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Biomedical subjects

P A Small

Publications and source records attributed to P A Small.

At least 55 records · Page 3Linked to original sources
PubMed1980

Adherence of Pseudomonas aeruginosa to tracheal cells injured by influenza infection or by endotracheal intubation.

Adherence of Pseudomonas aeruginosa to normal, injured, and regenerating tracheal mucosa was examined by scanning electron microscopy. Uninfected and influenza-infected murine tracheas were exposed to six strains of P. aeruginosa isolated from human sources and one strain of platn origin. All of the strains tested adhered to desquamating cells of the infected tracheas, but not to normal mucosa, the basal cell layer, or the regenerating epithelium. Adherence increased when the incubation time of the bacteria with the trachea was prolonged. Strains isolated from human tracheas appeared to adhere better than strains derived from the urinary tract. After endotracheal intubation of ferrets, P. aeruginosa adhered only to the injured cells and to areas of exposed basement membrane. We call this phenomenon "opportunistic adherence" and propose that alteration of the cell surfaces or cell injury facilitates the adherence of this bacterium and that adherence to injured cells may be a key to the pathogenesis of opportunistic Pseudomonas infections.

Animals↗
PubMed1980

Heterotypic immunity to influenza in ferrets.

Heterotypic immunity to influenza virus in ferrets operated against heterotypic influenza viruses but not heterologous viruses. Contrary to prior reports, the protection conferred lasted for at least 18 months. This type of immunity limited virus shedding but did not prevent infection. These results suggest that this phenomenon could play a role in determining the severity of infections caused by type A influenza viruses in humans.

Age Factors↗
PubMed1980

Outcome of influenza infection: effect of site of initial infection and heterotypic immunity.

An infection established throughout the total respiratory tract of mice with a highly lung adapted influenza virus (H0N1) led to death from viral pneumonia. The 50% lethal dose (LD(50)) was approximately the same as the 50% infectious dose (ID(50)). An infection with the same virus initiated in the nasal mucosa spread to the trachea and lungs over a 3- to 5-day period but was not lethal except at very high infecting doses. The LD(50) was 30,000 times the ID(50). Mice that had recovered from a prior infection with A/PC/73(H3N2) demonstrated enhanced recovery (heterotypic immunity) when challenged with A/PR/8/34(H0N1). Heterotypically immune mice infected while anesthetized with this potentially lethal virus stopped shedding virus from the nose, trachea, and lungs by day 7 and recovered. Heterotypically immune mice, infected awake, stopped shedding virus from the nose by day 5, and, in fact, the virus did not spread to the trachea or lungs. Thus, some of the variation in the severity of influenza infections may be explained by two factors: the site of initial infection and previous infection with heterotypic influenza virus.

Anesthesia↗
PubMed1979

Experimental IgA nephropathy.

An animal model for IgA immune complex nephritis was developed. IgA immune complexes formed in vitro with an IgA anti-dinitrophenyl (DNP) derived from MOPC-315 plasmacytoma, and dinitrophenylated bovine serum albumin (DNP-BSA) produced mild focal glomerulonephritis in mice. Similar, but more severe pathological changes were produced with complexes formed in vivo either in normal mice or MOPC-315 tumor-bearing mice. In contrast to the focal nature of the PAS-positive glomerular lesions observed by light microscopy, immunofluorescent examination revealed IgA deposits in all glomeruli. This discrepancy between immunofluorescent and histopathologic findings as well as the distribution of the immune complexes within the affected glomeruli, are some of the features which bear resemblance between this experimental model and human IgA nephropathy. Fixation of complements by DNP-BSA-IgA immune complexes, formed in vitro or in vivo, was shown to occur in the glomeruli of mice with IgA immune complex nephropathy. The pattern of C3 glomerular deposits was similar to that of IgA. However, complement proved to be nonessential for complex deposition. This conclusion is based on the observation that decomplemented mice, although showing no deposition of C3 in their glomerulus, developed glomerular immunohistological changes similar to those observed in experimental mice that were not decomplemented. Polymeric IgA was observed to be critical for renal deposition of complexes and induction of nephritic histological changes. In contrast, monomeric IgA immune complexes failed to produce glomerular deposits. This finding raises the possibility that secretory IgA, which is predominantly polymeric, may play a role in human IgA-associated glomerulonephritis.

Animals↗
PubMed1979

Serum antibody prevents lethal murine influenza pneumonitis but not tracheitis.

