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Skin MS: Week 4 > Intro to Parasitic Infections > Flashcards

Intro to Parasitic Infections Flashcards

1
Q

Onchocerciasis

A

River Blindness (Robles disease in Latin America)

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2
Q

Onchocerca volvulus lifecycle

A

Blackfly takes blood meal (L3 larvae enter bite wound)
Go to subcutaneous tissues - adults in subQ, sexually reproduce to produce unsheathed microfilariae typically found in skin and lymphatics of CT, blackfly takes meal here, microfilariae penetrate blackfly’s midgut and migrate to thoracic muscles –> L1 larvae –> L3 larve –> migrate to head and blackfly’s proboscis

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3
Q

Drugs for onchocerciasis and what effective against

A

Ivermectin - effective against microfilariae (not adults)

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4
Q

Epidemiology of onchocerciasis

A

sub-Saharan Africa, tropical climates of the Americas, Yemen, Middle EAst
Transmitted by blackfly (near rivers and streams)

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5
Q

Onchocerciasis causative agent

A

nematode (roundworm) = Onchocerca volvulus

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6
Q

Sxs of onchocercaisis

A

Eye and skin disease
Nodules under skin (adults growing in SubQ)
Hyperpigmented skin (post-inflamm)
Severe itching, eye lesions, skin lesiosn (migration and inflammation by microfilariae, release of symbiont bacteria)
Keratitis
Destruction of elastic fibers –> skin looks thin

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7
Q

dx of onchocerciasis

A

skin snip method

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8
Q

symbiont bacteria of onchocerca volvulus

A

Wolbackia pipientis (causes inflammation when released by dead worms)

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9
Q

Onchocerciasis prevention

A

No vaccine. Aerial applications of larvicides to control blackflies and DEET application to prevent bites.

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10
Q

Onchocerciasis tx

A

Ivermectin (to avoid blindness, longterm damage to skin, continued transmission)
Well absorbed, affective against microfilariae. Retreatment required.
Doxy as co-tx for Wolbackia pipientis

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11
Q

Ivermectin mechanism

A

binds to and blocks glutamate-gated chloride channels that are present on invertebrate muscle and nerve cells

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12
Q

Leishmania life cycle

A

Sandfly takes blood meal - injects promastigote stage into skin (flagellar) - promastigotes phagocytized by macrophages and other types of mononuclear phagocytic cells - promastigotes transform into amastigotes - amastigotes multiply in cells of various tissues and infect other cells - sandlfy takes blood meal (ingests macrophages w/ amastigotes) - ingestion of parasitized cell - amastigotes transform into promastigote stage in gut of fly - diving in the gut and migrate to proboscis

** Requires uptake by phagocytic cell to achieve mammalian life cycle state - replicated in phagolysosome.

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13
Q

Leishmaniasis causative agent

A

Caused by the protozoan parasite Leishmania transmitted by the sand fly.

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14
Q

Leishmaniasis epidemiology

A

Leishmaniasis is found in East Africa, Asia, and Latin America and has multiple forms

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15
Q

Cutaneous leishmaniasis

A

leishmaniasis is most common, found in Old World (Asia, the Middle East, Africa) and New World (Latin America).
Symptoms: One or more skin sores. sores can change in size and appearance over time. Often volcano-like, with raised edge and central crater. sores can be painless or painful. Some people have swollen glands near the sores (for example, in the armpit if the sores are on the arm or hand).

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16
Q

Mucocutaneous leishmaniasis

A

very rare but results from a metastasis of an untreated case of cutaneous leishmaniasis

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17
Q

Visceral leishmaniasis

A

occurs mostly in Bangladesh, Brazil, Ethiopia, India, South Sudan and Sudan. Also called kala-azar. Life threatening!!!
Symptoms: weight loss, and an enlarged spleen and liver (usually the spleen is bigger than the liver). Some patients have swollen glands. Patients usually have low blood counts, including a low red blood cell count (anemia), low white blood cell count, and low platelet count. An emerging HIV opportunistic pathogen.

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18
Q

Leishmaniasis prevention

A

No vaccines or prevention (limit sandfly)

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19
Q

Dx leishmaniasis

A

Definitive diagnosis in laboratory : CDC will need to be involved. Usually still involves microscopic detection of the organism in a blood or tissue sample.
Serological tests will only be positive in the case of visceral leishmaniasis (same with tests that detect antigen directly).

