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    بعض اختصارات الميكروبيولوجي-5

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    تاريخ التسجيل : 22/03/2010
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    بعض اختصارات الميكروبيولوجي-5

    مُساهمة من طرف admin في الإثنين أغسطس 29, 2011 11:26 pm


    Protection from bite. Insect
    control.
    Leishmania tropica, Leishmania mexicana, and
    Leishmania braziliensis

    L. tropica and L. mexicana cause cutaneous
    leishmaniasis; L. braziliensis causes mucocutaneous leishmaniasis. L.
    tropica
    occurs primarily in the Middle East, Asia, and India, whereas L.
    mexicana
    and L. braziliensis occur in Central and South America. All
    are transmitted by sandflies. Forest rodents are the main reservoir. Diagnosis
    is made by observing amastigotes in smear of skin lesion. Treatment is sodium
    stibogluconate. No specific means of
    prevention.
    Acanthamoeba castellanii

    Ameba that causes meningoencephalitis. Also causes
    keratitis in contact lens wearers. Life cycle includes trophozoite and cyst
    stages. Found in freshwater lakes and soil. Transmitted via trauma to skin or
    eyes. Disease occurs primarily in immunocompromised patients. Diagnosis made by
    finding ameba in spinal fluid. Treatment with pentamidine, ketoconazole, or
    flucytosine may be effective. No specific means of
    prevention.
    Naegleria fowleri

    Ameba that causes meningoencephalitis. Found in freshwater
    lakes and soil. Life cycle includes trophozoite and cyst stages. Transmitted
    while swimming or diving in contaminated lake. Disease occurs primarily in
    healthy individuals. Diagnosis made by finding ameba in spinal fluid. Treatment
    with amphotericin B may be effective. No specific means of
    prevention.
    Babesia microti

    Sporozoa that causes babesiosis. Endemic in rodents along
    the northeast coast of the United States. Transmitted by Ixodes ticks to
    humans. Infects red blood cells, causing them to lyse, and anemia results.
    Asplenic patients have severe disease. Diagnosis is made by observing organism
    in red blood cells. Treat with combination of quinine and clindamycin. No
    specific means of prevention.
    Balantidium coli

    Only ciliated protozoan to cause human disease. Causes
    diarrhea. Acquired by fecal–oral transmission from domestic animals, especially
    pigs. Diagnosis is made by finding trophozoites or cysts in feces. Treat with
    tetracycline. No specific means of
    prevention.
    Cyclospora cayetanensis

    Coccidian protozoan. Causes diarrhea, especially in
    immunocompromised (e.g., AIDS) patients. Acquired by fecal–oral transmission. No
    evidence for animal reservoir. Diagnosis is made by finding oocytes in acid-fast
    stain of feces. Treat with trimethoprim-sulfamethoxazole. No specific means of
    prevention.
    Isospora belli

    Coccidian protozoan. Causes diarrhea, especially in
    immunocompromised (e.g., AIDS) patients. Acquired by fecal–oral transmission
    from either human or animal sources. Diagnosis is made by finding oocytes in
    acid-fast stain of feces. Treat with trimethoprim-sulfamethoxazole. No specific
    means of prevention.
    Microsporidia

    Group of spore-forming, obligate intracellular protozoa.
    Two important species are Enterocytozoon bieneusi and Septata
    intestinalis.
    Cause diarrhea, especially in immunocompromised, e.g., AIDS,
    patients. Acquired by fecal–oral transmission from human sources. Diagnosis is
    made by finding spores within cells in feces or intestinal biopsy specimens.
    Treat with albendazole. No specific means of
    prevention.
    Diphyllobothrium latum

    Disease

    Diphyllobothriasis.

    Characteristics

    Cestode (fish tapeworm). Scolex has two elongated sucking
    grooves; no circular suckers or hooks. Gravid uterus forms a rosette. Oval eggs
    have an operculum at one end. Life cycle: Humans ingest undercooked fish
    containing sparganum larvae. Larvae attach to gut wall and become adults
    containing gravid proglottids. Eggs are passed in feces. In fresh water, eggs
    hatch and the embryos are eaten by copepods. When these are eaten by freshwater
    fish, larvae form in the fish muscle.

    Transmission and Epidemiology

    Transmitted by eating raw or undercooked freshwater fish.
    Humans are definitive hosts; copepods are the first and fish the second
    intermediate hosts, respectively. Occurs worldwide but endemic in Scandinavia,
    Japan, and north-central United States.

    Pathogenesis

    Tapeworm in gut causes little damage.

