the community hospital using presently available equipment. Obstructive and central types of apnea can be differentiated. This technique may also be applicable to the study of sleep patterns in other types of pulmonary disease (ie COPD) .
REFERENCES 1 Gastaut H, Tassinari CA, Duron B: Etude polygrapbique des manifestations episodiques (hypniques et respiratoires ), diurnes et nocturnes dy syndrome de Pickwick. Rev NeuroI112:568-579, 1965 2 Zwillich CW: Uncovering the mysteries of sleep. Arch Intern Moo 138: 195, 1978 3 SacJcner MA, Landa J, Forrest T, et al: Periodic sleep apnea: Chronic sleep deprivation related to intermittent upper airway obstruction and central nervous system disturbance. Chest 67 : 164-171, 1975 4 GuillemJnault C, Eldridge FL, Tilkian AG, et al: Sleep apnea due to upper airway obstruction. Arch Intern Med 137:2~, 1977 5 Tilkian AG, Guilleminault C, Schroeder JS, et al: Sleepinduced apnea; studies during wakefulness and sleep. Ann Intern Moo 85:714-719, 1976 6 Farmer WC, Glenn WW, Gee BL: Alveolar hypoventilation syndrome. Studies of ventilatory control in patients selected for diaphragm pacing. Am J Med 64:39-49, 1978 7 Glenn WW, Gee JB, Cole DR. et al: Combined central alveolar hypoventilation and upper airway obstruction; treatment by tracheostomy and diaphragm pacing. Am J Moo 64 :50-60, 1978 8 Zwillich CW, Sutton ro, Pierson D, et al: Decreased hypoxic ventilatory drive in the obesity-hyperventilation syndrome. Am J Med 59:343-348, 1975
Yellow Nail Syndrome with Reduced Glucose Level in Pleural Fluid* Vito A. Angelillo, M.D., F.C.C.P.;-- and Walter J. O'Donohue, lr.• MD., F.C.C.P.t
~
first description of the yellow nail syndrome ap-
.I. peared in 1964, when Samman and White! reported
the association of slowly growing yellow nails with primary lymphedema. In 1966, Emerson' described the three clinical findings that constitute the full syndrome, ie, pleural effusions. yellow nails, and lymphedema. We report a case with aD three manifestations of this entity. In addition, the patient had a defect in cellmediated immunity and subsequently developed an empyema. An interesting finding in this patient was a very low level of glucose in the pleural fluid, which did not increase after loading with either oral or intravenously administered glucose.
CASE REPoRT A 30-year-old white man with profound mental retardation secondary to postnatal meningoencephalitis due to Hem0philus was hospitalized on July 3, 1977, with a history of a low-grade fever of 38°C (IOO.4°F) and a dry cough for one day. A chest roentgenogram revealed a massive left pleural effusion (Fig 1). A seizure disorder that bad been present since infancy was controlled with administration of pheuytoin sodium (50 mg orally four times daily) and phenobarbital (60 mg orally twice daily). Examination at the time of admission revealed the patient to be in DO acute distress. The blood pressure was 118/72 mm Hg, the temperature was 37.7°C (99.9-F), the respiratory rate was 28/min, and the pulse rate was 104 beats per miDute. Several teeth were broken or missing, and the trachea was deviated to the right. The chest was dull to percussion, with decreased vocal and tactile fremitns and decreased breath sounds on the left. The fingernails were yellow, with distal transverse ridges. The feet were clubbed, and there was pitting edem& from below the bees to the feet. On admission, an automated analysis of multiple blood chemical constituents (SMA-6) showed the following levels: sodium in serum, 133 mEq/L; potassinm, 4.5 mEq/L; cbJoride, 93 mEq/L; blood urea nitrogen, 10 mg/100 ml; glucose, 100 mg/100 ml, albumin, 2.62 mg/100 ml, and total protein concentration, 3.5 mg/100 ml. A complete blood cell count revealed a white blood cell count (WBC) of 13,000/01 mm, with 77 percent segmented neutrophils, 10 percent band
The yellow naB syadrome, consisting of deformed yellow
naBs, lymphedema, and pleanl . . . . . . II • nre dls-
order of ukDowa etioIoIY. The udeilyIJII ............. in this disease is beUeved to be hypoplasia of the lymphatic: syste.... To date, only 47 CMeS of die ydow ... syndrome have been reported. We report _ ..witIoal case, with • defect in ceIl-mediated immunity and development of an empyema. 11le pldleat aIIo ..... .,., low pcoee leyel in the pleural tbdd (10 . ./100 mI 01' less), which did Dot increase after IoadioI with oral 01' iotrayeocnaW I'dmiolstemlllluc:a& The ........... 101' low leyels!of &bJcose in the pleural Ihdd are ~uL -From the Division of PuhnODlllY Disease. Department of Medicine. Creighton University School 01 Medicine, Omaha. - - Assistant Professor of Medicine. tProfessor of Medicine. Reprint requests: Dr. AngeUllo, St. JOIef'h HotpittIl. Omtrha 68131
CHEST, 75: 1, JANUARY, 1979
7·3 ·n
FICURE 1. Chest roe ntge nogram rlwc 31s massive left p leural
effusion.
