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Flashcards in Parasitic Diseases Deck (113)
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1
Q

Epidemiology of parasitic diseases?

A
  • majority occur in tropical regions, where there is poverty, poor sanitation and personal hygiene
  • often entire communities may be infected with multiple, different organisms which remain untx b/c tx isn’t accessible
2
Q

Epidemiology of parasitic diseases?

A
  • majority occur in tropical regions, where there is poverty, poor sanitation and personal hygiene
  • often entire communities may be infected with multiple, different organisms which remain untx b/c tx isn’t accessible
3
Q

What does effective prevention and control of parasitic diseases require?

A
  • “mass intervention strategies” and intense community education. Examples include:
  • general improved sanitation: pit latrines, fresh water wells, piped water
  • vector control: insecticide impregnated bed nets, spraying of houses with residual insecticides, drainage, and landfill
  • mass screening and drug administration programs which may need to be repeated at regular intervals
4
Q

What are parasites?

A
  • organisms that infect and cause disease in other animals: protozoa, helminths, and arthropods
5
Q

How are protozoa transmitted?

A
  • can be passed directly from host -> host through sexual contact, by contaminated water, or through arthropod vector.
  • Direct or indirect transmission results from ingestion of highly resistant spores that are shed in feces of infected host
  • most are mobile by means of flagella, cilia or ameboid motion
6
Q

How are helminths transmitted?

A
  • wormlike parasites
  • transmission occurs primarily through ingestion of fertilized eggs or the penetration of the infectious larval stages through the skin
  • infections can involve many organs: liver, lungs, urinary and intestinal tract, circulatory, and nervous systems, and muscles
    3 main groups:
  • flatworms (platyhelminths)
  • thorny-headed worms (acanthocephalins)
  • roundworms (nematodes)
7
Q

What are the most common arthropods?

A

flies, fleas, ticks, mosquitoes, and lice

- transmission from arthropod to human occurs either mechanically or biologically

8
Q

Effects of parasitic infections?

A
  • typically, a parasitic infection doesn’t directly kill a host
  • the stress placed on the host’s resources can affect its growth, ability to reproduce and survival
  • This stress can sometimes lead to host’s premature death
9
Q

Pathogenesis of parasitic infection?

A
  • organisms attack a host and begin to multiply
  • multiplies and increasingly interferes with the normal life functions of the host
  • Host begins to feel ill as a sx of parasite’s invasion and activities
  • In many cases, the host’s immune system may be able to respond to the parasite and destroy it (immunocompetent person)
10
Q

What is unique about parasites?

A
  • complex life cycles
  • may spend part of their life cycle in a variety of differential species hosts
  • Host species may be animal (all types), insect, or other
  • May live only in water, or on veggies (grass, and soil)
11
Q

What does effective prevention and control of parasitic diseases require?

A
  • “mass intervention strategies” and intense community education. Examples include:
  • general improved sanitation: pit latrines, fresh water wells, piped water
  • vector control: insecticide impregnated bed nets, spraying of houses with residual insecticides, drainage, and landfill
  • mass screening and drug administration programs which may need to be repeated at regular intervals
12
Q

What are parasites?

A
  • organisms that infect and cause disease in other animals: protozoa, helminths, and arthropods
13
Q

How are protozoa transmitted?

A
  • can be passed directly from host -> host through sexual contact, by contaminated water, or through arthropod vector.
  • Direct or indirect transmission results from ingestion of highly resistant spores that are shed in feces of infected host
  • most are mobile by means of flagella, cilia or ameboid motion
14
Q

How are helminths transmitted?

A
  • wormlike parasites
  • transmission occurs primarily through ingestion of fertilized eggs or the penetration of the infectious larval stages through the skin
  • infections can involve many organs: liver, lungs, urinary and intestinal tract, circulatory, and nervous systems, and muscles
    3 main groups:
  • flatworms (platyhelminths)
  • thorny-headed worms (acanthocephalins)
  • roundworms (nematodes)
15
Q

What are the most common arthropods?

