Nocardiosis is a deep pseudomycosis, the causative agent of which causes purulent granulomatous lesion of the lungs, skin and internal organs. The pulmonary form of nocardiosis occurs in the form of bronchopneumonia, empyema of the pleura. With septic nocardiosis, brain abscesses and purulent meningitis usually occur. Nocardiosis of the skin is characterized by the development of pyoderma, abscesses of the skin and subcutaneous tissue, non-healing fistulas. Laboratory diagnostics includes examination of the material (sputum, bronchial flushes, exudate, pus, cerebrospinal fluid, blood, urine, biopsies) by microscopy, culture media, PCR. With nocardiosis, therapy with sulfonamide preparations and antibiotics is carried out; drainage or removal of abscesses is performed.
ICD 10
A43 Nocardiosis
General information
Nocardiosis (proactinomycosis, false tuberculosis) is a systemic infection caused by Nocardia microorganisms and occurring with damage to the respiratory organs, skin, and central nervous system. Previously, disease was attributed to fungal diseases, identifying it with streptotrichosis and cladotrichosis; currently, views on the nature of infection have undergone significant changes. 1500-2000 new cases of nocardiosis are diagnosed annually in the world, more than half of which occur in patients with immunodeficiency. The disease usually affects the adult population, men are 2 times more likely than women. Nocardiosis can occur in pulmonary, septic (generalized) and cutaneous forms.
Causes
Nocardia – microorganisms that cause nocardiosis occupy an intermediate position between fungi and bacteria. According to their microbiological properties, they are classified as facultative anaerobic gram-positive bacteria. When cultivated on nutrient media, nocardia form a thin mycelium, which later decomposes into rod-shaped and coccoid elements. In human tissues, the pathogen has the form of branched filaments of mycelium. The causative agents of human nocardiosis are most often N. asteroides, N. caviae and N. brasiliensis.
The habitat of nocardia in nature is soil and decomposing organic residues. A person can become infected with nocardiosis aerogenically (by inhalation of pathogens with dust particles), by contact (when skin wounds are contaminated with contaminated earth), less often by alimentary (when bacteria enter the damaged gastrointestinal mucosa with food). Improper care of soft contact lenses may be a possible cause of nocardial eye lesions. Susceptibility to infection is increased in persons with insufficient immunity (HIV-infected, recipients of internal organs and bone marrow, patients with lymphogranulomatosis, lymphomas and leukemias treated with corticosteroids, etc.), patients with lung cancer, tuberculosis, granulomatosis, pulmonary alveolar proteinosis, Cushing’s syndrome.
When ingested by inhalation, the causative agent is absorbed by alveolar macrophages, which causes the formation of a primary pulmonary focus in the form of multiple drainage microabsesses. In immunodeficient individuals with reduced functional activity of T-lymphocytes, there is a hematogenic spread of the pathogen and generalization of nocardiosis with the formation of multiple abscesses and granulomas in the heart, liver, spleen, lymph nodes, brain. When nocardia penetrates through the injured skin, infiltrates form at the entrance gate; then the purulent inflammation spreads to nearby tissues.
Symptoms
There are five forms of nocardiosis: pulmonary, systemic (involving 2 or more organs), extrapulmonary, cutaneous and central nervous system nocardiosis. In clinical practice, another classification is more often used, which distinguishes pulmonary, septic (generalized) and cutaneous nocardiosis. Nocardia can be the causative agents of actinomycotic mycetoma of the “Madura foot” type (actinomycetoma) – a disease mainly common in subtropical and tropical countries (Africa, Central and South America, India).
The main clinical form of infection is pulmonary nocardiosis, occurring in the form of abscessing pneumonia or necrotic pneumonitis. The gradual development of symptoms is characteristic: an increase in weakness and pain in the chest area, increased sweating at night, the occurrence of subfebrility and dry cough. At the height of the disease, the body temperature rises to 39-40 ° C, the cough becomes productive, with the separation of purulent sputum. X-ray examination of the lungs reveals focal or drainage changes in the lungs, involving several segments, pleural effusion, enlargement of the lymph nodes of the lung root. With the spread of purulent inflammation to nearby anatomical structures, pleural empyema, mediastinitis, pericarditis, chest wall abscesses may develop. Differential diagnosis of pulmonary nocardiosis should be carried out with tuberculosis, bacterial pneumonia and lung abscess, histoplasmosis, lung tumors.
In about a third of patients with pulmonary nocardiosis, the disease progresses into a generalized (septic) form. In most cases, metastatic purulent foci are found in the brain (brain abscess, purulent meningitis). Secondary nocardial foci may also occur in the bones (osteomyelitis), joints (purulent arthritis), kidneys (pyelonephritis), heart (pericarditis and endocarditis), eyes (keratitis, endophthalmitis), spleen and liver (abdominal abscesses). Septic nocardiosis usually develops in people with immunodeficiency and ends fatally.
The cutaneous form often occurs on the skin of the foot, where deep infiltrates, panniculitis, skin ulceration, long-term non-healing fistulas are formed. The suppurative process can capture subcutaneous tissue, muscles, bones, lymph nodes (lymphocutaneous nocardiosis). Nocardial skin lesions can be mistaken for cat scratch disease, actinomycosis, skin tuberculosis.
Diagnosis and treatment
Confirmation of the diagnosis is possible by comparing the clinical picture of nocardiosis with laboratory and instrumental data. In the pulmonary form, lung radiography reveals a picture of draining bronchopneumonia with decay cavities. In the disseminated form, CT and MRI reveal intracerebral abscesses and secondary purulent foci in the internal organs.
Isolation of the causative agent of nocardiosis from clinical material (sputum, bronchial flushes, exudate, blood, urine, pus, cerebrospinal fluid, biopsies) is performed using microscopy, bacteriological seeding, PCR. Additionally, serological studies (reaction of agglutination, precipitation, complement binding), skin allergic tests can be used.
Treatment should include prolonged chemotherapy and surgical drainage of purulent foci. For etiotropic chemotherapy of nocardiosis, sulfonamide preparations are used (sulfadimidine, sulfadiazine – for several months), sulfamethoxazole + trimethoprim, antibiotics (imipenem, amikacin, cefotaxime, ceftriaxone, tetracyclines – a course of 4-6 weeks). With nocardiosis, the question of drainage of the pleural cavity, surgical treatment of brain abscesses, opening of soft tissue abscesses, etc. may arise.
In pulmonary nocardiosis, the mortality rate is about 10%, in the septic form of infection – 50%. The isolated cutaneous form of nocardiosis is benign. Immunoprophylaxis of nocardiosis has not been developed. Preventing skin injuries, wearing protective clothing and shoes in contact with the ground, and increasing immune reactivity allows you to avoid infection with pathogenic microorganisms.