YnLOW _
SYIIDROM£ 83
Table l---Cllleore LeHl in
P""'" n.u ..... "Be
Glucose Level in Pleural
Date
Fluid, mg/IOO ml Therapy with Glucose
WBC, cells/cu mm (percent Polymorphonuclear Leukocytes)
7/4m
8
None
717m
1
Gluoola (1 bottle 1 br before tap)
1,000 (100)
7/8m
9
Intravenous 5 percent dextrose in water; 50 ml of 50 percent dextzoee 90 min before tap
4,000 (100)
240 (93)
7/Um Chest tube (fluid purulent) 7/16m 10 (fluid
clear)
None
cells, 10 percent lymphocytes, 1 percent IIlODOC)'tes, and 2 percent eosinophils. The hemoglobin level was 12.5/100 ml, with a hematocrit reading of 37.4 percent. The results eE clotting studies were within normal limits. A total of three thoracocenteses were performed. The level of protein in the ftuid was above 4.5 mg/loo m1 on each occasion. Table 1 summarizes the glucose level in the pleural ftuid before and after administration of glucose. Gram stain and subsequent culture were negative for bacteria, acid-fast bacilli, and fungi. CutaDeous tests with intermediate-strengtb purified protein derivative of tuberculin (PPD), mumps antigen, Candida, and second-strength PPD were all negative. Sensitization with dinitrochJorobenzene was carried out, and recha1Ienge demonstrated no reaction. The serum immunoelectrophoretic pattern was normal. Tests for rheumatoid factor in the serum and pleural ftuid were negative, as was the ftuorescent antinuclear antibody assay. A pleural biopsy revealed chronic jnflammation. A chest tube was inserted on July 11, 1977. At that time the ftuid was purulent, and Gram stain revealed grampositive cocci. Therapy was begun with cephalothin sodium (I gm intravenously every four hours). Cultures disclosed anaerobic streptococci and fusobacteria, both sensitive to cephalothin. On July 16, 1977, after five days of drainage via the chest tube, the glucose level in the pleural ftuid was 10 mg/loo ml. An open thoracotomy with decortication was performed on July 22, 1977. Histologic studies showed both acute and chronic inflammatory changes. Special staining reactions for acid-fast bacilli and fungi were uegative. There was no evidence of malignant disease. DISCUSSION
The yellow nail syndrome, originally described by Samman and White1 in 1964, consisted of deformed yellow nails and lymphedema. The complete syndrome is a triad that includes pleural elusions. The abnormalities may appear individually or in combination, and the time between the development of the various manifestations may range from months to years. A recent
84 AlCEUu.o, O'DONOHUE
reportS has stated that the use of the term, yellow nail syndrome, is unfortunate, because primary lymphedema and pleural effusion frequently exist without changes in the nails. The combinations of abnormalities in the 48 reported cases, including ours,· were as follows: yellow nails and lymphedema, 18 patients; yellow nails, lymphedema, and pleural effusions, 12 patients; yenow nails alone, II patients; lymphedema and pleural effusions, 7 patients; and yellow nails and pleural effusions, no patients. We would agree that the combination of lymphedema and pleural effusions without yellow nails should not be included under this syndrome. The pathogenesis of the yellow nail syndrome is not well understood. It is postulateds that the underlying abnormality is hypoplasia of the lymphatic system. Why this syndrome does not appear in infancy or early life is also unknown. The findings in the fingernails have also been attributed to defective lymphatic vessels. The changes have included not only the characteristic yellowgreen hue but also smoothness with transverse ridging, curving from side to side, defective cuticles, onycholysis, and a characteristic hump. In addition, a number of other abnormalities have been associated with the syndrome. S These include chronic pulmonary infections, an increased incidence of acquired lymphoreticular malignant diseases, and immunologic deficiencies. This last finding was seen in our patient.
