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260 Cards in this Set
- Front
- Back
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What controls the severity of worm disease?
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Mostly the size of the innoculum (eggs or larva)
Most worms do not multiply in humans |
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Classification of parasitic worms
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Roundworms
Intestinal Tissues Flatworms Tapeworms Flukes |
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What to order when you are looking for parasites in the stool?
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Ova an Parasites
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Roundworm structure
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Outer tube - impermeable cuticle
Within are tubular gonads and intestine Most release eggs, some larvae Built to eat and reproduce and nothing else |
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What causes really high eosinophilia?
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More than 5K over 60%
Tropical - series of infectious by mites, filariae, other parasites Eosinophilic leukemia Visceral larva migrans |
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Is this eosinophilia from worm infection?
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Is it really high?
History of pica Larva seen on biopsy Leukocytosis Constant |
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Pinworm
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Enterobius vermincularis
An intestinal roundworm |
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Pinworm lifecycle
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Ingestion of infectious (embryonate eggs)
Eggs hatch is small intestine Mature in 5-6 weeks in cecum Mating to produce 10,000 eggs Gravid female travels out Deposits eggs on perianal skin and dies Eggs are infectious in 6 hours and for 2 weeks |
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Pinworm symptoms and diagnosis
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Anal itch
Scotch tape of perianal skin To see egg - thick walled colorless shell, with developing larva |
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Treating pinworm
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Treat the whole family with mebendazole
Retreat about 3 weeks later |
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Epi of pinworm disease
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Common
30% of children and 15% of adults worldwide No reasonable sanitary measures can prevent occasional reinfection when young children are present |
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Ascaris
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Ascaris Lumbricoides
Intestinal roundworm 35 cm in length (female |
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Ascaris lifecycle
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Ingestion of embryonated eggs from human fecal veneer
Larva hatch in small intestine Penetrate into portal circulation Larvae are trapped in lung capillaries and break into alveoli Partially mature in alveloi Larvae ascend are swallowed Larve mature into adults in sm intestine Mate and begin producing eggs (2 months after ingestion of egg) Eggs excreted in feces Eggs infectious in 3 weeks |
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Ascaris diagnostic stage
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Egg in feces
(unmated femalees lay non-fertilized eggs) Unicellular embryo Thick, yellow/brown bile stained shell Lumpy bumpy surface |
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Ascaris symptoms
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Most infections are asymptomatic
Malabsorption Intestinal obstruction by masses of worms Biliary obstruction Pancreatic obstruciton Hemorrohagic pneumonitis -- from larval migration Fever, eosinopilia, abd pain, n/v Exit of adult worm through anus |
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Epi of ascaris infection
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Very common in tropics
Occasionally in US (southeast) Eggs remain infectious for months (destroyed by sunlight or heating, not freezing) |
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Ascaris in NE?
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Most pig ascaris
Ascaris suum from pig fecal contamination Infection does not last long in human colon |
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Treating and preventing ascaris
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Mebendazole
Piperazine - paralyzes worm and lets it get peristalsed out Prevention = sanitary disposal of feces |
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Hookworms
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Ancylostoma duodenale - Europe and asia
Necator americanus - Africa and Western hemisphere |
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Hookworm symptoms
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Lighter infections are often asymptomatic
Chronic/heavier cause anemia Esp w. iron deficiency Peripheral edema Developmental delay from chronic anemia in children |
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Hookworm lifecycle
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Infectious larva in soil or wet vegetation penetrate skin to enter blood
Larvae exit in alveoli and partially mature Late stage larva ascend and get swallowed Mature in small intestine Mating and egg laying Eggs excreted in feces Hatch in environment to release free-living larva that survive < 6 weeks |
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Diagnostic stage of hookworm
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Egg in feces
Thin shell with cells vs larva |
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Skin manifestation of hookworm
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Larvae produce a papul and erythema at site of entry
"Ground itch/Dew itch" |
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Gross appearance of hookworm
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Adult female is 1 cm long
Slightly smaller male |
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Pathogenesis of hookworm
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Attach to mucosa of small intestine by their anterior (mouth) end
Secrete an anticoagulant Suck blood ( 50 to 200 microliters per day) 100K eggs/day Live about 5 years |
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Epi of hookworm
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Tropical and warm temperate regions
Africa, South America, Asia Formerly common in southeastern US |
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Hookworm treatment and prevention
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Mebendazole
Iron or transfusions for anemia Sanitary disposal of human feces and the wearing of shoes |
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Strongyloides
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Strongyloidies stercoralis
