Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Medical Microbiology > Lecture 9 > Flashcards

Lecture 9 Flashcards

You may prefer our related Brainscape-certified flashcards:
Biology 101 flashcards USMLE® Step 1 flashcards
1
Q

How do microbes generally enter the urinary system?

A

Through the urethra

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How do microbes generally enter the reproductive system?

A

Women- Through the vagina
Men- Through the urethra

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Which parts of the urinary system is sterile?

A

Urinary bladder and upper urinary tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How can urine become contaminated?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the diseases caused by in the urinary system

A

Intestinal bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is Cystitis?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the symptoms of Cystitis?

A

Include Dysuria; difficult, painful, burning and urgent urination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the bacteria that are usually responsible for Cystitis?

A

E.Choli, Staph, saprophyticus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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

A

Klebsiella, Proteus, Enterococcus, Pseudomonas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How can Cystitis be treated?

A

Trimethoprim/sulfamethoxazole, ampicillin or fosfomycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is pyelonephritis?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Symptoms of pyelonephritis?

A

Fever, flank or backpain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

In most cases which bacteria is the cause of pyelonephritis?

A

E.Choli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Dangers of pyelonephritis?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Treatment of pyelonephritis?

A

intravenous administration of cephalosporins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How are STIs transmitted?

A

Sensitive to environmental stress, require intimate contact for transmission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Which bacteria is gonorrhea caused by and describe the bacteria?

A

Neisseria Gonorrhea–> Gram negative diplococci growth in pairs
gonnococcus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What happens due to gonorrhea in men?

A

disease results in discharge of pus in men

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Gonorrhea transmission mode?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Which parts of the body do the bacteria infect?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Gonorrhea: Modes of Transmission

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Gonorrhea: Clinical Manifestations in males

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Gonorrhea: Clinical manifestations in Females

A

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
Q

Pelvic Inflammatory disease?

A

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
Q

Opthalmia neonatorum causes in newborn?

A

Exposure of infant to infected secretions
in birth canal
* Ocular infections of newborn with
N. gonorrhoea

30
Q

Prophylaxis against N. gonorrhoeae
infections:

A

eyes of newborns treated
with tetracyline, erythromycin or
1 % AgNO2
Keratoconjunctivitis occasionally in
adults after autoinoculation:
* corneal scarring

31
Q

What are the virulence factors of Neisseria Gonorrhea?

A

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
Q

What is the diagnosis of gonorrhea?

A

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
Q

Gonorrhea: Epidemiology

A

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
Q

Gonorrhea: Treatment and Prophylaxis

A

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
Q

Ways of Prevention of Gonorrhea?

A
  • Public education
  • Condoms and prompt
    treatment
  • Cases have to be reported
  • No vaccine
36
Q

What are the different types of Chlamydia infections?

A

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
Q

Features of Chlamydia? How do Chlamydia Infections?

A

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
Q

C. trachomatis Infections

A

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
Q

Chlamydia Trachomatis infects what cells?

A

Infects human columnar epithelial cells

39
Q

Chlamydia Trachomatics has two body forms during life cycle? Talk about them?

A

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
Q

Life Cycle of C. Trachomatis.

A

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
Q

C. trachomatis Infections: Symptoms

A

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
Q

C. trachomatis Trachoma: Symptoms

A
  • 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
Q

what bacteria is Syphilis caused by?

A

Treponema Pallidum

44
Q

Describe Treponema pallidum

A

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
Q
  • Axial filaments in treponema pallidum
A
  • flagella between peptidoglycan
    layer/outer membrane
  • run parallel to cell body
  • movement by twisting of cell body
46
Q

Culture of Treponema pallidum

A

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
Q

Treponema pallidum: Pathogenesis

A
  • 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
Q

Primary Syphilis

A

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
Q

Secondary Syphilis

A

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
Q

Tertiary Syphillis

A

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
Q

Talk about human Papilloma virus

A

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
Q

Sexually transmitted HPVs:

A
  • 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
53
Q

Human Papilloma Virus (HPV): Cervical Cancer

A

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
Q

Human Papilloma Virus (HPV): Cervical Cancer

A

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

55
Q

High risk types for cervical cancer

A

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
Q

Structure of HIV and Infection of CD4+ Cell

A

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
Q

Entry of the Virus into the Cell

A
  • 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
Q

HIV Attachment and Entry

A

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
Q

HIV Entry

A

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.

60
Q

Latent HIV Infections

A
  • 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.
61
Q

The Three Stages of HIV Infection

A
  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
Q

Diagnostic and Preventive Methods

A

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
Q

HIV - The Virus

A

Membrane: host derived
* Three structural genes: gag – pol –env
* gag: group specific antigen
* pol: polymerase
* env: envelope
* Three polypeptides

64
Q

Group-Specific Antigens

A

p17: inner surface
p24: nucleocapsid
p9: nucleocapsid associated
with RNA
Retrovirus
Polyprotein

65
Q
A

Medical Microbiology (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions