Showing posts with label Parasitology. Show all posts
Showing posts with label Parasitology. Show all posts

27 July 2012

Myiasis



Myiasis is a universal term for extreme infection by parasitic fly larvae that feed on their host living/dead tissue.

Screwworm Myiasis
http://www.cfsph.iastate.edu
Flies and Myiasis
http://www.uwyo.edu/

Arthropods
Gregory L. Brower, D.V.M., Ph.D.
http://pathmicro.med.sc.edu

Medical & Veterinary Entomology
http://courses.washington.edu

Parasitic Infestations, Stings & Bites
Erik Austin, D.O., M.P.H.
http://www.atsu.edu

Tropical Ophthalmology
Dr. Steve Waller
http://www.pitt.edu/~super7/45011-46001/45191
http://www.pitt.edu/~super7/45011-46001/45171

Insects and Disease
https://www.msu.edu

Towards an ontology of vector-borne diseases
http://ontology.buffalo.edu/

Hurricane Related Infectious Disease Risks
David J. Weber, M.D., M.P.H.
http://www.unc.edu

Survey of Organisms in Microbiology
http://content.hccfl.edu

Biting Flies
http://www.uwyo.edu

Arthropod Disease
Surbhi Modi, MD, MPH
http://www.fpm.emory.edu


187 free full text articles

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05 May 2012

Pediculosis



Common Childhood Illnesses
Nancy Pares
Common Childhood Illnesses.ppt

Hygiene Skin
Hygiene Skin.ppt

Care of Patients with Skin Problems
CareofPatientswithSkinProblems.ppt

Parasitic Infestations, Stings & Bites
Erik Austin, D.O., M.P.H.
Parasitic Infestations, Stings & Bites.ppt

Dermatology
Dermatology.ppt

Communicable Diseases
Communicable Diseases.ppt

Personal Hygiene
Personal Hygiene.ppt

Metazoans and Exoparasites
Metazoans and Exoparasites.ppt

Antiviral, Antifungal and Antiparasitic Drugs
Linda Self
Antiviral_Antifungal_and_Antiparasitic_Drugs.ppt

Child with an Integumentary Alteration
Child with an Integumentary Alteration.ppt
43 free full text articles

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03 April 2010

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

Zoonotic Helminthiasis.ppt

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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 Ä… 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?

Parasitic Pathogens Affecting the CNS.ppt

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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

CYSTICERCOSIS.ppt

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08 October 2009

Emerging Infections and Medical Procedures



Emerging Infections and Medical Procedures

Parasitic Infections: Clinical Manifestations, Diagnosis and Treatment
By:Lennox K. Archibald, MD, PhD, FRCP, DTM&H
Hospital Epidemiologist
University of Florida

The Reality
* 1.3 billion persons infected with Ascaris (1: 4 persons on earth)
* 300 million with schistosomiasis
* 100 million new malaria cases/yr
* At UCLA, 38% of pediatric and dental clinic children harbored intestinal parasites

Case1
* 42-yr-old previously healthy, UF professor
* 6-week history of intermittent diarrhea, flatus and abdominal cramps
* Diarrhea: x8/day; pale; no blood or mucus
* No tenesmus
* Illness began slowly during camping trip to Colorado with loose stools
* Spontaneously remission for 5-6 days at a time, then recur
* His 8-yr-old son had had a mild course of watery diarrhea—ascribed to viral gastroenteritis by general practitioner
* Stool smear—no pus cells
* However, wet preps showed…

Diagnosis?
Giardiasis (G. lamblia)
* Should be suspected in prolonged diarrhea
* Contaminated water often implicated—outbreaks
* Campers who fail to sterilize mountain stream water
* Person-person in day care centers
* MSM
* Symptoms usually resolve spontaneously in 4-6 weeks

Giardiasis Tests of choice
* Examination of concentrated stools for cysts (90% yield after 3 samples)
o Usually no PMNs
* Stool ELISA, IF Antigen (up to 98% sensitive/90-100% specific)
* Consider aspiration of duodenal contents--trophozoites
* Treatment: Metronidazole for 5-7 days

Case 2
* 40 y/o male vicar returned from 2 years of missionary work in South Africa
* Excellent health throughout stay there
* 3 months after returning to U.S.
o Suddenly ill with abdominal distension
o Fever
o Periumbilical pain
o Vomiting
o Blood-tinged diarrheal stools
* Denied arthritis /known exposure to parasites
* Family history of “inflammatory bowel disease”
* Physical examination:
o Acutely ill
o Distended abdomen
o No hepatomegaly or splenomegaly
o Decreased bowel sounds
o Stool exam
+ Gross blood present
+ No pus cells
+ Negative for O&P, one negative C&S

Sigmoidoscopy revealed…
* Multiple punctate bleeding sites at 7 to 15 cm with normal appearing mucosa between sites
* This mucosa easily denuded when pressure applied to it, leaving large areas of bleeding submucosa
* Diagnosed with ulcerative colitis
* Started on corticosteroids
* Temperature rose to 40°C
* Abdomen distension increased and worsening of symptoms
* Emergency laparotomy for toxic megacolon

Diagnosis?
Entamoeba histolytica
* One of 7 amoebae commonly found in humans
* Only one that causes significant disease
* Causes intestinal (diarrhea and dysentery) and extraintestinal (liver primarily) disease
* In US
o Institutionalized patients
o MSM
o Tourists returning from developing countries
o Patients with depressed cell mediated immunity

Trophozoites with ingested RBC
Trophozoites in colon tissue (H & E stain)
Cyst (wet mount)

Amoebiasis: Clinical Manifestations
* Symptoms depend on degree of bowel invasion
o Superficial: watery diarrhea and nonspecific GI complaints
o Invasive: gradual onset (1-3 weeks) of abdominal pain, bloody diarrhea, tenesmus
* Fever is seen in minority of patients
* Can be mistaken for ulcerative colitis
* Steroids can dramatically worsen and precipitate toxic megacolon
* Amebic liver abscesses
o RUQ pain, pain referred to right shoulder
o High fever
o Hepatomegaly (50%)

Amoebic abscess—remember…
* Can occur in lung, brain, spleen
Amoebic Abscess
* Liquefaction of liver cells
* Do not contain pus
* Anchovy paste sauce
* Culture of contents usually sterile
* Liver affected:
o 53%-right lobe
o 8%-left lobe

Remember…
* That stool is merely a convenient vehicle passing by
* Amoebae live the bowel wall
* Direct observation preferable to mere examination of stool
* Trophozoites best seen in direct scrapings of ulcers

Amoebiasis Treatment
* Most respond to metronidazole
* Open surgical drainage should be avoided, if at all possible

Case 3
* Previously healthy 3-year-old girl
* Attends day-care center
* 7 day history of watery diarrhea
* Nausea
* Vomiting
* Abdominal cramps
* Low-grade fever

Case 4
* 34 year-old AIDS patient
* Debilitating, cholera-like diarrhea
* Severe abdominal cramps
* Malaise
* Low-grade fever
* Weight loss
* Anorexia

Diagnosis? Case 3 & 4

Three cysts stained pale red are seen in the center with this acid fast stain
Modified acid-fast stain of stool showing red oocysts of Cryptosporidium parvum against the blue background of coliforms and debris

