Mycobacteria: TB, Lepros, and Atypicals

Question 1

m. tuberculosis bacteriology

Answer 1

gram stain poorly, but are almost uniquely acid fast. grows slowly in vitro. humans are natural host and reservoir. can be intra or extracellular. produce no toxins. drug resistance is chromosomal. environmentally hardy. obligate aerobe.

Question 2

important structural components of m. tuberculosis

Answer 2

mycolic acids: acid fastness
wax D: adjuvant
Phosphatides: caseation necrosis
cord factor: virulence and serpentine appearance
phtiocerol dimycocerosate: lung pathogenesis

Question 3

m. tuberculosis pathogenesis

Answer 3

transmitted by inhalation of infected aerosols mainly.

Question 4

ghon complex

Answer 4

parenchymal focus and hilar lymph node lesions. forms when bacilli proliferate and spread through the lymphatics to a hilar node. exudative lesion

Question 5

proliferative lesions vs. exudative lesions in TB

Answer 5

prolif develop where bacillary load is small and host cellular immune responses dominate. exudative lesions predominate when large numbers of bacilli are present and host defenses are weak. these loose aggregates of immature macrophages, neutrophils, fibrin, and caseation necrosis are sites of mycobacterial growth

Question 6

risk factors for m. tuberculosis infection

Answer 6

crowded at-risk environments like prisons, homeless shelters, hospitals. HIV. immunosuppressed.

Question 7

m. tuberculosis diagnosis: exam

Answer 7

classic pulmonary TB = cough, weight loss, night sweats, fever, hemoptysis. Chest xray shows cavity formation, noncalcified round infiltrates. fiberoptic bronchoscopy most effective way to get cultures. nonpulmonary symptoms mimic a wide variety of diseases.

Question 8

TB scrfula

Answer 8

reactivation in lymph node. painless, enlarging, or persistent mass. symptoms: fever, weight loss, malaise. cervical lymph node affected in 2/3. mostly caused by m. tuberculosis in adults, but usually caused by atypicals in kids. do PPD and fine needle aspiration. surgery only after antibiotic treatment is well underway

Question 9

genitourinary TB

Answer 9

most common site for extrapulmonary infection. TB almost always reaches kidney during primary infection but usually doesnt present clinically. females present with infertility, menstrual disorders, pain. pregnancy rare, but leads to spont. abortion or ectopic preg. IV urography best option. can use CT, MRI, ultrasound. needs surgery.

Question 10

CNS tuberculosis

Answer 10

visualize by MRI with gadolinium. CSF analysis used to detect decreased glucose, elevated protein, slight pleocytosis. PCR assays can be used.

Question 11

skeletal TB

Answer 11

shows up as arthritis of one joint or pott disease (back pain, stiffness, paralysis of lower extremities)

Question 12

GI TB

Answer 12

abdominal pain, weight loss, anemia, fever with night sweats, obstruction, palpable mass. radiograph for calcified granulomas. mesenteric lymphadenopathy. use exploratory surgery

Question 13

miliary TB

Answer 13

hematogenous spread through body, many tiny noncalcified foci of infection appear like millet seeds. more likely to develop right after primary infection. highest risk in young and old. history of cough/respiratory distress. lymphadenopathy and hepatosplenomegaly. tachypnea. cyanosis. lesions on skin or choroidal tubercles in retina. tiny nodules best visualized by chest xray with bright spotlight.

Question 14

TB meningitis

Answer 14

nuchal rigidity. altered deep tendon reflexes. lethargy. cranial nerve palsy.

Question 15

pediatric TB

Answer 15

middle ear, skin, ocular structures. rule out TB if presents with pneumonia, pleural effusion, cavitary mass lesion in lung. gastric aspirates are used in lieu of sputum in kids younger than 6. begin treatment as soon as samples have been taken for culture. pediatric TB can be lethal before TST is positive

Question 16

tuberculin skin test

Answer 16

PPD, TST. positivity 2-10 weeks post infection. alternative is IFN gamma release assay (IRA) using TB peptides. either PPD or IRA can be false negative if patient is badly immunosuppressed or late in the course of TB. HIV+ patients must be regularly screened for TB and vice versa.

Question 17

M. tuberculosis lab

Answer 17

sputum smears and culture are specific but not sensitive. repeat often. urinalysis and urine cultures can be used if urinary complaints. cultures are needed for antibiotic resistance testing. rRNA and PCR are available. antibiotic resistance tests take 3-4 weeks. TB bacteremia can be detected from blood cultures.

