Exam 5 Flashcards

(136 cards)

1
Q

Fungi pathogens are most associated with:

A

Superficial Infections

Allergic Reactions

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2
Q

Are fungi thermotolerant?

A

No, optimal growth temperatures are well below body temperature

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3
Q

Fungal Pathogens two major growth forms:

A

Yeast

Mold

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4
Q

Ability to grow as yeast or hyphae

A

Dimorphism

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5
Q

Are Fungi Eukaryotes or Prokaryotes?

A

Eukaryotes

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6
Q

Glucan is a part of the Fungal Cell Wall. What are the two major types of glucan?

A
  1. B (1,3) glucan
  2. B (1,6) glucan

An important component for immune recognition by the host.

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7
Q

B (1,3) glucan and B (1,6) glucan are both synthesized by

A

B-(1,3)-glucan synthase enzyme

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8
Q

Chitin is also a part of the fungal cell. What is its importance?

A

Structural Component of the wall

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9
Q

Do Fungi produce ergosterol or cholesterol?

A

Ergosterol

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10
Q

Ergosterol is located where in the cell?

A

Fungal Plasma Membrane

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11
Q

Polyenes, Imidazoles, Triazoles, and Allylamines targets what?

A

Ergosterol and Ergosterol Synthesis in Plasma Membrane

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12
Q

_____ binds to ergosterol to form pores.

A

Polyenes

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13
Q

Amphotericin B and Nystatin are types of

A

Polyene

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14
Q

_______ and ______ inhibit fungal lanosterol 14-a-dmethylase to inhibit ergosterol synthesis. Toxic intermediate back up and increased membrance permeability.

A

Imidazoles and Triazoles

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15
Q

Ketoconazole, Itraconazole, Fluconazole, and Voriconazole are types of

A

Imidazoles and Triazoles

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16
Q

_______ inhibit fungal squalene epoxidase to inhibit ergosterol synthesis.

A

Allylamines

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17
Q

Terbinafine is a type of

A

Allylamine

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18
Q

Echinocandines targets

A

Cell Wall - B-(1,3) glucan synthase

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19
Q

__________ inhibits activity of B-(1,3)-glucan synthase depletion of glucans, decreased cell wall integrity.

A

Echinocandins

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20
Q

Caspofungin, Micafungin, and Anidulofungin are types of

A

Echinocandiin

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21
Q

Yeast can cause what disease?

A

Candidiasis, Cryptococcosis, and Pneumocytosis

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22
Q

Is Candididasis endogenous or exogenous?

A

Endogenous

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23
Q

Most common cause of candidemia?

A

C. albicans

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24
Q

Candida is a colonizer where?

