Common bacterial infections Flashcards
What is the cause of diphtheria?
CH 187: DIPHTHERIA
- By Corynebacterium diphtheria – aerobic gram(+)
bacilli
- Acute, contagious
Epid:Transmission
- skin transmission via airborne respiratory droplets (3
feet)
- direct contact with respiratory secretions, exudate
from skin lesion
- impt: asymptomatic respiratory tract carriage
- can remain in dust/fomites x 6mos
- CD exclusive inhalant of human mucus membranes
- Humans are the only known reservoir (exclusively in
skin and mucosa)
IP: 1-5 d
How is diphtheria transmitted?
Transmission
- skin transmission via airborne respiratory droplets (3
feet)
- direct contact with respiratory secretions, exudate
from skin lesion
- impt: asymptomatic respiratory tract carriage
- can remain in dust/fomites x 6mos
What is the pathophysiology of diphtheria?
Patho
- non-invasive organism
- remains in the superficial layers of skin/respiratory
mucosa inducing local inflammation
- lysogenic CD bacteriophage encodes exotoxin which
inhibits protein synthesis causing local tissue necrosis
- local signs of inflammation
- infection of pharynxà form dense, necrotic coagulum
(organism + RBC + WBC + epithelial cells + fibrin) –>
becomes gray, brown, leatherlike adherent
pseudomembrane
a. difficult to remove
b. reveals bleeding edematous submucosa –>
suffocation of aspirated membrane
c. Bull neck appearance –> intense soft tissue
edema and cervical adenitis (children with
small airway)
- Fatality due to airway compromise and toxin mediated
complications
What are the clinical manifestations of diphtheria?
CM:
1. Respiratory diphtheria (94%)
- Facial & pharyngeal (most common), laryngeal &
tracheobronchial
- Nose: shallow ulceration of external nares & upper lip
is characteristic
- Abrupt LG fever (rarely above 39C), sore throat, dev’t
of membrane (extend widely) à pharynx and
tracheobronchial tree, bull neck appearance
2. Cutaneous (10%)
- Superficial nonhealing ulcer, ecthymic with gray-brown
membrane (tender, erythema, and with exudate)
- Usually extremities
- Heals in 2-3 mos, w/ a scar
3. Systemic – cause 50-60% of deaths
a. Cardiac
- Myocarditis in 2/3s of pxs
- Occurs in 2nd-3rd week of infection
- Dysrhythmia, Vtach, HF
- The first sign of cardiac involvement is tachycardia
disproportionate to the degree of fever
b. Neurologic
- First few days
- Cranial neuropathies characteristically occur in the 6th
week: strabismus, BOV
- Local paralysis of the soft palate and posterior pharynx
à regurgitation of swallowed fluids
- Symmetric polyneuropathy: distal muscle weakness
with proximal progression
- 1st signs: Dysphagia and nasal speech
c. Others: otitis externa, conjunctivitis,
arthritis
- Recovery from myocarditis and neuritis usually slow
but complete
How is diphtheria diagnosed?
Dx
1. CBC - moderate leukocytosis
2. Throat swab membrane GS & C/S – specimen should
be collected beneath the membrane including the
membrane itself
- Repeat cultures of nose and throat 2x (24h apart) after
completion of tx to ensure eradication of org
3. Baseline ECG – detect myocarditis ASAP
- Repeat 2x/week for 4-6 weeks
- ST-T wave changes, variable heart block, dysrhythmia
4. Serum Troponin I – correlate with severity of
myocarditis
5. Soft tissue neck XR/CT/UTZ – prevertebral soft tissue
swelling, enlarged epiglottis, narrowing of subglottic
region
6. 2D echo – demonstrate valvular vegetations
How is diphtheria managed?
