Bacterial Infections Table 1: Classical Division of Non-tuberculous Mycobacteria According to Runyon8 Runyon Class I II III IV Description Photochromogens Scotochromogens Nonchromogens Rapid growers Growth Slow growing Slow growing Slow growing Rapid growing Pigment Production
Yellow-orange pigment following exposure to light Yellow-orange pigment with or without light None
None
Some Examples of the Mycobacterial Species per Group
M. Kansasii, M. marinum
M. scrofulaceum, M. gordonae, M. szulgai
M. avium-intracellulare complex, M. xenopi, M. terrae, M. ulcerans, M. Haemophilum
M. fortuitum, M. peregrinum, M. abscessus, M. Chelonae
Photochromogens are pigment producers in the presence of light, scotochromogens are pigment producers in the absence of light and nonchromogens do not produce pigments. M. = Mycobacterium. Source: Reproduced from Jarzembowski and Young, 2008.8
Table 2: Clinical and Bacteriological Classification of Leprosy Type
Skin Lesions Intermediate Tuberculoid (TL)
Single, may be loss of sensation Single, macule, loss of sensation
Multiple, irregular macules and plaques
Single
Borderline tuberculoid (BT) Multiple, macules, loss of sensation Single or multiple Borderline
Multiple
Borderline lepromatous (BL) Macules, plaques and papules Lepromatous (LL)
Multiple and symmetrical Papules, nodules and infiltration
Peripheral Nerve Involvement Bacillary Load None
-/+ -
-/+ +
++ Late, multiple and symmetrical +++
Non-tuberculous Mycobacteria Disease Human-to-human transmission of NTM is rare and infection usually occurs following environmental exposure. This may occur via inhalation or direct inoculation, as may occur with wound contamination or penetrating injuries. The risk of pulmonary disease is increased in immunocompromised individuals and in persons with chronic pulmonary disease such as cystic fibrosis, emphysema or bronchiectasis,7,8,11,38
but
Other factors may include strain-specific virulence, decreasing exposure to MTB, discontinuation of universal BCG vaccination and environmental changes that may favour certain NTM species.8,12,41
NTM
pathogens are frequently classified as either slow (groups I to III) and rapid (group IV; producing mature colonies in agar within seven days) growers (see Table 1).8
photochromogens (pigment producers in the presence of light), scotochromogens (pigment producers in the absence of light) and nonchromogens (see Table 1).
Leprosy
Although the mode of transmission remains controversial, leprosy is possibly transmitted by infectious respiratory and/or nasal secretions and rarely by direct skin contact.43
Children exposed to a close family
member with infective leprosy are at increased risk of M. leprae infection.16,44
In a study from the US, the attack rate among close
Due to long incubation times (two to five years), leprosy usually manifests in children older than six years. However, it may be present as early as three months after birth, suggesting intrauterine or perinatal exposure.44
contacts was 5 %.45 The slow-growing NTMs are subdivided into
has also been associated with prolonged ventilation in intensive care units.39
Disease Pathogenesis
In general, following exposure, mycobacteria may trigger host defences through a combination of innate and adaptive immune responses.47
Initial defence is provided by the innate immune response through macrophages, dendritic cells (DC) and natural killer (NK) cells, following recognition of pathogen associated molecular patterns (PAMP) by mycobacterial pathogen recognition receptors (PRRs) including toll-like receptors (TLRs).48
(IFN)-γ-mediated responses is well documented.47,48
The importance of interferon Infected alveolar
In most infected individuals, cell mediated immunity usually develops 4–8 weeks after primary infection. Activated T-lymphocytes and macrophages prevent further dissemination of MTB, leading to granuloma formation and regional (hilar) lymphadenopathy.47–49
macrophages present MTB antigens to T-lymphocytes and provide co-stimulatory cytokines such as IL-12 and IL-18, principally stimulating CD4+ T-lymphocytes to release IFN-γ that activates the infected macrophage and facilitates MTB eradication. Following inhalation, MTB replicates and spreads via the lymphatic system to regional lymphnodes.47
An efficient T-helper 1 (Th1) immune response Clinical cases of leprosy are
classified according to the Ridley-Jopling classification as tuberculoid (TL), lepromatous (LL) or borderline (BT, BB or BL) (see Table 2). Lepromatous cases are considered infectious while tuberculoid cases are non-infectious and borderline cases have variable infectivity.14–16,44 A more pragmatic classification only differentiates pauci- and multibacillary forms, which also reflects transmission risk. Armadillos
104
is required for the elimination of mycobacteria, as illustrated by the increased susceptibility of individuals with inherited deficiencies in their IFN-γ signalling an/or response pathway, low numbers of T-cell cells or using TNF-alpha blockers.47–49
The combined effects
of impairment of innate defences, relative immaturity of dendritic cells and suboptimal response of naive T cells with reduced Th-1 cytokine production may explain the vulnerability and potential for rapid disease progression observed in very young children and/or
EUROPEAN INFECTIOUS DISEASE
Treatment Classification Pauci-/multibacillary
Paucibacillary Multibacillary Multibacillary
Multibacillary Multibacillary
are the only animal species that can be infected with M. leprae and are often utilised for research purposes. In a recent study, the same unique M. leprae genotype was found in wild Armadillos and patients from Southwestern US where exposure to wild Armadillos is possible, suggesting that leprosy may possibly represent a zoonotic disease in this particular area.46
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