Clinical Parasitology 08
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Parasitic Infections: Clinical Manifestations, Diagnosis and Treatment Lennox K. Archibald, MD, PhD, FRCP, DTM&H Hospital Epidemiologist University of Florida
Transcript of Clinical Parasitology 08
Parasitic Infections:Clinical Manifestations,
Diagnosis and Treatment
Lennox K. Archibald, MD, PhD, FRCP, DTM&H
Hospital Epidemiologist
University of Florida
The Reality• 1.3 billion persons infected with 1.3 billion persons infected with
Ascaris (1: 4 persons on earth)Ascaris (1: 4 persons on earth)
• 300 million with schistosomiasis300 million with schistosomiasis
• 100 million new malaria cases/yr100 million new malaria cases/yr
• At UCLA, 38% of pediatric and At UCLA, 38% of pediatric and dental clinic children harbored dental clinic children harbored intestinal parasites 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
Case 1
• 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)
–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.
–Suddenly ill with abdominal distension–Fever–Periumbilical pain–Vomiting–Blood-tinged diarrheal stools
• Denied arthritis /known exposure to parasites• Family history of “inflammatory bowel
disease”
Case 2
• Physical examination:–Acutely ill–Distended abdomen–No hepatomegaly or splenomegaly–Decreased bowel sounds–Stool exam
Gross blood presentNo 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
Case 2
• 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
– Institutionalized patients–MSM–Tourists returning from developing countries–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
–Superficial: watery diarrhea and nonspecific GI complaints
–Invasive: gradual onset (1-3 weeks) of abdominal pain, bloody diarrhea, tenesmus
• Fever is seen in minority of patients
Amoebiasis: Clinical Manifestations
• Can be mistaken for ulcerative colitis
• Steroids can dramatically worsen and precipitate toxic megacolon
• Amebic liver abscesses
–RUQ pain, pain referred to right shoulder
–High fever
–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:
–53%-right lobe
– 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
Case 5
• 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
–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
– P. falciparum: 9-40 days
– Non-P. falciparum: may be prolongedP. vivax: 6-12 monthsP. malariae and ovale: years
• Fever is the hallmark of malaria
– Classically, 2-3 day intervals in P. vivax and malariae
– 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
– Cold stagePt feels cold and has shaking chills15-60 mins. prior to fever
– Hot stage39-41°CLassitude, loss of appetite, bone and joint achesTachycardia, hypotension, cough, HA, back pain,
N/V, diarrhea, abdo pain, altered consciousness– Sweating stage
Marked diaphoresis followed by resolution of fever, profound fatigue, and sleepiness
2-6 hours after onset of hot stage
Malaria: Clinical manifestations• Other symptoms depend on malaria strain• P. vivax, ovale and malariae: few other sxs• P. falciparum:
– Dependent upon host immune status– No prior immunity/splenectomy high levels
of parasitemia profound hemolysis– Vascular obstruction and hypoxia
Kidneys: renal failureBrain: (CNS) ― hypoxia, coma, seizuresLungs: pulmonary edema
– Jaundice & hemoglobinuria (blackwater fever)
Malaria: Clinical manifestations
• Always suspect malaria in travelers from developing countries who present with:
–Influenza-like illness
–Jaundice
–Confusion or obtundation
Diagnosis
• Giemsa-stained blood smear
–Thick and thin smears
• P. falciparum:
–Best just after fever peak
• Others:
–Smears can be performed at any time
• Examine blood on 3-4 successive days
Differences in strains• P. falciparum
–No dormant phase in liver
–Multiple signet ring trophs per cell
–High percentage (>5%) parasitized RBCs considered severe
Differences in strains
• P. vivax and ovale
–Dormant liver phase
–Single signet ring trophs per cell
–Schuffner’s dots in cytoplasm
–Low percent (< 5%) of parasitized RBCs
Differences in strains
• P. malariae–No dormant stage–Single signet ring trophs per cell–Very low parasitemia
Treatment• P. falciparum malaria can be fatal if not
promptly diagnosed and treated
• Non- P. falciparum malaria rarely requires hospitalization
• Widespread drug resistance dictates regimen (www.cdc.gov/travel; CDC malaria hot line: 770-488-7788).
