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W2P1 Flashcards

1
Q

Vector of Malaria

A

Anopheles mosquitoes

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2
Q

Vector of Dengue

A

Aedes mosquitoes

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3
Q

Vector for Chikungunya

A

Aedes mosquitoes

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4
Q

Vector for ZIKA

A

Aedes mosquitoes

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5
Q

Vector for Lyme disease

A

Ixodes ticks

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6
Q

Vector for Leishmaniasis

A

Sandflies

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7
Q

Vector for African Tryp

A

Tse Tse flies

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8
Q

Vector for American Tryp

A

Triatomine

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9
Q

Vector for Rickettsia

A

Lice
Ticks
Other arthropods

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10
Q

Arthropods

A

Arthropods are members of the phylum Arthropoda, which means “jointed leg.” Arthropods include insects, arachnids, and crustaceans

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11
Q

Anopheles Mosquito

- what is the life cycle**

A

Parasite of human RBCs- MALARIA
THE parasitic killer of human beings

90% of deaths in sub-Saharan Africa*
Transmitted by Anopheles mosquitoes

LIFE CYCLE
A. infection, a bite
B. Sporozoites released and invade hepatocytes = LIVER STAGE, they multiply
C. Meroziotes get released into the blood = BLOOD stage, they for a ring, asexual reproduction cycle. they they burst/hemolytic and infect other RBCs

D. Small percentage will enter sexual stage: gemtocytes which will then be passed on to next mosquito that bites infected host = TRANSMISSION stage

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12
Q

At what stage of Malaria cycle does the infected host start to feel symptoms?

A

During the LIVER STAGE there are NO symptoms, this is the incubation period it takes to mature

only once it enters the BLOOD stage (7-30 days later) do we get symptoms: high fever + shaking chills

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13
Q

Anopheles Mosquito

  • Vector for which illness
  • When does it bite?
  • Inactive in what conditions
A

vector for Malaria

Bite dusk to dawn
Only females
Inactive below 18°
Altitude sensitive

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14
Q

Anopheles Mosquito

  • vector for what
  • What are the known effective repellents?
  • don’t like what type of environment?
A

Vector for Malaria

DEET and picaridin are the ONLY effective repellents
Permethrin-treated clothes/nets/curtains
Don’t like cities*

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15
Q

Why are there prevalence differences in the areas where falciparum malaria occurs?

A

even though falciparum malaria exists in many places, only the places with EFFICIENT VECTORS lead to endemics and threats to human

so the TYPE OF VECTOR plays an important role**

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16
Q

Aedes Mosquito

  • vector for
  • what environment is is emerging in
  • what are the two types
  • overtaking malaria as the…
A

Vector for DENGUE/CHIK/ZIKA/YF 


Emerging URBAN VECTOR-BORNE disease
- Very infectious* = Incidence 30X in last 50 years

Dengue vs dengue hemorrhagic fever
Overtaking malaria as leading cause of fever in returning travellers from several places

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17
Q

Dengue Fever vs Dengue Hemorrhagic Fever (DHF)

A

Despite the name, the critical feature that distinguishes DHF from dengue fever is not hemorrhaging, but rather plasma leakage resulting from increased vascular permeability

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18
Q

Aedes Mosquito

  • vector for
  • time it bites
  • inactive when
  • what are the ONLY effective repellents ?
  • where do they thrive
A

Vector for: DENGUE/CHIK/ZIKA/YF 


DAYTIME BITERS
Only females
Inactive below 18°
*DEET and picaridin are the ONLY effective repellents*
Permethrin-treated clothes/nets/curtains
Thrive in cities and elsewhere
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19
Q

Anopheles vs Aedes Mosquito, what are the

  • Differences
  • Similarities
A

Differences:

  1. Time it bites
    Anopheles - bites dusk to dawn, night time
    Aedes - bites in the DAYTIME
  2. Area of preference
    Anopheles - DON’T like cities
    Aedes- THRIVE in cities. #citygirls
Similarities
1. only females bite, hehehe
2. INACTIVE below 18 degrees
3. DEET and picaridin are the ONLY effective repellents
Permethrin-treated clothes/nets/curtains
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20
Q

ZIKA

  • what is it’s vector
  • which virus
  • why did it get attention
A

Aedes mosquitos
Flavivirus closely related to Dengue, YF, JEV, SLE

2015-2016: Exploded onto the scene, Americas
Association with rise in microcephaly cases, Brazil

1 Feb 2016: “Public Health Emergency of international concern” WHO

mid-2016: Causal link established for CONGENITAL syndrome

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21
Q

ZIKA infection in adults

A

Incubation usually 2 to 14 days

Resolves spontaneously

Approx 80% asymptomatic

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22
Q

ZIKA most severe in which type of patients?

