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Chapter 4
Tissue Nematodes
Tissue Nematodes
Intermediate host- Some are vectors
Long and thin- adapted to life in tissues
Nonfilarial worms
Dracunculus medinensis
Filarial (filamentous) worms- Live in lymphatics or subcutaneous tissues
Wucheria bancrofti
Loa loa
Onchocerca volvulus
Rule of Thumb
Blood and tissue parasites cause more pathology than lumen dwelling parasites
Drancunculus medinensis (Guinea Worm, Fiery Serpent)
Life Cycle
Human drinks unfiltered water containing copepods with L3 larva
Larva are released when copepods die. Larvae penetrate the host’s stomach and intestinal wall. They mature and reproduce
Fertilized female worm migrates to surface of skin causes blister, and discharges larvae
Female worm begins to emerge from skin one year after infection (through foot)
L1 larvae released into water from emerging female worm
Larva is consumed by a copepod
Larvae undergo two molts in the copepod and become an L3 larva
Copepods
is NOT a Vector!! (but is a intermediate host)
Because human infects itself by ingesting
Epidemiology
Almost eradicated
Related to the use of step wells from gathering water
Pathology and Clinical Manifestations
Lesions on foot or ankle
Worm grows up leg and sometimes damages knee joint (frozen joint due to scar tissue)
Secondary bacterial infection
Diagnosis
Observation- anterior portion of worm, ulcer, release of larvae
Treatment
Matchstick or rubber band
Metronidiozole (Flagyl)- does not kill but aids in removal (interfers with DNA replication, but carcinogen)
Prevention
Treat carriers
Stop carriers from using wells
Filter water to remove copepods
Kill copepods
Education
Wuchereria bancrifti- Bancroft’s filariasis or Elephatiasis
Life Cycle
A mosquito takes blood (L3 larva enters the skin)
Adults in lymphocytes
Adults produced sheathed microfilariae that migrate into lymph and blood channels
Mosquito takes a blood meal (ingests microfilariae)
Microfilariae shed sheaths, penetrate mosquitos midgut and migrate to thoracic muscles
L1 larva
L3 larva
Migrate to head and mosquitos proboscis
Epidemiology
Mosquito vector- Culex, Anopheles, Aedes
An estimated 120M people in tropical and subtropical areas of the world are infected with lymphatic filariasis
Mosquitos are very successful vectors but even they have problems
Pathology can Clinical Manifestations
Adult worms reside in lymphatic channels
3 Clinical Presentations
Asymptomatic- 70% of cases
Acute Filariasis- 25% of cases
Chronic Filariasis- 5% of cases
Lymphatic system return fluid from tissues to circulatory system
One of the main functions of the lymphatic system is to provide a return route to the circulatory system. The capillary flow rate is about 4L of fluid per day
Asymptomatic Filariasis (70% of cases)
Adult worms causing little to no blockage of lymph channels
Mild lymphatic inflammation
Some minor blockage on lymph channels
Some minor swelling of tissues
Acute Filariasis (25% of cases)
Adult worms causing pathology
Per-Endo (around or inside) lymphatic inflammation
Inflammation results in scarring and narrowing of the lymphatic lumen- lymph stasis
Chronic Filariasis (5% of cases)
Results from:
Repeated infections over 20yr period
Increased worm burdens
Blockage of collateral lymphatic circulation
Hypersensitivity to worm metabolites/allergens
Intense peri-endo lymphatic inflammation leading to lymphatic scarring'
Narrow lymphatic channels
Severe tissue swelling- lower limbs/genitalia
Elephantic skin due to lack of nourishment
Diagnosis
Microfilaria in blood- thick or thin blood smear or concentration technique, also serology- presence of worm
Treatment
Diethylcarbamazine
Polytherapy with diethylcarbamazine or albendazole with ivermectin
Compressed bandages
Surgery
Lymphatic Bypass surgery
Prevention
Mosquito control
Mass chemotherapy
Supportive treatment/psychotherapy
Loa loa- Eye Worm
Life Cycle
Fly (Genus: Chrysops) takes a blood meal (L3 larva enter skin)
Adults in subcutaneous tissue (under skin)
Adults produce sheathed microfilariae that are found in spinal fluid, urine, sputum, peripheral blood and in the lungs
Fly takes a blood meal (ingests microfilaria)
Microfilaria shed sheaths, penetrate fly’s midgut, and migrate to thoracic muscles
L1 larvae
L3 larvae
Migrate to head and fly’s proboscis
Epidemiology
40% of the 14.4M people who live in the area report that they have had eye worm in one time or another
Mostly found in central Africa
Pathology and Clinical Manifestations
Worms move freely through subcutaneous tissues
Attracted to warmth
