Mid - Vector Borne Infections

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Rickettsi prowazekii

Transmission

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Vector: Human body louse
Reservoir: Human

The louse becomes infected by feeding on an infected human. The R. prowazekii replicate in the louse gut and are expelled in the feces. Humans become infected after scratching the infected louse feces into the bite. Epidemic typhus occurs in crowded conditions with poor hygiene and often emerges during war and disaster situations.

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Rickettsia

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Gram negative coccobacilli or short bacilli that are obligate intracellular pathogen

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Rocky mountain spotted fever

Location

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Pathogen: Rickettsia rickettsii

RMSF occurs throughout the U.S., Mexico, Central and South America. In the U.S. it is most common in the S. Central and SE states, despite its namesake.

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Rocky mountain spotted fever

Transmission

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Pathogen: Rickettsia rickettsii

It is transmitted via tick salivary secretions (the American dog tick or the Rocky Mountain wood tick depending on the location). R. rickettsii is passed transovarially in the tick; therefore, the tick is both the vector and reservoir for RMSF. Small mammals may also be reservoirs.

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Rocky mountain spotted fever

Time of year

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Cases most frequently occur May-Sept

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Rocky mountain spotted fever

Clinical presentation

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After ~7 day incubation, there is the sudden onset of a flu-like illness including headache, myalgia, malaise, nausea, and fever. Subsequently a rash occurs that begins on the wrists/ankles and spreads to the trunk (centripetal). The rash can evolve from macules to papules, to petechiae (from hemorrhage). The palms/soles can become involved. This pathogen causes extensive injury to the microcirculation and, if left untreated, can result in multi-organ system damage and death.

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Rocky mountain spotted fever

Treatment

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Doxycycline (a tetracycline)

Front 8

Rickettsialpox

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Caused by R. akari

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Rickettsialpox

Transmission

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Transmitted by mice (reservoir) and their mites (vector).

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Rickettsialpox

Clinical Presentation

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At the site of the mite bite: papule->vesicle->eschar with surrounding erythema (this can be confused with cutaneous anthrax). About 10+ days later flu-like symptoms (HA, fever, chills, malaise) occur and a papulo-vesicular rash develops (looks like chicken pox). Without treatment, this disease is self-limited and is not fatal.

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Rickettsialpox

Treatment

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Doxycycline (a tetracycline)

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Rickettsi epidemic typhus

Clinical Presentation

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Pathogen: Rickettsi prowazekii

Severe illness. After ~1 week incubation, there is the abrupt onset of high fever, severe headache, and prostration. Cough is very common and myalgias can be intense. After 5 days, a rash begins on the trunk and spreads centrifugally, but spares the face, palms, and soles. The rash evolves from macular, to maculopapular to hemorrhagic/confluent without treatment. If severe/untreated, multiorgan system failure can result (often with prominent neurologic findings).

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Rickettsi epidemic typhus

Reactivitation

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Brill-Zinsser disease occurs when R. prowazekii reactivates (causing a milder illness) in older or immunocompromised individuals years after the initial infection.

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Rickettsi epidemic typhus

Treatment

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Pathogen: Rickettsi prowazekii

Doxycycline

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Human monocytic ehrlichiosis (HME)

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Ehrlichia chaffeensis

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Human granulocytic anaplasmosis (HGA)

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Anaplasma phagocytophilium

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Ehrlichia/Anaplasma

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Human ehrlichioses are tickborne infections caused by members of the Anaplasmataceae family. These species are small, obligate intracellular Gram negative bacteria that infect either monocytes (HME) or granulocytes (HGA),

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Human monocytic ehrlichiosis (HME)

Transmission

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across the south-central, SE, and mid-Atlantic states where its major reservoir (white-tailed deer) and its vector (lone star tick) coexist.

Infections occur most frequently April through September.

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Human granulocytic anaplasmosis (HGA)

Transmission

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HGA occurs in the U.S. in the NE, mid-Atlantic, Upper Midwest, and Pacific NW states, but also occurs
internationally (Europe and Asia). Ixodes ticks are the vector while small mammals (especially mice) are likely reservoirs.

Infections occur most frequently April through September.

