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Micro Final2 Flashcards

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1
Q

What common fungal infection (that is typically asymptomatic) can present with symptoms very similar to tuberculosis?

A

Cryptococcus: fever, cough, night sweats

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2
Q

What organism is this? What is being used to visualize it? How does it enter the body?

A

Cryptococcus; India ink; respiratory tract

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3
Q

What tissue does cryptococcus have a preference for after entering via the respiratory tract?

A

The CNS, so it causes fungal meningitis

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4
Q

What is the most significant virulence factor of cryptococcus?

A

The capsule

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5
Q

What is being used to visualize these budding yeast cells of cryptococcus?

A

Silver stain

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6
Q

Can cryptococcus have skin manifestations?

A

Yes, it can present with a non-blanching rash or skin lesions

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7
Q

How is cryptococcal infection diagnosed?

A

Visualization of organism from biopsy or CSF, or cryptococcal capsular antigen in blood or CSF

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8
Q

How is cryptococcus treated?

A

Amphotericin B, 5-fluorocytosine, and fluconazole

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9
Q

What organism can be spotted on this blood smear?

A

Histoplasma capsulatum, which is a fungus growing inside an RBC

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10
Q

What is the vector for infection by Histoplasma capsulatum? What environments predispose somebody to this?

A

Inhalation of microconidia; spelunking or construction work, or exposure to bat guano

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11
Q

A 65 y/o man entered a Mexican mine filled with bat guano, and the CT reveals these nodules. He does not have TB. What organism is most likely?

A

Histoplasmosa capsulatum

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12
Q

How can histoplasmosis be diagnosed? Does having AIDS increase or decrease the sensitivity of these methods?

A

Urine histoplasma antigen, bone marrow biopsy, other biopsies, or CSF antigen; AIDS patients show increased sensitivity

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13
Q

In this 50 year old AIDS patients with fever, weight loss, pancytopenia, and hemoptysis, the following organism is seen with silver stain in bronchoalveolar lavage. What is it?

A

Histoplasma

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14
Q

The following organism in the liver was better visualized with silver stain on the right. It was taken from a patient from an excavation site in Ohio. What immunological structure is this? What organism is it?

A

Granuloma; Histoplasma capsulatum

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15
Q

What three drugs are used to treat Histoplasma capsulatum?

A

Amphotericin, itraconazole, and voriconazole

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16
Q

Where is the greatest prevalence of histoplasmosis in the US?

A

Ohio river valley

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17
Q

Can serology be used to diagnose histoplasmosis?

A

Rarely

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18
Q

What other dimorphic fungal infection has a prevalence pattern in the US that overlaps with Histoplasma capsulatum?

A

Blastomyces dermatitidis

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19
Q

How does Blastomyces dermatitidis typically enter the body?

A

Inhalation of conidia (spores)

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20
Q

What respiratory symptoms are caused by Blastomyces?

A

Atypical chronic pneumonia with mass-like lesions, lobar infilrates

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21
Q

What dimorphic fungus can cause these skin manifestations?

A

Blastomyces dermatitidis

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22
Q

What is the shape of the conidia of Blastomyces?

A

Ovoid

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23
Q

What are two common localizations of Blastomyces infection?

A

Lungs and skin

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24
Q

Where is Coccioides immitis most prevalent in the US?

A

The Southwest

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25
Q

What disease is also called San Joaquin Valley Fever?

A

Coccidioidomycosis, caused by Coccidioides

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26
Q

What is the shape of Coccidioides conidia?

A

Rectangular arthroconidia

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27
Q

What is the infectious unit of Coccidioides?

A

A barrel-shaped arthroconidium: one of these packets

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28
Q

What are the primary clinical manifestations of Coccidioides?

A

A primary pulmonary infection, usually asymptomatic, but sometimes with flu-like symptoms two weeks post exposure

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29
Q

What are risky environments for Coccidioides exposure?

A

Excavations, construction, or military exercises in the southwest US

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30
Q

What are these fungal skin lesions caused by in this patient who was at an excavation two weeks ago in the southwest US?

A

They are an infection of Coccidioides

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31
Q

How is Coccidioides infection treated?

A

Amphotericin B, and fluconazole as well in immunocompromised hosts

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32
Q

What fungus is this morphology a characteristic sign of?

A

It is the mariner’s wheel of Paracoccidiodes brasiliensis

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33
Q

What is the typical worldwide origin of Paracoccidiodes infections?

A

South America

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34
Q

Do Paracoccidiodes infections occur equally in men and women?

A

No, more often in males

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35
Q

What is the route of primary infection by Paracoccidiodes?

A

Lungs

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36
Q

What are three drugs with which Paracoccidioides is treated?

A

Itraconazole, amphotericin B and TMP-SMX

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37
Q

Papular skin lesions present on this AIDS patient from Thailand. What is the most likely organism?

A

Penicillum marneffei

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38
Q

What two drugs are used to treat Penicillum marneffei?

A

Amphotericin and 5-fluorocytosine (flucytosine)

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39
Q

What fungal infection endemic in Southeast Asia produces these skin lesions? Is it common in immunocompetent hosts?

A

Penicillum marneffei; no, it is not common in the immunocompetent

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40
Q

What infection is this most likely to be, in an immunosuppressed patient from Bangladesh? What is expected to be seen on CT scan?

A

Mucormycosis; inflamed sinuses

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41
Q

What fungal infection is characterized by oral infections with broad ribbon-like hyphae with right angle branching?

A

Mucormycosis, caused by zygomycetes

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42
Q

Which is the most common fungus in the Zygomycetes family that causes oral and sinus infections, shown here?

A

Rhizopus

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43
Q

What is the hyphae pattern of Rhizopus?

A

Nonseptate ribbon-like hyphae with right angle branching

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44
Q

Why is diabetes mellitus a risk factor for mucormycosis?

A

Hyperglycemia and ketoacidosis causes impaired phagocytic chemotaxis

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45
Q

What fungal infection seen here can invade burn or trauma wounds and produces black necrotic lesions?

A

Zygomycetes, like Rhizopus

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46
Q

How is a zygomycete infection of a surgical wound treated?

A

Aggressive surgical debridement, amphotericin, and posaconazole

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47
Q

Are Rhizopus infections common in immunocompetent hosts?

A

No

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48
Q

When an opportunistic fungal infection shows septated hyphae with acute angle branching, which organism is suspected?

A

Aspergillus

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49
Q

What is an aspergilloma?

A

A fungus ball in the lung, walled off similar to a granuloma

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50
Q

What cell types prevent inhaled conidia of Aspergillus from becoming infectious in pulmonary tissue?

A

Macrophages and neutrophils

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51
Q

Will Aspergillus present in immunocompetent hosts?

A

Usually not

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52
Q

What is the most likely organism shown here, cultured from a heart valve in a 74 year old man with diabetes and an implanted defibrillator?

A

Aspergillus (septated acute branching hyphae)

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53
Q

What are the top three drugs used to treat Aspergillus?

A

Voriconazole, amphotericin B, caspofungin

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54
Q

What mainly determines survival in an invasive case of Aspergillus?

A

Immune recovery

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55
Q

What kind of organism is Pneumocystis jirovecii?

A

A fungus

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56
Q

What is this organism, visualized with silver stain in a lung biopsy of an AIDS patient complaining of dyspnea on exertion?

A

Pneumocystic jirovecii

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57
Q

What is the typical diagnostic test used for Pneumocystis jirovecii?

A

Direct fluorescence antibody (silver staining can also be used, but DFA is faster and more sensitive)

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58
Q

What is used to treat Pneumocystis jirovecii?

A

TMP-SMX

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59
Q

Is Pneumocystis jirovecii a typical infection in immunocompetent hosts?

A

No

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60
Q

What condition is this? What family of yeast causes it?

A

Athlete’s foot or tinea pedis; Trichophyton

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61
Q

When lesions similar to athlete’s foot present in the groin, what is it called?

A

Tinea cruris

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62
Q

What topical drugs are used to treat tinea pedis?

A

Miconazole and tolnaftate

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63
Q

What non-azole systemic therapy can be used against Trichophyton rubrum if topical antifungals fail?

A

Terbinafine (lamisil)

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64
Q

What is fungal onchomycosis?

A

Fungal infection of the nail

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65
Q

What is tinea corporis?

A

Ringworm

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66
Q

What organism causes ringworm?

A

Trichophyton verrucosum

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67
Q

What is the difference between a Tinea and a Taenia?

A

Tinea refers to cutaneous fungal infections, while taenia refers to tapeworms

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68
Q

What organism causes a superficial infection characterized by hypo or hyperpigmentation? How is it diagnosed?

A

Malassezia furfur; scrapings stained with KOH

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69
Q

What stains are used to visualize topical dermatophytes?

