Mycobacteria Flashcards
1
Q
mycobacteria
A
- NOT mycoplasma
- M tuberculosis
- atypical mycobacteria
- M leprae
2
Q
M tuberculosis intro
A
- has existed as a human disease since at least 3000 BC
- the most common infectious cause of mortality worldwide
- > 1/3 world pop infected
- was on the decline due to effective antibiotic treatment (4 drug regimens featuring isoniazid) until AIDS epidemic
- multidrug resistant (MDR) and extensively drug resistant (XDR) are becoming a public health emergency in US and abroad
3
Q
M. tuberculosis bacteriology
A
- mycobacterium gram stain very poorly but are almost uniquely acid fas
- cell wall has some peptidoglycan, arabinogalactin, and mycolic acid-makes it waxy
- grows very slowly in vitro and needs special nutrients
- humans are natural host and reservoir
- very slow growing even in human
- can be intra or extracellular
- produce no toxins
- drug resistance is chromosomal, no known plasmids
- resistant to acid and alkali-environmentally hardy
- important structural components
- pathogenic in guinea pigs
- strictly aerobic
4
Q
acid fast staining
A
- cover smear with carbolfuchsin. Steam over boiling water for 8 minutes, add additional stain if it boils off
- after cooling decolorize with acid alcohol for 15-20 sec
- stop decolorization action with water
- counterstain with methylene blue for 30 sec
- rinse briefly with water to remove excess methylene blue
- blot dry with lens paper and examine with oil immersion
- pos will be pink, neg will be blue
5
Q
important structural components of M tuberculosis
A
- mycolic acid-acid fastness
- phosphatides-caseation necrosis
- cord factor (trehalose dimycolate)-virulence, microscopic serpentine appearance
6
Q
M. tuberculosis pathogenesis
A
- transmitted primarily by inhalation of infected aerosols; rarely transdermal or GI infection
- aerosols are extremely infectious-ID50 t kill
7
Q
pathogenesis 2
A
- proliferates within mononuclear phagocytes, traveling to extrapulmonary sites, where it can establish latent (immunocompetent) or active (peds, HIV+, immunosenescence) extrapulmonary infection in:
- lymph nodes
- kidney
- bones
- meninges
- swallowing infectious sputum infects GI
8
Q
pathogenesis 3
A
- immunocompetent hosts develop latent/dormant infection-only 5-10% lifetime risk for active TB
- current or later immunosuppression allows reactivation
- non TB infections may activate quiescent TB-measles, varicella, pertussis
9
Q
pathogenesis 4
A
- CMI response terminates the unimpeded growth of M tuberculosis 2-3 weeks after initial infection
- CD4 T cells activate some infected macrophages to kill intracellular bacteria (TH1)
- CD8 T cells lyse other infected macrophages-creates caseating granulomas-TB can live there even though we keep sending ROS in
- also called tubercules
10
Q
pathogenesis 5
A
- mycobacteria cannot continue to grow within these granulomas, so the infectious process pauses (latency)
- TNF plays an important role in maintaining latency-TNFa antagonists may reactivate-Remicade
11
Q
pathogenesis 6
A
- 85% of active TB includes lungs
- bacilli proliferate locally and spread through lymphatics to a hilar node, forming the Ghon complex, launch from there to the bloodstream
12
Q
Ghon complex
A
- parenchymal focus and a hilar lymph node lesions
- exudative lesion plus hilar node
13
Q
TB pathway
A
- enters through inhalation and infects lungs
- forms lesions and replication
- forms Ghon complex
- spreads to GI via swallowing
- can get into blood
- in immunocompromised patient can cause meningitis or miliary TB
- in healthy forms granulomas (in places with high pO2)
- granulomas calcify
- can later become reactivated and infectious
14
Q
Scrofula
A
-reactivated neck node
15
Q
Genitourinary TB
A
-reactivated in kidney/ GU
16
Q
GI TB
A
- reactivated in GI
- used to get from M Bovus-unpasteurized milk
17
Q
skeletal TB
A
-reactivated in skeletal system
18
Q
risk factors for infection
A
- crowded at risk environments
- prisons, hospitals, homeless shelters
- HIV
19
Q
risk factor for poor outcome
A
- uncontrolled HIV
- steroids
- IFNgamma deficiency
- TNFa antagonists
- age <5
20
Q
diagnosis-classic active TB
A
- 75%
- present with cough, weight loss, fever, night sweats, hemoptysis chest pain
- may not be able to see acid fast pos in sputum
- chest radiograph
- cavity formation, indicates advanced infectoin, associated with a high bacterial load
- noncalcified round infilrations-may be confused with lung carcinoma
21
Q
diagnosis of scrofula
A
- painless, enlarging or persistent mass
- cervical lymph node affected in 2/3
- systemic symptoms include fever/chills, weight loss, malaise
- ~95% of mycobacterial cervical infections in adults caused by M TB
- in peds trend is reversed-92% of cases due to atypical mycobacterium-acquired by putting contaminated objects in their mouths
22
Q
GU diagnosis
A
- most common site for extrapulmonary infection
