MLS 440 Parasite
Plasmodium species
- causes malaria; transmitted by Anopheles mosquito -Plasmodium Life Cycle
Tissue Cestodes
1. Echinococcus granulosus (Hydatid tapeworm) Teania soliun
Blood trematodes
1. Schistosoma mansoni 2. Schistosoma japonicum 3. Schistosoma haematobium (bladder fluke)
Ciliates
A group of protozoans that move by waving tiny, hair-like organelles called cilia. This group only includes one organism: Balantidium coli
Trichostrongylus species
About 10 species, live in mucosa of small intestine, adult worm have no visible buccal cavity Epidemiology - 70% of humans in southwest Iran, and some of Egypt are infected Acquired via ingestion of contaminated plants Pathogenesis and spectrum of disease - larvae mature and migrate through lungs, symptom related to worm burden and damage in intestine Laboratory diagnosis - identification of eggs, hatched larvae in stool Resemble hookworm eggs but longer and more pointed Larvae are used to differentiate from Strongyloides stercoralis Therapy - antihelminthic drugs mebendazole and pyrantel pamoate Prevention - washing plants before eating them
LOA LOA
African eye worm worm," circulates in blood stream, lives in subcutaneous tissue Microfilariae up to 300 µm Epidemiology Rain forests of West and Central Africa, transmitted through bite of tabanid fly or deer fly Pathogenesis and spectrum of disease Often asymptomatic Develop into adult worms in 6-12 monts, can live in host for up to 17 years Typically discovered when it migrates in the subconjunctiva of the eye Episodic calabar swelling, localized transient angioedema from parasitic metabolites, swelling of extremitites, inflammation of joints and nerves, immune-mediated encephalopathy, nephropathy, and cardiomyopathy
BRUGIA MALAYI AND BRUGIA TIMORI
Also lymphatic filarial parasites Brugia timori - 300 µm long, 5-6 µm wide Brugia malay - 270 µm long, 5-6 µm wide Epidemiology - Far East but B timori limited to two islands of Timor and Indonesia Pathogenesis and spectrum of disease Nocturnal form found near areas of costal rice fields Nonperiodic form associated with swampy forests Same pathogenesis and spectrum as Wuchereria bancrofti except no involvement of gentials and faster progression Microfilariae seen in blood 3-4 months after infection Associated with zoonotic infections associated with cats, dogs, rabbits, and raccoons In US, disease is usually asymptomatic or have tender cervical, axillary, and inguinal regions with lymphatic mass with a live or a dead worm, if dead 🡪 granulomatous reaction
Echinococcus multilocularis
Alveolar Hydatid Epidemiology- found in Asia, Europe, and northern North America, including areas such as Alaska, Montana, and Minnesota. Foxes, coyotes, and dogs are the definitive host whereas rodents are the intermediate host Transmitted to humans through the ingestion of contaminated food or water and by handling infected animals
Blastocystis hominis
Amoeba, Sometimes Pathogenic, when numerous -Usually commensile -Oral-Fecal Transmission -Symptoms: diarrhea, cramps, nausea, fever, vomiting, abdominal pain -Seen in Central Vacuolated Form ( central body form), most common seen stool specimen. but also exists as granulated form, amoebic form, and cyst form. Epidemiology- Transmission of B. hominis is by the fecal-oral route from infective forms contained in the feces or through various sexual practices that may include accidental ingestion of fecal organisms. Flies and cockroaches can be responsible for mechanical transmission. Human-to-human and animal-to-human transmission is probably more common than suspected Pathogenesis and spectrum of disease- B. hominis can cause diarrhea, cramps, nausea, fever, vomiting, abdominal pain, and urticaria and may require therapy. Proteases of genetic subtype 3 could be considered a virulence factor responsible for protein degradation and subsequent pathogenesis
Protozoa from other body site
Amoeba- N. fowlei, Acanthamoeba spp, Flagellates- Trichomonas vaginalis, Trichomonas tenax Coccidia- Toxoplasma gondii
Necator americanus - New World Hookworm
Attach to intestinal mucosa via well- developed cutting plates Pathogenesis and spectrum of disease - iron deficiency anemia,
Ancylostoma duodenale - Old World Hook Worms
Attach to intestinal mucosa via well-developed mouthparts, teeth Pathogenesis and spectrum of disease - maturation in intestine without migration through lungs
liver and lungs trematodes
Clonorchic sinensis, Opisthorchis felineus, Opisthorchis viverrini
Intestinal Cestodes (tapeworms)
D. latum, T. solium,
Taenia multiceps
DH: Carnivores, esp. dogs. IH: Herbivorous mammals Note: Larval cysts call coenurus, inner layer becomes germinal layer to form protoscolices. Epidemiology-T. multiceps is most often found in Africa, although it may be seen in South America, the United States, and Canada. The adult worm is typically found in dogs and other canids. Many animals serve as the intermediate host, such as sheep, cattle, and deer. Human infection occurs from accidental ingestion of dog feces containing the eggs.
