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Rabies and Tetanus and Ticks
Oh my…
Heather Patterson
PGY3
November 7, 2007
Objectives
• Review
– basic pathophysiology
– clinical presentation
– management
• What this will not be:
– Didactic!
Describe the rash.
Rocky Mountain Spotted Fever
Etiology?
• Rickettsia rickettsee – found in Rocky Mountain
wood tick saliva
How many hours does the tick need to feed for
innoculation?
• 6 hours
Rocky Mountain Spotted Fever
• R. rickettsii:
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Obligate intracellular bacteria
Infect endothelial cells and vascular smooth muscle
Initiates the coagulation cascade
Cellular immune response and complement activation
↓
Increased vascular permeability
Rocky Mountain Spotted Fever
• Clinical Presentation
– Onset:
• Day 2-14 after bite (mean 7 days)
• Most often abrupt onset but can be gradual (33%)
– Symptoms:
• Sudden onset fever (>38.3) and rigors – may precede other
symptoms by 2-3 days
• Myalgias – tenderness in large muscle groups
• Headache
• Nausea,vomiting, anorexia (80%)
• Rash
Rocky Mountain Spotted Fever
• Classic Triad (3%):
– Fever
– Rash
– Tick bite
Rocky Mountain Spotted Fever
How does the rash present on day 2-4 post onset fever?
• 2-6 mm blanchable, pink macules
• Wrists, palms, ankles, soles
• Spreads cetripetally 6-12 h post onset
Rocky Mountain Spotted Fever
How does the rash present on day 4-6 post onset fever?
• Non-blanchable petechial rash
• Local edema surrounding petechie
Rocky Mountain Spotted Fever
How do we make the diagnosis?
– Based on clinical features
– Skin bx with assays– dx can be made in 4h
– Serology – drawn 2-3 wks post onset
Labs:
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Bands
Thrombocytopenia
↑Na
↑ Transaminases
Rocky Mountain Spotted Fever
• DDx:
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Meningococcus
Rubella
Measles
Disseminated gonoccocal
TSS
Mononucleosis
Enteroviral infections
Other infections: dengue, leptospirosis, typhus
Rocky Mountain Spotted Fever
• Must think of RMSF with unexplained fever even in
absence of rash, headache, tick bite, or travel to
endemic area
Rocky Mountain Spotted Fever
• Complications:
– Cardiac:
• Myocarditis
• 1 degree AV block, non-specific ST-T changes
• PAT, Afib
• CHF
– Resp:
• Interstitial pneumonitis
• Pulmonary edema, effusions, infiltrates
• ARDS
Rocky Mountain Spotted Fever
• Complications:
– Neuro:
• Eosinophilic meningitis
• Encephalomyelitis
• Vaculitis +/- thrombosis
• Mov’t disorders
– Other:
• Shock
• DIC
Rocky Mountain Spotted Fever
Treatment? Duration?
• Doxycycline
– 100mg po bid
– 2.2 mg/kg for kids
• Tetracycline
– 2g/d
• Chloramphenicol
– In pregnancy or kids <8y
• Treat for 2-5 days after afebrile OR min of 7-10 days
Rocky Mountain Spotted Fever
• Steriods:
– Unstable, encephalitis, cerebral edema or “extensive”
vasculitis
• Mortality:
– Untreated >30%
– Treated 3-7%
Case 2
Case 2
Lyme
Etiology?
• Borrelia burgdorferi – spirochete
• Vector – deer tick (deer, small rodents)
How many hours does the tick need to feed for
innoculation?
• 24-72 hours
Lyme Pathophysiology
• Hematogenous spread of spirochete
• Affinity for skin, synovial tissue, nervous tissue.
