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ENDO/ID FInal > ID > Flashcards

ID Flashcards

1
Q

Factors that increase risk for fungal infection

A
  • immunity
  • Recent of current use of antifungal medication
  • Risk of exposure
  • Neutropenia (Invasive candidiasis and aspergillosis)
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2
Q

List oppurtunistic

fungal infections

virus

Parasite

A

Fungus

  • Cryptococcus
  • Histoplasma
  • Candida
  • Pneumocystis

Virus - Cytomegalovirus

Parasite - Toxoplasma

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3
Q

pathogen responsible for Criptococcus

A

C. neoformans and C. gattii

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4
Q

transmission of Criptococcus

A

Transmission via air droplets and bird dropping

Spores are inhaled, lodge into the lung alveoli then disseminate hematogenously and cause infection

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5
Q

Si/Sx of Criptococcus

what is most common??

A

The most common is meningitis

  • Malaise (76%)
  • Headache (73%)
  • Fever (65%)
  • N/V(42%)
  • Cough/ SOB (31%)
  • Altered MS (28%)
  • Temperature above 38.4 (56%)
  • Papilledema (33%)
  • Meningeal signs (27%)
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6
Q

Dx & Tx of Criptococcus

A

Dx: cryptococcal antigen in CSF

Tx:

  • Amphotericin B (80%)
  • Fluconazole (50%).
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7
Q

Tranmission of Histoplasmosis

A

inhalation & Exposure to chicken coop

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8
Q

si/sx of Histoplasmosis

A

Fever

weight loss

skin ulcers

Hepato-splenomegaly

lymphadenopathy

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9
Q

Dx & Tx of Histoplasmosis

A

Dx: Urine: H. capsulatum antigen sensitivity 95%

Tx:

  • Amphotericin B an/or
  • Itraconazole total 12 weeks
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10
Q

the strain causing the disease is from the patient’s own GI flora

A

Candidiasis

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11
Q

2 types of canidiasis

CD4 counts?

A

Oropharyngeal candidiasis (OPC) - CD4 <300.

Esophagitis - CD4 <100.

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12
Q

types of Oropharyngeal candidiasis (OPC)

A
  • Erythematous
  • Hyperplastic
  • Angular Cheilitis
  • Pseudomembranous
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13
Q

tx of Candidiasis

avoid??

A

Itraconazole (97%) or Fluconazole (87%)

Avoid topical treatments (nystatin)

  • Lower cure rates
  • Higher relapses rates
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14
Q

the most common cause of dysphagia and odynophagia in AIDS.

A

Esophageal candidiasis

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15
Q

Dx & Tx of Esophageal candidiasis

A

Dx: EGD

Tx: Fluconazole - If unable to swallow use IV

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16
Q

pathophys of Pneumocystis Jirovecii

A

unique tropism for the lung and rarely invading the host.

•By attaching to the alveolar epithelium cause inflammation, interstitial edema and diffuse alveolar damage

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17
Q

si/sx of Pneumocystis Jirovecii

A

Gradual onset and progression of

  • Fever
  • dry cough
  • dyspnea.

Average 1 month before medical consultation

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18
Q

Dx of Pneumocystis Jirovecii

best imaging & best lab??

A

Best imaging test: HRCT chest.

  • If normal no PCP

Best lab test: BAL+ immunofluorescence

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19
Q

tx of Pneumocystis Jirovecii

A

TMT-SMX

Adjunctive steroids if PO2 <70

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20
Q

most important form of Cytomegalovirus

A

CMV can affect mainly retina ( the most important form of CMV), CNS and GI tract. Rare in lung.

CMV retinitis

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21
Q

si/sx of CMV retinitis

A
  • No pain but floaters, blurry vision, decreased peripheral vision
  • Light flashes or sudden vision loss can occur
  • Usually start in one eye but often involves both eyes
  • Blindness due to retina detachment 2-6 months if untreated
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22
Q

Dx & Tx of CMV retinitis

A

Dx: Perivascular fluffy yellow-white retinal infiltrate +/- hemorrhage

Tx: IV Ganciclovir , lifelong

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23
Q

pathogen for Toxoplasmosis

A

30% of people in USA are seropositive (IgG) for T. gondii.

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24
Q

The annual risk of of developing Toxoplasmosis encephalitis among patients with a

  • CD4<100 and positive serology is ___%
  • ___% if CD4<50 if they do not receive prophylaxis
A

The annual risk of of developing Toxoplasmosis encephalitis among patients with a

  • CD4<100 and positive serology is 30%
  • 75% if CD4<50 if they do not receive prophylaxis
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25
Q

Si/sx of toxoplasmosis

A

HA

Confusion

Fever

Lethargy

Seizure

Focal Sign

AMS

Psychomotor Retardation

Menignismus

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26
Q

Dx toxoplasmosis

A

Best imaging: MRI brain

Bc CNS lymphoma may look similar then:

  • Obtain IgG serology for T. gondii
  • Order MRI brain and look for more than 1 lesion
  • If LP was done then order cytology for malignant cells and EBV PCR
  • Where available order PCR for T. gondii
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27
Q

Tx toxoplasmosis

A

Pyrimethamine+ Sulfadiazine + Leucovorin

Brain biopsy - if no clinical or radiological improvement after 14 days of anti-Toxoplasma therapy.

