Scenario 15 Flashcards
1
Q
What are the 3 classes of microorganisms?
A
Viruses, prokaryotes (bacteria/ mollicutes), eukaryotes (fungi, protozoa, nematodes, ectoparasites)
2
Q
What is the difference between a parasite and commensal?
A
Both live in/ on another organism but commensal does not injure the organism
3
Q
What colour is gram positive?
A
Purple/blue
4
Q
What colour is gram negative?
A
Red
5
Q
What classification are mycobacteria?
A
Gram positive but dont take up aq gram stain- walls made up of waxy my colic acid (use ziehl nelson stain)
6
Q
What are the properties of gram positive bacteria?
A
survive well on drying some produce spores/ toxins and have teichoic acids in their cell wall
7
Q
What are the properties of gram negative bacteria?
A
dont survive drying, no spores, have endotoxin in their cell wall (LPS)
8
Q
Is staph aureus gram negative or positive?
A
Gram positive coccus which forms clusters
9
Q
What are some distinguishing factors of staph aureus?
A
Grow readily on blood agar, golden colonies after 48 hours, coagulase and DNAase production
10
Q
What are the virulence factors of staph aureus?
A
Protein A- anti-phagocytic and secretes coagulase and exotoxins
11
Q
Where is it found/ transmitted?
A
Normal human flora, transmission from some carriers and close contact
12
Q
What infections does staph aureus cause?
A
Skin and soft tissue, ENT, pneumonia, bone and joint, sepsis, infective endocarditis, implanted prosthetics
13
Q
What toxin mediated problems does it cause?
A
Staphylococcal toxic shock and food poisoning
14
Q
What do you use to treat s aureus?
A
NOT penicillin- 90% resistant sue to beta lactamase, can use fluoxacillin or co-amoxiclav or macrolides (erythromycin) for MRSA use vancomycin
15
Q
How do you classify streptococcus pyogenes?
A
gram positive cocci in chains, grows readily on blood agar
16
Q
What are the virulence factors of s.pyogenes?
A
M protein in cell wall and endotoxins
17
Q
Where is it found and how is it transmittes?
A
In nose and throat of 1-5% of population and transmitted by close contact
18
Q
What infections does s.pyogenes cause?
A
pus forming, ENT and RT, skin and soft tissue (impetigo), puerpal fever, blood stream, streptococcal toxic shock
19
Q
What are some post infecitve manifestations of s.pyogenes?
A
non suppurative sequalae, acute rheumatic fever, acute glomerulonephritis
20
Q
How do you treat s.pyogene?
A
PENICILLIN OR AMOXICILLIN erythromycin, vancomycin if allergy
21
Q
How do you distinguish streptococcus pneumonia?
A
Gram positive cocci in pairs/short chains up to 4 cells long, produced pheumolysin in alpha haemolysis on blood agar
22
Q
What are the virulence factors of s. pneumo
A
pneumococcal teichoic acid c-polysaccharide and polysaccharide capsule which is anti-phagocytic
23
Q
Where is it found?
A
Commensal URT flora in humans, transmission by resp secretions
24
Q
What infections does s.pneumo cause?
A
URTIs, LRTIs, CNS (meningitis), sepsis, peritonitis, endocarditis
25
What is the treatment for s.pneumo?
2 vaccines in UK, penicillin (90%), erythromycin (not in meningitis), ceftriaxone in meningitis
26
What are some other gram positive bacteria?
Coagulase-negative staphylococci (normal skin flora, implanted prosthetics), Clostridium (spore forming rods, commensals in GIT produce endotoxins, difficile, tetani, botulinum, perfringens) Bacillus (rods, anthrax and cereus), cornyebacterium species (non spore forming rods, skin commensals)
27
What are the distinguishing factors of E coli?
gram negative bacilli, grow on blood agar, fements lactose, cell wall contains LPS, proteins and porins, motile (flagellae, fimbiae)
28
What are the virulence factors of E coli?
LPS, iron binding proteins, small polysaccharide capsule, fimbiae or pili, endotoxin priduction
29
Where is it found and how is it transmitted?
normal colonic flora, contaminated food/water, ascending infection
30
What infections does e coli cause?
UTI, diarrhoeal illness, intraabdominal infection, sepsis, pneumonia, meningitis
31
How do you treat e coli?
Amoxicillin
32
How do you distinguish pseudomonas aerginosa
Gram negative non sporing bacillus, non lactose fermenting, outer membrane with LPS, porins and proteins, large genome
33
What are the virulence factors of pseudomonas aerginosa
Endotoxins, exotoxins, iron binding proteins
34
Where is it found and how is it transmitted?
Soil and water, colonises UT, transmitted on medical equipment, water, spas and whirlpools
35
How do you treat p. aeruginosa?
