Infectious Disease Flashcards

1
Q

Leptospires have this type of flagella

A

2 periplasmic flagella

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2
Q

Most impt reservoir of leptospires

A

rodents

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3
Q

T/F

The vast majority of infections with Leptospira cause no or only mild disease in humans.

A

True

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4
Q

T/F

During the immune phase, the appearance of antibodies coincides with the disappearance of leptospires from the blood.

A

True
However, the bacteria persist in various organs, including liver, lung, kidney, heart, and brain

During the immune phase, resolution of symptoms may coincide with the appearance of antibodies, and leptospires can be cultured from the urine

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5
Q

Usual incubation period of leptospirosis

A

2-30

The incubation period is usually 1–2 weeks but ranges from 2 to 30 days.

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6
Q

2 phases of leptospirosis

A

The acute leptospiremic phase is characterized by fever of 3–10 days’ duration, during which time the organism can be cultured from blood and detected by (PCR).

During the immune phase, resolution of symptoms may coincide with the appearance of antibodies, and leptospires can be cultured from the urine.

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7
Q

Weil’s syndrome triad

A

Weil’s syndrome, encompasses the triad of hemorrhage, jaundice, and acute kidney injury.

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8
Q

Typical electrolyte abnormality in leptospirosis

A

Typical electrolyte abnormalities include hypokalemia and hyponatremia

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9
Q

Common ECG finding in leptospirosis

A

Cardiac involvement is commonly reflected on the electrocardiogram as nonspecific ST- and T-wave changes. Repolarization abnormalities and arrhythmias are considered poor prognostic factors

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10
Q

Most common radiologic finding in severe leptospirosis

A

The most common radiographic finding is a patchy bilateral alveolar pattern that corresponds to scattered alveolar hemorrhage.

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11
Q

Based on Harrisons , how is leptospirosis confirmed

A

A definitive diagnosis of leptospirosis is based on isolation of the organism from the patient, on a positive result in the PCR, or on seroconversion or a rise in antibody titer.

In cases with strong clinical evidence of infection, a single antibody titer of 1:200–1:800 (depending on whether the case occurs in a low- or high-endemic area) in the microscopic agglutination test (MAT) is required.

** In CPG At least 1:1600 is enough for diagnosis

Preferably, a fourfold or greater rise in titer is detected between acute- and convalescent-phase serum specimens.

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12
Q

In rare instances, a ______ reaction
develops within hours after the initiation of antimicrobial therapy for leptospirosis

A

Jarisch-Herxheimer

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13
Q

Treatment for leptospirosis

A
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14
Q

Based on CPG when do you suspect leptospirosis?

A
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15
Q

Based on CPG what are the lab results that may indicate severe leptospirosis?

A
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16
Q

Based on CPG what are the recommended tests for AKI in leptospirosis?

A
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17
Q

Based on CPG what is the IVF of choice for px with leptospirosis presenting with shock?

A

Plain NSS with K incorporation

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18
Q

Based on CPG, what are the indications for HD

A

Almost same values as severe lepto but K should be > 5

HD should be done DAILY in critically ill px

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19
Q

Based on CPG how do you manage oliguria in leptospirosis

A
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20
Q

Based on CPG, what is the 1st sign of pulmonary involvement in leptospirosis?

A

tachypnea >30

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21
Q

Based on CPG, what are the 2 most common pulmonary complications of leptospirosis?

A

Pulmonary hemorrhage and ARDS

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22
Q

Based on CPG, how do you treat the pulmonary complications of leptospirosis?

A

Methylprednisolone should be given as 1gm IV for 3 days then should be continued as oral prednisolone 1mg/kg/day for 7 more days

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23
Q

Based on CPG, recommended PRE exposure prophy for leptospirosis

A
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24
Q

Based on CPG, duration of POST exposure prophylaxis for leptospirosis

A
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25
Q

Which of the Plasmodium species can cause relapse

A
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26
Q

What stage of the Plasmodium species invade the RBCs?

