Pediatric Cryptosporidium parvum Pneumonia

　　1. Etiology

　　The pathogen is Pneumocystis carinii, which exists in the form of trophozoites and cysts, mainly in the lungs. It was previously considered a protozoan, but recent studies have found that the DNA of Pneumocystis carinii is homologous to that of fungi. Based on its ultrastructure and the analysis of the phylogenetic development of the ribosomal RNA of Pneumocystis, it is considered a fungus. However, its morphology and drug sensitivity are similar to those of protozoa. The disease is transmitted through air and droplets. Although Pneumocystis carinii is widely infected in humans and animals, only a few parasites usually寄生 in the alveoli (latent infection). When infected with immunodeficient children, such as weak infants, congenital immunodeficiency, and children receiving immunosuppressive drug treatment, they begin to rapidly proliferate and cause pneumonia. If the air in the nursery is contaminated with Pneumocystis carinii, it can cause cross-infection among newborns and lead to an outbreak. Older children and adults are mostly patients who receive a large amount of long-term hormone therapy, chemotherapy for malignant tumors (leukemia, lymphoma), or patients who receive immunosuppressive drug therapy after organ transplantation.

　　2. Pathogenesis

　　Two forms of Pneumocystis carinii can be seen in the alveolar cavity: one is a vesicle with a diameter of 5-8 nm, containing 8 polymorphic intravesicular sporozoites; the other form is the extravesicular trophozoite, which is the sporozoite after egressing from the vesicle. Pneumocystis carinii attaches to type I alveolar cells with fibronectin. Alveolar macrophages phagocytize and kill Pneumocystis carinii, releasing tumor necrosis factor. Pneumocystis carinii pneumonia has two histopathological types: one is infantile interstitial plasma cell pneumonia, which can be seen in weak infants aged 3 to 6 months, sometimes in an outbreak. There is extensive thickening of the alveolar septum, mainly with plasma cell infiltration. The other type is more common in children with immune injury, being a diffuse desquamative alveolitis. The alveoli contain a large number of Pneumocystis carinii, and alveolar macrophages show foamy changes. The infiltration of the alveolar septum is different from the infantile type, usually without plasma cell infiltration.

　　The complications of Pneumocystis carinii pneumonia are increasing, such as lung cystic lesions, spontaneous pneumothorax, upper lobe consolidation, etc. The manifestations change rapidly and are diverse. Without proper treatment, it can rapidly develop into acute respiratory distress syndrome. Acute respiratory distress syndrome refers to an acute respiratory failure syndrome characterized by progressive respiratory distress and refractory hypoxemia, based on diffuse lung capillary injury and increased permeability, with pulmonary edema, hyaline membrane formation, and atelectasis as the main pathological changes, caused by severe lung and extrapulmonary diseases.

　　Section 1: Symptoms and signs

　　It can be divided into two types

　　1. Infantile type

　　It mainly occurs in infants aged 1 to 6 months and belongs to interstitial plasma cell pneumonia. The onset is gradual, and the main symptoms are poor feeding, restlessness, cough, increased respiratory rate, and cyanosis, while fever is not significant. There are few rales on auscultation. The respiratory distress gradually worsens within 1 to 2 weeks, with few pulmonary signs and not proportional to the severity of respiratory distress symptoms, which is one of the characteristics of the disease. The course of the disease is 4 to 6 weeks, and about 25% to 50% of children will die without treatment.

　　2. Pediatric type

　　It mainly occurs in individuals with weakened immune function due to various causes, with an acute onset. Unlike the infantile type, almost all patients have fever, in addition, common symptoms include accelerated breathing, cough, cyanosis, tracheal retraction, nasal flaring, and diarrhea. The course of the disease develops rapidly, and most patients die without treatment.

　　Section 2: X-ray examination

　　Diffuse granular shadows in both lungs can be seen, extending from the hilum to the periphery, appearing like frosted glass, accompanied by bronchial emphysema. Later, they become dense string-like, interspersed with irregular patchy shadows. In the later stage, there is persistent emphysema, more pronounced in the peripheral part of the lung, which may be accompanied by mediastinal emphysema and pneumothorax.

　　The prevention of PCP with SMZ-TMP has been successful. Harris et al. treated 229 high-risk pediatric tumor patients with PCP, with SMZ-TMP 20-4mg/(kg·d) orally, starting the medication for the prevention of CNST (on the 28th day) and maintaining it for at least 1 year; for ANLL or solid tumor patients, the medication was administered simultaneously with the start of chemotherapy, and none of the patients developed PCP. However, 10 high-risk patients were not given prophylactic medication, and 5 of them developed PCP, indicating that this dose of prophylaxis is reliable. The Department of Pediatrics of the 301st Hospital improved its understanding of this disease after the occurrence of PCP in children with leukemia and formulated a prophylactic program in 1988, which involved giving SMZco 20mg/(kg·d) orally in two doses, three days a week for three days and then stopping for four days. Subsequently, only one high-risk child with a predisposition to PCP developed the disease, and this child was the one who did not consistently take SMZco, indicating that the 3-day continuous therapy can achieve the same prophylactic effect, which will not increase the infection rate of other pathogens or side effects, and can greatly reduce the incidence of systemic fungal infections in patients. For patients who have completely recovered from PCP, prophylactic measures must still be taken, otherwise, re-infection may occur. In adults, for patients who cannot tolerate TMPSMZ, alternative medications include pentamidine, clindamycin/pyrimethamine; sulfaquinoxaline alone or in combination with TMP and pyrimethamine is widely used in patients with AIDS or those who have undergone transplantation; pyrimethamine combined with sulfadoxine has been successfully used for the prevention of Pneumocystis carinii pneumonia.

