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Extraintestinal helminths Flashcards

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1
Q

Extraintestinal nematodes (3)

A

Trichinella, Dracunculus, Toxocara (Dog nematode)

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2
Q

Nematodes- filarial worms (4)

A

Wuchereria, Loa, Onchocerca, Brugia malayi

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3
Q

Extraintestinal trematodes/flukes (4)

A

Liver/lung – Clonorchis, Fasciola, Paragoniumus
Blood – Schistosoma

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4
Q

Trichinella spiralis species (5)

A
  1. pseduospiralis - mammals and birds
  2. nativa - artic bears
  3. nelsoni - African predators, scavengers
  4. britovi – carnivores Europe, Asia
  5. papuae – wild and domestic pigs in Papua New Guinea and Thailand
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5
Q

Trichinella spiralis symptoms

A

Low level infection is asymptomatic. With intestinal tissue invasion, symptoms begin 1 week post infection- GI symptoms – diarrhea, pain, vomiting. Symptoms of striated Muscle tissue invasion begins 2 weeks post infection. Includes peri-orbital and facial edema, conjunctivitis, fever, myalgia, splinter hemorrhage, rash, peripheral eosinophilia. Rare life-threatening symptoms include myocarditis (have a preference for cardiac muscle), CNS involvement, pneumonitis

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6
Q

Trichinella spiralis life cycle (5 steps)

A
  1. Domestic cycle results from consumption of an undercooked pork product. The sylvatic cycle results from consumption of unusual game. People consume contaminated muscle that is not cooked appropriately.
  2. Larva released in the small intestine, invade the mucosa
  3. Adults mature in the small intestine, they are very small worms
  4. Males and females mate, larva deposited in mucosa
  5. Larvae migrates through the mucosa, enters the circulation, then enters striated muscle. Then forms an encysted structure. Takes a week after females mature to make larvae, muscle invasion 2 weeks after infection
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7
Q

Trichinella spiralis

A

This species is found worldwide and is most common in the US and parts of Europe. Associated with contaminated food products, especially meat. Unusual game can be problematic. This organism is unusual because it is not found in the gastrointestinal tract, it is identified using muscle biopsies (especially the deltoid and calf muscles). They travel through the circulation and end up in the muscle in an encysted form.

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8
Q

Trichinella spiralis infectious stage

A

Ingestion of undercooked meat

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9
Q

Trichinella spiralis diagnostic stage

A

Encysted larvae in striated muscle

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10
Q

Identification of Trichinella spiralis

A

Larvae are encapsulated in the muscle tissue and are used for diagnosis of infection

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11
Q

Trichinella spiralis adult worm structure

A

Found in the intestinal tract of the host, and they develop in the small bowel mucosa. Females are 2.2 mm in length while males are 1.2 mm. The small bowel life span is approximately 4 weeks

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12
Q

Trichinella spiralis diagnosis

A

Eosinophilia can indicate a parasitic infection but is non-specific. Serology is generally best and can be done around 4 weeks post infection. Muscle biopsy is taken for H & E staining, but is very invasive and you must be able to find the encystment. Species specific PCR is available. History of consumption of unusual game will increase the suspicion of this infection

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13
Q

Trichinella spiralis treatment (3)

A

Varies with stage of roundworm
1. Thiabendazole = intestinal worm
2. Albendazole - encysted larvae
3. Mebendazole = recommended antiparasitic therapy

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14
Q

Dracunculus medinensis

A

Roundworm, known as Guinea worm disease. Found in rural areas in a narrow belt of African countries- Africa, Chad, Ethiopia, Mali, South Sudan. There is an ongoing eradication campaign, this disease can be eliminated with clean drinking water. People are exposed when rhabditiform larvae is released in water. There is no treatment, as treating to kill the worm causes anaphylaxis for the patient. Therefore, the worm must be physically removed using a stick to role and eventually remove it. The worms can be up to 100cm in length

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15
Q

Dracunculus medinensis symptoms

A

There is a localized, painful ulceration/blister on and inflammation of the foot, secondary bacterial infection may occur. These lesions can be debilitating. The worm is a whitish filament (~1 to 3 weeks incubation – up to 1 year), can be removed from center of ulceration. The presentation is typical & well known in endemic areas, so no lab confirmation is needed. No serologic test is available.

