Lecture 9 Flashcards

(66 cards)

1
Q

How do microbes generally enter the urinary system?

A

Through the urethra

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2
Q

How do microbes generally enter the reproductive system?

A

Women- Through the vagina
Men- Through the urethra

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3
Q

Which parts of the urinary system is sterile?

A

Urinary bladder and upper urinary tract

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4
Q

How can urine become contaminated?

A

Urine and lower urethra can become contaminated by the microbiota of the skin.

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5
Q

What are the diseases that can happen in the urinary system?

A

Urethritis–>Inflammation of the urethra
Cystitis–> infection of the urinary bladder
Ureteritis–> Infection of the ureter
Pyelonephritis–> Infection of the kidneys

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6
Q

What are the diseases caused by in the urinary system

A

Intestinal bacteria

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7
Q

What is the diagnosis of infections in the urinary system?

A

Painful urination
Bladder does not feel empty after urination
Cloudy or slightly bloddy urine.
>1,000 bacteria of one species/ml or 100 coliforms/ml of urine

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8
Q

What is Cystitis?

A

Common urinary bladder infection in females; eight times higher in females than in males.

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9
Q

What are the symptoms of Cystitis?

A

Include Dysuria; difficult, painful, burning and urgent urination

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10
Q

What are the bacteria that are usually responsible for Cystitis?

A

E.Choli, Staph, saprophyticus

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11
Q

What are the other bacteria that can also be responsible for cystitis?

A

Klebsiella, Proteus, Enterococcus, Pseudomonas

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12
Q

How can Cystitis be treated?

A

Trimethoprim/sulfamethoxazole, ampicillin or fosfomycin

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13
Q

What is pyelonephritis?

A

Inflammation of one or more kidneys
Developed in 25% of untreated cystitis patients.

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14
Q

Symptoms of pyelonephritis?

A

Fever, flank or backpain

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15
Q

In most cases which bacteria is the cause of pyelonephritis?

A

E.Choli

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16
Q

Dangers of pyelonephritis?

A

Scar formation on kidneys can impair their function.
Potentially life thretening

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17
Q

Treatment of pyelonephritis?

A

intravenous administration of cephalosporins

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18
Q

What are the various sexually transmitted diseases(STI)?

A

Neisseria Gonorrheae– Gonorrhea
Chlamydia trachomatis–>Chlamydia Infection
Treponema Pallidum–> Syphilis
Papillomavirus–> Ovarian cancer
HIV–> AIDS

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19
Q

How are STIs transmitted?

A

Sensitive to environmental stress, require intimate contact for transmission

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20
Q

Which bacteria is gonorrhea caused by and describe the bacteria?

A

Neisseria Gonorrhea–> Gram negative diplococci growth in pairs
gonnococcus

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21
Q

What happens due to gonorrhea in men?

A

disease results in discharge of pus in men

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22
Q

Gonorrhea transmission mode?

A

Humans only reservoir
Disease generally transmitted by someone who is an asymptomatic carrier or has only minimal symptoms

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23
Q

Efficiency of transmission in male and female?

A

30-40% chance of transmission from infected female to uninfected male
50-80% transmission from infected male to uninfected female

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24
Q

Which parts of the body do the bacteria infect?