  • symptoms in these patients
  • similar to rubella because…
A

CONGENITAL ISSUES, i.e. VERTICAL TRANSMISSION

mother infected can have baby with
- seizures, microcephaly, facial distortions, delays in cognitive development

First time we face infectious epidemic teratogen since rubella

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23
Q

How is ZIKA transmited

A

Primarily vector borne transmission

HOWEVER can also be transmitted SEXUALLY so important to use protection after travelling to high risk countries for atleast 6 months

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24
Q

Where should you check for ticks

A
  • In and around the hair
  • in and around the ears
  • under the arms
  • bra lin
  • inside belly button
  • groin area
  • back of the knees
  • any creases
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25
Q

Lyme disease Life Cycle

- what season is risk of human infection greatest?

A
  • In late spring and summer
  • these are the BLACK LEGGED ones

This life cycle is more complex

  1. eggs
  2. Larva : a distinct juvenile form many animals undergo before metamorphosis into adults in BIRDS AND MICE
  3. Nymph: dear and other mammals
  4. Adults: in dear and humans
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26
Q

What is the #1 vector borne disease in NA

A

Lyme Disease

  • southern border of Canada, along american border*
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27
Q

Clinical manifestations of Lyme disease in UNTREATED infections

A

these are experts at evading immune system so they will manifest as MULTIPLE stages of infection

Early infection

a. localized stage = Erythema Migrans
b. disseminated stage, if untreated = meningitis, bell’s palsy

Late infection
- prolonged arthritis attacks

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28
Q

Treatment of Lyme disease

- word on retreatment?

A

Give Oral antibiotics THEN Treat symptomatically*
- if they have meningitis give X, carditis give Y, arthritis give Z etc

10% of treated pts continue to have subjective symptoms
MSK, neuro, fatigue, etc.

4 dbpc-RCT = NO BENEFIT FROM MORE ABX
- no such thing as chronic lyme disease? no point in giving MORE treatment, it is ineffective

High complication rate (line infections, PE, allergy, GB, c.diff)

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29
Q

Methods to PREVENT ticks

A
  • to prevent i.e. Lyme disease

Preventing tick bites

  • extra vigilance in the summer months
  • habit to scan body for ticks latched on
  1. Avoid direct contact
    - Avoid wooded and busy areas with high grass and leaf litter
    - walk in the center of trails
  2. Repel Ticks with DEET or PERMETHRIN
  3. Find and remove ticks from your body
    - bath and shower right away
    - full body scan
    - examine gear and pets
    - tumble clothes in a dryer on high heat to kill remaining ticks
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30
Q

Lyme should be considered as able to cause many ______

A

Lyme should be considered as able to cause many NEUROPATHOLOGIES

Seropositivity is the sine qua non of diagnosis

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31
Q

Antibiotic-Refractory Lyme

  • when does it occur
  • chronic symptoms?
A

Antibiotic-refractory Lyme occurs rarely

  • No ongoing infection in these cases*
  • Strong evidence support auto-immunity (HLA associations, demonstrable sterilization, strain-dependent)

Post-Lyme syndrome (among proven treated cases) must be distinguished from other “Chronic Lyme” suspicions

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32
Q

Lyme Disease is a real infection with:

A
  • known cause
  • well characterized diagnostic methods
  • effective treatments
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33
Q

Intestinal Nematodes

- list all 5 we learned about

A 
Trichuris
Enterobius
Ascaris
Strongyloides*
hookworm
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34
Q

What is special about strongyloides

A

Stronglyoides needs special consideration

All these nematodes have a life span, if you don’t get re-infected, the worm will get old and just DIE, you’ll be rid of it.

Strongyloides is the EXCEPTION, it will multiply in the human host and NEVER go away. Can become a high burden, especially if you are immunosuppressed

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35
Q

Systemic nematodes

- List the ones we’ve learned about

A
  1. Trichinella
  2. Toxocara
  3. Filaria
    • lymphatic
    • Loa loa
    • Onchocerca
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36
Q

Intestinal Helminths are what kind of worm?

