Parasitology review

November 5, 2009

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Types of Life Cycle• Direct life cycle

– Only one animal (human) host needed for entire life cycle.– Pinworm, hookworm, head lice

• Indirect life cycle – More than one animal host required for complete life cycle– beef tapeworm (human + ox)– fluke (human + snail)– filariasis (human + mosquito/fly)– malaria (human + anopheline mosquito)

• VectorsAnimals, usually arthropods (insects/ticks/mites) that transmit infection

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Types of host in indirect life cycles

• Definitive host – Host where sexually mature adult forms.– Malaria (mosquito); Toxoplasma (cat)

• Intermediate host – host(s) in which larvae form

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Reservoir Hosts

Wild or domestic animals that maintain parasite life cycle.I.e. stage of life cycle is not restricted to humans with animals and humans acting as alternative hosts

Many wild animal hosts : Trypanosoma brucei (African trypanosomiasis)Water buffalo : Schistosoma japonicum (Borneo)Dogs : Leishmania infantum

Pathology mainly due to blood cyclemerozoite – trophozoite- schizont- merozoite

Liver phase of malaraiaSporozoites invade hepatocytes

–Multiply greatly (1 sporozoite gives rise to several thousand merozoites) –Merozoites released in 1-2 weeks (depends on species)These will infect RBCs

Dormant forms hypnozoites derived from sporozoites (Gr. hypno = sleep). These activate and grow in hepatocytes at various times after original mosquito bite to give relapse

Reactivation–P. vivax and P. ovale ~5 years reactivation due to hypnozoites–P. malariae >20 years due to reactivation of persistently infected

RBCs –P. falciparum does NOT have hypnozoites and does not cause relapse

Malaria - cycle in blood

trophozoite

Red cell phase• RBC infection to cell lysis takes ~48 h (tertian malaria) except for P. malariae (72 h)

• falciparum – Potentially deadly. Infected RBCs become sticky and block capillaries

in CNS (cerebral malaria) and GI (diarrhea). Persons with sickle cell trait (HbA+S) are resistantShortest incubation period (7-10 days)Relapses not seen

• vivax – Most common form. Incubation 10-17 days– Persons who are Duffy-negative are resistant

• ovale • (like vivax but not binding via Duffy)

• malariae fever every 4th day– Infections can last for years– Longest incubation period (18-40 days)

Damage due to P. falciparum

• Blocking of capillaries• Anemia (mainly of inflammation)+ some red

cell lysis• 5% RBCs can be infected• Fever

Leishmaniasis

• Old World and New World diseases caused by different species

• Infective form is flagellated is released into skin by a sandfly and is phagocytosed to form the intracellular amastigote.

• The amastigotes lack flagella and divide within macrophages. This is the diagnostic form

• Transmitted to sandflies ingesting blood containing amastigotes within monocytes

Visceral Leishmaniasis

• Human main source for L. donovani

• Dogs, main source for L. infantum

LeishmaniasisVisceral disease (most serious) affects all organs where grows in fixed macrophages or macrophages that enter organ

• Cutaneous disease (chronic sore). Several species: differ in Old and New World

• Mucocutaneous disease in South and Central America. Single species that has potential to eat away face

• Controlled by Th1 activity (IFN- activation of macrophages)

Diagnostic stage

African Trypanosomiasis

• Extracellular blood protozoan that divides longitudinally• Transmitted by tsetse fly• Wild animals provide major reservoir

African Trypanosomiasis

Surface coating has antigenic VSG (variable surface glycoprotein). Different VSGs are expressed by organisms within a population. This allows a replacement population to be generated after an effective antibody response against the dominant VSG. This enables evasion of host response

African Trypanosomiasis

Infection occurs in 3 stages.

• chancre may develop at inoculation site.

• hemolymphatic stage fever, lymphadenopathy, and pruritus.

• meningoencephalitic stage

invasion of the central nervous system causing headaches, somnolence, abnormal behavior, and leading to loss of consciousness and coma.

