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Parasitic Infections: Clinical Manifestations, Diagnosis and Treatment

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Giardia 200,000,000 - Trypanosomes 25,000,000 65. Leishmanias 1,200,000 1. Parasites ... Giardia. Giardiasis (G. lamblia) Should be suspected in prolonged diarrhea ... – PowerPoint PPT presentation

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Title: Parasitic Infections: Clinical Manifestations, Diagnosis and Treatment


1
Parasitic InfectionsClinical Manifestations,
Diagnosis and Treatment
  • Lennox K. Archibald, MD, PhD, FRCP, DTMH
  • Hospital Epidemiologist
  • University of Florida

2
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

3
  • 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

4
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

5
Giardia
6
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

7
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

8
Entamoeba histolytica
9
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

10
Cyst (wet mount)
11
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

12
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

13
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)

14
Amoebic abscessremember
  • Can occur in lung, brain, spleen

15
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

16
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

17
Amoebiasis (Entamoeba histolytica)Treatment
  • Most respond to metronidazole
  • Open surgical drainage should be avoided, if at
    all possible

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Cryptosporidium
20
Cryptosporidium parvum
  • Causes secretory diarrhea 10 liter/day
  • Significant cause of death in HIV/AIDS
  • Animal reservoirs
  • Incubation period 5-10 days

21
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)

22
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

23
Malaria
24
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

25
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

29
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

30
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

31
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)

32
Malaria Clinical manifestations
  • Always suspect malaria in travelers from
    developing countries who present with
  • Influenza-like illness
  • Jaundice
  • Confusion or obtundation

33
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

34
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

37
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

38
Differences in strains
  • P. malariae
  • No dormant stage
  • Single signet ring trophs per cell
  • Very low parasitemia
  • All developmental stages
  • RBCs normal size

39
Early troph--ring
Mature troph
Schizont
Gametocyte
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41
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).

42
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

43
Prevention
  • Chloroquine
  • Mefloquine
  • Doxycycline
  • Atovaquone plus proguanil (AP)
  • Screens, nets
  • 30-35 DEET
  • permethrin spray for clothing and nets

44
And dont forget baggage malaria!
45
Leishmaniasis
46
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

47
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

48
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

49
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

50
Hepatosplenomegaly
51
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

52
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

53
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

56
Toxoplasmosis
57
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

58
Transmission
  • Eating oocysts excreted by cats harboring sexual
    stages of parasite
  • Outbreaks traced to inadequately cooked meat of
    herbivores (raw beef)
  • Mutton

59
Toxoplasma gondii life cycle
60
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

61
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

62
Toxoplasma gondii Clinical manifestations
  • Immunocompromised hosts
  • Non-AIDS (transplants, hematologic malignancies)
  • CNS 75
  • Myocardial 40
  • Pulmonary 25

63
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

64
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

65
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

66
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

67
Ascaris lubricoides
68
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

69
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)

70
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

74
  • Strongyloides

75
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

76
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

77
SummaryClinical Findings
  • Defective cell-meditated immunity steroids,
    burns, lymphomas, AIDS (?)
  • Gl symptoms in about two-thirds
  • Abdominal pain
  • Bloating
  • Diarrhea
  • Constipation
  • Wheezing, SOB, hemoptysis

78
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

79
Summary-Clinical Findings
  • Eosinophilia 60-95
  • Less if on steroids

80
Hookworm
81
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)
86
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

87
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.

88
Cutaneous larva migrans (creeping eruption)
  • Usually not associated with systemic symptoms

89
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

93
EchinococcosisHydatid Disease
94
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

95
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

96
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
104
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).

105
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

106
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

107
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

108
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

114
Blood smear
115
Tsetse fly
116
Treatment
  • Suramin
  • Melasoprol

117
American trypanosomiasis
118
Blood smear
119
Reduviid bug(assassin bug)
120
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

121
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

122
Chagas Disease
  • Public health implications in the US
  • Chronic
  • Cardiomyopathy
  • Megaesophagus
  • Magacolon
  • Blood transfusion
  • Transplant
  • Solid organ
  • Musculoskeletal allograft tissue

123
Tape worms
124
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

125
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.

126
Beef Tapeworm
127
Treatment
  • Praziquantel
  • Albendazole
  • Niclosamide

128
Cystercercosis
129
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

130
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

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General rules of treatment of metazoa
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This is just the beginning of a great adventure
in infectious diseases
  • Sine qua non
  • history and physical examination

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