Infectious diseases and STIs Flashcards
Live attenuated vaccines
BCG measles, mumps, rubella (MMR) influenza (intranasal) oral rotavirus oral polio yellow fever oral typhoid
inactivated vaccines
rabies
hepatitis A
influenza (intramuscular)
Toxoid vaccines
tetanus
diphtheria
pertussis
subunit and conjugate vaccines
ins to make them more immunogenic pneumococcus (conjugate) haemophilus (conjugate) meningococcus (conjugate) hepatitis B human papillomavirus
HIV count for live vaccines
CD4 >200
viral meningitis with low CSF glucose
mumps
BV cause and gram stain
Gardnerella vaginalis
Gram positive coccobacilli
raised pH due to outcompeting lactobacilli. clue cells.
BV treatment
oral metronidazole 5-7days
migrating rash on buttocks and feet
Strongyloides stercoralis
Larvae penetrate the skin and are carried via the blood to the lungs where they are coughed up and swallowed. Adult worms reproduce in the GI tract (causing symptoms of bloating, discomfort and diarrhoea) and larvae are passed in the stool. Auto-infection can occur through the GI tract or peri-anal skin. Larva currens is the characteristic skin eruption of Strongyloides stercoralis. It causes an urticarial band that typically starts in the peri-anal area. The rash rapidly migrates, more quickly than the rash of cutaneous larva migrans.
Strongyloides stercoralis treatment
ivermectin and albendazole are used
infective bloody diarrhoea cause
Campylobacter
E.coli 0157
shigella
Campylobacter presentation
prodrome: headache malaise
diarrhoea: often bloody
abdominal pain: may mimic appendicitis
incubation period 1-6 days
campylobacter gram stain
gram negative bacillus
campylobacter management
usually self-limiting
the BNF advises treatment if severe or the patient is immunocompromised. Clinical Knowledge summaries also recommend antibiotics if severe symptoms (high fever, bloody diarrhoea, or more than eight stools per day) or symptoms have last more than one week
the first-line antibiotic is clarithromycin
ciprofloxacin is an alternative although the BNF states that ‘Strains with decreased sensitivity to ciprofloxacin isolated frequently’
campylobacter complications
Guillain-Barre syndrome may follow Campylobacter jejuni infections
Reiter’s syndrome
septicaemia, endocarditis, arthritis
leprosy cause
Mycobacterium leprae
Mycobacterium leprae features
patches of hypopigmented skin typically affecting the buttocks, face, and extensor surfaces of limbs
sensory loss
The degree of cell mediated immunity determines the type of leprosy a patient will develop.
Low degree of cell mediated immunity → lepromatous leprosy (‘multibacillary’)
extensive skin involvement
symmetrical nerve involvement
High degree of cell mediated immunity → tuberculoid leprosy (‘paucibacillary’)
limited skin disease
asymmetric nerve involvement → hypesthesia
hair loss
leprosy management
rifampicin, dapsone and clofazimine
genital warts cause
HPV, especially types 6 & 11. It is now well established that HPV (primarily types 16,18 & 33) predisposes to cervical cancer.
