POST LAB EXPERIMENT 13,14, 17, 18, 19, 20, 21 Flashcards
(172 cards)
1
Q
is prone to progression with involvement of deeper tissues and organs
A
Streptococcus pyogenes
2
Q
Streptococcal pyogenic exotoxins (SPEs) may be released and produce
A
scarlet fever
3
Q
Other complications that result from S. pyogenes infections are the
A
poststreptococcal diseases
rheumatic fever
acute glomerulonephritis
4
Q
is an example of a pathogen that induces the production of several different antibodies.
A
S. pyogenes
5
Q
contains antigenic structural components and produces antigenic enzymes, each of which may elicit a specific antibody response from the infected host.
A
S. pyogenes
6
Q
In the course of an infection, the extracellular products act as antigens to which the body responds by producing specific antibodies
A
S. pyogenes
7
Q
Most infected patients by S. pyogenes demonstrate increased concentration of antibody against
A
SLO
8
Q
ANTI-STREPTOLYSIN O DETERMINATION
Titer production begins at about [?] after the onset of infection.
A
7 days
9
Q
ANTI-STREPTOLYSIN O DETERMINATION
The concentration of antibody (titer) begins to rise about 7 days after the onset of infection and reaches a maximum after [?].
A
4 to 6 weeks
10
Q
ANTI-STREPTOLYSIN O DETERMINATION
A rise in titer of [?] in 1 to 2 weeks is of greater diagnostic significance than a single titer.
A
50 Todd units*
11
Q
ANTI-STREPTOLYSIN O DETERMINATION
An elevated titer indicates a relatively [?].
A
recent infection
12
Q
ANTI-STREPTOLYSIN O DETERMINATION
Peak titers are seen at the time of [?] of acute rheumatic fever, but these titers are no longer at their peak during the [?] of acute rheumatic fever.
A
acute polyarthritis
carditis
13
Q
Virulence factors of Streptococcus pyogenes.
A
M protein
Exoantigens/exotoxins
14
Q
Major virulence factor
A
M protein
15
Q
They are proteins excreted by the bacterial cell as they metabolize during the course of streptococcal infections
A
Exoantigens/exotoxins
16
Q
It is a filamentous molecule consisting of two alpha-helical chains twisted into a ropelike structure that extends out from the cell surface.
A
M protein
17
Q
There is a net-negative charge at the amino-terminal end that helps to inhibit phagocytosis.
A
M protein
18
Q
It limits deposition of C3 on the bacterial surface, thereby diminishing complement activation
A
M protein
19
Q
Immunity to group A streptococci appears to be associated with antibodies to the
A
M protein
20
Q
Exoantigens/exotoxins examples
A
Pyrogenic exotoxins A, B, and C
21
Q
are responsible for the rash seen in scarlet fever and also appear to contribute to pathogenicity.
A
Pyrogenic exotoxins A, B, and C
22
Q
Pyrogenic exotoxins A, B, and C Antibodies are produced to the following exoantigens:
A
SLO
(DNase B)
hyaluronidase
nicotinamide adenine dinucleotidase (NADase)
streptokinase
23
Q
is a stepwise method involving the use of a series of serum dilutions. ASO titer of serum is determined as the serum dilution that inhibits nearly 50% of SLO-induced hemolysis. Therefore, the method gives stepwise ASO titers for various sera.
A
Rantz-Randall method
24
Q
Therefore, the method gives stepwise ASO titers for various sera.
A
Rantz-Randall method
25
[?] FOR DETECTING ANTIBODIES AGAINST Helicobacter pylori
ICT RAPID ASSAY
26
Virulence factors of Helicobacter pylori.
CagA
Vacuolating cytotoxin/VacA
27
-Highly immunogenic
CagA
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The severity of the disease is related to injection of the [?] protein into the gastric epithelial cells.