Intestinal roundworm In some cases can multiply extensively in humans and produce a life-threatening disease (hyperinfection) |
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Strongyloides lifecycle
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Infectious larva penetrate skin and enter blood stream
Exit at alveoli and partially mature Late larva ascend and get swallowed Mature into hermaphroditic adults in intestine One month into infection: Adults burrow into muscosa and lay eggs Eggs hatch in intestine and Mature to infectious larva or Mature into larva that excreted and live free |
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How does strongyloides autoinfection work
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Larva that hatch in intestine
Mature into infectious Burrow right into blood stream Go to lungs Back to intestine where they mature to adults |
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Free living strongyloides
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Male and female live free in soil
Mate and lay eggs in soil Lay eggs in soil Some larva grow up into infectious kind |
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Diagnostic stage of strongyloides
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Larva (0.25 cm) in feces
Short buccal cavity Hourglass shaped esophagus Genital promordium Anus |
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Size of strongyloides adults
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2 mm
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Symptoms of strongyloides infection
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Many are asymptomatic
Heavy infections - Diarrhea, nausea, abdominal pain Eosinophila Can be chronic because of autoinfection Mild cutaneous and pulmonary symptoms |
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Symptoms of strongyloides chronic autoinfection
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Years of eosinophilia
Recurrent gram negative bacteremia from E. Coli carried by larva penetrating the intestinal mucosa |
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Hyperinfection with strongyloides
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Occurs when autoinfection cycle gets out of control
Immunocompromised Life threatening High fever, dyspnea, gram negative septicemia |
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Treatment of strongyloidies infection
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Treat all infections to avoid possible hyperinfection
Ivermectin Albendazole Thiabendazole |
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Preventing strongyloides infection
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Controlling fecal contamination
Shoes |
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Epi of strongyloides
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South America
Africa Asia Tropical/temperate |
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Larva migrans
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Human infection by larva of intestinal roundworm from another species
Accidental hosts Larva cannot live in intestine or mature Wander around until they die Either visceral or cutaneous |
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Visceral larva migrans
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Ascaris-like intestinal roundworm of dog, cat, racoon
Kids eat eggs from dog fecal contamination Larva penetrate to portal circulation Exit at liver and wander through the tissues |
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Visceral larva migrans symptoms
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Many are asymptomatic
Marked eosinphilia Fever Hepatomegaly |
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Pathology in visceral larva migrans
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Eosinophilic granulomata surrounding dead larva in various organs
Retinal involvement may mimic retinoblastoma |
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Treating and preventing visceral larva migrans
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Treat with albendazole, diethylcarbamazine
Most cases self-limted in less than a year (granulomata) Avoid dog feces Treat dogs for roundworms |
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Cutaneous larva migrans
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Creeping eruption
Dog/cat hookworm Human infected by infectious larva Intracutaneous tunnels moving 1 cm/day Itching and inflam response Scarring |
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Cutaneous larva migrans treatmetn
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Disease is self-limiting
Larva die in less than 2 months Treat with local or systemic thiabendazole |
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Cutaneous larva migrans epi
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Worldwide distribution
Prevalent in southeastern USA |
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Preventing cutaneous larva migrans
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Treat dogs for hookworm
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Which roundworms are viviparous?
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Release live larva rather than eggs
Trichinella spiralis Dracunculus medinesis (guinea worm) Filarial infections Wuchereria bancrofti (elephantiasis) Onchocerca volvulus (river blindness) |
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Trichinella
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Trichinella spiralis
Tissue roundworm Transmitted via consumption of skeletal muscle |
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Trichinella life cycle
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Consumption of undercooked pork (bear, etc) with encysted trichinella
Larva released in small intestine Invade mucosa and mature Male fertilizes female about 2 days into infection Female burrows into intestinal mucosa Five days into infection, females begins to release live larva, which enter blood and are disseminated throughout body Larva release for about 1 month Larva enter striated muscle cells Grown for 3 weeks Die and are calcified in 2 years |
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Pathology of trichinella cysts
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Intracelluar
Enclosed by fibrous capsule of host cell origin Calcified |
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Diagnostic stage of trichinella
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Larval form in muscle
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Symptoms of trichinella
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Light infections asymptomatic
Heavy infections: Diarrhea, gastronenteritis from mucosal infection early Pain from skeletal muscle invasion during week 1-4 Death from invasion of other tissues that do not support encystment (heart/brain) Eosinophilia, periorbital edema, diploplia, muscle pain, HA, fever Variable |
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Treating trichinella?
