VBSC 402W

Oxyurids – Pinworm Morphology

Oxyurids – Pinworm Morphology

• Tail – sharp, pin

• Esophageal bulb

• Lips – 3

• Male – 0 or 1 spicule

• Flat egg – 1 side

Oxyurids – Pinworms

• Oxyuris equi –

• Enterobius vermicularis –

• Enterobius gregorii –

• Skrjabinema ovis –

• Skrjabinema caprae –

Oxyurids – Pinworms

• Oxyuris equi – horse

• Enterobius vermicularis – human

• Enterobius gregorii – human

• Skrjabinema ovis – sheep

• Skrjabinema caprae – goat

Oxyuris Equi

• ___ life cycle, ___l transmission

• PPP

• Migrate to ____- reproduction

• Lay eggs

• • Unique:

• Infective stage –

Oxyuris Equi

• Direct life cycle, fecal oral transmission

  • Definitive host: horse

• PPP 5 months

• Migrate to large intestine - reproduction

• Lay eggs perianal area, carried out with feces

  • embryonate and L1 --> L3 in environment

• + Retroinfection

  • Unique: because eggs are sticky, eggs may hang out in environment while staying on the perineum. Can crawl back in, go up to the colon, and go back through sexual reproduction

• Infective stage – L3, in egg

Enterobius vermicularis

• • Definitive host:

• Infective stage –

• Diagnostic stage –

Enterobius vermicularis

• Direct fecal-oral life cycle

  • Definitive host: human

• Infective stage – L3, in egg

• Diagnostic stage – Egg (in perianal folds)

  • scotch tape test - medical/clear tape, touch perineum and put on microscope

Oxyurids – Pinworm Disease Pathogenesis

• Severe –

Oxyurids – Pinworm Disease Pathogenesis

• Most asymptomatic

• Pruritis ani (itchy perineum)

• Severe – colonic mucosa inflammation

• Susceptible to most anthelmintics

Spiruids

2 Suborders

• Suborder Camallanoidea

  • Superfamily Camallanoidea

  • Superfamily

• Suborder Spirurida

  • 10 Superfamilies – all animals, humans, zoonotic

    • 1. Gnathostomatoidea –

    • 2. Physalopteroidea – vertebrate stomach/intestinal worm

    • 3. Rictularoidea

    • 4. Thelazoidea

      • Thelaziidae - Eye/lacrimal/conjunctival worm

      • Pneumospiruridae – carnivore lung parasite

    • 5. Spiruroidea –

    • 6. Habronematoida – equine stomach, cutaneous Habronemiasis

    • 7. Acuarioidea – birds

    • 8. Aproctoidea

    • 9. Diplotriaenoidea

    • 10. Filaroidea –

Spiruids

2 Suborders

• Suborder Camallanoidea

  • Superfamily Camallanoidea

  • Superfamily Dracunculoidea – Guinea Worm

• Suborder Spirurida

  • 10 Superfamilies – all animals, humans, zoonotic

    • 1. Gnathostomatoidea – carnivore stomach worm

    • 2. Physalopteroidea – vertebrate stomach/intestinal worm

    • 3. Rictularoidea

    • 4. Thelazoidea

      • Thelaziidae - Eye/lacrimal/conjunctival worm

      • Pneumospiruridae – carnivore lung parasite

    • 5. Spiruroidea – esophageal/stomach worm

    • 6. Habronematoida – equine stomach, cutaneous Habronemiasis

    • 7. Acuarioidea – birds

    • 8. Aproctoidea

    • 9. Diplotriaenoidea

    • 10. Filaroidea – human, animal filarial worm! Public health concern!