Cryptosporidium parvum
* Causes secretory diarrhea: 10 liter/day
* Significant cause of death in HIV/AIDS
* Animal reservoirs
* Incubation period: 5-10 days

Cryptosporidium parvum
* Infants & young children in day-care
* Unfiltered or untreated drinking water
* Farming practices: lambing, calving, and muck-spreading
* Sexual practices: oral contact with stool of an infected individual
* Nosocomial setting with other infected patients or health-care employees
* Veterinarians: contact with farm animals
* Travelers to areas with untreated water
* Living in densely populated urban areas
* Owners of infected household pets (rare)

Diagnosis and Treatment
* Best diagnosed by stool exam
* No known effective treatment
* Nitazoxamide shortens duration of diarrhea

Case 5
* Mr. & Mrs. R. were sailing with their 3 children in Jamaica
* Living primarily on the boat with several day trips to a small coastal island
* On island, ate several types of tropical fruit
* Both became suddenly ill with fevers, chills, muscle aches, and loss of appetite.
* Sought treatment locally, and were diagnosed with hepatitis, likely due to ingestion of toxic fruit

Case 5
* Two days later, Mr. R. became jaundiced and passed dark urine
* He progressively worsened, became comatose and died
* In the meantime, Mrs. R. was transferred to SUF for liver transplant
* None of the children were sick despite having eaten the same fruits and other foods.
* The family had taken chloroquine prophylaxis against malaria, but the parents stopped the medicine 2 weeks prior to becoming ill because of side effects.

Falciparum vs. Vivax
* Location: Falciparum confined to tropics and subtropics; vivax more temperate
* Falciparum infects RBC of any age; others like reticulocytes
* Falciparum-infected RBCs stick to vascular endothelium causing capillary blockage

Malaria: Genetic susceptibility
* Two genetic traits associated with decreased susceptibility to malaria
* Absence of Duffy blood group antigen blocks invasion of Plasmodium vivax
o Significant number of Africans
* Persons with sickle cell hemoglobin are resistant to P. falciparum
* Sickle cell disease and trait

Malaria: Clinical manifestations
* Non-specific, flu-like illness
* Incubation
o P. falciparum: 9-40 days
o Non-P. falciparum: may be prolonged
+ P. vivax: 6-12 months
+ P. malariae and ovale: years
* Fever is the hallmark of malaria
o Classically, 2-3 day intervals in P. vivax and malariae
o More irregular pattern in P. falciparum
* Fever occurs after the lysis of RBCs and release of merozoites

Malaria: Clinical manifestations
* Febrile paroxysms have 3 classic stages
o Cold stage
+ Pt feels cold and has shaking chills
+ 15-60 mins. prior to fever
o Hot stage
+ 39-41°C
+ Lassitude, loss of appetite, bone and joint aches
+ Tachycardia, hypotension, cough, HA, back pain, N/V, diarrhea, abdo pain, altered consciousness
o Sweating stage
+ Marked diaphoresis followed by resolution of fever, profound fatigue, and sleepiness
+ 2-6 hours after onset of hot stage
* Other symptoms depend on malaria strain
* P. vivax, ovale and malariae: few other sxs
* P. falciparum:
o Dependent upon host immune status
o No prior immunity/splenectomy  high levels of parasitemia  profound hemolysis
o Vascular obstruction and hypoxia
+ Kidneys: renal failure
+ Brain: (CNS) ― hypoxia, coma, seizures
+ Lungs: pulmonary edema
o Jaundice & hemoglobinuria (blackwater fever)
* Always suspect malaria in travelers from developing countries who present with:
o Influenza-like illness
o Jaundice
o Confusion or obtundation

Diagnosis
* Giemsa-stained blood smear
o Thick and thin smears
* P. falciparum:
o Best just after fever peak
* Others:
o Smears can be performed at any time
* Examine blood on 3-4 successive days

Differences in strains
* P. falciparum
o No dormant phase in liver
o Multiple signet ring trophs per cell
o High percentage (>5%) parasitized RBCs considered severe

Differences in strains
* P. vivax and ovale
o Dormant liver phase
o Single signet ring trophs per cell
o Schuffner’s dots in cytoplasm
o Low percent (< 5%) of parasitized RBCs
* P. malariae
o No dormant stage
o Single signet ring trophs per cell
o Very low parasitemia

Treatment
* P. falciparum malaria can be fatal if not promptly diagnosed and treated
* Non- P. falciparum malaria rarely requires hospitalization

Treatment
Uncomplicated malaria
* P. vivax, ovale, malariae, chloroquine-susceptible falciparum
o Chloroquine
o Primaquine for dormant liver forms
* Chloroquine-resistant falciparum
o Quinine plus doxycycline
o Mefloquine
o Atovaquone plus proguanil (AP)
o Artemisins (common in SE Asia due to multi-drug resistance)

Treatment Severe malaria
* Drug options
o Quinidine gluconate—only approved parenteral agent in US
o Artemisin
Prevention
* Mefloquine
* Doxycycline
* Nets
* 30-35% DEET
* Permethrin spray for clothing and nets

And don’t forget baggage malaria!
Case 5
* Mrs. R. was treated with IV quinidine and improved rapidly.
* In retrospect, Mr. R. had died from untreated blackwater fever
o Few parasites in peripheral blood
o Acute renal failure

Case 6
* A 24-year-old white male army officer
* Referred to the VA ID clinic with a 3-month history of a lesion on his right leg, developing approximately 2 weeks after returning from Iraq
* Recent travel history: 1 month in Kuwait and 2 months traveling between Kuwait and Iraq
* Recalled being bitten numerous times by small flying insects and other nasty “bugs”

Physical examination essentially normal except for:
* Non-tender (20 × 15 mm) scaly erythematous plaque with a moist central erosion of the left popliteal area.
* There was no lymphadenopathy and no mucosal lesions were noted

Diagnosis?
An intact macrophage practically filled with amastigotes (arrows),

Leishmaniasis
* Tropical areas where phlebotomine sandfly is common: South America, India, Bangladesh, Middle East, East Africa
* Sandfly introduces flagellated promastigote into human  ingested by macrophages  develops into nonflagellated amastigote
* Cutaneous
o Most common among farmers, settlers, troops and tourists in Mid East (L. major and tropica), Central and South America (L. mexicana, braziliensis, amazonensis, and panamensis)
o L. mexicana reported in Texas
* Visceral (kala azar)
o Anemia, leukopenia, thrombocytopenia, hypergammaglobulinemia common

Leishmaniasis: Diagnosis
* Biopsy and Giemsa stain with amastigotes
* Species most prevalent in different places
# L. donovani – India
# L. infantum – Mid East
# L. chagasi – Latin America
# L. amazonensis -- Brazil

Visceral Leishmaniasis
* Dissemination of amastigotes throughout the reticulendothelial system of the body
o Spleen
o Bone marrow
o Lymph nodes
* Opportunistic infection in AIDS patients
* Ineffective humeral response

Hepatosplenomegaly
Splenic aspirate
* Most satisfactory method
* Spleen must be at least 3cm below LCM
* Aspirate stained with Giemsa