    Laboratory Diagnosis

    Eggs visible in stool.

    Treatment

    Praziquantel.

    Prevention

    Adequate cooking of fish. Proper disposal of human
    waste.
    Echinococcus granulosus

    Disease

    Hydatid cyst disease.

    Characteristics

    Cestode (dog tapeworm). Scolex has four suckers and a
    double circle of hooks. Adult worm has only three proglottids. Life cycle: Dogs
    are infected when they ingest the entrails of sheep, e.g., liver, containing
    hydatid cysts. The adult worms develop in the gut, and eggs are passed in the
    feces. Eggs are ingested by sheep (and humans) and hatch hexacanth larvae in the
    gut that migrate in the blood to various organs, especially the liver and brain.
    Larvae form large, unilocular hydatid cysts containing many protoscoleces and
    daughter cysts.

    Transmission and Epidemiology

    Transmitted by ingestion of eggs in food contaminated with
    dog feces. Dogs are main definitive hosts; sheep are intermediate hosts; humans
    are dead-end hosts. Endemic in sheep-raising areas, e.g., Mediterranean, Middle
    East, some western states of the United States.

    Pathogenesis

    Hydatid cyst is a space-occupying lesion. Also, if cyst
    ruptures, antigens in fluid can cause anaphylaxis.

    Laboratory Diagnosis

    Serologic tests, e.g., indirect hemagglutination.
    Pathologic examination of excised cyst.

    Treatment

    Albendazole or surgical removal of cyst.

    Prevention

    Sheep entrails should not be fed to
    dogs.
    Taenia saginata

    Disease

    Taeniasis.

    Characteristics

    Cestode (beef tapeworm). Scolex has four suckers but no
    hooks. Gravid proglottids have 15–20 uterine branches. Life cycle: Humans ingest
    undercooked beef containing cysticerci. Larvae attach to gut wall and become
    adult worms with gravid proglottids. Terminal proglottids detach, pass in feces,
    and are eaten by cattle. In the gut, oncosphere embryos hatch, burrow into blood
    vessels, and migrate to skeletal muscles, where they develop into
    cysticerci.

    Transmission and Epidemiology

    Transmitted by eating raw or undercooked beef. Humans are
    definitive hosts; cattle are intermediate hosts. Occurs worldwide but endemic in
    areas of Asia, Latin America, and eastern Europe.

    Pathogenesis

    Tapeworm in gut causes little damage. In contrast to
    Taenia solium, cysticercosis does not occur.

    Laboratory Diagnosis

    Gravid proglottids visible in stool. Eggs seen less
    frequently.

    Treatment

    Praziquantel.

    Prevention

    Adequate cooking of beef. Proper disposal of human
    waste.
    Taenia solium

    Diseases

    Taeniasis and cysticercosis.

    Characteristics

    Cestode (pork tapeworm). Scolex has four suckers and a
    circle of hooks. Gravid proglottids have 5–10 uterine branches. Life cycle:
    Humans ingest undercooked pork containing cysticerci. Larvae attach to gut wall
    and develop into adult worms with gravid proglottids. Terminal proglottids
    detach, pass in feces, and are eaten by pigs. In gut, oncosphere (hexacanth)
    embryos burrow into blood vessels and migrate to skeletal muscle, where they
    develop into cysticerci. If humans eat T. solium eggs in food
    contaminated with human feces, the oncospheres burrow into blood vessels and
    disseminate to organs (e.g., brain, eyes), where they encyst to form
    cysticerci.

    Transmission and Epidemiology

    Taeniasis acquired by eating raw or undercooked pork.
    Cysticercosis acquired only by ingesting eggs in fecally contaminated food or
    water. Humans are definitive hosts; pigs or humans are intermediate hosts.
    Occurs worldwide but endemic in areas of Asia, Latin America, and southern
    Europe.

    Pathogenesis

    Tapeworm in gut causes little damage. Cysticerci can expand
    and cause symptoms of mass lesions, especially in brain.

    Laboratory Diagnosis

    Gravid proglottids visible in stool. Eggs seen less
    frequently.

    Treatment

    Praziquantel for intestinal worms and for cerebral
    cysticercosis.

    Prevention

    Adequate cooking of pork. Proper disposal of human
    waste.
    Hymenolepsis nana

    H. nana infection is the most common tapeworm in the
    United States. Infection is usually asymptomatic. It is endemic in the
    southeastern states, mostly in children. It is called the dwarf tapeworm because
    of its small size. It is also different from other tapeworms because the eggs
    are directly infectious for humans without the need for an intermediate animal
    host. Diagnosis is made by finding eggs in feces. Treat with praziquantel. No
    specific means of prevention.
    Schistosoma (S. mansoni, S. japonicum, & S.
    haematobium)


    Disease

    Schistosomiasis.