Gnathostoma spinigerum
Dogs and cats definitive host, eggs passed in feces Epidemiology - when feces deposited in water, larvae hatch and infect copepods 🡪 intermediate hosts...etc... 🡪 humans are accidental host after eating contaminated fish Pathogenesis and spectrum of disease Worms are incapable of maturation inside humans 🡪 migrate aimlessly causing tissue damage and inflammation, resembles visceral larva migrans Not usually fatal Laboratory diagnosis ID larvae in tissue by head with four rows of cephalic hooklets, body covered with transverse rows of spines Therapy - supportive corticosteroid therapy, surgical excision
Tissue nematodes
Draculucus, Onchocera volvulus, Loa Loa, Wuchereria, elephantiasis, Toxocara
ENTAMOEBA HISTOLYTICA: Epidemiology Pathogenesis and spectrum of disease Asymptomatic infection Intestinal disease hepatic disease Metastatic amoebiasis
E. histolytica is considered the etiologic agent of amebic colitis & extraintestinal abscesses (amebic liver abscess), whereas nonpathogenic E. dispar produces no intestinal symptoms and is not invasive in humans. Infection is acquired through the fecal-oral route from infective cysts contained in the feces. Flies and cockroaches have been implicated as mechanical vectors of contaminated fecal material. Pathogenesis and Spectrum of Disease The pathogenesis of E. histolytica is related to the organism's ability to directly lyse host cells and cause tissue destruction. The presentations of disease are seen with invasion of the intestinal mucosa or dissemination to other organs (most often the liver) or both. Asymptomatic Infection- individuals harboring E. histolytica may have either a negative or a weak antibody titer and negative stools for occult blood. Asymptomatic patients identified with E. histolytica are at risk for the development of invasive amebiasis. Intestinal Disease-the incubation time ranges from 1 to 4 weeks. Tissue invasion by E. histolytica requires a contact-dependent process that involves colonic mucins and amoebic lectins in the plasma membrane that mediate adherence to the host mucosa. Invasive intestinal amebiasis has various clinical forms, all of which are generally acute: amoebic diarrhea without dysentery, dysentery (bloody diarrhea), or colitis, ameboma, and amoebic liver abscess. The digestive action of these proteases contributes to the development of amoebic ulcers and tissue damage in the intestinal tract. Amoebic ulcers often develop in the cecum, appendix, or adjacent portion of the ascending colon Dysentery may last for months, it varies from severe to mild and may lead to weight loss and prostration. In rare severe cases, symptoms may begin very suddenly and include profuse diarrhea, fever, and dehydration with electrolyte imbalances Hepatic Disease- Blood flow from the mesenteric veins surrounding the intestine returns blood, via the portal vein, to the liver, most commonly the upper right lobe. Amoebae in the submucosa can be carried by the bloodstream to the liver. Symptoms may be gradual or sudden; upper right abdominal pain and fever (38°C to 39°C) Liver may be enlarged and tender, liver function tests may be normal or slightly abnormal (jaundice is rare). The most common complication is rupture of the abscess into the pleural space. An abscess also can extend into the peritoneum and through the skin. Hematogenous spread to the brain, lung, pericardium. Pyogenic abscess depends on the bacterial source and the patient's underlying condition. An amoebic abscess tends to be more prevalent in those with suppressed cell-mediated immunity, males, and younger individuals. Metastatic Amebiasis Extraabdominal amebiasis may occur after liver involvement: Thoracic amebiasis Pericardial involvement Cerebral amebiasis
Intestinal protozoa: Trophozoites of common Amoebas
ENTAMOEBA HISTOLYTICA,E. dispar, E. hartmanni, Entamoeba coli, Endomilax nana, Iodamoeba butschlii
Dracunculus medinensis - Guinea worm
Epidemiology - Dracunculiasis, used to be worldwide, close to eradication Ingestion of freshwater from stagnant ponds with larvae-infected copepods Larvae penetrate small intestine 🡪 thoracic musculature, mature in 2-3 months, gravid female 10-14 months Gravid female migrates to lower extremities 🡪 blister on skin which erupts when placed in water 🡪 larvae released Pathogenesis and spectrum of disease Blisters cause burning, itching, systemic symptoms: fever, nausea, vomiting, diarrhea, headache, urticaria, and eosinophilia Dead worms may calcify 🡪 secondary inflammatory symptoms Laboratory diagnosis - find larvae or adult worms in specimens, serology helpful before blister is formed Therapy - removal of adult worms by attaching to stick and slowly turning, metronidazole or thiabendazole help with retraction
Capillaria philippinensis
Epidemiology - Northern Phillipines, reproduces in intestines, autoinfection and superinfection similar to Strongyloides stercoralis Ingestion of uncooked fish with infective larvae Defacation in fields where snails, shrimp, and crabs collected to eat Pathogenesis and spectrum of disease Depends on worm burden, burrow into mucosa, rapid weight loss from malabsorption and fluid loss 🡪 death from electrolyte loss (mostly potassium) and organ failure Laboratory diagnosis - ID of eggs, worms, or larvae Eggs are similar to T. trichiura but smaller and thick, striated shell, less prominent polar plugs Therapy - albendazole, mebendazole Prevention - cooking seafood
Hookworms - Ancylostoma duodenale and Necatur americanus
Epidemiology - eggs and rhabditiform larvae of these two indistinguishable via microscopy Differentiation based on buccal capsule and adult male copulatory bursa Filariform larvae (infective stage) penetrate skin 🡪 blood stream 🡪 lungs 🡪 bronchial tree over epiglottis, swallowed 🡪 attach to mucosa of small intestine Secrete anticoagulants and ingest blood
Parastrongylus costaricensis
Epidemiology - found in cotton rat and black rat Endemic in Central and South America Pathogenesis and spectrum of disease Life cycle similar to Parastrongylus cantonensis Ingestion of salad contaminated with slugs or snails Larvae make inflammatory lesions in bowel wall 🡪 tissue inflammation, necrosis, vomiting, diarrhea RLQ pain similar to appendicitis Laboratory diagnosis - histologic ID of larvae or eggs in tissue sections Therapy - traditional antihelminthic therapy
Entamoeba coli
Epidemiology- Transmission occurs through the ingestion of mature cysts from contaminated food or water. Pathogenesis and spectrum of disease- E. coli are typically considered nonpathogenic and do not cause disease. Laboratory diagnosis- Unless the mature cyst with eight nuclei is seen, the morphologies of E. histolytica, E. dispar, E. moshkovskii, and E. coli are similar in the trophozoite and immature cyst stages. Definitive identification relies on examination of permanent stained smears. Therapy- Specific treatment is not recommended for the nonpathogenic E. coli. If few E. histolytica, E. dispar, or E. moshkovskii organisms are present among many E. coli organisms, extended microscopic examination or the use of speciesspecific immunoassay or nucleic acid-based testing may be required to make the correct identification. Prevention- adequate disposal of human excreta and improved personal hygiene
Giardia duodenalis
Epidemiology- Transmission of G. duodenalis occurs by ingestion of viable cysts. Contaminated food or drink may be the source, intimate contact with an infected individual may also result in transmission of the organism. Organism is found more frequently in children or in groups living in close quarters. Pathogenesis and spectrum of disease- The incubation period for giardiasis ranges from approximately 12 to 20 days. Giardiasis may not be recognized as the cause, because the infection mimics acute viral enteritis, bacillary dysentery, bacterial or other food poisonings, acute intestinal amebiasis, or "traveler's diarrhea" (toxigenic Escherichia coli). Lack of blood, mucus, and cellular exudate is consistent with giardiasis -asymptomatic infection- The organisms feed on the mucous secretions and do not penetrate the mucosa -intestinal disease- symptomatic patients may have irritation of the mucosal lining, increased mucus secretion, and dehydration, nausea, anorexia, malaise, low-grade fever, and chills, sudden onset of explosive, watery, foul-smelling diarrhea, epigastric pain, flatulence, and diarrhea with increased amounts of fat and mucus in the stool but no blood, weight loss -chronic disease- loose, foul-smelling stools and possibly increased distention and foul flatus. Between episodes of mushy stools, the patient may have normal stools or may be constipated. Abdominal discomfort includes marked distention and belching with a rotten-egg taste, upper intestinal discomfort, heartburn, and belching, giardiasis must also be differentiated from duodenal ulcer, hiatal hernia, and gallbladder and pancreatic disease. -antigenic variation- Variation of the surface antigen during human infections with G. duodenalis has been documented: The variant specific surface proteins (VSPs). VSPs are resistant to the effects of intestinal proteases, which allows the parasites to survive in the protease-rich small intestine.