Chagas’ Disease - Trypanosoma cruzi• South American (and Central American) trypanosoma.

Transmitted by reduviid bugs that pick up flagellated form from blood

• In addition to blood form, amastigotes (no flagellum) are produced and these live intracellularly

• Major cause of cardiomyopathy . Also megaesophagus with or without megacolon following destruction of myenteric plexus. Other sites may be involved too

Chagas’ Disease

Reduviid (kissing) bug. Fecal drops with parasite rubbed into skin wound orparasite enters throughconjunctiva

Toxoplasmosis• Definitive hosts are felines (cats etc) where T. gondii grows within the gut

epithelium. When infected, these release oocysts in their feces for about 3 weeks. It takes about 3 days for oocysts to become infective (embryonate)

• Embryonated oocysts ingested by mammalian intermediate host

• Oocyst wall digested in small intestine. Parasites penetrate intestinal wall and are picked up by macrophages, then spread throughout body via blood.

• The tachyzoite stage in macrophages divides extensively, when released can

infect other macrophages or almost any nucleated cell

• Progressive disease controlled by T-cell mediated immunity (Th1) which prevents spread of infection in organ. Area where infection occurred and somewhat controlled is a pseudocyst (especially brain but the other sites)

• If pseudocysts are eaten, infectious toxoplasma can cause infection in humans (mainly associated with not fully cooked meat)

Toxoplasmosis• Humans infected by eating:

– oocysts (from cat feces) – pseudocysts (uncooked flesh of an intermediated host)

• Congenital disease serious – Can occur if mother is not immune and becomes infected shortly before

or during pregnancy (Torch syndrome). Chorioretinitis often seen.– Keep cats indoor and don’t handle cat feces

• AIDS – reactivation of pseudocysts can occur. Toxoplasma is the most

common reason for ring-enhancing lesion in brain seen in contrast enhanced CT or MRI scan

• Diagnosis: – serology (IgG in absence of IgM antibody suggests immunity and

no ongoing infection)

pseudocyst

Ring-enhanced lesions in AIDS

Giardiasis

• In USA, most common protozoal pathogen reported causing GI infection

• Acquired by ingesting cysts (usually in water or other fecal-oral).

• Cysts are present in feces (human and several animals including beaver)

• Infection causes diarrhea and can lead to chronic malabsorption syndrome. Giardia attaches to upper small bowel

• IgA deficient people very susceptible• Diagnosis; detection of trophozoites and/or cysts in feces

(specific antibody-based stains available for trophozoites)

Cysts (above) and trophozoites of Giardia

Immunofluorescence

Cryptosporidiosis

• Cryptosporidium parvum is a common cause of diarrhea but persons typically recover very fast. It grows within the GI tract, hardly ever disseminates

• Incidence of diarrhea increases with communal bathing at swimming pools during summer months

• In AIDS, C. parvum can cause a chronic, potentially lethal, diarrhea.

• Infection from ingesting oocysts (1 oocyst is enough to establish infection)

• Diagnosis via microscopy for oocysts in feces (C. parvum oocysts are acid fast). Antibody-based stains are available

Oocysts of Cryptosporidium in feces

Entamoeba histolytica

• Infects ~ ½ billion people• Causes intestinal and extraintestinal infection• Infection is fecal-oral – cysts transmit disease.

