block 6- sexually transmitted diseases Flashcards

You may prefer our related Brainscape-certified flashcards:
1
Q

problems with sti’s

A
  • Pregnancy complications
  • Infertility
  • Impact on health
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

challenges in reducing sti’s

A

-asymptomatic transmission= people have it but don’t know as they have no symptoms and so pass it on
-stigma= people don’t want to talk about and so don’t get checked
-antimicrobial resistance

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

spirochaetes

A
  • group of bacteria with a unique spiral shape that helps them move in a corkscrew motion. They are long, thin, and have flexible bodies, which allow them to twist and spin through different environments, such as mucus or tissue.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

treponema pallidum

A
  • a type of spirochaetes
    -important for global health
    -obligate pathogen that can never be cultured in the lab as it only lives in humans
    -small genome=limited metabolic capability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

syphilis

A

-Transmission may be sexual or
congenital
- Congenital syphilis is
systemic and serious= bacteria in the baby via the mother. serious because babies have weak immune system
- STI has three stages of disease
with different symptoms:
-primary disease=
-secondary syphilis
-latent syphilis which can develop into tertiary syphilis
- Slow disease with latent periods

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

symptoms of primary syphilis

A
  • trponema pallidium multiples at the site of infection
  • 3 weeks incubation so usually don’t see the affects at first. painless. chacre (like a sore) appears and last for 2-6 weeks
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

symptoms of secondary syphilis

A

-After 2-24 weeks without
symptoms, there is bacteraemia
- Fever, headache, lesions, body rashes too

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

tertiary syphilis symptoms

A

-localised
symptoms after 3-30 years
-If syphilis remains untreated, it can eventually damage organs, including the heart, brain, nerves, eyes, and bones. This can lead to serious health issues like heart disease, mental health problems, blindness, or even death.

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

virulence/immune evasion in a chronic infection

A
  • Untreated Treponema pallidum infection lasts for years
  • No LPS and few outer membrane proteins – less stimulatory to the immune system - “stealth”
  • Some T. pallidum antigens may modulate the immune response (influence T cell differentiation)
  • Antigenic variation in outer membrane proteins= the pathogen can change its surface proteins (outer membrane proteins) to look different to the immune system. This helps it evade detection by the immune system because ach time it changes, the immune system has to start over in recognizing and fighting it.
  • Invades central nervous system (less immune surveillance)
  • Adhesion to extra cellular matrix proteins makes it easier to spread to tissues
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

diagnosis, treatment and prevention of syphilis

A

-Blood tests for antibodies
- Screening of all pregnant women
- Penicillin cures infection and prevents transmission

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

william Hinton test

A

-using bacterial
antigen to detect antibody) for rapid diagnostics with fewer false
positives

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

Jane Hinton(daughter of william)

A

-developed selective medium (agar) for isolation of Neisseria that is still used in diagnostics and antimicrobial susceptibility testing
-agar is supplemented with blood
(chocolate agar – brown colour) and antimicrobials:
- Nystatin (anti-fungal); vancomycin (anti-Gram-positives);
colistin (anti-Gram-negatives), trimethoprim and
sulfamethoxazole

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

Neisseria gonorrhoeae

A

-gram-negative beta proteobacteria
-oval(coffee bean) shaped diplococcus
-can be cultured in the lab
-micoscropy can be used to see the puss too
-only transmitted by intimate contact as it can only survive in humans
-obligate pathogen ,small genome

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

what happens when a person is infected with N.gonorrhoeae

A

-N. gonorrhoeae colonies the mucosa
- Adhesion to the surface
- Competition with microbiome
- Invasion of epithelial cells
- Release of virulence factors
- N. gonorrhoeae stimulates the innate immune system
- Influx of neutrophils that phagocytose bacteria
- Symptoms: pain and discharge (80% of female patients
have no symptoms), infertility, miscarriage

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

virulence factors of N.gonorrhoeae

A

-Adhesion: Opa protein and pili
- Release of peptidoglycan, lipooligosaccharides and outer membrane
vesicles, which stimulate the innate immune system
- Lipooligosaccharide (LOS) is like LPS but missing the O antigen
- Looks more like human glycosylation patterns – molecular mimicry for immune evasion
- Glycosylation on the surface helps adhesion, serum resistance, survival inside human cells

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

peptidoglycan-derived cytotoxin

A

-Peptidoglycan fragments released by N. gonorrhoeae damage epithelium of
Fallopian tubes, which may affect
fertility

17
Q

diagnostic and prevention of gnoherria

A

– Nucleic acid amplification tests
- Microscopy
- Culture, oxidase test, catalase test
- Prevent in new-borns by screening and treating pregnant women
- Prevent in communities by protected sexual intercourse and screening
programmes to identify asymptomatic carriers

18
Q

treatment and antimicrobal resistance of gnorroheria

A
  • intravenous penicillin
  • Azithromycin and a cephalosporin
  • A cephalosporin and a fluoroquinolone
  • Increasing cases of antimicrobial resistance (requiring second line
    treatments, drug combinations, antimicrobial susceptibility testing)
  • GP/pharmacy awareness
    “Super-gonorrhoea” &
    Clinical trials of new drug
19
Q

latent stages symptoms

A

-There are no noticeable symptoms during this stage, but the bacteria are still in the body. Some people may stay in this stage for years.
-Timing: This stage can last for years, and some people may never have symptoms again.

