- Email: [email protected]
Disseminated Legionella pneumophila infection in an infant with severe combined immunodeficiency
760
Brief clinical and laboratory observations
Disseminated
The Journal of Pediatrics May 1982
Legionella pneumophila infection
in an
infant with severe combined immunodeficiency Ernest Cutz, M.D., F.R.C.P.(C),* Paul S. Thorner, M.D., C. Pandu Rao, M.D., Sandu Toma, M.D., F.R.C.P.(C), Ronald Gold, M.D., F.R.C.P.(C), and Erwin W. Gelfand, M.D., C.M., F.R.C.P.(C), Toronto, Ont., Canada
LEGIONNAIRE DISEASE, unrecognized before 1976, has since received global attention, with over 1,000 cases reported. ~ A l t h o u g h most individuals who developed the disease were previously healthy, this infection frequently occurs in i m m u n o c o m p r o m i s e d patients? Most cases have been described in adults, but children can be affected. 3,4 W e report a case of fatal Legionnaire disease in an infant with severe combined immunodeficiency who developed disseminated infection involving the lungs, liver, and brain. CASE REPORT The patient was a 5-month-old first-born male infant of a non-consanguinous marriage whose growth and development had been normal until one month before admission, when he developed fever, cough, and coryza. Treatment with amoxicillin, followed by erythromycin, was without effect. On admission, he was noted to be well developed and well nourished. He appeared acutely ill with a temperature of 39.6~ and had mild respiratory distress. Chest radiograph revealed bilateral lower lobe infiltrates. Cloxacillin a n d ampicillin therapy was started. Cultures of pharyngeal secretions grew parainfluenza virus type 3, Staphylococcus ~aureus, and Haemophilus influenzae (type unknown). He became afebrile, and antibiotic therapy was discontinued after seven days. However, three days later, fever and respiratory distress recurred. Despite therapy with Cefamandole, a right-sided effusion developed which required chest tube drainage. Cultures and Gram stains were negative, Cefamandole therapy was discontinued, and treatment with ampicillin and chloramphenicol was begun. The possibility of an underlying immunodeficiency was raised. The family history was negative. No tonsils or lymph nodes were evident on physical examination, and no thymus shadow was visualized on the chest radiograph. Additional studies revealed a peripheral lymphopenia, and only 3% of peripheral blood mononuclear cells formed rosettes with sheep erythrocytes. Peripheral blood lymphocytes failed to proliferate in response to phytohemagglutinin or concanavalin A, and serum levels of all immunoglobulin classes (other than lgM) were decreased (IgG 50 mg/dl,
From the Departments of Pathology, Immunology, Infectious DBeases and Paediatrics, The Hospital for Sick Children, Toronto and The University of Toronto, and Division of Bacteriology, Public Health Laboratory, Ontario Ministry of Health. *Reprint address." Department of Pathology, The Hospital for Sick Children, 555 University Ave., Toronto. Ont., Canada M5G IX8.
lgA < 5 mg/dl, IgM 37 mg/dl, IgE < 10 ng/ml). Red blood cell adenosine deaminase and nucleoside phosphorylase activities were normal. The infant's condition further deteriorated, requiring assisted ventilation and oxygen. A lung biopsy was performed and revealed a heavy infestation with Pneumoeystis carinii organisms and growth of parainfluenza virus type 3, for which he was given trimethoprim-sulfamethoxazole. After 72 hours there was no improvement and treatment with pentamidine isothionate was begun. Subsequent studies of the lung biopsy revealed numerous Dieterle-positive blunt rods. Despite the addition of erythromycin, the infant's pulmonary condition progressively deteriorated, and he died one week after the lung biopsy and four weeks following admission. Abbreviations used CDC: Centers for Disease Control SCID: severe combined immunodeficiency disease METHODS Tissues from the lung biopsy as well as lung and other tissues obtained at autopsy were processed for routine histology including Dieterle stain 5 and electron microscopy. For the growth of Legionella, lung tissue specimens were inoculated undiluted and as serial dilution inoeula on four plate media (F-G, CYE, C Y E with antibiotics, and Greaves) and then incubated at 36~ in 3% CO2. 6,7 Direct fluorescent antibody examination of lung, liver, spleen, brain, a n d bone m a r r o w tissues was carried out according to the instructions of the Centers for Disease Control, A t l a n t a , Ga, 7 using reagents received from the C D C or prepared in our laboratory for Legionella pneumophila serogroups 1 to 6, L. boxemanii, L. micdadei, L. dumoffii, and L. gormanii. RESULTS The sections of lung biopsy showed a diffuse interstitial process with intra-alveolar exudate composed of amorphous debris and a mixture of macrophages and polymorphonuelear leukocytes. A well-circumscribed area of coagulative necrosis within the lung p a r e n c h y m a was present, showing dense infiltrate of granulocytes and m a c r o p h a g e s (Figure). The stains for microorganisms revealed large numbers of Pneumocystis carinii organisms within the
0022-3476/82/050760+03500.30/0 9 1982 The C. V. Mosby Co.
