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Mycobacterium Tb Flashcards

1
Q

What type of bacterium is mycobacteria

A

It is a long slender straight or a slightly curved, red in colour with beaded appearance with blue background
These are obligate aerobes which grow slowly and have a doubling time of 18 hours.
it is an acid-fast bacteria due to long chain fatty acids called
mycolic acids in their cell wall. they have a cord factor which is correlated with the virulence of the organism

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2
Q

How mycobacterium can be stained

A

We use zeihl Neelson method of staining as they resist decolourization by acid or acid alcohol mixture
They are neither gram positive nor gram negative and stain poorly with gram stains

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3
Q
A
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4
Q

Other acid fast bacteria

A

M. Leprae 5% h2so4
Nocardia 1% h2so4

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5
Q

Pathogenic classification of mycobacteria

A
  1. Always pathogenic:
    m tuberculosis
    M leprae
    M bovis
  2. Potentially pathogenic
    Saprophytic or rarely pathogenic
  3. Atypical mycobacteria
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6
Q

Calssify atypical mycobacteria and why are they called so
Runyon classification

A

Group 1 photochromogens
Group 2 scotochromogens
Group 3 non chromogen
Group 4 rapid growers

These bacteria are called atypical because they have different characteristics than that of typical Mycobcteria and they do have different disease manifestations

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7
Q

Photochromogens

A

Produce yellow orange pigment both in presence of light and dark.
M. Kansasi: pulmonary disease
M. Marinum: swimming pool granuloma
M.simiae
M.asiaticum

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8
Q

Group 2 scotochromogens

A

Produce pigment both in presence of light and dark.

M scrofulaceum
M. Gordonae
M. Xenopi

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9
Q

Group 3 non chromogens

A

Do not produce pigment either in presence or absence of light
M. Avium intracellulare complex which causes pulmonary tb in aids patient.
M. Malmaens

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10
Q

Group 4 rapid growers

A

Grows quickly
Colony appears in 3 days
M. Fortuitum
M.chelonei
M. Flavecens

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11
Q

Saprophytic mycobacteria

A

M. Gordonae
M. Flavescens
M. Gastri
M. Terrae
M. Smegmatis

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12
Q

Mode of transmission of tb

A

Humans are the national reservoir of Michael back to tradition Tuberculosis
2. inhalation: During coughing sneezing talking spitting from smear positive person via respiratory tract: droplet infection
airborne
3. ingestion of raw or unpasteurised milk is Mycobacterium bovis and by direct contact with tubercular lesion occurs in the skin of the persons doing autopsy

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13
Q

Pathogenesis of tb

A

The incubation period is several weeks to many years. progression of disease depends on personal, immune and nutritional status, virulence of The Strain and infective disease Tuberculosis develops if the immune system weakens as in malnutrition
Aids
diabetes
cancer
treatment with immune suppressant drugs.
following inhalation
Mycobacteria reaches lungs after being ingested by alveolar macrophage.
2 types of lesions are produced exudative and productive Spread Mycobacterium :
may multiply within the macrophage leading to lysis of the cell and spread to the adjacent area by direct extension.
phagocytes with Ingested Mycobacteria may act as a vehicle transporting the infection to various parts. infection may spread to regional lymph nodes through lymphatics causing lymphangitis. The the bacteria may reach the bloodstream and then cause erosion of the vein by caseating tubercle

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14
Q

According to site of involvement tb

A

Pulmonary
Extra pulmonary

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15
Q

Sited of extra pulmonary tb

A

Cervical lymphnodes
Tonsils
Intestine
Skin
Serous cavities
Joint
Bones
Brain
Meninges

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16
Q

Organ that escapes from tb

A

Cardiac muscle
Skeletal muscle
Thyroid gland
Pancreas

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17
Q

Diagnose tb

A

Clinical features and lab diagnosis
Cf-
1.General cond: fatigue, weakness, fever, night sweats and anaemia of chronic infection
2. Pulmonary tb: chronic cough and haemoptysis
3. Scrofula: cervical lymphadenitis
4. Miliary tb
5. Meningitis
6. Lymphadenitis
7. Gi tb
8. Renal tb
9. Oropharyngeal tb

Lab diagnosis
Specimen
Microscope exam
Culture
Biochem test
Serological test
Gene x pert
Tuberculin test
Igra test

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18
Q

Specimen for mycobacterium tb

A
  1. Sputum for pulmonary tb
    :3 samples to prevent contamination. Bacilli may not be present in every sample
    Day 1 on spot specimen and container is given
    Day 2 overnight morning sample and spot sample

2.Csf
3. Aspirated fluid
4.morning urine for renal tb
5. Endometrial tissue for uterine tb
6. Gastric washing in children
7. Blood for serology

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19
Q

Microscopic exam m. Tb

A

2 types of afb stain
1. Zeihl neelson stain
2.Fluroschrome stain: smear is stained with auramin and rhodamin and seen under fluorecence microscope
Bacilli appear brilliant yellow against dark bg.