A

Merozoites invade RBCs to become trophozoites

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27
Q

Phenotype resistant to P. vivax

A

Most West Africans and people with origins in that region are the Duffy-negative FyFy phenotype and are generally resistant to P. vivax malaria

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28
Q

The most effective mosquito vectors of malaria are those

A

Anopheles gambiae species complex in Africa, that are long-lived, occur in high densities in tropical climates, breed readily, and bite humans in preference to other animals.

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29
Q

P. ___ and P. ___ show a marked predilection for young RBCs and P. ____for old cells;

A

vivax and ovale - young
malariae- old

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30
Q

Genetic abnormalities/ conditions with reduced risk of dying from severe P. falciparum malaria

A

The geographic distributions of the thalassemias, sickle cell disease, hemoglobins C and E, hereditary ovalocytosis, and (G6PD) deficiency closely resemble that of falciparum malaria before the introduction of control measures. This similarity suggests that these genetic disorders confer protection against death from falciparum malaria

Hemoglobin S–containing RBCs impair parasite growth at low oxygen tensions, and P. falciparum– infected RBCs containing hemoglobin S or C exhibit reduced cytoadherence because of reduced surface presentation of the adhesin PfEMP1

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31
Q

T/F
In malaria, the corneal reflexes are
preserved even when patients are in deep coma

A

False

preserved except in deep coma

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32
Q

Pathophysiology of hypoglycemia in severe malaria

A

Hypoglycemia, an important and common complication of severe malaria, is associated with a poor prognosis and is particularly problematic in children and pregnant women. Hypoglycemia in malaria results from both a failure of hepatic gluconeogenesis and an increase in the consumption of glucose by the host and, to a much lesser extent, the malaria parasites.

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33
Q

Manifestations of severe malaria

A
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34
Q

Features indicating poor prognosis in severe malaria

A
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35
Q

T/F

Transfusion associated malaria may still have relapses from P. vivax and ovale

A

False

there is no preerythrocytic stage of development, and thus there are no relapses of P. vivax and P. ovale infections

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36
Q

Plasmodium species associated with Quartan malaria

A

P. malariae

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37
Q

Identify the stages of P. falciparum

A

A. Young trophozoite. B. Old trophozoite. C. Trophozoites in erythrocytes and pigment in polymorphonuclear cells. D. Mature schizont. E. Female gametocyte. F. Male gametocyte

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38
Q
A

A. Young trophozoite. B. Old trophozoite. C. Mature schizont. D. Female gametocyte. E. Male gametocyte

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39
Q

disadvantage of RDTs for diagnosis of P. falciparum

A

A disadvantage of RDTs is that they do not quantify parasitemia

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40
Q

In severe malaria, a poor prognosis is indicated by a predominance of more mature P. falciparum parasites (i.e., >___% of parasites with visible pigment) in the peripheral-blood film or by the presence of phagocytosed malarial pigment in >__% of neutrophils (an indicator of recent schizogony)

A

20%

5%

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41
Q

What are the diagnostic tests used for malaria

A
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42
Q

First line tx for uncomplicated P. falciparum malaria

A

The World Health Organization (WHO) recommends artemisinin-based combination therapy (ACT) as first-line treatment for uncomplicated P. falciparum malaria in malaria-endemic areas

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43
Q

Tx for severe falciparum malaria

A

Artesunate therefore is now the drug of choice for all patients with severe malaria everywhere

Severe falciparum malaria constitutes a medical emergency requiring intensive nursing care and careful management. Adjunctive treatments such as high-dose glucocorticoids, urea, heparin, dextran, desferrioxamine, antibody to tumor necrosis factor α, high-dose phenobarbital (20 mg/kg), mannitol, or large-volume fluid or albumin boluses have proved either ineffective or harmful in clinical trials and should not be used. In acute renal failure or severe metabolic acidosis, hemofiltration or hemodialysis should be started as early as possible

44
Q

Tx to prevent relapse for P. vivax and P. ovale

A

Need to add primaquine in addition to chloroquine or amodiaquine

Primaquine eradicates hepatic forms of P. vivax and P. ovale;

Note: primaquine should NOT be given in severe G6PD deficiency

45
Q

When a patient with severe malaria is unconscious, what lab test/s should you request for?