genital warts management
- topical podophyllum / cryotherapy
2. Imiquimod
ribavarin machanism
Guanosine analog which inhibits inosine monophosphate (IMP) dehydrogenase, interferes with the capping of viral mRNA
ribavarin indications
Chronic hepatitis C, RSV
ribavarin adverse effects
Haemolytic anaemia
Aciclovir mechanism
Guanosine analog, phosphorylated by thymidine kinase which in turn inhibits the viral DNA polymerase
aciclovir indications
HSV, VZV
aciclovir adverse efects
Crystalline nephropathy
gancyclovir mechanism
Guanosine analog, phosphorylated by thymidine kinase which in turn inhibits the viral DNA polymerase
gancyclovir adverse effects
Myelosuppression/agranulocytosis
amantadine mechanism
Inhibits uncoating (M2 protein) of virus in cell. Also releases dopamine from nerve endings
amantadine adverse effects
Confusion, ataxia, slurred speech
oseltamivir mechanism
Inhibits neuraminidase
foscarnet mechanism
Pyrophosphate analog which inhibits viiral DNA polymerase
foscarnet adverse effects
Nephrotoxicity, hypocalcaemia, hypomagnasaemia, seizures
interferon-a mechanism
Human glycoproteins which inhibit synthesis of mRNA
interpheron-a side effects
Flu-like symptoms, anorexia, myelosuppression
cidofovir mechanism
Acyclic nucleoside phosphonate, and is therefore independent of phosphorylation by viral enzymes (compare and contrast with aciclovir/ganciclovir)
cidofovir adverse effects
Nephrotoxicity
prodrome: irritable, conjunctivitis, fever
Koplik spots (before rash): white spots (‘grain of salt’) on buccal mucosa
rash: starts behind ears then to whole body, discrete maculopapular rash becoming blotchy & confluent
diarrhoea occurs in around 10% of patients
measles
measels type of virus and spread
RNA paramyxovirus
spread by droplets
infective from prodrome until 4 days after rash starts
incubation period = 10-14 days
Measels management
- notifiable disease
- supportive
- if a child not immunized against measles comes into contact with measles then MMR should be offered (vaccine-induced measles antibody develops more rapidly than that following natural infection)
this should be given within 72 hours
measels complications
otitis media: the most common complication
pneumonia: the most common cause of death
encephalitis: typically occurs 1-2 weeks following the onset of the illness)
subacute sclerosing panencephalitis: very rare, may present 5-10 years following the illness
febrile convulsions
keratoconjunctivitis, corneal ulceration
diarrhoea
increased incidence of appendicitis
myocarditis
black lump cause
Anthrax is caused by Bacillus anthracis, a Gram positive rod
Bacillus anthracis produces a tripartite protein toxin
protective antigen
oedema factor: a bacterial adenylate cyclase which increases cAMP
lethal factor: toxic to macrophages
from infected carcasses
anthrax management
ciprofloxacin
lyme cause
Borrelia burgdorferi
lyme investigations
NICE recommend that Lyme disease can be diagnosed clinically if erythema migrans is present
erythema migrans is therefore an indication to start antibiotics
enzyme-linked immunosorbent assay (ELISA) antibodies to Borrelia burgdorferi are the first-line test
if negative and Lyme disease is still suspected in people tested within 4 weeks from symptom onset, repeat the ELISA 4-6 weeks after the first ELISA test. If still suspected in people who have had symptoms for 12 weeks or more then an immunoblot test should be done
if positive or equivocal then an immunoblot test for Lyme disease should be done
lyme management
doxycycline if early disease. Amoxicillin is an alternative if doxycycline is contraindicated (e.g. pregnancy)
people with erythema migrans should be commenced on antibiotic without the need for further tests
ceftriaxone if disseminated disease
Jarisch-Herxheimer reaction is sometimes seen after initiating therapy: fever, rash, tachycardia after first dose of antibiotic (more commonly seen in syphilis, another spirochaetal disease)
gram positive colour
purple
gram positive rods
Actinomyces Bacillus antracis Clostridium Corynebacterium diphtheriae Listeria monocytogenes
gram positive cocci
makes catalase: Staphylococci
does not make catalase: Streptococci
staphylococci that make coagulase
makes coagulase: S. aureus
does not make coagulase: S. epidermidis (novobiocin sensitive), S. saprophyticus (novobiocin resistant)
streptococci that causes haemolysis
partial haemolysis (green colour on blood agar): α-haemolytic
- s.pneumoniae
- strep viridans
complete haemolysis (clear): β-haemolytic
- Group A (bacitracin sensitive) S.pyogenes
- Group B (bactiracin resistant) strep agalactiae
no haemolysis: γ-haemolytic
Enterococcus
dengue fever bloots
low platelet count and raised transaminase level
dengue fever spread
transmitted by the Aedes aegypti mosquito
incubation period of 7 days
varicella zoster in pregnancy management
if there is any doubt about the mother previously having chickenpox maternal blood should be urgently checked for varicella antibodies
if the pregnant woman <= 20 weeks gestation is not immune to varicella she should be given varicella-zoster immunoglobulin (VZIG) as soon as possible
RCOG and Greenbook guidelines suggest VZIG is effective up to 10 days post exposure
if the pregnant woman > 20 weeks gestation is not immune to varicella then either VZIG or antivirals (aciclovir or valaciclovir) should be given days 7 to 14 after exposure
Fetal varicella syndrome features
risk of FVS following maternal varicella exposure is around 1% if occurs before 20 weeks gestation
studies have shown a very small number of cases occurring between 20-28 weeks gestation and none following 28 weeks
features of FVS include skin scarring, eye defects (microphthalmia), limb hypoplasia, microcephaly and learning disabilities
bacteria found in soil
Clostridium tetani
why do you cramp in tetanus
Tetanospasmin prevents release of GABA
management of tetanus
supportive therapy including ventilatory support and muscle relaxants
intramuscular human tetanus immunoglobulin for high-risk wounds (e.g. compound fractures, delayed surgical intervention, significant degree of devitalised tissue)
metronidazole is now preferred to benzylpenicillin as the antibiotic of choice
most common organism animal bites
Pasteurella multocida.
