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Objective To investigate the risk factors of delayed hemolysis after treatment in patients with malaria .Methods Eighty-nine cases of malaria were retrospectively analyzed .The incidence rate , time from treatment to delayed hemolysis and clinical features of delayed hemolysis after treatment in patients with malaria were investigated .The characteristics of demography ,etiology and laboratory data were compared between delayed hemolysis group and non-delayed hemolysis group .The t test ,χ2 test and Fisher exact test were used for comparison between groups .Results A total of 89 cases of malaria infection were included and 8 cases were diagnosed with delayed hemolysis after treatment among them , with incidence rate of 8 .99% .Patients developed delayed hemolysis after anti-malarial treatment with a median of 7 .5 d and patients recovered from hemolysis after the usage of glucocorticoid with a median of 2 .5 d .The 8 cases were all infected with Plasmodium f alciparum ,and 4 of which had high parasitemia . None of the patients with delayed hemolysis came from epidemic area ,while 28 of the patients without non-delayed hemolysis came from epidemic area .The difference was statistically significant (P=0 .042 , Fisher unilateral exact test) .The average level of minimum hemoglobin was (44 .87 ± 11 .58) g/L in patients with delayed hemolysis ,which was significantly lower than that of non-delayed hemolysis group (108 .35 ± 19 .72) g/L (t= -8 .923 , P< 0 .01) .Conclusion Plasmodium falciparum infection , hyperparasitemia and having no immunity against malaria may be risk factors of delayed hemolysis after treatment .
ABSTRACT
Infectious disease hospitals are obliged to cope with public health emergencies such as outbreak of infectious diseases.Such hospitals are required to make early detection,early containment,proper management,reasonable preplans,timely training,targeted drills,reasonable deployment of hospital resources,appropriate protection for hospital staff.General hospitals should also cope with prevention and control of infectious diseases to some extent,and work with infectious disease hospitals hand in hand to better cope with such outbreaks.
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Objective To obtain the antigen and antibody of JC virus(JCV)VP2.Methods The JCV VP2 gene were amplified from a cerebrospinal fluid sample by polymerase chain reaction (PCR)and confirmed by sequencing.Then,the gene was cloned into plasmid pET32a(+)to construct recombinant prokaryotic expression vector pET-32a(+)-VP2.The recombinant plasmid was transformed into the competent E.coli BL21.Induced with isopropyl-β-D-1-1 thiogalactopyranoside (IPTG),E.coli BL21 were subsequently crushed by ultrasound.The gene expression in the supernatant was analyzed by Western blot.Thereafter,the expressed protein was purified by isoeleetric point method.The polyclonal antibody against JCV VP2 protein was obtained from the BALB/c mouse immunized with the purified protein.Results The VP2 fusion protein was expressed in the E.coli BL21.The recombinant fusion protein was expressed by IPTG induetion with relative molecular mass of 58.5×10~3.Sodium dodecyl sulphate-polyacrylamide gel electrophoresis(SDSPAGE)analysis showed that the expression level was highter after 6-10 h of IPTG induction.The recombinant protein had good antigenicity which was confirmed by BALB/c mice immunized with the protein.Conclusions The successful expression and purification of VP2 fusion protein and the antibody will be valuable for the study on the biological function of VP2 and JCV epidemiologieal investigation.
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Objective To discuss the clinical characteristics and prognosis of 15 children with hand foot and mouth disease (HFMD) and acute flaccid paralysis (AFP) who were admitted to Beijing Ditan Hospital during the outbreak of HFMD in 2008. Method The epidemiology, clinical manifestations, cerebrospinal fluid (CSF),magnetic resonance imaging and prognosis of 15 children with HFMD and AFP were retrospectively reviewed. The recovery of the patients' affected extremities were monitored for 4 weeks. Results The mean age of these patients was (22.47 ± 20.68) months (range: 5～72 months). Acute paralysis developed (3.47 ± 1.68) days after the onset of fever and progressed to maximum severity within (1～2) days. Poliomyelitis-like syndrome was observed in all cases. Of the 15 cases, 10 had monoplegia of lower limbs, two had paraplegia, one had monoplegia of upper limbs and two had quadriplegia. In these cases, the muscle power varied from level 0 to level 4, and six even showed no muscle power in their affected extremities. Thirteen cases developed neurologic complications (encephalitis, meningitis or ataxia) and three had transient urinary retention. Cerebrospinal MRI examination in eight cases showed hyperintense lesions on T2-weighted images, predominantly in the impaired anterior horn regions of the spinal cord (C2～C7 for cases with upper extremity impairments and T12～L1 for cases with lower extremity impairments), and displayed long T1 signals and long T2 signals. In addition, the midbrain, brain-stem or medulla was also involved in four cases who also contracted encephalitis or meningitis. The muscle strength in 11 patients with single lower extremity impairment showed improvements in the distal limb muscles within 4～8 days, and the other cases showed recovery 2～3 weeks later. Conclusions HFMD in combination with AFP most commonly occurs in children aged less than 2 years old. Acute paralysis develops during the early stage of infection and progresses to a maximum severity within 2 days. In most cases described here, paralysis occurred in a single lower extremity and recovered more rapidly than those with all four limbs affected or with single upper extremity impairment . MRI examination is particularly valuable for the diagnosis and prognosis of AFP because of its high sensitivity and accuracy.