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Albendazole is recommended but not proven
Steroids may be useful |
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Preventing trichinella
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Fully cook meat
On a public health level: Ban feeding uncooked pork scraps to pigs (ie don't feed pigs garbage) |
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Trichinella epi
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Worldwide (except Australia and some pacific islands)
Falling markedly in US |
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Definitive host
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Adults present in host
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Intermediate host
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Larval forms in host
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Accidental host
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Host does not play a role in life cycle
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Filariases
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Blood sucking inset is the intermediate host
Humans are definitive host and harbor both adult worm and their newborn larva (microfilariae) |
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Filiarial roundworm lifecycle
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Human bitten by insect
Mature larva injection Larva mature to adults Male and female mate Female releases first stage larvae (microfilaria) Microfiliaria circulate in blood or migrate in tissues A blood sucking insect is infected and microfilariae develop into the insect to become mature larva |
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Wuchereria
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Wuchereria bancrofti
Wuchereria/Elephantiasis Filariasis Pathology arises from adult worms in lymphatics |
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Wuchereria intermediate host
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Mosquitos
Infection by biting humans with microfilaria circulating in blood |
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Wuchereria infection symptoms
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Light infections are asymptomatic
Heavy chronic infection: Lymphatic obstruction Elephantiasis |
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Diagnostic stage of wuchereria
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Microfilaria in blood
Can be difficult because in chronic disease there may not be many microfilaria in the blood |
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Wuchereria epi
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All tropical regions
Could be eradicated with universal chemotherapy over 5 years |
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Treating wuchereria
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Ivermectin
Diethylcarbamazine Albendazole |
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Tropical pulmonary eosinphilia
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Rare (0.5%), potentially fatal complication of wucherereia
Pulmonary infiltrates |
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Preventing wuchereria
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Prevent mosquito bites
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Dirofilia
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Dog heartworm
Humans are accidental host Get infection from mosquitos that are carrying dog heartworm larva |
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Onchocerca
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Onchocera volvulus
River blindness Filariasis Major pathlogy is from microfilariae, which migrate in tissues |
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Onchocerca intermediate host
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Black fly
genus Simulium |
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Onchocerca disease
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Adult worms (35 cm female) found in subcutaneous nodules at stie of black fly bite
Microfilariae cause dermatitis w/ sever itching Blindess from chronic keratitis and fibrosis of cornea, atrophy of irus, chorioretinitis all from microfilaria migration - autoimmunity? |
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Onchocerciasis epi
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Focal areas of
tropical Africa Central/South America |
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Diagnosing onchocerciasis
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MIcrofilaria in skin snip or adult worms in biopsy of nodules
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Treating and preventing onchocerciasis
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Once a year ivermectin
Kills microfilaria Does not kill adult worms though Surgery to take out nodules does not work because of missed nodules Prevent via black fly control/bite avoidal |
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Flukes
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Trematodes
Parasitic flatworms Reproduce sexually in definitive host Reproduce asexually in snail (obligatory intermediate host) Blood flukes - sexual Tissue flukes - hermaphroditic |
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Schistosomes
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Blood flukes
Separate male and females Three important in humans: Schisotosoma mansoni Schistosoma haemtaobium Shistosoma japonicum |
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Schistomsome lifecycle
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Free swimming cercariae penetrate human skin in freshwater
Cercariae transform into larval worms Migrate to lungs then hepatoportal system, where the mature further Enter venules and lay eggs Some of eggs are excreted Hatch into ciliated form Infects snail species Multiply extensively to yield many cercariae |
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Localization of different shistosomes
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Mansoni - lower intestine
Japonicum - intestine Hematobium - bladder |
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Shistosome diagnostic stage
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Egg is feces, urine or rectal biopsy
Mansoni - lateral spine Hematobium - terminal spine Japonicum - small lateral spine |
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Shistosome symptoms
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Acute - 6 weeks after exposure - fever, flu-like, hepatosplenomegaly, lymphadenopathy, eosinophilia
Chronic - damage caused by immune response to eggs: portal HTN, CNS damage, bladder tumors (haematobium) |
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Shistosomes and portal htn
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Eggs trapped in liver cause pipestem fibrosis
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Complications of S. haematobium
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Urinary tract disease
Bladder tumors - from chronic inflammation Obstruction -- hydro Calcified eggs in bladder wall reduces compliance |
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Pathology in schistosomes
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Most eggs do not make it to lumens
Become trapped in veins or tissues Provoke intense cell-mediate immune response Granulomas form Compromised blood flow |
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How long to adult schistosomes live?
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Decades
Cloak themselves in human antigens to avoid an immune response |
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Suspect schistosomiasis in patients with
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Eosinophilia, hepatosplenomegaly, blood vomit, hematuria
With appropriate geographic history And history of prolonged freshwater contact |
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Where are the schistosomes
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Mansoni: North Africa, Middle East, South America, some Caribbean islands
Haematobium: Africa and Middle East Japonicum: China, Japan, SE Asia |
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Treating schisto
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Praziquantel
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Preventing schisto
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Avoid contact with contaminated water
Life cycle broken by sanitary disposal of feces and urine |
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Schistosome dermatitis
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Swimmer's itch
Human is accident host Cercariae penetrate skin but die there and cause itchy dermatitis Worldwide distribution, species based on snail, can be in fresh or salt water |
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Cercaria penetration of tissue
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By elaborating proteases
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Schistosome egg antigens get what reaction
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Eosinophilic infiltrate
Il 4, 5, 13 Granuloma formation Dense fibrosis |
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Changing immune response to schisto over time
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Initially a TH1 response
fever, flu-like symptomes Chronic disease is driven by TH2 eosinophilic granulomas |
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Adult tape worm structure
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Scolex - head - specialized for attachment to intestinal mucosa
Neck - grows to form new proglottids Proglottids - segments involved in egg formation, most caudal is most mature - hermaphroditic immature, mature, gravid |
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How do tape worms feed
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Absorption through entire surface of worm from intestinal contents
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Human tapeworms
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Humans are definitive host
Taenia saginata - beef tapeworm Taenia solium - pig tapeworm Diphyllobothrium, latum - fish tapeworm |
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Treating tapeworms in humans
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Praziquantel
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Taenia saginata
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Beef tapeworm
Giant tapeworm of humans |
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Taenia saginata lifecycle
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Humans ingest cysticerci (encysted larva) in undercooked beef
Larvae attach to wall of small intestine Grow to mature 12 to 30 foot hermaphroditic adults (2-3 months) Mature proglottids passed into feces Cow ingests eggs Larva hatch, penetrate intestinal wall Become encysted in muscle |
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How many eggs are in a taenia saginata proglottid?
