pyomyositis affects the massive skeletal muscles and is most frequently caused by staphylococcus bacteria ( 1 ) .
necrotizing fasciitis is a localized spread of infection that follows events such as trauma or surgery ( 2 ) , and which is commonly affected by group a streptococcus .
rhabdomyolysis comprehensively affects the skeletal muscle and , like pyomyositis and necrotizing faciitis , shows serum creatinine kinase elevation ; however , rhabdomyolysis occurs as a systemic disease and is not associated with the focal manifestation of abscesses ( 3 ) .
the pathogenesis of infectious rhabdomyolysis is thought to be associated with the systemic or local metabolic changes related to a systemic or local infection ( 4 ) ; however , the mechanisms underlying its pathogenesis have not been established . in addition , gram - negative bacillus rhabdomyolysis is rare , and its microbiological pathology remains to be elucidated .
we diagnosed the patient , a 64-year - old japanese man with multiple myeloma , with bacteremia caused by morganella morganii .
he was admitted to our institute due to septic shock at the sudden onset of a febrile episode .
his vital signs at admission were as follows : blood pressure , 82/60 mmhg ; heart rate , 78/min ; body temperature , 39.1 ; respiration rate , 20/min ; and spo2 , 95% ( room air ) .
the laboratory findings at the time of his diagnosis showed massive myolysis and a significantly elevated level of creatinine kinase ( ck ; 3,582 u / l ) ; thereafter , an isotype analysis of the patient 's ck confirmed that the elevated ck was derived from the patient 's skeletal muscle ( 98.8% ) .
the status of the patient 's multiple myeloma , which had been diagnosed 5 years earlier , was stage iiia , igg  type .
he had undergone treatment with a variety of chemotherapies : melphalan ( mp ; 12 mg / day for 4 days + prednisolone 60 mg / day for 6 days , repeated triweekly ) , vad ( vincristine 0.4 mg / m for 4 days as a continuous infusion + doxorubicin 10 mg / m for 4 days as a continuous infusion + dexamethasone 40 mg / day , days 1 - 4 , 9 - 12 , and 17 - 20 , repeated monthly ) , bd ( bortezomib 1.3 mg / m on days 1 , 4 , 8 , and 11 + dexamethasone 40 mg / day for 4 days , repeated monthly ) , and thalidomide ( 100 mg / day ) .
his last treatments were lenalidomide 20 mg / day , and igg gradually increased 6 months before the current infectious episode .
after the patient 's admission for sepsis caused by m. morganii , rehydration was immediately performed via central venous catheterization and a catecholamine infusion ( dopamine 3 mg / kg / h ) was administered ; at the same time , antimicrobial treatment with meropenem ( 0.5 g three times a day ) was initiated .
cervical to pelvis computed tomography ( ct ) was performed on the day of admission , but there were no clear findings explaining the patient 's massive myolysis . on day 2 of the patient 's hospitalization ,
the patient 's vital sign were as follows : blood pressure , 61/45 mmhg ; heart rate , 87/min ; and body temperature , 36.8. we started hemodialysis combined with endotoxin absorption the same day .
however , respiratory failure occurred , necessitating mechanical ventilation , on the night of day 2 .
the patient died of multi - organ failure two days after undergoing intubation . before his death , rhabdomyolysis developed day - by - day and was reflected in the remarkable elevation of the patient 's ck level .
the final ck value was 19,790 u / l ( normal range : 40 - 200 u / l ) ( figure ) .
we found that the m. morganii was sensitive to all of the broad spectrum beta - lactams , including carbapenems and cephalosporins , but only resistant to cefotiam , minomycin , and ciprofloxacin .
his muscle damage manifested as with elevated levels of ck , aspartate aminotransferase ( ast ) , alanine aminotransferase ( alt ) , and lactate dehydrogenase ( ldh ) after the onset of the disease ( day 1 ) , with increasing leukocytes and c - reactive protein ( crp ) .
the days in the x - axis indicate the days after the patient s admission .
the patient visited our outpatient clinic for a routine follow - up examination 6 days before his admission .
infectious rhabdomyolysis is caused by various pathogens including viruses , bacteria and fungi ( 3 ) .
the clinical entity of infectious rhabdomyolysis was established in 1982 ( 5 ) , and a review ( 3 ) identified the predisposing risk factors for rhabdomyolysis : alcohol ingestion , compression injury , and generalized seizures . regardless of the pathogen that causes infectious rhabdomyolysis , the underlying mechanism of the disease is metabolic .
the most frequent differential diagnosis is necrotizing fasciitis , which occurs when the infection spreads into the deep fascial layers ( 2 ) .
