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Microbiology Exam 7 > Bacteremia > Flashcards

Bacteremia Flashcards

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1
Q

Spontaneous bacteremia

A

common event (flossing, brushing teeth) that creates small lacerations allowing small amt of bacteria to enter the blood (minutes)

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2
Q

Transient bacteremia

A

trauma to a heavily colonized mucosal surface resulting in bacteria entering into the blood (hours)

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3
Q

Intermittent/Recurrent bacteremia

A

foci of infection (staph abscess) causing there to be bacteria in the blood occasionally

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4
Q

Continuous bacteremia:

A

certain diseases cause there to be bacteria in the blood continuously

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5
Q

Causes of Continuous bacteremia:

A

• Infective endocarditis, typhoid fever, anthrax, rickettsia, pyelonephritis, bacterial meningitis

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6
Q

Organs that clear bacteria from blood

A

liver & spleen

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7
Q

_______________ kill bacteria in the liver and spleen

A

Kupffer cells + PMNs

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8
Q

Asplenics are particularly susceptible

A

bacteremia, particularly those w/ capsules

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9
Q

Agents of bacteremia

A

CoNS, S. aureus, Enterococcus, GNRs, Strep, Candida

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10
Q

Risks for bacteremia

A

HA-bacteremia: CVC, catheters (Staph, E.coli)

CA-bacteremia:acute pyelonephritis

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11
Q

Catheter associated bacteremia agents

A

E.coli, GNR

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12
Q

CVC associated bacteremia agents

A

Staph

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13
Q

Common cause of bacteremia in children < 2

A

S. agalactiae, E. coli, K. pneumo

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14
Q

Common cause of bacteremia in elderly

A

GNR

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15
Q

Pathogenesis of catheter associated bacteremia

A

spread from skin to catheter, biofilm formation

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16
Q

S/S Bacteremia

A

Sepsis, severe sepsis, septic shock

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17
Q

Diagnosis of Bacteremia

A

Blood specimen collected 2-3 separate times over a 24hr period , >15m apart, before Abx Tx, before/during fever spike

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18
Q

Native Valve Endocarditis

A

most common, occurs in pts w/o hx of IVDU or prosthetic valve

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19
Q

Native Valve Endocarditis valves affected

A

mitral, aortic

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20
Q

Risks for Native Valve Endocarditis

A

mitral valve prolapse, congenital or acquired heart defects, rheumatic heart disease

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21
Q

Pathogenesis of Native Valve Endocarditis

A

turbulent BF -> deposition of fibrin/proteins/etc -> contamination of damaged heart valve secondary to bacteremia

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22
Q

Agents of Native Valve Endocarditis

A

Strep —> CoNS, S. aureus, GNR, S. pneumo, GAS

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23
Q

Prosthetic Valve Endocarditis

A

occurs in pts w/ prosthetic valves

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24
Q

Early Prosthetic Valve Endocarditis d/t

A

Contamination of valve during surgery

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25
Q

Agents of Early Prosthetic Valve Endocarditis

A

Strep —> CoNS, S. aureus, GNR, S. pneumo, GAS

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26
Q

Late Prosthetic Valve Endocarditis d/t

A

secondary to bacteremia

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27
Q

IVDU Endocarditis

A

least common, acute disease d/t contamination of the valve secondary to bacteremia

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28
Q

Most common valve affected by IVDU Endocarditis

A

tricuspid

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29
Q

Agents of IVDU Endocarditis

A

CoNS, S. aureus, Enterococci, S. pneumo, GAS, polymicrobic

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30
Q

Pathogenesis of IE

A

deposition of fibrin & platelet aggregation -> NBT -> bacteremia & secondary infection -> vegetation/biofilm -> large/small emboli

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31
Q

Immunopathology d/t IE

A

Hypergammaglobulinemia

Type III HSN reaction -> acute vasculitis & glomerulonephritis

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32
Q

Subacute IE Sx

A

low virulent; slow progression, immune pathology d/t Type III HSN, vasculitis, glomerulonephritis;
Fever, wt loss, anemia, leukocytosis, splenomegaly, mild heart murmur, Roth’s spots, CHF, emboli + Peripheral STIGMATA