An interesting finding in this case was a very low level of glucose in the pleural fluid (less than 10 mg/1oo ml). The level was 9 mg/1oo ml initially and after two attempts at loading with glucose was 1 mg/100 ml and 8 mg/100 ml. Reductions of this magnitude in the glucose level of the pleural fluid are unexpected except in rheumatoid arthritis, tuberculosis, and rarely in malignant disease. In rheumatoid pleural effusions, the low glucose content has been attributed to a reduction in the transport of glucose from the blood to the pleural fluid. 5 , 6 The mechanism of transport may be inhibited by certain products of inflammation. Two other proposed mechanisms for low glucose levels in the pleural fluid include excessive utilization by inflammatory cells and active transfer of glucose out of the effusion. Studies have shown that it may take as long as four hours after intrapleural injection of glucose for levels to return to basehne.s Our patient underwent thoracocentesis between one and two hours after loading with glucose; therefore, transfer of glucose out of the effusion does not seem likely. Increased utilization of glucose in infected effusions has been demonstrated. In citro studies of leukocytic kinetics have shown the utilization of glucose to be 0.24 ± O.09ltmoles per 10 million cells per hour (±SE).7 Paradoxically, the uptake of glucose decreases as the concentration of leukocytes Inereases.! Thoracocentesis performed 60 to 90 minutes after loading with glucose would not allow enough time for utilization to lower the level of glucose in the pleural fluid to 1 mg/loo ml and 8 mg/100 mi. Although low concentrations of glucose may be found in empyemic fluid, in this case, all three thoracocenteses were performed at times when the effusion was nonpurulent and when Gram
CHEST, 75: 1, JANUARY, 1979
stains were negative. No parenchymal infiltrates were observed on chest roentgenograms; and, therefore, there is no evidence that this was a parapneumonic effusion. Reduced concentrations of glucose in the pleural fluid have been reported to occur occasiona1Iy with parapneumonic effusions.' It is possible that the large volume of fluid present caused enough pulmonary collapse to decrease pulmonary circulation, such that diffusion of glucose into the pleural Huid was impaired;10 however, it is most likely that a true defect in the transport of glucose was present, since the glucose level in the pleural fluid was 10 mgll00 mI on July 16, 1977, five days after insertion of the chest tube and partial reexpansion of the lung. The Huid at this time was clear in appearance, Was negative on Gram's stain, and had a low cell count as well. In general, the yellow nail syndrome is believed to be benign, and treatment is largely symptomatic. Pleurectomy or pleurodesis may be indicated for large uncontrollable effusions. 2 This syndrome may also be included in the list of diseases that are associated with a glucose level in the pleural fluid of less than 10 mg/l00 mI.
Endocarditis due to Strain of Card;olxJder;um 110m;,.;. Resistant to Erythromycin and Vancomycin· Richard B. Prioril Ph.D.; Vincent A.
Robert L. Perkins, M.D.