Cyclospora cayetanensis
Epidemiology- Transmission thought to be by fecal oral route. Outbreaks linked to contaminated water and various types of fresh produce (raspberries, basil, baby lettuce leaves, and snow peas) Pathogenesis and spectrum of disease- some patients are asymptomatic, others report a flulike illness, marked by nausea, vomiting, anorexia, weight loss, and explosive diarrhea lasting 1 to 3 weeks. The onset of symptoms after infection generally averages 7 to 8 days, and the symptoms last 2 to 3 weeks. In immunocompromised and immunocompetent patients, C. cayetanensis infection can be associated with biliary disease
Chilomastix mesnili
Epidemiology- cosmopolitan distribution. Transmission occurs through ingestion of infective cysts. Pathogenesis and spectrum of disease- nonpathogenic and does not cause disease. Laboratory diagnosis- examination of permanent stained smears. Therapy- treatment is not recommended for C. mesnili. Both pathogens and nonpathogens can be found in the same patient and must be reported as they are acquired the same way Prevention- adequate disposal of human excreta and improved personal hygiene, preventive measures that apply to most of the intestinal protozoa.
Cryptosporidium species
Epidemiology- several transmission routes, such as direct contact with infected people or animals or consumption of contaminated water or food. The only extracellular stage in the Cryptosporidium life cycle is the oocysts; these are the environmental stage of the parasite and are immediately infectious when passed in the stool . Infection occurs mostly in children younger than 5 years, with peak occurrence of infections and diarrhea in children younger than 2 years. Calves and perhaps other animals serve as potential sources of human infection. Pathogenesis and spectrum of disease - Immunocompetent- (the most common symptom is diarrhea. Clinical symptoms include nausea; low-grade fever; abdominal cramps; anorexia; and 5 to 10 watery, frothy bowel movements per day, which may be followed by constipation). Immunocompromised- Hemodialysis patients with chronic renal failure and renal transplant patients with cryptosporidiosis can have chronic, life-threatening diarrhea Laboratory diagnosis: Routine methods- Oocysts in clinical specimens are difficult to see without special staining techniques, such as the modified acid-fast, Ziehl-Neelsen or Kinyoun's, or Giemsa method, or the newer immunoassay methods Antigen detection- direct fluorescent antigen (FA), direct fluorescent antibody (DFA) kits, Enzyme immunoassay (EIA molecular methods- PCR and PCR-related methods Antibody detection- antibody detection is not available on a routine basis Histology- developmental stages (sporozoites, trophozoites, merozoites, and oocysts) in the life cycle of Cryptosporidium spp. can be found at all levels of the intestinal tract, with the jejunum being the most heavily infected site. Hematoxylin and eosin staining is sufficient to demonstrate these parasites. Reporting results-Identification of oocysts in a patient's stool or a positive antigen test should be reported as Cryptosporidium positive. Therapy- Oral or intravenous rehydration and antimotility drugs for severe diarrhea. Nitazoxanide is the only drug approved by the FDA for the treatment of cryptosporidiosis in immunocompetent individuals. Paromomycin and spiramycin have been used in immunodeficient patients. In patients with AIDS is highly active antiretroviral therapy (HAART) Prevention- chlorine and related compounds can dramatically reduce the ability of oocysts to excyst or infect, high concentrations and long exposure times are required, making this approach impractical.
Pentatrichomonas hominis
Epidemiology- transmission probably occurs in the trophic form. If ingested in a substance such as milk, these organisms apparently can survive passage through the stomach and small intestine in patients with achlorhydria. Pathogenesis and spectrum of disease- P. hominis is considered nonpathogenic and does not cause disease. Laboratory diagnosis- can sometimes be seen on a permanent stained smear, but definitive identification can be difficult Therapy- Specific treatment is not recommended for this nonpathogen Prevention - adequate disposal of human excreta and improved personal hygiene
Balantidium coli
Epidemiology- widely distributed in hogs, particularly in warm and temperate climates, and in monkeys in the tropics. Human infection is found in institutionalized groups with low levels of personal hygiene. Pathogenesis and spectrum of disease- some asymptomatic, whereas others have severe dysentery, diarrhea, tenesmus, nausea, vomiting, anorexia, and headache. Insomnia, muscular weakness, and weight loss. B. coli may penetrate the mucosa on contact, developing ulcer. May migrate from the intestine to the lungs causing a pneumonia-like illness in immunocompromised patients Laboratory diagnosis- Routine stool examinations, particularly direct wet preparation examinations of fresh and concentrated material. Organism recognition and identification on a permanent stained smear is usually difficult. Reporting results- the organism is rarely identified. Care should be taken to not confuse the parasite with contaminating debris. Therapy- Tetracycline is the drug of choice. Iodoquinol or metronidazole, and Nitazoxanide may be used Prevention- increased attention to personal hygiene and sanitation measures, because the mode of transmission is ingestion of infective cysts through contaminated food or water.
Echinococcus granulosus
Epidemiology-E. granulosus is most common in cool, damp areas where sheep herds are prevalent, such as southern South America, Russia, East Africa, and the western United The eggs in the definitive host are passed through the feces and contaminate soil, water, or food States. The eggs are able to survive freezing conditions and can remain viable within the environment for several years. Pathogenesis and Spectrum of Disease- The cyst is very slow growing in humans. It is usually fluid-filled and has a germinal layer from which many thousands of scolices are budded. These are known as daughter cysts (brood capsules) The result is a unilocular cyst containing future adult worms Infection in the liver or lungs may be asymptomatic for many years Hydatid cysts occur within the liver. Cysts within the liver cause chronic abdominal pain and allergic reactions and may result in cholangitis (infection of the common bile duct) and cholestasis (interference with the flow of bile from the liver).
Intestinal Trematodes
Fasciolopsis buski (Giant Intestinal Fluke) > Eggs in stool (cannot differentiate from Fasciola hepatica
Dipylidium caninum
Flea tapeworm Infection is common worldwide. In the case of D. caninum, human infection is acquired through the accidental ingestion of fleas. Infection is most often seen in young children as a result of close contact with infected pets. The tapeworms are found in both wild and domestic dogs and cats.
