Parasitic Infections: Clinical Manifestations, Diagnosis and Treatment

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Parasitic InfectionsClinical Manifestations,
Diagnosis and Treatment

• Lennox K. Archibald, MD, PhD, FRCP, DTMH
• Hospital Epidemiologist
• University of Florida

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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

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• Infections Deaths (103/yr)
• Ascaris 900,000,000 20
• Hookworm 800,000,000 55
• Malaria 100,000,000 1500
• Trichuris 500,000,000 -
• Amoebae 480,000,000 75
• Filarias 280,000,000 -
• Schistosomes 200,000,000 750
• Giardia 200,000,000 -
• Trypanosomes 25,000,000 65
• Leishmanias 1,200,000 1

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Parasites

• Organisms that cannot survive outside their host,
  AND they cause some harm to the host.
• Contrast with commensal organisms
• Incredibly complex organisms
• Consider the struggle for survival from the
  perspective of a parasite

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Giardia
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Giardiasis (G. lamblia)

• Should be suspected in prolonged diarrhea
• Contaminated water often implicatedoutbreaks
• Campers who fail to sterilize mountain stream
  water
• Person-person in day care centers
• MSM
• Symptoms usually resolve spontaneously in 4-6
  weeks

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Giardiasis (G. lamblia)

• 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

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Entamoeba histolytica
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Entamoeba histolytica

• One of 7 amoebae commonly found in humans
• Only one that causes significant disease
• Causes intestinal disease (diarrhea and
  dysentery) and extra-intestinal disease (liver
  primarily)
• In US, often seen in institutionalized patients,
  MSM, tourists returning from developing
  countries, patients with depressed cell mediated
  immunity

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Cyst (wet mount)
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Entamoeba histolytica

• Diagnostic smear trophozoites in liquid stools,
  cysts in formed stools
• IHA important in liver abscess
• Intestinal 95 predictive of active infection
• Extra-intestinal 100 predictive of active I
  infection

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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

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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)

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Amoebic abscessremember

• Can occur in lung, brain, spleen

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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

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Amoebic Abscess

• Liquifaction of liver cells
• Do not contain pus
• Anchovy paste sauce
• Culture of contents usually sterile
• Liver affected
• 53--right lobe
• 8--left lobe

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Amoebiasis (Entamoeba histolytica)Treatment

• Most respond to metronidazole
• Open surgical drainage should be avoided, if at
  all possible

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Cryptosporidium
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Cryptosporidium parvum

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

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Cryptosporidium parvum

• Infants and younger children in day-care centers
• Unfiltered or untreated drinking water
• Farming practices lambing, calving, and
  muck-spreading
• Sexual practices that brings a person into oral
  contact with feces 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)

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Diagnosis and Treatment

• Best diagnosed by stool exam
• There is no known effective treatment-nitazoxamide
  shortens duration of diarrhea
• Infectious disease specialist - for consideration
  of antiparasitic and antiretroviral therapy
• Gastroenterologist - ERCP and sphincterotomy
  endoscopy sometimes required for diagnosis
• General surgeon - suspected acalculous
  cholecystitis

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Malaria
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Falciparum vs. Vivax

• Location Falciparum confined to tropics and
  subtropics vivax more temperate
• Falciparum infects RBC of any age others like
  reticulocytes only 2 infected cells
• Falciparum infected RBCs stick to vascular
  endothelium causing capillary blockage fewer
  schizonts in the periphery, heavy pigment
  deposition, cerebral and renal disease

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Falciparum vs. Vivax

• Vivax and Ovale may reinfect hepatocytes, leading
  to a persisting tissue phase, causing relapses
• Sickle cell trait protects against Falciparum

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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

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Malaria Clinical manifestations

• Non-specific, flu-like illness
• Incubation
• P. falciparum 9-40 days
• Non-P. falciparum may be prolonged
• P. vivax 6-12 months
• P. 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

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Malaria Clinical manifestations

• Febrile paroxysms have 3 classic stages
• Cold stage
• Pt feels cold and has shaking chills
• 15-60 mins. prior to fever
• Hot stage
• 39-41C
• Lassitude, loss of appetite, bone and joint aches
• Tachycardia, 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

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Malaria Clinical manifestations

• Other symptoms depend upon the strain of malaria
• 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 failure
• Brain hypoxia, CNS dysfunction, coma, seizures
• Lungs pulmonary edema
• Jaundice and hemoglobinuria (blackwater fever)

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Malaria Clinical manifestations

• Always suspect malaria in travelers from
  developing countries who present with
• Influenza-like illness
• Jaundice
• Confusion or obtundation

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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

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Diagnosis

• Key of diagnosis is to identify P. falciparum
• New assays
• ELISA for antigen, immunoassay for LDH, PCR
• Anemia, elevated LDH, increased reticulocytes,
  thrombocytopenia
• Elevated unconjugated bilirubin without increases
  in hepatic enzymes
• Elevated serum creatinine, proteinuria,
  hemoglobinuria, hypoglycemia

