Microbiology Flashcards
name the gram positive cocci clusters
staphylococcus aureus
staphylococcus epidermidis
where would gram positive cocci cluster be found?
skin
nasal
name the gram positive cocci chains
beta-haemolytic streptococci (pharyngitis, tonsilitis) streptococcus agalactiae streptococcus oralis streptococcus pneumoniae enterococcus faecalis
where would gram positive cocci chains be found?
mouth
upper respiratory tract
name the gram positive rods
clostridium difficile clostridium perfringens clostridium tetani lactobacillus acidophilus bacillus species listeria monocytogenes propionibacterium acnes
name the gram negative cocci
neisseria gonorrhoea
neisseria meningitidis (bacterial meningitis)
haemophilus influenza
name the gram negative non-enterobacteriaceae rods
escheria coli
klebsiella pneumoniae
salmonella enteriditis
proteus mirabilis
name the gram negative enterbacteriaceae rods
bacteroides fragilis
campylobacter jejuni
pseudomonas aeruginosa (aquatic environments)
name the non-gram staining acid and alcohol fast bacilli
mycobacterium tuberculosis
name the non-gram staining cell wall deficient bacteria
mycoplasma pneumoniae
legionella pneumoniae (aquatic, lung)
chlamydia tractomatis
name the non-gram staining spirochaete bacteria
treponema pallidum (syphilis)
describe otitis media
streptococcus pneumoniae
haemophilus influenza
fever
pain
glue ear
amoxicillin
describe sinusitis
streptococcus pneumoniae
haemophilus influenza
facial pain
localised tenderness
fever
amoxicillin if persistent/severe
describe acute epiglotitis
medical emergency haemophilus influenza (capsular type B)
respiratory obstruction
intubation
cefotaxime
Hib vaccine
describe pharyngitis
epstein barr virus - glandular fever
streptococcus pyogenes - strep throat
sort throat
fever
peritonsillar abscess
describe croup/aryngotracheobroncihitis
young children
parainfluenza 1 & 2
inspiratory stridor due to laryngeal narrowing
paracetamol
IV fluids
corticosteroids
adrenaline if hospitalised
describe infectious mononucleosis
epstein barr virus (herpes family)
babies asymptomatic fever sore throat lymphadenopathy splenomegaly hepatitis lethargy encephalitis - rare
describe streptococcus pyogenes (scarlet fever)
streptococcus pyogenes
anti-streptolysin O titre
pharyngitis
rheumatic fever
rheumatic heart disease
acute glomerulonephritis
penicillin
erythromycin
describe whooping cough
brodetella pertussis (gram negative coccobacillus)
catarrhal
paroxysms of cough
lobar collapse
secondary pneumonia
supportive treatment and macrolide (clarithromycin, erythromycin, azithromycin)
describe opportunistic pneumonia
pneumocystis jirovecii
immunocompromised
high fatality rate
co-trimoxazole
describe enteric fever salmonella
s typhi
s paratyphi
fever headache myalgia malaise sepsis 1 week, followed by diarrhoea
ciprofloxacin
cefotaxime
describe enterocolitis salmonella
salmonella enteritidis
nausea vomiting cramps non-bloody diarrhoea 2-7 days
ciprofloxacin
cefotaxime
describe the taxonomic status of hep B
DNA virus
comes from the family hepadnavirus
describe the taxonomic status of hep C
flavivirus
related to the flaviviruses that are mosquito-borne; yellow fever
describe the taxonomic status of HIV
retrovirus
lentivirus subfamily
what are the modes of transportation of BBVs?
penetrative sexual intercourse
blood transmission
vertical (breastfeeding)
if a patient has contracted 1 BBV then they should be tested for others
what is the main transmission mode of HIV?
penetrative sexual intercourse
what is the main transmission mode of HCV?
contaminated blood; particularly IV drug use
what is the main transmission mode of HBV?
vertical; post and perinatal
describe diagnostics
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
describe theranostics
tests specifically done to guide treatment
monitor treatment
response to treatment
drug resistance
development/disappearance of drug resistance
genotype of HVC; given different treatment
describe HBV
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
what are the symptoms and signs of HBV?