Balamuthia mandrillaris
General Found in soil, can cause meningoencephalitis Death within a week to several months No flagellated forms, only trophozoites and cysts, similar size as Acanthamoeba and similar appearance under microscope for tissue sections Electron microscope - cyst 3 layers wrinkled ectocyst, mesocyst, and inner endocyst Sometimes have more than one nucleolus under light microscope Pathogenesis and spectrum of disease Similar to GAE by Acanthamoeba, no association with freshwater Headache, nausea, vomiting, fever, visual disturbances, dysphagia, (problems swallowing foods/liquids), hemiparesis Symptoms few days to months
Fasciolopsis buski
Giant intestinal fluke 20-75mm long and 8-20 mm wide Oral sucker at anterior end, ventral sucker halfway down posterior end Eggs look same as Fasciola hepatica, oval, elongated, transparent, yellow-brown, operculum, ~130-140 µm long by 80-85 µm wide
Dirofilaria immitis
Heartworm
Heterophyes and Metagonimus yokoawai
Heterophyes flukes 1-1.7mm long to 0.3-0.4mm wide, broadly rounded posterior Metagonimus yokogawai flukes 1.0-2.5mm long by 0.4-0.8mm wide Eggs - small, yellow-brown, embryonated, operculated with minimal opercular shoulders, 26-30 µm long by 15-17 µm wide Epidemiology most common intestinal fluke in Far East Reservoir hosts cats, dogs, birds Ingestion of pickled/uncooked fish
Flukes
Ingestion of metacercariae encysted on freshwater vegetation or fish Found in small intestine, lay eggs that are released in feces
Leishmania species
Laboratory diagnosis Serologic tests-A rapid immunochromatographic dipstick test using the recombinant K39 antigen has become available for the qualitative detection of total anti-Leishmania immunoglobulins. Serologic assays are not very useful for the diagnosis of mucocutaneous and visceral leishmaniasis. Molecular methods - PCR methods have excellent sensitivity and specificity for direct detection, for identification of causative species, and for assessment of treatment efficacy Therapy- In simple cutaneous leishmaniasis, lesions usually heal spontaneously, although treatment options include cryotherapy, heat, photodynamic therapy, surgical excision of lesions, and chemotherapy. Standard therapy consists of injections of antimonial compounds; additional drugs have been used and include lipid-associated amphotericin B for Mediterranean and Indian disease.
Acanthamoeba species
Large karyosome no peripheral chromatin No flagellate stage, only troph and cyst stage Can cause GAE, amoebic keratitis, cutaneous lesions, or sinusitis Motile trophs have spinelike pseudopodia (25 - 40 µm), nucleus large karyosome (will "blink at you" under microscope) Cysts have large single nucleus with large karyosome, double wall with wrinkled outer wall
Pathogenesis and spectrum of disease lung fluke
Light infections asymptomatic Migration through muscle and tissue cause pain, immune response, tissue damage Lungs become infiltrated with eosinophils and neutrophils, serum IgE elevated Adult worms encapsulate 🡪 granuloma Chronic cough, blood-tinged sputum Larvae of Paragonimus Mexicana can migrate to subcutaneous tissue or lower abdomen Paragonimus larve can migrate to the brain, but extremely rare
liver fluke
Live in biliary ducts and also gallbladder if heavy infection Clonorchis sinensis - Chinese liver fluke China, Japan, Korea, Tiawan, and Vietnam Opisthorchis felineus and Opisthorchis viverrine - South-East Asian liver fluke Cambodia, Laos, Thailand, and Vietnam (O. viverrini) Northern Europe, Asia, reservoir hosts = dogs and cats Fasciola - sheep liver fluke F. hepatica - Europe, North and South America F. gigantica - Asia and Africa Affect economies of sheep and cattle Reservoir hosts = dogs, pigs, equines, and rats Epidemiology and lifecycle Lifecycle similar to that of intestinal flukes Eggs secreted in bile ducts and released in feces, finds water...many steps...metacercaria infect humans from raw or undercooked fish (Clonorchis and Opisthorchis) and raw freshwater vegetation such as watercress and water chestnuts (Fasciola)
ENTAMOEBA HISTOLYTICA
Living trophozoites (motile feeding stage) of E. histolytica vary in size from about 12 to 60 µm in diameter, invasive form maybe >20um. E. histolytica has directional and progressive motility with hyaline, fingerlike pseudopodia, motility maybe rapid. Motility is rarely seen even in a fresh direct wet mount from a patient with diarrhea or dysentery. The cytoplasm is generally more finely granular (ground glass), clear differentiation of ectoplasm and endoplasm and the presence of red blood cells (RBCs) in the cytoplasm was previously considered diagnostic for E. histolytica. Stain: peripheral chromatin stain- fine granules, uniform in size and usually evenly distributed. Karyosome- small usually compact, centrally located but may also be eccentric. As part of the life cycle, the trophozoites may condense into a round mass (precyst), and a thin wall is secreted around the immature cyst
Blood nematodes (filaria)
Loa loa, brugia timori, wuchereria bancrofti
MANSONELLA SPECIES
M. OZZARDI, M. STREPTOCERCA, M. PERSTANS
Ascaris lumbricoides
Most common, largest, worldwide but more often seen in tropics Eggs hatch in duodenum, go through intestinal wall, migrate to hepatic portal circulation Adults like to live in small intestine Eggs leave through feces, become infective 2-6 weeks later See life cycle in Figure 50-1 Epidemiology - need warm humid environment, found in areas with poor sanitation, fecal-oral route, can survive dry/freezing temperatures
Chilomastix mesnili
Non-pathogenic Flagellate Protozoa -lives in cecal region of large intestine -fecal-oral transmission -looks like yeast -"Pear Shaped"
Entamoeba hartmanni
NonPathogenic Amoeba Oral-Fecal transmission, motility- usually non progressive. Not seen in unstained preparation, may contain bacterial inclusion. Epidemiology- Transmission occurs through the ingestion of mature cysts from contaminated food or water Pathogenesis and spectrum of disease- E. hartmanni is considered nonpathogenic and does not cause disease. Laboratory diagnosis- Definitive identification relies on examination of permanent stained smears and measurements made with the calibrated microscope.
