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MD1 > Microbiology > Flashcards

Microbiology Flashcards

1
Q

Acid Fast

A

Thick waxy walls
Peptidoglycan base layer
Additional layers of arabinogalactan, mycolic acid, and lipid
Slow bacterial growth

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2
Q

Adenovirus

A 
dsDNA
No envelope
Icosahedral capsid
Decrease MHC-I expression (bind in ER)
Small RNA prevent PKR
Cytokine interference
DISEASES:
Pharyngoconjunctival fever
Pneumonia
Intestinal illness (mesenteric adenitis, intussusceptoins)
Hepatitis
Conjunctivitis - pink eye
Haemorrhagic Cyctitis

TREATMENT:
Ribavirin
Cidofovir

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3
Q

Coronavirus

A

ssRNA +
Envelope
Helical capsid

DISEASES:
Common cold
Gastroenteritis
Severe acute respiratory syndrome (SARS)
Severe LRTI
Encephalitis (via olfactory bulb)

TREATMENT:
No treatment

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4
Q

Hepatitis A

A 
Picornavirus
ssRNA +
No envelope
Icosahedral capsid
Single serotype worldwide

DISEASES:
Incubation 15-30 days
Symptoms 2-3 weeks
Hepatitis (jaundice, pale faeces, dark urine)

TREATMENT:
Normal IgG response
Inactivated Vaccine

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5
Q

Hepatitis B

A

dsDNA (circle, gapped)
Envelope
Icosahedral capsid

DISEASES:
Incubation 60-90days
Acute (adults) and chronic (children) hepatitis
can be acquired by child at time of delivery (maternal blood)
Cirrhosis
Hepatocellular carcinoma
Acute: HbsAg, anti-HBc IgM, 
Chronic: HbsAg, anti-HBc IgG

TREATMENT:
Interferon alpha for HBeAg +ve carriers
Nucleoside/Nucleotide analogues (Lamivudine or Adefovir)
Vaccination + Hep B Ig

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6
Q

Hepatitis D

A

ssRNA
Envelope
Heterogeneous satellite capsid
Requires Hep B to provide envelope proteins

DISEASES:
Acute and chronic hepatitis
Cirrhosis

TREATMENT:
Treat hep B

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7
Q

Hepatitis C

A 
Flavivirus
ssRNA +
Envelope
Icosahedral capsid
High genomic deversity

DISEASES:
Incubation 6-7weeks
Acute and chronic hepatitis
Cirrhosis

TREATMENT:
OLD: Peg-INFalpha + Ribavirin
NEW: RNA polymerase inhibitors, Protease inhibitors (Simeprevir) = curative

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8
Q

Hepatitis E

A 
ssRNA +
No Envelope
Icosahedral capsid
Spread by enteric-oral route
Fatality 15%-25% pregnant women

DISEASES:
Sporadic acute hepatitis
Incubation 40 days

TREATMENT:
Supportive

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9
Q

Bacillus anthracis

A 
Gram-positive
Rods
Endospore-forming 
Aerobic
Has protein capsule (polypeptide)
Environmental (soil)

DIAGNOSIS:
PCR
Fluroescent antibody stain

DISEASES:
Anthrax

TREATMENT:
β-lactam antibiotics (penicillin)
Fluroquinolones (ciprofloxacin)
Tetracycline (doxycycline)

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10
Q

Candida albicans

A

Diploid Fungus
Yeast
Opportunistic pathogen (immunosuppressed)
Part of normal skin, mouth, intestine flora
Typically invades mucosal surfaces (white discharge and growth)

DIAGNOSIS:
Culture on SDA
Germ tubes (pseudohyphae) visible on microscopy

DISEASES:
Candidiasis (mucocutaneous, chronic, systemic)
Thrush

TREATMENT:
Topical antifungals (nystatin, miconazole)
Fluconazole for disseminated disease

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11
Q

Clostridium perfingens

A 
Gram Positive
Rods
Strict anaerobe
Spore forming
Normally found in environment and GI tract

DIAGNOSIS:
Haemolytic on HBA
Naglers test positive
Degrades litmus milk

DISEASES:
Gas Gangrene
Food poisoning

TREATMENT:
Wound debridement and cleaning
Penicillin prophylaxis (or metronidazle, imipenem)
Hyperbaric oxygen

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12
Q

Enterococcus faecium

A 
Gram Positive
Cocci (diplococci and chains)
Facultative anaerobe
Heat & Salt tolerant
GIT commensals

DIAGNOSIS:
Alpha haemolytic
Optochin resistant

DISEASES:
Urinary Tract Infection
Endocarditis
Septacaemia (following surgery and immunocompromisation)

TREATMENT:
Resistant to cephalosporins
Vancomycin Resistant Enterococcus (VRE)
Linezolid or daptomycin for VRE

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13
Q

Escherichia coli

A 
Gram Negative
Rods
Facultative anaerobe
Motile (some strains)
Some capsulated
Normal gut flora
DIAGNOSIS:
Lactose fermenter 
Grows on bile-containing selective media
DISEASES:
Urinary Tract Infection
Diarrhoea
Neonatal meningitic
Septacaemia
TREATMENT:
Antibiotic sensitivities vary widely (often plasmid mediated)
Use susceptibility testing
Amoxicillin
Cephalosporins
Amioglycosides
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14
Q

Gram Negative Cell Wall

A

PINK
Outer membrane stabalised by Lipopolysaccharide (PAMP / endotoxin)
Has periplasmic space with peptidoglycan wall

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15
Q

Gram Positive Cell Wall

A

PURPLE
Large amount of peptidoglycan and teichoic acids
peptidoglycan made of n-acetyl-glucosamine and n-acetal-muramic acid joined by pentapeptide bridges

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16
Q

Haemophilus influenzae

A

Gram Negative
Rods (coccobacilli) - very very tiny
Facultative anaerobe
May have capsule (polysaccharide)

DIAGNOSIS:
Catalase positive
Oxidase positive
Latex agglutination
X+V growth (grows on CHA not HBA)
DISEASES:
Otitis media!!
URTI & LRTI
Adult Meningitis!!
Epiglottitis (Type B)
Osteomyelitis
Chronic bronchitis
Grey/creamy expectorate with wheeze and cough 
TREATMENT:
Penicillin resistant
Ampicillin (if susceptible)
Cephalosporins (cefotaxime, ceftriaxone)
Rifampicin
Fluroquinolones
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17
Q

Klebsiella pneumonia

A 
Gram negative
Rods
Non-motile
Facultative Anaerobe
Has capsule
Normal flora of skin and GI.
Opportunistic pathogen

DIAGNOSIS:
Lactose fermenter
Bile tolerant
Oxidase Negative

DISEASES:
Urinary tract infections
Respiratory tract infections

TREATMENT:
Surgical clearing
Ampicillin (and other antibiotics)
Multiple antibiotic resistances (usually plasmid mediated)
Susceptibility testing generally required

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18
Q

Myocbacterium tuberculosis

A 
Gram Positive - Acid Fast (thick waxy walls – mycolic acid)
Rods
Highly aerobic
Slow growing
Infect respiratory system

DIAGNOSIS:
Ziehl-Neelsen Stain
PCR

DISEASE:
Tuberculosis
(esp. AIDS & immunocompromised)

TREATMENT:
Combination of antimycobacterial drugs

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19
Q

Neisseria (gonorrhoeae & meningitidis)

A

Gram Negative
Cocci (diplococci - often intracellular)
N. meningitis has capsule
Complement immunity (MAC) important
Gonnorrhoea typically asymptomatic (80% of females)
Gonnorrhoea likes to grow in columnar epithelium