50% asymptomatic
initially; prodromal fever, malaise
chronic; chronic active hepatitis, liver cirrhosis, hepatocellular carcinoma
what is the name of the HBV virus particle?
the Dane particle
describe the tolerogen affect of the HBV E antigen
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
what factors affect chance of becoming chronic carriers?
neonates that are infected at birth by maternal virus; >90% chance
affected >5yrs; 10% chance
what antigens are associated with HBV?
HBsAg; grossly over-produced
HBeAg
what factors affect the chance of perinatal transmission?
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
what does core antibody hepatitis B and core antibody IgG identify?
past or present infection
will always remain positive for hep B core antibody
what does IgM presence indicate in HBV?
acute/recent infection
occurred within the last 6 months
what does E antigen indicate in HBV?
highly infectious
very active, disease-causing levels of virus
what does anti-hepatitis B surface antigen indicate?
this is the antibody to the surface antigen
immunity; natural (infection and recovery), vaccine-induced
what does hepatitis B DNA indicate?
determines response to treatment; falls if treatment is working
describe high-grade HBV infections
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
describe low-grade HBV infections
much lesser risk of transmission; <1% risk via needle stick
less likely to develop clinical effects
E antigen negative
E antibody positive
describe the HBV vaccine
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
what is the treatment of HBV?
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
what theranostic tests are used in HBV?
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
describe hepatitis C
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
describe the different genotypes of hepatitis C
6 genotypes
1; very common in NI, poor response to treatment
3; much easier to treat, responds much better to treatment
how many people are infected with hepatitis B?
350 million; 5%
how many people are infected with hepatitis C?
170 million; 2.5%
describe the signs and symptoms of acute and chronic HCV
acute; mostly asymptomatic chronic; 70% develop chronic infection, remain infected for decades/life, 50% develop chronic active hepatitis cirrhosis liver failure hepatocellular carcinoma
describe HCV markers
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
how is current HCV infection diagnosed?
antibody positive
PC positive
how is past HCV infection diagnosed?
antibody positive
PCR negative
what is the treatment of HCV?
interferon and ribavirin
aim of treatment; cure
liver transplantation; last option, hep C recurs in the graft in almost 100% of cases
what theranostic tests are used in HCV?
genotype; determine the duration of treatment
hep C RNA by PCR; determines response to treatment
describe HIV
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
how many people are infected with HIV?
40 million; 0.5%
about 4.3 million people are newly infected each year
what diseases are caused by HIV?
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
what are the key opportunistic infections in AIDS?
CMV; retinitis JC polyomavirus; encephalopathy EBV; lymphoma mycobacteria; TB toxoplasma; CNS infection cryptosporidia; blood diarrhoea candida; oesophageal infection pneumocystis; pneumonia cryptococcus; meningitis
describe HIV diagnosis
look for HIV antibody; indicates infection
4-assay approach to ensure specificity
viral load; measures the amount of RNA in the blood
what is the treatment of HIV?
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
what are the theranostic assays used in HIV?
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
what investigations are performed on a patient with suspected hepatitis?
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
interpret these investigation results; HBsAg negative HB core antibody (IgG) positive anti-HbsAg positive HCV antibody positive HCV PCR positive
past HBV infection
current HCV infection
define gastroenteritis
a clinical syndrome characterised by nausea, vomiting and abdominal discomfort
define dysentery
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
what are the key agents of bacterial diarrhoea?
campylobacter salmonella shigella E. coli (including VTEC) vibrio cholerae
what are the pathogenesis and key agents of toxin ingestion?
disease is caused by ingestion of performed toxin in food clostridium perfringes bacillus cereus staphylococcus aureus clostridium botulinum (neurotoxin)
what is the cause of antibiotic associated diarrhoea?
clostridium difficile
what are the viral causes of diarrhoea?
norovirus; winter vomiting disease
rotavirus; predominant in children
what are the parasitic causes of diarrhoea?
cryptosporidium
giardia lamblia
describe clostridium difficile
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
describe pseudomembranous colitis
most severe form of clostridium difficile infection
pseudomembrane present on the colon surface made of inflammatory cells, fibrin and necrotic gut cells
how is clostridium difficile diagnosed?