Iodamoeba butschlii
Nonpathogenic , seen worldwide. Epidemiology- Transmission of I. bütschlii occurs through the ingestion of mature cysts from contaminated food or water. Pathogenesis and Spectrum of Disease- I. bütschlii is considered nonpathogenic and does not cause disease. Laboratory diagnosis- definitive identification relies on the examination of permanent stained smear Therapy - Because these nonpathogenic amoebae are acquired through fecal-oral contamination, both pathogens and nonpathogens can be found in the same patient. It is always important to report pathogens and nonpathogens, because they are acquired in similar way Prevention- adequate disposal of human excreta and improved personal hygiene, preventive measures
Trichuris trichiura - whipworm
Often asymptomatic; loose stools, anemia, *rectal prolapse in children (heavy infection)* Epidemiology - No tissue migration phase Asia, Africa, South America, southern United States Coinfections with Ascaris lumbricoides or hookworm in children Poor hygiene, contract via ingestion of embryonated eggs, mature in intestine Diagnostic stage = eggs containing unsegmented ovum which pass in feces Pathogenesis and spectrum of disease severity depends on worm burden Bleeding, weight loss if heavy infestation Inflammatory reaction, peripheral eosinophilia
Lung Flukes
Paragonimus - 10 species that affect humans, Paragonimus westermani most common Live in lungs, eggs may be found in sputum or feces (if swallowed) Epidemiology and life cycle Many in Far East Paragonimus mexicanus - Mexico and South America, reservoir host wild pigs, dogs, and rodents Paragonimus africanus and Paragonimus uterobilateralis - West Africa Paragonimus kellicotti - North America, ingestion of undercooked crustaceans (crayfish) containing metacercaeria Paragonimus westermani - reservoir host dogs and cats Adult flukes encapsulate in lungs, eggs stimulate cough, eggs swallowed Eggs vary in size by species - 80-120 µm long by 40-70 µm wide When metacercaria ingested, migrate through intestinal wall 🡪 through diaphragm 🡪 into lungs
Plasmodium knowlesi
Pathogenesis and spectrum of disease Patients who have been diagnosed with high numbers of P. malariae organisms by microscopy should receive intensive management as appropriate for severe P. falciparum malaria, assuming the infection is actually caused by P. knowlesi. These infections can be as severe as those caused by P. falciparum, with fatal outcomes.
Plasmodium vivax
Pathogenesis and spectrum of disease Patients with no prior exposure to the malaria :Symptoms such as headache, photophobia, muscle aches, anorexia, nausea, and sometimes vomiting Patients with prior exposure to the malaria: the parasites can be found in the bloodstream several days before symptoms appear Coma and sudden death or other symptoms of cerebral involvement have been reported, particularly in patients with varying degrees of primaquine resistance. Patients can exhibit cerebral malaria, renal failure, circulatory collapse, severe anemia, hemoglobinuria, abnormal bleeding, acute respiratory distress syndrome, and jaundice. Acute cerebral malaria involves changes in mental status and if untreated may result in fatality within 3 days.
Plasmodium ovale
Pathogenesis and spectrum of disease Symptoms include a lower fever and a lack of typical rigors. The geographic range is usually described as being limited to tropical Africa, the Middle East, Papua New Guinea, and Irian Jaya in Indonesia P. ovale infections in Southeast Asia may cause benign and relapsing malaria in this area. In both Southeast Asia and Africa, two different types of P. ovale circulate in humans. Human infections with variant-type P. ovale are associated with a higher level of parasitemia.
Plasmodium falciparum
Pathogenesis and spectrum of disease attack occurs 8 to 12 days after infection and is characterized by 3 to 4 days of vague symptoms such as aches, pains, headache, fatigue, anorexia, or nausea. This stage is followed by fever, a more severe headache, and nausea and vomiting, with occasional severe epigastric pain. Severe or fatal complications- Blackwater fever is a complication of malaria that is a result of red blood cell lysis, releasing hemoglobin into the bloodstream and urine, causing discoloration Disseminated intravascular coagulation (DIC) is a rare complication and is seen with a high parasitemia, pulmonary edema, anemia, and cerebral and renal complications. Vascular endothelial damage from endotoxins and bound parasitized blood cells may lead to clot formation in small vessels. Cerebral malaria - Extreme fevers, 41.7°C (107°F) or higher, may occur . Without vigorous therapy, the patient usually dies
Dipylidium caninum
Pathogenesis and spectrum of disease- The flea is the intermediate host in which infective cysticercoids (larval form) develop; humans, dogs, and cats are the reservoir hosts. The adult worm develops and matures within the reservoir host. Humans usually have very mild symptoms such as indigestion, appetite loss, weight loss, perianal itching, persistent diarrhea, and vague abdominal pain. Human infection is usually self-limited.
Sarcocystis species
Pathogenesis and spectrum of disease- When humans (intermediate host) ingest oocysts from other animal stool sources, the sarcocysts that develop in human muscle are 7 to 16 mm long and cause few, if any, problems. Painful muscle swellings measuring 1 to 3 cm in diameter are associated with erythema of the overlying skin; these occur periodically and last 2 days to 2 weeks. Symptoms also include fever, diffuse myalgia, muscle tenderness, weakness, eosinophilia, and bronchospasm. Different types of skeletal and cardiac muscle sarcocysts have been found in humans. Infections in humans can manifest primarily as intestinal disease if infected meat is ingested or as muscular disease if sporocysts are ingested Laboratory diagnosis - presumptive diagnosis of intestinal disease may be based on the patient's symptoms, particularly with documented ingestion of raw or poorly cooked meat. Confirmation of the diagnosis may depend on finding human fecal specimens containing sporocysts, which are passed in the stool 11 to 18 days after ingestion of beef or pork. A muscle biopsy in a patient with a history of travel to or residence in a tropical location Results and reporting -Identification of Sarcocystis spp. is very rare. However, it is possible to differentiate the two species based on morphologic characteristics.
Blood and tissue protozoa
Plasmodium (P. falciparum, P. vivax, P. ovale, P. malariae) Toxoplasma gondii Trypanosoma cruzi Leishmania species
List the subgroups of Protozoans, Helminths and Arthropods
Protozoa - Intestinal. other sites, blood and tissue Helminths - i. Nematodes Intestinal ii. Nematodes, Tissue iii. Nematodes, Filarial iv. Cestodes, intestinal
ENTAMOEBA HISTOLYTICA
Reporting of results -the full taxonomic name of the infecting organism including genus and species as well as the life cycle stage or form present, trophozoite or cyst should be reported. Therapy- Two classes of drugs: luminal amebicides, such as paromomycin, iodoquinol, or diloxanide furoate and tissue amebicides such as metronidazole, tinidazole, or dehydroemetine Asymptomatic infection- Patients found to have true E. histolytica in the intestinal tract, even if asymptomatic, should be treated to eliminate the organisms. Both diloxanide furoate and iodoquinol or paromomycin can be used to treat cysts in the lumen of the gut. both luminal and tissue amoebicides is emphasized in patients with amoebic liver abscesses. Prevention- Humans are the reservoir host for E. histolytica, and infection can be transmitted to other humans, primates, dogs, cats, and possibly pigs. Accidental consumption of sewage contaminated water Amoebiasis is considered a zoonotic waterborne infection. The cyst stages are resistant to environmental conditions and can remain viable in the soil for 8 days at 28°C to 34°C, for 40 days at 2°C to 6°C, and for 60 days at 0°C. Proper disposal of contaminated feces is considered the most important preventive measure.
