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MBBS2 Diseases > Scenario 15: Infections > Flashcards

Scenario 15: Infections Flashcards

1
Q

What is the cytopathic effect?

A

The changes to a cell following viral infection: altered shape, lysis, membrane fusion, altered membrane permeability, inclusion bodies, apoptosis

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2
Q

Name three different detection systems for immunoassays

A

CLIA- chemiluminescent immunoassay
EIA- enzyme immunoassay
ELISA- enzyme linked immunosorbent assay

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3
Q

When is the antibody detectable in rubella?

A

Not until 17 days post rash

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4
Q

How is Varicella-Zoster transmitted?

A

Respiratory droplets/inoculation of mucus membrane

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5
Q

How do CD4 T cells become depleted with HIV infection?

A

Direct cell killing by virus (apoptosis, cell permembility etc.) cytotoxic T cell mediated killing, immune hyperactivation (by microbial translocation and indirect cell death) increased turnover rates drains T memory pool

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6
Q

Give a helical ss (+) RNA non enveloped virus

A

Coronavirus

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7
Q

Which viruses cause persistent infection with continued production of infectious viruses and immune evasion?

A

Hepatitis B, HIV

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8
Q

What are the problems with the tuberculin skin test?

A

Positive in those who have had BCG, loss of skin sensitivity through age or immunocompromised giving false negative

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9
Q

What are the properties of mycobacteria?

A

Gram positive in structure but cannot show up in gram stain due to presence of waxy mycolic acids in cell wall

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10
Q

What dermatomes are involved in Zoster?

A

50% thoracic, 20% cranial, 14% trigeminal, 16% lumbosacral

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11
Q

What vaccine is there for H influenzae?

A

Hib vaccine for capsule strain B introduced into childhood immunisation schedule

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12
Q

Which viruses survive well outside the cell and which do not?

A

Non enveloped viruses tend to survive well and may be bile resistant. Enveloped viruses often survive transiently outside the host, spread by close and intimate contact

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13
Q

How does PCR detect viral gene sequences?

A

Harnesses specific nature of genetic code, using specific primers to anneal the target. Amplifies signal generated by labelled reagents

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14
Q

Name 2 gram postive non spore forming rods

A

Listeria, corynebacterium diphtheriae

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15
Q

What is the classic manifestation of post primary TB?

A

Fibrotic, upper lobe, cavitatory

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16
Q

What infections do Chlamydia psittaci and pneumoniae cause?

A

Pneumonia. Multi system disease: hepatitis, haemolytic anaemia and cardiac involvement for psittaci

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17
Q

What are 5 modifications of PCR?

A

Multiplex: simultaneous amplification of different targets
Nested PCR: enhanced sensitivity
RNA detection: initial reverse transcriptase step
Quantitative PCR: measure amount of NA detected
Real Time: sophisticated adaption detects and quantifies target in real time without the need to reopen the reaction tube

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18
Q

Give a icosahedral ss (+) RNA non enveloped virus

A

Picornavirus

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19
Q

Which viruses are cleared followed acute phase of cell death?

A

Influenza, viral gastroenteritis, poliovirus, meleases

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20
Q

What is Zoster, what are the signs and symptoms?

A

Reactivation of latent VZV (shingles), painful eruption of many vesicles, unilateral, ophthalmic division of trigeminal nerve involved in 50% (Hutchinson’s sign on tip of nose) post-herpetic neuralgia (elderly)

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21
Q

Describe the structure of HIV

A

Outer layer: lipid bilayer with protruding Env spikes (heterotrimers of SU3TM3)
Inside the envelope lie shells of Gag proteins. The matrix associates with the membrane, there is a conical capsid and the nucleocapsid which contains the viral RNA genome with copies of the viral enzymes.

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22
Q

What is the function of exfoliatin toxin?

A

Staphylococcal scaled skin syndrome, phage mediated

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23
Q

What infections is a solid organ transplant at risk of?

A

Wound, respiratory and intravascular catheter infections as well as UTI in renal transplant, billary in liver transplant, mediastinitis, invasive fungal infection and herpes virus infections in cardio-pulmonary transplants

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24
Q

What are the pathogenic factors for H influenzae?

A

Endotoxin, virulence factor is large polysaccharide capsule (labelled a-f type) adhesions in cell wall for colonisation, IgAse inactivates IgA on mucosal surfaces

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25
Q

What are some pros of aciclovir?

A

Effective chain termination due to lack of 3’ OH group, selective for virally infected cells, competitive inhibitor of DNA polymerase

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26
Q

What effects can viruses have on host cells?

A

Rounding and detachment from surface, nuclear distortion, cell fusion, inclusion body formation, organelle fragmentation, lysis and necrosis, inhibition or stimulation of cell division, transformation, activation of cell signalling pathways, induction of cytokines and interferon synthesis, apoptosis, display of viral antigens on cell surface, viral antigen secretion, interference with host molecules (MHC) viral encoded cytokines

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27
Q

What gene change makes MRSA resistant to beta lactams?

