Immuno - Microbial Infection Flashcards
(77 cards)
1
Q
What are the 5 main types of infectious agents?
A
- Viruses
- Bacteria
- Fungi
- Protozoa
- Helminths (parasites)
2
Q
What are viruses?
A
Obligate parasite - only survive by infecting other cells (not cells in their own right)
3
Q
How does viruses contain genetic material?
A
RNA/DNA
4
Q
What is host specificity?
A
Capability of infecting one or more specific hosts
5
Q
How do viruses come out of cells?
A
- Budding out of cell - host cell remains intact (Enveloped virus)
- Cytolysis - host cell ruptures (Non-enveloped virus)
6
Q
What are the routes of infection for viruses?
A
- Faecal-oral
- Airborne
- Insect vectors
- Blood borne
7
Q
What is are examples of viruses?
A
- HIV - Retrovirus
- Polio
- HPV - human papilloma virus
- Smallpox - Variola virus
(Eradicated) - Influenza
- Rhinovirus
- Adenovirus
- Coronavirus
8
Q
What are bacterias?
A
Prokaryotes
9
Q
What are the characteristics of a prokaryote?
A
- No internal membranes (except non-pathogenic photosynthetic bacteria)
- HAPLOID (single copy of chromosome)
- cytoskeleton poorly defined
10
Q
What is the main structural determinant of prokaryotes?
A
The cell wall that contains peptidoglycan
11
Q
How do prokaryotes divide?
A
Binary fission (exponential increase)
12
Q
How would haploid gene of prokaryote affect mutation effect?
A
Only that one gene mutated to have bigger phenolytic effect
13
Q
How do viruses replicate?
A
- Binding
- Fusion
- Reverse transcriptase
- Integration with host DNA
- Transcription
- Translation into particle
- Assembly
14
Q
What use are the structures on bacteria?
*Note not all bacterias have these features
A
- Pilus (adhere to surfaces)
- Capsule (Prevent desiccation/hinder phagocytosis)
- Flagella (swimming)
15
Q
What are examples of bacterias?
A
- Shigella
- Mycobacterium tuberculosis (TB)
- Neisseria Meningitidis (Commensal to pathogen)
- Hospital-acquired infections (Nosocomial)
- Helicobacter pylori
- E. coli
16
Q
What is Shigella?
A
Invasive pathogen via faecal-oral transmission that affects the GI tract
- it moves without flagella by being pushed by host actin
17
Q
How does shigella bacteria get pushed around by host actin?
A
It nucleates host actin at tail of bacteria therefore push forward into cytoplasm of neighbouring cells
(infects whole monolayer of cells without going outside)
18
Q
What are serogroups?
A
A group of bacteria containing a common antigen
19
Q
Where and how does Neisseria meningitidis affect the body?
A
- Colonisation in naso-pharynx (no harm)
- Community acquired multiple serogroups - (invade tissues - non-blanching rash)
- Septicaemia
- Meningitis (penetrate blood-brain barrier - found in cerebrospinal fluid)
20
Q
What is Septicaemia?
A
Fatal rapid progressing bacterial disease
- Go into septic shock
- Severe inflammatory response
21
Q
What is non-blanching rash caused by?
A
Neisseria meningitidis - rapid onset needing immediate medical attention
- Can be left with severe disabilities
- Common (babies, young adult)
- Vaccine is available for different serogroups
22
Q
What are some hospital-acquired infections (bacteria)?
A
- Clostridium difficile
- MRSA - Methicillin Resistant Staphylococcus aureus
23
Q
Why are hospital-acquired bacterial infections so difficult to treat?
A
A lot of AMR - Antimicrobial resistance
24
Q
What diseases do Helicobacter pylori cause?
A
- Peptic ulcer
- Gastric cancer
25
Why do some pathogens mutate so quickly even with similar mutation rates as humans?
Have short replication/generation time
26
What are mutation rates?
How quickly a novel trait is developed
27
Why do viruses mutate so quickly?
Error prone replication (Low efficiency correction)
28
How is pathogenic E.Coli spread?
Originate in animals
| Spread via faecal-oral route
29
What is the current problem with TB?
- Drug therapy take too long
- BCG vaccine don't work well in endemic regions
- Current diagnostics miss too many cases (fail to break transmission chain)
30
What can we improve with TB treatment?
- New drugs (shorten treatment)
- Better vaccines
- Better tools for early diagnosis (Imaging tools eg PET-CT scan [high resolution] show area of inflammation - help understand pathogenesis of TB)
31
What is fungi?
Single-celled eukaryote
32
What does fungi cause?
Cutaneous, mucosal &/ systemic mycoses [divided base on location]
33
What forms do fungi come in?
Yeast
| Filament
34
How do fungi replicate?
Bud or divide
| Filaments (hyphae) have cross walls or septa
35
What are some examples of fungal disease?
- Candida albicans
| - Aspergillus fumigators
36
What is protozoa?
Unicellular eukaryote (including intestinal, blood and tissue parasites)
37
How do protozoa replicate?