A

I THINK

Roundworms

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37
Q

Round Worm Characteristics

- how many larval stages

A

Round in cross section

Digestive system complete – mouth to anus

Acellular cuticle

Four larval stages

Subcuticular layer of muscle

Separate sexes

Terms: egg (ova)
embryo
larva
adult

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38
Q

Alternative name for Trichuris Trichiuria

A

Whipworm
(head is the thinner part)

[This is an intestinal nematode under Helmints]

39
Q

Trichuris trichiura

  • Geography
  • route of transmission
  • Presentation in what organ

Clinical presentation in
Canada VS Tropics

A

Geography: tropical esp. SE Asia, 
 Phillipines, Dominica

Risk: fecal oral transmission

Presentation: colon

Presentation in

CANADA:
asymptomatic

no eosinophilia

TROPICS
[worm load dependent]
diarrhea
hypertrophic osteoarthropathy
* dysentery

* prolapsed rectum
* iron deficiency anemia
  • because: We get eosinophilia when worms are migrating through tissues but NOT when worms are just chilling and livin in the lumen





40
Q

Life Cycle of Trichuris Trichiura

A
  1. Human feces used as fertilizer in soil
  2. 2-3 weeks in soil before it becomes infective
  3. humans eat plants the grew in that fecal contaminated soil and get infected themselves
  4. trichuris then lives in our colons* until we poop again and the cycle continues
41
Q

Enterobius vermicularis

is what kind of worm

A

pinworm

42
Q

Enterobius vermicularis

Geography
Risk
Presentation

Symtpoms in
Canada vs Tropics

A

Geography…universal
Risk……… small children
Presentation… colon, anus

THE SAME
Canada
 asymptomatic
 perianal itch
recurrent UTIs 
in female children

Tropics 
asymptomatic
 perianal itch
recurrent UTIs 
in female children

43
Q

life cycle of Enterobus

A

lays eggs at night in
 perianal folds

eggs become infective
 in 4-6 hours

eggs can survive in
 carpet for 2 weeks

eggs laid by adult after
 2 months in colon

adult female lives 2-3 
 months

44
Q

What can be used to diagnose Enterobius Vermicularis?

A

aka pinworm

you can use the pinworm paddle

45
Q

Ascaris lumbricoides

- what type of worm

A

roundworm

46
Q

Ascaris lumbricoides
Geography
Risk
Presentation

symptoms in Canada Vs the Tropics

A

Geography…. World wide in the tropics
Risk………… Fecal oral
Presentation.. small intestine

Symptoms

Canada
 asymptomatic

Tropics 
abdominal pains
?
malnutrition?
 
small intestine obstruction
 
biliary tree obstruction
 
perforation of intestine suture
47
Q

Life cycle of Ascaris lumbricoides

A

18-24 days to embryonate

2-3 mo to start egg production


live 1-2 years


48
Q

What are the two Hookworms we learned about

A

Ancylostoma duodenale

Necator americana

49
Q

Ancylostoma duodenale/ Necator americanum



A

Geography…. worldwide in tropics



Risk….. Contact with feces contaminate soil



Presentation….
Canada
: asymptomatic

eosinophilia

Tropics
 minor abdominal pains

iron deficiency
anemia 
malnutrition


50
Q

Life cycle of Ancylostoma duodenale/ Necator americanum

A

eggs in human feces

grow in soil

human steps in contaminated soil and gets infected

51
Q

Difference between roundworms, whipworms and hookworms in terms of AGE of peak intensity

A

The first two: roundworms and whipworms are feceal oral, so as kids your at higher risk…. as you get older, adults eat less poop so the infection rate is lower in adults

However, hookworms is through contact in the soil, and in this case, adults are as likely to walk bare foot as are children so the risk relative to age is still high in adults.

52
Q

Strongyloides stercoralis

A

Geography…scattered tropical
Risk……contact with feces contaminated soil immunocompromised (not AIDS) 
 HTLV1

Presentation…..
Canada
 
asymptomatic

dyspepsia

cutaneous larva currens

eosinophilia

disseminated strongyloides
Tropics 

asymptomatic

dyspepsia

cutaneous larva currens

eosinophilia

disseminated strongyloides
*chronic diarrhea, weight loss* [the only difference]
53
Q

Diagnosis for Strongyloides Stercoralis

A

Diagnosis
Agar plate culture
Serology * [The other ones don’t have serology cause they stay in the lumen ]

THIS ONE does have serology

The actuall disease has to do with disseminating into other parts of the body but its home is the intestine

Treatment
Ivermectin
Albendazole

54
Q

Disseminated Strongyloidiasis in the Immunocompetent vs immunosuppressed (HTLV1, Steroids etc)

A

Immunocompetent
limits adults and larvae to submucosa of small intestine
severely limits autoinfective cycle

Immunosuppressed (HTLV1, steroids etc.)
no limit to dissemination of larvae (wandering through body)
larvae carry intestinal bacteria
peritonitis
pneumonitis
meningitis
necrosis of intestine wall

55
Q

Which two are the larger nematodes that you’d actually be able to SEE passed in the stool?

