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CONGENITAL PNEUMONIA
275
practical standpoint we believe that the treathave outlined is applicable to all cases of prolonged accidental hypothermia whether euthyroid or otherwise, and perhaps the sole importance of recognising severe myxoedema would rest on one’s views on the use of From
a
ment we
tri-iodothvronine in that situation. HELEN DUGUID. R. G. SIMPSON. J. M. STOWERS.
Maryfield Hospital, Dundee. Geriatric Unit, Perth. Royal Infirmary, Aberdeen.
CONGENITAL PNEUMONIA SIR,-Dr. Barter’s survey (Jan. 20) of the problem of " congenital pneumonia " contains many lines of thought but may not clarify the issue. Although important observations were not made, I feel the credit for the first diagnosis of this condition should be given to Semmelweis. In 1847 he discovered why mothers died, often with their newborn babies. In 1856-57 when 16 mothers died, but their babies remained healthy, he rightly concluded that the maternal infection had occurred after the child had been delivered. Transplacental infection of the foetus in utero by common
organisms has come to be doubted in recent years. It is always a risk with infections that readily cause a bacterxmia-notably, and pyelonephritis, acute bronchitis and pneumonia, and the extraction of septic teeth. Pregnant women need rapid antibiotic protection should these develop. Nobody doubts the transplacental spread of the spirochaete of syphilis. I have seen one clear case of congenital tuberculosis. Congenital pneumonia due to bacteria of one sort or another is a very real condition. Dr. Barter shows that our thought on the problem is often confused. The problem is not infection or hypoxia (many of us prefer to call that asphyxia), but the correct diagnosis of every case. This may be a very difficult
pyelitis
matter.
By pneumonia the average doctor understands a bacterial infection of the lungs. Pathologists have confused the issue by failing to make clear that in the foetus and newborn we are dealing with one of three conditions when a " histological pneumonia" is present. These are: (1) " drowning in pus "; (2) inhalation of pus or other substances followed by a true pneumonia; and (3) a pneumonia following bacteraemia before or after rupture of the membranes.’ Because this differential diagnosis may
be very difficult I
am not
offering
exact
figures.
There is little doubt that " drowning in pus " is the "
com-
form of histological pneumonia "; this is the pure type resulting from asphyxia. The polymorphs inhaled into the lungs are typically degenerate and so the diagnosis may be clear. When a bacterial infection follows inhalation of the pus the diagnosis is more difficult, and reactions must be looked for in the lungs, lymph-nodes, and thymus. The diagnosis of the primary infective type is helped by the maternal history of an infection, a slight ante-partum haemorrhage about a week before abortion, and by the quality of the polymorphs in the air spaces of the lungs. It is essential to realise that the presence of polymorphs in a lesion is no proof of bacterial infection. The premenstrual endometrium is infiltrated with polymorphs but is not " septic ". Decidua and placental tissue in abortions are usually heavily infiltrated with polymorphs, but most of these are not " septic abortions ". The comparative absence of polymorphs in decidua always means that an ectopic gestation must be excluded. Polymorphs are easily fooled, they respond to the leukotaxin effect of breaking-down protein as regularly as they do to bacterial infection. The polymorphs in the air spaces of the fcetal lungs in the form of histological pneumonia which is the result of drowning in pus " are derived from the exudate on the placenta and membranes; they are also found in the foetal nose, pharynx, and alimentary canalsometimes as far as the anus. monest
"
1.
Osborn, G.
R. Proc. R. Soc. Med.
1958, 51, 840.
Polymorph infiltration of the umbilical cord is even more to interpret than that of the lungs. There may be gross suppuration at the umbilicus with demonstrable bacteria in a baby dying of hyaline-membrane disease, but no evidence of infection anywhere else. The umbilical cord is just as subject to the leucotaxin effect of its breakdown products as other tissues. The cord can be damaged in many ways beside foetal asphyxia. I doubt if I would be prepared to conclude anything important from the presence, or absence, of polymorphs in a frozen section of the cord at the time of delivery. Too much importance is being attached to early rupture of the membranes in foetal pneumonia ". Taking gross injuries of the foetus as the criterion of a criminal abortion by the passage of an instrument, I have found that such cases do not show a higher incidence of foetal histological pneumonia difficult
"
"
"
than the rest. Doubtless this would in the pre-antibiotic era. Derbyshire Royal Infirmary, Derby.
