Immune compromise

Introduction

Introduction In the past decade or two, with the increase in tumor incidence and treatment progress, the improvement of the diagnosis and treatment of autoimmune and other immune-related diseases, the breakthrough and development of organ transplantation, especially the HIV/AIDS epidemic, immunocompromised host (immunocompromised host) .ICH) Increasing and accumulating has become a huge global challenge. Infection is the most important factor affecting the course and prognosis of ICH. The lung is the main target organ of infection. There are still many problems in the diagnosis and treatment of ICH lung infection, which requires in-depth study. On the other hand, if the existing research results and techniques can be promoted and fully utilized, it is still possible to make the majority of clinical patients diagnose and obtain effective treatment and improve the prognosis.

Cause

Cause

Although ICH has increased susceptibility to infection by various pathogenic microorganisms, there are significant differences in the distribution of pathogens between different types of immune damage. Pulmonary infection in patients with cellular immune damage is dominated by intracellular parasites such as Listeria, Nocardia, Salmonella other than Salmonella typhi, Mycobacterium, Legionella, and fungi, viruses (mainly herpesviruses including cytomegalovirus) ), parasites (Pneumocystis carinii, toxoplasma, faecalis).

Humoral immunodeficiencies include immunoglobulin (Ig) deficiency or hypoxia, reduction of complement, and splenectomy. The pathogens of lung infection are mainly Streptococcus pneumoniae and Haemophilus influenzae. Neutrophil deficiency, especially when it is below 500/mm3, Pseudomonas aeruginosa is the most common pathogen, followed by Escherichia coli, Klebsiella, Serratia, Aeromonas and other G-bacilli, fungi More common. If the barrier damage causes damage to the defense mechanism, the infection is mostly Staphylococcus, Pseudomonas aeruginosa and colonization of adjacent sites.

However, the epidemiology of ICH lung infection pathogens is also restricted by many other factors, such as cell immunosuppression, and the pathogen distribution of different causes or underlying diseases and immune damage varies greatly. In terms of bacterial pneumonia after solid organ transplantation, the incidence of heart-lung combined transplantation was the highest (22.2%), liver transplantation was second (16.7%), single heart transplantation was again (5.2%), and kidney transplantation was the lowest (1.5%). Generally speaking, early bacterial pneumonia in the early stage of transplantation is a multi-line virulence pathogen, such as G-bacteria, Streptococcus pneumoniae, and Staphylococcus aureus, which account for more than 80%. Pneumonia within 3 to 4 weeks after surgery is rarely an opportunistic pathogen. After 6 months, if there are no additional risk factors such as rejection, the need for intensive immunosuppressive therapy, fatal pneumonia and other serious infections are relatively rare, and the pathogens are similar to the community infection of the general population. Solid organ transplantation receptor cytomegalovirus (CMV) infection is more common in the first to fourth months after surgery, while pneumonia peaks in the fourth month; Pneumocystis carinii pneumonia (PCP) mostly occurs after surgery from February to June, not Seen for less than 6 weeks; fungal infections are usually 2 to 3 weeks after surgery, but liver transplant recipients can be as early as week 1. Unlike solid organ transplantation, the bone is associated with early post-transplantation (<1 month = infection is mainly sepsis, and lung infection is relatively rare.

G+ and G-bacillus bacteria and Candida albicans are the main pathogens, and coagulase-negative staphylococci have increased in recent years. In the medium term (January to March), although bacterial and fungal infections still occur, CMV pneumonia is the most common, followed by PCP. Later (>3 months), herpesviruses other than CMV are the most common, but rarely invade the internal organs; The infection is still mainly bacterial, especially Streptococcus pneumoniae and Staphylococcus aureus. It is believed that the humoral immunodeficiency in the late stage of transplantation is mostly systemic due to malignant tumors such as leukemia and lymphoma. Pulmonary infection is also common. However, patients with leukemia are inferior to perineal infections. There is a certain correlation between the pathogens of leukemia and lymphoma without chemotherapy and the type of immune damage. For example, granulocyte leukemia is prone to purulent infection, and lymphoma is prone to tuberculosis and fungal infection. However, this correlation is mostly absent in patients receiving chemotherapy. Before the chemotherapy, more than 1/3 of the infections of granulocytopenia are local infections of sensitive bacteria; if they have been treated with various antibiotics, they may be mostly resistant to Pseudomonas aeruginosa, Klebsiella pneumoniae and fungi, etc. The underlying disease is very serious, and even if antibiotics have not been used, there are more resistant bacteria. Those who received chemotherapy were more likely to have sensitive bacteria in the initial induction stage, such as Staphylococcus and Escherichia coli. Due to repeated application of antibiotics, the infections were mostly resistant to G-bacilli and fungi. The good efficacy of hormones on lymphocytic leukemia and lymphoma will reduce the risk of infection, but long-term use of hormones in the intensive phase can cause PCP, fungi and other opportunistic infections. Failure to achieve remission or disease recurrence, continued chemotherapy under conditions of low white blood cell counts may lead to drug-resistant G-bacilli and fungal sepsis and pneumonia.

