Journal of Infection (I992) z4, I91-195
CASE REPORT
Paecilomyces lilacinus i n f e c t i o n i n a c h i l d w i t h c h r o n i c granulomatous
disease
C h r i s t o p h e r C. S i l l i m a n , *ll D a v i d W. Lawellin,T Jacob A. Lohr,~: B r a d l e y M. Rodgers~ a n d Leigh G. D o n o w i t z ~
Departments of * Pediatrics and t Microbiology, University of Colorado School of Medicine and t The Kempe Research Center, The Children's Hospital, Denver, Colorado, and Departments of ~;Pediatrics and ~ Surgery, University of Virginia Health Sciences Center, Charlottesville, VA, U.S.A. Accepted for publication I I September I99I Summary Chronic granulomatous disease (CGD) is a rare inherited disorder in which neutrophils do not appropriately generate cytotoxic superoxide anion, the respiratory burst, in response to invading bacteria or fungi as a part of normal host defence. We report the case of a child with CGD who had two abdominal wall abscesses caused by Paecilomyces lilacinus, an organism not previously known to cause infections in patients with CGD. The abdominal wall is a location that is rarely associated with Paecilomyces infections. Parenteral amphotericin B eradicated the infection in an immunocompromised child whereas this regimen has heretofore largely been unsuccessful in the treatment of this infection. Paecilomyces species and other fungi from immunocompromised hosts and thought to be laboratory contaminants, need to be carefully investigated for they may become pathogens in this clinical setting.
Introduction Chronic granulomatous disease is a rare disorder affecting approximately i in I ooo ooo persons. 1 T h e u n i f y i n g abnormality in this heterogeneous condition is the absence of the respiratory burst in neutrophils due to the failure of the electron transport chain to produce cytotoxic superoxide anion in these phagocytes. 2 T h e disease is characterised by recurrent, life-threatening infections with catalase-positive bacteria, and recalcitrant inflammation that leads to granuloma formationfl, ~ T h e largest subgroup of patients with C G D inherits this disease in an X-linked m a n n e r with a lesser proportion d e m o n s t r a t i n g an autosomal recessive m o d e of inheritance. 2'~ T h e phenotypic expression of this disorder is based u p o n its genetic heterogeneity, t'4 Paecilomyces species are c o m m o n saprophytic fungi f o u n d in soil, tap water, and in the case o f Paecilomyces lilacinus, as a c o n t a m i n a n t in sterile solutions.5-9 It is in the latter context that the majority of infections have occurred w h e n ocular lens implants were packaged in a buffer contaminated with the fungus 5, 6 T h e present case is the first reported infection with P. lilacinus in a II Address correspondence to : Dr C. C. Silliman, Department of Pediatrics, Box C-222, University of Colorado School of Medicine, 4200 East Ninth Ave, Denver, CO 80262, U.S.A. oI63-4453/92/o2ot9I +05 $03.00/0
© I992 The British Society for the Study of Infection
192
C.C. SILLIMAN ET AL.