Volume 1O0 Number 5
Brief clinical and laboratory observations
76 1
alve01i, and Dieterle stain showed numerous blunt rodshaped bacilli, with features of Legionella pneumophila (Figure, inset). These organisms were most numerous in the area of necrosis, but extended to adjacent tissue. Results of Gram" stain and Ziehl-Neelsen stain were negative. By electron microscopy, bacterial organisms with triple layer cell membranes and cytoplasmic empty vacuoles were identified within the cytoplasm of macrophages or lying free in the alveolar spaces. The ultrastructural features of these organisms were similar to those previously described in cases of Legionnaire disease? At autopsy, the lungs were diffusely consolidated and contained numerous abscess cavities, involving all lobes. One abscess cavity had penetrated through the pleural space, resulting in an empyema. The microscopic changes were similar to those seen in the lung biopsy. Although only occasional Pneumocystis carinii organisms were seen, numerous Dieterle-positive bacilli were present. A single large abscess and numerous microabscesses were identified in the liver. Microscopically the lesions consisted of an infiltrate of macrophages and polymorphonuclear leukocytes with a central area of necrosis. Numerous blunt rod organisms, both within cells and extracellularly, were seen on Dieterle staining. A search for similar lesions in other organs revealed a single microabscess in the midbrain, where the morphology resembled a granuloma.
Legionella pneumophila, serogroup 6, grew after five days incubation of lung specimen on CYE media only (with and without antibiotics) yielding two to five colonies. On subculture, the isolate grew well on all media used. Direct fluorescent antibody examination showed the presence of Legionella serogroup 6 bacilli in the lung (> 50/ smear), liver (> 50/smear), spleen (< 10/smear), and brain (> 3/smear); no bacilli were seen in bone marrow tissue. The diagnosis of severe combined immunodeficiency was confirmed at autopsy; the thymus was small and lacked Hassall corpuscles. No lymph nodes were identified and lymphoid tissue was absent from the posterior pharynx, appendix, and gastrointestinal tract. The spleen was of normal weight but showed marked depletion of the periarteriolar sheath areas. DISCUSSION The primary disease in this patient appeared to be severe combined immunodeficiency disease, a condition in which occurrence of opportunistic and mixed infection is common. In our patient, at least three different infectious agents were documented: parainftuenza type 3 virus, which in itself can lead to fatal pneumonitisg; Pneumocystis
Figure. An area of consolidation with central necrosis (asterisk) and a heavy cellular infiltrate in lung biopsy sample. (HematoxyInset: Numerous Dieterle-positiveorganisms lin and eosin, • in the section of lung biopsy. (Dieterle stain, xS00.)
carinii, and Legionella pneumophila. Legionella pneumonitis has been recognized with increasing frequency in immunosuppressed patients, including those with lymphoma, leukemia, or various solid tumors, and following renal transplantation.2 A recent survey indicates increasing reports in infants and young children?,4 These reports, however, only describe seroreaetivity to the Legionella organisms. The diagnosis of Legionella pneumophila infection is not readily made, since routine bacterial cultures are negative and special media are needed to grow the organisms.7 Rapid diagnostic techniques include fluorescent antibody staining of sputum, tracheal aspirates, pleural fluid, and tissues obtained by needle aspiration or lung biopsy. The pathologic features of the pneumonitis have been well defined.8 Although the presence of abscess formation was not described in the initial reports, this complication is now being recognized? Pleural reactions
762
Brief clinical and laboratory observations
The Journal of Pediatrics May 1982
may include fibrinous pleuritis or pleural effusions, but
REFERENCES
e m p y e m a has not been reported. In several reports, the organisms have been identified in hilar lymph nodes, and in the sinusoids of the spleen and liver1~ no cellular reaction or inflammatory response to the organisms was documented. In our patient, the lesions in the liver and brain resembled those found in the lungs, indicating t h a t under certain circumstances the bacilli m a y become disseminated and cause multisystem disease. T h e precipitating factors in our patient likely include the profound immunodeficiency associated with S C I D , and potentially the co-presence of parainfluenza virus and Pneumocytis carinii. T h e present case illustrates severat i m p o r t a n t points. It documents Legionella pneumophila infection in an infant. The features not reported thus far include disseminated infection with m a r k e d tissue reaction in several organs, including liver and brain. I m m u n o c o m p r o m i s e d patients appear to be at the highest risk. Since m a n y of these patients develop mixed infections, Legionella pneumophila should be included in the differential diagnosis, with appropriate studies being carried out when confronted with progressive respiratory failure of unknown etiology.