Can wonder across eye
Form subcutaneous nodules- groups of entwined worms
Host forms a capsule due to hypersensitivity reaction- Calabar Swelling
Diagnosis
Observation
History of exposure
Microfilaria in blood
Treatment
surgical removal of Calabar swellings
A single does of Ivermectin
Onchocerca volvulus- River Blindness
Life Cycle
Blackfly (genus Simulium) takes a blood meal (L3 larva enter)
Larva enter subcutaneous tissue
Adults in subcutaneous tissue (benign tumors)
Adults produced unsheathed microfilariae that typically are found in skin and in lymphatics of connective tissues, but also occasionally in peripheral blood, urine, and sputum
Blackfly takes a blood meal (ingests microfilariae)
Microfilariae penetrate blackfly’s midgut and migrate to thoracic muscles
L1 larva
L3 larva
Microfilariae migrate to head and blackfly’s proboscis
Epidemiology
The Global Burden of Disease Study estimated that in 2017 at least 20.9 million people infected worldwide
Pathology and Clinical Manifestations
-Damage caused by microfilaria
Benign tumors
associate with head- Adult releases microfilaria which migrate in skin causing hanging groin and across the eye causing corneal damage leading to blindness
Collections of worms causing a hypersensitivity reaction
Skin
Migrating microfilaria causes skin to be detached and loose elasticity and malnourished resulting in parchment skin and hanging groin
Eyes
Corneal damage caused by migrating larva
Though that Wolbachia, an endosymbiotic bacteria is responsible for the inflammatory reaction that caused river blindness
Mutualism
Essential metabolites (bacteria); food and shelter (nematode)
Diagnosis
Skin biopsy for microfilaria
Treatment
Nodulectomy- remove benign tumor
Ivermectin
Promising treatment with doxycycline that kills adult worms by killing the Wolbachia bacteria which is intracellular and has a endosymbiotic relationship with the parasite
Prevention
Remove vector and treat carriers
Chapter 5
Cestodes: General Characteristics and Intestinal Tapeworms
Remember
Many intestinal tapeworms produce little or moderate pathology and draw nourishment from host food
Cestode General Characteristics and Morphology
Flat and ribbon like— an old fashioned tape measurer
Hermaphroditic- male and female reproductive track on same organism
General morphology
Scolex
Neck
Proglottids (+ Neck = Strobila)
Scolex
Orientation of the worm, biological holdfast, not for support or physical anchor, not for feeding
Rostellum, hooks (sometimes armed), suckers
Neck
Budding area for growth of worm, area where proglottids bud off ( where the worm grows)
Undifferentiated stem cells that give rise to the proglottids
Proglottids
Worm segments that are sexually immature (growing), sexually mature (reproducing), or gravid (sacs of eggs, no uterus or ova) depending on age
Absorption of Nutrients
Tapeworms are highly specialized and lack a digestive tract
Food is digested by the host and tapeworms absorb nutrients directly across their tegument using- pinocytosis, diffusion, facilitated diffusion, and active transport
Nutrients: amino acid, monosaccharides, absorbance assisted by microvilli and microtriches
Intestinal Tapeworms
Adult worms found in the small intestine of the definitive host (because this is where nutrients is absorbed)
Hymenolepsis nana- Dwarf Tapeworm
Taenia saginata- Beef Tapeworm
Taenia solium- Pork Tapeworm
Diphyllobothrium latum- Fish Tapeworm
Hymenolepsis nana- Dwarf Tapeworm
1-3 inches long
Scolex- 4 sockers and hooks on rostellum
Eggs free in host gut as proglottids usually disintegrate in the gut as eggs pass in feces
Life Cycle
Direct- Ingestion of eggs or mouse pills
Indirect- Ingest larvae via ingestion of insects (Tenebrio beetle)
Internal Autoinfection- Eggs laid and hatch in intestine
Life Cycle Steps
Embryonated eggs in feces
Egg ingested by insect and cysticercoid develops in insect
Humans and rodents are infected when they ingest cysticercoid infected arthropods
Instead of 2/3, Embryonated eggs ingested by humans from contaminated food, water, hands
Onchosphere hatches cysticercoid develops in intestinal villus
Scolex
Adult in ileal portion of the small intestine
Eggs can be released through the genital atrium of the gravid proglottids. Gravid proglottids can also disintegrate released eggs passed in stools
Autoinfection
can occur if eggs remain in the intestine. The eggs then release the hexacanth embryo, which penetrates the intestinal villus continuing the cycle
Epidemiology
This parasite does not need an intermediate host
Person to person contact like pinworm
