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MSII Micro Unit 6 > Parasites > Flashcards

Parasites Flashcards

1
Q

Some characteristics of parasitic diseases

A

-high prevalence in developing countries; in lower socioeconomic population -low morality and morbidity -limited drug-development -no vaccines

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2
Q

Why Don’t North Americans suffer from parasites

A
  • high standards of education- better housing, higher standard of living -general good health- poor health=more susceptible to disease
  • nutrition= adequate diet
  • sanitation- sewers and septic systems keep raw sewage out of streams
  • temperate climate- parasites do better in the warmth of the tropics
  • absence of certain vectors
  • intermediate hosts such as the tsetse fly, certain snails, etc
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3
Q

Ectoparasite

A

-Parasite which lives on the outside of the host (infestation)

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4
Q

Endoparasite

A

-parasite which lives within the body of the host

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5
Q

Direct Life Cycle

A

-only humans are host -infective stage like ovum, cyst, larva passed out of the body that infects another healthy person -example: E. histolytica, Giardia, Ascaris lumbricoides

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6
Q

Indirect Life Cycle

A

-multiple hosts or involvement of vector - definitive host, intermediate host -example: Taenia solium (pork tapeworm), Malaria

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7
Q

Importance of Vectors in Parasitic Diseases

A

-the geographic distribution and occurrence of many parasitic disease is directly related to the distribution of various vectors that are responsible for the transmission of the parasite and the distribution of secondary or intermediate hosts -Mosquito, Sand-fly, Tick-bone

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8
Q

Parasite Classification

A
  • 3200 varieties of parasites in two major categories
  • Parasitic Protozoa- Unicellular: Ameba- like Entamoeba Flagellates- like Giardia, Leishmania Ciliates
  • Balantidium Sporozoa- like Plasmodium, Cryptosporidium
  • Parasitic Helminths- Multicellular Nematodes (roundworms)- like Ascaris, Pinworm

Cestodes (flatworms/tapeworms)- like Taenia solium (pork), Taenia saginata (beef) Trematodes (flukes)

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9
Q

Blood borne parasites

A

-malaria -babesia -trypanosomes -leishmania -filarial infections

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10
Q

Global impact of malaria

A

-50 million cases per year -1-3 million deaths per year -reasons: increased global travel, drug resistance by the parasite, Plasmodium falciparum has replaced P. vivax as the main type of malaria in much of Africa -Malaria control efforts have decayed- India had a few as 700,000 cases of malaria at its low point a couple of decades ago, Recently about 50 million cases occurred per year

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11
Q

Causes of Malaria

A
  • the single cell protozoan that causes malaria derives from the genus Plasmodium
  • human malaria is caused by either: P. falciparum, P. vivax, P. ovale, and P. malaria
  • P. falciparum is by far the most lethal of the strains, causes the most deaths
  • P. vivax is the most common strain, cause of large percentage of cases in the US
  • malaria parasites are transmitted to humans through the bite of an infected female mosquito of the genus Anopheles
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12
Q

Distribution of Plasmodium Species

A
  • 104 malaria-endemic countries
  • P. vivax: all malarious areas except sub- Saharan Africa
  • P. malariae: all malarious areas, but spotty
  • P. ovale: tropical areas of western Africa; occasionally, western Pacific and Southeast Asia
  • P. falciparum: predominates in sub-Saharan Africa, but also occurs in Southeast Asia, Southeast Asia, South
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13
Q

Genetic and Immunological Protection

A
  • the absence of Duffy antigen in RBC, predominates in West Africans, prevents P. vivax malaria -patients with hereditary elliptocytosis, in those with glycophorin C deficiency (Leach phenotype) as well as in those who are heterozygous for sickle cell disease are less susceptible to infection
  • certain thalassaemias or glucose-6-phosphate dehydrogenase deficiency offer a degree of protection
  • untreaated infected patients eventually develop curative immunity against the parasitizing strain
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14
Q

Hemoglobin Variants

A

-a number of genes, including those for sickle hemoglobin S and C, the thalassemias provide protection against malaria infection -Hemoglobin C (HbC) is one of the commonest structural hemoglobin variants in human populations

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15
Q

Duffy Antigen Negativity

A
  • duffy antigen is the erythrocyte receptor for P. vivax merozoite invasion
  • erythrocytes lacking Duffy antigen are resistant to P. vivax invasion, which accounts for the extremely low incidence of vivax malaria in West Africa, where Duffy antigen negativity is highly prevalent
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16
Q

