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Scientific Basis of Clinical Practice > Microbiology > Flashcards

Microbiology Flashcards

1
Q

name the gram positive cocci clusters

A

staphylococcus aureus

staphylococcus epidermidis

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2
Q

where would gram positive cocci cluster be found?

A

skin

nasal

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3
Q

name the gram positive cocci chains

A 
beta-haemolytic streptococci (pharyngitis, tonsilitis)
streptococcus agalactiae
streptococcus oralis
streptococcus pneumoniae
enterococcus faecalis
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4
Q

where would gram positive cocci chains be found?

A

mouth

upper respiratory tract

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5
Q

name the gram positive rods

A 
clostridium difficile
clostridium perfringens
clostridium tetani
lactobacillus acidophilus
bacillus species
listeria monocytogenes
propionibacterium acnes
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6
Q

name the gram negative cocci

A

neisseria gonorrhoea
neisseria meningitidis (bacterial meningitis)
haemophilus influenza

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7
Q

name the gram negative non-enterobacteriaceae rods

A

escheria coli
klebsiella pneumoniae
salmonella enteriditis
proteus mirabilis

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8
Q

name the gram negative enterbacteriaceae rods

A

bacteroides fragilis
campylobacter jejuni
pseudomonas aeruginosa (aquatic environments)

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9
Q

name the non-gram staining acid and alcohol fast bacilli

A

mycobacterium tuberculosis

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10
Q

name the non-gram staining cell wall deficient bacteria

A

mycoplasma pneumoniae
legionella pneumoniae (aquatic, lung)
chlamydia tractomatis

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11
Q

name the non-gram staining spirochaete bacteria

A

treponema pallidum (syphilis)

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12
Q

describe otitis media

A

streptococcus pneumoniae
haemophilus influenza

fever
pain
glue ear

amoxicillin

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13
Q

describe sinusitis

A

streptococcus pneumoniae
haemophilus influenza

facial pain
localised tenderness
fever

amoxicillin if persistent/severe

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14
Q

describe acute epiglotitis

A 
medical emergency
haemophilus influenza (capsular type B)

respiratory obstruction

intubation
cefotaxime
Hib vaccine

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15
Q

describe pharyngitis

A

epstein barr virus - glandular fever
streptococcus pyogenes - strep throat

sort throat
fever
peritonsillar abscess

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16
Q

describe croup/aryngotracheobroncihitis

A

young children
parainfluenza 1 & 2

inspiratory stridor due to laryngeal narrowing

paracetamol
IV fluids
corticosteroids
adrenaline if hospitalised

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17
Q

describe infectious mononucleosis

A

epstein barr virus (herpes family)

babies asymptomatic
fever
sore throat
lymphadenopathy
splenomegaly
hepatitis
lethargy
encephalitis - rare
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18
Q

describe streptococcus pyogenes (scarlet fever)

A

streptococcus pyogenes
anti-streptolysin O titre

pharyngitis
rheumatic fever
rheumatic heart disease
acute glomerulonephritis

penicillin
erythromycin

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19
Q

describe whooping cough

A

brodetella pertussis (gram negative coccobacillus)

catarrhal
paroxysms of cough
lobar collapse
secondary pneumonia

supportive treatment and macrolide (clarithromycin, erythromycin, azithromycin)

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20
Q

describe opportunistic pneumonia

A

pneumocystis jirovecii

immunocompromised
high fatality rate

co-trimoxazole

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21
Q

describe enteric fever salmonella

A

s typhi
s paratyphi

fever
headache
myalgia
malaise
sepsis
1 week, followed by diarrhoea

ciprofloxacin
cefotaxime

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22
Q

describe enterocolitis salmonella

A

salmonella enteritidis

nausea
vomiting
cramps
non-bloody diarrhoea
2-7 days

ciprofloxacin
cefotaxime

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23
Q

describe the taxonomic status of hep B

A

DNA virus

comes from the family hepadnavirus

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24
Q

describe the taxonomic status of hep C

A

flavivirus

related to the flaviviruses that are mosquito-borne; yellow fever

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25
Q

describe the taxonomic status of HIV

A

retrovirus

lentivirus subfamily

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26
Q

what are the modes of transportation of BBVs?

A

penetrative sexual intercourse
blood transmission
vertical (breastfeeding)

if a patient has contracted 1 BBV then they should be tested for others

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27
Q

what is the main transmission mode of HIV?

A

penetrative sexual intercourse

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28
Q

what is the main transmission mode of HCV?

A

contaminated blood; particularly IV drug use

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29
Q

what is the main transmission mode of HBV?

A

vertical; post and perinatal

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30
Q

describe diagnostics

A

which infection
which virus
past/current infection
acute/chronic infection
how long the infection has been present for
infectivity
how much virus is circulating in blood at that time

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31
Q

describe theranostics

A

tests specifically done to guide treatment
monitor treatment
response to treatment
drug resistance
development/disappearance of drug resistance
genotype of HVC; given different treatment

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32
Q

describe HBV

A

discovered in 1970 as a cause of serum hepatitis
infects the hepatocytes
immune system reaction to the presence of the virus
patient immunosuppressed; no immune response and no disease
up to 6 months incubation period

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33
Q

what are the symptoms and signs of HBV?

A

50% asymptomatic
initially; prodromal fever, malaise
chronic; chronic active hepatitis, liver cirrhosis, hepatocellular carcinoma

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34
Q

what is the name of the HBV virus particle?

A

the Dane particle

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35
Q

describe the tolerogen affect of the HBV E antigen

A

E antigen is the soluble form of the core antigen of HBV
it crosses the plasma in pregnancy
allows the foetus immune system to recognise it as a self-antigen; clonal detection of lymphocytes recognising E antigen
the baby recognises HBV important epitopes as being self-antigens, get no immune response and get chronic infection

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36
Q

what factors affect chance of becoming chronic carriers?

A

neonates that are infected at birth by maternal virus; >90% chance
affected >5yrs; 10% chance

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37
Q

what antigens are associated with HBV?

A

HBsAg; grossly over-produced

HBeAg

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38
Q

what factors affect the chance of perinatal transmission?

A

S and E Ag positive; 70-90% of infants infected
S Ag positive only; <10% of infants infected

in the absence of post exposure prophylaxis

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39
Q

what does core antibody hepatitis B and core antibody IgG identify?

A

past or present infection

will always remain positive for hep B core antibody

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40
Q

what does IgM presence indicate in HBV?

A

acute/recent infection

occurred within the last 6 months

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41
Q

what does E antigen indicate in HBV?

A

highly infectious

very active, disease-causing levels of virus

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42
Q

what does anti-hepatitis B surface antigen indicate?

A

this is the antibody to the surface antigen

immunity; natural (infection and recovery), vaccine-induced

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43
Q

what does hepatitis B DNA indicate?