Spiruida, Superfamily Dracunculoidea

Spiruida, Superfamily Dracunculoidea

• Largest nematode – 2.5 ft female (Guineaa worm, females larger)

• No lips, underdeveloped buccal area

• SQ tissues of carnivores, humans (but oral exposure)

• Guinea Worm

Dracunculus medinensis (Guinea Worm)

• Infectious stage –

• Diagnostic stage –

• Life cycle:

  • No ___. Release ___

  • ___consumed by ___

  • Larval stage molts to ___

  • Stays in ___, ___with ___

  • ___in ___, ___, ___released

  • ___ to ___

• PPP

Dracunculus medinensis (Guinea Worm)

• Infectious stage – L3

• Diagnostic stage – Adult worm in blister

• Ovoviviparous

• Indirect life cycle

  • Intermediate host – Copepod

  • Definitive host: human

• Life cycle:

  • No eggs. Release L1 filariform directly from subcutaneous blister bursting when exposed to water

  • L1 consumed by copepod

  • Larval stage molts to L3 larvae (infective form)

  • Stays in copepod, humans consume copepod with L3 larvae in water (copepods are too small to be visible)

  • L3 in stomach, copepod digested, L3 released

  • L3 migrate out of stomach and intestinal wall to lower leg, mature and create a blister

• PPP 12-14 months

Spiruida – Dracunculoidea – Guinea Worm signs

• • Treatment -

• 3 conditions necessary for disease

  • 1.

  • 2.

  • 3.

• Challenge is

Spiruida – Dracunculoidea – Guinea Worm

• 2ndary bacterial infections

• Aberrant migration

• Dying nonemergent worms

  • Treatment - must physically remove the adult worm across week (do not come out on their own). No anthelmintics or treatments (killing 2.5 ft worm would cause hypersensitivity immune response, hyper shock, overwhelming immune system)

• 3 conditions necessary for disease

  • 1. Infected individual in water

  • 2. Copepods present

  • 3. Drink water

• Challenge is 12-14 month PPP. Have to wait full lifecycle to determine an area is negative

Spiruida – Dracunculoidea – Guinea Worm Control

• Control strategies

  • • ___ - biggest progress

Spiruida – Dracunculoidea – Guinea Worm Control

• Slow removal

• No medications

• Control strategies

  • Education

  • Safe drinking water supply

    • Clean water from copepods (does not remove other bacteria/protozoa). Copepods are not visually able to be seen but big enough that simple filtration eliminates (straw, weave) - biggest progress

  • Early case containment

  • Vector control (not elimination)

Spiruida, Suborder Spirurida

• L1 –

• Esophagus -

• Some oviparous (__) some ovovivparous (__)

Spiruida, Suborder Spirurida

• Lots of species and variation!

• Intermediate host – Arthropod

• Indirect lifecycle

• Deep tissue/intestinal parasites

• L1 – dorsal cuticular hooks/spines

• Pseudolabia – 2 lateral lips

• Esophagus - anterior muscular, posterior glandular

• Some oviparous (thick-shelled) some ovovivparous (filaroidea)

Suborder Spirurida, Superfamily Gnathostomoidae

• Females – 11-54 mm length

• Parasite

Suborder Spirurida, Superfamily Gnathostomoidae

• 2 lateral lips

• Swollen head – 4 circles of spines

• Fat spiny body

• Females – 11-54 mm length

• Parasite of carnivores

Suborder Spirurida Superfamily Gnathostomoidae

Life Cycle

• Indirect lifecycle

• 1st Intermediate host –

• 2nd intermediate host –

• Paratenic host –

  • Human -

• Definitive host –

• Infective stage –

• Diagnostic stage –

Suborder Spirurida Superfamily Gnathostomoidae

Life Cycle

• Indirect lifecycle

• 1st Intermediate host – copepod

• 2nd intermediate host – fish, amphibian

• Paratenic host – snakes, birds, humans, pigs

  • Human - dead end host

    • Eat IH/PH —> aberrant migration, dormant, abscess (visceral larval migrans)

• Definitive host – carnivore (dog, cat, pig)

• Oviparous. egg hatches in water, L1 in water is eaten by copepod (shallow water), molt to L2

• 2nd intermediate ingest copepod, mature and ensyst in smaller fish/amphibian as L3

• Definitive host (usually dog, sometimes cat) eat, mature and sexually reproduce

• Infective stage – L3

• Diagnostic stage – L3

Suborder Spirurida, Superfamily Spirurodea

• Spirocerca lupi

Suborder Spirurida, Superfamily Spirurodea

• Spirocerca lupi

  • 6 lips, developed buccal capsule

  • Stout worm

  • Eggs – embryonated when laid

  • Esophageal worm

Suborder Spirurida, Superfamily Spirurodea

Spirocerca lupi

• Adults – esophagus

• Eggs – shed in feces – embryonated!