Mgt
1. Neutralization of free loosely bound toxin with
diphtheria antitoxin (DAT)
- 40K-60K U <2d of sx
- 80K-120K U >2 d of Sx
2. Eradication of the organism
- Pen G 100,000-150000 U/k/d q6h x 10d
- Erythromycin 40-45 mkd q6h x 14d
3. Supportive – IV hydration, intubation (MV,
tracheostomy), bed rest
4. Complete immunization (convalescent) – protection
lasts 10 yrs
- Vax does not eliminate carriage of CD in the pharynx,
nose or skin
- Infection does not confer immunity
- Only effective way of preventing cases and outbreaks
- If unimmunized à complete vaccination
a. 6wk-6yo: DTaP (5)
b. >6yo: Tdap-Td-Td
c. 11-12 yo: Tdap q10y
5. Carriers – sx free but with CD in nasopharynx
- Erythromycin 40-45 mkd q6h x 7d
- Benzathine penicillin (<30kg) 600,000 U IM single dose;
(>30kg) 1.2M U IM single dose
- F/u after 2 weeks & if carrier state persists, give
additional 10d course of erythromycin and consider
tonsillectomy/adenoidectomy
6. Patient contact – household and hospital contact
(unimmunized or partially immunized)
- Nasopharyngeal GS/CS
- Erythromycin 40-45mkd qid x 7d
- Benzathine penicillin (<30kg) 600,000 U IM single dose;
(>30kg) 1.2M U IM single dose
7. Infection control – strict isolation precaution for the
duration of tx (10d)
- Droplet precautions
- Vaccinate all hospital workers
Acute spastic paralysis
Tetanus
What is the etiology of tetanus?
Etiology:
- Clostridium tetani
- Anaerobic gram (+)
IP: 2-14d, but may occur months after an injury
Acute spastic paralysis
- Favorable prognosis: long incubation period, absence
of fever, localized disease
- Unfavorable prognosis: onset of trismus <7d afer
injury, generalized tetanic spasms occurring <3d after
onset of trismus, cephalic tetanus
How is tetanus transmitted?
Transmission
- Associated with traumatic injury (penetrating wound
from a dirty object
- Introduced spores germinate, and produce tetanus
toxin
What is the pathophysiology of tetanus?
Patho:
Traumatic injury –> bacterial spores enter injury –> spores
converted to vegetative forms w/c produce tetanospasmin –>
blood/LN dissemination –>
- SC & brain: binds to NMJ (retrograde axonal transport)
à GABA inhibition –> blocks inhibition of antagonistic
muscles –> spasmic paralysis
- ANS: Ach inhibition –> autonomic dysfunction
- Note: vs botulism: Ach inhibition –> flaccid paralysis
What are the clinical manifestations of tetanus?
CM
3 main components: muscle rigidity, muscle spasm & autonomic
dysfunction
1. Neonatal or umbilical tetanus – most common form
- Occurs within 3-12d of birth
- Progressive difficulty in feeding to jaw stiffness
- Generalized weakness
- Hunger, crying, paralysis, stiffness and rigidity to touch,
spasms, opisthotonos
- Cyanosis or pallor, apneic episodes
- unsterile umbilical cord stump, unsanitary delivery of
baby, mom incomplete immunization hx
- constipation and urinary retention
2. Generalized tetanus
- Most common presentation
- Tetanic paralysis usually more severe in the 1st week,
stabilizes in the 2nd week, then ameliorates gradually in
the next 1-4 wks
- Progressive stiffness of voluntary ms:
a. Trismus: masseter muscle spasm or lockjaw
b. Risus sardonicus: orbicularis oris, sardonic
smile of tetanus
c. Opisthotonos: neck and back; arched
posture of extreme hyperextension
d. Board-like abdomen: trunk
e. Flexed arms and extended legs: extremities
- Laryngeal & respiratory muscle spasm can lead to
Headache, restlessness, irritability, fever, followed by
stiffness, difficulty chewing, dysphagia, neck muscle
spasm
- Accumulation of secretions because of inability to
swallow
- Intact sensorium, severe pain during each spasm
- Fever: usually absent, if present HG due to energy
generated from tetanic spasm
- Seizures: sudden tonic contractions of the muscles
- Smallest disturbance by sight, sound, or touch may
trigger a tetanic spasm
a. May be so violent to cause upper airway
obstruction and vertebral fractures
- Dysuria and urinary retention from bladder sphincter
spasm
- Hyperactive DTR
- Sympathetic overactivity (SOA): Autonomic sx: resting
tachycardia, arrhythmia, labile hypertension, sweating,
depression of bowel motility and bladder dysfunction
a. Occurs a few days after onset of spasms
3. Localized tetanus
- Chronic form, prodrome of gen tetanus
- May reflect partial immunity to tetanospasmin
- Painful spasms of muscles adjacent to wound site
- May precede generalized tetanus
a. Cephalic tetanus: rare form
b. Involve bulbar musculature. Results in
retracted eyelids, deviated gaze, trismus,
risus sardonicus, spastic paralysis of tongue
and pharyngeal membrane
c. Affecting muscles innervation CN 3,4,7,9,10
d. Follows head injury, OM, FB in nose
What are the diagnostics for tetanus?