    Characteristics

    Trematode (blood fluke). Adults exist as two sexes but are
    attached to each other. Eggs are distinguished by spines: Schistosoma
    mansoni
    has large lateral spine; Schistosoma japonicum has small
    lateral spine; Schistosoma haematobium has terminal spine. Life cycle:
    Humans are infected by cercariae penetrating skin. Cercariae form larvae that
    penetrate blood vessels and are carried to the liver, where they become adults.
    The flukes migrate retrograde in the portal vein to reach the mesenteric venules
    (S. mansoni and S. japonicum) or urinary bladder venules (S.
    haematobium
    ). Eggs penetrate the gut or bladder wall, are excreted, and
    hatch in fresh water. The ciliated larvae (miracidia) penetrate snails and
    multiply through generations to produce many free-swimming cercariae.

    Transmission and Epidemiology

    Transmitted by penetration of skin by cercariae. Humans are
    definitive hosts; snails are intermediate hosts. Endemic in tropical areas:
    S. mansoni in Africa and Latin America, S. haematobium in Africa
    and Middle East, S. japonicum in Asia.

    Pathogenesis

    Eggs in tissue induce inflammation, granulomas, fibrosis,
    and obstruction, especially in liver and spleen. S. mansoni damages the
    colon (inferior mesenteric venules), S. japonicum damages the small
    intestine (superior mesenteric venules), and S. haematobium damages the
    bladder. Bladder damage predisposes to carcinoma.

    Laboratory Diagnosis

    Eggs visible in feces or urine. Eosinophilia occurs.

    Treatment

    Praziquantel.

    Prevention

    Proper disposal of human waste. Swimming in endemic areas
    should be avoided.
    Clonorchis sinensis

    Disease

    Clonorchiasis.

    Characteristics

    Trematode (liver fluke). Life cycle: Humans ingest
    undercooked fish containing encysted larvae (metacercariae). In duodenum,
    immature flukes enter biliary duct, become adults, and release eggs that are
    passed in feces. Eggs are eaten by snails; the eggs hatch and form miracidia.
    These multiply through generations (rediae) and then produce many free-swimming
    cercariae, which encyst under scales of fish and are eaten by humans.

    Transmission and Epidemiology

    Transmitted by eating raw or undercooked freshwater fish.
    Humans are definitive hosts; snails and fish are first and second intermediate
    hosts, respectively. Endemic in Asia.

    Pathogenesis

    Inflammation of biliary tract.

    Laboratory Diagnosis

    Eggs visible in feces.

    Treatment

    Praziquantel.

    Prevention

    Adequate cooking of fish. Proper disposal of human
    waste.
    Paragonimus westermani

    Disease

    Paragonimiasis.

    Characteristics

    Trematode (lung fluke). Life cycle: Humans ingest
    undercooked freshwater crab meat containing encysted larvae (metacercariae). In
    gut, immature flukes enter peritoneal cavity, burrow through diaphragm into lung
    parenchyma, and become adults. Eggs enter bronchioles and are coughed up or
    swallowed. In fresh water, eggs hatch, releasing miracidia that enter snails,
    multiply through generations (rediae), and then form many cercariae that infect
    and encyst in crabs.

    Transmission and Epidemiology

    Transmitted by eating raw or undercooked crab meat. Humans
    are definitive hosts; snails and crabs are first and second intermediate hosts,
    respectively. Endemic in Asia and India.

    Pathogenesis

    Inflammation and secondary bacterial infection of
    lung.

    Laboratory Diagnosis

    Eggs visible in sputum or feces.

    Treatment

    Praziquantel.

    Prevention

    Adequate cooking of crabs. Proper disposal of human
    waste.
    Ancylostoma duodenale & Necator
    americanus


    Disease

    Hookworm.

    Characteristics

    Intestinal nematode. Life cycle: Larvae penetrate skin,
    enter the blood, and migrate to the lungs. They enter alveoli, pass up the
    trachea, then are swallowed. They become adults in small intestine and attach to
    walls via teeth (Ancylostoma) or cutting plates (Necator). Eggs
    are passed in feces and form noninfectious rhabditiform larvae and then
    infectious filariform larvae.