• Indirect lifecycle

• Intermediate hosts – dung beetles

• Paratenic hosts -birds, reptiles, mammals

• Definitive host – dog

Spirocerca lupi Life cycle

• Esophagus –

• Eggs -

Spirocerca lupi Life cycle

• dung beetles ingest egg, egg develops from L1-L3, dog ingests dung beetle with L3 larva

• L3 enter, adults nodulate in esophagus, sexual reproduction, will release eggs

• Paratenic may also ingest dung beetle with L3, paratenic host then eaten by definitive

• Juveniles penetrate stomach wall to gastric artery to aorta

• Esophagus – reproduction

• Eggs - lumen

Suborder Spirurida, Superfamily Spirurodea, Spirocerca disease

• • Unique to Spirocerca lupi -

Suborder Spirurida, Superfamily Spirurodea, Spirocerca disease

• Aberrant migration

• Vomiting – stomach wall lesions

• Aortic lesions – aneurysms, hemorrhage

• Spondylosis, hypertrophic pulmonary osteoarthropathy, spondylitis

  • Unique to Spirocerca lupi - create spondylitis of the skeletal system via an immune system response, cause most common clinical sign bringing in dogs (limping, pain). "arthritic lesions"

• Esophageal sarcomas

• Europe, Africa, and Asia mostly. Sometimes US

Ascarid Morphology

Ascarid Morphology

• Large stout nematodes – 45 cm!

• 3 lips surround small buccal capsule

• No copulatory bursa

• Eggs w thick shell, last long in environment

Toxocara spp.

Modes of Infection

• Direct ingestion of eggs (Egg + ___) –

  • egg hatches in ___, migrate to ___, ___, ___(__), ___ (adult)

  • PPP canis –

  • PPP cati –

• Transplacental –

  • __ in Mom___, ___, ___(__),___ (adult)

• Transmammary –

  • __ in Mom to___, molt to __in___, ___

• Ingestion of paratenic host –

  • Larva ___

  • L__ ___, ingested by ___/___

Toxocara spp.

Modes of Infection

• Direct ingestion of eggs (Egg + L3) – T. canis, cati

  • Fecal excretion of unembryonated egg, embryonate, mature to L3 larvae in embryonated egg

  • egg hatches in stomach, migrate to liver, trachea (L3), cough/swallow, stomach (L4), small intestine (adult)

  • PPP canis – 14-28 days

  • PPP cati – 56 days

• Transplacental – T. canis only

  • L2 in Mom crosses placental to fetal liver, trachea (L3), cough/swallow, stomach (L4), small intestine (adult)

• Transmammary – T. canis, cati

  • L2 in Mom to mammary gland, molt to L3 in mammary gland, L3 ingested

• Ingestion of paratenic host – T. canis, cati

  • Larva hatch and get into tissue

  • L3 encysts in tissues of mouse, ingested by dog/cat

Toxocara spp.

• Diagnostic stage –

  • Also

• Infective stage –

  • take ___ to mature/embryonate to __ in environment

  • PPP –___ (eggs)

  • PPP –___ (placental/mammary)

• In humans; diagnostic stage is ___ ; infective stage is i___ or ingestion via___

• In people: ___ host - ___ , larva___ ,

Toxocara spp.