Leishmaniasis: treatment
* Only drug approved in US is Amphotericin B
* Treatment of cutaneous disease depends on anatomic location
* Many spontaneously heal and do not require treatment

Remember..
* The factors determining the form of leishmaniasis:
o Leishmanial species
o Geographic location
o Immune response of the host

Case 7
* 38-year-old businessman
* Previously fit
* 2-week history of fever since returning from Brazil business trip
* Flu-like symptoms and myalgia
* Had consumed steak tartare in Brazil
* Results all unremarkable---normal WBC and ESR; negative smears; CXR and urine OK
* Continued to have fever, tachycardia and myalgia

Case 8
* A 29-yr-old man with AIDS (CD4 count=59) presents with a 2 week history of headache, fevers and new onset seizures
* He had not been taking any antiretroviral medications

Cases 7 & 8
What parasite could
cause this picture?
AIDS Patient
Toxoplasma gondii cyst in brain tissue with H & E stain (100x)
For the businessman…
* Toxoplasma serology was positive at a very high titer
* Responded to treatment with sulphonamide + pyrimethamine
* No relapse

Transmission
* Eating oocysts excreted by cats harboring sexual stages of parasite
* Outbreaks traced to inadequately cooked meat of herbivores (raw beef)
* Mutton

Toxoplasma gondii
* Worldwide distribution
* Human infection
o Ingestion of cysts in undercooked meat of herbivores
o Water/food contaminated with oocysts
o Congenitally
o Infected organs, blood (less common)
* Prevalence of latent infection in US about 10%; France about 75%
o Generally higher in less-developed world
o 50% in AIDS patients; up to 90% of AIDS patients in developing world

Toxoplasma gondii: Immunocompetent hosts
* Latent infection (persistence of cysts) is generally asymptomatic
* Cervical lymphadenopathy (10-20%)
* Mono-like presentation (<1% of all mono-like illnesses)
* Chorioretinitis
* Very rare: myocarditis, myositis

Toxoplasma gondii: Immunocompromised hosts
* Often life-threatening
* Almost always reactivation of latent infection
* AIDS
o Encephalitis most common manifestation
o Usually subacute onset/focal (if CD4< 200)
o Mental status changes, seizures, weakness, cranial nerve abnormalities, cerebellar signs,
o Can present as acute hemiparesis/language deficit
o Usually multiple ring-enhancing lesions on CT/MRI
* Pneumonitis
* Chorioretinitis

Toxoplasma gondii: Clinical manifestations
* Immunocompromised hosts
o Non-AIDS (transplants, hematologic malignancies)
+ CNS 75%
+ Myocardial 40%
+ Pulmonary 25%

Toxoplasma gondii: Clinical manifestations
* Congenital
* Acute infection asymptomatic in mother
* Clinical manifestations range: no sequelae to sequelae that develop at various times after birth
o Chorioretinitis
o Strabismus
o Blindness
o Epilepsy, mental retardation, pneumonitis, microcephaly, hydrocephalus, spontaneous abortion, stillbirth

Toxoplasma gondii: diagnosis
* Clinical suspicion crucial
* Serology is primary method of diagnosis
o IgM, IgG
* Histopathology
o Tachyzoites in tissue sections or body fluid (difficult to stain)
o Multiple cysts near necrotic, inflammatory lesions

Toxoplasma gondii: Treatment
* Immunocompetent adults are usually not treated unless visceral disease is overt or symptoms are severe and persistent
* Immunodeficient patients
o Latent disease: not treated
o Active disease: pyrimethamine + sulfadiazone + folinic acid

Toxoplasma gondii: Treatment
* Congenital:
o Treatment of acute infected pregnant women decreases but does not eliminate transmission
+ Spiramycin
o If fetal infection is documented, treat with pyrimethamine + sulfadiazone + folinic acid
o Postnatal treatment: pyrimethamine + sulfadiazone + folinic acid
Case 22
* 25-year-old Caucasian woman presented with 1-week history of fever, chills, sweating, myalgias, fatigue
* No travel abroad
* Had gone cranberry picking in Massachusetts approx 3 weeks earlier
* PE: anemic, hepatosplenomegaly
* Blood workup: hemolytic anemia, reduced platelets

Thick smear
Thin smear
Maltese cross
Diagnosis??
Babesiosis
* Babesiosis caused by hemoprotozoan parasites of the genus Babesia
* >100 species reported
* Few actually cause human infection
* Babesia microti
* Life cycle involves two hosts:
o Deer tick, Ixodes dammini, (definitive host) introduces sporozoites into white-footed mouse
* Once ingested by an appropriate tick gametes unite and undergo a sporogonic cycle resulting in sporozoites
* Humans enter cycle when bitten by infected ticks
Deer are the hosts upon which the adult ticks feed and are indirectly part of the Babesia cycle as they influence the tick population
* Clindamycin* plus quinine
* Atovaquone* plus azithromycin*
* Exchange transfusion in severely ill patients with high parasitemia
* Approved by FDA

Case 9
* 6-year-old son of seasonal farm worker
* Presents with cough and fever, wheeze
* CXR reveals a lobar pneumonia
* Admitted for initial therapy
* After 2 days of antibiotics, with good defervescence, a worm is found in his bed
* Stool exam reveals …

Diagnosis?
Ascaris lumbricoides
* In GI tract, few symptoms in light infections
o Nausea
o Vomiting
o Obstruction of small bowel or common bile duct.
* Pulmonary: symptoms due to migration
o Alveoli (verminous pneumonia)—cough, fever wheeze, dyspnea, X-ray changes, eosinophilia
Effects of Adult Ascaris Worms
* Depends on worm load
* Effects
o Mechanical: obstruction, volvulus, intussusception, appendicitis, obstructive jaundice, liver abscesses, pancreatitis, asphyxia
* Toxic and Metabolic
o Malnutrition (complex)

Ascaris lumbricoides Diagnosis
* Characteristic eggs on direct smear examination
* If treating mixed infections, treat Ascaris first
o Mebendazole
o Pyrantel
* Control:
o Periodic mass treatment of children, health education, environmental sanitation
Case 10
* 11-year-old female
* Doing poorly in school
* Not sleeping well
* Anorectic
* Complains of itching in rectal region throughout the day
* A Scotch-tape test reveals…
Diagnosis?
Enterobius (Pinworm)
* 18 million infections in U.S.
* Incidence higher in whites
* Preschool and elementary school most often
* Mostly asymptomatic
* Nocturnal anal pruritis cardinal feature due to migration and eggs
* May have insomnia, possible emotional symptoms
* DS-eggs or adults on perineum {scotch tape}
* Mebendazole 100 mg. Repeat in 2 weeks. Pyrantel pamoate 11 mg/kg; repeat 2 weeks
* 69-year-old male was admitted to VA Hospital
* Far East Prisoner of War (FEPOW)
* COPD--steroids for 3 years
* 2-month history of nausea, vomiting and anorexia
* 25 pounds weight loss

Case 11
On the day of admission…

* Fever, confusion, and not able to get out of bed---transported to the hospital
* Initial blood work:
o Elevated WBC
o Raised eosinophil count 4 times normal
* Underwent UGI endoscopy
* Duodenal biopsy obtained