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20
Q

Culture m. Tb

A
  1. Solid media: lowenstein jensen media containing egg and malachite green
    Egg is used for enrichment
    Dye. Malachite green inhibits the normal flora present in sputum sample.
    Requires 3-6 weeks for growth to appear.
    Colonies are dry wrinkled and tenacious.
    At first white and later buffy coloured
  2. Semisynthetic agar media
    Middle brook 7H10
    7H11
  3. Liquid media
    Middle brook 7H9 and 7H12
    Bactec media
    Others: dubos media and tissue culture media
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21
Q

Biochemical test m tuberculosis

A

M.tuberculosis produces niacin
Niacin +
Catalase+

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22
Q

Serological test m tb

A

Elisa
Pcr

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24
Q

Gene xpert

25
Tuberculin test
Certain degree of resistance is offered by the host that limits the spread and multiplication of the organism which is provided by CD 4 +t cells and at the same time some delayed hyperensitivity reaction mediated against tuberculo protein of mycobacterium Tuberculosis occurs assessed by tuberculin test Reagent: ppd Method 5-T U of ppd is 0.1 ml is injected intradermally in the flexor aspect of forearm. reading is taken 48 to 72 hrs after. Induration is measured not erythema Interpretation: Positive: >10mm Negative <5mm Borderline. 6-10mm In hiv >5mm
26
False negative test in tuberculin test
1.Injection of ppd in deeper layer. 2. improper storage and handling of ppd reagent. 3 acute viral infection 4. overwhelming infection 5.measles 6.hodgkins disease 7.Immunosuppressive disease 8.faulty technique
27
Bcg vaccine source and efficacy
Strain of m.bovis called bacillus calmette gurein Efficacy is 0-70 % 0.05 ml 1 dose in the lower part of left deltoid Intradermal at birth within 6 weeks
28
Cellular constituents of m tb
Cell wall 1. Lipid containing mycolic acid, waxes-d , phosphatids Mycolic acid is responsive for acid fastness 2. Protein: tuberculin 3. Cho- polysaccharide Cell memb made of lipid bilayer Virulence factors like Cord factor helps the virulent strains to grow in a sepentine cord like fashion Arabinogalactan Lipoarabinomannan Heat shock protein
29
Pr and sec tb
Pr tb occurs in children Sec tb adults Pr tb results from exogenous source Sec tb results from endogenous source Pr tb site is base of the lung Sec tb site is apex of the lung Pr tb produces exudative lesion Sec tb produces productive lesion
30
Why secondary lesions occur at apex of lung
Because it is well oxygenated Sec infection occurs after reactivation of tubercle bacilli that survived pr lesion.
31
How long does it take to grow
It grows slowly having a doubling time of 18 hours So specimen must be held for 6-8 weeks before being recorded as negative
32
TREPONEMA MORPHOLOGY
These are thin walled,long, slender helically coiled , fexible, spiral or cork screw shaped rods with tapered ends motility: they show cork screw motili,ty a rapid rotation along the long axis, flexion, bending and snapping about the full length they are actively motile through axial filaments that lie under the outer sheath rotating steadily around their endoflagella. locomotive even in high viscosity. They differ from other bacteria by the location of their flaggilla that is they are endoflagellated. they are seen only by dark field microscopy ,silver impregnation and immune of florescence. they can easily swim through gel like material.
33
Species of treponema
T.palidium T. Endemicum T.pertenue T. Carateum
34
Calssify syphilis
A. Congenital B. Acquired: Primary Secondary: early latent and late latent Tertiary: benign tertiary Neurosyphillis Cardio syphillis
35
Pathogenesis of pr syphillis
Treponema enters through mucus membrane Or ulcer of skin. it will then spread to the regional lymphnode and inguinal lymph node It multiplies in the lymph node reaches the bloodstream and gets seeded into the body. 2. OR It may multiply at the inoculation site and form papule , it turns into a vesicle and then ruptures and produces ulcer with a clean hard base known as hard chancre
36
Fate of pr syphillis
40% secondary syphillis 30% complete resolution 30% latent phase without passing into sec syphillis
37
Secondary syphilis
It develops when the Cmi is decreased or HI is hyper active. Lesions are Rich in spirochetes And highly infectious. subsides within few weeks due to cmi. 10 to 90 days after primary syphillis, if untreated it gives rise to maculo popular rash mouth ulcer condylomalata alopecia
38
Fate of sec syphillis
Full recovery if treatment is given 40% tertiary syphilis 30% complete cure with treatment 30% latent life long
