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CDHB

Tuberculosis (TB) - Early Recognition and Initial Management

TB is managed within the departments of Respiratory and Infectious Diseases. The following is a guide to the timely recognition and early management of TB for the generalist pending Specialist referral. A specialist TB nurse can be contacted through Cardio-Respiratory Integrated Specialist Services (CRISS). The TB nurse works both in the hospital and in the community, can coordinate TB treatment including directly observed treatment (DOTS) in the community, and educates patients and staff on isolation procedures, TB disease and TB medications. Remember that TB is a notifiable disease.

Incidence

The annual incidence of TB in New Zealand has fallen to 7-10 per 100,000 with 20 to 30 cases annually in Canterbury. There are marked differences between ethnic groups with higher incidences of TB in Maori (x5), Pacific Islanders (x10), and Asian ethnicity (x25) compared to Pakeha. 70% of cases of TB in NZ occur in people born outside NZ. In NZ 1% of patients diagnosed with TB also have HIV infection.

Diagnosis

A delay in diagnosis is often due to TB not being considered in the differential. This leads to prolonged infection risk as well as increased morbidity and mortality.

• Risk situations for TB include:
  • Previous residence in high-incidence TB country - especially if recent arrival in NZ.
  • Prolonged close contact with an infectious case, usually domestic contact over weeks or months. Consider possibility of institutional contact, i.e., refugee camps, prisons, rest homes.
  • Previous TB, especially inadequate treatment of previously active TB, e.g., a drug regimen that did not include both isoniazid (available since 1950) and rifampicin (available since 1965), noncompliance (treatment not directly observed), or an unknown treatment regimen.
  • Radiological or pathological evidence of previously unrecognized, and therefore untreated, naturally remitting TB, such as abnormal calcification on radiograph, or granulomatous inflammation on surgically resected tissue.
  • Immunosuppression by disease or medication - including TNF-alpha inhibitor treatment.
• Clinical scenarios:
  • Pulmonary TB:
    • Approximately 2/3 of TB cases are pulmonary TB.
    • May be asymptomatic initially but with radiological change and still have active disease. Will eventually progress to becoming symptomatic.
    • Cough - dry or productive, haemoptysis.
    • Chronic respiratory symptoms with chest X-ray abnormality, particularly bilateral upper zone pleuropulmonary fibrosis with cavitation, calcified pulmonary nodules, or calcified intrathoracic lymph nodes.
    • Persistent or recurrent pleural effusion - usually lymphocytic exudate.
  • Lymphadenopathy or lymph node suppuration.
    • Patients typically have chronic unilateral non-tender lymphadenopathy without systemic symptoms. This usually involves the cervical nodes, but other node groups may be affected. Rarely nodes become fluctuant or develop a draining sinus.
    • TB lymphadenitis should be considered in patients from high endemic countries with chronic lymphadenopathy and any lymph node aspirates or biopsies taken from such patients should be sent for TB culture as well as cytology / histology.
  • Chronic spinal osteomyelitis, persistent septic arthritis.
    • TB causing osteomyelitis (typically spinal) or septic arthritis usually presents with local pain which becomes increasingly severe over weeks to months. Joint disease may also present with swelling and progressive loss of joint function. In patients with subacute presentation TB should be considered and diagnostic samples should be sent for TB culture as well as routine bacteriology, especially if the patient is from a high risk country or at risk of TB exposure in the past.
  • Chronic diarrhoea with/without ascites. Often with systemic symptoms of weight loss, fever and malaise.
  • Sterile pyuria - if other common causes excluded.
  • Pyrexia of unknown origin.
  • Chronic meningitis.
    • Patients present with a subacute febrile illness associated with headache and often progressing through personality change, confusion, cranial neuropathies and long tract signs to coma and paralysis. They may have features of meningism as well as vomiting, lethargy and seizures. Approximately 1/3 of patients will have miliary tuberculosis.
    • The CSF typically shows a mononuclear pleocytosis, low glucose and high protein. Demonstration of acid fast bacilli (AFB) in the CSF is the most effective way to make the diagnosis and diagnostic yield of both AFB stain and TB culture increases with repeated (up to 4) LPs.
    • CSF PCR for TB is available but has poor sensitivity despite high specificity. A large volume (e.g., 10 mL) of CSF is needed for TB testing.
• Disseminated or miliary TB is rare but has a high associated mortality.
• All patients diagnosed with extrapulmonary TB should have CXR and consideration as to whether they have concomitant pulmonary involvement as this frequently co-exists and requires respiratory isolation.