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33
Q

Skin manifestations/Peripheral Stigmata of Subacute IE

A

petechiae on mucosa (conjunctiva), Janeway’s Lesions, Osler’s Nodes, Splinter hemorrhages, clubbing

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34
Q

Janeway’s Lesions

A

painless, petechial lesion on palms and soles

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35
Q

Osler’s Nodes

A

painful, petechial lesions on fingers & toes

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36
Q

Acute IE Sx

A

high virulent; rapid septic emboli -> ischemic event: Stroke, MI, Liver or Kidney Failure; Fever, significant heart murmur, w/o other S/S of immunopathology

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37
Q

Diagnosis of IE

A

transesophageal ECHO, blood specimen (2-3X), MIC/MBC/Cidal, Culture

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38
Q

Failure to culture for IE d/t HACEK

A
  • Haemophilus
  • Aggregaitbacter
  • Cardiobacterium hominis
  • Eikenella corrodens
  • Kingella kingae
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39
Q

Treatment of IE

A

10X MBC

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40
Q

Prevention of IE

A

abx prophylaxis for procedures w/ risk of bacteremia (tooth extraction, cardiac, GI); Amoxicillin 30m before, 2hrs after

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41
Q

Old World visceral leishmaniasis causative agents

A

L. donovani donovani, L. donovani infantum, L. donovani archibaldi

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42
Q

New World visceral leishmaniasis causative agents

A

L. donovani chagasi

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43
Q

L. donovani characteristics

A

Small, round protozoan parasite of the macrophage family; obligate intracellular

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44
Q

Promastigote form

A

carried by sandflies & infects humans/reservoirs

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45
Q

Amastigote form

A

carried by humans/reservoirs & infects sandflies

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46
Q

Life Cycle of L. donovani

A

sandfly bites a human -> promastogotes are released & engulfed by macrophages -> divide, fill cytoplasm, cause macrophage cell lysis -> release of amastigotes -> taken up by new macrophages

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47
Q

L. donovani has a Predilection for

A

mononuclear cell populations, spleen, liver, bone marrow -> histiocyte and macrophage destruction

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48
Q

Vector of L. donovani in the Old World

A

Sandflies (Phlebotomus)

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49
Q

L. donovani infection in US

A

immigrants, travelers, troops

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50
Q

L. donovani is common

A

in India, Bangladesh, Middle East, Mediterranean, Africa, C. & S. America

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51
Q

Vector of L. donovani in the New World

A

Lutzomyia spp

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52
Q

Immune Response to L. donovani

A

CMI: Th1 cells produce IFN-gamma which activates macrophages to restrict intracellular growth

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53
Q

L. donovani has what affect on the immune system

A

amastigotes drive the immune response towards Th2 (production of Ab) & away from Th1, resulting in suppressed CMI & high levels of circulating Ig. Abs are ineffective

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54
Q

Visceral Leishmaniasis incubation period

A

~3-6mo

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55
Q

Manifestations of Visceral Leishmaniasis: Insidious

A

Insidious onset: hepatosplenomegaly, weight loss, fever, malaise, LAD, scaly skin/ashen appearance, cachexia

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56
Q

Manifestations of Visceral Leishmaniasis: Abrupt

A 
Dromedary fever (intermittent high fever w/ 2X/d spikes, weak & feverish, but does not feel very ill!!!
Generalized LAD and HSM eventually develop; intermittent fever continues for wks/mos while pt becomes emaciated & weak; Uncontrolled hemorrhage & anemia
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57
Q

Post-Kala-azar Dermal Leishmaniasis:

A

1-2yrs later; multiple erythematous macules -> large, non-tender nodules may appear on the face & upper body; Lesions are filled w/ Leishmaniae-infected histiocytes

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58
Q

Mortality of Visceral Leishmaniasis is d/t

A

secondary infection

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59
Q

Diagnosis: Labs w/ Visceral Leishmaniasis

A

Granulocytopenia, anemia, elevated gamma-globulins

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60
Q

Visceral Leishmaniasis Microscopy

A

Biopsy of bone marrow + Giemsa Stain - intracellular amastigotes in macrophages is a confirming diagnosis

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61
Q

Leishman Intradermal Skin Test

A

used retrospectively (post-infection); Negative during active infection d/t CMI anergy