TreatmentUncomplicated malaria
• P. vivax, ovale, malariae, chloroquine-susceptible falciparum–Chloroquine–Primaquine for dormant liver forms
• Chloroquine-resistant falciparum–Quinine plus doxycycline–Mefloquine–Atovaquone plus proguanil (AP)–Artemisins (common in SE Asia due to
multi-drug resistance)
TreatmentSevere malaria
• Drug options
–Quinidine gluconate—only approved parenteral agent in US
–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
–Few parasites in peripheral blood
–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”
Case 6
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
Leishmaniasis
• Cutaneous
–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)
–L. mexicana reported in Texas
• Visceral (kala azar)
–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
–Spleen
–Bone marrow
–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:
–Leishmanial species
–Geographic location
–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
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
– Ingestion of cysts in undercooked meat of herbivores
– Water/food contaminated with oocysts– Congenitally– Infected organs, blood (less common)
• Prevalence of latent infection in US about 10%; France about 75%– Generally higher in less-developed world– 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
– Encephalitis most common manifestation– Usually subacute onset/focal (if CD4< 200)– Mental status changes, seizures, weakness,
cranial nerve abnormalities, cerebellar signs, – Can present as acute hemiparesis/language
deficit– Usually multiple ring-enhancing lesions on
CT/MRI• Pneumonitis• Chorioretinitis
Toxoplasma gondii: Clinical manifestations
• Immunocompromised hosts
–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–Chorioretinitis–Strabismus–Blindness–Epilepsy, mental retardation, pneumonitis,
microcephaly, hydrocephalus, spontaneous abortion, stillbirth
Toxoplasma gondii: diagnosis
• Clinical suspicion crucial
• Serology is primary method of diagnosis
–IgM, IgG
• Histopathology
–Tachyzoites in tissue sections or body fluid (difficult to stain)
–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
–Latent disease: not treated
–Active disease: pyrimethamine + sulfadiazone + folinic acid
Toxoplasma gondii: Treatment• Congenital:
–Treatment of acute infected pregnant women decreases but does not eliminate transmissionSpiramycin
–If fetal infection is documented, treat with pyrimethamine + sulfadiazone + folinic acid
–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
Babesiosis• Babesia microti
• Life cycle involves two hosts:
–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
Babesiosis
Deer are the hosts upon which the adult ticks feed and are indirectly part of the Babesia cycle as they influence the tick population
Babesiosis
• 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–Nausea–Vomiting–Obstruction of small bowel or common
bile duct.• Pulmonary: symptoms due to migration
–Alveoli (verminous pneumonia)—cough, fever wheeze, dyspnea, X-ray changes, eosinophilia
Effects of Adult Ascaris Worms
• Depends on worm load• Effects
–Mechanical: obstruction, volvulus, intussusception, appendicitis, obstructive jaundice, liver abscesses, pancreatitis, asphyxia
• Toxic and Metabolic–Malnutrition (complex)
Ascaris lumbricoidesDiagnosis
• Characteristic eggs on direct smear examination
• If treating mixed infections, treat Ascaris first–Mebendazole–Pyrantel
• Control: –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:–Elevated WBC–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
–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:
–Abdominal pain
–Bloating
–Diarrhea
–Constipation
• Wheezing, SOB, hemoptysis
Summary—Clinical Findings• Skin rash or pruritis in ~ one-third
–Larva currens (racing larva)
–Intensely pruritic
–Linear or serpiginous urticaria with flare that moves 5-15 cm/hr
–Usually buttocks, groin, and trunk
–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
–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.
Cutaneous larva migrans (creeping eruption)
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
Case 17• 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
Case 17
• 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 – South America, Caribbean, Africa, Mid East
• S. japonicum – China and Philippines
• S. haematobium– Africa, Mid East
Schistosomiasis: Clinical manifestations
• Three stages of disease, corresponding to life cycle within human hosts
• Swimmer’s itch– Within 24 hours of cercariae penetration
• Serum sickness syndrome (Katayama fever)– 4 to 8 weeks later when worms mature and
release eggsFever, headache, cough, chills, sweating,
lymphadenopathy, hepatosplenomegaly usually resolves spontaneously
Elevated IgE and eosinophilsMost common with S. japonicum
Chronic Schistosomiasis
• Granulomatous reaction to egg deposition in intestine, liver, bladder, lungs
• S. mansoni, japonicum
– Chronic diarrhea, abdominal pain, blood loss, portal hypertension, hepatosplenomegaly, pulmonary hypertension
– Eosinophilia is common
– Liver function tests are usually normal
• S. Haematobium
– Hematuria, bladder obstruction, hydronephrosis, recurrent UTIs, bladder cancer
Schistosomiasis: Diagnosis and Treatment
• Detection of characteristic eggs in stool, urine or tissue biopsy is diagnostic
–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. mansoniStool
S. haematobiumUrine
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
–More rarely: myocarditis, encephalitis
• Years later: chronic Chagas Disease (10-30%)
–Heart: primary targetCardiomyopathy associated with CHF,
emboli, arrythmias
–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
–Cardiomyopathy–Megaesophagus–Megacolon
• Blood transfusion• Transplant
–Solid organ–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
– Definitive for T. saginata
– Intermediate for Echinococcus granulosus (hydatid)
– 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
Case 21
• 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
Cystercercosis
• 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.
Cysticercosis• Clinical manifestations
– Adult worms rarely cause sxs– Larvae penetrate intestine, enter blood, and
eventually encyst in the brain.Cerebral ventircles hydrocephalusSpinal cord compression, paraplegiaSubarachnoid space chronic meningitisCerebral cortex seizures
– Cysts may remain asymptomatic for years, and become clinically apparent when larvae die
– Larvae may encyst in other organs, but are rarely symptomatic
Cysticercosis
• Diagnosis– CT and MRI preferred studies
Discrete cysts that may enhanceUsually multiple lesions
–Single lesions especially common in cases from India
Older lesions may calcify– CSF
Lymphs or eos, low glucose, elevated protein– Serology
Especially in cases with multiple cysts
Cysticercosis
• Treatment–Complex and controversial
–Praziquantel and albendazole may kill cysts, but death of larvae can increase inflammation, edema and exacerbate sxs
–When possible, surgical resection of symptomatic cyst is preferred
–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)
1) Helminths (worms)Nematodes
– Intestinal– Extra-intestinal
Flatworms (platyhelminths)– Cestodes (tapeworms)– Trematodes (flukes)
2) 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 Permethrin, Ivermectin
This is just the beginning of a great adventure in infectious diseases
Sine qua non:
history and physical examination