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50K - 100K
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Diagnostic stage of taenia saginata
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Mature proglottid in feces
15-20 lateral branches/side Free eggs may also be seen |
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Symptoms of taenia saginata infection
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None
Unless you feel a motile multi-proglottid segment force its way out |
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Epi of taenia saginata
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Anywhere that cows/human feces interact
Highly prevalent in Africa |
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Preventing taenia saginata
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Cooking beef
Protecting cows from human feces |
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Taenia solium
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Pork tapeworm
Humans are only definitive host and can be intermediate host |
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Taenia solium lifecycle
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Humans ingest encysted larva (cysticerci) in raw or undercooked pork
Larva attach to wall of small intestine Mature to 12 to 30 foot hermaphroditic adults Several months after infection Mature proglottids (50K eggs) are passed in human feces Pigs ingest eggs/proglottids from human feces Larva hatch, penetrate intestinal wall and encyst in muscle |
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Cystocercosis
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Humans ingest eggs from human fecal contamination
Cysticerci formed in human tissues: lungs, brain, eye, connective in tissues Can cause life threatening disease |
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Diagnostic stage of taenia solium
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Mature prolottid in feces
Gravid proglotid has 8 to 13 lateral branches (less than saginata) |
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Symptoms of taenia solium infection
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Adult worm infection is usually asymptomatic
Cystocercosis can damage eye, heart, brain -- seizures, causes eosinophilia |
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Radiology of neurocystocercosis
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Calcified cysts - easy to see
Live cysts - more difficult |
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Treating taenia solium infection
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Praziquantel needed, preventing future fecal contaminants that could lead to cystocercosis
Treat neurocystocercosis with albendazole or praziquantel |
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Preventing taenia solium infections
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Cook pork
Protect pigs and humans from human fecal contamination |
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Diphyllobothrium latum
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Fish tapeworm
Giant tapeworm of humans |
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Diphyllobothrium lifecycle
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Human ingest raw freshwater fish w/ encysted larvae
Larvae attach to wall of lower small intestine Mature in a few months Proglottids release eggs that are excreted in feces Egg hatches into free-living cilated stage in fresh water Ciliated stage is eat by copepod (small curstacean) Develops into a later stage larva Copepod is eaten by fish Larva encysts in fish muscle |
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Diagnostic stage of diphyllobothrium
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Egg in feces
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Symptoms of diphyllobothrium
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B12 deficiency
Diphyllopbothrium has high affinity for B12 |
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Where is diphyllobothrium
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Great Lakes and Alaska
Worldwide, prevalent in Finland |
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Preventing diphyllobothrium infection
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Cooking or freezing fish
Keeping human feces out of freshwater where the fish/copepods live |
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Definitive host of diphyllobothrium
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Humans
Cats, dogs, pigs |
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Anisikiasis
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Marine mammal ascarid worm, passed through the fish
Humans are accident host Ingested larva cause eosinophilic granuloma of the stomach wall |
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Echinococcus granulosus
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Dog tapeworm
Causes serious cystic disease in humans |
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Echinoccous granulosus life cycle
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Sheep (dog food) ingests eggs from dog fecal contamination
Early larvae hatch in intestine Penetrate intestinal mucosa to enter portal circulation Most are trapped in liver Develop into cysts with inner germinal layer Germinal layer grows vesiculates and differentiates to form larval scolices (asexual multiplication) Cyst can be 20 cms Sheep viscera fed to dogs In dog intestine, larval scolices attach to small intestine wal and mature into small tapeworms 500 eggs released per segment |
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Humans in Echinococcus granulosus
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Accidental host
Get disease by eating food contaminated by dog feces Form hydatid cysts (w/ scolices in the = hydatid sand) - mostly in liver and lung |
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Symptoms of echinococcus granulosus infection is humans
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Mostly asymptomatic, calcified cysts seen on routine xray
Symptoms by gradual expansion - hepatic cysts: pain and hepatomegaly Pulmonary - cough + dyspnea Space filling lesions Symptoms of rupture -- anaphylactic shock, new cyst formation |
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Diagnosis of E. granulosus
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Xrays
Serology of antibodies |
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Geography of echinococcus
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Prevalent diease in sheep and cattle livestock in areas of South America, Eastern Europe, South Africa, and the Mediterranean basin
Alaska - wild animals |
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Treating echinococcus granulosus
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Symptomatic patients treated with surgical excision
Contents of cysts must be sterilized (with ethanol) prior to removal to prevent releasing new scolicies (which would makes more cysts) Can also give albendazole or praziquantel |
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Preventing ecchinococcus granulosus
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Avoiding dog feces in endemic areas
Preventing/treating dog infections |
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Echinococcus multilocularis
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Dog/fox tapeworm
Humans are accidental intermediate host Endemic to far north climates (MN, AK) Rodents are usual intermediate host Cysts are multi-compartmental alveolar usually in liver, can give rise to metastatic growth at distant sites like lung and brain Surgical cure more difficult Can also treat with albendazole |
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When does ascaris/hookworms cause high eosinophilia?