A

When the patient is unconscious, the blood glucose level should be measured every 4–6 h. All patients should receive a continuous infusion of dextrose, and blood concentrations ideally should be maintained above 4 mmol/L. Hypoglycemia (<2.2 mmol/L or 40 mg/dL) should be treated immediately with bolus glucose.

The parasite count and hematocrit should be measured every 6–12 h. It has been recommended that if the hematocrit falls to <20%, whole blood (preferably fresh) or packed cells should be transfused slowly, with careful attention to circulatory status.

46
Q

What antimalarial drug is associated with hypoglycemia

47
Q

What antimalarial drug is associated with Hypotension

A

Chloroquine

48
Q

What anti malarial drug is associated with Agranulocytosis and should not be used with efavirenz

A

Amodiaquine

49
Q

What antimalarial drug is associated with Megaloblastic anemia

A

Pyrimethamine

50
Q

Artemisinin and derivatives (artemether, artesunate) do not have action on these stages of Plasmodium

A

kills all but fully mature gametocytes of P. falciparum. No action on liver stages

51
Q

Treatment for acute pulmonary edema in malaria

A

This syndrome is caused by increased pulmonary capillary permeability. Patients should be positioned with the head of the bed at a 45° elevation and should be given oxygen and IV diuretics. Positive-pressure ventilation should be started early if the immediate measures fail

52
Q

Treatment for hypoglycemia in malaria

A

An initial slow injection of 20% dextrose (2 mL/kg over 10 min) should be followed by an infusion of 10% dextrose (0.10 g/kg per hour). The blood glucose level should be checked regularly thereafter as recurrent hypoglycemia is common, particularly among patients receiving quinine

53
Q

Treatment for spontaneous bleeding in malaria

A

Patients who develop spontaneous bleeding should be given fresh blood and IV vitamin K.

54
Q

Treatment for convulsions in malaria

A

Convulsions should be treated with IV or rectal benzodiazepines and, if necessary, respiratory support.

55
Q

the only drug advised for pregnant women traveling to areas with drug-resistant malaria;

A

Mefloquine

this drug is generally considered safe in the second and third trimesters of pregnancy;

56
Q

When should pre exposure prophylaxis be taken when visiting a malaria endemic region

A

Travelers to a malaria endemic region should start taking antimalarial drugs 2 days to 2 weeks before departure so that any untoward reactions can be detected before travel and so that therapeutic antimalarial blood concentrations will be present if and when any infections develop

Antimalarial prophylaxis should continue for 4 weeks after the traveler has left the endemic area, except if atovaquone-proguanil or primaquine has been taken; these drugs have significant activities against the liver stage of the infection (causal prophylaxis) and can be discontinued 1 week after departure from the endemic area

57
Q

Atovaquone-proguanil is contraindicated in persons with _______

A

severe renal impairment (creatinine clearance rate, <30 mL/min).

58
Q

Serotypes of Salmonella that are only restricted to human hosts

A

The growth of serotypes Salmonella Typhi and Salmonella Paratyphi is restricted to human hosts, in whom these organisms cause enteric (typhoid) fever.

59
Q

T/F

All Salmonella infections begin with ingesting organisms, most commonly in contaminated food or water.

A

True

The infectious dose ranges from 200 colony-forming units (CFU) to 106 CFU, and the ingested dose is an important determinant of incubation period and disease severity

60
Q

Mean incubation period for S. typhi

A

The mean incubation period for S. Typhi is 10–14 days but ranges from 5 to 21 days, depending on the inoculum size and the host’s health and vaccination status.

The most prominent symptom is prolonged fever (38.8°–40.5°C [101.8°–104.9°F]), which can continue for up to 4 weeks if untreated

61
Q

When do yo usually see rose spots in typhoid fever

A

Rose spots make up a faint, salmon-colored, blanching, maculopapular rash located primarily on the trunk and chest. The rash is evident in ~30% of patients at the end of the first week and resolves without a trace after 2–5 days.

62
Q

When do you expect to see GI complications of typhoid fever?