A

determines response to treatment; falls if treatment is working

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44
Q

describe high-grade HBV infections

A

E antigen positive
E antibody negative
high risk of transmission; needle stick injury
33% risk of the individual picking up HBV from the needle stick if unvaccinated
more likely to develop chronic active hepatitis, cirrhosis, hepatocellular carcinoma

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45
Q

describe low-grade HBV infections

A

much lesser risk of transmission; <1% risk via needle stick
less likely to develop clinical effects
E antigen negative
E antibody positive

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46
Q

describe the HBV vaccine

A

genetically modified
recombinant protein expressed in yeast
surface antigen protein
targeted to neonates born to hep B positive women, healthcare workers, dialysis patients, young gay men, contacts of cases within households/relationships
all women are screened for HBV in pregnancy

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47
Q

what is the treatment of HBV?

A

lamivudine; suppression and reduces the amount of virus to a level where it does not cause disease
1st line
interferon; less successful, aims to cure high grade infection

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48
Q

what theranostic tests are used in HBV?

A

lamivudine resistance; sequence the virus genes
most patients treated with lamivudine will become resistant
hepatitis B DNA load; assesses response to lamivudine, rises when the treatment is no longer effective

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49
Q

describe hepatitis C

A

discovered in 1989
principle caused of post-transfusion hepatitis (95%)
key transmission route is blood transmission (including IV)
infects the hepatocytes and causes hepatitis via direct viral effects, killing of cells and the immune reaction

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50
Q

describe the different genotypes of hepatitis C

A

6 genotypes
1; very common in NI, poor response to treatment
3; much easier to treat, responds much better to treatment

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51
Q

how many people are infected with hepatitis B?

A

350 million; 5%

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52
Q

how many people are infected with hepatitis C?

A

170 million; 2.5%

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53
Q

describe the signs and symptoms of acute and chronic HCV

A 
acute; mostly asymptomatic
chronic; 70% develop chronic infection, remain infected for decades/life, 50% develop chronic active hepatitis
cirrhosis
liver failure
hepatocellular carcinoma
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54
Q

describe HCV markers

A 
hep C antibody; past or present infection
hep C (RNA) PCR; current infection
genotype test; determines which genotype of virus by looking at the sequence of the virus
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55
Q

how is current HCV infection diagnosed?

A

antibody positive

PC positive

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56
Q

how is past HCV infection diagnosed?

A

antibody positive

PCR negative

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57
Q

what is the treatment of HCV?

A

interferon and ribavirin
aim of treatment; cure
liver transplantation; last option, hep C recurs in the graft in almost 100% of cases

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58
Q

what theranostic tests are used in HCV?

A

genotype; determine the duration of treatment

hep C RNA by PCR; determines response to treatment

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59
Q

describe HIV

A

discovered in 1983
retrovirus
infects immune cells; CD4-positive, including CD-4 lymphocytes, macrophages
results in immunosuppression, loss of immune function, T-cell function reduction

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60
Q

how many people are infected with HIV?

A

40 million; 0.5%

about 4.3 million people are newly infected each year

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61
Q

what diseases are caused by HIV?

A

primary HIV infection; mild illness that occurs 10-25 days after exposure
glandular fever-like illness with swollen lymph nodes, lymphadenopathy, rash (maculopapular), fever
AIDS; approximately 8 years post-exposure, opportunistic infections, weight loss

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62
Q

what are the key opportunistic infections in AIDS?

A 
CMV; retinitis
JC polyomavirus; encephalopathy
EBV; lymphoma
mycobacteria; TB
toxoplasma; CNS infection
cryptosporidia; blood diarrhoea
candida; oesophageal infection
pneumocystis; pneumonia
cryptococcus; meningitis
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63
Q

describe HIV diagnosis

A

look for HIV antibody; indicates infection
4-assay approach to ensure specificity
viral load; measures the amount of RNA in the blood

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64
Q

what is the treatment of HIV?

A

anti-retroviral therapy (ART)
supression
combination of 2 drugs from 3 classes;
nucleoside reverse transcriptase inhibitors
non-nucleoside reverse transcriptase inhibitors
protease inhibitors
reduction in mother-baby transmission; elective caesarean section, ART to mother and baby, avoiding breastfeeding

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65
Q

what are the theranostic assays used in HIV?

A

HIV load; determines response to treatment
CD4 lymphocyte count; determine when to initiate treatment, sequence viral genes and look for mutations that determine drug resistance

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66
Q

what investigations are performed on a patient with suspected hepatitis?

A 
clotted blood sample
HAV IgM; not BBV, common cause of hepatitis
HBV sAg
hepatitis core antibody (IgG)
HCV antibody
HIV; can get hepatitis in primary infection
HBsAg
HB core antibody
anti-HbsAg
HCV PCR
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67
Q 
interpret these investigation results;
HBsAg negative
HB core antibody (IgG) positive
anti-HbsAg positive
HCV antibody positive
HCV PCR positive
A

past HBV infection

current HCV infection

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68
Q

define gastroenteritis

A

a clinical syndrome characterised by nausea, vomiting and abdominal discomfort

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69
Q

define dysentery

A

when there is blood, mucous and pus in stools
usually associated with abdominal pain
implies that there is a colon inflammation in association with the infection

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70
Q

what are the key agents of bacterial diarrhoea?

A 
campylobacter
salmonella
shigella
E. coli (including VTEC)
vibrio cholerae
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71
Q

what are the pathogenesis and key agents of toxin ingestion?

A 
disease is caused by ingestion of performed toxin in food
clostridium perfringes
bacillus cereus
staphylococcus aureus
clostridium botulinum (neurotoxin)
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72
Q

what is the cause of antibiotic associated diarrhoea?

A

clostridium difficile

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73
Q

what are the viral causes of diarrhoea?

A

norovirus; winter vomiting disease

rotavirus; predominant in children

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74
Q

what are the parasitic causes of diarrhoea?

A

cryptosporidium

giardia lamblia

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75
Q

describe clostridium difficile

A

gram positive rod
sporing
anaerobic
major cause of antibiotic associated diarrhoea, antibiotic associated colitis
present in 3% of the healthy population
antibiotic use triggers the development of illness

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76
Q

describe pseudomembranous colitis

A

most severe form of clostridium difficile infection

pseudomembrane present on the colon surface made of inflammatory cells, fibrin and necrotic gut cells

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77
Q

how is clostridium difficile diagnosed?

A

presence of toxin in faeces; difficult and slow to grow, does not tell you if somebody has a significant infection

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78
Q

how is clostridium difficile treated?

A

isolation
spores survive exposure to alcohol
stop antibiotics if possible
oral metronidazole or oral vancomycin

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79
Q

describe immunocompromised hosts

A

those patients who will more readily get an infection from a common primary pathogen
patients who will get infections with opportunistic pathogens

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80
Q

define a primary pathogen

A

one which commonly causes disease in aa health non-immune host
e.g. staphylococcus aureus, streptococcus pneumoniae

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81
Q

define an opportunistic pathogen

A

an organism which rarely causes disease in a healthy host but may cause serious disease in an immune-compromised individual
e.g. coagulase negative staphylococci, aspergillus

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82
Q

what are the causes of immunity?

