Tuberculosis Flashcards
what other condition is related to TB?
HIV
how is TB prevalence/ morbidity evolving?
decreasing
environment for TB development?
poor nutrition, social distress
what does TB initially do in alveoli?
slow dev., consumption by macrophages
where do the macrophages go?
they go to lymph nodes
what happens in lymph nodes?
T cells get cloned and go back to alveoli to activate macrophages
why are activated macrophages a problem?
they attack TB as well as damage tissue (balance between destroying Ag and alveoli tissue)
under which conditions could you get TB as a primary infection in the UK?
if no immunity (to BCG vaccine)
advanced TB CXR top apex typical characteristics?
empty on CXR
in what areas is TB still a problem (Britain)? why?
London, because of immigration
what is the responsible organism for TB? what are the two main (70%) strains? where does TB come from?
mycobacteria tuberculosis, mycobacterium bovis, ubiquitous in soil, water
what organisms are responsible for the remaining 30%?
M. avium-intracellulare (HIV), M. kansasii, M. malmoense, M. xenopii
which organism is responsible for leprosy?
M. leprae
what type of bacteria is mycobacteria? how does that impact where it prefers to go to in the lungs?
non-motile bacillus, aerobic (predilection for apices of lung)
how fast is its growth?
very slow growing (disease is slow, treatment is long)
what is mycobacterium’s cell wall like? is this common?
uniquely has a very thick cell wall; lipids, peptidoglycans, arabinomannans
what is mycobacterium resistant to?
acids, alkalis, detergents, neutrophil, macrophage destruction
is mycobacteria an acid (an alcohol) fast bacilli (AAFB)? what test to find out?
yes, Ziehl Neilson stain
how does mycobacterium tuberculosis get transmitted (‘open’ pulmonary TB)?
coughing, sneezing; respiratory droplets evaporate, droplets nuclei contain mycobacteria (1 cough=3500 nuclei), remains airborne for very long periods
how can outdoor mycobacteria get eliminated?
UV radiation and infinite dilution
what happens to the larger droplets nuclei when inhaled?
impact on large airway and cleared
what happens to the small (<5 micrometer) droplets nuclei when inhaled?
1-3,organisms impact in alveoli slowly proliferate
how does mycobacterium bovis?
consumption of infected cow’s milk, deposited in cervical, intestinal lymph nodes
what is the immunopatholgy for TB?
activated macrophages -> epitheloid cells -> Langhan’s giant cells, accumulation of macrophages, epitheloid & Langhan’s cells -> GRANULOMA
also central caveating necrosis (may later calcify)
why is the Th1 mediated immunological response a “two edged sword”?
- eliminates/ reduces number of invading mycobacteria
- tissue destruction is a consequence of activation of macrophages
what factors change chance of infection?
virulence, number (of bacteria)
what factors change susceptibility of being vulnerable to infection?
genetics, race, nutrition, age (susceptibility increased if elderly), immunosuppression
how does TB affect a susceptible host? (as opposed to a resistant host)
increased tissue destruction, organism proliferates instead of being contained, turns into a progressive disease
what is a primary infection?
infection when no preceding exposure or immunity
who is normally affected by primary infection? where are they affected?
usually children, 80% infected focus in alveolus (lymph nodes, gut)
how can TB spread from the alveoli?
spread via lymphatics to draining hilar lymph nodes; haematogenous seeding of mycobacteria to all organs of the body (lungs, bone, genitourinary (=reproductive) system)
what is the outcome of an infection in 85% cases?
initial lesion + local lymph node (primary complex), heals with or without scars, may calcify (Ghon focus + complex)
what are the symptoms for TB?
usually none, can be fever, malaise, Erythema nodosum, rarely chest signs
what is the outcome for TB infection in terms of immunity?
infection is associated with development of immunity to tuberculprotein
how do you test for tuberculin?
intra dermal administration of tuberculoprotein (PPD) results in lymphoctic and macrophage based areas of inflammation/induration after 48 hours
what are the three outcomes of a primary infection?
