Zoonotic Helminthiasis

ZOONOTIC HELMINTHIASIS
* Helminth: parasitic worm (Greek)
o Platyhelminthes (flukes, tapeworms)
o Nematodes (roundworms)

* Pathogenic helminths are some of most common parasites
* Worlwide distribution
* Toxocariasis (visceral/ocular larval migrans)
o Toxocara canis, T. cati
* Meningoencephalitis
o Balysascaris procyonis
* Trichinosis
o Trichinella spiralis
* Taeniasis
o Taenia soleum, T. saginata
* Hydatid disease
o Echinococcus granulosus, E. multilocularis

TOXOCARIASIS
* Agent:
o Toxocara canis - roundworm of dogs and cats
o Toxocara cati - roundworm of cats (less frequently involved)
* Other names for diseae:
o visceral larval migrans (VLM)
o ocular larval migrans (OLM)

TOXOCARIASIS
Egg
Adult female - head
* Life cycle:
Epidemiology
* Reservoir:
o dogs, cats, small mammals
* Distribution:
o worldwide, most attention in US and UK
o seroprevalence: 3%; 23% in some groups
* Transmission:
o direct or indirect by ingestion of infective eggs from fecal contamination or contaminated soil
o larvae in contaminated undercooked liver from poultry, beef

Clinical features
* Incubation period:
o children - weeks to months
o OLM may be 2-4 years later
* Symptoms:
o asymptomatic to chronic, mild disease (usually)
o predominantly in young children
o increasingly recognized in adults
o symptoms related to migration of larval stage through tissues
* Symptoms:
o VLM - may persist for year or longer
+ fever
+ anorexia
+ weight loss
+ cough
+ eosinophilia
+ rash
+ hepatosplenomegaly
+ death (rarely) due to severe cardiopulmonary and neurologic manifestations
* Symptoms:
o OLM
+ misdiagnosed as retinoblastoma, leading to surgical enucleation
+ endophthalmitis at entry of larva
+ loss of vision
+ eosinophilia rare
+ visceral manifestation rare
+ occurs in children and adults
Diagnosis
* Direct (fecal) examination no use - larva does not develop into adult, no ova passed in feces
* Antibody detection confirmatory only in presence of clinical signs and history
o EIA (enzyme immunoassay)
+ larval antigen extracts from
# embryonated eggs
# cultured TES (Toxocara excretory-secretory antigens) - preferred
+ 1:32

Treatment
* Supportive treatment
* Anthelmentics - effectiveness uncertain
o DEC (diethylcarbamazine)
o Albendazole
o Mebendazole
* Corticosteroids for severe eye problems

Prevention/Control
* Education, especially pet owners
* Routine examination of pets
* Effective deworming program for puppies and kittens
* Removal of feces from environment
* Routine hygiene after handling pets, soil

TAENIASIS
* Agent:
o Tanea soleum - pork tapeworm
o T. saginata - beef tapeworm
* Other names for disease:
o taeniasis - intestinal infection of either tapeworm in animals or humans
o cystiserciasis; cysticercosis - tissue infection with T. soleum larva

Epidemiology
* Reservoir:
o humans definitive host for both T. saginata and T. soleum
* Occurrence:
o worldwide
o highest in Latin America, Africa, SE Asia, Eastern Europe
o T. soleum rare in US, Canada, UK, but increasingly recognized in immigrants

Epidemiology
* Transmission:
Clinical features
* Incubation period:
o taeniasis - eggs appear in 8-14 weeks
o cystercosis - days to years
* Symptoms:
o Taeniasis
+ mild abdominal symptoms
+ occasionally appendicitis or cholangitis from migrating proglottids
+ passage of proglottids (active or passive)
Clinical features
* Cysticercosis:
TANEIASIS
Diagnosis
* Taeniasis
* Cysticercosis
Treatment
* Taeniasis
o praziquantel
* Cystercosis
o praziquentel if active cystercosis, but only under hospitalization due to acute inflammatory reaction; steroids given to control inflammation
o surgical
+ shunt - ventriculoperitoneal shunt to drain CSF
+ cyst removal
+ endoscopic fenestration (hole in cyst wall)

Prevention/Control
* Education
* Identification and immediate treatment of infected individuals
* Freezing meat at -5ºC (23ºF) for > 4 days effectively kills cysticerci
* Irradiation