A

non-specific; skin/mucosal integrity, mucosal clearing mechanisms, gut defence, complement system, phagocytosis
specific; cell-mediated and humeral (antibody) response

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83
Q

what are the causes of immunocompromise?

A

primar/secondary immunodeficiency diseases
stressed physiological states
iatrogenic input

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84
Q

name some primary immunodeficiencies

A

neutrophil defects; chronic granulomatous disease
humoral; B cell defects
cell-mediated; T cell defects
SCID

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85
Q

name some secondary immunodeficiencies

A 
AIDS
hyposplenism
cancer
diabetes
any severe systemic illness
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86
Q

name some stressed physiological states

A

pregnancy
neonates; especially preterm
elderly
nutritionally deficient

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87
Q

what are the causes of iatrogenic immunodeficiency?

A

drugs; corticosteroids, anti-cancer chemotherapy, immunosuppressive therapy post-transplant
irradiation
invasive devices; IV lines
surgical procedures; splenectomy

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88
Q

how is infection prevented in immunocompromised patients?

A 
avoiding risk activities/locations; hospital
protective isolation
vaccination
antimicrobial prophylaxis
restore underlying defect
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89
Q

how is the spectrum of infecting organism related to the type of illness and how ill the patient becomes?

A

as the CD4 T-cell count falls, the patient becomes susceptible to an increasing range of organisms;
from mycobacterium tuberculosis to pneumocystis, toxoplasmosis and to cytomegalovirus and mycobacterium avium-intracellulare

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90
Q

describe pneumocystis jiroveci/carinii

A

fungi
seen in HIV positive patients
cause pneumocystis pneumonia
diagnosed by direct microscopy following silver staining or immunofluorescence or by a polymerase chain reaction

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91
Q

what are the signs and symptoms of pneumocystis pneumonia (PCP) in HIV?

A 
non productive cough
dyspnoea
fever
perihilar infiltration
may progress to severe respiratory disease
extra pulmonary infection
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92
Q

what is the treatment of pneumocystis pneumonia (PCP) in HIV?

A

high dose cotrimoxazole
supportive therapy
ICU usually required

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93
Q

describe toxoplasma gondii in healthy patients

A

protozoal infections
usually asymptomatic or glandular fever-like illness
50% affected by middle age
zoonosis; from cats

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94
Q

describe toxoplasma gondii in HIV patients

A

cerebral toxoplasmosis
neurological symptoms; seizures, depressed consciousness
main cause of focal CNS lesions
ring enhancement on CT brain
may present as pneumonitis or chorioretinitis

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95
Q

how are infections prevented in HIV positive patients?

A

highly active antiretroviral therapy; boost CD4 count

antibiotic prophylaxis; prevent some classical opportunistic infections

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96
Q

what antibiotics are offered for which opportunistic infection?

A

cotrimoxazole; pneumocystis
rifabutin; mycobacterium avium intracellulare (MAI)
ganciclovir; cytomegalovirus

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97
Q

describe the causes and diagnosis of neutropenia

A

chemotherapy
bone marrow transplant
aplastic anaemia
high dose beta lactams

fever; cardinal sign
no pus/localisation

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98
Q

describe neutropenia

A

usually susceptible to most typical bacteria; pseudomonas, staphylococcus aureus, fungi
occurs after a number of days of therapy beginning
maximum risk; when neutrophils >0.1

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99
Q

describe cellular immune dysfunction

A

principally affects T cells

more susceptible to mycobacteria, legionella, listeria and viruses

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100
Q

what are the key opportunistic fungi associated with neutropenic patients?

A

aspergillus; mould, causes lung infection and may cause a brain infection is disseminates, difficult culture, high mortality
candida; yeast, easier to diagnose, high mortality

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101
Q

what are the risk factors for becoming infected with Candida albicans?

A

central lines
parenteral nutrition
broad-spectrum antibiotics
gut abnormalities; perforation, mucositis

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102
Q

what is the treatment of sepsis in neutropenia?

A

immediately commence a broad-spectrum bactericidal antibiotic combination; anti-pseudomona penicillin and an aminoglycoside (piperacillin and gentamicin)
fails; add in a glycopeptide (vancomycin or teicoplanin)
fails after 48hrs; anti fungal (in case aspergillus or candida are the pathogens)
support; oxygen, respiratory support, fluids

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103
Q

what is the treatment/prevention of infection in burns patients?

A

prophylaxis; silver sulphadiazine
excision of the necrotic area of burn
systemic agents; target organisms in the blood and deep tissue
topical agents; blood will often not adequately perfuse the dead tissue associated with burn injuries

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104
Q

what are the infection risks in those with a splenectomy?

A

particularly susceptible to capsulate bacteria; pneumococcus, haemophilus

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105
Q

what is the treatment/prevention of infection in those with a splenectomy?

A

vaccination; before or after surgery

long-term prophylactic antibiotics; targeted towards preventing pneumococcal infection (penicillin)

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106
Q

what are the infections risks in pregnancy?

A

ascending UTI; more common, may precipitate premature labour

listeria; common, can be devastating

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107
Q

what is the treatment/prevention of infection in pregnancy?

A

avoid high risk foods; soft cheese, pates

ampicillin and gentamicin; ampicillin added to the cephalosporin when treating meningitis in pregnant ladies

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108
Q

what organisms are associated with skin and soft-tissue infections?

A

staphylococcus aureus
beta-haemolytic streptococci
particularly group A streptococci; streptococcus pyogenes

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109
Q

what is the difference between staphylococci?

A

staphylococcus aureus; coagulase positive, pathogenic

all others; coagulase negative, less pathogenic

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110
Q

how does staphylococcus aureus cause infection?

A

produces adhesions which mediate attachment to cell receptors or to host connective tissue
produce enzymes; coagulase (activates fibrinogen), hyaluronidase (lyses fibrin clots)
produces Toxic Shock Syndrome Toxin One

111
Q

what is the most common bacterial cause of haemolytic uraemic syndrome?

A

E. coli

not the bacteria itself but the shiga toxin

112
Q

what are the commonest organisms associated with skin and soft tissue infections?

A

staphylococcus aureus

beta haemolytic streptococci; particularly group A streptococci (streptococcus pyogenes)

113
Q

what is the differentiating feature between staph aureus and other staphylococci?

A

coagulase positive

114
Q

what are the virulence factors of staph aureus?

A

production of adhesions which mediate attachment to cell receptors or host connective tissue
elaborates toxic shock syndrome toxin one, enterotoxin responsible for food poisoning, exfoliating toxin in neonates
coagulase; fibrinogen activation, important in abscess formation
hyaluronidase; lyses fibrin clots, assists in infection spread

115
Q

what are the carriage sites of staph aureus?

A

anterior nares
axilla
groin

116
Q

what are the virulence factors of strep pyogenes?

A

extracellular capsule is similar to host CT; evades host immune system
M proteins resist phagocytosis
streptokinase and hyaluronidase help spread infection
elaborates toxins; pyrogenic toxin, seen in necrotising fasciitis

117
Q

what is used to clinical detect the presence of a previous/recent streptococcal infection?

A

streptolysin O antibodies

118
Q

what are the non-suppurative sequelae of strep pyogenes?

A 
rheumatic fever
glomerulonephritis
relate to the organisms molecular mimicry
arise 1-3 weeks post-infection
immunologically mediated
119
Q

describe impetigo

A

common superficial skin condition
numerous vesicles which become pustular before breaking down to form thick golden crusts
more common in young children 2-5yrs
common in humid conditions; summer
highly infectious
may be caused by staph aureus or strep pyogenes

120
Q

what are the complications and treatment of impetigo?

A

post-streptococcal glomerulonephritis

limited number of lesions; topical, fusidic acid or mupirocin
more extensive lesions; systemic or oral flucloxacillin
personal hygiene
infection control; do not share towels, school exclusion

121
Q

define folliculitis

A

infection of the hair follicle
can occur anywhere on hairy skin
superficial infection
pus is found only in the epidermis

122
Q

define furuncles/boils

A

extend into the dermis
greater degree of inflammation
inflammatory nodule is frequently present with the overlying pustule
often with a hair emerging

123
Q

define carbuncles

A 
coalescence of multiple adjacent boils
forma large inflammatory mass
typically in the back of the neck
multiple senses can be seen discharging
more uncommon
associated with underlying predisposition
124
Q

what is the treatment of carbuncles?

A

incision and drainage
eradication of carriage from anterior nares using topical mupirocin may alleviate the condition
antibiotics are usually unnecessary

125
Q

what are the causes of folliculitis, furuncles and carbuncles?

A

staphylococcus aureus

underlying problem; diabetes in recurrent boils

126
Q

describe erysipelas

A

a form of cellulitis affecting the most superficial layers of the skin
cause; streptococcus pyogenes

127
Q

what are the symptoms and signs of erysipelas?

A

lesions that are raised above the level of the surrounding skin
abrupt onset
fever
chills
malaise
red hot and swollen skin
very clear line of demarcation
advancing edge can move as the disease progresses
common in infants and elderly
usually affects the lower limb (70%) or face (10%)

128
Q

what is the treatment of erysipelas?

A

penicillin

oral/IV depending on severity of the illness

129
Q

define cellulitis

A

acute spreading pyodermic inflammation of the dermis and subcutaneous tissue

130
Q

what are the symptoms and signs of cellulitis?

A

preceded by systemic malaise or flu-like symptoms
can affect any area of the skin; typically the lower limb
unilateral
advancing edge is diffuse
red hot and swollen skin
dimpled
may resemble the skin of an orange; peau d’orange

131
Q

what are the risk factors and causes of cellulitis?

A 
obesity
venous insufficiency
lymphoedema
trauma
athletes foot; inter-toe maceration
diabetes

mostly; staph aureus, strep pyogenes
aeromonas hydrophila; contact with fresh water

132
Q

what is the management of cellulitis?

A

culture any skin breaches
broad cultures if severe

mild; oral flucloxacillin (covers staph and strep)
moderate-severe; IV flucloxacillin +/- benzylpenicillin
allergic; clindamycin

133
Q

what are the common and occasional organisms associated with bites?

A

pasteurella multocida; dogs, cats
anaerobes; dogs, cats, humans
eikenella corrodens; humans

capnocytophaga canimorsis; dogs

134
Q

what is the management of bites?

A

prophylactic antibodies for high-risk wounds and patients; those more likely to succumb to complications (diabetics, asplenics, immunocompromised)
co-amoxiclav
penicillin allergic; ciprofloxacin and clindamycin

135
Q

describe surgical wound infections

A

depend on the type of surgery
staph aureus is the most common cause
contaminated/dirty wounds; coliform streps, anaerobes
prevention; strict adherence to infection control and prophylaxis

136
Q

what investigations are required to diagnose a surgical wound infection?

A

pus sample rather than swab sample
blood cultures; systemically unwell, pyrexia
clinical signs; pain, swelling, redness, purulent drainage, take time to incubate (up to 5 days after)
immediate post-op fever; consider a different cause

137
Q

describe the cause and management of clean surgery

A

staph aureus

flucloxacillin

138
Q

describe the cause and management of contaminated surgery

A

staph, strep, coliforms, co-amoxiclav

broader spectrum antibiotic; cefuroxime and metronidazole

139
Q

what are the features of arterial ulcers?

A 
reduction in peripheral pulses
reduction in ABPI
intermittent claudication
hairless, shiny skin
well defined border
140
Q

what is the management of arterial ulcers?

A

revascularisation; by-pass grafting, angioplasty

141
Q

what are the features of venous ulcers?

A

usually superior to medial malleolus
haemosiderin deposits
oedema

142
Q

what is the management of venous ulcers?

A

compression therapy

143
Q

describe pressure ulcers

A

occur over areas of bony prominence

144
Q

describe diabetic foot ulcers

A

usually on the plantar surface
associated with (diabetic) neuropathy
the leading cause of non-traumatic amputations

145
Q

what are the signs of infection?

A 
pain
redness
purulent exudate
delayed healing
poor quality granulation tissue
new/increased odour
local cellulitis
146
Q

what are the rules for sampling chronic infections?

A

swab after cleansing/removing slough and before antiseptics/antibiotics
tissue biopsy>swab
only sample when there are clinical signs of infection
positive swab result from a chronic wound is not a directive to treat

147
Q

what is the management of chronic wounds?

A

debridement; surgical, chemical, larvae
local antiseptics; cadexomer, silver products
complex dressings; keep wound bed moist, control exudate
antibiotics; systemic infection, failure of local measures
treat cause

148
Q

describe mild, moderate and severe foot ulcers

A

mild; <2cm radius of cellulitis
moderate; >2cm radius, deep infection
severe; deep infection, systemic sepsis

149
Q

define necrotising fasciitis

A

rare, life-threatening, rapidly progressive subcutaneous infection which tracks along the fascial planes
associated with toxin production, tissue necrosis, accumulation of gas in the tissues

150
Q

describe polymicrobial necrotising fasciitis

A

usually after trauma or surgery; particularly bowel
fournier’s gangrene; form of PNF that occurs in the uro/anogenital region following surgery or infection
causes; staph, strep, aerobic gram -, coliforms, anaerobes

151
Q

describe group A streptococcal necrotising fasciitis

A

may be mono-microbial, involving only group A strep
flesh-eating bacterial infection
may arise in previously fit and healthy individuals
causes; relatively minor trauma, cut, laceration, blunt trauma

152
Q

describe clostridium myonecrosis/gas gangrene

A

most commonly cause by clostridium perfringens

153
Q

what are the symptoms and signs of necrotising fasciitis?

A

pain out of keeping with the clinical finding
skin necrosis
ecchymosis
crepitus in the tissue
late symptoms; confusion, hypotension
diagnosis confirmation; surgical exploration

154
Q

what is the treatment of necrotising fasciitis?