A

KOH or calcafluor white

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70
Q

Are subcutaneous fungal infections common in the US?

A

No, they are more typical in the tropics

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71
Q

How do the fungi in this subcutaneous infection get under the epidermis?

A

Local trauma and implantation

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72
Q

What subcutaneous infection of the foot will produce black fungal grains on culture?

A

Eumycetoma, caused by Madurella fungi

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73
Q

What bacterium can cause a presentation similar to eumycetoma?

A

Actinomycetes like Nocardia, which is then called actinomycetoma

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74
Q

What subcutaneous infection is commonly caused by Madurella grisea? What is the most typical treatment?

A

An infection of the foot called Madura foot; surgical removal, including possibly amputation (voriconazole and posaconazole also show some preliminary efficacy)

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75
Q

What fungal infection is associated with rose thorn punctures?

A

Sporotrichosis

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76
Q

What outdoor activity is a risk factor for sporotrichosis infection?

A

Gardening

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77
Q

What organism causes this infection associated with gardening?

A

Sporothrix schenckii

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78
Q

What is the treatment for sporotrichosis?

A

Sporonox (itraconazole)

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79
Q

What is the pathway of spread of Sporothrix schenckii after the initial subcutaneous implantation?

A

Lymphatic, usually up the arm

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80
Q

What fungal infection likely produced these nodules? The patient denies gardening, touching fishtanks, or construction.

A

Exophiala jeanselmei

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81
Q

What is phaeohyphomycosis? What is a potential serious target tissue of the infection?

A

An infection with darkly-pigmented fungi, e.g. Exserohilum rostratum; meningitis

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82
Q

What is this fungus, which caused an outbreak of meningitis in 2012 after a contamination of pharmaceutical goods?

A

Exserohilum rostratum

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83
Q

What are three typically targeted cellular processes by antifungals?

A

The cell membrane which uses ergosterol instead of cholesterol, DNA synthesis, and the cell wall

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84
Q

What is the mechanism of fluconazole?

A

It inhibits ergosterol synthesis

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85
Q

What is the suffix used for drugs that inhibit ergosterol synthesis?

A

NAME?

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86
Q

What cellular process is targeted by flucytosine?

A

DNA synthesis

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87
Q

How do polyene antibiotics kill fungi?

A

They cause direct membrane damage

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88
Q

What part of the cell is attacked by the antifungal amphotericin?

A

The cell membrane

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89
Q

What drug is this? What is its mechanism?

A

Amphotericin; disruption of the fungal cell membrane

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90
Q

Is oral ketoconazole still typically used?

A

No

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91
Q

What are the two first generation triazoles?

A

Itraconazole and fluconazole

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92
Q

What are the two second generation triazoles?

A

Voriconazole and posaconazole

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93
Q

What kind of enzyme is responsible for converting lanosterol to ergosterol in fungi? What class of drugs inhibits it?

A

A cytochrome P450; azoles

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94
Q

Do azoles cross-react with mammalian cytochrome p450s?

A

Some cross-reactivity is seen

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95
Q

Is fluconazole fungicidal or fungistatic?

A

Fungistatic

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96
Q

Does fluconazole have an oral formulation? Is it narrow or broad spectrum?

A

Yes, there is an oral formulation; it is narrow spectrum

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97
Q

What organisms is fluconazole very effective against?

A

C. albicans and Cryptococcus

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98
Q

Do non-albicans *Candida *species respond to fluconazole?

A

Usually, no

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99
Q

What are common adverse effects of fluconazole?

A

Nausea, vomiting, rash

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100
Q

What sort of drugs have bad interactions with fluconazole, e.g., what tissue are those drugs metabolized by?

A

Drugs that are metabolized by or inhibit liver enzymes

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101
Q

Is itraconazole more or less orally bioavailable than fluconazole?

A

Less

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102
Q

Which azole is cleared renally instead of by the liver?

A

Fluconazole

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103
Q

Which triazole antifungal has the shortest serum half life?

A

Voriconazole

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104
Q

What is the advantage of second generation triazoles?

A

They are more broad spectum, e.g. include all Candida species, Aspergillus, Fusarium

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105
Q

Which triazole is not effective against Aspergillus?

A

Fluconazole

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106
Q

Which triazole has poor CSF penetration?

A

Itraconazole

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107
Q

What is a unique adverse effect of voriconazole compared to other triazoles?

A

Visual disturbances

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108
Q

What azole is used for invasive histoplasma, blastomycosis, and sporotrichosis?

A

Itraconazole

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109
Q

For invasive aspergillosis, what triazole is preferred?

A

Voriconazole

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110
Q

What triazole is preferred for mucormycosis?

A

Posaconazole

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111
Q

Which triazole uniquely produces osmotic diarrhea at high doses?

A

Itraconazole

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112
Q

What drug would be preferred to treat this fungal infection of the oral cavity and sinuses?

A

Posaconazole (the infection is mucormycosis caused by zygomycetes)

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113
Q

Does posaconazole have an oral formulation, an IV formulation, or both?

A

Only an oral formulation

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114
Q

What is the mechanism of terbinafine?

A

Interferes with ergosterol synthesis

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115
Q

What is terbinafine used to treat?

A

Superficial fungal infections, e.g. onychomycosis

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116
Q

What topical therapy can be used against oral thrush? What is its benefit?

A

Nystatin; it has little toxicity and is not absorbed by the body

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117
Q

What infections may be treated with clotrimazole?

A

Mucocutaneous candidiasis and dermatophyte infections (e.g. ringworm)

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118
Q

What is the meaning of “polyene macrolide”?

A

It has many double bonds (polyene) and a ring with more than 12 atoms (macrolide)

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119
Q

What drug is shown here and what is it doing?

A

Amphotericin B, forming a pore in a cell membrane to kill a fungus

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120
Q

What is the most significant delayed toxicity of amphotericin B?

A

Nephrotoxicity

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121
Q

What is amphotericin B the drug of choice for?

A

Cryptococcal meningitis, mucormycosis, histoplasmosis, and invasive fungal infection that does not respond to other therapy

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122
Q

What is flucytosine most commonly used to treat in the US?

A

Cryptococcal meningitis

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123
Q

What class of drugs does caspofungin belong to? What part of the fungus does it target?

A

Echinocandins; the cell wall

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124
Q

What three genuses of fungi are echinocandins very active against?

A

All Candida species, Pneumocystis jirovecii, and most Aspergilllus species

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125
Q

Do echinocandins have activity against systemic dimorphic endemic fungi, e.g. Coccidioides?

A

Not really, so they usually can only be used in conjunction with other drugs

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126
Q

Can caspofungin be given orally?

A

No

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127
Q

What are typical adverse effects of caspofungin infusion?

A

Intravenous site irritation, infusion related adverse effects consistent with histamine release

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128
Q

What are the two most common organisms causing fungal endophthalmitis?

A

C. albicans and Aspergillus

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129
Q

What is used to treat fungal endopthalmitis?

A

Intravitreal administration of amphotericin

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130
Q

What other fungal skin lesions are those caused by Penicillum marneffei difficult to distinguish from?

A

Cryptococcal lesions

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131
Q

What is another (more generic) name for the drug Sporonox?

A

Itraconazole

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132
Q

Are human parasites eukaryotes or prokaryotes? Can they be multicellular, unicellular, or both?

A

Eukaryotes; they can be both multicellular and unicellular

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133
Q

What are the two general classes of helminths?

A

Nematodes and platyhelminthes

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134
Q

What are the unicellular parasites classified as?

A

Protozoa

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135
Q

What are the presenting symptoms of malaria?

A

Fever, shivering, pain in the joints, headache, and vomiting

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136
Q

Approximately how many cases of malaria occur per year worldwide?

A

~200 million

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137
Q

Where do most cases of malaria occur today?

A

90% are in Africa

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138
Q

What parasite is visualized in these RBCs? It is found in a 45 year old UN employee.

A

Plasmodia falciparum, identifiable by the multiply infected red cells and heavy parasitemia

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139
Q

Which Plasmodium causes the worst type of malaria?

A

P. falciparum

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140
Q

Which mosquito transmits P. falciparum?

A

Anopheles mosquito

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141
Q

What are these called? What organism are they characteristic of?

A

Schizonts; Plasmodium ovale, since the RBC is enlarged and oval

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142
Q

What additional treatment is required against P. ovale and P. vivax?

A

Primaquine

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143
Q

What cell type within mosquitos is colonized by Plasmodium?

A

Gametes, which become oocysts

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144
Q

What tissue is the first area of replication for Plasmodium entering a human host?

A

The liver

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145
Q

Why is it possible for malaria to manifest months to years after exposure?

