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MEDICAL PARASITOLOGY

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Title: MEDICAL PARASITOLOGY


1
MEDICAL PARASITOLOGY
  • HELMINTHS PROTOZOA

2
INFORMATION EMPHASIS
  • Agent and Group ID general importance
  • Epidemiology (distribution, transmission, etc)
  • Pathogenic capability
  • Diagnosis
  • Control

3
BASIC TERMINOLOGY PRINCIPLES
  • Symbiosis Living together
  • Commensalism One symbiont benefits, other
    unaffected
  • Mutualism Both symbionts benefit
  • Parasitism One symbiont benefits, other is
    damaged

4
COMMON TERMS
  • Obligate vs Facultative Parasites
  • Endo- vs Ecto-parasites
  • Pseudo- vs Spurious Parasites
  • Zoonotic Parasites
  • Host-specific vs Non-host-specific Parasites
  • Definitive vs Intermediate Hosts
  • Paratenic/Transfer Hosts
  • Vectors

5
PARASITE SURVIVAL FACTORS
  • Parasites have successfully adapted to (all?)
    environmental niches in hosts
  • Parasites best adapted are least pathogenic
  • Parasite-host relationships are typically
    long-term/chronic/intimate

6
CONDITIONS NECESSARY FOR SUCCESSFUL ENDEMIC
PARASITISM
  • Reservoir of infection
  • Means of transmission from infected to
    susceptible, new hosts
  • Ability to invade and successfully reside in
    new hosts
  • Ability to reproduce

7
  • HELMINTH/WORM TERMINOLOGY
  • Adults sexually reproductive life cycle stage
  • Larvae developmental or asexually reproductive
    life cycle stage
  • Eggs stage protective of zygote /or embryo
  • Cysts usually a larval stage encapsulated in
    tissues of an intermediate host
  • Hypobiosis worms in temporary developmental
    arrest
  • Monoecious/hermaphroditic both sexes 1 body
  • Dioecious sexes separate males females
  • Parthenogenesis ability to produce offspring
    without fertilization of eggs

8
  • Helminths, continued
  • Worm-terms, continued
  • Oviparous production of eggs, discharged from
    uterus of female
  • Ovoviviparous production of eggs which hatch
    prior to discharge from uterus of female
  • Viviparous production of embryos/L1 larvae, no
    rigid encapsulation of embryo

9
  • Enteric helminths, continued
  • GENERALIZED NEMATODE LIFE CYCLE
  • Adults
  • Eggs Embryos L1
  • L2 larva
  • L3 larva
  • L4 larva
  • L5 juvenile

10
  • Enteric Helminths
  • Ascaris lumbricoides
  • SI roundworm transmitted fecal-oral via eggs
  • Pathogenic potential low to high, depending on
    host species and condition, number of eggs
    ingested, secondary bacterial agents carried
  • Clinical signs larval migration none,
    pneumonitis, asthmatic reaction. Adults SI
    blockage, plugging of bile duct, perforation of
    SI, appendix or other site, malnourishment
  • Reservoir human DH
  • Damage potential dependent on worm s, host
    susceptibility to larval and adult action

11
  • Enteric helminths, continued
  • lumbricoides, continued
  • Prevalence world-wide, temperate and tropical
    regions, possibly 1 billion infected
  • Diagnosis eggs in feces, observation of
    drop-out adult worms
  • Treatment piperazine, albendazole, mebendazole,
    pyrantel pamoate

12
  • Enteric helminths, continued
  • Ascaris lumbricoides life cycle

13
  • Extra-enteric helminths, continued
  • Toxocara canis, Toxocara cati, Balisascaris
    columnaris, others (Visceral Larval Migrans)
  • Transmission fecal-oral, ingestion of infective
    ova
  • Pathogenic potential high, dependent on s of
    larvae, migrational destination(s)
  • Clinical signs determined by s of larvae, sites
    infected cough, fever, hypereosinophilia,
    retinochoroiditis, epilepsy, myocarditis, other
  • Reservoir hosts canines, felines, mustelids,
    raccoons, badgers, oppossums, other
  • Damage potential high carriers of bacterial
    contaminants, direct toxicity tissue destruct.