39
Stages of syphillis with corresponding lesions produced
1. Primary: hard chancre 2 secondary: condyloma lata 3.
40
Benign tertiary syphilis
3 to 10 years after secondary syphilis due to delayed type of hypersensitivity response to treponema antigen. nonprogressive granulomatous lesion also known as gumma which has gum like consistency
41
Neurosyphillis
5 years after benign tertiary syphillis patient is asymptomatic sero reactive csf+ during incubation period even before the development of primary syphillis.bacteremia develops and 30% CNS invasion occurs 50% of the patients get spontaneous resolution rest develops neurosyphilis. so during late period they are also seroreactive CSF positive but no signs and symptoms. Pathology is end Arthritis obliterans leading to ishchaemic necrosi,s stroke Tabes dorsalis Classical features Paralytic dementia Taves dorsalis Meningocvascular syphillis Optic atrophy Generalised paresis
42
Cardiac syphilis
10 to 40 years after more common and more fatal than neuroscephilis end arteritis obliterans of vasavenorum causes median necrosis which will lead to destruction of elastic tissue and aneurysm. aneurysm is the bulging out of the great vessels and if it is ruptured it is fatal. it is commonly in ascending aorta, aortic arch, descending aorta rarely
43
Congenital syphilis
Foetus is not infected before 16 weeks of gestation presence of languor hands layer of Korean transmission is translacent Outcome Death of some infected fetus miscarriage stillborn live born develops interstetial keratitis Hutchinson's teeth saddle nose periostitis CNS anomalies 8th cranial nerve defect
44
Clinical features of sec syphilis
1. Low grade fever Anorexia Wt loss Malaise Meningitis Myalgia Pharyngitis Nephritis Hepatitis Headache
45
Difference btw chancre and chancroid
Chancre is flat dull red indurated ulcer Chancroid is non indurated irregular ulcer Chancre is caused by treponema palidium Chancroid is caused by h. Ducrei Chancre is painless Chancroid is painful Chancre has a clean hard base Chancroid has an unclean soft base
46
Disease transmission of syphilis
Sexual contact Transplacental Fresh blood transfusion Accidental inoculation Invades the intact mucous memb and abraded skin
47
Lab diagnosis of syphilis
Specimen: exudate from squeezing the base of hard chancre Serum: for serology Csf: for neurosyphilis Microscopic exam DGI to see cork screw motility and immunoflorecence to differentiate between pathogenic strains (apple green ) and non pathogenic that do not take stain. Serological test 1. Specific : TPHA FTA- AB test most specific and confirmatory TPI test 2. Non specific: A.Flocculation test . Vdrl Rpr rapid plasma reagin Trust toludene red unheated serum test B. Cft C. Newer tests Elisa Naat pcr Rt pcr These are non specific because antigens are derived not from treponema but beef heart Ag. Is cardiolipin Ab is reagin
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49
Lab diagnosis for neurosyphilis
Specimen: csf 1. Reactive serological test 2. Csf abnormality 3. Vdrl csf
50
Lab diagnosis of congenital syphilis
Specimen: placenta and umbilical cord Aspirates from lesions Nasal discharge Body fluid Serum Microscopic exam: Placenta and umb cord: dif and silver staining Specimen from lesion: dif and dgi Serology: quantitative vdrl Transplacentally acquired non treponemal ab will be present in infants and disappears in 2-3 months Increasing titre is diagnostic Specific test: fta-abs and elisa
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Screening test for syphillis
Vdrl It is confirmed by specific tests Advantages of vdrl: 1.screening for both diagnosis and mass screening of syphillis 2.to see the prognosis of disease Disadv: Lacks sensitivity in early and late syphilis False positive reaction may occur Prozone effect may cause false neg result
53
Adv of tpha and disadv
It is more sensitive than vdrl in detection of latent and late syphilis. It is highly specific Easy to perform Disadv It is time consuming Cant assess response to treatment
54
Adv and disadv of fta ab test
Adv: 1.Highly specific 2.Once + ve remains + for life 3.Positive test indicates infection whether present or past 4.It becomes positive before non specific tests Disadv: too costly Expertise is necessary
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56
It is an exagerrated and inappropriate immune response of tissue or body to an ag in a previously sensitized indivisual leading to gross tissue damage
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Micro Term 1 (3 decks)

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