Lyme
• Classification by stage of infection:
– Early Lyme Disease
– Acute Disseminated Infection
– Late Lyme Disease
Early Lyme Disease
• Onset:
– 1-36 days post innoculation
• Clinical features:
– Rash (90%) +/- 2º lesions
• Lymphadenopathy in same region
– Constitutional symptoms “flu-like”
• Low grade fever
• Malaise, lethary
– Migratory arthralgias and myalgias
CLUE:
Rash is present in 90%
Diagnostic
Early Lyme Disease
– Neuro
• h/a
• meningeal irritation
• photophobia
– GI:
• N/V
• RUQ pain
CLUE:
Rapidly changing and
intermittent symptoms in many
systems
Erythema Migrans
• Characteristics:
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Round/oval/triangular/linear
Confluent or targetoid
Sharply demarcated boarders
Flat or raised
Blanch with pressure
• Size:
– Spreads ~1-2cm/day
– Ave size 8-10cm
• Secondary lesions
– Smaller, migrate less, spare palms and soles
Lyme – Acute Disseminated
• Acute Disseminated Infection
– Onset
• Avg 4 wks post innoculation
• May overlap symptoms of early or late
– Neuro
• MC -Fluctuating meningoenceph
• Triad
– Cranial neuropathy (Bell’s)
– Peripheral neuropathy/radiculopathy
– Meningitis
• CSF
– N gluc, ↑prot/lymphs
CLUE:
•Multiple neuro features
in CNS/PNS
•Bilateral Bell’s = Lyme
until proven otherwise
Lyme
• Acute Disseminated Infection
– Joint:
• Intermittent large joint inflam arthritis
• Brief with spont remission
• Recurrent
– Cardiac:
• Dysrhythmias and blocks
• Uncommon
CLUE:
Cardiac: Fluctuating blocks,
slow spont resolution
Joint: shorter duration,
recurrent
Lyme - Late
• Late Lyme Disease
– Joint:
• More frequent episodes of arthritis
• Becomes chronic
– Neuro:
• Chronic encephalopathy
• Memory and learning abN
• Sensory abN
• Psych
Lyme - Diagnosis
• Erythema migrans
– endemic area
• ELISA test 89% Sens and 72% Spec
• Confirmed on Western Blot/PCR
• Isolation from tissues and body fluids takes weeks to grow
• Impractical clinically
Lyme - Treatment
• Prophylaxis?
– Risk of infection minimal to nonexistent if attached <24hrs
– If symptoms develop, ABx curative in most cases
• Uncomplicated
– PO ABx 14-21 days
– Doxycycline 100mg BID for adults
– Amoxicillin 50mg/kg divided TID for Peds
• Late or severe disease
– IV ABx x 30d
– Ceftriaxone/PenG/chloramphenicol
– Neurologic (other than Bell’s) or cardiac manifestations
Case 3
• 18mo F sleeping at the cottage. Parents go in to check
on her. There is a bat in the room.
• What do you do?
Rabies
• Bats are a major vector of rabies in North America
• Analysis has shown that rabies comes from bats even when there is absence
of a bite.
• CDC recommends:
– Postexposure prophylaxis for anyone exposed to a bat who is unable to
give a history of contact : ie sleeping, children etc
– Any contact with bat, including saliva
– Bat bites
Rabies
• What is the major animal vector in North America?
– Raccoon
• What are other common vectors:
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Bat
Skunk
Fox
Woodchuck
Other carnivores
Rabies
• What is rabies?
– Bullet shaped RNA rhabdovirus
– Previously thought to be a single virus
responsible for all rabies
– Antigen detection has shown that several
viruses and at least 6 serotypes exist
Rabies
• How is rabies transmitted?
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Saliva
Scratches
Aerosolized virus into respiratory tract
Secretions that contaminate MM
Corneal transplants
Rabies
• How does rabies affect the body?
(what tissue does it primarily affect?)
• The virus attacks nerve tissue
– Spreads along peripheral nerves and muscle
fibers to the CNS
– Encephalomyelitis
– Spreads from CNS throughout the PNS
especially to highly innervated areas
• Progression to generalized nervous system
failure and death
Rabies
• Rabies is a uniformly fatal disease once clinical symptoms
manifest
• Presents with 1 of 2 clinical forms
1) Encephalitic (furious) rabies
– 80-85%
– Hydrophobia, pharyngeal spasm, hyperactivity
– Paralysis, coma and death
2) Paralytic form
– Far less common
Rabies
5 clinical stages:
1) Incubation
- Ranges from 10d to 1yr (avg 20-60 days)
2) Prodrome
- Occurs 2-10d post-exposure last <2wks
- Nonspecific flu-like illness
3) Acute Neurologic Syndrome
- 2-7days after prodrome onset
- Dysarthria, dysphagia, salivation, diplopia, vertigo, nystagmus,
agitation, hallucinations, hydrophobia, hyperative DTR, nuchal
rigidity
4) Coma
- 7-10 days after neuro symptoms
- Prolonged apnea and generalized flaccid paralysis
5) Death
Rabies
• Prodrome:
– Sounds like all the other viral prodromes?
– If the patient has sustained a bite, are there
any clues to dx?
CLUE:
Tingling at the bite over first few
days
Rabies
• Questions
• Saliva contact?
• Skin breakdown?
• Provoked or unprovoked attack?
• Wild vs domestic animal?
• All suspicious warrant a call to the MOH on-call 264-5615
• Immediately if scratch or bite to head
• Urgently in all other cases
• Follow-up is with MOH or the clinical disease unit during the
day
Rabies
• Preexposure prophylaxis:
– Who gets this?
• Travel to area where dog
rabies is endemic
• Likelihood of being in
contact with virus or vectors