Sp~
M.D.; arad
Endocarditis caused by CardiobtJcterium Iaominis . . oIIIe"ed in a ~ patient with a proItIIetie cardiac valve who bad received proplayladle therapy with erytllromycin for deatal utnIctIoas. TIle orpaism ,.. resistant to erytbromydD ad vancomydD, with mba""
inhibitory CODCeDtndIons of 12.5p1!mI and 2514/11II, respectively, bnt was seDSitive to penidDiD G, tetracydiae, cepbalexiD, aDd cefador. 'Ibis C8Ie . . . . tllat currently recommended _tibiOtJe propIayiadle thenpy for endocarditis, especially ill ~rgic patIenU, may be inadequate for unnsnal padIoaeas such • C
hominis.
caused by Cardiobacterium hominls Endocarditis curs infrequently and first described 1964
0c-
fu:FERENCES
was
1 Samman PD, White WF: The yellow nail syndrome. Br J Dermatol 76: 154, 1964 2 Emerson PA: Yellow nails, lymphoedema, and pleural effusions. Thorax 21:247,1966 3 Beer DJ, Pereira W, Snider GL: Pleural effusion ass0ciated with primary lymphedema: A perspective on the yellow nail syndrome. Am Rev Respir Dis 117:595, 1978 4 Nakielna EM, Wilson J, Ballon HS: Yellow nail syndrome: Report of three cases. Can Med Assoc J 115:46, 1976 5 Lillington GA, Carr DT, Mayne JC: Rheumatoid pleurisy with effusion. Arch Intern Med 128:764, 1971 6 Dodson WH, Hollingsworth JW: Pleural effusion in rheumatoid arthritis impaired transport of glucose. N Eng} J Med275:1337, 1966 7 Martin SP, Gordon RM, Green R, et aI: The influence of glucose, fructose, and insulin on the metabolism of 1eukocytes of healthy and diabetic subjects. J Clin Invest 32:1171, 1953 8 Esmann V: Effect of cell concentration on the metabolism of normal and diabetic leukocytes in vitro. Metabolism 13:354, 1964 9 Potts DE, Levin DC, Sahn SA: Pleural fluid pH in parapneumonic effusions. Chest 70:328-331, 1976 10 Berger HW, Maher G: Decreased glucose concentrations in malignant pleural effusions in 13 patients. Am Rev Respir Dis 103:421, 1911
in
1
and subsequently by other investigators. i-I Since C hominis hasbeen isolated hom the respiratory tract in 68 percent of normal individuals,I dental sepsis was suggested to be the most likely origin of infection in one report.' In another report the precipitating factor in three cases of endocarditis due to C hominis (one with a prosthetic valve) was a dental procedure without antibiotic prophylactic therapy.s The present report describes a case of endocarditis caused by C hominls in a penicillin-allergic patient with a prosthetic valve who had received prophylactic therapy with erythromycin for dental extractions.
CASE REPoRT A 41-year-old woman who had been in good health noted the gradual onset of fatigue, night sweats, and loss of weight six months before admission. Three years previously, a StarrEdwards mitral valve prosthesis and a transvenous demand pacemaker were inserted because of atrial Butter with high-degree atriovenbicular block and rheumatic mitral stenosis. Two months before the onset of symptoms, extractions of carious teeth were perfonned on three occasions. Because of a history of an allergy to penicillin that was manifested by hives, prophylactic therapy with erythromycin (500 mg orally every six hours) had been given, beginning 24 hours prior to the procedures and afterwards for 48 hours. The patient denied fever, chills, pain in the chest, orthopnea, or other cardiovascular symptoms. Her medications included digoxin and warfarin (Cownadin). At physical examination the patient was thin, normotensive, and partially edentulous and had an oral temperature of 38°C (IOO.4°F). Examination of the heart revealed a loud metallic Brst heart sound and a grade 2/6 midsystolic mur-From the Division of Infectious Diseases, Department of Medicine, The Ohio State University College Of Medicine, Columbus. Re"rint requests: Dr. Prior, 413 West 12th Aoenueil Colum","43210
CHEST, 75: 1, JANUARY, 1979
ENDOCARDITIS RESISTANT TO ERYTHROMYCIN AID VANCOMYCIN 85