- Replicate in host by binary fission
| - Formation of trophozoites inside cell
38
What is special about the life cycle of protozoa?
Have 2 hosts
39
How is infection acquired with protozoa?
- Ingestion
| - Through a vector (insect or invertebrate)
40
What are some diseases caused by protozoa?
- Malaria
| - Leishmaniasis
41
What is malaria caused by?
Many plasmodium species (protozoa)
| 5 species infect humans
42
What is malaria?
An infection acquired via mosquito vector
| Blood and tissue parasites
43
How does plasmodium replicate in host?
Formation of trophozoites in cells
44
How does formation of trophozoites in cells help protozoa transmission?
1. Parasite replicate to form feeding structures which produce progeny
2. The progeny lyse structures and gets released into bloodstream (related to fever - a characteristic of malaria)
45
How to treat malaria?
Antimalarials
46
What is Leishmaniasis caused by?
Leishmania species - 3 infect humans (protozoa)
47
What is Leishmaniasis?
An infection acquired via sandfly vector
| Blood and tissue parasites
48
How does leishmania replicate inside host?
Formation of trophozoites in cells
49
What forms of Leishmaniasis are there?
- Leishmania donovani (visceral disease - aka Kala-azar)
- Leishmania tropica (cutaneous)
- Leishmania braziliensis (cutaneous)
50
How to treat cutaneous lesions of leishmania diseases?
No need , they heal on their own slowly
51
How to treat mucosal & visceral leishmania diseases?
Combination of drugs and treatment
52
What are helminths?
Multicellular eukaryotic parasites
| Metazoa
53
What is metazoa?
Contains cells differentiated into tissues & organs
54
What type of helminths are there?
- Roundworms (eg Ascaris)
- Flatworms (aka flukes)
- Tapeworm
55
Describe lifecycle of helminths.
Inside and outside of human host
- many do not need an intermediate vector
- transmitted by faecal-oral route
56
What can the obstruction of intestine by ascarid roundworms cause?
Malabsorption of nutrients
| Malnutrition
57
What is an inefficient treatment for helminths?
Chemotherapy
58
What is an example of helminth?
Flukes - 3 schistosoma species can infect human via intermediate vector causing Schistosomiasis
59
How are schistosomiasis transmitted?
When entering contaminated water
60
What is the lifecycle of schistosoma mansoni?
1. Cercaria released from infected snails burrow through skin and travel to liver
2. It releases eggs in the hepatic portal vein
3. Egg moves into gut and released in faeces
4. Miracidium hatches from egg and enters freshwater snail
61
What causes inflammation in schistosomiasis?
The movement of the egg, which has a spine, through tissue
62
How to treat Schistosomasis?
- Antimicrobial treatment
| - Programme to remove freshwater snail to limit disease
63
What is a feature of the disease Schistosomasis?
Enlarge distended(expanded) abdomen
64
What do we have to deal with at this age of pathology?
- Increased microbial resistance
| - Reduced no. of antibiotics
65
What is the full name of HIV?
Human Immunodeficiency virus
66
What does HIV cause?
AIDS - acquired immunodeficiency syndrome
67
What cells do HIV invade?
CD4+ T cells & monocytes
68
Why does immune system fail to fight HIV?
By affecting T-cells, HIV can replicated in activated T-Cells and paralyse main component of adaptive immune system
Latency in infection also means it remains invisible so replication can occur later and generate new virion
Antigenic mutation in T-cell epitope can affect binding capacity of MHC molecules to viral peptides
HIV hide from anti-HIV antibodies by expressing non-immunogenic glycans (polypeptide) on key antibody epitopes
69
How does TB spread?
Respiratory droplets
70
How does immune system deal with TB bacteria?
- Contain it within granuloma, does not eradicate them
- Infection = latent
- Risk of reactivation if person becomes immunocompromised
71
How does TB get contained in a granulomas?
A combination of innate and adaptive immune responses culminates it
Innate: early infiltration lead to it being organised into primary granuloma w/ centrally located macrophages
- lead to formation of larger solid granuloma when adaptive immunity is initiated
Macrophage in centre will often be infected and some combined to form giant multi-nucleated cell
72
How does TB grow extracellularly?
When infection continues and centre of granuloma liquefies
73
What is severe malaria caused by?
Excessive RBC rupture - anaemia
Excessive inflammation
Accumulation of infected RBC in small blood vessel - lead to organ damage
74
How does malaria transmission get blocked in body?
Complement-fixing antibody against parasite gametocytes and gamete antigen can prevent infection in mosquito
75
What does Candida albicans cause?
Fungal infection - mucosal and systemic (more serious, in immunosuppressed patients)
eg mucosal in women - vulvovaginal candidiasis (Thrush)
76
What are the different forms of Candida albicans?
- A budding yeast
- Pseudohyphae
- Filament hyphae
Dependent on environmental factors
77
How is immunity established against Candida albicans?
Pattern recognition receptor [Dectin-1 & signalling molecule CARD9] expressed by innate myeloid cells (Monocytes. dendritic cells (APCs), neutrophils)
