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having observed no occurrence of pcp in our pediatric renal transplant unit for the last 20 years and only 1 case in all german pediatric renal transplant units during the last 10 years , we encountered 3 consecutive incidents of pcp during a 5-month period .
the first patient was a 13-year - old girl , who had received her second renal graft because of cystic kidney disease ; pcp developed 4 months after transplantation .
the second patient , a 14-year - old boy , fell ill in the ninth posttransplant month ; he had bilateral vesicoureteral reflux as underlying renal disease .
the third patient was a 13-year - old girl , who had a transplant 2 years before contracting pcp because of cystic renal dysplasia occurring in the context of bardet - biedl syndrome .
all 3 children had been given cyclosporine a ( average dose 6.7 mg / kg / day ) , mycophenolate mofetil ( 1,060 mg / m / day ) , and methylprednisolone ( 3.2 mg / m / day ) , as maintenance immunosuppression .
all 3 children had been treated with methylprednisolone pulses for acute rejection episodes 2 , 3 , and 15 months before pcp was diagnosed .
clinically , all patients showed nonspecific symptoms , such as mild fever , dyspnea , and dry cough in the absence of auscultatoric anomalies .
laboratory tests showed an elevation of lactic dehydrogenase activity , c - reactive protein concentration in blood , and pronounced hypercalcemia ( 2.73.5
mmol / l ) , which was interpreted as an extrarenal production of 1.25-dihydroxyvitamin d3 by activated alveolar macrophages .
we found a significant reduction of s - adenosylmethionine concentration in plasma ( 6 nmol / l ; normal range 86128
nmol / l ) , which appears to be specific to pcp , unlike bacterial or other atypical pneumonias ( 8) .
we measured the blood count of cd4 and cd4/drt lymphocytes in the third patient to indicate the degree of immunosuppression , since antirejection therapy had been administered 15 months before the occurrence of pcp .
the number of cd4 t cells was normal at the time of pcp diagnosis ( 1,100 cells/l ; normal range 5051,151 cells/l ) , while the number of activated t - helper cells was slightly decreased ( 24 cd4/drcells/l ; normal range 2987/l ) .
only in the course of pcp did the numbers of cd4 and cd4/drt lymphocytes drop significantly ( 308 cd4 t cells/l and 8 cd4/drcells/l ) .
chest radiographs and thorax computed tomographic scans of the 3 children showed typical signs of interstitial pneumonia , e.g. , ground - glass opacity .
diagnosis of pcp was confirmed by the presence of cysts and vegetative forms in bronchoalveolar lavage fluid , proved by immunofluorescence staining , and through detection of pneumocystis dna by means of polymerase chain reaction ( pcr ) . in spite of intensive antimicrobial therapy , 2 of our 3 renal transplant patients died , at 10 and 28 days , respectively , after the onset of pcp . to determine if pcp could have been caused by patient - to - patient transmission , we closely examined the course of pcp in the infected children ( figure ) . patient 1 stayed on the same ward and same floor , but not in the same room ( distance between the rooms ' doors 10 m ) , as an infant with a yet - unclassified mitochondriopathy and pneumonia , which later was diagnosed as pcp .
patient 2 's hospital stay overlapped that of patient 1 ; the patients were on the same ward and same floor , in rooms with doors separated by 8 m , before the onset of pcp .
patient 3 spent her holiday with patient 2 in a summer camp organized by our pediatric nephrology division .
course of pneumocystis pneumonia ( pcp ) in 3 pediatric renal transplant recipients and 1 infant suffering from a yet - unclassified mitochondriopathy .
r , acute rejection episode ; rtx , renal transplantation ;  , contact ; # , , joint holiday ; > , start of pcp symptoms ;  , hospitalization ; x , diagnosis of pcp ; d , death . proceeding on the assumption that pcp in the 4 children resulted from patient - to - patient transmission , we investigated the genotypes of p. jirovecii with the multitarget single - strand conformation polymorphism ( sscp ) method .
this typing procedure is based on the amplification by pcr of 4 variable regions of the genome , followed by the detection of polymorphisms by means of sscp .
these 4 genomic regions are as follows : internal transcribed spacer number 1 of the nuclear rrna genes operon ( its1 ) , the intron of the nuclear 26s rrna gene ( 26s ) , the variable region of the mitochondrial 26s rrna gene ( mt26s ) , and the region surrounding intron number 6 of the -tubulin gene ( -tub ) .