14
  • Extra-enteric helminths, continued
  • T. canis, T. cati, B. columnaris, et.al.
  • Prevalence worldwide, sanitation dependent,
    cold/cool temperate regions to equator
  • Diagnosis serology, lesion/abcess pathological
    examination (gross histo), high eosinophil
    count is strongly suggestive
  • Treatment systemic anthelmintics have been used
    with varying degrees of success, depending on
    diagnostic timing fenbendazole other
    benzimidazoles, probably avermectins

15
Toxocara canis life cycle
16
  • Enteric helminths, continued
  • Ancylostoma duodenale Necator americanus
    (hookworms)
  • Transmission via contact of skin with L3 larva
  • Pathogenic potential population dependent, each
    worm sucks blood from mucosa in SI, larval
    migration usually insignificant
  • Clinical signs minor reaction (ground itch),
    dependent, at larval entry pneumonitis via
    migrating larvae, if large s eosinophilia,
    occult blood in stools, diarrhea, anemia, edema,
    et.al.
  • Reservoir humans, possibly other anthropoids
  • Damage potential depends on condition
    sensitivity of host, and s of worms

17
  • Enteric helminths, continued
  • Duodenale N. americanus, continued
  • Prevalence world-wide, in tropics, subtropics,
    and warm temperate regions some zonal variation
    by species
  • Diagnosis by ID of ova in feces
  • Treatment albendazole, mebendazole, pyrantel
    pamoate, piperazine (probably)

18
Hookworm Life Cycle
19
  • Extra-enteric helminths, continued
  • Ancylostoma caninum, A. braziliense, Uncinaria
    stenocephala, et.al. (cutaneous larval migrans)
  • Transmission penetration of skin by direct
    contact with infective L3 larvae
  • Pathogenic potential low, transient
  • Clinical signs serpiginous tracks/creeping
    eruption on skin near invasion sites
  • Reservoir hosts canines, felines, other animals
    with host-specific species of hookworms
  • Damage potential limited to numbers of worms
    involved, host sensitivity to cutaneous trauma

20
  • Extra-enteric helminths, continued
  • caninum, A. braziliense, U. stenocephala, et.al
  • Prevalence worldwide distribution, tropical,
    subtropical, warm cool temperate, sub-arctic
    (Uncinaria)
  • Diagnosis visual observation of characteristic
    tracks/burrows on skin surface
  • Treatment albenazole, other benzimidazoles

21
  • Enteric helminths, continued
  • Trichuris trichiura (whipworm)
  • Transmission fecal-oral via embryonated ova
  • Pathogenic potential low to moderate, dependent
    on worm numbers location in LI
  • Clinical signs dependent on worm s none,
    bloody(frank)/mucoid diarrhea, abdominal pain
    distention, rect. prolapse, anemia, weakness,
    eosinophilia
  • Reservoir mainly human, others possible but host
    specificity not well documented
  • Damage hinges on results numbers of worm
    mucosal perforations, bacterial/viral
    involvement, degrees of blood loss, worm location

22
  • Enteric helminths, continued
  • T. trichiura, continued
  • Prevalence worldwide tropical, subtropical, warm
    temperate sanitation dependent SE USA, spotty in
    other states with large populations of infected
    immigrants
  • Diagnosis microscopic ID of ova in feces
  • Treatment albendazole is drug of choice

23
Trichuris trichiura life cycle
24
  • Enteric helminths, continued
  • Capillaria phillipinensis
  • Transmission ingestion of larvae in fresh and
    brackish-water fish
  • Pathogenic potential high due to worm site and
    autoinfection factors
  • Symptoms abdominal pain, borborygmus, diarrhea
    early anorexia, nausea, vomiting, et.al
  • Reservoir unknown probably many fish-eating
    mammals
  • Damage potential high populations build via
    autoinfection adults and larvae migrate through
    mucosal tissue in (mainly) jujunal SI