presence of toxin in faeces; difficult and slow to grow, does not tell you if somebody has a significant infection
how is clostridium difficile treated?
isolation
spores survive exposure to alcohol
stop antibiotics if possible
oral metronidazole or oral vancomycin
describe immunocompromised hosts
those patients who will more readily get an infection from a common primary pathogen
patients who will get infections with opportunistic pathogens
define a primary pathogen
one which commonly causes disease in aa health non-immune host
e.g. staphylococcus aureus, streptococcus pneumoniae
define an opportunistic pathogen
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
what are the causes of immunity?
non-specific; skin/mucosal integrity, mucosal clearing mechanisms, gut defence, complement system, phagocytosis
specific; cell-mediated and humeral (antibody) response
what are the causes of immunocompromise?
primar/secondary immunodeficiency diseases
stressed physiological states
iatrogenic input
name some primary immunodeficiencies
neutrophil defects; chronic granulomatous disease
humoral; B cell defects
cell-mediated; T cell defects
SCID
name some secondary immunodeficiencies
AIDS hyposplenism cancer diabetes any severe systemic illness
name some stressed physiological states
pregnancy
neonates; especially preterm
elderly
nutritionally deficient
what are the causes of iatrogenic immunodeficiency?
drugs; corticosteroids, anti-cancer chemotherapy, immunosuppressive therapy post-transplant
irradiation
invasive devices; IV lines
surgical procedures; splenectomy
how is infection prevented in immunocompromised patients?
avoiding risk activities/locations; hospital protective isolation vaccination antimicrobial prophylaxis restore underlying defect
how is the spectrum of infecting organism related to the type of illness and how ill the patient becomes?
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
describe pneumocystis jiroveci/carinii
fungi
seen in HIV positive patients
cause pneumocystis pneumonia
diagnosed by direct microscopy following silver staining or immunofluorescence or by a polymerase chain reaction
what are the signs and symptoms of pneumocystis pneumonia (PCP) in HIV?
non productive cough dyspnoea fever perihilar infiltration may progress to severe respiratory disease extra pulmonary infection
what is the treatment of pneumocystis pneumonia (PCP) in HIV?
high dose cotrimoxazole
supportive therapy
ICU usually required
describe toxoplasma gondii in healthy patients
protozoal infections
usually asymptomatic or glandular fever-like illness
50% affected by middle age
zoonosis; from cats
describe toxoplasma gondii in HIV patients
cerebral toxoplasmosis
neurological symptoms; seizures, depressed consciousness
main cause of focal CNS lesions
ring enhancement on CT brain
may present as pneumonitis or chorioretinitis
how are infections prevented in HIV positive patients?
highly active antiretroviral therapy; boost CD4 count
antibiotic prophylaxis; prevent some classical opportunistic infections
what antibiotics are offered for which opportunistic infection?
cotrimoxazole; pneumocystis
rifabutin; mycobacterium avium intracellulare (MAI)
ganciclovir; cytomegalovirus
describe the causes and diagnosis of neutropenia
chemotherapy
bone marrow transplant
aplastic anaemia
high dose beta lactams
fever; cardinal sign
no pus/localisation
describe neutropenia
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
describe cellular immune dysfunction
principally affects T cells
more susceptible to mycobacteria, legionella, listeria and viruses
what are the key opportunistic fungi associated with neutropenic patients?
aspergillus; mould, causes lung infection and may cause a brain infection is disseminates, difficult culture, high mortality
candida; yeast, easier to diagnose, high mortality
what are the risk factors for becoming infected with Candida albicans?
central lines
parenteral nutrition
broad-spectrum antibiotics
gut abnormalities; perforation, mucositis
what is the treatment of sepsis in neutropenia?
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
what is the treatment/prevention of infection in burns patients?
