M23- Anaerobes Flashcards
What Neisseria species is commonly isolated from plaque?
N. subflava
where is the location of Neisseria?
Oropharynx, Nasopharynx & occasionally anogenital mucosal membranes
Describe the characteristics of Neisseria.
• 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
Name the r pathogenic specie of Neisseria.
- N. gonorrhoeae
- N. meningitidis
What diseases does N. gonorrhoeae cause?
– Urethritis (gonorrhea)
– Cervicitis
– Pelvic inflammatory disease
– Pharyngitis
What diseases does N. meningitidis?
– Meningitis
– Bacteremia
– Pnuemonia
Describe N. gonorrhea.
– 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
Name the key virulence factors of gonorrhea.
– 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
What makes it hard to make an effective vaccine for gonorrhea?
phase variation
-changes amino acid antigens
Describe the infection of gonorrhea.
– 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
Describe the identification of gonorrhea.
– Swabs of infected material
– Gram stain,intracellular Gm-ve diplococci
– Cooked Blood Agar
– Oxidase+ve,glucose+ve,-ve maltose & sucrose
Describe the treatment of gonorrhea.
Penicillin (resistance increasing problem)
-threat level is urgent
what is the oral presentation of gonorrhea?
usually asymptomatic
what is meningitis?
Infection & inflammation of membranes covering the
brain & spinal cord (meninges & CSF)
-bacterial and viral
what organisms can cause meningitis?
N. meningitidis, S.pnuemoniae & H.influenza
what is the only organism that causes large scale epidemics of meningitis?
N. meningitidis
Describe N. meningitidis and its spread.
– 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
Describe features of the main disease of meningitis?
-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).
Describe the identification of meningitis.
- 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
Describe the treatment and control of meningitis.
• 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
If family members have previously had it, how does this effect the risk of meningitis?
Increases the risk
Give 4 types of meningitis.
- 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
what gram +ve cocci causes caries and actinomyocosis?
Actinomyces species
What gram -ve cocci cause periodontal infections?
- Fusobacterium species
- Prevotella species
- bacteriodes
what is clostridia?
Anaerobic/ aerotolerant Gm+ve Bacilli
What does clostridia form?
endospores
Where is clostridia found?
Found in GI tract & environment
Name 3 clostridial diseases and the species that causes them.
- C. difficile - Pseudomembraneous colitis
- C. botulinum - Botulism
- C. tetani - tetanus
What is the habitat of C. tetani?
– Soil
– Humans (0% to 25%)
what is the appearance of C. tetani?
– Terminal spores
– drumstick or tennis racquet
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
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
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
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
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
Describe clostridium botulinum.
- Gram-positive,
- Obligate anaerobe,
- Sub-terminal (slipper) endospores
- Four groups (I, II, III, IV)
- Produce neurotoxin
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)
Describe how botulism is food borne.
- Refrigeration <3 ̊C
- Incomplete cooking/reheated food
- Preparation of canned food
How does botulism cause infection in wounds?
Contamination with bacteria/ spores
How does botulism infect infants?
spores consumed and organism grows in gut
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
Describe the symptoms of botulism in infants.
- Lethargy/poorly
- Constipated
- Weak cry
- Poor muscle tone
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
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
Describe the antibiotic therapy of pseudomembraneous colitis.
C. difficile proliferates in absence of normal flora
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
what are key to the virulence of pseudomembranous colitis?
toxins
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)
What are the reasons for C. difficile epidemic?
– strains producing more toxins
– antibiotic resistance
– Increased sporulation
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
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
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
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)
