|Year : 2022 | Volume
| Issue : 2 | Page : 122-126
Pulmonary nocardiosis: A case presentation
Hilda Mercy Priyadarsini1, Thilagavathi2, Mary Jancy Joy1
1 Assistant Professor, College of Nursing, Christian Medical College, Vellore, Tamill Nadu, India
2 Charge Nurse, Christian Medical College, Vellore, Tamill Nadu, India
|Date of Submission||01-Dec-2021|
|Date of Decision||20-Oct-2022|
|Date of Acceptance||04-Nov-2022|
|Date of Web Publication||24-Jan-2023|
Mrs. Hilda Mercy Priyadarsini
College of Nursing, Christian Medical College, Vellore, Tamil Nadu
Source of Support: None, Conflict of Interest: None
Nocardiosis is a rare, Gram-positive bacterial infection caused by aerobic actinomycetes in the genus Nocardia. Nocardia species are not the part of normal human flora. Although the occurrence of Nocardiosis is predominant in immunosuppressed individuals, it has not failed to affect immunocompetent individuals. The organ that is most commonly affected is the lung but if left undiagnosed or untreated the infection can spread to other vital organs such as the brain and spinal cord and result in significant mortality. A thorough knowledge and a quick assessment skill are necessary to care for patients affected with such deadly diseases. The aetiology, risk factors, clinical manifestations, diagnosis and medical and nursing management of patients affected with Nocardiosis are discussed using a case study approach.
Keywords: Immunocompetent individuals, immunosuppressed, nocardiosis
|How to cite this article:|
Priyadarsini HM, Thilagavathi, Joy MJ. Pulmonary nocardiosis: A case presentation. Indian J Cont Nsg Edn 2022;23:122-6
| Introduction|| |
Nocardia are thin, Gram-positive, weak, acid-fast, aerobic, branching, filamentous, slow-growing bacteria, found in soil, decaying vegetable matter and aquatic environments and dust particles.,, Nocardiosis was initially named after the French microbiologist, Edmond Nocard in 1888. Nocardiosis occurs worldwide and it is currently considered the global health problem due to the rapid increase in the number of cases detected.,,,,,,, National Organization for Rare Diseases is accepted reports about 500–1000 new cases of Nocardiosis each year in the USA, whereas the global incidence is well known. Males are reported to be more affected than females. Around 54 species of Nocardia are reported to cause infections in humans and known to gain entry into the human body through various routes such as:
- Inhalation – Airborne transmission (predominant)
- Ingestion of contaminated food
- Direct inoculation of the organism through traumatised sites
- Use of unlicensed cosmetic injections (Nocardia cyriacigeorgica) causing cutaneous disease
- Haematogenous dissemination causing bacteraemia
- Nosocomial transmission through articles contaminated with these organisms.
The organisms can affect any part of the body but the most common site of infection is the lungs. If left untreated, it can spread to other parts of the body including the brain and spinal cord. Nocardia species result in rapid progression of the disease due to its ability to overcome the immune response of the host through suppression of phagocytosis and through resistance to human neutrophils. Early diagnosis and appropriate interventions may help in reducing the severity and improving the quality of life of patients. The risk for death is much higher for patients with compromised immune systems with more than 85% of death after developing Nocardiosis of the brain or spinal cord. Hence, it is important that the health-care team is equipped with adequate knowledge regarding the modes of transmission, specific assessment skills and management strategies in dealing with patients affected with this deadly organism.
Some common risk factors are:
- Deficient cell-mediated immunity such as persons with organ transplantation
- Malignancy and inflammatory bowel disease
- Diabetes mellitus
- AIDS, autoimmune diseases, chronic granulomatous disease, structural lung disease, chronic obstructive pulmonary disease and tuberculosis
- Prolonged corticosteroid therapy
- Hospitalisation – Nosocomial infections.
The clinical manifestations present as pulmonary, central nervous or cutaneous problems.
Chest pain, cough, bloody sputum, sweats, chills, weakness, lack of appetite, weight loss and laboured breathing are the pulmonary manifestations reported by most patients. Individuals can also have complaints of central nervous system (CNS) symptoms which include headache, weakness, confusion and seizures. Severe disseminated disease may present with signs of septicaemia as a result of infection from skin ulcers and nodes.
Clinical manifestations vary based on the site of infection. Pulmonary Nocardiosis is clinically determined with the findings of inflammatory bronchial mass or pneumonia with fever, productive cough, dyspnoea or chest pain.