　　1. Blood routine examination

　　The blood routine shows normal or slightly elevated white blood cell count, with an increase in neutrophils, about half of the cases with a decrease in lymphocytes, and a slight increase in eosinophils.

　　2. Other

　　Blood gas analysis shows significant hypoxemia and increased alveolar-arterial oxygen pressure difference, NBT test is positive, the etiological examination of sputum and tracheal aspirate smears is mostly negative, chest X-ray films show early reticulate, flocculent, and string-like blurred shadows around the hilum, with the progression of the disease, small patchy blurred shadows and nodular shadows appear, which can also merge into larger patchy shadows. Nodular shadows are often multiple, and pulmonary lesions generally develop from the hilum along the bronchi to the periphery of the lungs. The lungs at the top and bottom are rarely involved or involved lightly, which is a characteristic of the disease. If the lesions are close to the pleura, they can cause local mild reactive pleural thickening, and pleural effusion usually does not occur.

　　1. Avoid high-protein diets

　　The main component of lean meat, fish, and eggs is protein.

　　2. Avoid foods high in sugars

　　Sugars are a heat supplement substance with a simple function and basically do not contain other nutrients. If children with infantile pneumonia consume too much sugar, the bactericidal effect of white blood cells in the body will be suppressed. The more sugar consumed, the more obvious the suppression will be, and the illness will worsen.

　　3. Avoid spicy foods

　　Spicy foods are stimulating and easily transform into heat, damaging the body's fluids. Therefore, children with infantile pneumonia should not add chili oil, pepper, and other spicy seasonings to their diet.

　　4. Avoid greasy and heavy foods

　　Children with infantile pneumonia often have low digestive function. If they eat greasy and heavy foods, it will further affect their digestion. Necessary nutrition will not be supplemented in time, leading to a decrease in resistance and exacerbation of the illness.

　　5. Avoid cold and raw foods

　　Overeating cold foods such as watermelons, ice cream, frozen fruit juices, ice lollies, popsicles, cold drinks, bananas, and unripe pears can easily disrupt the body's yang energy. If the yang energy is damaged, it will be weak in resisting pathogens, and the illness will be difficult to heal. Therefore, these foods should be avoided, especially for children with gastrointestinal symptoms.

　　6. Avoid drinking tea

　　Children with infantile pneumonia often have fever, and they should avoid drinking tea. Tannins in tea have astringent effects, and traditional Chinese medicine believes that it is not conducive to the external dispersion of evil qi on the body surface, which is also not suitable for feverish children.

　　7. Avoid taking cooling herbs randomly

　　Herbal remedies such as Jinyincha, Qingguo, and Banlangen decoction are beneficial for children with infantile pneumonia. However, they should not be taken for a long period of time, especially for those with weak constitutions. Otherwise, it may harm the body's vital energy and exacerbate the original symptoms.

　　8. Avoid using acidic drugs and foods

　　Schisandra, black plum, vitamin C, sour fruits, oranges, vinegar, etc., are sour in taste, can contract, and hinder sweating and relieve the exterior.

　　9. Avoid the abuse of antipyretics

　　Using excessive antipyretics as soon as fever occurs is not only harmful to the body but may also conceal the condition, delaying treatment. Therefore, antipyretics should be used with caution in children with fever, and it is forbidden to use too much medication to prevent a sudden drop in body temperature, profuse sweating, and collapse.

　　1. Treatment

　　Perform pathogen treatment. The first-line drug is trimethoprim (TMP) 20mg/(kg·d) plus sulfamethoxazole (SMX) 100mg/(kg·d), taken twice a day, for 2 weeks, with efficacy similar to pentamidine (pentamidine), but with far fewer adverse side effects, mainly skin allergies and gastrointestinal reactions. Some also advocate using sulfamethoxazole (SMX) 100mg/(kg·d) for 2 weeks, then reduced to half the dose and used for another 2 weeks, and finally reduced to 1/4 the dose and used continuously for 2 months, with an efficacy rate of up to 75%. This drug can be used for chemoprophylaxis in high-risk children receiving immunosuppressive drugs, with a dose of trimethoprim (TMP) 5mg/(kg·d) and sulfamethoxazole (SMX) 25mg/(kg·d), both taken twice a day or administered continuously for 3 days a week, with a 4-day break, for 6 months. Supportive therapy includes the use of human blood gamma globulin to enhance immunity. Oxygen therapy may be necessary if needed. If this disease occurs during the use of adrenal cortical hormones, the dose should be reduced or the medication discontinued. To prevent cross-infection in high-risk children, it is recently recommended to practice respiratory isolation until the end of treatment.

　　2. Prognosis

　　Poor prognosis. This disease has a mortality rate of about 50% with isolated supportive therapy (such as oxygen therapy, antibiotics, blood transfusion, good nursing care, etc.). The mortality rate of immunodeficient individuals is almost 100%. Foreign reports indicate a mortality rate of 10% to 50%, with an average of about 40%. However, it is believed that with timely and active treatment, the cure rate can reach as high as 70%. The cause of death is insufficient pulmonary and cardiac function. After the application of specific chemical therapy in 1958, the prognosis has improved, and the mortality rate has decreased from 50% to 2.3% to 3.5%. After treatment, the lesions are usually resolved in the short term without leaving scars, but some patients may have residual pulmonary fibrosis.