Life Cycle of the Malarial Parasite

A
  • sporozoites in salivary gland -oocysts in stomach wall
  • male and female gametocytes
  • liver phase -release of merozoites from liver- these enter red cells where both sexual and asexual cycles continue
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17
Q

Malaria Symptoms

A
  • the time from the initial malaria infection until symptoms appear (incubation period) generally ranges from: 9-14 days for Plasmodium falciparum 12-18 days for P. vivax and P. oval 19 to 40 days for P. malariae 11 to 12 days for P. knowlesi
  • symptoms can appear in 7 days. Sometimes, the time between exposure and signs of illness may be as long as 8 to 10 months with P. vivax and P. ovale
  • in early stages, malaria symptoms are sometimes simlar to those of many other infections caused by bacteria, viruses, or parasites (fever, chills, headache, sweats, fatigue, nausea and vomiting
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18
Q

Stages of malaria paroxysm

A
  • the malarial paroxysm will usually last 4-8 hrs and begins with a sudden onset of chills in which the pt experiences an intense feeling of cold despite having an elevated temp- cold stage- intense shivering
  • immediately following cold stage is the host stage- the pt feels an intense heat accompanied by severe headache. Fatigue, dizziness, anorexia, myalgia, and nausea
  • next a period of profuse sweating will ensue and the fever will start to decline. The patient is exhausted, will sleep
  • this will cycle
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19
Q

Plasmodium falciparum

A
  • a much more acute and severe than malaria caused by other Plasmodium species
  • almost all deaths directly attributable to malaria are caused by severe manifestations of P. falciparum infection, including cerebral malaria,severe anemia, respiratory failure, renal failure, and severe malaria of pregnancy
  • an important feature of the pathogenesis of P. falciparum its ability to sequester in the deep venous microvasculature
  • P. falciparum is the only one that can infect all cells- young and old- organ damage in kidneys, liver, brain, GI tract
  • cerebral malaria in particular can lead to coma and convulsions
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20
Q

Malaria of Pregnancy

A
  • placental colonization by infected RBCs results in maternal morbidity and mortality, intrauterine growths retardation, premature delivery, low birth weight, and increased newborn mortality
  • selective accumulation of mature parasites in the placenta appears to involve their interaction with syncytoitrphoblastic chondroitin sulfate A (CSA), hyaluronic acid and immunoglobulins
  • this is in contrast to the sequestration of infected erythrocytes in the systemic microvasculature, where CD36 is the major endothelial receptor
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21
Q

Mosquirix Vaccine

A
  • a completely effective vaccine is not yet available for malaria, although several vaccines are under development
  • the RTS, S/ASO1 is in phase III clinical trials
  • targets an outer membrane protein of the early blood phase of P. falciparium
  • initial results found it efficent against severe malaria 6 mon-2 years 34% -initial trial vaccine 50% efficacy in first 3-4 months
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22
Q

Babesia

A
  • world-wide distribution
  • multiple species involved with infecting humans
  • transmitted by a large variety of ticks
  • B. microti most common in US however, additional species- Midwestern US
  • Clinical Disease- infections acquired in the Northeast US clinically present with a similar picture of P. vivax
  • individuals infected in the Midwest and West coast present with a fulminate, febrile, hemolytic disease
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23
Q

Life cycle of Babesia

A
  • in the mouse there is a sporozoites they then go between Trophozoite and Merozoite and then gamete
  • the tick takes a blood meal and sporozoites introduced into host and ingests gametes, there is then fertilization in get, then ookinete enters salivary gland and then sporogony and sporozoties which then transfer into human or dog after blood meal
  • then the sporozoites infect RBCs -then trophozoite and merozoite and transmitted from human to human via blood transfusion
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24
Q

Distribution of Lyme Disease and Babesia

A
  • the prevalence and distribution of Lyme disease (Borrelia burgdorferi) and Babesia are the same
  • the transmission vector for both diseases are the same
  • the blacklegged tick or deer tick spreads the disease in the north eastern, mid-Atlantic, and north-central US, and the western blacklegged tick spreads the disease on the Pacific Coast
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25
Q