25
  • Enteric helminths, continued
  • C. phillipinensis, continued
  • Prevalence high/moderate in Phillipine areas
    where eating raw fish is a cultural event
  • Diagnosis microscopic ID of ova in feces,
    differentiation from whipworm eggs (Trichuris)
  • Treatment mebendazole drug of choice, other
    benzimidazoles also efficacious

26
  • Enteric helminths, continued
  • Enterobius vermicularis (pinworm)
  • Transmission by ingestion of embryonated ova
  • Pathogenic potential 0/low
  • Clinical signs occasional anal itching from
    night-time exit migration of female worm for
    oviposition occasional host skin pruritis to egg
    glue rare migration disintegration of female
    worms into urogenital tract of female, with
    lesions in abdominal cavity via oviducts
  • Reservoir hosts human (family friends)
  • Damage potential 0 no tissue invasion/insult, no
    apparently toxic by-product production

27
  • Enteric helminths, continued
  • E. vermicularis, continued
  • Prevalence world-wide, arctic to equator
  • Diagnosis microscopic ID of ova /or worms on
    transparent cellophane tape swab of perineum
  • Treatment albendazole, and others

28
Enterobius vermicularis life cycle
29
  • Extra-enteric Helminths
  • Strongyloides stercoralis
  • Transmission ingestion of, or skin contact with
    L3 larva, possibly congenital transmammary
  • Pathogenic potential very high due to
    autoinfection, infection site, parasite-host
    incompatibility
  • Clinical signs skin reaction at larval entry
    (ground itch), pneumonitis re primary larval
    migration, diarrhea/dysentery, malabsorption,
    mucosal ulceration, frank or occult bloody stool
  • Reservoir hosts none necessary, free-living
    agent with invasion capability (facultative P)

30
  • Extra-enteric helminths, continued
  • S. stercoralis, continued
  • Damage potential high/extreme direct damage to
    SI villar epithelium extensive worm population
    buildup intensifies, eventually colonizes colonic
    mucosa, nutritional absorption restricted/eliminat
    ed, dehydration intense
  • Prevalence free-living colonies numerous,
    distribution similar to hookworms, human
    infections rare, sporadic, but significant
  • Diagnosis isolation, microscopic ID of ova,
    larvae in feces or intestinal biopsies
  • Treatment albendazole, ivermectin, others

31
Strongyloides stercoralis life cycle
32
  • Extra-enteric helminths, continued
  • Trichinella spiralis
  • Transmission ingestion of encysted larvae in
    meat
  • Pathogenic potential moderate in majority of
    infected hosts of infective larvae, host
    tolerance are major factors
  • Clinical signs occasional diarrhea during early
    stages fever, eosinophilia, muscle
    pain/stiffness during larval invasion of muscle
  • Damage potential low/moderate in healthy
    hosts, high in those in which myocarditis,
    encephalitis or chronic pneumonitis occur

33
  • Extra-enteric helminths, continued
  • T. spiralis, continued
  • Prevalence low to high, dependent on cultural
    preferences regarding meat selection
    preparation no climatic factors are involved
  • Diagnosis serologic testing, histologic ID of
    larvae in muscle biopsy
  • Treatment corticosteroids, mebendazole,
    albendazole

34
Trichinella spiralis life cycle
35
  • Extraenteric helminths, continued
  • Dracunculus medinensis
  • Transmitted by ingestion of copepod IH
  • Clinical signs skin blister followed by ulcer
    with anterior end of female worm visible,
    cutaneous bulge of skin over body of worm,
    various immune responses (rashes, asthma)
  • Reservoir hosts canines, many other mammals
  • Damage potential low to moderate, depending on
    sensitivity of host to worm excretions and other
    worm-related antigens
  • Prevalence worldwide, from equator into cool
    temperate climatic areas

