Bacteria Flashcards
Pathogenesis of stash areus
- patient factors
- interaction with host
Break in mucosa, inhalation, ingestion etc. Naturally found on skin and nares
Immuni compromised?
- coagulase: converts fibrinogen to fibrin
-spreads quickly: hyuronidase: breaks down hyularonic acid in CT
- exotoxins: proteases- DNA ribonuclease to break down host DNA
Staphylococcus areus
- presentation
- conditions
- treatment
Often Immune compromised patients
- skin lesions: impetigo, boils, ABSCESS
- SPUR: severe persistent, unusual, recurrent
- conditions: HAP pneumonia, meningitis, impetigo
- complications: endocarditis (BSI), TSS SEPSIS
MRSA: glycopeptides- vancomycin (systemic) , erythromycin/Vancouver (local)
Others: amoxicillin
Clostridium difficile
- pathogenesis
- bacteria type?
- interaction with host
- risk factors
Gram positive anaerobic bacilli with spores
- opportunistic infection when normal flora eliminated by antibiotics for another infection (amoxicillin, cephalosporins, clindamycin)
- RF: age, pathological state etc
- exotoxin A : causes inflammation = excessive histamine= fluid loss= widens intracellular spaces
- exotoxin B: escapes though these gaps and kills host cells (disrupts protein synthesis)
Clostridium difficile
- presentation
- conditions
- complications
- treatment
Antibiotic associated DIARRHOEA
Pseudo membranous colitis
Complication: severe diarrhoea–> renal failure–> cognitive impairment
Perforated toxic mega colon–> peritonitis–> septic shock
Treatment: discontinue causative antibiotics, give metinodazole , vancomycin
Streptococcus pneumoniae
- type of bacteria
- patient factors? RF?
Mechanism of infection
Gram positive, pairs/chains. Capsulated
Direct contact. Normal flora in URT.
Patient factors: age, pathological state, (smoking HIV obesity, spleen, chemo) time: more common in winter,
How does streptococcus pneumonia lead to infection?
What conditions..
Treatment
Bacterial Pneumonia, - most common CAP
Can lead to meningitis/septicaemia , pericarditis, if enters blood stream
Pneumonia occurs when bacteria colonise lungs. Not easily phagocytosis (thick capsule)
Pus accumulates= symptoms
Treat: supportive. And broad spectrum antibiotics
Viridans strep- type, conditions, when
Positive cocci Breach in dental --> endocarditis Occurs if there is poor dental hygiene --> Harmless bacteraemia--> accumulates on heart valves Treat: penicillin, replace valve Complication--> heart failure
Coagulase negative strep- conditions?
Positive cocci- clusters
Prosthetics infections malaise, fever etc
Localised infection and Inflammation = pain
Prosthetic >1 year then strep viridans, enterococcus faecalis, staph areus, candidia
Escheridia coli
Describe
Pathogenesis
Conditions
Gram negative anaerobic, spore forming, rod Faecal oral. Different strains- some harmless. Conditions: -gastroenteritis (colonises GI tract) -Peritonitis(e coli from bowel perforation/surgery) = cramping, bloating, diarrhoea - cystitis: UTI
Other strains: travellers diarrhoea, shigella, cholera like illness
E coli infection
Treatment
Complications
Supportive: fluids, o2, immodium
Specific: board spec antibiotic,
Complications: peritonitis–> liver damage, septic shock, death :O
Prevention: gastroenteritis very infectious!