DIAGNOSIS:
Extremely fastidious (rich growth medium needed) 
Growth on CHA
Cervical swab in charcoal
GNC visible inside WBCs
Thayer Martin Agar growth
DISEASES:
meningitis
septicaemia (rash)
Gonorrhoea (2-7 day incubation)
Pelvic inflammatory disease
Chlamydia co-infection common
Neonatal gonococcal opthalmia

TREATMENT:
Highly antibiotic resistant (freely shares genes)
Penicillin
Ceftriaxone (third generation cephalosporin)
+ azithromycin

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20
Q

Pseudomonas aeruginosa

A 
Gram Negative
Rod
Has capsule
Aerobic (or facultative)
Motile (flagella, pili)
Environmental (soil, skin, gut flora)
Produces endotoxin A (LPS) - block protein synthesis
Oportunistic pathogen
Produces biofilm after quorum-sensing (slows growth, loses O-antigen, less invasive, more adherent, non-motile, increased resistance due to slowed growth and biofilm)
DIAGNOSIS:
Lactose non-fermenter
Clear colonies on MAC
Catalase & Oxidase positive
Blue-green pigment
Growth on Citrimide
DISEASES:
Pneumonia
Sepsis
External otitis (swimmers ear)
UTI
Skin and burns (post)
Cystic Fibrosis infections (deadly) (LPS usuall binds to CFTR)
Urinary tract infections
Endocarditis
TREATMENT:
Heavy resistance (chromosomal β-lactamase & acquired from other bacteria) – need to test 
Beta-lactam + Aminoglycoside
Ticarcillin & Tobramycin
Prevention!! - hand hygiene
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21
Q

Rotavirus

A

dsRNA (segmented)
No envelope
Icosahedral triple/double capsid
uses trypsin (in gut) to shed outer layers so virus has access to receptors

DISEASES
Diarrhoea
Gastroenteritis
Dehydration (death)

TREATMENT:
Supportive
Vaccination

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22
Q

Salmonella (enterica & typhi)

A

Gram Negative
Rods
Motile
Facultative anaerobes
From food chain (poultry, eggs, milk, meat)
Invade sub-mucosa or systemic
Typhi survive within macrophages (migrate via lymph to liver/spleen/bone/intestine)
patients deficient in IFN-gamma are susceptible to infection (latent liver/bone infections)

DIAGNOSIS:
Non-lactose fermenting
Oxidase negative
Growth on MAC (white/clear colonies)
Growth on DCA 
O,H antigens
Vi antigen (S. typhi & paratyphi)

DISEASES:
Diarrhoea
Septacaemia (S. typhi)
Anaemia w/ slight splenomegaly (S. typhi)
Intestinal haemorrhage (late stage S. typhi)
Typhoid fever (S. typhi)
S. typhi induces apoptosis of macrophages (can hide inside them)

TREATMENT:
Susceptibility tests (antibiotics)
Antibiotic resistance is increasing
Ciprofloxacin

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23
Q

Shigella

A 
Gram Negative
Rods
Facultative Anaerobe
4 species (dysenteriae, flexneri, boydii, sonnei)
Closely related to salmonella.
same species as E.Coli
Humans only reservoirs

DIAGNOSIS:
Negative motility
Non-lactose fermenting,
Growth on Mac (white/clear colonies)

DISEASES:
Causes dysentery (intestinal infection)
Presence of blood in faeces
Induces macrophage apoptosis 
S. dysenteriae has shiga toxin

TREATMENT:
Ampicillin, fluroquinolones (e.g. ciprofloxacin)
Some Shigella resistant to antibiotics so administer sparingly

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24
Q

Staphylococcus aureus

A 
Gram Positive
Cocci (grapelike clusters)
Facultative anaerobe
Some capsulated
Normal flora of skin, upper respiratory tract & pathogen (gastroenteritis, sinusitis, skin infections) 
TSStoxin - binds MHCII
Primary defense is innate (via neutrophils)
Adaptive immune response is weak

DIAGNOSIS:
“golden staph” – white or yellow colonies on HBA
b-Hemolysis when grown on HBA
Catalase positive (produces catalase enzyme – converts H2O2 to water and oxygen)
Coagulase positive (fibrin clot formation)
Ferments mannitol anaerobically

DISEASES:
Skin infection
Pneumonia
Toxic Shock Syndrome
Endocarditis
Osteomyelitis
Post-op wound infection
Catheter associated infection
Gastroenteritis (ingested heat stable toxin - food poisoning 2-6hr incubation)
UTI (kidney abcess via blood)

TREATMENT:
Penicillin (may be resistant due to β-lactams)
Flucloxacillin (for penicillin resistant bacteria)
Combination with gentamicin (may cause kidney damage)
Aminoglycosides not effective
Possible methicillin and vancomycin reisistance

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25
Q

Staphylococcus epidermidis

A

Gram Positive
Cocci
Opportunistic (part of normal human skin flora and some mucosal)
Facultative anaerobe
Infection associated with device-related sepsis (forms biofilms well)

DIAGNOSIS:
Forms white colonies on HBA
Non-haemolytic
Catalase positive (produces catalase enzyme)
Coagulase negative
Lactose fermenter
Novobiocin sensitive (otherwise its S. saprophyticus)

DISEASES:
Wound infections (can produce biofilms) - IV catheters

TREATMENT:
Often resistant to penicillin, amoxicillin, and methicillin
Vancomycin with aminoglycoside (gentamicin) are drugs of choice
Treat for a long time due to biofilm

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26
Q

Streptococcus pneumoniae

A

Gram Positive
Cocci (diplococci)
Pyogenic
Polysaccharide capsule
Normal flora of mouth & respiratory tract, may cause HCAIs involving neutropaenia or humoral immune defects (encapsulated)
Naturally transformable (takes up DNA easily)
Modified penicillin-binding proteins are the basis for penicillin resistance (not penicillinase)

DIAGNOSIS:
Alpha-haemolytic (greening)
Capsule may present as 'halo' on gram stain
Facultative Anaerobe
Catalase negative
Optochin susceptible
DISEASES:
Pneumonia (typically lobar)
Septacaemia
Meningitis
Otitis media

TREATMENT:
Penicillin
Vancomycin (if resistant to penicillin, quinolones, tetracyclines, and cephalosporins)
Pneumococcal conjugate vaccine

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27
Q

Streptococcus pyogenes

A

Gram Positive
Cocci (chains)
Group A Strep (group A antigen on cell wall)
Normal flora of skin, mouth and pharynx (strep throat) & pathogen (gastroenteritis)
Pyogenic
Has capsule (hyalurinoc acid) - not antigenic

DIAGNOSIS:
Beta haemolytic
Catalase negative
Facultative anaerobe
Bacitracin sensitive
No growth on MAC

DISEASES:
URTI
Skin, throat, and soft tissue infection (pharyngitis, cellulitis, lymphadenitis)
Scarlet fever, necrotizing fasciitis (‘flesh eating’)
Rheumatic Fever (M-proteins)
Glomerulonephritis (Type III hypersensitivity)
Septacaemia
Osteomyelitis
Toxic Shock Syndrome

TREATMENT:
Penicillin (long term due to likelyhood of reinfection)
Tetracyclines, cehpalosporin (cefotaxime), or vancomycin/genatmicin
Hygiene

(NB: Strep agalactiae similar - causes neonatal meningitis but also grows on MAC and is bacitracin resistant)