A

surgical emergencies
aggressive and repetitive debridement
intensive care support
antibiotics; benzylpenicillin (strep), ciprofloxacin (aerobic gram -, coliforms), clindamycin (staph, strep, anaerobes, reduce/prevent toxin formation)

155
Q

describe dermatophyte infections

A

infection with a ringworm fungus

tinea barbae, capitis, corporis, pedis (athletes foot)

156
Q

what are the causes of dermatophyte infections?

A 
trichophyton
microsporum
epidermophyton
frequently zoonotic
human-human spread; shared towels, hair brushes, direct contact
157
Q

describe the diagnosis of dermatophyte infections

A

clinical appearance
microbiological confirmation
woods light; tinea capitis

158
Q

describe the treatment of dermatophyte infections

A

topical imidazoles
resistant; oral terbinafine
2-4 weeks
repeated treatment often necessary

159
Q

what are the risk factors for MRSA infection?

A 
elderly
repeated hospitalisation
prolonged stay in hospital
those in long-term care facilities, residential homes, nursing homes
in close proximity to those with MRSA
surgical wound
IV device; venflon, catheter
some classes of antibiotics; quinolones, cephalosporins
160
Q

what is the treatment of MRSA infection?

A

mild; tetracyclines, trimethoprim, fusidic acid, rifampicin
severe; glycopeptides, vancomycin, teicoplanin, rifampicin, fucidin
new antibiotics; linezolid, daptomycin, tigecycline

161
Q

describe community associated MRSA

A

no known risk factors
frequently produces a toxin; panton-valentin leukocidin
associated with skin and respiratory infection
commonly spread by skin-skin contact
sensitive to a much wider range of antibiotics

162
Q

describe meningitis

A

infection in the subarachnoid space
inflammation of the leptomeninges
a medical emergency
require lumbar puncture

163
Q

what are the clinical features of meningitis

A 
headache
neck stiffness
photophobia
fever
irritability
vomiting
purpura
non-blanching rash
infants; less specific, not feeding well, Hugh pitched cry, bulging fontanelle
164
Q

describe the CSF findings in viral meningitis

A

high lymphocytes and protein
normal neutrophils
nothing identified on gram stain

165
Q

describe the CSF findings in bacterial meningitis

A

high neutrophils and protein
low glucose
gram stain may show causative organism

166
Q

describe the CSF findings in TB meningitis

A 
high WCC; predominantly lymphocytes
slightly high neutrophils
very low glucose
high protein
gram stain negative
ziehl neelsen stain for TB may be positive
167
Q

describe the pathophysiology of bacterial meningitis

A

nasopharyngeal area becomes colonised with bacteria
bacteraemia in the bloodstream or local invasion
progresses to meningitis
neisseria meningitidis; intracellular infection
haemophilus influenzae; inter-cellular infection
can evade complement attack with a polysaccharide capsule
CSF; no immunoglobulin or complement
bacteria grow in the CSF

168
Q

describe the breakdown of the blood brain barrier

A 
bacterial replication
release of IL2, IL6, TNF
polymorphs are attracted to site of infection
endothelial disruption
albumin leak
increased cerebral blood flow
cerebral oedema
169
Q

describe meningitis in infants

A

most commonly group B strep, E. coli, listeria

very small infants acquired the infection from organisms that colonise the maternal vagina

170
Q

describe meningitis in toddles

A

NHS bacteria;
neisseria meningitidis
strep pneumoniae
haemophilus influenzae (less common because of theHiB vaccine)

171
Q

describe meningitis in >4yrs and adults

A

neisseria meningitidis

strep pneumoniae

172
Q

describe strep pneumoniae

A

affects the extremes of age
seeing more penicillin resistance
gram positive streptococcus
seen on blood agar; zone of green haemolysis around them
can cause meningitis, pneumonia and septicaemia

173
Q

describe haemophilus influenzae

A

affects young children
may be resistant to penicillins
requires factors V and X to grow on nutrient media
grows best on chocolate
smells like semen
invasive strains are often capsulated
may cause pneumonia, meningitis, epiglottitis

174
Q

describe neisseria meningitidis

A

affects children and young adults
always penicillin sensitive
sensitive to the 2nd and 3rd generation cephalosporins
gram negative diplococcus
oxidase positive
identified by sugar fermentation with maltose and glucose

175
Q

what is the treatment of meningitis?

A

infant; ampicillin and cefotaxime
toddlers; ceftriaxone,
>4yrs to adults; ceftriaxone
immunotherapy; dexmethasone, given at the same time as the antibiotic, reduces the risk of cerebral oedema, reduces the long-term risk of deafness and neurological improvement

176
Q

describe the prevention methods for meningitis

A

HiB vaccine; haemophilus influenzae
meningococcal type C vaccine; decrease in meningococcal meningitis due to group C disease
meningococcal polysaccharide vaccine; covers type A and C neisseria

prophylaxis; rest of the family
HiB vaccine; all kissing and living contacts
inform the consultant in communicable disease control

177
Q

what are the causes of viral meningitis?

A 
enterovirus; 80%
HSV 1 and 2
varicella
cytomegalovirus
mumps
adenovirus
HIV

more common than bacterial meningitis
good prognosis

178
Q

describe enteroviral meningitis

A

causes 80% of viral meningitis
70 different serotypes of enteroviruses; including coxsackieviruses, echoviruses, enteroviruses
broad range of infections; URTI, conjunctivitis, pharyngitis, pneumonia, myocarditis, gastroenteritis, neurological disease
presentation; mild meningeal irritation (stiff neck), mild photophobia (severe encephalitis)

179
Q

what is the treatment of viral meningitis?

A

supportive
acyclovir; HSV, treatment not proven
vaccine; mumps, measles

180
Q

what are the non-viral causes of aseptic meningitis?

A 
fungi
TB
syphilis
brucella
mycoplasma
parameningeal infection; brain abscess, protozoa, helminths

nothing grown in the lab and nothing identified by PCR initially

181
Q

what questions should be asked in a CNS infection history?

A 
travel; epidemics
work
sexual history
contacts
animal contact
vaccination history
history regarding symptoms which are not CNS symptoms
182
Q

describe TB meningitis

A

insidious illness
usually affects those <6yrs
usually occurs 3-6 months after initial TB infection/exposure
50% of children will have evidence of TB elsewhere; lungs, liver

183
Q

what are the clinical features of TB meningitis?

A 
personality change
irritability
unexplained temperature
drowsiness
neck stiffness
cranial nerve palsies
cranial nerve involvement
decreased level of consciousness
184
Q

describe the investigations required for a diagnosis of TB meningitis

A 
positive tuberculin
positive Mantoux test
FHx of TB in recent months
lumbar puncture; CSF often looks, clear, may be under pressure
gastric washings
185
Q

what is the treatment of TB meningitis?

A 
4 drugs;
rifampicin
pyrazinamide
ethambutol
aminoglycoside 
after 2 months; treatment rationalised to rifampicin and isoniazid which continue for up to a year
186
Q

what are the bugs which would only cause infection in an immunocompromised host?

