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Infectious Disease 2 > Exam Review 3 > Flashcards

Exam Review 3 Flashcards

1
Q

Which antimalarials block blood schizonticide?

A

Chloroquine, quinine (IV), mefloquine, sulfadoxine-pyrimethamine, artemisinins

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2
Q

Which antimalarials block hypnozoites?

A

Primaquine

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3
Q

Which antimalarial blocks the liver stage?

A

Atovaquone- proguanil

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4
Q

Which antimalarial blocks gametocytocide?

A

Artemisinins

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5
Q

Which medications inhibit the apicoplast?

A

doxycycline, azithromycin, clindamycin, fosmidomycin

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6
Q

What is quinine/quinidine?

A

Antimalarial derived from bark of Chinchona tree; blocks trophozoites, gametocytes of ovale, malariae, vivax
NOT falciparum; used in severe malaria; Oral, iv, im regimen; narrow therapeutic range (can cause worsening of hypoglycemia, Qt-interval prolongation, hypotension, hearing loss)

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7
Q

What is chloroquine?

A

Antimalarial that used to be used a lot; Now rarely used because of resistance (almost universal resistance in falciparum); remains drug of choice for P. ovale and P. vivax, as well as P. falciparum in Middle East or Central America

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8
Q

What are artemisinins?

A

Antimalarials that are highly potent, have rapid action, kill gametocytes, reduce transmission, and have no clinical resistance to date. HOWEVER, they’re expensive, typically have to be used with other drugs, and they have a short half-life

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9
Q

What are problems with artemisinin combined therapy?

A

Pharmacokinetic properties mismatched; Manslaughter with counterfeit drugs!

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10
Q

What is primaquine?

A

Uniquely broad spectrum (tissue schizontoid, asexual blood stages (vivax, NOT falciparum), gametocidocide); Used as treatment or prevention of relapse; Long regimen (2 weeks); Massive hemolysis in severe G6PD-deficiency - phenotypic screening prior

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11
Q

What is the WHO guideline for uncomplicated falciparum malaria?

A

Artemisinin combination therapy - primarily artemether + lumefantrine

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12
Q

What is the CDC guideline for uncomplicated falciparum malaria?

A

Atovaquone-proguanil (3 days) - don’t use if taken prophylactically

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13
Q

What does the CDC recommend for severe malaria?

A

Quinidine gluconate iv (3d, 7d SE Asia)
plus one of the following: doxycycline, tetracycline or clindamycin (7d); Investigational protocol:
Artesunate (from CDC), followed by either atovaquone proguanil, doxycycline, or mefloquine

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14
Q

What does the WHO recommend for severe malaria?

A

Artesunate iv or im; Quinine gluconate iv or im

– plus 7 days tetracycline, doxycycline or clindamycin

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15
Q

When should chemoprophylaxis for malaria be given?

A

Aimed at preventing severe P. falciparum

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16
Q

What should be given as chemoprophylaxis for malaria?

A

Atovaquone-proguanil (best tolerated, but expensive); can give Mefloquine (some resistance) or doxycycline (but causes photosensitivity, tricky in tropics…; can cause GI upset, yeast infections)

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17
Q

What is the timing for chemoprophylaxis for malaria?

A

Chloroquine, mefloquine, and doxycycline don’t prevent initial infection, need to be continued for 4 weeks; Atovaquone-proguanil affects blood and liver stages, only needs to be continued for 1 week

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18
Q

What is the problem with prophylactic mefloquine?

A

While it’s efficacious and only requires weekly dosing, it’s not tolerated by some (causes neuropsychiatric issues!); start 1 week in advance of travel

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19
Q

How can malaria be prevented in endemic areas?

A

Mosquito netting, indoor residual spraying

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20
Q

What is babesiosis?

A

Caused by intraerythrocytic protozoa Babesia; Emerging human infection (only over past 50 years appreciated); currently can get from tick or from blood transfusion; dependent on deer and mouse - humans are dead-end hosts

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21
Q

What are the species of babesia?

A

~ 100 Babesis species, at least 3 in US; B. microti in North-East (NE, CT, NY, P) - hundreds of cases reported; B. duncanii - West Coast (rare); B. divergens - very rare (more common in Europe; more severe disease, up to 45% mortality)

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22
Q

How does babesiosis present?

