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PMMI > Exam 5 > Flashcards

Exam 5 Flashcards

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
Q

Is Candidiasis opportunistic? (Needs Conditions (DM, Malnutrition, Immunosuppressive, Trauma) to infect)

A

Yes

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26
Q

Candidemia is

A

bloodstream infection of candida

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27
Q

Manifestations of Candidiasis

A

In immunocompetent hosts:
Thrush, Vaginitis, Cutaneous Lesions
In immune suppressed hosts
Esophagitis, Chronic Mucocutaneous Candidiasis (CMCC), Disseminated

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28
Q

Candidiasis virulence and pathogenesis

A

Adherence factors - allows yeast and hyphae to attach to tissues
“Yeast-to-hyphal” transition - phenotypic switching

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29
Q

Treatment of Candida species

A

Triazole (static)

Echinocandins (Cidal)

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30
Q

C. glabrata is resistant to what class of drugs?

A

Triazoles

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31
Q

Clinical Manifestations of Cryptococcosis

A

Subacute to Chronic Meningitis, Pneumonia, Skin Ulcers, and Bone Lesions

Can occur during defective T-lymphocyte function (AIDS, carcinoma, leukemia, Hodgkin’s lymphoma

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32
Q

Emerging Cryptococcosis pathogen

A

Cryptococcus gattii

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33
Q

Clinical Manifestations of Cyptococus gattii

A

Causes tumor-like lesions “cryptococcomas” in lungs, brain, and soft tissue.
More tolerant to antifungal compounds

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34
Q

Virulence and Pathogenesis of Cryptococcosis

A

Polysaccharide Capsule

Melanin deposited in cell wall (provides stress protection for intracellular survival)

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35
Q

Cyptococcus species are susceptible to

A

Triazoles

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36
Q

Pneumocystosis predisposing agents

A

AIDS, Pulmonary Infections

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37
Q

Pneumocystosis virulence an pathogenesis

A

Major Surface Glycoprotein (MSG) - acts as an attachment factor to several host proteins
Histologically - alveoli are filled with foamy exudate

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38
Q

Clinical manifestations of Pneumocystosis

A

Pneumonitis

Lesions outside the lung are common in AIDS patients

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39
Q

Treatment of Pneumocystis

A

Bactrim and Clindamycin

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40
Q

Bactrim and Clindamycin are treatment options for Pneumocystis but which drug has a higher incidence of adverse effects in AIDS patients?

A

TMP-SMX (Bactrim)

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41
Q

Are fungi opportunistic or true pathogens?

A

True Pathogens

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42
Q

Fungi are also thermal dimorphism

A

Body Temp = Yeast

Room Temp = Mold

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43
Q

Type of ENDEMIC Thermal Dimorphic Mycoses

A

Blastomyces dermatitidis
Coccidioides immitis
Histoplasma capsulatum

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44
Q

Endemic Dimorphic Mycoses: Pathogen for Histoplasmosis

A

H. capsulatum, endemic to the eastern US, near MS and OH river valleys

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45
Q

Endemic Dimorphic Mycoses: H. capsulatum and B. dermatitidis transmission

A

inhalation of airborne conidia (spores)

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46
Q

Endemic Dimorphic Mycoses: Histoplasmosis Virulence and Pathogenesis

A

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)

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47
Q

Endemic Dimorphic Mycoses: Histoplasmosis Clinical manifestations

A

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

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48
Q

Endemic Dimorphic Mycoses: Blastomycosis Clinical Manifestations

A

Respiratory Infection - asymptomatic or mild, resolves spontaneously
Systemic Blastomycosis - Defects in CMI are predisposing
Chronic Cutaneous Blastomycosis - ulcerated lesions, exposed or mucocutaneous tissues

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49
Q

Endemic Dimorphic Mycoses: Coccidioidomycosis pathogen

A

Coccidioides Immitis

Located to the desert southwest US, Mexico, and Guatemala

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50
Q

Endemic Dimorphic Mycoses: Coccidioides immitis initiates

A

Infectious Arthroconida

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51
Q

Endemic Dimorphic Mycoses: Coccidioidomycosis Virulence and Pathogenesis

A

Arthroconidia - highly infectious, but NOT highly virulent

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52
Q

Endemic Dimorphic Mycoses: Coccidioidomycosis Clinical Manifestations

A

Respiratory Infections

  • Symptomatic Patients - VALLEY FEVER with malaise, cough, chest pain, fever
  • Filipinos, African/Native Americans & Hispanics are at greatest risk of dissemination
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53
Q

Treatment of Endemic Dimorphic Pathogens
Blastomyces dermatitidis
Coccidioides immitis
Histoplasma capsulatum

A

Triazoles

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54
Q

Endemic Dimorphic Mycoses: Pathogen of Sporotrichosis

A

Sporothrix schenckii

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55
Q

Endemic Dimorphic Mycoses: Sporotrichosis is associated with

A

Decaying Vegetation.. Enters blood via splinter, thorn pricks (gardeners and landscapers)

56
Q

Endemic Dimorphic Mycoses: Sporotrichosis is widely present in

A

Soil

57
Q

Endemic Dimorphic Mycoses: Clinical Manifestation of Sporotrichosis

A

Skin Lesion begins as a painless papule (normally on hand or finger)
Papule larges and slowly ulcerates
Primary pulmonary Sporotrichosis

58
Q

Treatment of Sporotrichosis

A

Triazoles

59
Q

Characteristics of opportunistic mold

A

Monomorphic (produce hyphae in vitro and vivo, regardless of temperature

60
Q

Opportunistic Mold can cause what diseases?