not
have been the
case
G. R. OSBORN.
SIR,-Dr. Barter supports the view of Dominguez et al.1 that leucocytic infiltration of the umbilical cord may indicate prenatal hypoxia rather than prenatal infection. We agree with him that clinical and morphological evidence of hypoxia is often present in infants dying of congenital pneumonia. Moreover, anomalous features of this disease, such as the common absence of pleurisy, of bronchiolar damage, and of fibrinous exudation, must raise doubts about its infective nature. But whether congenital pneumonia is hypoxic or infective in origin we feel that examination of the cord for leucocytes is an important part of the investigation of these infants. We have been trying for some time to find a simple, rapid, and reliable technique for making cord smears which could be used and interpreted by the clinician instead of the frozen-section method advocated by Benirschke and Clifford. The following method appears satisfactory: A microscope slide is cleaned in alcohol, dried and flamed. A piece of cord is cut free and stripped of blood as far as possible. From the centre of this a segment about 0-5 cm. long is cut. Any blood persisting on the cut surfaces or in the vessels is gently syringed away with normal saline. The segment is then pressed firmly on the glass slide and heated over a flame for a few seconds. Several imprints are taken in this way from both cut surfaces. The preparation is then fixed in acetic alcohol and stained with 0-1% Azure A in 30% alcohol.
If a significant polymorph infiltration is present in the cord, these cells will readily be found in the smear, among the endothelial and other normal mononuclear cells. It is important to be certain that no blood from the vein or arteries remains, otherwise the smear will be difficult to interpret. Radcliffe Infirmary, Oxford.
W. AHERNE PAMELA A. DAVIES.
MOSAICISM IN A MONGOL SIR,-Clarke et al. described a girl of normal intelligence and mongoloid characteristics in whom they found that cells cultured from peripheral blood were normal, whereas 30% of cells from skin cultures were trisomic for chromosome 21, the remaining 70% being normal. We recently examined cells cultured from the peripheral blood of a typical mongol, an adult male of imbecile grade, with typical mongol palm prints, born to a young mother. Of 45 cells counted, 48% were normal and 52% 21-trisomic with 47 chromosomes in the karyotype. Other tissues have not yet been examined. As Clarke et a]. observed, this type of 46/47 mosaicism may arise from anaphase lagging during mitosis of an originally 21-trisomic zygote, or from somatic non-disjunction of a normal 1. Dominguez, R., Segal, A. J., O’Sullivan, J. A. J. Amer. med. Ass. 1960. 2. 3.
173, 346. Benirschke, K., Clifford, S. H. J. Pediat. 1959, 54, 11. Clarke, M., Edwards, J. H., Smallpiece, V Lancet, 1961, i, 1028.
practical standpoint we believe that the treathave outlined is applicable to all cases of prolonged accidental hypothermia whether euthyroid or otherwise, and perhaps the sole importance of recognising severe myxoedema would rest on one’s views on the use of From
a
ment we
tri-iodothvronine in that situation. HELEN DUGUID. R. G. SIMPSON. J. M. STOWERS.
Maryfield Hospital, Dundee. Geriatric Unit, Perth. Royal Infirmary, Aberdeen.
CONGENITAL PNEUMONIA SIR,-Dr. Barter’s survey (Jan. 20) of the problem of " congenital pneumonia " contains many lines of thought but may not clarify the issue. Although important observations were not made, I feel the credit for the first diagnosis of this condition should be given to Semmelweis. In 1847 he discovered why mothers died, often with their newborn babies. In 1856-57 when 16 mothers died, but their babies remained healthy, he rightly concluded that the maternal infection had occurred after the child had been delivered. Transplacental infection of the foetus in utero by common
organisms has come to be doubted in recent years. It is always a risk with infections that readily cause a bacterxmia-notably, and pyelonephritis, acute bronchitis and pneumonia, and the extraction of septic teeth. Pregnant women need rapid antibiotic protection should these develop. Nobody doubts the transplacental spread of the spirochaete of syphilis. I have seen one clear case of congenital tuberculosis. Congenital pneumonia due to bacteria of one sort or another is a very real condition. Dr. Barter shows that our thought on the problem is often confused. The problem is not infection or hypoxia (many of us prefer to call that asphyxia), but the correct diagnosis of every case. This may be a very difficult
pyelitis
matter.
By pneumonia the average doctor understands a bacterial infection of the lungs. Pathologists have confused the issue by failing to make clear that in the foetus and newborn we are dealing with one of three conditions when a " histological pneumonia" is present. These are: (1) " drowning in pus "; (2) inhalation of pus or other substances followed by a true pneumonia; and (3) a pneumonia following bacteraemia before or after rupture of the membranes.’ Because this differential diagnosis may
be very difficult I
am not
offering
exact
figures.