a variable region amplified from a bronchoalveolar lavage fluid specimen can generate either 2 bands ( simple pattern ) or > 2 bands ( complex pattern ) .
while a simple pattern corresponds to a single allele of the genomic region , the presence of > 2 bands ( complex pattern ) indicates the existence of several alleles for a given region , most probably attributable to coinfection with multiple p. jirovecii types ( 10 ) .
our analysis showed that all 3 renal transplant patients had acquired the same 2 strains of pneumocystis , types 1 and 2 .
the infant with mitochondriopathy had been infected with > 2 strains , which possibly included types 1 and 2 ( table ) .
in contrast , 3 unrelated cases in patients ( patients 4 , 5 , and 6 ) from the same hospital harbored other p. jirovecii types .
the index of discrimination of the method was high ( 0.93 ) ( 10 ) , and the probability that patients 1 , 2 , and 3 were infected with the same strains by chance is extremely low .
we observed that the proportion of coinfecting strains within the clinical specimen was more important than the amount of template dna to detect or not detect a strain by means of the sscp typing method .
a coinfecting strain has to represent 11% of the population to be detected ( 11 ) .
coinfecting strains are missed when very low amounts of template dna are used , sometimes resulting in a negative pcr ; however , this was not the case for the specimens analyzed in the present study .
* bold letters signify the most abundant simple pattern with the complex one , as shown by silver staining .
the index patient had more strains than the other patients ( table ) but generated smaller amounts of pcr products with the 4 different pcr tests used , which suggests a lower amount of dna template .
although excluding a common source of p. jirovecii is difficult , the results strongly suggest that all 3 kidney transplant recipients had infected each other , and the infant could have acted as index patient .
this transmission may have occurred directly from 1 patient to another but also indirectly through immunocompetent carriers . indeed ,
carriage of p. jirovecii dna in the nose of immunocompetent relatives and healthcare workers in close contact with a pcp patient has been described ( 12 ) .
to our knowledge , this report is the first published on an outbreak of pcp in a pediatric renal transplant unit , probably attributable to patient - to - patient transmission .
however , we can not exclude that the cases described were infected by the same environmental source .
the presence of p. jirovecii in the air of hospital corridors has been described ( 13 ) , making an environmental reservoir in the hospital possible .
other potential sources of p. jirovecii could be asymptomatic p. jirovecii carriers , such as immunosuppressed patients ( 14,15 ) .
our findings at the molecular level suggest that p. jirovecii may be transmitted nosocomially and be acquired by immunosuppressed pediatric transplant recipients .
the incubation periods of p. jirovecii infection ( 17 , 15 , and 19 weeks for patients 1 , 2 , and 3 , respectively ) would be longer than those ( 212 weeks ) suggested by the previously described clusters of pcp ( 3,7,16 ) .
this finding may reflect a difference between adults and children . until the outbreak of pcp outlined in this article , pediatric renal transplant recipients in our hospital and other pediatric renal transplant units in germany were not given pcp prophylaxis routinely because of possible side effects , such as a rise of serum creatinine values , myelosuppression , and lyell syndrome .
we had not observed any case of pcp in our transplant recipients for the last 20 years without prophylaxis . in the light of the high death rate for pcp , prophylactic treatment with trimethoprim - sulfamethoxazole
is highly recommended for the first 6 posttransplant months and during the 4 months after antirejection therapy , in accordance with the guidelines for adults ( 1 ) . according to these guidelines , patient 3 ,
in whom pcp developed 15 months after steroid pulse therapy , would not have been protected by prophylaxis . whether prophylaxis should be given for a longer period of time
remains unknown , particularly since immunosuppression did not appear to be intensive in this patient at the onset of pcp , as indicated by the normal cd4 t - lymphocyte count in peripheral blood and the only slightly decreased number of activated t - helper cells .
we describe an outbreak of pneumocystis jirovecii pneumonia in a pediatric renal transplant unit , likely attributable to patient - to - patient transmission . 
 single - strand conformation polymorphism molecular typing showed that 3 affected patients had acquired the same 2 strains of pneumocystis , which suggests interhuman infection . 
 an infant with mitochondriopathy was the probable index patient .