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                                                                          Chapter 3: Respiratory infections 103


                  wall components interfere with the fusion of the lyso-  Secondary tuberculosis
                  somes with the phagocytic vacuole, so that the bacteria     Secondary tuberculosis is a reactivation of infection
                  can survive intracellularly.                   occurring in a previously latently infected individual.
                    The most common pattern of TB is a primary pul-  It usually occurs due to reactivation of a healed pri-
                  monary infection:                              marylesionduetoaweakeningofthehostdefence,e.g.
                    The mycobacteria are inhaled into the alveolar spaces  diabetes mellitus, malnutrition, immunosuppression

                    ofthelung.Conditionsforgrowtharemostfavourable  (drugs, HIV). It may occur at any time from weeks
                    just below the pleura in the apex of the upper lobe or  up to years after the original infection. Occasionally it
                    the apical lobe of the lower lobe. Here the inflam-  may be due to re-infection from an external source. It
                    matory process forms the ‘Ghon focus’ usually just  differs from primary infection in its immunopathol-
                    beneath the pleura. Bacteria spread to the draining  ogy. The lymph nodes are rarely involved, and there is
                    lymph nodes at the lung hilum, and excite an immune  reactivation of the immune response in the tissues.
                    response there also. This pattern forms the primary     Inthelung,thebacteriahaveapreferencefortheapices
                    complex with infection at the periphery of the lung  (higher pO 2 ), and form an apical lung lesion known
                    and enlarged peribronchial lymph nodes.      as an Assmann focus. It begins as a small caseating
                    The outcome of the primary infection depends on the  tuberculous granuloma, histologically similar to the

                    balance between the virulence of the organism and  Ghon focus, with destruction of lung tissue and cavi-
                    the strength of the host response (see Table 3.11). If  tation. T cells are re-induced by the secondary infec-
                    the host can mount an active cell mediated immune  tion, with activation of macrophages, and exactly as
                    response the infection may be completely cleared.  with primary TB the outcome is a balance between the
                    In the vast majority of cases there is an intermediate  virulence of the infection and the strength of the host

                    responseandtheactivatedmacrophagesaggregateand  immune system.
                    wall off a central area of caseous (cheese-like) necro-     In patients with a vigorous immune reaction there
                    sis. These are called granulomas or tubercles. Collagen  is healing of the apical region with collagen de-
                    is deposited around these, often becoming calcified.  position and eventually calcification by the same
                    Twenty per cent of these tubercles contain viable my-  process as the healing of the primary infection re-
                    cobacteria, but clinically the infection becomes latent.  sulting in a latent apical fibrocaseous tuberculosis
                    If the immune response is very poor, there is progres-  lesion.

                    sion of the caesating granulomas in the lymph nodes     In patients with a poor immune response the le-
                    which erode into a bronchus or blood vessel caus-  sion enlarges with caseous necrosis destroying lung
                    ing further dissemination. This is called a ‘progres-  tissue, thinning of the collagen wall and increasing
                    sive primary infection’. Occasionally the Ghon focus  the risk of erosion of a bronchus or blood vessel.
                    may rupture through the pleura causing a tuberculous
                    pleurisy.
                                                                Patterns of progressive TB infection
                   Table 3.11 Predisposing factors towards extension or  See Fig. 3.3.
                   containment of infection.                    1 Tuberculous Bronchopneumonia: If an infected
                                                                 lymph node in primary tuberculosis, or an enlarging
                   Predisposing to      Predisposing
                   extension of infection  to containment        secondary tuberculous lesion erodes into a bronchus,
                                                                 tuberculous caseous material containing live tuber-
                   Exposure to large numbers  Exposure to a small number
                    of highly virulent   of poorly virulent      cle bacilli spreads infection throughout that segment
                    organisms            organisms               of lung. Coughing disperses these bacilli into the at-
                   Poor immune system eg  Good immune response, e.g.  mosphere, transmitting TB to other people. Without
                    malnutrition, extremes of  healthy immunised  treatment, extensive caseating lesions develop rapidly,
                    age, intercurrent disease  individual        leading to a high mortality. This disease is sometimes
                                        Use of appropriate antibiotics
                                                                 called ‘galloping consumption’.
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