Agent
Echinococcus granulosus
E. multilocularis
E. vogeli
E. oligarthrus
Disease
Cystic hydatid disease;
unilocular echinococcosis
Alveolar hydatid disease;
multilocular echinococcosis
Polycystic alveolar disease
Rare in humans

UNILOCULAR ECHINOCOCCOSIS
Hydatid “sand”-protoscolices from fluid aspirate of hydatid cyst
Note: normally invaginated; evaginates in saline (right)

Epidemiology
* Transmission:

Clinical features
* Incubation period: months to years
* Symptoms:
o cysts grow slowly, asymptomatic until noticeable mass effect
o compatible with slow-growing tumor
o symptoms depend on location, size, and number of cysts
o anaphylactoid reaction if cyst ruptures/leaks

MULTILOCULAR ECHINOCOCCOSIS
Epidemiology
Clinical features
POLYCYSTIC ECHINOCOCCOSIS
Clinical features
Diagnosis
Serological diagnosis
Treatment
DIPHYLLOBOTHRIASIS
Epidemiology
* Occurrence:
Clinical features
Diagnosis
Treatment
Prevention and Control
ANISAKIASIS
Epidemiology
* Occurrence:
Clinical features
Diagnosis
* Direct examination:
o parasite coughed up
o Fiber optic exam
o laparotomy
* Radioallergosorbent (skin test) developed but not available commercially

Treatment
* surgical excision
Prevention and control
* Avoid ingestion of raw/undercooked fish
* Heating for 10 minutes @ 140ºF (60ºC)
* Freezing:
o “blast freezing” for 15 hours @ -31ºF (-35ºC)
o regular freezing for 7 days @ -10ºF (-23ºC)
* irradiation
* proper cleaning/evisceration as soon as caught

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Parasitic Pathogens Affecting the CNS

Parasitic Pathogens Affecting the CNS
By:Mark F. Wiser
Department of Tropical Medicine
School of Public Health

Protozoa Affecting the CNS
Rare cases
Free-living ameba
Rare invasion of the brain
Entamoeba histolytica
Cerebral Malaria
Plasmodium falciparum
African Sleeping Sickness
African Trypanosomes
Associated with congenital defects and AIDS
Toxoplasma gondii
Disease

Protozoan
Amebas Affecting the CNS
* Entamoeba histolytica
o normally found in large intestine
o can become invasive (primarily liver)
* Free-living Amebas

GAE; skin or lung lesions
Balamuthia mandrillaris
GAE; skin or lung lesions; amebic keratitis
Acanthamoeba species
PAM

Naegleria fowleri
Diseases
Ameba

Toxoplasma gondii
* cosmopolitan distribution
* seropositive prevalence rates vary
o generally 20-75%
* generally causes very benign disease in immunocompetent adults
o congenital transmission
o AIDS associated
* tissue cyst forming coccidia
o predator-prey life cycle
o felines are definitive host
o infects wide range of birds and mammals (intermediate hosts)

Definitive Host
* adult forms
* sexual reproduction

Intermediate Host
* immature forms
* asexual reproduction

chronic stage = bradyzoites
acute stage = tachyzoites
* ingestion of sporulated oocysts (cat feces + incubation)
* ingestion of zoites (undercooked meat)
* congenital infection (only during acute stage)
* organ transplants
o chronic infection in donor
o immunosuppression
* blood transfusions (only during acute stage)

Human Transmission
Acquired Postnatal Toxoplasmosis
* 1-2 week incubation period
* acute parasitemia persists for several weeks until development of tissue cysts
o often asymptomatic (>80%)
o a common symptom is lymphadenopathy without fever
o occasionally mononucleosis-like (fever, headache, fatigue, myalgia)
* likely persists for life of patient
* immunosuppression can lead to reactivation (eg, organ transplants)

Congenital Toxoplasmosis
* 1o infection must occur during or shortly before pregnancy
o can only occur once
o 1/3 will pass infection to fetus
* incidence ~1 per 1000 births
* severity varies with age of fetus
o move severe early in pregnancy
o more frequent later in pregnancy
* infection can result in: spontaneous abortion, still birth, premature birth, or full-term ą overt disease
* typical disease manifestations include: retinochoroiditis, psychomotor disturbances, intracerebral calcification, hydrocephaly, microcephaly