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16
Q

Dracunculus medinensis life cycle (6 steps)

A
  1. Human host drinks unfiltered water containing copepods with L3 larvae
  2. Larvae are released when copepods die. Larvae penetrate the host’s stomach and intestinal wall. They mature and male and female worms reproduce in the intestine. Once the female is fertilized, it migrates out of the intestine, down the leg to the foot
  3. Fertilized female worm migrates to the surface of the skin, causes a blister, and discharges larvae
  4. L1 larvae are released in water from the emerging female worm
  5. L1 larvae are consumed by a copepod
  6. Larvae undergoes 2 molts in the copepod and becomes an L3 larvae, and the cycle begins again
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17
Q

Dracunculus medinensis infectious stage

A

Larvae undergoes 2 molts in the copepod and becomes an L3 larvae, and the cycle begins again. Humans are infected when they consume unfiltered water containing the L3 larvae

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18
Q

Dracunculus medinensis diagnostic stage

A

L1 larvae are released in water from the emerging female worm. The female worm begins to emerge from the skin one year after infection

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19
Q

Dracunculus medinensis transmission

A

The worm can sense changes in temperature. If people are putting the infected foot in the water, the blister will rupture and the female worm will enter the water. Fluid discharged by the worm - rhabditiform larvae, which are consumed by copepods. When people drink the water, copepods will deliver the infectious organism into the host.

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20
Q

Copepods

A

Small crustaceans, associated with almost ALL sea and freshwater habitats.

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21
Q

Visceral larva migrans (VLM)

A

Preschool children - ova hatches and larvae invade multiple tissues (liver, heart, lungs, brain, muscle) resulting in fever, anorexia, weight loss, cough, wheezing, rashes, hepatosplenomegaly. Since humans are incidental hosts, the larvae are migrating in an attempt to continue their life cycle, but they can’t. Typically diagnosed through serology

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22
Q

Ocular larva migrans (OLM)

A

Older children or young adults - Death is rare by severe cardiac, pulmonary or neurologic disease. Larvae produce various ophthalmologic lesions, misdiagnosed as retinoblastoma, resulting in surgical enucleation. Rare eosinophilia or visceral manifestations. Typically diagnosed through serology

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23
Q

Toxocara canis and T. cati

A

Nematode, T. canis is a dog roundworm, and T. cati is a cat roundworm. They are bound found worldwide. They are asymptomatic, possible eosinophilia and positive serology. Can cause visceral larva migrans or ocular larva migrans. Humans are incidental hosts and are most commonly exposed through soil contaminated with dog feces. Especially problematic with little kids in inner city areas due to people walking their dogs in playgrounds or other areas shared by children. Ova usually are not produced within the host, so we don’t look for them

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24
Q

Toxocara canis and T. cati life cycle (5 steps)

A
  1. Embryonated eggs and larvae are passed in dog/cat feces. Dogs ingest fecal material that contain infected eggs. The eggs hatch and penetrate the gut of the dog- they can migrate or remain in the small intestine
  2. The adults form in the small intestine, mate, produce eggs, and dogs shed the eggs in fecal material
  3. Humans accidentally become infected by consuming the larvae
  4. After ingestion, the larvae penetrate the intestinal wall and get into the circulation
  5. The larvae is carried in the body to various tissues- liver, heart, lungs, eyes. The larvae do not undergo any further development after this point but can cause severe local reactions
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25
Q

Toxocara canis is most problematic in which animals?

