USMLE Forum Archives - USMLE Step 3 - TICK BORN DISEASES
TICK BORN DISEASES
meduploader - 05-12-09 06:05
Lyme disease
Advise Patients to avoid exposure to vector ticks in endemic areas and to promptly remove attached ticks.
Wear protective clothing
Use insect repellant containing diethyltoluamide (DEET) or a tick-killing spray containing permethrin, the latter to be applied to clothing, not skin
Acute, localized Lyme disease:
Erythema migrans and other symptoms (e.g., fever, fatigue, headache, arthralgias, myalgias) occuring within 30 days of possible tick exposure ( this is sufficient to diagnose Lyme disease)
Acute, disseminated Lyme disease :
Multiple, secondary erythema migrans lesions, Acute carditis (heart block) , CNS Disease (e.g., cranial neuropathy, radiculoneuropathy, lymphocytic meningitis) and brief episodes of monoarticular or oligoarticular inflammatory arthritis occuring within weeks to months after tick exposure
Late Lyme disease:
Occuring within months to years after possible tick exposure
Chronic (>1 year) inflammatory monoarthritis or oligoarthritis
Nervous system complications : peripheral neuropathy or encephalomyelitis
Erythema migrans in an endemic area is sufficient for diagnosis  do not get serology ( can be negative in acute disease - ). Start therapy as next step – oral doxycycline or amoxicillin or cefuroxime.
Disseminated Lymes  Get serologic testing. Use 2 step approach – first ELISA. If ELISA indeterminate, get western blot.
Arthritis, Carditis ( except third degree block, cranial nerve palsy without meningitis  Rx similar to erythema migrans
Third degree block or Meningitis/ neuroborreliosis  Rx with ceftriaxone IV
Babesiosis
An Ixodes tick–borne illness caused by Babesia microti, an intracellular protozoan that infects RBCs.
Fever, chills, headache, myalgia, and fatigue.
Severe hemolytic disease can manifest with abdominal pain, jaundice, splenomegaly, and dark urine.
Older, asplenic, or immunocompromised patients (including HIV + ive patients) present with more severe
symptoms.
Peripheral blood smears show intracellular parasites in 1–10% of RBCs (or up to 85% if severe). The classic “Maltese cross” tetrads may be seen, but more commonly Babesia parasites look like Plasmodium falciparum signet-ring forms with no other parasitic stages seen
Labs show hemolytic anemia, mild leukopenia, thrombocytopenia, elevated LFTs, and hemoglobinuria.
Antibody tests are available.
PCR may be more sensitive for detecting low levels of parasitemia.
Most infections are self-limited.
For sicker, asplenic, or immunocompromised patients, use clindamycin plus quinine or atovaquone plus azithromycin. Doxycycline and most antimalarial drugs are ineffective.
Exchange transfusion has been used as adjunctive therapy in patients with a high degree of hemolysis or parasitemia (> 10%) or with the more severe European forms of the disease.
COMPLICATIONS
Patients may develop shock or ARDS. Deaths in the United States have occurred in patients both with and without spleens.
Coinfection with Borrelia burgdorferi (Lyme disease) and/or Anaplasma phagocytophilum (human granulocytotropic anaplasmosis) should be suspected in any patient with babesiosis.
Rocky mountain spotted fever
Rickettsia rickettsii. The vector is the Dermacentor
tick, which needs to feed for only 6–10 hours before injecting the organism (a much shorter attachment time than for Lyme disease).
Think of Rocky Mountain spotted fever and start treatment early in patients with a recent tick bite (especially in the mid-Atlantic or South Central states) along with fever, headache, and myalgias followed by a centripetal rash.
The rash first appears on the wrists and ankles and then spreads centrally and to the palms and soles.
Diagnosis is made clinically (symptoms and signs plus recent tick bite); treatment should be started as soon as Rocky Mountain spotted fever is suspected.
Diagnosis can be made by biopsy of early skin lesions or confirmed retrospectively by serologic testing.
Labs may show thrombocytopenia, elevated LFTs, and hyponatremia. The Weil-Felix test (for antibodies cross-reacting to Proteus) is no longer considered reliable.
Rx: Doxycycline, chloramphenicol (for pregnant or doxycycline-allergic patients).
COMPLICATIONS
Pneumonitis, pulmonary edema, renal failure, and death after 8–15 days.