Toxoplasmic Encephalitis
* common complication associated with AIDS during the 1980's
* recrudescence of latent infection
* multifocal disease associated with immunosuppression
* lesions detectable with CT or MRI
* little spread to other organs
* symptoms include: lethargy, apathy, incoordination, dementia
* progressive disease  convulsions
* usually fatal if untreated

Diagnosis
* various serological tests
* active (acute) vs chronic infection
o compare samples at 2 week intervals
o IgM > IgG; Ab titers
* seldom by direct parasite demonstration
o biopsy
o inoculation into mice or cell culture (only acute stage)
* CT scans or MRI for toxoplasmic encephalitis

Prevention
But dog contact is highly correlated with Toxoplasma transmission.
Several studies show no correlation between cat contact and Toxoplasma.

An Enigma
Some Helminths Affecting the CNS
Taenia solium and Cysticercosis
* adult tapeworm infects GI tract of humans
* larval stages infect tissues causing cysticercosis or neurocysticercycosis
* most common parasitic disease of the CNS
* endemic throughout much of the developing world
o especially prevalent in Central and South America, Sub-Saharan Africa, Southeast Asia and Central and Eastern Europe
* prevalence of 3.6% in some regions of Mexico
* greatest cause of acquired epilepsy worldwide

Cysticercosis in the United States
* has become an important parasitic disease, particularly in California
* estimated that 1000 new cases of neurocysticercosis will be diagnosed each year
* increasing prevalence attributed to the migration of large numbers of rural immigrants from developing countries
* also improvements in neuro-imaging leading to better diagnosis

http://www.dpd.cdc.gov/dpdx/
Disease States
* Taeniasis = adult tapeworm in small intestine
o Usually asymptomatic (eggs or proglottids in feces)
o Vague abdominal symptoms occasionally report
* Cysticercosis = T. solium larvae in human tissues (eg, muscle)
o Usually asymptomatic
o Painless subcutaneous nodules in arms and chest
* Neurocysticercosis (NCC) = cysts in the central nervous system
o Most severe manifestation

Pathogenesis of Cysticerci
* larva (cysticercal cysts) survive up to 5 years
* living larva produce little inflammation
* death of larva leads to inflammation and edema resulting in symptoms
* cellular reaction eventually destroys parasite and leaves a calcified nodule

Clinical Manifestations
* presentation is varied—depends on stage, number, size and location of cysts
* seizures/convulsions most common symptoms
* blocked circulation of CSF can lead to intracranial hypertension or hydrocephalus
* occasionally large cysts can mimic tumors
* can also cause a variety of mental and motor changes

Diagnosis
* onset of epileptic seizures
* person from endemic area
* CT scans and MRI are most useful
o 1-2 cm cystic lesions
o with or without edema and inflammation
* some serological tests available
o problems with sensitivity and specificity

Treatment
* symptomatic treatment (eg, antiepileptic drugs)
o spontaneous cures noted especially in children
* praziquantel and albendazole kill the cysts faster
o limited clinical benefit
o administer with corticosteroids (anti-inflammatory)
* surgical excision of cysts was previous treatment

Prevention and Control
* Enhanced personal hygiene
* Thorough cooking/ freezing of pork to kill cysticerci
* Enhanced environmental sanitation
o proper disposal of human feces
* Agricultural inspection of pork
* Vaccination of pigs?

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Cysticcercosis

CYSTICERCOSIS
By:Palak Parikh

EPIDEMIOLOGY
* Found in approximately 50 million people worldwide (probably an underestimate)
* Endemic in several countries in Central and South America, sub-Saharan Africa, India, and Asia
* Prevalence in this country often higher in rural areas
* 221 deaths identified in the US from 1990-2002 (62% had emigrated from Mexico)

CYSTICERCOSIS TRANSMISSION
* Caused by the larval stage of Taenia solium, the pork tapeworm
* Humans develop by ingestion of T. solium eggs; they can spread infection by:
o Egg-containing feces contaminating water supplies in endemic areas
o Contaminating food directly, as eggs are sticky and can often be found under the fingernails of tapeworm carriers.