A

The parasite can spend a long time replicating in the liver before being released into the bloodstream

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146
Q

What is the structure indicated with a white arrow, known as the resting stage of Plasmodium?

A

A hypnozoite

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147
Q

What is the basis of the malaria rapid diagnosis test?

A

Antibodies that bind to malaria antigens in the blood

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148
Q

What is the second most lethal cause of malaria?

A

Plasmodium vivax

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149
Q

What are most P. falciparum strains now resistant to which complicates treatment?

A

Chloroquine

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150
Q

How are hypnozoites significant to the prognosis of a malaria case? Which species of malaria does not have them?

A

Being a latent form of the parasite, they can cause a relapse after a round of treatment; Plasmodium falciparum does not have them so it will not relapse after a successful treatment with RBC schizonticides

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151
Q

What is the most feared complication of P. falciparum infection? What are the symptoms?

A

Cerebral malaria; seizure, altered mental status, and hypoglycemia

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152
Q

What are these? Which Plasmodium are they helpful in identifying?

A

Banana-shaped gametocytes; P. falciparum

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153
Q

Are schizonts seen in peripheral blood smears of a patient with P. falciparum?

A

Usually not

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154
Q

What is this structure that merozoites like Plasmodium use to enter the red blood cell?

A

The parasitopherous vacuole

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155
Q

Why can cerebral malaria cause ischemia of the brain?

A

Parasitized RBCs attach to endothelial cells and sequester in cerebral capillaries, because of the knobs shown on this EM

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156
Q

What is visualized in pathological examination of cerebral malaria?

A

Ring hemorrhages

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157
Q

What is the pigment that is deposited in tissue following malaria infection?

A

Hemozoin

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158
Q

Why is primaquine necessary for treatment of P. vivax and P. ovale?

A

It acts against hypnozoites, a dormant form of the parasite, which would otherwise cause relapse of the malaria after months or years

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159
Q

Which malaria parasite is seen here?

A

P. vivax, due to the prevalence of schizonts (and they are not oval shaped as in P. ovale although the distinction is minute)

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160
Q

Which two Plasmodium species may be hard to differentiate on peripheral blood smear?

A

*P. ovale *and P. vivax

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161
Q

What kind of drug is primaquine? What tissue does it primarily act upon to kill Plasmodium?

A

Tissue schizontocide; liver

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162
Q

Is primaquine effective against the erythrocytic forms of Plasmodium?

A

No, so a chloroquine is required as well

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163
Q

When is primaquine contraindicated?

A

In the case of a G6PD deficiency, which would cause hemolytic anemia

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164
Q

What human diseases are also protective against malaria?

A

Sickle cell disease and thalassemia

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165
Q

Does *Plasmodium malariae *have a hypnozoite form? How long can the organism persist in blood after the initial infection?

A

No; for 20-30 years

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166
Q

Does P. malariae present with schizonts in the peripheral blood smear? What is particularly distinguishable about its blood smear appearance?

A

Yes, there are schizonts; there are also band forms of infected RBC’s

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167
Q

Is quinine still effective against all four species of Plasmodium? Is it available as an IV formulation?

A

Yes; No, instead IV quinidine is used

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168
Q

What herbal remedy based on “Chinese wormwood” was recently approved as a powerful antimalarial?

A

Artemesinin

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169
Q

What was the most important component of malaria control efforts in the early 20th century?

A

Eliminating breeding sites for the mosquito vector

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170
Q

What is this parasite, transmitted by the same ticks that carry Anaplasma and Borellia burgdorferi?

A

Babesia microti

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171
Q

What is the animal reservoir (not the vector) of Babesia?

A

White footed mice and small rodents

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172
Q

What drugs are used to treat Babesia?

A

Atovaquone and azithromycin

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173
Q

Where are most cases of babesia in the United States from?

A

Coastal vacation areas with more ticks, e.g. eastern LI, Shelter Island

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174
Q

What are the clinical manifestations of babesiosis in an immunocompetent host?

A

Mild flu-like illness after 1-6 weeks, including malaise/fatigue/fever, chills and sweats

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175
Q

Do most patients with babesiosis recall a tick bite?

A

No

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176
Q

How could a bedbound 85 year old man with hemolytic anemia in East Harlem get babesia?

A

Blood transfusions are a vector for parasite transmission

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177
Q

Which species of nematode parasites are generally the largest?

A

Ascaris lumbricoides

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178
Q

How many people in the world are infected with Ascaris lumbricoides? Although many are asymptomatic, what is a clinical presentation usually a result of?

A

25%; obstruction of the intestine

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179
Q

Are children more or less at risk to develop complications from infection by Ascaris lumbricoides?

A

More, because their intestine is smaller and more prone to blockage

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180
Q

How does Ascaris lumbricoides stay in the upper GI tract? How many eggs are produced daily?

A

They do not attach to the wall, but instead contract their muscles against the fecal stream and peristalsis; about 2000 eggs/day

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181
Q

What life stage of Ascaris lumbricoides can penetrate the intestinal wall to enter the bloodstream? What tissues are then affected?

A

Larvae; they move through the liver and then into the right heart and lungs, and then are coughed up and re-ingested, at which point they are young adults and resistant to gastric acidity

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182
Q

What are the two clinical manifestations of Ascaris lumbricoides?

A

Intestinal obstruction and nutrient impairment

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183
Q

What are the two most commonly used drugs for treating nematode infections?

A

Albendazole and mebendazole

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184
Q

What is the mechanism of benzimidazoles? What are two used in mass treatment campaigns?

A

They inhibit the assembly of microtubules and uptake of glucose by helminths; albendazole and mebendazole

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185
Q

What can be used to treat the nematodes Ascaris lumbricoides, Necatur americanus, Ancylostoma duodenale, Strongyloides, Enterobius, and Trichuris?

A

Benzimidazoles

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186
Q

What is the common suffix for benzimidazoles? What are they used to treat?

A

-bendazole, e.g. Albendazole; nematode parasites

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187
Q

How is Ascaris transmitted between humans?

A

Ingestion of eggs from fecally contaminated soil or food

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188
Q

What is the difference between the methods of Necatur americanus and of Ascaris lumbricoides in staying within the small bowel?

A

Necatur attaches to the intestinal with small teeth, while Ascaris swims upstream. Necatur’s mouth is pictured:

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189
Q

What is the layman name for Necatur americanus and Ancylostoma duodenale?

A

Hookworm

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190
Q

How long can adult hookworms be?

A

9mm-13mm

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191
Q

What is the typical clinical presentation of a patient with hookworm?

A

Childhood anemia

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192
Q

How does hookworm enter the body?

A

It penetrates the skin such as the bare foot, or can enter via the pulmonary or digestive tracts

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193
Q

What is this condition called, caused by a zoonotic parasite that is moving around the surface of the foot?

A

Cutaneous larva migrans

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194
Q

What is cutaneous larva migrans?

A

A migrating rash caused by a zoonotic parasite under the skin

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195
Q

Why do parasites involved in cutaneous larva migrans stay under the skin and not enter the bloodstream?

A

They are zoonotic and cannot complete their lifecycle in a human host, so they wander around the dermis layer leaving itchy tracks

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196
Q

What is the name of the dog hookworm? What condition does it cause?

A

Ancylostoma braziliense; Cutaneous larva migrans, a creeping eruption caused by worms under the skin

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197
Q

Where are zoonotic hookworms common in the US?

A

Southeastern US and tropical areas

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198
Q

How are zoonotic (e.g. dog) hookworms treated?

A

Ivermectin or albendazole

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199
Q

How is a case of human hookworm infection diagnosed? How is it treated?

A

Visualization of eggs in the stool; mebendazole or albendazole

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200
Q

Why are there tracks of bacteria in this streaked sputum culture of a patient with dyspnea and wheezing from Peru?

A

Because of Strongyloides, a nematode leaving tracks of bacteria as it moves around the plate

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201
Q

How does Strongyloides enter the body? Where does it* *replicate? How does it get there?

A

It penetrates the skin as a larval form; it replicates in the small intestine; the larvae migrate from the skin to the circulation to the lungs, where they are coughed and reingested, entering the GI tract

202
Q

How is Strongyloides diagnosed?

A

Visualization of larvae or eggs in the stool

203
Q

How may Strongyloides enter a patient with a PMH of GI issues that has never traveled to places where this parasite is endemic?

A

Small bowel transplant from somebody who had the parasite

204
Q

Where is Strongyloides endemic?

A

Southeastern US and the tropics

205
Q

What is the most serious manifestation of Strongyloides infection? What is the major risk factor for this presentation as opposed to other less serious presentations?

A

Hyperinfection syndrome; being immunocompromised

206
Q

How is Strongyloides treated?

