Block 9 Week 4 Flashcards

1
Q

Types of Eukaryotic Parasites

A

Protozoa:
- single celled eukaryotes

Helminths:
- parasitic worms
- adults can be seen with naked eye
- Many are intestinal worms that are soil transmitted and can infect the GI tract.

Arthropods:
- multicellular eukaryotics

  • hard ticks, soft ticks, scabies, mites, bed bugs, fleas
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2
Q

Malaria

A
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3
Q
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4
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5
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6
Q

African Trypanosomiasis (sleeping sickness)

A
  • African Trypanosomiasis (sleeping sickness) is caused by Trypanosoma brucei parasites in sub-Saharan Africa and is transmitted by the bloodsucking testes fly ( genus Glossina).
  • 50,000 people die annually from the infection.
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7
Q

Two forms of the disease

A

There are two forms of the disease:
- East African HAT (human african trypanosoma) caused by Trypanosoma brucei rhodesiense (T.b. rhodesiense). This variant has a faster tempo and leads to death if untreated in several weeks to a few months. Whereas Gambiense can last from months to years.

  • West African variant caused by T.b. gambiense. Gambiense variant is more more prevalent and accounts for 95% of cases.
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8
Q

Two stages of African Trypanosomiasis ?

A

Early stage (stage 1) (hemolymphatic stage) :

  • 1-3 weeks after bite.
  • Parasites spread in the bloodstream, lymph nodes and systemic organs.
  • This causes nonspecific symptoms such as malaise (feeling of discomfort), headache, arthragalia (pain in joint) , headache and fatigue .

Late stage (stage 2) (Encephalitic stage):

  • the parasites cross the blood brain barrier to enter the CNS

Symptoms and signs vary but include:
- characteristic sleep disturbance

  • alteration in sleep/wake cycle urge to sleep
  • motor disturbances: pyramidal weakness, extrapyramidal features, cerebral ataxia (poor muscle control, clumsy),

Neurological disturbances

Untreated or unsuccessfully treated patients will rapidly deteriate with seizures and cerebral edema, incontinence and death.

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9
Q

Symptoms of Arfrican Trypanosomiasis ?

A

Symptoms of sleeping sickness may include:
- fever
-headache
- joint pain
- itching
- swollen lymph nodes

This is followed by neurological symptoms, as the infection progresses such as:
- confusion
-sleep disturbances
- seizures

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10
Q

Treatment of African Trypanosomiasis ?

A

Treatment of sleeping sickness typically involves a combination of drugs:
Early stage of disease:

  • pentamidine
  • suramin

Later stages of disease requires more toxic drugs:

-melarsoprol

  • eflornithine
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11
Q

South American Trypanosomiasis(Chagas disease)

A
  • parasitic disease common in central and south america.
  • Caused by a protozoan called Trypanosoma cruzi
  • T. Cruzi is transmitted through the feces of insect Triatomine.
  • Triatomine is a type of Reduviid bug also known as ‘kissing bug’ because it often bites your face.
  • Transmission: parasites in bug feces
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12
Q

Lifecycle of T.Cruzi

A
  1. Epimastigote T.cruzi in bug midgut. Reproduce through binary fission.
  2. Over time Epimastigote becomes a Trypomastigote and loses ability to divide. But gains ability to invade human cells.
  3. Trypomastigotes from bug feces to human through contact.
  4. In human trypomastigote loses its flagellum and we now call this Amastigote. Multiply intracellulary through binary fission.
  5. Become blood trpomastigotes. They can move through blood and lymph to other tissues.
  6. Blood trypomastigotes invade more cells then again becomes amastigotes.
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13
Q

Transmission Chags disease

A
  • Also through infected blood and organ donations
  • From a mother to a child during pregnancy.
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14
Q

After bite their is an incubation period

A
  • Bite: Chagoma
  • Next to eye: Romanas sign
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15
Q

Chagas disease has an Acute and Chronic phase.

A
  • Acute phase resolves when T.Cruzi Trypomastigotes are cleared from the blood.
  • Over time antibodies against T.Cruzi decrease. This indicates that the infection has been cleared.
  • However in some individuals this does not happen and they go on to the chronic phase of teh infection.