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28
Q

Most common tick-borne illness in the US & Europe

A

Lyme Dz

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29
Q

pathogen responsible for lyme

US

Europe & Asia

A

Borrelia burgdorferi in the US

Borrelia afzelii and Borrelia garinii in Europe and Asia

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30
Q

Si/Sx of Lyme

Early Localized Disease

Early Disseminated Disease

Late Lyme Disease

Post Lyme Syndrome

A

Early Localized Disease-7-14 days after bite

  • Erythema migrans (EM) – bullseye rash

Early Disseminated Disease

  • Neurologic – meningitis, facial nerve palsies, radiculopathy (TRIAD)
  • Carditis – heart block
  • Ocular manifestation

Late Lyme Disease

  • Arthritis - knee
  • Neurologic fts Lyme encephalopathy – subtle cognitive disturbances & polyneuropathy
  • Fibromyalgia

Post Lyme Syndrome

nonspecific symptoms that may persist for month after treatment of Lyme Disease

  • Headache
  • Fatigue
  • Arthralgia
  • Cognitive difficulties
  • Musculoskeletal pain
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31
Q

Dx Lyme

A

Spirochetemia on blood culture

ELISA (Enzyme linked immunosorbent assay)

  • Most common initial serologic test
  • Available for IgM (early), IgG (late), and combined IgM and IgG antibody detection
  • If + or indeterminate –> send for western blot

Western Blot Test

  • Provides more information regarding which agent of B. burgdorferi are reacting to the serum antibody
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32
Q

Tx of lyme

A

Doxycycline

Later in dz –> IV abx

Alt: amoxicillin or ceftriaxone

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33
Q

Criteria for Lyme prophylaxis (ALL):

A
  1. Attached tick identified as adult or nymph I. scapularis and attached for >36 hours
  2. Prophylaxis can be started within 72 hours of the time the tick was removed
  3. Ecologic information indicated local rate of infection of ticks is ≥ 20%
  4. Doxycycline is not contraindicated
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34
Q

Babesiosis pathogen & transmsission

A

Ixodes scapularis ticks – typically in nymph stage, size of a poppy seed

During nymph stage the tick searching for a blood meal, B.microti

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35
Q

si/sx of babeosis

A

Babesia can infect and destroy RBCs -> hemolytic anemia

Jaundice, dark urine

Rash is UNCOMMON

Life threatening to asplenic patients

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36
Q

Dx of babeosis

A

peripheral blood smear

  • On smear may look like Malaria – look for the tetrads and extra cellular mezozites.
  • no hemozoin pigments.
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37
Q

Tx of babeosis

A

Atovaquone + Azithromycin;

OR

Clindamycin + Quinine

Educate the patient to not donate blood products

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38
Q

transmission of Ehrlichiosis

A

Lone star tick

Blacklegged tick

Blood transfusions

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39
Q

si/sx of Ehrlichiosis

A
  • Malaise, rigors, nausea, high fevers and headache
  • Rash – infrequent!!!, if present consider other tick-borne co-infections
  • Immunocompromised patients can have severe presentations
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40
Q

dx & Tx of Ehrlichiosis

A

Dx:

Peripheral Smear – see the bacteria in leukocytes

(PCR)– identify specific genes unique anaplasmosis – most sensitive in the 1st week of illness

(IFA_)_ – not commonly used, measures the antibody to the bacteria. Can take 3 weeks for results

Tx: Doxycycline

  • Rifampin for pregnant & families
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41
Q

Dx differentiation b/w

Ehrlichiosis

Anaplasmosis

A

Ehrlichiosis: Peripheral Smear – see the bacteria in leukocytes

Anaplasmosis: Peripheral Smear – see bacteria in monocytes

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42
Q

Males >40 years in age

Weakened immune system

Residence or time spent in tick habitats, contact with the white tail deer and white-footed mouse

A

Anaplasmosis

Spread from the bite of an infected tick

Rare cases can be spread thru blood transfusions

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43
Q

si/sx of anaplasmosis

early

late

A

Bites are usually PAINLESS

People don’t remember being BITTEN

Early Illness (1-5 days)

  • Fevers, chills, Severe headache, myalgia, N/V, diarrhea, anorexia

Late Illness

  • Respiratory failure
  • Bleeding problems
  • Organ Failure , Death (RARE <1%)
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44
Q

Dx & Tx of anaplasmosis

A

Dx:

Peripheral Smear – see the bacteria in the monocytes

(PCR)– identify specific genes unique anaplasmosis – most sensitive in the 1st week of illness

(IFA) – not commonly used, measures the antibody to the bacteria. Can take 3 weeks for results