Ehrlichosis
Tick-borne illnesses transmitted by rickettsia-like bacteria. There are two main types:
Human monocytic ehrlichiosis (HME): Caused by Ehrlichia chaffeensis; found in southern states such as Arkansas and Missouri (where Rocky Mountain spotted fever is also present).
Human granulocytic anaplasmosis (HGA): Formerly known as human granulocytic ehrlichiosis. Caused primarily by Anaplasma phagocytophilum; found in the Northeast and upper Midwest (where Lyme disease and babesiosis are also present).
Dx
Leukopenia and thrombocytopenia; often elevated LFTs.
Peripheral blood buffy-coat smear may show morulae (meaning “mulberries” in Latin), a cluster of organisms in the cytoplasm of WBCs. The test is insensitive, especially for HME.
Acute and convalescent antibody titers are most sensitive (> 95% of patients develop antibodies within four weeks of symptom onset).
PCR.
Rx: Doxycycline (chloramphenicol or rifampin in pregnancy).
Malaria
Four species of Plasmodium, viz, P. falciparum, P. vivax, P. ovale, and P. malariae can cause malaria.
Most of the deaths are due to falciparum malaria whereas Vivax and ovale are responsible for several
relapses.
Cyclical fever is hallmark of malaria and it coincides with RBC lyses by the parasites.
Fever occurs every 48 hours with P. vivax and P. ovale and
Every 72 hours with P. malariae, whereas
Periodicity is generally not seen with P. falciparum.
The typical episode consist of a cold phase characterized by chills and shivering, followed by a hot phase
characterized by high grade fever, followed 2-6 hours later by a sweating stage characterized by
diaphoresis and resolution of fever
In people from endemic areas, anemia and splenomegaly are common findings. Vitals would show
hypotension and tachycardia
Dx: Order blood smears in all febrile travelers or returned immigrants from endemic areas. Giemsa- or Wright-stained thick and thin smears are the best diagnostic tests.
P. falciparum must be distinguished from other species because it requires hospital admission and is the only species with significant drug resistance. P. falciparum is usually characterized by > 1%
parasitized RBCs, > 1 parasite/RBC, banana-shaped gametocytes, and lack of mature schizonts. It is also associated with travel to Africa, severe disease, and symptoms that occur within two months of travel.
P. vivax is as widespread as but generally less virulent than P. falciparum.
P. malariae and P. ovale are much less common causes of malaria.
TREATMENT
Treat P. vivax, P. ovale, and P. malariae with chloroquine. Treat P. vivax and P. ovale with primaquine as well to eradicate chronic liver stages (if patients have normal G6PD levels).
For P. falciparum, assume chloroquine resistance (unless acquired in Central America, Haiti, or the Middle East) and treat with quinine plus doxycycline, quinine plus sulfadoxine/pyrimethamine (Fansidar), Fansidar alone, mefloquine, or atovaquone/proguanil (Malarone). Artesunate and artemisinin compounds are the fastest-acting malaricidal agents, but they are unavailable in the United States. Repeat blood smears at 48 hours to document a > 75% ↓ in parasitized RBCs. Exchange transfusion may be
used for severe malaria or in the presence of > 15% parasitemia.
In the United States, IV quinidine is often used because IV quinine may be unavailable. Primaquine may lead to severe hemolytic anemia, so screen for G6PD deficiency before using it. Adverse effects of mefloquine include irritability, bad dreams, GI upset, and, to a lesser extent, seizures and psychosis. Sulfadoxine/pyrimethamine is a sulfa drug and may lead to Stevens-Johnson syndrome. Atovaquone/proguanil has GI toxicities. Halofantrine (rarely used in the United States) may lead to QT prolongation.
Doxycycline leads to photosensitivity and GI upset. During pregnancy, chloroquine is safe, and quinine, sulfadoxine/pyrimethamine, and doxycycline may be used despite potential fetal risks because morbidity and mortality are so high.
PREVENTION
Avoid mosquito bites (use bed netting, window screens, insecticides, and insect repellents with 30–35% DEET). Chloroquine is effective in Central America, Haiti, and parts of the Middle East. For most other areas, the CDC recommends mefloquine or atovaquone/proguanil. For Southeast Asia (the Thai-Burmese and Thai-Cambodian border areas), use doxycycline or atovaquone/proguanil, as resistance to all other antimalarials is common.
meduploader - 05-12-09 06:05
Lyme disease
Advise Patients to avoid exposure to vector ticks in endemic areas and to promptly remove attached ticks.
