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Query: UMLS:C0032285 (pneumonia)
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A number of practical office and bedside clues to cardiac disease in infants and children have been passed on through the years. They relate to the history, to the inspection and palpation components of the physical examination, and to knowledge of the specific cardiac defects that are likely to be associated with certain clinical syndromes. With the possible exception of coarctation of the aorta, the clues are not diagnostically specific. In many instances, however, they serve to narrow a broad array of diagnostic possibilities to 2 or 3 and, with the aid of other clues and auscultation, they can often be distinguished from one another. When a primary care physician is confronted with a child who has an incidental murmur that is "probably" innocent but could be organic, useful clues favoring an organic murmur are a history of congenital heart disease in a first-degree relative; a history of maternal rubella syndrome, alcohol use, or teratogenic drug use during pregnancy; a history of inappropriate sweating; a history of syncope, chest pain, or squatting; maternal diabetes mellitus; premature birth; birth at a high altitude; cyanosis; abnormal pulsations; recurrent bronchiolitis or pneumonia; chronic unexplained hoarseness; asymmetric facies with crying; and a physical appearance suggestive of a clinical syndrome.
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PMID:Clues in diagnosing congenital heart disease. 157 99

An active transmissible virus exists in the blood of measles patients during the eruptive stage of the disease. This virus produces in rabbits after intravenous injection a specific reaction analogous in all essential features to that of the human infection. Following a definite incubation period of from 2 to 5 days the animals infected show pyrexial, leucocytic, and cutaneous alterations. Fully 90 per cent of such inoculated rabbits react in a remarkable manner. The earliest constant symptom of the infection is a rise in temperature, which on the average occurs 4 days after inoculation and most probably marks the end of the incubation period. Concomitantly with this temperature rise there is a diminution in the total number of circulating leucocytes. This decrease in the number of white blood elements may be relative or may appear in the form of a well defined leucopenia. The most striking objective signs are the coryza, conjunctival injection, enanthemata, and exanthemata. The mucous membrane lesions are similar in their physical appearance to the so called Koplik spots seen in man. They occur on the buccal side of the oral cavity ranging in number from two to eight discrete hemorrhagic areas with paler centers. They appear as a rule coincidently with the temperature rise or shortly thereafter. The exanthematous lesions though occurring only in about 40 per cent of the infected animals complete the clinical syndrome in this particular experimental host. The rash may appear as early as the 3rd and as late as the 7th day after inoculation. In its early stage it is of the macular variety, appearing as a diffuse eruption which later develops into a more papular type of lesion. At this time the cutaneous manifestations appear as slightly raised, flattened, purplish red, discrete areas in the skin of the face, neck, chest, and abdomen. Repeated passage of the virus of measles through the rabbit seems to increase its virulence. A number of animals infected with such passage virus succumb in the fourth and subsequent generations, undoubtedly as the direct result of the action of the specific excitant, as in none of the animals was there cultural evidence of secondary intercurrent infection. In the animals dying presumably as a result of the specific virus grave nephritic changes were evident. It is a noteworthy fact that the pneumonia so common in fatal cases of human measles was not evident in any of the experimental animals. We believe this to be of considerable significance, especially in elucidating the direct etiological factor of the fatal pneumonias so often present in human measles cases. Apparently such infections in man can be explained purely on the basis of the destruction of normal defense barriers by the specific excitant of the infectious disease, and the lack of host resistance to the ordinary pyogenic microorganism.
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PMID:STUDIES UPON EXPERIMENTAL MEASLES : II. THE ENANTHEMATOUS, EXANTHEMATOUS, PYREXIAL, AND LEUCOCYTIC SYNDROME PRODUCED IN THE RABBIT BY INTRAVENOUS INOCULATION OF BLOOD FROM CASES OF HUMAN MEASLES. 1986 66

Marfan syndrome is rarely diagnosed in the neonatal period because of variable expression and age-dependent appearance of clinical signs. The prognosis is usually poor due to high probability of congestive heart failure, mitral and tricuspid regurgitations with suboptimal response to medical therapy and difficulties in surgical management. The authors have studied two cases of Marfan syndrome in the newborn period. Two cases of neonatal Marfan syndrome, one male and one female, were diagnosed by characteristic physical appearance. Both infants had significant cardiovascular abnormalities diagnosed by ultrasonography. Genetic DNA analysis in the second case confirmed the mutations in the fibrillin-1 gene located on chromosome 15q21 which is responsible for the development of Marfan syndrome. The boy died at six weeks of age with signs of rapidly progressive left ventricular failure associated with pneumonia. The second infant was having only mild signs of congestive heart failure and has been treated with beta blockers. At the age of 4 years her symptoms of congestive heart failure had worsened due to progression of mitral and tricuspid insufficiency and development of significant cardiomegaly. Mitral and tricuspid valvuloplasy had to be done at that time. Early diagnosis of Marfan syndrome in the newborn period can allow treatment in the early stages of cardiovascular abnormalities and may improve the prognosis. It also helps to explain to the family the serious health problem of their child.
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PMID:Neonatal Marfan syndrome: Report of two cases. 2875 79