child with CGD ; moreover the site of the infection, the abdominal wall, is unusual, and the eradication of this pathogen with amphotericin B is novel. Case r e p o r t
SM was a 4-year-old white male in whom CGD was diagnosed at 7 months of age by an abnormal Nitroblue Tetrazolium (NBT) test following presentation with cervical adenopathy and tonsillitis which was refractory to appropriate oral antimicrobial therapy. Genetic studies on this patient and his family confirmed X-linked inheritance. Neutrophil function studies revealed superoxide anion production of 2 nmol/min/2"5 x lO 6 cells (normal being 15 n m o l / min/2"5 × lO 6 cells) in response to opsonised zymosan. Following resolution of this adenopathy with parenteral antibiotics, the patient was maintained on oral antibacterial prophylaxis with 4 o m g trimethoprim and 2 o o m g sulfamethoxazole administered twice daily. In 1986, at 29 months of age, the patient was hospitalised because of a paronychial infection of the left thumb as a result of mild trauma. Aspergillus fumigatus was isolated from the infected site. Blood cultures were negative. Eradication of this organism was achieved with a 4-week course of amphotericin B. T h e patient presented at 42 months of age with fever, shortness of breath, and fatigue. An infiltrative pneumonia was confirmed by chest radiograph and A. fumigatus was grown from the bronchial washings. Blood cultures were negative. T h e patient received 4o doses of amphotericin B during a 7-week period together with three times weekly granulocyte transfusions for 3 weeks. This treatment resulted in clinical and radiographic resolution of the pneumonia. At 55 months of age the patient required surgical extraction of his left, second molar tooth which he had fractured while eating a piece of candy. He was given oral penicillin pre-operatively and oral dicloxaciltin peri-operatively. One week after the extraction two small furuncles appeared on the right upper quadrant of the abdomen. These lesions were 2 cm by 2 cm in area, smooth, well-circumscribed, closed, raised, non-tender and indurated with a purple hue. T h e patient was afebrile and asymptomatic. T h e furuncles were refractory to a 2-week course of oral dicloxacillin followed by 2 weeks of intravenous nafcillin. Fine needle aspiration of both lesions was then performed. Histopathology revealed granulomatous inflammation without microscopic evidence of fungal or bacterial infection. Bacterial cultures were negative. Fungal cultures were positive from broth only. This fungus was referred to the mycology laboratory for identification and was initially reported to be a Penicillium species (see Microbiology for further description). T h e patient's WBC count and ESR were normal as were anti-aspergillus IgG and IgE serologies. Four weeks after the initial culture, a second biopsy was performed on one of the furuncles and the fungus isolated was also reported to be a Penicillium species. T h e patient received a 2-month course of amphotericin B with initial daily doses of 0"5 m g / k g for 3 weeks followed by I'O m g / k g dose given 3 times weekly on an outpatient basis (a total of 25"5 m g / k g of amphotericin equal to 825 mg for the entire treatment course).
Paecilomyces infection in a child with CGD
I93
Another needle biopsy of the affected sites was culture negative at the completion of anti-fungal therapy. T h e patient remained in his usual state of health for 4 months but then he had a relapse or reinfection of pulmonary A. fumigatus which also involved the ribs and chest wall. None of the cultures or histopathological specimens was positive for Paecilomyces species. T h e patient died of the aspergillus infection some months later. Microbiology T h e initial culture of the biopsy materials was undertaken by the Pediatric Microbiology Laboratory. Subsequently all tissue specimens, which included the skin lesion biopsy, wound tissue biopsy, and abdominal wall aspirate, were sent to the General Microbiology Laboratory and cultured for routine bacteria, acid-fast bacilli, and fungi. Cultures for routine and acid-fast bacteria were negative, but moulds were recovered from specimens for routine bacteriology and fungus. From the latter, two to four colonies on two plates were recovered from the fluid aspirated from the abdominal wall abscess, one colony from one plate of the skin lesion biopsy, and two to four colonies on three plates from the wound tissue. In each case the fungus was subcultured on to Sabouraud-dextrose agar. Mature colonies (I to 3 weeks old, were woolly and lavender coloured with a tan reverse. Microscopic examination revealed hyaline septate hyphae with branched conidiophores from which flask-shaped phialides arose bearing chains of globose to subglobose conidia. T h e conidial structure resembled a brush (penicillus), and the organism was presumptively identified as a Penicillium species. Antifungal therapy was instituted based upon this diagnosis. T h e culture was referred to the Center for Disease Control for determination of the species and was identified as Paecilomyces lilacinus (Thorn) Samson, I974 (Penicillium lilacinus). 9 Discussion T h e clinical manifestations of C G D are a result of the inability of the affected phagocytes to kill phagocytised microbes. 2 Infections are common in the lymph nodes, liver, bone, and lungsfl '3 Staphylococcus aureus and catalase positive bacteria are the most common bacterial pathogens responsible for recurrent infections in these patients; however, less common microbes such as Aspergillus species and other fungi may be responsible for a significant number of life-threatening infections in children with C G D ) T h e present report is the first description of a patient with CGD infected by Paecilomyces lilacinus. This fungus has also been referred to as Penicillium lilacinum which may account for the original identification of the fungal pathogen as a Penicillium species. 8'9 T h e taxonomic distinction between Penicillium species and Paecilomyces species can be found elsewhered-9 More important is the fact that Penicillium species are susceptible to amphotericin B; while most Paecilomyces species are resistant) T M Therefore, proper identification of the fungal pathogen is clinically important. Paecilomyces species have a worldwide distribution as saprophytes in the soil and on decomposing vegetation. 1°,11 T h e y are frequent contaminants of clinical specimens and are rare pathogens. ~1 Most human infections occur in 10
JIN24
194
C.C. S I L L I M A N ET AL.