A

mecA gene altered pbp, produces beta lactamases

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28
Q

What is DOTS therapy?

A

Directly Observed Therapy Short course. 1) Detect cases 2) Standardise treatment 3) Drug supply and management system 4) Monitoring and evaluation system and impact measurement 5) Political support

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29
Q

What does the Tat HIV accessory protein do?

A

Activates viral transcription

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30
Q

How is the HIV-1 sequence diversified?

A

Copying error (drift), recombination (shift) Both together produce clades (diverse viruses with phenotypic differences)

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31
Q

What are the symptoms of a defect in humeral immunity?

A

Various infections: frequent ear and sinus infections, repeated pneumonia, deep skin or organ abscesses, infant fails to thrive, persistent oral infection with oral candida, chronic enterovirus, increased autoimmune and connective tissue disorders

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32
Q

What antibiotics can be used to treat H influenzae?

A

15% resistance to amoxicillin, use in UTRI if sensitive, co-amoxiclav if resistant, IV ceftriaxone used if invasive infection

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33
Q

What are the complications of Varicella Zoster at the primary stage?

A

Severe hamorragic varicella, pneumonia (adults), acute cerebellar ataxia (children), encephalitis, secondary bacterial infection.

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34
Q

What exotoxins does Streptococcus pyogenes produce?

A

Streptokinase, streptolysins, streptococcal pyrogenic exotoxins

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35
Q

What does the host resistance factor SAMHD1 do?

A

Suppresses RT in myeloid cells by hydrolysing dNTPs

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36
Q

How can ganciclovir be activated?

A

When it is triphosphorylated

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37
Q

What antibiotics can be used to treat TB?

A

Highly antibiotic resistant. Need quadruple therapy for 2 months: isoniazid, rifampicin, pyrazinamide, ethambutol. Then dual therapy for 4 months: isoniazid, rifampicin.

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38
Q

What is the difference between MDR and XDR TB?

A

MDR TB is resistance to 2 first line drugs isoniazid and rifampicin. XDR is resistance to all 4 first line agents: isoniazid, rifampicin, pyrazinamide, ethambutol as well as another agent

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39
Q

How does a retrovirus replicate?

A

Uses reverse transcriptase to copy RNA template into double stranded DNA copy. Integration: covalent insertion of viral cDNA into the genome of the infected cell to form the provirus. The cell now has viral DNA integrated into it and will produce virions which bud off and mature

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40
Q

What the pathogenic factors of M tuberculosis?

A

Replicate inside macrophages, inhibit cell apoptosis, mycolic acids stimulate host cell hypersensitivity, antibodies formed are ineffective, granuloma formation with caseous necrosis

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41
Q

What are the 3 enzyme activities of reverse transcriptase?

A

RNA dependant DNA polymerase, RNAase H (cleaves RNA from RNA/DNA hybrid), DNA dependant DNA polymerase

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42
Q

What does salmonella cause?

A

Diarrhoea, vomiting, systemic upset, rarely bloodstream infection in immunocompromised

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43
Q

How can we test for past exposure to TB?

A

Tuberculin skin test: purified protein derivative injected intradermally. This will cause a hypersensitivity reaction if the patient has significant past exposure to TB.

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44
Q

What endotoxins does Staphylococcus aureus have?

A

Haemolysins, Panton Valentine leucocidin, toxic shock syndrome toxin, enterotoxins, exfoliatin toxin

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45
Q

What is the characteristic colour of Staphylococcus aureus?

A

Golden

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46
Q

What does the host resistance factor tetherin do?

A

Inhibits release of viruses from cell surface

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47
Q

What antibiotics can be used in MRSA?

A

Vancomycin (glycopeptide class)

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48
Q

Give a icosahedral ds DNA enveloped virus

A

Herpesvirus

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49
Q

If we see gram positive cocci in clusters under the microscope which bacteria would this be typical of?

A

Staphylococcus aureus

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50
Q

What is the difference between immunosuppression and immunodeficiency?

A

Both are immunocompromised. The immunodeficient have a congenital or acquired absence of normal immune response. The immunosuppressed have a lack of immune system mediated by drugs therapy, or as a side effect of therapy.

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51
Q

Name the coliforms

A

E coli, Klebsiella, Proteus, Enterobacter, Serratia

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52
Q

What fragments can we identify Staphylococcus aureus by in the laboratory?

A

Coagulase and DNAase production

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53
Q

What infections can M pneumoniae cause?

A

Community acquired atypical pneumonia, fever, malaise, dry cough, rashes, cardiac, neurological problems, cold aggutin disease

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54
Q

What do coagulase negative staphylococci usually infect?

A

Implanted prosthetic devices

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55
Q

What antivirals can be used to treat herpes virus?

A

Aciclovir, ganciclovir

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56
Q

How does Varicella-Zoster resurface to cause shingles?