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Differences in strains

• P. falciparum
• No dormant phase in liver
• Multiple signet ring trophs per cell
• High percentage (gt5) parasitized RBCs considered
  severe
• Development stages other than early ring trophs
  and mature gametocyte not seen

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Differences in strains

• P. vivax and ovale
• Dormant liver phase
• Single signet ring trophs per cell
• Schuffners dots in cytoplasm
• Low percent (lt 5) of parasitized RBCs
• All developmental stages seen
• RBCs often enlarged in later stages

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Differences in strains

• P. malariae
• No dormant stage
• Single signet ring trophs per cell
• Very low parasitemia
• All developmental stages
• RBCs normal size

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Early troph--ring
Mature troph
Schizont
Gametocyte
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Treatment

• P. falciparum malaria can be fatal if not
  promptly diagnosed and treated
• Pts with no immunity against P. falciparum
  require hospitalization
• Pregnant women, young children, elderly
• Non- P. falciparum malaria rarely requires
  hospitalization
• Widespread drug resistance dictates regimen
  (www.cdc.gov/travel CDC malaria hot line
  770-488-7788).

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Treatment

• Uncomplicated malaria
• Drug options
• Chloroquine phosphate
• Mefloquine
• Quinine sulfate plus doxycycline
• Atovaquone plus proguanil (AP)
• Artemisin derivatives
• P. vivax, ovale, malariae, chloroquine-susceptible
  falciparum
• Chloroquine
• Primaquine

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Prevention

• Chloroquine
• Mefloquine
• Doxycycline
• Atovaquone plus proguanil (AP)
• Screens, nets
• 30-35 DEET
• permethrin spray for clothing and nets

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And dont forget baggage malaria!
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Leishmaniasis
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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
• Intracellular parasite controlled by Th1-type
  CD8 response

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Leishmaniasis Clinical Manifestations

• 3 forms visceral, cutaneous, mucosal
• A single species can produce more than one
  syndrome, and each syndrome is caused by multiple
  different species
• Visceral (kala azar)
• Species most prevalent in different places
• L. donovani India
• L. infantum Mid East
• L. chagasi Latin America
• L. amazonensis -- Brazil

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Leishmaniasis

• Cutaneous
• Lesions primarily on exposed areas
• Incubation 2 weeks 2 months
• Dry or moist in appearance
• Ulcers with sharp, raised borders, commonly
  pizza-like
• Dx biopsy (always biopsy the border of lesion)
• Mucosal
• Usually L. braziliensis
• Rarer, usually involves the nose
• Stuffiness, discharge, epistaxis ? nasal septum
  destroyed

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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

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Hepatosplenomegaly
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Splenic aspirate

• Most satisfactory method
• Spleen must be at least 3cm below LCM
• PT not more than 5 secs longer than controls
• Platelets gt40,000
• 21 gauge needle
• Aspirate stained with Giemsa

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Leishmaniasis treatment

• Only drug approved in US is Amphotericin B
• Outside US pentavalent antimony (sodium
  stibogluconate)
• Treatment of cutaneous disease depends on
  anatomic location
• Many spontaneously heal and do not require
  treatment

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Leishmaniasis treatment

• If no mucosal disease and areas of no cosmetic
  concern
• 15 paromomycin or 12 methylbenzethonium
  chloride
• Mucosal, progressive lesions or cosmetically
  sensitive locations
• Pentavalent antimony or ketoconazole

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Remember..

• The factors determining the form of
  leishmaniasis
• Leishmanial species
• Geographic location
• Immune response of the host

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Toxoplasmosis
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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

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Transmission

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

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Toxoplasma gondii life cycle
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Toxoplasma gondii Immunocompetent hosts

• Latent infection (persistence of cysts) is
  generally asymptomatic
• Cervical lymphadenopathy (10-20)
• Mono-like presentation (lt1 of all mono-like
  illnesses)
• Chorioretinitis
• Very rare myocarditis, myositis

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Toxoplasma gondii Immunocompromised hosts

• Often life-threatening
• Almost always reactivation of latent infection
• AIDS
• Encephalitis most common manifestation
• Usually subacute onset/focal (if CD4lt 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

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Toxoplasma gondii Clinical manifestations

• Immunocompromised hosts
• Non-AIDS (transplants, hematologic malignancies)
• CNS 75
• Myocardial 40
• Pulmonary 25

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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

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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

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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

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Toxoplasma gondii Treatment

• Congenital
• Treatment of acute infected pregnant women
  decreases but does not eliminate transmission
• Spiramycin
• If fetal infection is documented, treat with
  pyrimethamine sulfadiazone folinic acid
• Postnatal treatment pyrimethamine sulfadiazone
  folinic acid

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Ascaris lubricoides
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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

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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)

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Ascaris lumbricoidesDiagnosis

• Characteristic eggs on direct smear examination
• If treating mixed infections, treat Ascaris first
• Mebendazole 100 mg bid x 3 days
• Pyrantel 10 mg/kg single dose
• Control
• Periodic mass treatment of children, health
  education, environmental sanitation

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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

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• Strongyloides

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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

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Disseminated Strongyloidiasis

• High mortality?75
• 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

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SummaryClinical Findings

• Defective cell-meditated immunity steroids,
  burns, lymphomas, AIDS (?)
• Gl symptoms in about two-thirds
• Abdominal pain
• Bloating
• Diarrhea
• Constipation
• Wheezing, SOB, hemoptysis

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SummaryClinical 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

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Summary-Clinical Findings

• Eosinophilia 60-95
• Less if on steroids

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Hookworm
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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

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Cutaneous larva migrans (creeping eruption)
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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

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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.