A

Gastrointestinal bleeding (6%) and intestinal perforation (1%) most commonly occur in the third and fourth weeks of illness and result from hyperplasia, ulceration, and necrosis of the ileocecal Peyer’s patches at the initial site of Salmonella infiltration

63
Q

What are the neurologic manifestations associated with Typhoid fever

A

meningitis, Guillain-Barré syndrome, neuritis, and neuropsychiatric symptoms (described as “muttering delirium” or “coma vigil”), with picking at bedclothes or imaginary objects

64
Q

Chronic carriage of Salmonella is common among which subsets of patients

A

Chronic carriage is more common among women, infants, and persons who have biliary abnormalities or concurrent bladder infection with Schistosoma haematobium

65
Q

Definitive diagnostic test for typhoid fever

A

The definitive diagnosis of enteric fever requires the isolation of S. Typhi or S. Paratyphi from blood, bone marrow, other sterile sites, rose spots, stool, or intestinal secretions.

The diagnostic sensitivity of blood culture is only ~60% and is lower with low blood sample volume and among patients with prior antimicrobial use or in the first week of illness, reflecting the small number of S. Typhi organisms (i.e., <15/mL) typically present in the blood

Bone marrow culture is >80% sensitive, and, unlike that of blood culture, its yield is NOT reduced by up to 5 days of prior antibiotic therapy

Stool cultures, although negative in 60–70% of cases during the first week, can become positive during the third week of infection in untreated patients.

66
Q

If blood, bone marrow, and intestinal secretions are all cultured, the yield is >___ for Salmonella

67
Q

Antimicrobial tx for Typhoid fever

A

If drug susceptible, use FQ

68
Q

How do you prevent typhoid fever?

A

Two typhoid vaccines are commercially available in the United States:

(1) Ty21a, an oral live attenuated S. Typhi vaccine (given on days 1, 3, 5, and 7, with revaccination with a full four-dose series every 5 years); and

(2) Vi CPS, a parenteral vaccine consisting of purified Vi polysaccharide from the bacterial capsule (given in a single dose, with a booster every 2 years)

69
Q

S. Enteritidis infection associated with what food?

A

chicken eggs

70
Q

Treatment of choice for non typhoidal salmonellosis (NTS)

A

Because of increased resistance to conventional antibiotics such as ampicillin and TMP-SMX, extended-spectrum cephalosporins and fluoroquinolones have emerged as the agents of choice for the treatment of MDR NTS infections

71
Q

Bacteremia and metastatic infection are most common with which non typhoidal salmonellosis (NTS) species?

A

Salmonella Choleraesuis and Salmonella Dublin

72
Q

Endovascular infection should be suspected if there is high-grade bacteremia (>___% of three or more blood cultures positive) of non typhoidal salmonellosis (NTS) species

A

50%

Echocardiography, CT, and indium-labeled white cell scanning are used to identify localized infection

73
Q

Antimicrobial tx for NTS

A

Preemptive antibiotic treatment should be considered for patients at increased risk for invasive NTS infection, including neonates (probably up to 3 months of age); persons >50 years of age with known or suspected atherosclerosis; and patients with immunosuppression, cardiac valvular or endovascular abnormalities, or significant joint disease

74
Q

Duration of tx for NTS with endocarditis, arteritis

A

If the patient has endocarditis or arteritis, treatment for 6 weeks with an IV β-lactam antibiotic (such as ceftriaxone or ampicillin) is indicated

75
Q

Vectors of dengue viruses

A

Mosquitoes (predominantly Aedes aegypti, A. albopictus)

Dengue virus is under flaviviruses

76
Q

Pathogenesis of encephalitis in arthropod borne viruses

A

Viremia leads to multifocal entry into the CNS, presumably through infection of olfactory neuroepithelium, with passage through the cribriform plate, “Trojan horse” entry with infected macrophages, or infection of brain capillaries

77
Q

the most nonspecific of the disease syndromes caused by arthropod-borne and rodent-borne viruses

A

Fever and myalgia syndrome

Treatment is supportive, but acetylsalicylic acid is avoided because of the potential for exacerbated bleeding or Reye’s syndrome

78
Q

The most clinically significant flaviviruses that cause the fever and myalgia syndrome are

A

dengue viruses 1–4

79
Q

Duration of incubation of dengue

A

After dengue virus infection and an incubation period averaging 4–7 days, three evolving phases are described: a febrile phase, a critical phase, and a recovery phase.

