Mycobacteria Flashcards
Which 3 groups of mycobacteria did we talk about?
- M. Tuberculosis
- Atypical mycobacteria
- M. Leprae
Are mycobacterium and mycoplasma the same?
No, mycoplasma is a bacteria without a cell wall and normally doesn’t cause deathly infections unlike mycobacterium.
M. Tuberculosis is the most common infectious cause of mortality worldwide. M. Tb can’t be gram stained. Explain the acid fast stain.
- Smear patient’s sputum on slide and fix it via heat
- Cover whole smear with carbol fuschin dye
- Steam over boiling water (necessary to get stain into mycolic acid)
- Decolorize with acid alcohol
- Rinse, add acid
- Counter stain with methylene blue.
M. Tb will appear fuchsia, non tb will stain blue
M. Tb is an obligate aerobe. It is very slow growing in cultures and in human host which creates a problem in diagnosis and treatment. Explain.
Since there is multidrug resistant tb, it is impt to so anti microbial sensitivity assay before prescribing abx. But tb grows so slowing in vitro (1-2 wks). Performing the assay will also take a few weeks so giving appropriate treatment could be delayed as long as a little over a month.
Does m. Tb secrete toxins?
No toxins
How is m. Tb transmitted?
Inhalation of infected aerosols
Why are guinea pigs impt in clinical testing of m. Tb?
M. Tb is pathogenic in guinea pigs but other mycobacteria that can mimic TB are not pathogenic in guinea pigs so this is a good way to differentiate real tb from mimics
Tb can be extra cellular and intracellular and are very environmentally hardy. Explain.
Tb is extracellular as its being inhaled. Tb can be phagocytosed by naive macrophages and not get killed (hence is also an intracellular pathogen). It is environmentally hardy because resistant to acid and alkali
What are three structural components of mycobacteria tuberculosis?
- Mycolic acids
- Phosphatides (caseation necrosis)
- Cord factor gives tb it’s microscopic serpentine appearance and is a virulence factor
Does tb get its abx resistance via plasmids?
No, drug resistance is chromosomal
M tuberculosis pathogenesis
- Via inhalation
- Replication in lungs
- Form ghon complexes that actively proliferate and want to go to blood
- Additional sites of proliferation in lungs causing development of infectious sputum
- Swallow infectious sputum causes GI infection
- Ghon complexes breach blood
- Some will use macrophages like Trojan horses (salmonella typhi), some will be free bacteria in blood
What are two potentially fatal consequences of m tuberculosis in patients under 5 and/or immuno suppressed or the very old?
Miliary tb -millet seeds all over body
Tb meningitis
If patient is healthy, s/he can close off tb with help of active immunity, forming
Tb granulomas which have oxygen! Impt because tb is an obligate aerobe. These granulomas can calcify over the years.
Immunosuppression can cause reactivation of tb
In neck - scrofula In kidneys - genitourinary tb In gut - GI tb In spine/long bone - skeletal tb In lungs - reactivating pulmonary tb
M tuberculosis can travel to which 4 extrapulmonary sites via hematogenous spread
Kidneys, meninges, bones and lymph nodes
What are the 2 phases used to explain the cellular pathogenesis of tb?
First, tb will grow for 2-3 wks. Then the 1st phase of cell-mediated immunity to stop the growth involves cd4 helper T cells activate infected macrophages to kill intracellular bacteria. The 2nd phase is when cd8 suppressor T cells lyse other infected macrophages.
Dormant tb is holed up in granulomas. Which 3 other infections can cause reactivation of TB?
Measles, varicella and pertussis
What are tubercles and when are they found in tb infection?
Tubercles are caseating granulomas that develop when cd8 cells lyse infected macrophages (2nd phase of cell mediated immunity against tb).
Should you give patients with dormant tb the drug remicade?
No, remicade is a TNF-alpha antagonist. Should not be given to patients with latent tb bc TNF-alpha helps maintain dormancy.
What is the role of TNF-alpha in tb?
TNF-alpha can maintain the latency/dormancy of tb
Risk factors of tuberculosis
Crowded at-risk environments like prisons, homeless shelters and hospitals
What are some risk factors for poor outcome of tb?
- under 5 y.o
- immunosuppression (HIV, cancer)
- steroids
- IFN-gamma deficiency (cannot activate macrophages)
- on remicade
75% of Tb is classic active pulmonary TB. What are some symptoms?
cough, weight loss, fever, night sweats, hemopytesis, and chest pain. (Consumption)
Classic active pulmonary TB is easily diagnosed. What are two ways?
1) Acid fast stain
2) CXR - will show non-calcified round infiltratres; cavity formation
Scrofula is when there’s TB reactivation in lymph nodes causing neck enlargement. What if you see children with scrofula?