REFERENCES 1 Gastaut H, Tassinari CA, Duron B: Etude polygrapbique des manifestations episodiques (hypniques et respiratoires ), diurnes et nocturnes dy syndrome de Pickwick. Rev NeuroI112:568-579, 1965 2 Zwillich CW: Uncovering the mysteries of sleep. Arch Intern Moo 138: 195, 1978 3 SacJcner MA, Landa J, Forrest T, et al: Periodic sleep apnea: Chronic sleep deprivation related to intermittent upper airway obstruction and central nervous system disturbance. Chest 67 : 164-171, 1975 4 GuillemJnault C, Eldridge FL, Tilkian AG, et al: Sleep apnea due to upper airway obstruction. Arch Intern Med 137:2~, 1977 5 Tilkian AG, Guilleminault C, Schroeder JS, et al: Sleepinduced apnea; studies during wakefulness and sleep. Ann Intern Moo 85:714-719, 1976 6 Farmer WC, Glenn WW, Gee BL: Alveolar hypoventilation syndrome. Studies of ventilatory control in patients selected for diaphragm pacing. Am J Med 64:39-49, 1978 7 Glenn WW, Gee JB, Cole DR. et al: Combined central alveolar hypoventilation and upper airway obstruction; treatment by tracheostomy and diaphragm pacing. Am J Moo 64 :50-60, 1978 8 Zwillich CW, Sutton ro, Pierson D, et al: Decreased hypoxic ventilatory drive in the obesity-hyperventilation syndrome. Am J Med 59:343-348, 1975
Yellow Nail Syndrome with Reduced Glucose Level in Pleural Fluid* Vito A. Angelillo, M.D., F.C.C.P.;-- and Walter J. O'Donohue, lr.• MD., F.C.C.P.t
~
first description of the yellow nail syndrome ap-
.I. peared in 1964, when Samman and White! reported
the association of slowly growing yellow nails with primary lymphedema. In 1966, Emerson' described the three clinical findings that constitute the full syndrome, ie, pleural effusions. yellow nails, and lymphedema. We report a case with aD three manifestations of this entity. In addition, the patient had a defect in cellmediated immunity and subsequently developed an empyema. An interesting finding in this patient was a very low level of glucose in the pleural fluid, which did not increase after loading with either oral or intravenously administered glucose.
CASE REPoRT A 30-year-old white man with profound mental retardation secondary to postnatal meningoencephalitis due to Hem0philus was hospitalized on July 3, 1977, with a history of a low-grade fever of 38°C (IOO.4°F) and a dry cough for one day. A chest roentgenogram revealed a massive left pleural effusion (Fig 1). A seizure disorder that bad been present since infancy was controlled with administration of pheuytoin sodium (50 mg orally four times daily) and phenobarbital (60 mg orally twice daily). Examination at the time of admission revealed the patient to be in DO acute distress. The blood pressure was 118/72 mm Hg, the temperature was 37.7°C (99.9-F), the respiratory rate was 28/min, and the pulse rate was 104 beats per miDute. Several teeth were broken or missing, and the trachea was deviated to the right. The chest was dull to percussion, with decreased vocal and tactile fremitns and decreased breath sounds on the left. The fingernails were yellow, with distal transverse ridges. The feet were clubbed, and there was pitting edem& from below the bees to the feet. On admission, an automated analysis of multiple blood chemical constituents (SMA-6) showed the following levels: sodium in serum, 133 mEq/L; potassinm, 4.5 mEq/L; cbJoride, 93 mEq/L; blood urea nitrogen, 10 mg/100 ml; glucose, 100 mg/100 ml, albumin, 2.62 mg/100 ml, and total protein concentration, 3.5 mg/100 ml. A complete blood cell count revealed a white blood cell count (WBC) of 13,000/01 mm, with 77 percent segmented neutrophils, 10 percent band
The yellow naB syadrome, consisting of deformed yellow
naBs, lymphedema, and pleanl . . . . . . II • nre dls-
order of ukDowa etioIoIY. The udeilyIJII ............. in this disease is beUeved to be hypoplasia of the lymphatic: syste.... To date, only 47 CMeS of die ydow ... syndrome have been reported. We report _ ..witIoal case, with • defect in ceIl-mediated immunity and development of an empyema. 11le pldleat aIIo ..... .,., low pcoee leyel in the pleural tbdd (10 . ./100 mI 01' less), which did Dot increase after IoadioI with oral 01' iotrayeocnaW I'dmiolstemlllluc:a& The ........... 101' low leyels!of &bJcose in the pleural Ihdd are ~uL -From the Division of PuhnODlllY Disease. Department of Medicine. Creighton University School 01 Medicine, Omaha. - - Assistant Professor of Medicine. tProfessor of Medicine. Reprint requests: Dr. AngeUllo, St. JOIef'h HotpittIl. Omtrha 68131
CHEST, 75: 1, JANUARY, 1979
7·3 ·n
FICURE 1. Chest roe ntge nogram rlwc 31s massive left p leural
effusion.