80
Q

What is a positive tourniquet test in dengue

A

A positive tourniquet test—i.e., the detection of 10 or more new petechiae in one square inch of the upper arm after a 5-min blood pressure cuff inflation to midway between systolic and diastolic pressure—may demonstrate microvascular fragility associated with dengue but is more likely to be associated with severe disease.

81
Q

When do rashes appear in dengue?

A

Near the time of defervescence on days 3–5, a maculopapular rash begins on the trunk and spreads to the extremities and the face.

82
Q

The most significant flaviviruses that cause VHF are the mosquito-borne _____ and ____

A

dengue viruses 1–4 and yellow fever virus

83
Q

Subset of people that may be given Dengvaxia

A

A tetravalent live attenuated dengue vaccine based on the attenuated yellow fever virus 17D platform (CYD-TDV, or Dengvaxia) was licensed in 2015 and registered in 20 countries for individuals 9–45 years of age. However, retrospective analysis of phase 3 trials in Latin America and Asia suggested protection from severe dengue only in previously seropositive individuals; indeed, the risk of severe dengue was actually increased in seronegative vaccine recipients over that in nonvaccinated seronegative individuals, a result suggesting that a “first serologic hit” from the vaccine predisposes naïve recipients to more severe natural dengue infection.

84
Q

The clinical manifestations of tetanus occur only after tetanus toxin has reached _________

A

presynaptic inhibitory nerves

85
Q

. Serum anti-tetanus immunoglobulin G also may be measured in a sample taken before the administration of antitoxin or immunoglobulin; levels >_____ (measured by standard enzyme-linked immunosorbent assay) are deemed protective and do not support the diagnosis of tetanus

86
Q

Antimicrobial therapy for tetanus

A

Metronidazole (400 mg rectally or 500 mg IV every 6 h for 7 days) is preferred for antibiotic therapy. An alternative is penicillin (100,000–200,000 IU/ kg per day), although this drug theoretically may exacerbate spasms and in one study was associated with increased mortality

87
Q

Two types of antitoxin preparations available for tetanus

A

Antitoxin should be given early in an attempt to deactivate any circulating tetanus toxin and prevent its uptake into the nervous system.

Two preparations are available: human tetanus immune globulin (TIG) and equine antitoxin.

TIG is the preparation of choice, as it is less likely to be associated with anaphylactoid reactions. A single IM dose (500–5000 IU) is given, with a portion injected around the wound.

Equine-derived antitoxin is available widely and is used in low-income countries; after hypersensitivity testing, 10,000–20,000 U is administered IM as a single dose or as divided doses.

88
Q

Factors associated with poor prognosis in tetanus

89
Q

Schedule for tetanus vaccination

A

0,1,6 months

followed by one dose in subsequent pregnancies (or intervals of at least 1 year), to a total of five doses to provide long-term immunity.

90
Q

Individuals sustaining tetanus-prone wounds should be immunized if their vaccination status is incomplete or unknown or if their last booster was given >__ years earlier

91
Q

T/F

Giardia remains a pathogen of the proximal large bowel and does not disseminate hematogenously

A

proximal SMALL bowel

92
Q

How is giardiasis diagnosed?

A

Giardiasis is diagnosed by detection of parasite antigens in the feces, by identification of cysts in the feces or of trophozoites in the feces or small intestines, or by nucleic acid amplification tests (NAATs).

Cysts are oval, measure 8–12 μm × 7–10 μm, and characteristically contain four nuclei. Trophozoites are pear-shaped, dorsally convex, flattened parasites with two nuclei and four pairs of flagella

93
Q

Treatment for giardiasis

A

Cure rates with metronidazole (250 mg thrice daily for 5 days) are usually >90%.

Tinidazole (2 g once by mouth) may be more effective than metronidazole.

Nitazoxanide (500 mg twice daily for 3 days) is an alternative agent for treatment of giardiasis.

Paromomycin, an oral aminoglycoside that is not well absorbed, can be given to symptomatic PREGNANT patients, although information is limited on how effectively this agent eradicates infection.