1. Tsai TF, and Fraser SW: The diagnosis of Legionnaires' disease, Ann Intern Med 89:413, 1979. 2. Saravolatz GD, Bureh KH, Fisher E, et al: The compromized host and Legionnaires' disease, Ann Intern Med 90:533, 1979. 3. Ryan ME, Feldman S, and Pruitt B: Legionnaires' disease in a child with cancer, Pediatrics 64:951, 1979. 4. Simpson RM, Cogswell J J, Mitchell ER, et al: Legionnaires' disease in an infant, Lancet 2:740, 1980. 5. Chandler FW, Hicklin MD, and Blackmon JA: Demonstration of Legionnaires' disease in tissue, N Engl J Med 297:1218, 1977. 6. Greaves PW: New methods for the isolation of Legionella pneumophila, J Clin Pathol 33:581, 1980. 7. Jones GL, and Herbert GA, editors: Legionnaires: The disease, the bacterium and methodology, Atlanta, 1979, Cen'ter for Disease Control. 8. Winn WC, and Myerowitz RL: The pathology of the Legionella pneumonias, Hum Pathol 12:401, 1981. 9. Jarvis WR, Middleton P J, and Gelfand EW: Fatal parainfluenza pneumonia in severe combined immunodeficiency disease, J PEDIATR 94:423, 1979. 10. White HJ, Felton WW, and Sun CN: Extrapulmonary histopathologic manifestations of Legionnaires' disease, Arch Pathol Lab Med 104:287, 1980.
Atypical neonatal respiratory syncytial virus infection Andrew Unger, M.D., Lionel Tapia, M.D., Linda L. Minnieh, M.S., and C. George Ray, M.D.,* Tucson, Ariz.
RESPIRATORY SYNCYTIAL VIRUS infection in young infants commonly presents as a pneumonitis and m a y be associated with apnea, lethargy, and poor feeding; presentation with fever and rash is rare. 1,2 Two examples of R S V infection in neonates are described in which fever with rash dominated the clinical presentation, but respiratory symptoms were absent. Both infants were born during a community-wide R S V outbreak. CASE REPORTS Patient l. This 9-day-old female breast-fed infant presented to a Tucson hospital in January, 1981, with a chief complaint of fever. The patient was a term product of an uncomplicated pregnancy, labor, and delivery; Apgar scores were 8 at one minute and 9 at five minutes. Thirty-six hours prior to admission her appetite diminished. Rectal temperature was recorded as 38.7~ 10 hours prior to admission; two hours later the temperature was 39.4~ and
From the University of Arizona Health Sciences Center. *Reprint address:" Department of Pathology. University of Arizona College of Medicine. Tucson. AZ 85724.
an erythematous, truncal rash became evident. During this period of time, no contacts of the patient had been ill. On admission, temperature was 38.0~ (R), pulse 152/minute, respirations 38/minute, blood pressure 75 systolic/palpation. The infant was lethargic when undisturbed, but vigorous when examined. There was no evidence of respiratory infection, otitis media, or other organ system disease. A finely granular, scarlatiniform rash covered the entire body except the palms and soles. The CBC Abbreviations used RSV: respiratory syncytial virus R: rectal NP: nasopharyngeal CMV: cylomegalovirus FA: immunofluorescenee showed a WBC count of 12,000/mm 3 with normal differential count, hemoglobin and hematocrit, and platelet count of 200,000/ mm 3. The CSF had 10 WBCs/mm 3, all mononuclears, and normal glucose and protein concentrations. Chest radiograph was interpreted as normal. Blood, CSF, and urine:for bacterial cultures, and CSF, nasopharyngeal-throat swabs, rectal swab, and urine for viral cultures were obtained. Intravenous ampicillin and gentamiein therapy was begun.