A

Incubation 1 – 6 weeks; Two ends of the spectrum: Mild flu-like illness in young and healthy vs. Life-threatening, malaria-like in asplenic, immunocompromised elderly; Generally non-specific: Fever (intermittent or sustained), severe chills, Fatigue, malaise, arthralgias, myalgias, SOB, (not as much GI symptoms)

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23
Q

What are complications of B. microti?

A

multi-organ failure

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24
Q

How is babesiosis diagnosed?

A

Historically xenodiagnosis; now microscopy clues, IFA test, PCR

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25
Q

How is babesiosis treated?

A

Not necessary in asymptomatic; If treated, prolonged courses; evaluate for Lyme; if mild microtii - atovaquone plus azithromycin; if severe, clindamycin plus quinine; b divergens requires immediate complete RBC exchange transfusion (plus cindamycin and quinine)

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26
Q

What is impetigo?

A

Highly contagious, bacterial infection of superficial epidermal layers; Mostly Staphylococcus aureus or Streptococcus pyogenes; 3 clinical presentations (Non-bullous, Bullous, Ecthymatous)

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27
Q

What are the clinical presentations of impetigo?

A
  1. Bullous: flaccid bullae with clear yellow fluid that becomes purulent, & ruptured leaves a thick brown crust, caused by exfoliative toxin producing S. aureus (Exotoxin A & B); 2. Non-bullous: papules surrounded by erythema that progress to pustules, which enlarge & rupture into thick, adherent crusts with gold appearance; 3. Ecthymatous: “punched-out” ulcer with black eschar surrounded by raised margin
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28
Q

How is impetigo treated?

A

Local care, bacterial culture; if healthy w/ limited infection: topical antibiotic; if complicated or widespread: oral antibiotic (1st gen cephalosporin or beta lactam-beta lactamase combo)

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29
Q

What is bacterial folliculitis?

A

superficial infection of hair follicles presenting as perifollicular pustules; Majority of bacterial folliculitis due to S. aureus; Exposure to hot tub/swimming pool  Pseudomonas; Acne patients treated with antibiotics  gram-negative bacteria

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30
Q

How is bacterial folliculitis treated?

A

antibacterial washes, topical antibiotics if localized, Oral antibiotics if widespread, resistant or recurrent, extensive surrounding cellulitis, immunosuppression, risk for MRSA (Methicillin-resistant S. aureus), systemic signs of infection; bacterial culture should be sent

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31
Q

What is cellulitis?

A

Bacterial infection of dermis often begins with portal of entry; can be associated with lymph node or lymphatic channels; Erysipelas is superficial cellulitis with marked dermal lymphatic involvement

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32
Q

What are risk factors for cellulitis?

A

Local trauma (bug bites, laceration, abrasion, puncture wound), Underlying skin lesion (furuncle, ulcer), Inflammation (local dermatitis, radiation therapy), Edema and impaired lymphatics in affected area, Preexisting skin infection (impetigo, tinea pedis); NOTE: Cellulitis from the following is rare: hematogenous spread of infection or direct spread of subjacent infections (fistula from osteomyelitis)

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33
Q

How should cellulitis be treated?

A

Outpatients with non-purulent cellulitis: empirically treat for β-hemolytic streptococci (Group A) and MSSA; Outpatients with purulent cellulitis: empirically treat for community-associated MRSA

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34
Q

What is venous stasis dermatitis?

A

presents with erythema, scale, pruritus, erosions, exudate, and crust; usually located in the lower third of the legs, superior to medial malleolus; can occur bilaterally or unilaterally; edema often present, as well as varicose veins and hemosiderin deposits (pinpoint yellow-brown macules)

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35
Q

How should an abscess be managed?

A

I&D: 1. Analgesia and sedation; 2. Incision; 3. Manual expression of contents; 4. Lysis of intracavitary septae; 5. Saline irrigation; 6. Wound stenting

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36
Q

What are dermatophyte infections?

A

Superficial fungal infections caused by organisms that invade and proliferate in keratin-containing layers of hair, skin & nails; classified by site

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37
Q

What are common complications of tinea pedis?

A

Cellulitis, Tinea corporis

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38
Q

How is dermatophyte infection diagnosed?

A

Microscopic evaluation of scale treated with potassium hydroxide (KOH) solution; Take skin scrapings for KOH exam from MARGIN;

39
Q

What is the treatment for dermatophyte infection?

A

Topical treatment is usually appropriate as first-line agent for tinea pedis and tinea corporis; Oral medications considered when involvement is extensive, tinea corporis transmitted by an animal, fungal infection of hair or nails

40
Q

What is tinea versicolor?