A

Puppies- they are usually infected by their mothers. The parasite may be encysted and not cause problems in older dogs, but when a dog is pregnant, it will be immunocompromised and the infection will reactivate. The infection can be transmitted across the placenta and the puppies will be infected

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26
Q

Toxocara canis and T. cati ova structure

A

Not diagnostic for a human as they are only found in the definitive host. Subspherical, thick-shelled and have a pitted surface. Size range: 60 to 85um

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27
Q

Toxocara canis and T. cati adult worm structure

A

4-6 cm-males, 6-10 cm-females
Toxocara have three “lips” on the anterior end of the worm. They also possess large cervical alae (longitudinal ridge) with striations

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28
Q

Toxocara canis and T. cati diagnosis

A

Must look for adult worms in humans, ova will not be present since humans are incidental hosts. Serology- acute and convalescent can be done, ELISA can be conducted for a secretory antigen

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29
Q

Wuchereria bancrofti

A

Nematode, lymphatic filarial (thread like) worm. Found in Asia (mostly India), Africa, South America, Brazil, Haiti, Dominican Republic, Pacific islands.Transmitted by Anopheles mosquito

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30
Q

Wuchereria bancrofti symptoms

A

After a bite from an infected mosquito – Anopheles or Aedes. Larvae develop in lymphatics and nodes of lower extremities. Symptoms- fever, inguinal or axillary lymphadenopathy, testicular and/or inguinal pain, skin exfoliation, limb or genital swelling - ~6 months to develop then leads to Elephantiasis.

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31
Q

Wuchereria bancrofti life cycle (6 steps)

A
  1. A mosquito feeds on a human and infectious larvae enter the skin
  2. Filaria larvae develop within the lymphatics
  3. In the lymphatics, male and female worms mate and produce microfilaria
  4. Microfilaria enter the bloodstream and circulate
  5. A mosquito ingests microfilariae with a blood meal
  6. Microfilariae develop to infective larvae in the mosquito and the cycle repeats
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32
Q

Microfilaria

A

Early stage (embryonic)
of a nematode filariae larvae

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33
Q

Filariae

A

Filamentous nematodes, adults are parasites in the blood or tissues of birds or mammals and as larvae usually develop in biting insects (as fleas or mosquitoes) that belong to the superfamily Filarioidea

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34
Q

Wuchereria bancrofti adult worm structure

A

Long, threadlike filarial worm. 40mm in length for males, 80-100mm females. The microfilaria may have a sheath-like covering. Found primarily in lymphatic vessels, less commonly in blood vessels. Thick and thin blood smear used to diagnose- gently curved body, tail tapered to a point. Nuclear column (the cells that constitute the body of the microfilaria), is visualized individually and do not extend to the tip of the tail.This is important for identification. Microfilariae circulate in the blood at limited times. They are easiest to detect at night- nocturnal periodicity (10 pm to 2 am)

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35
Q

Brugia malayi

A

Nematode, lymphatic filarial worm. It is found in Asia and spread from person to person by mosquito. Transmitted after a bite from infected mosquito – Mansonia and Aedes

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36
Q

Tropical pulmonary eosinophilia syndrome

A

Common in Asia. Cough, wheezing, dyspnea and increased eosinophils. Due to Brugia malayi

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37
Q

Brugia malayi symptoms

A

Most people are asymptomatic and never develop symptoms. Symptoms include- tropical pulmonary eosinophilia syndrome, lymphatic drainage. A low number of people develop lymphedema in their legs. Skin hardening, thickening = Elephantiasis. Increased susceptibility to bacterial and fungal infections due to the folds of the skin

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38
Q

Brugia malayi life cycle (8 steps)

A
  1. Mosquito takes a blood meal and larvae enter the skin
  2. Adults develop in the lymphatics. Males and females mate
  3. Adults produce sheathed microfilariae that reach the bloodstream.
  4. Mosquito takes a blood meal and ingests microfilariae
  5. Microfilariae shed sheaths, penetrate the mosquito’s midgut, and migrate to thoracic muscles
  6. L1 larvae
  7. L3 larvae
  8. Migrate to head and mosquito’s proboscis, and the cycle begins again
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39
Q

Brugia malayi infectious stage

A

Mosquito takes a blood meal and larvae enter the skin

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40
Q

Brugia malayi diagnostic stage

A

Adults produce sheathed microfilariae that reach the bloodstream.