Babesia Infection

A
  • more than 100 species of Babesia have been reported to infect vertebrates, including mammals and birds
  • because Babesia is an obligate parasite of erythrocytes, the pathogenesis of babesiosis results, in part, from the modification and rupture of these host cells by the pathogen -asynchronous replication of Babesia explains the lack of periodicity in parasitemia and associated symptoms -because erythropoiesis is increased, severe anemia despite low level parasitemia is best explained by the clearance of nonparasitized erythrocytes
  • clinically Babesia infection is characterized by the presence of hemolytic anemia and nonspecific flu-like symptoms (fever, chills, body aches, weakness, fatigue). Some patients have splenomegaly, hepatomegaly, or jaundice
26
Q

Anaplasma phagocytophilum (Human Granulocytotropic Anaplasmosis)

A
  • 92% of cases are reported from southern New england, NY, NJ, Wisconsin, and Minnesota -the distribution is almost identical to that of Lyme disease because of the shared Ixodes spp. tick vectors
  • between 4% and 36% of patients with serologic evidence of A. phagocytophilum infection also have serologic evidence of Borrelia burgdorferi or Babesia microti infection
  • a major proven reservoir host is the white-footed mouse, Peromyscus leucopus; however, other small mammals, such as sciurids (squirrels) in the western US and ruminants have been found naturally infected or have serologic evidence of infection
27
Q

Anaplasmosis

A

-the first symptoms of anaplasmosis typically begin with 1-2 weeks after the bite of an infected tick (fever, headache, muscle pain, malaise, chills, nausea/abdominal pain, cough, confusion -anaplasmosis can be a serious illness that can be fatal if not treated correctly, even in previously healthy people. Severe clinical presentations may include difficulty breathing, hemorrhage, renal failure or neurological problems

28
Q

Chagas Disease (American Trypanosomiasis)

A

-caused by the parasite Trypanosoma cruzi which is transmitted to animals and people by insect vectors and is found only in the Americas (mainly, in rural areas of Latin America where poverty is widespread). Chagas disease (T. cruzi infection) is also referred to as American trypanosomiasis -the parasite is transmitted by various species of bloodsucking triatomine insects or kissing bugs

29
Q

Trypanosome Infections

A

-American trypanosomiasis-

Trypanosome cruzi- most frequent in the US

  • predominately seen in Mexico but cases observed in Southern to Middle Texas region
  • recently reported in Southern California- differences observed in contact time of the Reduvid bug (required up to 1 hour)
  • two forms of disease: acute- death within a few weeks, chronic- symptoms may not present until 5-15 years later
  • generally notice some swelling under one eye
30
Q

Leishmaniasis

A
  • a vector-borne disease that is transmitted by sandflies and caused by obligate intracellular protozoa of the genus Leishmania. Human infection is caused by about 21 of 30 species that infect mammals
  • infective stage transmitted by the sand fly by regurgitation with multiplication occuring in the histiocytes
  • Leishmaniasis is a highly focal disease with widely scattered foci. The parasite may survive for decades in asymptomatic infected people, who are of great importance for the transmission since they can spread visceral leishmaniasis indirectly through the sandflies
31
Q

Leishmania Lifecycle

A
  • the Leishmania parasite is spread by certain species of tiny blood feeding sand flies
  • a sand fly becomes a host for the Leishmania parasite when it takes a blood meal from an already infected organism
32
Q

Lesihmaniasis Clinical Manifestations

A
  • in cutaneous lesihmaniasis chronic skin ulcers occur commonly. Certain Leishmania species may cause lesions to occur at sites other than where the initial bite occured
  • in mucocutaneous leishmaniasis there is the metastatic spread of primary lesions to the mouth, nose, pharynx where the destruction of the mucosa occurs, this may be accompanied by secondary bacterial infection
  • in visceral lesihmaniasis there is often fever, weight loss, anorexia, splenomegaly and hepatomegaly
33
Q

Gastrointestinal Parasitic Disease

A
  • parasites found in the human GI tract can be largely categorized into two groups, protozoa (single celled) and helminths (multicelled)
  • parasitic infections, caused by intestinal helminths, and protoxoan parasites are among the most prevalent infections in humans in developing countries
  • in developed countries, protozoan parasites more commonly cause GI infections compared to helminths
  • intestinal parasites cause a significant morbidity and mortality in endemic countries
  • estimates suggest that as much as 90% of certain populations have one or more GI parasites
  • intestinal parasites that remain prevalent in the US include Enterobius vermicularis, Giardia lamblia, Ancylostoma duodenale, Necator americanus, and Entamoeba histolytica, and Cryptosporidium parvum
34
Q