A

caused by Malassezia species; clinical manifestations when yeast transforms to mycelial form; Characterized by well-demarcated, tan, salmon, or hypo/hyper-pigmented patches, most commonly on trunk; scale often not visible, but seen when rubbed – diagnostic

41
Q

How is tinea versicolor treated?

A

topical or oral antifungals

42
Q

What is Molluscum contagiosum?

A

Viral infection due to pox virus; Benign, usually asymptomatic (no systemic manifestations); Characterized by 2 to 20 discrete, 5-mm-diameter, skin-colored to translucent, dome-shaped papules, some with central umbilication; Spread via skin-to-skin contact, fomite exposure, & autoinoculation; Lesions commonly occur on trunk, face, & extremities but rarely generalized

43
Q

Who typically is at risk for Molluscum contagiosum?

A

Young children (especially those with atopy) (NOT a sign of immunocompromise); Sexually active adults (STD); Immunosuppressed individuals (Adults with chronic MC outside the genital area should be evaluated for immunosuppression)

44
Q

How is Molluscum contagiosum treated?

A

Various treatment options available: cantharidin, curettage, cryotherapy, topical retinoids, imiquimod; Children: spontaneous remission frequently occurs (“no treatment” is an option)

45
Q

What causes warts?

A

HPV that infects skin and mucosal epithelia

46
Q

How can warts be treated?

A

Majority common warts spontaneously resolve in 1-2 years without scar; Most treatments are destructive or aim at stimulating the immune response to HPV (Cryotherapy, Salicylic acid, Topical tretinoin, Podophyllin, Imiquimod); No specific antiviral therapy for cure; high recurrence rates

47
Q

What is the Hutchinson’s sign?

A

Herpes zoster of nasal tip; must Refer to ophthalmology patients with V1 Zoster due to risk of ocular disease and permanent loss of sight

48
Q

What are trematodes?

A

Dorsoventrally flattened; 1st intermediate host always a snail

49
Q

What are Schistosomes?

A

Bisexual flukes (dioecious) – Dorsoventrally flattened male clasps a cylindrical female in a ventral groove; Live in Blood vessels; Penetrate skin of definitive host

50
Q

What is the peak age group for Schisto?

A

Peaking in the age group of 15 to 20 years; Decline in intensity - not in prevalence - as patients get older

51
Q

What is the life cycle of Schisto?

A
  1. Eggs in fresh water; 2. Snail as intermediate host; 3. Cercariae released in fresh water; 4. penetrate the human skin; 5. larvae migrate to the lungs, then to the heart and the liver; 6. worms pair off; 7. worms migrate to the bowel or else cause chronic schisto; 8. eggs are excreted
52
Q

What are the clinical presentations of acute Schisto?

A

Cercarial Dermatitis (Pruritic, papular rash found on skin at the site of the cercarial penetration), Occurs within 24 hours of exposure - Usually on lower legs (“Swimmer’s itch”); Symptoms 4 to 8 weeks after exposure of Katayama Fever (Fever, sweats, chills, cough, diarrhea and headaches) - most likely to occur in new travelers

53
Q

What are the physical and lab findings of acute schisto?

A

Lymphadenopathy and hepatosplenomegaly, Skin lesions – urticaria, Respiratory symptoms 2/3 – interstitial pneumonitis, Eosinophilia, Hyperglobulinemia

54
Q

What is the treatment for acute schisto?

A

Presumptive - Praziquantel works only against adult worms, so retreatment necessary

55
Q

How is acute schisto diagnosed?

A

Eggs may or may not be present stool/urine, so dx with eosinophilia and positive serology

56
Q

What is chronic schisto?

A

Eggs in the intestinal wall that induce inflammation and microabscess formation; Symptoms/signs: Diarrhea (more common in children), Pain in the left lower quadrant, Occult blood in stool or visible, Colonic polyposis; Eggs can also embolize liver, causing granulomatous inflammatory response and periportal collagen deposits, portal hypertension and bleeding; hepatosplenic disease

57
Q

How is chronic schisto diagnosed?

A

Gold standard – eggs in patient’s stool; Serologic tests – FAST ELISA - not useful in someone from an endemic area

58
Q

What is urinary schisto?

A

Usually seen in children - Eggs deposit around the lower end of ureters and in the bladder wall; Symptoms are seen large percentage infected; causes fetal head sign; can cause squamous cell carcinoma; caused by S. haematobium

59
Q

What are the symptoms of urinary schisto?

