Bacteremia Flashcards
(213 cards)
1
Q
Spontaneous bacteremia
A
common event (flossing, brushing teeth) that creates small lacerations allowing small amt of bacteria to enter the blood (minutes)
2
Q
Transient bacteremia
A
trauma to a heavily colonized mucosal surface resulting in bacteria entering into the blood (hours)
3
Q
Intermittent/Recurrent bacteremia
A
foci of infection (staph abscess) causing there to be bacteria in the blood occasionally
4
Q
Continuous bacteremia:
A
certain diseases cause there to be bacteria in the blood continuously
5
Q
Causes of Continuous bacteremia:
A
• Infective endocarditis, typhoid fever, anthrax, rickettsia, pyelonephritis, bacterial meningitis
6
Q
Organs that clear bacteria from blood
A
liver & spleen
7
Q
_______________ kill bacteria in the liver and spleen
A
Kupffer cells + PMNs
8
Q
Asplenics are particularly susceptible
A
bacteremia, particularly those w/ capsules
9
Q
Agents of bacteremia
A
CoNS, S. aureus, Enterococcus, GNRs, Strep, Candida
10
Q
Risks for bacteremia
A
HA-bacteremia: CVC, catheters (Staph, E.coli)
CA-bacteremia:acute pyelonephritis
11
Q
Catheter associated bacteremia agents
A
E.coli, GNR
12
Q
CVC associated bacteremia agents
A
Staph
13
Q
Common cause of bacteremia in children < 2
A
S. agalactiae, E. coli, K. pneumo
14
Q
Common cause of bacteremia in elderly
A
GNR
15
Q
Pathogenesis of catheter associated bacteremia
A
spread from skin to catheter, biofilm formation
16
Q
S/S Bacteremia
A
Sepsis, severe sepsis, septic shock
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
18
Q
Native Valve Endocarditis
A
most common, occurs in pts w/o hx of IVDU or prosthetic valve
19
Q
Native Valve Endocarditis valves affected
A
mitral, aortic
20
Q
Risks for Native Valve Endocarditis
A
mitral valve prolapse, congenital or acquired heart defects, rheumatic heart disease
21
Q
Pathogenesis of Native Valve Endocarditis
A
turbulent BF -> deposition of fibrin/proteins/etc -> contamination of damaged heart valve secondary to bacteremia
22
Q
Agents of Native Valve Endocarditis
A
Strep —> CoNS, S. aureus, GNR, S. pneumo, GAS
23
Q
Prosthetic Valve Endocarditis
A
occurs in pts w/ prosthetic valves
24
Q
Early Prosthetic Valve Endocarditis d/t
A
Contamination of valve during surgery
25
Agents of Early Prosthetic Valve Endocarditis
Strep ---> CoNS, S. aureus, GNR, S. pneumo, GAS
26
Late Prosthetic Valve Endocarditis d/t
secondary to bacteremia
27
IVDU Endocarditis
least common, acute disease d/t contamination of the valve secondary to bacteremia
28
Most common valve affected by IVDU Endocarditis
tricuspid
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Agents of IVDU Endocarditis
CoNS, S. aureus, Enterococci, S. pneumo, GAS, polymicrobic
30
Pathogenesis of IE
deposition of fibrin & platelet aggregation -> NBT -> bacteremia & secondary infection -> vegetation/biofilm -> large/small emboli
31
Immunopathology d/t IE
Hypergammaglobulinemia
| Type III HSN reaction -> acute vasculitis & glomerulonephritis
32
Subacute IE Sx
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
33
Skin manifestations/Peripheral Stigmata of Subacute IE
petechiae on mucosa (conjunctiva), Janeway's Lesions, Osler's Nodes, Splinter hemorrhages, clubbing
34
Janeway's Lesions
painless, petechial lesion on palms and soles
35
Osler's Nodes
painful, petechial lesions on fingers & toes
36
Acute IE Sx
high virulent; rapid septic emboli -> ischemic event: Stroke, MI, Liver or Kidney Failure; Fever, significant heart murmur, w/o other S/S of immunopathology
37
Diagnosis of IE
transesophageal ECHO, blood specimen (2-3X), MIC/MBC/Cidal, Culture
38
Failure to culture for IE d/t HACEK
* Haemophilus
* Aggregaitbacter
* Cardiobacterium hominis
* Eikenella corrodens
* Kingella kingae
39
Treatment of IE
10X MBC
40
Prevention of IE
abx prophylaxis for procedures w/ risk of bacteremia (tooth extraction, cardiac, GI); Amoxicillin 30m before, 2hrs after
41
Old World visceral leishmaniasis causative agents
L. donovani donovani, L. donovani infantum, L. donovani archibaldi
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New World visceral leishmaniasis causative agents
L. donovani chagasi
43
L. donovani characteristics
Small, round protozoan parasite of the macrophage family; obligate intracellular
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Promastigote form
