M23- Anaerobes Flashcards

(53 cards)

1
Q

What Neisseria species is commonly isolated from plaque?

A

N. subflava

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

where is the location of Neisseria?

A

Oropharynx, Nasopharynx & occasionally anogenital mucosal membranes

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

Describe the characteristics of Neisseria.

A

• Gramnegative
– Diplococci; oval (bean shaped) organisms in pairs or small clumps
– Non motile, do not form endospores
• Aerobes
– Oxidase +ve and usually Catalase +ve
• Produce cytochrome oxidase
• Pathogenic & Non-Pathogenic Species
– 10 species, 2 of which are pathogenic
– Pathogens fastidious (i.e. Cooked blood Agar) non pathogenic species do not require blood & serum

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

Name the r pathogenic specie of Neisseria.

A
  • N. gonorrhoeae

- N. meningitidis

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

What diseases does N. gonorrhoeae cause?

A

– Urethritis (gonorrhea)
– Cervicitis
– Pelvic inflammatory disease
– Pharyngitis

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

What diseases does N. meningitidis?

A

– Meningitis
– Bacteremia
– Pnuemonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe N. gonorrhea.

A

– frequent cause of STD (Peak 20-24 yrs in Males, 16-19 yrs in females)
– Sensitive to desiccation, fatty acids and temperature
– Acute & chronic pathology

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

Name the key virulence factors of gonorrhea.

A

– Simple Capsule & Pili which extend through capsule.
( Phase variation of Pili via gene conversion)
– Pili & Opa Proteins facilitate adhesion (urethra, rectum, cervix, pharynx, conjunctiva)
– Pili enable organism to resist phagocytosis
– IgA protease produced

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

What makes it hard to make an effective vaccine for gonorrhea?

A

phase variation

-changes amino acid antigens

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

Describe the infection of gonorrhea.

A

– Localised infection of genital urinary tract producing pus, tissue invasion & localised inflammation.
– Acute & easier to diagnose in Males
– Asymptomatic carriers act as reservoir (female more often than male)
– Pharyngitis; oral-genital contact symptoms mimic a mild viral or streptococcal sore throat.
– Non-venereal seen in newborn as conjunctivitis

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

Describe the identification of gonorrhea.

A

– Swabs of infected material
– Gram stain,intracellular Gm-ve diplococci
– Cooked Blood Agar
– Oxidase+ve,glucose+ve,-ve maltose & sucrose

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

Describe the treatment of gonorrhea.

A

Penicillin (resistance increasing problem)

-threat level is urgent

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

what is the oral presentation of gonorrhea?

A

usually asymptomatic

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

what is meningitis?

A

Infection & inflammation of membranes covering the
brain & spinal cord (meninges & CSF)
-bacterial and viral

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

what organisms can cause meningitis?

A

N. meningitidis, S.pnuemoniae & H.influenza

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

what is the only organism that causes large scale epidemics of meningitis?

A

N. meningitidis

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

Describe N. meningitidis and its spread.

A

– Acute suppurative Meningitis
– Meningococcemia (severe blood infection)
– Reservoir nasopharynx of 5-10% of the population
– Spread; infected carrier; via respiratory secretions to case
– Not highly communicable but crowded conditions concentrate carriers e.g. Dormitory, School, Prison, University
– Greatest threat to children <5 year old

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Describe features of the main disease of meningitis?

A

-Aerosolisation of respiratory tract secretions, (winter & early spring)
– Colonisation & penetration of epithelium
– 2 to 10 day incubation
– Possible mild disease, fever & non specific symptoms
– Absence of effective host immune response, severe disease
– Abrupt onset, malaise, high fever (>40 ̊C) & possible rash (bloodstream)
– Progresses to headache, stiff neck, & sensitivity to bright lights
– Fever, Vomiting & diarrhoea, confusion/drowsiness, difficulty supporting own weight.
– Coma can occur within a few hours (e.g. 4 hours).

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

Describe the identification of meningitis.

A
  • Non-motile, Gm -Ve diplococcus (kidney bean shape)
  • Cultured on CBA or Chocolate agar with increased CO2 (48 hrs)
  • Oxidase +ve, Ferments Glucose & Maltose
  • 12 serogroups A, B & C responsible for 90% of the disease
  • Diagnosis through cerebrospinal fluid (CSF) and serogroup specific anticapsular antibody reactions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Describe the treatment and control of meningitis.

A

• Suspected Meningitis is a medical emergency – (cannot wait for definitive diagnosis)
• High fever, headache & rash treated with Large intra-veinous doses of Penicillin G or Ampicillin
• Cefotaxmine or Spectinomycin if resistant
• Prophylaxis Rifampicin (e.g. family members)
• Meningococcal ACWY
– 99% drop in cases (955 UK deaths to around 13)
• Meningococcal B – new vaccine for 73% of these European strains

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

If family members have previously had it, how does this effect the risk of meningitis?

A

Increases the risk

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

Give 4 types of meningitis.

A
  • MenB - 53% - 396 cases - 40% infants and toddlers
  • MenW - 30% - 225 cases - 62%> 25
  • MenC - 5% - 37 cases - 59%>25
  • MenY - 11% - 80 cases - 79% >25
23
Q

what gram +ve cocci causes caries and actinomyocosis?

A

Actinomyces species

24
Q

What gram -ve cocci cause periodontal infections?