A

listeria monocytogenes; found in raw milk, soft cheeses

cryptococcus; yeast

187
Q

what are the viral causes of encephalitis?

A 
majority of cases are caused by viruses;
HSV 1; most common cause
arboviruses; region specific
Hendra and nipah viruses
Japanese B
rabies
enteroviruses
influenzae A
VZV
188
Q

what are the non-viral causes of encephalitis?

A 
neisseria monocytogenes
listeria
scrub typhus
leptopsirosis
melioidosis
malaria
TB
borrelia
brucella
189
Q

what is the management and investigations required to diagnose encephalitis?

A

high dose acyclovir and antibiotics; before samples return from the lab

CSF, throat, stool samples; sent to the lab for bacteriology, virology, PCR
neural imaging
EEG

190
Q

describe herpes simplex encephalitis

A

most common cause of encephalitis
long term sequelae; occur in 50%, 80% untreated, significant mortality
associated with reactivation or primary infection

191
Q

describe the clinical presentation of herpes simplex encephalitis

A 
headache
fever
decreased LOC
confusion
dysphagia
192
Q

what is the treatment of herpes simplex encephalitis?

A

acyclovir 14-21 days

193
Q

what are the CNS complications of measles infection?

A

post infectious encephalitis (PIE); 1/1000, autoimmune response
measles inclusion body encephalitis (MIBE); in immunocompromised patients, 1-6 months after measles exposure, fatal
subacute sclerosing panencephlaitis (SSPE); 1/250,000, most commonly in children infected <2yrs, progressive neurodegenerative condition, no cure, fatal

194
Q

describe demyelinating encephalopathies

A

all naturally-occurring demyelinating disease are viral
subacute sclerosing pan encephalitis (SSPE)
measles inclusion body encephalitis (MIBE)
measles
progressive multifocal encephalopathies; JC virus, most common in immunosuppressed
rubella encephalitis

195
Q

describe the slide features of progressive multifocal encephalopathy

A

characteristic demyelination

oligodendrocytes affected

196
Q

what are the clinical features of a brain abscess?

A 
persistent headache; often localised
drowsiness
confusion
stupor
general/focal seizures; depend on where the brain abscess is
nausea and vomiting
facial motor or sensory neural impairment; gives an indication as to where the abscess is
papilloedema
ataxia
197
Q

describe the pathophysiology of a brain abscess?

A

causative organisms often linked to the source of infection
45-50%; contiguous suppurative focus, otitis media, infection crossing into the CNS
10%; associated with trauma
25%; haematogenous spread from a distant focus

198
Q

what are the causative organisms of a brain abscess?

A

large number are polymicrobial
source of infection gives an indication of the causative organism

staph aureus
streptococci
bacteroides
fusobacterium
enterobacteriae
pseudomonas
other anaerobes
haemophilus influenzae
strep pneumoniae
neisseria meningitidis
mycobacterium
fungi
protozoa
toxoplasma
199
Q

what is the treatment of a brain abscess?

A

Hx; find the causative organism
treating blindly; penicillin G, cefotaxime, ceftriaxone (streptococci)
metronidazole; penicillin resistant anaerobes (gram negative bacilli)
vancomycin; suspected staph aureus, following neurosurgery or trauma
cefepime, ceftazidime; pseudomonas aeruginoas suspected
HIV infection; consider toxoplasma

200
Q

describe prion diseases

A

transmissible spongiform encephalopathies
both human and animal forms of the diseases
aberrant protein folding
no treatment
invariably fatal
cause neurodegeneration

201
Q

describe the different types of prion diseases

A

sporadic CJD; dementia, ataxia, myoclonus
diagnosis made on the detection of 14-3-3 protein in CSF
familial TSE; autosomal dominant
familial CJD
GSSS
FFI
kuru

202
Q

describe bovine spongiform encephalopathy

A 
new variant CJD
usually occurs in younger patients
60%; psychiatric problems initially
50%; 14-3-3 and tau protein in CSF
MRI; high T2 signal in the post thalamus
203
Q

define a fever/pyrexia of unknown origin (F/PUO)

A

a fever 38.3 or greater for at least 3 weeks with no identified cause after 3 days of hospital evaluation or 3 outpatient visits

not necessarily due to infection; neoplasms, CT disease

204
Q

describe the non-classical PUOs

A

nosocomial PUO; >38.3, several times, hospitalised
neutropenic PUO; >38.3, several occasions, neutrophil count <500
HIV-associated PU; >38.3, HIV positive

do not require a fever for 3 weeks
these patients can progress very rapidly; pace of investigations needs to be faster
empiric treatment is more likely to be justified

205
Q

describe the history required in PUO

A

travel; where, what activities, exposures
malaria prophylaxis where relevant
vaccinations against potential travel-acquired infections
hobbies
work; animal or environment contact
FHx; familial fevers, chronic infection (particularly TB)

206
Q

describe the investigations performed in PUO

A

blood cultures; always done in febrile patients, 3 sets
blood tests; FBC, ESR, CRP, U&E, LFTs, bone p
HIV testing
basic culture; urine, MSSU, sputum
CXR

further investigations based on history, exam and findings;
echocardiography
US abdomen
CT/MRI spine
bone marrow biopsy
culture and histology sample of lesions
207
Q

what is the management of PUO?

A

specific aetiology; specific targeted therapy
no specific aetiology; watch and wait approach if the patient is clinically stable
clinically unstable; empiric antibiotics
NSAIDs; treatment trial, sometimes useful without a clear diagnosis, empirical use discouraged

208
Q

what are the clinical features of lower tract respiratory infections?

A

cough; cardinal symptom, new cough, change in pre-existing cough
sputum; mucoid, purulent, clear
haemoptysis
dyspnoea; at rest, on exertion
wheeze; inspiratory, expiratory
chest pain; stabbing, worse on inspiration, clinical sign of lobar pneumonia
fever
confusion
systemic signs; consistent with SIRS of the body to any insult
sort throat
coryza; runny nose, can be a sign of L or URTI

209
Q

what are the main types of LRTI?

A

90%;
COPD
non-pneumonic LRTI
CAP

paediatric or hospital AP
CAP in those significantly immunosuppressed (HIV, AIDs, cancer)
bronchiectasis
cystic fibrosis

210
Q

describe COPD

A

occurs in patients with a pre-existing lung condition
long history of structural disease
often have a cough and sputum production when well

211
Q

define an exacerbation of COPD

A

2/3 of the Anthonisen criteria;
increased dyspnoea
increased sputum production
increased sputum volume

212
Q

describe community acquired pneumonia in primary care

A

at least two symptoms of an acute lower respiratory tract infection
cough is the cardinal symptom, plus one other LRTI symptom
there should be at least one systemic feature of LRTI; >38.3, muscle aches, malaise, shivering, sweating
new focal chest signs on auscultation
no other explanation

213
Q

describe community acquired pneumonia in secondary care

A

symptoms and signs of LRTI
new x-ray shadowing for which there is no other explanation
primary reason for patient’s admission
should be managed as pneumonia

214
Q

what are the causes of CAP?

