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Tuberculosis Flashcards

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1
Q

How many percentage of the world’s population have TB?

A

30%

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2
Q

How many people develop TB annually

A

About 8 to 10 million

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3
Q

How many children U15 develop TB and what percentage?

A

1 million (11%)

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4
Q

How many people die from TB annually? How many children are included in this number?

A

About 3 million people die from TB annually including 250,000 children

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5
Q

Majority of children with TB infection develop clinical symptomatology - True/False

A

False - Majority of children with TB infection develop NO clinical symptomatology

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6
Q

What is the lifetime risk of progression of TB in older children

A

5 to 10%

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7
Q

What is the difference between smear negative and smear positive TB and what is the significance of this difference?

A

Patients with sputum smear–negative TB are less infectious than patients with sputum smear–positive TB

Nevertheless, patients with smear-negative, culture-positive pulmonary TB are capable of transmitting M. tuberculosis

In a case where only smear positive cases are reported, it leads to underestimation of the burden of TB in children.

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8
Q

What is the percentage of smear negative cases of TB in U12 children

A

95%

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9
Q

There is decreased risk of progression and development of extra pulmonary disease in the first 2 years of life - True/False

A

False - There is INCREASED risk of progression and development of extra pulmonary disease in the first 2 years of life

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10
Q

What are the factors responsible for the resurgence in the incidence of TB globally?

A

Worsening economic situations

Multidrug resistance

HIV pandemic

Large number of displaced persons living in poor conditions as a result of conflicts and wars

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11
Q

What are the pathogens that can cause TB

A

M. TB
M. bovis
M. africanum
M. microti
M. canetti

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12
Q

How can M. bovis infection be acquired?

A

Drinking unpasteurized milk

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13
Q

What type of TB does M. bovis cause?

A

Abdominal TB

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14
Q

Why is M. TB referred to as an acid fast bacilli?

A

They have a waxy outer capsule so they do not take up the usual stains for bacteria but absorb carbol fushcin stain when heated and resist decolourization by acid and alcohol – “acid fast bacilli”

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15
Q

What are the predisposing factors for developing TB?

A

Very young and very old, adolescents and pregnant women

Malnutrition

Over crowding

Immunosupression from drugs or disease e.g HIV, diabetes, malnutrition, steroid use.

Measles, pertussis, kwashiorkor

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16
Q

How is M. TB acquired?

A

Inhalation of infected droplets
Drinking infected milk
Abrasions on the skin
Conjunctival sac and genitalia
Congenital via placenta transmission

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17
Q

What happens when the tubercle bacilli enter the alveolar spaces of the lungs?

A

The tubercule bacilli are engulfed by macrophages.

The macrophages destroy some of these tubercules while some multiply in the macrophages, causing their death.

The organisms are then released and they attract more macrophages as well as lymphocytes from the blood stream, forming a small focus of granulomatous infiltration called a tubercule

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18
Q

What is the primary complex?

A

The primary focus + regional lymph glands

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19
Q

What is the fate of the primary complex?

A

It usually heals with or without calcification

It may become dormant with possible later reactivation

It may be complicated by acute dissemination (especially in infants) and give rise to miliary TB or TB meningitis

The local lesion may heal but organisms disseminated to other sites e.g the bones, joints, liver, kidney etc may cause disease at a later date

