. Biology of Reproduction, lecture on Sexually Transmitted Diseases

Biology of Reproduction

Fall 1998

text: Human Reproductive Biology 2nd Edition - R.E. Jones: Read pages 454-492 for this lecture
Summers
end

XXV. Sexually Transmitted Diseases (STD's, venereal diseases (venus))
                         back to XXIV. Pheromones

	A. typically require moist membranes at the transitions (openings)
	    between external and internal

		1. mouth, oral cavity, eyes, anus, urethra, penis, vulva, vagina

			a. usually passed only by vaginal, oral, and anal coitus

		2. bacterial, viral, retroviral, fungal

			a. immunity develops only slowly, if at all

	B. Bacteria

		1. Chlamydia trachomatis

			a. the most common STD

				i. ~ 5 106/yr (U.S.)

			b. very small bacteria

				i. live inside cells

					(1) unlike other bacteria	

					(2) once thought to be viral

				ii. gram-negative

			c. nonspecific urethritis

				i. cervix is the main site of infection in women

					(1) associated with cervical cancer

					(2) urethra (in men and women), vagina, vulva
					     & cervix become irritated and red

				ii. spotting between menstruation, vaginal discharge,
				     frequent (& painful in men) urination

				iii. other causes include Ureaplasma urealyticum 
				      (related to Chlamydia) and Hemophilus vaginalis

			d. many have no symptoms (30% of men, 50-70% of women)

				i. early detection difficult

					(1) may lead to sterility in females, abnormal &
					     nonmotile sperm in men, lung and eye infections
						 in newborn if passed during delivery

				ii. treated with tetracycline, erythromycin,
				     not penicillin

					(1) both sexual partners should be treated

						(a) even without symptoms both are usually infected 

			e. Lymphogranuloma venereum, tropical strain
			    of  C. trachomatis which can also be
				transmitted on clothing

				i. may lead to Reiter's syndrome

		2. Neisseria gonorrhoeae    (flow of seed)

			a. 2nd most common STD (~2 106/yr U.S.)

			b. gram negative, diplococcus (occurs in pairs) bacterium

				i. 16 strains

			c. females usually (75%) asymptomatic

				i. vaginal discharge, vaginitis, cervicitis,
				    urethritis (with painful urination), and cystitis

					(1) may infect uterus, fallopian tubes (salpingitis),
					     heart, brain, spinal cord, eyes skin and joints

				ii. males (70-90%) have urethral discharge, red glans,
				     urethritis (with scar tissue and painful urination),
					 pain in the groin and with erections, and low fever

					(1) may lead to infection of bladder (cystitis),
					     prostate, epididymis and testes

			d. penicillin was an effective treatment

				i. some strains resistant

					(1) these strains produce penicillinase

					(2) spectinomycin and tetracycline can be used

				ii. without treatment ® infertility, spontaneous
				     abortion & newborn blindness

		3. Treponema pallidum 

			a. named for the shepherd Syphilis in an
			    Italian poem (by Hieronymous, 1520)

			b. spirochete bacterium

				i. survives only in ¯ O2 conditions

				ii. probably evolved from Treponema pertenue,
				      nonvenereal syphilis of the axilla, mouth,
					  nostrils, crotch and anus

			c. four stages

				i. 1o = chancre where bacteria entered body

					(1) heals in 1-5 wks

				ii. 2o = spreading rash; blemishes may burst
				    and are very infectious

					(1) begins 2 wks to 6 mo; lasts 2-6 wks

				iii. Latent Stage = no symptoms

					(1) can last for years

					(2) after ~ 1 yr infected individual can no
					    longer transmit

						(a) many (50%) never leave latent stage

				iv. 3o stage = bacteria have invaded entire body

					(1) large tumor like sores (gummas) of skin,
					     muscle, digestive tract, liver, lungs, eyes,
						 heart, endocrine  and nervous systems

						(a) severe damage to heart and valves;
						      neurosyphilis ® severe damage of brain
							and spinal cord ® paralysis, blindness
							& psychotic behavior