    Transmission and Epidemiology

    Filariform larvae in soil penetrate skin of feet. Humans
    are the only hosts. Endemic in the tropics.

    Pathogenesis

    Anemia due to blood loss from GI tract.

    Laboratory Diagnosis

    Eggs visible in feces. Eosinophilia occurs.

    Treatment

    Mebendazole or pyrantel pamoate.

    Prevention

    Use of footwear. Proper disposal of human
    waste.
    Ascaris lumbricoides

    Disease

    Ascariasis.

    Characteristics

    Intestinal nematode. Life cycle: Humans ingest eggs, which
    form larvae in gut. Larvae migrate through the blood to the lungs, where they
    enter the alveoli, pass up the trachea, and are swallowed. In the gut, they
    become adults and lay eggs that are passed in the feces. They embryonate, i.e.,
    become infective in soil.

    Transmission and Epidemiology

    Transmitted by food contaminated with soil containing eggs.
    Humans are the only hosts. Endemic in the tropics.

    Pathogenesis

    Larvae in lung can cause pneumonia. Heavy worm burden can
    cause intestinal obstruction or malnutrition.

    Laboratory Diagnosis

    Eggs visible in feces. Eosinophilia occurs.

    Treatment

    Mebendazole or pyrantel pamoate.

    Prevention

    Proper disposal of human
    waste.
    Enterobius vermicularis

    Disease

    Pinworm infection.

    Characteristics

    Intestinal nematode. Life cycle: Humans ingest eggs, which
    develop into adults in gut. At night, females migrate from the anus and lay many
    eggs on skin and in environment. Embryo within egg becomes an infective larva
    within 4–6 hours. Reinfection is common.

    Transmission and Epidemiology

    Transmitted by ingesting eggs. Humans are the only hosts.
    Occurs worldwide.

    Pathogenesis

    Worms and eggs cause perianal pruritus.

    Laboratory Diagnosis

    Eggs visible by "Scotch tape" technique. Adult worms found
    in diapers.

    Treatment

    Mebendazole or pyrantel pamoate.

    Prevention

    None.
    Strongyloides stercoralis

    Disease

    Strongyloidiasis.

    Characteristics

    Intestinal nematode. Life cycle: Larvae penetrate skin,
    enter the blood, and migrate to the lungs. They move into alveoli and up the
    trachea and are swallowed. They become adults and enter the mucosa, where
    females produce eggs that hatch in the colon into noninfectious, rhabditiform
    larvae that are usually passed in feces. Occasionally, rhabditiform larvae molt
    in the gut to form infectious, filariform larvae that can enter the blood and
    migrate to the lung (autoinfection). The noninfectious larvae passed in feces
    form infectious filariform larvae in the soil. These larvae can either penetrate
    the skin or form adults. Adults in soil can undergo several entire life cycles
    there. This free-living cycle can be interrupted when filariform larvae contact
    the skin.

    Transmission and Epidemiology

    Filariform larvae in soil penetrate skin. Endemic in the
    tropics.

    Pathogenesis

    Little effect in immunocompetent persons. In
    immunocompromised persons, massive superinfection can occur accompanied by
    secondary bacterial infections.

    Laboratory Diagnosis

    Larvae visible in stool. Eosinophilia occurs.

    Treatment

    Ivermectin is the drug of choice. Thiabendazole is an
    alternative.

    Prevention

    Proper disposal of human
    waste.
    Trichinella spiralis

    Disease

    Trichinosis.

    Characteristics

    Intestinal nematode that encysts in tissue. Life cycle:
    Humans ingest undercooked meat containing encysted larvae, which mature into
    adults in small intestine. Female worms release larvae that enter blood and
    migrate to skeletal muscle or brain, where they encyst.

    Transmission and Epidemiology

    Transmitted by ingestion of raw or undercooked meat,
    usually pork. Reservoir hosts are primarily pigs and rats. Humans are dead-end
    hosts. Occurs worldwide but endemic in eastern Europe and west Africa.

    Pathogenesis

    Larvae encyst within striated muscle cells called "nurse
    cells," causing inflammation of muscle.

    Laboratory Diagnosis

    Encysted larvae visible in muscle biopsy. Eosinophilia
    occurs. Serologic tests positive.

    Treatment

    Thiabendazole effective early against adult worms. For
    severe symptoms, steroids plus mebendazole can be tried.

    Prevention

    Adequate cooking of
    pork.
    Trichuris trichiura

    Disease

    Whipworm infection.

