Biology 216 - Lect 27
Tuberculosis and Leprosy
I. TB - M. tuberculosis and M. bovis - tubercle bacillus
	Consumption; Egyptian mummies (2400 BC); 
	1700s healthy climate, sanatorium (isolation, rest, diet)
	Koch's Postulates; Vaccine 1920s; Streptomycin 1940s; 1999 Genome sequence
	A. Bacteriology - same as MOTT
		M. tuberculosis - man only
		M. bovis - catttle and man; invasion through GI
		Obligate aerobes - tendency to colonize apex of lung
		Very slow growers - 4 - 6 weeks (generation of 24 hr)
		No exotoxins; Lipids make up 10 % of cell weight (60 % of cell wall)
		Sulfatides - sulfur lipids which inhibit phago-lysosome fusion
		Muramyl dipeptide active adjuvant; Freund's, wax D and MDP
	B. Pathogenesis and disease
		1. Epidemiology - A disease of civilization
			Perspective - 1800s 1% of city population 
				die from TB/yr  (Ex. New York 100,000)
			10 million/yr worldwide (3 million deaths); 
			Estimated 2 billion infected.
			US - 28,000/yr epidemic (reverse trend downward) 
			(15 million infected) - Plan for elimination by 2010
				Incidence highest in crowded states (CA, NY, FL,TX).
			Control: antibiotics, living conditions, inexpensive screening 
			(skin test and x-ray), case workers.
			Increase: immigration (1/4 of new cases, crowded, 
				homeless shelters, prisons.
			Abandoned control in 1970s: not much time in med school, 
				no new drugs, less research 
			Currently #2 reportable infectious killer in US (AIDS is #1)
		2. Transmission - M. bovis no longer major due to 
				cattle control in developed countries 
			Elimination of cattle, pasteurization.
			Airborne - coughed, dried secretions, small droplets
				 from active or cavitation TB.
			Outbreaks - teacher, bus driver w/active TB, health care workers
		3. Infection vs disease
			Man is highly susceptible to infection (skin test +), 
				but resist disease.
				(less than 5 % symptomatic in one year),10 % chance 
				of TB in lifetime (highest first 2 years)
			Disease depends on dose and host ability 
				to respond and wall off
				(Crowding, nutritional inadequacy, alcoholism, 
				young and very old, AIDS)
				35 % of AIDS patients have TB -> 
					death in 1 month from TB symptoms
				Genetics - Native Americans, Inbred mouse strains.
		4. Primary TB - primary focus in alveoli (mild or asymptomatic)
			Macs phagocytize, TB multiply within, 
				drain to hilar nodes, blood, miliary, bones...
			CMI by 4th week stops spread, tubercle walls off, 
				active Macs kill (TB reduced numbers)
				T-cells -> IFN alpha important (stimulate Macs)
				TB more virulent in IFN negative mice,
			+ skin test and + x-ray (both may be + for life)
			Healthy patient - flu-like.
			Unhealthy - miliary TB, impair function of lung, 
				fatigue, fever, wasting (By Mac -> TNF alpha)
			Fever, cough, bloody sputum, wasting (consumption) 
		5. Secondary (Reactivation/reinfection) TB
			TB survive in tubercle (90 % latent)
			Decreased CMI (alcoholism, cancer, age, AIDS) years later
			Tubercle liquifies - spread, lung dysfunction, 
				chest pain, fever, weight loss
			Cavitation susceptible to Nocardia
			New foci controlled, but massive pathophysiology 
				- 50 % fatal w/o and 6 % w/ treatment.
				MDRTB - 50 % fatal
	C. Diagnosis:Early diagnosis important to treat and stop spread. 
			History (socioeconomic,  HIV..), x-ray,
		1. Skin test - for DTH to TB antigen after 4 weeks 
			of infection, BCG, specific anegy in active TB.
			- Intradermal injection of TB Ag (Mantoux)(tuberculin syringe) 
				or multiple puncture (less reliable antigen delivery)
			- High population of sensitized T-cells in circulation, 
				immobilized, cytokines -> Macs attracted.
			- 48 - 72 hr induration/red (raised and hard)
				and erythema (red) - measure diameter.
			- Antigen - 	OT (old tuberculin) - dialyzed TB
					PPD - AmSO4 ppt of OT
					 (less Ag, more specific)
			- Interpretation - 	
			Greater than 10 mm = + (present or past infection) 
			5 - 9 mm = atypical Mycobacteria
			0 = negative, injection too deep, 
				anergy (compromised, severe TB, measles 
			(Test for general anergy w/mumps, tetanus skin test)
			- Skin test dose is not immunizing dose
			- Suggested treatment if skin positive, even if not active TB
		2. Direct exam of specimen (sputum)
			- Solubilize (2 % N-acetyl-L-cys) and 
				decontaminate (2 % NaOH), then neutralize in 15 min.
			- Acid fast stain - Scan 100 fields under oil 
				(3 sweeps through slide) picks up all Mycobacteria

Finding

Report

0

No AFB

3 - 9/slide

+ rare (repeat specimen)