Almost all infection is human-human• ~90-95% infections asymptomatic• Colitis most common disease (flask shaped ulcers

in colon mucosa)• If invade portal venous system, can cause liver

abscess. Abscess also can form elsewhere such as lung and brain

Entamoeba histolytica types of disease and diagnosis

• Colitis – diagnose using feces or mucosal biopsy (Serology can help but is not positive all the time)

• Extraintestinal diseases (e.g. liver abscess) – visible by imaging. (could be hydatid cyst, tumor or Entamoeba)

For differential, serology is needed since finding E. histolytica in intestine does not prove it is causing an extraintestinal abscess (antibody and antigen tests available). Serology test for an antibody or lectin antigen

Material drained from abscess is just necrotic cells. You cannot see Entamoeba in it since the live amebae are penetrating and attacking the surrounding liver tissue

• Typical therapy is metronidazole then paromomycin

Entamoeba histolytica

Multinucleate cyst with chromatoid body trophozoite (will ingest RBCs)

Trichomoniasis• Major STD. Often asymptomatic in men, can be

asymptomatic in women• Infection in women characterized by vaginal discharge +

soreness. • Diagnosis made by from wet mount with motile

protozoan seen. Also with various stains including antibody-based stains

• Metronidazole is usual treatment

Trichomonas vaginalisFlagella present. No cyst stage

Drugs for Malaria– Chloroquine

• Oral. Used as prophylaxis and for acute attacks – all types of malaria. Kills schizonts in blood, not in liver

• BUT much P. falciparum is now resistant so rarely able to be first choice for prophylaxis or treatment of falciparum malaria

– Mefloquine• Oral. First line prophylaxis where chloroquine resistance is present. Resistance to

mefloquine is emerging in SE Asia. Used for acute malaria (as alternative to quinine)– Primaquine

• Kills schizonts in tissues but not in blood • (good for eradicating liver stages of vivax and ovale)

– Quinine• Oral for active disease (can be i.v. in severe disease). Fairly toxic. Usually used with

doxycycline or clindamycin to reduce time of use. Kills schizonts in blood- not in liver. Problems in G6PDH deficiency. Can cause intravascular hemolysis (Blackwater fever)

– Antifolates • Doxycycline (can be used as prophylaxis in areas with resistance to mefloquine and

chloroquine)

– A variety of other drugs available with varying effectiveness and side effects

Drugs for other protozoa• Metronidazole (oral)

– Amebiasis, giardiasis, trichomoniasis– Bacteroides fragilis, Clostridium difficile– Free radicals produced during its metabolism. Requires high redox

potential (not found in non-anaerobic microbes)– Reported effective in cutaneous forms of leishmaniasis

• Paromomycin– Aminoglycoside that can be used for luminal amebiasis– ? ? Some efficacy for cryptosporidioisis in AIDS– Being investigated and looks effective as cheap alternative for visceral

leishmaniasis (replacing liposomal amphotericin B or sodium stibogluconate which is toxic and tends to prolong cardiac QT interval)

Drugs for toxoplasmosis and trypanosomiasis

• Toxoplasmosis– Antifolates

• Pyrimethamine + sulfadiazine• Pyrimethamine + clindamycin• Given with folinic acid (=leucovorin) to offset hematologic toxicity. Folinic acid is

converted to tetrahydrofolate directly (not requiring dihydrofolate reductase)

• Trypansomiasis– Pentamidine - only the blood stages of African trypanosomiasis. Also used for Pneumocystis– Melasoprol - CNS stages of african trypanosomiasis – Nifurtimox - Both Chagas and African trypanosomiasis (+ mucocutaneous leishmaniasis).

Highly toxic

TapewormsAdult in intestinal lumen has a scolex that attaches to intestine wall, followed by the neck region and strobila composed of proglottids.

•immature near neck • mature, •gravid (with fertile eggs)

Eggs (+ proglottids) in feces give diagnosis

scolex

Matureproglottid

Gravid proglottid

TapewormsLarval forms derived from eggs that are ingested

In correct host, eggs hatch within small intestine and larva penetrates through intestinal wall and migrates into tissues where it forms a mature infective larva. This is the damaging form of tapeworm disease

The infective larva, when eaten by a definitive host, develops into the adult tapeworm within the intestine

Adult Tapeworms Site in human Source Human Diagnosis

Beef intestine larva in beef eggs(+proglottids) in fecesT. saginata

Pork intestine larva in pork eggs(+proglottids) in fecesT. solium These have humans as their sole definitive host