A

Virus becomes latent in posterior horn cells of spinal column after acute chickenpox infection. No signs of virus for years until immunosuppression allows it to resurface as shingles

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57
Q

Describe the bacteroides species

A

Gram negative rod, anaerobic, sensitive to metronidazole

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58
Q

How does pulmonary TB appear on a CT?

A

White area with black cavity communicating with airway

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59
Q

What tumours does HPV cause?

A

Cervical carcinoma, anogenital and vulvo-perineal tumours

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60
Q

What antibiotics can be used to treat E coli?

A

Amoxicillin only if sensitivity confirmed, trimethoprim or nitrofurantoin for UTI, co-amoxiclav for UTI or sepsis (community acquired) piperacillin-tazobactam for sepsis (hospital acquired)

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61
Q

How is HIV transmitted across mucosal surfaces?

A

Breaches genitoanal mucosal barriers by attaching to CCR5 surface molecules on activated T cells

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62
Q

What causes a defective barrier to infection?

A

Age extremes, loss of skin integrity (burns, eczema) deficient production or drainage of fluid, malnutrition and mineral/vitamin deficiencies

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63
Q

Why would we use PCR for detection of M tuberculosis?

A

It is faster than culture which can take 3-6 weeks (incubated for 12 weeks before declared negative) useful if positive to rule out other conditions however if a negative result TB must not be ruled out as it is not as sensitive as culture.

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64
Q

How can S aureus be transmitted?

A

Infected from own endogenous S aureus, transfer by hand, close contact, infected surfaces (fomites) in hospital/community

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65
Q

What does the Vif HIV accessory protein do?

A

Critical regulator of virus infectivity

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66
Q

Describe Helicobacter pylori

A

Small curved gram negative rod. Colonises the stomach living under the mucus layer and produces urease to increase pH locally. CagA protein associated with virulence. Causes gastritis, duodenal ulceration, gastric lymphoma. Antigen detection in stool. PPL and dual/triple antibiotic action required.

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67
Q

How is syphilis transmitted?

A

Sexually or congenitally

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68
Q

Give a icosahedral ss (+) RNA enveloped virus

A

Flaviavirus, retrovirus

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69
Q

What antibiotics can be used to treat S pneumoniae?

A

Penicillin, macrolides: erythromycin, clindamycin for penicillin allergic NOT in meningitis, ceftriaxone for meningitis

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70
Q

What are some possible defects in humeral immunity?

A

Immunoglobulin deficiency, hypogammaglobulinemia, congenital B cell deficiencies,

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71
Q

How can we minimise the risk of rejection and infection from a solid organ transplant?

A

Screen organ to prevent use of HIV, hepatitis positive organs, give antimicrobial prophylaxis to prevent severe disease

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72
Q

Give a helical ds DNA enveloped virus

A

Baculovirus

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73
Q

How is negative stranded viral RNA replicated?

A

Negative stranded RNA must first be converted to +RNA (mRNA) by RNA dependant RNA polymerase. mRNA is then translated into proteins, -RNA is synthesised. Structural proteins package progeny -RNA and RDRP into virions.

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74
Q

Name 3 anaerobic gram postive spore forming rods

A

Clostridium tetani, clostridium botulinum, clostridium difficle

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75
Q

What is the late stage of syphilis?

A

There may be a latent phase through which 2/3 do not progress and then cardiovascular, gummatous and neurosyphilis.

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76
Q

What causes functional hyposplenism/asplenism?

A

Sickle cell disease

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77
Q

What does the host resistance factor SERINC do?

A

Interferes with viral entry

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78
Q

What are the memory cells that the body has after primary Varicella Zoster infection?

A

VZV specific IgG and VZV IgA antibodies as well as VZV specific CD8 and CD4 T cells

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79
Q

How is aciclovir activated?

A

By addition of phosphate group by viral thymidine kinase activity so it can be it’s active triphosphate form

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80
Q

What is miliary TB?

A

Uncontained infection- may occur at primary infection or if immunocompromised later in life

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81
Q

What are the post infective manifestation of S pyogenes?

A

Non suppurative sequelae (molecular mimicry- antibodies cross react with similar antigens) acute rheumatic fever (carditis, pancreatitis, polyarthritis, endocarditis) Acute glomerulonephritis- Bright’s disease (fluid overload, oedema, hypertension, oliguria)

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82
Q

What does a complement deficiency manifest as?

A

Similar to hyposplenism, at risk of infection from capsulate bacteria like Streptococcus pnuemoniae, Haemophilis influenzae, Neisseria meningitidis. Increases incidence of immune complex disease such as systemic lupus erythematosus, glomerulonephritis, vasculitis

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83
Q

Give a icosahedral ds RNA non enveloped virus

A

Reovirus

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84
Q

How can VZV be diagnosed?