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62
Q

Treatment for Visceral Leishmaniasis

A

Pentavalent antimony, Sodium Stibogluconat

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63
Q

Treatment for relapsed Visceral Leishmaniasis

A

Pentamidine isoethionate or Amphotericin B

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64
Q

Cutaneous Leishmaniasis Old World Agents

A

L. tropica, L. major, L. aethiopica

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65
Q

Cutaneous Leishmaniasis New World Agents

A

L. mexicana, L. amazonenesis, L. peruviana

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66
Q

Mucocutaneous Leishmaniasis Agents

A

L. braziliensis, L. guyanensis, L. panamensis

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67
Q

Incubation period of Cutaneous Leishmaniasis

A

1-3mo

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68
Q

Cutaneous Leishmaniasis Sx

A

1 dry ulcer or multiple wet ulcers; at site of infection, erythematous papule that gradually increases in size & evolves into a painless, non-pruritic plaque or ulcer, no systemic S/S

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69
Q

Leichmaniasis Recidivans – Hyperergic Variant:

A

Tubercles or nodules appearing over/around scars of healed ulcers; DTH response

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70
Q

Diffuse Cutaneous Leishmaniasis – Anergic Variant

A

anergic & the organisms disseminate throughout the skin; Th2 response

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71
Q

Mucocutaneous Leishmaniasis Sx

A

initial lesion is similar to the cutaneous form, but metastatic spread occurs to the nasal or oral mucosa (during or mos/yrs after primary lesion has healed)

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72
Q

Mucocutaneous Leishmaniasis Secondary lesions on mucosa

A

have intense mononuclear infiltrate w/ few/no parasites; Inflammatory cells release proteases -> erodes oronasal or oropharyngeal mucosa -> ulceration of the ST and cartilage -> loss of lips, soft part of nose, nasal septum, and soft palate

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73
Q

Trypansoma cruzi

A

Obligate intracellular protozoan hemoflagellate w/ a “C” or “U” shaped appearance

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74
Q

Chagas’ Disease locations

A

C. & S. America are infected

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75
Q

Trypansoma cruzi found in human peripheral blood

A

Trypomastigote form

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76
Q

Trypansoma cruzi Life Cycle

A

Metacyclin form invades cells locally -> transform to amastigote forms -> multiply & fill cytoplasm -> differentiate to trypomastigotes
Trypomastigotes lyse the host cell -> hematogenous spread to distant site

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77
Q

Trypansoma cruzi immune response

A

CMI; invades SM and evades CMI

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78
Q

Acute Chagas

A

Mild, localized inflammatory reaction at inoculation site; followed by parasitemia (fever, LAD, HSM, malaise) lasting 4-6wks

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79
Q

Chagoma Sign

A

erythematous subcutaneous nodule may form at inoculation site

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80
Q

Romana Sign

A

edema of the conjunctiva or eyelids if inoculation is via the oral, nasal, or ocular mucosa

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81
Q

Indeterminant Phase of Chagas

A

vague GI or Cardiac Sx, life-long persistent low-grade parasitemia

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82
Q

Chronic Chagas

A

occur years/decades after an acute infection d/t chronic inflammatory responses (Th1-mediated) to persisting antigens of organisms, resulting in fibrosis

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83
Q

Sx of Chronic Chagas

A

biventricular enlargement w/ thinning of the ventricular walls, conduction system defect, dysarrhythmias, cardiomyopathy, thromboembolism; Megacolon or Megaesophagus may develop: dysphagia, regurgitation, aspiration, constipation

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84
Q

Acute Chagas Diagnosis

A

peripheral blood smears: motile parasites on direct examination “C” shaped

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85
Q

Chronic Chagas Diagnosis

A

Serology to detect specific Abs

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86
Q

Treatment of Chagas

A

Nifurtimox & Benzidiazole (50% efficacy)

87
Q

Acute chagas, which organs are heavily parasitized

A

heart & GI

88
Q

West Africa Sleeping Sickness Agent

A

T. brucei gambiense

89
Q

T. brucei vector

A

Tetse Fly

90
Q

T. brucei evades immune system by

A

antigenic variation of VSG intracellularly

91
Q

Primary Lesion of African Trypanosomiasis

A

chancre may form at bite site (painful, well-circumscribed, rubbery, red lesion, 2-5cm)