A

flies, fleas, ticks, mosquitoes, and lice

- transmission from arthropod to human occurs either mechanically or biologically

16
Q

Effects of parasitic infections?

A
  • typically, a parasitic infection doesn’t directly kill a host
  • the stress placed on the host’s resources can affect its growth, ability to reproduce and survival
  • This stress can sometimes lead to host’s premature death
17
Q

Pathogenesis of parasitic infection?

A
  • organisms attack a host and begin to multiply
  • multiplies and increasingly interferes with the normal life functions of the host
  • Host begins to feel ill as a sx of parasite’s invasion and activities
  • In many cases, the host’s immune system may be able to respond to the parasite and destroy it (immunocompetent person)
18
Q

What is unique about parasites?

A
  • complex life cycles
  • may spend part of their life cycle in a variety of differential species hosts
  • Host species may be animal (all types), insect, or other
  • May live only in water, or on veggies (grass, and soil)
19
Q

Protozoa species?

A
  • Sarcodina (amebas)
  • Sporozoa ( non- motile sporozoans)
  • Mastigophora (flagellates)
  • Ciliata (ciliates)
20
Q

Metazoa (helminth) species?

A
  • flatworms (platyhelminthes): flukes (Trematoda), and tapeworms (Cestoda)
  • roundworms (nemathelminthes)
21
Q

What are protozoa and what kind of disease state do they cause?

A
  • single cell (unicellular) organisms
  • historically been the cause of more disease and death than any other category of disease-causing organisms:
  • Malaria
  • African sleeping sickness
22
Q

What is a trophozoite?

A
  • term for the live adult protozoa
  • cysts, spore or “eggs” are non-adult forms
  • Most of these diseases are spread by the fecal-oral route
23
Q

What is the cause of Giardiasis?

A
  • Giardia lamblia, a flagellate, is a common pathogenic protozoan
  • infects duodenum and jejunum of humans
24
Q

Epidemiology of Giardiasis?

A
  • occurs worldwide
  • humans are infected by ingestion of fecally contaminated water or food containing giardia cysts
  • it is also spread by direct person-person contact, which has caused outbreaks in institutions such as day care centers
  • Oral-fecal transmission
    At high risk: infants, kids
    ->especially internationally adopted kids
25
Q

How long can Giardia lambda cysts survive in water?

How are humans infected?

A

up to 3 months

  • outbreaks among campers in wilderness areas suggest that humans may be infected with guard harbored by rodents, deer, cattle, sheep, horses, or household pets
  • life cycle: 2 forms: cysts: infectious form, and trophozoites: mature form
  • localize to the small bowel, adhere and once they get back into cyst form -> go into stool
26
Q

What will a biopsy of small bowel show?

A
  • parasites attach to the bowel wall and may cause irritation and low-grade inflammation of duodenal or jejunal mucosa so a bx of the small bowel will show:
  • crypt hypertrophy
  • villous atrophy or flattening
  • epithelial cell damage
27
Q

Sx forms of giardiasis?

A
  • a large portion of infected pts are asymptomatic but sx forms are:
    1. acute diarrhea
    2. chronic diarrhea
    3. malabsorption syndrome
28
Q

Presenting sxs of Giardiasis?

A
  • presenting sxs can be diarrhea, malaise, steatorrhea, abdominal cramps, bloating, flatulence, N/V, and wt loss
  • pts with chronic infection often experience major wt loss, malabsorption and depression
  • the stools may be watery, semisolid, greasy, bulky, and foul-smelling at various times during the course of the infection
29
Q

Giardiasis encystment?

A
  • as the parasites pass into the colon they typically encyst
  • cysts are found in the stool
  • > often in enormous numbers
30
Q

Work up of Giardiasis?