CagA
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CAUSES DUODENAL OR GASTRIC ULCERS-IF UNTREATED IT MAY LEAD TO GASTRIC CARCINOMA
CagA
30
Once the [?] protein is in the epithelial cells, changes occur in the function of the cell’s signal transduction pathways and in the structure of the cytoskeleton.
CagA
31
The [?] gene codes for a toxin precursor.
VacA
32
Epidemiological studies have shown that if the [?] genes are present in the strain of bacteria infecting the individual, there is a higher risk of developing gastric or peptic ulcers or gastric carcinoma.
CagA and VacA
33
– widely believed that it started in west Africa and the practice of bushmeat trading.
1930s
34
Meat of wild animals were being sold and transported in the market
1930s
35
– The disease is renamed as Acquired Immune Deficiency Syndrome (AIDS), sexual and through blood transfusion transmission were established
1982
36
– discovered that HIV can be passed from mother to child through breastfeeding
1986
37
– 8-10 million (est) with HIV worldwide
1990
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– 33 million were living with HIV and 14 million have died from AIDS
1999
39
- continued efforts are being done by global and local organizations, collaboration with pharmaceuticals to reduce
2000s
40
– improved treatment, approval of PrEP
2010s
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– UNAIDS reported that AIDS-related deaths have fallen 30% since its peak
2013
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transcribe HIV infection
Human Immunodeficiency Virus
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Human Immunodeficiency Virus types
HIV-1 and HIV-2
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– most advanced stage of HIV infection
AIDS (acquired immunodeficiency syndrome)
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This abbreviation can mean the virus or the infection
AIDS (acquired immunodeficiency syndrome)
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is responsible for all of the infection worldwide
HIV-1
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is the responsible for the epidemic
HIV-1 group 1 M Strain
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endemic to west Africa, less common and less infectious
HIV-2
49
HIV TRANSMISSION
Body fluids (◉ Blood ◉ Breast milk ◉ Semen ◉ Pre-seminal fluid ◉ Rectal fluid ◉ Vaginal fluid )
Contact with mucous membrane
Unprotected anal or vaginal sex
Sharing needles
Breastfeeding During pregnancy or birth
50
Transmission is caused by exposures such as high-risk sexual behaviors and other activities
HIV
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These body fluids must come in contact with the damaged/wounded mucous membrane in order for transmission to happen
HIV
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Risky sexual activities and other modes of transmission
HIV
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During pregnancy, transmission to the child happens because the blood of an infected mother can pass through the placenta and infect the child.
HIV
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Mother to child transmission is greatest during vaginal delivery when a baby passes through the birth canal and is exposed to the mother’s blood and other fluids
HIV
55
HIV infection cannot be transmitted through the following methods
56
Enumerate and describe the principles and clinically significant results of other serologic tests for diagnosing infection with HIV
Screening and Confirmatory tests
57
can be caused by one of four single-stranded, positive-sense RNA viruses (serotypes virus type 1 to virus type 4) of the Flavivirus genus.
Dengue
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Dengue
After an incubation period of 3 to 7 days, signs and symptoms start suddenly and follow three phases:
o initial febrile phase
o Critical phase
o final recovery phase
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Critical phase at about the time that the fever subsides (?) final spontaneous recovery phase
defervescence
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Most dengue virus infections are [?], with a wide variety of clinical manifestations.
asymptomatic
61
Signs and symptoms range from mild febrile illness to severe and fatal disease.
Dengue
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[?] after entering in the body invades the local macrophages and multiply there.
Dengue
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Infected local cells then migrate from site of infection to lymph nodes, where monocytes and macrophages are recruited, which become targets of infection.
Dengue
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Consequently, infection is amplified and virus is disseminated through the lymphatic system. As a result of this primary viremia, several cells of the mononuclear lineage, including blood-derived monocytes
Dengue
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Dengue
Viremia develops within [?]. During this period, virus travels throughout the body.