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
what are the infection risks in those with a splenectomy?
particularly susceptible to capsulate bacteria; pneumococcus, haemophilus
what is the treatment/prevention of infection in those with a splenectomy?
vaccination; before or after surgery
long-term prophylactic antibiotics; targeted towards preventing pneumococcal infection (penicillin)
what are the infections risks in pregnancy?
ascending UTI; more common, may precipitate premature labour
listeria; common, can be devastating
what is the treatment/prevention of infection in pregnancy?
avoid high risk foods; soft cheese, pates
ampicillin and gentamicin; ampicillin added to the cephalosporin when treating meningitis in pregnant ladies
what organisms are associated with skin and soft-tissue infections?
staphylococcus aureus
beta-haemolytic streptococci
particularly group A streptococci; streptococcus pyogenes
what is the difference between staphylococci?
staphylococcus aureus; coagulase positive, pathogenic
all others; coagulase negative, less pathogenic
how does staphylococcus aureus cause infection?
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
what is the most common bacterial cause of haemolytic uraemic syndrome?
E. coli
not the bacteria itself but the shiga toxin
what are the commonest organisms associated with skin and soft tissue infections?
staphylococcus aureus
beta haemolytic streptococci; particularly group A streptococci (streptococcus pyogenes)
what is the differentiating feature between staph aureus and other staphylococci?
coagulase positive
what are the virulence factors of staph aureus?
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
what are the carriage sites of staph aureus?
anterior nares
axilla
groin
what are the virulence factors of strep pyogenes?
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
what is used to clinical detect the presence of a previous/recent streptococcal infection?
streptolysin O antibodies
what are the non-suppurative sequelae of strep pyogenes?
rheumatic fever glomerulonephritis relate to the organisms molecular mimicry arise 1-3 weeks post-infection immunologically mediated
describe impetigo
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
what are the complications and treatment of impetigo?
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
define folliculitis
infection of the hair follicle
can occur anywhere on hairy skin
superficial infection
pus is found only in the epidermis
define furuncles/boils
extend into the dermis
greater degree of inflammation
inflammatory nodule is frequently present with the overlying pustule
often with a hair emerging
define carbuncles
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
what is the treatment of carbuncles?
incision and drainage
eradication of carriage from anterior nares using topical mupirocin may alleviate the condition
antibiotics are usually unnecessary
what are the causes of folliculitis, furuncles and carbuncles?
staphylococcus aureus
underlying problem; diabetes in recurrent boils
describe erysipelas
a form of cellulitis affecting the most superficial layers of the skin
cause; streptococcus pyogenes
what are the symptoms and signs of erysipelas?
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%)
what is the treatment of erysipelas?
penicillin
oral/IV depending on severity of the illness
define cellulitis
acute spreading pyodermic inflammation of the dermis and subcutaneous tissue
what are the symptoms and signs of cellulitis?
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
what are the risk factors and causes of cellulitis?
obesity venous insufficiency lymphoedema trauma athletes foot; inter-toe maceration diabetes
mostly; staph aureus, strep pyogenes
aeromonas hydrophila; contact with fresh water
what is the management of cellulitis?
culture any skin breaches
broad cultures if severe
mild; oral flucloxacillin (covers staph and strep)
moderate-severe; IV flucloxacillin +/- benzylpenicillin
allergic; clindamycin
what are the common and occasional organisms associated with bites?
pasteurella multocida; dogs, cats
anaerobes; dogs, cats, humans
eikenella corrodens; humans
capnocytophaga canimorsis; dogs
what is the management of bites?
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
describe surgical wound infections
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
what investigations are required to diagnose a surgical wound infection?
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
describe the cause and management of clean surgery
staph aureus
flucloxacillin
describe the cause and management of contaminated surgery
staph, strep, coliforms, co-amoxiclav
broader spectrum antibiotic; cefuroxime and metronidazole
what are the features of arterial ulcers?
reduction in peripheral pulses reduction in ABPI intermittent claudication hairless, shiny skin well defined border
what is the management of arterial ulcers?
revascularisation; by-pass grafting, angioplasty
what are the features of venous ulcers?
usually superior to medial malleolus
haemosiderin deposits
oedema
what is the management of venous ulcers?
compression therapy
describe pressure ulcers
occur over areas of bony prominence
describe diabetic foot ulcers
usually on the plantar surface
associated with (diabetic) neuropathy
the leading cause of non-traumatic amputations
what are the signs of infection?
pain redness purulent exudate delayed healing poor quality granulation tissue new/increased odour local cellulitis
what are the rules for sampling chronic infections?