36
  • Extraenteric helminths, continued
  • D. medinensis, continued
  • Diagnosis observation of skin ulcer, at bottom
    of which end of female worm is visible
  • Treatment removal of worm by gentle extraction
    from burrow by winding on a stick, with
    concomitant use of metronidazole or thiabendazole

37
Dracunculus medinensis life cycle
38
  • Filarid helminths
  • Filarid Helminth Life Cycle
  • DH Vector
  • Adults microfilariae L1 L2 larva
  • L4 larva L3 larva
  • L5 larva

39
  • Filarid helminths
  • Wuchereria bancrofti (filariasis/elephantiasis)
  • Transmission by mosquito vectors
  • Pathogenic potential moderate - high, long term
  • Clinical signs variable re host factors and worm
    species/strains none, renal disease, hematuria,
    proteinuria, hyperimmune reactivity,
    eosinophilia, lymphangitis (soft edematous
    swelling of extremeties, followed by eventual
    hardening)
  • Reservoir hosts humans, some monkeys
  • Damage potential variable immune reactions to
    worms worm products varies with individuals,
    long-term, plugging of lymph vessels

40
  • Filarid helminths, continued
  • W. bancrofti, continued
  • Prevalence throughout tropical and subtropical
    countries, into some warm temperate areas
  • Diagnosis recovery and microscopic ID of
    microfilaria from blood samples
  • Treatment diethylcarbamazine, followed by
    ivermectin for prevention of reinfection

41
Wuchereria bancrofti life cycle
42
  • Filarid helminths, continued
  • Brugia malayi, et.al.
  • Transmission by mosquito species different from
    those involved with W. bancrofti
  • Pathogenic potential essentially similar to that
    described for W. bancrofti
  • Clinical signs similar to those of W. bancrofti
  • Damage potential similar to that of W. bancrofti
  • Prevalence similar to W. bancrofti, regional
    differences dependent on vector habitat
    preferences
  • Diagnosis microscopic diff of microfilariae from
    other species
  • Treatment diethylcarbamazine Ivermectin

43
  • Filarid helminths, continued
  • Loa loa (african eyeworm)
  • Transmission via chrysops/mango fly vectors
  • Pathogenic potential moderate, dependent on host
    sensitivity factors
  • Clinical signs eosinophilia, few obvious signs
    except when adults are migrating across eye
    occasional swellings, edema in local sites
  • Reservoir hosts monkeys known, possibly et.al
  • Damage potential low, minor host response
    normally
  • Prevalence tropical, rain forest vector habitat
  • Diagnosis ID of microfilaria, extraction of
    adult
  • Treatment Diethylcarbamazine ivermectin

44
Loa loa life cycle
45
  • Filarid helminths, continued
  • Mansonella spp., Dipetalonema spp., et.al.
  • Transmission by midges blackflies
  • Pathogenic potential low to zero
  • Clinical signs usually non-existent
  • Reservoir hosts humans, monkeys
  • Damage potental low, dependent on host
    sensitivity to specific worms
  • Prevalence tropical, subtropical, warm temperate
    regions where vectors exist
  • Diagnosis ID of microfilariae in blood
  • Treatment Diethylcarbamazine ivermectin, when
    warranted

46
  • Filarid helminths, continued
  • Onchocerca volvulus (river blindness)
  • Transmitted by blackfly vectors
  • Pathogenic potential moderate, dependent on death
    decomposition of microfilariae
  • Clinical signs adult clusters cause subcutaneous
    nodules, microfilariae cause blindness
  • Reservoir hosts large domestic animals, probably
    others
  • Damage potential low/moderate, depending on host
    sensitivity, toxicity of worm strain, number
    and death/decomposition rate of larvae in eye