Wear protective clothing
Use insect repellant containing diethyltoluamide (DEET) or a tick-killing spray containing permethrin, the latter to be applied to clothing, not skin
Acute, localized Lyme disease:
Erythema migrans and other symptoms (e.g., fever, fatigue, headache, arthralgias, myalgias) occuring within 30 days of possible tick exposure ( this is sufficient to diagnose Lyme disease)
Acute, disseminated Lyme disease :
Multiple, secondary erythema migrans lesions, Acute carditis (heart block) , CNS Disease (e.g., cranial neuropathy, radiculoneuropathy, lymphocytic meningitis) and brief episodes of monoarticular or oligoarticular inflammatory arthritis occuring within weeks to months after tick exposure
Late Lyme disease:
Occuring within months to years after possible tick exposure
Chronic (>1 year) inflammatory monoarthritis or oligoarthritis
Nervous system complications : peripheral neuropathy or encephalomyelitis
Erythema migrans in an endemic area is sufficient for diagnosis  do not get serology ( can be negative in acute disease - ). Start therapy as next step – oral doxycycline or amoxicillin or cefuroxime.
Disseminated Lymes  Get serologic testing. Use 2 step approach – first ELISA. If ELISA indeterminate, get western blot.
Arthritis, Carditis ( except third degree block, cranial nerve palsy without meningitis  Rx similar to erythema migrans
Third degree block or Meningitis/ neuroborreliosis  Rx with ceftriaxone IV
Babesiosis
An Ixodes tick–borne illness caused by Babesia microti, an intracellular protozoan that infects RBCs.
Fever, chills, headache, myalgia, and fatigue.
Severe hemolytic disease can manifest with abdominal pain, jaundice, splenomegaly, and dark urine.
Older, asplenic, or immunocompromised patients (including HIV + ive patients) present with more severe
symptoms.
Peripheral blood smears show intracellular parasites in 1–10% of RBCs (or up to 85% if severe). The classic “Maltese cross” tetrads may be seen, but more commonly Babesia parasites look like Plasmodium falciparum signet-ring forms with no other parasitic stages seen
Labs show hemolytic anemia, mild leukopenia, thrombocytopenia, elevated LFTs, and hemoglobinuria.
Antibody tests are available.
PCR may be more sensitive for detecting low levels of parasitemia.
Most infections are self-limited.
For sicker, asplenic, or immunocompromised patients, use clindamycin plus quinine or atovaquone plus azithromycin. Doxycycline and most antimalarial drugs are ineffective.
Exchange transfusion has been used as adjunctive therapy in patients with a high degree of hemolysis or parasitemia (> 10%) or with the more severe European forms of the disease.
COMPLICATIONS
Patients may develop shock or ARDS. Deaths in the United States have occurred in patients both with and without spleens.
Coinfection with Borrelia burgdorferi (Lyme disease) and/or Anaplasma phagocytophilum (human granulocytotropic anaplasmosis) should be suspected in any patient with babesiosis.
Rocky mountain spotted fever
Rickettsia rickettsii. The vector is the Dermacentor
tick, which needs to feed for only 6–10 hours before injecting the organism (a much shorter attachment time than for Lyme disease).
Think of Rocky Mountain spotted fever and start treatment early in patients with a recent tick bite (especially in the mid-Atlantic or South Central states) along with fever, headache, and myalgias followed by a centripetal rash.
The rash first appears on the wrists and ankles and then spreads centrally and to the palms and soles.
Diagnosis is made clinically (symptoms and signs plus recent tick bite); treatment should be started as soon as Rocky Mountain spotted fever is suspected.
Diagnosis can be made by biopsy of early skin lesions or confirmed retrospectively by serologic testing.
Labs may show thrombocytopenia, elevated LFTs, and hyponatremia. The Weil-Felix test (for antibodies cross-reacting to Proteus) is no longer considered reliable.
Rx: Doxycycline, chloramphenicol (for pregnant or doxycycline-allergic patients).
COMPLICATIONS
Pneumonitis, pulmonary edema, renal failure, and death after 8–15 days.