A

Ivermectin, thiabendazole or albendazole

207
Q

Which three intestinal nematodes have a life cycle that passes through the lungs? What is similar about the method of entry of these nematodes?

A

The hookworms Necatur americanus and Ancylostoma duodenale and the worm Strongyloides stercoralis; they all enter the body by penetrating skin

208
Q

What are these tiny ovoid structures inside this nematode?

A

Eggs

209
Q

Where is pinworm prevalent throughout the US?

A

The entire country

210
Q

What are symptoms of pinworm infection?

A

Perianal itching or vaginitis

211
Q

What is the scientific name for pinworm?

A

Enterobius vermicularis

212
Q

What is the most common intestinal nematode infection in the US?

A

Pinworm (Enterobius vermicularis)

213
Q

What are risk factors for pinworm infection?

A

Humidity, crowding, and a high proportion of school age children

214
Q

What is this organism that is migrating to the perianal region to lay eggs and is prevalent throughout the US?

A

Pinworm (E. vermicularis)

215
Q

What is the method of transmission for Enterobius vermicularis?

A

Fecal-oral

216
Q

What is the “Scotch Tape” test? What parasite is it used to diagnose?

A

Tape is applied to the perianal area and examined microscopically for ova; this will detect pinworm (Enterobius vermicularis)

217
Q

How is pinworm treated?

A

Mebendazole, albendazole, or pyrantel pamoate

218
Q

If albendazole and mebendazole are not available, what else can be used to treat pinworm? What is its mechanism of action?

A

Pyrantel pamoate; it is a neuromuscular junction blocker that paralyzes them

219
Q

What organism are these eggs from? What telltale feature is used to identify them?

A

Whipworm (Trichuris trichiura); the polar plugs

220
Q

What parts of the world are endemic for Trichuris trichiura infection?

A

Warm moist climates, so SE Asia, sub-Saharan Africa, and the Caribbean

221
Q

Does Trichuris trichuria pass through the human lungs in its life cycle?

A

No

222
Q

What organism is this? What is a severe complication of infection that is preceded by tenesmus?

A

Whipworm (Truichuris trichiura); rectal prolapse

223
Q

How is Trichuris trichiura transmitted?

A

Fecal-oral (ingestion of eggs in stool)

224
Q

How is whipworm (Trichuris trichiura) treated?

A

Mebendazole or albendazole

225
Q

What nematode infection causes elephantiasis of the limbs? What is the mechanism for this? Does the elephantiasis subside after the parasite is killed?

A

Filariasis; lymphedema due to lymphatic blockage by the parasite; no, the damage to the lymphatics is permanent

226
Q

What is the vector for infection by parasites that cause filariasis? What parts of the world are still endemic for it?

A

Mosquitos; tropical regions

227
Q

When is a blood sample to diagnose filariasis taken? Why?

A

During the night time; because the adult worms release microfilariae at the time of mosquito feeding

228
Q

What condition is this, caused by the parasite on the right?

A

Lymphatic filariasis, caused by a variety of nematodes, most significantly Wuchereria bancrofti and Brugia species

229
Q

What manifestation of infection is produced by Onchocerca volvulus? How is it transmitted between humans;

A

River blindness, caused by the organism migrating to the eye; subcutaneous infection by blackfly bites

230
Q

What disease is caused by Wuchereria bancrofti?

A

Lymphatic filariasis, which produces elephantiasis of limbs

231
Q

Where is Onchocerca volvulus endemic?

A

Africa, Latin America, and the Middle East

232
Q

How is Dracunculis medinensis transmitted? How can an endemic community prevent this?

A

Drinking water contaminated with larvae; filtering the water through a nylon mesh

233
Q

What extraocular symptoms associate with river blindness? How long can these symptoms persist without treatment?

A

Subcutaneous nodules and dermatitis where the microfilariae are being produced by adult females under the skin; 9 years

234
Q

How long does it take for the guinea worm to produce a blister on the skin? How does the worm get from the site of infection to the skin?

A

About 1 year; it penetrates the stomach and intestinal wall, and travels via the abdominal cavity and retroperitoneal space toward the skin

235
Q

What is the scientific name for the guinea worm?

A

Dracunculis medinsis

236
Q

How is an infection by Dracunculis medinsis treated?

A

Mechanical extraction of the worms from the skin, and topical treatment with antibiotics if superinfection is suspected (no antihelminthics are available)

237
Q

When does the Dracunculis medinsis female release eggs from a skin lesion?

A

When the lesion is brought into contact with water, which the patient usually does to relieve the local discomfort

238
Q

What is the structure of a cestode?

A

They are flat ribbonlike worms. The head or scolex is followed by an elongating chain of proglottids, segments that comprise independent reproductive units

239
Q

How long can cestodes become?

A

Up to 12m

240
Q

What kind of a worm is this?

A

A cestode or “tapeworm”

241
Q

What is the reservoir for tapeworm? How is tapeworm transmitted to humans?

A

It lives in the muscles of livestock or fish; humans are infected by ingesting raw or undercooked infected meat

242
Q

What is the scientific name for the fish tapeworm?

A

Diphyllobothrium latum

243
Q

What is the typical treatment for flatworms?

A

Praziquantel

244
Q

What is the morphological difference between the scolex of the beef and the fish tapeworm?

A

The fish tapeworm (Diphylobothrium latum) has hooks on its scolex, while the beef tapeworm (Taenia saginata) has no hooks on its scolex

245
Q

Does the pork tapeworm have a scolex with hooklets? What is its scientific name?

A

Yes;* Taenia solium*

246
Q

What countries would rarely harbor Taenia solium infections?

A

Muslim countries

247
Q

What is the number one cause of adult-onset seizures in the developing world?

A

Parasitic infection

248
Q

What is a tapeworm infection of the brain called?

A

Neurocysticercosis

249
Q

What parasitic infection of the brain is seen here?

A

Neurocysticercosis (tapeworm)

250
Q

What organism causes neurocysticercosis?

A

Taenia solium (pork tapeworm)

251
Q

How is Taenia solium infection of the brain ventricles treated?

A

Surgical removal is indicated if the infection is within the ventricles

252
Q

When is albendazole indicated for neurocysticercosis?

A

For 5-100 lesions and when the ventricles are not involved

253
Q

What is the mechanism of praziquantel?

A

It damages the worm integument and allows for Ca++ influx

254
Q

What organism causes a hydatid cyst?

A

Echinococcus granulosus, the dog tapeworm

255
Q

What organism is the reason for sandbox covers? How does it enter the body?

A

Echinococcus granulosus, the dog tapeworm; ingesting eggs from dog feces

256
Q

What organism is associated with a salty taste in the mouth while coughing?

A

Dog tapeworm (Echninococcus granulosus) which creates hydatid cysts that rupture and spill scolices that taste salty

257
Q

What treatment is used to remove Echinococcus granulosus? What animal(s) harbor this tapeworm?

A

Surgical excisions, like the PAIR procedure, or albendazole when this is not possible; Dog and sheep

258
Q

What differentiates the progression of intestinal infection as opposed to neurocysticercosis in the event of Taelia solium exposure?

A

Whether it was in undercooked pork (which causes GI manifestation) or in food contaminated by feces of an infected human (neurocysticercosis course)

259
Q

What parasites are shared between snails and humans? Are they segmented like tapeworms?

A

Trematodes (flukes); no

260
Q

What structure is seen on the egg of a trematode?

A

A lid-like structure called an operculum

261
Q

What determines the different manifestations of splenomegaly, hepatomegaly, hematuria, or CNS involvement for cases of schistosomiasis?

A

The particular species of trematode involved, which differs based on the location of the exposure

262
Q

What is the major strategy for preventing outbreaks of schistosomiasis?

A

Preventing contamination of the water supply by snails, which harbor the sporocysts

263
Q

How do trematodes enter the body in the course of causing schistosomiasis? Where in the body do they mature?

A

They penetrate the skin upon exposure to water containing cercariae released by infected snails; they mature in the liver

264
Q

How do trematodes return from humans to their animal reservoir (freshwater snails)?

A

Excretion of eggs in feces and urine

265
Q

What kind of immune response is generated in response to trematode eggs during schistosomiasis?

A

A Th2 response

266
Q

What are the four clinically relevent species of Schistosoma? How are they all treated?

A

S. mansoni, S. hematobium, S. japonicum, S. mekongi; Praziquantel

267
Q

What led to an outbreak in hepatitis C near the Aswan dam in Egypt?

A

Tartar emetic was administered to prevent schistosomiasis because of the increase in freshwater snails, but many syringes were reused, spreading HCV

268
Q

What is the common name of Opistorchis sinensis? How does it enter a human host? What cancer does it increase the risk of?

