BIOL 4106 - Exam 3

Scolex

The anterior end of the tapeworm

Equipped with a holdfast organ: suckers, hooks, grooves

Types of suckers:

1. Acetabula: 4 cup-shaped with a cup-shaped muscular wall

2. Bothria: 2 “slit-like“ shallow pits/grooves

Rostellum

Protruding dome-shaped area on the most anterior end of scolex

Cestode Neck

The region between scolex and strobila segments

Contains stem cells that give rise to new proglottids (Praziquantel)

Cestode Strobila

Long chain of proglottids (segments)

Each has sets of reproductive organs of both sexes

Strobilization

Growth of strobila

Proglottids closet to scolex are most immature

The more posterior, the more mature

Gravid Proglottids

“Gravid“ = Filled with eggs

Proglottids “cross fertilize“

How Proglottids are Shed

1. Intact gravid proglottid – [Taenia spp]

   • detaches and shed intact in feces

2. Proglottid disintegrates as shed and eggs go out with feces – [Hymenolepsis spp]

3. Eggs shed from attached proglottid through uterine pore – [Diphyllobothrium spp]

   • senile (empty) proglottids detach in a short chain which is shed in feces

Cestode Tegument (Cuticle)

Absorption: All nutrients absorbed through the tegument

• Covered in microvilli called “microtriches” even on the sucker

  • Increases the absorptive area of the tegument

Excretion of wastes

Osmoregulation (water balance)

Monecious

Cestodes = Hermaphroditic

Sperm are transferred between mature proglottids that lie next to each other

Dipylidium Egg

Thin shell

Operculated in [Diphyllobothrium latum]

In egg packets for [Dipylidium caninum]

• Diphyllobothrium sp, Dipylidium caninum, Hymenolepsis sp

Taenia Egg

Thick striated shell

Hexacanth embryo within

• Taenia sp and Echinococcus sp

Cestode Life Cycle

Egg → Onchosphere → Metacestode → Adult

Onchosphere: Hexacanth larva in egg

Metacestode: Juvenile (larval form of tapeworm)

IH: Herbivore

DH: Carnivore

• Hymenolepsis nana doesn’t follow this; only needs one host

Pseudophyllidan Life Cycle

Egg → Onchosphere = Coracidium → Procercoid → Plerocercoid → Adult

• Coracidium: Ciliated free-swimming oncosphere, has hooks

• Procercoid (1st IH):

  • Usually in copepod

  • First metacestode stage

• Plerocercoids (2nd IH):

  • Fish will eat 1st IH

  • Procercoid → Penetrates gut wall → muscle → Plerocercoids

  • Infective Stage for DH

Sparganum

Term for plerocercoid of Diphyllobothrium (Spirometra) mansonoides

What is difference between procercoid and plerocercoid?

Plerocercoid develops a scolex and has some strobilia formation (a true juvenile cestode)

Cyclophyllidian Life Cycle

Egg → Onchosphere → Metacestode → Adult

• Egg has to be eaten by IH

• Eggs can be viable in soil for a while

• Onchosphere uses hooks penetrate thru gut wall → tissues → metacestode

4 Basic Metacestode Forms in Cyclophyllidians

1. Cysticercoid

• Solid cyst with a single, inverted scolex within

• IH is an invertebrate

  • [Dipylidium sp] and [Hymenolepsis sp]

2. Cysticercus (“bladder worm”)

• Fluid-filled cyst (“bladder” worm) with a scolex inverted and invaginated

• IH is a vertebrate

  • [Taenia sp]

3. Coenurus

• Fluid-filled cyst with several inverted scolices, each on a stalk

• IH is usually a vertebrate

  • [Multiceps sp]

4. Hydatid Cyst

• IH is a vertebrate

• Grows slowly but can get very large containing quarts of antigenic fluid with 1000s of scolices

• Cyst is lined with germinal epithelium which gives rise to:

1. Individual protoscolices (scolex without bladder)

2. Daughter capsules (each with many protoscolices within)

“Hydatid Sand” – a granular deposit in hydatid cysts consisting of liberated daughter capsules and free protoscolices