A
  • stool sample-fecal smear: this is to look for ova and parasites, The dx depends upon finding the distinctive cysts in formed stools, or cysts or the protozoa in liquid stools. A series of 3 or more stool exams on alt. days is therefore recommended
  • stool enzyme-linked immunosorbent assay (ELISA) has been shown to be both a specific and sensitive rapid dx tool
  • Exam of duodenal contents: may be necessary to establish the dx, as cyst production may be sporadic and not found in the stool by an ovum and parasite fecal smear examination
31
Q

Giardiasis tx?

A

metronidazole (Flagyl): 250 mg 2x daily for 5 days will clear over 90% of Giardia lamblia infections (can become lactose intolerant while having giardiasis -> this will go away after 1 week of tx)
- oral tinidazole and nitazoxinide are alternatives

32
Q

Prevention of giardiasis?

A
  • avoid contaminated water sources
  • hikers or campers should boil water or use iodine or filtration with a large pore sized filter
  • adequate disposal of diapers and frequent hand washing for daycare centers
33
Q

What causes cryptosporidiosis?

A
  • a coccidian protozoan parasite (Cryptosporidium hominis)
  • associated with contaminated water supplies
  • unknown as human pathogen prior to 1976
  • one of the most common causes of waterborne illness in the US
34
Q

Where do the cryptosporidium localize to?

A
  • the intracellular spheres are found in great numbers just under the outer membrane of the cells lining the stomach or intestine
  • oocysts, passed into feces in enormous numbers, are the infective agents
  • get into digestive tract but also can get into resp. tract
35
Q

Site of cryptosporidium infection?

A
  • epithelial cells of GI tract
  • Has affected other tissues such as respiratory tract tissues and conjunctiva of the eye
  • infectious dose
36
Q

Sxs of Cryptosporidium?

A
  • some individuals can be asymptomatic
  • incubation period: 7-10 days (range 3-28)
  • sxs include:
    stomach cramps, pain, watery diarrhea, dehydration, vomiting, and fever
    severe sxs: profuse, watery diarrhea, severe malabsorption, electrolyte imbalance and marked wt loss
37
Q

Dx of Cryptosporidium?

A
  • usually made by examining stool specimens. 3 stools may be required. Microscopy with an acid fast stained stool smear is usually dx (acid fast stain**)
  • enzyme immunoassay for greatest sensitivity and specificity or molecular methods using PCR
38
Q

What is usually dx test for cryptosporidium?

A
  • acid fast stain on stool
39
Q

Tx of Cryptosporidium?

A
  • Nitazonxanide: can be used for pediatric patients
    adults: 500 mg q 12 hours
    children (1-3): 100 mg q 12 hours
    children (4-11): 200 mg q 12 hours
40
Q

Prevention of cryptosporidium?

A
  • water purification and filtration (resistant to chlorine)
  • routine testing:
    use of 1 micron filter to remove cysts
    boil water
    the sporocysts are resistant to most chemical disinfectants, but are susceptible to drying and the UV portion of sunlight
  • drink bottled water when traveling abroad
  • wash hands frequently
  • this protozoan is susceptible to freezing
  • want person to avoid swimming pools after infection has resolved -> can infect pool water
41
Q

What is the common parasite found in large intestine of humans?

A

Entamoeba histolytica is common parasite in large intestine of travelers
- mostly a disease of travelers

42
Q

What are the 3 stages of intestinal amebiasis?

A
  • the active amoeba
  • the inactive cyst
  • the intermediate precyst
43
Q

What are the 2 strains that cause intestinal amebiasis?

A
  • Entamoeba histolytica

- Dientamoeba fragilis

44
Q

Pathogenesis of Entamoeba histolytica?

