Tick borne infections
1 / 115

Tick-borne Infections - PowerPoint PPT Presentation

  • Updated On :

Tick-borne Infections. Pola de la Torre, M.D. Assistant Professor of Medicine Division of Infectious Diseases. Ticks. Blood-sucking arthropods (eight legged) of the class Arachnida. Three families: -Ixodidae (hard ticks) -Argasidae (soft ticks)

I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
Download Presentation

PowerPoint Slideshow about 'Tick-borne Infections' - cricket

An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.

- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript
Tick borne infections l.jpg

Tick-borne Infections

Pola de la Torre, M.D.

Assistant Professor of Medicine

Division of Infectious Diseases

Ticks l.jpg

  • Blood-sucking arthropods (eight legged) of the class Arachnida.

  • Three families:

    -Ixodidae (hard ticks)

    -Argasidae (soft ticks)

    -Nuttalliellidae (characteristics of both)

Ixodes l.jpg

  • Three-stage life cycle




  • Require a blood meal at each stage.

  • Peak questing periods

    -Larvae: August and September.

    -Nymphs: May through July.

    -Adults: Spring and Fall.

Ticks12 l.jpg

  • The host’s epidermis is penetrated by the tick’s chelicerae.

  • The resulting defect guides the tick’s hypostome into place to begin withdrawal of blood.

  • Hard ticks can secrete a liquid cement from salivary glands so that it can remain in place for the 7-14 days required for a blood meal.

  • After several hours of attachment disease transmission can take place.

Removing attached ticks l.jpg
Removing Attached Ticks

  • Use forceps and detach the intact tick

    without leaving the mouth parts in the skin.

  • Monitor for signs and symptoms of tick-borne diseases for up to 30 days.

The pathogen l.jpg
The Pathogen

  • Causative agent

    -Rickettsia rickettsii

    -Nonmotile pleomorphic weakly gram-negative


    - Intracellular obligate that resides more

    in the cytosol (less so in the nucleus) of

    host cells.

    -Can be seen with Gimenez or acridine

    orange stains.

Epidemiology l.jpg

  • In 1908 the role of a tick bite in transmitting RMSF was described.

  • The seasonal distribution of disease parallels tick activity.

  • The tick is both the vector and the main reservoir.

  • Most cases are diagnosed in late spring and summer.

Epidemiology18 l.jpg

  • Dermacentor variabilis

    -Two thirds of US and the Far West

  • Dermacentor andersoni

    -Western states

  • Rhipicephalus sanguineus


  • Amblyomma cajennense

    -South America

Pathogenesis l.jpg

  • Rickettsiae enter through the skin and spread via the lymphatics and small blood vessels to the systemic and pulmonary circulation.

  • They attach to (Omph A, Omph B, rickettsial phospholipase) vascular endothelium.

  • After induced phagocytosis, rickettsiae escape from the phagosome into the cytosol.

Pathogenesis21 l.jpg

  • Rickettsiae proliferate intracellularly by binary fission and are released to infected adjacent cells (the maculopapular rash).

  • The effect of this endothelial cell injury is increased vascular permeability which results in edema, hypovolemia, hypotension, and hypoalbuminemia.

  • Hyponatremia results from secretion of ADH in response to the hypovolemia.

Pathogenesis22 l.jpg

  • Vascular injury and the subsequent host response correspond to the distribution of rickettsiae.

    -Interstitial pneumonia, interstitial

    myocarditis, perivascular glial nodules of

    the CNS and similar vascular lesions in

    the rash, GI tract, pancreas, liver,

    skeletal muscles, and kidneys.

Pathogenesis23 l.jpg

  • Significant hemorrhage is rare.

  • Platelets are consumed in the localized lesions and thrombocytopenia can be seen in 32-52% of patients.

  • A procoagulant state occurs but true DIC is rare and occlusive vascular thrombosis is not the basic pathophysiologic event.

Clinical manifestations l.jpg
Clinical Manifestations

  • Incubation period: 2-14 days (median 7d).

  • Usually begins with fever, myalgia, and HA.

  • Temp >102 F in 63% during the first 3 days and in 90% later.