92
Q

Hemolymphatic Stage of African Trypanosomiasis

A

invade the lymphatics resulting in febrile attacks lasting 3-7d, followed by asymptomatic interval

93
Q

Hemolymphatic Stage of African Trypanosomiasis Sx

A

fever, malaise, HA, arthralgia, LAD, rash

94
Q

Winterbottom’s Sign

A

Posterior cervical lymph node enlargement w/ African Trypanosomiasis Hemolymphatic Stage

95
Q

Meningoencepphalitic Stage of African Trypanosomiasis Sx

A

delayed & prolonged pain sensation (Kerandel’s Sign), increasing loss of energy -> unresponsive, loss of motor control, difficult to arouse

96
Q

Kerandel’s Sign

A

delayed & prolonged pain sensation; Meningoencepphalitic Stage of African Trypanosomiasis

97
Q

T. brucei Diagnosis

A

“S” shaped protozoan on wet mount

98
Q

Meningoencephalitic stage diagnosis

A

elevation of WBCs (>5) in CSF, elevated protein & intracranial pressure, + Mott Cells

99
Q

Mott Cells

A

large eosinophilic plasma cells containing IgM – is an uncommon, but characteristic finding in CSF

100
Q

Treatment of African Trypanosomiasis w/o CNS involvement

A

Suramin or Pentamidine

101
Q

Treatment of African Trypanosomiasis w CNS involvement

A

Malarsoprol or Eflornithine

102
Q

Toxoplasma gondii

A

protozoan, obligate intracellular, 2 life forms in humans

103
Q

Tachyzoite

A

invasive, rapidly proliferating trophozoite found in any nucleated cell, predilection for mononuclear phagocytes

104
Q

Bradyzoite

A

pseudocysts found in muscle and brain, dormant/slow replication; Host’s CMI response forms tissue pseudocysts

105
Q

Life Cycle of T. gondii

A

intermediate host ingests either a mature oocyst or pseudocyst -> sporozoites (from oocyst) or trophozoites (from pseudocyst) invade the GIT epithelium
-> picked up by macrophages -> tachyzoites multiply rapidly -> lyses cell & spread hematogenously to all tissues -> small necrotic foci lead to CMI response -> pseudocyst

106
Q

Leading cause of death d/t food-borne illness in the US

A

T. gondii

107
Q

2nd leading cause of CNS infection in AIDS pts

A

T. gondii

108
Q

Most common cause of intraocular inflammation & posterior uveitis in immunocompetent pts WW

A

T. gondii

109
Q

Transmission of T. gondii

A

cat feces, undercooked pork

110
Q

Primary Toxoplasmosis Sx

A

asymptomatic, cervical LAD or fever, fatigue, chills, HA, sore throat, mono-like Sx

111
Q

Severe Primary Toxoplasmosis Sx

A

Mono-like Sx, lymphadenitis, retinochoroiditis, myocarditis, polymyositis, uveitis, hepatitis, or pneumonia

112
Q

Primary Toxo, Acute Ocular Toxoplasmosis Sx

A

red eye, blurred or reduced vision, eye pain, photophobia, tearing, floaters; progression to Retinochoroiditis

113
Q

incubate period of T. gondii

A

5-20d

114
Q

Retinochoroiditis Sx

A

sudden or gradual impaired vision d/t yellowish-white cotton patch lesions on retina

115
Q

Latent T. gondii infection

A

pseudocysts remain in tissues (lymph nodes, brain, eyes, lung, & muscle)

116
Q

Congenital Toxoplasmosis Risk of fetal infection

A

female acquires primary infection DURING pregnancy, esp 2nd or 3rd trimester higher risk for infection

117
Q

Congenital Toxoplasmosis Risk of fetal disease

A

female acquires primary infection DURING pregnancy, esp 1st or 2nd trimester higher risk of disease

118
Q

Congenital Toxoplasmosis S/S

A

stillbirth, spontaneous abortion, hydrocephalus, encephalitis, retinochoroiditis, HSM, lymphadenitis, fever, atypical pneumonia, rash, diarrhea, jaundice, splenomegaly