Asexual reproduction is often referred to as “budding” from the cyst

Two Types of Hydatid Cysts

1) Unilocular: Seen in [Echinococcus granulosus] infections

2) Multilocular: Daughter capsules bud externally

• As daughter cysts bud outward, the multilocular cyst invades the tissues of infected organs

• Makes this form highly invasive like an aggressive metastatic tumor as parasite tissue replaces host organ tissue

• Seen in [E. multilocularis] infections

Adult Tapeworms in DH

Metacestode form excysts in the gut

• Hymenolepsis diminuta can increase its size to over a million times greater than the initial size

Once mature size for species is attained, growth then becomes the production of proglottids to replace the gravid ones that are shed

No real pathology associated with adults in the intestinal lumen attaching to the gut lining

Absorb nutrients from digested nutrients in the lumen provided by the host

• Cestodes eat when you eat!

Pseudophyllidae

[D. latum] & [D. mansonoides]

Scolex with bothria

Proglottids remain attached and shed eggs through pore

• Genital pores are central

Eggs are operculated (look like trematode eggs)

1st IH: Crustacean – copepod

2nd IH: Fish

DH: Can be a human

Diphyllobothrium latum

Distribution: Worldwide

1st IH: Copepod (Procercoid Stage)

• Eggs in FW → Coracidium → Eaten by copepod

2nd IH: FW fish; minnow/salmon (Plerocerocid Stage)

• FW fish can eat FW fish many times and stay as plerocercoid; must be eaten by DH to → Adult

DH: “Fish-eating“ carnivores

• Transmission: Eating raw FW fish containing plerocercoids

• Niche: SI

• No pathology unless the person already has anemia → worsens Vitamin B12 anemia deficiency

Morphology: Large worm

• Proglottids are wider than longer

• Eggs: operculated

Dx: Long strings of exhausted (senile/empty) proglottids in feces

Prevention: Don’t eat raw FW fish (salmon)

Diphyllobothrium mansonoides (Spirometra mansonoides)

1st IH: Copepods

2nd IH: Any vertebrates (NOT FISH)

• Can get infected by procercoids and plerocercoids

• Infection is “Sparganosis”

  • Painful nodules that can go to eye → brain

• Humans are accidental 2nd IH

  • Drink water with infected copepods

  • Eating raw 2nd IH

  • Applying IH skin on a lesion (East Asia)

    • Frog or snake skin on wounds to heal

DH: Cats or Dogs only

No treatment (;-;)

Prevention: Don’t eat raw or undercooked meat (snake) and don’t wear frog skins

Taenia saginata

“Beef Tapeworm“

Distribution: Anywhere that consumes beef and lack of sanitation

IH: Cattle (herbivore)

• Egg with hexacanth → Eaten by cattle → Hatch in SI → Hexacanth uses hooks and penetrates gut wall → enters the bloodstream → striated skeletal muscle tissue → develops into cysticercus (measly beef) → Eaten by human

DH: Man

• Scolex everts from cysticercus → SI wall

• Usually asymptomatic

Niche: SI

Morphology:

• No rostellum

• 4 acetabular

• Immature and mature proglottids are slightly wider than longer

  • Gravids are much longer than wide

  • Lateral genital pore

Dx:

Prevention: Freezing and cooking

Taenia solium

“Pork Tapeworm”

Distribution: SE Asia, Mexico, South and Central America, Eastern Europe, Micronesia, Philippines

IH: Pig and Human

• Infective stage: Eggs containing hexacanth

• Can cause Cysticercosis → Space occupying lesion → Neurocysticercosis

• Parasites dying 2 years later will release antigens and cause pathology

DH: Human

• Infective Stage: Undercooked pork (measly pork) containing cysticercus → Adults in SI → Eggs in feces

• Usually asymptomatic

Morphology: Gravid proglottid is longer than wide

Dx: Proglottids

• Neurocysticercosis: CAT scans, MRI, antigen capture ELISA using CSF fluid

Prevention: Don’t eat measly pork or feces

Taenia pisiformis

IH: Rodents and Rabbits

• Larval predilection site for cysticercus: Peritoneum of rodent/rabbit

DH: Dog and cats only

• Not infective for humans

Morphology:

• Scolex has 4 suckers and a double row of hooks on the rostellum

• Segments are more rectangular

• Genital pores occur in irregular alternating sequences on either lateral margin