Chronic phase:
- Amastigotes linger in infected cells

  • elevated level of T.Cruzi antiboodies ( even though typomastigotes are not usually in the blood)
  • Chronic phase can be asymptomatic or symptomatic.
  • Most common symptom is CARDIOMYOPATHY (heart gets large)

NERVE DAMAGE

GI symptoms: Eg megaesopgagus, megacolon

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16
Q

DIAGNOSIS

A
  • Acute phase using a blood smear or PCR
  • No ‘gold standard’ for diagnosing chronic phase of infection.
  • Serology - looks for number of antibodies
  • chest x-ray (look at size of heart)
  • Barium swallow : look at colon

Advanced stages: ECG to identify arhytmia

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17
Q

Treatment

A

For acute phase:
Antiparasitic medication:
- Benznidazole/ Nifurtomox
( post infection and continuing for 2-4 months)

Chronic phase:
- managing symptoms of cardiomyopathy eg with pacemakers or anticoagulation medication.

Advanced stages: may need heart transplant

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18
Q

Leishamania

A
  • Human leishmaniasis characterised by ulcers (eg. skin, oral, nasal mucosa), systemic illness.
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19
Q

Leishmaniasis

A

Cause: Leishmaniasis

Spread: female sandflies of genus Lutzomyia/Phlebotomus

  • Lipophosphoglycan layer can help it survive the immune system
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20
Q

Types / Spectrum of diseases caused by Leishmania spp.

A

Asymptomatic

Cutaneous leishmaniasis:
- Most common

  • usually caused by L.major, L.tropica, L.aethiopica

Visceral leishmaniasis:
- most sever, systemic involvement

  • usually caused by L.donovani. L.infantum

-resists host complement system , prevents natural killer cells

-infected macrophages spread infection causing:
splenomegaly, liver dysfunction, panycytopenia, lymphadenopathy

Mucosal leishmaniasis:
- mucosal and skin ulcers
- usually caused by L.braziliensis

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21
Q

Toxoplasmosis

A
  • Toxoplasmosis gondii is a protozoan parasite infects most species of warm blooded animals including humans.
  • The only known definitive hosts for Toxoplasmosis gondiia re members of family Felidae (domestic cats )
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22
Q

Lifecycle of Toxoplasmosis Gondii

A

SEXUAL REPRODUCTION:
- cat consumes infected animal meat
- parasite survives transit through stomach
- infects small intestine epithelial cells
- parasites undergo sexual development, reproduction-> millions of thick-walled, zygote containing, oocytes produced.

FELID SHEDDING:
- infected epithelial cells rupture
- release oocytes into intestinal epithelium
- this is released in feces
- spread to soil, water, food

  • Oocysts highly resilient: can survive, remain infective for moths in cold dry climates.

INFECTION OF THE INTERMEDIATE HOST:
- ingestion of oocysts by humans.
- oocyst wall dissolves by proteolytic enzymes in stomach, small intestine
- frees sporozites from within oocyst
- parasites invade intestinal epithelium surrounding cells
- differentiation into tachyzoites (motile, quick -multiplying phase)

ASEXUAL REPRODUCTION IN INTERMEDIATE HOST:
- tachyzoites replicated inside specialized vacuoles until host cell dies, ruptures -> release, hematogenous spread of tachyzoites to all tissues

FORMATION OF TISSUE CYSTS:
- host immune response -> tachyzoite conversion -> bradyzoites (semi dormant slow dividing stage) -> inside host cells known as tissue cysts -> can form in any organ: predominately brain, eyes, striated muscle (including cardiac muscle)

  • Tissue cysts maintained in host tissue for remainder of life via periodic cyst rupture
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23
Q

Toxoplasmosis signs and symptoms

A

Initial infection in immunocompetent host:
- mild flu-like symptoms (eg. swollen lymph nodes, headache, fever, fatigue, muscle aches, pains)

Chronic infection in healthy hosts:
- asymptomatic in healthy hosts

Immunocompromised host:
-Active infection: headache, confusion, poor coordination, seizures, cough, dyspnea

  • Reactivation of latent infection: worsening of immunosuppression due to progression of underlying disease (e.g. HIV/AIDS, iatrogenic immunosuppression) -> loss of immune balance -> progression to active infection
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24
Q

Diagnosing Toxoplasmosis

A
  • CT scan with contrast
  • T2 weighted MRI
  • Fundoscopy
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25
Q

Varied intestinal protozoan

A
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26
Q

AMOEBIASIS: what is does

A
  • caused by Entamobea histolytica
  • trophozoites bind to intestinal epithelial cells in colon, release lytic enzymes, epithelial cell lysis.
  • trophozoites lyse inflamed/attracted immune cells.
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27
Q

Consequences of Amoebiasis ?