47
  • Filarid helminths, continued
  • O. volvulus, continued
  • Prevalence variable, 5 to 80 in endemic areas
    near streams needed by blackfly reproduction
  • Diagnosis observation of adults in prominent
    subcutaneous nodules, skin biopsy and histologic
    examination for microfilariae
  • Treatment surgical removal of adults,
    diethylcarbamazine, ivermectin for larvae

48
Onchocerca volvulus life cycle
49
  • Filarid helminths, continued
  • Dirofilaria immitis (canine heartworm infection)
  • Transmission by mosquito vector
  • Pathogenic potential in human (unnatural host)
    low/moderate, dependent on host sensitivity
  • Clinical signs usually absent in humans,
    dependent on location of worm
  • Reservoir hosts canines (dogs, coyotes, etc.)
  • Damage potential low in humans, dependent on host
    sensitivity, s of worms, location of worms
  • Prevalence wide tropical, subtropical, warm and
    cool temperate regions
  • Diagnosis usually biopsy of dead, encysted worm
  • Treatment surgical removal

50
  • Flatworms/Platyhelminths
  • Flatworm-related Terminology
  • Cestodes/tapeworms segmented flatworms
  • Trematodes/flukes leaf-shaped (except for
    schistosomes), single-unit flatworms
  • Oncosphere/hexacanth egg-encased embryo of
    cyclophyllidean tapeworms
  • Coracidium egg-encased embryo of
    pseudophyllidean tapeworms
  • Miracidium egg-encased embryo of flukes
  • Cysticercoid, cysticercus, coenurus, hydatid
    cysts cyclophyllidean tapeworm larval types in
    IHs

51
  • Flatworm helminths, continued
  • Flatworm terms, continued
  • Procercoid, plerocercoid larvae of
    pseudophyllidean tapeworms
  • Scolex organ of attachment, adult tapeworms
  • Proglottids tapeworm body segments
  • Strobila tapeworm body (all segments)
  • Sporocyst, redia larvae of fluke species
  • Cercaria end stage of asexual reproduction of
    flukes
  • Metacercaria encysted cercaria infective to DH

52
  • Flatworm helminths, continued
  • Trematodes/Flukes
  • Generalized Fluke Life Cycle
  • Adults in DH
  • Egg Miracidium (embryo) Snail primary IH
  • Sporocyst /or Redia larva
  • Cercaria
  • Vegetation/secondary IH
  • Metacercaria

53
  • Flatworm helminths, continued
  • Fasciolopsis buski (intestinal fluke)
  • Transmission ingestion of metacercaria on
    aquatic vegetation
  • Pathogenic potential 0/low
  • Clinical signs none, rash, intestinal discomfort
  • Reservoir hosts numerous, herbivores
  • Damage potential low, minor SI mucosal damage
  • Prevalence high, 10 m infections annually in
    oriental and asian, tropical/subtropical areas
  • Diagnosis ID of eggs in fecal sedimentation
  • Treatment prazyquantel, niclosamide

54
Fasciolopsis buski life cycle
55
  • Flatworm parasites, continued
  • Echinostoma spp. (spiny-mouthed flukes)
  • Transmission ingestion of metacercaria in snail
    secondary IH
  • Pathogenic potential low/moderate
  • Clinical signs dependent, none/mild irritation
  • Reservoir many snail-eating mammal DHs
  • Damage potential low some SI abrasion
  • Prevalence oriental, asian tropical/subtropical
    countries
  • Diagnosis microscopic ID of ova in fecal sed
  • Treatment praziquantel, niclosamide

56
  • Flatworm helminths, continued
  • Heterophyes spp., Metagonimus spp.
  • Transmission ingestion of metacercaria in fish
    secondary IH
  • Pathogenic potential low early, rising to high
    over time, re worm s, infection longevity
  • Clinical signs none early, myocarditis,
    seizures, neurologic defecits, other, in chronic
    infections
  • Reservoir hosts most piscivorous mammals
  • Damage potential dependent on tissue-infested
    ova lodged in various organs, emitting toxins
    produced by embryos egg s determine level of
    damage

