2016年 · 第54卷第02期

Mycoplasma pneumoniae (Mycoplasma pneumoniae,MP), a clinically common pathogenic microorganism belonging to the genus Mycoplasma (Mycoplasma), Mycoplasmaceae (Mycoplasmaaceae), Mycoplasma (Mycoplamatales), finally classified into the class of flexible membranes (Mollicutes)。 Mycoplasma is a class of cell-wallless, pleomorphic microorganisms that cannot be found by sterilizing filters or conventional Gram staining. It is also the smallest prokaryotic microorganism known to grow and reproduce on inanimate medium. In 1898, Nocard successfully isolated this microorganism from cattle with lung disease for the first time, named it pleuropneumonia microorganism (PPO), then renamed it pleuropneumonia-like microorganism (PPLO), and then the so-called Eaton virus. Human understanding of MP has experienced twists and turns for more than 60 years. It was not until 1962 that Chanock used cell-free medium to isolate the microorganism from the sputum of patients with SARS that it was identified as a non-viral living organism and named it Mycoplasma pneumoniae^[1]。

Mycoplasma pneumoniae (Mycoplasma pneumoniae,MP) infection has a wide range of clinical involvement, and there are many different views on some doubtful and confusing questions. At present, several hot issues that clinicians are interested in are discussed in depth.

The study of mycoplasma began when humans explored the pathogen of infectious diseases in livestock. In 1898, Nocard and Roux in France used artificial medium containing animal serum to isolate it from the lesions suffering from bovine pneumonia for the first time. At that time, it was named pleuropneumonia organism (PPO). Subsequently, the same microorganisms were isolated from different types of animal specimens in various regions. Because of the morphology and culture characteristics similar to PPO, they were collectively called pleuopneumonia-like organisms (PPLO). Over the next 50 years, evidence has grown that PPLO is associated with many animal diseases and may cause disease in humans. With the development of nucleotide determination and DNA hybridization technology, it is finally realized that PPLO is indeed a unique life form, which lacks the ability to form cell walls in all environments, and is completely different from bacterial L-form. It was officially named Mycoplasma in 1956 (Mycoplasma), and established an independent new class in the microbial taxonomy, Phyllomembranaceae (Mollicutes)。 At present, there are five kinds of mycoplasmas that have proven pathogenic effects on humans, including Mycoplasma pneumoniae, Ureaplasma, Mycoplasma hominis, Mycoplasma genitalium and Mycoplasma fermentum (Table 1)^[1]。

Mycoplasma pneumoniae (Mycoplasma pneumoniae(MP) infection is a global infectious disease that affects different tissues and organs in children of all age groups, with respiratory tract infections being the most common. MP respiratory tract infection has certain infectivity, and patients are the main source of infection. It spreads through the respiratory tract through droplets, and people of all ages are generally susceptible to it. This article summarizes the epidemiological characteristics of MP infection.

Mycoplasma pneumoniae (Mycoplasma pneumoniaeThe pathogenic mechanism of MP) infection has not been completely defined, and the amount of initially infected MP bacteria, the immune status of the host, and the distribution of normal respiratory flora may affect the progression of MP infection^[1]。 At present, it is believed that MP can cause direct damage to respiratory epithelium through adhesion and cytotoxicity, and can also cause pneumonia and other system damage through immune mechanism^[2]。 The main pathogenic mechanisms of MP infection are presented.

Mycoplasma pneumoniae (Mycoplasma pneumoniaeThe clinical manifestations of MP) infection are diverse. Infections can occur both in the upper and lower respiratory tracts and lungs, and can also involve the extrapulmonary system. The clinical symptoms of MP infection are not characteristic, and the severity of the disease varies greatly, which may be life-threatening or lead to serious sequelae, while some patients can self-relieve. Clinicians need to raise awareness of this disease.

Off-label use of drugs refers to the application of drugs beyond the scope of the drug instructions provided by manufacturers approved by the national drug regulatory authorities, including beyond the applicable age, dosage, dosage form, route of administration or indication, etc. However, "off-label use" does not mean irrational use, illegal use or experimental use of drugs^[1], usually after extensive clinical observation and supported by literature and evidence-based medical evidence. In the field of pediatrics, off-label medication faces certain risks and legal problems.

A 7-year-old and 11-month-old child came to the neurology clinic of Beijing Children's Hospital in December 2013 because she was "unwilling to talk and communicate with others for 2 weeks". Two weeks before seeing the doctor, the child was unwilling to talk without obvious inducement, and he could take the initiative to talk about things he was interested in, but it was significantly reduced compared with before. He did not communicate with others, accompanied by laughter, and often talked to himself. Good limbs movement, steady walking, no obvious posture abnormalities and dysphagia, choking and coughing after drinking water, normal diet, reduced sleep, and no abnormalities in urine and defecation. There was no history of fever, poisoning and vaccination in the past 1 month. The child was the first birth, the first birth, the full-term natural birth, the mother's pregnancy period was normal, the birth weight was 3.3 kg, the perinatal hypoxia and asphyxia were denied, and the developmental milestone was normal. Two years ago, the parents found that the child's reaction was slower than that of children of the same age, and the attention test in other hospitals was severe abnormal, and the IQ test was 66~74. No treatment was given. Family history denied. Physical examination: clear consciousness, cooperation with physical examination, normal development, moderate nutrition, no abnormalities in hair and skin, no deformities in face and head, little eye contact, no nystagmus, and normal hearing on rough test. Medical examination showed no abnormalities. The muscle strength and tone of the limbs were normal, the sensory system was not abnormal, the tendon reflex was normal, the pathological signs were negative, and the physical examination of co-taxic exercise was not abnormal.

The child was a male, 3 years and 4 months old. He was admitted to hospital in April 2015 due to "fever for 5 days with rash and yellowing skin for 3 days". Five days before admission, the child had fever, the maximum body temperature was 40 ℃, and red maculopapular rash was scattered all over the body, and the rash was mild itching. Skin yellowing appeared 3 days ago, gradually aggravated, accompanied by irritability. For 2 days, the stool was clay-like, and the urine was dark yellow. No cough, expectoration, abdominal pain, abdominal distension. Out-of-hospital anti-infective treatment did not improve for 1 day, and he was admitted to our hospital for treatment. Poor spirit, sleep and appetite since the onset of the disease. Formerly healthy.

Kawasaki disease is an acute febrile and eruptive disease with systemic vasculitis as the main lesion, which is characterized by extensive inflammation of small and medium vessels, with the most serious damage to cardiovascular system. Damage and dysfunction of vascular endothelial cells are the initial links of vasculitis. Inflammatory immune injury of vascular endothelial cells mainly refers to the expression and release of adhesion molecules such as intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), E-selectin, P-selectin, L-selectin, and cell adhesion molecules related to carcinoembryonic antigen by endothelial cells under the action of a series of stimulating factors. The above adhesion molecules cause circulating monocytes and neutrophils to adhere to the surface of endothelial cells, and then enter the cell inner membrane, and activate complement binding to damage endothelial cells. In this paper, the mechanism of immune damage of vascular endothelial cells in Kawasaki disease was reviewed from the aspects of cytokines and immune signaling pathways.

Pediatric clinical research increasingly emphasizes ethical management, and research topics must be reviewed and approved by the ethics committee before they can be applied for project establishment and organization. So what does the ethics committee do, and why does clinical research need the supervision of the ethics committee?