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Pneumocystis carinii infection in melanesian children
914
The ]ournal of P E D I A T R I C S
Pneumocystis carinii infection in Melanesian cbiMren B. Ryan, ~ M.R.C.P.(Edin.), D.G.O., D.C.H. PORT
IViORESBY~
NEW
GUINEA
tion which was thought to be probably bronchiectatic in origin, and a grossly enlarged heart. Splenectomy was eventually agreed to; after transfusion this was performed July 7, 1960. After a stormy postoperative period during which he developed pneumonia and intermittent heart bloc, he appeared to be greatly improved. Following the operation, the wound discharged intermittently and he was again anesthetized. The wound was probed and a piece of silk suture removed. On the following day he had obviously again developed pneumonia which did not appear to be responding to antibiotics. However, these had been given for only a little over 24 hours when he suddenly collapsed and died. It was noted at this time that his brother was suffering from an acute upper respiratory infection and it was thought that he may possibly have had the same infection. It seemed reasonable to suppose that the resistance may have been lowered by the anesthetic and that the absence of the spleen may have conduced to a fatal outcome2 A postmortem examination showed edematous lungs in which large dark friable areas were present. Microscopic examination revealed excessive hyperemia and thickening of the alveolar walls with areas of collapse alternating with some areas of emphysema. The thickened walls contained infiltrations with plasma cells, and a number of alveoli
I N F E C T I O N with Pneumocystis carinii has been reported from America, 1-* England,S, 6 Europe,~ and Australia, a but as far as I know, it has not been described in the Far East or Melanesia. At least 3 cases have been admitted to the Port Moresby General Hospital over a period of 12 months. REPORTS
OF C A S E S
Case 1. L. K., aged 5 years, a male child of Milne Bay, was admitted on June 6, 1960, with a diagnosis of hemolytic anemia for which he had been hospitalized a year previously. At that time he was emaciated and had an enormously enlarged spleen and hepatomegaly. He had suffered from frequent respiratory infections while in the hospital and had been treated by transfusion, cortisone, and hematinics, but the condition had failed to improve. Splenectomy had been refused, and he had returned to his village. On readmission, the condition was the same as previously, and he was found to be suffering from a congenital hemolytic anemia of unknown causation. He also appeared to have a chronic pulmonary infee-
From the Public Health Department, Territory of Papua and New Guinea. ~Address, General Hospital, Port Moresby, New Guinea.
914
Volume 60 Number 6
contained eosinophilic material in which Pn. carinii were found. Other organs such as the liver, heart, and bone marrow showed the typical changes of hemolytic anemia. Case 2. J. L., a male infant, aged 3 months, was admitted on Jan. 11, 1960. The mother of this child stated that he weighed 7 pounds at birth and had become ill several weeks before entering the hospital. He had lost his appetite, become irritable, and begun to lose weight. A few days before admission, he had developed a cough and the mother noticed that the breathing had been rapid. On examination, the child was obviously poorly nourished (weight 8 pounds) with tachypnea and cyanosis. Edema of the legs and hands was marked and the face also appeared puffy. The heart appeared normal and, although percussion of the chest suggested an underlying pneumonia, no adventitious sounds could be heard. Radiologic examination showed numerous areas of consolidation in both lung fields. Blood examination was essentially normal and there was no albuminuria, but blood culture produced a coagulase positive staphylococcus sensitive to most antibiotics. A serum protein examination was requested but apparently not performed. Treatment with chloramphenicol and oxytetracycline appeared to produce some improvement, but tachypnea persisted. Two days after admission, edema of the face was more marked and cyanosis had increased. As the child appeared to be developing congestive cardiac failure, he was given digitalis and there was an immediate improvement-edema disappeared from the face and hands but persisted in the feet. Chloramphenlcol was added to the other drugs on July 11, 1960, but there was no further improvement. On Oct. 11, 1960, nine days after admission, the condition was obviously deteriorating-cyanosis was increasing in spite of high concentrations of oxygen, edema had also returned and did not respond to diuretics. The patient collapsed and died later the same night.
