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Year : 2014  |  Volume : 15  |  Issue : 1  |  Page : 24-26

Fatal Raoultella ornithinolytica sepsis and purpura fulminans in a preterm newborn

Department of Pediatrics, Suleyman Demirel University Medical School, Isparta, Turkey

Date of Web Publication2-May-2014

Correspondence Address:
G Sandal
Suleyman Demirel University, Faculty of Medicine, Department of Pediatrics Isparta
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2319-7250.131833

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Raoultella ornithinolytica is a Gram-negative encapsulated aerobic bacillus belonging to family Enterobacteriaceae. It is an extremely rare causative organism of infections in humans. We reported R. ornithinolytica sepsis and purpura fulminans in a preterm female baby. Our case is the second newborn case of human infection by R. ornithinolytica that has been reported in the literature.

Keywords: Preterm newborn, purpura fulminans, Raoultella ornithinolytica

How to cite this article:
Sandal G, Ozen M. Fatal Raoultella ornithinolytica sepsis and purpura fulminans in a preterm newborn. Indian J Paediatr Dermatol 2014;15:24-6

How to cite this URL:
Sandal G, Ozen M. Fatal Raoultella ornithinolytica sepsis and purpura fulminans in a preterm newborn. Indian J Paediatr Dermatol [serial online] 2014 [cited 2022 Jan 16];15:24-6. Available from: https://www.ijpd.in/text.asp?2014/15/1/24/131833

  Introduction Top

Raoultella ornithinolytica is a Gram-negative encapsulated aerobic bacillus belonging to family Enterobacteriaceae. It is found in aquatic environments, fish and insects. [1] R. ornithinolytica is a histamine-producing bacterium that causes fish poisoning. [2] The signs of histamine fish poisoning, most commonly include marked, red skin flushing, headache, abdominal cramps and rarely, tachycardia, hypotension and bronchospasm. [3] Herein we reported R. ornithinolytica sepsis and purpura fulminans in a preterm female baby. Our case is the second newborn case of human infection by R. ornithinolytica has been reported in the literature.

  Case report Top

A female baby weighing 1730 g was born to 27-year-old, gravida 2 and para 2 mothers. At 35 weeks of gestation, the mother underwent caesarean section for severe olygohydramnios. At the delivery room, 1 st min APGAR score was 8 and 5 th min APGAR score was 9. In prenatal ultrasonography (USG), intrauterine growth restriction determined. There was no history of infection, gestational diabetes and hypertension during pregnancy.

Her weight, height and head circumference was 1730 g (10-25 p), 43 cm (10-25 p) and 30 cm (10-25 p) respectively. On cardiovascular, respiratory, abdominal and neurologic examinations, no significant signs were detected. The following laboratory investigations were performed and were normal: Serum urea, creatinine, electrolytes, calcium, phosphate, uric acid, liver function and hematologic parameters. Viral titers did not support congenital infection. Anteroposterior chest radiography, cranial and renal ultrasonographic findings were normal. The initial blood culture was reported as negative.

On day 2 of intensive care, oral feeding started. However, feeding intolerance developed. On day 12 of intensive care, total enteral feeding could be achieved. On day 14 of intensive care, the infant was less active and had apneic episodes, with tachycardia and lowered pulse oximetry readings, which returned to normal levels. She had poor peripheric circulation. There was flushing including upper and lower extremities. The clinical picture worsened with the development of multisystem failure and septic shock. The purpura fulminans developed on all the extremities and right ear cartilage.

The patient had leukopenia (3.9 × 10 3 leukocytes/mm 3 ) with a left shift, thrombopenia (17 × 10 3 /mm 3 ) and disseminated intravascular coagulation (DIC) (prothrombin time and activated partial thromboplastin time were 21.3 (9.4-12.5) and 106 s (26-55 s), respectively. Plasma D-dimer level was 1480 μg/L (64-246 μg/L) by latex immunoassay. Protein C activity was 7% (normal: 70-140%), protein S activity 4.3% (normal: 58-127%) and antithrombin III (AT III) activity 25% (normal: 75-125%). Serum C-reactive protein value was 40 mg/L (normal: 0-5). She became hypotensive (blood pressure, 36/20 mm Hg; heart rate, 170/min) and oliguric (urea, 21 mg/dL; serum creatinine, 1.29 mg/dL; K, 6.2 mg/dL). Biochemical studies revealed abnormal liver function tests (serum glutamic-oxalo-acetic transaminase, 117 u/L; serum glutamate pyruvate transaminase, 64 u/L; lactate dehydrogenase, 1134 u/L; albumin, 1,8 g/dL; total bilirubin 10 mg/dL, direct bilirubin: 0,7 mg/dL). Blood fibrinogen and homocysteine levels were normal. Factor V Leiden and prothrombin 20210 gene mutations were not found.