Diagnosis
Strongyloides: Crucial Aspects of Life Cycle
* Infection acquired through penetration of intact skin
* Infection may persist for many years via autoinfection
* In immunocompromised patients, there is risk of dissemination or hyperinfection
o Hyperinfection syndrome

Disseminated Strongyloidiasis
* High mortality75%
* Penetration of gut wall by infective larvae
* Gut organisms carried on the surface of larvae results in polymicrobial sepsis, meningitis
* Larvae disseminate into all parts of body: CNS, lungs, bladder, peritoneum

Summary—Clinical Findings
* Defective cell-meditated immunity: steroids, burns, lymphomas, AIDS (?)
* Gl symptoms in about two-thirds:
o Abdominal pain
o Bloating
o Diarrhea
o Constipation
* Wheezing, SOB, hemoptysis

Summary—Clinical Findings
* Skin rash or pruritis in ~ one-third
o Larva currens (racing larva)
o Intensely pruritic
o Linear or serpiginous urticaria with flare that moves 5-15 cm/hr
o Usually buttocks, groin, and trunk
o In dissemination, diffuse petechiae and purpura

Summary-Clinical Findings
* Eosinophilia 60-95%
* Less if on steroids

Case 12
* 57 year old farmer from Dixie County
* Presents with profound SOB
* Physical examination: anemic otherwise unremarkable
* Laboratory examination reveals a profound anemia (hct 24) with aniso and poikilocytosis
* Remainder of laboratory examination normal.

Diagnosis?
Hookworm
* Hookworm responsible for development of USPHS
* Caused by two different species (North American and Old World)
* Very similar to strongyloides in life cycle
* Attaches to duodenum, feeds on blood
* Elaborates anticoagulant, attaches and reattaches many times
* Loss of around 0.1 ml/d of blood per worm

Case 13
* 8-yr-old schoolgirl visiting the U.S. from Malaysia
* 1 week history of epigastric pain, flatulence, anorexia, bloody diarrhea
* No eosinophilia noted
* Clinical diagnosis of amoebic dysentery made
* However, microscopy of stool prep…

Diagnosis?
Trichuris trichiura (Whipworm)
* Common in Southeast U.S.
* Frequently coexists with ascaris
* Entirely intraluminal life cycle—eggs are ingested
* Frequently asymptomatic
* Severe infections: diarrhea, abdominal pain and tenesmus
* Rectal prolapse in children
* DS-eggs in stool
* Mebendazole 100 mg bid x 3 days

Case 14
* 18-year-old trailer park handyman seen in ER
* Worked under trailers wearing shorts and no shirt
* Developed intensely pruritic skin rash
* Unable to sleep
* WBC 18,000
* 65% eosinophils.

Case 15
* An 8 year old boy
* Presents with skin lesions and itching after spending the summer at a beach condo in St. Augustine with his family (mother, father, younger sister, dog and cat).
* Legs show several raised, reddened, serpiginous lesions that are intensely pruritic.

Diagnosis ?
Cutaneous Larva Migrans
* Caused by filariform larvae of dog or cat hookworm (Ancylostoma braziliense or Ancylostoma duodenale
* Common in Southeast U.S.
* Red papule at entry with serpiginous tunnel
* Intense pruritis
* Self limiting condition
* Diagnosis clinical
* Topical or oral thiabendazole 25 mg/kg bid for 3-5 days
* May use ethyl chloride topically

Cutaneous larva migrans (creeping eruption)
* More common in children
o Larvae penetrate skin and cause tingling followed by intense itching.
* Eggs shed from dog and cat bowels develop into infectious larvae outside the body in places protected from desiccation and extremes of temperature
* Shady, sandy areas under houses, at beach, etc.
Usually not associated with systemic symptoms

Cutaneous larva migrans (creeping eruption)
* Diagnosis and treatment
* Skin lesions are readily recognized
* Usually diagnosed clinically
* Generally do not require biopsy
# Reveal eosinophilia inflammatory infiltrate
# Migrating parasite is generally not seen
* Stool smear will reveal eggs

Visceral Larva Migrans
* Infection with dog or cat round worms
* Toxocara canis; Toxocara catis
* Underdiagnosed based on seroprevalence surveys
* Heavy infections associated with fever, cough, nausea, vomiting, hepatomegaly, and eosinophilia
* Uncommon in adults
* Ocular type more common in adults
* Diagnosis-ELISA
* Thiabendazole: 25 mg/kg bid X 5 days

Case 17
* A 34 yr-old woman from Saudi Arabia
* Radiation and cyclophosphamide, adriamycin, vincristine and prednisone for diffuse large B cell lymphoma of the neck.
* Mild eosinophilia (AEC=500) at the time of diagnosis
* 4 months after initiation of chemo, c/o intermittent diffuse abdominal pain, bloating, constipation and occasional rectal bleeding.
* Absolute eosinophil count: 1000
* No evidence of lymphoma found on re-staging
* Completed chemo, was deemed to be in complete remission, but had persistence of GI complaints.
* Upper endoscopy was unrevealing.
* Colonoscopy and biopsy revealed granulomatous inflammation, prominent eosinophilic infiltrate, surrounding a collection of eggs.

Chronic intestinal schistosomiasis
* The patient was treated with praziquantel and did not have relapse of symptoms at 2-year follow-up
* AEC=250

Schistosomiasis: Epidemiology and life cycle
* Cercariae in fresh water penetrate human skin.
* Cercariae mature to schistosomulae, which enter the bloodstream, liver and lung.
* Mature worms migrate to the venous system of the small intestine (S. japonicum), large intestine (S. mansoni) or bladder venous plexus (S. haematobium).

Schistosomiasis: Epidemiology and life cycle
* Worms release eggs for many years into stool or urine, resulting in fresh water contamination.
* Freshwater snails are infected by miracidia and are necessary for the production of cercariae and human infection.
* S. mansoni
o South America, Caribbean, Africa, Mid East
* S. japonicum
o China and Philippines
* S. haematobium
o Africa, Mid East

Schistosomiasis: Clinical manifestations
* Three stages of disease, corresponding to life cycle within human hosts
* Swimmer’s itch
o Within 24 hours of cercariae penetration
* Serum sickness syndrome (Katayama fever)
o 4 to 8 weeks later when worms mature and release eggs
+ Fever, headache, cough, chills, sweating, lymphadenopathy, hepatosplenomegaly  usually resolves spontaneously
+ Elevated IgE and eosinophils
+ Most common with S. japonicum

Chronic Schistosomiasis
* Granulomatous reaction to egg deposition in intestine, liver, bladder, lungs
* S. mansoni, japonicum
o Chronic diarrhea, abdominal pain, blood loss, portal hypertension, hepatosplenomegaly, pulmonary hypertension
o Eosinophilia is common
o Liver function tests are usually normal
* S. Haematobium
o Hematuria, bladder obstruction, hydronephrosis, recurrent UTIs, bladder cancer

Schistosomiasis:
Diagnosis and Treatment

* Detection of characteristic eggs in stool, urine or tissue biopsy is diagnostic
o Urine is best between 12N and 2Pm, passed through 10 µm filter to concentrate eggs
* Antibody tests are available, but limited by sensitivity, specificity
* Praziquantel is the drug of choice