Fish intestine larva in fish eggs(+proglottids) in fecesD. latumMay absorb beaucoup vitamin B12 and, if enough, cause megaloblastic anemia (rare)Has a number of wild animals as reservoir definitive hosts

Control of adult tapeworm infection in humansCooking meat to kill larva

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Egg shape and size allows you to identify a helminth. Fecal preps

Fluke eggsOften have a cap“operculum”

Roundworms

Tapeworms

Flukes

Urine and feces

Sputum and feces

Human Larval tapeworm disease

• Acquired from ingesting eggs from feces • i.e. fecal oral • Controlled by good sanitation

• Hydatid cyst. Many intermediate hosts including humans. (Dogs are definitive hosts)

• Cysticercosis. Pigs and humans can both be intermediate hosts infected via eating Taenia solium eggs in feces of humans with adult pork tapeworm

Cysticercosis• Taenia solium eggs release larvae in

small intestine• Larvae penetrate intestinal wall and

spread to multiple sites including muscle, liver and CNS

• Muscle infection – myalgias, see calcifications by X-ray

• Brain infection - seizures etc. Especially after a few years when aging cysticercus begins to swell

• Fairly common in parts of Mexico where incidence of pork tapeworm is high and hygiene standards can be low

Neurocysticercosis

Calcified cysticerci in muscle

Larval disease caused by Echinococcus granulosus (hydatid cyst)

• Many animals, including humans, can act as intermediate hosts.

• Herding animals with dogs associated as an occupational risk

• Larva forms a large ball like structure filled with fluid and protoscolices (hydatid sand). On rupture of the cyst, protoscolices can form new cysts. Antigens in fluid may also cause anaphylaxis leading to death.

• When protoscolices eaten by dog, adult tapeworm forms in dog intestine

• Diagnosed by imaging and serology

40From: www.biosci.ohio-state.edu/

Cyst/contents in offal eaten by dog in which adult form develops from protoscolex

Dog intestine

Eggs indog feces

Eaten by sheep,humans etc

HUMANS, SHEEP, GOATS, Camels etc. (not dogs)

Flukes• All flukes have a mollusc (a water snail) as an intermediate

host. Therefore all show an indirect life cycle. • Eggs released from humans hatch in water and release a larva

that infects the snail. • In the snail, the organism divides and the numbers of larvae

increase substantially• The larval form released from the snail is motile and named a

cercaria• Humans are either infected via ingestion of encysted cercaria

(liver fluke and lung fluke) or the cercariae may infect directly through the skin (i.e. for schistosomes)

• After infection larvae enter human circulation by penetrating small intestine wall (lung and liver flukes) or after some time as a schistosomulum in the skin and then migrate through tissues before arriving at target site and becoming adults (eosinophilia seen)

• Liver flukes (bile duct), Lung flukes (lungs), Schistosomes (blood vessels in mesentery or around bladder)

Liver fluke (Fasciola)

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Lung fluke – Paragonimus westermani

Eggs in sputum may be swallowed

Tissue invasion with migration to lung cavities where adults mature

Metacercariae in lobsters, crabs, shrimp are eaten

Schistosoma mansoni

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Water snail host of certain schistosome species (limited snail species are hosts)

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Schistosomes • Contact with water

leads to infection through skin by cercaria

• The cercaria then undergoes transition to a schistosomulum

47http://www.path.cam.ac.uk/~schisto/SchistoLife/Human.skin.html

5 min 10 min 20 min

5 min: schistosomule penetrated surface of epidermis10 min: broken through basement membrane of epidermis20 min: migration in dermis. Search for blood vessel and time for antigen coating (2 days)

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Schistosomes • transition to schistosomulum