A

Chinese liver fluke; ingestion of raw freshwater fish; Bile duct cancer

269
Q

How can humans be infected with Fasciola hepatica? Where does it reside in humans?

A

Ingestion of raw watercress; in the bile ducts

270
Q

What is the common name of Fasciola hepatica? How is it treated?

A

Liver fluke; triclabendazole

271
Q

What is the only trematode not treated with praziquantel? What is it treated with?

A

Liver fluke (Fasciola hepatica); triclabendazole

272
Q

What is the pathogenetic mechanism of most forms of schistosomiasis?

A

Inflammatory reaction to the eggs

273
Q

What parasites must spend part of their lifecycle in a snail?

A

Trematodes

274
Q

What are the two most likely intestinal protozoa to present in the US?

A

*Entamoeba histolytica *and Giardia lamblia

275
Q

What is the primary reservoir for Entamoeba histolytica? What organ(s) does it attack?

A

Humans; the liver, lungs, the GI wall, and in rare cases, the brain. Large cysts are formed:

276
Q

What organism causes the majority of amebiasis cases in developing countries?

A

Entamoeba histolytica

277
Q

How is Entamoeba histolytica transmitted?

A

Fecal-oral

278
Q

What type of colitis is this? What organism is likely responsible?

A

Amebic colitis; Entamoeba

279
Q

In what extraintestinal tissues can Entamoeba form abscesses?

A

Liver, lungs, and brain

280
Q

What is a condition caused by *Entamoeba *that manifests as stool with blood mucous and pus (that may have been the cause of Thomas Jefferson’s death)?

A

Amebic dysentery

281
Q

How is Entamoeba treated?

A

Metronidazole (or tinidazole)

282
Q

What is the amoeba that causes infection via direct inoculation into nares, pictured here causing a fatal infection of the brain?

A

Balamuthia

283
Q

What is the prognosis for infection by free living amoeba?

A

Almost invariably, death

284
Q

What kind of organisms are Acanthamoeba, Balamuthia, and Naegleria? Do they spread host-to-host or through the enviroment?

A

Free-living amoeba; they can spread in the environment as a trophozoite or cyst form

285
Q

What dramatic infection seen here is caused by a contamination of contact lens solution?

A

Acanthamoeba keratitis

286
Q

What form of *Giardia lamblia *is seen on the right side of this picture that is capable of surviving in the environment?

A

The cyst form

287
Q

What kind of symptoms are produced by Giardia lamblia?

A

GI symptoms: nausea, diarrhea, fatigue and weight loss

288
Q

How many Giardia cysts are necessary to cause in infection via ingestion?

A

Only 10

289
Q

What triggers the transformation from the cyst form back into the trophozoite form for Giardia entering the body?

A

The gastric acid exposure in the stomach

290
Q

Why does* Giardia* cause malabsorption and lactase deficiency?

A

It inhibits several digestive enzymes and absorbs nutrients from the host’s GI tract, while also causing loss of the intestinal brush border

291
Q

What infectious organism is this, present on an intestinal wall and causing chronic diarrhea and malabsorption even after successful treatment?

A

Giardia

292
Q

How is Giardia lamblia infection treated?

A

Tinidazole or metronidazole

293
Q

How is Giardia lamblia transmitted?

A

Fecal-oral

294
Q

How is Trichomonas vaginalis transmitted?

A

Sexual contact

295
Q

Do males develop symptoms of Trichomonas vaginalis?

A

Usually no

296
Q

What sexually transmitted protozoan commonly causes vaginitis and cervicitis, with no cyst form or mitochondria?

A

Trichomonas vaginalis

297
Q

What are these curious little spiral organisms that cause fever, myalgias, orbital edema, and eosinophilia? How are they transmitted to humans?

A

Trichinella spiralis; eating undercooked meat

298
Q

What tissue do Trichinella spiralis organisms enter to cause a brisk inflammatory response (fever, myalgias)? How do they get there from the GI tract?

A

Muscle; penetration of the bowel wall and entering circulation

Here is the organism in muscle:

299
Q

What form of Cryptosporidium is ingested to cause the infection?

A

The cyst form

300
Q

How is *Cryptosporidium *diagnosed?

A

Visualization of parasites with acid fast or an immunostain of the stool sample

301
Q

What properties do Cryptosporidium, Isospora, Cyclospora, and *Microsporidium *share in common?

A

They are all intestinal spore-forming protozoa

302
Q

What spore-forming protozoa caused an outbreak affecting >400k people in Milwaukee in 1993? What caused it?

A

Cryptosporidium; contamination of the water supply

303
Q

In AIDS patients, what does Cryptosporidium manifest as?

A

Wasting syndrome (HIV-related cachexia)

304
Q

Is Cryptosporidium larger or smaller than other spore-forming protozoans?

A

Smaller than most, hence the name *Cryptosporidium parvum *meaning “small”

305
Q

What nucleated, single-celled obligate intracellular protozoan without mitochondria presents as an opportunistic infection in AIDS patients and immunosuppressed patients?

A

Microsporidium

306
Q

What is the treatment for Microsporidia and Cryptosporidia?

A

Since they are usually symptomatic in immunocompromised patients, the immune system is reconstituted, e.g. with antiretrovirals in AIDS patients to bring up the CD4+ count

307
Q

In Africa, what insect transmits sleeping sickness, also called African trypanosomiasis?

A

The Tsetse fly

308
Q

What organism causes Chagas disease in South America?

A

Trypanosoma cruzi

309
Q

What parasite pictured here is transmitted by the sandfly?

A

The Leishmania species

310
Q

What are the sympotoms of cutaneous leishmaniasis?

A

Clusters of skin lesions and palpable subcutaneous nodules (the lymph nodes)

311
Q

What are these skin lesions and this slide of skin scrapings indicative of?

A

Leishmaniasis

312
Q

What organism is the vector Leishmaniasis?

A

The sandfly

313
Q

What organism is the vector for Chagas disease, also called South American trypanosomiasis?

A

The kissing or Riduviid bug

314
Q

Where is Leishmaniasis endemic?

A

Many countries in the New and Old Worlds, including Central and South America, Europe, Asia, and the Middle East

315
Q

Besides cutaneous leishmaniasis, how else can the parasite manifest clinically?

A

Mucocutaneous or visceral symptoms

316
Q

What tissues are targeted in mucocutaneous leishmaniasis?

A

The nose, oropharynx and larynx

317
Q

What two drugs are used to treat Leishmaniasis?

A

Pentavalent antimonials (heavy metals) or amphotericin B

318
Q

What compound has demonstrated preliminary efficacy against New World cutaneous Leishmaniasis but is not yet FDA approved?

A

Miltefosine

319
Q

What species causes the diseases called Dum Dum fever or Kala Azar?

A

Leishmania species

320
Q

What fungi mimics the histologic appearance of Leishmania?

A

Histoplasma capsulatum

321
Q

What are the animal reservoirs for Leishmaniasis?

A

Rodents and canines

322
Q

What are the three categories of manifestations of Leishmaniasis?

A

Cutaneous, mucocutaneous, and visceral

323
Q

What protozoan parasite can be seen here, which is distributed by the Chinch bug?

A

Trypanosoma cruzi

324
Q

How far north is the distribution of the Chinch (Chagas) bug that causes South American trypanasomiasis?

A

As far north as Mexico

325
Q

Does T. cruzi enter the body via oral secretions of the chinch bug?

A

No, the trypomastigotes enter from feces secreted by the chinch bug and travel into the bite wound or a mucosal membrane

326
Q

The acute phase of what Central and South American parasitic infection is seen here? What is this sign called?

A

Trypanosoma cruzi; Romana’s sign or chagoma

327
Q

What three organs are enlarged in the chronic progression of South American trypanosomiasis?

A

The heart, esophagus, and colon

328
Q

Do trypomastigotes replicate in the blood in African, South American, or both localizations of trypanosomiasis?

A

Only African

329
Q

What are the two treatments of choice for acute Chagas disease? What is their mechanism?

A

Benznidazole or nifurtimox; they form oxygen radicals within the parasite

330
Q

How is Chagas disease diagnosed?

A

Peripheral blood smear showing trypomastigotes or xenodiagnosis and culture (of the offending insect vector, the Riduviid bug)

331
Q

What organisms cause African sleeping sickness?

A

Trypanosoma brucei gambiense and Trypanosoma brucei rhodesiense

332
Q

What is the prognosis of untreated African sleeping sickness?

A

Death

333
Q

How does Trypanosoma brucei evade the immune system?

A

It alters its antigenic surface proteins if it is discovered by white blood cells

334
Q

How does African trypanosomiasis kill its host?

A

It enters the CNS and performs irreversible damage to the brain

335
Q

What is the first sign of infection with African sleeping sickness? What is its name?