A
  • fecal-oral transmission
  • cyst is ingested: the trophozoite emerges from the ingested cyst in the stomach and duodenum.
  • Each of which divides again to produce 8 small trophozoites per infective cyst
  • these pass to the cecum and produce a population of lumen-dwelling trophozoites
  • *** disease results when trophozoites of Entamoeba histolytic invade the intestinal epithelium
  • mucosal invasion with the aid of the proteolytic enzymes occurs through the bowel wall
  • causes discrete ulcers with a pinhead-sized center and raised edges, from which mucus, necrotic cells, and amoebas pass
  • Subsequent spread may coalesce colonies of amoebas, undermining large areas of mucosal surface
  • trophozoites may penetrate the muscular coats and occasionally the serosa, leading to perforation into the peritoneal cavity
  • secondary bacterial invasion, and accumulation of neutrophilic leukocytes can occur.
45
Q

Extraintestinal infection of Entamoeba histolytic amebiasis is what?

A
  • metastatic, amoebas spread through the blood
  • rarely occurs by direct extension from the bowel
  • By far the most common form is amoebic hepatitis, or liver abscess (4% or more common of clinical infections): this is assumed to be due to micro emboli including trophozoites carried through portal circulation.
46
Q

What factors determine the invasion of amoebas in Entamoeba histolytica amebiasis?

A
  • number of amoebas ingested
  • pathogenic capacity of the parasite strain
  • host factors such as gut motility and immune competence
47
Q

Clinical findings of amebiasis?

A
  • sxs vary greatly depending upon the site and intensity of lesions:
  • extreme abdominal tenderness
  • fulminating dysentery and dehydration occur in serious disease
  • in less acute disease, onset of sxs is usually gradual: episodic diarrhea, abdominal cramps, N/V, and urgent desire to defecate (takes 1-3 weeks)
  • more frequently there will be weeks of cramps and general discomfort, loss of appetite, wt loss, and malaise
48
Q

Lab test for Amebiasis?

A
  • stool specimens:
    fluid feces: fresh and warm for immediate exam of trophozoites. After a saline purge for cysts and trophozoites
  • formed feces for cysts
  • serology is available (EIA -> enzyme immunoassay)
49
Q

Tx of Amebiasis?

A
  • E. histolytica should be differentiated from morphologically similar species and tx appropriately.
  • Given small but substantial risk of invasive disease and the potential to transmit the infection to others, WHO recommends tx all cases of proven E. histolytica regardless of sxs
  • Asymptomatic intestinal infection: Paromomycin 10 days of 30 mg/Kg divided into 3 doses and diloxanide furoate 500 mg tid x 10 days
  • symptomatic: paromomycin as above after metronidazole (flagyl) 750 mg, 3x a day, for 5-10 days, tx should be followed by administration of diolxanide to eradicate any potential intestinal reservoirs
  • w/ early tx prognosis is good
50
Q

Prevention of amebiasis?

A
  • avoid contaminated food and water
  • wash and cook veggies
  • hand washing
  • chemoprophylaxis isn’t available
  • a potential vaccine is currently being developed
51
Q

is there an effective vaccine for malaria?

A
  • no, only immunity is a result of multiple infections
52
Q

How many malaria cases are there in the world?

A
  • about 3.3 billion people (half world’s pop) are at risk for malaria
  • 250 mill malaria cases and nearly one million deaths each year
  • In Africa, 1 in 5 childhood deaths are due to effects of malaria
  • An African child has an average b/t 1.6-5.4 episodes of malaria fever each year
53
Q

What is the vector for Malaria?

A
  • mosquitoes of the genus Anopheles -> only females carry this!
  • 5 species that infect humans (Plasmodium falciparum most serious)
  • endemic in SE US until 1940s (most cases in US now are airport malaria)
  • Spread by bite of mosquito that was previously infected from a human blood meal
  • parasited multiply within liver cells and RBCs
54
Q

How long does it take for malaria to reach body system after bite? How long does it take to be systematic?

A

1-2 hours

- 13-35 days to be sx

55
Q

What are the four species responsible for human malaria?

A
  • plasmodium vivax: most widely distributed
  • Plasmodium malariae- comparatively rare - temperate areas and subtropics
  • Plasmodium ovale: relatively uncommon, found in Asia, Europe and S. America
  • Plasmodium falciparum: predominates throughout all tropical areas -> very often lethal
56
Q

What does plasmodium vivid attack?