• Diagnostic stage – Eggs in feces

  • Also may see adult worms in feces or vomit

• Infective stage – embryonated eggs

  • take 2-4 weeks to mature/embryonate to L3 in environment

  • PPP – 4-5 weeks (eggs)

  • PPP – 2-3 weeks (placental/mammary)

• In humans; diagnostic stage is seeing larva in tissue biopsy of organs/conjunctiva; infective stage is ingestion of embryonated eggs or ingestion via undercooked paratenic

• In people: aberrant host - visceral larval migrans, larva get into stomach, intend to migrate to liver and trachea to get to SI, instead get stuck in organs (liver, brain, skin, eyes)

Parascaris equorumi

• PPP -

Parascaris equorumi

• Foals <1 year

• Not associate with VLM in humans

• PPP - >10 weeks

• Immature eggs in feces, eggs develop to infective stage (embryonate) in environment in 2 weeks, remain infective for years. Swallow, go to liver, go to trachea, cough up and swallow, small intestine

Ascarid Disease Pathogenesis

• Contamination with eggs!

  • Eggs extremely resistant to ___

  • Eggs survive

  • Abnormal hosts –

  • Control:

• • Adult worms –

• Inflammatory response in ___ – related to ___ and ___

  • Ascaris pneumonitis –

Ascarid Disease Pathogenesis

• Contamination with eggs!

  • Eggs extremely resistant to disinfectants

  • Eggs survive months-years in soil, fomites

  • Abnormal hosts – could transport eggs

  • Control: Clean feces (eggs not infective until embryonated & matured), Anthelmintics targeting mothers (for Toxocaria canis and cati), Baylisarcarcis: stop pets from hunting, cook food thoroughly, wash hands around potential exposure in environment

• Minimal GI damage to mucosa

  • Malnutrition, intestinal obstruction, Intestinal rupture

  • Adult worms – vomit or fecal excretion

• Inflammatory response in liver, lungs – related to number of larva and organ affected

  • Milk spots – 2ndary fibrosis

    • white spots on liver, called that as these are young animals on milk. mostly in commercial and wild swine

  • Ascaris pneumonitis – inflammation in alveoli

Visceral Larval Migrans

• Humans –

  • Accidental egg ingestion

  • Larvae

  • ___ is Susceptible!

  • Treatment difficult –

  • Control parasite sources –

Visceral Larval Migrans

• Humans – aberrant host of intestinal roundworm larvae

  • Accidental egg ingestion

    • Toxocara canis

    • Baylisascaris procyonis

  • Larvae burrow through small intestine; enter circulatory system

  • Any Organ is Susceptible!

    • Eye – blindness

    • Liver

    • Brain – neurologic problems

  • Treatment difficult – surgical removal

  • Control parasite sources – environment!

Filaroidea superfamily

• ____ reproduction

Filaroidea superfamily

• All vertebrates except fish

• Reduced buccal capsule, lips

• Spiral flexure – male

• Indirect life cycle

• Intermediate host – blood sucking arthropod

• Ovoviviparous reproduction

• Microfilaria - pre-juveniles free in blood/lymph

1. Genus Onchocerca

• Microfilaria – ___ & ___

• Microfilaria –

• Adults –

  • Parasite (adult mother) releasing microfilaria is___ and ___ dependent, releasing microfilaria ___ and ___

1. Genus Onchocerca

• Rudimentary – no lips, spines, ring around mouth

• Non-divided esophagus

• No caudal alae

• Microfilaria – sheathed & unsheathed

• Microfilaria – time dependent

• Adults – connective tissues, heart, arteries, body cavities

  • Parasite (adult mother) releasing microfilaria is time-dependent and temperature dependent, releasing microfilaria at times mosquitos are more active (dusk and dawn) and season

1. Onchocerca volvulus

• ___ life cycle

• Microfilaria – ___– can live___

• Adults – ___ - can live in ___for ___

• Infective stage –

• Diagnostic stage —

Life cycle

• ___-___ host, injects ___ into ___ . ___ hangs around in ___ (especially ___ ). Cause ___ from___ . Adults mature, sexually reproduce, release ___ , remain in ___ until ___ takes a bloodmeal. ___ --> ___ --> ___ --> ___ inside ___ host (___ )

1. Onchocerca volvulus

• Indirect life cycle

• Intermediate host – blackfly

• Ovoviviparous

• Microfilaria – unsheathed– can live 2 years!