LIFE CYCLE
* Once eggs ingested, embryos are released in the small intestine and invade the bowel wall.
* They then disseminate hematogenously to other tissues and develop into cysticerci over 3 weeks to 2 months.
* Cysticerci – liquid-filled vesicles consisting of a membranous wall and a nodule containing the invaginated scolex.
* Scolex – head armed with suckers and hooks and a rudimentary body.

PATHOGENESIS
* Cysticerci initially viable but do not cause much inflammation in surrounding tissues – asymptomatic infection
* Host develops immune tolerance to cysticerci, which remain in this stage for several years.
o Postulated mechanisms of tolerance:
+ Taenia elaborate substances that inhibit or divert complement pathways away from parasite
+ Humoral antibodies do not kill mature taenia.
+ Poorly defined factors may interfere with lymphocyte proliferation and macrophage function, inhibiting normal cellular immune defenses.
* Clinical manifestations occur when inflammatory response develops around degenerating cysticercus.

SYMPTOMATIC DISEASE
* Divided into:
o Neurocysticercosis
o Extraneural cysticercosis

NEUROCYSTICERCOSIS
* 80% of infections are asymptomatic
* Symptoms mainly due to mass effect, inflammatory response, or obstruction of foramina and ventricular system of brain.
* Most common symptoms:
o Seizures
o Focal neurological signs
o Intracranial hypertension
* Peak estimated to occur 3-5 years after infection

NEUROCYSTICERCOSIS
* Increased risk of seizures with a single calcific granuloma.
* Risk of seizures highest when lesions are degenerating and are surrounded by inflammation.
* Encephalitis and diffuse brain edema most common in children and young females.
* 1-3% of cases involve the spinal cord, with thoracic lesions the most common.

NEUROCYSTICEROSIS IN ENDEMIC COUNTRIES
* Most common cause of adult-onset seizures
* Risk of seizures in seropositive individuals 2-3 times higher than seronegative controls.
* Punctate calcifications most frequent finding on neuroimaging of brain.

EXTRANEURAL CYSTICERCOSIS
* Typically involves:
o Eyes – in 1-3% of all infections
o Muscle
o Subcutaneous tissue – nodules most common in patients from Asia and Africa than from Latin America

DIAGNOSIS
* Serologic testing
* Peripheral eosinophilia only if cyst is leaking
* CT scan or MRI
o Pathognomonic Lesion: Scolex – mural nodule within a cyst
* Brain biopsy (only in symptomatic patients with equivocal serology and radiologic tests)

SEROLOGIC TESTING
* ELISA
* Complement fixation (CF)
* Radioimmunoassay
* Enzyme linked immunoelectrotransfer blot (EITB) assay – test of choice

EITB ASSAY
* Enzyme-linked immunoelectrotransfer blot assay
* Test of choice for detecting anticysticercal antibodies
* Uses affinity-purified glycoprotein antigens
* Higher sensitivity (83-100%) and specificity (93-98%) than ELISA
* Can be performed on serum or CSF but has a higher sensitivity on serum.
* Detected 94% of pathologically confirmed NCC with 2 or more lesions compared to only 28% with a single lesion in one study.

CT VS MRI
* MRI preferred since it is more sensitive in detecting:
o small lesions
o brainstem or intraventricular lesions
o perilesional edema around calcific lesions
o scolex
o degenerative changes in the parasite
* CT scan cheaper and better at detecting:
o small areas of calcifications.
o cysticercal infestation of extraocular muscles.

* Perform CT scan first followed by MRI in patients with inconclusive findings or in those with negative CT scans where strong clinical suspicion persists.

PERUVIAN STUDY
POTENTIAL TREATMENTS
* Albendazole (15 mg/kg/day) X 15 days + corticosteroids (30-40 mg prednisolone or 12-16 mg dexamethasone daily) – per UpToDate
* Praziquantel (50 mg/kg/day) X 15 days + corticosteroids (30-40 mg prednisolone or 12-16 mg dexamethasone daily) – per UpToDate
* Corticosteroids alone
* Anticonvulsants in patients who present with seizures or are at high risk for seizures
* Surgery

ALBENDAZOLE VS PRAZIQUANTEL
* Albendazole
o Destroys 75-90% of parenchymal brain cysts
o Does not interact with anticonvulsants
o Levels not adversely affected w/ co-administration of corticosteroids
* Praziquantel
o Destroys 60-70% of cysts 3 months after administration
o Decreased efficacy compared to Albendazole
o Available for oral administration
o Does not cross the blood-brain barrier well, so CSF levels only approx 20% of plasma levels.
o Involves cytochrome P-450 hepatic metabolism, which is induced by corticosteroids, phenytoin, and phenobarbital

* No blinded randomized controlled trials comparing albendazole to praziquantel.
Because of the above, praziquantel is generally considered second-line therapy.