24 hours
66
Bone marrow cells have also been shown to be susceptible to infection with
DENV
67
In severe case, viral load is very high and many vital organs are affected.
Dengue
68
Dengue Virus infected macrophages produces a number of signaling proteins such as (?), other mediators which are responsible for many symptoms such as flue like syndrome and pain.
interferons, cytokines, chemokines, TNF
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These mediators affect hemostatic system of body.
Dengue
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Fluid from blood vessels starts to leak out so that the blood volume decreases resulting in low blood pressure.
Dengue
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Decrease in blood pressure causes insufficient supply of blood and Oxygen to vital organs such as brains.
Dengue
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also infects bone marrow, so that bone marrow cannot produces sufficient platelets.
Dengue
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Since platelets are needed for blood clotting, infection causes blood clotting defect and increase the risk of bleeding.
Dengue
74
Dengue
Laboratory diagnostic testing is by detection of viral components in serum or directly by [?].
serologic testing
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DENGUE Diagnostics tests
a. Viral Isolation
b. Dengue NS1 test
c. RT-PCR
d. IgM-capture ELISA (MAC-ELISA)
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- Gold standard; 6-10 days to replicate viral cell culture
a. Viral Isolation
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- is a highly conserved glycoprotein essential for virus viability.
b. Dengue NS1 test
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Detects the acute phase infection
b. Dengue NS1 test
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- Molecular detection of dengue genomic RNA
c. RT-PCR
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- First detectable IgM only appears 4-5 days
d. IgM-capture ELISA (MAC-ELISA)
81
Diagnosis of acute infection
b. Dengue NS1 test
d. IgM-capture ELISA (MAC-ELISA)
82
Currently, no effective antiviral agents are available to treat [?].
dengue infection
83
Treatment is supportive.
dengue infection
84
If patients have severe bleeding, a blood transfusion can be lifesaving.
dengue infection
85
There are four types of human malaria:
• Plasmodium falciparum
• Plasmodium vivax
• Plasmodium malariae
• Plasmodium ovale
86
are the most common
Plasmodium falciparum and Plasmodium vivax
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is the deadliest
P. falciparum
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In recent years, some human cases of malaria have also occurred caused by [?], a monkey malaria that occurs in certain forested areas of Southeast Asia.
Plasmodium knowlesi
89
[?], a bloodborne parasite, is transmitted exclusively through the bite of Anopheles mosquitoes.
Malaria
90
Transmission is more intense in areas in which the mosquito lifespan is longer, and where it prefers to bite humans rather than other animals.
Malaria
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This allows the parasite to have time to complete its development inside the mosquito.
Malaria
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The intensity of transmission depends on factors related to the parasite, vector, human host, and environment.
Malaria
93
In many areas, transmission is seasonal, with a peak during and just after the rainy season.
Malaria
94
All the important vector species of Anopheles bite at night
Malaria
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• The malaria parasite life cycle involves [?] hosts.
2
96
During a blood meal, a malaria-infected female Anopheles mosquito inoculates [?] into the human host.
sporozoites
97
• infect liver cells.
Sporozoites
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• There, the sporozoites mature into [?].
schizonts
99
• The schizonts rupture and release (?). This initial replication in the liver is called the (?)
merozoites
exoerythrocytic cycle
100
• [?] infect RBCs. There, the parasite multiplies asexually (called the [?]). The merozoites develop into [?]. Some then mature into [?].