YnLOW _
SYIIDROM£ 83
Table l---Cllleore LeHl in
P""'" n.u ..... "Be
Glucose Level in Pleural
Date
Fluid, mg/IOO ml Therapy with Glucose
WBC, cells/cu mm (percent Polymorphonuclear Leukocytes)
7/4m
8
None
717m
1
Gluoola (1 bottle 1 br before tap)
1,000 (100)
7/8m
9
Intravenous 5 percent dextrose in water; 50 ml of 50 percent dextzoee 90 min before tap
4,000 (100)
240 (93)
7/Um Chest tube (fluid purulent) 7/16m 10 (fluid
clear)
None
cells, 10 percent lymphocytes, 1 percent IIlODOC)'tes, and 2 percent eosinophils. The hemoglobin level was 12.5/100 ml, with a hematocrit reading of 37.4 percent. The results eE clotting studies were within normal limits. A total of three thoracocenteses were performed. The level of protein in the ftuid was above 4.5 mg/loo m1 on each occasion. Table 1 summarizes the glucose level in the pleural ftuid before and after administration of glucose. Gram stain and subsequent culture were negative for bacteria, acid-fast bacilli, and fungi. CutaDeous tests with intermediate-strengtb purified protein derivative of tuberculin (PPD), mumps antigen, Candida, and second-strength PPD were all negative. Sensitization with dinitrochJorobenzene was carried out, and recha1Ienge demonstrated no reaction. The serum immunoelectrophoretic pattern was normal. Tests for rheumatoid factor in the serum and pleural ftuid were negative, as was the ftuorescent antinuclear antibody assay. A pleural biopsy revealed chronic jnflammation. A chest tube was inserted on July 11, 1977. At that time the ftuid was purulent, and Gram stain revealed grampositive cocci. Therapy was begun with cephalothin sodium (I gm intravenously every four hours). Cultures disclosed anaerobic streptococci and fusobacteria, both sensitive to cephalothin. On July 16, 1977, after five days of drainage via the chest tube, the glucose level in the pleural ftuid was 10 mg/loo ml. An open thoracotomy with decortication was performed on July 22, 1977. Histologic studies showed both acute and chronic inflammatory changes. Special staining reactions for acid-fast bacilli and fungi were uegative. There was no evidence of malignant disease. DISCUSSION
The yellow nail syndrome, originally described by Samman and White1 in 1964, consisted of deformed yellow nails and lymphedema. The complete syndrome is a triad that includes pleural elusions. The abnormalities may appear individually or in combination, and the time between the development of the various manifestations may range from months to years. A recent
84 AlCEUu.o, O'DONOHUE
reportS has stated that the use of the term, yellow nail syndrome, is unfortunate, because primary lymphedema and pleural effusion frequently exist without changes in the nails. The combinations of abnormalities in the 48 reported cases, including ours,· were as follows: yellow nails and lymphedema, 18 patients; yellow nails, lymphedema, and pleural effusions, 12 patients; yenow nails alone, II patients; lymphedema and pleural effusions, 7 patients; and yellow nails and pleural effusions, no patients. We would agree that the combination of lymphedema and pleural effusions without yellow nails should not be included under this syndrome. The pathogenesis of the yellow nail syndrome is not well understood. It is postulateds that the underlying abnormality is hypoplasia of the lymphatic system. Why this syndrome does not appear in infancy or early life is also unknown. The findings in the fingernails have also been attributed to defective lymphatic vessels. The changes have included not only the characteristic yellowgreen hue but also smoothness with transverse ridging, curving from side to side, defective cuticles, onycholysis, and a characteristic hump. In addition, a number of other abnormalities have been associated with the syndrome. S These include chronic pulmonary infections, an increased incidence of acquired lymphoreticular malignant diseases, and immunologic deficiencies. This last finding was seen in our patient.