- cleared (slight tissue damage, no impact)
- contained latent (no progression but more tissue damage)
- progressive disease
what happens in 1% of primary infection which will lead to a very poor prognosis?
primary infection progresses, primary focus continues to enlarge -> cavitation, enlarged hilar lymph compress bronchi, lobar collapse, enlarged lymph node discharges into bronchus -> tuberculous bronchopneumonia
how can a post primary disease happen?
- reactivation of mycobacterium from latent primary infection disseminated by the blood stream around the body
- new re-infection from outside source; different host response because of previous sensitisation, if insufficient immunity present: tissue damage, progressive
what diseases are caused by a post primary disease?
- pulmonary disease (1-5 years, maybe 30-40)
- pleural TB, miliary, meningeal (6-12 month)
- lymph nodes, usually cervical
- bone and joint (spine, hip) (1-5 years, maybe 30-40)
- genito-urinary
- males; infertility- vas deferens (10-15 years, maybe 30-40)
- females; infertility- uterus, Fallopian tubes (10-15 years, maybe 30-40)
- pericardium; constrictive pericarditis
- abdomen; ascites, ileal TB -> obstruction
- adrenal -> Addison’s disease
- skin; lupus vulgaris (10-15 years, maybe 30-40)
what are the symptoms for post-primary pulmonary TB?
may be no symptoms for many months, respiratory: cough, sputum, haemoptysis, pleuritic pain, breathlessness, systemic: malaise, fever, weight loss (‘night sweats’)
typical past medical history for a patient with post-primary pulmonary TB?
diabetes, immunosuppressive disease (HIV), previous TB, previous gastric surgery, malignancy
typical drug history for a patient with post-primary pulmonary TB?
immunosuppressive drug (corticosteroid therapy)
typical past social history for a patient with post-primary pulmonary TB?
alcohol, IV drug abuse (IVDA), poor social circumstances (malnutrition, vagrants), immigrants from high incidence areas
typical signs for a patient with post-primary pulmonary TB?
- may be none at all- extensive TB can be present without physical signs
- if more advanced, may be crackles, bronchial breathing
- finger clubbing is rare unless very chronic infection
how do you diagnose TB on a CXR?
- ‘patchy’ shadowing, often on apices/ upper zones or apex of lower lobes (related to high ventilation + poor perfusion of O2), often bilateral
- cavitation if advanced
- may calcify if chronic or healed TB
how to investigate TB sputum?
- sputum smear (Ziehl Neilsen stain, immediate answer if many AAFB)
- sputum culture (up to 8 weeks)
- sputum PCR
how to get sputum if none is produced spontaneously?
induce production
what further investigations are initiated if sputum negative?
- CT scan of thorax
- bronchoscopy with bronchoalveolar lavage, transbronchial biopsy, Z-N stain, culture, PCR, biopsy history
- pleural aspiration and biopsy if pleural effusion, fluid cytology (lymphocytes), fluid for AAFB and culture, biopsy histology, 1 biopsy sent in saline for culture
what was “the Sanatorium regime”?
improving immunity by offering fresh air, sunshine, bed rest and good food (vitamin D & cathelecidin (LL-37)
how do you manage TB?
multi-drug therapy is essential, legal requirement to notify all cases, low threshold for HIV testing, AIDS defining condition
what happens if you treat a patient with a single agent treatment?
drug resistant organisms within 14 days
how long does TB therapy last?
6 months
what drugs are used for TB treatment for the 2 months?
rifampicin, isoniazid, ethambutol, pyrazinamide
what drugs are used for TB treatment for the 4 months?
rifampicin, isoniazid
when is a patient following the treatment rendered non-infectious?
after 2 weeks
what are the side effects of rifampicin?
orange ‘irn bru’ urine, tears, induced liver enzymes, prednisolone, anticonvulsants, oral contraceptive pill contraindication, hepatitis
what are the side effects of isoniazid?
hepatits, peripheral neuropathy (pyridoxine B6)
what are the side effects of ethambutol?
optic neuropathy (check visual acuity)
what are the side effects of pyrazinamide?
gout
why is contact tracing used for TB? how is first targeted?
identify source, identify transmission, duration of contact, close household contacts; casual contacts if close contacts have been infected with virulent organism/high transmission
what does likelihood of infection with TB depend on?
duration of contact + intensity of contact
