Infectious Etiologies of Rhabdomyolysis: Three Case Reports and Review

Author(s): Upinder Singh and W. Michael Scheld

Source: Clinical Infectious Diseases, Vol. 22, No. 4 (Apr., 1996), pp. 642-649
Published by: Oxford University Press
Stable URL: http://www.jstor.org/stable/4459345 .
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642

InfectiousEtiologies of Rhabdomyolysis:Three Case Reports and Review

Upinder Singh and W. Michael Scheld From the Departmentof Internal Medicine, Division of Infectious
Diseases, Universityof VirginiaHealth Sciences Center,
Charlottesville,Virginia

Rhabdomyolysiscan be precipitatedby trauma,ischemia,metabolicdefects,electrolyteabnormali-

ties, drugs,and a wide varietyof infectiousdiseases.At our institution,recentcases of rhabdomyolysis
induced by influenza prompted us to review the infectious etiologies of this entity. In addition, a
thorough literature search revealed numerous case reports but no general review on this subject.
This study describesrepresentativerecent cases from our institutionand details the wide variety of
infections that can cause muscle damage. The pathophysiologicalmechanisms, muscle histology,
and correlationwith renal dysfunctionare also discussed.

Rhabdomyolysisis a syndromecharacterizedby elevated imbalances(potassiumlevel, < 2.5 mEq/L; or phosphorus

serum concentrationsof creatinephosphokinase(CPK) and level, < 1.5 mEq/L),drugingestion,or otherknownprecipi-
myoglobinurialeadingto renaldysfunction.This entityshould tantsof rhabdomyolysiswere excludedfrom our analysis.
be clinicallydifferentiatedfrompyomyositisand myonecrosis We did a thoroughsearchof the literaturefrom 1966 via
in thatno focal purulentabscessesarepresentandno localized MEDLINEwith use of the termsrhabdomyolysis andmyoglo-
site of muscle injuryis evident.Patientswith rhabdomyolysis binuria.Referencesin primaryarticlesthat pertainedto our
oftenhave swollen,painfulmuscles,however,andradiological topic were also used in the analysis. Only English-language
studies such as CT and MRI may prove useful in excluding articleswerereviewedin detail;informationfromthesearticles
myonecrosisand abscess formation. was utilizedto createtables 1, 2, and3. Pertinentdemographics
Numerousprecipitatingfactorsof rhabdomyolysis havebeen (e.g., patientage, peak CPK level, and renal function)were
described; in 1982 Gabow et al. [1] reviewed 77 cases of extractedfromthe reportedcases, whereavailable.
rhabdomyolysis and found that alcohol ingestion (67% of
cases), compressioninjury (39%), and generalizedseizures
(24%) were the most common precipitatingetiologies. In 5% Case Reports
of the cases, influenza-likeillness (3%)and sepsis (2%)repre-
Case 1
sentedthe infectiousetiologiesnoted.Althoughthe association
between skeletal muscle damageand viral infectionsis well A 68-year-oldwomanpresentedto our centeron 4 Septem-
known, numerousother infectiouscauses of rhabdomyolysis ber 1988 becauseof respiratoryfailure.One week beforead-
have since been reported(most of them in the past decade). mission she had had anorexia,malaise, cough productiveof
Ourpurposewas to review the recentliteratureand compilea white sputum,and shortnessof breath.She had a historyof
comprehensivelist of the infectionsthathave been reportedto smoking(100 packsper year)but denieda historyof diabetes
cause rhabdomyolysis.The putative mechanismsof muscle mellitus,hypertension,coronaryarterydisease,or renalinsuf-
damageand associationwith renal failureare also discussed ficiency;she was not receivingany medications.
briefly. Hertemperature was 37.6?C,systolicbloodpressurewas 90
mm Hg, respiratory ratewas 44, andpulseratewas 130. Physi-
Materials and Methods cal examination revealeddecreasedbreathsoundson the right
and bilateralrales. Laboratorystudiesdisclosedthe following
A retrospectivechartreviewof inpatientstreatedat the Uni- significantdata: serum sodium, 136 mEq/L;potassium,5.7
versity of Virginia Health Sciences Center (Charlottesville) mEq/L;chloride, 110 mEq/L;bicarbonate,19 mEq/L;blood
since 1988 was conductedon the basis of dischargediagnosis ureanitrogen(BUN), 46 mg/dL;creatinine,5.6 mg/dL;WBCs,
codes. Patients with hypotension (systolic blood pressure, 9,200/uL; hematocrit,51.2%; platelets, 144,000/,4L;CPK,
< 90 mm Hg), severeacidosis(serumpH, < 7.15), electrolyte 6,538 U/L;lactatedehydrogenase(LDH), 1,705 U/L;aspartate
aminotransferase (AST), 280 U/L; alanine aminotransferase
44
(ALT), U/L; alkalinephosphatase(ALP),19 U/L;prothrom-
Received 7 August 1995; revised20 November1995. bin time, 13.3 seconds;and partialthromboplastintime, 44.6
Reprintsor correspondence:Dr. Upinder Singh, Departmentof Internal seconds.An arterialblood gas determination while the patient
Medicine,Division of InfectiousDiseases, MR 4 Building,Room 2115, 300 was breathing50% FIO2revealeda pH of 7.18, Pco2 of 47,
ParkPlace, Charlottesville,Virginia22908.
and Po2 of 60. The urine was positive for myoglobin,and a
ClinicalInfectiousDiseases 1996;22:642-9
? 1996by TheUniversityof Chicago.All rightsreserved. chestradiographshowedmultilobarinfiltrateson the rightwith
1058-4838/96/2204-0008$02.00 a possiblerighthilarmass.Gramstainingof a sputumspecimen
CID 1996;22 (April) Infectious Etiologies of Rhabdomyolysis 643