common in children
Mouse pills
Tenebrio Beetle can serve as intermediate host
Mouse Life Cycle
Growth and maturation in small intestine
Ova released in gravid proglottids into feces, ingested by beetle
Infective cysticercoid develops in beetle, ingested by rat
Pathology and Clinical Manifestations
Adult Worms in small intestine
Asymptomatic to mild symptoms- irritation to gut wall
Allergic reactions to worm metabolites (nervousness, headache, dizzy, diarrhea
Oncosphere penetrates villus and develops into cysticercoid
Diagnosis
Eggs in stool
Treatment
Praziquantel and Niclosamide
Prevention
Personal hygiene
Mass chemotherapy
Taenia Tapeworms- Morphological Differences
Taenia saginata- Beef tapeworm- little pathology
Taenia solium- Pork tapeworm- high degree of potential pathology (due to human physiology being similar to a pig)
Taenia saginata- Beef Tapeworm
Very long proglottids: 5-10 meters, but up to 25m
Scolex: 4 suckers, no hooks
Proglottids- IMPORTANT: longer than wide, more than 15 uterine branches, found whole in stool, mobile in stool, can migrate out of anus
Life Cycle
Eggs or gravid proglottids in feces and passed into environment
Cattle become infected by ingesting vegetation contaminated by eggs or gravid proglottids
Oncospheres hatch, penetrate intestinal wall, and circulate the musculature
Oncospheres develop into cysticerci in muscle
Humans infected by ingesting raw or undercooked infected meat
Scolex attaches to intestine
Adults in small intestine
Epidemiology
Cattle infection due to grazing areas polluted with sewage, cattle in feed lots infected by feed lot workers
Eat undercooked beef
Endemic in all beef eating areas
In US about 0.37% of cattle infected
Pathology and Clinical Manifestations
Adult worm in small intestine
No real problem
No weight loss
Can potentially cause intestinal blockage
Diarrhea can be present due to reactions to worm metabolites
Since little pathology was sold as weight loss treatment before there was FDA
Diagnosis
Proglottids in stool
Treatment
Single oral dose of praziquantel
Single dose of niclosamide
Prevention
Inspect beef
Cook beef at 56C- denatures protein
No sewage in grazing areas
Importation of canned not fresh beef (also a good treatment for cancer, bacterial, and viral infections)
Taenia solium- Pork Tapeworm
Long worm: 8-10m
Scolex: suckers and hooks
Proglottids: less than 13 uterine branches
Life Cycle
Eggs or gravid proglottids in feces and passed into environment
Embryonated eggs and/or gravid proglottids ingested by pigs or humans
Oncospheres hatch, penetrate intestinal wall and circulate to musculature in pigs or humans
Oncosphere develop into cysticerci in muscles of pigs or humans (can cause cysticercosis)
Humans acquire the infection by ingesting raw or undercooked meat from infected animal host
Scolex attaches to intestine
Adults in small intestine
Cysticercosis
Cysticerci may develop in any organ, being more common in subcutaneous tissue, brain, and eyes
Epidemiology
Endemic in areas of high pork consumption and lax meat inspection
Pathology and Clinical Manifestations
Adult worm in small intestine- asymptomatic to mild symptoms like Taenia saginata
DANGER- ingestion of eggs can result in autoinfection or self-contamination or infection of people in close proximity resulting in…
Cystercercus cellulosae: ingestion of embryonated eggs- oncosphere hatches in gut- enters circulation- travels to any organ in body. Pathology and danger are determined by the organ system affected
Organ/tissue Affected
Intramuscular: encystment in muscle, calcification, dead end for parasite, usually found in X-ray
Brain: no encystment: can grow into grapelike clusters. Causes Jacksonian epilepsy. Surgery needed with death common
Eye: appears to be a floater in vitreous humor, no encystment, can get into sub-retinal space. Death of organisms results in massive inflammation causing loss of eye
Lungs, Liver, etc
Diagnosis
Proglottids in feces for adult worm
X-Ray, CT scan, MRI for cysticercus cellulosae
Treatment
Praziquantel
If cysts are present, caution, since antibiotic is cysticidal and can cause inflammation around dying cysts in those with cystercosis, which may lead to seizures and other serious symptoms
Surgery may be required to clear cyst
Prevention
Proper disposal of feces
Cook or freeze pork
Inspect pork
Diphyllobothrium latum- Fish Tapeworm
Long worm: 5-10 meters
As with all of these large tapeworms there is one worm per person
As with all these large tapeworms this worm is very long lived
Scolex-Bothrium- leaf-like suckers or sucking groove