Dx
1. CBC – usually N, or mod leukocytosis
2. RBS, Na, K, Cl, Ca, Mg - r/o abN
3. CXR – r/o aspiration PN
4. BUN, Crea, CSF, septic workup (neonates), ABG, 12L
ECG
5. wound d/c GS/CS – not indicated because only (+) in
30%. Does not indicate whether organism contains
toxin
6. CSF/ lumbar puncture – not nec. Usu N or only inc
opening pressure
7. Elev CK, aldolase
8. Spatula test – using a spatula/tongue depressor, touch
oropharynx eliciting reflex spasm of masseters and bite
the spatula (+ result)
9. EMG – continuous discharge of motor subunits and
absence of the silent interval normally observed after
an action potential
Scoring system for Neonatal tetanus
Staging system for non-neonatal generalized tetanus
Ablett Classification of severity of tetanus
Management of tetanus
- neutralization of circulating/unbound toxin: TIG 250U
or ATS 1500-3000IU, ideally HTIG 500U IM
a. If TIG unavailable: human IVIG, equine, or
bovine-derived tetanus antitoxin
b. Upon d/c, tetanus toxoid - Active Vaccination
DTaP, DTwP, Tdap, Td - Elimination of exotoxin production
e. Wound care: Wound excision &
debridement
a. Abx
i. Metronidazole po/iv 30mkd x
10d – DOC
ii. Pen G x 10d
Neonates 100K U/k/d q12
Children 100L U/k/d q6
Adult 5M q6
iii. Alt for allergy: erythromycin,
tetracycline - Prevention and control of spasms:
a. For generalized tetanus: muscle relaxants
and NM blockers (Pancuronium,
vecuronium)
b. BZDs, MgSO4
c. Control of sz (Pb) - Severe: Intubation to prevent aspiration, early
tracheostomy - Control of autonomic dysfuntion – MgSO4 to suppress
cathecholamine release - Quiet, dark, secluded setting
How is tetanus prevented?
Prevention
1. Vaccination with DTaP, Tdap, Td
2. Pregnant women: 1 dose Tdap during each pregnancy,
at 27-36 weeks AOG
3. Tetanus prophylaxis in wound mgt
a. Clean minor wounds and <3doses of Td:
Tdap or Td
b. Clean minor wounds and >3 dose of Td
within the past 10 yrs: no need for toxoid
c. All other wounds and <3 doses of Td: Tdap
or Td and TIG
d. All other wounds and > 3 dose of Td within
the past 5 years: no need for toxoid/TIG
What is botulism and its cause?
- Acute, flaccid, paralysis
- Gram (+), spore-forming, obligate anaerobe whose
natural habitat is soil, dust, and marine sediments - Strains endure sev hrs of boiling, survive food
preservation; but the toxin is heat labile at >85C for
5min (canned foods) - Botulinum toxin is the most poisonous substance
known, lethal dose = 10-6 mg/kg - Most striking epidemiologic fx is its age of distribution
= 95% cases infants between 3wks to 6mos age, peak
2-4 mos - Risk factors: breastfeeding, ingestion of honey, slow
intestinal transit time (<1 stool/d), contaminated water - Represents a medical and public health emergency
What is the pathophysiology of botulism?