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Early migration through lung
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When does strongyloides cause high eosinophilia?
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Hyperinfection
Sporadic in chronic infection |
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When does trichinella, larva migrans, filariasis, shisto cause high eosinphilia?
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Migratory periods
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Parasites causing chronic eosinohilia
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Hookworm
Strongyloidies w/ autoinfection cycle Taenia solium with adults Echinococcus - leakage of cyst contents Onchocerciasis Schistosomiasis - sometimes |
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Helminth chemo tages
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Nueral and neuromuscular transmission
Cytoskeletal structure (microtubules) Energy metabolism |
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Parasitic protozoa
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Single celled eukaryotes
Multiply in humans Not usually cause of eosinphilia E. histolytica, giardia, trichomonas |
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Entamoeba histolytica
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Parasitic extracellular protazoan
Anaerobic |
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Enatmoeba histolytica life cycle
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Human ingests cysts from human fecal contamination
Cysts open in intestine Progeny parasites multiply as trophozoites in large intestine Trophozite becomes a cyst with decreasing water content in stool Cysts excrete in stool Resistant to most environmental conditions Survive for weeks |
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Trophozoite
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Actively multiplying stage of parasitic protazoa
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Diagnostic stage of E. histolytica
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Cyst in formed stools
Motile trophozoite in diarrhea Can also look for antibody against surface lectin |
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E. histolytica symptoms
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Symptomatic = invasive disease of colon mucosa = ulcerations by scope - flask-shaped
Dysentery Amebic abscess - spread to liver - pain, fever, enlarged and tender liver --not always secreting cysts still use serology |
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Treating E. histolytica infection
Preventing |
Metronidazole +
Avoid fecal contamination |
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Where is E. histolytica?
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Worldwide
Not usually in NE (?) |
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E. histolytica sterile abscess?
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Not sterile
Protozoa at edge Lack PMNs because trophozoites kill them |
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Routes of getting amebiasis
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Contaminated food or water
Sexual transmission Contaminated GI procedures |
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Entamoeba coli infection
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Does not cause disease
Marker that someone has consumed contaminated food though |
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E histolytica virulence factor
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Surface lectin allows binding to colonic mucosa and protection from complement
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Amebic meningoencephalitis
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Naergleria
Caused by several free living amebas Ameba get into nose from swimming in stagnant water Invade through cribiform plate Cause necrotic lesions at base of brain Rapidly fatal - meningitis/encephalitis picture Rare Try treating with amphotericin B |
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Avoiding food and water born infections
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Boil water
or filter it, halogen it Avoid contact with freshwater in schisto areas Avoid fruits you can't peel Cook your meat |
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Giardia
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Giardia lamblia
Flagellated extracellular protozoan parasite |
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Giardia lifecylce
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Humans or animals can be hosts
Ingest cyst from fecal contamnation Cysts open in small intestine Released parasites multiply as trophozoites in duo and jej Trophozoites encyst as stool dehydrates Excreted in feces |
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Diagnostic stage of giardia
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Cyst in stool or trophozoite in diarrhea
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Symptoms of giardia
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Totally limited to GI tract
Incubation 1-3 weeks Diarrhea, foul smelling greasy stools, abdominal discomfort, nausea Weight loss from malabsorption |
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Who is more likely to get chronic giardia?
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Congenital defects in IgA
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Where is giardia?
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Endemic to most or all parts of the world
Also pops up as epidemic when municipal water supplies are contaminated |
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Preventing giardia
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Filtration of water supplies (chlorination does not kill)
Avoiding contaminated water - like municipal water from reservoir where beavers live |
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Treating giardia
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Metronidazole
(Nitazoxanide) |
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Trichomonas vaginalis
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Flagellate extracellular protozoan parasite
Sexually transmitted |
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Trichomonas life cycle
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Trophozoites in vagina of female or urethra prostate of male are transmitted by sexual contact or poor hygiene
Multiply by binary fission No cyst stage Relatively hardy trophozoites |
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Diagnostic stage
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Motile trophozoite in vaginal secretions/urine
Can try prostatic secretions, urine in men, but this is rarely done |
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Symptoms of trichomonas infection
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10-20% of infected women have symptoms
Inflammation, itching, burning, purulent discharge Men ? a few with urethritis |
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Treating/preventing trichomonas infection
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Metronidazole
Must include sexual partners Prevention requires mechanical barriers |
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Trichomonas infection increases risk of...