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
what is the management of chronic wounds?
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
describe mild, moderate and severe foot ulcers
mild; <2cm radius of cellulitis
moderate; >2cm radius, deep infection
severe; deep infection, systemic sepsis
define necrotising fasciitis
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
describe polymicrobial necrotising fasciitis
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
describe group A streptococcal necrotising fasciitis
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
describe clostridium myonecrosis/gas gangrene
most commonly cause by clostridium perfringens
what are the symptoms and signs of necrotising fasciitis?
pain out of keeping with the clinical finding
skin necrosis
ecchymosis
crepitus in the tissue
late symptoms; confusion, hypotension
diagnosis confirmation; surgical exploration
what is the treatment of necrotising fasciitis?
surgical emergencies
aggressive and repetitive debridement
intensive care support
antibiotics; benzylpenicillin (strep), ciprofloxacin (aerobic gram -, coliforms), clindamycin (staph, strep, anaerobes, reduce/prevent toxin formation)
describe dermatophyte infections
infection with a ringworm fungus
tinea barbae, capitis, corporis, pedis (athletes foot)
what are the causes of dermatophyte infections?
trichophyton microsporum epidermophyton frequently zoonotic human-human spread; shared towels, hair brushes, direct contact
describe the diagnosis of dermatophyte infections
clinical appearance
microbiological confirmation
woods light; tinea capitis
describe the treatment of dermatophyte infections
topical imidazoles
resistant; oral terbinafine
2-4 weeks
repeated treatment often necessary
what are the risk factors for MRSA infection?
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
what is the treatment of MRSA infection?
mild; tetracyclines, trimethoprim, fusidic acid, rifampicin
severe; glycopeptides, vancomycin, teicoplanin, rifampicin, fucidin
new antibiotics; linezolid, daptomycin, tigecycline
describe community associated MRSA
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
describe meningitis
infection in the subarachnoid space
inflammation of the leptomeninges
a medical emergency
require lumbar puncture
what are the clinical features of meningitis
headache neck stiffness photophobia fever irritability vomiting purpura non-blanching rash infants; less specific, not feeding well, Hugh pitched cry, bulging fontanelle
describe the CSF findings in viral meningitis
high lymphocytes and protein
normal neutrophils
nothing identified on gram stain
describe the CSF findings in bacterial meningitis
high neutrophils and protein
low glucose
gram stain may show causative organism
describe the CSF findings in TB meningitis
high WCC; predominantly lymphocytes slightly high neutrophils very low glucose high protein gram stain negative ziehl neelsen stain for TB may be positive
describe the pathophysiology of bacterial meningitis
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
describe the breakdown of the blood brain barrier
bacterial replication release of IL2, IL6, TNF polymorphs are attracted to site of infection endothelial disruption albumin leak increased cerebral blood flow cerebral oedema
describe meningitis in infants
most commonly group B strep, E. coli, listeria
very small infants acquired the infection from organisms that colonise the maternal vagina
describe meningitis in toddles
NHS bacteria;
neisseria meningitidis
strep pneumoniae
haemophilus influenzae (less common because of theHiB vaccine)
describe meningitis in >4yrs and adults
neisseria meningitidis
strep pneumoniae
describe strep pneumoniae
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
describe haemophilus influenzae
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
describe neisseria meningitidis
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
what is the treatment of meningitis?
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
describe the prevention methods for meningitis
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
what are the causes of viral meningitis?
enterovirus; 80% HSV 1 and 2 varicella cytomegalovirus mumps adenovirus HIV
more common than bacterial meningitis
good prognosis
describe enteroviral meningitis
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)
what is the treatment of viral meningitis?
supportive
acyclovir; HSV, treatment not proven
vaccine; mumps, measles
what are the non-viral causes of aseptic meningitis?
fungi TB syphilis brucella mycoplasma parameningeal infection; brain abscess, protozoa, helminths
nothing grown in the lab and nothing identified by PCR initially
what questions should be asked in a CNS infection history?
travel; epidemics work sexual history contacts animal contact vaccination history history regarding symptoms which are not CNS symptoms
describe TB meningitis
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
what are the clinical features of TB meningitis?
personality change irritability unexplained temperature drowsiness neck stiffness cranial nerve palsies cranial nerve involvement decreased level of consciousness
describe the investigations required for a diagnosis of TB meningitis
positive tuberculin positive Mantoux test FHx of TB in recent months lumbar puncture; CSF often looks, clear, may be under pressure gastric washings
what is the treatment of TB meningitis?
