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Clinical Pathology - > CP19 - Mycobacterial Diseases > Flashcards

CP19 - Mycobacterial Diseases Flashcards

1
Q

what are mycobacteria?

A

rod shaped bacilli

gram positive

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2
Q

how are mycobacteria different to other bacterial species?

A
  1. thick and way cell wall because it contains mycolic acids
  2. slow growing in comparison to other bacteria because they have different requirements for growth
  3. therefore, don’t respond well to the gram stain very well
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3
Q

why are mycobacteria called acid fast bacteria?

A

they take up stains quickly in the presence of acid or alcohol. types of stains used for them -

  1. ziehl nelson
  2. phenol auramine
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4
Q

are mycobacteria intracellular or extracellular?

A

intracellular pathogens

therefore they cannot be killed by macrophages. the bacteria multiply within them

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5
Q

why does mycobacterial disease have latent phase?

A

due to the immune response in the body. it cannot kill the bacteria, but keeps it at bay.
bacteria cause disease-like symptoms when immunity is weakened

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6
Q

why do mycobacteria cause chronic infections?

A

they take longer to breed and their clinical presentation therefore varied from other bacteria
they do not colonise to a specific part of the body
therefore, antimicrobials used are different
therapy lasts about 6 months

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7
Q

what are the key pathogens causing mycobacterial disease?

A

M tuberculosis complex - TB
M. tuberculosis
M. bovis

M. leprae - Leprosy

Atypical mycobacteria:
M. avian complex - associated with HIV
M. kansasii
M. marinum - fish tank granuloma, in people who own tropical fish

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8
Q

what fraction of the population is affected by TB?

A

1/3 - either carriers or symptomatic

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9
Q

why are there high occurrences of co-infection of TB and HIV in sub saharan africa?

A

TB acts synergistically with HIV

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10
Q

what is the pathogenesis of TB?

A
  1. inhalation of infected respiratory droplets
  2. taken to the periphery of the middle zone of the lung
  3. macrophages recognise the bacilli and inhale them
  4. macrophages are unable to kill TB
  5. macrophages are carried back to the hilar lymph nodes (clinical presentation at this point)
  6. multiplication of TB inside macrophages. dissemination via the lymphatic system and blood stream, but growth is slow
  7. body responds to dissemination by the formation of tubercles or granuloma - this is a cell mediated response
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11
Q

what is the clinical presentation of primary TB?

A

asymptomatic, or influenza like symptoms
chest xray and skin test at this point is also normal
6-8 weeks later, the skin test will test positive due to the activation of the immune system

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12
Q

what is a granuloma?

A

a structure that contains epithelia cells and giant cells in the centre. activates macrophages to kill the bacteria
lymphocytes infiltrate from the surroundings and cause caseous necrosis
results in fibrosis/calcification of lesions.
TB either dies, or is latent for a long time

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13
Q

what are the risk factors for the reactivation of TB?

A
  1. lowered immunity
  2. old age, men
  3. malnutrition
  4. alcoholism
  5. debilitating illness
  6. HIV infection
  7. silicosis
  8. chronic renal failure
  9. gastrectomy
  10. Anti-TNF agents eg. infliximab - suppress the immune system
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14
Q

what helps to maintain the wall of a granuloma?

A

TNF alpha

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15
Q

what happens when a patient is actively infected with TB in the lung?

A

the tubercles join, causing the cavities to enlarge
causes caseous necrosis
cavity allows a larger organism load, this translates to a greater risk of transmission
when the patient coughs, these droplets leave the patient and are transmitted to other people

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16
Q

why does TB reactivate in lung apices?

A

this is the place with the highest oxygen content in the body

17
Q

what are the symptoms of TB?

A 
chronic productive cough (more than 2-3 weeks)
possibly haemoptysis
weight loss 
fever, relatively low grade
night sweats
18
Q

risk factors for disseminated/military TB

A

extremes of age
immunocompromised
when it is a primary disease
when secondary infection erodes into blood vessels

19
Q

which sites are affected in disseminated TB?

A 
pleura
lymph nodes
kidneys
epididymis
bones - especially spine
intestines
brain/meninges
pericardium
20
Q

what are the symptoms of TB meningitis?

A

insidious onset

  1. unidentified fever
  2. personality change
  3. focal neurological deficit
  4. mild headache and mild symptoms of meningism
  5. may also have pulmonary fever, night sweats, anorexia, etc. but not always
21
Q

how is TB diagnosed?

A 
index of suspicion
radiology - Chest Xray
histology - ZN stain
skin testing - mantoux test - look for skin induration, which indicates TB exposure 
blood test
microbiology
22
Q

why are skin and blood tests done?

A

to look for latent disease as opposed to active disease

23
Q

why are microbiology tests carried out?

A
  1. to confirm diagnosis
  2. to look for dug sensitivities
  3. molecular typing to analyse spread and update understanding
24
Q

what sample is used for microbiology testing?

A

early morning sputum
3 specimens
because they would have all pooled together during the night

25
Q

what needs to be done if patients are not producing sputum?

A
  1. induce sputum by giving them saline via nebulisers
  2. do a bronchoscopy for bronchial aspirates
  3. collect gastric aspirates if they have swallowed their sputum
26
Q

what is a clinical sign of renal TB?

A

sterile pyuria - white cells in urine. this is not common

to check - collect 3 samples of early morning urine

27
Q

how is TB meningitis investigated?

A

lumbar puncture and cell count
high lymphocytes
high protein count
low glucose

28
Q

how is TB treated?

A 
lengthy, required combined tablets 
for non meningeal TB - isoniazid
rifampicin
pyrazinamide 
ethambutol
next 4 months
isoniazid
rifampicin
29
Q

why are so many drugs used for treatment?

A

to ensure a spectrum of species is covered

30
Q

how is meningeal TB treated?

A

12 months of therapy. initial treatment corticosteroids

31
Q

what are the second line agents to treat TB, if the bacteria is resistant to first line agents?

A

amikacin
ethionamide
cycloserine
moxifloxicin

32
Q

how can TB be controlled?

A

identify and treat the active disease early

recognise latent infection

33
Q

whats the vaccination for TB?

A

BCG (Bacille Palmette Guerin) against M. bovis

34
Q

what are atypical mycobacteria?

A

don’t spread from person to person

35
Q

how are atypical mycobacterial infections managed?

A

similar diagnosis and treatment, although treatment may be more prolonged
an additional macrolide may be needed

36
Q

what is another term for leprosy?

A

Hansen’s disease

37
Q

what is the species that causes leprosy?

A

M. leprae

38
Q

what are the 2 extreme clinical forms of leprosy?

A

tuberculoid - males and plaques, inflammation around the ulnar and common peroneal nerve, if immune system is dealing with the organism
lepromatous - if immune system is unable to deal with it. accumulates in SubCutaneous tissue, earlobes, face, called lenience facies

39
Q

how is leprosy treated?

A

dapsone, rifampicin, clofazimine

Clinical Pathology - (15 decks)

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