Pneumocystis carinii pneumonia

Introduction to Pneumocystis carinii Pneumocystis cariniipneumonia pneumonia (Pneumocystis cariniipneumonia PCP), also known as Pneumocystis carinii pneumonia, also known as interstitial plasma cell pneumonia, is a rare form of pneumonia, mainly in children with low immunity. At present, the preferred drug is trimethoprim (TMP) 20mg / (kg · d) plus sulfamethoxazole (SMZ) 100mg / (kg · d), divided into 2 times, even for 2 weeks, the efficacy and Pentane oxime is similar, but the adverse side effects are far less common, manifested as skin allergies and gastrointestinal reactions. It also advocates SMZCo100mg/(kg·d) for 2 weeks, then reduces it to half amount for another two weeks, then reduces it to 1/4 amount for 2 months, and the effective rate is 75%. This medicine can be used as a chemopreventive agent in application. Prevention of this disease in high-risk children with immunosuppressive agents, the dose is TMP5mg / (kg · d) and SMZ 25mg / (kg · d), are divided into 2 oral or weekly for 3 days, stop for 4 days, use 6 Months. basic knowledge The proportion of illness: 0.002% Susceptible people: good for children Mode of infection: droplet spread Complications: spontaneous pneumothorax Acute respiratory distress syndrome

Causes of Pneumocystis carinii pneumonia

The pathogen is Pneumocystis carinii, trophozoites and cysts, mainly in the lungs. It was thought to belong to the protozoa in the past. Recently, some scholars have analyzed the ultrastructure and the development of the ribosomal RNA of Pneumocystis: In the fungi, the main path of infection of PCP is airborne and in vivo activity in the activation of Pneumocystis carinii. Host response to verification and immune response including alveolar macrophages phagocytosis of Pneumocystis carinii, peribronchial and vascular areas Lymphocyte infiltration, type II alveolar cell proliferation, local and systemic antibody increase.

In 1951, Vanek first reported that such Pneumocystis carinii was found in cases of premature infantile interstitial plasma cell pneumonia. Due to the widespread use of immunosuppressive agents in recent decades and chemotherapy for patients with malignant tumors, the disease is more More common, especially after the emergence of acquired immunodeficiency disease (AIDS) in the past 10 years, PCP has received more attention. According to the US CDC data, 1200 children with AIDS were reported from 1981 to 1990, the most common and most serious opportunity. The infection is PCP, the incidence rate is 39%, and in adult AIDS patients up to 80%, Pneumocystis carinii is mainly seen in five patients:

1 premature baby and newborn.

2 children with congenital immune defects or secondary immunocompromised.

3 malignant tumors such as leukemia, lymphoma patients.

4 Organ transplantation for children treated with immunosuppressive agents.

5 AIDS children as early as the 1950s, a small number of PCP cases were found in Beijing. In the 1980s, Beijing Children's Hospital reported that 16 cases of PCP occurred in the remission period of children with leukemia. PCP occurred and T-lymph was confirmed according to animal models and patient observations. The relationship between cellular immune function and low is closely related. At present, it is considered that the risk of PCP is very high when CD4 (helper T cell) count is 200/mm3, but this standard is not applicable to children who are especially younger than 1 year old.

Pneumocystis carinii pneumonia prevention

Close attention should be paid to high-risk groups. Note the isolation of immunosuppressors from patients to prevent cross-infection. For patients with a risk of developing K. cerevisiae, drug prevention can effectively prevent potential infections from turning into clinical diseases and recurrence after treatment. Spraying inhalation can be used as a second-line prophylaxis.

Pneumocystis carinii pneumonia complications Complications spontaneous pneumothorax acute respiratory distress syndrome

The complications of Pneumocystis carinii pneumonia are increasing, such as cystic lesions of the lungs, spontaneous pneumothorax, consolidation of the upper lobe, etc., and their performance changes rapidly and diversely. If they are not properly treated, they can rapidly develop into acute respiration. Distress syndrome.

Pneumocystis carinii pneumonia symptoms common symptoms irritability, difficulty breathing, weight loss, diarrhea, low fever, purpura, chest dry cough

The naked eye is widely affected by extensive invasion. The texture and color, such as the liver, the foamy substance in the alveolar and bronchioles, is a mixture of necrotic and immunoglobulin. The alveolar space is interspersed with plasma cells and lymphocytes, resulting in increased alveolar septa. Thick, up to 5 to 20 times normal, occupying 3/4 of the entire lung volume, the cyst begins to be located in the alveolar septal macrophage cytoplasm, and then the encapsulated alveolar cells fall off into the alveolar space; or in the capsule The sporozoites proliferate and mature. After the cyst wall breaks, the sporozoites are discharged into free trophozoites into the alveolar space. There are plasma cells, lymphocytes and tissue cells in the alveolar exudates.