20
Q

outer membrane proteins in N.menigitidus

A
  • In N. meningitidis five classes of OMPs depending on molecular weight
  • PorA and PorB are porins; anti-PorA antibodies
    are bactericidal for N.meningitidis; PorB affects maturation of phagosome
  • Opa proteins are important for adherence and rearrangement of cytoskeleton
  • Factor H-binding protein (fHBP) is critical forsurvival in the human
    hos
21
Q

two partner secretion systems

A

-gram neg proteins have two membranes and so need a special secretion system
-composed of TpsA and TpsB.
-TpsA= secreted through the I inner membrane via the SecA system.
-TpsB= outer membrane protein interacts with TpsA
-and aids its transport through the outer membrane
-Up to 5 Tps in N. meningitidis
* These systems are involved in adhesion and biofilm production

22
Q

N.meninitidis infection and diseases

A

-* Septicaemia
* Meningitis (mainly affects babies, young children,
young adults)
* Pneumonia (elderly patients)
* Urogenital infections

23
Q

N.meningitidis septicaemia

A

-Meningococcemia is an acute
and potentially life-threatening
infection of the bloodstream
leading inflammation of the
blood vessels (vasculitis). It
has a high mortality rate.
Symptoms:
high fever
characteristic rash
headache
neck stiffness
coma

24
Q

meningitis

A

-N.meningitidis septicaemia can lead to this
-It is Inflammation of the meninges, the
protective membranes of the brain and spinal cord.
Symptoms:
* Headache
* High fever
* Neck stiffness
* Intolerance of light
* Characteristic rash

25
Q

strategies used by bacterial pathogens t cross the blood-brain barrier

A

-Transcellular Transport

Passive or adhesion-induced transcytosis: Bacteria pass through endothelial cells directly by attaching and triggering cell transport mechanisms.
Tight Junction Opening

Passage through opened tight junctions: Bacteria can break through the tight junctions between endothelial cells, making the barrier easier to cross.
Direct Cytotoxic Effect

Disruption of the endothelial barrier: Bacteria can damage the cells of the barrier directly, allowing easier passage.
Leukocyte-Facilitated Transport

Infected phagocytes: Bacteria might use white blood cells to enter the brain by hitching a ride through the barrier.

26
Q

age-specific meningitis

A

-N. meningitidis and H.
influenzae are the major causative agents of
meningitis in babies
-bactericidal power of blood s not in babies as it can’t kill pathogens= higher chance of meningitis for young babies hene the importance of vaccinating babies

27
Q

Diagnostics of meningitis and Neisseria meningitidis

A

-ctrA and sodC specific primers
Oxidase test, catalase
test,
-utilisation of sugars
-Specimens of spinal fluid or
blood
-agar testing, Pcr

28
Q

treatment of meningitis

A

-* Intravenous administration of penicillin
* Azithromycin
* Cephalosporins (ceftriaxone)
* Fluoroquinolones
* Increasing numbers of drug-resistant strains

29
Q

surveillance and prevention of N. meningitis infection

A
  • Detect and confirm outbreaks
  • Determine antimicrobial resistance profiles and
    circulating strains
  • Vaccination
  • Chemoprophylaxis with ciprofloxacin
30
Q

haemophillus infuenzae

A
  • Gamma-proteobacterium,
    polymorphic rods and long filaments
  • Catalase and oxidase positive
  • Reduces nitrate to nitrite and
    ferments glucose
  • An aerobic bacterium but can grow
    in anaerobic conditions.
  • First sequenced bacterial genome ~1.8 Mb (1995)
31
Q

capsules of influenza

A

Six capsular types (a-f)
* The most important type is b (Hib); it is a polymer of
ribosyl-ribitol-phosphate
* PCR amplification of capsular locus or by capsular
serotyping can be used for confirming capsular types
* Capsulated strains mainly cause invasive diseases

32
Q

fimbriae

A
  • Four types of fimbriae in H. influenzae
  • They are encoded by 5 genes (ghfA-E)
  • Fimbriae promote binding to columnar and ciliated
    columnar epithelial cells
33
Q

diagnostic of H.influenzae

A
  • Clinical samples should not be stored particularly at
    4°C
  • Chocolate agar is used for cultivation of H. influenzae;
    addition of bacitracin helps to control contamination by
    other bacteria
  • H. influenzae requires both haemin and NAD
  • PCR tests (hpd and bexA gene specific primers)
34
Q

cultivation of H.influenza

A
35
Q

treatment of H.infuenza

A
  • Ampicillin or amoxicillin
  • Chloramphenicol
  • Tetracycline
  • Cephalosporin
36
Q
A