S. mansoni
Stool
S. haematobium
Urine
S. japonicum

Case 18
* 15-yr-old girl
* Fever, rash, swelling around the eye and hands, severe headaches
* Fatigue, aching muscles and joints
* Swollen lymph nodes on the back of neck
* Weight loss
* Progressive confusion, personality changes
* Sleeping for long periods of the day
* Insomnia
* Had been on a safari with parents to West Africa
* Dusky red lesion developed within 1 week
* Vaguely remembered being bitten by a fly

Diagnosis?
Investigations
* Blood films
* Lumbar puncture

Blood smear
African trypanosomiasis
Trypanosoma brucei gambiense
Tsetse fly
Treatment
* Suramin
* Melasoprol

Case 19
* 6-yr-old boy recently arrived from Brazil
* Swelling around the eye
* Conjunctivitis
* Fever
* Enlarged lymph nodes
* Hepatosplenomegaly
* Had stayed in a hotel—adobe style with thatched roof

Diagnosis?
Blood smear
Reduviid bug (assassin bug)
Chagas disease:
Clinical manifestations
* Local edema is followed by fever, malaise, anorexia
o More rarely: myocarditis, encephalitis
* Years later: chronic Chagas Disease (10-30%)
o Heart: primary target
+ Cardiomyopathy associated with CHF, emboli, arrythmias
o GI tract: mega-esophagus, megacolon

Chagas disease: Diagnosis and treatment
* Acute disease is diagnosed by seeing trypomastigotes on peripheral blood smear
* Chronic disease is diagnosed by ELISA detecting IgG antibody to T. cruzi
* Treatment slows the progression of heart disease

Chagas Disease
* Public health implications in the US
* Chronic
o Cardiomyopathy
o Megaesophagus
o Megacolon
* Blood transfusion
* Transplant
o Solid organ
o Musculoskeletal allograft tissue

Case 20
* 20-yr-old male
* Abdominal pain and nausea for several months
* More common in the morning
* Relieved by eating small amounts of food
* Some diarrhea and irritability
* Weight loss
* Pruritus ani
* Passage of white “bits”

Diagnosis?
Taenia saginata
* Ingestion of raw or poorly cooked beef
* Cows infected via the ingestion of human waste containing the eggs of the parasite
* Cows contain viable cysticercus larvae in the muscle
* Humans act as the host only to the adult tapeworms
* Up to 25 meters in the lumen of intestine
* Found all over the world, including the U.S.

Beef Tapeworm
Treatment
* Praziquantel
* Albendazole
* Niclosamide
Tapeworms (Cestodes)
* Adult worms inhabit GI tract of definitive vertebrate host
* Larvae inhabit tissues of intermediate host
* Humans
o Definitive for T. saginata
o Intermediate for Echinococcus granulosus (hydatid)
o Both definitive and intermediate for T. solium
* Adult worms shed egg-containing segments in stool ingested by intermediate host larval form in tissues

Case 21
* A 33 year-old Indian man was admitted with a grand mal seizure
* 2 yrs PTA, he had vertigo and CT revealed an enhancing calcified lesion in left temporal-parietal region
* FHx: Brother had grand mal seizure several years earlier
* Throughout his life, he has eaten a diet heavy in pork
* Difficulty speaking and loss of consciousness while on the phone
* Co-workers noticed generalized tonic-clonic seizures lasting 10 minutes.
* CT revealed new localized edema around the previously identified lesion and a second contiguous ring enhancing lesion.
* He received phenytoin (Dilantin, an antiseizure med) and 5 days of corticosteroids.

Case 21
* ELISA titer was positive for antibodies against Taenia solium.
* The neurosurgeons tell you that resection is impossible because of the extent and location of the lesion

Cystercercosis
* Human infected with the larval stage of Taenia solium
* Humans can serve as definitive or intermediate host
* Eggs are ingested, or possibly get to stomach by reverse peristalsis
* Probably much more common than is reported, since most infections are asymptomatic
* Symptoms depend on location of cysts, but frequently include motor spasms, seizures, confusion, irritability, and personality change
* In the eye, often subretinal or in vitreous. Movement may be seen by the patient. Pain, amaurosis, and loss of vision may occur.
* Clinical manifestations
o Adult worms rarely cause sxs
o Larvae penetrate intestine, enter blood, and eventually encyst in the brain.
+ Cerebral ventircles  hydrocephalus
+ Spinal cord  compression, paraplegia
+ Subarachnoid space  chronic meningitis
+ Cerebral cortex  seizures
o Cysts may remain asymptomatic for years, and become clinically apparent when larvae die
o Larvae may encyst in other organs, but are rarely symptomatic

* Diagnosis
o CT and MRI preferred studies
+ Discrete cysts that may enhance
+ Usually multiple lesions
# Single lesions especially common in cases from India
+ Older lesions may calcify
o CSF
+ Lymphs or eos, low glucose, elevated protein
o Serology
+ Especially in cases with multiple cysts
* Treatment
o Complex and controversial
o Praziquantel and albendazole may kill cysts, but death of larvae can increase inflammation, edema and exacerbate sxs
o When possible, surgical resection of symptomatic cyst is preferred
o Corticosteroids vs. edema and inflammation; antiseizure meds

Case 21

* He was not treated with praziquantel or albendazole
* He continued to receive dilantin for seizures and was treated with corticosteroids for edema

Classification of Parasitic Diseases
* Protozoa: amoeba; flagellates; ciliates
* Metazoa (two phyla)
o Helminths (worms)
+ Nematodes
# Intestinal
# Extra-intestinal
+ Flatworms (platyhelminths)
# Cestodes (tapeworms)
# Trematodes (flukes)
o Arthopods (ectoparasites): scabies, lice, fly larvae

General rules of treatment
* Protozoa: require species-specific treatment
* Metozoa: species-specific

General rules of treatment of metazoa
Nematodes
Intestinal
Mebendazole or Albendazole
Tissue
Albendazole
Filiariae
Ivermectin, doxycycline
Cestodes
Praziquantel, Albendazole, Niclosamide
Trematode
Praziquantel
Ectoparasites

Emerging Infections and Medical Procedures.ppt

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Differentiating Babesia from Malaria



Differentiating Babesia from Malaria
By:Devak Desai

Case Presentation
* Middle aged hypertensive and asplenic man presented with a pruritic rash on his right buttock accompanied by flu-like symptoms.
* 1010, arthralgias, myalgias, some nausea, and general malaise, and decreased appetite.
* Reports walking through a wooded area on Martha’s Vineyard, an island off the coast of Mass.
* PE shows a well nourished man with no significant findings other than an erythmatous oropharynx without exudate.

Laboratory Data
* Normal WBC differential
* Blood smear: numerous intraerythrocytes involving 2.7% of RBCs
* Direct Combs test was negative
* Positive serologic test for Lyme Disease

Peripheral Blood Smear
* Numerous erythrocytes are infected with the predominantly ring or pear-shaped form of Babesia microti.
* Pleomorphic rings with 1-3 chromotin dots per parasite.
* 3 dots is unique for Babesia.