immunocompromised hosts. I1 Paecilomyces species have been reported to cause endocarditis following valve replacement, endophthalmitis when intraocular implants were contaminated with the fungus during storage, and infections of the lung, sinuses kidney, cornea, and skin. 5'~'I2-I7 Paecilomyces species, especially P. lilacinus and P. marquandii, are highly resistant to amphotericin B, whereas P. variotti is sensitive to amphotericin B and fluorocytosine, s,II,I~ Identification of the species of Paecilomyces is clinically important because of this difference of sensitivity patterns to antifungal agents. 11 In the present case, histopathological examination of the biopsy material from the site of infection did not demonstrate any evidence of fungal or bacterial infection. However, clinical and laboratory data support this report's conclusion that this was a case of infection rather than contamination or colonisation; i.e. isolation of Paecilomyces lilacinus from the original sterile specimen collected by fine needle aspiration from a closed lesion, repeated isolation of this unusual fungus in the absence of other pathogens, and progression of the infection while the patient was having antibacterial therapy but resolution when given anti-fungal treatment. Although the treatment regimen was based upon the original identification of the pathogen as a Penicillium species, amphotericin B proved effective in eradicating this Paecilomyces lilacinus infection. This response to amphotericin B is novel because Paecilomyces lilacinus is highly resistant in vitro to amphotericin B; however, the correlation between in vitro and in vivo fungal susceptibilities to antifungal agents has not been adequately established. Is Paecilomyces and Penicillium species are common laboratory contaminants. 7-9,II Reports of either species in an immunocompromised host should alert the physician and laboratory personnel to a possible fungal infection with either of these two organisms. Careful attention to identification of the fungal pathogen must follow so that proper antifungal treatment can be implemented. As in the case cited, all suspected pathogenic isolates should be sent to a reference laboratory for confirmation of their identification. In the case of unusual infections, rare fungi can be referred to the Center for Disease Control by the state reference laboratories for complete identification to the genus level. References i. Segal AW. Variation on the theme of chronic granulomatous disease. Lancet 1985; i: 1378-1382. 2. Gallin JI, Buescher ES, Seligmann BE, Nath J, Gaither T, Katz P. Recent advances in chronic granulomatous disease. Ann Intern Med 1983 ; 99: 657-674. 3. Rudolf A M (ed.) Pediatrics. I8th ed. Norwalk : Appleton Century Crofts, 1988 : lO65-1o66. 4. Smith RM, Curnutte JT. Molecular basis of chronic granulomatous disease. Blood 1991 ; 77(4) : 673-687 • 5. O'Day DM. Fungal endophthalmitis caused by Paecilomyces lilacinus after intraocular lens implantation. Am J Ophthal 1977; 83: 13o-131. 6. Miller GR, Rebell G, Magoon RC, Kulvin SM, Forster RK. Intravltreal antimycotic therapy and the cure of mycotic endophthalmitis caused by a Paecilomyces lilacinus contaminated pseudophakos. Ophthal Surg 1978 ; 9 : 54-62. 7- Barron GL. The genera of Hyphomycetes from soil. Baltimore: Williams and Wilkins, 1968. 8. Gordon MA. Paecilomyces lilacinus (Thom) Samson, from systemic infection in an armadillo (Dasypus novemcinctus). Sabouraudia. J Med Vet Mycol 1984; 22:lO9-116.