>10/slide

++ Few

1/field

+++ Numerous

		3. Culture and ID - work in hood
		     	Inoculate media with glycerol (C-source 
				for building triglycerides) and egg (slants)
			Ex. 7H11, Lowenstein Jensen - Support variety 
				of Mycobacteria; Satisfactory for niacin
				test; Malachite green inhibit others; 
				May add antibiotics.
			3-4 weeks growth - dry, cream colored
			ID - pigment, niacin, tween hydrolysis..., 
			DNA hybridization (probe for TB)
			Antibiotic sensitivity
		4. BACTEC - liquid culture with 14C-substrate -> 
			14C-CO2 -> fluorescence -> detector (14 days)
			Can be used to test antibiotics
		5. PCR - Primers for TB specific IS6110
                6. Mycophage with luciferase: 
                   Infect isolate, grow in antibiotic -> ?
	D. Treat
		1. Combination antibiotics, long term (up to 2 years); 
			Less than 20 % finish -> resistance
			Possible subq implants being considered; 
			Single pill with all antibiotics.
			Non-contagious after 1 - 2 weeks; 
			Lungs take months to improve.
			Outpatient treatment when not communicable.
			Used to have sanatoria; may return in the future; 
				in hospital - negative pressure isolation room.
			MDR - 50 % mortality.
	E. Prevention - Dosage and host immunity 
			most important considerations.
		1. INH treat contacts and skin test+ converts.
		2. Better housing, sanitation, nutrition, health
		3. Animal control (M. bovis - treat, moniter, pasteurize)
		4. Vaccine - BCG (bacillus of Calmette and Guerin) - 
			live attenuated (1921), enters Macs, then dies
			One of safest vaccines known; 3 Billion doses given; 
			Given orally; 10 cents/dose
			Efficacy in question - effective in children, 50 % in adults,
				not effective in preventing reactivation TB.
			Given to exposed and high risk in some countries.
				(Controversy - health care workers)
			Not given to immunocompromised 
				- disseminated disease in AIDS
			Not given in US -> conversion to skin test +; 
				eliminates tool for diagnosis and epidemiology.
			Work on cloning protective Ag into BCG
			Experimental treatmentof tumors
				- BCG attracts and immobilizes Macs	
II. M. leprae - leprosy (Hansen's disease)
	A. Bacteriology - Obligate intracellular parasite
		 (Never grown in lab)
		Few generations in Mac tissue culture; 
			mouse foot pad; armadillo blood (endemic)
			(2 week generation time)
		In vivo growth very slow - incubation period of years.
		Prefers low temp - colonize skin, 
			mucus membrane, peripheral nerves.
                Sequenced: 1999
	B. Pathogenesis - 10 - 15 million world total (mostly tropics).
		1. Transmission - person -> person by nasal 
				secretion or skin (children especially susceptible)
			Lepromatous shed 10(8)/day in nasal.
			Survive dessication.
			Infection through cuts, mucus membranes (ex URT)
			Infection requires - high number, compromised
				 and prolonged exposure (not very contagious)
			Predisposition - crowding, genetic, CMI, nutrition.
		2. Very long incubation - ave 4 yrs
			Proliferate in Mac and Schwann 
			(affect peripheral nerves and tissues)
			 - damage from CMI
			Usually asymptomatic or minor skin lesion (blotch) 
			- CMI protective.
		3. Clinical - 2 major forms with intermediate forms 
			a. Tuberculoid leprosy - early loss of skin pigmentation 
				Large granuloma formation, may destroy nerve cell ->
				Paralysis of muscles, anaesthesia (numbness)
				Lesions on face, trunk, skin -> deformity
				Good CMI - walled off, few organisms shed, 
					slow progressive healing, scaring.
			b. Lepromatous leprosy (high # and low CMI) - severe form
				Anergy to leprosy (specifically) by glycolipid -> Ts
				Evidence - Ts low in tuberculoid, high in lepromatous
				No granuloma formation, no walling off, 
					lesions coalesce, large # in macs and schwann
					(less nerve damage since no granuloma)
				Lesions coalesce -> loss of nasal, lips, 
					earlobe, digits; Highly contagious.
				Susceptible to secondary infection
				Ab/Ag complex deposition -> renal failure, 
					pulmonary blockage
	C. Diagnosis - symptomology, h istory of contact
		1. AFB in scrapings of lesion (low # in tuberculoid)
		2. Skin test - Lepromin (ground material) - 
			prognostic of patient CMI
		3. Cannot grow in lab; Serology available.
	D. Treatment
		1. Long term antibiotics (1 - 5 years), combination, 
			relapse may occur
			Some resistance to Dapsone
			Prophylaxis of close contacts to lepromatous patient.
	E. Prevention 
		1. Chemoprophylaxis for close contacts (lepromatous);
			 Isolation of patient if lepromatous.
		2. BCG vaccine - cross reacts (questionable efficacy)
		3. Cloned surface Ag into E. coli
			Expression when subcloned behind lac promoter
			Currently experimental work on this as vaccine
			Other experimental vaccines: 
				TB/leprosy genes into vaccinia virus