4 drugs; rifampicin pyrazinamide ethambutol aminoglycoside after 2 months; treatment rationalised to rifampicin and isoniazid which continue for up to a year
what are the bugs which would only cause infection in an immunocompromised host?
listeria monocytogenes; found in raw milk, soft cheeses
cryptococcus; yeast
what are the viral causes of encephalitis?
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
what are the non-viral causes of encephalitis?
neisseria monocytogenes listeria scrub typhus leptopsirosis melioidosis malaria TB borrelia brucella
what is the management and investigations required to diagnose encephalitis?
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
describe herpes simplex encephalitis
most common cause of encephalitis
long term sequelae; occur in 50%, 80% untreated, significant mortality
associated with reactivation or primary infection
describe the clinical presentation of herpes simplex encephalitis
headache fever decreased LOC confusion dysphagia
what is the treatment of herpes simplex encephalitis?
acyclovir 14-21 days
what are the CNS complications of measles infection?
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
describe demyelinating encephalopathies
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
describe the slide features of progressive multifocal encephalopathy
characteristic demyelination
oligodendrocytes affected
what are the clinical features of a brain abscess?
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
describe the pathophysiology of a brain abscess?
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
what are the causative organisms of a brain abscess?
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
what is the treatment of a brain abscess?
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
describe prion diseases
transmissible spongiform encephalopathies
both human and animal forms of the diseases
aberrant protein folding
no treatment
invariably fatal
cause neurodegeneration
describe the different types of prion diseases
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
describe bovine spongiform encephalopathy
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
define a fever/pyrexia of unknown origin (F/PUO)
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
describe the non-classical PUOs
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
describe the history required in PUO
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)
describe the investigations performed in PUO
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
what is the management of PUO?
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
what are the clinical features of lower tract respiratory infections?
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
what are the main types of LRTI?
90%;
COPD
non-pneumonic LRTI
CAP
paediatric or hospital AP
CAP in those significantly immunosuppressed (HIV, AIDs, cancer)
bronchiectasis
cystic fibrosis
describe COPD
occurs in patients with a pre-existing lung condition
long history of structural disease
often have a cough and sputum production when well
define an exacerbation of COPD
2/3 of the Anthonisen criteria;
increased dyspnoea
increased sputum production
increased sputum volume
describe community acquired pneumonia in primary care
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
describe community acquired pneumonia in secondary care
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
what are the causes of CAP?
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
describe non-pneumonic respiratory tract infections
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
what is the difference between pneumonia and acute bronchitis?
<38 HR <100 RR <24 no focal signs of consolidation on CXR ; pneumonia is very unlikely
what are the features of non-pneumonic LRTI?
normal; temperature, HR, BP
no confusion
no comorbidity
<50yrs
how do you know when to admit a patient with CAP to hospital?
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
what investigations should be performed in CAP?
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
what is the treatment of CAP?
antibiotics;
after sending microbiological samples
within 4 hours; improves 30 day mortality
what is the treatment of non-severe CAP (at home)?
oral amino penicillin; amoxicillin 0.5-1g TDS, ampicillin 0.5-1g QID
or
oral macrolide; erythromycin 500mg QID, clarithromycin 500mg BD
what is the treatment of non-severe CAP (in hospital)?
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
what is the treatment of severe CAP (hospital/ICU)?
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
describe the pathophysiology of TB infection
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
describe chronic pneumonia
most common form of TB
may present following an acute-on-chronic deterioration
what are the symptoms and signs of TB?
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
what are the risk factors for developing TB?
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
what investigations are required to diagnose TB?
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
what is the treatment of TB?