57
  • Flatworm helminths, continued
  • Heterophyes, Metagonimus, continued
  • Prevalence high in oriental, asian and other
    countries where endemic, and cultural
    consumption of raw fish is common
  • Diagnosis microscopic ID of ova in feces via
    sedimentation concentration
  • Treatment nothing effective against systemically
    lodged ova prazyquantel, tetrachloroethylene X
    adults

58
Heterophyidae life cycle
59
  • Flatworm helminths, continued
  • Paragonimus westermani (lung fluke)
  • Transmission ingestion of metacercaria in
    crustacean secondary IH
  • Pathogenic potential moderate to high dependent
    on worm s, species toxicity, level of tissue
    damage
  • Clinical signs none, fever, cough, bloody
    sputum, chest pain, bronchitis, dyspnea
  • Reservoir huge, almost any crustacean-eating
    mammal
  • Damage potential early migration through tissues
    minor encapsulation in lungs major

60
  • Flatworm helminths, continued
  • P. westermani, continued
  • Prevalence worldwide, dependent on human
    consumption of raw crustaceans
  • Diagnosis microscopic ID of ova in sputum or
    sedimentation-concentrated feces ID of ova in
    needle biopsy of encapsulations in lungs
  • Treatment praziquantel, bithionol

61
Paragonimus westermani life cycle
62
  • Flatworm helminths, continued
  • Fasciola hepatica (sheep, et.al., liver fluke)
  • Transmission ingestion of metacercaria on
    vegetation
  • Pathogenic potential moderate/high dependent on
    worm s length of infection period
  • Clinical signs none early, fever, chills, pain,
    jaundice, eosinophilia, liver enlargement, other
  • Reservoir huge, almost any herbivorous or
    omnivorous animal is suitable host
  • Damage potential moderate to high depending on
    worm s migration through tissues liver
    parenchyma, mechanical toxic effects,
    hyperplasia of biliary epithelium, cirrhosis

63
  • Flatworm helminths, continued
  • F. hepatica, continued
  • Prevalence millions of human infections
    probable, worldwide distribution dependent on
    aquatic vegetation production and consumption
  • Diagnosis microscopic ID of ova in fecal
    sedimentation
  • Treatment bithionol, praziquantel

64
Fasciola hepatica life cycle
65
  • Flatworm helminths, continued
  • Clonorchis sinensis, Opisthorchis spp. (oriental
    liver flukes)
  • Transmission ingestion of metacercaria in fish
    secondary IH
  • Pathogenic potential 0 early, low/moderate late
    infection, depending on worm s
  • Clinical signs similar to those described for F.
    hepatica, but usually less intense until worms
    reach very large population levels
  • Reservoir huge, nearly all piscivorous mammals
    in endemic areas
  • Damage potential moderate, similar but usually
    smaller magnitude than F. hepatica

66
  • Flatworm helminths, continued
  • C. sinensis, O. spp., continued
  • Prevalence high in oriental other countries
    where fish are eaten raw sporadic in many
    countries, dependent on local cultural factors
    some outbreaks tied to transport of fresh fish in
    non-endemic areas
  • Diagnosis microscopic ID of ova in feces
    processed by sedimentation concentration
  • Treatment praziquantel, albendazole

67
Clonorchis/Opisthorchis life cycle
68
  • Flatworm helminths, continued
  • Dicrocoelium dendriticum (terrestrial liver
    fluke)
  • Transmission ingestion of metacercaria in ant
    secondary IH primary IH is a terrestrial
    snail/slug
  • This agent is mentioned only to provide an
    example of adaptability, and is confined to warm,
    moist areas of the world where gastropod
    secondary IHs mingle with scavenging,
    arthropod-ingesting DHs most of the internal
    factors described for other liver flukes are
    applicable to D. dendriticum

69
  • Flatworm helminths, continued
  • Schistosomes/Bloodflukes
  • Generalized schistosomal life cycle
  • Male Female Adults in DH
  • Egg Miracidium
    embryo Snail IH
  • Sporocyst larvae
  • Cercaria

