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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated an immunodeficient child in whom chronic progressive poliomyelitis developed after she had received live oral poliovirus vaccine. Poliovirus, Type II, was isolated from throat and stool during life and from several sites within the brain at autopsy. The brain isolate was classified as vaccine-like on the basis of temperature sensitivity and antigenic markers. However, in the monkey neurovirulence test, the brain isolate produced moderately severe lesions throughout the spinal cord and brainstem and appeared nonvaccine-like. Thus, the brain isolate demonstrated a dissociation between the antigenic and neurovirulence markers. Our observations suggest that, under unusual circumstances, such as immunodeficiency, attenuated poliovirus can produce a chronic progressive neurologic disease. This case also emphasizes the need to diagnose immunodeficiency as early as possible, so that live-virus vaccines will not be administered.
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PMID:Chronic progressive poliomyelitis secondary to vaccination of an immunodeficient child. 19 6

Paralytic poliomyelitis was observed in a child with a sex-linked defect in immunoglobulin synthesis. Evidence is presented that this was secondary to administration of oral, live poliovaccine. The demonstration of a familial sex-linked gammaglobulin deficiency and the failure to document a defect in cell-mediated immunity in this child extends the risk of vaccine associated poliomyelitis to virtually all forms of immunodeficiency. The critical host factors in the pathogenesis of poliovirus vaccine infection and in particular its unfavorable outcome appear to include either a deficiency in the humoral (B cell) system or in the cell-mediated (T cell) system.
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PMID:Vaccine-associated poliomyelitis in a child with sex-linked agammaglobulinemia. 19 20

The value and special problems of application of killed and life polio vaccines are compared and discussed. The vaccination with life polio vaccine will be continued generally. Killed polio vaccine may be useful in children with immunodeficiency only.
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PMID:[Will Salk's polio vaccination be used again?]. 63 10

Four infants underwent radical thymectomy for a suspected malignancy of the thymus. Histology revealed no malignant cells. The patients did clinically well as long as 14 years after the operation. There was laboratory evidence for a cellular and humoral immunodeficiency. Affected were mainly the response to oral poliomyelitis vaccinations and the skin tests of delayed type hypersensitivity.
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PMID:Immunological decay in thymectomized infants. 124 40

An explanation is provided for the male predominance in incidence of infectious diseases in children. A theoretical and mathematical model for predicting sex ratios for different prevalences of increased susceptibility to infectious disease in males is presented. The theoretical model states that males are more likely to experience symptomatic disease due to an increased prevalence of a factor such as immune deficiency. Variables are the proportion infected, the ratio of symptomatic (clinical) to asymptomatic (subclinical) infections, and the prevalence of males with increased susceptibility to infectious disease. Data included incidence of viral hepatitis, shigellosis and salmonellosis between 1966-85 and viral meningitis between 1971-85 by age and sex for Israeli Jews and nonJews. Other data for shorter time periods included poliomyelitis (1958-62), measles (1976-85), and diphtheria (1958-70). Single years of age were used for those 0-4 years. In diseases where vaccination has reduced the case load, the male to female incidence ratio was estimated with incidence density computed for the whole time period. The results of the analysis showed that male incidence 5 years in all 3 bacterial and 4 viral diseases was higher. The incidence ratios showed an excess of 20-100% for infectious diseases. This consistent pattern is not apparent in the literature because sex differences may be difficult to detect among symptomatic diseases; i.e., measles. There is also a lower symptomatic to nonsymptomatic infection ratio and small sex incidence ratio for shigellosis, salmonellosis and viral hepatitis. Where the symptomatic to nonsymptomatic ratio is about 1:50 or 1:100, the male to female incidence ratio will be much higher at about 2:1 and more readily detected. The immunodeficiency prevalence among males as an explanation for the susceptibility of males for diseases was not supported by an excess frequency of 2-3% in overt symptoms, although it is still considered a viable hypothesis. It is suggested that the inconsistencies in reports on male predominance in infectious diseases may be an artifact of statistics showing variability in the proportion of symptomatic infectious diseases. The implications are that comparisons should be made between the sexes. The disease rates may be biased by different proportions of males in the study and placebo groups in vaccine testing. Sex differences and disease should be examined further.
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PMID:The male predominance in the incidence of infectious diseases in children: a postulated explanation for disparities in the literature. 142 96

In order to evaluate the response to immunization of HIV-infected children we studied the humoral response to an enhanced potency inactivated poliovaccine (E-IPV) of 43 children born of HIV seropositive mothers. All these subjects have been followed for 32 (15-48) months in order to ascertain their infection status. After a course of 2 doses of E-IPV, 88% of children had neutralizing antibody (n.a.) titers greater than 1:4 to the 3 poliovirus serotypes and 100% to at least 2 polio strains. No statistically significant differences both as rates of n.a. positive subjects and as antibody levels were found between HIV infected children and those who lost HIV antibodies. The poorest response was observed in subjects with full-blown immunodeficiency (CD4 less than 1000/mm3, reduced response to PWM). Sixteen children also received a booster dose of vaccine one year after the completion of the primary cycle. Infected and non-infected subjects responded to the same extent with high levels of n.a. to this immunization. Interestingly, the recall dose was also able to induce high n.a. titers in those HIV infected children who showed significant decreases of n.a. titers in the months following the end of the primary cycle.
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PMID:Antibody response to inactivated polio vaccine (E-IPV) in children born to HIV positive mothers. 164 38