An interesting finding in this case was a very low level of glucose in the pleural fluid (less than 10 mg/1oo ml). The level was 9 mg/1oo ml initially and after two attempts at loading with glucose was 1 mg/100 ml and 8 mg/100 ml. Reductions of this magnitude in the glucose level of the pleural fluid are unexpected except in rheumatoid arthritis, tuberculosis, and rarely in malignant disease. In rheumatoid pleural effusions, the low glucose content has been attributed to a reduction in the transport of glucose from the blood to the pleural fluid. 5 , 6 The mechanism of transport may be inhibited by certain products of inflammation. Two other proposed mechanisms for low glucose levels in the pleural fluid include excessive utilization by inflammatory cells and active transfer of glucose out of the effusion. Studies have shown that it may take as long as four hours after intrapleural injection of glucose for levels to return to basehne.s Our patient underwent thoracocentesis between one and two hours after loading with glucose; therefore, transfer of glucose out of the effusion does not seem likely. Increased utilization of glucose in infected effusions has been demonstrated. In citro studies of leukocytic kinetics have shown the utilization of glucose to be 0.24 ± O.09ltmoles per 10 million cells per hour (±SE).7 Paradoxically, the uptake of glucose decreases as the concentration of leukocytes Inereases.! Thoracocentesis performed 60 to 90 minutes after loading with glucose would not allow enough time for utilization to lower the level of glucose in the pleural fluid to 1 mg/loo ml and 8 mg/100 mi. Although low concentrations of glucose may be found in empyemic fluid, in this case, all three thoracocenteses were performed at times when the effusion was nonpurulent and when Gram
CHEST, 75: 1, JANUARY, 1979
stains were negative. No parenchymal infiltrates were observed on chest roentgenograms; and, therefore, there is no evidence that this was a parapneumonic effusion. Reduced concentrations of glucose in the pleural fluid have been reported to occur occasiona1Iy with parapneumonic effusions.' It is possible that the large volume of fluid present caused enough pulmonary collapse to decrease pulmonary circulation, such that diffusion of glucose into the pleural Huid was impaired;10 however, it is most likely that a true defect in the transport of glucose was present, since the glucose level in the pleural fluid was 10 mgll00 mI on July 16, 1977, five days after insertion of the chest tube and partial reexpansion of the lung. The Huid at this time was clear in appearance, Was negative on Gram's stain, and had a low cell count as well. In general, the yellow nail syndrome is believed to be benign, and treatment is largely symptomatic. Pleurectomy or pleurodesis may be indicated for large uncontrollable effusions. 2 This syndrome may also be included in the list of diseases that are associated with a glucose level in the pleural fluid of less than 10 mg/l00 mI.
Endocarditis due to Strain of Card;olxJder;um 110m;,.;. Resistant to Erythromycin and Vancomycin· Richard B. Prioril Ph.D.; Vincent A.
Robert L. Perkins, M.D.
