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nagasaki flashcard extravaganza > Bacteria - gram +ve > Flashcards

Bacteria - gram +ve Flashcards

Tetanus, Diphtheria

1
Q

What are the symptoms of tetanus?

A

Tetanus (lockjaw)
Trismus
Difficulty feeding
Tonic muscle spasms - think in neonate if mum unvaxed
Respiratory difficulties
Cardiovascular instability (sympathetic nervous system)
Localised tetanus - eg to a limb
Cephalic tetanus

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2
Q

What is the microbiology of tetanus?

A

Gram-positive obligate anaerobe
* Thin film on blood agar due to motility
* Terminal spore: ‘tennis racquet’ shape
* Highly resistant spores

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3
Q

What is the source of tetanus?

A

Widespread in soil

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4
Q

What is the epidemiology of tetanus

A

Ubiquitous organism
Global decline in cases over last 20 years Majority of cases: South East Asia and South America
Commonest in neonates (via umbilicus)

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5
Q

What is the clinical syndrome of tetanus

A

1 Generalized
* Remember the acronym ‘ROAST’ r – Rigidity
O – Opisthotonus A – Autonomic
dysfunction
S – Spasms (painful)
T – Trismus
* Risk factors
- Puncture wound
- Devitalized tissue
- Delay to
- debridement
Contact with soil or
- manure
Animal bites
- Clinical evidence of
sepsis
2 Neonatal
* Accounts for 50% of * cases
Only in the context
of lack of maternal
* immunity
* 1–10 days postpartum
Mortality 90%
(i) Initially subtle
signs: irritability,
poor feeding
(ii) Later spasms, opisthotonus,
hypersympathetic
state
(iii) Mental retardation
in survivors
3 Localized
* Muscle rigidity near * site of injury
May be mild and
* persist for months
Can progress to generalized form:
important to recognize and treat
4 Cephalic
* Rare
* Associated with head
injury or middle-ear * infection
* Incubation 1–2 days
Presents with cranial nerve palsies

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6
Q

What is the vaccinology of tetanus?

A

Toxoid vax

  • ≥ 5 doses of tetanus vaccine (inactivated tetanus toxoid)
  • Maternal vaccination protects against neonatal tetanus
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7
Q

What is the management of tetanus?

A
  • Debridement: to clear organism/spores
  • Tetanus immunoglobin (rarely given intrathecally)
  • Antibiotics: metronidazole/penicillin
  • Benzodiazepines: to prevent spasms
  • Airway management: early airway protection ± tracheostomy - common cause of death is laryngeal spasm
  • Manage autonomic instability:
  • sedation, pacing, atropine
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8
Q

What is the incubation of tetanus?

A

Around 8 days in severe disease
1-10 days of life for neonatal tetanus

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9
Q

What is the pathophysiology of tetanus?

A

Spores germinate under anaerobic conditions at the site of a wound and the growing bacteria produce two toxins: tetanolysin and tetanos- pasmin. Tetanospasmin undergoes proteolytic cleav- age and binds and enters the presynaptic terminal. There, tetanospasmin cleaves the protein that allows fusion of synaptic vesicle with the membrane and thus prevents transmitter release. Tetanospasmin is able to travel retrogradely via axons to cell bodies and cross synapses, thus reaching the spinal cord, brain and autonomic nervous system. It primarily affects inhibitory glycine or γ-aminobutyric acid (GABA) neurones, leading to increased firing and lack of nor- mal relaxation and causing the classical spasms of tetanus.

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10
Q

What is the microbiology of diphtheria?

A

C.diptheriae - 4 biovars
Small Gram-positive bacilli

Three varieties: var. gravis/var. mitis/var. intermedius
* Family Mycobacteriaceae
* Non-motile, non-sporing, non-branching
* Irregular club-shapes,
Y-shapes, ‘Chinese letter’ arrangements

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11
Q

What is the epidemiology of diphtheria?

A
  • Remains common in developing world
  • Can survive for months in the environment
  • Spread via naso-pharyngeal secretions
  • Incidence highest in young children (3–6 months) after waning of maternal antibody
    Asymptomatic upper respiratory tract colonization is common—reservoir for spread
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12
Q

What are the symptoms of diphtheria?

A

Membranous pharyngitis with fever
Membrane – grey, thick, fibrinous, firmly adherent Enlarged anterior cervical lymph nodes Surrounding oedema – “bull neck”
Laryngeal – increasing hoarseness and stridor Nasal – discharge initially clear then bloody
Cutaneous – vesicles that ulcerate with an eschar. May be reservoir of infection

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13
Q

What are the complications for diphtheria?