A

HSV/VZV Dx in skin lesions found by electron microscopy, immunofluorescence, tissue culture, PCR

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85
Q

What kind of samples can be sent to the microscopic laboratory?

A

Swabs, blood and bodily fluid (urine, pus, faeces, sputum, synovial or pleural fluid, bronchial washings, CSF) biopsies, prosthetic material, serum/plasma, worms insects or arachnids

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86
Q

What can we use to treat VZV?

A

Aciclovir, PO or IV, valaciclovir, PO, famciclovir, PO

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87
Q

What does cidofovir inhibit to have an anti viral effect?

A

CMV and HHVs, adenovirus, HPV nucleotides

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88
Q

What is the aim of treatment of herpes virus?

A

To control outbreaks as the virus cannot be eradicated

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89
Q

How is cytomegalovirus spread?

A

Horizontally: social contact, sexually, blood transfusion, organ transplantation
Vertically: intrauterine, perinatal

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90
Q

What does the Vpu HIV accessory protein do?

A

Immune modulator, virus release

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91
Q

What antibiotics can be used to treat Streptococcus pyogenes?

A

Penicillin, amoxicillin, erythromycin and clindamycin for penicillin allergic (some resistance) vancomycin (severe infections in penicillin allergic)

92
Q

What is the primary phase of syphilis?

A

Chancre at site of infection (firm round painless) on genitals or mouth (may go unnoticed on cervix/anal margin)

93
Q

What are the group A streptococci?

A

Streptococcus pyrogenes

94
Q

Give a complex enveloped ds DNA virus

A

Poxvirus

95
Q

Which drugs cause T cell defects?

A

Anti-TNF and anti-CD20 monoclonal antibody treatments

96
Q

How is E coli transmitted?

A

Ascent into urinary tract, intraabdominal infection from colonic perforation, contaminated water or food, farm animals, person to person

97
Q

What is the classification of herpes virus?

A

Large double stranded DNA genome, icosahedral capsid, lipid envelope derived from host cell bearing virus encoded glycoproteins

98
Q

What happens in primary (usually childhood) TB infection?

A

Bacteria division in lung focus and enlarged draining lymph nodes may rupture, lymphatic and hematogenous dissemination to distant sites can occur, usually host can contain the infection. May be no symptoms or non specific, cough, fever

99
Q

What 3 polyproteins do retroviruses synthesise?

A

Gag: group specific antigen (viral core proteins, matrix, capsid and nucleocapsid
Pol: polymerase (enzymes: protease, reverse transciptase and intergrase)
Env: envelope glycoprotein (surface and transmembrane)

100
Q

When is the antibody detectable in parvovirus?

A

Coincides with rash and arthralgia

101
Q

What does the shingles vaccine do?

A

Lowers risk of shingles in those over 60, decreases risk of post hepatic neuralgia, and decreases burden of illness

102
Q

What infections does Chlamydia trachomatis cause?

A

STI- urethritis, LGV, PID, infertility
Eye infection- blindness
Congenital infection- eye infection, pneumonia

103
Q

What infections does P aeruginosa cause?

A

Sepsis and bloodstream infection (neutropenia, infection of IV lines, skin of burns patients, UTI) UTI (urinary catheter associated) Pneumonia (ventilator associated, immunosuppressed, CF) Skin and soft tissue (burns, neutropenic patients, hot tub folliculitis) Eyes (keratinitis after contact lense use, endophthalmitis after cataract implant surgery)

104
Q

What types of haemopoietic stem cell grafts are there?

A

Stem cell autograft, matched allograft, matched unrelated donor

105
Q

Which viruses cause latent infection with viral persistence after initial clearance?

A

Herpes viruses e.g. simplex, varicella zoster

106
Q

What are the vaccines for S pneumoniae?

A

One for adults at risk, one in childhood immunisation scheme

107
Q

Describe botulism

A

C botulinum toxin ingested from food or absorbed through wound, imported into CNS and inhibits Ach release at NMJ. Flaccid paralysis, respiratory failure.

108
Q

What does complement do?

A

Activates neutrophils, macrophages, mast cells, monocytes, dendritic cells, B and T cells and therefore activates opposition, lysis of pathogens, chemotaxis, inflammation cell activation, clearance of immune complexes and apoptic cells, augments the antibody response, promotes T cell response, eliminates self reactive B cells, enhances immunological memory

109
Q

How can we clinically stain mycobacterium?

A

Cannot use gram stain due to waxy mycolic acids in cell wall, so use auramine staining which is more sensitive than ZN. If auramine positive then use Ziehl-Neelsen. If ZN positive then presence of AAFB reported.

110
Q

Name a reverse transcriptase inhibitor which is non nucleoside based.

A

Nevirapine

111
Q

Name a reverse transcriptase inhibitor which is nucleoside based.

A

Zidovudine

112
Q

What colour will a gram positive organism stain?

A

Blue/purple

113
Q

Describe the Nesseria species

A

Gram negative diplococci, live on mucus membranes, survive and replicate into neutrophils

114
Q

Give the two most clinically important gram negative cocci.