A

Hematuria – 10 -12 weeks after exposure; Dysuria and hematuria – early and late; Late manifestations: Calcifications in bladder, Obstruction of the ureter, Proteinuria – nephrotic range, Renal Failure

60
Q

How can urinary schisto be diagnosed?

A

Eggs in urine (Viability test – hatching test), Eggs in bladder biopsy, FAST ELISA

61
Q

How is urinary schisto treated?

A

Pyrazinoisoquinoline; Action Unknown

62
Q

What is the pathogenesis of polio?

A

Humans are only known reservoir, Spread by fecal-oral transmission, Peaks during warm months in temperate climates

63
Q

What is post-polio syndrome?

A

Complication after 30-40 years; Not an infectious process

64
Q

What are the clinical features of polio?

A

May range from clinically inapparent illness (90% of infections) to paralytic polio; Abortive poliomyelitis (8% of cases): Fever, headache, sore throat, no neurological sequelae; Nonparalytic poliomyelitis (1-2%): Severe headache, neck stiffness (“aseptic meningitis”) w/ full recovery after 2-10 days; Spinal paralytic poliomyelitis (less than 1%): weakness and flaccid asymmetric lower limb paralysis, can involve respiratory muscles, recover from paralysis (often incomplete) can occur, 10% fatality rate; Bulbar paralytic poliomyelitis (less than 0.1%): Cranial nerve paralysis (mostly CN 9, 10), Vasomotor and respiratory centers involved, may be fatal due to respiratory muscle paralysis, 50% fatality rate

65
Q

What are the types of polio vaccines?

A

Inactivated poliovirus vaccine, IPV: injected, does not cause disease, does not produce intestinal immunity, currently used; Oral poliovirus vaccine, OPV: easier to administer, produces intestinal immunity, usually reverts during intestinal replication, no longer used in US

66
Q

What are enteroviruses?

A

Usually no GI symptoms; Common childhood infections; Worldwide distribution, summer peaks in temperate
climates; Diagnosed clinically or viral culture or PCR

67
Q

How can enteroviruses affect the CNS?

A

Aseptic meningitis; Encephalitis (Echovirus and Coxsackievirus); Chronic meningoencephalitis; Enterovirus paralysis (Infrequently associated with echovirus and
Coxsackievirus infections, Less severe than poliomyelitis, Not permanent)

68
Q

How does enteroviral meningitis present?

A

Prodrome: fever, chills, malaise, URI; presents as headache, fever, stiff neck, photophobia; NOTE: 90% of viral aseptic meningitis in community due to
group B Coxsackieviruses; Diagnosed by PCR of spinal fluid; Therapy is supportive

69
Q

What is Enterovirus exanthems?

A

Morbilliform - fine, erythematous, maculopapular; seen on face, arms, trunk; Associated with echovirus 9

70
Q

What is hand, foot, and mouth disease?

A

Distinct vesicular eruptions in mouth, on hands and
feet; Associated with Coxsackievirus A16 or enterovirus
71; may cause neurologic disease; large outbreaks in Asia

71
Q

What is rotavirus?

A

Single most important cause of severe diarrheal
illness in infants and young children worldwide -
30-50%; Seven different serogroups, infect many different
animals. A, B, C infect humans; Segmented dsRNA genome = reassortment; High mortality in developing world due to dehydration

72
Q

What is rotavirus pathogenesis?

A

Transmitted by fecal-oral contamination; only requires 10-100 infectious particles; Repeated infections with our without illness can occur with same or different strains; Increasing levels of immunity with repeated
exposures or vaccination; Young children 3 mo - 2 yo primarily affected; disrupts tight junctions and microvillar network; secretes enterotoxin

73
Q

What are the symptoms of rotavirus?

A

Self-limiting disease, vomiting, watery diarrhea, low
grade fever; Asymptomatic infections play a role in spread; Incubation period 1-3 days; Vomiting followed by 4-8 days of diarrhea; Recovery usually complete unless fluid/electrolyte replacement is not done - particularly risky for children under 2

74
Q

What are the vaccines for rotavirus?

A

RotaTeq: human - bovine reassortant; Rotarix - infectious attenuated human isolate

75
Q

What is norovirus?

A

Caliciviridae; (+) strand RNA virus; Causes 50% of all food-borne outbreaks of gastroenteritis (23 million/yr US)

76
Q

What is the pathogenesis of norovirus?