A

Mucosal cells in urethra (males), cervix, rectum, pharynx, and eyes

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25
Gonorrhea: Modes of Transmission
Sexual Intercourse: * Vaginal or anal sex with infected partner * Oral sex Without Sexual Intercourse: * Touching infected parts with fingers e.g. eyes * From mother to baby at birth * Incubation Period: * 1- 14 days
26
Gonorrhea: Clinical Manifestations in males
80-90% infected males show symptoms: * Men with asymptomatic urethritis are an important reservoir for transmission * White, yellow or green thick discharge of pus from tip of penis * Urethral itch and pain or burning sensation when passing urine * Disease can heal spontaneously * Complications in Males: * Scarring of urethra: blockage of urine flow * Infection of testes: sterility * Scarring of vas deferens: sterility * Dissemination to joints, heart, pharynx
27
Gonorrhea: Clinical manifestations in Females
Disease in females more insidious * only 50% show symptoms * In vaginal region, only cervix infected * Strong smelling vaginal discharge, either thin and watery or thick and yellow * Pain or burning sensation when passing urine * Complications: * Pelvic Inflammatory Disease * Ophthalmia neonatorum
28
Pelvic Inflammatory disease?
In 15% of infected woman Gonococci ascend from the cervix to the fallopian tube all the way to the pelvic peritoneum. Bacteria can cause inflammation Scarring of fallopian tube can result in their blockage Reduced fertility or infertility Ectopic pregnancy-Life threatening
29
Opthalmia neonatorum causes in newborn?
Exposure of infant to infected secretions in birth canal * Ocular infections of newborn with N. gonorrhoea
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Prophylaxis against N. gonorrhoeae infections:
eyes of newborns treated with tetracyline, erythromycin or 1 % AgNO2 Keratoconjunctivitis occasionally in adults after autoinoculation: * corneal scarring
31
What are the virulence factors of Neisseria Gonorrhea?
Adherence due to pili mediate binding to mucosal cells of the cervix and urethra. Evasion of host defenses due to IgA protease and change of pili variant overtime(antigenic variation) Cell damage as lipopolysaccharides cause inflammation
32
What is the diagnosis of gonorrhea?
In males: Gram stained smear of pus from urethra gram negative diplococci in phagocytotic leukocytes In females: Cultivation of bacteria on Thayer Martin or Chocolate Agar Novel Detection Methods: * ELISA to detect gonococci * Monoclonal antibodies against gonococcal surface protein * DNA probes against gonococci
33
Gonorrhea: Epidemiology
Sharp decrease in cases after introduction of penicillin Increase of cases after introduction of birth control pills. Results in decreased glycogen production in vaginal region Lactobacilli usually grow on glycogen and convert it to lactic acid Reduced glycogen production leads to increased pH in vaginal region At higher pH gonococci have a better chance of growing and proliferating in genital region.
34
Gonorrhea: Treatment and Prophylaxis
Azithromycin--> class of macrolides subclass of azalides; single or two oral doses Ceftriaxone--> Cephalosporin; one intramuscular injection Doxycycline (tetracycline): two doses per day for one week; also kills chlamydia
35
Ways of Prevention of Gonorrhea?
* Public education * Condoms and prompt treatment * Cases have to be reported * No vaccine
36
What are the different types of Chlamydia infections?
C. trachomatis: Causes urogenital infections, trachoma, conjunctivitis, and pneumonia. Noted as a sexually transmitted disease. C. pneumoniae: Causes bronchitis, sinusitis, pneumonia, and possibly contributes to atherosclerosis. Transmission occurs through airborne infection. C. psittaci: Causes pneumonia, specifically known as psittacosis. Transmission also occurs through airborne infection.
37
Features of Chlamydia? How do Chlamydia Infections?
Small obligate intracellular pathogens * once considered to be viruses * Possess an inner and outer membrane similar gram-negative bacteria but do not have a peptidoglycan layer * Although synthesizing most of their metabolic intermediates, they are unable to generate their own ATP energy parasites
37
C. trachomatis Infections
Only infecting humans (one strain infecting mice) * Appr. 127 Mio cases / year worldwide * major cause of human eye and genital disease * significant cause of blindness worldwide * transmission by vaginal, anal or oral sex, and from mother to baby during birth
38
Chlamydia Trachomatis infects what cells?
Infects human columnar epithelial cells
39
Chlamydia Trachomatics has two body forms during life cycle? Talk about them?