119
Q

Gold Standard Diagnostic test for Toxoplasmosis

A

Sabin-Feldman IgG Dye test

120
Q

Other Diagnostic tests for Toxoplasmosis

A

IFA, TORCH, IgG/IgM Avidity test

121
Q

Treatment for Toxoplasmosis, only targets actively dividing organisms

A

Pyrimethamine & Sulfonamides

122
Q

Tx for 1st trimester pregnant female w/ Toxoplasmosis or Congenital

A

Spiramycin

123
Q

Schistosoma mansoni

A

WW, feces shedding

124
Q

Schistosoma japonicum

A

Orient, feces shedding

125
Q

Schistosoma haematobium:

A

Africa, Asia, Portugal, Urine shedding

126
Q

Schistosoma characteristics

A

Blood flukes/helminths, diecious

127
Q

Life Cycle of Schistosoma

A

Cercariae penetrate human hair follicles -> in humans, schistosomulae migrate through the lungs to the hepatoportal system -> mature, mate, produce ova in the mesenteric v.

128
Q

Immune response to Schistosoma

A

Humoral (IgE), ADCC (eosinophils)

129
Q

Schistoma evades immune reponse by

A

Acquisition of blood group & host antigens on surface, masking them from host immunity; Metabolic products from adult inhibit T cell proliferation

130
Q

Vector of Schistoma

A

snail

131
Q

Primary Schistoma Sx

A

Schistosomal dermatitis: itchy papular eruption

132
Q

Lung Involvement Schistoma Sx

A

Eosinophilic infiltration; Peripheral eosinophila; Acute phase exposure Sx: fever, n/v, abdominal pain, diarrhea – a syndrome known as “Katayama fever”

133
Q

“Katayama fever”

A

fever, n/v, abdominal pain, diarrhea d/t Schistoma larvae traveling through lungs

134
Q

Chronic Stage of Schistoma

A

Toxic hepatitis, irregular fluctuating fever, urticaria; intestinal hemorrhage & pseudodysentery; Eosiniophilic granulomatous (Th2) response to ova in liver and local tissue -> HSM, pulmonary schistomiasis, ascites

135
Q

Schistosome Dermatitis aka “Swimmer’s Itch”

A

Schistosoma species that have an animal other than humans as a definitive host (waterfowl), may enter humans -> larvae die -> severe allergic dermatitis at site of penetration

136
Q

Tx for Swimmer’s Itch

A

antihistamines, corticosteroids

137
Q

Diagnosis for Schistoma

A

Presence of ova in GI/liver biopsy or fecal sample

138
Q

Labs for Schistoma

A

high IgE & eosinophilia

139
Q

Treatment for Schistoma

A

Praziquantel

140
Q

Major Agents of Osteomyelitis

A

S. aureus & CoNS; GNRs, GAS, GBS, Anaerobes

141
Q

Osteomyelitis + Sickle Cell

A

Salmonella

142
Q

Osteomyelitis + Children

A

S. aureus, GAS, H. influenza, Kingella kingae

143
Q

Osteomyelitis + Unregulated Diabetic

A

Mucomycoses

144
Q

Osteomyelitis + Chronic, persistent, recurrent d/t SCV

A

S. aureus, P. aeruginosa, E. coli

145
Q

Osteomyelitis + Immunocompromised

A

Aspergillus, MAC, Candida

146
Q

Osteomyelitis + puncture wound

A

P. aeruginosa

147
Q

Osteomyelitis causes

A

Trauma or surgery to bone or surrounding ST; Foreign body (artificial joint, pins, plates) for biofilm formation; Bacteremia or ST infection (cellulitis); IVDU or Nosocomial infections

148
Q

Osteomyelitis caused by trauma/surgery Sx

A

Fever, chills, malaise, bone pain, swelling/pain of ST overlying affected bone

149
Q

Osteomyelitis d/t Diabetic Foot most often affects which bones

A

Metatarsal head, Tarsal bone, Phalange involvement

150
Q

Osteomyelitis d/t bacteremia

A

Fever, chills, malaise, bone pain, localized pain & swelling of ST

151
Q

Children’s Osteomyelitis d/t bacteremia most often infects

A

metaphyseal areas of long bones – tibia, femur (Brodie Abscess – tibia osteomyelitis)

152
Q

Adult’s Osteomyelitis d/t bacteremia most often infects

A

infects vertebrate (fever + back pain)