A "cleavage cassette" specifying a decapeptide human immunodeficiency virus (HIV) protease cleavage site was introduced into six different locations of beta-galactosidase (beta-D-galactoside galactohydrolase, EC 3.2.1.23) in Escherichia coli. Four of these constructs retained beta-galactosidase activity despite the insertion of the cleavage cassette. Of these four constructs, one was cleaved by HIV protease, resulting in the inactivation of beta-galactosidase both in vivo and in vitro. This cleavage was inhibited by pepstatin A, a known inhibitor of HIV protease. Thus, beta-galactosidase has been converted into an easily assayed substrate for HIV protease. An analogous construct of beta-galactosidase containing a polio protease cleavage site was cleaved likewise by polio protease, suggesting that this system may be generic for monitoring cleavage by a variety of proteases.
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PMID:beta-Galactosidase containing a human immunodeficiency virus protease cleavage site is cleaved and inactivated by human immunodeficiency virus protease. 212 94

The acute aseptic meningitis syndrome is an entity that presents a diagnostic challenge to the clinician. Although many infectious and noninfectious etiologies exist for this syndrome, viruses, especially nonpolio enteroviruses, are the classic and most important agents encountered. The incidence of polio and mumps meningitis has declined dramatically in the vaccine era, but recently described pathogens, such as human immunodeficiency virus and Borrelia burgdorferi (Lyme disease agent) are now important considerations in the differential diagnosis. Specifically treatable entities (eg, mycobacterial or fungal meningitis, herpes simplex encephalitis, parameningeal infection) that may mimic aseptic meningitis in their initial presentations must not be overlooked. A careful approach to the patient and a rational use of laboratory studies are the basis for establishing a specific diagnosis and assuring a favorable outcome.
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PMID:The acute aseptic meningitis syndrome. 227 91

The Centers for Disease Control reported that 109,167 cases of AIDS had been diagnosed since 1981 and that approximately 40,000 persons were living with AIDS at the time of this writing. These numbers, however, are the tip of an iceberg that consists of approximately 1.5 million Americans who are infected by the human immunodeficiency virus (HIV). As we described in earlier articles of this series, the HIV infection/AIDS epidemic has invaded the domain of the American family through heterosexual transmission, vertical transmission, drug abuse, and sexual abuse of children. Therefore, physicians for children are now facing the prospects of having to deal with this disease in their practices. If there is something unique about pediatrics and other specialties of the medical profession dealing with infants and children, it is that "prevention" of disease can be and has been used effectively. One only needs to remember the 1950s, when the poliomyelitis epidemic was causing the same, if not greater, concerns in the lives of the American families. The development and application of the "polio" vaccines has virtually eliminated the threat of poliomyelitis in our society. Similarly, the incidence of diphtheria, tetanus, and smallpox has decreased to the point that these diseases present practically no threat to the US population. Armed with these positive experiences, we need to examine what we can do today to curb the spread of the HIV infection/AIDS among infants and children, and by extension, among the general population of our country.
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PMID:Pediatric AIDS: prevention of HIV infection in infants and children. 240 77

Dextran sulfate (DS) is a potent inhibitor of the growth of human immunodeficiency virus type 1 (HIV-1) in the H9 cell. Its minimal inhibitory concentration is about 1 microgram/ml. Its therapeutic index is greater than or equal to 200 which is higher than that of 38 for zidovudine. At the ID100 range, DS blocks the synthesis of HIV-1 antigens completely for at least 21 days; zidovudine at the subtoxic concentration of 3 micrograms/ml is incapable of achieving such a complete blockage. DS is still active when added to H9 cell cultures 4 hr after the addition of HIV-1. DS does not inactivate extracellular HIV-1 and is incapable of inducing interferons. It interferes partially with the infection of the H9 cells by the HIV-1. It inhibits the activity of HIV-1 reverse transcriptase. These activities may account, at least in part, for the inhibitory activity of dextran sulfate against the HIV-1. DS has a narrow antiviral spectrum; it is noninhibitory to the herpes simplex, vesicular stomatitis, polio, or adeno viruses. Dextran is not inhibitory to HIV-1. After sulfonation, the sulfonated dextran is highly inhibitory. Therefore, the sulfate group in the DS molecule appears to be essential for its anti-HIV-1 activity. The molecular weights of DS within the range 4000 to 12,000 do not appear to influence its anti-HIV potency.
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PMID:Dextran sulfate as an inhibitor against the human immunodeficiency virus. 246 37


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