A

GI tract, vaginal mucosa, and skin

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25
Is Candidiasis opportunistic? (Needs Conditions (DM, Malnutrition, Immunosuppressive, Trauma) to infect)
Yes
26
Candidemia is
bloodstream infection of candida
27
Manifestations of Candidiasis
In immunocompetent hosts: Thrush, Vaginitis, Cutaneous Lesions In immune suppressed hosts Esophagitis, Chronic Mucocutaneous Candidiasis (CMCC), Disseminated
28
Candidiasis virulence and pathogenesis
Adherence factors - allows yeast and hyphae to attach to tissues "Yeast-to-hyphal" transition - phenotypic switching
29
Treatment of Candida species
Triazole (static) | Echinocandins (Cidal)
30
C. glabrata is resistant to what class of drugs?
Triazoles
31
Clinical Manifestations of Cryptococcosis
Subacute to Chronic Meningitis, Pneumonia, Skin Ulcers, and Bone Lesions Can occur during defective T-lymphocyte function (AIDS, carcinoma, leukemia, Hodgkin's lymphoma
32
Emerging Cryptococcosis pathogen
Cryptococcus gattii
33
Clinical Manifestations of Cyptococus gattii
Causes tumor-like lesions "cryptococcomas" in lungs, brain, and soft tissue. More tolerant to antifungal compounds
34
Virulence and Pathogenesis of Cryptococcosis
Polysaccharide Capsule | Melanin deposited in cell wall (provides stress protection for intracellular survival)
35
Cyptococcus species are susceptible to
Triazoles
36
Pneumocystosis predisposing agents
AIDS, Pulmonary Infections
37
Pneumocystosis virulence an pathogenesis
Major Surface Glycoprotein (MSG) - acts as an attachment factor to several host proteins Histologically - alveoli are filled with foamy exudate
38
Clinical manifestations of Pneumocystosis
Pneumonitis | Lesions outside the lung are common in AIDS patients
39
Treatment of Pneumocystis
Bactrim and Clindamycin
40
Bactrim and Clindamycin are treatment options for Pneumocystis but which drug has a higher incidence of adverse effects in AIDS patients?
TMP-SMX (Bactrim)
41
Are fungi opportunistic or true pathogens?
True Pathogens
42
Fungi are also thermal dimorphism
Body Temp = Yeast | Room Temp = Mold
43
Type of ENDEMIC Thermal Dimorphic Mycoses
Blastomyces dermatitidis Coccidioides immitis Histoplasma capsulatum
44
Endemic Dimorphic Mycoses: Pathogen for Histoplasmosis
H. capsulatum, endemic to the eastern US, near MS and OH river valleys
45
Endemic Dimorphic Mycoses: H. capsulatum and B. dermatitidis transmission
inhalation of airborne conidia (spores)
46
Endemic Dimorphic Mycoses: Histoplasmosis Virulence and Pathogenesis
Inhaled Conidia/spores convert to yeast phase at body temperature Initial infection is pulmonary Reticuloendothelial system is the focus of the infection (lymph nodes, spleen, bone marrow)
47
Endemic Dimorphic Mycoses: Histoplasmosis Clinical manifestations
Dependent on intensity of exposure and immune status of host Low inoculum = asymptomatic Heavy inoculum = primary pulmonary infection Progressive (chronic) pulmonary histoplasmosis Dissemination - higher incidence in children and immunocompromised Calcified Nodules, Granuloma
48
Endemic Dimorphic Mycoses: Blastomycosis Clinical Manifestations
Respiratory Infection - asymptomatic or mild, resolves spontaneously Systemic Blastomycosis - Defects in CMI are predisposing Chronic Cutaneous Blastomycosis - ulcerated lesions, exposed or mucocutaneous tissues
49
Endemic Dimorphic Mycoses: Coccidioidomycosis pathogen
Coccidioides Immitis | Located to the desert southwest US, Mexico, and Guatemala
50
Endemic Dimorphic Mycoses: Coccidioides immitis initiates
Infectious Arthroconida
51
Endemic Dimorphic Mycoses: Coccidioidomycosis Virulence and Pathogenesis
Arthroconidia - highly infectious, but NOT highly virulent
52
Endemic Dimorphic Mycoses: Coccidioidomycosis Clinical Manifestations
Respiratory Infections * Symptomatic Patients - VALLEY FEVER with malaise, cough, chest pain, fever * Filipinos, African/Native Americans & Hispanics are at greatest risk of dissemination
53
Treatment of Endemic Dimorphic Pathogens Blastomyces dermatitidis Coccidioides immitis Histoplasma capsulatum
Triazoles
54
Endemic Dimorphic Mycoses: Pathogen of Sporotrichosis
Sporothrix schenckii
55
Endemic Dimorphic Mycoses: Sporotrichosis is associated with
Decaying Vegetation.. Enters blood via splinter, thorn pricks (gardeners and landscapers)
56
Endemic Dimorphic Mycoses: Sporotrichosis is widely present in
Soil
57