Entamoeva species

A
  • some species are pseudopod forming
  • species include: E histolytica and E. dispar
  • E harmanni
  • E polecki
  • E coli
  • E gingivalis
35
Q

E histolytica

A
  • spreading occurs via the fecal-oral route, usually by poor hygiene during food preparation or by the use of night soil, and oral-anal sexual practices
  • crowding and poor sanitation contribute to its prevalence in Asia, Africa, and Latin America
  • approximately 10% of world pop infected, 90% asymptomatic -50 million symptomatic cases, 100,000 fatal
  • the stable reservoir of infective cause complicates eradication -after malaria, it is likely that E. histolytica is the world’s second leading protozoan cause of death
36
Q

Life cycle Entamoeba histolytica

A

-the life cycle of Entamoeba histolytica involves trophozoites (the feeding state of parasites) that live in the host’s large intestine and cysts that are passed in the host’s feces

37
Q

Amebiasis and E. histolytica

A
  • amebiasis can cause both intraluminal and disseminated disease
  • in the intestinal lumen, E. histolytica can disrupt the protective mucus layer overlying the colonic mucosa
  • the resulting epithelial ulcerations can bleed and cause colitis, usually two to six weeks after initial infection. Acute progression to malaise, weight loss, severe abdominal pain, profuse bloody diarrhea, and fever can occur
  • trophozoites that penetrate the intestinal wall spread through the body via the portal circulation
  • amebic liver abscesses form because of toxin release and hepatocyte damage, and usually develop within five months after infections. Abscesses may rupture into the pleural space, peritoneum, or pericardium
38
Q

Hepatic Disease Due to E. histolytica

A
  • infection may result in hematogenous spread of the organisms from the submucosa to the liver via the portal system, resulting in amebic abscesses of the liver
  • occurs in up to 5% of patients who have symptomatic intestinal amebiasis
  • the abscess can be visualized radiologically, sonically or by radionuclear scan and the majority of patients have a single abscess in the right lobe of the liver
  • the most common complication is rupture of the abscess into the pleural space
  • presents with fever, RUQ or epigastric pain and/or shoulder pain, rarely diarrhea
39
Q

Giardia lamblia

A
  • Giardiasis is a zoonosis, and corss-infectivity among beaver, cattle, dogs, rodents, and bighorn sheep ensures a constant reservoir
  • Giardiasis is one of the common causes of travelers’ diarrhea and is worldwide in distribution
  • Giardia is arguably the most common parasite infection of humans worldwide, and the second most common in the US after pinworm
40
Q

Giardia Transmission

A
  • in the US, giardiasis is one of the most common parasitic infections
  • many cases of travelers diarrhea are caused by this
  • transmission may occur directly between children or sex partners or indirectly through contaminated food or water
  • the cysts are hardy, can survive several months in cold water
41
Q

Clinical Presentation of Giardia

A

-acquisition of the parasite requires oral ingestion of Giardia cysts -after the ingestion of G. lamblia cysts, there is an incubation period of 1 to 2 weeks before the onset of symptoms -symptomatic giardiasis is characterized by the acute onset of diarrhea, abdominal cramps, bloating, and flatulence -the patient usually expresses feelings of malaise, nausea, and anorexia and may complain of sulfuric belching. Vomiting, fever, and tenesmus occur less commonly -initally, stools may be profuse and watery, but later they are commonly greasy and foul smelling and may float

42
Q

Cryptosporidium parvum

A
  • since the first reports of human cases in 1976, cryptosporidium has been found worldwide
  • outbreaks of crytosporidiosis have been reported in several countries, the most remarkable being a waterborne outbreak in Milwaukee in 1993
  • watery diarrhea is the most frequent symptom, and can be accompanied by dehydration, weight loss, abdominal pain, fever, nausea and vomiting
  • in immunocompetent persons, symptoms are usually short lived (1-2 weeks); they can be chronic and more severe in immunocompromised patients, especially those with CD4 counts
43
Q

Crytosporidiosis

A
  • mean incubation period between infection and onset of symptoms is approximately 7-14 days
  • the severity and duration of illness varies depending on the immune status of the hosts
  • in immunocompetent patients, cryptosporidia cause a self-limiting, usually watery, diarrhea lasting 10-14 days but the clinical presentation varies from asymptomatic shedding of oocysts to severe disease that may last up to 3 months
  • in immunocompromised patients, particularly individuals with HIV infection, cryptosporidiosis is a more severe, often chronic and incurable illness that can be life-threatening
44
Q