demonstratedmore than three polymorphonuclear cells and Case3

more thanthreegram-positivecocci.
A 74-year-oldmanwith a historyof metastaticprostatecan-
Thepatientwas intubated,andempiricaltherapywithbroad-
cer,inferiormyocardialinfarction,andchronicobstructivepul-
spectrumantibiotics(ticarcillin/clavulanic
acid, erythromycin,
monarydisease presentedto anotherinstitutionbecause of a
and clindamycin)was startedfor presumedsepsis secondary
3-day historyof shortnessof breath,cough, myalgias,and fe-
to post-obstructivepneumonia.She requiredtherapeuticsup- ver. His wife had recentlyhad a "flulike" illness.
portwithpressoragents,andher conditiondeteriorated rapidly At the time of admission,his CPKlevel was 1,365U/L, and
with the developmentof anuricrenalfailure,disseminatedin- his LDH level was 1,150 U/L;arterialblood gas determination
travascularcoagulation,abdominaldistensionwith ileus, and at this time revealeda pH of 7.25, Pco2 of 40, and Po2 of 92.
possiblemesentericischemia.In concordancewith the wishes Gramstainingof sputumdemonstratedmore than two gram-
of her family,furtheraggressivecarewas not pursued,andshe
positive cocci in clusters,and empiricaltherapywith intrave-
died the day afteradmission.
nous cefotaximeand erythromycinwas started.Upon transfer
Subsequently,sputumandbloodcultures(one of two bottles to ourcenter,physicalexaminationshowedvital signs of blood
on day 2) becamepositive for Streptococcuspneumoniaeand
pressureof 120/70 mm Hg, pulse rateof 110, and respiratory
Clostridiumperfringens,respectively. rate of 16 and bilateralrales. Laboratorystudies disclosed
the following significantdata: serum sodium, 145 mEq/L;
potassium,4.5 mEq/L;chloride,96 mEq/L;bicarbonate,32
Case2 mEq/L; BUN, 93 mg/dL; creatinine, 7.9 mg/dL; WBCs,
10,500/pL; hematocrit,32%; platelets, 204,000//1L; AST,
A 57-year-oldwoman with a medical history of insulin-
3,605 U/L; ALT, 2,246 U/L; ALP, 186 U/L; LDH, 10,885
dependentdiabetes mellitus and mild chronic renal insuffi- U/L;andCPK,3,324 U/L. The chestradiograph revealedbilat-
ciency presentedto our centerwith a chief complaintof short- eral lower-lobeinfiltrates.
ness of breath.Five daysbeforeadmissionshe hadhada cough,
He was admittedto the medical intensive care unit, and
shortnessof breath,fatigue, myalgias,nausea,and vomiting.
Hermedicationsincludedinsulin,acetaminophen,and furose- therapywithcefotaxime,erythromycin, andmetronidazolewas
started.Blood culturesbecamepositive for Pseudomonasspe-
mide.
cies, andnasopharyngeal culturesbecamepositivefor influenza
Physical examinationrevealed a temperatureof 36.7?C, virustype A H3N2. The patientsubsequentlyhadrenalfailure
bloodpressureof 133/99mmHg, pulserateof 104,andrespira-
requiringhemodialysis, disseminatedintravascularcoagula-