Laboratory diagnosis of Plasmodium species
Routine methods Antigen-based tests Serologic tests Molecular methods Automated instruments
Blastocystis hominis: laboratory diagnosis
Routine methods- Routine stool examinations are very effective in recovering and identifying B. hominis The permanent stained smear for identification If the fresh stool is rinsed in water before fixation (for the concentration method), B. hominis organisms, other than the cysts, are destroyed, and a false-negative report may result. Antigen detection- Fecal immunoassays to detect B. hominis antigen have been developed but are of little clinical use. Currently used-- is the enzyme-linked immunosorbent assay (ELISA). Serologic detection- ELISA and fluorescent antibody tests have been developed to detect serum antibody to B. hominis infections. Result: the presence of B. hominis should be quantitated in the report (i.e., rare, few, moderate, or many). It is not important to state the life cycle stage or form of the organism present Therapy- metronidazole (Flagyl) appears to be the most appropriate drug. TMP-SMX (trimethoprimsulfamethoxazole) and iodoquinol are also recommended with variable success. Resistance to metronidazole has been reported. Prevention- improved personal hygiene and sanitary conditions, in addition to proper disposal of fecal material.
ENTAMOEBA HISTOLYTICA: laboratory diagnosis
Routine methods-Microscopic examination of a direct saline wet mount. the most important technique for the recovery and identification of protozoan organisms is the permanent stained smear Sigmoidoscopy specimens may be very helpful for identifying organisms. Antigen detection- enzyme immunoassay reagents. Antigen screening test kits -RIDASCREEN Entamoeba and the Triage Micro Parasite Panel Histology- histologic diagnosis of amebiasis can be made when the trophozoites in the tissue are identified. Hematoxylin and eosin staining also allows visualization Molecular methods- The polymerase chain reaction assays (PCR) identify unique ribosomal ribonucleic acid (rRNA) or specific episomal (small circular nucleic acid) sequences to differentiate the organisms. Multiplex assays improve diagnostic testing : xTAG Gastrointestinal Panel Serologic detection -In patients suspected of having extraintestinal disease, serologic tests are diagnostically more effective and a valuable tool in conjunction with either antigen or nucleic acid-based testing
richomonas vaginalis
Sexual intercourse, men asymptomatic Can survive on damp towels or underclothes but transmission this way is rare Pregnancy complications, cervical cancer association, predisposition to HIV infection Trophozoite 7 - 23 µm long, 5 - 15 µm wide Axostyle protrudes through bottom of organism (see videos), undulating membrane ends halfway down Humans are the only natural host: vagina and prostate, feed on mucosal surfaces Pathogenesis and spectrum of disease Large number of trophs in tissues and secretions, inflammation Vaginal/vulval pruritis and discharge sudden, often after menstruation Odor, erythema, vaginitis, dysuria, some women asymptomatic Sometimes Dystension of fallopian tubes with pus, endometriosis, infertility, low birth weight, cervical erosion
Toxoplasma gondii
Sulfadiazine + pyrimethamine Protozoan parasite, cats are definitive host, reservoir for infection, oocysts excreted in feces Oocysts survive more than a year, resistant to disinfectant, freezing, drying Killed by heating to 70ºC for 10 minutes 3 infectious stages - tachyzoites (groups or clones), bradyzoites (in tissue cysts), and sporozoites (in ooysts from cat feces) Intramuscular cysts up to 100 µm in size, lungs, liver kidneys, more commonly in brain, eyes, skeletal and cardiac muscle Cysts persist for life of host, no inflammatory response Tachyzoites 2-3µm wide, 4-8 µm long, Giemsa - cytoplasm = blue, nucleus = red Cysts in chronic infections, contain bradyzoites, stain PAS positive
Babesia species
These blood protozoa appear as pear-shaped forms (piroplasms) in the red blood cell and use a tick as their intermediate host. Pathogenesis and spectrum of disease- Babesiosis is caused by B. microti and B. duncani or B. duncani. Mild disease resembles influenza-like illness, whereas severe disease is clinically similar to malaria, and symptoms include high fever, myalgias, malaise, fatigue, hepatosplenomegaly, and anemia Risk factors for severe disease include increasing age, splenectomy, and a compromised immune system
Toxocara canis (Visceral Larval Migrans)
Toxocara canis - intestinal ascarid of dogs
Toxocara cati (Ocular Larval Migrans)
Toxocara cati - intestinal ascarid of cats
Enterobius vermicularis (pinworm)
Transmission via food contaminated w/ eggs; intestinal infection; causes anal pruritis (the Scotch tape test) Tx: Mebendazole/pyrantel pamoate Female lays eggs around anus at night 🡪 itching, infective within hours, can auto-reinfect but otherwise asymptomatic Infections via ingestion or inhalation Epidemiology - Spread in group settings of children Pathogenesis and spectrum of disease Can migrate to other tissues 🡪 pelvic, cervical, peritoneal granulomas Single worm to thousands
Blood nematodes
Transmitted by mosquitos, midge, or fly Infect subcutaneous tissues, deep connective tissues, body cavities, and lymphatic systems, and of course can be found in the blood Infective larvae are injected into blood stream when vector feeds on human Larvae are motile and migrate to lymphatic system Female worm produces large numbers of microfilariae Depending on species, the membrane of the egg can be maintained as a sheath that is useful for ID Can remain in host for many years causing chronic, debilitating conditions and severe inflammatory responses Different species migrate via a defined circadian rhythm To ID: presence/absence of sheath, arrangement of nuclei within tail
Plasmodium malariae
What type of Plasmodium affects • Only mature RBCs? Pathogenesis and spectrum of disease Proteinuria is common in P. malariae infections and may be associated with clinical signs of nephrotic syndrome Kidney problems result from deposition within the glomeruli of circulating antigen-antibody complexes. A membrane proliferative type of glomerulonephritis is the most common lesion seen in quartan malaria Chronic glomerular disease associated with P. malariae infections is usually not reversible with therapy
Entamoeba coli
Worldwide NonPathogenic Amoeba -Amoebic Lifecycle -Mature cysts most diagnostic on permanent stains, NO ingestion of RBCs, ingestion of bacterial yeast and other debris, -Oral-Fecal transmission -Off center karyosome, random peripheral chromatin, >4 nuclei, 15-20 um, usually range 20-25um. Motility - Sluggish, nondirectional, blunt, granular pseudopodia. Often visible in unstained preparation.
