TUBERCULOSIS

EPIDEMIOLOGY

 World Health Organization estimates that tuberculosis

remains the second leading cause of death from an infectious
disease worldwide (after HIV) and that almost one-third of the
world’s population (2.5 billion people) is infected with M.
tuberculosis.
 The highest numbers of cases are in Asia, Africa, and the
eastern Mediterranean region .
 The global burden of tuberculosis is influenced by several
factors including: the HIV pandemic; the development of
multidrug resistant (MDR ) tuberculosis; and the
disproportionate access of populations in low -resource
settings worldwide to both diagnostic tests and ef fective
medical therapy.
 ETIOLOGY

There are 5 closely related mycobacteria in

the Mycobacterium tuberculosis complex:
 M. tuberculosis, Mycobacterium bovis,
Mycobacterium africanum, Mycobacterium
microti, and Mycobacterium canetti.
M. tuberculosis is the most important cause of
tuberculosis disease in humans.
 3 MAJOR CLINICAL STAGES

EXPOSURE INFECTION DISEASE

 RISK FACTORS

1. Absence of BCG
vaccination
2. Close contact
3. Age <5 yo
4. Severe malnutrition,
measles and Childhood TB
immunosuppressive
drugs and illness
5. HIV infection
TREATMENT
 PREVENTION

Contact screening and

TB infection control mass treatment

BCG vaccination
 HANSEN DISEASE
(MYCOBACTERIUM
LEPRAE)

Leprosy is a heterogeneous, chronic mycobacterial

infection primarily affects the upper airways, skin, and
peripheral nerves.
 ETIOLOGY
 Mycobacterium leprae is the etiologic agent of leprosy
 Obligate intracellular acid -fast Gram-positive bacillus of the
family Mycobacteriacea
 1-8um in length
 Grows optimally at 27 -33 degrees celsius
 IP: between natural infection and overt clinical disease in human
ranges from 3 months to 20 years with a mean of 4 years for
tuberculoid leprosy and 10 years for lepromatous leprosy
 EPIDEMIOLOGY
 Continues to affect 2 million people worldwide
 245,000 new cases were reported globally in 2009
 80% of cases occurring Southeast Asia, Africa and
South America
 Age (with 2 incidence peaks: 10-14 years and 30 years
old)
 Gender ( male:female ratio is 2:1)
 5% of people is genetically susceptible to infection
 Exact mechanism of transmission is not fully
understood but is thought to occur primarily via the
respiratory route
 PATHOGENESIS
Only bacterium known to infect nerves
Colonizes the perineural space and gain
entry into the endoneural space
Binds to the laminin-2 glycoprotein present
in the basal lamina of Schwann cells in
peripheral nerves
Taken up by the Schwann cells where it
replicates slowly intracellularly over
several years
 CLINICAL
MANIFESTATIONS
Classic manifestations:
Hypopigmentation
Erythematous
Infiltrative skin lesions with or without neurologic
symptoms such as hypoesthesia or anesthesia, weakness,
autonomic dysfunction and peripheral nerve thickening

SKIN INVOLVEMENT
Macules or plaques
Insidious hypopigmented macules are the initial lesions
More pronounced in cooler areas (earlobes & nose)
Scalp, axillae or perineum are the less frequent site
NERVE INVOLVEMENT
Peripheral nerves are most commonly
affected early in the disease course and
should be palpated for thickness and
tenderness and evaluated for both motor &
sensory function
Posterior tibial nerve (medial malleolus)
most common nerve affected
Ulnar nerve (elbow), median (wrist), lateral
popliteal (fibular neck), and facial nerves
 OTHER INVOLVEMENT

Ocular involvement leading to vision loss

results from both direct bacillary invasion
of the eye and optic nerve damage
Lagophthalmos occurs when there is
destruction of the facial nerve
 3 TYPES OF LEPROSY REACTIONS

1. Type 1 reactions (reversal reactions) occurs in 1/3 of

patients with borderline disease and are caused by a
spontaneous increase in T-cell-mediated reactivity to
mycobacterial antigens.
Characterized by:
Acute edema
Increased erythema
Warmth & painful inflammation of preexisting
cutaneous plaques or nodules with acute swelling and
tenderness of peripheral nerves that can quickly
progress to cause nerve abscess and necrosis
Corticosteroid is essential to prevent continued nerve
damage.
2. Type 2 reactions (erythema nodosum leprosum
ENL) occur in borderline lepromatous and lepromatous
forms, as these patients have the highest levels of
M.leprae antigens and antibodies
Development of new painful, erythematous
subcutaneous nodules with an accompanying systemic
inflammatory response
High fever and signs of toxicity and in severe cases
may present features similar to septic shock
Migrating polyarthralgia, painful swelling of lymph
nodes and spleen, iridocyclitis, vasculitis, orchitis and
rarely nephritis.
3. Lucio’s phenomenon (erythema necroticans) uncommon but
potentially fatal reaction distinct from types 1 & 2 that occurs in
patients with untreated lepromatous leprosy most common in
Mexico. It is a necrotizing vasculitis caused by M.leprae directly
invading the endothelium.
Clinical Manifestations:
 Violaceous or hemorrhagic plaques
 Ulcerations in the absence of systemic complaints
 Secondary bacterial infections are common
Nontuberculous Mycobacteria
Atypical mycobacteria or mycobacteria other
than TB
Exists as saprophytes in soil and tap water
Progresses slowly, over years
Usually takes several years to cure
Characterized by granulomas that are non-
caseating, ill-defined, irregular, serpiginous or
even absent with only chronic inflammatory
changes
M. Avium Complex
Infections are acquired from birds
Causes pediatric lymphadenitis

M. Avium Hominissuis
Mainly found in humans and pigs
Causes adult pulmonary disease

M. Marinum
From fish & other cold-blooded animals
Causes fish-tank granuloma following skin injury
in an aquatic environment
M. Fortuitum & M. Chelonae
Causes nosocomial surgical wound and
venous catheter-related infections

M. Ulcerans
Causes Buruli ulcer disease

M. Abscessus
Associated with cystic fibrosis