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41
Q

Brugia malayi Microfilaria

A

Circulate in the blood- they are sheathed, 175-230 µm. Have a tapered tail, significant gap between the terminal and subterminal nuclei. Exhibit a nocturnal periodicity and an accurate diagnosis is best achieved on smears collected at night (10 PM-2 AM). There is a space between the terminal and sub-terminal cells of the nuclear column- the last few cells are found after the space at the tip of the tail, differentiating it from other species

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42
Q

Loa loa

A

A nematode, also called the African eye worm. Found in Africa and transmitted by a bite from a tabanid fly (horse fly).

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43
Q

Loa loa diagnosis

A

Microfilariae of L. loa exhibit diurnal periodicity and a diagnosis is best made from blood collected during the mid-day (10 AM-2 PM). The diagnosis is made from microfilaria from thick or thin blood smears or adults in the subconjunctiva.

44
Q

Loa loa symptoms

A

Often asymptomatic. Patients may experience episodic angioedema (Calabar swellings). Transient swelling marking path of adult microfilaria migration. Helps confirm diagnosis
Subconjunctival migration- you can see the worm moving in the inner eye

45
Q

Loa loa life cycle (8 steps)

A

Stages in humans and in flies
1. The fly (genus Chrysops) takes a blood meal, and larvae enter the bite wound
2. Adults in subcutaneous tissue- can produce 200-300 microfilaria per day
3. Adults produce sheathed microfilariae that are found in spinal fluid, urine, sputum, and peripheral blood in the lungs
4. The fly takes a blood meal (ingests microfilaria)
5. Microfilaria shed their sheaths, penetrate the fly’s midgut, and migrate to thoracic muscle
6. L1 larva- a larva molt/stage of maturation
7. L3 larva- a larva molt/stage of maturation
8. Migrate to head and the fly’s proboscis

46
Q

Loa loa infectious stage

A

The fly (genus Chrysops) takes a blood meal, and larvae enter the bite wound

47
Q

Loa loa diagnostic stage

A

Adults produce sheathed microfilariae that are found in spinal fluid, urine, sputum, and peripheral blood in the lungs

48
Q

Loa loa adult worm

A

Often isolated from the subconjunctiva. The female worm is 40-70mm length,0.45-0.60mm width, and the male worm is 30-34mm length, 0.35-0.40mm width. Has an uninterrupted column of nuclei extend in to the tip of the tail- no space at the end. Exterior sheath does not stain well with Giemsa so it is difficult to detect

49
Q

Mansonella streptocerca

A

A nematode and filarial worm, found in the tropics of west and central Africa. M. perstans is found in the Endemic West, East & Central Africa, Central & S. America. M. ozzardi is found in S. America, Haiti

50
Q

Mansonella streptocerca symptoms

A

Mild to asymptomatic, especially in endemic regions. These infections are rarely observed outside of endemic regions. A complicating feature of Mansonella infections is that their geographic distribution overlaps that of other filarial diseases that may have similar clinical manifestations. It is difficult to be certain that symptoms identified in cross-sectional studies of patients in endemic areas were due to Mansonella or to co-infection with other parasites. Transmitted by a vector, midges spread the infection

51
Q

Mansonella streptocerca diagnosis

A

Serology – Problematic – cross-reactive with other filarial worms since there is a lot of protein overlap in the microfilaria. Molecular analysis- qRT-PCR to differentiate from other filarial worms. Microscopy- do a
blood smear, hooked end
skin snip (2mm) place in saline, 30-60 mins then prep. The hooked end is unusual and will help with identification

52
Q

Mansonella streptocerca life cycle (8 steps)

A
  1. A midge (genus Culicoides) takes a blood meal and larvae enter the bite wound
  2. Adults located in dermis, less than 1 mm from the skin. Males and females mate and produce microfilaria
  3. Adults produce unsheathed microfilaria which reside in the skin but can reach the peripheral blood
  4. The midge takes a blood meal and ingests microfilaria
  5. Microfilaria penetrate the midge’s midgut and migrate to the thoracic muscles
  6. L1 larva
  7. L3 larva
  8. Migrates to the head of the midge and to its proboscis
53
Q