Endosymbiont
a cell that lives within a host cell and soon became one with it, forming the mutually-beneficial eurkaryote instead of two separate prokaryotes. alpha-proteobacterium that lives as an endosymbiont inside of Wuchereria bancrofti, Brugia species, and Onchocerca volvulus
Flagellates (Mastigophora)
a group of protozoans that move using a whip-like organelle called a flagellum. 4 common flagellates of the intestine - Giardia duodenalis, D. fragilis, Chilomastix mesnili, Pentatrichomonas hominis.
Giardia duodenalis
a parasite found in improperly treatred water. easily spread in day care centers. fever, loose stools, ab cramps, N
Hookworms
a type of parasite. Hookworms usually enter the body through bare feet and move through the body to the small intestines where they attach themselves with a series of hooks around their mouths. Laboratory diagnosis ID of eggs of rhabditiform larvae in stool Eggs oval, thin-shelled, clearly visible 4-8-cell stage embryo Characteristic clear space between shell and embryo Rhabditiform larvae 250-300µm with long buccal capsule, inconspicuous primordial genitalia Filariform larvae about 500 µm, pointed tail, esophageal:intestinal ratio of 1:4 Must differentiate from Strongyloides stercoralis Store stool at room temp to allow eggs to hatch for differentiation Therapy - albendazole, mebendazole, iron supplementation Prevention - avoid contaminated soil and beaches, wear shoes Results and reporting - report any amount, treatment is recommended even if asymptomatic
Define Parasite terminology: Definitive host, intermediate host, endoparasite, ectoparasite
a. Definitive host: host in which the sexual reproduction of a parasite occurs b. Intermediate host: required host in the life cycle in which essential larval development must occur before a parasite is infective to its definitive host or to additional intermediate host. c. Endoparasite: parasite that lives within the body d. Ectoparasite: organism that lives on or within the skin
Describe the major divisions of parasite
a. Protozoa (amebae, flagellates, ciliates, sporozoans, coccidia, microsporidia): unicellular eukaryotic organisms most of which are microscopic b. Nematode or round worms: nonsegmented elongated, cylindrical worms with a well developed digestive tract and reproductive system also called helminths c. Platyhelminthes or flatworms (cestodes, trematodes): tape worms, have a long segmented ribbonlike body with a specialized structure for attachment or scolex at the anterior end. d. Pentastomids or tongue worms: flat worms are dorsoventrally flattened and require at least one intermediate host normally freshwater snail e. Acanthocephala or thorny headed worms f. Arthropoda ( insects, spiders, mites, ticks): small invertebrate animals
Amoebae
also called Sarcodina, type of cell or organisms with ability to alter shape, primarily by extending and retracting pseudopods (cytoplasmic protrusion)
Taenia saginata
beef tapeworm Epidemiology Cattle are the intermediate hosts, and humans are infected through the ingestion of cysticerci (larval form with an unarmed scolex) in raw or undercooked beef Pathogenesis and Spectrum of Disease - ingestion of undercooked or raw meat infected with larvae In about 3 months, the worm may grow up to 4 to 5 m in length, and gravid segments begin to break off and pass in stool intermediate bovine host may ingest the segments Humans then ingest the infected meat of the intermediate host Humans typically are asymptomatic, or have very mild indigestion, loss of appetite, vomiting, and abdominal discomfort. A rare case of severe infection may result in intestinal obstruction and appendicitis.
Naegleria fowleri
brain eating amoeba. Trophozoite (water, moist soil), cyst stages Enter nasal cavity after aspiration of water, dust, aerosols 🡪 brain via migration across olfactory nerves Does not survive in chlorinated water Troph's - amoeboid (~15 µm) or flagellate forms (7 - 35 µm) Large central karyosome, no peripheral nuclear chromatin, cytoplasm granular with vacuoles Flagellated forms don't divide by amoeboid forms can Cysts have thick double wall (7 - 15µm)
WUCHERERIA BANCROFTI
causes elephantiasis Transmitted via mosquito: Culex fatigans, Anopheles, or Aedes species Adult worm and microfilariae have sheath that stains faintly or not at all About 298 µm long by 2.5 µm wide Tail is pointed, no nuclei present Epidemiology - most common identified filarial worm in humans Tropics and subtropics Humans are definitive host Two forms with different periodicities: nocturnal found in blood between 10pm and 4am, second form only in Pacific Islands, present in blood at all times but more frequently during day and afternoon
Trypanosoma species
causes sleeping sickness General characteristics- Trypanosomal forms are ingested by the tsetse fly (Glossina spp.) when a blood meal is taken. While feeding, the fly introduces the metacyclic trypanosomal forms into the next victim in saliva injected into the puncture wound. The entire developmental cycle in the fly takes about 3 weeks, and once infected, the tsetse fly remains infected for life. In fresh blood, the trypanosomes move rapidly among the red blood cells. An undulating membrane and flagellum may be seen with slower-moving organisms. The trypomastigote forms are 14 to 33 mm long and 1.5 to 3.5 mm wide. With a blood stain, the granular cytoplasm stains pale blue. The centrally located nucleus stains reddish. At the posterior end of the organism is the kinetoplast, which also stains reddish.
Hymenolepis nana
dwarf tapeworm, most common US tapeworm, direct infection Epidemiology- generally found in children. Although it is most prevalent in the southern United States. Common in populations living in conditions of poverty or poor hygiene, in daycare centers, and in persons living in institutional settings or prisons.
intestinal nematodes
enterobius vermicularis (pinworm) ascaris lumbricoides (giant roundworm) strongyloides stercoralis (threadworm) ancylostoma duodenale necator armericanus (hook) trichinella spiralis
Diphyllobothrium latum
fish tapeworm- causes Vit B12 deficiency D. latum can be found wherever freshwater fish are eaten raw or marinated. This includes fish such as burbot, pike, perch, ruff, and salmon. In the United States, D. latum is generally found in and around the Great Lakes.