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Cutaneous larva migrans (creeping eruption)

• Usually not associated with systemic symptoms

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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

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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

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EchinococcosisHydatid Disease
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Echinococcosis

• Clinical manifestations
• Most patients are asymptomatic
• Dxd incidentally on an imaging study
• Sxs generally develop when the hydatid cyst
  reaches 8-10 cm (often over decades)
• Compress vital structures
• Erode into biliary tract or bronchus
• Cysts can become superinfected
• Leakage or rupture can result in anaphylactic
  reaction ? fever, hypotension

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Echinococcosis

• Diagnosis
• US, CT or MRI
• Characteristic hydatid cyst with septated
  daughter cysts
• May see head of the tapeworm
• ELISA
• Highly sensitive for liver cysts, less so for
  other organs

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Echinococcosis (Treatment)

• Surgical resection of cyst
• To reduce risk of spread
• Aspirate cyst
• Instill hypertonic saline, iodophor, 95 ethanol
  to kill germinal layer and daughter cysts
• No cidal agents in cases with biliary
  communication ? risk of sclerosing cholangitis
• Percutaneous aspiration-injection-reaspiration
  (PAIR)
• Albendazole before and after surgery or PAIR

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Schistosomiasis
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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).

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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

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Schistosomiasis Clinical manifestations

• Three stages of disease, corresponding to life
  cycle within human hosts
• Swimmers itch
• Within 24 hours of cercariae penetration
• Serum sickness syndrome (Katayama fever)
• 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

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Schistosomiasis Clinical manifestations

• Chronic schistosomiasis
• Results from granulomatous reaction to egg
  deposition in intestine, liver, bladder, lungs
  (less common) and CNS (less common).
• 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

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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

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S. haematobium Urine
S. japonicum
S. mansoni Stool
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African trypanosomiasis

• Trypanosoma brucei gambiense

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Blood smear
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Tsetse fly
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Treatment

• Suramin
• Melasoprol

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American trypanosomiasis
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Blood smear
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Reduviid bug(assassin bug)
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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 target
• Cardiomyopathy associated with CHF, emboli,
  arrythmias
• GI tract mega-esophagus, megacolon

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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
• Both acute and chronic disease can be treated
  with nifurtimox or benznidazole
• Treatment slows the progression of heart disease

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Chagas Disease

• Public health implications in the US
• Chronic
• Cardiomyopathy
• Megaesophagus
• Magacolon
• Blood transfusion
• Transplant
• Solid organ
• Musculoskeletal allograft tissue

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Tape worms
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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

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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.

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Beef Tapeworm
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Treatment

• Praziquantel
• Albendazole
• Niclosamide

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Cystercercosis
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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

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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.

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Cystercercosis

• Clinical manifestations
• Adult worms rarely cause symptoms
• Larvae penetrate intestine, enter blood, and
  eventually encyst in the brain.
• Cerebral ventricles ? hydrocephalus
• Spinal cord ? compression, paraplegia
• Subarachnoid space ? chronic meningitis
• Cerebral 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

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Cysticercosis

• Diagnosis
• 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
• CSF
• Lymphs or eos, low glucose, elevated protein
• Serology
• Especially in cases with multiple cysts

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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

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Babesiosis
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Babesiosis

• Babesiosis caused by hemoprotozoan parasites of
  the genus Babesia
• gt100 species reported
• Few actually cause human infection

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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

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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

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Babesiosis

• Clindamycin plus quinine
• Atovaquone plus azithromycin
• Exchange transfusion in severely ill patients
  with high parasitemia
• Approved by FDA

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Classification of Parasitic Diseases

• Protozoa amoeba flagellates ciliates
  apicomplexa microspors (primitive intracellular
  parasites)
• Metazoa (two phyla)
• Helminths (worms)
• Nematodes
• Intestinal
• Extra-intestinal
• Flatworms (platyhelminths)
• Cestodes (tapeworms)
• Trematodes (flukes)
• Arthopods (ectoparasites) scabies, lice, fly
  larvae

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General rules of treatment

• Protozoa require species-specific treatment
• Metozoa species-specific

143
General rules of treatment of metazoa
144
This is just the beginning of a great adventure
in infectious diseases

• Sine qua non
• history and physical examination

145
Thank you

• Lennox K. Archibald, MD, PhD, FRCP
• lka1_at_ufl.edu