Life Cycle
Unembryonated eggs passed in feces
Eggs embryonate in water
Coracidia hatch from eggs and are ingested by crustaceans
Procercoid larvae in body cavity or crustations
Infected crustacean ingested by small freshwater fish. Procercoid larva released from crustacean, develops into plerocercoid larvae
Predator fish eats infected small fish
Human ingests raw or undercooked infected fish
Adults in small intestine
Proglottids release immature eggs
Epidemiology
Found in temperature regions in areas with high freshwater fish consumption
= Great Lakes and Pacific Northwest, Finland, Baltic region, Russia
Scandinavians brought the parasite to the USA
Pathology and Clinical Manifestations
Mild attachment damage
Some allergic reaction to metabolites
Worm has great affinity for Vitamin B12- Pernicious anemia is common in those infected
Diagnosis
Eggs in stool
Treatment
Praziquantel
Niclosamide
Prevention
Cook fish
Prevent sewage from contaminating water
Chapter 6
Cestodes: Tissue Tapeworms
Tissue Cestodes
Echinococcus granuloses- Unilocular (1 chamber) Hyatid Disease
Enchinococcus multilocularis- Multilocular Hyatid Disease (more pathogenic, less common)
Enchinococcus granulosus -Hyatid Cyst Disease
Small worm, only ¼ inches long, composed of Scolex-Neck-Three Proglottids (immature, mature, gravid)
Life Cycle
Normal life cycle has two players: Dog (definitive host) and Sheep (intermediate host)
Humans play the role of sheep when they ingest the eggs
Life Cycle Steps
Adults in small intestine of dogs
Embryonated eggs passed in feces (ingested by humans causes pathology)
Oncosphere hatches; penetrates intestinal wall after sheep ingests
Hyatid cyst in liver, lungs, etc
Protoscolex from cyst ingested by dogs
Scolex attaches from intestine
Adults in small intestine
Hyatid Cyst
Contains Brood Capsule
Brood Capsule hold Protoscolex
Protoscolex: Become adults in host
Epidemiology
Enchinococcus spp. are zoonotic tapeworm currently infecting 2-3 million persons worldwide causing US $200-800 million in annual economic losses related to human infections
1990-2017 US had 41 deaths
Pathology and Clinical Manifestations
Cyst expands/grows as a sphere (perfect sphere due to its strong membrane) in soft tissue- increasing in diameter
Pea to golf ball to baseball to softball to volleyball etc
Parasite fibrous capsule is very strong and resilient with no weak spots so it expands uniformly
Organs Effeted
Liver: mechanical damage as cyst grows causing pressure atrophy
Brain: very serious
Heart valves: very serious
Lungs
Allergic reaction to hyatid fluid can cause anaphylaxis if cyst ruptures
Diagnosis
Observation
X-ray, CT scan, MRI
Treatment
Based on size, location, manifestations, and overall health of patient
Surgery most common
Risk of surgery from leakage of fluid include anaphylaxis and dissemination of infectious solices, cholangitis (inflammation of bile duct), hyperatremia (electrolyte imbalance, increase in sodium concentration)
Prevention
Treat dogs
Cook sheep organs before feeding them to dogs
Enchinococcus multilocularis- Alveolar hyatid disease
Normal life cycle involves dog/fox (definitive host)— Moles/voles/rodents (intermediate host)
Humans play role of the moles/voles/rodents when they ingest eggs
Life Cycle
Egg (Humans ingest eggs and are infected)
Rodents ingest egg
Mestacestode in rodent liver
Fox/dog ingest eggs through rodents
Adult in the intestine
Epidemiology
Northern USA possible
Easting wild blackberries/blueberries/mushrooms contaminated with eggs
Almost all cases confined to Northern Hemisphere in Europe, Russia, China, Japan, and North America
Pathology and Clinical Manifestations
Alveolar hyatid cyst forms: Multi-locular cyst that spreads because the cyst wall is weak and germinal layer is neoplastic-like
Cavitation of infected organ results- organ replaced by cyst. Slow in developing may take 5 to 15 years
Diagnosis
Indirect: X-Ray, CT scan, MRI
Liver Function
Observation
Treatment
Surgery: same as E. granulosus, except if any germinal layer is left it will regrow the cyst, similar to neoplasia- matastaiss cell travel to other tissues/organs
Prevention
Treat/control infected dogs
Wash fruits
Non-surgical options induce cyst drainage, scolicidal solution and continuous treatment with albendazole- parasitostatic not parasitocidal
Chapter 7
Trematodes: General Characteristics and Trematodes Infective in the Metacercarial Stage
Trematodes
Flukes- Looks like flukes of an anchor
Trematodes (trematos) literally mean pierced with holes- refers to sucker on the worms