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20
Q

Signs of early manifestation of TB

A

Evidence of primary lesion

Erythema nodosum

Phlycternular conjunctivitis

Poncet’s arthritis

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21
Q

Signs of TB within 3 months

A

Military TB
TB meningitis

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22
Q

Signs of TB within 1 year

A

Pleural effusion

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23
Q

Signs of TB within 3 years

A

Bone and joint lesions

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24
Q

Signs of TB within 5 years

A

Progressive pulmonary disease

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25
Signs of TB after 5 years
Renal TB
26
What is the basis of the tuberculin skin sensitivity test?
Infection with mycobacterium TB or mycobacterium bovis leads to development of delayed hypersensitivity to the tubercular protein which forms the basis of the tuberculin skin sensitivity test
27
When does the tuberculin skin test become positive?
Within 4 to 8 weeks after exposure, either due to a natural infection or after BCG vaccination. The skin response is more after a natural infection.
28
What are the types of the tuberculin skin test
Mantoux test Head Tine BCG vaccination
29
Describe the mantoux test
Mantoux test 0.1ml of diluted tuberculin at a dose of 5 tuberculin units (TU) of purified protein derivative (PPD) is given intradermally into the volar aspect of the forearm and the reaction is read after 48 – 72hrs. The reading is based on the size of the transverse induration. Positive - ≥10mm 6 – 9mm - equivocal ≤ 5mm – negative ≥ 15mm or presence of any vessiculation should be regarded as due to TB infection
30
Describe the response of a patient that has naturally been exposed to TB to BCG vaccine
Children with natural TB infection will respond to BCG vaccination with an accelerated reaction i.e. induration within 48hrs, a pustule on the 3rd day and a scab by 5-6 days leading to scar formation within about 2 weeks.
31
What are the clinical features of primary TB
There may be no apparent illness Conversion of tuberculin test from negative to positive General symptoms: weight loss and failure to thrive, unexplained pyrexia, loss of appetite, lack of energy, sweating, abdominal pain. Other symptoms: erythema nodosum, phlyctenular conjunctivitis, Poncet’s arthritis.
32
What are the types of TB
Pulmonary TB Extra pulmonary TB
33
List the types of extra pulmonary TB
TB lymphadenitis Abdominal TB TB meningitis Bone and joint TB TB of the spine Renal TB TB epididymo-orchitis Female genital tuberculosis TB of the skin TB of the larynx TB of the nose and palate
34
Describe the clinical presents of pulmonary TB
Enlarged hilar glands causing obstructive emphysema, lung collapse, bronchiectasis, or endobronchial TB. Tuberculous bronchopneumonia Pericardial effusion or constrictive pericarditis Pleural effusion Pneumothorax Miliary TB Tracheal compression from enlarged mediastinal or paratracheal glands causing stridor.
35
How would you make a diagnosis of pulmonary TB
History of contact Positive tuberculin test Chest x-ray Detection of M.TB in pulmonary secretions i.e. sputum or gastric aspiration Therapeutic trial of anti-TB drugs
36
Describe TB lymphadenitis
Most commonly affected site is the neck Glands are initially discrete, rubbery in consistency and slightly tender but soon become matted together and may break down to form discharging ulcers or sinuses.
37
How would you make a diagnosis of TB lymphadenitis?
Detection of organisms from exudates from ulcers or sinuses Biopsy of the lymph nodes for microbiology and histology Therapeutic trial of anti-TB drugs
38
Abdominal TB only occurs with M. bovis infection - True or False
False - May occur as a secondary disease from infection with M.TB or as a primary disease from infection with M. bovis.
39
What organs are affected in abdominal TB
Organs affected: mesenteric and retroperitoneal lymph nodes, peritoneum, omentum and gut
40
Describe the pathology of abdominal TB
Lymph nodes may become massively enlarged and present as abdominal tumors There may be ascites Intestinal obstruction may occur Involvement of the bowel may result in chronic malabsorption or TB enteritis
41
What are the clinical features of abdominal TB
Insidious onset with malaise, low grade fever, weight loss, diarrhoea, constipation Abdominal distension Symptoms of intestinal obstruction like colicky pain, vomiting and constipation Occasionally, chronic diarrhoea, weight loss, abdominal distension and other signs suggestive of malabsorption. Signs: vague sense of fullness and increased resistance to palpation described as “doughy abdomen”
42
How would you diagnose abdominal TB
Tuberculin skin test is usually positive Evidence of PTB on chest x-ray is supportive Plain abdominal x-ray may reveal calcification of lymph nodes Aspiration of the ascitic fluid shows that it is an exudate Demonstration of the organism in ascitic fluid Therapeutic trial of anti-TB drugs
43
What is the most common cause of death in very young children with TB
TB meningitis
44
When is the greatest incidence and most severe manifestations of TB meningitis
first 2-3 years of life
45
Describe the pathogenesis of TB meningitis