Neissaria menigitidis. Type Virulence factors Pathogenesis Complications
Gram negative cocci
Direct contact with respiratory secretions- kissing, sneezing
Normal flora of URT
- colonises meninges (lining of brain) = headaches and non specifically I’ll
–> BSI = rash
Virulence:
- potent endotoxins (immune over reaction = vasodilation and permeability= decrease TPR = SEPTIC SHOCK
- renal and resp failure
- And disseminated intra vascular coagulation–> Ischaemic necrosis –> multi organ failure
- Also increase ICP
Neissaria menigitidis
Presentation
Treatment
Fever chills sweats- quick onset- 24hrs - then purperic rash, photophobia, fever, neck pain Identification: Treat: o2, fluids, adrenaline Measure lactate and urging Blood cultures and Broad spec: cefriaxone
Salmonella typhi - basics
Gram negative rod Faecal oral Typhoid fever Gastroenteritis (food borne) Pneumonia --> sepsis and intestinal perforation/haemorrhage --> endocarditis
Treat: supportive, antipyrexials,
Ciprofloxacin, cefriaxone
Legionella pneumophillia basics
Gram negative rod
Droplet- hot tubs air con, stagnant water
Fever, SOB, pneumonia, productive cough, death
Legionaries disease oft confused with:
Pointaic fever (no pneumonia )
Pseudomonas aerinoginosa
- type
- pathogenesis
Mechanism of infection
Gram negative bacilli, facultative anaerobes (prefers anaerobic but can be both)
- inhalation: respiratory infection
- other route e,g, UTI cystitis
RF: cystic fibrosis, HIV,neutropenia ,immunecomp etc,
Pathogenesis: opportunistic infection - needs disease to take hold. Can survive in thick cystic fibrosis mucus (facultative anaerobes)
Colonises bronchi first –> pneumonia
Most common HAP
Pseudomonas aerinoginosa
Virulence
Virulence factors
- blocks eukaryotic protein synthesis= oncosis
- biofilm like layer: mucopolysaccharide capsule- reduced phagocytosis = harder to destroy (especially if a splenic as spleen destroys capsule)
Pseudomonas aerinoginosa
Treatment
Supportive
Specific: tobamycin (IV)
Don’t let ct sufferers meet!
Mycobacterium tuberculosis
- features
Gram stain resistant, obligate aerobes Has thick, mycolic acid capsule Slow growing - slow for cultures Non motile 7 species
M. Tuberculosis
Mechanism of infection and virulence
Mycolic acids: resist phagocytosis
Frustrated phagocytosis–> multiplies inside –> destroys macrophage –> reduces host response
Produces IL 12–> (NK –> IFN A and CD4 cells –> TNF A) –> recruit macrophages –> langhans cells in granuloma
Intense immune response –> local tissue destruction –> cavitation
Systemic–> fever and weight loss etc
M tuberculosis
Patient: risk factors?
Transmission?
How does it develop into active to
Droplets. Long term exposure. Schools, families, overcrowding, prisons, hospitals,homeless,
Reaches lymph nodes = primary complex
–> active Tb (immune comp)
Or –> latent TB (Th contain infection) infected but not a case
- -> post primary TB (mature and reactivation)
- -> self cured, 95%
Investigating TB
MANAGEMENT
investigate: varying symptoms, most have lung involvement Military = systemic - culture - CXR - NAAT, IGRA, TST
antibiotics: rifamycin, isoniazid (4mths), pyradizonamide, ethambutol (2 mth)
MDRTB, XDRTB
SE: liver toxicity, monitor compliance,, contract tracing
Norovirus
Structure
Transmission
Non enveloped
SsRNA
Isocahedral
Direct, indirect (air, facael oral)
Norovirus
- disease, presentation
Investigation
Gastroenteritis: vomiting
Noroviral infection: treatment and prevention
Fluids, supportive, at home if not too bad
Wash everything! Very contagious and veery dangerous in very old and very young
Normally only lasts 1-4 days
No high risk food prep in hospital etc, short cuts through kitchens, infection wards separate.
Norovirus, pathogenesis
Multiplies in small intestine and irritates lining
Adenovirus
Type of virus?
Ds DNA non enveloped
Isocahedral
Direct, faecal oral, droplet
Adenovirus
Mechanism of infection
Infections..
Respiratory tract to pharynx/URTI–> nasolacrimal duct
Or to –> GI tract
Leads to repiratory infection/conjunctivitis/gastroenteritis
- enlarged tonsils, inflamed pharynx ,fever, malaise etc
Adenovirus
Treatment
Pain relief- paracetamol
Fluids
Antivirals if lethal strain
Influenza A
Structure, mechanism of infection
-ssRNA
Circular capsid, enveloped
Different subtypes e.g. H1N1
Influenza A
Pathogenesis? Diseases cause?