Trichomonas vaginalis

A
  • infection with T. vaginalis is acquired primarily through sexual intercourse
  • T. vaginalis is site specific and usually cannot survive outside the urogenital system
  • after introduction, proliferation begins, with resulting inflammation and large numbers of trophozoites in the tissues and the secretions
45
Q

T. vaginalis infection

A
  • the infection in men is generally asymptomatic, but 25-50% of infected women exhibit symptoms, which include dysuria, vaginal itching and burning and in severe infections, a foamy, yellowish-green discharge with foul odor
  • in many women the infection becomes symptomatic and chronic, with periods of relief in response to therapy -recurrences of infection and disease may be caused by reinfection from an asymptomatic sexual partner or by failure of the drug metronidazole to eliminate the parasite completely -symptomatic infections in men are rarely reported but include prostatitis, urethritis, epididymitis and urethral stricture
46
Q

Major Intestinal Nematodes-

A
  • Ascaris lumbricoides
  • Trichuris trichirura (whipworm)
  • Necator americanus, Ancylostoma duodenale (hookworm) -Strongyloides stercoralis
  • Enterobius vermincularis (pinworm)
47
Q

Ascariasis

A
  • ascaris lumbricoides is the most common helminthic infection of humans, infecting more than 1/2 of worlds population
  • the white or pinkish adult worms (15-35 cm) live and mate in the lumen of the small intestine, primarily the jejunum
  • each female worm has a daily output of 200,000 ova or more -eggs embryonate and become infective only on soil in warm, humid environments
  • heavy infections can also cause intestinal ostruction, intussusception, volvulus, blockage of the bile ducts and cholangitis and intestinal perforation
48
Q

Ascaris Lifecycle

A
  • the eggs pass in the feces and embryonate in the soil in 10-14 days
  • upon ingestion the egg hatches in the intestine and the liberated larva penetrates the mucosa and passes to the liver via the portal vessels and then to the lungs
  • after a few weeks the larva penetrates the alveolar air sac, passes up the pulmonary tree, is coughed up and swallowed
  • the worms become sexually mature in the small intestines and produce eggs in 60-75 days
49
Q

Trichuriasis

A

-found in humid tropical environments and temperate zones, including the southeastern US during warm and humid months -most infected people harbor fewer than 20 worms, but a small proportion, usually children in the 5- to 15- year age group, harbor more than 200 worms -also called the human whipworm

50
Q

Trichuria Lifecycle and Clinical Manifestations

A
  • infection results in the ingestion of eggs from soil
  • most persons with trichuriasis have no symptoms or only peripheral blood eosinophilia
  • in persons with heavy infections, the mucosa is inflammed, edematous and friable
  • heavy infections, especially in small children, can cause GI problems (abdominal pain, diarrhea, rectal prolapse) and possibly growth retardation
51
Q

Hookworm (Ankylostomiasis)

A
  • the human hookworms include two nematode (roundworm) species: ancylostoma duodenale, necator americanus
  • human infection with the two species of hookworm, Ancylostoma duodenale and Necator americanus, is estimated to affect approximately 1/4 of worlds population
  • a low prevalence of the infection still exists in pockets of the SE US
52
Q

Hookworm Lifecycle

A
  • eggs are passed in the stool and with moisture, warmth, shade the larvae hatch in 1 to 2 days
  • the released rhabditiform larvae grow in the feces and/or the soil, and after 5-10 days and two molts they become filariform (third-stage) larvae that are infective
  • on contact with the human host, the larvae penetrate the skin and are carried through the veins to the heart and then to the lungs
  • they penetrate into the pulmonary alveoil, ascent the bronchial tree to the pharynx, and are swallowed
  • the larvae reach the small intestine where they reside and mature into adults
53
Q

Hookwork Clinical Manifestations

A
  • most persons harbor light infections and are asymptomatic -person infected with adult hookworms may experience chronic abdominal pain and persistent eosinophilia
  • the major manifestations of hookworm disease are iron-deficiency anemia and protein energy malnutrition resulting from blood loss
  • the development of anemia depends on the intensity and duration of the infection, the infecting species of worm, and iron stores, intake and requirements
  • blood loss is gradual, allowing the body to adapt to chronic anemic state. Feature of hookworm-induced anemia include microcytic/hypochromic erythrocytes
54
Q