0022-3476/82/050762+03500130/0 9 1982 The C. V. Mosby Co.
Brief clinical and laboratory observations
Disseminated
The Journal of Pediatrics May 1982
Legionella pneumophila infection
in an
infant with severe combined immunodeficiency Ernest Cutz, M.D., F.R.C.P.(C),* Paul S. Thorner, M.D., C. Pandu Rao, M.D., Sandu Toma, M.D., F.R.C.P.(C), Ronald Gold, M.D., F.R.C.P.(C), and Erwin W. Gelfand, M.D., C.M., F.R.C.P.(C), Toronto, Ont., Canada
LEGIONNAIRE DISEASE, unrecognized before 1976, has since received global attention, with over 1,000 cases reported. ~ A l t h o u g h most individuals who developed the disease were previously healthy, this infection frequently occurs in i m m u n o c o m p r o m i s e d patients? Most cases have been described in adults, but children can be affected. 3,4 W e report a case of fatal Legionnaire disease in an infant with severe combined immunodeficiency who developed disseminated infection involving the lungs, liver, and brain. CASE REPORT The patient was a 5-month-old first-born male infant of a non-consanguinous marriage whose growth and development had been normal until one month before admission, when he developed fever, cough, and coryza. Treatment with amoxicillin, followed by erythromycin, was without effect. On admission, he was noted to be well developed and well nourished. He appeared acutely ill with a temperature of 39.6~ and had mild respiratory distress. Chest radiograph revealed bilateral lower lobe infiltrates. Cloxacillin a n d ampicillin therapy was started. Cultures of pharyngeal secretions grew parainfluenza virus type 3, Staphylococcus ~aureus, and Haemophilus influenzae (type unknown). He became afebrile, and antibiotic therapy was discontinued after seven days. However, three days later, fever and respiratory distress recurred. Despite therapy with Cefamandole, a right-sided effusion developed which required chest tube drainage. Cultures and Gram stains were negative, Cefamandole therapy was discontinued, and treatment with ampicillin and chloramphenicol was begun. The possibility of an underlying immunodeficiency was raised. The family history was negative. No tonsils or lymph nodes were evident on physical examination, and no thymus shadow was visualized on the chest radiograph. Additional studies revealed a peripheral lymphopenia, and only 3% of peripheral blood mononuclear cells formed rosettes with sheep erythrocytes. Peripheral blood lymphocytes failed to proliferate in response to phytohemagglutinin or concanavalin A, and serum levels of all immunoglobulin classes (other than lgM) were decreased (IgG 50 mg/dl,
From the Departments of Pathology, Immunology, Infectious DBeases and Paediatrics, The Hospital for Sick Children, Toronto and The University of Toronto, and Division of Bacteriology, Public Health Laboratory, Ontario Ministry of Health. *Reprint address." Department of Pathology, The Hospital for Sick Children, 555 University Ave., Toronto. Ont., Canada M5G IX8.
lgA < 5 mg/dl, IgM 37 mg/dl, IgE < 10 ng/ml). Red blood cell adenosine deaminase and nucleoside phosphorylase activities were normal. The infant's condition further deteriorated, requiring assisted ventilation and oxygen. A lung biopsy was performed and revealed a heavy infestation with Pneumoeystis carinii organisms and growth of parainfluenza virus type 3, for which he was given trimethoprim-sulfamethoxazole. After 72 hours there was no improvement and treatment with pentamidine isothionate was begun. Subsequent studies of the lung biopsy revealed numerous Dieterle-positive blunt rods. Despite the addition of erythromycin, the infant's pulmonary condition progressively deteriorated, and he died one week after the lung biopsy and four weeks following admission. Abbreviations used CDC: Centers for Disease Control SCID: severe combined immunodeficiency disease METHODS Tissues from the lung biopsy as well as lung and other tissues obtained at autopsy were processed for routine histology including Dieterle stain 5 and electron microscopy. For the growth of Legionella, lung tissue specimens were inoculated undiluted and as serial dilution inoeula on four plate media (F-G, CYE, C Y E with antibiotics, and Greaves) and then incubated at 36~ in 3% CO2. 6,7 Direct fluorescent antibody examination of lung, liver, spleen, brain, a n d bone m a r r o w tissues was carried out according to the instructions of the Centers for Disease Control, A t l a n t a , Ga, 7 using reagents received from the C D C or prepared in our laboratory for Legionella pneumophila serogroups 1 to 6, L. boxemanii, L. micdadei, L. dumoffii, and L. gormanii. RESULTS The sections of lung biopsy showed a diffuse interstitial process with intra-alveolar exudate composed of amorphous debris and a mixture of macrophages and polymorphonuelear leukocytes. A well-circumscribed area of coagulative necrosis within the lung p a r e n c h y m a was present, showing dense infiltrate of granulocytes and m a c r o p h a g e s (Figure). The stains for microorganisms revealed large numbers of Pneumocystis carinii organisms within the
0022-3476/82/050760+03500.30/0 9 1982 The C. V. Mosby Co.