management animal bites
cleanse wound. Puncture wounds should not be sutured closed unless cosmesis is at risk
current BNF recommendation is co-amoxiclav
if penicillin-allergic then doxycycline + metronidazole is recommended
bacteria in human bites
Common organisms include: Streptococci spp. Staphylococcus aureus Eikenella Fusobacterium Prevotella
canned food IVDU, ascending flacid paralysis
Clostridium botulinum
Clostridium botulinum gram stain
gram positive anaerobic bacillus
how does botulism cause paralysis?
produces botulinum toxin, a neurotoxin which irreversibly blocks the release of acetylcholine
botulism management
botulism antitoxin and supportive care
antitoxin is only effective if given early - once toxin has bound its actions cannot be reversed
gram negative cocci
Neisseria meningitidis + Neisseria gonorrhoeae, also Moraxella catarrhalis
gram positive rods
ABCD L Actinomyces Bacillus anthracis (anthrax) Clostridium Diphtheria: Corynebacterium diphtheriae Listeria monocytogenes
gram negative rods
Escherichia coli Haemophilus influenzae Pseudomonas aeruginosa Salmonella sp. Shigella sp. Campylobacter jejuni
basic makeup of ART
Antiretroviral therapy (ART) involves a combination of at least three drugs, typically two nucleoside reverse transcriptase inhibitors (NRTI) and either a protease inhibitor (PI) or a non-nucleoside reverse transcriptase inhibitor (NNRTI). This combination both decreases viral replication but also reduces the risk of viral resistance emerging
Nucleoside analogue reverse transcriptase inhibitors (NRTI) examples, side effects
examples: zidovudine (AZT), abacavir, emtricitabine, didanosine, lamivudine, stavudine, zalcitabine, tenofovir
general NRTI side-effects: peripheral neuropathy
tenofovir: used in BHIVAs two recommended regime NRTI. Adverse effects include renal impairment and ostesoporosis
zidovudine: anaemia, myopathy, black nails
didanosine: pancreatitis
Non-nucleoside reverse transcriptase inhibitors (NNRTI) examples and side effects
examples: nevirapine, efavirenz
side-effects: P450 enzyme interaction (nevirapine induces), rashes
Protease inhibitors (PI) examples and side effects
examples: indinavir, nelfinavir, ritonavir, saquinavir
side-effects: diabetes, hyperlipidaemia, buffalo hump, central obesity, P450 enzyme inhibition
indinavir: renal stones, asymptomatic hyperbilirubinaemia
ritonavir: a potent inhibitor of the P450 system
PCP cause
Pneumocystis jiroveci
Pneumocystis jiroveci type
Pneumocystis jiroveci is an unicellular eukaryote, generally classified as a fungus but some authorities consider it a protozoa
CD4 count for prophylaxis in HIV
all patients with a CD4 count < 200/mm³ should receive PCP prophylaxis with co-trimoxazole
PCP management
co-trimoxazole
IV pentamidine in severe cases
aerosolized pentamidine is an alternative treatment for Pneumocystis jiroveci pneumonia but is less effective with a risk of pneumothorax
steroids if hypoxic (if pO2 < 9.3kPa then steroids reduce risk of respiratory failure by 50% and death by a third)
PCP investigations
CXR: typically shows bilateral interstitial pulmonary infiltrates but can present with other x-ray findings e.g. lobar consolidation. May be normal
exercise-induced desaturation
sputum often fails to show PCP, bronchoalveolar lavage (BAL) often needed to demonstrate PCP (silver stain shows characteristic cysts)
herpes investigation
nucleic acid amplification tests (NAAT) is the investigation of choice in genital herpes and are now considered superior to viral culture
HSV serology may be useful in certain situations such as recurrent genital ulceration of unknown cause
herpes management
general measures include:
saline bathing
analgesia
topical anaesthetic agents e.g. lidocaine
oral aciclovir
some patients with frequent exacerbations may benefit from longer-term aciclovir
herpes in pregnancy
elective caesarean section at term is advised if a primary attack of herpes occurs during pregnancy at greater than 28 weeks gestation
women with recurrent herpes who are pregnant should be treated with suppressive therapy and be advised that the risk of transmission to their baby is low
Suppressive treatment is often considered from 36 weeks to reduce asymptomatic shedding and risk of transmission during delivery.