Paecilomyces infection in a child w i t h C G D
I95
9. Samson RA, Paecilomyces and some allied hyphomycetes. In Studies in mycology. No. 6. Baam, The Netherlands: Centraalbureau voor Schimmelcuhures, I974: 119. IO Rockhill RC, Klein MD. Paecilomyces lilacinus as the cause of chronic maxillary sinusitis. J Clin Microbiol I98O; 1I : 737-739. I I. Weitzmann I. Saprophytic molds as agents of cutaneous and subcutaneous infection in the immunocompromised host. Arch Dermatol I986; I22: I161-1168. 12. Takayasu S, Akagi M, Schimuzi Y. Cutaneous mycosis caused by Paecilomyces lilacinus. Arch Dermatol I977; 113: 1687-I69O. 13. Harris LF, Dan BM, Lefkowitz LB, Alford RH. Paecilomyces cellulitis in a renal transplant patient: successful treatment with intravenous miconazole. South Med J I979; 72: 897-898. 14. Sherwood JA, Dansky AS. Paecilomyces pyelonephritis complicating nephrolithiasis and a review of Paecilomyces infections. J Urol 1983 ; 13o : 526-528. I5. Gordon MA, Norton SW. Corneal transplant infection by Paecilomyces lilacinus. Sabouraudia 1985 ; 23 : 295-3Ol. I6. Jade KB, Lyons MF, G n a n n JW. Paecilomyces lilacinus cellulitis in an immunocompromised patient. Arch Dermatol 1986; I22: II69-II7O. 17. Fenech FF, Mallia CP. Pleural effusion caused by Penicillium lilacinum. Br J Dis Chest 1972 ; 66 : 284-290. 18. Stevens DA. Antifungal drug susceptibility testing. A critical review. Mycopathologica 1984; 87: 137-14o.
10-2
CASE REPORT
Paecilomyces lilacinus i n f e c t i o n i n a c h i l d w i t h c h r o n i c granulomatous
disease
C h r i s t o p h e r C. S i l l i m a n , *ll D a v i d W. Lawellin,T Jacob A. Lohr,~: B r a d l e y M. Rodgers~ a n d Leigh G. D o n o w i t z ~
Departments of * Pediatrics and t Microbiology, University of Colorado School of Medicine and t The Kempe Research Center, The Children's Hospital, Denver, Colorado, and Departments of ~;Pediatrics and ~ Surgery, University of Virginia Health Sciences Center, Charlottesville, VA, U.S.A. Accepted for publication I I September I99I Summary Chronic granulomatous disease (CGD) is a rare inherited disorder in which neutrophils do not appropriately generate cytotoxic superoxide anion, the respiratory burst, in response to invading bacteria or fungi as a part of normal host defence. We report the case of a child with CGD who had two abdominal wall abscesses caused by Paecilomyces lilacinus, an organism not previously known to cause infections in patients with CGD. The abdominal wall is a location that is rarely associated with Paecilomyces infections. Parenteral amphotericin B eradicated the infection in an immunocompromised child whereas this regimen has heretofore largely been unsuccessful in the treatment of this infection. Paecilomyces species and other fungi from immunocompromised hosts and thought to be laboratory contaminants, need to be carefully investigated for they may become pathogens in this clinical setting.