A
  • Fusobacterium species
  • Prevotella species
  • bacteriodes
25
what is clostridia?
Anaerobic/ aerotolerant Gm+ve Bacilli
26
What does clostridia form?
endospores
27
Where is clostridia found?
Found in GI tract & environment
28
Name 3 clostridial diseases and the species that causes them.
- C. difficile - Pseudomembraneous colitis - C. botulinum - Botulism - C. tetani - tetanus
29
What is the habitat of C. tetani?
– Soil | – Humans (0% to 25%)
30
what is the appearance of C. tetani?
– Terminal spores | – drumstick or tennis racquet
31
Describe the development of tetanus.
• Small wound introduces spores (position) • Germinate&growin absence of O2 • Infection remains localised with minimal inflammation • Incubation 4 days to several week • Toxin produced during stationary phase & released upon lysis
32
Describe the actions of the tetanus toxin.
- TeNT (tetanus neurotoxin) - AB toxin - B subunit binds neuronal membranes - A subunit internalised - A subunit moves from peripheral nerves to CNS by retrograde axonal transport - crosses synaptic cleft - localised in pressynpatic cleft - blocks release of GABA - prevents synapse inhibitor - Unregulated excitatory synaptic activity - spastic paralysis
33
What are the symptoms of tetanus?
``` • Irritability, drooling • Headache • Fever, sweating • Exaggerated reflexes, back spasms, Lock Jaw • Musclespasms – Difficulty swallowing – Rigidity of the back • General Muscle rigidity ```
34
Describe prompt intervention of tetanus.
– Administer antitoxin : >Tetanus immune globin (TIG) and 3 tetanus toxoid injections to non-immunised > Tetanus toxoid to boost already immunised – Clean wound & undertake debridement – Penicillin
35
Describe the control of tetanus.
– Immunisation with Tetanus Toxoid (Formalin inactivated toxin) part of original DPT triple vaccine (5 diseases) – 2, 4, 6 months with booster at 5 years. – Immunity declines, boosters every 10 years recommended
36
Describe clostridium botulinum.
* Gram-positive, * Obligate anaerobe, * Sub-terminal (slipper) endospores * Four groups (I, II, III, IV) * Produce neurotoxin
37
Describe the neurotoxin of clostridium botulinum.
– Targets SNARE proteins at neuromuscular junction – Prevents vessicles anchoring & releasing acetylocholine. – Flacid muscle paralysis (stops the particular signal being sent to muscle from being switched on)
38
Describe how botulism is food borne.
- Refrigeration <3 ̊C - Incomplete cooking/reheated food - Preparation of canned food
39
How does botulism cause infection in wounds?
Contamination with bacteria/ spores
40
How does botulism infect infants?
spores consumed and organism grows in gut
41
Describe the symptoms of botulism in adults.
- 18-36 hrs after exposure - Double/blurred vision - Drooping eyelids - Slurred speech - Dry mouth/difficulty swallowing - Muscle weakness - Respiratory failure/Paralysis
42
Describe the symptoms of botulism in infants.
- Lethargy/poorly - Constipated - Weak cry - Poor muscle tone
43
Describe botox.
* Purified type-A toxin * Injection of minute quantities as therapy * Paralysis of muscle for up to 6 months * Facial muscle paralysis & wrinkle reduction
44
Describe the carrier statistics of pseudomembraneous colitis caused by clostridium difficile.
* 1-3% carriers of organism or inactive spores | * 20% of hospitalised patients are carriers
45
Describe the antibiotic therapy of pseudomembraneous colitis.
C. difficile proliferates in absence of normal flora
46
Describe pseudomembranous colitis.
• Ampicillin, Cephalosporins & Clindamycin • Toxin A enterotoxin • Toxin B cytotoxin • Mild to severe – Diarrhoea (2 days- 6 weeks after Antibiotic treatment) – Nausea, fever, abdominal pain – Mild 5-10 bowel movements – Severe >10, nausea vomiting, high fever, rectal bleeding
47
what are key to the virulence of pseudomembranous colitis?
toxins
48
Describe the action of toxin A and B in pseudomembranous colitis.
* Toxins A& B bind & internalised into intestinal epithelial cells * Impair function of intestinal epithelial cells (diarrhoea) * Stimulate Cytokine release & activation of macrophages & monocytes (Inflammation)
49
What are the reasons for C. difficile epidemic?
– strains producing more toxins – antibiotic resistance – Increased sporulation
50
what is the treatment for pseudomembranous colitis?
• Stop predisposing Antibiotic treatment • Fluid replacement • 1st line is metronidazole orally • Severe cases/ no response/ 2nd or more relapse – Metronidazole &/or – Oral Vancomycin
51
Describe the prevention of pseudomembranous colitis.
* Early diagnosis & awareness of the problem * Surveillance of episodes to pick up outbreaks * Single room/cohort isolation: separate toilets etc • Handwashing (PPE e.g. gloves & aprons) * Prudent antimicrobial prescribing by all * Education all healthcare staff & patients * Cleaning of healthcare premises & equipment
52
Give a C.difficile summary.
* Produces spores (survive in environment) * Toxins * Spores not inactivated by alcohol hand gels * Especially over 65 age group at risk * New strain: ribotype O27 may behave differently – more deaths, better survival, more easily spread? * Risk factors: antibiotics, increasing age, long hospital stay, serious underlying diseases, major surgery * Relapsing course; 30% have 2nd episode, this increases with each relapse
53
Give the summary slide.
``` • Neisseria – Meningitis & Gonorrhea – Diagnosis & treatment • Clostridia & spores – Tetanus • Symptoms & toxin – Botox • toxin – C. difficile • Antibiotics • Infection control • High risk individuals (>65 & >85 years old) ```