Other diagnostic procedures include;
- Isolation and identification of the organism from clinical specimens (e.g. sputum, the sample from bronchoalveolar lavage, blood, skin or abscess aspirates) depending on the system involved
- Gram staining/modified acid-fast staining, culture and histopathological studies
- Histopathology: Tissue specimens show necrosis, abscess formation, mixed cellular infiltrate of polymorphonuclear leucocytes, lymphocytes, plasma cells and haemosiderin-laden macrophages
- Chest radiograph: This may reveal consolidation, ground-glass opacities, interlobular septal thickening and/or cavitation
- Computed tomography (CT): Common computed tomography (CT) thorax findings may include irregular nodules/cavitation/diffuse pulmonary infiltrates/lung abscesses or pleural effusion
- Magnetic resonance imaging of the brain – If CNS is involved
- Cerebrospinal fluid analysis – If nocardial meningitis is suspected.
Nocardiosis is primarily treated with antimicrobial therapy as follows.
Sulfonamides are the mainstay of therapy for the majority of the Nocardia species. Trimethoprim-sulfamethoxazole (TMP-SMX) is considered the first-line monotherapy.
For mild-to-moderate pulmonary disease (without the involvement of other organs)
Following is the dosage of TMP-SMX, recommended for patients with normal renal function:
- For immunocompetent patients: 5–10 mg/kg orally of the TMP component per day in two divided doses
- For immunocompromised patients: 15 mg/kg orally of the TMP component per day in three or four divided doses.
For patients with severe infection
A dose of 15 mg/kg intravenous (IV) of the TMP component per day in three or four divided doses along with amikacin (7.5 mg/kg IV every 12 h) or imipenem (500 mg IV every 6 h) along with amikacin is the standard mode of treatment. Dosing must be adjusted in patients with impaired renal function. Patients on sulfonamide therapy need to be monitored for adverse drug reactions such as benign skin rashes or potentially lethal toxidermias (most frequent), acute liver injury, pulmonary reactions and blood dyscrasia.
If the patient is allergic to sulfonamides, the alternative agents considered are:
- Imipenem and meropenem
- Third-generation cephalosporins (ceftriaxone and cefotaxime)
- Extended-spectrum fluoroquinolones (e.g. moxifloxacin)
- Clarithromycin (as a single agent or as part of the combination regimen).
Induction IV therapy will be followed by oral antibiotic regimen with sulfonamides (TMP-SMX), minocycline or amoxicillin-clavulanate for patients with normal renal function.
Lung cavitation, abscess formation, pleural effusion, empyema, brain abscess, meningitis and osteomyelitis are some complications that increase the chances of mortality in nocardiosis.
There are no specific ways to prevent Nocardiosis infection. However, immunocompromised people need to protect their skin by wearing shoes and protective clothing while at risk of being exposed to soil/outside environment. Inhalation of organism can be prevented by wearing mask at high-risk places such as factories or any dusty environment. Any open wound or cut must be well covered while working in the soil. Hospitals should maintain strong infection control practices to avoid outbreaks of Nocardiosis.
| Case Presentation|| |
Mrs. J, a 32-year-old homemaker from an urban area, presented with history of intermittent fever for a week and intermittent haemoptysis associated with breathlessness on exertion for 3 months. She did not have any complaints of chest pain, paroxysmal nocturnal dyspnoea, pedal oedema, loss of weight or appetite. There was no history of previous infections or hospitalisation. High-resolution CT findings revealed bilateral bronchiectasis and focal calcified nodular soft tissue involving the right middle lobe, lower part of the anterior segment of the left upper lobe, lingula, medial basal segment and anterior and posterior basal segments of the left lower lobe. The bronchoalveolar lavage sample had tested positive for Nocardia Cyriacigeorgica in 2020. She was started on tablet SMX and TMP DS for 2 weeks at the time. Although her breathlessness on exertion persisted, the haemoptysis settled after the treatment with above-mentioned antibiotics for 2 weeks. She did not report for further follow-up, after that last visit to the outpatient Department. Two months later, she returned to the emergency department with a history of intermittent fever for a week and worsening breathlessness at the rest for the past 2 days which required immediate hospitalisation. At the time of admission into the emergency department, she was conscious and oriented and had tachycardia, tachypnoea and fever. The blood pressure (BP) was 100/70 mmHg and SpO2 was 90% on room air. There was no pallor, icterus, cyanosis, clubbing, lymphadenopathy or oedema. Bilateral crepitation was heard in mammary, inter and infrascapular and infra-axillary regions but no heart murmurs were noted. The CT scan repeated 2 months after the initial CT, done in 2020 showed bilateral patchy, confluent ground-glass opacities, consolidations and fibrotic changes in the right middle lobe and lower lobe indicating the severity and worsening of pulmonary damage.