A
  • reticulocytes

- may become symptomatic 6-12 months after leaving an area with malaria, can be dormant for years

57
Q

What does Plasmodium malariae attack?

A
  • attacks mature red cells, after the acute infection, the infection becomes chronic and can persist for years
58
Q

What is unique about Plasmodium ovale?

A
  • can be dormant for years
59
Q

What cells does Plasmodium falciparum invade?

A

invades all red cells irrespective of age of red cells -> cells agglutinate forming thrombi and emboli

60
Q

Where is Plasmodium knowlesi found?

A
  • newly identified

- found in SE Asia (70% of cases of malaria)

61
Q

What are the typical Malaria sxs and when do they start?

A
  • onset 10-14 days up to 1 month with P. falciparum, 18-42 days occasionally 6 months to a year with other types
  • chills
  • night sweats
  • fever
  • HA
  • muscle pain
  • cough and chest pain
  • splenomegaly in chronically infected pts
  • hepatomegaly in chronically infected pts
62
Q

What is congenital malaria and when should it be considered?

A
  • it should be considered in febrile newborns and infants from women who could have been infected during their pregnancy
  • malaria infection during pregnancy can result because the mother become infected during pregnancy, but it can also result from an infection acquired months or years before
63
Q

What are ways to prevent malaria?

A
  • vector control: reduce stagnant water, spraying with insecticide
  • Application of DEET
  • Mosquito nets
  • vaccines: under development, no completely effective vaccine
64
Q

Malaria tx and prophylaxis?

A
  • chloroquine (most strains of Plasmodium show resistance) -> safe during pregnancy
  • Atovaquone & proguanil (Malarone)
  • Hydroxycholoroquine (Plaquenil)
  • Doxy (can be used with cholorquine)
  • Mefloquine (Larium): safe with pregnancy
65
Q

What 2 malaria txs and prophylaxis are safe with pregnancy?

A
  • Chloroquine and Mefloquine
66
Q

When should malaria be considered?

A
  • in all cases of fever in an area with high transmission of malaria
67
Q

What are the DOC for tx of Malaria?

A
  • first loading dose of chloroquine or atovaquone should be admin. immediately after collecting the blood specimen, even w/o waiting for its report
  • In areas with high transmission of P. falciparum malaria -> chloroquine alone as presumptive tx may not be enough -> Atovaquone should be first choice
68
Q

DOC for Malaria prophylaxis?

A

-chloroquine phosphate 500 mg weekly, continue 6 weeks after leaving area:
+ Fansidar (25 mg pyrimethamine and 500 mg sulfadoxine) weekly in areas with chloroquine resistant P. falciparum

or

Primiquine phosphate 26.3 mg daily, start 1-2 days before travel and continue 7 days after leaving area

69
Q

What causes Toxoplasmosis?

A
  • Toxoplasma gondii
  • it’s a coccidian protozoan of worldwide distribution that infects a wide range of animals and birds but doesn’t appear to cause disease in them
  • Felines are the only animals that can complete its reproductive cycle
70
Q

How prevalent is Toxoplasmosis in the U.S.?

A
  • it is considered to be the 3rd leading cause of death attributed to food borne illness in the US
  • more than 60 mill men, women and children in the US carry the Toxoplasma parasite
  • Very few have symptoms because the immune system usually keeps the parasite from causing illness
71
Q

Pathogenesis of Toxoplasmosis (in the cat -> human)?

A
  • oocysts develop in the cat GI tract, pass into the gut lumen of the cat, and pass out via the feces
  • These cysts can then be ingest by other creatures, including humans (changing the litter box)
72
Q

Pathogenesis of Toxoplasmosis once the human is infected?