Tx: Doxycyline

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45
Q

tick borne illness that:

Loves endothelial cells –> inc permeability –> leaky blood vessles

A

Rocky Mountain Spotted Fever

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46
Q

Si/Sx of Rocky Mountain Spotted Fever

A

SICK FAST!!! 4-10 days after bite

*Blanching erythematous rash with macules (3rd-5th day of illness)

“Spotless” RMSF may be severe and have fatal outcomes

  • Rash initially involves wrists and ankles, spreading centrally to arms, legs and trunk. Involves palms and soles!
  • Facial flushing, conjunctival injection and hard palate lesions may occur
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47
Q

Dx of rocky mtn spotted fever

A

CXR = interstitial infiltrates on chest x-ray, consistent with early pulmonary edema

Echo - minimal myocardial dysfunction

(IFA) assay for IgG R. Rickettsii antigen

  • Frequently negative in first few weeks of illness. IgM only available thru some labs and not as specific

Positive PCR helpful but does not rule out if negative as may not have large amounts of DNA in blood because invasive of endothelial.

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48
Q

Tx of rocky mtn spotted fever

A

Doxycycline

Chloramphenicol – safe in preg up to 3rd tri

Continue abx for 3 days after patient becomes afebrile

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49
Q

Complications of rocky mtn spotted fever

A
  • Encephalitis
  • Noncardiogenic pulmonary edema
  • Adult respiratory distress syndrome
  • Cardiac arrhythmias
  • Coagulopathy
  • Gastrointestinal bleeding
  • Skin necrosis
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50
Q

si/sx of rabies

Encephalitic

Paralytic

A

Encephalitic (furious) rabies (80%) –

  • Hydrophobia & Aerophobia (fear of breathing)
  • Hyperactivity of muscle subsiding to paralysis
  • “goose flesh”

Paralytic (dumb) rabies (<20%) –

  • hypo reflexive
  • CN palsy
  • ascending paralysis
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51
Q

dx of rabies

A

_Rabies serum antibody tite_r – will not be positive until later in course

Spinal tap – elevated protein, normal glucose, anti-rabies antibiodies

Skin biopsy –> Saliva

CT head = Cerebral edema

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52
Q

Tx of rabies

A

Pre-exposure Vaccination: 3 IM injections given at days 0, 7 , and 21 or 28

Post-exposure Vaccination:

  • Immunocompetent: 4 IM
  • Immunocompromised: 5 IM

NEED vaccine on day 0

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53
Q

*Anopheles mosquito→P. falciparum & P. vivax

transmitted from a female Anopheles gambiae mosquito

  • P. falciparum most commonly transmitted disease
  • 2nd is P. vivax
A

Malaria

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54
Q

sporozoites goes to the liver within 1 to 2 hours and can remain dormant for years asymptomatic for 12 - 35 days –> invade RBCs

A

Malaria

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55
Q

Si/sx of malaria

mild

severe

A

Mild: Cycle of cold, hot, sweating occurring Every 2 days or every 3 days (cyclical fever!!)

Severe Clinical Presentation

  • “cerebral malaria” – confusion, obtunded, seizures, coma
  • Hemolysis, hemoglobinuria
  • ARDS – inflammation in lungs which impairs O2 exchange
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56
Q

dx malaria

A

Rapid diagnostic test (RDT) : if + →blood smear

  • Evidence of hemozoin – breakdown products of the red cells seen in digestive tracts of the parasites

Smear for speciation & degree of parasitemia

If negative at first, continue testing each day for 2 more days

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57
Q

tx of malaria

A

Chloroquine

Malarone (atovaquone + proguanil) - NIGHTMARES

Coartem (arthemether + lomefantone)

Mefloquone

Quinine + Doxycycline, Clindamycin or Tertacycline

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58
Q

Most severe encephalitis in America

A

EEE

Dead-end hosts are HUMANS, EQUINE, SWINE, PHEASANTS

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59
Q

partho of EEE

A

After a bite, EEE virus is inoculated in dermal tissue, it stats affecting dendritic and Langerhans cell which migrate to Lymphoid tissues. There is replicated

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60
Q

si/sx of EEE

A

“Encephalitis”

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61
Q

dx of EEE

A

CBC – leukocytosis (lymphocyte predominant)

ELISA and IFA

Radiologic findings:

  • Brain MRI T2 weighted images can report f_ocal lesions in basal ganglia, thalamus and cortex._

Pro Tip: early involvement of the thalamus and basal ganglia can help differentiate between Herpes simplex and EEE

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62
Q

tx of EEE

A

No antiviral drug has proven beneficial

Supportive care

Steroids worse outcomes!!-avoid

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63
Q

pathophys of west nile

A

Enters through dermal layer and replicates in dermal dendritic cells and keratinocytes. Then there is visceral-organ dissemination phase followed by third phase which it spreads to CNS

Unclear how it enters the CNS.