– hyaluronidase helps in skin penetration– cercaria loses tail– fresh water to salt water organism physiology– glycolysis switch to fermentation– tegument takes up host components including RBC

antigens, HLA, Ig

• Once complete (~2 days) schistosomulum migrates from skin via lung to liver

49http://www.path.cam.ac.uk/~schisto/SchistoLife/Schistosomule.html

Immature schistosomulum feeds on plasma while maturing to young adult

migrates via lungs to liver where adults mate

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Schistosomes • 3 main species. Mate, produce eggs

– S. mansoni: mesenteric veins– S. japonicum: mesenteric veins– S. haematobium: veins around bladder

– Eggs released (100s - 1000s a day) migrate into intestinal lumen or bladder. Eggs produce proteases allowing migration through host tissue.

– ~50% eggs die within host tissue.

– The dead eggs induce inflammation and that eventually causes tissue damage

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Portal hypertensionAscitesEsophageal varicesCor pulmonale

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Schistosoma haematobium– hematuria in early disease

(school urines: East Africa who/tdr/crump)– evential fibrosis of bladder and obstructive

uropathy– renal failure and hydronephrosis can occur.– Bladder carcinoma also found

•Diagnosis

– Eggs are characteristic

Main speciesS. mansoni (Tropical Africa, S. and Central

America, Caribbean) Lateral spineS. japonicum (Asia)

eggs in fecesS. haematobium (Tropical Africa, Near East)

eggs in urine, and some in feces Terminal spine.

(Additional 2 less common species with more localized distributions)55

Schistosomes

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Schistosomes • Control (~200 million persons affected)

Specificity for snail host prevents spread outside snail’s geographical range

– Sanitation (avoiding excretion into open water where snails live)

– Snail reduction • (also control irrigation projects that allow snail spread)

– Reduction in carriage in population by using medication. But S. mansoni also in some rodents

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Immunity • Main target is schistosomulum and enzymes involved in

skin penetration.

• Low worm load may give minimal disease but stimulate some (not total) resistance to further infection - (Concomitant immunity)

• Macrophages, eosinophils, neutrophils all involved in resistance.

• IgE receptors on macrophages and activated eosinphils.

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Cercarial dermatitis • Infection of skin by cercariae that are

not adapted to humans (e.g. in ducks, these mature into adult schistosomes)

• cercariae penetrate skin (pin prick)• fail to form functional schistosomulum

and die• inflammatory reaction in skin (treatable

with antinflammatory drugs• serious problem locally for swimmers in

ponds, quarries etc

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Parasitic Helminths Basic Life Cycle

Tapeworms, Flukes, Nematodes

Egg

Larval stage(s)

Adult

61http://www.wormatlas.org

Nematodes: unsegmented roundworms

crawl

Body cavity and full digestive system Cuticle

shed during moltsallows minimal transport of nutrients

Muscular system for motilityAdult parasites usually separate sexes

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Parasitic Nematodes• Intestinal nematodes

– adults live in GI tract, maturing usually in small intestine or colon.

– some species get to intestine after larval migration via internal organs (e.g. lung)

– usually direct infection by eggs or larvae • (but hookworms & Strongyloides infect through skin)

• Almost all intestinal worms have direct life cycle Most cannot replicate without humans

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Pinworm (Enterobius)

Extremely common, most notable in young children

400,000,000 worldwideDirect life cycle

Female 8-13 mmMale 2-5 mm

Image from OSUwww.emedicine.com/med/images/18381.jpg

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Pinworm (Enterobius)Eggs ingested

Larvae hatch in small intestine (2 molts) and migrate to colon

Mature and mate

Females (containing ~10,000 eggs) migrate out of anus and lay eggs on anal skin after explosive evagination of uterus

Eggs become infective (embryonate) after 6 h

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Pinworm (Enterobius)

INTENSE ANAL ITCHING – main symptom!but many persons with low level carriage are asymptomatic

Diagnosis: characteristic eggs on anal skin - detected using clear sticky tape (Scotch tape test). Sometimes worms seen in feces