A

Complications
Local tissue necrosis
Myocarditis (heart block) (1-6 weeks)
Breathless, angina, syncope Bradyarrhythmia, tachyarrhythmia
ST segment abnormalities, 1st, 2nd and CHB
Demyelinating peripheral neuritis (10 days – 3 months) Palatal palsy, cranial nerve palsy
Limb weakness
Respiratory muscle paralysis

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14
Q

What is the transmission of diphtheria?

A

Human to human
Resp occasionally direct contact
Cutaneous can be lesion

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15
Q

What is the treatment of diphtheria?

A

Diphtheria antitoxin (horse serum) - within 4 days
Antibiotics
Benzyl Penicillin
Macrolides (erythromycin; clarithromycin; azithromycin) - some resistance
Parenteral then oral
Check susceptibilities
14 days
Confirm eradication of carriage
Immunisation primary course or booster
Follow up 3-6 months

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16
Q

What is the incubation of diphtheria?

A

2-5 days

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17
Q

What is the microbiology of anthrax?

A

Gram +
Rod-shaped bacillus
Aerobic

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18
Q

What is the testing for anthrax?

A

Culture on blood agar:
White, non-haemolytic, non-motile
Grows quickly to large ‘medusa-head’ colonies Penicillin sensitive

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19
Q

What is the epidemiology of anthrax

A

2000k pa
Turkey, US, Croatia

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20
Q

What is the IPC of anthrax

A

Spreads after sick animals killed so need surveillance and safe slaughtering policies
Lab safety v important

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21
Q

What is the treatment for anthrax?

A

Penicillin +/- cipro OR doxy

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22
Q

what is the clinical syndrome of anthrax

A

Depends of route…

  1. CUTANEOUS ANTHRAX
    Contact with infected animal hide or meat; also injecting drug users
    * Incubation 12 hours–12 days
    * > 95% of cases
    Papule itching, erythema, oedema
    Vesicle/eschar
    regional adenopathy
    ± Chills, headache, sepsis

2 Ingestion of infected meat
OROPHARYNGEAL OR GASTROINTESTINAL ANTHRAX
Severe sore throat
± ulceration, membrane
Neck sweling
massive oedema, dysphagia
Sepsis
OR
Nausea and vomiting
Bloody diarrhoea and bloody ascites
Sepsis

3 Inhalation of spores
PULMONARY ANTHRAX +/- MENINGITIS
* N.B. Bioterrorist agent Fever, myalgia, cough
Severe pneumonia
rapid onset
Bloody effusions and haemoptysis
+/- Tracheal compression, mediastinal widening
AND/OR
Haemorrhagic meningitis ~ 100% mortality

23
Q

What is the micro of pneumococcus?

A

Gram positive diplococci
Encapsulated
Lab confirmations:
Greenish discolouration and a-hemolysis of blood agar
Soluble in bile salts
Susceptible to optochin

24
Q

What is the global burden of pneumococcus?

A

Nearly 2·37 million deaths in 2016
- Sixth leading cause of mortality for all ages and
- The leading cause of death among children younger than 5 years.

25
Q

What are the clinical syndromes of pneumoccocus?

A

Non invasive - pneumonia, sinusitis, otitis media

Invasive - meningitis, bacteraemia

26
Q

Who is at risk for pneumococcal disease?

A

Very young and old

Immunocompromised (especially splenectomy, HIV infection)

Underlying CLD
Smoking
Overcrowding
Cold
Alcoholism

27
Q

What is the vaccinology of pneumococcus?

A
  • Vaccines recommended for high-risk groups (age < 2, > 65, and other high-risk groups, e.g.
  • splenectomy, sickle cell, HIV)
  • Polysaccharide vaccine: 23-valent
    Pneumococcal conjugate vaccine (PCV): 13-valent

Conjugate has a better immune response
Polysaccharide has no response in children

28
Q

How is pneumococcal disease diagnosed?

A

CXR: lobar pneumonia
Pleural effusion (upto 57%)-only 10% have enough fluids to aspirate
Empyema: 2-8%

Urine immunochromographic - Binax Now (not useful in children due to colonisation)

29
Q

How is pneumococcal disease managed?

A

Follow local guidelines and antibiotic resistance pattern Penicillin- Amoxycillin, Amoxycillin-Clavulanate Ceftriaxone
In meningitis: Ceftriaxone with or without Vancomycin
*Benefits of dexamethasone for pneumococcal meningitis is not consistent among studies in developing countries.