70
  • Flatworm helminths, continued
  • Schistosoma mansoni, S. japonicum, S. haematobium
    (blood flukes)
  • Transmission direct penetration of skin by
    fork-tailed cercaria in water
  • Pathogenic potential high, based on worm
    populations and location in veins, capability of
    eggs to erode tissue, other
  • Clinical signs none early or if worm s low,
    transient skin reaction at entry, malaise, fever,
    skin rashes, cough, acute hepatitis, abcesses,
    hepatomegaly, cardiomyopathy, haematuria
  • Reservoir limited?, monkeys, rodents, humans

71
  • Flatworm helminths, continued
  • S. mansoni, S. japonicum, S. haematobium,
    continued
  • Damage potential high, dependent on location of
    adults, excretions of adults and miracidia in
    ova, population s, egg locations s, damage is
    accumulative over time
  • Prevalence distribution worldwide in tropical,
    subtropical, temperate regions human infections
    nearly equal to prevalence of malaria,
  • Diagnosis microscopic ID of ova in feces, urine
    or biopsy specimen
  • Treatment praziquantel, oxamniquin, bilarcil

72
Schistosoma species life cycle
73
  • Flatworm helminths, continued
  • Shistosoma spp.
  • Transmission cercarial penetration of skin in
    water
  • This group of schistosomes do not develop to
    adulthood in humans. They are parasites of birds
    and other animals, but will infect humans when in
    contact in water. They cause a cutaneous larval
    migrans referred to as swimmers itch, which is
    transitory and usually eliminated by the immune
    response

74
  • Flatworm helminths, continued
  • Generalized Pseudophyllidean Life Cycle
  • Adults in DH SI
  • Egg Coracidium
  • Procercoid larva Copepod primary IH
  • Plerocercoid larva Fish secondary IH
  • Adults in DH SI

75
  • Flatworm helminths, continued
  • Pseudophyllidean tapeworms
  • Diphyllobothrium latum (broad fish tapeworm)
  • Transmission ingestion of plerocercoid larva in
    uncooked fish
  • Pathogenic potential low, dependent on host
    sensitivity, location of worm in SI
  • Clinical signs usually none, pernicious anemia
    if worm is anchored near pyloric sphincter
  • Reservoir hosts various wild domestic
    fish-eating mammals dogs, cats, bears, seals,
    other
  • Damage potential low strong affinity for B12

76
  • Flatworm helminths, continued
  • D. latum, continued
  • Prevalence worldwide, where freshwater or
    brackish water fish are consumed raw
  • Diagnosis observation of proglottid chains in
    stools microscopic ID of ova in feces
  • Treatment prazyquantel, niclosamide

77
Pseudophyllidean (Diphyllobothrium latum) life
cycle
78
  • Flatworm helminths, continued
  • Generalized Cyclophyllidean Life Cycle
  • Adults in DH SI
  • Egg with Onchosphere/Hexacanth Embryo
  • Larva (Cysticercoid, cysticercus, coenurus,
    hydatid) in IH
  • Adults in DH SI

79
  • Flatworm helminths, continued
  • Cyclophyllidian tapeworms
  • Taenia solium (pork tapeworm)
  • Transmitted by ingestion of cysticercus larvae in
    uncooked pork (adult worm in SI) ingestion of TW
    eggs in human fecal contamination
    (cysticercus/larval development in tissues)
  • Pathogenic potential low as adult in SI
    low/moderate as larvae in tissues
  • Clinical signs usually none with adult
    infection, dependent on location with larval
    infection
  • Reservoir hosts humans and pigs
  • Damage potential 0 to low with adults,
    low/moderate with larvae, location dependent