Endemic Dimorphic Mycoses: Clinical Manifestation of Sporotrichosis
Skin Lesion begins as a painless papule (normally on hand or finger) Papule larges and slowly ulcerates Primary pulmonary Sporotrichosis
58
Treatment of Sporotrichosis
Triazoles
59
Characteristics of opportunistic mold
Monomorphic (produce hyphae in vitro and vivo, regardless of temperature
60
Opportunistic Mold can cause what diseases?
Aspergillosis | Mucormycosis (Zygomycosis)
61
Opportunistic Mold: Pathogen for Aspergillosis
Aspergillus fumigatus
62
Opportunistic Mold: Aspergillus fumigatus is present
Air vents and Construction and Remodeling efforts can aerosolize Common contaminant in clinical laboratories
63
Opportunistic Mold: Clinical Manifestations of Aspergillosis
Allergic bronchopulmonary aspergillosis (ABPA) * Elevated serum IgE * Asthma type response Aspergilloma *colonization of paranasal sinuses and the lower airways Occurs in pre-formed cavitary lesions (CF, Chronic Bronchitis, TB) ASYMPTOMATIC Invasive Aspergillosis * Requires pre-existing pulmonary disease or immunosuppression * Colonization of airways leads to localized tissue invasion by hyphae Disseminated Disease * Requires immunocompromised host * Acute Pneumonia
64
Opportunistic Mold: Treatment of Aspergillus spp
Triazoles and Echinocandins
65
Opportunistic Mold: Mucormycosis (Zygomycosis) pathogenesis
Rapidly growing hyphae invade tissue
66
Opportunistic Mold: Mucormycosis (Zygomycosis) Clinical Manifestations
Pulmonary Mucorcycosis Rhinocerebral Mucorcycosis Primary Cutaneous Mucorcycosis (Contaminated Bandages) Disseminated
67
What constitutes a parasite?
Protozoans: single cell organism Helminths: Multicellular flatworms and roundworms
68
How do we become infected by parasites?
Fecal-Oral Food-Borne Vector-Borne Skin-penetrators
69
What kind of hosts do parasites use?
Definitive - contains the sexually mature stages Intermediate - maturational stage Reservoir - an animal which can substitute for humans in a parasite's life cycle Paratenic - maintains the parasite through space and time * *Some parasites use more than 1 host * *Some parasites can convert one type of host to another
70
KEY Parasite Concepts
Parasitic Infection Tend To Be Chronic EXCEPT: Malaria Travel History is often very important to diagnosis Elevated eosinophilia with contributing history may indicate parasitic infection *IgE responses to worm infections attract eosinophils
71
The protozoan parasites
Malaria: Plasmodium spp Blood-Borne Flagellates: Trypanosoma Protozoan infections in AIDS patient: Toxoplasma gondii Sexually Transmitted: Trichomonas Vaginalis
72
Properties of Protozoans
Single Celled, Eukaryotic Organism May be intracellular or extracellular Can live in GI, tissues, or vasculature
73
How do Protozoan exert their effects?
Interfering with nucleic acid synthesis orrrr carbohydrate metabolism
74
This pathogen causes Malaria
Plasmodium spp
75
In Malaria, a parasite growing within RBCs can cause
``` High Fever, Chills, and Profuse Sweating Fever Anemia Tissue Hypoxia Renal Failure Lung Edema Coma ```
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The Plasmodium pathogen is carried by what?
Female Anopheles Mosquito and Human *Different species burst RBC at different times P. vivax and P. ovale Q48H = Tertian malaria P. malariae Q 72 H = Quartan Malaria P. falciparum Q 36-48 H
77
Plasmodium Life Cycle
Mosquito takes a blood meal *injects sporozodes* After Infection of Liver Cell becomes Schzont
78
Malaria - Immunity
Host quickly mounts an immune response Limits multiplication without eliminating infection = premunition Leads to prolonged recovery period marked by recurrent exacerbations Recovery likely requires the concerted effort of T- and B- lymphocytes
79
Which Malaria strands can form intrahepatic cysts that are dormant and survive the host's immunologic attack?
P. vivax and P. ovale
80
P. vivax and P. ovale only infects
immature cells (reticulocytes)
81
P. malariae infects
Senescent Cells
82
P. falciparum infects
Mature RBC (most aggressive infection)
83
Parasites degrade hemoglobin within an acidic food vacuole for
Protein Requirements and Synthesize folate de novo
84
For Malaria, Chloroquine is used for treatment how?
Inhibits heme utilization by erythrocyte forms and ONLY KILLS ERYTHROCYTE FORM (Schizonts)
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For Malaria, Primaquine is used for treatment and kills what Pathogen?