Patho
- Toxin blocks NM transmission and causes death
through airway and respiratory muscle paralysis
- Botulinum toxin is carried by the bloodstream to
peripheral cholinergic synapses, where it binds
irreversibly, blocking acetylcholine release, and causing
impaired NM and autonomic transmission
How is botulism transmitted?
Transmission
Infant botulism – ingestion of spores
Foodborne botulism – ingestion of preformed botulinum toxin
contained in improperly preserved or inadequately cooked food
Wound botulism – spore germination from traumatized tissue
Inhalational botulism – aerosolized botulinum toxin is inhaled
What is the classic triad of botulism? What are the clinical manifestations?
- Classic triad
a. Acute onset of symmetric flaccid
descending paralysis with clear sensorium
b. No fever
c. No paresthesia - Symmetric, descending, flaccid paralysis – beginning in
the CN musculature. Multiple bulbar palsies. - Infant botulism
- poor feeding, weak suck, feeble cry, drooling,
obstructive apnea
- generalized weakness and hypotonia, diminished
spontaneous movt
- loss of head control is a prominent sign
- first sx may be dec freq or absence of defecation
- respiratory arrest from sudden airway occlusion by
unswallowed secretions or obstructive flaccid
pharyngeal musculature - Food-borne/ wound botulism
- Onset of neuro sx follows a characteristic pattern of
diplopia, BOV, ptosis, dry mouth, dysphagia,
dysphonia, dysarthria, dec gag and corneal reflex
- Toxic acts only on the motor nerves
- No paresthesia
- Nausea, vomiting, diarrhea
- Constipation once flaccid paralysis is evident
- Begins 12-36h after ingestion of food (range 2h-8d)
- Fever in wound botulism - Inhalational botulism
- Mild (min ptosis, flattened facial expression, minor
dysphagia, dysphonia) to fulminant (rapid extensive
paralysis, frank apnea, fixed, dilated pupils) - Fatigability with repetitive muscle activity – clinical
hallmark of botulism
How is botulism diagnosed?
Dx
1. Botulinum toxin – serum, wound, enema fluid, feces
2. EMG – distinctive finding: facilitation (potentiation) of
the evoked muscle action potential at high frequency
(50 Hz) stimulation
- Infant: BSAP (brief, abundant, motor unit action
potentials) is characteristic
- N nerve conduction velocity and sensory nerve fxn
3. CBC, BCS, CRP – r/o sepsis
how is botulism managed?
Mgt
1. Human botulism IG IV (BIG-IV) 50-100 mg/kg SD – given
ASAP
- Shortens mean hospital stay from 6wks to 2 wks
2. Equine heptavalent (A-G) botulism antitoxin – for older
pxs
3. Abx – not part of tx of uncomplicated infant/foodborne
botulism
- Reserved for tx of secondary infections, absence of
antitoxin tx
- DOC: TMP-SMX 20mkd IV q6/8
- Avoid aminoglycosides because may potentiate the
blocking action of botulinum toxin at the NMJ
4. Proper positioning
- Supine on rigid-bottomed crib/bed, head titled at 30
degrees. Small cloth roll under the cervical vertebrae
to tilt the head back so the secretions drain to the
posterior pharynx and away from the airway and
improve respiration
. Prophylactic ET intubation – indications: diminished
gag and cough reflex and progressive airway
obstruction by secretions
6. NGT feeding until sufficient oropharyngeal strength
and coordination enable BF/bottle feeding – EBM is
most desirable food
7. Hydration
8. Stool softeners (lactulose) – mitigate constipation
What are the complications of botulism? Prognosis?
Complic
1. Nosocomial infections
2. PN, UTI, OM
3. strabismus
Prognosis
- full and complete recovery (~4wks).
How is botulism prevented?
Prevention
- Avoiding suspicious foods (canned foods improperly
preserved)
- Heat all canned foods to 85C for >5min
- Avoid honey until 1 yo
- Continue BF
What is Staphylococcus aureus? How is it transmitted?
- Gram (+) aerobic bacteria, coagulase (+)
- Most common cause of pyogenic infections of the skin
and soft tissues
Transmission:
Autoinoculation or direct contact