tory rateof 40. Tachypneawith paradoxicalabdominalmove- tion, andunstableventriculararrhythmias. In compliancewith
ment was noted with respiration,and she had bilateralrales.
the wishes of his family, no furtherinterventionalmeasures
Laboratorystudiesdisclosedthe followingsignificantdata:se- were taken,and he died. An autopsywas not performed.
rumsodium,142 mEq/L;potassium,6.7 mEq/L;chloride,114
mEq/L;bicarbonate,23 mEq/L;BUN, 60 mg/dL;creatinine,
4.7 mg/dL;glucose, 173 mg/dL;WBCs, 14,200/tL; hemato- Literature Review and Discussion
crit,25%;platelets,347,000/tL; lacticacid,0.9 mmol/L;AST, ViralInfections
46 U/L; ALT, 60 U/L; ALP, 169 U/L; LDH, 459 U/L; and
CPK, 203 U/L. The urine was positive for myoglobin,and a Table 1 [2-69] lists the spectrumof viral infectionsthat
chest radiographrevealedbilateralpulmonaryinfiltrates.The have been reportedto cause rhabdomyolysis.Influenzais the
initial arterialblood gas determinationwhile the patientwas most commonviral etiology followed by HIV infectionand
breathing4 L of oxygen was remarkablefor a pH of 7.20, enteroviralinfection.The presentingsymptomsin the patients
Pco2 of 47, and Po2 of 65. whose cases are reportedin table 1 includedmyalgias,weak-
The patientwas intubated,and empiricalantibiotictherapy ness, muscle tenderness,and edema.A review of viral causes
withcefuroximeanderythromycin was startedafterappropriate of rhabdomyolysisby Tanakaet al. [61] in 1989 revealeda
culturewas performed.A renal ultrasonogramand a cardiac similarpreponderanceof influenzavirus infections;42 cases
echocardiogramwere unremarkable. Nasopharyngealcultures of virus-inducedrhabdomyolysiswere documentedin the En-
becamepositivefor influenzavirustype A; all otherblood and glish-languageandJapanese-language literature,and influenza
sputumcultureswere negative.HerCPKlevel peakedat 1,263 accountedfor 14 (33%)of 42 of these reportedcases.
U/L, andthe LDH level peakedat 831 U/L. Herrenalfunction In our review of the literature,influenzaviruswas the etio-
did not improve,however,and she requiredhemodialysis.The logic agent in 25 (42%) of 59 cases associatedwith a viral
remainderof herhospitalcoursewas long andcomplicated.She infection. For each period (1966-1975, 1976-1983, 1984-
was dischargedin stableconditionandunderwenthemodialysis 1988, and 1989 to present)studiedin the MEDLINEsearch
threetimes a week. The etiology of the renaldysfunctionwas of the literature,influenzawas repeatedlyone of the most
thoughtto be multifactorial,includingdiabeticrenal insuffi- common infectious precipitantsof rhabdomyolysiswith the
ciency, prerenalazotemia,and rhabdomyolysis. exceptionof 1984-1988, duringwhich surprisinglyfew cases
644 SinghandScheld CID 1996;22(April)

Table 1. Viral causes of rhabdomyolysis.