Host Infection Cycle
* Infection begins when sporozoites are released from the deer tick’s salivary gland during a blood meal.
* Sporozoites replicate directly in RBCs.
* Attachment and adsorption seems mediated through the C3b receptor.
* During invagination a clear vacuole appears.
* Babesia divided by asynchronous budding.
* The replicating structures are now called trophozoites.
* This is an asynchronous process with varying degrees of hemolysis.

Life cycle of Babesia spp. in the tick and vertebrate hosts
High Power
* Ring shaped trophozites
* The intraerythrocytic trophozoites multiply by binary fission or schizogony, forming two to four separate merozoites.
* White eccentric “food vacuole” in a ring form.
* Very transient stage in Malaria. Very rarely seen.

the famous Maltese Cross
* Presence of 4 daughter merozoites in a tetrad is pathomnemonic.
* However, rarely seen.
* Never seen in malaria.

Multiply infected RBCs
* RBCs can be infected with multiple organisms at the same time. Up to 12 parasites may infect a single RBC.
* Plasmodium has up to 3 parasites/RBC.
* Unremarkable RBCs.

Other Sightings
* Parasite with a peripheral nuclear band
* Basket cell
* Syncytium of extracellular parasites
* Far more common in Babesia infections

Malaria Review
Epidemiology
* There are >100 specicies of this intracellular parasite.
* Babesia microti is the predominant human pathogen, endemic to the NE and Midwest.
* 10-20% of adults are seropositive in endemic areas
* Natural parasite reservoir is rodents
* Carried by the hard-bodied Ixodes Deer tick.
* Also carries agents for Lyme Disease, and Ehrlichoisis.
* Can also be transferred transplacentally and through blood transfusion.

Clinical presentation
* Ranges from asymptomatic infection to fatal illness (rare)
* No direct correlation between parasitemia and severity.
* More severe infection tends to occur in immunnocompromised, elderly, and the very young.
* The extreme end of the spectrum is often described as a malaria-like infection; symptoms may include malaise, chills, mylagia, anemia, fatigue, and fever (as high as 1040).
* Some cases also described emesis, night sweats, weight loss, and hematuria.

Special Case – Splenectomy
* Most important risk factor for infection, esp. severe.
* Illness appears suddenly, with hemoglobinuria as the presenting symptom followed by jaundice due to severe hemolysis.
* Parasitemia can reach 80% of RBCs
* Can be a medical emergency.
* In the most severe cases, patients develop a shock-like picture, with renal failure and pulmonary edema.
* Chronic disease with many relapses over months to years may occur if not treated.

Co-Infection
* It is estimated from serologic surveys that as many as 13% of Lyme disease patients in babesia-endemic areas are coinfected with B. microti
* The initial symptoms of both babesiosis and Lyme disease overlap significantly.
* Like babesiosis, Lyme disease also presents with nonspecific symptoms of fever,fatigue, and other flu-like symptoms.
* Patients coinfected with B. microti and B. burgdorferi experience more severe symptoms, but does not increase the duration of Babesia parisitemia.
* Doxycycline will not kill Babesia.

Diagnosis
* Diagnosis is based on clinical suspicion and history of exposure.
* Thick and thin smears remain most clinically used
* However, it is necessary to examine 200 to 300 oil immersion fields before declaring a specimen negative.
* Various PCR detection assays are available for detection of B microtic and other species.
* More sensitive but also more time consuming and expensive.
* Indirect fluorescent antibody test can also be used as a confirmatory test.
* Can have false negatives (HIV) or false pos (autoimmune)

Treatment
* Current treatment is Quinine plus Clindamycin
* Better alternative treatment is Atovaquone plus Azithromycin
* This combo is almost as effective with fewer side effects.
* 72% receiving quinine and clindamycin had side effects attributed to the drugs—diarrhea, tinnitus, or vertigo
* 15% receiving atovaquone plus azithromycin experienced side effects (usually diarrhea or rash).
* For severe cases (asplenic) with high levels of parasitemia, RBC exchange transfusions may also be necessary.

Summary
* History: check for recent travel
* Symptoms: Babesia is milder and tends not to be cyclic.
* Smear: Babesia has no schizonts, gametocyes, or ameboid trophozoites.
* Lab tests: PCR or indirect antibody test.

Conclusion
* Major deterrents to the diagnosis of babesiosis include the low index of suspicion by physicians (except in endemic areas), non-specific flu-like signs, and the use of automated cell readers that cannot detect merozoites in erythrocytes
* Disease is increasing in prevalence due to more people living in rural tick infested areas and as the number of immunocompromised in increasing.
* Also environmental such as the exponential rise in deer populations.
* Blood transfusion risk becoming an increasing problem.
References

Differentiating Babesia from Malaria.ppt

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25 September 2009

Ectoparasites



Ectoparasites

* What are ectoparasites?
o Insects and arachnids which feed through or upon the skin
* How do they affect human health?
o Transmit disease
o Cutaneous irritation
o Allergic reaction

Biological Classification of Ectoparasites
* Superkingdom Eucaryotae
* Kingdom Animalia
* Phylum Arthropoda
o Class Insecta
o Class Arachnida

Bedbugs
* Class Insecta
* Family Cimicidae
* Order Hemiptera
* Genus Cimex
o Cimex lectularius
o Cimex hemipterus

Bedbugs - Data
* Size = 4-5 mm long/3 mm wide
* Color = varies with maturity and feeding state
o Adult = reddish brown
o Nymphs = yellowish white
* Other names = chinches, wall lice, red coats
* Feeding Apparatus – long sharp proboscis extends from anterior head into a groove under the thorax
* Feeding Pattern – nocturnal, gregarious, blood feeder
* Reproduction – fertile adult female lays yellowish-white eggs
o Eggs hatch into nymphs in 37 – 128 days depending on temperature
* Habitat – places where they can easily access humans at night
o Wood bedsteads, mattresses, loose wall paper, under rugs, etc

Bedbug - Epidemiology
* Distribution – bedbugs move from one human residence to another in various ways
o Water pipes
o Adjacent walls
o Clothing
o Travel bags/luggage
o Laundry
o Furniture

Bedbugs- Health Effects
* Bedbugs have never been associated with any disease transmission
o Their effect on humans is tied to the reaction to the bites
o Reaction varies with the individual
o Most severe reaction are due to cutaneous puncture and the effect of the salvia
+ Causing swelling (welts), irritation, allergic inflammation

Mosquitoes
* Class Insecta
* Order Diptera
* Family Culicidae
* Genus Aedes
* Genus Anopheles
* Genus Culex
* Genus Psorophora

Mosquitoes - Data
* Size = 3 – 5 mm long;
o A few species are much larger = 9 mm long
* Color – dark interspersed with while bands
* Females are blood feeders while males are plant feeders
o Females only mate once; then produce fertile ova for life
o Mosquito life expectancy ~ 5 weeks

Mosquitoes – Life Cycle
* Egg
o Female mosquitoes lay their eggs (oviposit) in aquatic settings
o Standing water, tree holes, buckets, tires, etc
o Generally do not oviposit in large bodies of water like lakes
* Larvae – aquatic life stage
o Hatches from eggs and actively feeds on aquatic debri
* Pupae – aquatic life stage
o Developmental stage – metamorphosis – not feeding
* Adults – male and female

