An assessment of nucleic acid amplification testing for active mycobacterial infection



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Site of infection

Clinical symptoms

Pleural TB

Blood-tinged sputum producing chronic cough, pleurisy, chest pain.

TB lymphadenitis

Enlarged cervical or supraclavicular lymph nodes.

Tuberculous meningitis

Persistent or intermittent headache for 2–3 weeks; mental status changes, coma.

Head and neck TB

The presenting complaints can include lump in the neck, nasal obstruction, sore throat or discomfort, external nasal lesions and otitis media.

Skeletal TB

Clinical presentation includes localised pain associated with fever and weight loss. Spine is most common site (Pott disease). Back pain, stiffness, lower extremity paralysis (50%).

Tuberculous arthritis

Involves the joints. Hips and knees more commonly affected. Pain precedes radiographic changes.

Cutaneous TB

Lesions show a wide spectrum of morphology including tuberculous chancre, TB verrucosa cutis, lupus vulgaris, scrofuloderma, orificial TB, miliary TB, metastatic TB abscess, and most cases of papulonecrotic tuberculid.

Pericardial TB

Clinical features include cough, weight loss, fever, night sweats and anorexia.

Genitourinary TB

The kidneys are the most common site of infection causing flank pain, dysuria and frequent urination. Men may present with a painful scrotal mass, prostatitis, orchitis or epididymitis. In women the condition may mimic pelvic inflammatory disease. Causes 10% of sterility in women worldwide and 1% of women in industrialised countries.

Renal TB

Renal TB is usually a complication of a previous primary pulmonary infection. MTB form cortical granulomas, and on reactivation spread into the medulla, causing papillitis. Advanced disease leads to cortical scarring, and infundibular and pelvic strictures. The end result of diffuse disease is destruction, loss of function and calcification of the entire kidney.

Gastrointestinal TB

TB may infect any site along the gastrointestinal tract. TB can manifest as non-healing ulcers of the mouth or anus, difficulty swallowing, abdominal pain (e.g. peptic ulcer), malabsorption, painful diarrhoea or haematochezia. Can also affect the liver, spleen and pancreas.

Ocular TB

Ocular TB can affect nearly every ocular tissue. Clinical manifestations include vitritis, macular oedema, retinal periphlebitis, choroiditis uveitis, retinal vasculitis and serpiginous-like choroiditis.

TB in the breast

Breast TB is rare and can present as clinical suspicion of carcinoma due to the development of granulomas; it can also present as mastitis. At later stages it erodes through the skin, causing ulceration and discharging sinus tracts.

TB from joint replacement surgery

MTB prosthetic joint infection is most often caused by reactivation of prior tuberculous arthritis.

Sources: Abbara & Davidson (2011); Abes, Abes & Jamir (2011); Al-Mezaine et al. (2008); Al-Serhani (2001); Bani-Hani et al. (2005); Berbari et al. (1998); Cruz-Knight & Blake-Gumbs (2013); Kakkar et al. (2000); Muttarak, ChiangMai & Lojanapiwat (2005); Reuter et al. (2006)

Some people have a high risk of infection due to an increased likelihood of exposure to an infected individual (CDNA 2013), such as:



  • new arrivals and recently returned travellers from countries with a high TB incidence

  • contacts of an active case within the past 5 years

  • people living in overcrowded conditions, such as some Indigenous Australians in localised areas (e.g. Northern Territory, Queensland) or in institutions

  • healthcare workers who serve or have served high-risk populations.

The fate of the mycobacteria in a newly infected individual is dependent on the person’s immune system. A healthy immune system may clear the bacterium or, alternatively, exposure can lead to latent TB or progress to primary active TB (Cruz-Knight & Blake-Gumbs 2013). Most infections in humans are asymptomatic and latent, and can persist for a lifetime. In the healthy host, progression to active TB occurs in approximately 10% of those infected. For half of these patients this progression occurs within 2 years, and in the other half it can occur up to decades later (CDNA 2013; Zumla et al. 2013). Once infected, some patients are more susceptible to progression to active TB than others (CDNA 2013). These include:

  • children younger than 5 years of age, adolescents and the elderly

  • people who are malnourished

  • people who are immunocompromised due to:

    • diseases such as HIV, diabetes and renal failure

    • immunomodulating therapies, such as corticosteroids, anti-TNF inhibitors and anti-cancer treatments.

Patients with a respiratory infection that is unresponsive to standard treatment should be suspected of having TB if they belong to one of these high-risk populations. Standardised TB treatment for an appropriate period of time will cure over 98% of drug-sensitive cases (HKCS/BMRC 1987). Deaths from TB in Australia are usually due to co-morbidities or delays in diagnosis and treatment (CDNA 2013). The success of treatment and the prevention of drug resistance and relapse relies heavily on the compliance of the healthcare provider in prescribing the right drug combination, dose and duration of treatment, as well as on patient adherence to treatment.

The aim of government policy is to prioritise screening of higher risk groups such as Aboriginal and Torres Strait Islander peoples and persons born overseas (including immigrants, students, healthcare workers), engage in regional TB control programs and ensure that there is a high standard of diagnosis and treatment (National Tuberculosis Advisory Committee 2012).



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