Pentatrichomonas hominis
harmless commensal in intestine
Cutaneous Larva Migrans (CLM)
hookworms of dogs and cats, AKA creeping eruption Epidemiology Eggs shed in feces of cats or dogs into sandy soil 🡪 children playing in infected sandboxes Pathogenesis and spectrum of disease Penetrate skin and migrate through subcutaneous tissue, pruritic papules, vesicular elevated linear tracks, migrate several millimeters each day 🡪 edema Peripheral eosinophilia, scratching can lead to scar tissue formation Systemic involvement rare but can cause eosinophilic enteritis Laboratory diagnosis - evidence of visible tracks and history of exposure , sometimes larva found in sputum with Charcot-Leyden crystals Therapy - ivermectin, thiabendazole
Microsporidia
microscopic protozoans that cause disease in insects Microsporidia are obligate intracellular, spore-forming parasites. More than 160 microsporidial genera and 1300 species have been identified
Clonorchis sinensis and Opisthorchis viverrine
often asymptomatic Heavy infections: fever, abdominal pain, jaundice, eosinophilia, increased serum IgE, obstruction of biliary ducts, cirrhosis, cholecystitis, and cholangiocarginoma
Trichinella spiralis
parasitic nematode occurring in the intestines of pigs and rats and human beings and producing larvae that form cysts in skeletal muscles. Epidemiology - 11 species of Trichinella Mammals are definitive host for adult and intermediate host for encysted larvae Eating undercooked meat with encysted larvae, usually pork but also bear, walrus, horsemeat, others Larvae resistant to pH of stomach 🡪 intestine, invade mucosa 🡪 migrate to lymphatic system/mesenteric venules 🡪 body tissues, preferring striated muscle 🡪 larvae eventually die, encysted capsules become calcified Pathogenesis and spectrum of disease Trichinosis - disease of the muscle (encysted larvae), intestinal stage ~1 week, diarrhea can last 14 weeks Periorbital edema, fever, muscle pain/tenderness, headache, myalgia, eosinophilia, sometimes splinter hemorrhages below fingernails Larvae can migrate to: brain (do not encyst), meninges - neurologic symptoms and myocardium - myocarditis, dysrhythmias 🡪 sudden death
Taenia solium
pork tapeworm Epidemiology- T. solium has a worldwide distribution. Higher rates of illness have been seen in Latin America. In the United States, typically among Latin American immigrants and Mexican agricultural workers. The tapeworm is more prevalent in underdeveloped communities with poor sanitation and when pork is ingested undercooked or raw.
Parastrongylus cantonensis -
rat lung worm Epidemiolgy Worldwide, endemic in Southeast Asia and Asian Pacific Islands, rodents are definitive host, infective larvae passed in feces Humans infected by ingestion of intermediate or paratenic host Pathogenesis and spectrum of disease Worm burden dictates severity May migrate to CNS causing meningitis or meningoencephalitis: headache, fever, eosinophilia, increased CSF protein, neurologic manifestations Migrate to eye 🡪 blindness Disease often self-limiting Laboratory diagnosis - histologic ID of adult female, spiral, winding "barber pole" appearance of uterus Serologic tests available Therapy - mebendazole May make inflammatory response worse 🡪 more systemic damage If found in eye surgical removal is needed
Hymenolepis diminuta
rat tapeworm Epidemiology- H. diminuta is an uncommon tapeworm in humans and is typically found in rodents including rats and mice. H. diminuta can infect humans after contamination of grains and flours with rodent feces. Pathogenesis and spectrum of disease-H. diminuta rarely infects humans but may do so if a human accidentally ingests an arthropod infected with cysticercoids. Symptoms may include diarrhea, anorexia, nausea, headache, and dizziness. The infection is more common in children, causing mild diarrhea, remittent fever, and abdominal pain.
ONCHOCERCA VOLVULUS
river blindness Lives in tissue nodules in host Microfilariae ~330 µm long by 5-9 µm wide Epidemiology Africa, Central America, and South America Transmitted by bite of black fly Pathogenesis and spectrum of disease Onchocerciasis - AKA river blindness Subcutaneous infection localized to skin, lymph nodes, and eyes Pruritis, edema, and erythema Hypopigmentation or hyperpigmentation Enlargement of lymph node in groin area 🡪 'hanging groin" 🡪 hernia Heavy infections can have organism in eyes 🡪 blindness, increased risk of death
Fasciola
sheep liver fluke Fever, abdominal pain, nausea, diarrhea, enlargement/tenderness of liver, jaundice, nonproductive cough, eosinophilia, and elevated IgE Severe infections - biliary duct obstruction, cirrhosis, cholecystitis, and cholangiocarcinoma Larve can migrate and penetrate peritoneal cavity Adult flukes can be found in intestinal walls, lungs, heart, or brain
Endolimax nana
smallest of the amoebas 6-12um, usually range 8 - 10um. Sluggish, non progressive motility, bacterial inclusion present. Epidemiology - Transmission occurs through the ingestion of mature cysts from contaminated food or water. E. nana is also found in warm, moist climates and in other areas with a low standard of personal hygiene and poor sanitary conditions. Pathogenesis and spectrum of disease- E. nana is considered nonpathogenic and does not cause disease Laboratory diagnosis- definitive identification of E. nana relies on examination of permanent stained smears.
Strongyloides stercoralis
threadworm Epidemiology - endemic in tropical and subtropics AKA threadworm, lives in intestine or free living in environment Filariform larvae (infective) penetrate skin and migrate to heart and lungs through bloodstream Swims up bronchial tree, swallowed 🡪 digestive tract for maturation Autoinfection through penetration of intestinal mucosa Females use asexual reproduction (there are no males) Rhabditiform larvae (noninfective) when free-living, males and females present but can change into infective filariform larvae at any time Direct penetration of skin, person-person transmission in institution
Spirometra mansonoides
zipper tapeworm Epidemiology- Spirometra is found worldwide; most human cases of sparganosis are found in Asia. Sparganosis is endemic in animals throughout North America but rare in humans Adult Spirometra live in the intestine of dogs and cats Eggs are shed in feces, hatch in water, and release free-swimming ciliated coracidia. Humans are accidental hosts; they acquire sparganosis after ingestion of contaminated water or by consuming undercooked fish Spargana can live up to 20 years in the human host.
Sporozoa (Apicomplexa)
• Non-motile protozoa; Obligate intracellular parasites; All have complex life cycles, usually involving one or 2 species which serve as vectors (carriers); Undergo both sexual and asexual reproduction
