Bacteriology & Microbiology Flashcards

1
Q

What is bacterial conjugation and how does it occur

A

A form of bacterial reproduction by passing DNA fragment, the fertility factor, from one F+ bacterium to a F- through a conjugation tube formed as the two cell membranes fuse together.

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2
Q

What are the processes in which bacteria transfer DNA fragments between each other

A
  • Trasnformation - Bacteria picking up DNA fragments from the environment usually released by dead bacteria
  • Transduction - The carrying of bacterial DNA from one cell to another by a virus.
  • Mutation

These are ways inwhich antibiotic resistance is passed down

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3
Q

What strains of bacteria can produce and secrete spores

A
  • Bacillus
  • Clostridium
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4
Q

What are bacterial spores (endospores)

A

Endospores are small fragments of bacterial DNA encased by a tough cell wall that is resistant to extreme conditions such as temperature, pH, drying and ohter chemicals.

They are released when environmental conditions become unfavourable as means of survival for the bacteria.

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5
Q

Gram positive bacteria characteristics

A
  • HIGH amounts of peptidoglycan (thick cell wall)
    ∴ sensetive to penicillin and lysosomes
  • Not sensetive to mechanical pressure
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6
Q

Gram negative bacteria characteristics

A
  • LOW amounts of peptidoglycan (Thin cell wall)
    ∴ NOT sensetive to penicillin
  • Two cytoplasmic membranes
    ∴ Inner phospholipid bilayer
    ∴ Outer leaflet of outer membranes is mainly composed of lipopolysaccharides
  • Periplasmic enzymes in periplasmic space
  • Sensetive to mechanical pressure
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7
Q

What catalyses the synthesis of peptidoglycan and how antibiotic resistance an occur

A

Penicillin binding protein and they can mutate into a strain that is no longer sensetive to penicillin drugs

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8
Q

TRUE OR FALSE

Gram positive bacteria contain periplasmic enzymes that can hydrolyze drugs

A

FALSE
Only gram negative bacteria contain periplasmic enzymes

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9
Q

Why does the inhibition of PBPs in gram negative bacteria not necessarily lead to apoptosis

A

Bc their defence is not mainly dependent on the peptidoglycan wall as they have other means of defence also.

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10
Q

What are endotoxins and what complications do the present in pharmaceutics

A

Endotoxins are lipopolysaccharides most commonly found in the outer membrane of gram negative bacteria cell and they are pyrogenic (cause fever). Some medications can consist of endotoxins which, when administered, increase the endotoxin concentration in the body = Harmful

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11
Q

How can we test for endotoxins in medication

A

BP test for pyrogens
* 3 rabbits are administered with the drug
* Temp is taken every 30 minutes for 3 hours
* An increase to their temp indicates pyrogen presence

Limulus amoebocyte lysate test
* Horseshoe crab blood is mixed with a product sample
* Coagulation of the blood indicates presence of endotoxins

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12
Q

What are the limitations of the BP test for pyrogens

A
  • Rabbits may be tolerant to pyrogens (to a certain degree)
  • Biological variations
  • Test is unsuitable for many classes of drugs
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13
Q

What are the limitations of the Limulus amoebocyte lysate test

A
  • Test cannot be conducted on viscous products
  • Only sensetive to gram negative endotoxins
  • Certain chemicals can inhibit the interaction between LAL substrate and the endotoxin
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14
Q

What enzyme targets and inhibits penicillin drugs and how

A

penicillinase / β-lactamase
* They target the β-lactam ring in penicillin chemical structures and break it down

they are the same

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15
Q

What is horizontal transmission and give examples

A

The spread of pathogens to the same or different species in a population through non-hereditary means (i.e droplet inhalation etc)

Examples: Polio, thypoid, covid-19

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16
Q

What is vertical transmission and give examples

A

The transmission of disease from mother to child (hereditary)
Examples: HIV, Rubella

