CP19 - Mycobacterial Diseases Flashcards
what are mycobacteria?
rod shaped bacilli
gram positive
how are mycobacteria different to other bacterial species?
- thick and way cell wall because it contains mycolic acids
- slow growing in comparison to other bacteria because they have different requirements for growth
- therefore, don’t respond well to the gram stain very well
why are mycobacteria called acid fast bacteria?
they take up stains quickly in the presence of acid or alcohol. types of stains used for them -
- ziehl nelson
- phenol auramine
are mycobacteria intracellular or extracellular?
intracellular pathogens
therefore they cannot be killed by macrophages. the bacteria multiply within them
why does mycobacterial disease have latent phase?
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
why do mycobacteria cause chronic infections?
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
what are the key pathogens causing mycobacterial disease?
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
what fraction of the population is affected by TB?
1/3 - either carriers or symptomatic
why are there high occurrences of co-infection of TB and HIV in sub saharan africa?
TB acts synergistically with HIV
what is the pathogenesis of TB?
- inhalation of infected respiratory droplets
- taken to the periphery of the middle zone of the lung
- macrophages recognise the bacilli and inhale them
- macrophages are unable to kill TB
- macrophages are carried back to the hilar lymph nodes (clinical presentation at this point)
- multiplication of TB inside macrophages. dissemination via the lymphatic system and blood stream, but growth is slow
- body responds to dissemination by the formation of tubercles or granuloma - this is a cell mediated response
what is the clinical presentation of primary TB?
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
what is a granuloma?
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
what are the risk factors for the reactivation of TB?
- lowered immunity
- old age, men
- malnutrition
- alcoholism
- debilitating illness
- HIV infection
- silicosis
- chronic renal failure
- gastrectomy
- Anti-TNF agents eg. infliximab - suppress the immune system
what helps to maintain the wall of a granuloma?
TNF alpha
what happens when a patient is actively infected with TB in the lung?
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
why does TB reactivate in lung apices?
this is the place with the highest oxygen content in the body
what are the symptoms of TB?
chronic productive cough (more than 2-3 weeks) possibly haemoptysis weight loss fever, relatively low grade night sweats
risk factors for disseminated/military TB
extremes of age
immunocompromised
when it is a primary disease
when secondary infection erodes into blood vessels
which sites are affected in disseminated TB?
pleura lymph nodes kidneys epididymis bones - especially spine intestines brain/meninges pericardium
what are the symptoms of TB meningitis?
insidious onset
- unidentified fever
- personality change
- focal neurological deficit
- mild headache and mild symptoms of meningism
- may also have pulmonary fever, night sweats, anorexia, etc. but not always
how is TB diagnosed?
index of suspicion radiology - Chest Xray histology - ZN stain skin testing - mantoux test - look for skin induration, which indicates TB exposure blood test microbiology
why are skin and blood tests done?
to look for latent disease as opposed to active disease
why are microbiology tests carried out?
- to confirm diagnosis
- to look for dug sensitivities
- molecular typing to analyse spread and update understanding
what sample is used for microbiology testing?
early morning sputum
3 specimens
because they would have all pooled together during the night
what needs to be done if patients are not producing sputum?
- induce sputum by giving them saline via nebulisers
- do a bronchoscopy for bronchial aspirates
- collect gastric aspirates if they have swallowed their sputum
what is a clinical sign of renal TB?
sterile pyuria - white cells in urine. this is not common
to check - collect 3 samples of early morning urine
how is TB meningitis investigated?
lumbar puncture and cell count
high lymphocytes
high protein count
low glucose
how is TB treated?
lengthy, required combined tablets for non meningeal TB - isoniazid rifampicin pyrazinamide ethambutol next 4 months isoniazid rifampicin
why are so many drugs used for treatment?
to ensure a spectrum of species is covered
how is meningeal TB treated?
12 months of therapy. initial treatment corticosteroids
what are the second line agents to treat TB, if the bacteria is resistant to first line agents?
amikacin
ethionamide
cycloserine
moxifloxicin
how can TB be controlled?
identify and treat the active disease early
recognise latent infection
whats the vaccination for TB?
BCG (Bacille Palmette Guerin) against M. bovis
what are atypical mycobacteria?
don’t spread from person to person
how are atypical mycobacterial infections managed?
similar diagnosis and treatment, although treatment may be more prolonged
an additional macrolide may be needed
what is another term for leprosy?
Hansen’s disease
what is the species that causes leprosy?
M. leprae
what are the 2 extreme clinical forms of leprosy?
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
how is leprosy treated?
dapsone, rifampicin, clofazimine