[Dipylidium caninum] is also a most common tapeworm of dogs

Echinococcus granulosus

Distribution: Europe, Africa, New Zealand, SW USA, Asia (Russia), South America, Canadian Arctic (Inuits)

• The northern variety in Canada involves caribou and moose as IH

IH: Grazing herbivores or humans

• Humans get hydatid cysts from ingesting eggs in dog feces

DH: Dogs and other Carnivores

Life Cycle:

Eggs with hexacanth oncosphere → IH → Hatches in SI → Pentrates gut wall → Bloodstream → Organs → Hydatid Cysts

• The liver is most common

Morphology: Adult tapeworm

• Smallest tapeworm

• Scolex has 4 suckers and armed rostellum with hooks

• Composed of scolex, neck, and 3 proglottids

• Gravid proglottid disintegrates and eggs pass out with feces

Dx: NEVER BIOPSY

• Radiographs, CAT scans, and MRI

• Case history: dogs/sheep or travel to an endemic region

Prevention:

• Keep sheep dogs dewormed

• Don’t feed raw infected meat to dogs!!

Cyclophyllidae

[Taenia sp.], [Dipylidium sp.], [Hymenolepsis sp.], [Echinococcus sp.]

Scolex with 4 acetabula (suckers)

• No rostellum: T. saginata & H. diminuta

• Rostellum with hooks (armed rostellum)

• Genital pores lateral

• Eggs with thick, striated shells and containing a hexacanth embryo

Echinococcus multilocularis

IH: Rodent such as field mice, vole (and humans)

• Trappers and fur handlers get it from eggs on fur or feces

DH: Wild carnivores such as foxes and other wild canids

Forms multilocular/alveolar hydatid cysts that create an aggressive, progressive, and destructive invasion of tissue

• Replaces normal tissue with parasite tissue

Rx: No effective treatment; surgery

Hymenolepsis nana

“Dwarf Tapeworm“

Distribution: Cosmopolitan parasite

IH: Arthropods such as grain beetle (OPTIONAL)

DH: Rodents and Humans

Life Cycle:

Humans as DH = Ingest grain beetle with cysticercoid → Scolex everts → Intestinal wall → Adult

Humans as IH = Eggs ingested → Onchospheres hatch in duodenum → Penetrates gut wall → Forms cysticercoid → Emerges from host tissue into gut lumen → Adult

Morphology:

Adults:

• Scolex with retractable armed rostellum

• Genital pores unilateral

• Gravid segment disintegrates and eggs pass out with feces

Eggs:

• Thin outer membrane and thick inner membrane

• Polar filaments on the inner membrane

Dx: Eggs in feces

Prevention: Get rid of rodents

Hymenolepsis diminuta

Distribution: Worldwide

IH: Grain beetle

DH: Rat and humans

Morphology: Larger than H. nata

Adults: Unarmed rostellum

Eggs: No polar filaments (not cloudy)

Dx: Eggs in feces

Dipylidium caninum

“Cucumber Tapeworm“

Distribution: Worldwide

IH: Flea

DH: Dogs and sometimes Humans

• Humans get it from ingesting fleas with cysticercoid

• No clinical disease

Life Cycle: Egg with hexacanth onchosphere → Flea → Cysticercoid → Dog/Humans → Cysticercoid → SI → Adults

Morphology:

Adult:

• Scolex with 4 suckers

• Armed retractable rostellum

• Proglottid long with double genital pores (bilateral)

• Gravid proglottid shed intact

  • Proglottids can crawl out the anus and onto clothing or bedding

Egg: Contained in packets of 8-15 eggs within proglottids

General Nematode Morphology

Bilaterally symmetrical

Usually tapered at both ends

External cuticle

• Protective covering

• Alae = lateral thickenings

Nematode Reproduction

Dioecious

Nematode Infective Stade for DH

J3 for most nematodes

Some species: Egg containing infective J3 stage

• Two exceptions: Ascarids, Trichinella

Some species: J1’s hatch from egg, molt 2x → J3 stage (infective stage)