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20
Q

Leishmaniasis - should be treated?

A

Should be treated. While cutaneous sores often heal on their own, they can leave disfiguring scars and possibly lead to mucocutaneous form even years later.

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21
Q

Leishmaniasis tx options

A

Pharmacology: Need drugs that can get into the macrophage, and furthermore, into the phagolysosome
Organic antimonials: Sodium stibogluconate and Meglumine antimoniate. Competing theories for mechanism of action. Incidence of treatment failures is increasing and resistance occurs. Must be administered intramuscularly.
Miltefosine. Mechanism not well understood. good alternative for drug-resistant leishmaniasis. Highly bioavailable and absorbed well.
Liposomal Amphotericin B. Only for visceral leishmaniasis. Only liposomal formulation of this anti-fungal is shown to be effective (injection necessary). Binds to ergosterol to form pores in membranes.

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22
Q

Romana’s sign

A

swelling of child’s eyelid - marker of acute chaga’s disease

d/t bug feces into eye or bite wound on same side of face as swelling

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23
Q

Chagas disease - causative agent

A

flagellated protozoan parasite Trypanosoma cruzi

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24
Q

T. cruzi lifecycle

A

Triatomine bug takes blood meal and passes metacyclic trypomastigotes in feces/enter bite wound or mucosal membrane –> metacyclic trypomastigotes penetrate various cells at bite wound site - inside cells, transform into amastigotes - amastigotes multiply by binary fission in cells of infected tissues –> intracellular amastigotes transform into trypomastigotes then burst out and enter blood stream (and can infect other cells) –> triatomine takes blood meal - multiply in midgut - passed through feces

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25
Q

Acute Chagas

A

symptoms are often asymptomatic but often mild, typical innate immune response to an infection. Often acquired early in life. Occasionally severe.
Without treatment at the acute stage, individuals do not entirely clear the parasite, go on to the chronic stage.

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26
Q

Chronic Chagas

A

T. cruzi replicates intracellularly (immune evasion), but does exit cell in an additional life stage to find a new cell. The presence of parasites and a continuous low-grade immune response (inflammatory) is what is thought to contribute to the following:
Myocarditis
Megaesophagus
Megacolon
Also, symptoms can reappear in chronic indeterminate individuals if they become immunocompromised

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27
Q

Dx Chagas

A

Identification of parasites in blood (acute or recurring infection only). Chronic infection is usually diagnosed with more than one serological test.

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28
Q

Should treat chagas ds?

A

Yes! Drugs are effective in acute stages, use and effectiveness in chronic stages where cardiomyopathy has developed is controversial. Permanent damage.

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29
Q

Chagas tx

A

nitroaromatics: Nifurtimox & Benznidazole are well absorbed from GI tract, no IV administration necessary.
Nifurtimox induces oxidative stress due to inhibition by NAD(P)H-dependent dehydrogenases with subsequent impairment of mitochondria membrane potential, Benznidazole has similar mechanism

30
Q

Nifurtimox/Benznidazole

A 
Chagas disease (T. cruzi)
well absorbed from GI tract, no IV administration necessary.
Nifurtimox induces oxidative stress due to inhibition by NAD(P)H-dependent dehydrogenases with subsequent impairment of mitochondria membrane potential, Benznidazole has similar mechanism
31
Q

Nifurtimox/Benznidazole specificity

A

This drug class requires a bacterial-like Type I nitroreductase to turn it from a prodrug to the active form. Trypanosomes have one, typical eukaryotic cells do not.

32
Q

African Sleeping Sickness Causative agent

A

Trypanosoma brucei

ALWAYS EXTRACELLULAR

33
Q

T. brucei lifecycle

A
  1. Tsetse fly takes blood meal - injects metacyclic trypomastigotes –> injected metacyclic trypomastigotes transform into blood stream trypomastigotes which are carried to other sites –> multiply by binary fission in various body fluids –> trypomastigotes in blood taked up by tsetse fly again –> transform into procyclic trypomastigotes in midgut - multiply –> leave midgut and transform into epimastigotes - multiply in salivary gland = metacyclic trypomastigotes
34
Q

Tsetse Fly transmits two subspecies of Trypanosoma brucei that infect humans:

A

Trypanosoma brucei gambiense, West Africa
Less severe, longer lasting
African Sleeping Sickness

Trypanosoma brucei rhodesiense, East Africa
More acute illness

35
Q

First Stage ASS

A

First stage: possible chancre at site of bite, fever, headache, swollen lymph nodes, muscle and joint aches, possibly rash or itchiness

36
Q

Second Stage ASS

A

Second stage: CNS involvement, neurological symptoms include Somnolence (extreme sleepiness, esp. at inappropriate times), altered gait, tremors, cranial neuropathies, urinary incontinence, personality changes

37
Q

Time scale ASS:

A

gambiense: CNS involvement after 1-2 yrs, death usually in 3 if not treated
rhodesiense: CNS involvement after a few weeks, death in a few months if not treated

38
Q

T. b. gambiense antigenic variation

A

“Waves” of parasitemia are a major challenge to the immune system.
Not intracellular so immune system should find - organisms switch surface proteins/antigens to proliferate and evade immune system

39
Q

Dx ASS

A

Positive diagnosis is finding organisms in blood (special labs do this test), and in CSF if in second stage

40
Q

Tx ASS?

A

YES

The earlier the better! Sleeping sickness is Invariably fatal unless treated (waves of parasitemia)

41
Q

ASS prevention

A

No vaccine or preventative is available

42
Q

ASS meds

A

Suramin: Has an inhibitory effect on enzymes of the pentose phosphate and glycolytic pathways. Selectively accumulates in trypanosomes.

Pentamidine: Possible mechanism: interference with DNA replication of its unique mitochondrial genome. Selectively accumulates in trypanosomes.

Eflornithine: inhibits ornithine decarboxylase, which turns over faster in human cells than in trypanosomes

Melarsoprol: Unknown mechanism, may relate to metabolism

43
Q

Nitrofurtimox and ASS

A

Has good absorption from GI tract (other don’t - give IV) but can’t cross BBB to CSF (co-treat with eflornithine)

44
Q

Lymphatic filariasis (elephantitis) causative agent

A

tissue nematode Wuchereria bancrofti

transmitted by female mosquito

45
Q

Wuchereria bancrofit lifecycle

A

Mosquito takes blood meal - L3 larvae enter skin –> adults into lymphatics - sexually reproduce to produce sheathed microfilaraie that migrate into lymph and blood channels –> mosquito takes blood meal and microfilariae –> shed sheaths, penetrate mosquito’s midgut and migrate to thoracic muscles –> L1 larvae –> L3 larvae –> migrate to head and proboscis

46
Q

Lymphatic filariasis epidemiology

A

Endemic to tropical areas in Asia, Africa, the Western Pacific, and parts of the Caribbean and South America.

47
Q

Lymphatic filariasis shortened lifecycle

A

Larvae enters skin and gains access to the lymphatic system where it matures to adult worms. The adult worms only live in the human lymph system

48
Q

Lymphatic filariasis clinical presentation

A

lymphedema and elephantiasis and in men, swelling of the scrotum, called hydrocele. Lymphatic filariasis is a leading cause of permanent disability worldwide.
Most individuals infected never develop clinical symptoms, or if they do, these symptoms appear years after initial infection. However, it may impact functioning of the lymphatic system, which in turn means the individual cannot fight bacterial infections as effectively.

49
Q

Lymphatic filariasis dx

A

most typical is blood smear. Microfilariae that cause lymphatic filariasis circulate in the blood at night. Blood collection should be done at night to coincide with the appearance of the microfilariae. Alternately, elevated levels of antifilarial IgG4 in the blood can be detected with a serological assay.

50
Q

LF prevention

A

No vaccines or preventatives, but MDA have been successful at wiping out the disease in certain foci, also important is mosquito control.

51
Q

Tx LF?

A

Depends on whether infection in active or not
Lymphedema and elephantiasis are not indications for DEC treatment because most people with lymphedema are not actively infected with the filarial parasite. Hygiene assistance suggested. The treatment for hydrocele is surgery

52
Q

LF tx

A

Diethylcarbamazine (DEC) administered orally, kills microfilaria and some adult worms. No longer FDA approved. Mechanism of action is on the arachidonic acid metabolic pathway in microfilaria. Generally well tolerated; however, DEC should not be administered to patients who may also have onchocerciasis as DEC can worsen onchocercal eye disease. In patients with loiasis, DEC can cause serious adverse reactions, including encephalopathy and death. Doxycycline????