Surface proteins HA and NA
H: Haemagglutinin- Helps virus enter cell by binding to the envelope
N: neuraminidase- cleaves glycoproteins to allow viral release from a cell after replication = spreads
Symptoms - due to cytokine over reaction
Disease- flu. Fever, aches, pains, dry cough,
–> chest infection, siniusitis (meningitis)
Influenza A treatment
Pain release, antipyrexials,
- neuraminidase inhibitor (oseltamivir - tamiflu)
- Antiviral (acyclovir)
Influenza a prevention
Flu vaccine - but change raking fie to high mutation rate
- antigenic drift (small changes)
- antigenic shift (large changes, change in subtype and the therefore treatment)
HIV
- structure?
Spread?
+ ssRNA
circular capsid
Enveloped
Bodily fluids
HIV- mechanis, of infection
Enters blood stream, Binds and fuses to CD4T cells, macrophages and dendritic cells Binds using glycoproteins Penetrates and releases enzymes ssRNA--> DNA (reverse transcriptase) --> host DNA (integrase) Transcription and translation--> vesicle Cell lysis Mature (use viral proteases)
= decline in T cells. = more susceptible to infection
HIV
- presentation
Often asymptomatic, any are non specific and 2-6 weeks later= Unknowningly spread infection
Fever malaise, headache, sore throat,
AIDS defining infections
- opportunistic oral Candida albicans
- TB - extra pulmonary
- pneumocystis pneumonia - caused by opneumocytis jirovecci
Kaposi sarcoma
Acute HIV: flu like, fevers, muscle ache etc, vomiting. –> AIDS illnesses –> weight loss, lymph enlargement, fatigue etc
HIV treatment
Treat AIDS defining illness
- cd4 count checked. Take action if
HIV - duration, complications,
Asymptomatic and then stage 1 (CD4>500) --> 4(AIDS) CAn live for years without it taking over- have class 1 MHCs that can present to CD8 T cells instead which destroy it
Most people have average life expectancy with treatment
Hep B
Structure
Transmission
dsDNA
Isocahedral
Enveloped
Fluids and blood
Hep B
Mechanism of infection
Pathogenesis, virulence factors
Presentation
How does it cause disease
Nucleocapsid core with envelope with surface antigen HBcAg
Virus enters blood stream
Surface antigen Binds to receptor on hepatocyte
Nucleocapsids: enter cell and reach nucleus
Replicate within
Tkillers recognise and destroy (and kill cell)
Hepatitis: liver failure, jaundice, fatigue, abdominal pain, Nausea, joint pain
Hep B
Describe the duration of the illness and the serotypes you would see in the blood
Normally self resolves after 6 months but can become chronic
HBsAg- surface antigen, within 6 days (ALT/DNA levels rising too)= infections
HBsAg: e antigen: highly infections period
IgM released (1st antibody, immune system started to fight back)
HBsAb: antibody to e antigen= end of infections period. Virus inactive :) patient recovered
HbsAb: surface antigen antibody - memory cells in vaccinated/ resistant people
IgG- core antibody persists for life
What is chronic HepB
Complications?
Hepatitis b infection >6mths
HBsAg persisted
Can lead to cirrhosis
Of hepatocellular carcinoma
Treatment hepatitis b
Investigations
Stop drinking, non essential medications
Fever reducers , pain relief
Vaccinate- prevention better, or (within 24hrs infection)
Normally self resolves but can give antiretroviral drugs in chronic infection or pefinterferon Alfa 2a to stimulate immune system
FBC, u snd Es , LFTs, CRP, Hep C antibody test, PCRl
Hepatitis c
Structure
Transmission
+ssRNA
Icosahedral
Enveloped
Blood NOT FLUIDS
Hep c Pathophysiology Treatment Investigations Complications
Virus travels to liver and replicates within hepatocytes but often asymptomatic. Most don’t know
Investigations: FBC, u snd Es , LFTs, CRP, Hep C antibody test, PCR
May have dark urine and RUQ pain, helatomegaly?