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28
Q

Yersinia pestis

A

Gram Negative
Rods
Facultative anaerobe

DIAGNOSIS:
Lactose non-fermenting (MAC white colonies)
Immunofluorescence
Growth on CIN agar

DISEASES:
Bubonic plague
Induce macrophage apoptosis
Invasive pathogen (gastroenteritis and infects mesenteric lymph nodes - haemorrhagic and necrotic lesions)
Reiter’s syndrome - arthritisi/urethriris/conjunctivitis following GI infection

TREATMENT:
Streptomycin
Tetracycline
Fluroquinolones
Doxycycline 
Gentamicin
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29
Q

Influenza Virus

A

ssRNA -
Envelope
Helical capsid
Antigenic Drift

PATHOGENESIS:
Haemagglutinin attaches to sialic-acid receptors (alpha2-6)
Endocytosis
H+ causes confirmational change (via M2)
Replication
Budding
Neuraminidase cleaves sialic-acid from glycoproteins
Tryptase clara activates HA (becomes infectious)
If uncleared can move down airways (lead to secondary bacterial infection)

DISEASES:
Influenza (1-5 day incubation, 5-6 infectious)
Fever
Malaise & loss of appetite
Sore Throat
Cough
Pneumonia

TREATMENT:
Zanamivir (neurominidase inhibitor)
Amantidine/Rimantadine (M2 ion channel block)
Vaccination

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30
Q

Papillomavirus

A

dsDNA
No envelope
Icosahedral capsid

DISEASES:
Warts (sexually transmitted)
Carcinoma (cervix)

TREATMENT:
Freezing
Lazer
Cidofovir

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31
Q

Measles

A 
Paramyxovirus
ssRNA -
Envelope
Helical capsid
Interferes with surface proteins (prevent T cell activation)

PATHOGENESIS
Respiratory, infects local macrophages & lymphocytes (Koplick spots), drains to LN and amplifies (spleen/liver), returns to lung and mouth.

DISEASES:
Fever
Nasal discharge
Rash
Subacute Sclerosing PanEncephalitis (SSPE) - slow growth between neural cells over 30 years (no budding)  - (via blood)

TREATMENT:
Vaccination

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32
Q

Mumps

A

Paramyxovirus
ssRNA -
Envelope
Helical capsid

DISEASES:
Parotitis (salivary gland inflammation)
Aseptic Meningitis (via blood)
Incubation: 12-25days

TREATMENT:
Vaccination

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33
Q

Respiratory Syncytial Virus (RSV)

A 
Paramyxovirus
ssRNA -
Envelope
Helical capsid
Decrease MCH-I expression
DISEASES:
Common cold
Bronchiolitis
Pneumonia
Incubation: 2-8 days

TREATMENT:
Aerosolized ribavirin

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34
Q

Parvovirus

A 
ssDNA
No envelope
Icosahedral capsid
Incubation period 4-21 days
shortens lifespan of RBC progenitors in bone marrow

DISEASES:
Erythmea
Slap-cheek rash
Fever
Arthopathy/arthralgia (joint inflammation)
Acute aplastic crisis (chronic haemolytic anaemia)
Fetal Death (febrile convulsions) - due to RBC destruction
Hydrops foetalis

TREATMENT:
Intravenous IgG

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35
Q

Enterovirus

A 
Include Coxsackie, Echo, Polio
Fecal-oral transmission
Picornavirus
ssRNA +
No envelope
Icosahedral capsid
Replicate in pharynx and GIT

DISEASES:
Aseptic meningitis
Rashes

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36
Q

Poliovirus

A 
Picornavirus
ssRNA +
No envelope - lyses cells
Icosahedral capsid (hardy - enterovirus)
Low Neuroinvasiveness
High Neurovirulence
PATHOGENESIS:
Gut lymphoid tissue invasion
Migration to regional lymph
Viremia
Crosses BBB (8-12 days)
Replicates in anterior horn cells (has receptor)
Excreted in faeces (5-45 days)

DISEASES:
Aseptic meningitis (via blood)
Paralytic poliomyelitis

TREATMENT:
Vaccination (Sabin, Salk)

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37
Q

HIV

A 
ssRNA +
Retroviridae
Envelope
Icosahedral capsid
Antigenic Drift
Decrease MHC-I expression
PATHOGENESIS
Binds to CXCR4 and CCR5
dsDNA integrated to host DNA
replicated in nucleus
assembles and buds at plasma membrane
DISEASES:
Mononucleosis
Aseptic Meningitis (via blood/monocytes)
AIDS -> Encephalitis -> Dementia
Weight loss

TREATMENT
Zidovudine, tenofovir and nevirapine:
nucleoside nucleotide, and non-nucleoside reverse transcriptase inhibitors.
Control maternal disease & lower viral load

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38
Q

Rhabdovirus

A 
ssRNA -
Envelope
Helical capsid
Obligatory nerve cell growth
Highly Neuroinvasive
HIghly Neurovirulent
PATHOGENESIS:
puncture wound
replicates in myocytes
retrograde travel via axonal fibres 
replicates in spinal neurons
retrograde to brain & salivary glands (acinar)
DISEASES:
Rabies (incubation 12-70days)
Meningitis/Encephalitis (via axons)
Aggression
Thirst
Seisures
Paralysis
Coma
Death

TREATMENT
Human rabies specific
Vaccination during window of opportunity (cell mediated immunity takes approx 10 days)

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39
Q

Rubella

A 
Togavirus
ssRNA +
Envelope
Icosahedral capsid
25-50% asymptomatic
spread in nasopharyngeal secretions
inbubation 14-21 days
DISEASES:
Mild rash (face, trunk, limbs)
low grade fever
lymphadenopathy (behind ears and neck)
rash 
Congenital rubella syndrome (slows down rate of cell division causing microcephaly, patent ductus arteriosus, cataracts, deafness, neurological, IDDM, thrombocytopaenia, etc.)

TREATMENT:
Vaccination

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40
Q

Corynebacterium diphtheriae

A

Gram Positive
Rods
Facultative anaerobe

DIAGNOSIS:
Catalase positive
PCR

DISEASES:
Diphtheria (throat or skin)

TREATMENT:
Antitoxin
Penicillin
Immunization

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41
Q

Clostridium tetani

A 
Gram Positive
Rods
Spore forming
Strict Anaerobe
Environmental (soil)

DIAGNOSIS:
Ground glass appearance on HBA

DISEASES:
Tetanus (lockjaw)
Muscle spasms / convulsions

TREATMENT:
Anti-toxin
Metronidazole
Anti spasmolytic drugs
Immunization with toxoid
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42
Q

Clostridium botulinum

A

Gram Positive
Rods
Spore forming
Strict anaerobic

DISEASES:
Botulism - inhibit ACh release.
Muscle paralysis and respiratory failure.
Typically due to ingestion of preformed toxin

TREATMENT:
Trivalent antitoxin
Penicillin and metronidazole for wounds

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43
Q

Legionella pneumophilia

A

Gram Negative
Rod
Aerobic
Lives in air-conditioning systems

DISEASES:
Legionnaires (atypical pneumonia)

TREATMENT:
Fluroquinolone

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44
Q

Pneumocystis JirovecIi (Carinii)

A

Fungus (originally classified as protazoa)
Lives extracellularly within alveoli
AIDS defining pathogen (pneumocystis pneumonia)

DISEASE:
Pneumonia-like (diffuse interstitial)

TREATMENT:
Co-trimoxazole

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45
Q

Coxsackie Virus

A

Picornavirus
ssRNA+
No envelope
Icosahedral capsid

DISEASES:
Aseptic Meningitis (via blood)
Encephalitis
Herpangina
Myopericarditis
Hand-foot-mouth disease
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46
Q