A

Ascaris Lumbricoides and pinworm [Enterobius Vermicular]

56
Q

Trichinosis

A

NOT a tropical disease. due to poor animal food hygiene

Trichinosis is a food-borne disease caused by a microscopic parasite called Trichinella. People can get this disease by eating raw or undercooked meat from animals infected with the parasite. Often these infected meats come from wild game, such as bear, or pork products.

57
Q

Two Types of Trichinella

A

Trichinella spiralis

Trichinella nativa

58
Q

Trichinella Life cycle

A

Starts through CONSUMPTION of contaminated food. It multiplies in the small intestine and travels to the STRIATED MUSCLE

(where we bite into when we eat animals) - walrus, pig, human- ANY CARNIVORE

  • cooking the meat/vegetables reduces infectivity
59
Q 
Trichinella spp.
Reservoir
Location 
Longevity 
Biology
Transmission
A

reservoir…muscles of all carnivorous
animals (bear, walrus, rat, man, pig)

location…encysted in individual striated
muscle cells

longevity…years

biology…T. nativa resists freezing

transmission…raw meat ingestion

60
Q

Trichinella spp.

A

reservoir…muscles of all carnivorous
animals (bear, walrus, rat, man, pig)

location…encysted in individual striated
muscle cells

longevity…years

biology…T. nativa resists freezing

transmission…raw meat ingestion

61
Q

Trichinella spp.

Classic vs Diarrheic Symptoms

A

Myopathic (classic)

muscle pain, weakness
fever
edema

CK
eosinophils
trichinella IgG
trichinella IgM
positive muscle biopsy
 EMG abnormal

Diarrheic

diarrhea
no fever*
no edema*

normal CK
eos
trichinella IgG

neg muscle box
EMG normal

62
Q

Diagnosis of Trichonella

A 
DIAGNOSIS
Symptoms
Eosinophilia
CK
Serology
biopsy

TREATMENT
albendazole
prednisone

63
Q

Which is a zoonosis?

A 
Trichinellosis
Strongyloides stercoralis
Trichuris trichiura
Ancylostoma duodenale
Enterobius (pinworm)
Ascaris lumbricoides
64
Q

How are HOOKWORMS different form the other ones we learned about?

A

Most of the other worms mentioned are commensal, they just occupy space and share your meals

HOOKWORM however is DIFFERENT: it bites into the mucousa and LIVES IN YOUR BLOOD

Hence why you get iron deficiency anemia

65
Q

Why do you get Dyspensia and Eosinophillia with Strongyloides

A

Eosinophilia: OFTEN present, because it is a continious cycle where it leaves the small bowel (unlike others where it stays in one place

same reason it causes dyspensia

66
Q

Toxocara canis

  • Distribution
  • Presenation
A 
visceral larva migrans
weakness
		pruritis
		rash/uriticaria
		dyspnoea
		abdominal pain
		dizziness
		cough
		weight loss
		fever and 
EOSINOPHILIA
67
Q 
Toxocara canis (visceral larva migrans)
CT
Laparoscopy 
Biopsy 
Serology
A

CT…………..scattered hypodense abscess-like
1-7 cm lesions

Laparoscopy…gray/yellow/tan round to “sinuous”
nodules on liver surface

Biopsy……..necrotic eosinophilic granulomas

Serology……sensitivity ~78 %

68
Q

Which Nematodes have SEVER eosinophil levels

A

Trichinella

Ancylostoma/Necator Americanum

Toxocara

Fasciola

69
Q

Which nematodes have NO eosinophil levels

A

giardia

amoeba

70
Q

Filariasis

  • location
  • require WHAT?
A

Nematoda
Systemic round worms
I.E. Loa, onchocerca, Wuchereria

a roundworm

Adult filaria live in body cavities, lymphatics,
and subcutaneous tissues

larvae (microfilaria) live in blood or dermis

all require an insect or crustaean vector

microfilaria (150-350 µ long) (4 – 10 µ wide)

adults 2 cm – 120 cm, 1mm wide or less

71
Q

River blindness is caused by?