Nematode Life Cycle

Consists of 4 juvenile stages and an adult stage

Egg containing J1 → J2 → J3 → J4 → Adult

• Stages are separated by ecdysis (molting) of cuticle

Hypobiosis

A developmental arrest in the parasite cycle

Development in the host will stop until certain conditions occur that are conducive to parasite survival

Oxyurida

[Enterobius vermicularis]

Cephalic alae

Medium to small worms with very pointed tails

Thin-shelled ovoid eggs that are flattened on one side

Direct life cycle

Ascaridida

[Ascaris lumbricoides] [Toxocara canis], [Toxocara cati], [Baylisascaris procyonis]

3 prominent lips

Direct life cycle

Eggs thick shelled, rough coated and very environmentally resistant

Strongylida

[Necator americanus], [Ancyclostoma duodenale], [Ancyclostoma caninum], [Ancylostoma braziliensis]

Long slender worms

Well-developed copulatory bursa in males

Usually oviparous (Lay eggs directly)

Eggs thin-shelled (release in morula stage – not embryonated yet)

Rhabditida

[Strongyloides stercoralis] & [Strongyloides fulleborni]

Small worms

Buccal cavity is small

Filariform esophagus – J3 (must become parasitic to survive)

Rhabditiform esophagus – free-living stages

Tail conical in both sexes

Trichurida

[Trichuris sp] & [Trichinella sp]

Anterior end is more slender than posterior

Buccal cavity reduced or absent

Stichosome esophagus

Eggs with polar plugs [Trichuris sp]

Enterobius vermicularis

“Pinworm“

Distribution: Temperate regions

DH: Humans (direct life cycle)

• Most common in elementary or daycare

• Niche: Large Intestine and Rectum

• Transmission: Ingestion or inhalation

Morphology:

Adult = cephalic alae & bulbed esophagus

• Crawl out at night and lay eggs → Worm dies

Eggs = Thin-shelled and flat on one side

• Can be airborne

• Reinfection it possible as J3 hatch and crawl back into rectum

Disease: Intense itching in perineal regions

Dx: “Scotch Tape” test

• First thing in the morning immediately

Ascaris lumbricoides

“Human roundworm“

Distribution: Worldwide, more in tropical rural areas with low sanitation

DH: Humans (direct life cycle)

• Niche: Upper small intestine

  • Does not attach to host tissue

Life Cycle:

Eggs in feces → J1 → J2 while in egg → Soil → Ingestion → Small intestine (J3) → Liver → Lungs (J4) → Cough into Stomach (J4) → SI (J5)

Morphology:

Adults = Huge with 3 distinct lips on the cephalic end

• Female: Straight tail

• Male: Curled tail

Eggs = Thick-shelled with a rough, bumpy surface

• Can survive forever and chemical-resistant

• Conditions need to be 37ºC, pH 7, low oxygen, and high CO2 to hatch

Dx: Eggs in feces

Ascaris Migratory Phase

Causes most host response

Molting substances very antigenic

Eosinophilia and increased levels of IgE

Ascaris Intestinal Phase

Few symptoms

Can obstruct the intestine or biliary, crowding effect, perforate intestine (peritonitis)

In children: stunting in growth, malabsorption, and intestinal blockage

Toxocara canis

Cosmopolitan ascarid of dogs and other canids

Life cycle in dog like A. lumbricoides in man with migratory phase from gut to liver to lung and back to gut

Can be transmitted to puppies two additional ways:

• J3’s transplacentally transmitted from the infected mother to fetus

• J3’s via a transmammary route from infected mother to nursing puppies

Can cause Visceral Larval Migrans and Ocular Lavaral Migrans

Toxocara cati

Roundworm of cats

Life cycle similar to Toxacara canis, except no transplacental transmission

Can cause Visceral Larval Migrans and Ocular Lavaral Migrans

Visceral Larval Migrans, Ocular Larval Migrans

Ingestion of eggs → J3 in bloodstream → Inflammation and granulomas in affected organs

CNS, liver, lungs, and eyes most seriously affected

Children are usually affected more

Ocular: Retinal granulomas → Detachment of retina → Blindness

Dx: Immunological tests (ELISA) for J2 antigens

Baylisascaris procyonis

Raccoon ascarid 🦝

Dogs can develop patent infections as definitive hosts

• Increases the risk of spreading to humans

Has a liking for CNS in aberrant (wrong) host

Eggs are as resistant as ascarid eggs

Small children are most often infected

CNS signs are indicative of an eosinophilic meningoencephalitis

Rx: None

• Usually fatal in humans, especially small children

Distribution:

1st IH:

2nd IH:

DH:

Morphology:

Dx:

Prevention:

New World Hookworm

Necator americanus

Old World Hookworm

Ancyslostoma duodenale

Canine Hookworm

Ancylostoma caninum/braziliensis

Hookworm

Distribution: Worldwide

DH: Humans or canine

• Niche: Small Intestine (mucosa and blood)

  • Anemia, iron deficiency, impaired physical and mental development, low birth weight/fetal development

Life Cycle: Direct

• J3 penetrates directly into skin → Bloodstream → Lungs → Small Intestine (J4) → Adult

• J3 in soil are filariform larvae

Morphology:

Adults

• “Hooked” anterior end

• Club esophagus

• Copulatory bursa

Eggs

• Thin shelled

• Unembryonated in fresh feces

Clinical Disease: “Ground itch/dew itch“

• Dermatitis is caused by repeated infections that are very pruritic (itchy)

• Infantile ancylostomiasis: Transplacental and transmammary transmission

  • Severe anemia, dysentery (black), fail to thrive

Dx: Eggs in feces

Prevention: Sanitation, education, wear shoes

Difference between Ancylostoma duodenale & Necator americanus

Ancylostoma duodenale

Morphology: Cutting teeth, larger worm

Pathology: More pathology, more blood loss, produce more eggs, hypobiosis (arrest development)

Transmission:

1. Skin penetration of J3

2. Oral ingestion

3. Transplacental of J3

4. Transmammary of J3 (vertical transmission)

Necator americanus

Morphology: Cutting plates

Pathology: Same but not as much (no hypobiosis)

Transmission: Skin penetration

Cutaneous Larval Migrans (CLM)

From J3 of dog or cat hookworms

Creates “creeping eruption” that’s very pruritic

• Scratching can cause bacterial infection

[Ancylostoma braziliense] & [Ancylostoma caninum]

Strongyloides stercoralis

Distribution: Worldwide

DH: Dogs, cats, and humans

• Infective stage: Filariform J3

Life Cycle: Heterogonic OR Homogonic

Transmission: Skin penetration, ingestion from soil or water, autoinfection, transmammary

• Autoinfection: J1 in gut long enough to be J3 and enter bloodstream

  • Compromised people get hyper infection

  • Given corticosteroids → Immunosupressed → Speeds molting process

Morphology:

• Adults are very small

• NO eggs

• Only females can be parasitic

Pathology: Adult females in intestine

• Local inflammation

• Heavy infection: Watery, mucoid diarrhea

Dx: J1 in stool

Heterogonic Life Cycle

Free-living phase

J1 →→ Adults (male and female) → Embryonated eggs → J1 →→ J3

J3 will continue to become an adult

Homogonic Life Cycle

J1 →→ Adults (male and female) → Embryonated eggs → J1 →→ J3

A female J3 will become a filariform J3 → Skin → Bloodstream → Lungs (J4) → Esophagus → SI → Adults (J5) in gut mucosa → Eggs in gut lumen → J1 in feces

Strongyloides fulleborni

Distribution: Papua New Guinea and Africa

DH: Humans

Pathology: “Swollen Belly Syndrome“ (SBS)

• Diarrhea

• Abdominal distension

• Malabsorption

• Affected mental and physical development

• Reversible with Rx

Dx: Eggs in stool

Differential Diagnosis for Strongyloides

S. stercoralis → J1 in stool (No eggs!)

S. fulleborni → Eggs in stool

Trichuris trichiura

Distribution: Worldwide

DH: Humans (direct life cycle)

• Transmission: Ingestion of eggs with J3

• Egg with J3 → Small Intestine (J3) →→ Adult → Colon

Morphology:

Adults: Stichosome esophagus (thin head), wider body, whip-like appearance

Eggs: Bipolar plugs with a thick brown shell

Pathology: Feeds on mucosa and blood, invade colon epithelium

• Usually in children

• Acute dysentery

• Prolapsed rectum with mucosal swelling

• Chronic colitis

Dx: Eggs in feces (barrel-shaped eggs with polar plugs)