hepatitis b complications
chronic hepatitis (5-10%). 'Ground-glass' hepatocytes may be seen on light microscopy fulminant liver failure (1%) hepatocellular carcinoma glomerulonephritis polyarteritis nodosa cryoglobulinaemia
hep b management
pegylated interferon-alpha used to be the only treatment available. It reduces viral replication in up to 30% of chronic carriers. A better response is predicted by being female, < 50 years old, low HBV DNA levels, non-Asian, HIV negative, high degree of inflammation on liver biopsy
whilst NICE still advocate the use of pegylated interferon firstl-line other antiviral medications are increasingly used with an aim to suppress viral replication (not in a dissimilar way to treating HIV patients)
examples include tenofovir, entecavir and telbivudine (a synthetic thymidine nucleoside analogue)
diarrhoea by incubation period
1-6 hrs: Staphylococcus aureus, Bacillus cereus*
12-48 hrs: Salmonella, Escherichia coli
48-72 hrs: Shigella, Campylobacter
> 7 days: Giardiasis, Amoebiasis
most common cause of travellers diarhoea
E.coli
infected rice
Bacillus cereus
hep A PEP
Human Normal Immunoglobulin (HNIG) or hepatitis A vaccine may be used depending on the clinical situation
hep B PEP
HBsAg positive source: if the person exposed is a known responder to HBV vaccine then a booster dose should be given. If they are in the process of being vaccinated or are a non-responder they need to have hepatitis B immune globulin (HBIG) and the vaccine
unknown source: for known responders the green book advises considering a booster dose of HBV vaccine. For known non-responders HBIG + vaccine should be given whilst those in the process of being vaccinated should have an accelerated course of HBV vaccine
hep C PEP
monthly PCR - if seroconversion then interferon +/- ribavirin
HIV PEP
the risk of HIV transmission depends heavily on the incident (e.g. needle stick, type of sexual intercourse, human bite etc) and the current viral load of the patient
please see the BHIVA link for charts which outline the risk depending on the incident. Generally, low-risk incidents such as human bites don’t require post-exposure prophylaxis
a combination of oral antiretrovirals (e.g. Tenofovir, emtricitabine, lopinavir and ritonavir) as soon as possible (i.e. Within 1-2 hours, but may be started up to 72 hours following exposure) for 4 weeks
serological testing at 12 weeks following completion of post-exposure prophylaxis
reduces risk of transmission by 80%
needlestick transmission rates Hep B, C and HIV
B- 20-30%
C- 0.5-2%
HIV- 0.3%
virus associated with nasopharyngeal malignancy
EBV
malignancies associated with EBV
Burkitt’s lymphoma*
Hodgkin’s lymphoma
nasopharyngeal carcinoma
HIV-associated central nervous system lymphomas
GP management meningococcal meningitis
intramuscular benzylpenicillin
meningococcal meningitis management
Intravenous benzylpenicillin or cefotaxime
chloramphenicol if anaphylaxis to penicillin
(pretty much all meningitis chloramphenicol is the right answer)
meningococcal meningitis prophylaxis in contacts
close contact within the 7 days before onset
oral ciprofloxacin or rifampicin or may be used
why do people get gonorrhoea multiple times?
