Recurrent purpura fulminans associated with drug-resistant Streptococcus pneumoniae infection in an asplenic girl.

We report a case of purpura fulminans associated with drug-resistant Streptococcus pneumoniae that responded to ceftriaxone therapy. Ultrasonography of the abdomen and splenic scan revealed the absence of a spleen.     

肺炎链球菌3型相关溶血尿毒症综合征一例临床分析

目的 探讨儿童肺炎链球菌相关溶血尿毒症综合征(SP-HUS)的临床特点.方法 回顾性分析1例3型肺炎链球菌相关HUS患儿的临床、辅助检查特点和随访情况,并复习文献,探讨SP-HUS的诊断要点.结果 患儿女,1.5岁,以发热、咳嗽伴气促5d入院.右肺呼吸音低于左侧,叩诊浊音.辅助检查:血常规示WBC 3.7×109/L,Hb 83 g/L,PLT 11 × 109/L.CRP＞180 mg/L.红细胞形态检查示红细胞大小不一,易见红细胞碎片.尿常规示红细胞计数42.66/HP,尿潜血阳性(+++),尿蛋白(++++).血培养、胸腔积液培养和痰培养均为肺炎链球菌.采用简易棋盘式肺炎链球菌分型试剂盒进行血清型分型证实为3型.Coombs试验示直接抗人球蛋白试验阳性.血补体C3 0.699 g/L,补体C4 0.064 g/L.胸部X线片示右侧胸腔积液,右肺感染.胸部CT示两肺多发感染,右肺下叶多发肺气囊.入院后考虑SP-HUS,予去甲万古霉素针、头孢哌酮舒巴坦针静脉滴注抗感染,连续性肾脏代替治疗,洗涤红细胞纠正贫血等治疗后,血小板恢复正常,溶血停止,贫血纠正,肝肾功能及尿常规正常;肺部病灶好转,直接Coombs试验转阴,补体C3、C4恢复正常.3个月后随访,肝肾功能及尿常规均正常.结论 肺炎链球菌感染出现溶血性贫血、血小板减少、急性肾衰竭、Coombs试验阳性时应考虑SP-HUS可能.肺炎链球菌3型感染与HUS相关.     

Purpura fulminans in a newborn infant with galactosemia

An 11-day-old neonate presented with purpura fulminans and was subsequently diagnosed with galactosemia. Neonatal purpura fulminans occurs predominantly in patients suffering from inherited protein C deficiency or disseminated intravascular coagulation associated with septicemia. Hemostatic changes in patients with liver disease may result in bleeding or, rarely, thrombosis. We suppose that in the present patient, deficiency of protein C, secondary to liver disease, was responsible for the development of purpura fulminans. Treatment consisted of blood and blood products and galactose-free formula. The patient recovered with residual mild psychomotor retardation and the lesions with minimal scarring. In conclusion, galactosemia also should be kept in mind as an uncommon cause of purpura fulminans in newborn infants.     

Internal carotid artery occlusion associated with Mycoplasma pneumoniae infection in a child

We describe a seven-year-old girl with severe pneumonia probably associated with Mycoplasma pneumoniae who developed right-sided hemiparalysis and right central facial paralysis soon after the onset of the disease. Cerebral magnetic resonance imaging revealed left corpus striatum acute infarction and magnetic resonance angiography demonstrated left internal carotid artery occlusion. She also had positive antiphospholipid and anticardiolipin antibodies and increased fibrinogen and D-dimer levels.     

Lung abscess in a child with Mycoplasma pneumoniae infection

Mycoplasma pneumoniae is a common cause of community-acquired pneumonia in children, while lung abscess is a severe complication of bacterial pneumonias caused mainly by pyogenes. Here we report a previously healthy 10-year-old boy admitted to our unit for a right upper lobe pneumonia, with a 15-day history of fever and cough insensitive to oral amoxicillin and intramuscular ceftriaxone. Chest computed tomography scan revealed that the right upper lobe consolidation was an abscess and that a similar formation was present in the right mid region. Serology allowed the diagnosis of M. pneumoniae infection. The clinical picture rapidly improved after initiation of oral clarithromycin, and radiographic resolution, without sequelae, was observed after 1-month treatment. Lung abscess in children is a rare complication of M. pneumoniae infection and only three previous cases have been described in the literature, all associated with a delayed diagnosis and late initiation of macrolide therapy. A long-term treatment with oral macrolide allows a prompt recovery and restitution ad integrum of the lung.     