A

Neisseria meningitidis and neisseria gonorrhoeae

115
Q

What organisms would PCR be appropriate to detect?

A

Chlamydia trachomatis, neisseria gonorrhoeae, norovirus, respiratory viruses (influenza A&B, parainfluenza, rhinovirus)

116
Q

What is HAART?

A

Highly active antiviral treatment

117
Q

What are the 5 current targets of anti HIV viral therapy?

A
  1. Protease inhibitor 2. Fusion inhibitor 3. RT inhibitor 4. Chemokine receptor antagonist 5. Intergrase inhibitor
118
Q

What is in the cell wall and capsule of Streptococcus pneumoniae?

A

Pneumoccocal teichoic acid (C-polypeptide) in cell wall, antiphagocytic polysaccharide capsule

119
Q

What is the reproductive number of a virus?

A

Infectiousness, average number of cases arising from a single index

120
Q

Which organisms cause TB in humans?

A

Mycobacterium tuberculosis and less commonly mycobacterium bovis

121
Q

What are enterobacteriaceae?

A

Gram negative rods which may be normal flora of the human colon. They are facultative anaerobes. Can cause infection when in the wrong place (e.g. urinary system, blood stream, appendicitis)

122
Q

How is Zoster different in the immunocompromised host?

A

Higher incidence, most severe, extensive, prolonged rash, pneumonitis, hepatitis, mengoencehalitis

123
Q

What kind of organisms are Bacillius?

A

Gram positive aerobic spore forming rods

124
Q

What is congenital syphilis?

A

Mothers most likely to transmit syphilis to baby early on, infected babies may be born very sick with hepatitis, thrombocytopenia, osteitis and desquamative rash. Hutchinson’s teeth- barrel shaped, notched incisors, deafness, interstitial keratitis

125
Q

Name a reverse transcriptase inhibitor which is nucleotide based.

A

Tenofovir

126
Q

How do we do PCR on RNA viruses?

A

Reverse transcriptase transcribes RNA into complementary cDNA which is then amplified by PCR

127
Q

Describe Treponema pallidum

A

Long fine spiral rods, can be seen in dark ground microscopy only, cannot be cultured or gram stained, serological diagnosis.

128
Q

What sub family of herpesvirus is EBV in?

A

Gammaherpesviridae

129
Q

When is the incubation period of the virus?

A

Interval between exposure and appearance of rash/sign (prodrome)

130
Q

When is the eclipse phase of a virus?

A

Period from viral entry until new infectious virions are released

131
Q

What does aciclovir inhibit to have an anti viral effect?

A

HSV and VZV DNA polymerases

132
Q

What structures does E coli have?

A

Gram negative cell wall, LPS endotoxin containing membrane, proteins, porins, flagellae, fimbriae or pili for adhesion

133
Q

How do DNA viruses replicate?

A

Large DNA viruses encode many of the enzymes needed for replication whereas smaller DNA viruses use host cell DNA enzymes e.g. polymerase

134
Q

What is the function of haemolysins?

A

Provide nutrients for dividing bacteria

135
Q

How do interferon gamma release assays (IGRAs) work?

A

Work on principle that lymphocytes which are sensitised to Mtb will produce IFNy when incubated with Mtb derived antigen whereas unexposed lymphocytes will not. Unaffected by prior BCG

136
Q

What does ganciclovir inhibit to have an anti viral effect?

A

CMV DNA polymerase

137
Q

What is the origin of the HIV virus?

A

SIVcpz from monkeys which crossed to humans in the African Bushmeat Trade

138
Q

What is the function of toxic shock syndrome toxin?

A

Superantigen activity, non-specific polyclonal activation of T cells

139
Q

What are the pathogenic factors of P aeruginosa?

A

Endotoxin, Exotoxins (exotoxin A, elastase, leucocidins) iron binding proteins, mucoid types

140
Q

What are the most common extra pulmonary manifestations of TB?

A

Lymph nodes, meningitis, renal, interstitial, bone, miliary (flecks)

141
Q

What does Hameophilus influenzae need added to agar to be grown in the lab?

A

Needs media enriched with growth factors X&V derived from blood heated blood agar

142
Q

What are the 8 basic steps of viral replication?

A
  1. Attachment to target cell 2. Penetration to cell interior 3. Uncoating to prime for transcription 4. Transcription to produce viral RNA 5. Translation to produce viral proteins 6. Replication- DNA or RNA driven by viral proteins 7. Assembly- new virons formed 8. Release and dissemination
143
Q

What is C difficile associated with?

A

Inflammatory diarrhoea, colitis, toxic megacolon associated with prior antibiotic use and disruption of normal flora

144
Q

Describe the structure of reverse transcriptase

A

A heterodimer of p66 and p51 subunits

145
Q

How is positive stranded viral RNA replicated?