• Adults – SQ tissues - can live in SQ for 15 years!

• Infective stage – L3

• Diagnostic stage – microfilariae in skin biopsies

Life cycle

• Blackfly - intermediate host, injects L3 larvae into human. L3 hangs around in subcutaneous tissues (especially eyes). Cause nodules from immune system. Adults mature, sexually reproduce, release microfilaria, remain in subq until blackfly takes a bloodmeal. Microfilaria --> L1 --> L2 --> L3 inside intermediate host (blackfly)

Onchocerciasis

• associated with ___

• ___, ___. ___

• ___ – needs ___, ___

• ___ – needs ___, ___

Onchocerciasis –___

• ___ – benign ___, can cause ___

• ___– ___

• ___/Decreased ___– ___ invade ___, ___

Onchocerciasis

• associated with rivers

• Warm, wet. Central Africa

• Black fly larva – needs clean, fast-moving water

• Black fly adult – needs stream-side vegetation, high humidity

Onchocerciasis – River Blindness

• Not fatal

• Onchocercomas – benign collagenous SQ nodules, can cause elephantiasis

• Dermatitis – Dying microfilariae in skin

• Blindness/Decreased vision – microfilariae invade cornea, immune response damages retina

Knowing the lifecycle of Onchocerca volvulus, what would be a good control measure?

Knowing the lifecycle of Onchocerca volvulus, what would be a good control measure?

• Mass drug administration/community-directed

• Cleaning riverbanks of vegetation (destroy breeding ground)

• Insecticide sprays

• Community education

2. Wuchereria bancrofti & Brugia malayi

• ___ life cycle

• Intermediate host – ___

• ___

• Microfilaria – ___

• Adults – ___

• Microfilaria – shed into ___

Life cycle

• ___ inject ___ , ___ get into ___ and get into ___ . Adults sexually reproduce, release ___ into ___ and ___ ___ . ___ ingests ___ -->___ --> ___ in ___ ___ . Same for ___ and ___

2. Wuchereria bancrofti & Brugia malayi

• Indirect life cycle

• Intermediate host – mosquito

• Ovoviviparous

• Microfilaria – sheathed

• Adults – lymphatic ducts

• Microfilaria – shed into circulation

Life cycle

• Mosquito inject L3, L3 get into subq and get into lymphatics. Adults sexually reproduce, release microfilaria into lymphatic and peripheral blood. Mosquito ingests microfilariae --> L1 --> L3 in intermediate mosqutio. Same for W. bancrofti and B. malayi

Wuchereria –

• Both ___ and ___

Disease

• 1. ___ phase

• 2. ___ phase

• 3. ___ phase –

• Control w: ___ , ___ , ___

Wuchereria – Elephantiasis

• Both W. bancrofti and B. malayi

• Lymphatic filariosis

• Obstruction of lymphatic vessels/ducts. Balance btwn interstitial and circulating fluid. Fluid moves out of lymphatic vessels into tissues

Disease

• 1. Asymptomatic phase

• 2. Inflammatory/acute phase

• 3. Obstructive/chronic phase – host inflammatory immune response to adult worms

• Even if parasite is killed, damage is permanent

• Control w: bednets, insecticides, MDA,

3. Genus Dirofilaria

• Microfilariae –

• Adults –

3. Genus Dirofilaria

• Thin worms

• Simple mouth – no lips coiled tail

• Caudal alae (male) – large papillae,

• Non-divided esophagus

• Microfilariae –unsheathed

• Adults – connective tissues, heart

Dirofilaria immitis

• Adults can live

• Lifecycle of ___ from exposure (___ PPP)

Life cycle

• Intermediate host - ___

• Definitive host - ___

• Infective stage - ___

• Diagnostic stage - ___

• Humans - ___

• ___ injects ___, migrate through wound into ___, ___ mature in ___ in ___ , ___ migrate through ___ and mature to ___ in ___ ___ (___ ). Immature migrate to ___ (early as___ post infection). Sexual maturity in___

  • ___ to reproduce in blood

Dirofilaria immitis

• Adults can live 5-7 years!