A

Aspergillosis

Mucormycosis (Zygomycosis)

61
Q

Opportunistic Mold: Pathogen for Aspergillosis

A

Aspergillus fumigatus

62
Q

Opportunistic Mold: Aspergillus fumigatus is present

A

Air vents and Construction and Remodeling efforts can aerosolize
Common contaminant in clinical laboratories

63
Q

Opportunistic Mold: Clinical Manifestations of Aspergillosis

A

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
Q

Opportunistic Mold: Treatment of Aspergillus spp

A

Triazoles and Echinocandins

65
Q

Opportunistic Mold: Mucormycosis (Zygomycosis) pathogenesis

A

Rapidly growing hyphae invade tissue

66
Q

Opportunistic Mold: Mucormycosis (Zygomycosis) Clinical Manifestations

A

Pulmonary Mucorcycosis
Rhinocerebral Mucorcycosis
Primary Cutaneous Mucorcycosis (Contaminated Bandages)
Disseminated

67
Q

What constitutes a parasite?

A

Protozoans: single cell organism
Helminths: Multicellular flatworms and roundworms

68
Q

How do we become infected by parasites?

A

Fecal-Oral
Food-Borne
Vector-Borne
Skin-penetrators

69
Q

What kind of hosts do parasites use?

A

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
Q

KEY Parasite Concepts

A

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
Q

The protozoan parasites

A

Malaria: Plasmodium spp
Blood-Borne Flagellates: Trypanosoma
Protozoan infections in AIDS patient: Toxoplasma gondii
Sexually Transmitted: Trichomonas Vaginalis

72
Q

Properties of Protozoans

A

Single Celled, Eukaryotic Organism

May be intracellular or extracellular

Can live in GI, tissues, or vasculature

73
Q

How do Protozoan exert their effects?

A

Interfering with nucleic acid synthesis orrrr carbohydrate metabolism

74
Q

This pathogen causes Malaria

A

Plasmodium spp

75
Q

In Malaria, a parasite growing within RBCs can cause

A 
High Fever, Chills, and Profuse Sweating
Fever
Anemia
Tissue Hypoxia
Renal Failure
Lung Edema
Coma
76
Q

The Plasmodium pathogen is carried by what?

A

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
Q

Plasmodium Life Cycle

A

Mosquito takes a blood meal injects sporozodes

After Infection of Liver Cell becomes Schzont

78
Q

Malaria - Immunity

A

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
Q

Which Malaria strands can form intrahepatic cysts that are dormant and survive the host’s immunologic attack?

A

P. vivax and P. ovale

80
Q

P. vivax and P. ovale only infects

A

immature cells (reticulocytes)

81
Q

P. malariae infects

A

Senescent Cells

82
Q

P. falciparum infects

A

Mature RBC (most aggressive infection)

83
Q

Parasites degrade hemoglobin within an acidic food vacuole for

A

Protein Requirements and Synthesize folate de novo

84
Q

For Malaria, Chloroquine is used for treatment how?

A

Inhibits heme utilization by erythrocyte forms and ONLY KILLS ERYTHROCYTE FORM (Schizonts)

85
Q

For Malaria, Primaquine is used for treatment and kills what Pathogen?

A

Liver schizonts of P. vivax and P. ovale

86
Q

Prevention Protocols for Malaria

A

Prevent mosquito bit with pesticides, repellants

87
Q

Mefloquine can be used for Malaria Chemoprophylaxis > 2 weeks before, weekly while in country , and 4 weeks after return, what is the MOA?

A

Inhibition of Lipid Trafficking and Nutrient Uptake

88
Q

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?

A

Inhibition of Mitochondrial Protein Synthesis

89
Q

Atovaquone-Proguanil can be used for Malaria chemoprophylaxis 1-2 days before, daily while in county, 7 days after return, what is the MOA?

A

Combo electron transport chain and DHFR inhibitor

90
Q 
\_\_\_\_\_\_\_\_\_ and \_\_\_\_\_\_\_\_\_ can be used for Malaria prophylaxis and pregnancy.
Atovaquone-proguanil
Chloroquine
Mefloquine
Doxycycline
A

Mefloquine

Chloroquine

91
Q

Blood-Borne Flagellates: Chagas’ Disease (Trypanosoma cruzi) can be transmitted by

A

Reduviid bug (“kissing bug”)

Feeds on sleeping human and defalcates near wound which then Chagoma develops

92
Q

Pathogen for Chagas’ Disease

A

Trypanosoma cruzi

93
Q

Chagas’ Disease ranges from what regions?