A

Fecal-oral spread; Retain infectivity passing through stomach; Blunting of villi in proximal jejunum, but site of
replication not known; Basis for vomiting, diarrhea not known

77
Q

What is the epidemiology of norovirus?

A

Affects all ages; Year round, peaks in cold weather; Outbreaks often occur in semi-closed environments
(nursing homes, hospitals, cruise ships), the military,
schools and at recreational activities (sports events,
camping trips, travel) that favor person-to-person
spread; Incubation period 10-51 hr; Viral shedding: Peaks 1-3 days after illness onset, but may persist for 56 days; Immunity: short term homologous only; reinfection
may occur

78
Q

What are the symptoms of norovirus?

A

Sudden onset of vomiting (more common
in children) and diarrhea (more common in adults); 30% asymptomatic infections; Severity: Less than other diarrheal infections but can lead to dehydration; Duration of illness: 28-60 hr; sometimes longer, especially in immunocompromised or with underlying illness

79
Q

What is a hypnozoite (malaria)?

A

Delayed replication (i.e. dormant); Merozoites produced months after initial infection; P. vivax and P. ovale only; Not sensitive to chloroquine, quinine, mefloquine or artemisinin

80
Q

What is the typical clinical presentation of malaria?

A

Prodromal body aches, fatigue 2 – 3d prior; 1. Cold stage: feeling of intense cold and shivering for 15-60min; 2. Hot stage: intense heat, dry burning skin, throbbing headaches; 3. Sweating stage: profuse, declining temperature, 2 – 4 hours, exhausted and weak (sleep); this is a cyclical pattern!

81
Q

What is the parasitic cycle in malaria?

A
  1. Merozoite; 2. Ring; 3. Trophozoite; 4. Schizont
82
Q

What is the cyclical timing for P vivax? P ovale? P malaria? P knowlesi?

A

48 hr in P vivax, P ovale, 72 hr in P malaria, 24 hr in P knowlesi; P falciform can have any pattern

83
Q

What is P vivax?

A

Malaria found in mainly South-East Asia, Americas; Host Duffy receptor required (almost never encountered in (West) Africa); Very acute febrile illness; Almost no fatalities – beware exceptions!; Recurrent infections (hypnozoites)

84
Q

What is P ovale?

A

Malaria w/ oval erythrocytes with fimbriated edges; found in Sub-Sahara Africa & Western Pacific islands; Recurrent infections (hypnozoites); Lower parasitemia; Difficult to distinguish from P. vivax

85
Q

What is P malariae?

A

Mild disease; Chronic stage: very low parasitemia, no evidence of persistent liver stages; Quartan 72 hr life cycle; Rare Nephrotic syndrome

86
Q

What is P knowlesi?

A

Severe disease - Malaysia in 2002 saw increase of “atypical malaria”; Only primate parasite with
24h erythrocytic cycle

87
Q

What is P falciparum?

A

Severe malaria; Extensive parasite sequestration & organ dysfunction: anemia, Coma / Cerebral malaria, Acute respiratory distress syndrome (ARDS), Lactic acidosis, Severe jaundice, Hypoglycemia (decreased gluconeogenesis), Hyperparasitemia

88
Q

What can travel clues tell you about malaria type?

A

Interval to development of symptoms: less than 10 days: P. falciparum; 10 – 60 days: Any species; more than 60 days: very unusual for P. falciparum; more than 3 years: P. malariae

89
Q

How is malaria diagnosed?

A

Giemsa stain; BinaxNow - rapid detection test;

90
Q

What affects malaria immunity?

A

PfEMP1 - protective immunity takes years, immunity lost within 1 year of leaving endemic area; Antibodies are limited to geographic regions; pregnancy causes new receptors (CSA) and wipes away immunity

91
Q

What is cerebral malaria?

A

coma more than 1 hour after seizure or treatment for hypoglycemia and P. falciparum parasitemia; fatal if not treated! if treated, fatal in 10-20%

92
Q

What is malarial retinopathy?

A

may aid in diagnosis (particularly of cerebral malaria - but not all patients have this); White centered hemorrhages, Macular whitening, Orange discoloration of vessels

93
Q

How does sickle cell affect malaria?

A

six-fold reduction in death, impaired parasite growth at lower oxygen tension

94
Q

What is a var gene?

A

unique to P. falciparum, Protein insertion RBC

Infectious Disease 2 (6 decks)

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