Volume 1O0 Number 5
Brief clinical and laboratory observations
76 1
alve01i, and Dieterle stain showed numerous blunt rodshaped bacilli, with features of Legionella pneumophila (Figure, inset). These organisms were most numerous in the area of necrosis, but extended to adjacent tissue. Results of Gram" stain and Ziehl-Neelsen stain were negative. By electron microscopy, bacterial organisms with triple layer cell membranes and cytoplasmic empty vacuoles were identified within the cytoplasm of macrophages or lying free in the alveolar spaces. The ultrastructural features of these organisms were similar to those previously described in cases of Legionnaire disease? At autopsy, the lungs were diffusely consolidated and contained numerous abscess cavities, involving all lobes. One abscess cavity had penetrated through the pleural space, resulting in an empyema. The microscopic changes were similar to those seen in the lung biopsy. Although only occasional Pneumocystis carinii organisms were seen, numerous Dieterle-positive bacilli were present. A single large abscess and numerous microabscesses were identified in the liver. Microscopically the lesions consisted of an infiltrate of macrophages and polymorphonuclear leukocytes with a central area of necrosis. Numerous blunt rod organisms, both within cells and extracellularly, were seen on Dieterle staining. A search for similar lesions in other organs revealed a single microabscess in the midbrain, where the morphology resembled a granuloma.
Legionella pneumophila, serogroup 6, grew after five days incubation of lung specimen on CYE media only (with and without antibiotics) yielding two to five colonies. On subculture, the isolate grew well on all media used. Direct fluorescent antibody examination showed the presence of Legionella serogroup 6 bacilli in the lung (> 50/ smear), liver (> 50/smear), spleen (< 10/smear), and brain (> 3/smear); no bacilli were seen in bone marrow tissue. The diagnosis of severe combined immunodeficiency was confirmed at autopsy; the thymus was small and lacked Hassall corpuscles. No lymph nodes were identified and lymphoid tissue was absent from the posterior pharynx, appendix, and gastrointestinal tract. The spleen was of normal weight but showed marked depletion of the periarteriolar sheath areas. DISCUSSION The primary disease in this patient appeared to be severe combined immunodeficiency disease, a condition in which occurrence of opportunistic and mixed infection is common. In our patient, at least three different infectious agents were documented: parainftuenza type 3 virus, which in itself can lead to fatal pneumonitisg; Pneumocystis
Figure. An area of consolidation with central necrosis (asterisk) and a heavy cellular infiltrate in lung biopsy sample. (HematoxyInset: Numerous Dieterle-positiveorganisms lin and eosin, • in the section of lung biopsy. (Dieterle stain, xS00.)
carinii, and Legionella pneumophila. Legionella pneumonitis has been recognized with increasing frequency in immunosuppressed patients, including those with lymphoma, leukemia, or various solid tumors, and following renal transplantation.2 A recent survey indicates increasing reports in infants and young children?,4 These reports, however, only describe seroreaetivity to the Legionella organisms. The diagnosis of Legionella pneumophila infection is not readily made, since routine bacterial cultures are negative and special media are needed to grow the organisms.7 Rapid diagnostic techniques include fluorescent antibody staining of sputum, tracheal aspirates, pleural fluid, and tissues obtained by needle aspiration or lung biopsy. The pathologic features of the pneumonitis have been well defined.8 Although the presence of abscess formation was not described in the initial reports, this complication is now being recognized? Pleural reactions
762
Brief clinical and laboratory observations
The Journal of Pediatrics May 1982
may include fibrinous pleuritis or pleural effusions, but
REFERENCES
e m p y e m a has not been reported. In several reports, the organisms have been identified in hilar lymph nodes, and in the sinusoids of the spleen and liver1~ no cellular reaction or inflammatory response to the organisms was documented. In our patient, the lesions in the liver and brain resembled those found in the lungs, indicating t h a t under certain circumstances the bacilli m a y become disseminated and cause multisystem disease. T h e precipitating factors in our patient likely include the profound immunodeficiency associated with S C I D , and potentially the co-presence of parainfluenza virus and Pneumocytis carinii. T h e present case illustrates severat i m p o r t a n t points. It documents Legionella pneumophila infection in an infant. The features not reported thus far include disseminated infection with m a r k e d tissue reaction in several organs, including liver and brain. I m m u n o c o m p r o m i s e d patients appear to be at the highest risk. Since m a n y of these patients develop mixed infections, Legionella pneumophila should be included in the differential diagnosis, with appropriate studies being carried out when confronted with progressive respiratory failure of unknown etiology.
