Congenital pneumonia: Causes, Symptoms, Diagnosis & Treatments
Causes
One of the most important diseases in infant infections is pneumonia. In developed countries, mortality and morbidity due to neonatal pneumonia is high. In developed countries, incidence is 1% in full term infants, ill infant in normal weight, and incidence in 10% in low birth weight infants. Neonatal pneumonia can be divided into early onset and late onset, and in the case of congenital pneumonia, early onset. Early-onset pneumonia acquires pathogens from the mother within three days of birth through the following three pathways: If the infected amniotic fluid is aspirated from the uterus, the pathogen is transmitted through the placenta, or the infant is aspirated during vaginal organism during or immediately after birth.
Congenital pneumonia can be a bacterial or a virus. Bacterial pneumonia causes inflammation of pleura or infiltration or destruction of bronchopulmonary tissue. Viral pneumonia is mainly caused by interstitial pneumonia. The main cause is bacteria, among which aerobic bacteria is mainly responsible for causing bacteria. Group B streptococcus (GBS) is the leading causative organism. In developing countries, Escherichia coli, GBS, Klebsiella spp, Staphylococcus aureus, Streptococcus pneumonia are the causative organisms. Other unusual pathogens include Listeria monocytogenes and Mycobacterium tuberculosis, both of which can be transplacental. Among early-onset viral pneumonia, Herpes simplex virus (HSV) is the most common causative organism. Other adenoviruses, enteroviruses, and mumps viruses can be the cause and are transmitted mainly to the fetus through the placenta. In rare cases, pneumonia occurs congenitally by Candida sp. Or other fungi, or by toxoplasmosis or syphilis.
In GBS pneumonia, the most common congenital pneumonia, beta-hemolysin acts as a pore-forming cytolysin and its concentration is directly related to its ability to damage the lung epithelium. Increased permeability due to damage contributes to alveolar edema and hemorrhage. Congenital pneumonia, especially in premature infants, is more severe because of the lack of surfactant phospholipids that prevent beta-hemolysin-associated lung epithelial cell injury. Risk factors for congenital pneumonia include maternal factors such as premature rupture of fetal membranes (PROM) over 18 hours, maternal amnionitis, premature delivery, fetal tachycardia and maternal intrapartum fever, and fetal factors such as airway anomalies or severe underlying disease.
Symptoms
Clinical manifestations may include respiratory distress, lethargy, apnea, tachycardia, poor perfusion, and even septic shock at birth or shortly after birth. In some cases, pulmonary hypertension may occur. Temperature instability, metabolic acidosis, and abdominal distension. However, it is not a pneumonia-specific symptom. Diagnosis is made by clinical symptoms and chest X-ray. Bilateral alveolar densities are seen with air bronchogram as imaging findings. However, there are cases of irregular patchy infiltrates or normal lung findings. The causative organisms are identified through blood, pleural fluid, tracheal aspirates (if possible), culture and gram stain, PCR (suspected viral or nonbacterial infection). However, needle aspiration or bronchoscopy is necessary to obtain pleural fluid or tracheal aspirates, but it is difficult to perform for neonates with poor condition.
Diagnosis & Treatments
Early diagnosis and treatment can prevent permanent damage. Initial treatment should be accompanied by the use of empirical antibiotics and oxygen supply and mechanical ventilation if necessary, depending on the severity of the repiratory distress. Until the results of the bacterial culture test, parenteral administration of empirical antibiotics to the bacteria of the mother's acidity is recommended. Ampicillin and gentamicin are used as empirical antibiotics. Drug dose is determined by weight, renal function, postnatal age, and postmenstrual age. Ampicillin is effective for group B streptococci, most other strains of streptococci, L. monocytogenes, and some gram-negative bacteria, and synergistic effect when used with gentamicin. Gentamicin resistance is replaced by other aminoglycoside antibiotics such as amikacin. However, third-generation cephalosporins may cause rapid resistance and should not be used as empirical antibiotics when early onset sepsis or pneumonia is suspected. Once the causative organism has been identified, antibiotics can be used. In the case of a viral infection, conservative treatment is performed except in certain cases. If herpes simplex virus pneumonia is suspected, acyclovir (60 mg / kg per day in divided doses for 21 days) is administered IV (but the result is fatal even after treatment). Respiratory syncytial virus pneumonia is only treated with Ribavirin, The efficacy is not proven precisely and is therefore not commonly used. RSV prophylaxis is recommended for high-risk neonates (who have chronic lung disease or are born less than 29 weeks of gestational age).
The prognosis of congenital pneumonia depends on the severity of the disease, the gestational age at birth, the presence of underlying disease, and the type of causative organism. However, in developed countries, In children born with preterm or chronic lung disease or immunodeficiency, mortality due to congenital pneumonia increases.