A

Extracellular proliferation of parasites at the site of the Tsetse fly bite(s); Winterbottom’s sign

336
Q

How long does it take for African sleeping sickness to progress to the CNS stage?

A

Months to years

337
Q

What causes the daytime somnolence of African trypanosomiasis?

A

Disruption of normal circadian rhythms

338
Q

Is Toxoplasmosis rare or relatively common in the US?

A

It is relatively common but typically asymptomatic

339
Q

If Toxoplasma gondii does cause symptoms in an immunocompetent host, what are they typically?

A

Mononucleosis-type illness and lymphadenopathy

340
Q

Can a congenital infection of toxoplasmosis have severe effects on the neonate?

A

It is rare, but yes there can be severe effects, including mental retardation, hydrocephalus, and blindness

341
Q

In immunocompromised or immunosuppressed hosts, what can Toxoplasma gondii infections manifest as?

A

Encephalitis and pneumonia

342
Q

What organism is this, which is transmitted by eggs glued to a mosquito which drop during feeding and burrow into the skin of the host?

A

The botfly, Dermatobia hominis

343
Q

What is the major determinant of the risk of infection by opportunistic pathogens (that can be measured via blood tests)?

A

CD4 count

344
Q

What type of infections would defects in cell mediated immunity increase risk for? What about defects in neutrophils?

A

Cell-mediated: viral pathogens; Neutrophils: bacteria and fungi

345
Q

How can the severity of immunosuppression in a transplant be quantified?

A

The dose and type of immunosuppressents and the recency of rejections or graft-versus-host disease

346
Q

What is typically the only effective therapy for eliminating opportunistic pathogens in an immunocompromised patient and hence the primary objective?

A

Restoring immune function

347
Q

How can immune function be restored in a neutropenic patient that is experiencing an opportunistic infection?

A

Granulocyte colony stimulating factor (GCSF) or other growth factors

348
Q

What are the first typical opportunistic pathogens to appear in an AIDS patient once the CD4 count drops below 500/μL?

A

Bacterial pneumonia or pulmonary TB, mucocutaneous candidasis, shingles, oral hairy leukoplakia, and Kaposi’s sarcoma

349
Q

Does chronic herpes simplex infection typically begin to appear in AIDS patients with lower or higher CD4 counts than those that present with oral hairy leukoplakia?

A

Lower

350
Q

What are the final opportunistic pathogens that attack AIDS patients when their CD4 count drops below 50/μL?

A

Disseminated Mycobacterium avium and cytomegalovirus

351
Q

An AIDS patient presenting with hypoxemia and this CXR is likely experiencing what opportunistic infection, particularly if he responds to TMP/SMX? Is a DFA for this organism in sputum always sufficiently sensitive?

A

Pneumocystic jirovecii pneumonia; no, the DFA may not be sensitive enough with sputum

352
Q

What opportunistic pathogen are all of these lab detection methods being used to identify?

A

Pneumocystic jirovecii

353
Q

What staining can be used to detect Mycobacterium avium? What must be noted about the culture requirements for this organism?

A

Acid fast; culture requires a special medium and may take weeks

354
Q

What disease symptoms are caused by Mycobacterium avium in AIDS patients?

A

A disseminated disease called MAC that causes fevers, chills, sweats, weight loss, and diarrhea, with infection of many organs

355
Q

What is this infection, common in AIDS patients, that presents with ring-enhancing lesions in the brain after fever and headache for a week?

A

Toxoplasmosis

356
Q

A 35 year old man with AIDS presents with fever and headache for a week and has no ring enhancing lesions in the brain, but instead an India ink stain of CSF reveals the following. What organism is this? What treatment is recommended?

A

Cryptococcus neoformans; amphotericin B and flucytosine

357
Q

What viral infection is common in AIDS patients that causes weakness of the extremities, and patchy T2 hyperintensities without enhancement near the gray-white junction in a brain MRI?

A

JC (John Cunningham) virus

358
Q

What is the genomic makeup of JC virus? Does it have an envelope?

A

Double-stranded DNA virus; no envelope

359
Q

Does JC virus normally cause disease in immunocompetent individuals?

A

No

360
Q

How does JC virus enter the body? Where does it create a latent infection?

A

Enters via respiratory tract; latent infection of kidney

361
Q

Why does JC cause weakness of the extremities?

A

Reactivation of the virus can lead to viremia and infection of oligodendrocytes which causes demyelination

362
Q

When HIV/AIDS patients have a dropping CD4 count, what drugs are normally started to prevent TB? What about PCP and CNS toxoplasmosis? *Mycobacterium avium *complex?

A

TB - isoniazid;

PCP and CNS toxoplasmosis - TMP/SMX;

Disseminated Mycobacterium avium - Azithromycin

363
Q

What infections are a solid organ transplant recipient most at risk of within the first month?

A

Bacterial surgical site infection and nosocomial infections

364
Q

When do most opportunistic infections, excepting EBV and community acquired infections, appear in an immunosuppressed solid organ transplant recipient? When can EBV and community acquired infections be expected?

A

1-12 months after the transplant; EBV and community acquired infections appear more than 6 months afterward

365
Q

What is given as prophylaxis during a period of high immunosuppression in a solid organ transplant recipient to preven infection by Pneumocystis jirovecii?

A

TMP-SMX

366
Q

What is done to prevent CMV infection in a solid organ transplant recipient?

A

CMV is monitored by PCR frequently and ganciclovir is started and immunosuppression decreased if it turns positive

367
Q

Is prophylaxis available for solid organ transplant recipients to prevent EBV infection?

A

No, it is monitored by PCR and immunosuppression is decreased if the PCR is positive

368
Q

What are the main pathogens that chemotherapy patients with neutropenia are most at risk for?

A

Gram-negative bacteria e.g. Pseudomonas, Candida, and *Aspergillus *and other filamentous fungi

369
Q

What is the laboratory definition of neutropenia?

A

Absolute neutrophil count below 500 cells/mm3

370
Q

What is the approach to a patient that develops fever after neutropenia from chemotherapy?

A

1) Broad spectrum antibiotic wtih activity against Pseudomonas, e.g. cefepime
2) possible vancomycin, aminoglycosides or fluconazole if MRSA, gram negatives, or Candida respectively are suspected
3) if neutropenia is prolonged, start antifungal against Aspergillus

371
Q

What happens to the risk of invasive pulmonary aspergillosis if neutropenia contines for more than a few weeks?

A

It trends close to 80%

372
Q

When a patient receives a fully ablative bone marrow transplant, does he or she retain any of the past immune memory? What about vaccines?

A

All past immune memory is lost; past vaccines are no longer protective

373
Q

What family of viruses do both JC virus and BK virus belong to? Are they rare or ubiquitous?

A

Polyoma viruses; they are ubiquitous and cause diseased in immunodeficient hosts

374
Q

What is the organism pictured here that is responsible for this skin infection in a child? Acid fast staining is employed in the upper right. What does this infection reveal about the immunocompetency of the child?

A

Nocardia; the child is immunodefecient, perhaps due to a disorder of phagocytic function (chronic granulomatous disease)

375
Q

What laboratory features do Nocardia and Actinomyces share? How can they be differentiated?

A

Both are gram-positive, branching, filamentous and slow-growing rods;

while Nocardia is a strict aerobe, Actinomyces can grow in either condition, and Nocardia is weakly acid-fast staining while Actinomyces does not stain

376
Q

In patients with primary immunodeficiency, does the opportunistic pathogen that eventually presents reveal something about which kind of immunodeficiency the patient has?

A

Yes, depending on the organism, severity, and recurrence

377
Q

What eye infection is this? How painful is it?

A

Acanthamoeba keratitis; extremely painful

378
Q

What is the most common retinal infection in the US?

A

Toxoplasmosis gondii

379
Q

How can infection spread from the upper respiratory tract to the eye?

A

Via the nasolacrimal duct

380
Q

What are two methods of parenteral transmission of ocular infections?

A

Transplacental passage and direct contact in the birth canal during delivery

381
Q

What two organisms are significant for eye infection related to contact lens hygiene?

A

Acanthamoeba and Pseudomonas aeruginosa

382
Q

What bacterium is associated with eye infections following trauma with soil or vegetable matter?

A

Bacillus cereus

383
Q

What eye infection is associated with faulty sterilization of surgical instruments?

A

Mycobacterium chelonei

384
Q

What are two significant bacterial causes of conjunctivis?

A

*Strep pyogenes *and Neisseria gonorrhoeae

385
Q

What are two significant viral causes of conjunctivitis?

A

Adenovirus and Herpesvirus

386
Q

What is the presentation of Neisseria gonorrhoeae infection of the eye?