64
Q

cayse of west nile

A

Culex species of mosquito most common

West Nile can infect birds, dogs and other mammals

Humans are “Dead-end” hosts

65
Q

si/sx of west nile

A

50% maculopapular rash on trunk

Virus incubation 2-14 days

Fever – typically 5 days, headache 10 days, fatigue – 1 month

Patients with features of encephalitis progress rapidly.

Neuro changes, muscular weakness, seizures, flaccid paralysis

66
Q

Dx & Tx of west nile

A

Dx:

CBC – leukocytosis

Serological detection in blood and CSF – IgM antibody

If high suspicion and initial negative, repeat in 10 days

May see hyponatremia when CNS is involved

Lumbar Puncture: CSF shows elevated protein, + leukocytes, normal glucose levels.

Tx:

Supportive care – will recover

As they recover, may need PT and OT as loss of gross and fine motor skills.

67
Q

pathogen responisble for tularemia

A

Francisella tularensis – infected animals

Inhale, touch, rub eye

68
Q

si/sx of tularemia

A

RAPID ONSET

Late presentation specific manifestations:

Ulceroglandular tularemia – skin lesion with adenopathy

Glandular tularemia – tender regional lymphadenopathy

Oculogladular tularemia – infection involving the eye

Pharyngeal tularemia – infection involving mouth or throat

Pneumonic tularemia – pulmonary involvement

Typhoid tularemia – systemic illness

69
Q

dx of tularemia

A

F. tularensis serology – initial presentation and 2-4 weeks after

Culture and gram-stain – rarely positive

70
Q

tx of tularemia

mild

severe

severe complications

A

Mild illness:

  • Doxycycline
  • Ciprofloxacin

Severe illness:

  • Streptomycin
  • Gentamicin

Severe complications : Meningitis & Endocarditis

71
Q

si/sx of plague

Bubonic plaque (80-95%)

Septicemic Plague

Pneumonic plague

A

Bubonic plaque (80-95%)

  • Skin lesions: eschars, pustules, necrotic lesions
  • Purpura with associated intravascular coagulation
  • Intense pain and swelling LNs (bubo)
  • If untreated this can progress to disseminated infection (sepsis), meningitis, or secondary pneumonic plague

Septicemic Plague (10-20%) - Extremely ill

  • Fever
  • GI symptoms (N/V/D) & Abdominal pain

Pneumonic plague – Sudden dyspnea

  • High fever
  • Pleuritic chest pain
  • Cough +/- blood sputum
  • Rapidly fatal unless appropriate treatment is started within the first day
72
Q

dx plague

A

Chest x-ray -

  • Bronchopneumonia
  • Consolidation
  • Cavities
  • Pleural effusions

Culture and staining

Blood serology

Rapid test

73
Q

Tx of plague

A

Drug of choice: Streptomycin IM

  • Alt: Doxycycline or Tetracycline

ISOLATION

74
Q

3 important diagnostic clues of plague

A
  1. Presence of fever in a person with known contact with dead rodents or travel to plague-endemic region
  2. Presence of fever, hypotension, and unexplained regional lymphadenitis
  3. Presence of clinical findings of pneumonia in association with hemoptysis and sputum containing gram negative rods
75
Q

•Intense pain and swelling LNs makes you think??

A

Bubonic plaque

76
Q

Erythema migrans (EM) – bullseye rash

dx?

A

Lyme

77
Q

hemolytic anemia, Jaundice, dark urine

dx?

A

Babesiosis

78
Q

Blanching erythematous rash with macules

Rash initially involves wrists and ankles, spreading centrally to arms, legs and trunk. Involves palms and soles
dx?

A

Rocky Mountain Spotted Fever

79
Q

Hydrophobia & Aerophobia & “goose flesh”

Dx

A

Encephalitic rabies

80
Q

Encephalitic rabies has (hypo/hyper) reflexia

Paralytic rabies has (hypo/hyper) reflexia

A

Encephalitic rabies has HYPERreflexia

Paralytic rabies has HYPOreflexia

81
Q

Cycle of cold, hot, sweating – cyclical fever!!

Dx

severe prrsentaion?

A

malaria

Severe Clinical Presentation: “cerebral malaria” – confusion, obtunded, seizures, coma

82
Q

50% maculopapular rash on trunk

dx?

A

West Nile

83
Q

Main HIV risk for males vs frmales

A

MSM main risk for males

heterosexual transmission for females

84
Q

HIV Transmission Risk Fx:

A

↑Viral load

Lack of circumcision

STDs

Sexual partner number, practices

(Genetic)

85
Q

HIV Risk Factor Estimator

↑ risk with:

↓ risk with:

A

↑ risk with:

  • Anal sex
  • STD (either partner)
  • Acute HIV

↓ risk with:

  • Condom use
  • Pre-exposure prophylaxis
  • ART plus undetected viral load
  • (Not on the estimator) Circumcision
86
Q

Dx HIV

A

Antibody/p24 antigen screen; (+) proceed per algorithm

Viral load as baseline

CD4 count

Ag/HIV1,2 Ab) – look for HIV antibody

  • (-) and suspect very recent infection, repeat in a few days
  • or jump to RNA viral load

(+), check:

  • HIV1,2 Ab differentiation assay
  • HIV1 viral load (RNA)
87
Q

Si/Sx of HIV infection

Early

Latency

AIDS

A

Early Infection – Shortly after acquisition.