Mansonella streptocerca infectious stage

A

A midge (genus Culicoides) takes a blood meal and larvae enter the bite wound

54
Q

Mansonella streptocerca diagnostic stage

A

Adults produce unsheathed microfilaria which reside in the skin but can reach the peripheral blood

55
Q

Mansonella streptocerca adult worm

A

The adult worm is not sheathed. It has a hook at the end. The morphology can indicate this infection especially in endemic areas

56
Q

Onchocerca volvus

A

A filarial worm and nematode that causes river blindness. It is transmitted by simulium- a black fly bite. Found mainly in Africa, focal in Latin America and the Middle East

57
Q

Onchocerca volvus symptoms

A

This infection is the leading cause of blindness. Symptoms-
pruritus, dermatitis, onchocercomata (subcutaneous nodules), and lymphadenopathy. People exhibit punctate lesions (dots in the cornea) which are associated with the location of the microfilaria. When the microfilaria die, they can cause scarring and lesions. Ocular lesions can progress to blindness. If someone has 5 or less nodules, they are considered to have mild disease, but 10-15 nodules is severe disease. Nodules tend to be on the head and the upper torso

58
Q

Onchocerca volvus life cycle

A
  1. The black fly takes a blood meal and introduces the infectious larvae into the circulation
  2. The larvae in the subcutaneous tissues will develop into adults. The adults can remain in the tissue for many years and will form nodules. Nodules can remain in the tissue for 15 years and the males and females will still be producing microfilaria
  3. The microfilaria can migrate through the skin, causing skin rashes. They can also migrate through the circulation and cause symptoms depending on where they are in the body
59
Q

Onchocerca volvus infectious stage

A

The black fly takes a blood meal and introduces the infectious larvae into the circulation

60
Q

Onchocerca volvus diagnostic stage

A

Microfilaria can be found in the circulation or in a skin biopsy (when the nodules are biopsied). The microfilaria may also be found in urine and sputum

61
Q

Onchocerca volvus adult worm

A

Has a long nuclear column that does not go to the tip of the worm. Is not sheathed. Knowing which regions are endemic is important for identification because it can look similar to other filarial worms

62
Q

Clonorchis sienensis

A

Called the Chinese liver fluke (trematode). Endemic to Asia, Korea, China, Taiwan, and Vietnam. There are non endemic areas including the United States- may be found in Asian immigrants, or following ingestion of imported, undercooked or pickled freshwater fish containing metacercariae. The adult flukes usually aren’t found and would have to be surgically removed

63
Q

Clonorchis sienensis symptoms

A

Causes inflammation and intermittent obstruction of the biliary ducts. Acute phase - abdominal pain, nausea, diarrhea, and eosinophilia. Chronic infection - cholangitis, cholelithiasis, pancreatitis, and cholangiocarcinoma can develop, which may be fatal.
Serologic testing is not available in US

64
Q

Clonorchis sienensis life cycle (6 steps)

A
  1. The embryonated eggs are passed in the feces, which end up in a water source
  2. Eggs are ingested by the snail and undergo several molting stages
  3. Free-swimming cercariae encyst in the skin or flesh of fresh water fish
  4. Metacercariae in the flesh or skin of fresh water fish are ingested by the human host
  5. Excyst in the duodenum
  6. Adults mature in biliary duct
65
Q

Clonorchis sienensis infectious stage

A

Metacercariae in the flesh or skin of fresh water fish are ingested by the human host. Humans are incidental hosts

66
Q

Clonorchis sienensis diagnostic stage

A

The embryonated eggs are passed in the feces

67
Q

Miracidia

A

A free-swimming ciliated larval stage in which a parasitic fluke passes from the egg to its first host, typically a snail.