153
Q

Radiographs: (+) several weeks post initiation of infection

A

Focal loss of trabecular pattern, periosteal reaction & frank bone destruction

154
Q

What imaging modalities identifies Osteomyelitis earlier

A

CT, MRI +/- contrast, Bone scan (inflammation)

155
Q

Tx for Osteomyelitis

A

prolonged Tx w/ ABX

156
Q

Agents of SA in Children < 4y/o

A

S. aureus, GBS, GAS, S. pneumo, GNRs

157
Q

Agents of SA in Children > 4y/o

A

S. aureus, CoNS, GAS, Enterococci,

N. gonorrhoeae, GNRs

158
Q

Agents of SA in Elderly

A

GBS, GAS, S. pneumo, Peptostreptococcus, anaerobic & facultative anaerobic GNRs (Bacteroides), Candida

159
Q

Agents of SA in Subacute or Chronic SA

A

MTB, Coccidioides immitis, Bastomyces dermatitis, Borrelia burgdorferi, T. pallidum

160
Q

Agents of SA in Immunodeficient pts (hypogammaglobulinemia) esp during bacteremia

A

Mycoplasma & Ureaplasma

161
Q

Viral Agents of SA

A

Hep B, Rubella, HPV-B19. Mumps

162
Q

Viral Agents of SA act via

A

direct or cause a Type III HSN

163
Q

> 24mo post-surgery - hematogenous dissemination acquired from sepsis, skin infection, or urosepsis; agent causing SA

A

S. aureus

164
Q

Pathogenesis of SA

A

PMNs respond to joint infection -> release degradative & lysosomal enzymes; Bacteria also release exotoxins & degradative enzymes
Damage to the articular cartilage occurs -> effusion

165
Q

Prosthetic joints pathogenesis of SA

A

-> biofilm S. aureus

166
Q

Acute SA Sx

A

fever + joint pain, limited movement, tenderness, swelling of joint

167
Q

Disseminated Gonococcal Infection -> SA Sx

A

occurs in untreated gonorrhea, several days after onset of genital infection
Fever, joint Sx, rash

168
Q

Granulomatous Arthritis

A

insidious onset, slow progression w/ granuloma formation

169
Q

Diagnosis of SA - Arthrocentesis

A 
o	(+) Culture
o	WBCs elevated (25,000-100,000)
•	PMNs if extracellular bacteria
•	Monocytic if viral, MTB, mycoses
o	RBCs may be present
o	Reduced glucose
o	Elevated protein & lactate
170
Q

Diagnosis of SA - X-ray

A

ST swelling, joint-space widening, displacement of tissue planes by distended capsule

171
Q

Tx for SA

A

IV Tx for ~1wk, then oral Tx if compliance is guaranteed

172
Q

Agents causing RA

A
  • RT infection: Chlamydia & Mycoplasma
  • GU infection: Chlamydia & N. gonorrhoeae
  • GI infection: Campylobacter, Yersinia, Salmonella, Shigella
173
Q

Incubation of RA

A

S/S occur 7-14d post-infection

174
Q

Risk Factors for RA

A

Male, HLA-B27

175
Q

RA Sx

A

Arthralgias: painful, asymmetric, involving < 3-4 joints, but only 1 at a time, typically involving LE joints
Acute conjunctivitis, sterile urethritis, afebrile (unless mucosal infection causes fever)

176
Q

Diagnosis of RA - Arthrocentesis

A 
o	(-) Culture
o	WBCs elevated (2,000-50,000)
•	PMNs 
o	RBCs may be present
o	Elevated Abs, complement, protein
o	Normal glucose level
177
Q

Diagnosis of SA - X-ray

A

ST swelling, joint-space widening, displacement of tissue planes by distended capsule

178
Q

HIV-M Clade C

A

accounts for 50% of infections WW

179
Q

HIV-M Clade B

A

predominates in US

180
Q

HIV characteristics

A

ssRNA (+) sense

181
Q

HIV 3 genes

A

gag, pol, env

182
Q

GP120 – Surface Glycoprotein function

A

envelope protein that mediates attachment w/ the host cell’s CD4

183
Q

GP41 – Transmembrane Glycoprotein function

A

envelope protein that mediates fusion of the viral envelope w/ the cytoplasmic membrane