94
Q

T/F

T. vaginalis can also infect men

A

Many men infected with T. vaginalis are asymptomatic, although some develop urethritis and a few have epididymitis or prostatitis. In contrast, infection in women, which has an incubation period of 5–28 days, is usually symptomatic and manifests with malodorous vaginal discharge (often yellow), vulvar erythema and itching, dysuria or urinary frequency (in 30–50% of patients), and dyspareunia

95
Q

How is trichomoniasis diagnosed?

A

Detection of motile trichomonads by microscopic examination of wet mounts of vaginal or prostatic secretions has been the conventional means of diagnosis. Although this approach provides an immediate diagnosis, its sensitivity for the detection of T. vaginalis is only ~50–60% in routine evaluations of vaginal secretions.
Direct immunofluorescent antibody staining is more sensitive (70–90%) than wet-mount examinations. T. vaginalis can be recovered from the urethra of both males and females and is detectable in males after prostatic massage.

NAATs are FDA approved and are highly sensitive and specific for urine and for endocervical and vaginal swabs from women

96
Q

Treatment for trichomoniasis

A

Metronidazole (either a single 2-g dose or 500-mg doses twice daily for 7 days) or tinidazole (a single 2-g dose) is effective.

Reinfection often accounts for apparent treatment failures, but strains of T. vaginalis exhibiting high-level resistance to metronidazole have been encountered. Treatment of these resistant infections with higher oral doses, parenteral doses, or concurrent oral and vaginal doses of metronidazole or with tinidazole has been successful.

97
Q

T/F

There is only one antigenic type of rubella virus, and humans are its only known reservoir.

98
Q

Duration of shedding period of rubella

A

Individuals with acquired rubella may shed virus from 7 days before rash onset to ~5–7 days thereafter.

99
Q

Lymphadenopathy, particularly occipital and postauricular, may be noted during the ___week after exposure to Rubella

100
Q

What are the transient and permanent manifestation of congenital rubella syndrome?

101
Q

Diagnostic test for rubella

A

Laboratory assessment of rubella virus infection is conducted by serologic and virologic methods. For acquired rubella, serologic diagnosis is most common and depends on the demonstration of IgM antibodies in an acute-phase serum specimen or a fourfold rise in IgG antibody titer between acute- and convalescent-phase specimens. To detect a rise in IgG antibody titer indicative of acute disease, the acute phase serum specimen should be collected within 7–10 days after onset of illness and the convalescent-phase specimen ~14–21 days after the first specimen. The enzyme-linked immunosorbent assay IgM capture technique is considered most accurate for serologic diagnosis, but the indirect IgM assays also are acceptable. After rubella virus infection, IgM antibody may be detectable for up to 6 weeks. In case of a negative result for IgM in specimens taken earlier than day 5 after rash onset, serologic testing should be repeated.

102
Q

Classic triad of congenital rubella syndrome

A

The classic triad of CRS—clinical manifestations of cataracts, hearing impairment, and heart defects—is seen in ~10% of infants with CRS

Hearing impairment is the most common single defect of CRS.

103
Q

Among women infected with rubella virus during the first 10 weeks of gestation, the risk of delivering an infant with Congenital Rubella syndrome is __%.

104
Q

When should administration of Ig for Rubella be considered?

A

Administration of immunoglobulin should be considered only if a pregnant woman who has been exposed to a person with rubella will not consider termination of the pregnancy under any circumstances. In such cases, IM administration of 20 mL of immunoglobulin within 72 h of rubella exposure may reduce—but does not eliminate—the risk of rubella

105
Q

The most effective method of preventing acquired rubella and CRS is through ____

A

vaccination with an RCV (Rubella containing Vaccine)

One dose induces seroconversion in ≥95% of persons ≥1 year of age. Immunity is considered long-term and is probably lifelong. The most commonly used vaccine globally is the RA27/3 virus strain.

106
Q

Contraindications for rubella containing vaccines

A

Because of the theoretical risk of transmission of live attenuated rubella vaccine virus to the developing fetus, women known to be pregnant should not receive RCV.

In addition, pregnancy should be avoided for 28 days after receipt of RCV. In follow-up studies of ~3000 unknowingly pregnant women who received rubella vaccine, no infant was born with CRS. Receipt of RCV during pregnancy is not ordinarily a reason to consider termination of the pregnancy