1, symptoms and signs can be divided into two types:

1 Infant type: mainly occurs in small infants from 1 to 6 months. It is an interstitial plasma cell pneumonia. The onset is slow. The main symptoms are poor feeding, irritability, cough, respiratory rate and purpura, but fever is not significant. There is not much Luoyin during auscultation. The difficulty of breathing is gradually worsened within 1~2 weeks. The lung signs are less than the serious disproportionate symptoms of respiratory distress. It is one of the characteristics of this disease. The course of disease is 4-6 weeks. If it is not treated, it is about 25%. ~50% of children died.

2Children's type: mainly occurs in children with low immune function caused by various reasons. The onset is rapid. Unlike other infants, almost all patients have fever. In addition, common symptoms are accelerated breathing, cough, sable, three concave, and nose. Fans and diarrhea, the course of disease develops rapidly, and more deaths when not treated.

2, X-ray examination showed diffuse granular shadows on both sides, stretching from the hilum to the surrounding, showing a frosted glass, with a bronchial inflatable image, which later became a dense cord, with irregular patchy shadows, and lasting Emphysema, more prominent around the lungs, may be associated with mediastinal emphysema and pneumothorax.

Examination of Pneumocystis carinii pneumonia

The white blood cell count was normal or slightly higher. In about half of the cases, lymphocytes decreased, and eosinophils increased slightly. Blood gas analysis showed significant hypoxemia and alveolar arterial oxygen pressure difference, and pulmonary function tests showed progressive decline.

Relying on the self-tracheal aspirate or lung biopsy section staining, the agglomerates of foamy eosinophils in the alveoli are rich in protozoa, and stained with silver nitrate of urotropine, a dark brown circle or ellipse with a diameter of 6-8 m can be found. The shape of the capsule is located outside the cell. In recent years, high-intensity saline inhalation has been used to increase the detection rate of pathogens. The rate of cysticercosis has reached 90% in bronchoalveolar lavage and bronchopulmonary biopsy. The cysticercosis method has Toluidine. Blue, cyclohexamethylene silver, Grdm-wright, Grimss and immunofluorescent antibody staining, etc. In recent years, ELISA has been used to detect Pneumocystis IgG antibodies and latex particle agglutination test for cysticercosis antigens, or molecular biology techniques such as PcR Make a quick early diagnosis.

Diagnosis and identification of Pneumocystis carinii

For malnutrition, low immune function, long-term use of glucocorticoids, tumor chemotherapy, organ transplantation and AIDS, such as low fever, diarrhea, weight loss, followed by dry cough, difficulty breathing, X-ray chest radiographs have typical changes, pay attention to PCP, Respiratory secretion, fiberoptic bronchoscopy specimens or even lung biopsy pathogen examinations are helpful for diagnosis.

Relying on the self-tracheal aspirate or lung biopsy section staining, the agglomerates of foamy eosinophils in the alveoli are rich in protozoa, and stained with silver nitrate of urotropine, a dark brown circle or ellipse with a diameter of 6-8 m can be found. The shape of the capsule is located outside the cell. In recent years, high-intensity saline inhalation has been used to increase the detection rate of pathogens. The rate of cysticercosis has reached 90% in bronchoalveolar lavage and bronchopulmonary biopsy. The cysticercosis method has Toluidine. Blue, cyclohexamethylene silver, Grdm-wright, Grimss and immunofluorescent antibody staining, etc. In recent years, ELISA has been used to detect Pneumocystis IgG antibodies and latex particle agglutination test for cysticercosis antigens, or molecular biology techniques such as PcR Make a quick early diagnosis.

The disease needs to be differentiated from bacterial pneumonia, viral pneumonia, fungal pneumonia, ARDS and lymphocytic interstitial pneumonia (LIP), especially in which LIP and this disease are more likely to occur in children with AIDS, but LIP is mostly chronic, mainly cough and dry rales, with enlarged lymph nodes and enlarged salivary glands. EBV-DNA1 can be detected in lung biopsy specimens, but PCP cannot be detected.

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