This paper reports studies showing the effects of serum antibody upon influenza infection at two different sites: the trachea and lung. Tracheal desquamation, pulmonary consolidation, death, and virus shedding were examined after infection of mice with a lethal A/Port Chalmers/1/73 (H3N2) influenza virus. Immune serum administered intraperitoneally before infection prevented death and pulmonary consolidation and also significantly lowered lung virus shedding as compared with controls receiving normal serum. However, this protection did not extend to the ciliated epithelium of the trachea because serum antibody did not prevent desquamation of the trachea or significantly decrease viral yield from the trachea. These results indicate that serum antibody is protective against severe pulmonary parenchymal disease but not for disease of the ciliated epithelium.

Animals↗
PubMed1979

Murine influenzal tracheitis: a model for the study of influenza and tracheal epithelial repair.

The murine model of influenza virus infection is generally a lethal pneumonitis produced by a highly mouse-adapted virus. However, we infected mice with a less adapted virus and produced a nonlethal disease that involved the airways without producing gross pneumonitis. Changes that occurred in the tracheal epithelium were studied by scanning and transmission electron microscopy. Complete desquamation of the epithelium occurred within 3 days after infection, regeneration began within 5 days, and repair was complete within 2 wk after infection. This model is proposed as an alternative to the lethal pneumonitis for the study of murine influenza and also as a model for the study of repair of the respiratory ciliated epithelium.

Animals↗
PubMed1978

Local and systemic immunity to influenza infections in ferrets.

To establish whether immunity to influenza infection in the ferret is local or systemic, two sites of challenge were utilized: the nose and the anatomically isolated tracheal pouch. Infection of either site did not spread to the other site, and challenge of either site resulted in seroconversion by 13 days. Simultaneous challenge of both sites 21 days after the primary infection revealed that prior infection of the pouch prevented subsequent reinfection of the pouch, but not infection of the nose. Thus, systemic immunity did not prevent the initiation of nasal influenza infection in the ferret. However, the duration of virus shedding from the nose was reduced to half of that seen when ferrets were infected for the first time, showing that the prior pouch infection did lead to a more rapid recovery from the subsequent nasal infection. Passively administered anti-influenza antibody did not prevent or modify the nasal infection, but it did prevent the pouch infection. This is consistent with the observation that an initial infection of the nose prevented pouch infection upon challenge 21 days later. The prior nasal infection also prevented the subsequent nasal infection. These data suggest that immunity to acquisition of influenza infection in the ferret is a local phenomenon, whereas recovery from active infection is influenced by systemic immune mechanisms.

Animals↗
PubMed1978

Specific immunity to influenza virus in ferret organ cultures.

Ferret tracheal organ cultures prepared from animals previously infected intranasally with influenza A virus required approximately 130 times more homologous virus (A/PR/8/34(HON1) or A/Port Chalmers/1/73 (H3N2)) to become infected in vitro than similar cultures from normal ferrets. Also, these cultures from convalescent ferrets required 9 times more heterologous virus (A/PR/8/34(HON1) or Sendai) to become infected in vitro than similar cultures from normal animals challenged in vitro with the hererologous virus. We conclude that these tracheal rings are specifically immune. Once tracheal rings are infected, they continue to shed viruses for at least 60 days, the longest period any cultures were kept. Virus sheeding in the intact ferret lasts normally 5-7 days. Thus recovery in the intact ferret seems to be dependent upon factors which are not present, or at least not functional, in the tracheal explant. This is consistent with the hypothesis that recovery is dependent upon systemic rather than local phenomena. Bladder tissue from normal and previously infected ferrets was also cultured and challenged with homologous and heterologous virus. The bladder from previously infected ferrets exhibited specific immunity, although the immunity was more varible.

Animals↗
PubMed1978

The secretory immunological system of the fowl. VI. The effect of chemical bursectomy on immunoglobulin concentration in tears.

The effect of chemical bursectomy (3-5 mg testosterone cypionate injected at 12 days in ovo followed by 4-0 mg cyclophosphamide intraperitoneally at days 1 and 2 post-hatching) on concentration of immunoglobulins in tears and serum of chickens was investigated. Tears and serum samples were collected from bursectomized and normal control birds between days 26 and 120 post-hatching and were assayed for IgA, 7SIg and IgM concentrations using double gel-diffusion and radial immunodiffusion. No immunoglobulins other than passively acquired 7SIg were detected in the sera or tears of 23 out of 30 bursectomized birds throughout the time period. Sera were also assayed for natural agglutinins; normal birds had titres for rabbit erythrocytes which gradually increased from a mean of 1:24 at day 26 to 1:280 at day 120, while bursectomized chickens had titres of less than 1:8 throughout the experimental period. It was concluded that chemical bursectomy effectively abolished the secretory immunoglobulins normally present in tears as well as serum immunoglobulins.

Agglutinins↗
PubMed1977

Local immunity against Newcastle disease virus in the newly hatched chicken's respiratory tract.

