Shigella sonnei enterocolitis and rhabdomyolysis

Margaret-Mary G. Wilson, M.B.,B.S.,

M.R.C.P(U.K.)
Katalin Scherer, M.D.
Division of Geriatric Medicine, Department of Internal Medicine, St. Louis University Health Sciences Center and the GRECC, Veteran's Administration Medical Center, St. Louis.

 

Corresponding Author:

Margaret-Mary G. Wilson, MRCP (UK),

Division of Geriatric Medicine,
Saint Louis University Health Sciences Center,
1402, S. Grand Blvd, Rm M238,
Saint Louis, MO 63104.
Tel No.: (314) 577-8462.
Fax No: (314) 771-8575.
Email the author

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Subject Index: Rhabdomyolysis, enterocolitis, Shigellosis, Shigella Sonnei

ABSTRACT

Systemic complications of shigellosis occur infrequently in the United States. In this report, we describe a case of rhabdomyolysis and acute renal failure resulting from infection with shigella sonnei in a healthy older adult. Rhabdomyolysis complicating shigellosis is rare. The occurrence of rhabdomyolysis in patients with shigellosis increases the risk of acute renal failure, mandating increased awareness of this potential complication of shigella infections.

INTRODUCTION

Shigellosis is a common cause of acute diarrhea in adults [Maurelli et al, 1977]. In developing countries, systemic complications of shigellosis occur frequently in children. These include acute renal failure, hemolytic-uremic syndrome, toxic megacolon and neurological complications [Goldfarb et al, 1982; Keutschet al 1996]. We report rhabdomyolysis due to shigellosis in an older man. This is the first documented case that we could find of rhabdomyolysis complicating Shigella sonnei enterocolitis reported in the United States.

CASE REPORT

An 83-year-old heterosexual African-American man with a history of mild hypertension controlled on amlodipine, presented with a three-day history of mucoid, non-bloody diarrhea. The diarrhea occurred approximately twelve times a day in moderately large volumes. There was associated cramping peri-umbilical discomfort and tenesmus. There was no history of fever, chills, nausea, vomiting, dizzy spells or loss of consciousness associated with his presenting symptoms. He denied recent use of antibiotics, foreign travel or known ingestion of contaminated foods. Family members and recent social contacts were reportedly in good health. He had not used any medications to alleviate his symptoms prior to presentation. He was a retired janitor and led a sedentary life with no history of recent unusual physical exertion. He did not drink alcohol, smoke or use any recreational drugs. He was married but not sexually active and unaware of his HIV status. Review of his family history was significant only for hypertension among several paternal relatives.
The patient was a well-nourished man with dry oral mucus membranes. He had a blood pressure of 100/60 supine and a heart rate of 94/min with significant orthostatic changes. The rest of his physical examination did not reveal any notable findings. A digital rectal examination revealed no structural abnormality. Direct inspection revealed brown, loose and mucoid stool. There was no blood visible on gross examination and the stool specimen tested negative for occult blood. His complete blood count was as follows: hematocrit 38%, WBC 19,300/mm3, platelets 199,000/ mm3 with 86% segmented neutrophils, 10% lymphocytes and no bandemia. The peripheral smear was normal with no fragmented red blood cells. Serum biochemistry was as follows: Sodium 136 mmol/L, potassium 3.8 mmol/L, BUN 28 mg/dl, creatinine 1.8 mg/dl, chloride 108 mmol/L, bicarbonate 19 mmol/L, glucose 110 mg/dl, calcium 8.6 mg/dl, phosphorus 3.0 mg/dl, magnesium 1.8 mg/dl, creatine phophokinase (CPK) 13,205 U/L, CPK-MB fraction 11.5 U/L, Troponin I < 0.2 ng/ml. Liver function tests were normal except for an AST of 77 U/L. Serum haptoglobin, thyroid stimulating hormone, prothrombin time and partial thromboplastin time were normal. A 12 lead electrocardiogram revealed only left ventricular hypertrophy. The calculated fractional excretion of sodium was 0.7%. Urinalysis revealed a Ph of 5, specific gravity 1013, 2+ protein, 6 coarse granular casts, moderate amounts of blood, 5 red blood cells and 4 white blood cells. A urine toxicology screen was negative. A urine culture and two sets of blood cultures were negative. He was HIV negative. Stool tests were negative for Clostridium difficile, Entameba histolytica, Giardia lamblia, Salmonella typhi and Campylobacter. Stool culture of a sample passed on admission grew Shigella sonnei resistant to ampicillin, but sensitive to ciprofloxacin, ceftriaxone and azithromycin.
The patient was started on high flow intravenous half normal saline alkalinized with sodium bicarbonate. He was oliguric for the first 12 hours after admission, but thereafter resumed normal urine output. He was started on oral azithromycin following receipt of the stool culture results. His CPK level returned to normal over the next 96 hours. Repeat investigations yielded a BUN of 19, a serum creatinine of 0.9 and a normal urinalysis. His diarrhea subsided 4 days after admission. A repeat stool culture done two weeks after discharge was negative for Shigella Sonnei.