necrotizing fasciitis is generally caused by infection , and the initial entry site is sometimes trivial . in contrast
, rhabdomyolysis is caused by the following two critical conditions : ( 1 ) physical distress ( for example , distress due to or involving excessive exercise , seizure , muscle compression , hyperthermia , or hypothermia ) ; and ( 2 ) systemic metabolic disorders ( for example disorders due to hypoxia , acidemia , drug abuse , infection , or inflammation ) .
the localization of a soft - tissue infection can be distinguished by systemic imaging , especially by sensitive mri ( 6 ) . in the reported cases of rhabdomyolysis , the local radiological findings are faint . in the present case ,
our evaluation of the present case raised an important question : what is the microbiological mechanism underlying the development of rhabdomyolysis accompanied by systemic infection ( 3,7 ) ?
thus , rhabdomyolysis is relatively common among patients with miscellaneous bacterial infections including , but not limited to , legionella ( 4 ) , pneumococcal ( 8) , and salmonella ( 7 ) .
we underscore that patients these types of infectious rhabdomyolysis share the following common findings : 1 ) the patients were immunocompromised due to malignancy or a severe wound ; 2 ) precedent or concomitant acute renal failure were observed in the patient 's clinical course ; and 3 ) metabolic abnormalities such as dehydration or acidemia due to single / multi - organ failure existed as the underlying pathogenesis .
thus , ischemia or hypoxia caused by systemic infection are considered to be involved in the mechanism underlying the development of rhabdomyolysis .
m. morganii is rarely pathogenic in humans , but it sometimes develops into an opportunistic infection in a compromised host . although there are no reported cases of infectious rhabdomyolysis caused by m. morganii , arranz - caso et al .
the authors noted that gram - negative bacterial pyomyositis can occur in an immunocompromised case followed by enteric organism translocation .
gram - negative bacterial infection does not favor pyomyositis , which is usually raised by gram - positive bacteria .
our case suggests that infectious rhabdomyolysis may be underdiagnosed as a comorbidity of gram - negative bacterial infections , even if the causative organism is an opportunistic pathogen such as m. morganii . regarding myolysis / rhabdomyolysis complicated with a systemic bacterial infection and the accumulation of muscle damage
the non - bacteremic mechanism includes alterations of systemic metabolism ( i.e. , hypoxia , acidosis ) and an intracellular metabolism in situ ( e.g. , disturbances of glycolysis and oxidation in muscle cells ) ( 7 ) .
the non - bacteremic mechanism of rhabdomyolysis accompanied by systemic infection is similar , regardless of the pathogen that is involved ( 3,7 ) .
the common mechanisms underlying muscle damage arise from a combination of hypoxia , dehydration , and acidemia in the tissue ( 4 ) . in general , rhabdomyolysis develops during the course of systemic infection in up to 5% of bacterial and viral cases ( 7 ) .
rhabdomyolysis is a specific term describing the excess leakage of enzymes derived from muscular tissue , which can result in multi - organ failure . in our patient , the apparent infection focus was not identified by repeated systemic ct .
this negative finding caused a delay in our differentiation of the cause of the patient 's rhabdomyolysis .
we treated the patient with meropenem , to which the causative pathogen , m. morganii , is sensitive ; however , an adequate antimicrobial therapy can not always rescue a patient from advanced multiple - organ deterioration .
rhabdomyolysis should thus be recognized as a more aggressive clinical situation than local myolysis , and one that requires intensive care .
furthermore , non - specific myolysis / rhabdomyolysis can occur due to any pathogen ( 7 ) ; thus , it may be underdiagnosed during the infection .
myalgia and scant laboratory signs of myolysis / rhabdomyolysis ( usually appearing as liver damage in laboratory data ) can be misdiagnosed in patients with the overlapping leakage of transaminases due to various etiologies .
clinicians should keep in mind that abnormal liver function test results may be linked to a muscular problem .
clinicians should be aware of the possibility of systemic infection - associated myolysis / rhabdomyolysis and closely observe immunocompromised patients .
this is the first report of lethal rhabdomyolysis caused by m. morganii as a complication in a non - hiv patient .
short description : fatal rhabdomyolysis caused by m. morganii can occur in a multiple myeloma patient without hiv .
 a 64-year - old japanese man with multiple myeloma was admitted to our institute due to fever and hypotension . 
 he had received multiple courses of chemotherapy just before his febrile episode . 
 blood culturing detected morganella morganii . at the time of the diagnosis , 
 his laboratory findings revealed massive rhabdomyolysis with a significantly increased creatinine kinase level ( ck ; 3,582 u / l ) ; 98.8% of which corresponded to the ck - mb isotype . 
 we diagnosed the patient with sepsis caused by m. morganii , complicated with severe rhabdomyolysis . 
 he died of multi - organ failure 2 days later . 
 clinicians should closely observe patients with possible systemic infection - associated rhabdomyolysis . 