Pneumocystis carinii injection
9 15
Postmortem examination showed the bronchi to be filled with hemorrhagic fluid. Both lungs were heavy, firm, and reddened, and crepitus was not present. Microscopic examination showed infiltration of the septa with plasma cells. The alveoli were filled with a foamy network and small round bodies were seen in the cystic spaces present. Subsequently these were shown to be Pn. carinii. Case 3. A. K., a 6-month-old female child from Kikori, was admitted in April, 1961. She had been an inpatient at another hospital 4 months previously, apparently suffering from pneumonia. The mother stated the child was well until 2 days before admission, when she developed fever and cough. She was breast fed. On examination, she was seen to be an emaciated, feeble child, with panting respiration and inspiratory retraction of the lower intercostal spaces and suprasternal notch; moist sounds were heard over both lung-fields. The weight was 9 pounds. Respiration became more and more difficult over the next 2 days and tracheostomy was performed on the third day, but without improvement. The temperature of 101.4 ~ F. on admission subsided within 24 hours, but rose to 104 ~ F. before the operation. The throat swab grew hemolytic streptococci. The child died 3 hours after the operation. Full autopsy was refused but a piece of Iung was obtained by a slight downward extension of the tracheostorny wound. The pathologist reported that a small piece of thymus was normal, except for a few areas of plasma cell infiltration; but in a piece of lung, there were areas of compensating emphysema, beside other areas which were completely involved partly with hemorrhage and partly showing thickening of the alveolar walls with plasma cell infiltration and the presence of either edema or masses of Pn. carlnii. DISCUSSION
All of the cases reported showed the presence of Pn. carinii post mortem, and the sec-
9 1 6 Ryan
ond case was typical of this infection in its clinical course. Whether Patient 1 did, in fact, die from the effect of Pneumocystis infection is not certain, as the course of the disease was so swift and his brother appeared to be suffering from a virus infection at the time. It is quite conceivable that the absence of the spleen, the heart also being affected, and his having had a general anesthetic 2 days before death may all have lowered the resistance to a relatively mild virus infection. In the third case the course of the disease was apparently short, but the accuracy of the history obtained is open to doubt. T h e point of recording these cases is to emphasize the fact that Pnemnocystis infection exists in New Guinea.
Dr. V. S. Prince, pathologist, Port IVforesby General Hospital, reported on the histology of Case 2 and Professor R. E. J. ten Seldam of the Pathology Department of the University of Western Australia, reported on Cases 1 and 3. The complete histologic findings in Case 1 will be reported elsewhere. This paper is printed by
June 1962
permission of the Director, Department of Public Health, Territory of Papua and New Guinea. REFERENCES
!. Anderson, C. D., and Battle, H. J.: Fatal Pneumoeystis Pneumonia in an Adult, Am. J. Clin. Path. 34: 365, 1960. 2. Dauzler, G., Willis, T., and Barnett, R. N.: Pneumocystis Carlnii Pneumonia in an Infant, Am. J. Clin. Path. 26: 787, 1956. 3. Nelson, W. E.: Textbook of Paediatrics. ed. 7, Philadelphia, 1959, W. B. Saunders Company, p. 798. 4. Rubin, E., and Zak, F. G.: Pneumoeystis. Carinii Pneumonia in the Adult, New England J. Med. 262: 1315, 1960. 5, McKay, E., and Richardson, J.: Pneumocystis Carinii Pneumonia Associated With Hypogammaglobulinaemia, Lancet 2: 713, 1959. 6. Baar, H. S.: Interstitial Plasma-Cellular Pneumonia Due to Pneumocystis Carinii, J. Clin. Path. 8: 19, 1955. 7. Vanek, J., Jirovec, O., and Luke% J.: Interstitial Plasma Cell Pneumonia in Infants, Ann. paediat. 180: 1, 1953. 8. Reye, R. D: K., ten Seldam, R. E. J.: J. Path. Bact. 72: 451, 1956 (Quoted by Williams et al., 1960). 9. Smith, C. H., Erland~on, M. E., Sehulman, L, and Stern, G.: Hazards of Severe Infections in Splenectomised Infants and Children, Am. J. Med. 22" 390, 1957.