Liver schizonts of P. vivax and P. ovale
86
Prevention Protocols for Malaria
Prevent mosquito bit with pesticides, repellants
87
Mefloquine can be used for Malaria Chemoprophylaxis > 2 weeks before, weekly while in country , and 4 weeks after return, what is the MOA?
Inhibition of Lipid Trafficking and Nutrient Uptake
88
Doxycycline can be used Malaria chemoprophylaxis 1-2 days before, daily while in country, 4 weeks after return and normally least expensive, What is the MOA?
Inhibition of Mitochondrial Protein Synthesis
89
Atovaquone-Proguanil can be used for Malaria chemoprophylaxis 1-2 days before, daily while in county, 7 days after return, what is the MOA?
Combo electron transport chain and DHFR inhibitor
90
``` _________ and _________ can be used for Malaria prophylaxis and pregnancy. Atovaquone-proguanil Chloroquine Mefloquine Doxycycline ```
Mefloquine | Chloroquine
91
Blood-Borne Flagellates: Chagas' Disease (Trypanosoma cruzi) can be transmitted by
Reduviid bug ("kissing bug") Feeds on sleeping human and defalcates near wound which then Chagoma develops
92
Pathogen for Chagas' Disease
Trypanosoma cruzi
93
Chagas' Disease ranges from what regions?
Texas, Mexico, Central America, South America
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Chagas' Disease survives in
wild animal reservoirs like rodents, opossums, armadillos
95
Systemic spread of Chagas Disease causes
acute phase with fever, malaise, swollen lymph nodes (can spread to heart and CNS) Intermediate phase has no symptoms, but parasite remains for life
96
Chronic Disease for Chagas can develop years later and cause
Cardiac Arrhythmia, Increase Heart Size | Dilation of Esophagus and Colon, dysfunction
97
Treatment of Chagas' Disease
Nifutimox - produces oxidative stress in parasite Benznidazole - DNA binder Both reduce severity of acute disease, but no activity in chronic infections
98
Toxoplasmosis pathogen
Toxoplasma gondii
99
Toxoplasma gondii is acquired through
interaction with infected cat, ingestion of contaminated pork, transfusions, transplacental Cat is the definitive host where sexual reproduction occurs in the GI
100
Toxoplasmosis Common Manifestations
Reactivation of latent infection upon immunosuppression * AIDS, immunosuppressive regimens for cancer or transplantation * Leads to disseminated infection with myocarditis and encephalitis * Fatal Primary Infection in Pregnant Woman * Risk of transmission is highest in the third trimester * Abortion, stillbirth, microcephaly, psychomotor retardation
101
Treatment of Toxoplsmosis for Trophozoites
Pyrimethamine/sulfadiazine Interferes with the regeneration of tetrahydrofolic acid from dihydrofolate by competitively inhibiting the enzyme dihydrofolate reductase
102
Treatment of Toxoplasmosis for Cysts
Atovaquone Block pyrimidine biosynthesis
103
Pathogen for Trichomoniasis
Trichomonas vaginalis * Trophozoite form is flagellated * Lacks a cyst form, but can survive a few hours outside of host
104
Primary Manifestation for Trichomoniasis
Vaginits * Discharge, Vulvar itching, burning sensation, dysuria * Lasts weeks to month * Can increase the risk of preterm birth and enhance susceptibility to HIV infections
105
Treatment of Trichomoniasis (T. vaginalis)
Metronidazole *likely effective through alkylation of DNA
106
Nematodes are also called
Nonsegmented, Roundworms
107
Cestodes are also called
Tapeworms
108
Trematodes
Flukes
109
Nemotodes are covered by a
Flexible, Durable outer cuticle that is resistant to chemicals Females are reproductive factories Most females release shelled eggs, some release live larvae
110
Key Players in the Infection
Infective Ovum (microscopic) * Contains single larva * Eggshell is chemically resistant Larvae (microscopic) * Eosinophilic pneumonitis after extravasation * MOST SYMPTOMATIC Phase Adult Males & Females * Inhibit Duodenum * Mate about 2x per year * Each female produces 200,000 ova per day * Ova released into fecal stream
111
Helminths: Pathogenesis of Ascariasis
Pulmonary Phase * Eosinophil-rich pneumonitis (cough, bloody sputum) Intestinal Phase * Symptoms proportional to adult worm burden * Significant cause of malnourishment * Small children have intestinal or biliary obstruction, leading to perforation
112
Helminths: Treatment of Ascariasis