  • Other S/S frequent early before the onset of rash: nausea, vomiting, abdominal pain, diarrhea, abdominal tenderness.

Clinical manifestations25 l.jpg
Clinical Manifestations

  • The major diagnostic sign-The Rash:

    -Small fraction on the first day.

    -49% during the first 3 days.

    -Usually appears 3-5 days after the onset

    of fever and occurs in 84-91% overall.

  • Rash typically begins around the wrists and ankles but may start on the trunk or be diffuse on the onset.

Clinical manifestations26 l.jpg
Clinical Manifestations

  • Involvement of the palms and soles often

    appears late and although thought to be characteristic occurs in only 36-82% with


  • Skin necrosis or gangrene in 4%.

  • Finding a eschar at the site of the bite rare.

Clinical manifestations30 l.jpg
Clinical Manifestations

  • HA quite severe.

  • Focal neurologic deficits, transient deafness, meningismus, and photophobia may suggest meningitis or meningoencephalitis.

  • CSF: 1/3 have increased leukocytes, elevated protein in 1/3, glucose low in only 8%.

  • Generally, neurologic involement portends a bad prognosis.

Clinical manifestations31 l.jpg
Clinical Manifestations

  • Retinal vein engorgement, arterial occlusion, flame hemorrhage, and papilledema without increased CSF pressure.

  • Prerenal azotemia.

  • ATN.

  • Pulmonary edema.

Clinical manifestations32 l.jpg
Clinical Manifestations

  • Classic RMSF

    -Without appropriate therapy death occurs

    8-15 days after onset of symptoms.

    -Labs nonspecific: WBC generally WNL

    but with increased immature myeloid

    cells, anemia in 5-30%, thrombocytopenia,

    coagulopathy is infrequent.

    -Hyponatremia in 50%.

    -Increased LDH, CK, other enzymes related to diffuse tissue injury.

Clinical manifestations33 l.jpg
Clinical Manifestations

  • Fulminant RMSF

    -Death within the first 5 days

    -Diagnosis difficult

    Antibodies haven’t developed

    Characteristic lesions appear different

    -Black males with G6PD deficiency, older

    age, possibly alcoholism.

Diagnosis l.jpg

  • Before the onset of rash the diagnosis is

    clinical and epidemiologic.

  • Differential Dx: typhoid fever, measles,

    rubella, respiratory tract infection,

    gastroenteritis, acute abdomen,

    enteroviral infection, meningococcemia,

    disseminated GC, secondary syphilis,

    leptospirosis, immune complex vasculitis, ITP,

    TTP, EBV, drug reaction, ehrlichioses, other

    rickettsial diseases.

Diagnosis35 l.jpg

  • Serology (retrospective)

    -A fourfold increase in titer between acute

    and convalescent stages is diagnostic.

    -A titer of ≥64 detectable between 7 and

    10 days after the onset of illness.

Treatment l.jpg

  • Doxycycline 100 mg q12 hours

  • Chloramphenicol 50-75 mg/kg/day

  • Usually 7 days and continued for 2 days

    after the patient has become afebrile.

Lyme disease please no lymes l.jpg

Lyme Disease(Please, no Lymes!)

The pathogen38 l.jpg
The Pathogen

  • Tick-borne spirochete Borrelia burgdorferi

  • Lyme disease or borreliosis was recognized in 1976 following a cluster of affected children in Lyme Connecticut were thought to have juvenile rheumatoid arthritis.

The pathogen42 l.jpg
The Pathogen

  • After injection of B.burgdorferi by the tick and an incubation period of 3-32 days, the organism first multiplies at the site of the bite in the skin.

  • Within days to weeks the organism disseminates through the body.

Clinical manifestations43 l.jpg
Clinical Manifestations

  • Early Infection: Stage 1(Localized)

    -About 70-80% develop EM (expands slowly at 1 cm/day) at the site of the bite.

    -Most patients do not remember the bite

    because the small size of the nymphal I.


Clinical manifestations55 l.jpg
Clinical Manifestations

  • Early infection: Stage 2 (Disseminated)

    -Within several days to weeks of the

    onset of EM, may develop multiple

    annular secondary lesions.

    -Some develop malar rash, conjunctivitis,

    or, rarely, diffuse urticaria.