A

Essentially equivalent to mRNA and can often be translated to proteins. Therefore protein synthesis is the first step and viral polymerase is synthesised. The polymerase synthesises a negative strand of RNA which is copied back. This produces structural proteins which are used to package progeny +RNA into virons

146
Q

How do RNA viruses replicate?

A

Many encode their own RNA-dependant-RNA-polymerase which uses complementary RNA as template. Retroviruses however encode reverse transcriptase and make dsDNA from RNA for genome synthesis (lack proofreading ability)

147
Q

What is the secondary phase of syphilis?

A

2-8 weeks after primary infection, dissemination of treponemes. Systemic illness, fever, rash, alopecia, mucous ulcers

148
Q

What are the side effects of TB drugs?

A

Nausea, fatigue, rashes. Isoniazid only: peripheral neuropathy prevented by pyridoxine. Ethambutol: rarely optic neuritis

149
Q

What sub family of herpesvirus is Varicella Zoster in?

A

Alphaherpesviridae

150
Q

How do viruses conceal themselves from the host immune system?

A

Prevent APCs, MHC trafficking, antigen processing, cell killing. Herpesviruses use latency. Retroviruses use integration into genome

151
Q

What are some cons of aciclovir?

A

Poor oral bioavailability, frequent oral dosing required 5x day, CNS toxicity, most of drug excreted unchanged in urine, bad for renal failure, nephrotoxicity due to precipitation in tubules

152
Q

Describe the process of a ZN stain

A 
Dry the smear of sputum on glass slide
Apply carbon fusion and heat
Wash with acid/alcohol mixture
Apply counter stain methylene blue
Wash
View under microscope
Only acid/alcohol fast bacteria seen
153
Q

Describe M pneumoniae

A

Sterols in cell wall, no gram stain reaction, can be cultured, colonise respiratory and genital tract

154
Q

Why is ganciclovir less effective than aciclovir?

A

Only acts via inhibition of CMV polymerase, not an obligatory chain terminator

155
Q

What does Mycobacterium leprae cause?

A

Leprosy

156
Q

Describe tetanus

A

C tetani enters through wound, toxin (tetanospasmin) acts to prevent inhibitory neurotransmitter release in CNS. Spasms, autonomic instability.

157
Q

What are the properties of gram negative bacteria?

A

Do not survive well on drying, no spores, have endotoxin in their cell wall

158
Q

What are the different targets for antiviral therapy?

A

Attachment (binding inhibitor) Virus entry (fusion inhibitors) Nucleic acid synthesis (polymerase and intergrase inhibitors) Assembly/maturation (protease inhibitors) release (protease inhibitors, neuraminidase inhibitors)

159
Q

What does the Rev HIV accessory protein do?

A

Mediates unspliced RNA nuclear export

160
Q

What are the principal steps of retroviral cDNA integration? (formation of provirus)

A

1) Full length dsDNA reverse transcript cleaved at 3’
2) Strand transferred to target DNA
3) Short duplication of target sequence and gap repair
Occurs randomly throughout genome, areas of gene area favoured

161
Q

What are the properties of gram positive bacteria?

A

Survive well on drying, may produce spores, produce endotoxins, have teichoic acid in cell wall

162
Q

What kind of bacteria is Pseudomondas aeruginosa?

A

Gram negative aerobic non sporing bacillus which does not ferment lactose

163
Q

What antibiotics can be used to treat P aeruginosa?

A

Piperacillin-tazobactam for hospital acquired sepsis, gentamicin added to severe cases, ciprofloxacin is only oral agent

164
Q

What does the Nef HIV accessory protein do?

A

Immune modulator, T-cell activation, virus infectivity

165
Q

Why is LPS of E coli pathogenic?

A

Endotoxin LPS binds to binding protein on host cell and stimulates release of TNFa, IL-1, IL-6, causing cell recruitment, fever, hypotension and shock

166
Q

What are some causes of neutropenia?

A

Haemopoietic stem cell therapy, chemotherapy, immune suppressive therapy, haematological malignancy disease, congenital diseases

167
Q

What is the mechanism of antibiotic resistance to penicillins in S pneumoniae?

A

Altered pbp

168
Q

How is the host protected against viral challenge?

A

Innate mechanisms- natural anti-viral activities
Cell mediated immunity- eliminates infected cells
Antibodies- systemic or mucosal, block initial infection,
Intrinsic mechanisms- intracellular (e.g. anti HIV properties of APOBEC and TRIM proteins)

169
Q

How is P aeruginosa transmitted?

A

Contaminated medical equipment, poor quality drinking water, can survive on hands, inadequately maintained spas, whirlpools, cedarwood hot tubs

170
Q

What are the basic principles of serological techniques?

A

Detection of antibody based on the idea that adding a specific viral antigen to patient serum will bind to the virus specific antigen if it is present. The antigen/antibody complex can then be indicated. Technique can be reversed to detect presence of viral antigen

171
Q

How can a virus be resistant to aciclovir?