Merozoites
erythrocytic cycle
ring-stage trophozoites
schizonts
101
• The schizonts rupture, releasing.
merozoites
102
• Some trophozoites differentiate into.
gametocytes
103
• During a blood meal, an Anopheles mosquito ingests the male (?) and female (?) gametocytes, beginning the
microgametocytes
macrogametocytes
sporogonic cycle
104
• In the mosquito’s stomach, the microgametes penetrate the macrogametes, producing.
zygotes
105
• The zygotes become motile and elongated, developing into.
ookinetes
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• The ookinetes invade the (?) of the mosquito where they develop into.
midgut wall
oocysts
107
The oocysts grow, rupture, and release [?], which
travel to the mosquito’s [?].
sporozoites
salivary glands
108
Inoculation of the [?] into a new human host perpetuates the malaria life cycle.
sporozoites
109
for P. vivax
• 12 to 17 days
110
for P. falciparum
• 9 to 14 days
111
for P. ovale
• 16 to 18 days or longer
112
for P. malariae
• About 1 month (18 to 40 days) or longer (years)
113
However, some strains of P. vivax in temperate climates may not cause clinical illness for
months to > 1 year after infection
114
Manifestations common to all forms of malaria include
Fever and rigors—the malarial paroxysm
Anemia
Jaundice
Splenomegaly
Hepatomegaly
115
is caused by hemolysis of infected RBCs, released merozoites and other malaria antigens, and the inflammatory response they elicit.
Malarial paroxysm
116
The classic paroxysm starts with malaise, abrupt chills and fever rising to [?], rapid and thready pulse, polyuria, headache, myalgia, and nausea. After [?], fever falls, and profuse sweating occurs for [?], followed by extreme fatigue.
39 to 41° C
2 to 6 hours
2 to 3 hours
117
Fever is often hectic at the start of infection.
Malarial paroxysm
118
In established infections, malarial paroxysms typically occur every [?] depending on the species
2 to 3 days
119
serologic tests for diagnosing malaria:
Microscopy - Thick and Thin Smear
Indirect Fluorescent Antibody Test
120
remains the ―gold standard‖ for laboratory confirmation of malaria.
Microscopic examination
121
A blood specimen collected from the patient is spread as a thick or thin blood smear, stained with a Romanovsky stain (most often Giemsa), and examined with a 100X oil immersion objective.
Thick and Thin Smear
122
Malaria antibody detection is performed using the
indirect fluorescent antibody (IFA) test
123
can be used to determine if a patient has been infected with Plasmodium.
indirect fluorescent antibody (IFA) test.
124
Because of the time required for development of antibody and also the persistence of antibodies, [?] is not practical for routine diagnosis of acute malaria.
serologic testing
125
a chronic systemic inflammatory disease primarily involving the joints
rheumatoid arthritis
126
The serum and synovial fluid contain
rheumatoid factor
127
Rheumatoid factors are synthesized within
lymphoid infiltrates
128
- immunoglobulin complex activates the complement
Rheumatoid factor
129
Pain occurs in small joint and later in large joints
rheumatoid arthritis
130
IgM Ab directed against Fc portion
IgG
131
3 classes:
IgM, IgG and IgA
132
Immune complexes consisting of the rheumatoid factor
IgM, IgG and IgA
133
immunoglobulin activate the complement cascade and lead to a number of inflammatory phenomenon’s affecting the joints.
IgM, IgG and IgA
134
Initially swelling and pain occur in small joints and later it involves the larger joints.
Rheumatoid Arthritis
135
Advance cases –
joint deformities
136
Invasive pannus consists of
macrophages, mast cells and fibroblasts
137
Synovial fluid contains organized lymphoid tissues (?)
CD4+ T cell, B cells and macrophages
138
Increase [?] in synovial fluid
neutrophil count
139
In advanced cases (?) occur and the patients are crippled.
permanent joint deformities
140
In [?], the synovial membrane is infiltrated with inflammatory cells and forms an invasive pannus consisting of macrophages, mast cells, and fibroblasts.
Rheumatoid Arthritis
141
The junction between the [?] is a focus for enzymatic degradation.
invasive pannus and the joint cartilage
142
Organized lymphoid tissues (?) are present around the synovial blood vessels.
CD4+ T cells, B cells and macrophages
143
The synovial fluid of RA patients contains large numbers of neutrophils (up to ?).