A

Hyperacute conjunctivitis with profuse yellow exudate, and it can perforate the eye

387
Q

What broad category of eye infection is this?

A

Blepharoconjunctivitis: the eyelids are inflamed (blepharitis) along with the conjunctiva

388
Q

What is always treated concurrently with N. gonorrheae infection of the conjunctiva?

A

Chlamydia, since coinfection rates are ~30%

389
Q

What kind of conjunctivitis is caused by chlamydia? How is it treated?

A

Inclusion conjunctivitis (named after the inclusion bodies seen in histological preparations); oral tetracycline, doxycycline, erythromycin, or azithromycin

390
Q

What is the leading cuase of preventable blindness in the world, mostly in developing countries? What is the vector for it? What bacterium causes it? How is it treated?

A

Trachoma; housefly; Chlamydia trachomatis; topical and oral tetracycline

391
Q

How is trachoma different from inclusion conjunctivitis, since both are caused by Chlamydia species?

A

Trachoma is on the inner surface of the eyelid, while inclusion conjunctivitis affects the conjunctiva

392
Q

What is the #1 risk factor for bacterial keratitis in the US?

A

Contact lens wear, particuarly overnight use

393
Q

What are the two most common organisms causing bacteria keratitis?

A

Staph aureus and Pseudomonas aeruginosa

394
Q

How does bacteria enter the cornea to cause keratitis, which is exacerbated by contact lens wear overnight?

A

Corneal abrasions

395
Q

What condition is seen here that was caused by contaminated contact lens wear overnight?

A

Bacterial keratitis, probably due to Pseudomonas or Staph

396
Q

How is bacterial keratitis diagnosed?

A

Culture of the bacterium from exudate or the offending contact lens source

397
Q

How is bacterial keratitis treated?

A

Topical antibiotics because they penetrate the cornea better than orals: fluoroquinolones like moxifloxacin, or vancomycin and tobramycin

398
Q

What is the primary adverse effect of topical antibiotics applied to the cornea?

A

The preservative can be toxic to the epithelium

399
Q

Are topical antibiotics on the cornea absorbed systemically?

A

Only in minute quantities, but still check for allergies and contraindications

400
Q

Which herpesviruses affect the eye?

A

Herpes simplex virus 1 and 2, varicella zoster virus, EBV, CMV, and Kaposi sarcoma-associated virus (HHV-8)

401
Q

What tissue is this? What infection is this?

A

This is the cornea; Herpes simplex keratitis

402
Q

What stain was used here to visualize a multinucleated epithelial cell in a case of keratitis? What virus is suspected?

A

Giemsa stain; Herpes simplex

403
Q

Should a topical or oral antiviral be used against herpes simplex keratitis?

A

Either can be used

404
Q

What two topical antivirals can be used for herpes simplex keratitis?

A

Trifluridine and ganciclovir

405
Q

What virus has caused this outbreak, which comes with a risk of keratitis?

A

Herpes zoster (varicella zoster virus)

406
Q

Is fungal keratitis more frequent in warmer or cooler areas of the US?

A

Warmer areas

407
Q

What is an environmental and a pharmacological risk factor for fungal keratitis?

A

Trauma to the cornea with a plant or vegetable is the leading risk factor, followed by topical steroid use

408
Q

What type of keratitis is likely here, which followed trauma to the eye with vegetable material?

A

Fungal keratitis

409
Q

What is the most common cause of fungal keratitis in the southern US? How is it treated?

A

Filamentus Fusarium; Natamycin drops

410
Q

Besides amphotericin B and Natamycin, what class of antifungals is also used against fungal keratitis?

A

Triazoles, e.g. ketoconazole, fluconazole, itraconazole, and voriconazole

411
Q

What part of this eye is inflamed? What does this layer cover?

A

The conjunctiva; it covers the sclera, the white part of the eye

412
Q

What part of the eye is inflamed in keratitis?

A

The cornea

413
Q

What is an infection of the whole eyeball called? What is the incidence post surgery? How is it treated

A

Endopthalmitis; 1/1000 after surgery; intravitreal injection of antibiotics or vitrectomy

414
Q

What is this emergency condition called?

A

Endopthalmitis, in this case caused by Staph

415
Q

What are the key clinical signs of inhalational anthrax?

A

Widened mediastinum with fever and sepsis

416
Q

What agent of bioterrorism presents with a widened mediastinum with fever and sepsis?

A

Inhalational anthrax

417
Q

What agent of bioterrorism creates a localized skin lesion with a depressed black scab?

A

Cutaneous anthrax

418
Q

What potential agent of bioterrorism causes a vesicular/pustular rash starting on the hands, covering the body and with all lesions at the same stage of development?

A

Smallpox

419
Q

What is the bacterium that causes anthrax?

A

Bacillus anthracis

420
Q

What is the gram staining and shape of anthrax? Does it form spores? Is it an aerobe or an anaerobe?

A

Large gram positive rod; spore forming; facultative anaerobe

421
Q

What are the three methods of infection by anthrax?

A

Inhalation, ingestion or inoculation through skin

422
Q

Does Bacillus anthracis have a capsule? What two toxins does it produce?

A

Yes; edema toxin and lethal factor

423
Q

How does anthrax lethal toxin cause cell death?

A

It is a zinc metalloprotease that stimulates inflammatory cytokine production

424
Q

How long does it take for cutaneous anthrax to manifest? What is the prognosis with treatment?

A

1-2 weeks; good prognosis with treatment (very rare mortality)

425
Q

Which manifestation of anthrax is responsible for the most deaths? How long does it take for symptoms to present?

A

Inhalational anthrax; up to 60 days after inhalation

426
Q

Where does anthrax replicate after spores are inhaled?

A

Macrophages phagocytose the spores and carry them to lymph nodes, where germination occurs weeks later

427
Q

Can anthrax spores be aerosolized? Can infections be spread person to person?

A

Yes, and they are odorless and colorless; no infectivity between humans

428
Q

What antibiotics are used against anthrax?

A

Penicillin and ciprofloxacin

429
Q

What organism causes plague? How is it transmitted to humans from its reservoir in rats?

A

Yersinia pestis, a member of Enterobacteriaceae; fleas

430
Q

What is this bacterium with the “safety-pin” appearance, transmitted via fleas?

A

Yersinia pestis or plague

431
Q

What is the genomic makeup of the variola virus (Smallpox)? How infectious is it? How is it spread between persons?

A

Large DNA virus; very infectious, only a few virions produces symptoms; spread via droplets or aerosols or direct/indirect contact

432
Q

What disease is caused by the variola virus?

A

Smallpox

433
Q

How long is it before the variola virus produces symptoms? What are they?

A

8 days; fever, malaise, headache, back ache, delirium

434
Q

What is the mortality of smallpox? What causes death?

A

15-40%; usually secondary to circulating immune complexes or bacterial superinfection

435
Q

Why do we not vaccinate for smallpox?

A

The last naturally occurring case was in 1977 in Somalia

436
Q

How is the chickenpox rash different from the smallpox rash?

A

The chicken pox rash has lesions in different stages (papules, vesicles, and crusts) and rarely involves the palms and soles, while the smallpox rash always presents with lesions in the same stage with no crusing and some are usually umbilicated.

Left, chickenpox; right, smallpox

437
Q

What vaccine did Edward Jenner discover in the 18th century that was active against smallpox? How quickly must it be given after smallpox exposure to confer immunity?

A

The cowpox virus given as a vaccine provides immunity against smallpox; Within 4 days

438
Q

Is there a proven treatment for smallpox?

A

No, although Cidofovir, a DNA polymerase inhibitor, may have some efficacy

439
Q

What poxvirus outbreak occurred in 2003 as a result of owners of pet prairie dogs?

A

Monkeypox

440
Q

What spore-forming bacillus that is naturally found in soil produces flaccid paralysis and is associated with improperly canned foods?

A

Clostridium botulinum

441
Q

How toxic is the botulinum toxin produced by Clostridium botulinum?

A

Very, 1 gram could kill a million people

442
Q

What are symptoms or signs of inhalational botulism?

A

Double/blurred vision, drooping eyelids, slurred speech, difficulty swallowing, and muscle weaknesses or flaccid paralysis, including paralysis of respiratory muscles

443
Q

What is the treatment for inhalational botulism?

A

Supportive and use of antitoxin

444
Q

What organism causes tularemia? What is its shape and gram staining? How is it transmitted naturally?

A

Francicella tularensis; Poorly staining gram negative coccobacilli; by ticks

445
Q

What are the three major causes of viral hemorrhagic fevers?

A

Filoviruses like Ebola and Marburg virus, and Arena viruses like Lassa fever

446
Q

How are most round worms treated, as a general rule?

