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Microbiology > Chapter 37-39 > Flashcards

Chapter 37-39 Flashcards

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1
Q

What family is the flu in?

A

Orthomyxoviridae—Influenza A, B, and C virus

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2
Q

what determines subtype of flu?

A

surface glycoproteins hemagglutinin (HA) and neuraminidase (NA)

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3
Q

How many known subtypes of the flu are there?

A

*18 known H subtypes
* 11 known N subtypes
* 130+ combinations found in nature to date
* 198 possible combinations by reassortment

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4
Q

Antigenic drift

A

smaller genetic changes that result in
subtle surface protein (antigen) changes.
* These surface antigens are the N and H proteins
* Cause of new influenza strains

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5
Q

Antigenic shift

A

larger protein sequence change made
possible by the linear, segmented nature of the RNA genome.
* Responsible for major epidemics and pandemics.
* Interspecies influenza virus reassortment
(ex: swine flu to humans bc NA and HA change)

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6
Q

what is the life cycle of the flu?

A

attachment, entry, synthesis, assembly and release

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7
Q

Attachment of the flu

A

the hemagglutinin (H) protein on the surface of the virus binds to sialic acid residues
* targets cells in the respiratory tract (nasal passages and throat)

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8
Q

how does the flu enter cells?

A

the virion is taken into the cell by receptor-
mediated endocytosis
- the entire virus particle is surrounded by an endosome
-maturation of the endosome (lowering the pH) allows the viral and endosome membranes to fuse
-fusion allows RNP (viral ribonucleoprotein) to enter the cytoplasm and into the nucleus

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9
Q

Flu virus synthesis

A

viral (-) RNA is replicated in the nucleus (matured into mRNA) using vRdRP
-mRNA is transported and translated in the cytoplasm & at rough ER
-proteins involved in replication are transported back into the nucleus
-Envelope proteins coat new virions

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10
Q

flu assembly and release

A

-H and N proteins are inserted in host cell membrane
-RNA viral genome components get
coated with proteins (forming nucleocapsid) and associates with inner face of membrane
-host cell membrane buds and protrudes outward
-fusion of the cell membrane, directed
by matrix protein results in mature virion

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11
Q

how can flu symptoms be lowered?

A

Neuraminidase inhibitors reduce duration of symptoms.
* Oseltamivir (Tamiflu)
* Zanamivir
* Peramivir

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12
Q

what kind of HIV is prevalent in different countries?

A

HIV-1 is widespread in United States.
HIV-2 is widespread in Africa

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13
Q

what is a retrovirus?

A

can reverse transcribe their +ssRNA into dsDNA (can directly translate and doesn’t have to go from antisense –> sense like flu)
-the reverse transcribed dsDNA from HIV integrates into human genome

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14
Q

what type of virus is HIV?

A

Lentivirus (genus of retrovirus)

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15
Q

what cells do HIV target?

A

immune cells

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16
Q

what makes HIV attach to a host immune cell?

A

Strains infecting macrophages- CCR5
strains infecting T-cells- CXCR-4

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17
Q

how is HIV diagnosed?

A

concentration of CD4+ T cells (flow cytometry) used to monitor patient

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18
Q

HIV life cycle

A

Can direct synthesis of viral DNA–> synthesis of viral particles–>virion released through budding

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19
Q

what happens to amount of detectable HIV in blood?

A

It decreases overtime because virus moves from blood into lymphoid tissues (bc it wants to spread to immune cells)

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20
Q

what happens if HIV crosses the blood brain barrier

A

it can cause CNS disease

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21
Q

what is the 1st stage of HIV infection

A

acute stage 2-8 weeks
most asymptomatic (fever, headache, weight loss, etc.)
replicate quickly
test positive between 4-10 weeks

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22
Q

what is the 2nd stage of HIV infection

A

clinic latency
can last up to 10 years or longer
- low level viral replication
- CD4+ T cells start to decline

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23
Q

What is the 3rd stage of HIV

A

AIDs
-significant decline in CD4+ T cells
<200 cells per microliter or
<14% relative to total lymphocytes