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Whipworm - Trichuris• Similar life cycle to pinworm except adults live in colon and

females release ~5000 eggs/day directly into feces. • Eggs take ~3-4 weeks to become infectious (embryonate) in soil• Infection by ingesting embryonated eggs

• Often coinfecting with hookworm and Ascaris1 billion personsExtremely heavy infections

can cause rectal prolapse

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Ascaris lumbricoides• Worldwide 1.5 billion

• (in USA, mainly in South)• Direct life cycle• Adults are large

– 8-14 inch female (200,000 eggs/day)– 6-12 inch male

• Infection after ingestion of embryonated eggs

• Eggs released in feces require 2-4 wk. incubation in soil to become embryonated. Widely spread when human feces used as fertilizer

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Ascaris lumbricoides - A long journey home

• Infection via oral route: embryonated eggs

• Larvae hatch in small intestine (pH bile) and enter lamina propria and mesenteric capillaries

• Migrate via liver, heart to lung• Enter alveoli and then migrate up bronchioles, bronchi and trachea

to epiglottis and then swallowed

http://workforce.cup.edu/buckelew/Ascaris%20lumbricoides%20larvae.htmImage from Thomas P. Buckelew, Ph.D.

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Ascaris lumbricoides - A long journey home

• Larval migration and molt in lung induces IgG antibody and eosinophilia

• After entry to small intestine, larvae mature (2 molts) into adults. Mating occurs with 6 weeks

• Adults feed on digested food in intestine

From OSU website

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Ascaris lumbricoides• Problems

– Larval migration: (no effective drug). Large number can cause pneumonitis & liver enlargement– Adult worms: rarely problem. If many, can cause intestinal blockage.– Aberrant migration known.

• Bile duct, liver,• penetrate intestinal wall – peritonitis

• Diagnosis– Eggs in feces characteristic– Occasionally whole worms expelled– Many carriers asymptomatic

• Control– Sanitation (but eggs resist disinfectants)

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Ascaris lumbricoides• Diagnosis:

– Eggs characteristic– Occasionally whole worms expelled– Many carriers asymptomatic

• Control:– Sanitation– Eggs resist disinfectants and sewage treatment

• Treatment:– mebendazole, albendazole

• also pyrantel pamoate, ivermectin, tribendimine

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Trichinosis - Trichinella spiralis

• Infection after ingestion of larvae in meat.

• Several million humans were infected in USA most usually due to T. spiralis in pork (16.1% population in 1943; 4.2% in 1970)

• Main source now is wild animals. 72 cases reported to CDC (1997-2001)

• In most environments kept in circulation by rodents being eaten by carnivores

• In Arctic animals, variety of Trichinella survives deep freezing

• Adults are very small and have short life (~7 days) in intestine. Not usually seen.

• Female releases larvae that penetrate intestinal wall

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Trichinosis - Trichinella spiralis• Released larvae enter lamina propria, then blood/lymph, and migrate

around body. • Penetrate into cells• In skeletal muscle “encysted” in a Nurse cell and survive many years. In

other tissues, larvae die.

http://phil.cdc.gov/

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TrichinosisSigns and Symptoms

Intestinal - First weekNausea, vomiting, cramps, diarrhea (sometimes bloody)

Extraintestinal – Second weekMuscle invasion (myalgia, weakness, malaise)Other organs may be invaded, may see petechiaeMyocarditis (uncommon) is potentially fatalCNS invasion can cause fits, paralysis, coma etc.By 3rd week, larvae begin to encyst

Eosinophilia in 2nd week peaking in 3rd week

Serum creatinine phophokinase and LDH levels

Diagnosis No eggs are passed!! Serology for antibody and muscle biopsy to see larvae

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Hookworm• 2 species - Widespread in tropics and important

cause of anemia. 1.3 billion infected, 12% morbidity. – 65,000 die, 0.005%

• Adults (~1 cm) in intestine live 4-5 years– Ancylostoma - 0.1-0.2 ml blood per day– Necator - 0.01- 0.02 ml blood per day

– Heavy infections can have >1000 worms

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Hookworm

• Adults in small intestine• Females release 10,000-

30,000 eggs/day• Eggs hatch within 2 days on

warm sandly soil• Larvae feed on debris and

molt twice– Filariform larvae climb on

vegetation (grass etc)

Hookworm

• Adults in small intestine, release eggs (10,000/30,000 per day).