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17
Q

What are anthroponoses and how are they transmitted

A

Diseases that are transmitted from human to human. They are transmitted via…
* Droplet inhalation
* Fecal-oral spread
* Venereal spread (sex)

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18
Q

What are arthropod-borne diseases & zoonoses and how are they transmitted

A

Diseases that are caused by pathogens that are transmitted by animals or arthropods. Methods of transmission include…
* Vector (biting)
* Vertebrate reservoir - Diseases that reside in animals and can jump to humans
* Vector-vertebrate reservoir

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19
Q

What bacterium causes lyme disease and what does it look like

A

Borrelia burgdorferi
* Starts as an expanding annular rash

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20
Q

What causes gonorrhoea and what are some key characteristics

A

Neisseria gonorrhoeae
* Can be transmitted both horizontally and vertically
* Vertical transmission causes destructive eye disease (Ophthalmia neonatorum)

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21
Q

What are the complication of local spread gonorrhoea

A

Female
* Damage to fellopian tubes
* Pelvic inflammatory disease
* Anorectal infection

Male
* Occasional epididymitis

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22
Q

What are the systemic complications of gonorrhoea

A
  • Skin lesions
  • Endocarditis
  • Arthritis
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23
Q

What causes the bubonic plague and what are the mortalities for each stage

A

Yersinia pestus
* Bubonic plague - 1-15% (treated) |40-60% (untreated cases)
* Septicemic plague - 40% (treated) |100% (untreated)
* Pneumonic plague - 100% if not treated within 24hrs

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24
Q

How is bubonic plague transmitted

A
  1. Rat flea / wild rodent flea
  2. Flea bites human
  3. Bubonic plague infects (no human transmission)
  4. Pneumonic plague develops (rapid human-human transmission)
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25
Q

What are the three stages of borrelia burgdorferi

A
  1. Expanding annular rash (at the site of the bite)
  2. Headache, fever
  3. Arthritis
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26
Q

What is pneumonia and what are the different causes

A

Inflammation of the lungs caused by viral pathogens such as parainfluenza in children. In adults the causes are more commonly bacterial but can also be viral.

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27
Q

How is cholera spread and when are cases at their highest

A

Cholera spreads through contaminated water sources and this most commonly happens when disasters occur such as earthquakes, tsunamis and hurricanes.

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28
Q

Describe the mode of action of cholera

A
  1. Vibrio cholera introduced into the system
  2. Cholera toxin released
    Contains α & β subunits
  3. β-subunit binds to GM1 receptors in intestinal tract
  4. α-subunit diffuses into the cell
  5. Binds to and activates Gas, which stimulates adenylyl cyclase
  6. Production of cAMP
  7. cAMP activates CFTR
  8. CFTR pushes Cl- out of the cell (Na+ and water also follows) into the intestinal tract = Watery diarrhoea
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29
Q

What are the complications of Gastrointestinal anthrax

A
  • Haematemesis
  • Severe diarrhoea
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30
Q

What are the complications of pulmonary anthrax

A

Initially presents with flu-like symptoms ollowed by severe respiratory problems that are fatal. Mortality ~100 % if not treated prior to symptoms presenting

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31
Q

What are the complications of cutaneous anthrax

A

Initially presents as an itchy skin lesion OR a dark blister which develops into a large, painless necrotic ulcer after ~ a week of exposure

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32
Q

What is Staphylococcus aureus and its most common complications

A

A spherical, gram-positive bacterium that lives on the skins and nasal membrane. It consists of different strains caused by different Staphylococcal toxins. Common complication include…
* Boils
* Pimples
* Wound infections
* Pneumonia
* Toxic shock syndrome

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33
Q

What is MRSA

A

Methicillin resistant staphylococcus aureus is resistant to many antibacterials including penicillins and can be treated with vancomycin. It is usually confined and contracted in hospitals.