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24
Q

what type of conditions can result from AIDs

A

-Kaposi’s sarcoma
- carcinomas of the mouth and rectum
- B-cell lymphomas
—immune suppression enables tumor-
causing agents
-opportunistic infections (vaginal candidasis, listeriosis, shingles, thrush, pneumonia)

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25
what are the treatments for HIV?
combination of 3 antiviral drugs- Antiretroviral therapy (ART) which inhibits reverse transcription and protease and the CCR5 antagonist prevents HIV entering into cell (rare case where patients were healed by chemotherapy and then a bone marrow transplant)
26
streptococcal pneumonia
caused my Streptococcus pneumoniae in upper respiratory tract rapid multiplication in alveolar spaces (air sacs)
27
what is the phylum/order/structure of streptococcus pneumoniae
phylum:Firmicutes order: lactobacillales gram positive (thick peptidoglycan) capsulated strains are pathogenic
28
how many healthy people have streptococcus pneumoniae
40-50% of children 20-30% of adults
29
what illnesses can streptococcus pneumoniae cause?
sepsis, otitis media (ear infection), sinusitis (sinus infection), meningitis (infection of brain and spinal cord tissues), and pneumonia
30
what are symptoms/ treatment of pneumonia?
chills, chest pain, labored breathing Diagnosis: chest x-ray, gram stain, culture antibiotic treatment or PCV (pneumococcal conjugate vaccine) which generates antibodies to opsonize cells
31
what is the 7th leading cause of death in the US
Community-acquired pneumonia
32
what are the virulence factors of streptococcus pneumoniae
- polysaccharide capsule (primary factor) interferes with phagocytosis - pili mediate adherence to host cells and stimulate inflammation - pneumolysin; Alveoli become filled with blood, fluid, and become inflammed - surface protein A protects pneumoniae against antimicrobial peptides
33
what is pneumolysin
a toxin released when S. pneumonia cells lyse; forms lytic pores in host membranes.
34
what is Atypical pneumonia caused by?
distinct species phylum Mycoplasmatota pneumoniae
35
what is significant about mycoplasmatota pneumoniae
lacks cell wall so it's resistant to B-lactam antibiotics -releases community acquired respiratory distress syndrome (CARDS) toxin - Tetracycline and macrolides are effective
36
streptococcus pyogenes
Lancefield group A streptococci
37
what are the virulence factors of streptococcal diseases
-extracellular enzymes- break down host molecules -Streptolysin O and S- kill host leuocytes -Capsules and M protein- limit phagocytosis -protein G- binds to antibodies so antigen binding site cannot affect bacterial cells - protein F- cell attachment protein
38
streptococcal pharyngitis
causes strep throat and tonsillitis sensitive to antibiotics
39
Group B Streptococcal disease
cause by gram positive streptococcus agalactia - common in immunocompromised adults and newborns - causes sepsis, pneumonia, and infections
40
GBS in infants
transmitted from mother during birth mother must get DNA tested for GBS before birth and get a penicillin IV if positive 5% mortality rate in newborns
41
where may toxin genes reside?
on plasmids and on chromosomes
42
enterotoxin
bacteria that is harmful to the GI tract food intoxication, bacteremia, and abscess formation
43
what is Staphylococcus aureus known for and how common is it?
-found in nose of 10-30% of healthy people -can cause minor skin infections or be deadly -regulate its virulence in order to respond to growth conditions
44
staphylococcus aureus structure
- gram positive - non-motile - usually in clusters - facultative anaerobe - b-hemolytic on blood agar
45
staphylococcus virulence factors (10 factors)