The blood culture and urine culture were performed. Because of patient's hemodynamic instability, lumbar puncture was not performed and cerebrospinal fluid culture was not taken. Chest radiography demonstrated signs of generalized condensation. Cranial and abdominal USG were normal.

On the clinical follow-up; she had intractable hypotension. She received volume replacement and vasoactive agents: Dopamine 20 μg/kg/min, dobutamine 20 μg/kg/min and epinephrine 0.4 μg/kg/min. Fresh frozen plasma was given at a dose of 10-20 mL/kg every 6-12 h. Replacement therapy was used with multiple transfusions of thrombocyte suspension and occasionally packed red cells. Broad-spectrum antibiotics (meropenem 40 mg/kg every 8 h and vancomycin 40 mg/kg every 8 h) were administered. Oxygenation was maintained by high-frequency oscillatory ventilation. The blood culture yielded a Gram-negative bacillus R. ornithinolytica (biotype 77563289). An antibiogram for R. ornithinolytica demonstrated susceptibility to aminoglycosides, cefepime, carbapenems, quinolones and trimethoprim-sulfamethoxazole. Meropenem therapy was continued. Netilmicin was added to treatment. Follow-up cultures were sterile. Despite aggressive treatment with broad antibiotic coverage, cardiopulmonary support with mechanical ventilation and multiple inotrope and blood product transfusions, ecchymotic and ischemic skin lesions became more extensive on the following days [Figure 1]. Multiple organ system failure secondary to sepsis was developed. Coagulation parameters did not correct with fresh frozen plasma transfusions. Finally, she died at 19 days of age due to persistent massive pulmonary hemorrhage and her parents refused autopsy.
Figure 1: Generalized purpura with necrotic bullae on the distal extremities and right ear cartilage

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  Discussion Top

R. ornithinolytica has been isolated from the gut of the fish, termites and aquatic environments. [1] An ability to convert histidine to histamine, leading to fish poisoning had been reported previously. [2],[3]

This bacterium was first described in 1989 by Kosako et al. [4] In 1994, Monnet and Freney used growth tests at 4° and 42° plus several four-carbon substrate assimilation tests to differentiate Klebsiella ornithinolytica and Klebsiella planticola, another species capable of producing large amounts of histamine. [5] Kanki et al. used Monnet and Freney's method to definitively identify, from fish and stool samples, 13 strains of R. ornithinolytica which all produced high levels of histamine. [2]

There are only four case reports of human infection by R. ornithinolytica in the literature and there are only one newborn case with R. ornithinolytica bacteremia. The first patient was an 82-year-old woman in whom the microorganism caused an enteric fever-like syndrome and the organism was isolated from blood. [1] The second patient was a 97-year-old female who presented with a giant renal cyst, which caused colic obstruction. The fluid culture isolated from the cyst was positive for R. ornithinolytica. [6] The third reported case was of R. ornithinolytica bacteremia in an infant with visceral heterotaxy. [7] The fourth case was a 44-year-old woman presented with the complaints of weakness, dyspnea and diabetic foot lesion and the organism was isolated from diabetic foot lesion. Our case is the second newborn case with R. ornithinolytica bacteremia. [8]

R. ornithinolytica is a histamine-producing bacterium that subsequently causes fish poisoning. [2] The signs of histamine fish poisoning, most commonly include marked, red skin flushing, headache, abdominal cramps and rarely, tachycardia, hypotension and bronchospasm. [3] In literature, only one case showed marked skin flushing, which was possibly related to a histamine reaction. Our case was presented with tachycardia, hypotension, red skin flushing (upper and lower extremities), septic shock and purpura fulminans.