Elementary Bodies Small (0.3-0.4 micrometer) infectious form and metabolically inactive. Have a rigid membrane as outer exterior to resist harsh outer environment conditions of the eukaryotic cells. bind to receptors of host cells to initiate infection. Reticulate Bodies: Noninfectious intracellular form Metabolically active replicating form fragile membrane lacking extensive disulphide bonds
40
Life Cycle of C. Trachomatis.
Binding of EBs to host cell receptors * Internalization by phagocytosis * Reorganization to become RBs * Inhibition of fusion of phagosome with lysosomes * Replication and reorganization into EBs * Between 100 - 500 progeny * C. psittaci: lysis of cells * C. trachomatis and C. pneumoniae: extrusion by reverse endocytosis
41
C. trachomatis Infections: Symptoms
Approximately 35 - 50% of nongonococcal urethritis due to C. trachomatis * Clinical manifestations from destruction of cells and host inflammatory response * Infection does not stimulate long lasting immunity * reinfection results in an inflammatory response and subsequent tissue damage * In appr. 80% of females infection asymptomatic * In only 25% of males infection asymptomatic
42
C. trachomatis Trachoma: Symptoms
* Trachoma from greek meaning rough which characterizes appearance of conjunctiva * Chronic infection or repeated reinfection results in inflammation of entire conjunctiva * Scarring of conjunctiva causes turning in of eyelids and eventual scarring, ulceration and blood vessel formation in cornea results in blindness Inflammation also interferes with flow of tears * important antibacterial defense mechanism secondary bacterial infections
43
what bacteria is Syphilis caused by?
Treponema Pallidum
44
Describe Treponema pallidum
Treponema (Greek): twisted thread pallidum (Greek): pale * Spirochete: * Gram negative, long, thin, helical * Motile: rapid rotation about its longitudinal axis * Locomotion by axial filaments
45
* Axial filaments in treponema pallidum
* flagella between peptidoglycan layer/outer membrane * run parallel to cell body * movement by twisting of cell body
46
Culture of Treponema pallidum
For research purposes cultivated in rabbits * Not possible to grow over longer periods in culture * viable organism can be maintained for 18 to 21 h in complex media * narrow optimal ranges of pH (7.2 to 7.4) and temperature (30 to 37°C) Culture of Treponema pallidum * Rapidly inactivated by mild heat, cold, desiccation, and most disinfectants * Long generation time (30 h)
47
Treponema pallidum: Pathogenesis
* Treponemal infections in distinct clinical stages: * Primary stage: * Multiplication of bacteria at initial site of entry * Secondary stage: * Dissemination of treponemes to other tissues * Tertiary stage: * After prolonged period, up to 30 years, immune reactions of body, affecting cardiovascular or central nervous system Treponema pallidum: Pathogenesis * Penicillin treatment effective on all stages of syphilis * No vaccine
48
Primary Syphilis
1 out of three people exposed gets infected Development of symptoms 10-60 days after exposure to Treponema pallidum Development of solitary and painless sore --> chancre at the site of infection On penis, labium, anorectal region, or around the mouth Healing of chancre within 4-6 weeks even without treatment Progression of syphillis to secondary stage if not treated in primary stage
49
Secondary Syphilis
1-6 weeks after healing of chancre red rashes or sores on palms of hands and soles of feet or all over the body Rash accompanied by fever , sore throat, headaches, joint pains, poor appetite, weight loss and hair loss superficial sores may occur on mouth vagina or anus sores contagious 2-6 weeks after onset of secondary syphillis host defences bring about healing about 25% of patients experience recurrence of secondary stages in the first several years of infection
50
Tertiary Syphillis
Without treatment of primary or secondary stage, < 50% of cases progress to tertiary stage * Most symptoms due to host immune reactions * Development of lesions, called ´gummas´ * rubbery masses of tissue in organs or on skin * ulceration causes extensive tissue damage * can affect cardiovascular or central nervous system * weakening of aorta * loss of motor control, personality changes, blindness
51
Talk about human Papilloma virus
Diverse group of DNA-based viruses * 118 different HPV types * Infection of skin and mucous membranes of humans and variety of animals * Some HPV types cause warts on skin * transmission by skin to skin contact * Group of about 30-40 HPVs typically transmitted through sexual contact and infection of anogenital region * About 25% of all women aged < 30 years infected
52
Sexually transmitted HPVs:
* Some types cause genital warts * Other types do not cause any noticeable signs of infection * Persistent infection with a subset of about 13 so-called "high-risk" types * different from the ones that cause warts * may lead to precancerous lesions ev. progression to cancer * HPV infection necessary factor in development of nearly all cases of cervical cancer