DISCUSSION

Shigellosis is an acute diarrheal syndrome caused by aerobic, gram negative, and non-motile rods that are members of the family Enterobacteriaceae, tribe Escherichieae, and genus Shigella. There are four Shigella species namely; Shigella dysenteriae, S. boydii, S. flexneri and S. sonnei. S. sonnei is the most frequent isolate in the United States [Keutsch et, 1996]. Shigellosis is worldwide in distribution but is most prevalent in developing countries. In the United States, endemic isolation rates range from 6-9 per 100,000 [Edwards, 1999]. High-risk groups include children aged less than 4yrs, Native Americans on Indian reservations, homosexual men, prisoners, and persons in military field groups. Persons with low levels of personal hygiene are also at increased risk due to an increased likelihood of faeco-oral contamination [Lee et al, 1991].
In healthy adults, shigellosis is usually a self-limiting illness ranging in duration from 3 - 10 days. The mortality rate in the United States, even in high-risk groups, is less than 1%. However, in developing countries, shigellosis often presents as an acute fulminant infection with systemic complications and mortality rates as high as 10%. Deaths in Shigellosis are usually due to septicemia, toxic megacolon or acute renal failure [Bennish et al, 1991]. Acute renal failure is a common complication of shigellosis among children in the developing world. Such cases have been attributed to acute tubular necrosis from severe dehydration, hemolytic uremic syndrome, thrombotic thrombocytopenic purpura and rhabdomyolysis [Goldfarb et al, 1982; Raghupathy et al, 1978]. However, we found only one prior case of rhabdomyolysis occurring in association with shigellosis in the developed world. This was documented in a 41-year-old woman in France who contacted S. flexneri enterocolitis during a one-week stay in the Dominican Republic [Paris et al, 1996].
Our patient is the first documented case of rhabdomyolysis occurring in association with S. sonnei infection in the United States. Evidence indicates that host factors are more important than species type in determining the severity of illness. Age related changes in host response might explain the predisposition of our patient to systemic complications of shigellosis [Keutschet al 1996, Thompson et al, 1984].
The absence of any other possible causes of rhabdomyolysis in this patient's clinical presentation suggests that infection with S. sonnei was the inciting factor for myonecrosis. Sporadic cases of rhabdomyolysis resulting from infections have been reported. However, these are most often due to viral infections, particularly influenza A. In virus-induced rhabdomyolysis, proposed pathogenetic theories include viral induced myolysis and toxin related muscle necrosis [Minow et al, 1974]. However, there is little data to substantiate these theories. Similarly, the pathophysiological mechanism responsible for myonecrosis in Shigellosis and other bacterial infections is unclear. Available evidence indicates that bacterial invasion of the intestinal mucosa by shigella may result in cytokine gene activation and subsequent activation of transcription factors. Indeed, studies have demonstrated increases in several cytokines studied. Significantly, IL-1, IL-6, IFN-gamma and TGF-beta producing cells increased in direct proportion to the severity of the enterocolitic inflammation [Raquib et al, 1995]. Thus, increased cytokine elaboration may play a role in the pathogenesis of myonecrosis in shigellosis. An alternative mechanism for myonecrosis could involve the direct effects of toxins. Shiga toxin, a cytotoxic protein toxin, has been implicated in the pathogenesis of HUS, TTP and neurological complications associated with shigellosis [Hoffman, 1993]. This toxin is produced predominantly by S. dysenteriae. There is currently little evidence to implicate this toxin in the pathogenesis of systemic manifestations of S. sonnei infections. Recently, two new shigella enterotoxins have been identified, namely SHET-1 and -2. Evidence suggests that these are produced in vivo although their precise role in the pathogenesis of disease in shigellosis remains unclear [Noriega et al, 1995].

CONCLUSION

The occurrence of rhabdomyolysis as a direct complication of shigella infection is rare. Available evidence precludes delineation of the underlying pathophysiological mechanism. However, awareness of the possibility of myonecrosis in the setting of shigellosis mandates heightened clinical suspicion for the presence of this complication. In order to reduce the risk of acute renal failure, physicians should have a low threshold for screening for rhabdomyolysis in patients presenting with clinical features consistent with shigellosis.

 

REFERENCES

 

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