30
Q

Tetanus causative organism

A

Clostridium tetanii
Gram positive tennis racquet, makes spores
Obligate anaerobe

31
Q

Tetanus transmission

A

Spores into minor cut

Spores into umbilical cord (dung)

Otitis media –> facilitated spore entry

32
Q

Tetanus pathophysiology

A

Clostridium tetanii –> toxin production

Toxin spreads up nerves and via blood into CNS

Blocks inhibitory neurotransmitters

Overactivation of motor and autonomic systems

33
Q

Tetanus incubation period

A

1-10 days (shorter = more severe disease)

34
Q

Tetanus signs

A

R - rigidity
O - opisthotonus
A - autonomic dysfunction
S - spasticity
T - trismus (first sign)

35
Q

How is tetanus diagnosed?

A

Clinically - clostridium tetanii often not isolated

36
Q

How is tetanus severity graded?

A

Modified Ablett score 1 - 4

1 = mild trismus, no spasticity

2 = moderate trismus, intermittent spasticity

3 = rigidity + respiratory compromise

4 = severe autonomic dysfunction

37
Q

How is tetanus managed?

A
  1. Urgent antitoxin / immunoglobulin
  2. Wound debridement (remove spores)
  3. Antibiotics (metronidazole, penicillin)
  4. Pacing and atropine
  5. Magnesium and benzos for spasticity
  6. Secure airway
38
Q

How is tetanus prevented?

A

Inactivated toxoid vaccine
5 doses as routine childhood schedule

Maternal vaccine in 3rd trimester for neonatal protection

39
Q

Anthrax causative organism

A

Bacillus anthracis

Gram +ve bacillus
Aerobic
Spore forming

40
Q

How is anthrax transmitted?

A
  1. Inhalation of spores
  2. Inoculation of spores into broken skin
  3. Ingestion of infected meat
41
Q

Clinical syndrome cutaneous anthrax

A

Incubation period 1-5 days

Papule –> vesicle –> ulcer –> eschar (painless), surrounding oedema +++

Self healing in 3/52, overwhelming sepsis may occur

42
Q

Clinical syndrome inhalational anthrax

A

Incubation period 1-5 days
Biphasic illness
Initial URTI

Rapid onset haemhorragic mediastinitis / haemhorragic meningitis

90% mortality
Bioterrorism (aerosolised spores)

43
Q

Clinical syndrome GI anthrax

A

Ingestion contaminated meat

Sore throat +/- membrane, considerable oedema –> dysphagia

Bloody diarrhoea, massive ascites

Mortality 50%

44
Q

How is anthrax diagnosed

A

PCR of eschar / serum / throat swab

Eschar swab –> gram +ve bacillus

Culture on blood agar –> “medusa head” colonies (spores)

45
Q

How is anthrax managed?

A

High dose ben pen + ciprofloxacin

10/7

(pen resistance +++, cover with cipro until sensitivities back)

46
Q

How can anthrax be prevented?

A
  1. Proper disposal animal carcass
  2. Cipro / doxy PEP
  3. Vaccinate animals yearly
  4. Vaccinate high risk persons (frequent booster required)
  5. Human : human tx rare, standard PPE only for nursing care
47
Q

Diphtheria causative organism

A

Corynebacterium diphtheriae

Gram +ve bacillus

48
Q

How is diphtheria transmitted?

A

Droplets containing corynebacterium diphtheriae

Direct contact with nasopharyngeal fluid of infected person

49
Q

What is clinical syndrome of diphtheria?

A

Illness caused by toxin. Resp and systemic effects. Short incubation

RESP:
Red oedematous mucosa with grey adherent membrane. “Bull neck” lymphadenopathy. Nasal speech from palatal paralysis

SYSTEMIC:
Myocarditis, RBBB, heart block. Peripheral neuritis from demyelination. Acute tubular necrosis

50
Q

How is diphtheria diagnosed?

A

Throat swab culture

ECG for heart block, ST changes, RBBB

51
Q

How is diphtheria managed?

A

Antitoxin (small subcut dose first to check for anaphylaxis)

High dose IV abx, multiple effective. Penicillin, erythromycin etc

Barrier nursing and isolation required

52
Q

What is the mortality rate of diphtheria?

A

Untreated 50%

Treated 10%

53
Q

How can diphtheria be prevented?

A

Vaccination: Purified toxin. routine childhood imm, 5 doses

Barrier nursing identified cases

nagasaki flashcard extravaganza (34 decks)

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