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HPV infection
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Diagnosing trichomonas
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Microscopy wet prep
Pap Culture Rapid EIA with stick |
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What the intracellular protozoans?
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Toxoplasmosis
Cryptosporidium Malaria Babesia Leshmania Trypanosomes |
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Toxoplasmosis
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Toxoplasma gondii
Obligate intracellular parasite Humans are accidental intermediate hosts |
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Toxoplasma natural lifecycle
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Cat eats intermediate host with tissue cysts on muscle and brain
Parasites grow intracelularly in feile intestinal mucosa and produce male and female gametes Gametes fuse to form zygote, excreted in feces Fecal cysts becomes infectious (sporulated oocyst) after 2 days at ambient temp Non-feline ingests cysts, gets acutely infected, then gets tissue cysts |
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Human toxo infections
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Eating undercooked meat with tissues cysts
Ingesting infectious fecal cysts form fecal feline contamination Acute infections with trophozoites Often asyptomatic Chronic infection with tissue cysts in muscle and brain |
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Diagnosing toxo
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Serologic, biopsy of lesions
Sabin-Feldman dye test - complement mediated lysis of parasites in presence of anti-toxo Abs ELISA/fluorescent Ab No diagnostic stage in human infection |
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Treating toxo
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Pyrimethamine (dihydrofolate reductase inhibitor) plus sulfadiazine (dihydrofolate synthesis inhibitor)
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Toxo symptoms
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Rare primary disease
Lymphadenitis, myalgia, HA, fatigue, fever, encephalitis, myocarditis, hepatitis, pneumo Tissue cysts that can reactivate when immunosuppressed |
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Toxo epi
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1 in 8 in US have been infected
Disease only seen in AIDS, neonates |
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Toxoplasmic encephalitis
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Opportunistic infection in AIDS with CD4<100
HA or confusion with focal deficits Ring enhancing CNS lesions Nearly all reactivation disease (although some are not seropos because they've lost all immunity with the AIDS) Therapeutic trial with pyrimethamine-sulfadiazine |
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Transplacental toxoplasmosis
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Primary infection during preg
Wide variation in fetal outcomes Earlier is worse Microcephaly, intracerebral calcifications, MR, blidness Visual defects (recurrent chorioretinitis) Treating during pregnancy can improve outcome |
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Prevention of toxo
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Cook meat and avoid cat fecal contamination
Esp during pregnancy |
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Toxoplasma trophyzoite AKA
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Tachyzoite
These multiply REALLY fast |
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Tissue response to toxo cysts
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Nothing
Sometimes a little inflammation when cysts break down |
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Chronic toxo and behavior change
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Definitely happens in mice
?schizophrenia, car accidents |
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"Spor" parasites
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Cryptosporidum, Cyclospora, Isospora, Microsporidia
Obligate intracellular parasites Mild-mod self-limited diarrhea in competent Severe, protracted diarrhea in suppressed hosts Fecal-oral via cyst |
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Cryptosporidium
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Obligate intracellular parasite
-just under epi surface Infectious cysts in feces of humans and animals Acute diarrheal disease - self limited except in immunosuppressed No chronic stage |
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Cryptosporidium diagnosis
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Acid-fast cysts in feces
Immunofluroesence ELISA or PCR |
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Treating/Preventing cryptosporidium
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Need large water filtration systems
No good drug for treatment |
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What causes malaria?
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Intracellular protozoan parasites of the genus Plasmodium
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Malaria lifecycle
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Mosquito injects sporozoites into humans
Sporozoites enter hepatocytes Divide intracellularly to yield merozoites Merozoites released into circulation Infect red blood ells Merozoites multiply in RBCs RBCs lyse and new ones are infcted Some gametophyes are produced and taken up by a mosquito as a blood meal In mosquiteo, gametes form zygote Zygote matures and produces many sporozites Sporozoites migrate to salivary gland |
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Stages of malaria in humans
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Liver (exoerythrogenic) stage - asymptomatic with no significant pathology
Erythrocytic stage - disease manifests |
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Stages of malaria in the RBC
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Ring stage
Cytoplasmic synthesis Nuclear replication (multinucleate cell) Cytoplasmic division |
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Types of malaria
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Plasmodium falciparum - more virulent
Plasmodium vivax Plasmodium malariae Plasmodium ovale |
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Diagnosing malaria
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Finding the erythrocytic forms in a blood smear
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Incubation period of malaria
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Usually 10-40 days
Can be longer in vivax (6-12 mos) because of a dormant liver stage |
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Symptoms of malaria
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Flu-like prodrome (HA, anorexia, fever, joint pains)
Attacks of rigors _--> HA w/ fever and n/v --> heavy sweat These cycles repeat as erythrocytic lysis occurs Anemia Splenomegaly from chronic |
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Plasmodium falciparum
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Most serious malaria. Emergency.