Mosquitoes – Health Effects
* Biological Vectors of Disease Pathogens
o Yellow Fever
o Dengue Fever
o Malaria
o Encephalitis
o Microfilariae = nematode larvae
* Mechanical Vectors of Disease Pathogens

Ticks
* Class Arachnida
* Order Acarina
* Family Ixodidae – hard ticks
* Genus Dermacenter
* Genus Amblyomma
* Genus Ixodes
* Genus Rhipicephalus

Tick Data
* Blood feeders – sole source of nutrients
o All vertebrates esp. mammals are hosts for ticks
o Heavy infestations result in significant blood loss
+ Some ticks ingest up to 2 gms of blood per feeding
+ Both male and female feed
* Ticks have longevity- live many years
o Ixodid ticks may live from 7-21 years
o This increases their role as reservoirs for pathogens

Ticks – Health Effects
* Dermatosis – inflammation at bite site
* Envenomization – toxic effect of tick salvia
* Exsanguination – loss of much blood
* Tick Paralysis – damage to peripheral nerves by the bite
* Otoacariasis – damage in the auditory canal
* Disease transmission – vectors of microbial pathoges

Tick - Life Cycle
* Four life stages – tick life history
o Egg – fully engorged females may lay up to 18,000 eggs
o Larva – hexapod, having six legs
o Nymph – sexually immature octapod, eight legs
+ Only one nymphal stage in Ixodid ticks
o Adult – sexually mature
* Host animals
o Some ticks have many hosts, some only one
o Host animal may change with development stage
o Some ticks may molt as many as five times; requiring a different host for each molt
* Ticks sometimes transmit pathogens transovarially

Ticks- Vectors of Microbial Diseases
* Bacterial Disease Transmission
o Rocky Mountain Spotted Fever
+ Dermacentor variabilis – American Dog Tick
+ Amblyomma americanum – Lone Star Tick
o Tularemia
+ Amblyomma americanum
o Lyme Disease
+ Ixodes ricinus
* Viral Disease Transmission
o Tick-Borne Encephalitis
o Colorado tick fever

Sucking Lice
* Class Insecta
* Order Anoplura
* Family Pediculidae
* Genus Pediculus
* Genus Pthirus

Sucking Lice Data
* Blood sucking ectoparasites of mammals
* Flat-bodied with no wings
o Legs adapted for clinging to hair and feathers
o 1.5 – 3.0 mm in length
* Six families having medical or veterinary importance
o One of these contains the species that affect humans
* Significant Human Lice
o Pediculus humanus capitis – head louse
o Pediculus humans humunas – body louse
o Pthirus pubis – pubic (crab) louse

Louse – Life Cycle
* Egg
* Nymphs
* Adults – male and female
o Female may lay 250- 300 eggs per day for 30 days

Sucking Lice – Health Effects
* Bacterial Disease Transmission
o Epidemic Relapsing Fever
+ Borrelia recurrentis
o Epidemic Typhus Fever
+ Rickettsia prowazeki
o Murine Typhus Fever
+ Rickettsia typhi
o Trench Fever
+ Rickettsia quintana

Biting Lice
* Class Insecta
* Order Mallophaga
* Family – there are no families of biting lice

that affect humans health in the world
Most are ectoparasites of birds

Mites
* Class Arachnida
* Order Acarina
* Family Dermanyssidae
* Genus Liponyssoides
* Genus Dermanyssus
* Class Arachnida
* Order Acarina
o Suborder – Trombidiformes
* Family Trombiculidae
* Genus Trombicula

Trombiculid Mites = Chiggers
* Eggs – hatch one week
* Larva – six legged
o Only parasitic stage in this family
o Not host specific – feeds on many hosts
o Leaves host when fully fed or engorged
* Nymph – eight legged
o Live in the soil and feed on insect eggs and soil debri
* Adult – eight legged
o Live in the soil and feed on insect egges and soil debri
o Male and females
o In North American – 1 -2 generations per year

Chigger Dermatitis
* Larval mites – chiggers- do not burrow into the skin
* Larval mites – chiggers – do not suck blood
o They attach to the surface of the skin or at the base of hairs and inject a digestive fluid into the tissues which lyses cells
o They ingest the cell fragments and cellular contents
* The digestive fluid causes the bite to itch
* Common North American Chiggers
o Trombicula alfreddugesi
o Trombiula splendens
o Trombicula batatas

Mites- Vectors of Microbial Pathogens
* Scrub Typhus
* Rickettialpox
* Hemorrhagic Fevers

Fleas
* Class Insecta
* Order Siphonaptera
* Family Pulicidae
* Genus Pulex
o Pulex irritans – human flea
* Genus Tunga
* Genus Ctenocephalides

Flea Data
* Blood sucking ectoparasites of vertebrates
* No wings – do not fly
* Adapted for jumping – strong posterior legs
* Many hosts
* Larvae feed on debri within the nest of the host

Flea – Life Cycle
* Egg – large in comparison to the adult flea
o Hatch in 9 – 15 days under ideal conditions
* Larva – small worm-like organisms which feed on dried blood, cutaneous and fecal debri
* Pupa – inactive, quiet stage, contained within a coccoon
* Adult – laterally compressed, wingless, legs adapted for jumping
o Piecing-sucking mouthparts
o Life expectancy –starved- 100 -125 days
o Life expectancy – fed – 500 – 600 days

Fleas – Health Effects
* Disease transmission
o Plague
o Murine typhus
o Myxomatosis in rabbits
o Cestode intermediate host
* Cutaneous infestation
o Adult flea burrows into skin
+ Chogoe flea of humans – Tunga penetrans

Fly Larvae
* Myaisis
o Infestation with the larvae of diptera or flies
o Cutaneous
o Intestinal
o Urogenital
Leeches

Ectoparasites.ppt

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29 April 2009

Excellent parasites atlas



Excellent parasites atlas with other useful diagnostic information on

heart and Muscle Parasites
Case reprots and updates in parasitology
Eye parasites
CNS parasites
Genito-Urinary parasites
Lung parasites
Skin parasites
Blood, Bone Marrow, Spleen Parasites
Liver & Bile Tree Parasites
Intestinal parasites (Helminths & Protozoa)

Get them from here

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Arthropoda images



Arthropoda images from Dept. of Parasitology, Faculty of Medicine, Chiang Mai University

Aedes aegypti
Anopheles
Assassin bug
Cimex hemipterus
Culex
Leptothrombidium spp.
Stomoxys
Parasarcophaga
Pediculus capitis
Pthirus pubis
Sarcoptes scabiei
Stomoxys
Tabanus
Hard tick
Soft tick
Xenopsylla cheopis
Sarcoptes scabiei
scabiasis

Arthropoda images

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Cestode images



Cestode images from Dept. of Parasitology, Faculty of Medicine, Chiang Mai University