No. of cases Rangeof CPK levels No. with ARF/total No. of deaths/total
Organism reported Age range (U/L) no. (%) no. (%)

Influenzavirus types A and B 25* 3-76 y 230-303,200 11/25 (44) 3/25 (12)
HIV 8 18-29 y 2,359-398,000 0/8 0/8
Coxsackievirus 8 11 mo to 67 y 8,500-600,900 4/8 (50) 2/8 (25)
Epstein-Barrvirus 5 6-23 y 4,500-482,000 1/5 (20) 0/5
Echovirus 4 17-30 y 19,600-890,000 1/4 (25) 0/4
Cytomegalovirus 2 21-27 y 4,800-74,850 1/2 (50) 0/2
Adenovirus 2 20-46 y 57,800-133,000 0/2 0/2
Herpessimplexvirus 1 20 y 126,600 1/1 (100) 0/1
Parainfluenzavirus 1 38 y 66,000 0/1 0/1
Varicella-zostervirus 3 15-22 y 84,000-1,977,600 1/3 (33) 0/3
Total 59 20/59 (34) 5/59 (8)

NOTE. ARF = acuterenalfailure;CPK = creatinephosphokinase.

* Threeseries with 10, 17, and 14 patients,respectively,were not includedbecauseof lack of clinical data.

werereported.Althoughthesetime categoriesarearbitrary, the secondaryto influenza.However,viralparticlesare occasion-

continuedpreponderance of influenzavirus infectionscausing ally difficultto differentiatefromglycogen by EM; therefore,
rhabdomyolysisis significant.From 1984 to 1988 a decrease thereis some doubtaboutthese observations.
in reportedcasesmayhavebeensecondaryto improvedpreven- Influenzavirus was subsequentlydemonstratedby hemag-
tive publichealthmeasures,suchas successfullarge-scalevac- glutinationandby directEM of culturedspecimensof the liver,
cinationsor increasingphysicianfamiliaritywith the associa- CSF, and muscle from a patientwith Reye's syndrome[25].
tion of influenza with rhabdomyolysis. Annual global In 1979 Gamboaet al. [15] definitivelydocumentedinfluenza
epidemics,physicianvigilance,andease of diagnosisprobably virus in a skeletalmuscle specimenfroma patientwith influ-
all contributeto the reportedpredominanceof this agent. enza virusinfection.Lightmicroscopyrevealednecroticmus-
Although the precise pathophysiologyunderlying virus- cle fibersin largeclusterssurrounded by morphologicallynor-
induced myoglobinuriais unknown, two mechanismshave mal appearingmuscle.InfluenzavirustypeB was isolatedfrom
been postulated:direct viral invasion and toxin generation. homogenizedmuscle by cell culturetechniques.Cytopathic
Some authorshave suggestedthatdirectviralinvasionof mus- changesconsistingof granularity andvacuolizationof the cyto-
cle fiberscausesmusclenecrosis.In 1977 Frankovaet al. [14] plasm,retraction,androundingof cell processeswith swelling
were able to demonstrateinfluenzavirustype A by tissue cul- of the cell body occurredin the infectedcell lines. Viralpres-
tureof specimensof the trachea,lung, liver, spleen,pancreas, ence was confirmedby immunofluorescence and EM. Subse-
and brainsfrom patientswho died of influenzavirus type A quently,Kessler et al. [31] also culturedinfluenzavirus type
infections,but no isolates were obtainedfrom muscle. How- A froma musclespecimenfroma 72-year-oldmanwith virus-
ever,in 1978Armstronget al. [2] did showthathumanskeletal inducedrhabdomyolysis.Recently,Poels et al. [57] reported
musclecells in tissuecultureweresusceptibleto influenzavirus isolationof echovirus6 in a tissuecultureof a musclespecimen
infection,and, in fact, infectiousprogenywere produced. from a patientwith simultaneousinfectionwith Epstein-Barr
Muscle biopsies of patientswith rhabdomyolysisthat have virus and echovirus.
showna lymphocyticinfiltrate[13, 21, 42, 52, 63] supportthe This evidence strongly suggests that direct viral invasion
hypothesisof directviral invasion.Morecompellingevidence may have a causativerole in precipitatingrhabdomyolysis.
is presentin somecases:musclebiopsiesof affectedindividuals Variousreportsdocumentingnormalresultsof musclebiopsies
have revealedviral inclusions,and, recently,DNA fromvari- or hyalinedegenerationandmyonecrosisbut no viralparticles
cella-zostervirus was identifiedby PCR analysis of muscle by immunofluorescence [56] and EM [66] are used to refute
specimens from patientswith rhabdomyolysis[69]. In 1977 this theory.Biopsiesof clinicallyaffectedmusculaturethatare
Fukuyamaet al. [50] foundpicomavirus-likecrystalsby elec- essentiallyunremarkable raise the possibilityof a circulating
tron microscopy(EM) of muscle fiber samples from an 11- "toxin" or cytokinecausingrhabdomyolysis. However,to date
month-oldgirl thoughtto be infectedwith CoxsackieB6 virus. no putativetoxins havebeen isolatedin cases of virus-induced
Porteret al. [52] describeda 67-year-oldmanwith concomitant rhabdomyolysis.
infectionwith Streptococcuspyogenes and picomavirus;both We believe that HIV-associatedrhabdomyolysisdeserves
viralparticlesandS. pyogeneswere seen withinmusclebiopsy specialmentionas it addsto the spectrumof clinicalpresenta-
specimens.Grecoet al. [16] documentedmyxovirus-likeparti- tionsof HIVinfection.A varietyof musculoskeletalsyndromes
cles by EM of a muscle specimenfroma patientwith myositis associatedwith HIV infection have been documented[37],
CID 1996;22(April) InfectiousEtiologiesof Rhabdomyolysis 645