80
  • Flatworm helminths, continued
  • T. solium, continued
  • Prevalence worldwide, where humans and pigs
    interact, and pork is eaten raw
  • Diagnosis observation of proglottid chains in
    stool for adult worms biopsy removal of larva
    from tissue site, microscopic ID of hooklets in a
    crush mount
  • Treatment prazyquantel, niclosamide X adults
    albendazole somewhat effective X cysticerci,
    untreated larval infections often subside
    (symptom-wise) within 2 to 5 years

81
  • Flatworm helminths, continued
  • Taenia saginata (beef tapeworm)
  • Transmission by ingestion of cysticercus larva in
    fresh, raw beef
  • Pathogenic potential 0/low
  • Clinical signs none, usually
  • Reservoir hosts bovine IHs, human DHs
  • Damage potential 0/low
  • Prevalence worldwide, wherever beef is eaten raw
    and cattle are exposed to human feces
  • Diagnosis sight of proglottid chains in stool
  • Treatment prazyquantel, niclosamide

82
Taenia species life cycle
83
  • Flatworm helminths, continued
  • Hymenolepis nana, H. diminuta, Dipyllidium
    caninum, others
  • Transmission ingestion of arthropod IH host
    containing cysticercoid larva
  • Pathogenic potential 0/very low
  • Clinical signs usually none, sensitive DH may
    show diarrhea, headache, abdominal pain,
    dizziness, anorexia, other nonspecific signs
  • Reservoir hosts rodents, dogs, normal DHs
  • Damage potential 0/very low
  • Prevalence world-wide, dependent on distribution
    of normal DHs

84
  • Flatworm helminths, continued
  • H. nana, H. diminuta, D. caninum, continued
  • Diagnosis complicated by small size of worms,
    making their observation in stools difficult
    eggs may sometimes be observed in fecal flotation
    examinations
  • Treatment prazyquantel, niclosamide

85
Hymenolepis nana life cycle
86
Hymenolepis diminuta life cycle
87
Dipyllidium caninum life cycle
88
  • Flatworm helminths, continued
  • Larval Tapeworm Infections
  • Echinococcus granulosus, E. multilocularis
    (unilocular/multilocular hydatidosis
    respectively)
  • Transmission ingestion of ova in feces of DH
  • Pathogenic potential high, dependent on larval
    type and organ involved
  • Clinical signs dependent on size of cyst, organ
    location related to pressure, abrasion, other
  • Reservoir hosts DH carnivores/omnivores, IH prey
    species primarily herd animals (sheep, etc)
  • Damage potential dependent on organ location,
    size of cyst moderate to high

89
  • Flatworm helminths, continued
  • E. granulosus, E. multilocularis, continued
  • Prevalence in humans spotty, dependent on human
    interaction with canine DH and herbivore IH
    distribution world-wide from equator to arctic,
    wherever predator-prey activity occurs
    (everywhere?)
  • Diagnosis microscopic ID of protoscoleces from
    needle biopsy of cyst, X-ray/other image
    detection of cyst in organ (liver, lung, brain,
    other) skin test, serotest
  • Treatment Surgical removal of cyst (unilocular),
    albendazole somewhat (variably) effective

90
Echinococcus species life cycle
91
  • Flatworm helminths, continued
  • Taenia spp. of carnivores
  • Transmission ingestion of eggs in DH feces
  • Pathogenic potential low to moderate, dependent
    on host sensitivity, s location of cysticerci
    in IH (human)
  • Clinical signs none, CNS-related abnormalities,
    subcutaneous nodules, et.al., site dependent
  • Reservoir hosts DH carnivores, IH prey
  • Damage potential dependent on worm species,
    larva type (cysticercus or coenurus), larva
    location host sensitivity, number of larvae

92
  • Flatworm helminths, continued
  • Taenia spp., continued
  • Prevalence worldwide, equator to arctic in
    normal carnivore DHs, prey IHs, spotty, somewhat
    infrequent/rare in humans
  • Diagnosis microscopic ID of larval biopsy
  • Treatment albendazole somewhat
    effective-seldom/never 100 curative

93
Cysticercosis-causing tapeworm life cycle
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