  • HIGH VL
  • Highly contagious.
  • CD4 dips (CD4 about 500) – still protect from opportunistic infections

Clinical latency – No or subtle symptoms.

  • VL drops.
  • CD4 usually partially recovers.

AIDS: HIV Infection + either

  • CD4 <200 regardless of symptoms, OR
  • AIDS-defining condition (at any CD4 count)
88
Q

who to test for HIV??

A

One-time: Anyone age 13-75

In all pregnancies

With ongoing risk factors (test yearly or more often)

With si/sx acute or chronic infection

89
Q

Note that 1 of ___ infected persons (~14%) in US unaware! Have low threshold to test.

A

Note that 1 of 7 infected persons (~14%) in US unaware! Have low threshold to test.

90
Q

tx of HIV

A

GENOME STUDY FIRST!!

Recommended starting regimes: use at least 3 drugs.

4 regimens recommended “for most people”

  • INSTI (integrase inhib) + two nukes

One regimen with INSTI + 1 nuke but only if

  • RNA <500k
  • no nuke resistance
  • no hep B coinfection.
91
Q

Early Complications of HIV (CD4 >_____)

A

Early Complications of HIV (CD4 >200)

  • Oral or vaginal candidiasis
  • Oral hairy leukoplakia (EBV)
  • Herpes Zoster (VZV)
  • Seborrheic dermatitis
  • Recurrent or atypical HSV
  • Kaposi’s sarcoma (HHV-8)
  • Extensive, recurrent condyloma (HPV)
92
Q

Late Complications of HIV (CD4

A

Late Complications (CD4 <200)

  • Pneumocystis jiroveci (carinii) infection
  • Cryptococcus neoformans infection
  • Toxoplasma gondii infection (reactivation)
  • Cytomegalovirus reactivation
  • Aspergillus infection
  • Mycobacterium avium infection (and other NTMs)
  • Cryptosporidiosis
  • Lymphomas
  • Wasting disease
93
Q

How does HIV present differently in Elderly??

A

Tend to have lower CD4 counts at presentation (delay in diagnosis) –Less rise in CD4

94
Q

define Immune Reconstitution Inflammatory Syndrome (IRIS)

A

Start tx with very low CD4 count Experience a rapid CD4 and virologic response when started on antiretroviral therapy and

•Develop new clinical pathologies from a new or previously diagnosed opportunistic organism

95
Q

pathogens responsible for Immune Reconstitution Inflammatory Syndrome (IRIS)

A

Mycobacterium avium, M. Tuberculosis

Cryptococcus, Leishmania

M. Leprae, Histoplasm

Kapsosi’s sarcoma, CMV, and JC virus (PML) are some of the organisms associated with IRIS

96
Q

who is at risk for Immune Reconstitution Inflammatory Syndrome (IRIS)

A

Usually occurs in patients with CD4 nadir <400

Occurs in up to 36% of those with TB who are started on antivirals at diagnosis

  • consider deferring ARV’s
97
Q

name the Integrase strand transfer inhibitors (INSTIs)

A

Raltegravir - N, HA, D, – ↑ transaminases & CPK

Elvitegravir

Dolutegravir - Impaired glucose tolerance

Bictegravir

Cabotegravir/rilpivirine

98
Q

name the nRTIs (Nucleos(t)ide reverse transcriptase inhibitors: “Nukes”

A

Tenofovir (TDF) - bone demineralization

Lamivudine (3TC) - Must check pt to make sure not HLA B*5701 positive

emtricitabine (FTC) - Must check pt to make sure not HLA B*5701 positive

Abacavir - hypersensitivity reaction

Zidovudine (AZT)

99
Q

All NRTIs Adverse Effects:

A

Lactic acidosis and hepatic steatosis (higher incidence with stavudine)

Lipodystrophy, fat redistribution (higher incidence with stavudine, zidovudine)

Rash

Drug-drug interactions

100
Q

HIV tx Can be added when all else failing.

A

Monoclonal anti-CD4 injection

101
Q

new HIV med thatv has NO ORALS

A

Cabotegravir + rilpivirine – 2

Cabotegravir + rilpivirine - 3

102
Q

pt taking abacavir what should you warn them about?

A
  • severe rash/fever reaction and to stop rx immediately should such occur
  • Ought not to occur if HLA B*5701 negative, but the world is not perfect.
103
Q

after initiating HIV therapy what do we need to monitor?

when?

A

Check basic labs and viral load in 2-4 weeks.

One expects at least 10-fold (“one log”) decline in viral load.