Incubation 2 weeks High parasitemia Primary attacks --> fever spikes --> low parisitemia in about three weeks Relapses over months |
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Severe symptoms of plasmodium falciparum infection
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Tissue ischemia:
Cerebral malaria: HA, coma, paralysis, death GI hemorrhage Tubular necrosis Parasite specific proteins are embedded in RBC membrane causing binding to endothelial cells (via integrin and thrombospondin receptors) At high parasitic loads -- occlude vessels |
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Where is p. falciparum?
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Tropically
Needs mosquitos and has not delayed stage to overwinter in |
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Diagnostics stages seen in p. falciparum infection
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Ring forms
Banana-shaped gametocytes -- really only falciparum |
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Plasmodium vivax
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Generally less severe malaria
Preferentially infects reticulocytes Lower parasitemia Anemia common Relapse/intial symptoms can be delayed for months because of dormant liver stage |
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Plasmodium vivax smear diagnosis
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Solitary rings in large erythrocytes
Schuffner's dots (invaginantions of RBC membrane) Gametocyte is round |
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Anti-malarial
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Inhibit growth of erythrocytic stages
Chloroquine (most falciparum resistant) Primythamine + sulfadoxine Atovoquine + proguanil (Malarone) Mefloquine Doxy Quinine Artemisinin |
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Drug to eradicate p. falciparum dormant stage (hypnozoite)
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Priamquine
Cannot be used with G6PD deficiency |
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Malaria prophy
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Bed nets, inset repellents
Mefloquine, cloroquine, doxy for travels to endemic areas |
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What determines where malaria is found?
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Where anopehles mosquito is found
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Immunity to malaria
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Slow to develop
Is species specific, may be strain specific Reinfection common |
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Genetic resistance to malaria
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Sickle cell - heterozygotes markedly reduced mortality
Need Duffy to be infected with vivax (this is only common in caucasians) PK deficiency, G6PD deficiency result in partial resistance |
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Eradicating malaria
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Difficult by possible
Mosquito control Mosquito bite protection Case finding and chemo to reduce number of infected humans |
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Malaria pigment
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Parasite breakdown of hemoglobin
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New ways to diagnose malaria
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PCR - reference labs only, most sens
Immunochromic dipstick assay - looking for antibodies to malaria proteins - used to r/o malaria |
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Malaria from transfusions
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Malaria can survive in blood
Happens but is rare now Defer blood from travelers to endemic areas for 1 year |
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Babesia
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Related to malaria
Transmitted by tick Erythrocytic cycle resembles P. facliparum |
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Who gets the worse babesiosis?
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Asplenic patients
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Where is babesia?
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Europe and US
Especially NE coastal islands Here |
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Babesia tick
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Ixodes
Black legged, hard tick Nymph transmits the best |
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Diagnostic stage of babesia
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Trophozoite in stained blood films
Look for tetrads of parasites in cross-shapped configuration Some red cells have ring stage tat can be mistaken for malaria |
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Symptoms of babesia
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Largely subclinical
Hemolytic anemia, fevers, chills Rarely have serious complications |
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Babesia not malaria
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See forms outside the cell
Less uniform size forms The cross-shapped - although that is rearely seen |
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Risks for developing serious babesia
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Old age
Immunosuppresion Aspelnia |
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Treating babesia
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Atovaquone + azithro/clinda + quinine
Exchange transfusion has been used in severe diseas |
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Babesia life cycle
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Sexual stages in tick
Sporozites injected by tick during bite Penetrates RBCs Forms tetrad in cell, merozoites Merozoites lyse Infect new RBCs Some gametocytes formed that infect ticks |
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Coinfections with ixophelles bite
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Borrelia burgorferi
Anaplasma phagycytophilium Babesia micro |
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Hemoflagellates
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Kinetoplast - darkly staining big mitochondria
Insect vectors Blood stage Definitive host not defined Lesishmania Typanosoma cruzi African trypanosomes |
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Amastigot
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Intracellular form of hemoflagellates
Rudimentary flaggellum only |
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Lesihmaniasis
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Different clinical forms, determined by species, site temperature and host immune status
Visceral (Kala Azar) Cutaneous Mucocutaneous |
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Leishmaniasis vector
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Sandfly
Dogs often reservoir |
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Leishmaniasis life cycle
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Sandflies (phlebotomus) regurgitate extracellular flagellated form
Flagellated form enters mono/mac Loses flagellum Multiples intracellularlly as amastigote Cell lysis and infection of new mononuclear phagocytes Uninfected sandfly ingests macrophages containing amastigotes |
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Leshmaniasis diagnosis
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Histology - current standard
Culture - low sensitivity, but can speciate PCR - research assay Serology - may not distinguish between infection and disease, esp visceral |
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Visceral leismaniasis symptoms
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Small percentage will get disease w/in months to years of infection
Wasting, hepatosplenomegaly High mortality in progressors |
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Distribution of visceral leishmaniasis
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Mid Africa
Around the Med Pockets in south america |
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Cutaneous leishmaniasis
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Incubation period 2-8 weeks
Papule at site of bite slowly becomse 1-2 cm in diamter Papule becomes ulcer that lasts 6 months to several years Scar and give reasonably good immunity |
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Geography of cutaneous leshmnaisis
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Northern south america
Mid africa South Asia |
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Mucocutaneous leishmaniasis
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South and central america
Starts out like cutaenous Weeks to years later, 3% of patients have dissmenation to produces progressive massive necrotizing lesion At mucocutaneous jcts of mouth or nose |
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Diagnosis of visceral lesihmaniasis
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Marrow biopsy
Original cutaneous lesion is often healed before visceral symptoms appear and few or now organisms can be found in blood |
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Why is speciation important in leschmania?