Introduction Chronic granulomatous disease is a rare disorder affecting approximately i in I ooo ooo persons. 1 T h e u n i f y i n g abnormality in this heterogeneous condition is the absence of the respiratory burst in neutrophils due to the failure of the electron transport chain to produce cytotoxic superoxide anion in these phagocytes. 2 T h e disease is characterised by recurrent, life-threatening infections with catalase-positive bacteria, and recalcitrant inflammation that leads to granuloma formationfl, ~ T h e largest subgroup of patients with C G D inherits this disease in an X-linked m a n n e r with a lesser proportion d e m o n s t r a t i n g an autosomal recessive m o d e of inheritance. 2'~ T h e phenotypic expression of this disorder is based u p o n its genetic heterogeneity, t'4 Paecilomyces species are c o m m o n saprophytic fungi f o u n d in soil, tap water, and in the case o f Paecilomyces lilacinus, as a c o n t a m i n a n t in sterile solutions.5-9 It is in the latter context that the majority of infections have occurred w h e n ocular lens implants were packaged in a buffer contaminated with the fungus 5, 6 T h e present case is the first reported infection with P. lilacinus in a II Address correspondence to : Dr C. C. Silliman, Department of Pediatrics, Box C-222, University of Colorado School of Medicine, 4200 East Ninth Ave, Denver, CO 80262, U.S.A. oI63-4453/92/o2ot9I +05 $03.00/0
© I992 The British Society for the Study of Infection
192
C.C. SILLIMAN ET AL.
child with CGD ; moreover the site of the infection, the abdominal wall, is unusual, and the eradication of this pathogen with amphotericin B is novel. Case r e p o r t
SM was a 4-year-old white male in whom CGD was diagnosed at 7 months of age by an abnormal Nitroblue Tetrazolium (NBT) test following presentation with cervical adenopathy and tonsillitis which was refractory to appropriate oral antimicrobial therapy. Genetic studies on this patient and his family confirmed X-linked inheritance. Neutrophil function studies revealed superoxide anion production of 2 nmol/min/2"5 x lO 6 cells (normal being 15 n m o l / min/2"5 × lO 6 cells) in response to opsonised zymosan. Following resolution of this adenopathy with parenteral antibiotics, the patient was maintained on oral antibacterial prophylaxis with 4 o m g trimethoprim and 2 o o m g sulfamethoxazole administered twice daily. In 1986, at 29 months of age, the patient was hospitalised because of a paronychial infection of the left thumb as a result of mild trauma. Aspergillus fumigatus was isolated from the infected site. Blood cultures were negative. Eradication of this organism was achieved with a 4-week course of amphotericin B. T h e patient presented at 42 months of age with fever, shortness of breath, and fatigue. An infiltrative pneumonia was confirmed by chest radiograph and A. fumigatus was grown from the bronchial washings. Blood cultures were negative. T h e patient received 4o doses of amphotericin B during a 7-week period together with three times weekly granulocyte transfusions for 3 weeks. This treatment resulted in clinical and radiographic resolution of the pneumonia. At 55 months of age the patient required surgical extraction of his left, second molar tooth which he had fractured while eating a piece of candy. He was given oral penicillin pre-operatively and oral dicloxaciltin peri-operatively. One week after the extraction two small furuncles appeared on the right upper quadrant of the abdomen. These lesions were 2 cm by 2 cm in area, smooth, well-circumscribed, closed, raised, non-tender and indurated with a purple hue. T h e patient was afebrile and asymptomatic. T h e furuncles were refractory to a 2-week course of oral dicloxacillin followed by 2 weeks of intravenous nafcillin. Fine needle aspiration of both lesions was then performed. Histopathology revealed granulomatous inflammation without microscopic evidence of fungal or bacterial infection. Bacterial cultures were negative. Fungal cultures were positive from broth only. This fungus was referred to the mycology laboratory for identification and was initially reported to be a Penicillium species (see Microbiology for further description). T h e patient's WBC count and ESR were normal as were anti-aspergillus IgG and IgE serologies. Four weeks after the initial culture, a second biopsy was performed on one of the furuncles and the fungus isolated was also reported to be a Penicillium species. T h e patient received a 2-month course of amphotericin B with initial daily doses of 0"5 m g / k g for 3 weeks followed by I'O m g / k g dose given 3 times weekly on an outpatient basis (a total of 25"5 m g / k g of amphotericin equal to 825 mg for the entire treatment course).
