Rabies and Tetanus and Ticks Oh my… Heather Patterson PGY3 November 7, 2007.

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


• 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


• 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


• Classic Triad (3%):– Fever– Rash– Tick bite


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


How does the rash present on day 4-6 post onset fever?

• Non-blanchable petechial rash• Local edema surrounding petechie


– 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?


• DDx:– Meningococcus– Rubella– Measles– Disseminated gonoccocal– TSS– Mononucleosis– Enteroviral infections– Other infections: dengue, leptospirosis,

typhus


• Must think of RMSF with unexplained fever even in absence of rash, headache, tick bite, or travel to endemic area


• Complications:– Cardiac:

• Myocarditis• 1 degree AV block, non-specific ST-T changes• PAT, Afib• CHF

– Resp:• Interstitial pneumonitis• Pulmonary edema, effusions, infiltrates• ARDS


• Complications:– Neuro:

• Eosinophilic meningitis• Encephalomyelitis• Vaculitis +/- thrombosis• Mov’t disorders

– Other:• Shock• DIC


• 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


• 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

Rabies and Tetanus and Ticks Oh my… Heather Patterson PGY3 November 7, 2007.

Documents

unexplained fever

post onset fever

sudden onset fever

rash present

lyme etiology

absence of rash

early lyme diseaseacute

abrupt onset