Rhinovirus

A

Picornavirus
ssRNA+
No envelope
Icosahedral capsid

DISEASES:
Common cold
Optimal growth at 33deg (URT)

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47
Q

Atypical pneumonia causative agents and clinical signs

A

Mycoplasma, coxiella, chlamydia pneumoniae, legionella
no cough, no mucus, no sputum, no abcesses, no consolidation
infection in INTERSTITUM (macrophages, lymphocytes, plasma cells)
Systemic symptoms predominate over respiratory
Walking patient CXR shows pneumonia

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48
Q

Acute pneumonia causative agents and clinical signs

A

Strep pneumoniae, H, influenzae, S. aureus, Klebsiella, Legionella
Inflammation in AIRWAYS
Acutely ill, high fever, evidence of consolidation, productive cough

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49
Q

Mycoplasma pneumoniae

A

No cell wall

DISEASES:
Atypical pneumonia

TREATMENT:
Doxycycline
Erythromycin
beta-lactams useless due to no cell wall

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50
Q

Protein Kinase R

A

Stimulated by IFN
requires viral RNA to help autophosphorylate
inactivates translational enzymes

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51
Q

Viral Immune Evasion

A

Antigenic Drift - Inflenza, HIV
Latency - HSV in neurones, EBV in B cells (inhibits proteosome)
Decrease MHC I - HIV, RSV, adenovirus (bind in ER)
(PKR) Small RNA - adenovirus, EBV
(PKR) RNA protection - reovirus, vaccinia
(PKR) eIF2a homologue - vaccinia
Cytokine production block - vaccinia, cowpox
Cytokine interference - adenovirus
TLR signal transduction - HSV
TAP block - HSV, CMV
TLR4 homologue - vaccinia
Surface Protein interference (TCell activation) - measles, CMV
MHC I homologue - CMV (inhibit death signal from NK)

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52
Q

Which sense RNA must bring its own RNA polymerase?

A

Negative

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53
Q

Diarrhoea Syndromes #1

  1. Non-specific gastro
  2. Dysentery
  3. Foodborne
  4. Travellers’ diarrhoea
A
  1. Viruses, bacteria protozoa
  2. Shigella, EIEC, protazoa
  3. S. Aureus, Salmonella, C. Perfringens, Bacillus, Vibrio, Listeria, viruses.
  4. ETEC, other bacteria, viruses, protazoa
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54
Q

Diarrhoea Syndromes #2
1. Antibiotic associated colitis

  1. Haemorrhagic colitis (blood no pus)
  2. Cholera-like (severe watery)
  3. Enteric fever (systemic infections)
A
  1. C. Difficle
  2. EHEC
  3. Vibrio Cholerae, ETEC
  4. Salmonella Thyphi, S. Paratyphi
55
Q

ETEC

A 
Enterotoxigenic
Colonisation factor antigen (adhesin in small bowel)
enterotoxins (LT/ST)
- heat stable
- heat labile (similar to cholera toxin)
Adhere to microvilli (CFA)

Symptoms:
Cholera-like: watery diarrhoea (Travellers)

Epidemiology:
infants in LDCs, travellers

56
Q

EPEC

A

Enteropathogenic
intimin, Bfp
T3SS (intimin&TIR)
Destroy microvilli

Symptoms:
non-specific gastro

Epidemiology:
Children in LDCs

57
Q

EHEC

A

Enterohaemorrhagic
intimin, Efa
Shiga toxins (interfere with protein synthesis)
Does not ferment sorbitol (unlike other E.coli)

Symptoms:
bloody diarrhoea
Shiga toxin cause HUS

Epidemiology:
any age (developed countries)
58
Q

EIEC

A

Enteroinvasive
- Shigella-like but does not have shiga-toxin so does not cause haemolytic uraemic syndrome or haemorrhagic colitis

Symptoms:
dysentery (similar shigella dysenterae)

Epidemiology:
any age (mainly LDCs)
59
Q

EAEC

A

Enteroaggregative

Symptoms:
watery diarrhoea

Epidemiology:
Children in LDCs

60
Q

Parasite Definitions

  • Definitive Host
  • Intermediate Host
  • Paratenic Host
  • Reservoir Host
A

Definitive Host
- host in which the parasite REACHES SEXUAL MATURITY

Intermediate Host
- host in which DEVELOPMENT OCCURS but parasite does not reach sexual maturity

Paratenic Host
- host in which parasite enters the body and does not undergo development but REMAINS INFECTIVE

Reservoir Host
- ANIMAL HOST for parasite that also INFECTS HUMANS

61
Q

Lice

Pediculus humanis, P. capitis, Phthirus pubis

A

Obligate blood sucking parasite
P. humanis - body louse, clothing spread
P. capitis - head louse, contact spread
P. pubis - ‘crabs’, contact spread

SYMPTOMS: itch, macules, 2nd degree infection
DIAGNOSIS: detection of eggs
TREATMENT: topical insecticides
SIGNIFICANCE: vector of rickettsia and spirochetes

62
Q

Mites (Sarcoptes scabei)

A

Live in tunnels in epidermis (fingerwebs etc.)
Lifecycle on single host
Contact spread

SYMPTOMS: itch, dermatitis, crusting (in immunosuppressed patients)
DIAGNOSIS: detection of mite in scrapings
TREATMENT: Ivermectin, topicals
CONTROL: sterilize clothes/bedding

63
Q

Ticks (Ixodes holocyclus)

A

Major infectious vector (bacteria, virus, rickettsia)
Some cause paralysis ( Guillian-Barre like neurotoxin)
Spread lime disease outside of Australia

SYMPTOMS: rapid ascending paralysis

64
Q

Entamoeba histolytica

A

Amoeba
Invades tissues in colon
Fecal-oral transmission
May cause liver / brain abscess (migration through colon wall)
Commensal or pathogen (ingests red cells)

DISEASES
Cause amoebic dysentery (large watery volume, very dehydrating)

DIAGNOSIS: faecal cysts, serology

TREATMENT: metronidazole  + paromomycin
reinfection common (low immune response)
65
Q

Giardia intestinalis/lamblia

A 
Flagellate, primitave eukaryote
Faecal-oral transmission
Zoonotic (possums)
Asymtomatic
lives in duodenum as trophozoite

SYMPTOMS: diarrhoea (acute to chronic), bloating, flatulence
DIAGNOSIS: cysts in faeces
TREATMENT: tinidazole
reinfection common (low immune response)

66
Q

Toxoplasma gondii

A

Obligate intracellular parasite (protozoan)
Primarily in cats & birds (infects all mammals)
Humans intermediate host (becomes cysts)
Infection persists for life
Can form cysts (organ transplant complications)
Congenital infection can be serious (rash, LN, hydrocephalus) - 70/80% asymptomatic at birth

SYMPTOMS: asymptomatic, CNS lesions, muscle cysts, occular disease in HIV
DIAGNOSIS: serology (screen pregnant)
TREATMENT: bactrim
CONTROL: cook food, avoid cats

67
Q

Enterobius vermicularis

A 
Pinworm (nematode)
Highly contagious
1cm long
female lays eggs outside of anus at night
(transferred to fingers / faeces)

SYMPTOMS: perianal itch
DIAGNOSIS: stickytape test
TREATMENT: antihelminthic
reinfection common (low immune response)

68
Q

Ascaris lumbricoides

A

Large intestinal roundworm (30-40cm)
Female lays 200,000 eggs per day
Embryonisation occurs in soil
FO route w/ fertalized egg (double layered)
Migrate from intestines to lungs (mature) and down oesophegus
Approx 2-3months from ingestion to oviposition
Adult can live 1-2 years