A
  • The oocyst opens in the human’s duodenum and releases the sporozoites
  • These pass through the gut wall, circulate in the body, and invade various cells, especially macrophages
  • They multiply, break out, and spread the infection to lymph nodes and other organs
  • They penetrate nerve cells, especially of the brain and eye, where they multiply slowly to form tissue cysts, initiating the chronic stage of disease
73
Q

Sources of toxoplasmosis?

A
  • 10% of lamb consumed by humans contain cysts
  • 25% of pork consumed by humans contain cysts
  • Direct contact with any material contaminated with infected cat feces may result in ingestion of oocysts - and it can be transmitted to food by infects
74
Q

Sxs of Toxoplasmosis?

A
  • in immune competent pts: most will be asymptomatic
  • immune compromised pts - can cause: hepatitis, pneumonia, blindness, and severe neuro disorders
  • sxs similar to those of the flu or mono, occur in immunocompetent pts such as:
    body aches
    swollen lymph nodes (bilaterally)
    HA
    fever
    fatigue
    occasionally a sore throat
75
Q

When does a congenital infection of toxoplasmosis develop?

A
  • develops only when non-immune mothers are infected during pregnancy
  • usually causes severe congenital defects
  • The incidence and severity of congenital toxoplasmosis varies with the trimester during which infection was acquired
  • B/C tx of the mother may reduce the incidence of congenital infection and reduce sequelae in the infant, prompt and accurate dx is important
76
Q

What can toxoplasmosis congenital infection lead to?

A
  • leads to stillbirths, chorioretinitis, intracerebral calcifications, psychomotor disturbances, and hydrocephaly or microcephaly
  • Prenatal toxoplasmosis is a major cause of blindness and other congenital defects
77
Q

Sxs of congenital infection of toxoplasmosis?

A

Sxs may include:

  • enlarged liver and spleen
  • diarrhea or vomiting
  • chorioretinitis
  • feeding problems
  • jaundice
  • low birth weight
  • vision problems
  • hearing loss
  • skin rash at birth
78
Q

Ways that a pregnant mother can contract toxoplasmosis?

A
  • a fetus may contract toxoplasmosis through the placental connection with its infected mother
  • the infected mother may be infected by improper handling of cat litter or handling or ingesting contaminated meat
79
Q

Toxoplasmosis Dx lab tests?

A
  • Specimes: serology ->
  • ***Sabin-Feldman dye test: gold std, but only a few labs run it
  • ELISA: std test for most labs -> this is very effective
80
Q

Tx of toxoplasmosis?

A
  • acute infections can be tx with combo of pyrimethamine and either sulfadiazine or clindamycin
  • Leucovorin should be given to all pts receiving pyrimethamine (protects bone marrow)
81
Q

What is the tx for toxoplasmosis in pregnancy?

A
  • spiramycin (Rovamycine) 1-2 grams BID is recommended, continued until delivery
82
Q

Prevention of Toxoplasmosis?

A
  • Transplacental infection of fetus has long been recognized. Domestic cats have been identified as hosts
  • Wear gloves when gardening or handling soil
  • Avoidance of human contact with cat feces is impt in control, particularly for pregnant women with negative serologic tests
  • Since oocysts usually take 48 hours to become infective, daily changing of cat litter (and its safe disposal) can prevent transmission
  • Pregnant women should avoid all contact with cats, particularly kittens
  • Don’t eat raw or undercooked meat
  • cover children’s sandboxes
83
Q

What helminths are we worried about in the US?

A
  • Nematodes:
    pinworms, hook worms, round worms
  • cestodes: tape worms
  • Trematodes: flukes (very rare in US)
84
Q

How is the pinworm spread?

A
  • (also known as Enterobius vermicularis)
  • spread fecal-oral route; self contamination and internal reinfection:
    worms reside in cecum, colon -> crawl out of anus at night
  • worldwide, but low morbidity
  • seen in school children age 5-1- and uncommon in children
85
Q

Sxs of pinworm infection?

A
  • itchy butt, squirming when sitting (rarely worms get in vaginal canal)
86
Q

Life cycle and transmission of Pinworm?