The ]ournal of P E D I A T R I C S
Pneumocystis carinii infection in Melanesian cbiMren B. Ryan, ~ M.R.C.P.(Edin.), D.G.O., D.C.H. PORT
IViORESBY~
NEW
GUINEA
tion which was thought to be probably bronchiectatic in origin, and a grossly enlarged heart. Splenectomy was eventually agreed to; after transfusion this was performed July 7, 1960. After a stormy postoperative period during which he developed pneumonia and intermittent heart bloc, he appeared to be greatly improved. Following the operation, the wound discharged intermittently and he was again anesthetized. The wound was probed and a piece of silk suture removed. On the following day he had obviously again developed pneumonia which did not appear to be responding to antibiotics. However, these had been given for only a little over 24 hours when he suddenly collapsed and died. It was noted at this time that his brother was suffering from an acute upper respiratory infection and it was thought that he may possibly have had the same infection. It seemed reasonable to suppose that the resistance may have been lowered by the anesthetic and that the absence of the spleen may have conduced to a fatal outcome2 A postmortem examination showed edematous lungs in which large dark friable areas were present. Microscopic examination revealed excessive hyperemia and thickening of the alveolar walls with areas of collapse alternating with some areas of emphysema. The thickened walls contained infiltrations with plasma cells, and a number of alveoli
I N F E C T I O N with Pneumocystis carinii has been reported from America, 1-* England,S, 6 Europe,~ and Australia, a but as far as I know, it has not been described in the Far East or Melanesia. At least 3 cases have been admitted to the Port Moresby General Hospital over a period of 12 months. REPORTS
OF C A S E S
Case 1. L. K., aged 5 years, a male child of Milne Bay, was admitted on June 6, 1960, with a diagnosis of hemolytic anemia for which he had been hospitalized a year previously. At that time he was emaciated and had an enormously enlarged spleen and hepatomegaly. He had suffered from frequent respiratory infections while in the hospital and had been treated by transfusion, cortisone, and hematinics, but the condition had failed to improve. Splenectomy had been refused, and he had returned to his village. On readmission, the condition was the same as previously, and he was found to be suffering from a congenital hemolytic anemia of unknown causation. He also appeared to have a chronic pulmonary infee-
From the Public Health Department, Territory of Papua and New Guinea. ~Address, General Hospital, Port Moresby, New Guinea.
914
Volume 60 Number 6
contained eosinophilic material in which Pn. carinii were found. Other organs such as the liver, heart, and bone marrow showed the typical changes of hemolytic anemia. Case 2. J. L., a male infant, aged 3 months, was admitted on Jan. 11, 1960. The mother of this child stated that he weighed 7 pounds at birth and had become ill several weeks before entering the hospital. He had lost his appetite, become irritable, and begun to lose weight. A few days before admission, he had developed a cough and the mother noticed that the breathing had been rapid. On examination, the child was obviously poorly nourished (weight 8 pounds) with tachypnea and cyanosis. Edema of the legs and hands was marked and the face also appeared puffy. The heart appeared normal and, although percussion of the chest suggested an underlying pneumonia, no adventitious sounds could be heard. Radiologic examination showed numerous areas of consolidation in both lung fields. Blood examination was essentially normal and there was no albuminuria, but blood culture produced a coagulase positive staphylococcus sensitive to most antibiotics. A serum protein examination was requested but apparently not performed. Treatment with chloramphenicol and oxytetracycline appeared to produce some improvement, but tachypnea persisted. Two days after admission, edema of the face was more marked and cyanosis had increased. As the child appeared to be developing congestive cardiac failure, he was given digitalis and there was an immediate improvement-edema disappeared from the face and hands but persisted in the feet. Chloramphenlcol was added to the other drugs on July 11, 1960, but there was no further improvement. On Oct. 11, 1960, nine days after admission, the condition was obviously deteriorating-cyanosis was increasing in spite of high concentrations of oxygen, edema had also returned and did not respond to diuretics. The patient collapsed and died later the same night.