    -These lesions usually fade within 3-4

    weeks (1 day -14 months).

Clinical manifestations58 l.jpg
Clinical Manifestations

-EM is often accompanied by malaise,

fatigue, HA, F, C, generalized achiness,

and regional lymphadenopathy.

-In 18% these symptoms are the

presenting picture.

-Some may have evidence of meningeal

irritations: HA, neck pain, mild


Clinical manifestations59 l.jpg
Clinical Manifestations

  • After several weeks to months, about 15% of untreated patients develop frank neurologic abnormalities.

    -Meningitis, encephalitis, cranial neuritis

    (including bilateral facial palsy), motor

    and sensory radiculoneuritis, mononeuritis multiplex, cerebellar ataxia or myelitis.

Clinical manifestations60 l.jpg
Clinical Manifestations

  • Meningitis

    -Lymphocytic pleocytosis of ~100 cells

    -Often elevated protein

    -Normal glucose

Clinical manifestations61 l.jpg
Clinical Manifestations

  • Within several weeks after the onset of illness, ~5% of untreated patients develop cardiac involvement which is brief (3 days-6 weeks).

    -Most common: fluctuating degrees of

    AV block.

    -Acute myopericarditis

    -Mild LV dysfunction

    -Rarely, cardiomegaly

    -No murmurs

Clinical manifestations62 l.jpg
Clinical Manifestations

  • Late Infection: Stage 3 (Persistent)

    -Months after the onset of disease

    -~60% begin to experience intermittent

    attacks of joint edema and pain primarily

    in the large joints.

    -Attacks of arthritis usually last from

    weeks to months separated with periods

    of remission.

Clinical manifestations63 l.jpg
Clinical Manifestations

  • Joint fluid cell counts: 500-110,000

    WBC’s most of which are polys.

  • During the second and third year of illness

    attacks may be longer and chronic arthritis develops in ~10% of untreated patients (≥1 year of continuous joint


  • However, even in untreated patients, chronic

    or intermittent arthritis usually resolves

    completely within several years.

Clinical manifestations64 l.jpg
Clinical Manifestations

  • Although most with acute or persistent infection respond to treatment, ~10% have continuing joint inflammation after 2-3 months of antibiotics.

  • B. burgdorferi DNA found in joint fluid prior to treatment, this is not the case after antibiotics.

Clinical manifestations65 l.jpg
Clinical Manifestations

  • Months to years after the onset of disease, ~5% of untreated patients can develop chronic neurologic manifestations.

    -Chronic axonal polyneuropathy

    -Lyme encephalopathy

    No inflammatory changes in the CSF, but

    intrathecal antibody production.

Clinical manifestations66 l.jpg
Clinical Manifestations

  • Also during this stage:

    -Migratory M-S pain is common.

    -Osteomyelitis, myositis, panniculitis,

    eosinophilic fasciitis.

    -Conjunctivitis the most common eye


Diagnosis67 l.jpg

  • Based on the recognition of a characteristic clinical picture, exposure in an endemic area, and a positive antibody (EXCEPT in those with EM).

  • Serologic testing

    -ELISA first!

    -Western Blot

Diagnosis68 l.jpg

  • Positive IgM

    -Two of three: 23, 39, 41.

    A combination of 23 and 41 may still be a false


  • Positive IgG

    -Five of ten: 18, 32, 38, 30, 41, 45, 58, 66, 93.

  • Approximately half of the normal population has IgG reactivity with the 41-kDa flagellar antigen of the spirochete.

Diagnosis69 l.jpg

  • In those ill for > one month, a positive IgM alone is likely to be a false positive.

  • After antibiotics titers decline slowly but IgG and even IgM may persist for many years after treatment.

Prevention of lyme disease after a recognized tick bite l.jpg
Prevention of Lyme Disease After a Recognized Tick Bite

  • A single dose of doxycycline 200 mg when ALL the following met:

    -The attached tick can be identified as an

    adult or nymphal I. scapularis that is

    estimated to have been attached for ≥36

    hours based on the degree of

    engorgement of the tick with blood or of

    certainty about the time of exposure to

    the tick.

Prevention cont d l.jpg
Prevention cont’d.