due to antigen variation of type IV pili (proteins which adhere to surfaces) and Opa proteins (surface proteins which bind to receptors on immune cells)
gonorrhoea management
a single dose of IM ceftriaxone 1g (i.e. no longer add azithromycin). If sensitivities are known (and the organism is sensitive to ciprofloxacin) then a single dose of oral ciprofloxacin 500mg should be given
if ceftriaxone is refused (e.g. needle-phobic) then oral cefixime 400mg (single dose) + oral azithromycin 2g (single dose) should be used
parvovirus exposure in pregnancy
If a woman is exposed early in pregnancy (before 20 weeks) she should seek prompt advice from whoever is giving her antenatal care as maternal IgM and IgG will need to be checked.
cerebral toxoplasmosis v lymphoma
Toxoplasmosis
Multiple lesions
Ring or nodular enhancement
Thallium SPECT negative
Lymphoma
Single lesion
Solid (homogenous) enhancement
Thallium SPECT positive
Progressive multifocal leukoencephalopathy (PML)
widespread demyelination
due to infection of oligodendrocytes by JC virus (a polyoma DNA virus)
symptoms, subacute onset : behavioural changes, speech, motor, visual impairment
CT: single or multiple lesions, no mass effect, don’t usually enhance. MRI is better - high-signal demyelinating white matter lesions are seen
Eron cellulitis criteria
I There are no signs of systemic toxicity and the person has no uncontrolled co-morbidities
II The person is either systemically unwell or systemically well but with a co-morbidity (for example peripheral arterial disease, chronic venous insufficiency, or morbid obesity) which may complicate or delay resolution of infection
III The person has significant systemic upset such as acute confusion, tachycardia, tachypnoea, hypotension, or unstable co-morbidities that may interfere with a response to treatment, or a limb-threatening infection due to vascular compromize
IV The person has sepsis syndrome or a severe life-threatening infection such as necrotizing fasciitis
criteria for cellulitis IV abx
Has Eron Class III or Class IV cellulitis.
Has severe or rapidly deteriorating cellulitis (for example extensive areas of skin).
Is very young (under 1 year of age) or frail.
Is immunocompromized.
Has significant lymphoedema.
Has facial cellulitis (unless very mild) or periorbital cellulitis.
cellulitis antibiotics
flucloxacillin as first-line treatment for mild/moderate cellulitis. Clarithromycin, erythromycin (in pregnancy) or doxycyline is recommended in patients allergic to penicillin.
NICE recommend that patients severe cellulitis should be offered co-amoxiclav, cefuroxime, clindamycin or ceftriaxone.
5 types of schistosomiasis
S. mansoni, S. japonicum and S. haematobium are the most common.
S. intercalatum and mekongi (intestinal schistosomiasis)
S. Haematobium features
These worms deposit egg clusters (pseudopapillomas) in the bladder, causing inflammation. The calcification seen on x-ray is actually calcification of the egg clusters, not the bladder itself.
Depending on the site of these pseudopapillomas in the bladder, they can cause an obstructive uropathy and kidney damage.
This typically presents as a ‘swimmer’s itch’ in patients who have recently returned from Africa. Schistosoma haematobium is a risk factor for squamous cell bladder cancer.
Features
frequency
haematuria
bladder calcification
schistosomiasis treatment
single oral dose of praziquantel
complications of S. mansoni adn japonicum
These worms mature in the liver and then travel through the portal system to inhabit the distal colon. Their presence in the portal system can lead to progressive hepatomegaly and splenomegaly due to portal vein congestion.
These species can also lead to complications of liver cirrhosis, variceal disease and cor pulmonale.
diptheria organism
Gram positive bacterium Corynebacterium diphtheriae
diptheria pathophysiology
releases an exotoxin encoded by a β-prophage
exotoxin inhibits protein synthesis by catalyzing ADP-ribosylation of elongation factor EF-2
diptheria presentations
Diphtheria toxin commonly causes a ‘diphtheric membrane’ on tonsils caused by necrotic mucosal cells. Systemic distribution may produce necrosis of myocardial, neural and renal tissue
Possible presentations
recent visitors to Eastern Europe/Russia/Asia
sore throat with a ‘diphtheric membrane’ - grey, pseudomembrane on the posterior pharyngeal wall
bulky cervical lymphadenopathy
may result in a ‘bull neck’ appearanace
neuritis e.g. cranial nerves
heart block
diptheria investigations
culture of throat swab: uses tellurite agar or Loeffler’s media
diptheria management
intramuscular penicillin
diphtheria antitoxin
list the 5 stages in the HIV life cycle that can be targeted.