R. ornithinolytica has been shown to be resistant to ampicillin and other commonly used antibiotics. [9] R. ornithinolytica bacteremia appeared to be limited and did not recur during therapy and a course of antibiotic treatment for 10-14 days with amoxicillin-clavulanic acid seemed to be curative. Two of the other four cases in the literature showed bacteremia caused by R. ornithinolytica and the all cases were recovered by antibiotic treatment and supportive therapy. The distinctive feature of our case was R. ornithinolytica that was markedly resistant to antimicrobial agents compared with previous reports.

Sepsis is associated with endothelial cell activation, a hemostatic profile characterized by activation of the coagulation pathway and subsequent activation of the fibrinolytic system, which then is followed by the inhibition of the fibrinolytic system. The resulting procoagulant state may manifest clinically as a coagulation-dominant DIC producing multiple organ system failure. Alterations in the levels of various mediators of coagulation and fibrinolysis have been reported to be associated with negative outcome in patients with sepsis. Given its pivotal role in the coagulation and fibrinolytic systems, protein C has been of particular interest as a factor in the hemostatic abnormalities of patients with sepsis. Protein C levels have been reported to be predictive of sepsis outcome. [10],[11],[12] Our case had acquired severe protein C, S and AT III deficiencies secondary to sepsis. We believe that this condition was worsened prognosis of sepsis. Despite prompt and efficiency antibiotherapy, invasive mechanic ventilation and supportive care, our case died due to DIC and multiple organ failure secondary R. ornithinolytica sepsis. The environmental cultures were taken, but we were unable to validate the origin of the organism.

  Conclusion Top

R. ornithinolytica is an extremely rare causative organism of infections in humans. R. ornithinolytica may cause highly fatal infection in neonates, especially in preterm infants.

  References Top

1.Morais VP, Daporta MT, Bao AF, Campello MG, Andrés GQ. Enteric fever-like syndrome caused by Raoultella ornithinolytica (Klebsiella ornithinolytica). J Clin Microbiol 2009;47:868-9.  Back to cited text no. 1
2.Kanki M, Yoda T, Tsukamoto T, Shibata T. Klebsiella pneumoniae produces no histamine: Raoultella planticola and Raoultella ornithinolytica strains are histamine producers. Appl Environ Microbiol 2002;68:3462-6.  Back to cited text no. 2
3.Ferran M, Yébenes M. Flushing associated with scombroid fish poisoning. Dermatol Online J 2006;12:15.  Back to cited text no. 3
4.Kosako Y, Tamura K, Sakazaki R, Miki K. Klebsiella ornithinolytica sp. nov., formerly known as ornithine-positive Klebsiella oxytoca. Curr Microbiol 1989;18:201-6.  Back to cited text no. 4
5.Monnet D, Freney J. Method for differentiating Klebsiella planticola and Klebsiella terrigena from other Klebsiella species. J Clin Microbiol 1994;32:1121-2.  Back to cited text no. 5
6.Vos B, Laureys M. Giant renal cyst as cause of colic obstruction. Rev Med Bru×2009;30:107-9.  Back to cited text no. 6
7.Mau N, Ross LA. Raoultella ornithinolytica bacteremia in an infant with visceral heterotaxy. Pediatr Infect Dis J 2010;29:477-8.  Back to cited text no. 7
8.Solak Y, Gul EE, Atalay H, Genc N, Tonbul HZ. A rare human infection of Raoultella ornithinolytica in a diabetic foot lesion. Ann Saudi Med 2011;31:93-4.  Back to cited text no. 8
9.Hostacká A, Klokocníková. Antibiotic susceptibility, serum response and surface properties of Klebsiella species. Microbios 2001;104:115-24.  Back to cited text no. 9
10.Yan SB, Helterbrand JD, Hartman DL, Wright TJ, Bernard GR. Low levels of protein C are associated with poor outcome in severe sepsis. Chest 2001;120:915-22.  Back to cited text no. 10
11.Petäjä J, Manco-Johnson MJ. Protein C pathway in infants and children. Semin Thromb Hemost 2003;29:349-62.  Back to cited text no. 11
12.Lorente JA, García-Frade LJ, Landín L, de Pablo R, Torrado C, Renes E, et al. Time course of hemostatic abnormalities in sepsis and its relation to outcome. Chest 1993;103:1536-42.  Back to cited text no. 12


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