Trichinella spiralis

DH: Humans

• Transmission: Ingestion of raw meat containing J1 in nurse cell complex (J1 = Newborn larvae)

• Niche: Eyes, tongue, jaw, diaphragm, and intercostals

Reservoir: Pigs (zoonotic disease)

• Urban cycle – pigs, rats, humans

• Sylvan cycle – wild animals

Morphology: Worms are slightly more slender anterior than posterior

• Female: larvae are visible in the uterus

Disease: Trichinosis or Trichinellosis

• Enteral Phase (short duration) → Gastroenteritis, diarrhea

• Parenteral Phase → Muscle pain, tenderness, eosinophilia

Dx: Muscle biopsy

Prevention: Cook your pork properly

T. spiralis Life Cycle

Enteral Phase: J1 → Columnar epithelium in upper SI →→ Adults [5 day post mating] → “newborn larvae“

• Pathology: Short-term enteritis

  • Molts damage columnar epithelium

  • Adults thread through cells → Cell damage

  • Releasing NBL → Local inflammatory response

Parental Phase: J1 → Bloodstream → Enter cells → Skeletal muscle fibers

• Nurse Cell Formation for J1

• Pathology: Association between parasite and host resulting in nurse cell complex

Effect on the body:

• Lose contractile myofilaments, DNA replication and becomes walled off

• Alters gene expression; arrests DNA and redirect to benefit the parasite

• Stimulates angiogenesis (blood vessel formation) called a “circulatory rete“ around nurse cell

Spirurina

Indirect life cycles

Vector: blood-sucking arthropod

Larvae are microfilaria, NOT J1

• Microfilaria found in the bloodstream

• Dx criteria: periodicity periods of high levels of microfilaria in circulation

  • Diurnal daytime (Loa loa)

  • Nocturnal night (W. bancrofti, Brugia sp)

Sexually dimorphic

• Male small and posterior end has a corkscrew appearance

• Female larger than male and is ovoviparous

J3 is infective stage for vertebrate host

Parasites of all vertebrates except fish

Wuchereria bancrofti

Distribution: Tropical and subtropical regions

Vector: Culicine and Anopheline mosquito

DH: Humans

Disease: Lymphatic Filariasis

Dx: Microfilariae in blood (night)

Brugia malayi

Distribution: India, Malaysia, and other parts of SE Asia

Vector: Mosquito (J1→J3)

DH: Humans (J3→ Sub Tissue → Lymphatic vessels → Adult → Microfilaria)

• Niche: Lymphatic vessels

  • In the lumen of vessels especially in the upper and lower extremities

  • Genitalia of males

Morphology:

Adults

• Thread-like

• Females produce microfilaria

• Produces 10,000 microfilaria per day

Microfilaria

• Circulate within bloodstream

• Infective stage for mosquito vector

• Periodicity of microfilaremia: active at night

Pathology: Host inflammatory and immune response

Dx: Microfilaria in blood smears

• Heavy infection – Thin stained smears

• Light infection – Concentration of microfilaria (Knotts test) then stain the smear

• OR detection of circulating adult antigens

Prevention: Vector control with insecticides

Clinical Symptoms of W. Bancrofti, Brugia sp

1. Endemic “normals”

   • No clinical signs

   • No microfilaremia detectable at any time

2. Asymptomatic microfilaremics

   • High leaves of microfilaria

   • No clinical signs

3. Acute lymphadenitis and filarial fevers

   • Circulating microfilaremia and recurrent bouts of fever and malaise with inflammation of the lymphatics including painful swollen lymph nodes

4. Chronic obstructive lymphadenitis

   • Repeated exposure to parasites

   • Elephantiasis – is the ultimate end point of chronic obstructive disease

   • Not everyone who develops chronic obstructive lymphadenitis → elephantiasis

5. Tropical pulmonary eosinophilia

   • Young men in southern India

   • Severe asthma-like syndrome with markedly elevated circulating eosinophilia

Onchocerca volvulus

Distribution: Africa, Central and South America (Mexico, Central American and regions of S. America)