104
Q

describe

HIVPost-exposure prophylaxis – I

HIV Post-exposure prophylaxis – II

A

Post-exposure prophylaxis – I

  • Occupational, e.g. healthcare worker, first responder – Sharps injury from HIV-positive or HIV-unknown
  • Splash, saliva, urine, etc: Negligible risk.

Post-exposure prophylaxis - II Sexual contact

  • We often end up giving rx even if statistics suggest low risk
  • Truvada plus an INSTI for almost all cases
105
Q

describe

  • Pre-exposure prophylaxis (PrEP) – I
  • Pre-exposure prophylaxis (PrEP) – II
A

Pre-exposure prophylaxis (PrEP) – I – Truvada (TDF)

  • Serodiscordant couples
  • Sex workers
  • Other patients with high risk for sexual exposure
  • Highly effective if taken daily – Requires close monitoring, harm reduction counseling regarding other STIs

PrEP - II

Issues – Very few end up adhering 100% on all days every week. Probably 4 days/week OK.

  • Take two pills 2 to 24 hours before sex
  • One pill 24 hours after the initial dose
  • One final pill 24 hours later
  • If pt has sex more than 24 hours after taking first dose (two pills), or over multiple days, continue taking one pill every day until pt has taken two doses following last anal sex encounter, at which point can stop.
106
Q

PrEP - II timeline for sexual intercourse

A

Take two pills 2 to 24 hours before sex

One pill 24 hours after the initial dose

One final pill 24 hours later

If pt has sex more than 24 hours after taking first dose (two pills), or over multiple days:

  • continue taking one pill every day until pt has taken two doses following last anal sex encounter, at which point can stop.
107
Q

Name the ssRNA viruses

A

Zika - Flavivirus-

Dengue Virus (DENV) - Flavivirus

CHIKV - Alphavirus

108
Q

transmission of Zika

A

Mosquito Bite - Aedes

  • Aedes aegypti mosquito- tropical
  • Aedes albopictus mosquito- temperate climates
  • Aedes can also carry Dengue and Chikungunya viruses

Maternal-Fetal

Sex

Blood transfusions (likely, not confirmed)

Organ transplants

Lab exposure

109
Q

transmission of dengue

A

Mosquito Bite - Aedes

Rare in organ donation or blood transfusion

maternal-fetal transmission - spread through breast milk

No Sex transmission

110
Q

transmission of CHIKV

A

Mosquito Bite-Aedes ONLY

111
Q

si/sx of Zika

A

Viremic period- Direct virus detection is 3-5 days after onset of symptoms

Symptoms (25%)- Resolve in 2-7 days

  • Fever
  • Maculopapular pruritic rash
  • Headache
  • Arthralgia _(small joints of hands/fee_t)
  • Myalgia
  • Conjunctivitis (non-purulent)
112
Q

which virus has 4 serotypes

A

dengue

113
Q

WHO 2009 revised classification of Dengue

A

Dengue w/o warning signs

Dengue w/ warning signs

Severe dengue –> Can lead to shock, internal bleeding and death in hours

114
Q

dengue Warning signs:

A
  • Abd pain
  • Persistent vomiting
  • Fluid accumulation
  • Mucosal bleed
  • Liver enlargement >2cm
  • ↑hematocrit w/ concurrent rapid ↓PLTs
115
Q

dx of Zika

A

rRT-PCR for Zika Virus RNA == Detects active infection

  • Serum, urine (some assays use whole blood)
  • ≤7 days of symptoms

Zika Virus IgM === If positive, need to do PRNT

  • Also test for Dengue Virus IgM
  • >7 days up to 12 weeks

Plaque Reduction Neutralization test (PRNT)

  • Will tell you if Recent Zika Virus or false positive test
116
Q

Tx of Zika

A

Supportive

acetaminophen

  • NSAIDS avoided until Dengue ruled out to reduce risk of bleeding
  • ASA avoided in children due to risk of Reye syndrome
117
Q

Complications of Zika

A

Fetal loss

Microcephaly

Guillian-Barre Syndrome

Brain ischemia

Myelitis

Meningoencephalitis

118
Q

phases of dnegue

A

Febrile Phase -3-7 days, after recover w/o complications

  • Sudden onset ↑ fever ≥38.5C (101.3F)
  • headache, eye pain, transient rash, vomiting, myalgia, arthralgia
  • Conjunctival injection, pharyngeal erythema, LAD, hepatomegaly, facial puffiness, petechiae -hemorrhagic features

Critical Phase- Lasts 24-48 hrs (appears days 3-7 @defervescence) à children & young adults

  • Systemic vascular leak syndrome- plasma leak, bleeding, shock, organ failure
  • Abdominal pain, lethargy, persistent vomiting, clinical fluid accumulation, mucosal bleed
  • Tachycardia, hypotension, AMS, oliguria, cool mottled skin, thready pulse

Recovery Phase - lasts 2-4 days

  • Plasma leakage and hemorrhage resolve
  • Additional pruritic rash may appear
  • profound fatigue that may takes days to weeks to recover
119
Q

dx of dengue

A

rRT-PCR for Dengue Virus RNA - Detects active virus infection within first 5 days