ranging from myopathyto polymyositis [36] to rhabdomy- esting and clinicallysignificant.Althoughthe specificnephro-
olysis. Maheet al. [41] anddel Rio et al. [35] describedpatients toxic mechanismis not known,aggressivemeasuresshouldbe
in whom rhabdomyolysisdevelopedin associationwith acute takento protectrenalfunction.Clinicaldataaddressingother
HIV infection and antigenemia.Clinical symptomssuch as concomitantrenal toxins (volume status, etc.) was not ad-
malaiseandmyalgiaswere presentin these patients,similarto dressed.
patientswith primaryviral infectionswith Epstein-Barrvirus Numerousviral infections can thereforecause rhabdomy-
andcytomegalovirus.Othercases of myoglobinuriain patients olysis. Thevirusmostcommonlyassociatedwiththissyndrome
with HIV infection have also been documented[32, 39, 40, is influenzavirus.Viralisolationfrominfectedmusclespoints
42, 45, 46]. to directviralinvasionas the pathogenicmechanism.The high
Dalakaset al. [34] reportedtwo cases of polymyositisassoci- incidenceof renalfailuredue to influenzavirus-inducedrhab-
atedwith HIV infection.A musclebiopsyrevealedOKT4and domyolysisis intriguing.
humanT cell leukemiavirus type III-positive inflammatory
cells surroundingmyofibrils,thus suggestingthat directviral
BacterialInfections
invasionor an associatedimmunologicmechanismis responsi-
ble for muscle damage.EM did not show any viral particles, Variousbacteriahavebeenreportedto causerhabdomyolysis
and,to date,the virushas notbeen isolatedfromhumanmuscle (table 2) [72-121]. Legionellaspecies are the most common
fibers. However, animal studies of monkeys infected with organismsfollowed by Streptococcusspecies, Francisellatu-
SAIDSD retrovirus(SRV-1) haveshownmyotropictendencies larensis,andSalmonellaspecies. In earlierreviewsof rhabdo-
of the virus and its ability to directly infect muscles [33]. myolysisby Grossmanet al. [17] in 1974 andby Chughet al.
Musclebiopsiesof patientswith HIV-inducedrhabdomyolysis [9] in 1979, no bacterialetiologies were identified.However,
revealed nonspecificinflammatorymyopathywith focal ne- by 1982 Gabowet al. [1] did note that "sepsis" accountedfor
crotic areasand regeneratingfibers[40]. 2% of cases of rhabdomyolysis.The possible bacterialagents
Therenaldysfunctionassociatedwithrhabdomyolysisarises involvedin these cases were not identified.
from a varietyof factors.Myoglobinobstructstubulesand is Ourreviewdocumentedonly one reportof bacterialinfection
a directrenaltoxin.Corticalischemiaanddecreasedglomerular resultingin rhabdomyolysisin the 1966-1977 period(patient
filtrationarealso injurious,andwhentheseconditionsarecom- with Herbicola lathyri [Enterobacteragglomerans]septice-
bined with hypovolemia,oliguricrenal failurecan result [70, mia). From 1976 to 1983, 14 cases were reported,most of
71]. In the previouslymentionedreviewby Tanakaet al. [61], whichweredueto Legionellaspecies.After1983the frequency