SYMPTOMS: GI obstruction, cholecystis, pneumonitis (possibly asthma-like), anaemia (loss of iron & protein)
DIAGNOSIS: eggs in faeces, obstruction imaging
TREATMENT: antihelminthic (benzimidazoles)
reinfection common (low immune response)
  • hookworms similar but less complications
  • Ancylostoma duodenale, Necator americanus
  • penetrate through skin (can cause local itching
69
Q

Strongyloides stercoralis

A 
Nematode
>100m infections worldwide (esp. Vietnam Vets)
Penetration of skin (usually feet)
Migrate via circulatory system
Bronchotracheal migration (causes pathology)
Live in small intestine epithelium
Female lays 50 ova/day
Embryonisation in colon
Produce eggs (hatch rapidly)
Autoinfection or larvae passed in stool

SYMPTOMS: migration may bring gram negative bacteria from gut (GN hyperinfection)
DIAGNOSIS: eggs in faeces, serology
TREATMENT: antihelminthic (ivermectin)
reinfection common (low immune response)

70
Q

Schistosoma mansonii

A

Fluke causing bilharzia
Lives in intestinal veins
transmitted by fresh water snails (penetrates skin)

SYMPTOMS: swimmers itch, hepatomegaly, splenomegaly, portal hypertension, pulmonary fibrosis
DIAGNOSIS: eggs in faeces, serology
TREATMENTS: antihelmintic
IMMUNITY: persistent (re)infections and immune evasion

71
Q

Echinococcus granulosus

A

Tapeworm
Zoonotic (sheeps, dogs)
Humans are accidental intermediate host (but don’t produce viable eggs)
Larval cysts known as HYDATID cysts (liver, lungs)

DIAGNOSIS: imaging, serology
TREATMENTS: surgery, PAIR (puncture, aspirate, inject, reaspirate), antihelmintics
IMMUNITY: vaccination (livestock) induces protection against egg infection

72
Q

Taenia saginta & solium

A

Tapeworm causing neurocystercercosis
Zoonotic (pork)
Humans can be both definitive and intermediate hosts
10m long, 300,000 eggs/day
T. solium forms cysts in subcutaneous and neural tissues

SYMPTOMS: cysts, epileptic foci
DIAGNOSIS: serology, imaging
TREATMENTS: antihelmintics (caution) - cyst breakdown can cause systemic immune response & seizure

73
Q

Helicobacter pylori

A

GNR
Catalase, Oxidase, Urease positive
Breaks down urea in food products to amonia

74
Q

Main GI Bacteria

A

Bacteroidetes (Bacteroides, Prevotella)
Firmicutes (Clostridia, Ruminococcus, Lactobaccillus)
Actinobacteria (Bifidobacterium)

Proteobacteria (E.Coli) relatively rare

75
Q

GI Immune Cells & Responses

A

Innate Lymphoid Cells (ICL’s)
resemble Th subsets (produce IFNg, IL-17, IL-22, IL-5, IL-13)
Include
- Lymphoid Tissue Inducer (LTI) cells - recruit DC/T/B cells to PP & ILF
- Intraepithelial Lymphocytes (IEL) - host protection, repair, promote tolerogenic DCs, IL-22, αβTCR (10%γδ)
- NK Cells (NK-22), produce IL-22

Also:
MAIT (mucosal associated invariant T cells) - rapid response to bacterial antigens
Invariant NKT cells - proinflamatory cytokines
Macrophages - low TLR expression and hyporesponsive

76
Q

Clostridium difficile

A

Gram Positive
Rods
Spore forming
Strict Anaerobe (hard to culture - PCR/EIA faster)

Diseases:
GI - pseudo-membranous collitis (toxin causes necrosis of epithelial cells)

Treatment:
Metronidazole / vancomycin
rePOOPulate

77
Q

Treponema pallidum (Syphillis)

A

Spirochete
oro-genital contact

DISEASES
First Degree
- painless chancre
Second Degree (6-8 weeks)
- maculopapular rash (palms/soles), alopecia, hepatosplenomegaly, lymphadenopathy
Third Degree (decades)
- chronic granulomas
- aortitis (vasa vasorum destruction)
- ataxia
- joint destruction
- neurosyphillis
Congenital syphilis
- stillbirth
- rash on feet / palms
- hepatosplenomegaly
- lymphadenopathy
DIAGNOSIS
serology treponemal (specific) and nontreponemal (nonspecific)
(EIA = positive for life, + RPR = current active infection)

TREATMENT
Penicillin G

78
Q

Common Aetological Agents of UTI

A

E.Coli
Proteus (GNR)
Staph saprophyticus

Other: (common nosocomial)
Klebsiella, Enterobacter, Pseudomonas

79
Q

Microbial Factors of UTIs

A

Adhesins (E.Coli: type 1 fimbrae, flagella, PAP - pyelonephritis associated pili)
Polysaccharide Capsule (E.Coli, Klebsiella)
Intracellular bacterial communities
Biofilm formation
Haemolysin (E.Coli) breaks down RBCs
Siderophores - greater affinity for iron than transferrin
Urease & Struvite stones (Proteus)

80
Q

Diagnosis of UTI (Quantitative)

A 
WBC > 10^5
RBC > 10^5
Squamous = 0
MSU Bacteria > 10^5 (esp if only one species)
Catheter Bacteria > 10^5
SPA Bacteria > 0

(transport under 1 hour, keep at 4deg for 18 hours)

81
Q

UTI treatment (Cystitis & Pyelonephritis)

A

CYSTITIS:
Alkalinise
Cephalexin OR co-amoxyclav OR trimethoprim
(3-5 days women, 14 days for men)

PYELONEPHRITIS:
Cephalexin OR co-amoxyclav OR trimethoprim (10 days)
w/ sepsis use ampi/amoxycillin + gentamicin

82
Q

What is the most common cause of meningitis?

A

Viruses, particularly enteroviruses
e.g. Coxsackie, echo
Also: mumps, VZV, influenza, HIV, HSV2

Viruses are typically self limiting and resolve on their own.
Bacteria should always be treated if meningitis is suspected (cefotaxime/ceftriaxone)

83
Q

Which three bacteria are the commonest cause of meningitis in Adults?

A

H. influenza* (GNR)
N. meningitidis (GNC)
S. Pneumoniae (GPC)

Normal commensals of nasopharynx
Good at evading immune system (polysaccharide capsule -> able to evade complement fixation)

84
Q

Which three bacteria are the commonest cause of meningitis in Neonates?

A

group B strep -s. agalactiae (GPC)
Listeria Monocytogenes (GPR)
E. coli / other GNRs

Common bacteria in birth canal
*type B in west, type A worldwide

Treat with IV 3rd generation cephalosporin (e.g. cefotaxime/ceftriaxone)
+ IV penicillin
+ IV gentamicin

85
Q

Common presenting symptoms of meningitis (Adult vs Child)

A 
ADULT
Fever
Vomiting/nausea
Headache
Stiff Neck
Altered Mental State
Photophobia
Seizures
CHILD
Fever
Irritable/unsettled
Refusing food/drink
Altered Mental State
Bulging fontanelle
86
Q

CSF meningitis diagnosis (NORMAL, VIRAL, BACTERIAL, TB)

A

NORMAL
pressure: 150mmH20
appearance: clear
WBC: 60% Blood

VIRAL
WBC: 100*10^6/L
Protein: 0.4-1g/L

BACTERIAL
pressure: raised
appearance: cloudy
WBC: 1000*10^-6L
Gram Stain: positive
Protein: >1g/L
Glucose: <30% Blood
  • NB: WBC count in sample rapidly decreases due to cell lysis
  • Glucose decreased in mumps
87
Q

CHA

A

Heated Horse Blood agar to lyse blood cells and release nutrients.
Good for fastidious organisms like H. influenzae and N. meningitidis

88
Q

HBA

A

Good for isolation of fastidious bacteria
b-haemoloysis (clear) = S. pyogenes, C. perfringens, B. cerus, S. aureus
a-haemoloysis (green) = S. pneumoniae, Viridans strep

89
Q

MAC

A 
Pink = lactose fermentater
Yellow/Clear = non lactose fermenters

Contains Bile salts so good for intestinal bacteria

90
Q

How does cholera toxin work?