    Characteristics

    Intestinal nematode. Life cycle: Humans ingest eggs, which
    develop into adults in gut. Eggs are passed in feces into soil, where they
    embryonate, i.e., become infectious.

    Transmission and Epidemiology

    Transmitted by food or water contaminated with soil
    containing eggs. Humans are the only hosts. Occurs worldwide, especially in the
    tropics.

    Pathogenesis

    Worm in gut usually causes little damage.

    Laboratory Diagnosis

    Eggs visible in feces.

    Treatment

    Mebendazole.

    Prevention

    Proper disposal of human
    waste.
    Dracunculus medinensis

    Disease

    Dracunculiasis.

    Characteristics

    Tissue nematode. Life cycle: Humans ingest copepods
    containing infective larvae in drinking water. Larvae are released in gut,
    migrate to body cavity, mature, and mate. Fertilized female migrates to
    subcutaneous tissue and forms a papule, which ulcerates. Motile larvae are
    released into water, where they are eaten by copepods and form infective
    larvae.

    Transmission and Epidemiology

    Transmitted by copepods in drinking water. Humans are major
    definitive hosts. Many domestic animals are reservoir hosts. Endemic in tropical
    Africa, Middle East, and India.

    Pathogenesis

    Adult worms in skin cause inflammation and
    ulceration.

    Laboratory Diagnosis

    Not useful.

    Treatment

    Thiabendazole or metronidazole. Extraction of worm from
    skin ulcer.

    Prevention

    Purification of drinking
    water.
    Loa loa

    Disease

    Loiasis.

    Characteristics

    Tissue nematode. Life cycle: Bite of deer fly (mango fly)
    deposits infective larvae, which crawl into the skin and develop into adults
    that migrate subcutaneously. Females produce microfilariae, which enter the
    blood. These are ingested by deer flies, in which the infective larvae are
    formed.

    Transmission and Epidemiology

    Transmitted by deer flies. Humans are the only definitive
    hosts. No animal reservoir. Endemic in central and west Africa.

    Pathogenesis

    Hypersensitivity to adult worms causes "swelling" in skin.
    Adult worm seen crawling across conjunctivas.

    Laboratory Diagnosis

    Microfilariae visible on blood smear.

    Treatment

    Diethylcarbamazine.

    Prevention

    Deer fly control.
    Onchocerca volvulus

    Disease

    Onchocerciasis (river blindness).

    Characteristics

    Tissue nematodes. Life cycle: Bite of female blackfly
    deposits larvae in subcutaneous tissue, where they mature into adult worms
    within skin nodules. Females produce microfilariae, which migrate in
    interstitial fluids and are ingested by blackflies, in which the infective
    larvae are formed.

    Transmission and Epidemiology

    Transmitted by female blackflies. Humans are the only
    definitive hosts. No animal reservoir. Endemic along rivers of tropical Africa
    and Central America.

    Pathogenesis

    Microfilariae in eye ultimately can cause blindness ("river
    blindness"). Adult worms induce inflammatory nodules in skin. See scaly
    dermatitis called "lizard skin." Also loss of subcutaneous tissue called
    "hanging groin."

    Laboratory Diagnosis

    Microfilariae visible in skin biopsy, not in blood.

    Treatment

    Ivermectin affects microfilariae, not adult worms. Suramin
    for adult worms.

    Prevention

    Blackfly control and
    ivermectin.
    Wuchereria bancrofti

    Disease

    Filariasis.

    Characteristics

    Tissue nematodes. Life cycle: Bite of female mosquito
    deposits infective larvae that penetrate bite wound, form adults, and produce
    microfilariae. These circulate in the blood, chiefly at night, and are ingested
    by mosquitoes, in which the infective larvae are formed.

    Transmission and Epidemiology

    Transmitted by female mosquitoes of several genera,
    especially Anopheles and Culex, depending on geography. Humans are
    the only definitive hosts. Endemic in many tropical areas.

    Pathogenesis

    Adult worms cause inflammation that blocks lymphatic
    vessels (elephantiasis). Chronic, repeated infection required for symptoms to
    occur.

    Laboratory Diagnosis

    Microfilariae visible on blood smear.

    Treatment

    Diethylcarbamazine affects microfilariae. No treatment for
    adult worms.

    Prevention

    Mosquito control.
    Toxocara canis

    Disease

    Visceral larva migrans.

    Characteristics

    Nematode larvae cause disease. Life cycle in humans:
    Toxocara eggs are passed in dog feces and ingested by humans. They hatch
    into larvae in small intestine; larvae enter the blood and migrate to organs,
    especially liver, brain, and eyes, where they are trapped and die.