Treat: smoking, drinking, excercise, antiviral (ribavirin), interferon (stimulates immune system)
–> cirrhosis, liver failure, liver cancer
varicella zoster
Structure
Transmission
Herpes family
Ds DNA
Enveloped
Trams,isisom: inhalation, direct contact with blisters
VZV
Pathogenesis
Who at risk
Immune compromised
Young children very common (chicken pox) much more serious in adults
Normal immune response:
Class 1 MHC –> cd8 T cells –> cytotoxic T cells
IgG antibodies persist = lifelong immunity
VZV
how does shingles occur?
Reactivation of the dormant virus
- lies dormant in dorsal ganglion of sensory nerves–> dermatome formation
- if immunecomp
Shingles : red rash (pox raised and itchy)
Aspergillus fumigatus
Mechanism of infection
In the air normally spores always present and inhaled
Rod shaped
Causes disease I’m immunocomprimised patients - opportunistic
Likes high O2 areas, carbon rich surfaces - starchy foods, organic material
Communised in the lungs–> chronic pulmonary aspergillosis
Aspergillus fumigatus
How does this body defend against this fungus
Cleared by mucocillary escalator –> pharynx –> swallowed
Alveolar macrophages :)
In ill patients: phagocyte deficiency–> multiplication of fungi :O
Aspergillosis- investigations and treatment
FBC, u snd Es , LFTs, CRP, PCR, CXR, sputum culture,
Antifungals: ampotericin
Colony stimulating factors in some cases
Ant pyrexials, pain relief
Avoid abundant spores
Plasmodium falcilarum
Structure, other strains,
Protozoa
P. Vivax
P. Ovale
P. Malariae
Via anopheles mosquito (saliva–> blood)
P falcilarum –> malaria?, how..
Blood stream by sporozites To liver Divide and rupture hepatocytes Thousands of merozites released --> rbc (hb used)--> oncosis and burst --> gameocytes released = haemolytic anaemia
Gameocytes adhere to endothelium in bra in–> cerebal malaria –> coma :O
Malaria, presentation investigate treat
Fever chills sweats 3 day cycle
Travel hx
Splenomegaly
3 blood smears, identify parasite strain,
FBC, u snd Es , LFTs, CRP, coagulation studies, head CT scan, PCRmof nucleic acid but too slow
Treat depends on strain: quinine/atovaquone-progunail
Or chloroquine in non resistant
Coma convulsions death
HIV diagnosis
Blood culture
PCR and antigen detection of genome
ELISA: antibody screening tests
Western blotting: antibodies
obligate anaerobes, where found in the body
Clostridium tetani (protective endospores) Bacteriodes - fragillis - oralis - melaniogenicus
Small bowel and COLON
Bacteria in colon
Anaerobes: clostridium tetani, difficile (antibiotics) perfringens (gas gangrene). Bacteriodes fragillis etc
Enterococcus faecalis
E. coli
Other Pseudomonas Klebsiella Salmonella Shigella Vibro cholera
In bowel/colon surgery what prophylaxis antibiotic would you give?
treat anaerobes, bacilli and cocci
Metronidazole: anaerobes
Gentamicin/cephalosporin: broad spec
Complications of bowel surgery and infections
Faecal peritonitis (peritoneum infected) Perinatal abscess (glands infected)
Most common UTI organisms
E.coli
Enterococcus faecalis
Gram neg: klebsiella, proteus, pseudomonas
Common mouth bacteria
Streptococci: gingivitis
Staphylococci:
Candidia
Lactobacili
Comps: infective endocarditis
Throat bacteria
Lots, think pneumonia and infections Staph strep Strep pyrogens--> tonsillitis (30% are bacterial) N. Meningitidis Haemophilius influenzae Candidia Lactobacilli
Nose bacteria
Staph
Strep
MRSA
Stomach
Helicobacter pylori in 50% pop
Duodenal (and gastric) ulcers in 20%
Other than that it’s sterile
Vagina
Lactobacili
Turn acidic
Perineal skin
Aerobic so no obligate anaerobes e,g, bacteriodes
E. coli, lactobacili, enterococcus faecalis