• Eggs hatch within 48 hours on warm, moist, sandy soil.

• Larvae feed on debris and molt twice

Hookworm vs. Strongyloides larvae

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Hookworm

• On contact with bare skin, filariform larvae PENETRATE skin, usually entering via hair follicle. Enter capillaries.

• Migrate via lung, bronchi and trachea to epiglottis and are swallowed (as for Ascaris)

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Hookworm • Migratory phase

– Eosinophilia

• Diagnosis– Characteristic eggs: do not distinguish hookworm species

• Prevention– good sanitation

• (avoid feces on soil- privies are adequate) – wearing shoes.

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Strongyloides• Tropical: Seen in Indochina and other areas of the

world• Similar to hookworm but differs by:

– Non-human reservoir hosts (monkey, dogs)– Eggs released but hatch within human intestine– rhabditiform larvae in feces (diagnostic). – Filariform larvae penetrate human skin (as in

hookworm)

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Comparison of hookworm and Strongyloides larvae

Hookworm

• Adults in small intestine, release eggs (10,000/30,000 per day).

• Eggs hatch within 48 hours on warm, moist, sandy soil.

• Larvae feed on debris and molt twice

Hookworm vs. Strongyloides larvae

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• Autoinfection possible – rhabditiform larvae molt in intestine (constipation)– resultant filariform larvae can directly reinfect via

colon mucosa or via skin– Large build up in immunosuppressed patients

Strongyloides

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Strongyloides

• Diagnosis– Rhabditiform larvae in feces. – Eggs NOT found in feces– String test – ELISA

– Long term survival of infection means screening must be done before immunosuppression for transplant, cancer etc.

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Nematode Parasites in Wrong Host• Larvae wander in tissues in absence of sensing correct

signals for migration. Intense inflammation and irritation. Eventual death

• Dog hookworm and other nematodes– Cutaneous larva migrans

• Dog ascaris and other species.– Infection after ingesting eggs– Visceral larva migrans (eye, brain are possible)– Many different species known to cause these

diseases including a nematode of raccoons

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Anisakis case: www.fujita-hu.ac.jp/~tsutsumi/case/case025.htm

Anisakis (from fish) Dog hookworm (Dermis.net)

Wandering larvae

Anisakis (from fish) Dog Hookworm (Dermis.net)

Anisakis case: www.fujita-hu.ac.jp/~tsutsumi/case/case025.htm

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Tissue nematodes – vector transmittedPrevalence

Lymphatic filariasis (elephantiasis) 120 millionOnchocerciasis (river blindness) 37 millionLoiasis (African eye worm) 13 million

Dracunculiasis (Guinea worm) 1 million(a deep tissue nematode: not truly a filarial species)

Many species of filarial nematodes contain essential bacterial endosymbionts: potential treatment target

Lymphatic filariasisWuchereria bancrofti and other species

http://www.filariasis.org/resources/countries_map_list.htm

Wuchereria bancrofti

There are several mosquito vectors Microfilaria in blood (above)

Adults in lymphatics. They release microfilariae

~270 m long

4-8 cm long

©TDR/WHO/Crump

www.filariasis.org

www.filariasis.org

Detection of filariasis in humans• Detection of microfilariae in blood. Requires testing at time

mosquitoes were biting (often middle of night). Still needed when not Wuchereria infections

• Most easy method now for detecting Wuchereria is via antigen in blood – can be done at any time of day/night

Rapid antigen detectionfor Wuchereria infections

Onchocerciasis – River blindness

Americas Africa (main area)