A
  • after ingestion, eggs hatch and release larvae in small intestine
  • adult worms establish in cecum and appendix
  • Gravid females migrate to rectum onto perianal skin to deposit eggs (usually at night)
  • one worm can produce 10,000 eggs
87
Q

Dx of pinworms?

A
  • stool for ova and parasites
  • pinworm prep (cellophane tape test):
    wrap 3” piece of clear scotch tape around glass slide (sticky side out) and touch the slide to the pt’s perianal skin in 4 quadrants
  • Examine under a microscope to find pinworm eggs. The best sample is collected either in early morning before bathing or several hours after going to bed
88
Q

Tx of pinworms?

A
  • Mebendazole (Vermox) >= 2 years: 100 mg PO single dose, may repeat in 2-3 weeks

or

Albendazole >=2 years: 400 mg PO single dose; may repeat in 2 weeks

  • Tx the whole family!!!
89
Q

Hygiene measure in tx of Pinworm?

A
  • infxn not indicative of poor personal hygiene, common childhood infection
  • Hand washing
  • discourage child from sucking thumb, biting nails, and scratching
  • trim nails
  • wash bedding and garments in hot water promptly and avoid shaking
90
Q

Epidemiology of Ascariasis (round worms)

A
  • Ascaris infection is very common, especially in the tropics, hundreds of millions of people are infected
  • in the US, most cases occur in the southern states
  • most common in children 2-10 y/o
91
Q

Transmission of round worms?

A
  • ingestion of contaminated food/water

- children playing in contaminated soil

92
Q

Life cycle of round worms?

A
  • when ingested ova hatch in small intestine and release larvae
  • migrate in blood or lymphatics to lungs within 4 days
  • after 10 days in the lung they mature, ascend the bronchial tree and get swallowed
  • mature worms attach to jejunum
  • female worms produce 200,000 fertilized eggs/day
93
Q

Clinical presentation of round worms?

A
  • cough, abdominal discomfort: anorexia, nausea, diarrhea
  • intestinal obstruction
  • biliary colic (can clog up duodenum and biliary duct)
94
Q

Lab dx of round worms?

A
  • dx is usually made microscopically by detecting eggs in the stools
  • the egg is oval with an irregular surface
  • occasionally, the pt sees adult worms in the stools
95
Q

Tx of round worms?

A
  • mebendazole 100 mg BID for 3 days or
  • Albendazole 200 mg PO single dose
    or
  • Pyrantel: 11 mg/kg PO single dose for pregnancy
  • alt second line: Ivermectin >15 kg 150 mc/kg single dose
  • may have to remove with surgery
    prevention: proper disposal of feces, and good handwashing
96
Q

when and where would you likely get infected by a hookworm (Necator americanus)?

A
  • an est. 576-740 mill people in world are infected with hookworm
  • once was widespread in US, particularly in the SE region
  • walking barefooted on soil predisposes to infection. An impt public health measure was requiring children to wear shoes to school
97
Q

Where at on the body is hookworm infection likely to occur?

A
  • humans are infected when filariform larvae in moist soil penetrate the skin, usually the feet or legs
98
Q

Pathogenesis of hookworm?

A
  • migrate into blood vessels and are carried by the blood to the lungs. Migrate into he alveoli and up the bronchi and trachea, and then are swallowed (takes 8-21 days)
  • they develop into adults in small intestine, attaching to wall with cutting plates (hooks)
  • They feed on blood from the capillaries of the intestinal villi
    (6-8 weeks after infection eggs will become detectable in the bowel, this can persist for years)
99
Q

What is the major damage due to from hook worm infection? Clinical findings?

A
  • due to loss of blood at the site of attachment in the small intestine. Put to 0.1-0.3 mL/ worm can be lost per day - blood is consumed by worm and oozes from site in response to anticoagulant made by worm
  • weakness and pallor accompany the microlytic anemia caused by blood loss
  • skin penetration produces a focal pruritic maculopapular eruption at site (ground itch) (this will resolve on its own in a few days)
  • mild cough and pharyngeal irritation
  • N/V, diarrhea, and midepigastric pain
100
Q

Dx of hookworm?