-Prophylaxis can be started within 72 hours of the time that the tick was removed.

-Ecologic information indicates that the rate of infection of these ticks with B. burgdorferi is ≥20%.

-Doxycycline is not contraindicated.

Treatment72 l.jpg

  • Early infection (local or disseminated)

    -Doxycycline 100 mg bid x 14-21 days

    -Amoxicillin 500 mg tid x 14-21 days

    -Cefuroxime axetil 500 mg bid x 14-21 d

    -Erythromycin 250 mg qid x 14-21 days

Treatment73 l.jpg

  • Arthritis (intermittent or chronic)

    -Doxycycline 100 mg bid x 30-60 days

    -Amoxicillin 500 mg qid x 30-60 days

    -Ceftriaxone 2 g qd x 14-28 days

    -PCN G 20 million U IV qid 14-28 days

Treatment74 l.jpg

  • Neurologic Abnormalities (early or late)

    -Ceftriaxone 2 g qd x 14-28 days

    -PCN G 20 million U IV qid x 14-28 days

    -Doxycycline 100 mg tid x 14-28 days

  • Facial palsy alone

    -Oral regimens may be adequate

Treatment75 l.jpg

  • Cardiac abnormalities

    -First degree AV block: oral

    -High degree AV block:

    Ceftriaxone 2 g qd x 14-21 days

    PCN G 20 million U IV qid x 28 days

Pathogen l.jpg

  • A protozoa that infects erythocytes and causes a malaria-like syndrome including fever, hemolysis, and hemoglobinuria.

  • Transmission is from a vertebrate reservoir to humans via an invertebrate vector (Ixodes scapularis).

  • In the USA, most cases cause by B. microti.

Epidemiology79 l.jpg

  • Most in the coastal regions of the NE but extends to NJ.

  • Isolated cases in VA, GA, MD.

  • Lakes region of the upper Midwest.

  • Blood transfusion.

  • Transplacental transmission.

Clinical manifestations80 l.jpg
Clinical Manifestations

  • Symptoms appear 1-4 weeks after the tick bite.

  • Gradual onset of malaise, fatigue, anorexia, and chills.

  • Then, fever to 40 C which may be intermittent or sustained.

  • Less frequent: myalgia. arthralgia, nausea, vomiting, cough, abdominal pain, depression, emotional lability, photophobia, conjunctival injection, and sore throat.

  • Mild hepatomegaly and splenomegaly in some, but no lymphadenopathy.

Clinical manifestations81 l.jpg
Clinical Manifestations

  • Hemolytic anemia, decreased haptoglobin, elevated retic counts.

  • Infected erythrocytes are usually 1-10% in those with an intact spleen, but can be as high as 85% in asplenic patients.

  • About 50% with mildly elevated LFT’s.

  • WBC WNL or mildly decreased and thrombocytopenia common.

  • Hemoglobinuria and proteinuria.

Clinical manifestations82 l.jpg
Clinical Manifestations

  • Increased risk of severe disease



    ->50 years of age

  • Approximately one-quarter of infected adults are asymptomatic or experience a mild viral-like illness that is incidentally diagnosed.

Clinical manifestations83 l.jpg
Clinical Manifestations

  • Complications

    -Acute respiratory failure




    -Renal failure

Diagnosis84 l.jpg

  • Based on epidemiologic, clinical, and laboratory information.

  • Microscopic identification of the organism on Giemsa stains of thin blood smears.

  • PCR detection of Babesia DNA in blood.

Diagnosis85 l.jpg

  • Serodiagnosis is insensitive during the first two weeks of infection.

    -~20-30% have positive responses of the

    IgM type.

  • Two-four weeks later ~70-80% have seroreactivity even after antibioitcs.

  • After one month, almost all patients with infection have IgG antibody positivity.

Treatment87 l.jpg

  • Not recommended in symptomatic patients whose serum contains antibody to Babesia but whose blood smear is negative (also, if PCR negative) and in asymptomatic individuals regardless of their serology, blood smear, or PCR.

  • Asymptomatic patients with positive smears and/or PCR should have these studies repeated and treated if parasitemia persists for > 3 months.