1. Tsai TF, and Fraser SW: The diagnosis of Legionnaires' disease, Ann Intern Med 89:413, 1979. 2. Saravolatz GD, Bureh KH, Fisher E, et al: The compromized host and Legionnaires' disease, Ann Intern Med 90:533, 1979. 3. Ryan ME, Feldman S, and Pruitt B: Legionnaires' disease in a child with cancer, Pediatrics 64:951, 1979. 4. Simpson RM, Cogswell J J, Mitchell ER, et al: Legionnaires' disease in an infant, Lancet 2:740, 1980. 5. Chandler FW, Hicklin MD, and Blackmon JA: Demonstration of Legionnaires' disease in tissue, N Engl J Med 297:1218, 1977. 6. Greaves PW: New methods for the isolation of Legionella pneumophila, J Clin Pathol 33:581, 1980. 7. Jones GL, and Herbert GA, editors: Legionnaires: The disease, the bacterium and methodology, Atlanta, 1979, Cen'ter for Disease Control. 8. Winn WC, and Myerowitz RL: The pathology of the Legionella pneumonias, Hum Pathol 12:401, 1981. 9. Jarvis WR, Middleton P J, and Gelfand EW: Fatal parainfluenza pneumonia in severe combined immunodeficiency disease, J PEDIATR 94:423, 1979. 10. White HJ, Felton WW, and Sun CN: Extrapulmonary histopathologic manifestations of Legionnaires' disease, Arch Pathol Lab Med 104:287, 1980.
Atypical neonatal respiratory syncytial virus infection Andrew Unger, M.D., Lionel Tapia, M.D., Linda L. Minnieh, M.S., and C. George Ray, M.D.,* Tucson, Ariz.
RESPIRATORY SYNCYTIAL VIRUS infection in young infants commonly presents as a pneumonitis and m a y be associated with apnea, lethargy, and poor feeding; presentation with fever and rash is rare. 1,2 Two examples of R S V infection in neonates are described in which fever with rash dominated the clinical presentation, but respiratory symptoms were absent. Both infants were born during a community-wide R S V outbreak. CASE REPORTS Patient l. This 9-day-old female breast-fed infant presented to a Tucson hospital in January, 1981, with a chief complaint of fever. The patient was a term product of an uncomplicated pregnancy, labor, and delivery; Apgar scores were 8 at one minute and 9 at five minutes. Thirty-six hours prior to admission her appetite diminished. Rectal temperature was recorded as 38.7~ 10 hours prior to admission; two hours later the temperature was 39.4~ and
From the University of Arizona Health Sciences Center. *Reprint address:" Department of Pathology. University of Arizona College of Medicine. Tucson. AZ 85724.
an erythematous, truncal rash became evident. During this period of time, no contacts of the patient had been ill. On admission, temperature was 38.0~ (R), pulse 152/minute, respirations 38/minute, blood pressure 75 systolic/palpation. The infant was lethargic when undisturbed, but vigorous when examined. There was no evidence of respiratory infection, otitis media, or other organ system disease. A finely granular, scarlatiniform rash covered the entire body except the palms and soles. The CBC Abbreviations used RSV: respiratory syncytial virus R: rectal NP: nasopharyngeal CMV: cylomegalovirus FA: immunofluorescenee showed a WBC count of 12,000/mm 3 with normal differential count, hemoglobin and hematocrit, and platelet count of 200,000/ mm 3. The CSF had 10 WBCs/mm 3, all mononuclears, and normal glucose and protein concentrations. Chest radiograph was interpreted as normal. Blood, CSF, and urine:for bacterial cultures, and CSF, nasopharyngeal-throat swabs, rectal swab, and urine for viral cultures were obtained. Intravenous ampicillin and gentamiein therapy was begun.
0022-3476/82/050762+03500130/0 9 1982 The C. V. Mosby Co.