Sp~
M.D.; arad
Endocarditis caused by CardiobtJcterium Iaominis . . oIIIe"ed in a ~ patient with a proItIIetie cardiac valve who bad received proplayladle therapy with erytllromycin for deatal utnIctIoas. TIle orpaism ,.. resistant to erytbromydD ad vancomydD, with mba""
inhibitory CODCeDtndIons of 12.5p1!mI and 2514/11II, respectively, bnt was seDSitive to penidDiD G, tetracydiae, cepbalexiD, aDd cefador. 'Ibis C8Ie . . . . tllat currently recommended _tibiOtJe propIayiadle thenpy for endocarditis, especially ill ~rgic patIenU, may be inadequate for unnsnal padIoaeas such • C
hominis.
caused by Cardiobacterium hominls Endocarditis curs infrequently and first described 1964
0c-
fu:FERENCES
was
1 Samman PD, White WF: The yellow nail syndrome. Br J Dermatol 76: 154, 1964 2 Emerson PA: Yellow nails, lymphoedema, and pleural effusions. Thorax 21:247,1966 3 Beer DJ, Pereira W, Snider GL: Pleural effusion ass0ciated with primary lymphedema: A perspective on the yellow nail syndrome. Am Rev Respir Dis 117:595, 1978 4 Nakielna EM, Wilson J, Ballon HS: Yellow nail syndrome: Report of three cases. Can Med Assoc J 115:46, 1976 5 Lillington GA, Carr DT, Mayne JC: Rheumatoid pleurisy with effusion. Arch Intern Med 128:764, 1971 6 Dodson WH, Hollingsworth JW: Pleural effusion in rheumatoid arthritis impaired transport of glucose. N Eng} J Med275:1337, 1966 7 Martin SP, Gordon RM, Green R, et aI: The influence of glucose, fructose, and insulin on the metabolism of 1eukocytes of healthy and diabetic subjects. J Clin Invest 32:1171, 1953 8 Esmann V: Effect of cell concentration on the metabolism of normal and diabetic leukocytes in vitro. Metabolism 13:354, 1964 9 Potts DE, Levin DC, Sahn SA: Pleural fluid pH in parapneumonic effusions. Chest 70:328-331, 1976 10 Berger HW, Maher G: Decreased glucose concentrations in malignant pleural effusions in 13 patients. Am Rev Respir Dis 103:421, 1911
in
1
and subsequently by other investigators. i-I Since C hominis hasbeen isolated hom the respiratory tract in 68 percent of normal individuals,I dental sepsis was suggested to be the most likely origin of infection in one report.' In another report the precipitating factor in three cases of endocarditis due to C hominis (one with a prosthetic valve) was a dental procedure without antibiotic prophylactic therapy.s The present report describes a case of endocarditis caused by C hominls in a penicillin-allergic patient with a prosthetic valve who had received prophylactic therapy with erythromycin for dental extractions.
CASE REPoRT A 41-year-old woman who had been in good health noted the gradual onset of fatigue, night sweats, and loss of weight six months before admission. Three years previously, a StarrEdwards mitral valve prosthesis and a transvenous demand pacemaker were inserted because of atrial Butter with high-degree atriovenbicular block and rheumatic mitral stenosis. Two months before the onset of symptoms, extractions of carious teeth were perfonned on three occasions. Because of a history of an allergy to penicillin that was manifested by hives, prophylactic therapy with erythromycin (500 mg orally every six hours) had been given, beginning 24 hours prior to the procedures and afterwards for 48 hours. The patient denied fever, chills, pain in the chest, orthopnea, or other cardiovascular symptoms. Her medications included digoxin and warfarin (Cownadin). At physical examination the patient was thin, normotensive, and partially edentulous and had an oral temperature of 38°C (IOO.4°F). Examination of the heart revealed a loud metallic Brst heart sound and a grade 2/6 midsystolic mur-From the Division of Infectious Diseases, Department of Medicine, The Ohio State University College Of Medicine, Columbus. Re"rint requests: Dr. Prior, 413 West 12th Aoenueil Colum","43210
CHEST, 75: 1, JANUARY, 1979
ENDOCARDITIS RESISTANT TO ERYTHROMYCIN AID VANCOMYCIN 85