15 (36%) of 42 patientswith virus-inducedrhabdomyolysis and varietyof bacteriareportedincreasedmarkedly.This ap-
had acute renal failure.The long-termoutcomeand possible parentincreasein the numberof bacterialinfectionscausing
recoveryof renalfunctionwere not documented.It is interest- rhabdomyolysisis probablydue to a varietyof factors.Culture
ing that althoughinfluenzavirus accountedfor only 33% of andidentificationof bacteriamay be improving.Morepatients
cases of rhabdomyolysis,53% of patientswith renal failure withsepsisaretherapeutically supportedthroughtheirillnesses,
hadthis infection.In addition,the conditionsof 57%of patients andsubsequentcomplications(rhabdomyolysis andacuterenal
with influenzavirusinfectionprogressedto renalfailure;these failure)areincreasinglyapparent.Thenumberof immunocom-
patients had CPK concentrationsranging from 261 U/L to promisedpatientswho aresusceptibleto a wide rangeof infec-
>50,000 U/L. However,most of these patients(11 of 14) had tions is also increasing.Physicianawarenessof the link be-
CPK levels of <20,000 U/L. tween bacterialinfectionand rhabdomyolysisis undoubtedly
We foundsimilarresultsin ourreview;renalfailureoccurred improvingas well. It is interestingto notethatalthoughEntero-
in 20 (34%) of 59 cases. Althoughinfluenzaaccountedfor bacteriaceaefrequently cause bacteremiaand sepsis, they
only 42%of cases, it was associatedwith renalfailurein 55% arenot commonlyassociatedwithrhabdomyolysis. In ourliter-
of patients;44% of patientswith influenzahad renal failure. aturereviewEnterobacterspecieswere implicatedin only nine
This rateis less thanthe rate(57%)of renalfailurewith influ- cases (15%).
enzareportedby Tanakaet al. [61], whichmaybe becauseless- The first documentedassociationbetween Legionella and
severe cases of disease are now diagnosedand management rhabdomyolysis was reportedin 1980by Posneret al. [80] who
techniqueshave improved.Renal biopsies of these patients describeda 61-year-oldman with a CPK level of 10,700 U/L
showedacutetubularnecrosisandmyoglobincastsobstructing and myoglobinuria.In the 14 case reportswe reviewed,the
tubules.Again, the range of CPK values in influenzavirus- CPKlevel rangedfrom606 U/L to >400,000 U/L; in most of
infectedpatientswas variable,but nine (82%) of 11 patients the cases (10 [71%] of 14), the CPK levels were <20,000
who hadrenalfailuredue to influenzavirusinfectionhadpeak U/L. Eleven (79%) of 14 of these patientshad renal failure,
CPK levels of <20,000 U/L. Gabowet al. [1] reportedearlier and four (29%) of 14 died. Thirteencases of Streptococcus
that peak CPK levels did not correlatewith the development species causingrhabdomyolysiswere found:8 due to S. pneu-
of renalfailure.The tendencyof influenzavirusto cause renal moniae,2 due to groupB streptococci,2 due to S. pyogenes,
dysfunctionirrespectiveof measurablemuscle injuryis inter- and 1 due to viridansstreptococci.Of these patients,54%had
646 Singh and Scheld CID 1996;22 (April)