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34
Q

What are some brief complications of having to use vancomycin

A

It is an expensive and toxic drug that can only be administered via intravenous infusion

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35
Q

What is SSSS and what causes it

A

Staphylococcus scaled skin syndrome is caused by an exfoliative toxin mainly in infants and young children

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36
Q

Briefly describe the various staphylococcal toxins and their complications

A
  • Alpha-toxin -> Disrupts smooth muscle in blood vessels ∴ prevents wound healing
  • Beta-toxin -> Neutral sphingomyelinase is a toxic enzyme that can harm many types of cells, including fibroblasts, erythrocytes, leukocytes, and macrophages
  • Delta-toxin -> Prevents wound healing
  • Gamma-toxin -> Prevents wound healing
  • Exfoliative toxin -> Causes SSSS
  • Enterotoxins -> Causes food poisoning
  • Toxic shock syndrome toxin-1 (TSST-1) -> Causes toxic shock syndrome
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37
Q

How do you treat Corynebacterium diphtheria

A

Antibiotic treatment + Antitoxin treatment

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38
Q

What are the complications of Corynebacterium diphtheria

A
  • Bacteria release a toxin which destroys epithelial cells in the pharynx
    -> Ulcer covered in necrotic exucate forms which obstructs airway
  • Toxin can also cause heart failure
  • If absorbed into the blood, it can cause myocarditis, polyneuritis and fever
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39
Q

What are enteric bacteria and give examples

A

Gram-negative, rod-shaped bacteria that reside in the intestinal tract. They are facultative anaerobes. Most are harmless but there are some pathogenic ones…
* E.coli
* Shingella dysenteriae

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40
Q

What is E.coli and its complications

A

E.coli is an enteric bacterium that is an indicator of faeces in water. Very few strains of E.coli are pathogenic. Enterohaemorrhagic E.coli (EHEC) ,more specifically Serotype O157, is a verotoxin-producing strain that causes haemorrhagic collitis and haemolytic-uremic syndrome that is transmitted via faecal-oral route.

Haemorrhagic collitis = Bloody diarrhoea

41
Q

What is shingella dysenteriae and its compliations

A

An enteric disease that is contracted and transmitted via the faecal-oral route

  • Causes bacillary dysentery (intestinal inflammation)
  • Leads to bloody diarrhoea
42
Q

Describe the mode of action of salmonella

A
  1. Bacteria ingested & absorbed by epithelial cells (in small testine)
  2. Migrate to lamina propria layer of the Ileocecal region
  3. Bacteria multiply in lymphoid follicles -> Feticuloendothelial hyperplasia
  4. Neutrophils and basophils are activated -> Confine infection to the GUT
  5. Inflammatory response results in the release of PGD
  6. Stimulate adenylyl cyclase -> cAMP production
  7. CFTR activation -> Cl- pushed out of cells (Na+ and H2O follows) into the GI tract
  8. Watery diarrhoea
43
Q

What are the different types of vaginitis and their presenting symptoms

A
  • Thrush - White & lumpy discharge (smells like cottage cheese)
  • Trichomoniasis - Yellow/green discharge
  • Chlamydia - Pain when urinating
44
Q

What causes syphillus and what are its stages

A

Treponema pallidum
* Primary stage (10-60 DAYS after infection): Chancre
* Secondary stage (2-4 months after): Headache, fever
* Tertiary stage (10-30 years after): Damage to nervous systems & bones

UNFINISHED

45
Q

What are the different strains of chlamydia and their key characteristics

A

Chlamydia Trachomatis
* Sexually transmitted
* Can be asymptomatic
* Leads to blindness

Chlamydia Pneumoniae
* Causes pneumonia

46
Q

What are the complications involved with Chlamydia trachomatis

A

Complication:
* Men - Systemic spread, Reiter’s syndrome
* Women - Ectopic pregnancy infertility, Systemic spread (dermatitis, arthritis)

47
Q

What pathogens cause meningitis

A
  • Neisseria meningitidis (children, teenagers)
  • Haemophilus influenza (Children < 5 years)
  • Streptococcus Penumoniae (All ages, specifically <2 years & elderly)
48
Q