Mrs. J was started on injection imipenem, injection amikacin and injection TMP-SMX and antipyretics. On her 1st day of admission, she required 2 L/min of oxygen. Since her oxygen demand increased rapidly, the oxygen supplementation was increased to 15 L/min. On day 2, she was swiftly shifted to the intensive care unit (ICU) for non-invasive ventilation, due to progressive tachypnoea and worsening hypoxaemia. She was swabbed for COVID-19, for which she tested negative. On day 3, her hypoxaemia further worsened requiring intubation and mechanical ventilation. From day 4, the ventilator supports were further maximised (FiO2 of 60% and positive end-expiratory pressure (PEEP) of 6 cm of H2o to FiO2 of 90% with 8 cm of PEEP) to combat worsening hypoxaemia and respiratory acidosis. She was nursed in prone position to treat hypoxaemia. Sedatives, narcotic analgesics and neuromuscular blocking agents were administered as continuous infusions. She also required inotropic support (injection noradrenaline, adrenaline and vasopressin) to maintain her BP above the target mean arterial pressure (MAP) of 70 mmHg. Her urine output was continuously monitored. She was administered parenteral fluids and enteral feeds as continuous infusion to meet her nutritional needs and her blood glucose levels were monitored every 2 h. Her family members were informed and kept updated of her condition by the ICU team. Family members were allowed to visit her in ICU and were encouraged to communicate with her. Despite intensive monitoring and therapy, she succumbed to her illness on the 10th day of hospitalisation.
| Nursing Care of Mrs. J Affected with Pulmonary Nocardiosis|| |
1. Nursing diagnosis
Ineffective airway clearance related to copious tracheobronchial secretions secondary to inflammatory and infectious processes, decreased energy and increased fatigue and ineffective cough reflex.
The patient maintains clear, open airway as evidenced by normal breath sounds, normal rate and depth of breathing and ability to cough out secretions effectively.
Mrs. J was able to maintain a patent airway as evidenced by the absence of obvious secretions in the endotracheal tube and the absence of adventitious breath sounds.
2. Nursing diagnosis
Impaired spontaneous ventilation related to respiratory muscle fatigue/acute respiratory failure/metabolic factors.
The patient maintains effective breathing pattern resulting in the absence of adventitious breath sounds and absence of use of accessory muscles and optimal gas exchange with arterial blood gases within normal limits.
Mrs. J was unable to maintain spontaneous ventilation as her respiratory distress progressed swiftly and required maximum ventilatory support with adjuncts such as proning therapy and neuromuscular blocking agents.
3. Nursing diagnosis
Impaired gas exchange related to ventilation-perfusion mismatch caused by collapse of alveoli.
Patient maintains optimal gas exchange as evidenced by arterial blood gas analysis within normal range, oxygen saturation 94% and greater, alert response mental response and relaxed breathing and heart rate (HR) within the baseline.
Mrs. J was unable to achieve satisfactory gas exchange due to worsening acute respiratory distress syndrome (ARDS). Her P/F ratio suggested worsening of ARDS to severe ARDS for day 3 of hospitalisation. She presented with haemodynamic instability as evidenced by drop in SpO2, PaO2, P/F ratio, hypotension, extensive chest infiltrates and she succumbed to death on the 10th day of her hospitalisation, despite maximum support.
4. Nursing diagnosis
Impaired cardiac output related to decreased contractility of cardiac muscle, decrease in preload secondary to high PEEP.
Patient maintains adequate cardiac output as evidenced by strong peripheral pulses, systolic BP within 20 mmHg of baseline, HR 60–100 beats/min with regular rhythm, urine output >0.5 ml/kg/h and warm, dry skin and normal level of consciousness.
Mrs. J was able to maintain adequate cardiac output during the initial 2 days of ICU hospitalisation. Since day 3, she gradually required increased ventilator support and high inotropic support. Since day 4, she started to present with signs of decreased cardiac output and impaired perfusion such as hypotension (MAP <65 mmHg requiring increase in doses of inotropes), delayed capillary refilling time >3 s, decrease in urine output, increased serum lactate levels and hypothermia.
5. Nursing diagnosis
Actual infection related to invasion of bacterial organisms.
Patient experiences reduction in infection/recovery from infection as evidenced by normal body temperature, normal white blood cell count and negative culture report.
Mrs. J's presented with signs of worsening of disease as evidenced by deranged leucocytes, worsening clinical and radiological findings of ARDS and resultant hypoxaemia, despite being started on antibiotics and intensive care. During her terminal stages of illness, she also presented with hypothermia.
6. Nursing diagnosis
Grieving is related to anticipatory loss or impending death.
- The family verbalises feelings regarding impending death and maintains functional support systems.
Family members were able to express their grief and were able to use the support from health-care team positively.
| Conclusion|| |
Mrs. J was provided with the best possible treatment and the family was given opportunity to understand about her condition, spend time with her during the terminal phase of her illness, and were assisted to set realistic expectations. Nurses played a vital role in providing quality care for Mrs. J as she passed through the difficult phase of illness and at the end of life. Although the outcome was death nurses ensured that the journey through the trajectory of illness was as comfortable as possible.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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