Resistant to co-amoxiclav, trimethoprim, nitrofurantoin use piperacillin-tazobactam and gentamycin
36
How do you distinguish Haemophilus influenzae?
Gram negative rod (sometimes coccobacillus) needs media with growth factors and cell membrane with LPS, proteins and porins
37
What virulence factors are present in haemophilus influenza?
Endotoxin, large polysaccharide capsule, IgAse, adhesins in cell wall
38
Where is h.influenzae found?
Mucosal surfaces transmitted with close contact and droplets
39
What infections does it cause?
Bloodstream infection in young children (capsulate) and ottis media, sinusitis, conjunctivitis all ages (not capsulate)
40
How do we treat H.i?
Vaccine in childhood, amoxicillin (15% resistance) chemoprophylaxis, IV ceftriaxone for invasive infections
41
What other gram negative bacteria are there?
Bacteroides (rod- colonise the mouth), neisseria (cocci in pairs, mucous membranes, inside neutrophils- meningococcus, gonococcus), legionella (rod, pneumonia), heliobacter pylori (rod, stomach)
42
What is the basic structure of a virus?
DNA or RNA core with protein coat, some have an envelope studded with glycoproteins
43
Where do non-enveloped viruses survive best?
Outside of cells and bile resistant
44
Where do enveloped viruses survive best?
In cells- only spread by close contact eg. Hep B HIV
45
Which viruses are RNA?
Retrovirus, coronvirus, picornavirus
46
Which viruses are DNA?
Adenovirus, herpesvirus, poxvirus
47
What are the steps in viral replication?
Attachment, penetration, uncoating, transcription, translation, replication, assembly, release
48
How do DNA viruses replicate?
Large replicate on their own, small encode only a few genes and use host cell DNA polymerase etc
49
How do RNA viruses replicate?
Most RNA viruses encode their own RNA-dependent RNA polymerase using complementary RNA as template
- Positive strand RNA- equivalent to mRNA can often be immediately translated into proteins then synthesise a -ve copy copied back into -ve mRNA messages to produce structural proteins to package progeny +ve RNA into visions
- Negative strand RNA- first converted into +ve RNA (.RNA) by RNA dependent RNA polmerase then same as abover
50
Why do RNA viruses replicate more quickly?
RDRP lacks proofreading ability and makes more mistakes
51
How do retroviruses replicate?
encode reverse transcriptase which makes dsDNA from RNA
52
What is a latent infection?
Viral DNA persists but doesnt replicate to produce new infectious virus e.g. herpes, varicella zoster
53
What is pathogenesis?
Process where infecion leads to disease
54
What are the virus properties that allow it to inhabit cells?
Concealment (prevent antigen presentation, latency, integration into genome- retrovirus), intefere with cytokine network (mimic receptors and inhibitory cytokines and interfeon), antigenic variation (mutation and antigenic shift), modulation of lymphocyte function (immuno suppression)
55
What is the eclipse phase?
Virus entry until new infectious virions released
56
What is the classification of family herpesviridae?
Large dsDNA icosahedral capsid and lipid envelope
57
What subfamiliy does varicella zoster belong to?
Alphaherpesviridae
58
Where is chicken pox latent?
Dorsal root or cranial nerve ganglion- reactivation= chicken pox
59
What is the incubation period for varicella?
10-21 days- prodrome (fever, pharyngitis, malaise)
60
What are the complications of varicella?
Sever haemorrhagic, pneumonia, acute cerebellar ataxia, encephalitis
61
What memory immunity is stored in varicella?
VZV specific IgA and IgG antibodies and CD8/4 T cells (needed to prevent reactivation)
62
What is zoster?
Reactivation of latent VZV painful vesicles (1-2 vesicles) most commonly thoracic
63
How is zoster transmitted?
Spread by resp and skin lesions and congenital infection of fetus in first 20 weeks
64
When should post exposure prophylaxis be given?
Pregnant, immunocompromised or neonate of seronegative mother
65
What treatment should be used in zoster?
First line antiviral agents- aciclovir, valaciclovir and famciclovir
66
How are virus' detected?
Electron microscopy , cytopathic effect, cmv, protein antigen, nucleic acid (PCR, ELISA)
Specific antigen response- serology, seroconversion
67
What is therapeutic index?
Minimum cell toxic dose/ minimum virus inhibitory dose= at least 10
68
What are examples of nucleoside analogues?
Aciclovir, ganciclovir
69
What are examples of nucleotide analogues?
Cidofovir
70
How does aciclovir work?
Nucleoside analogue, competitive substrate for viral DNA polymerase inhibiting viral DNA polymerase and terminating the chain
71
How is aciclovir selective to infected DNA?
Preferential monophosphorylation- infected has 40-50x more phosphorylation, cellular DNA less susceptible (no viral DNA polymerase), effective chain termination due to lack of OH group
72
What are the issues with aciclovir?
poor oral absorptuon, short half life (need 5 a day) 85% excreted in urine
Use valaciclovir- 80% taken up
73
Why are some cells resistant?