Cysticercus bovis
Cysticercus cellulosae
* Cyst
* Scolex

Dipylidium caninum
* Egg
* Living specimen
* Proglottid & Scolex

Echinococcus granulosus
* Adult
* Hydatid sand

Hymenolepis diminuta
* Egg
* Proglottid & Scolex

Hymenolepis nana
* Egg
* Proglottid & Scolex

Sparganum
Taenia saginata

* Living specimen 1
* Living specimen 2
* Living specimen 3
* Living specimen 4
* Proglottid
* Scolex

Taenia solium
* Whole worm specimen
* Proglottid
* Scolex

Taenia eggs

Cestode images

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Trematode images



Trematode images from Dept. of Parasitology, Faculty of Medicine, Chiang Mai University

Artefact

Paragonimus westermani
* Adult

Paragonimus heterotremus
* Adult

Paragonimus spp.
* Egg

Clonorchis sinensis
* Adult

Dicrocoelium dendriticum
* Adult
* Egg

Eurytrema pancreaticum
* Adult

Fasciola gigantica
* Adult

Fasciola spp.
* Egg

Opisthorchis viverrini

* Adult
* Egg
* Eggs compared with MIF
* Fish intermediate host
* Fish intermediate host II
* Cercaria
* Metacercaria

Echinostoma ilocanum
* Adult

Echinostoma malayanum
* Adult

Fasciolopsis buski
* Adult
* Egg

Hypoderaeum conoideum
* Adult

Haplorchis taichui

* Adult
* Cercaria

Heterophyes heterophyes
* Adult

Metagonimus yokogawai
* Adult

Gastrodiscoides hominis
* Adult

Phaneropsolus bonnei
* Adult

Prosthodendrium molenkampi
* Adult

Schistosoma haematobium

* Adult
* Egg

Schistosoma mansoni
* Adult male & female
* Egg

Schistosoma japonicum
* Adult
* Egg

Schistosoma spp.
* Fork-tailed cercaria

Trematode images

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Protozoa images



Protozoa images from Dept. of Parasitology, Faculty of Medicine, Chiang Mai University

Amoeba

* Endolimax nana
o Trophozoite- IH stain
o Cyst- IH stain
o Cyst- Wet mount/ Iodine stain
* Entamoeba histolytica
o Trophozoite- living
o Trophozoite- trichrome stain
o Trophozoite- trichrome stain VARIOUS FORMS
o Cyst, quadrinucleated- trichrome stain
o Cyst, binucleated- trichrome stain
o Cyst, uninucleated- trichrome stain
o Cyst, uninucleated- wet mount, Iodine stain
* Entamoeba coli
o Trophozoite- trichrome stain
o Trophozoite- living
o Cyst- trichrome stain
o Cyst- Wet mount/ Iodine stain
* Entamoeba gingivalis
o Trophozite- trichrome stain
* Iodamoeba butschlii
o Trophozoite- trichrome stain
o Cyst- trichrome stain
o Cyst- Wet mount/ Iodine stain

Flagellates

* Giardia lamblia
o Trophozoite- Giemsa stain
o Cyst- IH stain
o Cyst- Wet mount/ Iodine stain
* Chilomastix mesnili
o Trophozoite- IH stain
o Cyst- IH stain
o Cyst- Wet mount/ Iodine stain
* Trichomonas tenax
o Trophozoite- Giemsa stain
* Trichomonas vaginalis
o Trophozoite- Giemsa stain
* Trichomonas hominis
o Trophozoite- Giemsa stain
* Dientamoeba fragilis
o Trophozoite- Trichrome stain
* Trypanosoma brucei rhodesiense
o Trypomastigote
* Leishmania donovani
o Amastigote
o Promastigote

Ciliate

* Balantidium coli
o Trophozoite-IH stain
o Cyst- Wet mount/ Iodine stain

Malaria

THIN BLOOD FILM

* Plasmodium falciparum
o Early trophozoite (Ring form)
o Growing trophozoites
o Gametocytes, female
o Gametocytes, male
o Gametocytes, young
o Mixed stages
o Schizonts
o Exflagellation
o Oocyst- wet mount
o Sporozoite- Giemsa stain
* Plasmodium vivax
o Early trophozoite- Ring form
o Growing trophozoite- Amoeboid form
o Immature schizont
o Mature schizont
o Gametocyte, female
o Gametocyte, male
* Plasmodium malariae
o Early trophozoite- Ring form
o Growing trophozoite- Compact form
o Growing trophozoite- Band form
o Immature schizont
o Mature schizont
o Gametocyte, female
o Gametocyte, male
o Various stages
* Plasmodium ovale
o Mature schizont
o Gametocyte
o Various stages
* Mixed P. vivax/P. falciparum

THICK BLOOD FILM

* Plasmodium falciparum I
* Plasmodium falciparum II
* Plasmodium falciparum III
* Plasmodium vivax I
* Plasmodium malariae I
* Plasmodium malariae II

Other sporozoa

* Isospora belli
o Acid fast stain
o Wet mount/ Iodine stain
* Toxoplasma gondii
o Tachyzoite- Wet mount

* Sarcocystisbovihominis/suihominis
o Oocyst- Wet mount

* Sarcocystis spp.
o Sarcocyst- Section/ HE stain
o Sarcocyst- macroscopic cyst
* Cryptosporidium parvum
o Oocyst- Wet mount
o Oocyst- Acid fast stain
* Cyclospora cayetanensis
o Oocyst- Wet mount
o Oocyst with sporocyst- Wet mount
o Oocyst- Acid fast stain
o Comparing with Cryptosporidium

Microspora

* Enterocytozoon bieneusi
o Spores

Miscellaneous

* Pneumocystis carinii
o Cyst- TBO stain
o Cyst- MSN stain
o Cyst- Giemsa stain


Protozoa images

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Nematode images



Nematode images from Dept. of Parasitology, Faculty of Medicine, Chiang Mai University


Ancylostoma duodenale
* Adult

Angiostrongylus cantonensis
* Adults
* Larva
* First Intermediate host

Ascaris lumbricoides
* Adults- living (1)
* Adult living (2)
* Egg
o Fertilized
o Decorticated fertilized
o Unfertilized egg

Brugia malayi
* Microfilaria

Capillaria philippinensis
* Adult female
* Adult female 2
* Adult female showing vulva
* Adult male
* Adult male 2
* Adult male showing spicule
* Egg

Enterobius vermicularis
* Adult female
* Adult male
* Egg

Gnathostoma spinigerum
* Worms in dog stomach
* Adult
* Adult- head bulb
* Egg
* Larval development
* Advanced third-stage encystation
* Advanced third-stage larva 1
o Living
o Head bulb
* Advanced third-stage larva 2
o Living
o Head bulb
* Early third-stage larva in cyclops
* Skin test

Hookworm
* Egg
* Filariform larva
* Rhabditoid larva

Necator americanus
* Adult
* Copulating couple

Strongyloides stercoralis
* Parasitic female
* Parasitic female showing vulva
* Parasitic female (composite image)
* Adult -free living
* Filariform larva (tail)
* Rhabditiform larva
* Agar plate culture

Toxocara spp.
* Egg

Trichinella spiralis
* Adult female
* Adult male
* Larva
o compressed muscle
o muscle section
o from muscle digestion

Trichuris trichiura
* Adult female
* Adult male
* Egg

Wuchereria bancrofti
* Microfilaria

Nematode images

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