Paecilomyces infection in a child with CGD
I93
Another needle biopsy of the affected sites was culture negative at the completion of anti-fungal therapy. T h e patient remained in his usual state of health for 4 months but then he had a relapse or reinfection of pulmonary A. fumigatus which also involved the ribs and chest wall. None of the cultures or histopathological specimens was positive for Paecilomyces species. T h e patient died of the aspergillus infection some months later. Microbiology T h e initial culture of the biopsy materials was undertaken by the Pediatric Microbiology Laboratory. Subsequently all tissue specimens, which included the skin lesion biopsy, wound tissue biopsy, and abdominal wall aspirate, were sent to the General Microbiology Laboratory and cultured for routine bacteria, acid-fast bacilli, and fungi. Cultures for routine and acid-fast bacteria were negative, but moulds were recovered from specimens for routine bacteriology and fungus. From the latter, two to four colonies on two plates were recovered from the fluid aspirated from the abdominal wall abscess, one colony from one plate of the skin lesion biopsy, and two to four colonies on three plates from the wound tissue. In each case the fungus was subcultured on to Sabouraud-dextrose agar. Mature colonies (I to 3 weeks old, were woolly and lavender coloured with a tan reverse. Microscopic examination revealed hyaline septate hyphae with branched conidiophores from which flask-shaped phialides arose bearing chains of globose to subglobose conidia. T h e conidial structure resembled a brush (penicillus), and the organism was presumptively identified as a Penicillium species. Antifungal therapy was instituted based upon this diagnosis. T h e culture was referred to the Center for Disease Control for determination of the species and was identified as Paecilomyces lilacinus (Thorn) Samson, I974 (Penicillium lilacinus). 9 Discussion T h e clinical manifestations of C G D are a result of the inability of the affected phagocytes to kill phagocytised microbes. 2 Infections are common in the lymph nodes, liver, bone, and lungsfl '3 Staphylococcus aureus and catalase positive bacteria are the most common bacterial pathogens responsible for recurrent infections in these patients; however, less common microbes such as Aspergillus species and other fungi may be responsible for a significant number of life-threatening infections in children with C G D ) T h e present report is the first description of a patient with CGD infected by Paecilomyces lilacinus. This fungus has also been referred to as Penicillium lilacinum which may account for the original identification of the fungal pathogen as a Penicillium species. 8'9 T h e taxonomic distinction between Penicillium species and Paecilomyces species can be found elsewhered-9 More important is the fact that Penicillium species are susceptible to amphotericin B; while most Paecilomyces species are resistant) T M Therefore, proper identification of the fungal pathogen is clinically important. Paecilomyces species have a worldwide distribution as saprophytes in the soil and on decomposing vegetation. 1°,11 T h e y are frequent contaminants of clinical specimens and are rare pathogens. ~1 Most human infections occur in 10
JIN24
194
C.C. S I L L I M A N ET AL.