In general, no matter whether the whole body or the local infection is mainly bacteria, the proportion of special pathogens such as fungi increases in the lung infection. In autoimmune diseases such as systemic lupus erythematosus, if there is no active infection, G+ bacteria are more common, and active patients involving more than 2 organs are mostly G+ bacilli infection; when hormone and cyclophosphamide treatment further aggravate immunity When inhibited, opportunistic pathogens such as Aspergillus, Nocardia, Cryptococcus neoformans, Pneumocystis carinii, CMV, etc. are increased. It should be emphasized that in China, the rate of tuberculosis infection is high, and tuberculosis stimulation and re-ignition in immunosuppressed patients for any reason is quite common and should be vigilant.

Examine

an examination

Related inspection

Mixed lymphocyte culture test cyclic guanosine monophosphate anti-heat shock protein-60 antibody lung function test lung imaging

1. Pay attention to whether there is inhalation injury, tracheotomy or intubation, aspiration, pulmonary edema, atelectasis, shock, surgical anesthesia, wound invasive infection, suppurative thrombophlebitis.

2. Pay attention to whether there is difficulty in breathing, changes in body temperature, cough, increased sputum and sputum traits. Clinical symptoms should be distinguished from burn toxemia or sepsis.

3. Physical examination: patients with severe burns, burns on the chest, it is difficult to obtain accurate chest signs. Therefore, you should pay attention to check carefully, with or without breathing changes and voices.

4. In order to clear the infected bacteria, the airway secretions should be cultured regularly, preferably for bronchopulmonary lavage fluid to prevent pollution.

5. Chest X-ray examination. The diagnosis of most lung infections after burns depends on X-ray examination. Chest radiographs should be taken routinely after injury and reviewed regularly. X-ray findings of pneumonia can be divided into small lesions, large lesions and large lobe, and small focal pneumonia is the most common.

Diagnosis

Differential diagnosis

Because ICH complicated infection is more critical, empirical antibacterial therapy is started immediately on the premise of making pathogen diagnosis based on clinical and pathogenic epidemiological data, and on the premise of taking various test specimens, especially pathogen specimens. 48 to 72 hours without special effects, special diagnosis should be performed. Fiberoptic bronchoscopy is most useful. If the lesion is localized and near the pleura, percutaneous puncture can also be used. In a few cases, thoracotomy is also necessary, especially diffuse. Lesion. If accurate pathogen diagnosis is still undetermined, it may be modified to treat specific pathogens (Pneumocystis carinii, fungi, tuberculosis, etc.) after more aggressive antibacterial therapy and comprehensive and prudent re-evaluation. Empirical treatment should generally be directed to a single pathogen to avoid confusion.

As a microbiological phenomenon, pneumonia is not fundamentally different from those with healthy immune mechanisms. However, inhibition of host immune inflammatory response can significantly alter the clinical and X-ray manifestations of lung infections, while hormones and other immunosuppressive drugs can interfere with or mask the symptoms and clinical course of infection. To sum up, ICH pneumonia has the following characteristics: 1 Most of the onset is hidden and not easy to detect. However, some patients have acute onset, fulminant, rapid development to extremes, and even respiratory failure. 2 High fever is very common, and sometimes patients continue to receive hormone therapy, which is not enough to be flat. Although G-bacillus pneumonia has high fever, it rarely chills. This is considered to be a very characteristic symptom in immunosuppressive G-bacillus pneumonia. 3 cough and cough are relatively rare. According to the observation of G-bacteria pneumonia in patients with intensive chemotherapy, the incidence of cough symptoms is only 41%, mostly dry cough, and cough is less than 1/5. Chest pain is also uncommon. 4 lesions are mostly bilateral. Signs and signs of consolidation on the X-ray are rare, only about 50%. Especially in patients with granulocytopenia, the inflammatory response in the lungs is mild, and atelectasis can be an early or unique sign of infection. As the granulocytes recover, the inflammatory response worsens and the lesions on the X-ray only increase. 5 Even if the same cell immune damage, the PCP performance of patients with AIDS and non-AIDS immune damage can be very different, compared with the latter, the former has a latent onset and the treatment response is slow, the number of worms is large, and the diagnosis of sputum is easier to find. The clinical treatment effect is not associated with the elimination of the worm, and the recurrence rate is high. The incidence of allergic reactions was high with SMZco, while the side effects of pentamidine treatment were relatively small. 6 The inflammatory response to fungal infections is usually more bacterial than infection.

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