184
Q

Gag

A

encodes for matrix, capsid, nucleocapsid

185
Q

Pol

A

encodes RT, protease, integrase

186
Q

Env

A

encodes envelope glycoproteins GP120 & GP41 for attachment & fusion w/ host cells

187
Q

Co-receptors for CD4/GP120

A

CCR5 or CXR4

188
Q

GP120 binds CD4 on

A

T-helper cells, monocytes, macrophages, & dendritic cells

189
Q

M-Tropic HIV (R5 strain):

A

cause the Primary Infection by binding to CCR5 co-receptor found on CD4 T cells, macrophages, monocytes, dendritic cells; Do not form syncytia – non-syncytia producing (non-SI)

190
Q

T-Tropic HIV (X4 strain):

A

conversion as the infection proceeds by binding to CXCR4 co-receptor found on naïve CD4 Th cells; Form syncytia – (SI)

191
Q

DC-SIGN

A

dendritic cell ICAM that typically binds CD40 during Tcell activation, is bound by GP120 -> increased half-life & increases the affinity of HIV-1 glycoproteins for CD4 (it presents HIV to the T cell in lymph nodes

192
Q

Viremia peaks in blood 4-6 weeks after infection

A

coincides w/ CD4+ T cell reduction

193
Q

Seroconversion takes place ~4-6wks

A

Abs cause plateau of viremia -> rebound in CD4+ T cell count, but not back to normal

194
Q

Stage 1: HIV

A

(+), CD4+ T cell count > 500, CD4+ T cell % >29

195
Q

Stage 2: HIV

A

HIV (+), CD4+ T cell count 200-499, CD4+ T cell % 14-28

196
Q

Stage 3: AIDS

A

HIV (+), CD4+ T cell count <14

197
Q

Immune response to HIV

A

Neutralizing Antibodies + Cytotoxic T Lymphocytes (CTL)

198
Q

Sx of Primary HIV infection

A

10-20% w/ Sx: Fever, fatigue, rash, LAD, pharyngitis, arthralgia, n/v, diarrhea, night sweats, HA, etc; Sx resolve in ~2weeks

199
Q

Latent HIV Sx

A

No S/S, reduced CD4+ T cell count (500-1000)

200
Q

Opportunistic Infections in AIDS pts

A 
o	Toxoplasma gondii
o	Cryptosporidium parvum
o	Pneumocystic jiroveci
o	Candida
o	Cryptococcus neoformans
o	Histoplasma capsulatum
o	MTB
o	MAC
o	Salmonella
o	Bartonella
o	CMV, HSV, EBV, HHV-8, HPV, Poxvirus, JC virus
201
Q

Diagnosis of HIV

A

P24 antigen: present 2-3 weeks after infection

HIV Abs: 4-6wks

202
Q

Window Period of HIV:

A

period before Ab production where viremia is present, only marker is p24

203
Q

Confirmatory test for HIV

A

ELISA to detect Ab against HIV

204
Q

Monitor HIV Tx w/

A

CD4+ T cell levels: Flow Cytometry

Viremia: rtPCR to quantify viral RNA presence in blood

205
Q

Genotypic and Phentypic tests can determien

A

if there was a recent mutation in the HIV

206
Q

ART drugs

A

RT Inhibitors (NRTI, NNRTI), Protease inhibitor, Fusion inhibitor, Integrase strand transfer inhibitors

207
Q

RT Inhibitors NRTI

A

Nucleoside analogue RT inhibitor (NRTI): gets incorporated into the growing DNA chain & causes termination

208
Q

RT Inhibitors NNRTI

A

Non-Nucleoside analogue RT inhibitor (NNRTI): cause chain termination w/o getting incorporated into DNA

209
Q

Protease inhibitor

A

Prevent protease from cleaving viral proteins; Irreversible

210
Q

Fusion inhibitor

A

Inhibit p41 to block fusion of virus and host cell

211
Q

Integrase strand transfer inhibitors

A

Effective when used in combination w/ other ARTs

212
Q

HAART recommendations

A

2 RTIs + a PI (old recommendation)

2 NRTIs + NNRTI/PI/INSTI

213
Q

ART therapy for HIV

A

Asymptomatic Pts w/ CD4 < 500

All symptomatic Pts

Microbiology Exam 7 (2 decks)

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