TREATMENT
* One randomized, double-blind, placebo-controlled trial
o 120 pts with living cysticerci in the brain and seizures treated with antiepileptic drugs
+ Randomized to either albendazole (800 mg qd) and dexamethasone (6 mg qd X 10 days) or double placebo
+ Followed for 30 months or until they were seizure-free for 6 months after tapering of antiepileptic drugs
o Results:
+ Resolution of intracranial cystic lesions more common in treatment arm
+ Number of patients experiencing generalized seizures declined in the treatment arm
+ No significant change between the two groups in patients experiencing partial seizures

NEUROCYSTICERCOSIS
* Treatment in those with:
o 5-50 cysts (both antiparasitic and steroids)
o Steroids alone in patients w/ > 50 cysts
* No Treatment in those with:
o Asymptomatic nonviable neurocysticercosis
o Calcified cysts
o Single viable cysts
o Fewer than 5 cysts

ANTICONVULSANTS
* Recommended for patients who present with seizures
* Should be stopped if patient remains seizure-free during therapy to see if the patient remains asymptomatic
* Should be reinitiated chronically if the patient has recurrent seizures
* Should be considered in patients w/ multiple cysts who have no history of seizure activity

SURGICAL INTERVENTION
* Used in some patients with intracranial hypertension
* Shunting improves hydrocephalus, although recurrent blockages of shunts common
* Surgical intervention recommended for cysts:
o Located in the 4th ventricle
o Attached to middle cerebral artery
o Compressing the optic chiasm
o Located in the spine

TREATMENT OF EXTRANEURAL CYSTICERCOSIS
* None if pt asymptomatic
* Surgical excision for intraocular disease
* Medical therapy for involvement of extraocular muscles or optic nerve.
* NSAIDs for patients w/ symptomatic subcutaneous or intramuscular lesions.
* Excision of solitary lesions if NSAIDs fail or not tolerated.

BEFORE INITIATING MEDS…
* Apply PPD.
* Consider treating with a single dose of ivermectin before beginning corticosteroids, as many patients have risk factors for strongyloidiasis.
* Consult ophthalmology to rule out ocular cysticercosis.

PATIENT MONITORING
* Intermittent surveillance w/ imaging until cyst(s) resolve(s).
o Perhaps every 3-6 months if patient improving or earlier if patient symptomatic.
* Reimaging of brain 2 months after completion of treatment
* Consider antiparasitic therapy if cysts growing off therapy

POSSIBLE PREVENTION
* Human Tapeworm Infections
o Inspection of pork for cysticerci
o Freezing or adequately cooking meat to destroy cysticerci
o Administering antiparasitic agents to pigs
* Infection in Pigs
o Confining animals and not allowing them to roam freely
o Improved sanitary conditions
* Egg Transmission to Humans
o Good personal hygiene and hand washing prior to food preparation
o Identifying human carriers of tapeworms
o Mass community programs to treat tapeworm carriers.
* Possible Vaccine – porcine vaccine currently in the works

TAKE HOME POINTS
* Cysticercosis caused by the larval stage of Taenia solium, the pork tapeworm
* Pay special attention if pt from Central and South America, sub-Saharan Africa, India, and Asia, as neurocysticercosis is the most common cause of adult-onset seizures in these endemic areas.
* Order Head CT first to diagnose neurocysticercosis; if negative and suspicion still high, order Brain MRI.
* EITB test of choice for serology.
* Place PPD before starting treatment.
* Obtain Ophthalmology consult before starting treatment.
* Albendazole and Dexamethasone comprise first-line treatment for symptomatic cysticercosis. Consider concurrent anticonvulsants if pt presents with seizures.

REFERENCES
* aapredbook.aappublications.org
* UpToDate.
* www.dpd.cdc.gov
* www.e-radiology.net
* www.parasite-diagnosis.ch
* www.stanford.edu/class/cysticercosis/symptoms

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