*Capsule- polysaccharide slime layer that inhibits phagocytosis and promotes binding *Teichoic Acids- aid biofilm production and contribute to vancomycin resistance *Collagen-Binding Proteins- cell surface protein that aids binding and immune evasion *Haemolysins- lyse RBC * Coagulase- catalyze clot formation *Deoxyribonuclease- degrades DNA *Lipase- breaks down lipids *Staphylokinase- breaks blood clots and allows infection to spread *Enterotoxins- heat stable toxins involved in food poisoning and Toxic Shock Syndrome *b-lactamase- enzymes that degrade b-lactam antibiotics (penicillins,cephalosporins)
46
what are the most common infections from staphylococcus aureus
skin infections- cellulitis, Abcesses, Folliculitis, and impetigo -food poisoning - sinusitis, pneumonia - bacteremia - meningitis - TSS - HAI by colonizing medical implants
47
what does TSS result from?
Staphylococcus Aureus Antigen TSST-1 triggers overproduction of cytokines by T cells
48
Methicillin-Resistant Staphylococcus Aureus
resistant to B-lactam antibiotics -can be community or hospital acquired -must determine antibiotic sensitivity Vancomycin used for severe reactions
49
E coli. Gastroenteritis
most are harmless and provide assistance in the metabolism of the food we eat -5 categories or strains of diarrheagenic E. Coli
50
Enteric pathogens
diarrhea causing pathogen
51
What are the types of pathogenic E. Coli
ETEC, EHEC
52
Enterotoxic E. Coli
"travelers diarrhea" -induce secretion of water and electrolytes -AB toxins (A subunit is ADP-ribosyltransferases) -requires antibiotics
53
Enterohemorrhagic E. Coli
Fecal-oral transmission -Shinga toxin-producing E. Coli cause intestinal damage - cause of bloody diarrhea - usually no antibiotics -O polysacccharide (LPS) and H protein (flagella) antigens -Use type 3 secretion system to inject their proteins into host cytoplasm - host cytokines inflammatory response - blood and WBC enter stool - can cause hemolytic uremic syndrome (can lead to kidney failure)
54
Malaria is caused by
5 species of Plasmodium
55
what are the three stages of Malaria life cycle
Exoerythrocytic cycle, Erythrocytic cycle, and mosquito or sporogonic cycle
56
Exoerythrocytic cycle
-protozoan enters bloodstream via mosquito bite (anticoagulant and 100-1000s sporozoites) - sporozoites navigate to LIVER, entering hepatocytes - sporozoites asexually reproduce (schizogeny to form schizonts. schizonts--> Merozoites that exit hepatocytes and enter Blood stream)
57
Erythrocytic cycle
-enlarged cells form (trophozoites) - asexual repro to form schizionts -schizionts divide into merozoites that release when erythrocytes lyse - merozoites differentiate into haploid gametes (sex cells- 1 copy of chromosomes)
58
Sporogenic cycle
- sexual repro in mosquito - unruptured erythrocytes infected by gametes are ingested by mosquito - erythrocytes rupture inside mosquito and sexually repro - diploid zygote forms (ookinete) - ookinetes matures into oocyst - oocyst undergoes meiosis and 1000s haploid sporozoites are released
59
what are the symptoms, diagnosis type, and treatment of malaria?
-shaking chills, fever, and sweating - stained erythrocytes and serological tests - treatment depends on geographical location (chloroquine, amodiaquine, mefloquine) - vaccine approved for children that neutralize sporozoites
60
what is toxoplasmosis caused by? and how many people does it affect?
T gondii. 10% of US pop.
61
how is toxoplasmosis transmitted to humans?
disease asexually reproduces in mice and then sexually reproduces in cats - ingestion of oocytes while cleaning litter boxes - consumption of infected meat -Maternal-fetal transmission
62
what are toxoplasmosis symptoms, diagnosis, and treatment?
-lymph node swelling, tissue necrosis, in NB it can affect CNS - diagnosed by serological (blood) tests - treated by Pyrimethamine and Sulfadiazine
63
what causes candidiasis
caused by Candida albicans, C glabrata, or C auris -disease occurs in absence of competing microbiota (immunocompromised) -cause thrush, yeast infections, etc.
64
diagnosis and treatment of candidiasis
-diagnosis made through observation -mortality is about 25% when infection reaches the blood -topical agents used for lesions and genital or rectal candidiasis

Microbiology (12 decks)

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