6 months; isoniazid and rifampicin
supplemented in the 1st 2 months with pyrazinamide and ethambutol
full adherence required to avoid resistance and failure
how is TB preventioned?
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
define antibiotics
molecules which will kill or inhibit the growth of microorganisms at very low concentration
how do antibiotics not harm the patient?
selective toxicity; will block or inhibit an essential metabolic pathway in the microorganism which is absent or sufficiently different in mammalian cells
what are the modes of action of antibiotics?
blocking synthesis of the bacterial cell wall
inhibition of protein synthesis; inhibition of mRNA translocation
disruption of bacterial DNA
blockade of folate metabolism
describe antibiotics that block the synthesis of the bacterial cell wall
increased osmotic pressure, burst open and die
beta lactams; penicillins, cephalosporins, carbapenems
glycopeptides; vancomycin, teicoplanin
describe antibiotics that inhibit protein synthesis
all attack the bacterial ribosome macrolides; erythromycin, clarithromycin fusidic acid tetracyclines; doxycycline aminoglycosides; gentamicin
describe antibiotics that disrupt the bacterial DNA
inhibits the enzyme that allows DNA supercoiling
destroy the bacterial DNA
fluoroquinolones; ciprofloxacin
describe antibiotics that cause a blockade of folate metabolism
sulphonamides
trimethoprim; very widely used for UTI treatment
describe microbiological/ecological toxicity
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)
describe pharmacological toxicity
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
describe intrinsic resistance
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
describe antibiotic resistance acquisition
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
describe the antibiotic consumption thresholds
1; where resistant bacteria start to emerge as a larger proportion of the total population
2; sensitive bacteria are almost completely eradicated
what are the consequences of the antibiotic consumption thresholds?
a sharp rise in the prevalence of resistance
once resistance becomes totally established, reducing antibiotic consumption may not bring back the susceptible strains
describe linked resistance
resistance can be transferred
prescribing drug A can increase resistance to drugs B and C
how can we stop the promotion of resistance?
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
what are he uses of antibiotics?
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
describe an emerging infection
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
what current events encourage emerging infections?
global warming
changes in agriculture and irrigation; mosquitoes
urbanisation
social changes; travel
medical intervention; immunosuppression
advent of a big population of IV drug users
describe legionella pneumophila
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
describe E. coli 0157
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
describe coxiella burnettii
gram negative proteobacteria
causes Q fever; pneumonia, headache, mild pyrexia-like illness
very variable severity of disease
usually zoonosis; caught from animal placentas
describe extended-spectrum-betalactamase producers (ESBL)
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
describe vancomycin resistance enterococcus (VRE)
particularly a problem in specialist units; renal
can cause severe infection in those who are immunocompromised
describe healthcare associated infections
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
describe seasonal influenza
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
describe avian influenza
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
describe pandemic influenza
high mortality due to the new emergence of an influenza strain
describe the influenza virus
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
describe the nucleocapsid of influenza
segmented RNA genome
neuraminidase (N) and haemagglutinin (H) on the outside of the envelope of the virus
describe antigenic drift in relation to influenza
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
describe antigenic shift
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
describe genetic reassortment of viruses
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
what is the name of the influenza receptor?
sialic acid
how can pigs and cats be infected with the bird and human viruses?
they have both the alpha-2-6 (human) and alpha-2-3 (bird) forms of sialic acid within their respiratory cells
describe the formation of the H3N2 virus
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
define pandemic
a widespread epidemic of a disease, one that affects a whole country, continent etc.
what happens to a pandemic flu after a pandemic?
it becomes a seasonal flu until its replaced by another pandemic
describe avian influenza
bird flu H5N1 human infection approximately 500 human cases 55% mortality rate cases almost exclusively from close contact with sick poultry
describe swine flu
H1N1 2009
emerged in Mexico
traced as a reassortment virus that was derived from 3 known pig viruses; all from 10 years prior
what were the clinical features of swine flu
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
describe the clinical presentation of SARS
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
describe SARS
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
what were the consequences of SARS?
global fear
economic effects
<10% overall mortality rate
more people died due to cardiac events, strokes and reluctancy to go into hospitals for treatment
how was SARS controlled?
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
