Specific neurological infections pdf - وهاب رزاق

م هللاْسِب

الرحمن الرحيم

Specific

Neurological

Infections

Tetanus

Epidemiology:

1 per million per year in the US
Not uncommon in developing countries

Cause:

Clostridium tetani ( G+ve rods, anaerobe, spore forming)

a commensal in the gut of humans and domestic animals.

Habitat

: heat and anti-septic –resistant spores in soil (mainly

through fecal material of animals, and human!; and human
reservoir

Entry to human body

; in anaerobic conditions like T. necrosis,

spores form bacteria which produce exotoxin

• Tetanus is often associated with

rust

especially rusty nails. Although rust itself does
not cause tetanus, objects that accumulate
rust are often found outdoors or in places that
harbor anaerobic bacteria.

Pathophysiology

Exotoxin: tetano-spasmin
Blood-borne transport to local motor endplate
Retrograde axonal transport to CNS
Sites of action:
• Spinal cord and brainstem inhibitory neuron

( Renshaw cells)

Clinical features

Incubation period: 1-2 days to 1 month
Types:
Localized: benign course, resolution with no
residual effects, check for recruiting spasm and lock
jaw
Generalized: severe, mild fever, neck stiffness, then
bulbar involvement then limb & trunk; can be seen
in neonates (

tetanus neonatorum

)

Cephalic: bulbar and facial weakness and spasms,
worst prognosis

Risus sardonicus

( L: a sarcastic laugh)

opsithotonus

In the severe cases, violent spasms lasting for few
seconds to 3-4 minutes occur spontaneously , or
may be induced by stimuli such as movement or

noises

Spasms are painful and exhausting

Diagnosis

A clinical one!
Organism rarely isolable by the time of
presentation.

Hx of injury; dirty wounds

Causes of death

• Laryngospasm, apnea
• Heart failure, arrhythmia
• Shock
• Aspiration pneumonia

Treatment

•Immediate measures
•Antitoxin (3000-6000 units, IV )
•Antibiotic (Penicillin, metronidazole or
tetracycline , 10 day course)
•Nurse in quiet dark room
•Debridement of wound, Rx of secondary
infections
•ICU nursing ( environment, tracheostomy)
•muscle relaxants like diazepam, phenobarbitone

Prevention

Active immunization (DTP); 3 doses; routine in Iraq
Every 10 years, a booster should be administered
Toxoid is indicated in
• moderate/high risk wounds when patient hasn’t

received a booster in the last 5 years

• any open wounds when patient hasn’t received a

booster within last 10 years

Patients with moderate/high wounds should receive IM

anti-toxin

Summary

The only vaccine preventable disease that is
infectious but not contagious!
Mortality : 50%,
tetanus neonatorum :100% in developing
countries
Good prognosis:
Localized, early treatment

Rabies

Latin: madness, fury, rage

Rabies

A zonoosis
Maintenace hosts
wild: fox, raccoons, skunks, bats
Domestic: dogs, cats
Still common in developing countries
Mode of transmission
• Saliva ( bites, licks of broken skin or mucus

membrane)

• Iatrogenic (corneal transplants)

Aetiology

Pathophysiology

Causative agent: RNA virus, a Rhabdovirus

Retrograde axonal transport to CNS

Targets of infection: CNS( brainstem) and salivary

glands
Pathology:
• Rhombencephalitis
•

Negri bodies (hippocampus, Purkinji cells)

Clinical features

Incubation period: 4-8 weeks, as minimum as 9 days (multiple, necks,
face, scalp bites)
History of bite
Prodrome: fever, headache, parasthaesia around bite (characteristic)
Encephalitis versus paralytic phenotypes:

Furious/ rabid/ encephalitic rabies

: agitation, confusion, seizures,

insomnia, hallucinations, characteristic hydrophobia

Paralytic/ dumb

rabies: severe weakness, preserved sensorium

Coma
Death (100% of clinically evident cases) usually within 7 days of onset
of symptoms

Management

Diagnosis: a clinical one
PCR ( CSF, hair follicle, corneal smear preparation)
Post mortem examination for confirmation

What to do in established case?
Really nothing
Treatment is supportive and palliative,
isolation
Intensive care setting

Prevention

Wound washing with soap and benzyl ammonium chloride
Post-exposure:
Active: HDCV 1 ml IM, on day 0,3,7,14,28 (30), (90)
Passive: HRIG 20U/kg ½ IM, ½ infiltration around wound
If HRIG is not available, 0.1 ml of HDCV ID at 8 sites on day 1,
single boosters on day 7 & 28
If no human products available, observe the animal for 10 days
or euthanize if S&S of rabies!

Pre-exposure prophylaxis: HDCV 0.1 ml, two IM injections

Poliomyelitis

Greek: Polio: gray; Myelin: marrow

Dynasty

1403 - 1365 BC
Egypt

Poliomyelitis

Causative agent: 3 polioviruses….Enteroviridae.
( RNA viruses)
Mode of transmission: faeco-oral
Epidemiology: 3 countries are currently still
endemic ( Afghanistan, Pakistan and Nigeria),
reduced reports, from 350,000 cases in 1988 to
only 233 in 2012

infection

Inapparent polio

90-95%

Abortive polio

4-8%

(minor febrile illness)

Aseptic meningitis

(1-2%)

recovery

Paralytic polio

(0.5%)

Recovery with

residual deficit

Death

5-10% of

paralysed

Post-polio

syndrome

Clinical features

Incubation period: 3-35 days, average 6-20 days
Pre-paralytic: pharyngitis, headache, fever, muscle aches,
tenderness
Paralysis: peaks with maximal fever, within 24-48 hours, doesn’t
progress when fever is settled for two days, asymmetrical,
proximal, lower limbs mainly flaccid weakness (injection, physical
activity are risk factors)
Wasting apparent after 3 weeks, maximal by 12-16 weeks
Three phenotypes:
Spinal(79%);Bulbar( 2%); Bulbospinal (19%)

Management

Diagnosis:
Isolation of virus from stool or pharynx
Rarely isolable from CSF!
CSF examination: lymphocytic pleocytosis
Treatment:
Supportive: avoid IM injection, exercise.

Prevention:
Sabin vaccine (OPV) live attenuated, (herd immunity),

Salk (IPV)