A

streptococcus pneumoniae
chlamydia pneumoniae
chlamydia psittacosis
mycoplasma pneumoniae
legionella; not common, cause a large amount of mortality
tuberculosis; particularly from the Indian subcontinent, elderly, contact, FHx, cough >3 weeks

215
Q

describe non-pneumonic respiratory tract infections

A

previously referred to as acute bronchitis
a lower respiratory tract infection that is caused by viral pathogens or atypical pathogens
clinical diagnosis in a young, previously well patient with no other co-morbidities
can occur in others but cannot be diagnosed in primary care and is unsafe; diagnose CAP

216
Q

what is the difference between pneumonia and acute bronchitis?

A 
<38
HR <100
RR <24
no focal signs of consolidation on CXR
; pneumonia is very unlikely
217
Q

what are the features of non-pneumonic LRTI?

A

normal; temperature, HR, BP
no confusion
no comorbidity
<50yrs

218
Q

how do you know when to admit a patient with CAP to hospital?

A 
CRB 65
C; confusion
R; RR>30
B; SBP<90, DBP<60
age >65

0; home treated very safe
1-2; consider hospital referral
3-4; hospital admission urgently

includes urea >7mmol/L in secondary care

219
Q

what investigations should be performed in CAP?

A

sputum sample; gram stain, culture
blood culture
blood tests; WCC, PLT, CRP, urinary antigens
legionella pneumophila serogroup-1 antigen
pneumococcal antigen
serological tests; atypical agents, legionella

220
Q

what is the treatment of CAP?

A

antibiotics;
after sending microbiological samples
within 4 hours; improves 30 day mortality

221
Q

what is the treatment of non-severe CAP (at home)?

A

oral amino penicillin; amoxicillin 0.5-1g TDS, ampicillin 0.5-1g QID
or
oral macrolide; erythromycin 500mg QID, clarithromycin 500mg BD

222
Q

what is the treatment of non-severe CAP (in hospital)?

A

aminopenicillin; amoxicillin or ampicillin
plus
macrolide; clarithromycin or erythromycin
alternative; respiratory quinolone, moxifloxacin or levofloxacin

IV if vomiting;
penicillin; benzylpenicillin, amoxicillin, ampicillin
plus
macrolide; clarithromycin
alternative; levofloxacin
223
Q

what is the treatment of severe CAP (hospital/ICU)?

A

combination of a beta-lactam and a macrolide
beta-lactam; cephalosporin (discouraged), cefuroxime, cefotaxime, co-amoxiclav (augmentin)

2nd line; combination of benzylpenicillin and levofloxacin
only used when there is a high incidence of c. diff and you want to avoid that

224
Q

describe the pathophysiology of TB infection

A

infection requires prolonged close contact
>90% of those infected have no symptoms; latent tuberculosis infection
may cause active infection of any body system
can resemble any infectious/non-infectious pathology

should be considered in the differential of any CAP or chronic cough >3 weeks

225
Q

describe chronic pneumonia

A

most common form of TB

may present following an acute-on-chronic deterioration

226
Q

what are the symptoms and signs of TB?

A 
fever
night sweats
weight loss
raised temperature
cough
chest pain
dyspnoea
CXR; upper lobe consolidation, cavitation
higher lymphadenopathy
calcified lymph nodes
Mantoux test; positive test has a diagnostic odds ratio of ~13
227
Q

what are the risk factors for developing TB?

A

a personal, family or other contact history of TB
living or working in areas with endemic TB; Africa, India, Portugal, Estonia, inner London, HSC, prisons
immunosuppression

228
Q

what investigations are required to diagnose TB?

A

direct microscopy; poor sensitivity, shows infectiousness
culture; definitive diagnosis, full range of sensitivities, very slow
PCR; low sensitivity, fast
interferon gamma release assays; more sensitive in latent infection, do not react with previous BCG
histopathology; caseous necrosis epitheloid cells, multi-nucleated giant cells, calcification, acid-fast bacilli

229
Q

what is the treatment of TB?

A

6 months; isoniazid and rifampicin
supplemented in the 1st 2 months with pyrazinamide and ethambutol
full adherence required to avoid resistance and failure

230
Q

how is TB preventioned?

A

raising living standard
rapid diagnosis and fully adherent case treatment
notification, contact tracing and treatment
isolation in hospitalisation
controversial BCG vaccines
control of bovine TB by milk pasteurisation

231
Q

define antibiotics

A

molecules which will kill or inhibit the growth of microorganisms at very low concentration

232
Q

how do antibiotics not harm the patient?

A

selective toxicity; will block or inhibit an essential metabolic pathway in the microorganism which is absent or sufficiently different in mammalian cells

233
Q

what are the modes of action of antibiotics?

A

blocking synthesis of the bacterial cell wall
inhibition of protein synthesis; inhibition of mRNA translocation
disruption of bacterial DNA
blockade of folate metabolism

234
Q

describe antibiotics that block the synthesis of the bacterial cell wall

A

increased osmotic pressure, burst open and die
beta lactams; penicillins, cephalosporins, carbapenems
glycopeptides; vancomycin, teicoplanin

235
Q

describe antibiotics that inhibit protein synthesis

A 
all attack the bacterial ribosome
macrolides; erythromycin, clarithromycin
fusidic acid
tetracyclines; doxycycline
aminoglycosides; gentamicin
236
Q

describe antibiotics that disrupt the bacterial DNA

A

inhibits the enzyme that allows DNA supercoiling
destroy the bacterial DNA
fluoroquinolones; ciprofloxacin

237
Q

describe antibiotics that cause a blockade of folate metabolism

A

sulphonamides

trimethoprim; very widely used for UTI treatment

238
Q

describe microbiological/ecological toxicity

A

antibiotic administration upsets the natural balance of our normal bacterial flora in our GI tract and our body surface
nausea and vomiting
diarrhoea; pseudo-membranous colitis, c. diff takeover (superinfection)

239
Q

describe pharmacological toxicity

A

manifests as an allergy
can cause renal or liver toxicity
can interact with other drugs; warfarin and aminophylline
neurological toxicity; ciprofloxacin
visual damage; linezolid
bone marrow suppression; linezolid, sulphonamides

240
Q

describe intrinsic resistance

A

the antibiotic does not have any effect on a particular species of organism
no binding site for it to hang on to
cannot enter the bacterial cell
antibacterial/antimicrobial spectrum of the drug

241
Q

describe antibiotic resistance acquisition

A 
bacteria can acquire resistance genes from a variety of sources; other bacteria, very effective
mutation and darwinian evolution
reduced permeability to drugs
modification of a drug binding site
bypass folate metabolism pathway
produce enzymes that destroy the drug
kick the drug out of the cell; efflux
242
Q

describe the antibiotic consumption thresholds

A

1; where resistant bacteria start to emerge as a larger proportion of the total population
2; sensitive bacteria are almost completely eradicated

243
Q

what are the consequences of the antibiotic consumption thresholds?