53
Q

Toxoplasmosis causative agent

A

Caused by Toxoplasma gondii parasite

54
Q

Spread of toxoplasma gondii parasite

A

ingested as a tissue cyst (uncooked meat) or an Oocycst from unwashed produce or cat feces.
Also, in its life cycle, it forms muscle tissue cysts in its non-definitive hosts, which is one of the ways it is transmitted to humans.

55
Q

Toxoplasma is a ________ parasite

Intracellular encystment is in host _____ and ______ cells

A

neurotropic

muscle and brain cells

56
Q

Toxoplasmosis is opportunistic (2 populations?)

A 
Immunocompromised- cerebral abscesses, fever, confusion, HA, seizures, nausea, poor coordination
Ocular toxoplasmosis (headlight in fog lesion)

A fetus if the mother is first infected during that pregnancy –>
Stillbirth or miscarriage
Abnormal head size (small or large)
May seem normal at birth but later develop:
vision loss, mental disability, and seizures

The earlier in pregnancy the infection occurs, the more severe the symptoms

57
Q

Ocular toxoplasmosis

A

most common: red, painful, photophobic eye, with some decrease in visual acuity.”headlight in the fog” lesion with multiple surrounding healed chorioretinal scars in one eye (need not be immunocompromised to get ocular toxoplasmosis, but more likely)

58
Q

Toxoplasmosis dx

A

Serological testing is possible, but diagnosis requires some estimate of time of infection

59
Q

Toxoplasmosis prevention

A

Vaccines are not available

60
Q

Toxoplasmosis tx?

A

Not for most patients. Most will recover w/out tx, asymptomatic anyway
Pregnant women, newborns, and infants will need to be treated but note the caveats
Patients with ocular toxoplasmosis if the size, location, or characteristics of the lesion (actively growing) warrant it should be treated
The immunocompromised should be treated, until they have improvements in their condition
AIDS patients may require lifelong treatment as long as they remain immunosuppressed

61
Q

Apicomplexans

A

Toxoplasma, babesia, malaria

62
Q

Toxoplasmosis tx options

A

Some antimalarial combos also work on Toxoplasma and Babesia (apicomplexans)
High concentration in tissues over long times is desired -
Atovaquone

Folate antagonist combo**
Sulfadiazine (Fundamentals) and Pyrimethamine (anti-malarial)
Folinic acid often co-administered
Specificity…T. gondii cannot utilize presynthesized folinic acid

Pregnant women shouldn’t use these drugs unless extreme circumstances warrant its use, instead, the experimental spiramycin could be obtained from the FDA. Does not cross placenta. A macrolide - prevent peptidyltransferase from adding the growing peptide attached to tRNA to the next amino acid, inhibiting ribosomal translation, premature dissociation of the peptidyl-tRNA from the ribosome.

63
Q

Suramin

A
  • inhibitory effect on enzymes of PPP and Glycolytic pathways, trypanosomes (ASS)
64
Q

Pentamidine

A
  • interference w/ DNA replicatoin of unique mitochondrial genome (ASS)
65
Q

Eflornithine

A
  • inhibits ornithine decarboxylase, which turns over faster in human cells than trypanosomes (ASS)
66
Q

Melarsoprol

A
  • unknown MOA (ASS)
67
Q

African Sleeping Sickness Hallmarks

A

T. brucei
Enters into bloodstream
Bloodstream CNS

68
Q

Chagas hallmarks

A

T. cruzi
Enters mucosal tissue/dermal cells
bloodstream, cardiac, GI

69
Q

Leishmaniasis hallmarks

A

Leishmania spp
Enters via skin macrophage
Skin, systemic

70
Q

Toxoplasmosis hallmarks

A

Toxoplasma gondii
Enters via GI tract
GI, brain tissue, fetus, eyes

71
Q

Onchocerciasis hallmarks

A

Onchocerca volvulus
Enters via SubQ
Skin and Eyes

72
Q

Lymphatic filariasis

A

Wucheria bancrofti
Enters via skin
Lymphatic tissue

Skin MS: Week 4 (10 decks)

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