Dengue Virus antigen - active virus infection within first 7 days

Dengue Virus IgM - If positive, need to do PRNT

Plaque Reduction Neutralization test (PRNT) –

  • Will tell you if Recent Dengue Virus or false positive test
  • Can tell you serotype of Dengue

Dengue Virus IgG - Depends on primary vs secondary

120
Q

lab findings in dengue during

Febrile Phase:

Critical Phase:

Recovery phase:

A

Febrile Phase:

  • Leukopenia
  • thrombocytopenia
  • ↑ liver enzymes

Critical Phase:

  • Moderate to severe thrombocytopenia
  • US chest/abdomen for fluid

Recovery phase: Labs: Normalize

121
Q

tx dengue

A

Supportive

Fever management – Acetaminophen

  • No NSAIDS

Bleeding management- blood transfusions

Plasma leakage- volume replacement

Shock treatment

122
Q

dengue prevention

A

Vaccination – Dengvaxia (Sanofi)

  • Only for dengue seropositive or hx of Dengue
  • ONLY if had dengue in past
123
Q

si/sx of CHIKV

A

Incubation period: 3-7 days : Persistent and severe polyarthralgia is most prominent symptom

Acute phase: 7-10 days – show symptoms

  • Begin abruptly with ↑fever – Duration 3-5 days .w/ Malaise

Polyarthralgia - 2-5 days after fever onset

  • involves multiple joints- bilateral & symmetrical (hands, wrists, ankles
  • Pain is intense and disabling
  • Joint swelling, synovitis, joint effusions

Pruritic Macular or Maculopapular Rash

  • Appearing 3 days or later after illness onset
  • Starts on limbs and trunk
124
Q

Dx: CHIKV

Most common lab findings??

A

RT-PCT for Chikungunya RNA virus - Detects active virus infection within first 5 days

Chikungunya Virus IgM - Detects recent infection

Chikungunya Virus IgG - Detects prior infection

Most common lab findings:

  • lymphopenia & thrombocytopenia
125
Q

complications of chikv

A

Persistent debilitating and immobilizing arthritis

  • Some patients have persistent or relapsing disease (18 mo.-3 years)

Respiratory, renal and cardiovascular failure

126
Q

tx chikv

A

Supportive care

NSAIDS ok, but if suspect Dengue, then need to wait 14 days from symptoms and no fever for 48hrs or warning signs

Steroids - Avoid during acute infection

Methotrexate - Post-acute and chronic arthritis

  • After trial with with steroids & NSAIDs

Sulfasalazine if refractory to methotrexate

127
Q

etiology of ebola (EBV)

Ebola has 5 species:

A

Filoviridae family (Filo meaning thread-like)

  • Resembles rhabdoviruses (rabies) and paramyxoviruses (measles, mumps)

Ebola has 5 species

  1. Zaire
  2. Sudan
  3. Tai Forest (Ivory Coast)
  4. Bundibugyo
  5. Reston- animal reservoir only
128
Q

who is most at risk for ebola

A
  • Health care workers- most risk
  • Burial Preparation- most risk
129
Q

si/sx of ebola

A

Incubation period: 6-12 days post exposure

Symptoms: 2-21 days after contact (avg 8-10 days)

Symptoms start abruptly and progress from “Dry” to “Wet”

Dry symptoms (1-3 days)

  • Fever
  • aches/pains
  • HA, myalgia, arthralgia, abdominal
  • fatigue

Wet symptoms (3-10 days)

  • Diarrhea, vomiting
  • Volume loss contribute more to severe illness

Major hemorrhage is less common

Rash, red eye

130
Q

dx ebola

A

Abnormal CBC- Leukopenia, Thrombocytopenia,

Abnormal CMP- Hyponatremia, hypokalemia, renal insufficiency, Elevated AST/ALT

Coagulation abnormalities- PT/PTT/INR prolonged

  • Increase in fibrin degradation products i_n DIC_ (mostly in severe, fatal case)s

RT-PCR- Ebola viral RNA in serum

ReEbov- rapid immunoassay- detects virus antigen, used in field

  • Results in 15 minutes

Ebola IgG

131
Q

_____- Ebola viral RNA in serum

_______- detects virus antigen

  • used in field
  • Results in 15 minutes
A

RT-PCR- Ebola viral RNA in serum

ReEbov- rapid immunoassay- detects virus antigen

  • used in field
  • Results in 15 minutes
132
Q

tx ebola

A

2 Medications for Zaire Ebolavirus

  • Monoclonal Antibodies (Inmazeb, Ebanga)

Supportive care

133
Q

ebola complications

A

Internal and External Bleeding (5-7 days after symptoms)

  • Blood in stool, vomit, blood with coughing
  • Petechiae, purpura, ecchymosis, hematoma, mucosal bleeding

Death (fatality rate ~50%)