A

Virus TK absent or altered substrate specificity

172
Q

Which bacteria is an asplenic patient at risk of?

A

Encapsulated bacteria (Streptococcus pneumoniae, Haemophilus influenzae

173
Q

How can Varicella Zoster be transmitted?

A

Respiratory route (horizontal) congenital, perinatal (vertical)

174
Q

What are the group B streptococci?

A

Streptococcus agalactiae and C&G

175
Q

What tumours does EBV cause?

A

Burkitt’s lymphoma, nasopharyngeal carcinoma, Hodgkin’s lymphoma, lymphoproliferative disease/lymphoma in immunocompromised host

176
Q

What are the risk factors for TB?

A

HIV, alcohol, anti TNFa drugs, corticosteriods, cigarettes, lack of vitamin D, renal failure

177
Q

What is dangerous about infection in the immunocompromised patient?

A

Cardinal features may be absent, no single unifying diagnosis, delayed/absent response, agents of acute infection may cause chronic disease, serology complicated by passive acquisition of AB in blood/products

178
Q

How is M tuberculosis transmitted?

A

Exposure to droplet nuclei expectorated by someone with TB, smear-positive much more infectious than smear negative, close prolonged contact of at least 8 hours required, laboratory and post mortem hazard, BCG only partially protective

179
Q

Which organism causes ‘bull neck’?

A

Corynebacterium diphtheriae

180
Q

What tumours does HHV-8/KSHV cause?

A

Kaposi’s sarcoma

181
Q

Give some examples of enterobacteriaceae.

A

Escherichia coli, klebsiella, proteus, salmonella

182
Q

Name 2 aerobic gram postive spore forming rods

A

Bacillus anthracis, bacillus cerus

183
Q

What is the basic viral structure?

A

DNA or RNA core with protein coat, or capsid comprised of capsomeres. These together form the nucelocapsid. In some viruses there is an envelope of lipid bilayer derived from the host cell

184
Q

How do viruses interfere with host cytokine network?

A

Poxviruses mimic cytokine receptors, EBV mimics inhibitory cytokines, adeno-vaccinia and influenza inhibit interferon. Measles suppress mo derived cytokines.

185
Q

What are spike proteins?

A

Proteins on enveloped viruses used to attach to the cell, a carbohydrate side chain. Mediates viral entry into cells, targets for antibodies

186
Q

What is the function of Panton Valentine leucocidin?

A

Kills neutrophils, phage mediated

187
Q

What are the principal diagnostic methods in the microbiology laboratory?

A

Direct inspection of the sample (e.g. CSF turbidity, malodour, blood, pus or worm in stool), microscopy of wet preparation- gram stains, culture on agar and enrichment culture, automated liquid culture systems for blood, antigen/antibody detection methods in blood/other fluid, PCR to detect organisms in clinical material for rapid diagnosis/non culturable organisms

188
Q

What kind of virus is Varicella-Zoster virus?

A

Enveloped DNA virus

189
Q

What is the classic manifestation of progressive primary TB?

A

Consolidation of middle lobe with intrathoracic lymphadenopathy

190
Q

What are the consequences of having TB as a result of HIV infection?

A

The TB is more likely to be smear positive and disseminated and has a less characteristic clinical appearance, mortality is higher

191
Q

If we see gram positive cocci in pairs and chains under the microscope which bacteria would this be typical of?

A

Typical of streptococci

192
Q

What are the intra and extracellular phases of a viral life cycle?

A

Extracellular: viron is metabolically inert
Intracellular: virus genome expression occurs, acheieves production of new progeny virus

193
Q

What provides the thrust for chronic HIV infection?

A

T cell activation by viral products, active T cells are substrate for viral replication

194
Q

What surface components does Staphylococcus aureus have to bind to host cells?

A

Protein A which binds to the Fc portion of IgG and is antiphagocytic, various adhesion molecules to bind to proteins like collagen

195
Q

Name three organisms of the Spirocheaete family

A

The agents of Lyme disease (Borrelia burgforderi) leptospirosis (Leptospira interrogans) and syphilis (Treponema pallidum)

196
Q

What infections does Clostridium perfringens cause?

A

Food poisoning, intra-abdominal infections, appendicitis,

197
Q

Which virus causes chickenpox and shingles?

A

Varicella-Zoster

198
Q

How does the host recover from viral infection?

A

Innate mechanisms: macrophages, neutrophils, NK cells, interferon, complement
Cell mediated immunity: CTL’s, non-lytic mechanisms
Antibodies- neutralise further spread

199
Q

What does the Vpr HIV accessory protein do?

A

Cell cycle, virus nuclear import, resistance modulator

200
Q

Name the mycobacterium that causes a buruli ulcer.

A

M ulcerans

201
Q

What infections can S aureus cause?