Purpura fulminans in a Chinese boy with congenital protein C deficiency

Severe and recurrent purpura fulminans developed in a Chinese boy at one day of age. Results of coagulation studies performed on the patient during attacks were compatible with the diagnosis of disseminated intravascular coagulation. Subsequent investigations have revealed that the patient is homozygous and that his parents are heterozygous for protein C deficiency. Cryoprecipitate and fresh frozen plasma induced a remission, and administration of warfarin has been successful in preventing recurrence of attacks for as long as 8 months without infusion of any plasma components. None of the family members who are heterozygous for protein C deficiency have had thrombotic episodes.     

Purpura fulminans as a sequel to erythema nodosum in a child with homozygous Leiden mutation and acquired protein S deficiency

A 6-y-old boy presented with generalized, bruise-like swelling of both legs. Three weeks later, he developed purpura fulminans in one of the affected feet. Histology of the leg swelling was in accordance with erythema nodosum. The boy proved to be homozygous for the Factor V Leiden mutation and to have acquired protein S deficiency. He recovered, with partial loss of two toes. CONCLUSION: In contrast to what is often stated, erythema nodosum is not always a benign condition. On the basis of this report, we suggest that if extensive erythema nodosum develops in an individual without any known thrombophilic disorder, investigations with respect to the latter should be performed.     

Purpura fulminans. A case for heparin therapy

A 6.5-year-old boy developed purpura fulminans. He had no evidence of congenital protein C deficiency. He responded readily to heparin therapy with resolution of his coagulopathy. The coagulopathy resumed rapidly after heparin therapy was interrupted to allow for surgical procedures. Despite correction of his coagulopathy with heparin, surgical amputation of his leg was necessary because of inadequate perfusion.     

Haemolytic-uraemic syndrome associated with Streptococcus pneumoniae meningitis

We report the first case of Haemolytic-uraemic syndrome (HUS) associated with Streptococcus pneumoniae meningitis. This supports a common pathogenic mechanism in HUS following infections by neuraminidase-producing organisms and in pneumococcal meningitis. We recommend that HUS must be considered in cases of renal failure and/or anaemia associated with pneumococcal meningitis, and that bacterial meningitis be considered in all patients with HUS and central nervous system involvement.Abbreviations CSF cerebrospinal fluid - HUS haemolyticuraemic syndrome - RBC red blood cells - T-ag Thomsen-Friedenreich antigen     

Purpura fulminans in a case of protein C deficiency

We report a case of protein C deficiency which presented with purpura fulminans. The inheritance of protein C deficiency is discussed and the importance of warfarin (Coumadin) treatment in this condition is emphasized.Abbreviations DIC disseminated intravascular coagulation - PT prothrombin time     

Transverse myelitis associated with Mycoplasma pneumoniae infection.

A case of acute transverse myelitis associated with respiratory infection by Mycoplasma pneumoniae is described. Circulating antibodies to myelin were detected suggesting that mycoplasma related neurological damage is mediated by producing an immunological myelopathy.     

Recurrent Streptococcus pneumoniae meningitis in a child with traumatic anterior cranial base defect

Acute bacterial meningitis is a potentially life-threatening infection of the cranial and spinal leptomeninges. Recurrent episodes of meningitis are rarely seen, but when they occur, an extensive investigation has to be made to find out responsible factors. A single episode of acute meningitis may result from bacteriemia, but when followed by recurrent meningitis in pediatric patients, other possible routes of the bacteria invasion to the cerebrospinal fluid (CSF) should be considered. Patients with head injury have the highest risk of acquiring recurrent bacterial meningitis, followed by patients with a congenital anatomic lesion of the skull or duramater, such as meningomyelocele. The underlying cause is a transdural communication between the meningeal space and paranasal sinuses or skin. The first attack of meningitis may occur several weeks to 12 years after the head injury. In addition, recurrent bacterial meningitis may be due to disorders of the immune system, such as complement deficiency. We report a 14-year-old boy, who suffered from recurrent Streptococcus pneumoniae meningitis due to a well-defined defect at the ethmoid roof after a head trauma.