There is little doubt that " drowning in pus " is the "
com-
form of histological pneumonia "; this is the pure type resulting from asphyxia. The polymorphs inhaled into the lungs are typically degenerate and so the diagnosis may be clear. When a bacterial infection follows inhalation of the pus the diagnosis is more difficult, and reactions must be looked for in the lungs, lymph-nodes, and thymus. The diagnosis of the primary infective type is helped by the maternal history of an infection, a slight ante-partum haemorrhage about a week before abortion, and by the quality of the polymorphs in the air spaces of the lungs. It is essential to realise that the presence of polymorphs in a lesion is no proof of bacterial infection. The premenstrual endometrium is infiltrated with polymorphs but is not " septic ". Decidua and placental tissue in abortions are usually heavily infiltrated with polymorphs, but most of these are not " septic abortions ". The comparative absence of polymorphs in decidua always means that an ectopic gestation must be excluded. Polymorphs are easily fooled, they respond to the leukotaxin effect of breaking-down protein as regularly as they do to bacterial infection. The polymorphs in the air spaces of the fcetal lungs in the form of histological pneumonia which is the result of drowning in pus " are derived from the exudate on the placenta and membranes; they are also found in the foetal nose, pharynx, and alimentary canalsometimes as far as the anus. monest
"
1.
Osborn, G.
R. Proc. R. Soc. Med.
1958, 51, 840.
Polymorph infiltration of the umbilical cord is even more to interpret than that of the lungs. There may be gross suppuration at the umbilicus with demonstrable bacteria in a baby dying of hyaline-membrane disease, but no evidence of infection anywhere else. The umbilical cord is just as subject to the leucotaxin effect of its breakdown products as other tissues. The cord can be damaged in many ways beside foetal asphyxia. I doubt if I would be prepared to conclude anything important from the presence, or absence, of polymorphs in a frozen section of the cord at the time of delivery. Too much importance is being attached to early rupture of the membranes in foetal pneumonia ". Taking gross injuries of the foetus as the criterion of a criminal abortion by the passage of an instrument, I have found that such cases do not show a higher incidence of foetal histological pneumonia difficult
"
"
"
than the rest. Doubtless this would in the pre-antibiotic era. Derbyshire Royal Infirmary, Derby.
not
have been the
case
G. R. OSBORN.
SIR,-Dr. Barter supports the view of Dominguez et al.1 that leucocytic infiltration of the umbilical cord may indicate prenatal hypoxia rather than prenatal infection. We agree with him that clinical and morphological evidence of hypoxia is often present in infants dying of congenital pneumonia. Moreover, anomalous features of this disease, such as the common absence of pleurisy, of bronchiolar damage, and of fibrinous exudation, must raise doubts about its infective nature. But whether congenital pneumonia is hypoxic or infective in origin we feel that examination of the cord for leucocytes is an important part of the investigation of these infants. We have been trying for some time to find a simple, rapid, and reliable technique for making cord smears which could be used and interpreted by the clinician instead of the frozen-section method advocated by Benirschke and Clifford. The following method appears satisfactory: A microscope slide is cleaned in alcohol, dried and flamed. A piece of cord is cut free and stripped of blood as far as possible. From the centre of this a segment about 0-5 cm. long is cut. Any blood persisting on the cut surfaces or in the vessels is gently syringed away with normal saline. The segment is then pressed firmly on the glass slide and heated over a flame for a few seconds. Several imprints are taken in this way from both cut surfaces. The preparation is then fixed in acetic alcohol and stained with 0-1% Azure A in 30% alcohol.
If a significant polymorph infiltration is present in the cord, these cells will readily be found in the smear, among the endothelial and other normal mononuclear cells. It is important to be certain that no blood from the vein or arteries remains, otherwise the smear will be difficult to interpret. Radcliffe Infirmary, Oxford.
W. AHERNE PAMELA A. DAVIES.
MOSAICISM IN A MONGOL SIR,-Clarke et al. described a girl of normal intelligence and mongoloid characteristics in whom they found that cells cultured from peripheral blood were normal, whereas 30% of cells from skin cultures were trisomic for chromosome 21, the remaining 70% being normal. We recently examined cells cultured from the peripheral blood of a typical mongol, an adult male of imbecile grade, with typical mongol palm prints, born to a young mother. Of 45 cells counted, 48% were normal and 52% 21-trisomic with 47 chromosomes in the karyotype. Other tissues have not yet been examined. As Clarke et a]. observed, this type of 46/47 mosaicism may arise from anaphase lagging during mitosis of an originally 21-trisomic zygote, or from somatic non-disjunction of a normal 1. Dominguez, R., Segal, A. J., O’Sullivan, J. A. J. Amer. med. Ass. 1960. 2. 3.
173, 346. Benirschke, K., Clifford, S. H. J. Pediat. 1959, 54, 11. Clarke, M., Edwards, J. H., Smallpiece, V Lancet, 1961, i, 1028.