Ehrlichosis
Tick-borne illnesses transmitted by rickettsia-like bacteria. There are two main types:
Human monocytic ehrlichiosis (HME): Caused by Ehrlichia chaffeensis; found in southern states such as Arkansas and Missouri (where Rocky Mountain spotted fever is also present).
Human granulocytic anaplasmosis (HGA): Formerly known as human granulocytic ehrlichiosis. Caused primarily by Anaplasma phagocytophilum; found in the Northeast and upper Midwest (where Lyme disease and babesiosis are also present).
Dx
Leukopenia and thrombocytopenia; often elevated LFTs.
Peripheral blood buffy-coat smear may show morulae (meaning “mulberries” in Latin), a cluster of organisms in the cytoplasm of WBCs. The test is insensitive, especially for HME.
Acute and convalescent antibody titers are most sensitive (> 95% of patients develop antibodies within four weeks of symptom onset).
PCR.
Rx: Doxycycline (chloramphenicol or rifampin in pregnancy).
Malaria
Four species of Plasmodium, viz, P. falciparum, P. vivax, P. ovale, and P. malariae can cause malaria.
Most of the deaths are due to falciparum malaria whereas Vivax and ovale are responsible for several
relapses.
Cyclical fever is hallmark of malaria and it coincides with RBC lyses by the parasites.
Fever occurs every 48 hours with P. vivax and P. ovale and
Every 72 hours with P. malariae, whereas
Periodicity is generally not seen with P. falciparum.
The typical episode consist of a cold phase characterized by chills and shivering, followed by a hot phase
characterized by high grade fever, followed 2-6 hours later by a sweating stage characterized by
diaphoresis and resolution of fever
In people from endemic areas, anemia and splenomegaly are common findings. Vitals would show
hypotension and tachycardia
Dx: Order blood smears in all febrile travelers or returned immigrants from endemic areas. Giemsa- or Wright-stained thick and thin smears are the best diagnostic tests.
P. falciparum must be distinguished from other species because it requires hospital admission and is the only species with significant drug resistance. P. falciparum is usually characterized by > 1%
parasitized RBCs, > 1 parasite/RBC, banana-shaped gametocytes, and lack of mature schizonts. It is also associated with travel to Africa, severe disease, and symptoms that occur within two months of travel.
P. vivax is as widespread as but generally less virulent than P. falciparum.
P. malariae and P. ovale are much less common causes of malaria.
TREATMENT
Treat P. vivax, P. ovale, and P. malariae with chloroquine. Treat P. vivax and P. ovale with primaquine as well to eradicate chronic liver stages (if patients have normal G6PD levels).
For P. falciparum, assume chloroquine resistance (unless acquired in Central America, Haiti, or the Middle East) and treat with quinine plus doxycycline, quinine plus sulfadoxine/pyrimethamine (Fansidar), Fansidar alone, mefloquine, or atovaquone/proguanil (Malarone). Artesunate and artemisinin compounds are the fastest-acting malaricidal agents, but they are unavailable in the United States. Repeat blood smears at 48 hours to document a > 75% ↓ in parasitized RBCs. Exchange transfusion may be
used for severe malaria or in the presence of > 15% parasitemia.
In the United States, IV quinidine is often used because IV quinine may be unavailable. Primaquine may lead to severe hemolytic anemia, so screen for G6PD deficiency before using it. Adverse effects of mefloquine include irritability, bad dreams, GI upset, and, to a lesser extent, seizures and psychosis. Sulfadoxine/pyrimethamine is a sulfa drug and may lead to Stevens-Johnson syndrome. Atovaquone/proguanil has GI toxicities. Halofantrine (rarely used in the United States) may lead to QT prolongation.
Doxycycline leads to photosensitivity and GI upset. During pregnancy, chloroquine is safe, and quinine, sulfadoxine/pyrimethamine, and doxycycline may be used despite potential fetal risks because morbidity and mortality are so high.
PREVENTION
Avoid mosquito bites (use bed netting, window screens, insecticides, and insect repellents with 30–35% DEET). Chloroquine is effective in Central America, Haiti, and parts of the Middle East. For most other areas, the CDC recommends mefloquine or atovaquone/proguanil. For Southeast Asia (the Thai-Burmese and Thai-Cambodian border areas), use doxycycline or atovaquone/proguanil, as resistance to all other antimalarials is common.
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