One of the most important diseases in infant infections is pneumonia. In developed countries, mortality and morbidity due to neonatal pneumonia is high. In developed countries, incidence is 1% in full term infants, ill infant in normal weight, and incidence in 10% in low birth weight infants. Neonatal pneumonia can be divided into early onset and late onset, and in the case of congenital pneumonia, early onset. Early-onset pneumonia acquires pathogens from the mother within three days of birth through the following three pathways: If the infected amniotic fluid is aspirated from the uterus, the pathogen is transmitted through the placenta, or the infant is aspirated during vaginal organism during or immediately after birth.
Congenital pneumonia can be a bacterial or a virus. Bacterial pneumonia causes inflammation of pleura or infiltration or destruction of bronchopulmonary tissue. Viral pneumonia is mainly caused by interstitial pneumonia. The main cause is bacteria, among which aerobic bacteria is mainly responsible for causing bacteria. Group B streptococcus (GBS) is the leading causative organism. In developing countries, Escherichia coli, GBS, Klebsiella spp, Staphylococcus aureus, Streptococcus pneumonia are the causative organisms. Other unusual pathogens include Listeria monocytogenes and Mycobacterium tuberculosis, both of which can be transplacental. Among early-onset viral pneumonia, Herpes simplex virus (HSV) is the most common causative organism. Other adenoviruses, enteroviruses, and mumps viruses can be the cause and are transmitted mainly to the fetus through the placenta. In rare cases, pneumonia occurs congenitally by Candida sp. Or other fungi, or by toxoplasmosis or syphilis.
In GBS pneumonia, the most common congenital pneumonia, beta-hemolysin acts as a pore-forming cytolysin and its concentration is directly related to its ability to damage the lung epithelium. Increased permeability due to damage contributes to alveolar edema and hemorrhage. Congenital pneumonia, especially in premature infants, is more severe because of the lack of surfactant phospholipids that prevent beta-hemolysin-associated lung epithelial cell injury. Risk factors for congenital pneumonia include maternal factors such as premature rupture of fetal membranes (PROM) over 18 hours, maternal amnionitis, premature delivery, fetal tachycardia and maternal intrapartum fever, and fetal factors such as airway anomalies or severe underlying disease.
Symptoms
Clinical manifestations may include respiratory distress, lethargy, apnea, tachycardia, poor perfusion, and even septic shock at birth or shortly after birth. In some cases, pulmonary hypertension may occur. Temperature instability, metabolic acidosis, and abdominal distension. However, it is not a pneumonia-specific symptom. Diagnosis is made by clinical symptoms and chest X-ray. Bilateral alveolar densities are seen with air bronchogram as imaging findings. However, there are cases of irregular patchy infiltrates or normal lung findings. The causative organisms are identified through blood, pleural fluid, tracheal aspirates (if possible), culture and gram stain, PCR (suspected viral or nonbacterial infection). However, needle aspiration or bronchoscopy is necessary to obtain pleural fluid or tracheal aspirates, but it is difficult to perform for neonates with poor condition.
Diagnosis & Treatments
Early diagnosis and treatment can prevent permanent damage. Initial treatment should be accompanied by the use of empirical antibiotics and oxygen supply and mechanical ventilation if necessary, depending on the severity of the repiratory distress. Until the results of the bacterial culture test, parenteral administration of empirical antibiotics to the bacteria of the mother's acidity is recommended. Ampicillin and gentamicin are used as empirical antibiotics. Drug dose is determined by weight, renal function, postnatal age, and postmenstrual age. Ampicillin is effective for group B streptococci, most other strains of streptococci, L. monocytogenes, and some gram-negative bacteria, and synergistic effect when used with gentamicin. Gentamicin resistance is replaced by other aminoglycoside antibiotics such as amikacin. However, third-generation cephalosporins may cause rapid resistance and should not be used as empirical antibiotics when early onset sepsis or pneumonia is suspected. Once the causative organism has been identified, antibiotics can be used. In the case of a viral infection, conservative treatment is performed except in certain cases. If herpes simplex virus pneumonia is suspected, acyclovir (60 mg / kg per day in divided doses for 21 days) is administered IV (but the result is fatal even after treatment). Respiratory syncytial virus pneumonia is only treated with Ribavirin, The efficacy is not proven precisely and is therefore not commonly used. RSV prophylaxis is recommended for high-risk neonates (who have chronic lung disease or are born less than 29 weeks of gestational age).
The prognosis of congenital pneumonia depends on the severity of the disease, the gestational age at birth, the presence of underlying disease, and the type of causative organism. However, in developed countries, In children born with preterm or chronic lung disease or immunodeficiency, mortality due to congenital pneumonia increases.