Inoculation of 200 mean egg infectious doses (EID(50)) of lentogenic Newcastle disease virus strain B1 (NDV-B1) into the air sac of 4-day-old specific-pathogen-free chicks provided significant protection against challenge of the air sac with 100 chicken mean lethal doses (LD(50)) of velogenic NDV-H but no protection against reinfection when the challenge was by the eye. Conversely, inoculation of the eye with 200 EID(50) of NDV-B1 provided significant protection against challenge of the eye but not of the air sac with 100 chicken LD(50) of NDV-H. Birds that received both antiserum and intraocular immunization were subsequently protected against both eye and air-sac challenge. On the other hand, birds that received antiserum and air-sac immunization were protected only against air-sac challenge but not against ocular challenge. Low levels of passively administered antibody did not prevent infection of the eye or air sac but greatly reduced the mortality rate after inoculation of either the vaccine or the challenge viruses. Passively administered antibody also suppressed hemagglutination-inhibiting and virus-neutralizing antibody formation stimulated by air-sac infection but not antibody formation stimulated by ocular infection. These data are consistent with the hypothesis that local immunity is responsible for prevention of infection, since birds were immune to reinfection at one site and simultaneously susceptible at the other site of infection.

Air Sacs↗
PubMed1977

Respiratory allergy in the dog: induction by the respiratory route and the effect of passive antibody.

A technique for inducing hypersensitivity to prairie sage pollen (Artemisia gnopheles) in the dog was developed. The allergen induced skin reactivity in most dogs and respiratory hypersensitivity in 7 of the 17 animals tested. The respiratory hypersensitivity resembled naturally occurring respiratory allergies in both man and dog. The route of allergy induction resembles the natural route and it is felt that this system provides a useful model system for the study of respiratory allergies. Animals in which hypersensitivity was induced were used to investigate the role of passive 'blocking' antibody in respiratory allergy. It was observed that passive antibody will greatly inhibit the respiratory response to inspired allergen while completely inhibiting the cutaneous response. The results of these studies are discussed in relation to other studies.

Administration, Intranasal↗
PubMed1977

Construction of an improved tracheal pouch in the ferret.

A surgical technic is described for the construction of a subcutaneous tracheal pouch in the ferret and for sampling undiluted tracheal secretions at daily to weekly intervals during a period of many months. This technic is applicable to other species.

Animals↗
PubMed1976

Influenza infection in ferrets: role of serum antibody in protection and recovery.

The passive administration of ferret antiserum to Ao (H0N1) influenza virus failed to protect the recipient ferrets from subsequent infection with homologous virus. This susceptibility to infection was observed even when the passively acquired serum hemagglutination inhibition (HI) titer was similar to peak convalescent titers. It is therefore concluded that serum antibody alone is probably not a major factor in the prevention of influenza infection. This does not rule out a possible role for serum antibody in prevention of illness. Subsequent to infection, ferrets that had received passive antisera failed to develop high levels of serum HI antibody. In fact, many had no detectable serum antibody (less than 1:8). These animals shed virus for periods of time quite similar to those of infected control animals, which did develope serum antibody. From these data it was concluded that detectable serum HI antibody does not play a significant role in the recovery of ferrets from influenza infection. Interferon was present in high concentrations in the secretions a few days prior to cessation of virus shedding, but it is not clear whether this was the cause of the recovery or merely a concomitant event. Twenty-one days after initial infection two-thirds of the ferrets that had received passive antibody and all control animals were immune to reinfection with the homologous influenza virus. Since the former group had little or no detectable serum HI antibody but most members were immune, there must be some other host mechanism to account for the immunity.

Administration, Intranasal↗
PubMed1974

Antibody-mediated inhibition of dextran-sucrose-induced agglutination of Streptococcus mutans.

Immune sera to strains of Streptococcus mutans were found to inhibit agglutination of bacterial suspensions to which either high-molecular-weight dextran or sucrose was added. This inhibitory activity was shown to be mediated by antibody of the immunoglobulin G class. A semiquantitative assay was developed which demonstrated cross-inhibition of dextran/sucrose-induced agglutination among several strains of S. mutans. Antiserum to a partially purified glucosyltransferase was found to lack agglutination inhibition activity, consistent with the hypothesis that the dextran-binding antigen detected by the assay is immunologically distinct from the glucan-synthetic enzyme. A model for glucan synthesis and binding consistent with the reported data is described.

Absorption↗
PubMed1974

Dissemination of influenza virus between anatomically isolated sites in ferrets.

Influenza virus was shown to disseminate from the respiratory tract of nasally infected ferrets to a surgically formed, subcutaneous tracheal pouch. Conversely, ferrets infected via the pouch shed virus from the upper respiratory tract. These events occurred within the first 24 h after infection. Passively administered ferret antibody to virus did not prevent the dissemination.

Animals↗