Pneumocystis carinii injection
9 15
Postmortem examination showed the bronchi to be filled with hemorrhagic fluid. Both lungs were heavy, firm, and reddened, and crepitus was not present. Microscopic examination showed infiltration of the septa with plasma cells. The alveoli were filled with a foamy network and small round bodies were seen in the cystic spaces present. Subsequently these were shown to be Pn. carinii. Case 3. A. K., a 6-month-old female child from Kikori, was admitted in April, 1961. She had been an inpatient at another hospital 4 months previously, apparently suffering from pneumonia. The mother stated the child was well until 2 days before admission, when she developed fever and cough. She was breast fed. On examination, she was seen to be an emaciated, feeble child, with panting respiration and inspiratory retraction of the lower intercostal spaces and suprasternal notch; moist sounds were heard over both lung-fields. The weight was 9 pounds. Respiration became more and more difficult over the next 2 days and tracheostomy was performed on the third day, but without improvement. The temperature of 101.4 ~ F. on admission subsided within 24 hours, but rose to 104 ~ F. before the operation. The throat swab grew hemolytic streptococci. The child died 3 hours after the operation. Full autopsy was refused but a piece of Iung was obtained by a slight downward extension of the tracheostorny wound. The pathologist reported that a small piece of thymus was normal, except for a few areas of plasma cell infiltration; but in a piece of lung, there were areas of compensating emphysema, beside other areas which were completely involved partly with hemorrhage and partly showing thickening of the alveolar walls with plasma cell infiltration and the presence of either edema or masses of Pn. carlnii. DISCUSSION
All of the cases reported showed the presence of Pn. carinii post mortem, and the sec-
9 1 6 Ryan
ond case was typical of this infection in its clinical course. Whether Patient 1 did, in fact, die from the effect of Pneumocystis infection is not certain, as the course of the disease was so swift and his brother appeared to be suffering from a virus infection at the time. It is quite conceivable that the absence of the spleen, the heart also being affected, and his having had a general anesthetic 2 days before death may all have lowered the resistance to a relatively mild virus infection. In the third case the course of the disease was apparently short, but the accuracy of the history obtained is open to doubt. T h e point of recording these cases is to emphasize the fact that Pnemnocystis infection exists in New Guinea.
Dr. V. S. Prince, pathologist, Port IVforesby General Hospital, reported on the histology of Case 2 and Professor R. E. J. ten Seldam of the Pathology Department of the University of Western Australia, reported on Cases 1 and 3. The complete histologic findings in Case 1 will be reported elsewhere. This paper is printed by
June 1962
permission of the Director, Department of Public Health, Territory of Papua and New Guinea. REFERENCES
!. Anderson, C. D., and Battle, H. J.: Fatal Pneumoeystis Pneumonia in an Adult, Am. J. Clin. Path. 34: 365, 1960. 2. Dauzler, G., Willis, T., and Barnett, R. N.: Pneumocystis Carlnii Pneumonia in an Infant, Am. J. Clin. Path. 26: 787, 1956. 3. Nelson, W. E.: Textbook of Paediatrics. ed. 7, Philadelphia, 1959, W. B. Saunders Company, p. 798. 4. Rubin, E., and Zak, F. G.: Pneumoeystis. Carinii Pneumonia in the Adult, New England J. Med. 262: 1315, 1960. 5, McKay, E., and Richardson, J.: Pneumocystis Carinii Pneumonia Associated With Hypogammaglobulinaemia, Lancet 2: 713, 1959. 6. Baar, H. S.: Interstitial Plasma-Cellular Pneumonia Due to Pneumocystis Carinii, J. Clin. Path. 8: 19, 1955. 7. Vanek, J., Jirovec, O., and Luke% J.: Interstitial Plasma Cell Pneumonia in Infants, Ann. paediat. 180: 1, 1953. 8. Reye, R. D: K., ten Seldam, R. E. J.: J. Path. Bact. 72: 451, 1956 (Quoted by Williams et al., 1960). 9. Smith, C. H., Erland~on, M. E., Sehulman, L, and Stern, G.: Hazards of Severe Infections in Splenectomised Infants and Children, Am. J. Med. 22" 390, 1957.