- binding, fusion and entry into cell
- reverse transcription x2
- insetion into host cell DNA
- budding off (reproducing)
explain how entry inhibitors work in HIV
Entry inhibitors are a class of medication which interfere with the binding, fusion and entry of HIV-1 into host cells . An example of this type of medication includes maraviroc. Maraviroc works by targeting the CCR5 receptor on T-helper cells, reduces the HIV virus’ ability to enter the host CD4 cells. Indeed, some individuals may have a mutation of the CCR5 delta gene which results in natural protection from viral cell entry. Nevertheless, caution should be used when administering maraviroc as a tropism of the HIV virus can allow the HIV virus to target an alternative receptor CXCR4 - bypassing maraviroc’s mechanism of action.
explain how medications interfer with reverse transcription in HIV
HIV is an RNA virus and the genetic code be ‘reverse’ transcribed into DNA in order to be incorporated into the human cell. The conversion of RNA to DNA is not done by mammalian cells and is performed by a viral reverse transcriptase enzyme. This makes it an opportune target for drug therapies. Nulceoside reverse-transcriptase inhibitors act as nucleoside analogues which compete with natural deoxynucleotides for incorporation to DNA to prevent reverse transcription . Examples of this class of medications include emtricitabine and tenofovir disoproxil.
Reverse transcription can also be inhibited by non-nucleoside reverse-transcriptase inhibitors. These medications bind to the reverse transcriptase enzyme and inhibit its function (acting as allosteric modulators). Examples of this class of medications include efavirenz and nevirapine.
explain hiw integrase inhibitors work in HIV
Integrase inhibitors (of which raltegravir is one) block integrase enzymatic activity which is involved in inserting the viral genome into the DNA of the host cell . Integrase is a viral enzyme and hence is a reliable target.
explain how protease inhibitors work in HIV
protease inhibitors block the viral protease enzyme activity necessary to produce mature virions from budding from the membrane . Viral particles produced in the presence of protease inhibitors are mostly non-infectious and defective. Examples of this class of medications include ritonavir and lopinavir.
rabies features
prodrome: headache, fever, agitation
hydrophobia: water-provoking muscle spasms
hypersalivation
Negri bodies: cytoplasmic inclusion bodies found in infected neurons
rabies management
There is now considered to be ‘no risk’ of developing rabies following an animal bite in the UK and the majority of developed countries. Following an animal bite in at-risk countries:
the wound should be washed
if an individual is already immunised then 2 further doses of vaccine should be given
if not previously immunised then human rabies immunoglobulin (HRIG) should be given along with a full course of vaccination. If possible, the dose should be administered locally around the wound
doxycycline mechanism
Doxycycline is a tetracycline often prescribed for patients allergic to penicillin and with mild pneumonia. Tetracyclines inhibit the 30S subunit of ribosomes, which leads to an inability of bacteria to produce proteins. Tetracyclines are commonly confused with macrolides, which inhibit the 50S subunit of ribosomes.
tetracycline side effects
Discolouration of teeth, photosensitivity
aminoglycosides mechanism and adverse effects
Binds to 30S subunit causing misreading of mRNA Nephrotoxicity, Ototoxicity
chloramphenicol mechanism and adverse effects
Binds to 50S subunit, inhibiting peptidyl transferase Aplastic anaemia
protein synthesis inhibitors
30s
- aminoglycosides
- tetracyclines
50s
- chloramphenicol
- clindamycin
- macrolides
clindamycin mechanism and adverse effects
Binds to 50S subunit, inhibiting translocation (movement of tRNA from acceptor site to peptidyl site) Common cause of C. difficile diarrhoea
macrolides mechanism and adverse effects
Binds to 50S subunit, inhibiting translocation (movement of tRNA from acceptor site to peptidyl site) Nausea (especially erythromycin), P450 inhibitor, prolonged QT interval Commonly used for patients who are allergic to penicillin