68
Q

Metacercariae

A

Tailless encysted late larva of a trematode that is usually the form which is infective for the definitive host. Infective stage

69
Q

Clonorchis sienensis adult worm morphology

A

Flattened, 10-25 mm length by 3-5 mm width flukes. Hermaphroditic, with a single ovary situated anterior to two branches testes, also has a uterine horn. Adults reside in the biliary passages of the liver of the definitive host. Adult flukes are recovered during surgery

70
Q

Clonorchis sienensis ova structure

A

27-35µm by 11-20µm. Small, oval shaped, convex operculum, rests on visible “shoulders”. Abopercular end, a small knob or hook-like protrusion is often visible. Miracidium is visible in the egg. Eggs in the stool or in duodenal aspirate – diagnostic

71
Q

Paragonimus westermani

A

A fluke (trematode) found in the Americas, Africa and southeast Asia, and Japan. Infection has an acute and chronic phase. Biopsy may allow diagnostic confirmation and species identification when an adult or developing fluke is recovered. This fluke is larger and easier to find. Associated with consumption of contaminated crustaceans, like crab or crayfish. Associated with travel, especially to southeast Asia, along with people who have recently immigrated to the US

72
Q

Paragonimus westermani symptoms

A

Acute phase (invasion and migration) – diarrhea, abdominal pain, fever, cough, urticaria, hepatosplenomegaly, pulmonary abnormalities, and eosinophilia. During the chronic phase:
Pulmonary - cough, expectoration of discolored sputum, hemoptysis, and chest radiographic abnormalities.
Extrapulmonary - adult worms result in more severe manifestations, especially when the brain is involved.

73
Q

Paragonimus westermani life cycle (8)

A
  1. Unembryonated eggs develop to become embryonated
  2. Embryonated eggs develop in the environment
  3. Miracidia hatch and penetrate a snail
  4. Goes through several molting changes
  5. Cercariae invade the crustacean and encyst into the metacercariae
  6. Humans ingest inadequately cooked or pickled crustaceans containing metacercariae
  7. Excyst in the duodenum, can travel in the circulation and enter the abdominal wall, diaphragm, or lungs
  8. Adults in cystic cavities in lungs lay eggs, which are excreted in the sputum. The eggs cause an inflammatory response in the lungs, so hemoptysis may occur. Alternately eggs are swallowed and passed in the stool. The entire process takes about 90 days, and adults can live for 20 years
74
Q

Paragonimus westermani infectious stage

A

Cercariae invade the crustacean and encyst into the metacercariae

75
Q

Paragonimus westermani diagnostic stage

A

Unembryonated eggs develop to become embryonated

76
Q

Paragonimus westermani ova structure

A

80-120µm length by 45-70µm width. Yellow-brown, ovoid or elongate, thick shell, and often asymmetrical with one end slightly flattened. Operculum is clearly visible, Abopercular is thickened. Unembryonated when passed in sputum or feces
2 to 3 months until ovum appear in stool or sputum, occasionally in effusion fluid or biopsy material

77
Q

Paragonimus westermani adult worm

A

Large, robust, ovoid flukes. Hermaphroditic - lobed ovary located anterior to two branching testes, also a uterine. Oral and ventral suckers

78
Q

Fasciola hepatica

A

Common or sheep liver fluke (trematode). Areas where sheep and cattle are raised, and where humans consume raw watercress, including Europe, the Middle East, and Asia

79
Q

Fasciola gigantica

A

Tropical and subtropical regions. Case reports from Asia, Africa, Hawaii, Iran.

80
Q

Fasciola hepatica symptoms

A

Acute phase (migration of the immature fluke through the hepatic parenchyma) abdominal pain, hepatomegaly, fever, vomiting, diarrhea, urticaria and eosinophilia. Chronic phase (adult fluke within the bile ducts) intermittent biliary obstruction and inflammation. Rare ectopic infection

81
Q

Fasciola hepatica life cycle (8)

A
  1. Unembryonated eggs are passed in feces
  2. Embryonated eggs develop in water source
  3. Miracidia hatch and penetrate the snail host
  4. Miracidia is released
  5. Free-swimming cercariae encyst on water cysts
  6. Metacercariae on water plant ingested by human, sheep, or cattle
  7. Excyst in duodenum and can penetrate the intestinal wall
  8. Adults found in hepatic biliary ducts, lay eggs. This process takes 3-4 months
82
Q