carried by sandflies & infects humans/reservoirs
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Amastigote form
carried by humans/reservoirs & infects sandflies
46
Life Cycle of L. donovani
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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L. donovani has a Predilection for
mononuclear cell populations, spleen, liver, bone marrow -> histiocyte and macrophage destruction
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Vector of L. donovani in the Old World
Sandflies (Phlebotomus)
49
L. donovani infection in US
immigrants, travelers, troops
50
L. donovani is common
in India, Bangladesh, Middle East, Mediterranean, Africa, C. & S. America
51
Vector of L. donovani in the New World
Lutzomyia spp
52
Immune Response to L. donovani
CMI: Th1 cells produce IFN-gamma which activates macrophages to restrict intracellular growth
53
L. donovani has what affect on the immune system
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
54
Visceral Leishmaniasis incubation period
~3-6mo
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Manifestations of Visceral Leishmaniasis: Insidious
Insidious onset: hepatosplenomegaly, weight loss, fever, malaise, LAD, scaly skin/ashen appearance, cachexia
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Manifestations of Visceral Leishmaniasis: Abrupt
```
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
```
57
Post-Kala-azar Dermal Leishmaniasis:
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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Mortality of Visceral Leishmaniasis is d/t
secondary infection
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Diagnosis: Labs w/ Visceral Leishmaniasis
Granulocytopenia, anemia, elevated gamma-globulins
60
Visceral Leishmaniasis Microscopy
Biopsy of bone marrow + Giemsa Stain - intracellular amastigotes in macrophages is a confirming diagnosis
61
Leishman Intradermal Skin Test
used retrospectively (post-infection); Negative during active infection d/t CMI anergy
62
Treatment for Visceral Leishmaniasis
Pentavalent antimony, Sodium Stibogluconat
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Treatment for relapsed Visceral Leishmaniasis
Pentamidine isoethionate or Amphotericin B
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Cutaneous Leishmaniasis Old World Agents
L. tropica, L. major, L. aethiopica
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Cutaneous Leishmaniasis New World Agents
L. mexicana, L. amazonenesis, L. peruviana
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Mucocutaneous Leishmaniasis Agents
L. braziliensis, L. guyanensis, L. panamensis
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Incubation period of Cutaneous Leishmaniasis
1-3mo
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Cutaneous Leishmaniasis Sx
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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Leichmaniasis Recidivans – Hyperergic Variant:
Tubercles or nodules appearing over/around scars of healed ulcers; DTH response
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Diffuse Cutaneous Leishmaniasis – Anergic Variant
anergic & the organisms disseminate throughout the skin; Th2 response
71
Mucocutaneous Leishmaniasis Sx
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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Mucocutaneous Leishmaniasis Secondary lesions on mucosa
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
73
Trypansoma cruzi
Obligate intracellular protozoan hemoflagellate w/ a “C” or “U” shaped appearance
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Chagas’ Disease locations
C. & S. America are infected
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Trypansoma cruzi found in human peripheral blood
Trypomastigote form
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Trypansoma cruzi Life Cycle
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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Trypansoma cruzi immune response
CMI; invades SM and evades CMI
78
Acute Chagas
Mild, localized inflammatory reaction at inoculation site; followed by parasitemia (fever, LAD, HSM, malaise) lasting 4-6wks
79
Chagoma Sign
erythematous subcutaneous nodule may form at inoculation site
80
Romana Sign
edema of the conjunctiva or eyelids if inoculation is via the oral, nasal, or ocular mucosa
81
Indeterminant Phase of Chagas
vague GI or Cardiac Sx, life-long persistent low-grade parasitemia
82
Chronic Chagas
occur years/decades after an acute infection d/t chronic inflammatory responses (Th1-mediated) to persisting antigens of organisms, resulting in fibrosis
83
Sx of Chronic Chagas
biventricular enlargement w/ thinning of the ventricular walls, conduction system defect, dysarrhythmias, cardiomyopathy, thromboembolism; Megacolon or Megaesophagus may develop: dysphagia, regurgitation, aspiration, constipation
84
Acute Chagas Diagnosis
peripheral blood smears: motile parasites on direct examination "C" shaped
85
Chronic Chagas Diagnosis
Serology to detect specific Abs
86
Treatment of Chagas
Nifurtimox & Benzidiazole (50% efficacy)
87
Acute chagas, which organs are heavily parasitized
heart & GI
88
West Africa Sleeping Sickness Agent
T. brucei gambiense
89
T. brucei vector
Tetse Fly
90
T. brucei evades immune system by
antigenic variation of VSG intracellularly
91
Primary Lesion of African Trypanosomiasis
chancre may form at bite site (painful, well-circumscribed, rubbery, red lesion, 2-5cm)
92
Hemolymphatic Stage of African Trypanosomiasis
invade the lymphatics resulting in febrile attacks lasting 3-7d, followed by asymptomatic interval
93
Hemolymphatic Stage of African Trypanosomiasis Sx
fever, malaise, HA, arthralgia, LAD, rash
94
Winterbottom's Sign
Posterior cervical lymph node enlargement w/ African Trypanosomiasis Hemolymphatic Stage
95
Meningoencepphalitic Stage of African Trypanosomiasis Sx
delayed & prolonged pain sensation (Kerandel’s Sign), increasing loss of energy -> unresponsive, loss of motor control, difficult to arouse
96
Kerandel’s Sign
delayed & prolonged pain sensation; Meningoencepphalitic Stage of African Trypanosomiasis
97
T. brucei Diagnosis
“S” shaped protozoan on wet mount
98
Meningoencephalitic stage diagnosis
elevation of WBCs (>5) in CSF, elevated protein & intracranial pressure, + Mott Cells
99
Mott Cells
large eosinophilic plasma cells containing IgM – is an uncommon, but characteristic finding in CSF
100
Treatment of African Trypanosomiasis w/o CNS involvement
Suramin or Pentamidine
101
Treatment of African Trypanosomiasis w CNS involvement
Malarsoprol or Eflornithine
102
Toxoplasma gondii
protozoan, obligate intracellular, 2 life forms in humans
103
Tachyzoite
invasive, rapidly proliferating trophozoite found in any nucleated cell, predilection for mononuclear phagocytes
104
Bradyzoite
pseudocysts found in muscle and brain, dormant/slow replication; Host’s CMI response forms tissue pseudocysts
105
Life Cycle of T. gondii
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
Leading cause of death d/t food-borne illness in the US
T. gondii
107
2nd leading cause of CNS infection in AIDS pts
T. gondii
108
Most common cause of intraocular inflammation & posterior uveitis in immunocompetent pts WW
T. gondii
109
Transmission of T. gondii
cat feces, undercooked pork
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Primary Toxoplasmosis Sx
asymptomatic, cervical LAD or fever, fatigue, chills, HA, sore throat, mono-like Sx
111
Severe Primary Toxoplasmosis Sx
Mono-like Sx, lymphadenitis, retinochoroiditis, myocarditis, polymyositis, uveitis, hepatitis, or pneumonia
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Primary Toxo, Acute Ocular Toxoplasmosis Sx
red eye, blurred or reduced vision, eye pain, photophobia, tearing, floaters; progression to Retinochoroiditis
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incubate period of T. gondii
5-20d
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Retinochoroiditis Sx
sudden or gradual impaired vision d/t yellowish-white cotton patch lesions on retina
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Latent T. gondii infection
pseudocysts remain in tissues (lymph nodes, brain, eyes, lung, & muscle)
116
Congenital Toxoplasmosis Risk of fetal infection
female acquires primary infection DURING pregnancy, esp 2nd or 3rd trimester higher risk for infection
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Congenital Toxoplasmosis Risk of fetal disease
