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Microbiology > M23- Anaerobes > Flashcards

M23- Anaerobes Flashcards

1
Q

What Neisseria species is commonly isolated from plaque?

A

N. subflava

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2
Q

where is the location of Neisseria?

A

Oropharynx, Nasopharynx & occasionally anogenital mucosal membranes

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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

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4
Q

Name the r pathogenic specie of Neisseria.

A
  • N. gonorrhoeae

- N. meningitidis

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5
Q

What diseases does N. gonorrhoeae cause?

A

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

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6
Q

What diseases does N. meningitidis?

A

– Meningitis
– Bacteremia
– Pnuemonia

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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

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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

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9
Q

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

A

phase variation

-changes amino acid antigens

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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

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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

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12
Q

Describe the treatment of gonorrhea.

A

Penicillin (resistance increasing problem)

-threat level is urgent

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13
Q

what is the oral presentation of gonorrhea?

A

usually asymptomatic

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14
Q

what is meningitis?

A

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

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15
Q

what organisms can cause meningitis?

A

N. meningitidis, S.pnuemoniae & H.influenza

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16
Q

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

A

N. meningitidis

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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

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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).

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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
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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

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21
Q

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

A

Increases the risk

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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
Q

what is clostridia?

A

Anaerobic/ aerotolerant Gm+ve Bacilli

26
Q

What does clostridia form?

A

endospores

27
Q

Where is clostridia found?

A

Found in GI tract & environment

28
Q

Name 3 clostridial diseases and the species that causes them.

A
  • C. difficile - Pseudomembraneous colitis
  • C. botulinum - Botulism
  • C. tetani - tetanus
29
Q

What is the habitat of C. tetani?

A

– Soil

– Humans (0% to 25%)

30
Q

what is the appearance of C. tetani?

A

– Terminal spores

– drumstick or tennis racquet

31
Q

Describe the development of tetanus.

A

• 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
Q

Describe the actions of the tetanus toxin.

A
  • 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
Q

What are the symptoms of tetanus?

A 
•  Irritability, drooling
•  Headache
•  Fever, sweating
•  Exaggerated reflexes, back spasms, Lock Jaw
•  Musclespasms
–  Difficulty swallowing 
–  Rigidity of the back
•  General Muscle rigidity
34
Q

Describe prompt intervention of tetanus.

A

– 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
Q

Describe the control of tetanus.

A

– 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
Q

Describe clostridium botulinum.

A
  • Gram-positive,
  • Obligate anaerobe,
  • Sub-terminal (slipper) endospores
  • Four groups (I, II, III, IV)
  • Produce neurotoxin
37
Q

Describe the neurotoxin of clostridium botulinum.

A

– 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
Q

Describe how botulism is food borne.

A
  • Refrigeration <3 ̊C
  • Incomplete cooking/reheated food
  • Preparation of canned food
39
Q

How does botulism cause infection in wounds?

A

Contamination with bacteria/ spores

40
Q

How does botulism infect infants?

A

spores consumed and organism grows in gut

41
Q

Describe the symptoms of botulism in adults.

A
  • 18-36 hrs after exposure
  • Double/blurred vision
  • Drooping eyelids
  • Slurred speech
  • Dry mouth/difficulty swallowing
  • Muscle weakness
  • Respiratory failure/Paralysis
42
Q

Describe the symptoms of botulism in infants.

A
  • Lethargy/poorly
  • Constipated
  • Weak cry
  • Poor muscle tone
43
Q

Describe botox.

A
  • Purified type-A toxin
  • Injection of minute quantities as therapy
  • Paralysis of muscle for up to 6 months
  • Facial muscle paralysis & wrinkle reduction
44
Q

Describe the carrier statistics of pseudomembraneous colitis caused by clostridium difficile.

A
  • 1-3% carriers of organism or inactive spores

* 20% of hospitalised patients are carriers

45
Q

Describe the antibiotic therapy of pseudomembraneous colitis.

A

C. difficile proliferates in absence of normal flora

46
Q

Describe pseudomembranous colitis.

A

• 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
Q

what are key to the virulence of pseudomembranous colitis?

A

toxins

48
Q

Describe the action of toxin A and B in pseudomembranous colitis.

A
  • 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
Q

What are the reasons for C. difficile epidemic?

A

– strains producing more toxins
– antibiotic resistance
– Increased sporulation

50
Q

what is the treatment for pseudomembranous colitis?

A

• Stop predisposing Antibiotic treatment
• Fluid replacement
• 1st line is metronidazole orally
• Severe cases/ no response/ 2nd or more relapse
– Metronidazole &/or
– Oral Vancomycin

51
Q

Describe the prevention of pseudomembranous colitis.

A
  • 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
Q

Give a C.difficile summary.

A
  • 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
Q

Give the summary slide.

A 
•  Neisseria
–  Meningitis &amp; Gonorrhea 
–  Diagnosis &amp; treatment
•  Clostridia &amp; spores 
–  Tetanus
•  Symptoms &amp; toxin –  Botox
•  toxin
–  C. difficile 
•  Antibiotics
•  Infection control
•  High risk individuals (>65 &amp; >85 years old)

Microbiology (30 decks)

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