Table 2. Bacterial causes of rhabdomyolysis.

No. of Rangeof CPK levels No. with ARF/total No. of deaths/total

Organism cases Age range (U/L) no. (%) no. (%)

Legionellaspecies 14 26-61 y 1,850 to >400,000 11/14 (79) 4/14 (29)

Francisellatularensis 9 31-71 y 1,049-474,000 3/9 (33) 3/9 (33)
Streptococcuspneumoniae 8 36-81 y 244-105,700 4/8 (50) 2/8 (25)
Salmonellaspecies 6 32-84 y 1,870-24,360 4/6 (67) 0/6
Staphylococcusaureus 5 15-70 y 14,046-83,000 2/5 (40) 2/5 (40)
GroupB Streptococcus 2 17 d to 11 w 4,110-22,000 1/2 (50) 2/2 (100)
Streptococcuspyogenes 2 27-67 y 33,000-151,000 1/2 (50) 1/2 (50)
Listeriaspecies 2 38-51 y 5,000-149,500 1/2 (50) 0/2
Vibriospecies 2 38-51 y 9,260 NA 2/2 (100)
Staphylococcusepidermidis 1 18 y 13,600 1/1 (100) NA
Brucellaspecies 1 25 y 337,000 1/1 (100) 0/1
Bacillus species 1 50 y 14,130 1/1 (100) 1/1 (100)
Escherichiacoli 1 86 y 11,440 0/1 1/1 (100)
Herbicolalathyri 1 42 y 21,980 1/1 (100) 1/1 (100)
(Enterobacteragglomerans)
Leptospiraspecies 1 19 y 420,000 1/1 (100) 1/1 (100)
Polymicrobes(E. coli, 1 80 y 754 0/1 0/1
Clostridiumspecies,
Klebsiellaspecies)
Borreliaburgdorferi 1 81 y 29,988 1/1 (100) 1/1 (100)
Clostridiumperfringens 1 35 y >14,000 NA 1/1 (100)
Viridansstreptococci 1 20 y 3,100 1/1 (100) 1/1 (100)
Total 60 34/60 (57) 23/60 (38)

NOTE. ARF = acute renalfailure;CPK = creatinephosphokinase;NA = not available.

renal failureand 46% died. In 1985 Chun and Raff [89] re- Renalfailureoccurssecondaryto decreasedglomerularper-
viewed bacterialcausesof rhabdomyolysisand foundthatfour fusion and the toxic effects of myoglobinon tubules.Renal
(33%)of 12 cases were causedby Streptococcusspecies. Sal- biopsies reveal acute tubularnecrosis and pigment casts. In
monellainfectionsaccountedfor six cases in our review;four 1992 Shahet al. [82] reviewed45 cases of legionnaires'disease
of six patientshadacuterenalfailure,andtherewereno deaths. andacuterenalfailure.Of these45 patients,sevenhadrhabdo-
The proposedmechanismsof muscle injuryby bacteriain- myolysis causingacute renal failure;otherrenalpathological
cludetoxingenerationanddirectbacterialinvasion.Legionella findingsincludedacutetubulointerstitialnephritis,acutepyelo-
is believed to release an endotoxinor exotoxin [82, 85] that and
nephritis,mesangioglomerulonephritis, rapidlyprogressive
causesrhabdomyolysis.Biopsy specimensthatarenegativefor glomerulonephritis. These investigatorswere able to demon-
the organism[75, 80, 81] by immunofluorescence supportthis strateLegionellapneumophilaby EM and indirectimmuno-
hypothesis.Organismssuch as Streptococcusand Salmonella fluorescenceof renal tissue, thus raising the possibility that
cause muscle damageby directbacterialinvasion as well as directinvolvementby the organismresultsin renaldysfunction.
by decreasingthe oxidativeand glycolytic enzyme activityof Whetherthispossibilityalso appliesto muscledamageremains
skeletal muscle and by activatinglysosomal enzymes [54]. to be determined.
Staphylococcusaureus[25, 103],S. pyogenes [52], Vibriospe- Rhabdomyolysisis caused by a variety of bacteria,with
cies [111], and Bacillus species [114] have all been demon- Legionellaspeciesbeingthe mostfrequentlycitedagent.Direct
stratedin muscle biopsy specimens. bacterialinvasionandreleaseof endotoxinareproposedpatho-

Table 3. Miscellaneous infectious causes of rhabdomyolysis.

No. of Age range Rangeof CPK levels No. with ARF/total No. of deaths/total
Organism cases (y) (U/L) no. (%) no. (%)

Plasmodiumspecies 2 18-32 28,218-32,000 1/2 (50) 0/2

Candidaspecies 1 29 165,000 0/1 0/1
Aspergillusspecies 1 57 40,000 NA 1/1 (100)

NOTE. ARF = acute renalfailure;CPK = creatinephosphokinase;NA = not available.

CID 1996;22(April) InfectiousEtiologiesof Rhabdomyolysis 647

17. GrossmanRA, HamiltonRW, MorseBM, PennAS, GoldbergM. Non-

physiologicalmechanisms.Significantmorbidity(57%of cases
traumaticrhabdomyolysisand acute renal failure. N Engl J Med
with acuterenalfailure)and mortality(deathin 38%of cases)
1974;291:807-1 1.
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