What are the symptoms of Meningitis

A

Symptoms:
* Fever, headache
* Stiff neck *
* Sensetive to light
* Nausea, vomitting
* Confused

49
Q

What are the different presentations of Polio and their symptoms

A
  • Asymptomatic (~90%)
  • Abortive poliomyelitis -> Fever, headache, sore throat, vomitting
  • Nonparalytc poliomyelitis -> Progression of virus to the CNS= Back pain, muscle spasms + abortive symptoms
  • Paralytic poliomyelitits -> Occurs 3-4 days after first symptoms subside
50
Q

Explain the pathogenesis of paralyti poliomyelitis

A

Occurs when the virus spreads from the blood to the anterior horn cells of the spinal cord AND the motor cortex of the brain. The severity of paralysis depends on the exntent of the neuronal infection and which neurons are effected.

51
Q

Explain Alphaherpesvirus

A

A strain of the herpes virus that consists of HSV1 and HSV2, that target the mucoepithelialcells resulting in cold sores, and HSV3 is also known as the varicella-zoster virus (chickenpox)

52
Q

Explain gammaherpesvirus

A

HSV4 also known as the Epstein-barr virus that targets the B cells and mucoepithelial cells. It is characterised by a glandular fever and that the virus is sexually transmitted. The virus remains latent in B memory cells.

HSV8 also known as Kaposi’s sarcoma-related virus targets lymphocytes and causes cancer, most commonly in immunosuppressed patients

53
Q

Explain Betaherpesvirus

A

HSV5 also known as Cytomegalovirus

54
Q

TRUE OR FALSE

Herpes virus can be treated with antiviral treatment

A

FALSE
Herpes remains latent/dormant in your body and can reactivate throughout your lifespan. Reactivation will usually be indicated by cold sore formation

55
Q

What is viremia

A

The rapid replication and migrating to various tissues in the body by entering the bloodstream.

56
Q

Describe the varicella-zoster virus pathophysiology

A
  1. Virus breathed in
  2. Viral replication in lymph nodes
  3. Primary viremia - Not contagious or symptoms (Day4-6)
  4. Secondary viremia (VIRAL REPLICATION IN LIVER&SPLEEN) - contagious [Day 11-17]
  5. Fever, rash, itchy, small spots
  6. Virus becomes latent
  7. Reactivation in the form of shingles

There is a period inwhich you are contagious with no symptoms

57
Q

What are the symptoms of measles

A
  • Flat red spots (Maculopapular rash)
  • Fever
  • Cough
  • Sore red eyes
58
Q

What are the various complications of viremia in measles

A

It can cause Conjuctivitis and it also can impact
* Respiratory tract
* Urinary tract
* Small blood vessels
* Lymphatic system
* CNS

59
Q

What is rubella, how is it transmitted and what are its complications

A

A viral infection that is transmitted through human-human contact or droplet inhlation. It can be asymptomatic and can be self-limiting within 10 days. Symptoms typically present after 5 days of infection. Complications include…
* Placentitis and subsequent foetal damage (in pregnant women)
* Aching joints
* Spotty rash

60
Q

Symptoms of Mumps

A
  • Puffy cheeks
  • Tender/swollen jaw
61
Q

Mumps complications

A
  • Meningitis
  • Pancreatitis -> Vomitting, abdominal pain
  • Encephalitis
  • Orchitis -> Lead to sterility in men
62
Q

How is Rabies transmitted

A

Rabies is transmitted via saliva contamination, most commonly animal bites.

63
Q

Describe Rabies pathogenesis

A
  1. Virus enters body through animal bite
  2. Viral replication in muscle
  3. Virus enters Peripheral nervous system -> Travels up the spinal cord
  4. Infection of brain
  5. Descending infection to eyes, salivary glands and other organs
64
Q

How is rabies treated

A

Rabies wounds should be disinfected and can be possible treated prior to symptoms showing via post-exposure prophylaxis.
* Once symptoms shows, it is untreatable and fatal.
* Prophylaxis via vaccination is what is commonly used to prevent rabies infections when travelling.