• Lifecycle of 8 months from exposure (8 month PPP)

Life cycle

• Intermediate host - mosquito

• Definitive host - dog

• Infective stage - L3 larvae

• Diagnostic stage - adults in pulmonary arteries

• Humans - aberrant host, other dirofilaria sp do not complete life cycle in humans, become cutaneous granulomas. L3 stuck in skin

• Mosquito injects infective L3 larva, migrate through wound into dog host, L3 mature in subcutaneous tissues in 1-3 days, L4 larvae migrate through tissues and mature to sexually immature adults in subq 50-70 days (2 months). Immature migrate to heart and lungs (early as 70 days post infection). Sexual maturity in pulmonary artery.

  • Pulmonary artery takes deoxygenated blood form heart to lungs to be oxygenated

  • 6 months to reproduce in blood

Dirofilaria immitis - Epidemiology

• >60 ___species

• Development ___dependent

• ___ to begin

• Stops at __

• Reservoir population –

• ___ in 2010 —> dec incidence

• 2019 forward higher incidence -

Dirofilaria immitis - Epidemiology

• >60 mosquito species

• Development temperature dependent

• 2 weeks >80 F to begin

• Stops at <57 F

• Reservoir population – wild canids

• Heartworm preventatives developed in 2010 —> dec incidence

• 2019 forward higher incidence - Longer breeding seasons for mosquito, living longer, etc due to warming. More traveling

Dirofilaria immitis - Epidemiology

• 1.

• 2.

• 3.

• 4.

Dirofilaria immitis - Epidemiology

• 1. Susceptible host population

• 2. Stable reservoir of the disease

• 3. Stable mosquito population

• 4. Climate supportive of development

Heartworm disease

• Clinical Signs – ___, ___

• ___disease

• ___ – ___

• ___ – ___(___), ___(___), ___(___)

Dirofilaria immitus –

• ___disease –

• I

• ___ – ___, ___, ___, ___

Heartworm disease

• Clinical Signs – coughing, exercise intolerance

• Cardiopulmonary disease

• Pulmonary hypertension – right heart enlargement

• Heart failure – ascites (abnormal buildup of fluid in the abdomen), hydrothorax (fluid in the pleural space surrounding the lungs), hydroperitoneum (fluid in peritoneum)

Dirofilaria immitus – Caval Syndrome

• 2ndary hepatic disease – liver dysfunction

• Acute disease of extreme adult worm burden

• Increased venous pressure in liver

• RBC fragility – hemolysis, anemia, hemoglobinuria (free hemoglobin in the urine), bilirubinemia (biliruibin in bloodstream —> jaundice)

Dirofilaria immitus – Diagnosis

• Immunologic tests – ___

Dirofilaria immitus – Diagnosis

• Clinical signs

• Radiographic changes

• Cardiac changes

• Microfilarial tests – Knott test

• Immunologic tests – ELISA

Dirofilaria immitus Treatment & Prevention

• ___– 1st treatment

  • 1. Melarsomine dihydrochloride – “___”

  • 2. Thiacetarsemid – “___”

• ___- 2nd treatment

• Prevention – test 1st

  • 1. ___– monthly

  • 2. ___– monthly

  • 3. ___ – daily

Dirofilaria immitus Treatment & Prevention

• Surgical removal

• Cannot just treat and kill, would overwhelm immune

• Adulticide– 1st treatment

  • 1. Melarsomine dihydrochloride – “immiticide”

  • 2. Thiacetarsemid – “carparsolate”

• Microfilarial- 2nd treatment

• Prevention – test 1st

  • 1. Ivermectin – monthly

  • 2. Milbemycin oxime – monthly

  • 3. Diethyllcarbamazine (DEC) – daily