A

Intestinal mucosal ulcers -> collitis -> bowel necrosis -> perforation -> sepsis

Tissue destruction -> mucosa blood vessel injury-> malabsorption -> increases intestinal secretion -> bloody diarrhea, amebic dysentery

Blood vessel injury -> trophozites in blood stream -> extraintestinal amebiasis (liver, pulmonary, cardiac, brain)

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28
Q

Signs and symptoms of Amebiasis ?

A
  • bloody diarrhea
  • mucus in stool (severe dysentery)
  • abdominal pian
  • fever
  • weight loss
  • right-upper quadrant pain
  • jaundice (liver)
  • cough (pulmonary)
  • dehydration
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29
Q

Diagnostic Amoebiasis

A
  • X ray (liver)
  • CT scan, MRI, Ultrasound ( cystic intrahepatic cavity detection)

LAB:
- serology: Entamoeba antibody detection

  • PCR: Entamoeba DNA detection
  • Antigen detection: Enzyme linked immunosorbent assay ( ELISA)
  • Microscopic identification:
    cysts/trophozoites in stool/pus (eg. liver abscess)
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30
Q

Treatment

A
  • METRONDIAZOLE (amebic liver abcess)
  • Broad spectrum antibiotics
  • Antibacterial agents
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31
Q
A
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32
Q

Helminths

A
  • parasitic worms also known as helminths are large macroparasites
  • adults can generally be seen with the naked eye
  • many are intestinal worms that are soil transmitted and infect the G.I. tract.
  • Helminths is a term used to describe multicellular worm like parasites that can infect humans. This includes:
  • cestodes
  • trematodes
    -nematodes
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33
Q

TAPEWORMS aka CESTODES

A
  • Taenia saginata - spread from cows
  • Taenia solium - spread from pigs
  • ingest then tapeworms live off nutrient rich fluid
  • cysticercosis - newly hatched larvae burrow into different parts of the body
  • if the tapeworm goes to the brain this can cause seizures and death.
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34
Q
A
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35
Q

TREMATODES aka FLUKES

A
  • Schistomsomiasis (snail fever) live in fresh water snails and pop out as free swimming larva.
  • They get into humans which may be swimming outdoors and penetrate through hair follicles to get to capillary beds, where they feed off blood

-

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36
Q

NEMATODES aka ROUND WORMS

A
  • passed on when someone eats or drinks something contaminated with nematode eggs which are transmitted through feces
  • Eggs hatch into larvae in small intestine and causes GI symptoms such as malabsorption, diarrhea or abdominal pain
  • The nematodes then bore through the gut to get to the lungs
  • Then coughed up to the oral cavity
  • They are then swallowed and mature into adult worms in the intestines. Severe infections of 100s of these worms can lead to the complete obstruction of the intestines.
  • Most common species to infect humans are the ascaris species which causes ascariasis
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37
Q

Nematodes

A

Filarial worms - need an insect as an intermediate host

  • Black flies transmit Loa Loa which invades the skin and eyes
  • Mosquitos transmit Wurcheria Bancrofti which invades the lymphatic vessels and causes Elephantiasis
38
Q

Antihelminths

A

ALBENDENDAZOLE and MEBENDAZOLE inhibit the formation of microtubule.

Albendazole is the first line therapy for:
- Ascariasis, Pinworms, Hookworms & Whipworms.

Side effects:
- Teratogenic - cannot be used during pregnancy
- bone marrow suppression
-liver toxicity

39
Q

ASCARIASIS

A
  • intestinal roundworm parasite
  • Ascaris lumbricoides (nematode)

Lifecycle:
- Egg ingestion (human) -> larvae hatch -> invade intestinal mucosa -> portal circulation -> systemic circulation -> liver -> lungs -> larvae mature in alveoli (10-14 days) -> ascend bronchial tree, pharynx, swallowed -> larvae develop into adult form in small intestine.