A

Filaria- Onchocerca Volvulus

vector: black fly

(all require an insect or crustaean vector)

72
Q

Wuchereria bancrofti

Brugia malayi

A

These are a COMMON type of FILARIA that leads to
- lymphatic filariasis elephantiasis

and their vector is mosquito

73
Q

Clinical presentations of Wuchereria bancrofti

A
  1. assymptomatic
  2. inflammatory - lymphangitis - arms 25%
    - legs 11%
             - epididimitis, funiculitis 42%
         - ‘filarial fevers’
         - orchitis
         - filarial abscess
  3. Obstructive - elephantiasis
    • chyluria
    • hydrocoele
  4. Tropical pulmonary eosinophilia
74
Q

blood microfilaria

A

1 – direct examination (thick or thin smear)

2 – Knotts concentration technique

3 – millipore filtration

4 – antigen capture (Wb), PCR

serology

75
Q

Loa loa

  • presentation
A

Type of Filaris (the blood inhabiting one)
called the “eye worm”

Calabar swelling

76
Q

Immune tolerance: Age at first infection

A

Infected as a child, human worm, you develop tolerance

Then it develops as a lot of worms in the blood but immune system does NOTHING because fool us to think it is host

So you get no symptoms. When you get infected as a visitor to endemic area, you develop immune response and symptoms

So we see the infections in adults

But not in kids who have developed tolerance and no symptoms

77
Q

Onchocerca volvulus

A

Type of Filaris
“ River Blindness”

VECTOR: black fly

  • you get nodules
78
Q

Hyphae

A

Filamentous tubular structure with and with or without internal septae

79
Q

Mycelium

A

Mycelium

Group of hyphae, often used interchangeably with hyphae

80
Q

Yeast

A

Yeast

Unicellular round fungal cells that reproduce by budding

81
Q

Conidia

A

Asexual spores of ascomycetes (most pathogenic phylum)

82
Q

Conidiophore

A

Specialized hyphae that produce conidia

83
Q

The Big Two Morphologies

A

Yeast vs. Mold

84
Q

Antifungal agents

A

Antimicrobial agents must exploit differences between microorganisms and humans
Much greater challenge than with bacteria as fungi are eukaryotic and closely related to humans
Ribosomes and DNA replication enzymes are too similar for targetting
First antifungals developed were highly toxic

85
Q

The three targets of Antifungal Therapy

A

Cell membrane
Fungi use principally ergosterol instead of cholesterol

DNA Synthesis
Some compounds may be selectively activated by fungi, arresting DNA synthesis.

Cell Wall
Unlike mammalian cells, fungi have a cell wall

86
Q

List Cell Membrane Active Antifungals

A

Azoles
Allyamines
Polyenes

Azoles
Inhibit 14 alpha demethylase
Key enzyme to synthesize ergosterol
Toxic intermediates accumulate in the membrane

Allylamines
Inhibit squalene epoxidase early in ergosterol pathway
Polyenes
Binds to ergosterol in membranes
Forms pores allowing cell contents to leak out

87
Q

Polyenes

A

Nystatin
Highly toxic – topical only

Amphotericin B deoxycholate
Slightly less toxic but binds cholesterol
Renal failure, severe infusional toxicity
Lipid-based formulations of

Amphotericin
Reduced toxicity by using a lipid carrier intermediate in solubility between ergosterol and cholesterol
VERY expensive but broadest spectrum agents available

88
Q

Azoles

A

Yeast only activity
Fluconazole. Very non-toxic.

Yeast and mold activity
Itraconazole is oldest, but has poor absorption and erratic kinetics
Voriconazole, isavuconazole and posaconazole are newest and have excellent anti-mold activity, particularly Aspergillus species.

Toxicities
Hepatitis – all agents – VORI>ITRA>ISA>POSA>FLU
Visual hallucinations and skin cancer with voriconazole

89
Q

Allylamines

A

Terbinafine (lamisil)
Primarily used for superficial fungal infections

Most common topically

Oral is also available for extensive infections or nail infections
Can be used synergistically with azoles

Side effect – hepatitis

90
Q

Antifungal that targets DNA synthesis

A

5-Flucytosine (5-FC)

A prodrug converted by fungal cytosine deaminase into 5-flourouracil
Inhibits DNA chain synthesis
Type of chemotherapeutic
Toxicity is bone marrow suppression
Only useful in combination therapy for Cryptococcus

91
Q

Antifungal that targets Cell Wall Active Agents

A

Echinocandins

Caspofungin, micafungin, anidulafungin
Inhibit synthesis of cell wall β-glucan
Cause cell wall fragmentation
Not active on fungi with low levels of β-glucan
No significant toxicities or differences between agents
IV only

92
Q

Which antifungals are toxic to the liver?

A

azoles

93
Q

Which is the safest antifungal?

A

the ones that acts against the cell wall: Echinocandins

Block G (10 decks)

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