immunocompromised hosts. I1 Paecilomyces species have been reported to cause endocarditis following valve replacement, endophthalmitis when intraocular implants were contaminated with the fungus during storage, and infections of the lung, sinuses kidney, cornea, and skin. 5'~'I2-I7 Paecilomyces species, especially P. lilacinus and P. marquandii, are highly resistant to amphotericin B, whereas P. variotti is sensitive to amphotericin B and fluorocytosine, s,II,I~ Identification of the species of Paecilomyces is clinically important because of this difference of sensitivity patterns to antifungal agents. 11 In the present case, histopathological examination of the biopsy material from the site of infection did not demonstrate any evidence of fungal or bacterial infection. However, clinical and laboratory data support this report's conclusion that this was a case of infection rather than contamination or colonisation; i.e. isolation of Paecilomyces lilacinus from the original sterile specimen collected by fine needle aspiration from a closed lesion, repeated isolation of this unusual fungus in the absence of other pathogens, and progression of the infection while the patient was having antibacterial therapy but resolution when given anti-fungal treatment. Although the treatment regimen was based upon the original identification of the pathogen as a Penicillium species, amphotericin B proved effective in eradicating this Paecilomyces lilacinus infection. This response to amphotericin B is novel because Paecilomyces lilacinus is highly resistant in vitro to amphotericin B; however, the correlation between in vitro and in vivo fungal susceptibilities to antifungal agents has not been adequately established. Is Paecilomyces and Penicillium species are common laboratory contaminants. 7-9,II Reports of either species in an immunocompromised host should alert the physician and laboratory personnel to a possible fungal infection with either of these two organisms. Careful attention to identification of the fungal pathogen must follow so that proper antifungal treatment can be implemented. As in the case cited, all suspected pathogenic isolates should be sent to a reference laboratory for confirmation of their identification. In the case of unusual infections, rare fungi can be referred to the Center for Disease Control by the state reference laboratories for complete identification to the genus level. References i. Segal AW. Variation on the theme of chronic granulomatous disease. Lancet 1985; i: 1378-1382. 2. Gallin JI, Buescher ES, Seligmann BE, Nath J, Gaither T, Katz P. Recent advances in chronic granulomatous disease. Ann Intern Med 1983 ; 99: 657-674. 3. Rudolf A M (ed.) Pediatrics. I8th ed. Norwalk : Appleton Century Crofts, 1988 : lO65-1o66. 4. Smith RM, Curnutte JT. Molecular basis of chronic granulomatous disease. Blood 1991 ; 77(4) : 673-687 • 5. O'Day DM. Fungal endophthalmitis caused by Paecilomyces lilacinus after intraocular lens implantation. Am J Ophthal 1977; 83: 13o-131. 6. Miller GR, Rebell G, Magoon RC, Kulvin SM, Forster RK. Intravltreal antimycotic therapy and the cure of mycotic endophthalmitis caused by a Paecilomyces lilacinus contaminated pseudophakos. Ophthal Surg 1978 ; 9 : 54-62. 7- Barron GL. The genera of Hyphomycetes from soil. Baltimore: Williams and Wilkins, 1968. 8. Gordon MA. Paecilomyces lilacinus (Thom) Samson, from systemic infection in an armadillo (Dasypus novemcinctus). Sabouraudia. J Med Vet Mycol 1984; 22:lO9-116.
Paecilomyces infection in a child w i t h C G D
I95
9. Samson RA, Paecilomyces and some allied hyphomycetes. In Studies in mycology. No. 6. Baam, The Netherlands: Centraalbureau voor Schimmelcuhures, I974: 119. IO Rockhill RC, Klein MD. Paecilomyces lilacinus as the cause of chronic maxillary sinusitis. J Clin Microbiol I98O; 1I : 737-739. I I. Weitzmann I. Saprophytic molds as agents of cutaneous and subcutaneous infection in the immunocompromised host. Arch Dermatol I986; I22: I161-1168. 12. Takayasu S, Akagi M, Schimuzi Y. Cutaneous mycosis caused by Paecilomyces lilacinus. Arch Dermatol I977; 113: 1687-I69O. 13. Harris LF, Dan BM, Lefkowitz LB, Alford RH. Paecilomyces cellulitis in a renal transplant patient: successful treatment with intravenous miconazole. South Med J I979; 72: 897-898. 14. Sherwood JA, Dansky AS. Paecilomyces pyelonephritis complicating nephrolithiasis and a review of Paecilomyces infections. J Urol 1983 ; 13o : 526-528. I5. Gordon MA, Norton SW. Corneal transplant infection by Paecilomyces lilacinus. Sabouraudia 1985 ; 23 : 295-3Ol. I6. Jade KB, Lyons MF, G n a n n JW. Paecilomyces lilacinus cellulitis in an immunocompromised patient. Arch Dermatol 1986; I22: II69-II7O. 17. Fenech FF, Mallia CP. Pleural effusion caused by Penicillium lilacinum. Br J Dis Chest 1972 ; 66 : 284-290. 18. Stevens DA. Antifungal drug susceptibility testing. A critical review. Mycopathologica 1984; 87: 137-14o.
10-2