Mebendazole or Albendazole * Both inhibit sugar absorption in the parasite, energy loss In light infections, when females use up their stored sperm, they can wander * into the biliary/pancreatic duct system * Up on out of the GI system * Fever or pressurized airplane cabins also causes seeking behavior
113
Intestinal Nematodes
Ascaris lumbricoides Toxocara canis Strongyloides stercoralis Enterobius vermicularis (pinworm)
114
Helminths: Types of Larva Migrans (COMES FROM ANIMALS)
``` CLM = Cutaneous Larva Migrans (Dog Hookworm) VLM = Visceral Larva Migrans (Toxocara canis - dog Ascaris - Toxocariasis) - COMMON IN SE US! OLM = Ocular Larva Migrans ```
115
Routes of Transmission for Toxocara
Fecal - Oral Intrauterine Transmammary Predation - animal eat infected animal
116
T. Canis Life Cycle
Adult Helminths live in dog and cat small intestine Animals eat embroyonated eggs Eggs pass in feces and embroyonate in soil (Eggs are ingested) Larvae hatch in small intestin, and penetrate wall Larvae migrate to all organs via bloodstream EYE, CNS, LIVER
117
Helminths: Clinical Manifestation of VLM
* Typical Patient is < 5 years old and heavily infected * Presents with fever, hepato(spleno)megaly, lower respiratory symptoms * Host response to T. Canis is characterized by eosinophil-rich granulomas encapsulating migrating larvae * Pulmonary response includes bronchospasm, cough, wheezing, pneumonia
118
Helminth: Clinical Manifestation of OLM
Typical Patient 5 - 10 yearso ld Presents with unilater vision impairment Retinal granuloma formation can lead to blindness
119
Treatment of Larva Migrans (VLM & OLM)
Albendazole | Mebendazole
120
Pathogen for Strongyloidiasis
S. Stercoralis
121
Infection Route For Stronglyoides
Autoinfection Direct Cycle Indirect Cycle
122
Strongyloidiasis Clinical Manifestations
Acute Strongyloidiasis * Pruritic Rash at larval penetration site * Trachea irritation with a dry cough * Diarrhea and constipation, abdominal pains and anorexia Chronic Stronglyoidiasis (asymptomatic) * Most Common are GI and cutaneous * Diarrhea and constipatin, postpradial fullness, heartburn, and epigastric pain LARVA CURRENS along buttock, perineum, and thigh *Chronic Urticaria (Hives) Hyperinfection Syndrome and Disseminated Strogyloidiasis * Occurs in subclinical patients receiving hi-dose corticosteroids --> Asthma, COPD exacerbation, organ transplantation Hyperinfection: Larvae invade GI and Pulmonary Disseminated: Larvae invade numerous organ systems
123
Basis of Hyperinfection (Strongyloidiasis)
Under normal condition, T cell-mediated immunity limits the intestinal worm burden to relatively small number of adult females. (With time, adults will die and be digested) Immunosuppresion allows a greater number of females to establish in the gut * Increased number of eggs and hatched larvae * Larvae mature and reintiate the migration patten through lungs and GI
124
Treatment and Prevention of Strongylodiasis
Acute or Chronic Strongloidiasis - Ivermectin Hyperinfection Syndrome and/or Disseminated * Discontinue or taper steroids if possible and Ivermectin PREVENTION * Wear shoes when walking on soil * Avoid contact with feces and/or sewage
125
Pinworm or Enterobius vermicularis is a pathogen for
Enterbiasis
126
Lifecycle for Enterbiasis
Female migrates to perianal area (usually at night) to lay eggs Eggs are infectious within 4-6 hours Causes severe itching Ingested by humans
127
Treatment of Enterbiasis
Albendazole
128
This Cestodes (tapeworms) causes cysticercosis
Taenia solium (pork)
129
What does Cestodes inhabit? What is the head and body referred to?
Inhabit in the GI lumen Head is called scolex Body is called a strobila consisting of proglottids
130
Are Cestodes Asexual, Heterosexual, or Hermaphodites?
Hermaphodites
131
Outer Surface of Cestodes are called?
Tegument
132
Treatment of Cestodes
Rx Niclosamide
133
Taeniasis is aquired by
ingesting undercooked, contaminated meat. Starts by human release of eggs or proglottids Forms Cysticerci
134
What is Cysticercosis?
Acquired when human play the part of the pig, ingesting eggs rather than encysted larvae Eggs hatch in small intestine, larvae migrate through body and encyst in brain and skeletal muscle
135
Cysticercosis causes Neurocysticercosis which can lead to
Seizures, Obstructive Hydrocephalus, and Focal Neurologic Deficits. Cysts will grow slowly for up to 10 years before dying. Antigenic contents lead to local inflammation and enhanced seizures.
136
Treatment of Neurocysticercosis
Albendazole