Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0476273 (respiratory distress)
 19,632 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pathogenicity of a strain of simian herpesvirus SA8 in one month old conventional and gnotobiotic baboons was investigated. Intratracheal inoculation resulted in a mortality rate of 1/5 in the conventional and 1/4 in the gnotobiotic group. Disease became apparent after 3 days and was characterized by respiratory distress, reduced formula intake, weight loss and fever in both groups. Isolation of herpesvirus from the respiratory tract, lymphoid organs, kidneys, adrenals, and CNS was more frequent by explant culturing than by routine procedures. Although there was a significant difference in total white blood counts (WBC), with higher values in conventional vs. gnotobiotic infants, the absolute number of lymphocytes was not different. The lower number of WBCs apparently was due to fewer polymorphonuclear leukocytes in the gnotobiotic baboons. Infection resulted in a leukopenia 5 days post infection (p.i.) and a leukocytosis 10 days p.i. in both groups. The animals, which succumbed, had acute necrotizing fibrinous pneumonia. Intranuclear inclusion bodies typical for herpesviruses were present. All the surviving infant baboons had subacute interstitial pneumonia, when sacrificed 35 days p.i.
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PMID:Clinical, virological, and pathological features of herpesvirus SA8 infection in conventional and gnotobiotic infant baboons (Papio cynocephalus). 17 97

Infection of the newborn infant with Group B hemolytic streptococcus is increasing in importance as other pathogens decline. Such infection may appear within the first 48 hours of life and resemble respiratory distress syndrome, or around the tenth day, when signs of meningeal irritation may be present. Early onset disease may be due to any of the five serotypes of the Group B streptococcus and is fatal in a high percentage of cases. Late onset infection usually is due to serotype III. The epidemiologic aspects of early and late infection appear to differ, and a nosocomial source may be involved in the latter. Penicillin prophylaxis may be useful.
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PMID:Streptococcus group B: an old bug with new dangers. 33 Jun 10

Newborn infants with "early-onset" disease due to group B beta hemolytic streptococcus were studied over a 40-month period. Clinical presentations included asymptomatic bacteremia, mild transient illness, respiratory distress, meningitis, and overwhelming sepsis. Chronologically, 18 were ill at birth; 10 became ill after a symptom-free period; and four were asymptomatic. Sixty-six percent of the cases weighted less than 2500 grams, and 56% were born to mothers whose amniotic membranes were ruptured for over 20 hours. All 15 of the deaths occurred in low birth weight infants who were criticially ill from birth. A review of 128 consecutive deliveries of infants weighing under 2000 grams revealed 28 cases with prolonged ruptured membranes, and three of these 28 infants developed group B streptococcal infection. The infant of the colonized gravid woman in premature labor or with prolonged ruptured membranes is clearly at risk, and these results suggest that the management of "early-onset" disease should begin prior to delivery.
Infection 1978
PMID:Risk factors in early-onset neonatal group b streptococcal infections. 34 7

Amebiasis, that is, infection with Entameba histolytica, continues to be endemic in the United States, with liver abscess occurring as an infrequent but constant complication. Seven cases are reported, with epidemiologic investigation of two. Reliable findings in hepatic abscess include fever, abdominal pain, respiratory distress, tender abdomen, and large, tender liver. Anemia, elevated white count with left shift, and the radiographic findings of an elevated right hemidiaphragm are constant. Epidemiologically, amebiasis occurs in clusters in the United States with person-to-person transmission predominant in spread. Infection is associated with poor sanitation and crowding. Investigation of the families of two patients documented 9/21 carriers and an additional 3/21 who were seropositive, as well as crowding and poor sanitation. In this country, treatment of a patient with amebic disease should include investigation of his home and family.
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PMID:Amebic liver abscess in children: clinical and epidemiologic features. 51 19

The neonatal morbidity and mortality rate of 335 twin pairs born during the years 1965-1973 was investigated. 649 twins were born alive. 29 % of the twins were preterm. 31 % of the twins were small for date infants, and 41 % weighed less than 2 500 g. Mean birth weight was 2 590 g in A twins and 2 560 g in B twins. The neonatal mortality (0-28 days) was 7.1 %. The most common causes of death were the respiratory distress syndrome, intracranial haemorrhage and anoxia. Low one minute Apgar scores occurred more often in B twins than among A twins. Breech delivery gave low one minute Apgar scores more often than did spontaneous vertex delivery in both twins. Full term twins and infants weighing more than 2 500 g had fewer low one minute Apgar scores than the preterm infants and those with low birth weight. Neonatal disorders were equally common in both twins except the birth asphyxia and/or aspiration syndrome, which were more frequent in the B twins. The respiratory distress syndrome was diagnosed in 8 % of A twins and 12 % of B twins. Hypoglycaemia was recorded for 8 %, and hyperbilirubinaemia exceeding 15 mg % for 7 %. Infections occurred in 6 %. Transfusion syndrome was verified in 7 % and malformations in 6 %. Although mortality in twin pregnancies has declined, neonatal morbidity is very high. Twin pregnancies thus form a high risk group for obstetricians and pediatricians.
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PMID:Twin pregnancy. Neonatal morbidity and mortality. 106 Mar 59

A mortal case of atypical pneumonia due to Chlamydia psittaci with acute respiratory distress, septic shock and multiple organ failure is described. Infection has been caused by an ill parrot imported clandestinely. Antibody titration with the immunofluorescence technique allowed diagnosis.
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PMID:[Bilateral pneumonia caused by Chlamydia psittaci. Description of a clinical case]. 150 65