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Only some species cause mucocutaneous disease, definitely want to treat these
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Visceral leschmaniasis symptoms
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Protracted fever (non-prostating)
Hepatosplenomegaly Death in untreated |
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What causes visceral leishmania
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Leshmania donovani
Mostly human - sandfly - human |
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Chagas disease
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Trypanosoma Cruzi
Transmitted by reduviid bug Amastigote stage in tissue causes disease Acute and chronic Muscle infection |
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Preventing and treating leschmaniasis
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Avoid sandflies
Difficult to treat Many of the available drugs are toxic AmphB, paromomycin, fluconazole is okay |
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Reservoir for leschmania causing cutaneous leschmaniasis
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Domestic dogs
Rodents Other mammals Source of most fly infections |
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Diagnosing cutaneous leschmaniasis
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Microscopy of biopsy at margin of lesion looking for amastigote stage
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"oriental sore"
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Cutaneous leishmaniasis lesion of central asia, india, mediterranean, west africa
Usually on arms, legs, face |
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Chiclero ulcer
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Cutaneous leischmaniasis lesion of
Central and South America Often involves head |
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Treating leschmaniasis
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Must treat mucocutaenous and visceral
Often don't treat cutaneous (unless its really the first stage of mucocutaneous |
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Diagnosing mucocutaneous leschmaniasis
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Clinical
Biopsy at margin of lesion often fails PCR is reliable but not available |
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Geography of mucocutaneous leschmaniasis
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Central and South America
Dogs and other mammals are reservoir host |
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Trypanosoma cruzi
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Protozoan that causes Chagas disase
Intracellular and extracellular stages |
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Lifecycle of trypanosoma cruzi
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Infected reduviid bug bites, takes a blood meal and defecate
Feces contains infectious extracellular flagellated forms Enter at site site Enter cells (macros/monos, skeletal muscles, cardiac muscle) Multiply intracellularly as amastigotes Lyse and infect other cells (flagellated forms) or reduviids |
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Diagnostic stage of chagas disease
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Extracellular flagellated forms in blood
(hard to see in chronic disease) C-shaped |
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Symptoms of chagas disease
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Initial infection often mild/subclinical
Some have painless swollen lesion near eye at site of bite (Romana's sign) Some die in acute phase (CHF, meningitis) 10% of seropositive get chronic chagas dilated cardiomyopathy, mega-colon and esophagus, transplacental (3%) |
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Mega-colon in chagas
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Destruction of autonomic ganglia
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Diagnosing chronic chagas
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Look for flaggelated form in blood smear (probably won't work)
Culture blood on blood agar for 3 months Inject mice with blood and look for circulating forms Xenodiagosis Complement fixation - poor sensitiivty |
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Xenodiagnosis in chagas disease
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For diagnosing chronic disease
Feed lab-grown reduviid bug on patient Check bug rectum for fecal parasites 1-2 months later Will be replaced by PCR |
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Preventing chagas
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Better housing where the bugs can't live
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How to get chagas without insect bite?
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Blood transfusion in South or Central America
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Treating chagas
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Treat acute disease: nifurtimox, benznidazole
Treat cardiac arrythmias |
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African trypanosomiasis
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Sleeping sickness
Extracellular protozoan Flagellated |
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Life cycle of African trypanosomiasis
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Infected tsetse fly bites
Transmits trypanosome in saliva Trypnansomes multiply in blood, lymph, CSF, tissues Uninfected tsetse fly bites a person with parasitemia |
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Pathogenesis of African trypanosomiasis
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Ulcerating lesion at bite site from local multiplication
Two weeks later Parasitemia, fever, posterior cervical lymphadenopathy Invasion of CSF and parasite multiplication here -- products cause neural dysfnc |
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Diagnostic stage of african trypanosomiasis
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Flagellated form in
blood, lymph node biopsy, CSF |
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Symptoms of African typanosomiasis
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Ulcerating nodule
Fever Lymphadenopathy Splenomegaly Lethargy, coma, death |
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Reservoir for sleeping sickness
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Large mammals
Native cattle can survive disease (imported cannot) |
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Treating sleeping sickness
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Use toxic drugs
Need to treat or its fatal melarsoprol, suramin, eflornithine |
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Winterbottom's sign
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Posterior cervical adenopathy
Sign of african trypanosomiasis |