65
Q

What are the intial symptoms of ebola

A
  • High fever
  • Severe headache
  • Muscle/joint pain
  • Exhaustion
  • Nausea
  • Sore throat
66
Q

What are the secondary symptoms of ebola

A
  • Internal bleeding
  • External bleeding
  • Bloody diarrhoea
  • Red eyes

Bleeding from any body orifice

67
Q

How is ebola transmitted

A

Direct human contact with an individual’s bodily fluids (e.g. blood, saliva)

68
Q

Describe the pathogenesis of HIV

A
  1. GP120 binds to CD4+ on T-cells and macrophages
  2. Also binds to CCR5 OR CXCR4 on cell surface
  3. Fuses into the membrane
  4. Capsid containing RNA is transcribed (via reverse transcriptase) -> DNA
  5. Pro-virus integrates with host’s DNA
  6. Transcription results in replication of the provirus

LTR = Long-terminal repeats

69
Q

What is required for HIV to infect a cell

A
  • GP120 – CD4+ binding
  • GP41 – CCR5/CXCR4
70
Q

Describe HIV pathophysiology

A
  1. Virus infects macrophages - > becomes virus reservoir
  2. Transports to different tissues via different macrophages
  3. Macrophage dysfunction causes cytokine release -> dyregulates immune function
  4. Virus eventually start infecting CXCR4 on CD4+ T-cells
  5. CD4 T-cell CYTOLYSIS
71
Q

HIV complications

A

The eventual CD4 T-cell cytolysis can lead to…
* Immunodeficiency (loss of T-cells)
* Loss of cytokines = Less production of B-cells
* Patient susceptible to systemic oppportunistic infections (e.g. Kaposi’s sarcoma, Lymphoma)
* AIDS
* Dementia

72
Q

What are Rhinoviruses

A

Common cold, self-limiting infections that usually occur most in the spring and the fall.
* Only one viral particle is required to initiate infection
* Exacerbates asthma and COPD in patients

73
Q

Describe the pathogenesis of rhinovirus

A
  1. Viral capsid protein binds to ICAM-1 on nasal cells
  2. Penetrates the cell membrane
  3. Rapid viral replication leads to cell lysis
  4. Cytokines are released -> Innate immune response (Macrophages recuited, complement system activated)
  5. Swelling is induced by increased capillary permeability leading to a blocked nose
74
Q

TRUE OR FALSE

Anthrax is not contagious

A

TRUE
It is not passed person to person

75
Q

Influenza MoA

A
  1. Aerosol inoculation (breathed in)
  2. Haemagglutinin protein binds to Sialic acid on epithelial cells in the upper respiratory
  3. Uptaken via endocytosis -> Stored in endosome
  4. Viral envelop fuses with endosome membrane = Releasing genetic material
  5. Genetic material travels to the nucleus
  6. Viral RNA polymerase converts (-neg) stranded RNA into +(pos) stranded RNA
  7. Translation into viral proteins
  8. New virions assembled
  9. Budding exit
76
Q

Describe the pathophysiology of influenza

A
  1. Replication in respiratory tract
  2. Desquamination of goblet cells and cilliated cells -> Easier for secondary bacterial infection to occur
77
Q

Influenza symptoms

A

Initially headaches and then abrupt onset of fever, chills, myalgia, loss of appetite and a non-productive cough with the fever lasting between 3-8 days. Complete recovery occurs within 7 to 10 days of contracting the flu unless complications arise.

78
Q

What are the potential complications of influenza

A
  • Bacterial pneumonia
  • Myositis (inflammation of muscles)
  • Reye’s syndrome (swelling in the brain and liver)
79
Q

Treatment for influenza A and B

A

Zanamivir and Oseltamivir inhibit both A and B if administered with the first 24-48 hours of onset but the best way to prevent the virus is through immunisation via vaccines

80
Q

How is Hepatitis A contracted and is it contagious

A

It is contracted via the faecal-oral route and most commonly it is contracted from contaminated water, shellfish or other food. It is highly contagious.