Treatment88 l.jpg

  • Serious disease

    -Clindamycin 300-600 mg q 6 hours +

    quinine 650 mg q 6-8 hours for 7-10


  • Less side effects

    -Atovaquone 750 mg bid + azithromycin

    500mg followed by 250 mg qd.

  • Exchange transfusions with high levels of parasitemia significant hemolysis, or organ compromise.

Ehrlichia chaffeensis l.jpg

Ehrlichia chaffeensis

Human Monocytotrophic Ehrlichiosis

The pathogen90 l.jpg
The Pathogen

  • Small Gram negative bacteria of the family Anaplasmataceae.

  • Vectors

    -Amblyomma americanum

    -Dermacentor variabilis

    -Ixodes pacificus

Clinical manifestations94 l.jpg
Clinical Manifestations

  • In immunocompetent it is a mild to moderate multisystem illness with a median duration of 23 days. Two –thirds of infected patients are asymptomatic.

  • In severly immunocompromised it acts as an OI and can cause fatal overwhelming infection.

  • Peak incidence in May to July.

Clinical manifestations95 l.jpg
Clinical Manifestations

  • Median incubation period is 7 days.

  • Symptoms at onset

    -Nausea, vomiting, anorexia, weight loss.

  • Fewer than half have a rash that is maculopapular and may be petechial.

  • Severe illness

    -Cough, diarrhea, confusion, lymphadenopathy.

Clinical manifestations96 l.jpg
Clinical Manifestations

  • Severe complications

    -ARDS, ARF, CNS abnormalities,

    coagulopathy, GI hemorrhage, death.

  • CSF abnormalities

    -Lymphocytosis, increased protein, may

    demonstrate infected cells.

  • Nearly 50% have infiltrates on CXR

Clinical manifestations97 l.jpg
Clinical Manifestations

  • Thrombocytopenia


  • Mild-moderate leukopenia

    -Nadir 1300-4000

  • Elevated transaminases

Diagnosis98 l.jpg

  • PCR

  • Visualization of morulae in mononuclear cells (seen in ~7%) and IFA ≥1:64.

  • Four fold increase in IFA.

Treatment100 l.jpg

  • Doxycycline 100 mg bid x 7-14 days.

Anaplasma phagocytophilum l.jpg

Anaplasma phagocytophilum

Human Granulocytic Anaplasmosis

The pathogen102 l.jpg
The Pathogen

  • Obligate intracellular bacteria

    -Order Rickettsiales

    -Family Anaplasmataceae

  • Transmitted by the bite of Ixodes and occurs where Lyme endemic. Although contact with

    infected blood has been reported.

  • Bimodal distribution peaking in July and again in November.

Slide103 l.jpg

Average annual incidence of anaplasmosis (caused by Anaplasma phagocytophilum) by state, as reported to CDC, 2001--2002

Clinical manifestations106 l.jpg
Clinical Manifestations

  • Males > females.

  • Median age: 43-60.

  • Incubation period of 1-2 weeks.

  • Fever, HA, malaise, myalgias in the majority.

  • Less than 50%: nausea, vomiting, diarrhea, cough, arthralgias, stiff neck, and confusion.

  • Less than 10% have rash.

Clinical manifestations107 l.jpg
Clinical Manifestations

  • Majority well within 7 days when treated.

  • Untreated median duration 9 days (1-60 days).

  • Severe manifestations:

    -Respiratory insufficiency

    -Septic shock




Clinical manifestations108 l.jpg
Clinical Manifestations

  • Meningoencephalitis and CSF pleocytosis are rare.

  • Neurologic sequelae

    -Facial diplegia

    -Brachial plexopathy

    -Demyelinating polyneuropathy

Clinical manifestations109 l.jpg
Clinical Manifestations

  • Leukopenia.

  • Thrombocytopenia.

  • Mild elevation of transaminases.

Diagnosis110 l.jpg

  • PCR

  • Visualization of morulae in neutrophils (seen in 20-80%) and IFA ≥64.

  • Four fold increase in IFA.

Treatment111 l.jpg

  • Doxycycline 100 mg bid x 7-14 days.

  • Rifampin 300 mg bid if allergy to doxy or pregnant.