105/ml
144
LABORATORY DIAGNOSIS OF RA
Sheep cell agglutination test/Rose-Waaler test
Latex fixation test (Singer and Plotz)
Sensitized alligator erythrocyte test (Cohen et. Al)
Bentonite flocculation test (Bloch and Bunim)
145
Sheep cell agglutination test/
Rose-Waaler test
146
(Singer and Plotz)
Latex fixation test
147
(Cohen et. Al)
Sensitized alligator erythrocyte test
148
(Bloch and Bunim)
Bentonite flocculation test
149
When using RF latex tests, a titer of [?] or greater is generally considered a positive reaction.
80
150
A titer of [?] is considered a weakly positive reaction.
20 to 40
151
If there is no agglutination at [?], the specimen should be considered negative for RF, even is subsequent dilution shows agglutination.
1:20
152
used to describe a proliferation of cells that produces a mass rather than a reaction or inflammatory condition
neoplasms
153
are neoplasms and are described as benign or malignant.
Tumors
154
Most tumors are of
epithelial origin (ectoderm, endoderm, or mesoderm)
155
forms in the skin or tissue cells that line the body's internal organs, such as the kidneys and liver
carcinoma
156
grows in the body's connective tissue cells, which include fat, blood vessels, nerves, bones, muscles, deep skin tissues and cartilage.
sarcoma
157
The remaining tumors are of
connective tissue origin
158
Malignant neoplasms arising from tissue embryologically derived from ectoderm or endoderm are usually.
carcinomas
159
carcinomas Examples include:
• Squamous cell carcinoma of cervix
• Adenocarcinoma of stomach
• Hepatocellular carcinoma
• Renal cell carcinoma
160
Malignancies arising from mesoderm (connective tissues) are usually [?]. sarcomas Examples include:
• Leiomyosarcoma
• Chondrosarcoma
• Osteosarcoma
• Liposarcoma
161
The key distinction between benign and malignant tumors is the ability of [?] to invade normal tissue and metastasize to other secondary sites.
malignant tumors
162
Tumor Risk Factors:
• Smoking is responsible for one third of cancers.
• Other risk factors include a high-fat, low-fiber diet, obesity, and a sedentary lifestyle.
• Risk factors are important in specific cancers.
163
CAUSATIVE FACTORS IN HUMAN CANCER
• Environmental Factors
• Infectious diseases
• Cancer predisposing genes
164
Specific Tumor Markers
1. Alpha-fetoprotein
2. CA 125
3. Human epididymis protein 4
4. Thyroglobulin
5. Prostate-specific antigen (PSA)
6. Carcinoembryonic antigen
7. CA 19-9
8. CA 15-3
9. CA 27.29
10. HER2/neu
165
Other markers include the
beta subunit of human chorionic gonadotropin
166
Ten protein cancer biomarkers have been FDA-approved for clinical use:
Human Epididymis Protein 4
CA 27.29: Breast Carcinoma–Associated Antigen
HER2/neu
167
is recommended for monitoring patients for recurring epithelial ovarian cancer.
Human Epididymis Protein 4
168
Carcinoma of the breast often produces mucinous antigens
CA 27.29: Breast Carcinoma–Associated Antigen
169
is encoded by an oncogene and is over expressed in 15% to 20% of invasive breast cancers.
HER2/neu
170
• have the potential to uncover signature gene expression patterns for specific cancers and ultimately assist in the staging of tumors, prognosis, and treatment.
DNA microarray technology
171
• Three aspects of importance in Next Generation Sequencing (NGS) are:
1. Identification of
2. Detection of low levels of
3. Improved management of
somatic mutations
genomic alterations
cancer treatment
172
• The ability to isolate and characterize rare circulating tumor cells (CTCs) may provide critical insights into primary tumors, the process of metastasis, and monitor disease progression
Continuous Field-Flow Assisted Dielectropheresis (DEP)