81
Q

What is a picornavirus and give examples

A

Small, single stranded RNA that is not envolped and therefore has a ‘naked’ capsid structure.

Examples: Hepatitis A, Enterovirus

82
Q

Describe the Hepatitis A pathophysiology

A
  1. HAV is ingested
  2. Enters the bloodstream via the epithelial lining (of the intestines)
  3. Virus replicates in hepatocytes and kupffer’s cells (in the liver)
  4. Virus is released into the bile and into the stool
83
Q

TRUE OR FALSE

Hepatic cancer is a complication of Hepatitis A

A

FALSE
It is not

84
Q

Symptoms of Hepatitis A

A

Symptoms:
* Fever, Fatigue
* Nausea
* Loss of appetite
* Abdominal pain
* Jaundice (in 80% of adults)

85
Q

Briefly describe the structure of Hepatitis A

A

Small single-stranded RNA encased by a protein capsule and therefore means it had a naked capsid structure

86
Q

Hepatitis B Structure

A

Small, enveloped nucleocapsid, double-stranded DNA virus

87
Q

What are some key difference between HAV and HBV structures

A
  • HAV consists of a ‘naked capside’ whereas HBV consists of an enveloped nucleocapsid
  • HAV viral genome consists of mRNA whereas HBV contains DNA
88
Q

Hepatitis B and C symptoms

same symptoms

A

Symptoms:
* Jaundice
* Fever
* Dark urine
* Nausea, vomitting
* Abdominal pain

Hepatitis C patients are more likely to be asymptomatic

89
Q

How is hepatitis B trasmitted

A
  • Vertical transmission (mother-child)
  • Sexual transmission
  • Contact with infected bodily fluids
90
Q

How is Hepatitis C transmitted

A

Exposure to infected blood (blood-blood contact)
* Injection drug use
* Contaminated needle use
* Sharing of personal hygiene items with infected individual (razor, toothbrush)

Vertical transmission (mother-child)

91
Q

Describe the pathogenesis of Hepatitis B

A
  1. HBV binds to hepatocyte cell receptors
  2. Endocytosis of HBV -> HBV envelope fuses with endosome
  3. Nucleocapsid ‘uncoats’/dissasembles
  4. DNA transported to nucleus -> Transcribed to mRNA
  5. mRNA translated into proteins
    5b. mRNA is also reversely transcribed into DNA
  6. Formation of new viral structure
92
Q

What are the two possible immune response outcomes to HBV

A

Effective cell-mediated immune response
* Eradicates all HBV
* Acute Hep B
* Symptoms occur: Jaundice, nausea, abdominal pain etc

Limited cell-mediated immune response
* Virus stays
* Mild symptoms
* Chronic HBV

93
Q

What are chronic HBV complications

A
  • Fulminant hepatitis
  • Liver cancer
  • Cirrhosis
94
Q

HCV pathogenesis

A
  1. HCV binds to specific receptors on hepatocyte
  2. Viral entry via endocytosis
  3. Viral envelope fuses with endosome -> Releasing nuclecapsid
  4. Nucleocapsid ‘uncoats’ releasing ssRNA(+)
  5. Translation of ssRNA(+) via RER ribosomes creates viral proteins
95
Q

TRUE OR FALSE

HCV has negative-sense mRNA

A

FALSE
ssRNA(+)

96
Q

What can chronic Hepatitis C result in

A
  • Cirrhosis
  • Liver failure
  • Hepatocellular carcinoma
97
Q

What are the treatments for HBV

A
  • Passive immunisation via administration of Hep B immune globulin within a week of exposure
  • Drugs targetting polymerase: Lamivudine [for chronic HBV]
98
Q

TRUE OR FALSE

Influenza C is the usual cause of epidemics

A

FALSE
Influenza A and B cause epidemics