Fasciola hepatica diagnostic stage

A

Unembryonated eggs are passed in feces

83
Q

Fasciola hepatica infectious stage

A

Metacercariae on water plant ingested by human, sheep, or cattle

84
Q

Fasciola hepatica ova

A

The diagnosis is made by eggs in feces. Measure 130–150 µm long by 60–90 µm wide. Eggs of both species (hepatic and gigantica) are unable to be distinguished. Ellipsoidal, operculated, smooth shell. Unembryonated when passed in feces.

85
Q

Fasciola hepatica vs F. buski

A

F. buski eggs are difficult to distinguish from Fasciola spp. (abopercular end is roughened or irregular in buski). F. buski also has a round, cephalic end of the fluke

86
Q

Fasciola hepatica serology

A

Serology is helpful during the acute phase. 2-4 weeks antibody positive. Egg production not detected until 3 to 4 months

87
Q

Fasciola adult worms

A

F. hepatica can be up to 30 mm by 15 mm and F. gigantica can be up to 75 mm by 15 mm. Flattened, leaf-like appearance
F. buski-round cephalic end. Seen only from endoscopy or surgery

88
Q

Schistosoma distribution (4)

A
  1. S. mansoni - South America, Caribbean, Africa, Middle East
  2. S. haematobium - Africa, Middle East
  3. S. japonicum - Far East
  4. S. intercalatum – focally in east-central Africa
89
Q

Schistosoma diagnosis (4)

A
  1. Travel history (dictates parasite antigen screening)
  2. Presence of ova in appropriate patient samples
  3. Serology
  4. ELISA - Schistosoma mansoni adult microsomal antigen (MAMA)
90
Q

Acute schistosomiasis

A

Many infections are asymptomatic. Acute schistosomiasis (Katayama’s fever). S. mansoni and S. japonicum- fever, cough, abdominal pain, diarrhea, hepatosplenomegaly, eosinophilia. S. japonicum - CNS lesions with cerebral granulomatous disease may be caused by ectopic eggs in the brain. S. mansoni - granulomatous lesions around ectopic eggs in the spinal cord. The presence of eggs or adult worms has the ability to block blood flow

91
Q

Complications of continuing schistosomiasis

A

Continuing infection may cause granulomatous reactions and fibrosis in the affected organs, which may result in manifestations that include:
colonic polyposis with bloody diarrhea - Schistosoma mansoni mostly, portal hypertension with hematemesis and splenomegaly. S. mansoni and S. japonicum can cause cystitis and ureteritis with hematuria, which can progress to bladder cancer - S. haematobium. This is the only parasite found in the bladder, can get a urine sample to diagnose. Pulmonary hypertension, glomerulonephritis - S. mansoni, S. japonicum, more rarely S. haematobium

92
Q

Schistosoma

A

Flukes- all Schistosoma species require freshwater snails as their intermediate hosts. Adult worms are diecious. One of the most problematic flukes, they have the ability to migrate and live in other tissues and blood vessels. The cercariae live in freshwater and also have the ability to erode through the skin. We see the ova in the locations they migrate to. Several snail species can serve as intermediate hosts. Associated with contact with fresh water particularly: swimming, bathing, wading in river edges, and washing clothing in water in endemic areas puts individuals at risk.

93
Q

Schistosoma life cycle (9)

A
  1. Cercariae in the freshwater penetrates the skin
  2. Cercariae loses its tail and becomes a schistosomula
  3. The schistosomula is located in the circulation of the human host
  4. Adult males and females will mate depending on the species and where they have migrated to
  5. Haematobium is found in the urine, the other species (japonicum and mansoni) are found in the feces
  6. The eggs are introduced into a water source, where they mature
  7. The eggs hatch, releasing miracidia
  8. Miracidia penetrates snail tissue
  9. Cercariae develop and are released by the snail into the water, are free-swimming- cycle repeats
94
Q

