Tuberculosis Flashcards
How many percentage of the world’s population have TB?
30%
How many people develop TB annually
About 8 to 10 million
How many children U15 develop TB and what percentage?
1 million (11%)
How many people die from TB annually? How many children are included in this number?
About 3 million people die from TB annually including 250,000 children
Majority of children with TB infection develop clinical symptomatology - True/False
False - Majority of children with TB infection develop NO clinical symptomatology
What is the lifetime risk of progression of TB in older children
5 to 10%
What is the difference between smear negative and smear positive TB and what is the significance of this difference?
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.
What is the percentage of smear negative cases of TB in U12 children
95%
There is decreased risk of progression and development of extra pulmonary disease in the first 2 years of life - True/False
False - There is INCREASED risk of progression and development of extra pulmonary disease in the first 2 years of life
What are the factors responsible for the resurgence in the incidence of TB globally?
Worsening economic situations
Multidrug resistance
HIV pandemic
Large number of displaced persons living in poor conditions as a result of conflicts and wars
What are the pathogens that can cause TB
M. TB
M. bovis
M. africanum
M. microti
M. canetti
How can M. bovis infection be acquired?
Drinking unpasteurized milk
What type of TB does M. bovis cause?
Abdominal TB
Why is M. TB referred to as an acid fast bacilli?
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”
What are the predisposing factors for developing TB?
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
How is M. TB acquired?
Inhalation of infected droplets
Drinking infected milk
Abrasions on the skin
Conjunctival sac and genitalia
Congenital via placenta transmission
What happens when the tubercle bacilli enter the alveolar spaces of the lungs?
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
What is the primary complex?
The primary focus + regional lymph glands
What is the fate of the primary complex?
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
Signs of early manifestation of TB
Evidence of primary lesion
Erythema nodosum
Phlycternular conjunctivitis
Poncet’s arthritis
Signs of TB within 3 months
Military TB
TB meningitis
Signs of TB within 1 year
Pleural effusion
Signs of TB within 3 years
Bone and joint lesions
Signs of TB within 5 years
Progressive pulmonary disease
Signs of TB after 5 years
Renal TB
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
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.
What are the types of the tuberculin skin test
Mantoux test
Head
Tine
BCG vaccination
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
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.
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.
What are the types of TB
Pulmonary TB
Extra pulmonary TB
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
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.
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
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.
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
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.
What organs are affected in abdominal TB
Organs affected: mesenteric and retroperitoneal lymph nodes, peritoneum, omentum and gut
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
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”
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
What is the most common cause of death in very young children with TB
TB meningitis
When is the greatest incidence and most severe manifestations of TB meningitis
first 2-3 years of life
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
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
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
How does brain tuberculoma present
As space occupying lesion
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
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
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
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
How would you treat TB spine
Prolonged immobilization e.g. with the use of a spinal jacket + TB chemotherapy
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
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
What are the first line TB drugs
Rifampicin
Isoniazid
Pyrazinamide
Ethambutol
Streptomycin
Thiacetazone
What are the second line anti TB drugs
ethionamide
para-aminosalicylic acid
Ofloxacin/levofloxacin/moxifloxacin, Cycloserine/terizidone, Kanamycin/amikacin, Capreomycin
What are the bacterocidal TB drugs
Rifampicin
Isoniazid
Pyrazinamide
Streptomycin
What are the bacterostatic TB drugs
Thiacetazone
Ethambutol
Ethionamide
What are the doses of the first line TB drugs
Rifampicin 15mg/kg
Isoniazid 10
Pyrazinamide 35
Ethambutol 20
Streptomycin 15
What is the treatment for TB in Nigeria
2RHZE/4RH for TB and TB lymphadenitis
2RHZE/10RH for severe forms of TB
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
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
What is the supportive therapy for TB treatment
Improved Nutrition
Screening of immediate family members
Surgical intervention where necessary
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
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
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.