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Human monocytic ehrlichiosis (HME) / Human granulocytic anaplasmosis (HGA)

Clinical presentation

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The clinical presentation for ehrlichiosis is similar to that of the rickettsial diseases (e.g. RMSF); however, patients are very unlikely to have a rash with HGA and only 30% likely to have a rash with HME.
Note that thrombocytopenia, elevated transaminases, and leukopenia are common and are clues to the diagnosis.

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Human monocytic ehrlichiosis (HME) / Human granulocytic anaplasmosis (HGA)

Pathogenesis

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Are internalized by cell (monocyte or granulocyte) and avoid lysosomal fusion. They multiply and form clusters in cytoplasmic vacuoles (called ‘morulae’)

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Human monocytic ehrlichiosis (HME) / Human granulocytic anaplasmosis (HGA)

Diagnosis

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Someone presents with fever, thrombocytopenia, elevated transaminases, and leukopenia, in an endemic region during tick activity (Spring-Fall).

Acutely, the most rapid test is examination of a blood smear for morulae; however, this has a very low sensitivity because <10% with HME have visible morulae at presentation. ~60% of patients with HGA have morulae. Acutely, PCR is the diagnostic tool of choice with sensitivity 60-85% for HME and 67-90% for HGA.

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Human monocytic ehrlichiosis (HME) / Human granulocytic anaplasmosis (HGA)

Treatment

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Doxycycline

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Borrelia

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Spirochetal (helical) Gram negative bacteria

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Lyme Disease

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Caused by Borrelia burgdorferi. Predominant in the NE.

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Borrelia burgdorferi

Transmission

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Transmitted via the bite of Ixodes ticks (hard ticks). A tick must feed for >24 hours in order to transmit the spirochete. The white-footed mouse is the preferred host for immature/larval and nymphal ticks while the white-tailed deer is the preferred host for the adult tick. The nypmhal ticks are primarily responsible for transmission, which occurs most frequently in June, July, and August.

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Lyme disease

Clinical presentation - Stage 1

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Pathogen: Borrelia burgdorferi

Localized, stage 1 infection: 3 to 30 days after an infected tick bite, 70-80% of people develop an expanding rash called erythema migrans. Usually the tick bite goes unnoticed because the tick is so small. As the rash expands there may be an area of central clearing, giving it a bull’s eye appearance.

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Lyme disease

Clinical presentation - Stage 2

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In stage 2, disseminated infection, flu-like symptoms such as fever, headache, and myalgias frequently occur and may be the only symptoms. If untreated, the borrelia can cause disease in different organ systems:
1) cardiac (heart block, myopericarditis)—8% of untreated individuals
2) neurologic (Bell’s palsy (CN VII), meningitis, radiculopathy)—15% of untreated
3) musculoskeletal pain

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Lyme disease

Clinical presentation - Stage 3

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60% develop arthritis, usually of the knee or other large joint. This arthritis can last for weeks to months even with antibiotic therapy. Late neurologic Lyme disease can also occur which manifests as an encephalomyelitis, peripheral neuropathy, or encephalopathy.

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Lyme disease

Post Lyme disease syndrome

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Patient remains symptomatic months to years after appropriate antibiotic therapy.

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Lyme disease

Pathogenesis

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B. burgdorferi is introduced into the skin at the tick bite site. It multiplies at the site and spreads outward, causing the characteristic rash. OspC and OspA protein are used to bind to cells and ECM.

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Lyme disease

Diagnosis

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Bulls eye rash. In situations where the diagnosis is less certain, acute and convalescent antibodies can be obtained. In cases of CNS involvement, a lumbar puncture may be indicated (CSF usually reveals a lymphocytosis, elevated protein, and normal glucose). An important concept is that HGA and Babesia are transmitted via the same Ixodes tick vector and that co-infection may occur.

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Lyme disease

Treatment

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Erythema migrans is preferentially treated with doxycycline in adults, although amoxicillin and cefuroxime (a second generation cephalosporin) are alternatives for children, pregnant women, and those intolerant to doxycycline. Isolated Bell’s palsy, arthritis, and mild cardiac disease can be treated with the same oral regimen. When there is meningitis or radiculopathy or hospitalization is required for heart block or symptomatic cardiac disease, treatment with IV ceftriaxone, a third generation cephalosporin, is recommended.