POST LAB EXPERIMENT 13,14, 17, 18, 19, 20, 21 Flashcards
is prone to progression with involvement of deeper tissues and organs
Streptococcus pyogenes
Streptococcal pyogenic exotoxins (SPEs) may be released and produce
scarlet fever
Other complications that result from S. pyogenes infections are the
poststreptococcal diseases
rheumatic fever
acute glomerulonephritis
is an example of a pathogen that induces the production of several different antibodies.
S. pyogenes
contains antigenic structural components and produces antigenic enzymes, each of which may elicit a specific antibody response from the infected host.
S. pyogenes
In the course of an infection, the extracellular products act as antigens to which the body responds by producing specific antibodies
S. pyogenes
Most infected patients by S. pyogenes demonstrate increased concentration of antibody against
SLO
ANTI-STREPTOLYSIN O DETERMINATION
Titer production begins at about [?] after the onset of infection.
7 days
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 [?].
4 to 6 weeks
ANTI-STREPTOLYSIN O DETERMINATION
A rise in titer of [?] in 1 to 2 weeks is of greater diagnostic significance than a single titer.
50 Todd units*
ANTI-STREPTOLYSIN O DETERMINATION
An elevated titer indicates a relatively [?].
recent infection
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.
acute polyarthritis
carditis
Virulence factors of Streptococcus pyogenes.
M protein
Exoantigens/exotoxins
Major virulence factor
M protein
They are proteins excreted by the bacterial cell as they metabolize during the course of streptococcal infections
Exoantigens/exotoxins
It is a filamentous molecule consisting of two alpha-helical chains twisted into a ropelike structure that extends out from the cell surface.
M protein
There is a net-negative charge at the amino-terminal end that helps to inhibit phagocytosis.
M protein
It limits deposition of C3 on the bacterial surface, thereby diminishing complement activation
M protein
Immunity to group A streptococci appears to be associated with antibodies to the
M protein
Exoantigens/exotoxins examples
Pyrogenic exotoxins A, B, and C
are responsible for the rash seen in scarlet fever and also appear to contribute to pathogenicity.
Pyrogenic exotoxins A, B, and C
Pyrogenic exotoxins A, B, and C Antibodies are produced to the following exoantigens:
SLO
(DNase B)
hyaluronidase
nicotinamide adenine dinucleotidase (NADase)
streptokinase
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.
Rantz-Randall method
Therefore, the method gives stepwise ASO titers for various sera.
Rantz-Randall method
[?] FOR DETECTING ANTIBODIES AGAINST Helicobacter pylori
ICT RAPID ASSAY
Virulence factors of Helicobacter pylori.
CagA
Vacuolating cytotoxin/VacA
-Highly immunogenic
CagA
The severity of the disease is related to injection of the [?] protein into the gastric epithelial cells.
CagA
CAUSES DUODENAL OR GASTRIC ULCERS-IF UNTREATED IT MAY LEAD TO GASTRIC CARCINOMA
CagA
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
The [?] gene codes for a toxin precursor.
VacA
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
– widely believed that it started in west Africa and the practice of bushmeat trading.
1930s
Meat of wild animals were being sold and transported in the market
1930s
– The disease is renamed as Acquired Immune Deficiency Syndrome (AIDS), sexual and through blood transfusion transmission were established
1982
– discovered that HIV can be passed from mother to child through breastfeeding
1986
– 8-10 million (est) with HIV worldwide
1990
– 33 million were living with HIV and 14 million have died from AIDS
1999
- continued efforts are being done by global and local organizations, collaboration with pharmaceuticals to reduce
2000s
– improved treatment, approval of PrEP
2010s
– UNAIDS reported that AIDS-related deaths have fallen 30% since its peak
2013
transcribe HIV infection
Human Immunodeficiency Virus
Human Immunodeficiency Virus types
HIV-1 and HIV-2
– most advanced stage of HIV infection
AIDS (acquired immunodeficiency syndrome)
This abbreviation can mean the virus or the infection
AIDS (acquired immunodeficiency syndrome)
is responsible for all of the infection worldwide
HIV-1
is the responsible for the epidemic
HIV-1 group 1 M Strain
endemic to west Africa, less common and less infectious
HIV-2
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
Transmission is caused by exposures such as high-risk sexual behaviors and other activities
HIV
These body fluids must come in contact with the damaged/wounded mucous membrane in order for transmission to happen
HIV
Risky sexual activities and other modes of transmission
HIV
During pregnancy, transmission to the child happens because the blood of an infected mother can pass through the placenta and infect the child.
HIV
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
HIV infection cannot be transmitted through the following methods
Enumerate and describe the principles and clinically significant results of other serologic tests for diagnosing infection with HIV
Screening and Confirmatory tests
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
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
Critical phase at about the time that the fever subsides (?) final spontaneous recovery phase
defervescence
Most dengue virus infections are [?], with a wide variety of clinical manifestations.
asymptomatic
Signs and symptoms range from mild febrile illness to severe and fatal disease.
Dengue
[?] after entering in the body invades the local macrophages and multiply there.
Dengue
Infected local cells then migrate from site of infection to lymph nodes, where monocytes and macrophages are recruited, which become targets of infection.
Dengue
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
Dengue
Viremia develops within [?]. During this period, virus travels throughout the body.
24 hours
Bone marrow cells have also been shown to be susceptible to infection with
DENV
In severe case, viral load is very high and many vital organs are affected.
Dengue
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