A

a sharp rise in the prevalence of resistance

once resistance becomes totally established, reducing antibiotic consumption may not bring back the susceptible strains

244
Q

describe linked resistance

A

resistance can be transferred

prescribing drug A can increase resistance to drugs B and C

245
Q

how can we stop the promotion of resistance?

A

reduce precautionary prescribing
avoid prescribing for those with viral infections
avoid under-prescribing
avoid long treatment courses
use only agents which are active against the microbes we are trying to treat
learn to tell the difference between colonisation and infection

246
Q

what are he uses of antibiotics?

A

life-saving therapy; TB, endocarditis
reduced morbidity/mortality; pneumonia
safer surgery; intra abdominal prosthetic implant surgery; hip replacement
immunosuppression survival; leukaemia
rapid resolution of minor infections
avoidance of complications of minor infections

247
Q

describe an emerging infection

A

a newly evolved organism of pathogen
a pathogen that has been around a long time but has just been recognised
infectious agents that appear in a new niche; IV drug users
a recognised virus that has jumped species
animal-humans, with human-human spread
re-emergence
an infection that is new to a region or country

248
Q

what current events encourage emerging infections?

A

global warming
changes in agriculture and irrigation; mosquitoes
urbanisation
social changes; travel
medical intervention; immunosuppression
advent of a big population of IV drug users

249
Q

describe legionella pneumophila

A

gram negative bacillus
can survive in relatively warm conditions within an air-conditioning unit
spread through droplets and inhaled by individuals
causes legionnaires disease
this causes pneumonia particularly in the elderly or debilitated
clinical presentation is relatively indistinct/hard to distinguish from other causes of pneumonia
key assay; urinary antigen test that detects parts of the bacteria (serogroup 1 antigen)
serology tests for antibody
culture from respiratory samples

250
Q

describe E. coli 0157

A 
causes very severe disease
effects on the blood and kidneys
causes a haemolytic uraemia syndrome
relatively high death rate
relatively common in bovine gut
can contaminate raw meat readily at slaughter or subsequent processing
investigations; faecal culture
251
Q

describe coxiella burnettii

A

gram negative proteobacteria
causes Q fever; pneumonia, headache, mild pyrexia-like illness
very variable severity of disease
usually zoonosis; caught from animal placentas

252
Q

describe extended-spectrum-betalactamase producers (ESBL)

A

coliform organisms that are resistance to 3rd generation cephalosporins
large problem in intensive units; lots of antibiotics used
can be a big problem with patient-patient spread

253
Q

describe vancomycin resistance enterococcus (VRE)

A

particularly a problem in specialist units; renal

can cause severe infection in those who are immunocompromised

254
Q

describe healthcare associated infections

A

c. diff; causes enteric infection with diarrhoea, can be severe
norovirus; causes winter vomiting disease, causes outbreaks of vomiting and diarrhoea, seen both in hospitals and nursing homes

255
Q

describe seasonal influenza

A

influenza type A or B
happens every year
similar but more severe to those of the common cold
sudden high fever, headache and fatigue
complications; bacterial pneumonia (can be serious and even fatal)
greater risk of complications in certain individuals; infants, pregnant women, elderly, those with a variety of chronic health problems

256
Q

describe avian influenza

A

influenza type A
a disease of birds; zoonotic
caused by a variety of influenza viruses
severity of disease related to the virus subtype
human transmission occurs when there is extremely close contact with poultry and other birds
particularly rare
human transmission depends on strain

257
Q

describe pandemic influenza

A

high mortality due to the new emergence of an influenza strain

258
Q

describe the influenza virus

A 
an enveloped virus with a lipid envelope
relatively fragile
in an RNA virus
influenza A; birds and humans, currently H3N2, H1N1, H1N2
influenza B; exclusively human infection
259
Q

describe the nucleocapsid of influenza

A

segmented RNA genome

neuraminidase (N) and haemagglutinin (H) on the outside of the envelope of the virus

260
Q

describe antigenic drift in relation to influenza

A

the slow accumulation of mutations in the H protein that causes the virus to change throughout the influenza season from year to year
slow, stepwise change

261
Q

describe antigenic shift

A

very rare
complete change of the H protein
changes into a completely different protein, to which there is no prior immunity
usually associated with the advents of a pandemic

262
Q

describe genetic reassortment of viruses

A

the combination of 2 viruses to produce a virus that has components from 2 different viruses
con-infection of an individual cell
new virus emerges
perhaps with the ability to grow in human cells, infect humans and has antigens from the avian virus; no pre-existing immunity

263
Q

what is the name of the influenza receptor?

A

sialic acid

264
Q

how can pigs and cats be infected with the bird and human viruses?

A

they have both the alpha-2-6 (human) and alpha-2-3 (bird) forms of sialic acid within their respiratory cells

265
Q

describe the formation of the H3N2 virus

A

widely circulating human H2 virus which recombined with an avian H3 virus
segment mixing within a pig
H2; replicated well in humans
H3; had not been previously seen by humans, no herd immunity, rapid spread throughout population, severe mortality and morbidity

266
Q

define pandemic

A

a widespread epidemic of a disease, one that affects a whole country, continent etc.

267
Q

what happens to a pandemic flu after a pandemic?

A

it becomes a seasonal flu until its replaced by another pandemic

268
Q

describe avian influenza

A 
bird flu
H5N1 human infection
approximately 500 human cases
55% mortality rate
cases almost exclusively from close contact with sick poultry
269
Q

describe swine flu

A

H1N1 2009
emerged in Mexico
traced as a reassortment virus that was derived from 3 known pig viruses; all from 10 years prior

270
Q

what were the clinical features of swine flu

A

very young age profile; only 2% of cases over 65yrs
reduced mortality and severe morbidity
very high proportion of asymptomatic cases
key risk factors; pregnancy, obesity, neurodevelopment problems; increased mortality and rate of serious complications

271
Q

describe the clinical presentation of SARS

A

high fever followed by a dry cough and rapid progression to respiratory failure
more severe in older individuals than younger individuals
higher rate of transmission within hospitals
described as an atypical pneumonia; a pneumonia with a dry cough not producing sputum

272
Q

describe SARS

A

a coronavirus
a recognised world public health event by April 2003
believed to be a zoonotic coronavirus that had spread from the masked palm civet in china to humans

273
Q

what were the consequences of SARS?

A

global fear
economic effects
<10% overall mortality rate
more people died due to cardiac events, strokes and reluctancy to go into hospitals for treatment

274
Q

how was SARS controlled?

A

early case detection; due to rapid development of diagnostic tests
rapid isolation of infected individuals
knowledge and dissemination of routes of transmission
infection control measures were aimed at particular aspects of transmission
vigorous identification and management of close contacts and keeping people at home
international collaboration

Scientific Basis of Clinical Practice (10 decks)

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