A

Acts through second messenger
Causes cAMP to form in intestinal epithelium
- close Na+/Cl- chanels at tip of microvilli
- hypersecretion of ions from crypt

net water excretion

91
Q 
Definitions:
Neurotropic
Neuroinvasive
Neurovirulent
Primary Viral Encephalitits (acute)
Secondary Viral Encephalitis (post-infective)
A

Neurotropic: capable of replicating in nerve cells

Neuroinvasive: capable of entering or infecting the CNS

Neurovirulent: capable of causing disease within nervous system

Primary: direct viral infection

Secondary: results from complications of viral infection

92
Q

What is the most common cause of viral encephalitis?

A

HSV1&2
Rabies
Arbovirus (insect borne)
Enteroviruses

93
Q

How do the presenting features between viral meningitis and encephalitis differ?

A

Meningitis:
Headache, Fever, Neck Stiffness, Photophobia, Vomiting

Encephalitis
As above + personality & behavioural changes, partial paralysis, hallucinations, altered consciousness, coma, death.

94
Q

Herpesviridae (HSV)

A 
dsDNA - linear
Envelope
Icosahedral capsid
Obligatory nerve cell growth
Low Neuroinvasive
HIghly Neurovirulent
Antigentic Drift
TLR signal transduction
TAP block
PATHOGENESIS:
Infected saliva
Primary infection of mucosa (mouth/throat)
Replication locally and clearance (80%)
Primary disease (20%) of nerve endings
Migrate to ganglia (tigeminal/sacral)
Latency & reactivation
-> CNS temporal lobe
DISEASES:
cold sores
vesicular rash
temporal lobe encephalitis/meningitis (via axonal fibres & olfactory),
gential herpes

TREATMENT:
Antivirals (acyclovir)
Reduce stressors to prevent outbreaks (cold, UV, stress, immunosuppression, illness)

95
Q

Herpesviridae (VSV)

A 
dsDNA - linear
Envelope
Icosahedral capsid
Obligatory nerve cell growth
Low Neuroinvasive
HIghly Neurovirulent
PATHOGENESIS:
Infected conjunctiva/saliva (via resp/direct contact)
Replication in regional lymph
Primary viremia (4 days)
Replication in spleen/liver
Secondary viremia
Rash (10 days)
Axonal retrograde infection (latent in dorsal root ganglia)
Acute cerebellar ataxia (2-4 weeks)

DISEASES:
chickenpox (fever, lethargy, vesicular rash)
secondary bacterial infection (staph, s.pyogenes)
pneumonitis (tachypnea, cough, haemoptysis)
shingles
meningitis/encephalitis (acute cerebellar ataxia)
Reye’s Syndrome - cerebral oedema (associated w/ asprin during fever)
congenital varicella

TREATMENT:
Antivirals (acyclovir)
Reduce stressors to prevent outbreaks

96
Q

Herpesviridae (EBV, CMV)

A 
dsDNA - linear
Spherical lipid envelope
Icosahedral capsid
EBV latent in B cells (inhibit proteosome)
EBV small RNA inhibit PKR
CMV TAP block
CMV MHC-I homologue (prevent NK)
CMV surface protein interference (prevent T cell activation)
PATHOGENESIS:
latent infection (WBCs)
reinfection with different strains
shed in all body secretions
survives in environment for up to 24 hours

DISEASES:
EBV - Mononucleosis (Glandular fever), hepatitis
CMV - Mononucleosis, hepatitis, pneumonitis
Guillain-Barre Syndrome
congenital CMV - damage to developing organs (hepatosplenomegaly, rash)
postpartum CMV - sepsislike syndrome (hepatitis, pneumonitits)
Immunocompromised CMV - multi organ failure, graft damage

TREATMENT:
Antivirals (acyclovir, ganciclovir)
Reduce stressors to prevent outbreaks

97
Q

Anti-Streptolysin O Test (ASOT)

A

Test for Strep Gp A, C, G

Antibodies coat streptolysin (endotoxin) so it can’t lise the cell

If lysis occurs there are no antibodies pressent in serum
if lysis is stopped there must be antibodies to streptolysin present

98
Q

Anti-Nuclear Antibody (ANA) Test

A

Test for Antihuman dsDNA, or rNA
positive to autoimmune diseases like SLE and rheumatoid arthritis

Likely to see low complement levels in Type III autoimmunity given that they are used up faster than they can be replaced or host in naturally deficient

99
Q

Frequently Encountered Opportunistic pathogens

A 
E. coli
Staph aureus*
Klebsiella pneumoniae*
Enterococcus*
Pseudomonas Aeruginosa*
Enterobacter*
Serratia
Porteus*
Clostridium difficile

*may cause nosocomial epidemics

100
Q

Host factors affecting colonisation

A

LOCAL:

  • anatomical defects
  • surgical / wounds
  • burns (staph, pseudomonas)
  • catheters
  • foreign bodies

SYSTEMIC

  • Age
  • Leucopenia
  • Malignancy
  • Malnutrition
  • Diabetes (candidiasis may be first sign)
  • liver disease
  • certain infections (measles very immunocompromising)
  • antimicrobials (c. difficile)
  • primary (congenital) immunodeficiency
101
Q

Fungal Classifications

A

Unicellular (yeasts)

  • facultative anaerobes
  • reproduce asexually by budding
  • produce colonies on agar (may be confused with bacteria but are usually 2x larger and can see budding)

Fliamentous (moulds)

  • aerobes
  • reproduce by conidia (asexual spores)
  • produce mycelia on agar

Dimorphic
- most pathogenic

102
Q

Fungal Virulence Factors

A

Most are saphrophytes (live on organic material)

Dimorphic fungi

  • best adapted to grow in our tissues
  • filamentous in environment
  • yeast when invasive (facultative anaerobe)

Dermatophytes

  • ringworm fungi (e.g. microsporum - cause tinea)
  • very common
  • grow on skin, eat keratin, don’t usually invade

Subcutaneous mycoses

  • low grade pathogens
  • inoculated directly subcutaneously

Opportunists

Toxic fungi

  • e.g. poisonous mushrooms
  • aspergillus (aphlatoxin)
103
Q

Common Fungi and their associated diseases

A

Microsporum (dermatophyte)

  • causes tinea
  • lives off keratin in skin/hair

Madurella (fungi) (or Nocardia - bacteria)

  • cause myceroma (maduromycosis)
  • sulphur granules with yellow discharge

Candida Albicans

  • cause candidiasis (mucocutaneous, chronic, systemic)
  • chronic vaginal thrush
  • systemic in neonates or immunodeficient (AIDS)
  • opportunistic
  • germ tubes (pseudohyphae) visible on microscopy