Schistosoma infectious stage

A

Cercariae in the freshwater penetrates the skin

95
Q

Schistosoma diagnostic stage

A

Haematobium is found in the urine, the other species (japonicum and mansoni) are found in the feces

96
Q

Schistosoma mansoni ova

A

Large, 114-180µm length, 45-70µm width. Has a characteristic shape, with a prominent lateral spine near the posterior end.
Anterior end is tapered and slightly curved. Excreted in the stool, they contain a mature miracidium. Found in the inferior mesenteric veins (colon, rectum, sigmoid colon)

97
Q

Schistosoma japonicum ova

A

Large, more rounded than other species. They are 70-100µm in length, 55-64µm width. Spine is smaller and less conspicuous than other species- it has a rounded “hook”. The ova are shed in stool. Tend to be found in the superior mesenteric veins (small intestine).

98
Q

Schistosoma haematobium ova

A

Large, 110-170µm length, 40-70 µm width. Have a conspicuous terminal spine. Eggs contain a mature miracidium and are shed in urine. Found in the vesicular and pelvic venus plexus, uterus, cervix, lower genital tract, and bladder.

99
Q

Schistosoma intercalatum ova

A

Related to S. haematobium, but restricted to east-central Africa.
The eggs are similar to S. haematobium in general shape and in possessing a terminal spine. Usually longer (140-240 µm). Have an equatorial (central) bulge in addition to the spine and are shed in stool, not urine. Associated with the mesenteric plexus (lower bowel) same area as S. mansoni

100
Q

Echinococcus granulosus

A

A tapeworm (cestode). Humans are not the definitive host but can suffer pathological consequences as a result of infection. Associated with infections of dogs. Worldwide distribution with increased frequency in rural, grazing areas where dogs ingest organs from infected animals. E. granulosus is the most common, other species include Echinococcus multilocularis, Echinococcus vogeli, Echinococcus oligarthrus. Causes hyatidosis or cystic echinococcosis

101
Q

Echinococcus granulosus symptoms

A

Humans are only infected by larvae after ingestion of eggs from food, water or fomites contaminated with dog feces. Eggs hatch in the small intestine, releasing oncospheres that will ultimately form cysts in various tissues. Silent infection for years until proceeding to symptomatic enlarged cysts. Oncospheres cannot continue the life cycle because humans are a dead end host. Cyst-like structures form in the lung and liver. Hepatic involvement – mass formation, abdominal pain, biliary duct obstruction. Pulmonary involvement - chest pain, cough, and hemoptysis. May mimic tuberculosis. Rupture of cysts produces fever, urticaria, eosinophilia, anaphylactic shock, as well as cyst dissemination. Other organs (brain, bone, heart) can also be involved, with resulting symptoms.

102
Q

Echinococcus granulosus life cycle (6)

A
  1. Adult in small intestine
  2. Embryonated eggs in feces- excreted by the infected animal
  3. Oncosphere hatches and penetrates the intestinal wall
  4. Hydatid cyst in liver, lung, other tissues
  5. Protoscolex (next stage of development) makes up the cyst
  6. Scolex attaches to the intestine- this is where the adult worms live. This process takes around 8 days, but people can be infected for decades
103
Q

Echinococcus granulosus infectious stage

A

Embryonated eggs in feces

104
Q

Echinococcus granulosus diagnostic stage

A

Hydatid cyst in liver, lung, other tissues- this is a response of the parasite. Cysts fill will fluid and are filled with millions of protoscolexes

105
Q

Echinococcus granulosus ova

A

Eggs are not found in human stool, not diagnostic in humans. Eggs are however indistinguishable from the eggs of Taenia spp. Patient history and exposure is necessary for diagnosis

106
Q

Echinococcus granulosus cysts

A

Range from 2-20 cm. Migration from the intestinal lumen to other body sites and develop into hydatid cysts. Cysts can be found in any part of the body, but are most common in the liver, lung and central nervous system. Cysts can become very large, be under pressure, and therefore rupture. Scans for hydatid cysts or biopsies looking for cysts can be done for diagnosis

Clinical Microbiology (19 decks)

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