Also Yemen

Onchocerciasis – River blindness

• Major cause of blindness following continual inflammation of eye

• Larvae transmitted by bites from Simulium blackflies that live on rocks with fast moving water

• Adults live in subcutaneous nodules and release microfilariae that mainly are found in skin and connective tissues. Inflammation follows their death

• Severe itching of skin

Adult Onchocerca volvulus in nodules

http://www.icp.ucl.ac.be/~opperd/parasites/onch1.html

Tick paralysis (fairly rare)Toxin produced by female ticks:

several genera

Affects motor nerve conduction

Ascending paralysis

Tick typically attaches at back of neck.

Treatment: Remove tick and support patient

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Fed and unfed

Venoms from bees, yellow jackets, fire ants, spiders Direct venom effects damage and possibility for anaphylaxis

Many arthropods are vectors for pathogens

Irritation usually due to response against saliva, not to trauma

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Scabies • Mite (itch mite, Sarcoptes scabiei)

• Forms tunnels in epidermis

• After mating in skin pits, female mite tunnels within epidermis, leaving feces and eggs behind

• Irritation associated with immune inflammatory response. More rapid if already sensitized on previous occasion.

• Only short term survival off body

• In typical case <50 mites (often <20 on a person)

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Tunnels in the epidermis

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Scabies• Transmission requires close personal

contact. Mite survives only for a short time off the body

• Diagnosis– Symptoms and history (Ist infestation may take 2-

3 weeks to itch, second itches much sooner)– Skin scraping for mites, eggs and fecal pellets

– Mites and eggs are NOT visible to naked eye

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Scabies mite, eggs and feces in burrowsseen in skin scrapings

medent.usyd.edu.au/photos/mite_photos.htm

Morse et al: Atlas of Sexually Transmitted Diseases

Scabies DiagnosisEggs, fecal pellets and mites seen in skin scrapings

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Crusted scabies

Results of severe itching Include superinfection

Crusted (Norwegian) scabies

Immunosuppressed patientsMassive numbers of mites

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Scabies

Treatment

• Generally treated with lindane (care under nails)

• Ivermectin

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Lice

Head lice (Pediculus humanus)

Body lice ( “ “ )

Pubic lice or Crab lice (Pthirus pubis)

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Lice

nit (egg) glued to hair

larval stages hatch feed on blood molt

adults live in hair (clothing)feed on blood (itchiness response

to saliva)

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Head Lice• Pediculus humanus. (Can adapt to wigs)• Several million treatments sold per year• Showing increasing resistance to insecticides

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Body LicePediculus humanus corporis

Sign of poverty

Lice live within clothingVector for trench fever (Bartonella), epidemic typhus, (Rickettsia prowazekii)

Eggs in clothing.

http://www2.mf.uni-lj.si/~mil/clen1/jpeg/3b5.jpg

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Crab lice

• Pthirus pubis

• STD usually

• Lives in coarser hair– (eyelashes, armpit,

pubic)

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Treatment of liceCombing with fine-toothed comb

Insecticides in shampoo including malathion

Ivermectin: the heavy gun!

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Delusions of parasitosis

• Not uncommon

• Treat delusion

Guinea worm (Dracunculus)

Control using wells and/or filtered water

Burning sensation

Copyright: Carter Center and used by permission

Removing the Guinea Worm

Images from phil.cdc.gov Left and Upper right image copyright Carter Center and used by permission

No drug treatment effective

Treatments (main drugs) for helminthsNot all of them

• Nematodes– Ivermectin intensifies GABA-mediated neurotransmission– Mebendazole inhibits microtubule synthesis– Albendazole– Pyrantyl pamoate– Others (antibacterials being investigated for filariasis)

• Flukes and Adult Tapeworms – Praziquantel for most acts on Ca++ uptake– Oxamniquine (Schistosoma mansoni only)

• Larval tapeworms– Albendazole