A

Benzimidazoles, e.g. albendazole

447
Q

How are most flat worms treated, as a general rule?

A

Praziquantel

448
Q

How are most anaerobic protozoans like Entamoeba, Giardia, and Trichomonas treated, as a general rule?

A

Tinidazole and metronidazole

449
Q

Is the treatment for Ascaris different from that for hookworms?

A

No, both should be prescribed mebendazole or albendazole

450
Q

What drug can be used to treat all of: Enterobius, Strongyloides, Trichurius, hookworm, and Ascaris?

A

Albendazole

451
Q

Which roundworm species enter the body by penetrating the skin? Which one is significant for causing hyperinfection syndrome?

A

Strongyloides and hookworms; Strongyloides can cause hyperinfection syndrome

452
Q

What are adverse effects of albendazole?

A

Abdominal pain, reversible hair loss (alopecia), and liver damage (high liver enzymes)

453
Q

In the case of a severe hyperinfection syndrome caused by Strongyloides, what alterations in treatment may be made?

A

Ivermectin, albendazole, and thiabendazole are still administered but possibly as a rectal enema to increase exposure of the parasite to the drug

454
Q

What is the mechanism of ivermectin? What organisms is it the drug of choice for?

A

It is neurotoxic to the worm, keeping a chloride channel open and causing paralysis; Filiarisis causing river blindness, and sometimes Strongyloides

455
Q

What are two drugs that are active against filariasis?

A

Diethylcarbamazine (DEC) and ivermectin

456
Q

What class of organisms is praziquantel usually used for?

A

Flatworms (cestodes)

457
Q

When might albendazole be used instead of praziquantel for a tapeworm infection? Why?

A

In the case of neurocysticercosis (Taenia solium in the brain); albendazole has better CNS penetration

458
Q

What are all cases of schistosomiasis treated with?

A

Praziquantel

459
Q

What is this condition? What parasite spread by mosquitos is it indicative of, in conjunction with anemia?

A

Icterus; malaria

460
Q

How widespread is malarial resistance to chloroquine?

A

Very widespread (in red)

461
Q

What must be monitored when using IV quinidine?

A

Cardiotoxicity, since it can cause arrhythmias

462
Q

If a patient is taking quinine prophylaxis and they go into a coma, what adverse effect may have occured?

A

Hypoglycemia, because it stimulates pancreatic insulin secretion

463
Q

In the case of chloroquine resistance, what antibiotic can usually used for prophylaxis against and treatment of malaria? What is the adverse effect associated with this treatment?

A

Doxycycline in conjunction with quinine; photosensitivity

464
Q

Is mefloquine still used to treat or as prophylaxis for malaria?

A

While the weekly dosing is convenient, it has serious potential side effects (e.g., Stevens-Johnson syndrome) and is no longer preferred, only being used for pregnant women as it is the only non-teratogenic anti-malarial

465
Q

What is atovaquone and proguanil used to treat? What is the only side effect of concern?

A

Malaria; GI intolerance, so take it with food

466
Q

What antimalarial combination is an effective prophylaxis but may be too expensive for extended trips, and has few side effects except for GI intolerance?

A

Atovaquone and proguanil

467
Q

What treatment is used for severe, chloroquine resistant falciparum malaria?

A

IV quinidine and IV doxycycline

468
Q

What is IV artesunate used to treat, for which it was recently approved by the FDA? Is resistance to this drug yet known?

A

Malaria; no resistance yet reported

469
Q

When a malaria patient shows schizonts in a peripheral blood smear, what organism is less likely to be the culprit? What change should be made in treatment as opposed to the treatment for that organism?

A

P. falciparum is less likely and P. ovale and P. vivax are more likely; primaquine is used to kill schizonts

470
Q

What enzymatic deficiency is a contraindication for primaquine? Why?

A

G6PD deficiency; it can cause hemolytic anemia

471
Q

What is the preferred treatment for babesia? Why is it preferred over clindamycin and quinine?

A

Atovaquone with azithromycin; fewer side effects

472
Q

What is the drug of choice against Entamoeba histolytica infections? What is an important dietary guideline for patients on this drug?

A

Metronidazole; no alcohol should be consumed

473
Q

What can be added to metronidazole for treatment of amebiasis to kill cysts with infectious particles?

A

Iodoquinol

474
Q

What treatment options are shared by Giardia, Entamoeba, and Trichomonas? What is their mechanism?

A

Metronidazole and tinidazole; inhibition of DNA synthesis

475
Q

What is the major toxicity of amphotericin B?

A

Nephrotoxicity, with potential electrolyte abnormalities

476
Q

What insect-borne protozoan parasite infection can be treated with amphotericin B?

A

Leishmaniasis

477
Q

What is a typical FDA-approved treatment for Leishmaniasis that is not also used against fungi?

A

Pentavalent antimonials like sodium stibogluconate and meglumine antimonate

478
Q

What are sodium stibogluconate and meglumine antimonate used to treat?

A

Leishmaniasis

479
Q

How is South American trypanosomiasis treated? Is the drug available in the US?

A

Benznidazole and nifurtimox; only via the CDC

480
Q

Is the treatment for South American and African trypanosomiasis the same?

A

No

481
Q

What is the first line therapy for an AIDS patient presenting with ring enhancing lesions in a brain CT? What organism is implicated?

A

Pyrimethamine and sulfadiazene; Toxoplasma gondii

482
Q

What are pyrimethamine and sulfadiazene used to treat? What are the adverse effects associated with these drugs?

A

Toxoplasmosis, usually in an immunocompromised patient; pancytopenia and a skin reaction called Stevens-Johnson syndrome

483
Q

Can Pneumocystis jirovecii be grown in culture? How is it diagnosed? How is it treated?

A

No; direct fluorescence antibody; TMP-SMX

484
Q

Who will you need to call to treat kinetoplastids like Trypanosoma?

A

The CDC, since the treatments are not normally available in the US

485
Q

What is the top unnatural cause of death in low-income countries as reported by the WHO in 2008?

A

Lower respiratory infection

486
Q

What are the top two risk factors for the global distrubtion of disease in low and middle income persons?

A

Being underweight and unsafe sex

487
Q

What patient population does Doctors Without Borders focus on? How much does treatment cost?

A

Poorest, sickest patients worldwide; free to patient

488
Q

What is being done here on this patient that may have sleeping sickness in Sudan?

A

A lumbar puncture to retrieve CSF which can determine if the parasites have reached the CSF

489
Q

What is the relationship between severity and the risk of infection for the fetus over the course of a pregnancy?

A

Inverse

490
Q

Over the course of a pregnancy, during what period are infections worst for both mother and fetus? What period is typical for a better prognosis for the child at the expense of the fetus? What period is typical for a better prognosis for the mother at the expense of the fetus?

A

1st trimester – bad for mother and fetus;

3rd trimester – bad for mother, fetus may be savable;

2nd trimester – bad for fetus, mother is safer

491
Q

What viral pathogens are capable of vertical transmission?

A

5 H’s: HIV, Herpesviruses, Hep B, Hep C, HPV, …

Rubella,

and Parvovirus B19

492
Q

What protozoan parasite is most at risk of crossing from mother to fetus?

A

Toxoplasma gondii

493
Q

What bacteria can be transmitted from mother to fetus during pregnancy?

A

CLESS mnemonic:

Chlamydia,

Listeria,

E. Coli,

Syphilis,

and Strep (Group B)

494
Q

What is the key strategy for preventing neonatal infection of HIV? What viral co-infection is a risk for perinatal infection?

A

Decrease viral titers in the 3rd trimester; Hepatitis C

495
Q

What is the efficacy for antiretroviral treatment for vertical transmission of HIV to neonates? Is it more or less effective than C-section delivery alone?

A

Near 100%; much more effective

496
Q

What bacterium is a common colonizer of the human GU tract, found in 10-30% of pregnant women, and was the most common cause of sepsis and meningitis in infants <3mo old in the 1970s? How is vertical transmission prevented?

A

Strep agalactiae (group B Strep); screening at 26-28 weeks, and then treatment during labor or before C-section

497
Q

What is the prevention strategy for neonatal herpes?

A

Preventing maternal acquisition during pregnancy, and avoiding exposure to herpetic lesions during delivery

498
Q

For a pregant woman with active HSV displaying genital lesions, what is the recommendation for treatment or delivery?

A

C-section delivery

499
Q

What are the ToRCHSV infections?

A

A group of in utero infections that present similarly, including ocular findings and rash

500
Q

What in utero infections present similarly with ocular findings and a rash?

A

Use the mnemonic ToRCHSV:

Toxoplasma gondii

Rubella

Syphilis

Cytomegalovirus

HSV

Syphilis

Varicella

Microbiology (4 decks)

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