A

Texas, Mexico, Central America, South America

94
Q

Chagas’ Disease survives in

A

wild animal reservoirs like rodents, opossums, armadillos

95
Q

Systemic spread of Chagas Disease causes

A

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
Q

Chronic Disease for Chagas can develop years later and cause

A

Cardiac Arrhythmia, Increase Heart Size

Dilation of Esophagus and Colon, dysfunction

97
Q

Treatment of Chagas’ Disease

A

Nifutimox - produces oxidative stress in parasite
Benznidazole - DNA binder

Both reduce severity of acute disease, but no activity in chronic infections

98
Q

Toxoplasmosis pathogen

A

Toxoplasma gondii

99
Q

Toxoplasma gondii is acquired through

A

interaction with infected cat, ingestion of contaminated pork, transfusions, transplacental

Cat is the definitive host where sexual reproduction occurs in the GI

100
Q

Toxoplasmosis Common Manifestations

A

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
Q

Treatment of Toxoplsmosis for Trophozoites

A

Pyrimethamine/sulfadiazine

Interferes with the regeneration of tetrahydrofolic acid from dihydrofolate by competitively inhibiting the enzyme dihydrofolate reductase

102
Q

Treatment of Toxoplasmosis for Cysts

A

Atovaquone

Block pyrimidine biosynthesis

103
Q

Pathogen for Trichomoniasis

A

Trichomonas vaginalis

  • Trophozoite form is flagellated
  • Lacks a cyst form, but can survive a few hours outside of host
104
Q

Primary Manifestation for Trichomoniasis

A

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
Q

Treatment of Trichomoniasis (T. vaginalis)

A

Metronidazole

*likely effective through alkylation of DNA

106
Q

Nematodes are also called

A

Nonsegmented, Roundworms

107
Q

Cestodes are also called

A

Tapeworms

108
Q

Trematodes

A

Flukes

109
Q

Nemotodes are covered by a

A

Flexible, Durable outer cuticle that is resistant to chemicals

Females are reproductive factories
Most females release shelled eggs, some release live larvae

110
Q

Key Players in the Infection

A

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
Q

Helminths: Pathogenesis of Ascariasis

A

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
Q

Helminths: Treatment of Ascariasis

A

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
Q

Intestinal Nematodes

A

Ascaris lumbricoides
Toxocara canis
Strongyloides stercoralis
Enterobius vermicularis (pinworm)

114
Q

Helminths: Types of Larva Migrans (COMES FROM ANIMALS)

A 
CLM = Cutaneous Larva Migrans (Dog Hookworm)
VLM = Visceral Larva Migrans (Toxocara canis - dog Ascaris - Toxocariasis) - COMMON IN SE US!
OLM = Ocular Larva Migrans
115
Q

Routes of Transmission for Toxocara

A

Fecal - Oral
Intrauterine
Transmammary
Predation - animal eat infected animal

116
Q

T. Canis Life Cycle

A

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
Q

Helminths: Clinical Manifestation of VLM

A
  • 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
Q

Helminth: Clinical Manifestation of OLM

A

Typical Patient 5 - 10 yearso ld
Presents with unilater vision impairment
Retinal granuloma formation can lead to blindness

119
Q

Treatment of Larva Migrans (VLM & OLM)

A

Albendazole

Mebendazole

120
Q

Pathogen for Strongyloidiasis

A

S. Stercoralis

121
Q

Infection Route For Stronglyoides

A

Autoinfection
Direct Cycle
Indirect Cycle

122
Q

Strongyloidiasis Clinical Manifestations

A

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
Q

Basis of Hyperinfection (Strongyloidiasis)

A

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
Q

Treatment and Prevention of Strongylodiasis

A

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
Q

Pinworm or Enterobius vermicularis is a pathogen for

A

Enterbiasis

126
Q

Lifecycle for Enterbiasis

A

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
Q

Treatment of Enterbiasis

A

Albendazole

128
Q

This Cestodes (tapeworms) causes cysticercosis

A

Taenia solium (pork)

129
Q

What does Cestodes inhabit? What is the head and body referred to?

A

Inhabit in the GI lumen
Head is called scolex
Body is called a strobila consisting of proglottids

130
Q

Are Cestodes Asexual, Heterosexual, or Hermaphodites?

A

Hermaphodites

131
Q

Outer Surface of Cestodes are called?

A

Tegument

132
Q

Treatment of Cestodes

A

Rx Niclosamide

133
Q

Taeniasis is aquired by

A

ingesting undercooked, contaminated meat.
Starts by human release of eggs or proglottids
Forms Cysticerci

134
Q

What is Cysticercosis?

A

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
Q

Cysticercosis causes Neurocysticercosis which can lead to

A

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
Q

Treatment of Neurocysticercosis

A

Albendazole

PMMI (3 decks)

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