  • Shock from volume loss
  • Shock from blood loss
  • Multiorgan failure
134
Q

ebola Prophylaxis: Vaccine

A

rVSV-ZEBOV (called Ervebo®)

135
Q

list examples of each type of COVID vaccine:

mRNA Vaccines

Adenovirus Vector

Inactivated Virus

A

mRNA Vaccines

  • moderna
  • Pfizer

Adenovirus Vector

  • J&J
  • AstraZeneca/Oxford
  • Sputnik V

Inactivated Virus

  • Sinovac
  • Sinopharm
136
Q

how adenovorus vaccine work

A

Adenovirus is a dsDNA virus

Stable once assembled- standard Refrigerator

Issue is that if adenovirus carrying the vaccine is recognized by host from prior infection, then body will attack vaccine before it works

137
Q

how inactivated virus vaccines work

A

Virus is killed but spike protein remains intact

Injected into body and antigen presenting cells

T cells detect surface proteins and activates B cells

B cells make antibodies to the virus

138
Q

tx of COVID

A

Dexamethasone (High flow O2 or noninvasive vent)

Remdesivir Monotherapy (Low flow supplemental O2

Remdesivir with Dexamethasone (Low flow supplemental O2)

Remdesivir with Baricitinib (Low flow supplemental O2)

  • Immunomodulatory effect with potential antiviral effect
  • Used, if glucocorticoids CI

Adding Tocilizumab - Case by case basis

139
Q

si/sx of sepsis

A

Hypotension SBP <90

Tachycardia >90 bpm

Tachypnea >20

Fever >100.9

140
Q

risk fx for sepsis

A
  • ICU admission
  • Bacteremia
  • Advanced age ≥65 years
141
Q

dx sepsis

A

Leukocytosis <12 or leukopenia <4

Hyperglycemia >140

↑CRP, Cr, serum lactate, procalcitonin

Coag abnormalities

Thrombocytopenia <100

↓ PaO2

142
Q

tx sepsis

A

Supplemental oxygen

Aggressive IVF

Peripheral access/Central access

Empiric broad-spectrum ABX within 1 hour tailored to patient

Vasopressors

143
Q

Bacteremia common pathogens

A

S. aureus

s. pneumoniae

Group A Streptococcus

Enterobacteriaceae

Haemophilus influenzae

Pseudomonas aeruginosa

144
Q

Possible blood cx contaminants

A

Coagulase negative staphylococci

Corynebacterium species (also referred to as ‘diphtheroids’)

C. (formerly Propionibacterium) acnes

Bacillus species

Micrococcus species

145
Q

tx bacteremia

A

Empiric Antibiotics then NARROW

Antibiotic Prophylaxis

  • At least 2 weeks - From first negative blood cultures
146
Q

field mgt of Venomous Snake bites

A

1.Transport to a Medical Facility for ABCs and Antivenom

  1. Remove any areas of constriction (rings, clothing, ect)
  2. Clean with soap and water, cover with dry dressing
  3. Position bitten area - Neutral position at heart level, Can splint if needed
147
Q

Hospital Mgt of snake bites

A
  • ABCs- May need fluid resuscitation or vasopressors
  • Mark area every 15 minutes until stable
  • Labs: CBC, blood T&C, CMP, coags, CK, Other tests: ABG, ECG, CXR

•Specific antivenom administration - Call poison control, SnakeBite911 ER- phone app

•Acetylcholinesterase inhibitors if neurological dysfunction

148
Q

Cnidarians bite SHOULD NEVER …

A

Do not rub area as may worsen release of adherent cnidocysts

149
Q

how to remove spiculues of sea sponge

A

Dry skin

Use adhesive tape, commercial face peel or rubber cement

Vinegar 10-30 min q6-8h 4

Glucocorticoid or antihistamine cream

150
Q

first steo when stung by annelid worms

A

Remove spines -use forceps, tape, face peel or rubber cement

151
Q

complications of retained Sea Urchins spines

A

Can develop granulomas from retained spines

152
Q

Eye contact can cause blindness

A

Sea Cucumbers

153
Q

How Cone Snails cause death

A

Paralysis –> respiratory failure –> coma –> death

154
Q

Blue ringed Octopuses si/sx & tx

A

Within minutes, oral and facial numbness –> total flaccid paralysis

Apply circumferential pressure dressing- preserve arterial pulse

155
Q

most severe Scorpionfish that has antivenom

A

Stonefish > Scorpionfish > Lionfish

Stonefish antivenom available in severe cases

156
Q

where is venom in marine catfish

A

Venom in dorsal spine and pectoral spines

157
Q

Marine Vertebrate Sting Treatment

A
  1. Immerse affected part in non-scalding hot water for 30-90 min until pain relief
  2. Repeat pain = Repeat hot water immersion à Opioids and nerve blocks are ok
  3. Debride and clean wound (image if needed for FB)
  4. Mostly leave open to heal by secondary intention or delayed primary closure
  5. Consider tetanus and antibiotics

No evidence supports antihistamines or steroids

ENDO/ID FInal (4 decks)

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