Virus thymidine kinase absent or viral DNA polymerase altered
74
How does ganciclovir work?
Requires tri phosphorylation to active form. Works by inhibiton of CMV polymerase, not a chain terminator- need to add valine to be absorbed
75
Why is resistance to anti-retroviral therapy so high?
Error rate high so lots of mutations, selective pressure exerted if treatment stopped then resistant strain becomes latent
76
What are the targets for RNA anti-virals?
Viral proteases, viral surface proteins, immune modulation
77
What is advised after a splenectomy?
Prophylaxis and immunisation
78
What is defects in humoral immunity?
Immunoglobulin deficiency, congential B cell deficiencies
Frequent ear and sinus infection, infants fail to grow, pneumonias, obsesses, chronic enterovirus meninenephalitis, increased incidence of autoimmun and CT disorders
79
How do we prevent infection in defect in humoral immunity?
Ig replacement therapies
80
What infections are likely in people with congenital complement abnormalities?
Resembles hypospeism- streptoccocus pneumoniae, haemophilus influenzare, nisseria meningitidis)
81
What is defect in neutrophil number defined as?
less than 1x10^9 /l
May occur after haemopoetic stem cell transplantation, chemo, immunosuppresion, haematological malignancy, prolonged placement of catheters
82
What are the risks after solid organ transplantation?
Immediately after upper/lower RTIs but long term need lifelong immunosuppression, risk of transmitting infection i the organ and some inevitable CMV, toxoplasma- need prophylaxis
83
What is cytomegalovirus?
Transmitted by intimate contact 50% of adults, majority asymptomatic
If donor positive and recipient negative- primary infection
If donor negative recipient positive- reactivation
If both positive- recurrent infection
84
What is CD4?
A cell surface molecule which is on T helper cells and expressed on dendritic cells and macrophages. Stabilises a T helper 1 cells interaction with MHC class II and recruits signalling molecule, T helper 2 cells stimulate b cells for antibody production and aids CD8 T cells.
85
How are the number of CD4 cells depleted?
Direct cytopathicity of the virus, killing by specific cytotoxic T cells, memory pool particularly depleted
86
What is the host response in HIV infection?
CD4 count fails early and functional impairment of CTL response, cytotoxic T cells can kill HIV infected cells and HIV specific neutralising antibody response- antigenic diversity of HIV is a challenge
87
What is a primary immunodeficiency?
Innate defect at a genetic/ developmental level- failure to produce a class of antibody/ complement./ enzymes
88
What is a secondary immunodeficiency?
Factors not innate to the patient, nutrition, malignancies, aging, drugs, stress, splectomy
89
What are the steps of the formation of a HIV provirus?
Reverse transcriptase copies an RNA template onto dsDNA copy then covalent insertion of viral DNA into the genome of the infected cell (cant be cured)
90
What is the genetic organisation of a retrovirus?
9 genes synthesising 3 polyproteins
Gag- group specific antigen- viral core proteins, matrix, capsid
Pol- polymerase- enzymes, protease, reverse transcriptase, integrase
Env- envelope glycoprotein
91
What is the structure of a mature HIV-1 particle?
Outer envelope consists of a lipid bilayer and inside a shell of gag proteins, core contains two genomic RNA strands tRNA^lys and 50 copies of each viral enzyme
92
What are the basic steps of retroviral replication?
Attachment and receptor binding, membrane fusion and entry (requires CD4 and a chemokine receptor CDR5/CXCR4), uncoating and reverse transcription, nuclear import, intergration (RT makes a full length dsDNA which is cut in a stagerred cut at 3' end short replication of target sequence and gap repair), transcription, RNA processing, nuclear export, translation, assembly, budding (24hours)
93
What are the regulatory/accesory proteins
Adaptors that facilitate molecular interactions, good models for study, evasion of host mechanism, therapeutic targets
94
When should HAART be started?
When CD4 count reaches 300 (central to adaptive immunity)
95
What correlates with the recovery from acute infection and the suppression of the virus burden?
CD8 T cell response
96
What correlates with the disease stage?
CD4 T cells
97
What correlates with the tempo of the disease?
Viral set point
98
What are the current targets of HAART?
Protease inhibitors and RT inhibitors
99
What is the pathology of TB?
granulomatous inflammation with caseous necrosis in the centre (filled with pus) perhaps with visible acid fast bacili
100
What does it show on a CT scan?
Extensive consolidation with a cavity- cavitating pneumonia
101
How can you test for latent TB?
Mantoux test, interferon gamma release assay (more specific)
102
What is the treatment for TB?
Chemo- 4 drugs for 2 months then 2 drugs for another 2 months