A
  • made microscopically by observing eggs in the stools
  • occult blood in stools is frequent
  • ***Eosinophilia is typical
101
Q

Tx and prevention of hookworms?

A
  • both albendazole and mebendazole are effective

- prevention: disposing of sewage properly and wearing shoes

102
Q

What causes trichinosis?

impt properties of this organism?

A
  • Trichinella spiralis
  • any mammal can be infected, but pigs are most important reservoirs of human disease in US (except Alaska, where bear constitute as reservoir)
  • Humans are infected by eating raw or undercooked meat containing larvae encysted in muscle
103
Q

Where does Trichinosis end up in body?

A
  • the larvae excyst and mature into adults within mucosa of small intestine
  • eggs hatch within adult females, and larvae are released and distributed via the bloodstream to many organs; however they develop only in ***striated muscle cells
  • within these ***nurse cells they encyst within a fibrous capsule and can remain viable for several years but eventually calcify (this allows for concealment from immune system)
104
Q

Pathogenesis and clinical findings of Trichonisis?

A
  • a few days after eating undercooked meat, usually poor, the pt experiences diarrhea (severity is related to number of larvae ingested)
  • 1-2 weeks later: fever, muscle pain (most common complaint), periorbital edema and eosinophilia
  • **subungual splinter hemorrhages or conjuntival or retinal hemorrhages are an impt dx criterion
  • signs of cardiac and CNS disease are frequent, because the larvae migrate to these tissues as well
  • death (which is rare), is usually due to congestive heart failure or respiratory arrest
105
Q

Lab dx of Trichinosis?

A
  • muscle bx reveals larvae w/in striated muscle
  • serologic tests: ELISA, indirect immunofluorescence, and latex agglutination are reliable; results can be confirmed with western blot
106
Q

Tx and prevention of Trichinosis?

A

often self limited and not reqd
- symptomatic- steroids (help with discomfort) plus albendazole or mebendazole

  • prevention: the disease can be prevented by properly cooking pork or freezing the meat and by feeding pigs only cooked garbage
107
Q

What are the 2 impt human pathogens in the genus Tania (tapeworm)

A
  • T. solium (pork tapeworm)

- T. saginata (beef tapeworm)

108
Q

Morphology of tapeworm?

A
  • hav head, neck, and segmented body

- each segment is called a proglottid (each proglottid can reproduce eggs asexually)

109
Q

Lifecycle of tapeworms?

A

Cattle or pigs ingest vegetation that is contaminated w/ eggs or proglottids

  • humans become infected by eating infected undercooked meat
  • they attach to small intestine and develop proglottids
  • This occurs over 2 months and can survive for years in the small intestine
110
Q

Clinical findings of tapeworms

A
  • most pts with adult tapeworms are asymptomatic, but malaise and mild cramps can occur
  • in some, proglottids (segment or joint of tapeworm) appear in the stools and may even protrude from anus
111
Q

Dx of tapeworms?

A
  • ID of T. saginata consists of finding gravid proglottids with 15-20 uterine branches in the stop
  • eggs are found in stools less often than proglottids
112
Q

Tx and prevention of tapeworms?

A
  • Praziquantel (Biltricide): 5-10 mg/kg orally one time
  • prevention involves cooking meat adequately and disposing of waste properly so that cattle can’t consume human feces
  • most cases in USA are imported
113
Q

How should you be precautious when you go traveling to 3rd world countries?

A
  • use DEET, don’t drink the water, or us ice
  • Boil it, cook it, peel it or forget it
  • Be suspicious when your pts travel and come back ill or get ill soon thereafter
  • Be really suspicious of odd infectious signs in immunocompromised pts
  • wear shoes, especially when you vacation in South or in the tropics
  • give pts chipper for prophylaxis