female acquires primary infection DURING pregnancy, esp 1st or 2nd trimester higher risk of disease
118
Congenital Toxoplasmosis S/S
stillbirth, spontaneous abortion, hydrocephalus, encephalitis, retinochoroiditis, HSM, lymphadenitis, fever, atypical pneumonia, rash, diarrhea, jaundice, splenomegaly
119
Gold Standard Diagnostic test for Toxoplasmosis
Sabin-Feldman IgG Dye test
120
Other Diagnostic tests for Toxoplasmosis
IFA, TORCH, IgG/IgM Avidity test
121
Treatment for Toxoplasmosis, only targets actively dividing organisms
Pyrimethamine & Sulfonamides
122
Tx for 1st trimester pregnant female w/ Toxoplasmosis or Congenital
Spiramycin
123
Schistosoma mansoni
WW, feces shedding
124
Schistosoma japonicum
Orient, feces shedding
125
Schistosoma haematobium:
Africa, Asia, Portugal, Urine shedding
126
Schistosoma characteristics
Blood flukes/helminths, diecious
127
Life Cycle of Schistosoma
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
Immune response to Schistosoma
Humoral (IgE), ADCC (eosinophils)
129
Schistoma evades immune reponse by
Acquisition of blood group & host antigens on surface, masking them from host immunity; Metabolic products from adult inhibit T cell proliferation
130
Vector of Schistoma
snail
131
Primary Schistoma Sx
Schistosomal dermatitis: itchy papular eruption
132
Lung Involvement Schistoma Sx
Eosinophilic infiltration; Peripheral eosinophila; Acute phase exposure Sx: fever, n/v, abdominal pain, diarrhea – a syndrome known as “Katayama fever”
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“Katayama fever”
fever, n/v, abdominal pain, diarrhea d/t Schistoma larvae traveling through lungs
134
Chronic Stage of Schistoma
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
Schistosome Dermatitis aka “Swimmer’s Itch”
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
Tx for Swimmer’s Itch
antihistamines, corticosteroids
137
Diagnosis for Schistoma
Presence of ova in GI/liver biopsy or fecal sample
138
Labs for Schistoma
high IgE & eosinophilia
139
Treatment for Schistoma
Praziquantel
140
Major Agents of Osteomyelitis
S. aureus & CoNS; GNRs, GAS, GBS, Anaerobes
141
Osteomyelitis + Sickle Cell
Salmonella
142
Osteomyelitis + Children
S. aureus, GAS, H. influenza, Kingella kingae
143
Osteomyelitis + Unregulated Diabetic
Mucomycoses
144
Osteomyelitis + Chronic, persistent, recurrent d/t SCV
S. aureus, P. aeruginosa, E. coli
145
Osteomyelitis + Immunocompromised
Aspergillus, MAC, Candida
146
Osteomyelitis + puncture wound
P. aeruginosa
147
Osteomyelitis causes
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
Osteomyelitis caused by trauma/surgery Sx
Fever, chills, malaise, bone pain, swelling/pain of ST overlying affected bone
149
Osteomyelitis d/t Diabetic Foot most often affects which bones
Metatarsal head, Tarsal bone, Phalange involvement
150
Osteomyelitis d/t bacteremia
Fever, chills, malaise, bone pain, localized pain & swelling of ST
151
Children's Osteomyelitis d/t bacteremia most often infects
metaphyseal areas of long bones – tibia, femur (Brodie Abscess – tibia osteomyelitis)
152
Adult's Osteomyelitis d/t bacteremia most often infects
infects vertebrate (fever + back pain)
153
Radiographs: (+) several weeks post initiation of infection
Focal loss of trabecular pattern, periosteal reaction & frank bone destruction
154
What imaging modalities identifies Osteomyelitis earlier
CT, MRI +/- contrast, Bone scan (inflammation)
155
Tx for Osteomyelitis
prolonged Tx w/ ABX
156
Agents of SA in Children < 4y/o
S. aureus, GBS, GAS, S. pneumo, GNRs
157
Agents of SA in Children > 4y/o
S. aureus, CoNS, GAS, Enterococci,
| N. gonorrhoeae, GNRs
158
Agents of SA in Elderly
GBS, GAS, S. pneumo, Peptostreptococcus, anaerobic & facultative anaerobic GNRs (Bacteroides), Candida
159
Agents of SA in Subacute or Chronic SA
MTB, Coccidioides immitis, Bastomyces dermatitis, Borrelia burgdorferi, T. pallidum
160
Agents of SA in Immunodeficient pts (hypogammaglobulinemia) esp during bacteremia
Mycoplasma & Ureaplasma
161
Viral Agents of SA
Hep B, Rubella, HPV-B19. Mumps
162
Viral Agents of SA act via
direct or cause a Type III HSN
163
>24mo post-surgery - hematogenous dissemination acquired from sepsis, skin infection, or urosepsis; agent causing SA
S. aureus
164
Pathogenesis of SA
PMNs respond to joint infection -> release degradative & lysosomal enzymes; Bacteria also release exotoxins & degradative enzymes