Myxoma virus (MYX) is a leporipoxvirus of rabbits that induces a lethal syndrome characterized by disseminated tumorlike lesions, generalized immunosuppression, and secondary gram-negative bacterial infection. A MYX deletion mutant (vMYX-GF- delta M11L) was constructed to remove the entire myxoma growth factor (MGF) coding sequence and that for the C-terminal five amino acids of the partially overlapping upstream gene, M11L. Unexpectedly, this deletion completely abrogates the capacity of MYX to cause the characteristic disease symptoms of myxomatosis. Upon inoculation of rabbits with vMYX-GF- delta M11L, recipient animals developed only a benign, localized nodule reminiscent of a Shope fibroma virus-induced tumor in which a single primary lesion appeared at the site of injection and then completely regressed within 14 days, leaving the animals resistant to challenge with wild-type MYX. No evidence of the purulent conjunctivitis and rhinitis that always accompany wild-type MYX infection was observed. To ascertain whether the attenuation observed in vMYX-GF- delta M11L was due to a combined effect of the MGF deletion and alteration of the upstream M11L gene, two additional MYX recombinants were constructed: an MGF- virus (vMYX-GF-) containing an intact M11L gene and an M11L- virus (vMYX-M11L-) containing an intact MGF gene. Infection with vMYX-GF- resulted in moderated symptoms of myxomatosis, but all clinical stages of the disease were still detectable. In contrast, disruption of M11L alone dramatically reduced the virus virulence, resulting in a nonlethal syndrome whose clinical course was nevertheless distinct from that of vMYX-GF- delta M11L. Upon inoculation with vMYX-M11L-, rabbits developed primary and secondary tumors which were larger and more circumscribed than those of wild-type MYX recipients. Whereas wild-type MYX infection always includes severe, purulent conjunctivitis and rhinitis, vMYX-M11L- recipients remained healthy and displayed only minimal signs of respiratory distress. By about 30 days after infection, the tumors induced by vMYX-M11L- had completely regressed and these animals were immune to challenge with wild-type MYX. Histological analysis indicated that tumors induced by vMYX-M11L- are much more heavily infiltrated with macrophages and heterophils and that the sites of viral replication are more edematous and necrotic than those of wild-type infection, suggesting that the host was able to mount a more vigorous inflammatory response to vMYX-M11L- infection.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Deletion analysis of two tandemly arranged virulence genes in myxoma virus, M11L and myxoma growth factor. 162 52

A rat model is described in which animals develop respiratory cryptosporidiosis, a disease which is well documented in immunocompromised patients, especially those with AIDS. Our present lack of knowledge of the pathophysiology and immunology of Cryptosporidium parvum respiratory infections warrants the development of a laboratory animal model. Lewis rats immunosuppressed by subcutaneous injection of methylprednisolone acetate and inoculated intratracheally with 10(6) C. parvum oocysts developed a reproducible infection consisting of all known developmental stages in the epithelium lining airways from the trachea to the terminal bronchioles. Developmental stages were morphologically indistinguishable from those seen in gut epithelium. Infections were apparent at 4 days post-inoculation, and at 10-14 days post-inoculation, rats exhibited respiratory distress and severe weight loss and had enlarged, elastic lungs. Increased mucus production and exfoliative necrosis of the epithelium resulted in accumulation of large amounts of mucocellular exudate throughout the airways and patchy alveolitis involving alveoli emerging from respiratory bronchioles.
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PMID:An immunosuppressed rat model of respiratory cryptosporidiosis. 181 28

Infections due to gram-negative bacteria and other organisms can lead to septicemia and shock in some patients. Endotoxins, which cause these pathophysiological events, stimulate macrophages to elaborate tumor necrosis factor and other lymphokines. These lymphokines can augment free radical generation by polymorphonuclear leukocytes, macrophages and other cells, which may ultimately produce respiratory distress syndrome, multiorgan failure and irreversible shock seen in septicemia. This is supported by our results presented here that there is indeed an increase in free radical generation and lipid peroxidation in patients with septicemia. In addition, analysis of plasma lipid profile in these patients showed that gamma-linolenic, dihomogamma-linolenic and arachidonic acids of n-6 series and alpha-linolenic and eicosapentaenoic acids of the n-3 series are decreased in their plasma phospholipid fraction. These results suggest that free radicals, lipid peroxides, and alteration in essential fatty acid metabolism may have a role in the pathogenesis of septicemia.
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PMID:Free radical generation, lipid peroxidation and essential fatty acids in patients with septicemia. 201 12

From 1976 to 1983, the adult respiratory distress syndrome occurred in 14 patients during pregnancy or within a month postpartum. There were 8 survivors, giving a 43% mortality. All but 2 patients had obstetric-related precipitating events--labor problems, infections, eclampsia-toxemia, and obstetric hemorrhages. During emergency cesarean sections, 3 patients had respiratory problems that may have caused their respiratory distress syndrome. The average duration of mechanical ventilatory support was 16 days. Six patients had barotrauma with 1 patient sustaining an irreversible anoxic central nervous system injury. Infections were documented in 8 patients, 6 of whom had obstetric foci. There is a lack of information regarding the adult respiratory distress syndrome in this patient group. Though uncommon, it can cause substantial mortality and morbidity.
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PMID:Adult respiratory distress syndrome during pregnancy and immediately postpartum. 226 Feb 85


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