Cryptococcus neoformans & gattii

  • cause cryptococcosis
  • primarymild pulmonary infection (route of entry)
  • meningitis (AIDS defining illness)
  • gattii more virulent than neoformans
  • neoformans more common than gattii
  • opportunistic

Aspergillus

  • cause aspergillosis
  • saphrophytic fungus ball (e.g. previous TB cavitation)
  • allergic response (aphlatoxin)
  • systemic (in immunocompromised patient)
104
Q

Antifungal Treatments

A

Candida Albicans - fluconazole, amphotericin B

Cryptococcus - amphotericin B + 5-fluorocystosine

Aspergillus - voriconazole, amphotericin B

Dimorphic fungi - amphotericin B

Dermatophytes

  • topical
  • ternomafome
  • clotrimazole (canesten)
  • amorolfine
  • oral
  • terbinafine
  • fluconazole
  • only use for difficult to treat topical infections (nails) or widely disseminated
105
Q

Classifications of Osteomyelitis

A

Hematogenous

  • Asymptomatic bacteraemia
  • Septicaemia

Non Heamatogenous - Direct inoculation

  • Trauma
  • Surgery

Non Haematogenous - Local Invasion

  • Ulcer
  • Peridontal
  • Sinus
106
Q

Common aetiological agents of bone and joint infection

A 
GRAM POSITIVE
Staph aureus (Most common)
Step pyogenes (post chickenpox)
Group B strep (newborns - from mother)
Coagulase negative staph (post trauma/surgery)

GRAM NEGATIVE
Haemophilus influenzae type B (newborns until vaccination)
Kingella kingae
Other gram neative (newborns - from mother)

OTHER
TB, Fungi, Parasites

Treat w/ flucloxacillin for GPs and cefotaxime for GNs via IV for 3-5 days then oral for 3 weeks

107
Q

Plasmodium falciparum, vivax, ovale, malariae,

A

Malaria

Falciparum - Africa
Vivax - Asia, PNG, South America
Ovale & Malariae - limited, mild disease

0 hours - Skin infection by female (anopheles) mosquito
1-2 hours - sporozites get to liver
7-10 days - incubation (vivax lays dorment)
Release of merozites that infect RBCS
replication in blood stream (host is symptomatic)
reinfection of RBCs or mosquito takes up parasite

DISEASES:

  • ‘flu-like’ illness - fever, malaise
  • severe anaemia
  • cerebral complications (coma, convulsions)
  • lung damage -> acidosis
  • kidney failure / multiple system failure
  • clotting problems (RBC shape and adhesins)
  • splenomagaly
  • falciparum more deadly (infects all stages of RBCs, multiple parasites per RBC)\
  • potential hypoglycamia (parasite uses glucose)
DIAGNOSIS:
Thick film (screening) - no fixative, stain lyses RBCs
Thin film (speciation) - multiple ring forms / RBC = falciparum

TREATMENT:
Antimalarials
Artemisinin Combination Therapy (older - chloroquine)
Primaquine (for clearance of vivax from liver)
IV for 7-10 days if severe
Blood transfusion

108
Q

Increase risks for travellers

A
  • Exotic agents
  • Poor sanitation
  • Low immunisation (greater human reservoir)
  • Overcrowding
  • Cultural behaviours
  • Agriculture and animal handling
  • Risk taking behaviour (‘in the moment’)
  • Length of stay
  • Visiting friends / relatives (closer contact with locals in substandard accommodation)
109
Q

Incidence of Illness during Travel to Developing Countries

A 
20-60% Travelers Diarrhoea
5-20% Acute Respiratory Infection
2% Malaria
0.1% Dengue Fever
0.3% Animal bites with rabies risk
0.03-0.3% Hepatitis A
110
Q

Chlamydia trachomatis

A 
GNC/R
no cell wall (har dto see on gram stain)
oro-genital contact
most common STI (2-20%)
obligate intracellular parasite
(require cellular ATP to reproduce)

PATHOGENESIS:
lives in columnar epithelium
elimentary body infects columnar epithelial cells
formation of reticulate body and binary fusion
reorganisation into elementary bodies
lysis and release

DISEASES:
females: cervicitis (strawberry cervix, dysuria, irregular bleeding, pelvic inflammatory disease)
males: urethritis (dysuria, redness, clear discharge, prostatitis, testicular pain)
80% asymptomatic in females
neonatal chlamydia
- conjunctivitis (2-28 days) can be haemorrhagic
- pneumonia (2-8 weeks)
LGV serovar causes ulcerative lesions and inguinal lymphadenopathy

DIAGNOSIS:
Swabs
Urine

TREATMENT:
azithromycin or doxycycline
longer course of IV azithromycin for pelvic inflammatory disease

111
Q

Trichomonas vaginalis (trichomoniasis)

A 
protazoon
motile (flagellae)
sexually transmitted
frequently asymptomatic
frothy green-yellow vaginal discharge
cervical erythema
pH above 5.0 (usually lower)
itch, dysuria, abdominal pain
associated with increased risk of HIV acquisition

DIAGNOSIS:
vaginal swab ‘wet prep’ and culture
urine pcr

TREATMENT:
metronidazole or tinidazole

112
Q

Mycoplasma genitalium

A 
no cell wall
fastitious and difficult to culture
sexually transmitted
antibiotic resistant
prevalence 3-5%
DISEASES: 
men - urethritis
women - cervicitis, PID, endometritis
preterm labour and delivery
incrased risk of HIV

DIAGNOSIS:
nucleic acid amplification

TREATMENT:
azithromycin (30% failure rate)
moxifloxacin

113
Q

Effect of Group B Strep (strep agalactiae) on pregnancy

A 
lives in vagina (25-30%)
premature rupture of membranes
ascending infection or colonised during delivery
premature labour
pneumonia, septacaemia, meningitis
treatment: penicillin + gentamicin,
114
Q

Ro & Rt

Core group & Non-core group

A

Ro - basic reproductive rate
Ro = BcD
B = probability of transmission
- condoms, type of sex, organism load, treatments
c = rate of partner change
- core/noncore groups, mixing patterns
D = duration of infection
- symptom recognition, asymptomatic, chronic
number of secondary cases of an affection that arise from a primary case at t=0
Ro of 2 = one case leads to two secondary cases

Rt - affective reproductive rate (at time t)
Rt = BcD(x)
B = probability of transmission
c = rate of partner change
D = duration of infection
x = proportion susceptible (100% at t=0)
Rt of 1 = people curing infection at same rate as being infected

core group non core group
core group = many partners, high rate of STIs
noncore group = few partners, low rate of STIs
assortitive mixing - core group with core group (Ro&raquo_space; 1)
disassortitive mixing - core group with non-core (Ro < 1)

115
Q

Important HIV Genes

A

ENV GENE

  • surface glycoprotein gp120
  • transmembrane anchor gp41

GAG GENE

  • matrix layer (p17)
  • capsid layer (p24)
  • nucleocapsid (p7)

VIRAL ENZYMES (POL GENE)

  • reverse transcriptase (p66/51)
  • integrase (p32)
  • protease (p11)
116
Q

HIV replication

A

binds CD4

gp120 variable region opens

gp120 binds coreceptor (CCR5, CXCR4)

promotion of gp41 fusion with host plasma membrane

six-helix bundle forms to bring envelopes together

fusion of lipid bilayer of virus with cell
release capsid

ssRNA+

reverse transcription (high error rate)

cDNA

integrase enzyme translocates cDNA into nucleus of cell and cDNA becomes part of DNA = provirus (esp in latent memory T cells)