Vector: Simulium sp “Black fly“

DH: Humans

• Niche: Subcutaneous tissue of skin and eyes

Morphology:

• Adults cluster and intertwine together in pairs or groups in nodules (onchocercomas) in the subcutaneous tissues of skin

• Microfilaria has no sheath

Pathology: “River blindness“

• Lesions in eyes and skin

• Microfilaria or dying adults cause an inflammatory immune response

Dx: Biopsy of nodes or skin biopsy

• NOT RECOMMENDED: Mazotti Test

Rx: Excision of nodules to decrease reaching the eye

Prevention: Vector control

Clinical Disease of Ochocerca volvulus

1) Onchodermatitis (skin dermatitis)

• intense itching

• Rash consisting of numerous elevated and very itchy papules

• Skin becomes wrinkling, cracking and depigmentation: “leopard skin” or sowda (clinical term: lichenification)

2) Nodule formation around adults in skin:

• Nodule formed is called “onchocercoma”

• Antigenicity of worm products

• Formation of fibrous nodules with a network of blood vessels [similar to rete formation of nurse cell induction in T. spiralis]

• The host response is to encapsulate adults in this nodule

3) Ocular Lesions

• All parts of the eye become affected in chronic, long-term infections

• Conjunctivitis, keratitis, photophobia, and secondary glaucoma

  • Sclerosing keratitis (scarring and hardening of cornea) is a major cause of blindness

  • keratitis is a result of inflammatory response to microfilaria in eye; they can be found in choroid, retina, anterior chamber etc.

• Another cause of blindness can be the immune response to microfilaria in retina

4) Lymphadenopathy

Loa Loa

Distribution: West Africa and Sudan

Vector: Crysops spp “deer fly“

DH: Human

Life Cycle: Similar to W. bancrofti

Pathology:

1. Asymptomatic

2. Calabar swelling and angioedema

   • Increased immune response

   • Elevated levels of IgE and eosinophilia

   • Antigen elicit response

3. Endemic normals

   • Develop protective immunity

Dx: Microfilaria in blood smears

Prevention: Treat to decrease transmission (repeating doses)

“Dog heartworm“

Vector: Mosquito

DH: Dogs

Life Cycle: Microfilaria → Mosquito → J1-J3 → Bloodstream → Heart and Pulmonary Arteries → Adults

Clinical Signs:

• Soft cough and exercise intolerance

• Cardiopulmonary failure → Death

Dx: Microfilaria in blood

• Distinguish between Dirofilaria and Dipetalonema (nonpathogenic)

Prevention: Ivermectin (once a month)

Rx: Tricky, killing adults can cause fatal pulmonary emboli

Man can be an accidental host (not common)

• Find “coin lesions“ in lungs; nodules with a dead worm

Dracunculus medinensis

“fiery serpent” or “guinea worm”

Distribution: Middle East and Africa (Only 5 countries still have the parasite)

Vector: Copepod (Cyclops sp)

DH: Humans

Life Cycle: J1 → Copepod → J3 → Ingestion by human → Small Intestine (J3) → Connective tissue →→ Adult

• Female move to lower extremities to release J1 through an ulcer into water (no CLM)

Morphology: Females releases larvae in water

Pathology: Disfigures skin and subcutaneous tissues and site for 2nd bacterial infections

• Ulcerated lesions → Tetanus, gangrene etc.

Dx: Lesion with worm

Rx: Extraction by winding worm on a stick until entire worm removed

Prevention: Boil water OR Filter with fine mesh

Macracanthorhynchus hirudinaceus

“Thorny-headed Worms“

IH: Beetles

• Eats egg contain embryo called acanthor

• Acanthor → Acanthella → Infective Stage: Cystacanth

DH: Pigs

• Eats beetle with cystacanth → Gut wall with its proboscis into mucosa

• Trauma and damage of attachment and movement to different locations

• Penetration of gut wall → Fatal peritonitis

Morphology:

• Anterior proboscis covered with tegument

  • Thin muscular wall with embedded recurved, sclerotized hooks

  • Fluid-filled

  • Extended and retracted into a muscular receptacle (sac)

• Neck

• Trunk

Moniliformis moniliformis

DH: Rats and other rodents