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Human Papilloma Virus (HPV): Cervical Cancer
Most HPV infections rapidly cleared by immune system * no progression to cervical cancer * Slow process of transforming normal cervical cells into cancerous ones * occurring of cancer in people who have been infected with HPV for long time, usually over a decade or more * History of infection with one or more high-risk HPV types prerequisite for development of cervical cancer * women with no history of HPV infection do not develop cervical cancer
54
Human Papilloma Virus (HPV): Cervical Cancer
High risk types--> Are type 16, 18, 31 and 45 which are HPV virus can lead to cervical cancer, anal cancer, vulvar cancer, and penile cancer * HPV-induced cancers often have viral sequences integrated into cellular DNA * HPV oncogenes E6 and E7 promote tumor growth
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High risk types for cervical cancer
High-risk types 16 and 18 cause 65% of cervical cancer * High-risk types 31, 33, 45, 52 and 58 cause 20% of cervical cancer * HPV types 6 and 11 cause 90 percent of genital warts * Gardasil, prophylactic HPV vaccine, marketed by Merck * protection against high-risk types 16 and 18, and against genital wart types 6 and 11 * Gardasil 9, approved in 2014, marketed by Merck * protection against high-risk types 16, 18, 31, 33, 45, 52 and 58 * protection against genital wart types 6 and 11 * Cervarix, prophylactic HPV vaccine, marketed by GlaxoSmithKline * protection against high-risk types 16 and 18
56
Structure of HIV and Infection of CD4+ Cell
HIV is retrovirus with single-stranded RNA, reverse transcriptase, and a phospholipid envelope with gp120 spikes * HIV spikes attach to CD4+ and coreceptors on host cells; CD4+ receptor is found on T helper cells, macrophages, and dendritic cells.
57
Entry of the Virus into the Cell
* Co-receptors and HIV infection * CCR5 and CXCR4 are chemokine receptors * Cells with homozygous mutant CCR5 molecules are not infected by HIV * 1-3 in 100 Caucasians * No Africans * Persons with heterozygous mutant CCR5 molecules progress to AIDS more slowly * 25% of long term survivors are CCR5 mutants (deletions) * The same CCR5 mutation (called “delta 32”) is thought to be the mutation that rendered some people immune to plague in the middle ages
58
HIV Attachment and Entry
Mechanism of viral entry 1. Initial interaction between gp120 and CD4. 2. Conformational change in gp120 allows for secondary interaction with CCR5. 3. The distal tips of gp41 are inserted into the cellular membrane. 4. gp41 undergoes significant conformational change; folding in half and forming coiled-coils. This process pulls the viral and cellular membranes together, fusing them.
59
HIV Entry
Fusion of HIV virus envelope with cell membrane * Viral RNA transcribed to DNA by reverse transcriptase. * Viral DNA becomes integrated into host chromosome to direct synthesis of new viruses or to remain latent as a provirus.
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Latent HIV Infections
* HIV evades the immune system in latency: * inactive provirus * fully assembled virions in vacuoles * HIV may also escape immune system by using cell–cell fusion and by antigenic change.
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The Three Stages of HIV Infection
1. Acute and Asymptomatic Phase (appr. first three years) * Within first few months high virus titer (up to 10 million viruses per ml blood) and fall in CD4+ cells but recovery of numbers * After 2-3 months antibodies against HIV in blood * HIV titer in blood between 1000 to 10,000 per ml 2. Symptomatic Phase; early indications of immune failure * At least 100 billion HIVs generated each day; appr. 1 Mio mutated viruses generated per day * About 2 billion CD4+ cells produced per day to compensate for losses; Daily loss of about 20 million CD4+ cells per ml 3. AIDS Phase: CD4+ T-cell numbers have declined to less than 200 CD4+ cells/µl * Without medication progression from HIV infection to AIDS takes about 10 years; with early onset of medication appr. normal life expectancy
62
Diagnostic and Preventive Methods
Diagnosis * Seroconversion takes up to 3 months * HIV antibodies detected by ELISA * HIV antigens detected by Western blotting * RT-PCR for the detection of the retroviral RNA * Prevention * Use of condoms * Use of sterile needles (IDUs) * Health care workers use gloves, gowns, and masks
63
HIV - The Virus
Membrane: host derived * Three structural genes: gag – pol –env * gag: group specific antigen * pol: polymerase * env: envelope * Three polypeptides
64
Group-Specific Antigens
p17: inner surface p24: nucleocapsid p9: nucleocapsid associated with RNA Retrovirus Polyprotein
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