Damage to the articular cartilage occurs -> effusion
165
Prosthetic joints pathogenesis of SA
-> biofilm S. aureus
166
Acute SA Sx
fever + joint pain, limited movement, tenderness, swelling of joint
167
Disseminated Gonococcal Infection -> SA Sx
occurs in untreated gonorrhea, several days after onset of genital infection
Fever, joint Sx, rash
168
Granulomatous Arthritis
insidious onset, slow progression w/ granuloma formation
169
Diagnosis of SA - Arthrocentesis
```
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
Diagnosis of SA - X-ray
ST swelling, joint-space widening, displacement of tissue planes by distended capsule
171
Tx for SA
IV Tx for ~1wk, then oral Tx if compliance is guaranteed
172
Agents causing RA
* RT infection: Chlamydia & Mycoplasma
* GU infection: Chlamydia & N. gonorrhoeae
* GI infection: Campylobacter, Yersinia, Salmonella, Shigella
173
Incubation of RA
S/S occur 7-14d post-infection
174
Risk Factors for RA
Male, HLA-B27
175
RA Sx
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
Diagnosis of RA - Arthrocentesis
```
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
Diagnosis of SA - X-ray
ST swelling, joint-space widening, displacement of tissue planes by distended capsule
178
HIV-M Clade C
accounts for 50% of infections WW
179
HIV-M Clade B
predominates in US
180
HIV characteristics
ssRNA (+) sense
181
HIV 3 genes
gag, pol, env
182
GP120 – Surface Glycoprotein function
envelope protein that mediates attachment w/ the host cell’s CD4
183
GP41 – Transmembrane Glycoprotein function
envelope protein that mediates fusion of the viral envelope w/ the cytoplasmic membrane
184
Gag
encodes for matrix, capsid, nucleocapsid
185
Pol
encodes RT, protease, integrase
186
Env
encodes envelope glycoproteins GP120 & GP41 for attachment & fusion w/ host cells
187
Co-receptors for CD4/GP120
CCR5 or CXR4
188
GP120 binds CD4 on
T-helper cells, monocytes, macrophages, & dendritic cells
189
M-Tropic HIV (R5 strain):
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
T-Tropic HIV (X4 strain):
conversion as the infection proceeds by binding to CXCR4 co-receptor found on naïve CD4 Th cells; Form syncytia – (SI)
191
DC-SIGN
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
Viremia peaks in blood 4-6 weeks after infection
coincides w/ CD4+ T cell reduction
193
Seroconversion takes place ~4-6wks
Abs cause plateau of viremia -> rebound in CD4+ T cell count, but not back to normal
194
Stage 1: HIV
(+), CD4+ T cell count > 500, CD4+ T cell % >29
195
Stage 2: HIV
HIV (+), CD4+ T cell count 200-499, CD4+ T cell % 14-28
196
Stage 3: AIDS
HIV (+), CD4+ T cell count <14
197
Immune response to HIV
Neutralizing Antibodies + Cytotoxic T Lymphocytes (CTL)
198
Sx of Primary HIV infection
10-20% w/ Sx: Fever, fatigue, rash, LAD, pharyngitis, arthralgia, n/v, diarrhea, night sweats, HA, etc; Sx resolve in ~2weeks
199
Latent HIV Sx
No S/S, reduced CD4+ T cell count (500-1000)
200
Opportunistic Infections in AIDS pts
```
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
Diagnosis of HIV
P24 antigen: present 2-3 weeks after infection
| HIV Abs: 4-6wks
202
Window Period of HIV:
period before Ab production where viremia is present, only marker is p24
203
Confirmatory test for HIV
ELISA to detect Ab against HIV
204
Monitor HIV Tx w/
CD4+ T cell levels: Flow Cytometry
| Viremia: rtPCR to quantify viral RNA presence in blood
205
Genotypic and Phentypic tests can determien
if there was a recent mutation in the HIV
206
ART drugs
RT Inhibitors (NRTI, NNRTI), Protease inhibitor, Fusion inhibitor, Integrase strand transfer inhibitors
207
RT Inhibitors NRTI
Nucleoside analogue RT inhibitor (NRTI): gets incorporated into the growing DNA chain & causes termination
208
RT Inhibitors NNRTI
Non-Nucleoside analogue RT inhibitor (NNRTI): cause chain termination w/o getting incorporated into DNA
209
Protease inhibitor
Prevent protease from cleaving viral proteins; Irreversible
210
Fusion inhibitor
Inhibit p41 to block fusion of virus and host cell
211
Integrase strand transfer inhibitors
Effective when used in combination w/ other ARTs
212
HAART recommendations
2 RTIs + a PI (old recommendation)
| 2 NRTIs + NNRTI/PI/INSTI
213
ART therapy for HIV
Asymptomatic Pts w/ CD4 < 500
| All symptomatic Pts