Question 18

M. tuberculosis treatment

Answer 18

isolate infectious patients: negative pressure, high efficiency masks. 4 drug reginmen: isoniazid, rifampin, pyrazinamide, and ethambutol/streptomycin. for resistant TB, use a minimum of 1 susceptible injectable and at least 3 additional drugs. directly observed therapy recommended. pregos are at risk for hepatotox, ALT monitor them.

Question 19

BCG vaccine for TB

Answer 19

live attenuated M. bovis. prevents up to 70% of symptomatic infections. rarely used in US. watch for 3-6 mm PPD if vaccinated abroad or in military. can use IGRA to differentiate. not for the immunocompromised.

Question 20

why are atypical agents called atypical?

Answer 20

cause neither TB nor leprosy. environmentally acquired. PPD TST usually negative. less aggressive infections. systemic disease rare without predisposing condition. cutaneous infection common in adults, scrofula in kids.

Question 21

group 1: photochromogens

Answer 21

produce pigment when grown in light

M. kansasii is environmental in midwest, texas, england. produces pulmonary/systemic disease closely resembling TB.

m. marinum found in fresh and salt water, forms fish tank granulomas, ulcerating lesions on abrasions exposed to swimming water or aquariums. treat with tetracycline.

Question 22

group 2: scotochromogens

Answer 22

produce pigment when grown in dark or light.

m. scrofulaceum produces scrofula. reservoirs in water, can be harmless in respiratory tract. fix by surgically removing affected nodes.

Question 23

group 3: nonchromogens

Answer 23

m. avium/m. intracellulare are very difficult to distinguish, jointly called MAI, MAC. cause pulmonary disease indistinguishable from TB in severely immunocompromised people. environmentally wide spread. highly drug resistant. use clarithromycin in combo with ethambutol, rifabutin, or cipro.

Question 24

group 4: rapidly growing mycobacteria

Answer 24

culturable in 1 week or less.

m. fortuitum/m. chelonei: found in soil and water, cause problems in immunocomp, hip replacements, indwelling catheters, puncture wounds. treat with amikacin+doxicycin and surgery
m. abscessus: environmental. chronic lung infections, skin, bone joints. highly antibiotic resistant.
m. smegmatis: normal flora under foreskin

Question 25

m. leprae bacteriology

Answer 25

not culturable. reservoirs are humans and armadillos. 14 day doubling time. slowest growing human pathogen. prefers 30C for growth and sticks to periphery of humans. appears to be a stripped down version of M. tuberculosis

Question 26

m. leprae pathogenesis

Answer 26

causes leprosy. symptoms from both infection and immune response. exact mechanism of transmission is unclear. need prolonged contact with infectious case. rare zoonosis from armadillos. long incubation period. asymptomatic seroconversion. 5-10% of population is susceptible to symptoms immunologically.

Question 27

paucibacillary leprosy

Answer 27

tuberculoid form. vigorous CMI contains disease, but causes immunogenic problems.

Question 28

multibacillary leprosy

Answer 28

lepromatous form. inadequate CMI response. extensive skin involvement: >6 lesions, infiltrated nodules and plaques, bacilli may be visible on smears from lesion fluid. symmetric peripheral nerve damage from bacterial growth in schwann cells. lepromatin PPD negative

Question 29

m. leprae diagnosis: exam

Answer 29

hypoesthesia, skin lesions, and peripheral neuropathy. the first physical signs are usually cutaneous. tuberculoid: sharply demarcated hypopigmented macules on butt, face, limbs. superficial nerves near lesions enlarged. neuropathic pain and muscle atrophy. positive lepromatin.

lepromatous: bilaterally symmetric cutaneous macules. lesions have poor defined borders and raised centers. eye infection. loss of nasal cartilage. leonine facies. lepromatin PPD negative.

Question 30

m. leprae diagnosis: lab

Answer 30

a positive PPD meants that testee has been exposed and raises a strong CMI response against the antigen. a negative PPD means that testee has never been exposed or fails to raise a CMI response against the antigen even though their system has seen it before.

skin smear and punch biopsy. bacilli visible and foam cells if lepromatous. granulomatous changes with epithelial cells and lymphocytes if tuberculoid. PCR effective

Question 31

m. leprae treatment

Answer 31

tuberculoid: dapsone and rifampin.
lepromatous: dapsone + rifampin + clofazimine
peds: prophylaxis with dapsone
prevention: isolation
treat severe cases of erythema nodosum leprosum with thalidomide but not if pregnant