- TB almost always reaches the kidneys during the primary infection but does not present clinically; may be 20 years of latency before symptoms
- genital TB secondary to renal TB
23
Q
CNS diagnosis
A
- MRI, CSF tests
- abcsesses
24
Q
skeletal TB diagnosis
A
- MRI
- arthritis of one joint
- pott disease (spinal infection)-back pain, stiffness, paralysis of lower extremities
- don’t delay treatment
25
Q
GI diagnosis
A
- radiograph for calcified granulomas
- CT scans show lymphadenopathy with hypoattenuating center suggestive of necrosis
- exploratory surgery
26
Q
miliary TB
A
- 1.5% of TB cases
- hematogenous spread of TB throughout the body
- many tiny non calcified foci of infection appear like millet seeds in lung on chest xray
- miliary form more likely to develop right after primary infection, less likely as a reactivation
- highest risk is very young and old
- fatal if untreated
27
Q
TB meningitis
A
- develops in 5-10% of children under 2
- nuchal rigidity
- altered deep tendon relfexes
- lethargy
- cranial nerve palsies
- Brudzinski’s neck sign
28
Q
PPD
A
- tests for exposure
- 2-10 weeks post infection
- can use IFNgamma release assay using TB peptides-1 office visit and specific for TB, not vaccine
- either PPD for IGRA may be false neg if patient is badly immunosuppressed or late in course of TB
- HIV pts must be regularly screened for TB and vice versa
- results depend on history
29
Q
treatment
A
- isolate
- drugs for at least 3 mo-6 or 12 if CNS
- isoniazid
- monitor
- monitor pregnant woman blood
30
Q
prevention
A
- good housing and nutrition are disproportionately helpful- healthy CMI drives TB latent
- population load of TB can be significantly decreased by improved standard of living even without access to antibiotics
31
Q
BCG vaccine
A
- live attenuated M bovis
- prevents up to 70% of symptomatic infections
- seldom used in US
- watch for 3-6mm PPD+ if vaccinated abroad or in military-can differentiate with IGRA
- not for immunocompromised
32
Q
atypical mycobacteria
A
- cause neither TB nor leprosy
- environmentally acquired
- PPD TST usually neg
- less aggressive infections
- systemic disease very rare without predisposing condition-HIV, cancer, old age, infected surgical site, diabetes, lung disease
- cutaneous infection most likely in immunocompetent adults, scrofula in children
33
Q
photochromogens
A
- produce pigment when grown in light
- M kansaii is environmental in midwest, texas and england-pulm/systemic disease most closely resembling TB, killed by same antibiotics
- M marinum in fresh and salt water- fish tank granulomatous ulcerating lesions on abrasions exposed to swimming water or aquariums-tetracycline
34
Q
scotochromogens
A
- produce pigment when grown in dark or light
- M scrofulaceum produces scrofula
- reservoir is water, can be harmless in resp tract
- fix by surgically removing affected nodes
35
Q
nonchromogens
A
- M avium/M intracellulare difficult to distinguish, MAI MAC
- cause pulm disease indistinguishable from TB in severely immunocompromised patients
- environmentally widespread, found in soil and water
- highly drug resistant, use clarithromycin in combination with ethambutol, rifabutin or cipro
36
Q
rapidly growing mycobacteria
A
- culturable in less than 1 week
- M fortuitum/ chelonei- found in soil and water, cause problems in immunocompromised, prosthetic hips, indwelling catheters, puncture wounds-amikacin and doxy plus excision
- M abscessus-environmental, chronic lung infections, skin, bone joints- antibiotic resistant
- Smegmatis:normal flora under foreskin
37
Q
M leprae
A
- not culturable
- reservoirs are humans and armadillos
- 14 day doubling time, slowest growing human pathogen
- prefers 30 C for growth-periphery of humans
- genetically appears to be stripped version of M TB
38
Q
M Leprae pathogenesis
A
- causes leprosy/ Hansen disease
- symptoms from both infection and immune response
- worldwide incidence at historic lows, but still deemed PH prob in 9 countries-84% of cases
- 150 cases/ year in US
39
Q
leprae pathogenesis 2
A
- exact mechanism unclear
- requires prolonged contact with infectious cases
- rare zoonosis from armadillos
- extremely long incubation period-months to 50 years
- most common sequel of exposure is asymptomatic seroconversion, only 5-10% pop believed to be immunologically susceptible to symptoms
40
Q
presentations
A
- Paucibacillary-tuberculoid-CMI works with CD4 and TH1 but we react to immune system-6 lesions, infiltrated nodules and plaques, bacilli visible on smears
- symmetric peripheral nerve damage from bacterial growth in Schwann cells
- lepromatin PPD-
41
Q
lep PPD
A
-tests whether immune response it there-milder cases are PPD +
42
Q
leprosy treatment
A
- tuberculoid is dapsone and rifapin, 2 years
- lepromatous is dapsone and rifampin and clofazimine, 2 years
- peds is prophylaxis with dapsone if exposed