5’LRT (Long Terminal Repeats) act as HIV gene promotor

LRT has binding sites for proteins such as NFkb (causes upregulation during T cell activation)

transcription

translation

budding

cleavage of gag polyprotein into matrix and capsid (protease enzyme)

117
Q

HIV Infection Phases

A 
Acute HIV infection
- incubation 2-4 weeks
- clinical illness 1-4 weeks
- HIV antibodies (ELISA) detectible in 50% 
massive loss of (body) CD4 cells
- >60% of mucosal T-cells killed
- massive loss of memory T cells in GALT
- GI epithelial apoptosis
Fever
Myalgia
Nausea/vomiting/diarrhoea
Weight loss
Malaise
Rash
Oral Thrush
Headache

latent HIV infection (Asymptomatic)

  • equilibrium between viral replication and host defence
  • viral RNA levels constant
  • immune response & CD4 T cell loss
  • chronic immune activation
  • viral diversity
  • GIT distruption & infection -> activation of immune response

late phase

  • chronic immune activation
  • depletion of CD4 T cells = deficient B cell activation and neutrophil/macrophage killing ability
  • opportunistic infections & AIDS related illnesses
118
Q

AIDS Related Illnesses

A 
Pneumocystis jirovecii Pneumonia (PCP)
Candida albicans (oral thrush)
EBV (Hairy leukoplakia - tongue, and primary CNS lymphoma)
CMV (retina - blindness)
Cachexia/wasting
non-AIDS related illnesses in the era of HAART
- chronic inflammation
- T cell depletion
- lymphoid fibrosis
- cardiovascular
- hepatitis
- non-AIDS cancers
- liver disease
119
Q

HIV median Survival rate after <200 CD4 count

A

3.7 years

120
Q

HIV median survival rate after AIDS

A

1.3 years

121
Q

HIV median CD4 at AIDS

A

65 cells/uL

122
Q

HIV

  • TAT
  • TAR
  • REV
  • RRE
  • Vpr
  • Vpu
  • Nef
  • Vif
A

TAT
Transactivator of HIV Transcription
binds to TAR RNA
leads to phosphorylation of carboxy terminus of RNApolymerase II
increases rate of viral expression
promotes transcriptional elongation (longer RNA translated)
Inhibits promotor of MHC-I gene

TAR
transactivation response RNA element
very first RNA structure at 5’ end of genome
has stem, bulge, and loop

Rev
Regulator of structural gene expression through binding of RRE
allows switch from early stage of expression (TAT, REV) to late stage of expression (GAG, ENV, POL)

RRE
Rev-responsible RNA element

Vpr
virion protein for nuclear import of cDNA
cell growth cycle arrest
weak transcription transactivator

Vpu
regulator of particle release and ENV processing
promotes MHC-I and CD4 degradation (directs MHC-I to the proteosome and lysosome for destruction)
Antagonises tetherin and allows virus to escape

Nef
multifuncitonal protein important for in vivo pathogenesis
Downmodulates cell MHC-I and CD4
Directs MHC-I to the lysosome for destruction

Vif
Promotes infectivity of cell free virus
block cell defences targeting single stranded cDNA
binds APOBEC3G and targets it for death through proteosome

123
Q

HPV

A 
Human Papilloma Virus
HPV1,2,4 = skin infections
HPV16,18 = anogenital carcinomas
dsDNA
- early genes (E6,E7 - block p53 and Rb)
- late genes (capsid genes)
infects sqamous epithelium (basal first)
- 0 to 6 weeks - first lesion
- weeks to months - immune response
- (80-90%) DNA -ve clinical remission
- (10-20%) DNA +ve integrated into host DNA - CIN2/3 risk
124
Q

Streptococci Classifications

A 
beta-haemolytic - complete haemolysis
 Lancefield A - Strep pyogenes (M-types)
 Lancefield B - Strep agalactiae
alpha-haemolytic - 'greening' - RBCs release bile
 Strep pneumoniae (capsule types)
 Strep viridans (oral)
non-haemolytic
125
Q

Strep pyogenes virulence determinants

A
  • hyaluronic acid capsule (antiphagocytic)
  • M protein (acts as adhesin and antiphagocytic)
  • lipoteichoid acid acts as adhesin
  • streptokinase (fibrinolysis)
  • hyaluronidase (helps spreading)
  • C5a peptidase (acts on compliment)
  • SpeB (protease)
  • DNAses (break NETS - neutrophil traps)
  • streptolysin (haemolysis)
  • leukocidins (break down WBCs)
  • SpeA (pyrogenic superantigen)
  • toxins (superantigens)
126
Q

Staph aureus virulence factors

A
  • modified peptidoglycan (avoid phagocytosis)
  • techoic acids (act as adhesin)
  • polysaccharide capsule (antiphagocytic)
  • protein A (interferes with opsonisation)
  • staphylokinase (antiphagocytic)
  • aureolysin (protease)
  • hyaluronidase (helps spreading)
  • DNAase (break NETS)
  • toxins (superantigens)
  • leukocidins (breakdown WBCs) [Panton-Valentine leukocidin] & haemolysins
  • inhibit chemotaxis via CHIPS (block compliment)
  • biofilm formation and abcess formation
  • 90% resistant to penicillin
127
Q

Sterilization

A

Process that provides acceptably low probability that any microorganism or spore will not survive the treatment

‘sterility assurance’ = probability that a microorganism survives sterilisation and a proportion of sterilised articles may be unsterile (i.e. 1 in 1000)

More costly and damaging than disinfection

  • filtration for fluids
  • steam heat for objects
  • dry heat for glass
  • ionizing radiation for prepackaged articles
128
Q

Disinfection

A
  • process of removing or killing most, but not all, viable organisms.
  • cannot usually kill bacterial spores
129
Q

D Value

A
  • Decimal reduction time

- time it takes for 90% reduction in organisms due to disinfection/sterilisation

130
Q

Common Agents of Skin and Soft Tissue Infections

  • Bacteria
  • Fungi
  • Parasites
  • Arthropods
  • Viruses
A

BACTERIA:
S. aureus, S. pyogenes, clostridia

FUNGI:
Candida (yeast), and filamentous fungi

PARASITES:
Leishmania, schistosomes, hookworms

ARTHROPODS
Insects, ticks, mites

VIRUSES:
HSV, VZV, HPV, measles, rubella, enterovirus, Parvo B19, warts

  • also systemic infections:
    Enteric fever ‘rose spots’, petechiae in septicaemia, rash in syphilis, scarlet fever, toxic shock syndrome
131
Q

4 Pieces of information required to design appropriate sterilisation process

A
  1. Sterility Assurance - Level of sterility required
  2. D-value - how fast organism is killed
  3. Bioburden - how many organisms we start with
  4. Material - will the equipment survive the process
132
Q

HIV evasion of immunity

A
  • Sequence variation (esp gp160)
  • MHC I downregulation
  • Loss of effector cells (clonal exhaustion)
  • Latency
  • Privileged sites (brain, testes)
133
Q

Ebola

A

Filovirus
From bats
- ssRNA
Enveloped
Helical Capsid
Transmission during clinical illness (body fluids) (doesn’t persist on fomites)
Enters through broken skin / mucous membranes

SYMPTOMS (2-21 days after infection)

  • fever
  • headache
  • muscle pains
  • diarrhoea, vomiting
  • abdominal pain
  • maculopapular rash
  • haemorrhagic (late)

DIAGNOSIS

  • ELISA
  • PCR
  • Antibody (IgM/IgG)

TREATMENT

  • Blood transfusion (antibodies)
  • Zmapp (monoclonal antibodies)
  • Supportive treatment

MD1 (11 decks)

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