Children with scrofula are most likely not due to TB; most likely another mycobacterium.
What is the most common site of extrapulmonary infection of TB? What are some of the symptoms?
Genitourinary TB; symptoms include infertility/weird UTI.
Primary TB infection that infects the kidneys. Will the patients present with symptoms immediately?
No, it might not be until 20 years later before symptoms appear
TB meningitis is most common complication in what group of people? What are some signs/symptoms?
TB meningitis often affects children. Symptoms include high inflammation, nuchal rigidity, lethargy, and positive Brudzinski’s neck sign.
Describe a positive brudzinski’s neck sign and what does it test for?
Positive brudzinski’s neck sign is when you lift someone’s neck up and his/her knees pop up as well. It is a sign of meningitis.
What is Pott’s Disease?
When TB is reactivated in spine, causing back pain, stiffness, and paralysis of lower extremities.
GI TB is very rare due to which procedure? And why might it become more common?
GI TB is rare due to pasteurization. it might become more common due to a current trend of people drinking raw milk.
What are two ways to diagnose TB? How are they different?
1) PPD/Tuberculin Skin test to detect previous exposure
2) IGRA (IFN-gamma release assay) -specific for TB
* **PPD will read positive for ppl vaccinated against TB while IGRA won’t.
How to prevent TB?
Best way is to improve standard of living by providing good housing and nutrition.
What is the drug regimen for TB?
Normally a 4-drug regimen including ISONIAZID
BCG Vaccine
- live attenuated M. Bovis
- prevents up to 70% symptomatic infections, but may not prevent infection
- will test positive in tuberculin skin test, but not in IGRA
Eradication of TB seemed possible until
AIDS
In pediatric cases of TB, watch out for
1) Miliary disease
2) meningitis
What to do with patient with active TB?
4-drug regimen including IZONIAZID, isolate for 2 weeks and test for abx resistance
What’s the biggest difference between mycobacterium tuberculosis and atypical mycobacteria?
The biggest difference is atypical mycobacteria has environmental sources while m. tb has a human reservoir.
Group 1 Atypical Mycobacteria = Photochromogens can cause
fishtank granuloma (due to dealing with fishtanks)
Group 2 Atypical Mycobacteria = Scotochromogens can cause
scrofula (hence, mimic TB when patient is immunocompromised)
How do photochromogens and scotochromogens differ in terms of their production of pigment?
Photochromogens can produce pigment when grown in light while scotochromogens can produce pigment when grown in light or dark.
Group 3 Atypical Mycobacteria = Nonchromagens
can mimic TB when pt is highly immunosuppressed. Also, is highly resistant to drugs.
Group 4 Atypical Mycobacteria = Rapidly Growing Mycobacteria
are found part of normal flora
Is mycobacterium leprae culturable? What is the implication of this fact?
mycobacterium leprae is NOT culturable, making it extremely difficult to study
What are the 2 reservoirs of mycobacterium leprae?
- humans
2. armadillos
How long is the incubation period of m. leprae?
it is the slowest growing human pathogen with an incubation period of months to 50 years
What is the significance of m. leprae preferring to grow in 30 celsius?
M. leprae will cause skin infections (cooler)
There are 2 extremes of leprosy?
- Tuberculoid form aka paucibacillary leprosy
2. Lepromatous form aka multibacillary leprosy
Explain the role of CMI in the 2 extremes of leprosy.
In tubercoloid form, there’s a strong CMI response. The immune response is so strong that it can cause nerve damage. In lepromatous form, there’s inadequate CMI response, leading to extensive skin scarring. The nerve damage is due to bacterial infection.
In leprosy, the PPD test is used to? how does that differ from how it’s used for TB?
In m. leprae, the PPD test is used to assay and stage the disease whereas in m. TB, the PPD test is to detect previous exposure.
How will the PPD test read for people with the two different extremes of leprosy? Explain why this happens.
People with the tuberculoid form will test positive, while people with the lepramotous form will test negative. The PPD test indicates the level of CMI. It does not detect exposure to m. leprae.
What is the treatment for leprosy (Hansen’s Disease?
Dapsone and rifampin for 2 years, but it doesn’t fix the nerve damage
In atypical mycobacterial infection, what do you see in adults and in children?
In adults, you see cutaneous infections while in children, you see scrofula.
mycobacterium kansaii belongs to which group of mycobacteria
atypical mycobacteria and can cause systemic symptoms in immunosuppressed hosts.
About how many people are actually susceptible to getting leprosy after being infected with m. leprae?
about 5-10%. Most people will seroconvert and be asymptomatic and w/o disease.
