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Rabies and Tetanus and Ticks
Oh my…
Heather PattersonPGY3
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:– 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
– Based on clinical features– Skin bx with assays– dx can be made in 4h– Serology – drawn 2-3 wks post onset
Labs:– Bands– Thrombocytopenia– ↑Na– ↑ Transaminases
How do we make the diagnosis?
Rocky Mountain Spotted Fever
• DDx:– 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
• Doxycycline – 100mg po bid – 2.2 mg/kg for kids
• Tetracycline– 2g/d
• Chloramphenicol– In pregnancy or kids <8y
Treatment? Duration?
• 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:– 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:– 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?– 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 forms1)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
• Preexposure prophylaxis:– Who gets this?
• Travel to area where dog rabies is endemic
• Likelihood of being in contact with virus or vectors
Rabies