May occur as part of a miliary TB but more often arises in the absence of miliary TB Results from hematogenous seeding of the brain or spinal cord by tubercule bacilli during primary infection There is an inflammatory process in the meninges which tends to occur at the base of the brain involving the cranial nerves, obstructing CSF circulation with peri-arteritis and end-arteritis of the cerebral blood vessels which may impair blood supply to areas
46
Describe the clinical presentation of TB meningitis
Three phases General symptoms and signs: malaise, fever, poor appetite, apathy, irritability, headache, vomiting Signs of neurologic involvement: convulsion, signs of meningeal irritation, cranial nerve palsies, pyramidal signs, significant behavioural modification Coma Examination of the fundi occuli may show papilloedema and/or choroidal tubercules
47
How would you diagnose TB meningitis
Tuberculin skin test may be positive Chest x-ray may show evidence of PTB Sputum or gastric lavage may reveal mycobacteria FBC: marked lymphocytosis CSF studies: raised CSF pressure, or there may be a block, CSF may be xanthochromic CSF may be xanthochromic or turbid. A delicate “spider web” clot will form in the CSF left undisturbed for some hours. The organisms may be identified from a smear of this clot. CSF microscopy: in early disease, there is a mixture of polymorphs and lymphocytes, with polymorphs predominating but later, lymphocytes predominate. CSF protein is usually raised CSF glucose is usually low
48
How does brain tuberculoma present
As space occupying lesion
49
Describe bone and joint TB
Lesions are characterized by bone destruction without evidence of new bone formation Most common site is the spine Most common joints affected are the knees and hips
50
Describe TB of the spine
Usually originates in the body of the vertebrae leading to bone destruction The spinal processes and vertebral arches are usually spared The intervertebral disc spaces are usually involved with erosion and narrowing of the disc spaces
51
What are the clinical features of TB spine
Pain in the spine, exacerbated by impact on walking, running, jumping and bending With disease progression, the affected vertebral bodies collapse, causing angulation of the spinal column “gibbus” There may be spinal cord compression leading to increased muscle tone, exaggerated tendon reflexes and positive ankle clonus
52
How would you diagnose TB spine
Clinical evidence of spinal involvement X-ray of the spine: bone destruction without new bone formation with involvement of the disc spaces Positive tuberculin test Evidence of TB at other sites e.g. PTB There may be para-spinal abscess
53
How would you treat TB spine
Prolonged immobilization e.g. with the use of a spinal jacket + TB chemotherapy
54
Why type of TB is seen in PLWHIV
In addition to pulmonary lesions, there may be extra-pulmonary TB in 40-75% of cases. TB is usually atypical
55
What are the principles of drug treatment in chemotherapy of TB
Drugs must never be given singly Treatment must be continuous and long enough to kill off the bacilli i.e about 6-18 months At the onset, at least 3 drugs should be given Once a drug regimen has been started, it should not be altered unless there is toxicity
56
What are the first line TB drugs
Rifampicin Isoniazid Pyrazinamide Ethambutol Streptomycin Thiacetazone
57
What are the second line anti TB drugs
ethionamide para-aminosalicylic acid Ofloxacin/levofloxacin/moxifloxacin, Cycloserine/terizidone, Kanamycin/amikacin, Capreomycin
58
What are the bacterocidal TB drugs
Rifampicin Isoniazid Pyrazinamide Streptomycin
59
What are the bacterostatic TB drugs
Thiacetazone Ethambutol Ethionamide
60
What are the doses of the first line TB drugs
Rifampicin 15mg/kg Isoniazid 10 Pyrazinamide 35 Ethambutol 20 Streptomycin 15
61
What is the treatment for TB in Nigeria
2RHZE/4RH for TB and TB lymphadenitis 2RHZE/10RH for severe forms of TB
62
List the adverse effects of the first line TB drugs
Isoniazid Skin rash, hepatotoxic, peripheral neuritis, psychosis Rifampicin Hepatoxic, red urine, anorexia, nausea, abdominal pain, thrombocytopenia, drug interactions Pyrazinamide Hepatotoxic, arthralgia Ethambutol Optic neuritis Streptomycin Rash, anaphylaxis, oto-and nephrotoxic
63
What are the indications for corticosteroids in TB treatment
Compression of airway by enlarged glands TB meningitis TB pericarditis Miliary TB Endobronchial TB Large pleural effusion
64
What is the supportive therapy for TB treatment
Improved Nutrition Screening of immediate family members Surgical intervention where necessary
65
Define the various drug resistance in TB
Mono-drug resistance: Resistance to single drug Poly-drug resistance: Resistance to 2 or more drugs, but not to both INH and RMP MDR TB: Resistance to INH & RMP +/- other drugs XDR (extensively drug resistant)TB: MDR & 2nd-line injectable & quinolone Primary resistance: No previous anti-TB Rx or less than 1 month Acquired resistance: Previous anti-TB Rx >1 month
66
What are the causes of drug resistant TB
Poor management of drug-susceptible or mono-resistant TB cases, e.g. incorrect regimens, interrupting treatment (drug supplies, poor bio-availibility), poor adherence by patients Poor management of MDR-TB cases leads to transmission of MDR-TB strains, e.g. late diagnosis, not doing drug susceptibility in relapse/retreatment cases, poor infection control measures especially in high prevalence HIV settings
67
How would you prevent TB in a community
Case-finding and effective treatment. Contact tracing and INH chemoprophylaxis. BCG vaccination. Improvement in the general standard of living.

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