Respiratory Isolation

• Not all patients with TB need admission and some are treated in the community. Home isolation is often possible and the TB nurse from CRISS may be available to help assess the feasibility and safety of this and educate the patient and their family.
• If a case of pulmonary TB is suspected in the community but sputum results are still awaited, home isolation procedures should be put in place pending results.
• All suspected inpatient cases of pulmonary or laryngeal TB should be placed in respiratory isolation, ideally in an airborne isolation (negative pressure) room, pending confirmation (or exclusion) of the diagnosis.
• Staff must wear a fitted particulate respirator / N95 mask.
• Patients must wear a surgical mask if they need to leave the isolation room e.g., for investigations, transfer etc.
• See the CDHB Infection Prevention and Control Manual (search for "infection prevention" at http://cdhb.health.nz).
• Extrathoracic TB and pleural TB without pulmonary involvement are not infectious. However pulmonary TB commonly coexists with extrathoracic TB and infection risk should be investigated. For example 70% of patients with cervical or supraclavicular nodal TB will also have active pulmonary TB.

Multi Drug Resistant TB

Multi Drug Resistant TB (MDR TB) is diagnosed in NZ however <1% of cases are MDR TB. Suspect MDR TB in:

• Cases from high-incidence areas.
• Previously treated but relapsed disease.
• Contacts of a MDR case.

All suspected MDR TB cases must be strictly isolated in a negative pressure room.

• If MDR TB suspected and TB confirmed on initial samples, i.e., AFB-positive sputum, discuss with microbiology proceeding to rapid drug sensitivity testing. The geneXpert system™ can detect rifampicin resistance on AFB positive sputum within hours.
• All MDR TB must be treated in consultation with a specialist centre and must involve Respiratory or Infectious Disease team input.

Collection of Specimens

In cases of suspected TB an early and vigorous attempt should be made to collect relevant specimens for mycobacterial culture. In most cases treatment should not commence until the diagnosis is confirmed.

• Three spontaneous or induced sputum samples (contact Physiotherapy department) 8-24 hours apart, or bronchoalveolar lavage at bronchoscopy. Induced sputum has a higher yield than bronchoscopy. Bronchoscopy may be preferred if other differentials such as malignancy are being considered.
• Pleural fluid aspirate - positive culture in only 10-35% cases. Pleural biopsy increases yield to 60-80% and should be pursued if diagnosis uncertain.
• Joint fluid aspiration.
• Lymph node aspirate (positive in only 33% cases) or excisional biopsy of node.
• Early morning urine x3 for TB culture if sterile pyuria present.

Note: Acid fast bacilli or TB culture must specifically be requested when samples are sent for microbiology. Tissue should be sent in saline for TB culture.

Interferon Gamma Release Assay (IGRA) – Quantiferon-TB Gold

• The Mantoux test and IGRA both test for TB exposure/infection but do not distinguish latent TB infection from active disease.
• Latent TB is 'dormant' TB infection in the absence of active disease.
• These tests are never diagnostic for active TB and should not be performed routinely when investigating for active disease. Rather, positive cultures should be sought.
• A positive result may help increase clinical suspicion in occasional difficult cases. The sensitivity of IGRA in active disease may only be 80% and therefore cannot be used to exclude active disease.
• IGRA is not affected by past BCG vaccine (unlike the Mantoux test), is unaffected by most non-TB mycobacterial infection and requires one blood test.
• IGRA may be used in place of a Mantoux for the diagnosis of latent TB especially in BCG vaccinated individuals or the immunocompromised. In TB contact cases an IGRA may better predict those at risk of developing active disease.
• Active disease must be excluded before a diagnosis of latent TB can be made. If latent TB is diagnosed a decision must be made whether to treat. This should involve specialist input. Recent contacts of TB cases and those with impaired immunity due to illness or medications may require treatment to prevent progression to active disease.

General Information

• Certain antibiotics, not normally used to treat TB, have antimycobacterial activity and should be avoided if possible in suspected cases before adequate diagnostic specimen collection. Antibiotics with antimycobacterial activity include quinolones, aminoglycosides and amoxicillin/ clavulanate.
• All patients diagnosed with active TB should be offered HIV testing.
• The NZ Guidelines for TB (see below) have recently been updated and are available online. They are an excellent resource.

Reference: Guidelines for Tuberculosis Control in New Zealand 2010 www.moh.govt.nz.

Topic Code: 9589