Pathophysiology:
Pulmonary phase (early): caused by larval migration into the lungs -> pneumonitis

Intestinal phase: manifestations caused by adult-form presence -> mechanical obstruction ( degree worm - burden- dependent)

Risk:
- from eating egg contaminated food or water especially egg or chicken liver

  • infected soil (children)
  • fecal-oral route reinfection
40
Q

Signs and symptoms of Ascaris

A
  • often asymptomatic

Pulmonary phase (Loffler syndrome):
- develops 14-16days post infection
- dry cough, dyspnea, fever, wheezing, substernal discomfort, blood tinged sputum,

Intestinal phase:
- develops 6-8 weeks post infection
- abdominal discomfort, anorexia, nausea, vomiting, diarrhea

41
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A
42
Q

Taeniasis

A
  • Taeniasis in humans is a parasitic infection
  • Caused by the tapeworm species Taenia saginata (beef tapeworm),
    Taenia solium (pork tapeworm)
43
Q

(Larval) Cysticercosis

A
44
Q

Schistosomiasis ( Bilharzia)

A
  • Bilharziasis /snail fever
  • Schistosoma is a genus of trematodes, commonly known as blood flukes. They are parasitic flatworms responsible for a highly significant group of infections in humans termed schistosomiasis,
45
Q

Transmission of Schistosmiasis

A
  • Host: snails
  • Transmission: contaminated fresh water contact.
  • contact with cercariae in fresh water-> skin penetration -> schistosmulae -> migration to liver through circulation -> adult form -> migration to mesenteric venules/vesical venous plexus -> egg deposits -> inflammation -> fibrosis
  • High prevalence in sub-Saharan Africa
46
Q

Risk Factors

A
  • more common in individuals who are biologically male, rural areas
  • recent contact with fresh water bodies in endemic areas
47
Q

Signs and symptoms Schistomiasis

A

Acute infection:
- swimmers itch: urticarial rash esp. legs/feet

  • acute schistomiasis syndrome ( Katayama fever): non-specific symptoms fever, urticaria, chills, arthralgia, myalgia, headaches

Chronic infection:
on pic

48
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A
49
Q

Lymphatic Filariasis ( Elephantitis)

A
  • mosquito borne nematode infection

Transmission:
- introduction into human skin during mosquito blood meal -> lymphatic spread -> maturation into adult worm -> reproduction, microfilarial hematologic release ( commonly nocturnal release) -> further transmission after infected individuals mosquito bite

50
Q

Elephantitis Signs and Symptoms

A
  • fever, hydrocele (swelling in scrotum)

lymphatic disease:
-swelling of limb
- lymphedema

51
Q

Onchocerciasis (river blindness)

A
  • filarial nematode transmitted by blackflies
  • Leading preventable blindness cause in sub- Saharan Africa.
52
Q

Signs and symptoms River blindness

A

Cutaneous

  • pruritus
  • nodule development
  • focal darkening/depigmentation
  • epidermal atrophy, hyperpigmentation, hyperkeratosis

Ocular
- punctuate keratits -> fluffy corneal opacities -> eosinophilic infiltrate -> sclerosing keratitis -> corneal opacification

53
Q

Echinococcosis (Hydatid disease)

A
54
Q

Dracunaculiasis ( guinea-worm disease)

A
55
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Arthropds

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56
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Scabies

A
57
Q

Fungal infections

A
  • Fungi are all around us
  • 250,000 species
  • 1500 new species discovered annually
  • 1000 or so pathogenic to humans
  • 12 or so colonise humans
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59
Q

What are fungi types ?

A

Fungi types:
- Moulds
- Yeast
- Dimorphic

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76
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VACCINATIONS

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Benefits of vaccinations

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80
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Routine vaccinations

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Smallpox

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Polio virus

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86
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  • Live vaccines are always the gold standard for levels of protection
  • Live vaccine provide immunity for years
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HPV and the end of cervical cancer

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90
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The 40-year fight against HIV

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91
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COVID 19 - Vaccine -21

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