Enterobius vermicularis

A
  • enterobius vermicularis, or pinworm, is highly prevalent throughout the world (mostly temperate)
  • most common helminthic infection in US -pinworm infection is particularly common among children, institutionalized groups, and households; it is not associated with any specific socioeconomic level
  • most pinworm infections are asymptomatic
  • when present, symptoms are related largely to perianal and perineal pruritus and scratching
  • perianal pruritus, especially at night, may lead to excoriations and bacterial superinfection
  • occasionally, invasion of the female genital tract with vulvovaginitis and pelvic or peritoneal granulomas can occur -other symptoms include anorexia, irritability and abdominal pain
55
Q

Pinworm Lifecycle

A
  • gravid females migrate nocturnally outside the anus and oviposit while crawling on the skin of the perianal area
  • the larvae contained inside the eggs develop (the eggs become infective) in 4 to 6 hours under optimal conditions
  • retroinfection, or the migration of newly hatched larvae from the anal skin back into the rectrum, unknown how often this occurs -self-infection occurs by transferring infective eggs to the mouth with hands that have scratched the perianal area
56
Q

Human tapeworm infections

A
  • human taeniasis is a parasitic infection caused by T. saginata (known as beef tapeworm) or T. solium (pork tapeworm) -humans are the only hosts for these Taenia tapeworms. Humans pass the tapeworm segments and/or eggs in feces and contaiminate soil
  • cows and pigs become infected after feeding in areas that are contaiminated with Taenia eggs from human feces
  • once inside the cow or pig, the Taenia eggs hatch in the animal’s intestine and migrate to striated muscle to develop into cysticerci, causing a disease known as cysticercosis
  • humans become infected with tapeworms when they eat raw or undercooked beef or pork containing infective cystericerci
57
Q

Taenia saginata (beef) and Taenia solium (pork)

A
  • eggs of T. saginata and T. solium are ingested by bovids and swine and the larval or cysticercus stages develop in muscles -when the meat is eated insufficiently cooked the cysticerci are released and develop into the adults in the small intestine -most people with tapeworm infections have no symptoms or mild symptoms -patients with T. saginata have more symptoms because they are bigger- up to 10 meters, T. solium is usually 3 m
  • can cause digestive problems including abdominal pain, loss of appetite, weight loss, and upset stomach
  • active passing of proglottids (tapeworm segments) through anus and in the feces
58
Q

Taenia saginata- Beef Tapeworm

A
  • trasmitted to humans in the form of infectious larval cysts found in the meat of cattle
  • the T. saginata tapeworm is common in cattle-breeding areas of the world- also hosts can be Llamas, buffalo, and giraffes -comsuption of measly (cyst infected) uncooked or undercooked beef- rare streak or kebabs and steak tartare are dishes typically associated with T. saginata infection
  • in the definitive human host, adult T. saginata tapeworms are large (10 m) and can contain more than 1000 proglottids
59
Q

Taenia solium- the pork tapeworm

A
  • humans can serve as either intermediate or definitive hosts for T. solium
  • individuals who ingest T. solium eggs develop tissue infection with parasite cysts, a condition known as cysticercosis
  • some patients harbor both cysticerci and T. solium tapeworms, and it is possible for tapeworm-carrying individual to develop cysticercosis by autoinfection
  • areas in which T. solium infection is endemic include Mexico, Central America, South America, Southeast Asia, India, the Philippines, and southern Europe
60
Q

Cysticercosis

A
  • cystercosis is a tissue infection with larval cysts of the cestode T. solium in which the patient serves as an intermediate host for the parasite
  • infected subjects normally harbor multiples cysts in many parts of the body
  • neurocysticercosis is the term used for human CNS involvement with T. solium cysts
  • infection may involve any part of the CNS, but symptomatic disease is most often related to intracerebral lesions (causing mass effects, seizure, or both)
  • the symtpoms are due to obstruction of CSF or local meningeal irritation which leads to injury to local blood vessels, cranial nerves or the brain stem
61
Q

Diphyllobothrium latum- Fish Tapeworm

A

-human infection with D. latum is acquired by eating uncooked freshwater fish containing the parasite’s cysts- sushi and sashimi -takes 3-6 weeks after exposure for the tapeworm to mature. Once established parasite may survive 30 years or more

MSII Micro Unit 6 (8 decks)

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