    Transmission and Epidemiology

    Transmitted by ingestion of eggs in food or water
    contaminated with dog feces. Dogs are definitive hosts. Humans are dead-end
    hosts.

    Pathogenesis

    Granulomas form around dead larvae. Granulomas in the
    retina can cause blindness.

    Laboratory Diagnosis

    Larvae visible in tissue. Serologic tests useful.

    Treatment

    Albendazole or mebendazole.

    Prevention

    Dogs should be dewormed.
    Ancylostoma caninum & Ancylostoma
    braziliense


    The filariform larvae of A. caninum (dog hookworm)
    and A. braziliense (cat hookworm) cause cutaneous larva migrans. The
    larvae in the soil burrow through the skin, then migrate within the subcutaneous
    tissue, causing a pruritic rash called "creeping eruption." These organisms
    cannot complete their life cycle in humans. The diagnosis is made clinically.
    Thiabendazole is effective.
    Anisakis simplex

    The larvae of A. simplex cause anisakiasis. They are
    ingested in raw seafood, such as sashimi and sushi, and migrate into the
    submucosa of the intestinal tract. Acute infection resembles appendicitis.
    Diagnosis is not dependent on the clinical laboratory. There is no effective
    drug therapy. Prevention consists of not eating raw
    fish.
    Pediculus humanus & Phthirus pubis

    Disease

    Pediculosis.

    Characteristics

    Lice are easily visible. P. humanus has an elongated
    body, whereas P. pubis has a short body resembling a crab. Nits are the
    eggs of the louse, often attached to the hair shaft or clothing.

    Transmission

    Hair and body lice are transmitted from human to human by
    contact, especially fomites such as hats and combs. Pubic lice are transmitted
    by sexual contact.

    Pathogenesis

    Itching is caused by a hypersensitivity response to saliva
    of the louse.

    Laboratory Diagnosis

    Not involved.

    Treatment

    Permethrin.

    Prevention

    Personal items should be treated or
    discarded.
    Dermatobia hominis

    Disease

    Myiasis.

    Characteristics

    Fly larvae (maggots) cause the disease not the adult
    flies.

    Transmission

    Adult fly deposits egg in lesion. Egg hatches to form
    larva. Dermatobia deposits its egg on mosquito, and when the mosquito
    bites the eggs are then deposited on the skin.

    Pathogenesis

    Larva induces an inflammatory response.

    Laboratory Diagnosis

    Not involved.

    Treatment

    Surgical removal of larva.

    Prevention

    Limit exposure to flies and
    mosquitoes.
    Sarcoptes scabiei

    Disease

    Scabies.

    Characteristics

    Round body with eight short legs. Too small to be seen with
    naked eye.

    Transmission

    Person-to-person contact or fomites such as clothing.

    Pathogenesis

    Itching is caused by a hypersensitivity response to feces
    of the mite.

    Laboratory Diagnosis

    Microscopic examination reveals mites and their
    feces.

    Treatment

    Permethrin.

    Prevention

    Treat contacts and discard
    fomites.
    Dermacentor Species

    Disease

    Tick paralysis.

    Characteristics

    Certain species of ticks produce a neurotoxin.

    Transmission

    Ticks reside in grassy areas and attach to human
    skin.

    Pathogenesis

    Female tick requires a blood meal and toxin enters in tick
    saliva at bite site. Neurotoxin blocks release of acetyl choline at
    neuromuscular junction. Similar action as botulinum toxin.

    Laboratory Diagnosis

    Not involved.

    Treatment

    Removal of tick results in prompt reversal of
    paralysis.

    Prevention

    Remove ticks; wear protective
    clothing.
    Latrodectus mactans (Black Widow Spider)

    Disease

    Spider bite.

    Characteristics

    Black widow spiders have an orange-red hourglass on their
    ventral surface.

    Pathogenesis

    Neurotoxin causes pain in extremities and abdomen.
    Numbness, fever, and vomiting also occur.

    Laboratory Diagnosis

    Not involved.

    Treatment

    Antivenom should be given in severe
    cases.
    Loxosceles reclusa (Brown Recluse Spider)

    Disease

    Spider bite.

    Characteristics

    Brown recluse spiders have a violin-shaped pattern on their
    dorsal surface.

    Pathogenesis

    Dermotoxin is a protease that causes painful necrotic
    lesions

    Laboratory Diagnosis

    Not involved.

    Treatment

    Antivenom is not available in the United
    States.

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