W2P1 Flashcards

(93 cards)

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
Lyme disease Life Cycle | - what season is risk of human infection greatest?
- 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
26
What is the #1 vector borne disease in NA
Lyme Disease - southern border of Canada, along american border*
27
Clinical manifestations of Lyme disease in UNTREATED infections
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
28
Treatment of Lyme disease | - word on retreatment?
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)
29
Methods to PREVENT ticks
- to prevent i.e. Lyme disease Preventing tick bites - extra vigilance in the summer months - habit to scan body for ticks latched on 2. Avoid direct contact - Avoid wooded and busy areas with high grass and leaf litter - walk in the center of trails 3. Repel Ticks with DEET or PERMETHRIN 4. 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
30
Lyme should be considered as able to cause many ______
Lyme should be considered as able to cause many NEUROPATHOLOGIES Seropositivity is the sine qua non of diagnosis
31
Antibiotic-Refractory Lyme - when does it occur - chronic symptoms?
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
32
Lyme Disease is a real infection with:
- known cause - well characterized diagnostic methods - effective treatments
33
Intestinal Nematodes | - list all 5 we learned about
``` Trichuris Enterobius Ascaris Strongyloides* hookworm ```
34
What is special about strongyloides
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
35
Systemic nematodes | - List the ones we've learned about
1. Trichinella 2. Toxocara 3. Filaria - lymphatic - Loa loa - Onchocerca
36
Intestinal Helminths are what kind of worm?
I THINK Roundworms
37
Round Worm Characteristics | - how many larval stages
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
38
Alternative name for Trichuris Trichiuria
Whipworm (head is the thinner part) [This is an intestinal nematode under Helmints]
39
Trichuris trichiura - Geography - route of transmission - Presentation in what organ Clinical presentation in Canada VS Tropics
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
Life Cycle of Trichuris Trichiura
1. Human feces used as fertilizer in soil 2. 2-3 weeks in soil before it becomes infective 2. humans eat plants the grew in that fecal contaminated soil and get infected themselves 3. trichuris then lives in our colons* until we poop again and the cycle continues
41
Enterobius vermicularis | is what kind of worm
pinworm
42
Enterobius vermicularis Geography Risk Presentation Symtpoms in Canada vs Tropics
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
life cycle of Enterobus
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
What can be used to diagnose Enterobius Vermicularis?
aka pinworm | you can use the pinworm paddle
45
Ascaris lumbricoides | - what type of worm
roundworm
46
Ascaris lumbricoides Geography Risk Presentation symptoms in Canada Vs the Tropics
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
Life cycle of Ascaris lumbricoides
18-24 days to embryonate 2-3 mo to start egg production
 live 1-2 years

48
What are the two Hookworms we learned about
Ancylostoma duodenale Necator americana
49
Ancylostoma duodenale/ Necator americanum


Geography…. worldwide in tropics

 Risk….. Contact with feces contaminate soil

 Presentation…. Canada
: asymptomatic
 eosinophilia Tropics
 minor abdominal pains 
iron deficiency anemia 
malnutrition

50
Life cycle of Ancylostoma duodenale/ Necator americanum
eggs in human feces grow in soil human steps in contaminated soil and gets infected
51
Difference between roundworms, whipworms and hookworms in terms of AGE of peak intensity
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
Strongyloides stercoralis
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
Diagnosis for Strongyloides Stercoralis
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
Disseminated Strongyloidiasis in the Immunocompetent vs immunosuppressed (HTLV1, Steroids etc)
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
Which two are the larger nematodes that you'd actually be able to SEE passed in the stool?
Ascaris Lumbricoides and pinworm [Enterobius Vermicular]
56
Trichinosis
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
Two Types of Trichinella
Trichinella spiralis Trichinella nativa
58
Trichinella Life cycle
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
``` Trichinella spp. Reservoir Location Longevity Biology Transmission ```
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
Trichinella spp.
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
Trichinella spp. | Classic vs Diarrheic Symptoms
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
Diagnosis of Trichonella
``` DIAGNOSIS Symptoms Eosinophilia CK Serology biopsy ``` TREATMENT albendazole prednisone
63
Which is a zoonosis?
``` Trichinellosis Strongyloides stercoralis Trichuris trichiura Ancylostoma duodenale Enterobius (pinworm) Ascaris lumbricoides ```
64
How are HOOKWORMS different form the other ones we learned about?
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
Why do you get Dyspensia and Eosinophillia with Strongyloides
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
Toxocara canis - Distribution - Presenation
``` visceral larva migrans weakness pruritis rash/uriticaria dyspnoea abdominal pain dizziness cough weight loss fever and EOSINOPHILIA ```
67
``` Toxocara canis (visceral larva migrans) CT Laparoscopy Biopsy Serology ```
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
Which Nematodes have SEVER eosinophil levels
Trichinella Ancylostoma/Necator Americanum Toxocara Fasciola
69
Which nematodes have NO eosinophil levels
giardia amoeba
70
Filariasis - location - require WHAT?
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
River blindness is caused by?
Filaria- Onchocerca Volvulus vector: black fly (all require an insect or crustaean vector)
72
Wuchereria bancrofti | Brugia malayi
These are a COMMON type of FILARIA that leads to - lymphatic filariasis elephantiasis and their vector is mosquito
73
Clinical presentations of Wuchereria bancrofti
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
blood microfilaria
1 – direct examination (thick or thin smear) 2 – Knotts concentration technique 3 – millipore filtration 4 – antigen capture (Wb), PCR serology
75
Loa loa - presentation
Type of Filaris (the blood inhabiting one) called the "eye worm" Calabar swelling
76
Immune tolerance: Age at first infection
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
Onchocerca volvulus
Type of Filaris " River Blindness" VECTOR: black fly - you get nodules
78
Hyphae
Filamentous tubular structure with and with or without internal septae
79
Mycelium
Mycelium | Group of hyphae, often used interchangeably with hyphae
80
Yeast
Yeast | Unicellular round fungal cells that reproduce by budding
81
Conidia
Asexual spores of ascomycetes (most pathogenic phylum)
82
Conidiophore
Specialized hyphae that produce conidia
83
The Big Two Morphologies
Yeast vs. Mold
84
Antifungal agents
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
The three targets of Antifungal Therapy
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
List Cell Membrane Active Antifungals
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
Polyenes
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
Azoles
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
Allylamines
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
Antifungal that targets DNA synthesis
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
Antifungal that targets Cell Wall Active Agents
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
Which antifungals are toxic to the liver?
azoles
93
Which is the safest antifungal?
the ones that acts against the cell wall: Echinocandins