A

A range of skin and soft tissue infections (boils, abscesses etc) ENT infections, pneumonia, bone and joint infection (septic arthritis), bloodstream infections (spread from local infection/drug injection/IV lines) infection endocarditis (valve destruction) infection of prosthetic devices, toxic shock syndrome, staphylococcal food poisoning

202
Q

Name the mycobacterium that causes a ‘fishtank granuloma’

A

M marinum

203
Q

What colour will a gram negative organism stain?

A

Red

204
Q

What does the host resistance factor APOBEC3 do?

A

Catalyses C to U mutagenesis and inhibits RT

205
Q

If CSF is turbid what bacteria is this typical of?

A

Neisseria meningitidis

206
Q

What are the infections caused by Streptococcus pneumoniae?

A

URTI (sinusitis, otitis media, conjunctivitis), LRTI (pneumonia) CNS infection (meningitis), sepsis and bloodstream infection (pneumonia, meningitis), speenless or hypospelenic patients at risk of spontaneous bacterial peritonitis

207
Q

What is postprimary TB?

A

Reactivation of earlier primary infection. Chronic progressive infiltration of lung apices with cavitation and fibrosis. Symptoms are cough productive of bloodstained sputum, fevers, night sweats, weight loss. Patient may be smear positive and infectious to others

208
Q

Give a icosahedral ds DNA non enveloped virus

A

Adenovirus

209
Q

What infections can S pyogenes and other group A streptococcus cause?

A

ENT and respiratory infection (pharyngitis, tonsillitis, quinsy, scarlet fever, sinusitis, rarely pneumonia, otitis media) Skin and soft tissue infection (impetigo, cellulitis, erysipelas, necrotising fasciitis) Puerperal fever (infection of female genital tract post-partum) streptococcal toxic shock (mediated by superantigens)

210
Q

What tumours do hepatitis B and C cause?

A

Hepatocellular carcinoma

211
Q

What is the key virulence factor of S pyogenes?

A

M protein in cell wall- antiphagocytic

212
Q

How can viral infections be controlled?

A

Public health (sanitation, water and food, pest control) immunisation (HPV, VZV, rabies, yellow fever, japanese encephalitis, influenza, hepatitis A and B, smallpox, measles, mumps rubella), antiviral therapies

213
Q

What causes scarlet fever?

A

When pharyngitis is caused by a strain of group A streptococcus producing streptococcal pyrogenic exotoxins A&C- erthrogenic toxins-carried on a bacteriophage

214
Q

How can S aureus infections be treated?

A

Flucloxacillin, co-amoxiclav, macrolides for pencillin allergic (erythromycin, clarithromycin)

215
Q

Which viruses cause tumours?

A

EBV, HHV-8/KSHV, HPV, Hepatitis B and C

216
Q

What are the clinical features of the primary stage of Varicella Zoster virus?

A

Prodrome: fever, pharyngitis, malaise

Itchy painful lesions, appear in crops (macule then papule then vesicle then pustule then crusts)

217
Q

What are some symptoms of prolonged neutropenia?

A

Fevers of unknown cause, gram negative septicaemia, bacterial and fungal pneumonias, reactivation of TB,

218
Q

What are the pathogenic factors of E coli?

A

LPS, iron binding proteins, small antiphagocytic capsule, pili or fimbriae aid adherence to epithelial surfaces, exotoxin production

219
Q

When is CMV clinically significant?

A

In the immunocompetent with mononuclear syndrome, in the immunocompromised: immunoimmature, immunodeficient, immunosuppresseed

220
Q

What are the infections caused by H influenzae?

A

Invasive infections of children under 5: bloodstream infection (meningitis, cellulitis, epiglottitis, pneumonia, septic arthritis) Non invasive infections of all ages: otitis media, sinusitis, conjunctivitis, pneumonia (community acquired, infective COPD)

221
Q

What infections does E coli cause?

A

UTI, diarrhoeal illness, intraabodominal infection, septic shock and blood stream infection (secondary) pneumonia (HCA), neonatal bloodstream infection and meningitis, rarely bone/joint infection; post neurosurgical meningitis

222
Q

What are some congenital T cell defects?

A

DiGeorge’s disease, SCID, enzyme defects

223
Q

Describe Legionella pneumophila

A

Gram negative rod, lives intracellularly in amoebae, causes pneumonia and non specific flu like illness. Transmitted by inhalation of aerosolised contaminated water

224
Q

Give a helical ss (-) RNA non enveloped virus

A

Fliovirus, orthomyxovirus

225
Q

What are intravascular catheters are risk of infection from in neutropenia?

A

Coagulase negative staphylococci, gram negative rods like MRSA, VRE, Candida

226
Q

Give 3 examples of gram negative rods

A

Pseudomonas aeruginosa, legionella, haemophilus influenzae

227
Q

What is the function of enterotoxins?

A

Heat stable, short lived but profuse vomiting and diarrhoea, superantigen activity.

MBBS2 Diseases (7 decks)

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