						(b) death

					(2) not infectious

			d. several antibiotics are effective as treatment

				i. benzthine penicillin G, tetracycline, erythromycin

					(1) treatment during 3o stage may not
					     block tissue damage

				ii. untreated pregnant women can infect
				     a 6 mo + fetus at any stage

					(1) placenta protects < 6 mo

					(2) infection ® 30% miscarriage,
					    70% congenital syphilis

						(a) contagious in 1st and 2nd year of life

		4. other bacterial STDs: Hemophilus ducreyi = chancroid,
		   Hemophilus vaginalis ® vaginitis,
		   Calymmatobacterium granulomatis = granuloma inguinale

	C. Viruses

		1. none are curable

		2. Herpes simplex type 2

			a. Herpes genetalis comes from 1 of 25 herpes viruses

				i. Herpes simplex 1 = cold sores, fever blisters; 
					Herpes vericella-zoster = chicken pox, shingles;            
					Epstein-Barr = mononucleosis; 
					Herpes cytomegalovirus = cytomegalic inclusion
					 (fetal ­ liver/spleen)

					(1) all (incl 2) can be passed by nonsexual
					    contact, perhaps even inanimate contact

			b. tiny blisters ® painful sores ® itchy ulcers

				i. on penis or labia, clitoral hood,  cervix,
				    vaginal introitus, urethral meatus, or perineum

				ii. fever, enlargement of inguinal lymph nodes,
				     and blindness (touching sores then eyes) possible,
					 & positive correlation with cervical cancer

				iii. heal in 1-6 wks, but recurrence is common
				    & frequent associated with stress or menstruation

			c. vitamin A, zinc sulfate, 5-iodo-deoxyuridine,
			     2-deoxy-D-glucose, & acyclivor may improve
				 symptoms & ¯ recurrence

		3. Human papilloma virus = genital warts =
		    Condyloma acuminata (52 types)

			a. moist, soft, grainy warts
			    appearing 3 wks - 8 mo after contact

				i. on cervix, labia, vulva, perineum, penis, scrotum

			b. associated with cervical and penile cancers

				i. 95% of cervical cancer patients have hPV

			c. treated with liquid N2, solid CO2, podophyllin,
			    trichloracetic acid, laser surgery, or heat cauterization

		4. Hepatitis B can be sexually transmitted

	D. Retroviruses

		1. human immunodeficiency viruses type 1 and 2

			a. lentivirus subfamily	(lenti = slow)

				i. non-oncogenic retroviruses
				
					(1) persistent/chronically active infections

						(a) disease with long incubations periods

				ii. usually infect cells of the immune system

					(1) macrophages, T-cells

				iii. not cleared by the immune system

					(1) accumulated damage over years

				iv. can infect non-dividing cells

					(1) other retroviruses cannot

				v. large RNA genome (10 kb) for a retrovirus

					(1) large, heavily glycosylated envelope protein

					(2) Mg++ dependent reverse transcriptase

					(3) encode essential regulatory and accessory genes

						(a) \ regulation of their own expression
						     in an infected cell

				vi. replication is toxic to the infected cell

					(1) cell dysfunction and death

					(2) may be the reason the immune system
					    cannot eliminate infection

				vii. there are many types of lentivirus
				     causing immunodeficiency

					(1) SIV, FIV, EIAV, HIV

			b. continuous replication of HIV-1 ® development
			    of immunodeficiency

				i. rely on reverse transcriptase
				    to convert into DNA 'provirus'

					(1) integrated into the cellular genome

					(2) 3 coding regions = gag, pol, env

						(a) gag = encodes capsid proteins

							(i) core viral particle
							    containing RNA + enzymes

						(b) pol = viral enzymes
						     necessary for replication

							(i) reverse transcriptase,
							    integrase, protease

						(c) env = external glycoprotein

							(i) protrudes through lipid bilayer
							     viral envelope

							(ii) envelope produced by cellular
							      plasma membrane

							(iii) protruding  glycoprotein is
							       responsible for infectivity

							(iv) glycoprotein binds to cellular receptors

			c. treatment

				i. plasma HIV RNA indicates level of infection

					(1) treatment level based on [RNA + T-cell]

				ii. HIV RNA highly plastic

					(1) anti-retroviral drug resistant variants form quickly

				iii. combinations of anti-retroviral drugs must be used simultaneously

					(1) protease inhibitors (PI)

					(2) non-nucleoside reverse transcriptase inhibitors  (NNRI)

					(3) nucleoside analog reverse transcriptase inhibitors (RT)

					(4) durable suppression with 2 x RT + 1x PI
							
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