti-Salmonella resistance to parenteral or oral challenge with S. enteritidis. Heat-killed saline suspensions (200 mug, dry wt) of S. enteritidis or S. pullorum were unable to induce an effective antimicrobial resistance against a subsequent virulent Salmonella challenge. However, when the organisms were suspended in Freund complete adjuvant, both vaccines induced an antibacterial resistance to intravenous and intragastric challenge. Reduction of the antigenic dose from 200 to 40 mug did not greatly affect the protective value of the two killed vaccines against an intravenous challenge, but the level of protection observed with two 40-mug doses of S. pullorum was considerably reduced when the animals were infected intragastrically, suggesting that some quantitative differences existed between the sensitizing antigenic contents of the two test organisms.

Adjuvants, Immunologic↗
PubMed1973

Relative immunogenicity of streptomycin-sensitive and -resistant strains of BCG.

Normal, specific pathogen-free mice were vaccinated intravenously with increasing amounts of a streptomycin-resistant variety of BCG Tice (BCG SM(R)). The behavior of BCG SM(R) in the lungs, liver, and spleen was followed quantitatively for up to 50 days. One or two intravenous doses of 10(6) viable organisms were steadily eliminated from the tissues without producing detectable tuberculin sensitivity or raising resistance to a subsequent challenge with Mycobacterium tuberculosis strain Erdman. But mice receiving six weekly injections of 10(6) viable BCG SM(R) or a single injection of 10(6) BCG SM(R) by the intravenous route did develop effective levels of antituberculous resistance. Heat inactivation of the BCG SM(R) inoculum removed the organism's protective activity which could, however, be restored by incorporation of the organisms into Freund adjuvant. The ability of living BCG SM(R) to induce an effective antituberculous resistance when introduced into the tissues in an appropriate manner is discussed in terms of the mechanism of antituberculous immunity.

Animals↗
PubMed1973

Polyarthritis associated with Salmonella infection in rats.

Rats infected intravenously with Salmonella enteritidis develop a chronic destructive polyarthritis. The joint lesions resemble those of human rheumatoid arthritis in distribution and pathology. On the basis of histological and microbiological studies, involvement does not appear to be the result of intra-articular sepsis. Instead, the data favor the view that transient infection incites an immunological response that localizes in the joint and becomes destructive.

Animals↗
PubMed1973

Growth of Pasteurella multocida in vaccinated and normal mice.

Specific pathogen-free CD-1 mice are highly susceptible to infection by Pasteurella multocida strain 5A whether introduced intravenously, intraperitoneally, subcutaneously, or aerogenically. The growth of the challenge organism in the blood, liver, spleen, lung, and peritoneal cavity was quantitated hourly for up to 12 h. Unvaccinated mice died 9 to 12 h after intravenous challenge due to the uncontrolled growth of the organism in all tissues tested. The rate of removal of the bacteria from the blood and of phagocytosis by peritoneal macrophages was extremely slow. In the absence of specific opsonins, more than 90% of the unopsonized challenge inoculum remained in the extracellular growth phase throughout the challenge period. Vaccination of mice with two doses of 10(8) heat-killed (60 C for 60 min) P. multocida given 7 days apart protected the mice against 100 to 1,000 lethal challenge doses. Survival data and growth curves obtained for both actively and passively immunized mice indicated that a humorally mediated immune mechanism was involved. Peak resistance to challenge occurred 21 to 28 days after the mice received the second dose of antigen, and this correlated with an 8- to 16-fold increase in specific agglutinin titers over the same time. Resistance to aerogenic challenge by vaccinated mice was less effective than when other routes of infection were used. The significance of these findings is discussed.

Aerosols↗