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. |
