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
criteria for staphylococcal toxic shock syndrome
fever: temperature > 38.9ºC
hypotension: systolic blood pressure < 90 mmHg
diffuse erythematous rash
desquamation of rash, especially of the palms and soles
involvement of three or more organ systems: e.g. gastrointestinal (diarrhoea and vomiting), mucous membrane erythema, renal failure, hepatitis, thrombocytopenia, CNS involvement (e.g. confusion)
toxic shock syndrome pathophysiology
a severe systemic reaction to staphylococcal exotoxins, the TSST-1 superantigen toxin
TSS management
removal of infection focus (e.g. retained tampon)
IV fluids
IV antibiotics
enteric fever causes
The Salmonella group contains many members, most of which cause diarrhoeal diseases. They are aerobic, Gram-negative rods which are not normally present as commensals in the gut.
Typhoid and paratyphoid are caused by Salmonella typhi and Salmonella paratyphi (types A, B & C) respectively. They are often termed enteric fevers, producing systemic symptoms such as headache, fever, arthralgia.
typhoid transmission
typhoid is transmitted via the faecal-oral route (also in contaminated food and water)
typhoid features
initially systemic upset as above
relative bradycardia
abdominal pain, distension
constipation: although Salmonella is a recognised cause of diarrhoea, constipation is more common in typhoid
rose spots: present on the trunk in 40% of patients, and are more common in paratyphoid
typhoid complications
osteomyelitis (especially in sickle cell disease where Salmonella is one of the most common pathogens)
GI bleed/perforation
meningitis
cholecystitis
chronic carriage (1%, more likely if adult females)
opportunistic infections CD4 count 200-500
Oral thrush Secondary to Candida albicans
Shingles Secondary to herpes zoster
Hairy leukoplakia Secondary to EBV
Kaposi sarcoma Secondary to HHV-8
opportunistic infections CD4 count 100-200
Cryptosporidiosis Whilst patients with a CD4 count of 200-500 may develop cryptosporidiosis the disease is usually self-limiting and similar to that in immunocompetent hosts
Cerebral toxoplasmosis
Progressive multifocal leukoencephalopathy Secondary to the JC virus
Pneumocystis jirovecii pneumonia
HIV dementia
opportunistic infections CD4 count 50-100
Aspergillosis Secondary to Aspergillus fumigatus
Oesophageal candidiasis Secondary to Candida albicans
Cryptococcal meningitis
Primary CNS lymphoma Secondary to EBV
opportunistic infections CD4 count <50
Cytomegalovirus retinitis Affects around 30-40% of patients with CD4 < 50 cells/mm³
Mycobacterium avium-intracellulare infection
painful genital ulcer with a ragged border associated with unilateral tender inguinal lymphadenopathy points to?
Chancroid is caused by Haemophilus ducreyi.
what family of viruses does EBV belong to?
herpes virus
types of malaria (5)
falciparum (most common) vivax (second most common) Ovale malariae knowlesi
where does vivax and ovale come from?
Plasmodium vivax is often found in Central America and the Indian Subcontinent whilst Plasmodium ovale typically comes from Africa.
features of malaria
general features of malaria: fever, headache, splenomegaly
Plasmodium vivax/ovale: cyclical fever every 48 hours. Plasmodium malariae: cyclical fever every 72 hours
Plasmodium malariae: is associated with nephrotic syndrome.
why do people relapse with some kinds of malaria?
Ovale and vivax malaria have a hypnozoite stage and may therefore relapse following treatment.
malaria management
in areas which are known to be chloroquine-sensitive then WHO recommend either an artemisinin-based combination therapy (ACT) or chloroquine
in areas which are known to be chloroquine-resistant an ACT should be used
ACTs should be avoided in pregnant women
patients with ovale or vivax malaria should be given primaquine following acute treatment with chloroquine to destroy liver hypnozoites and prevent relapse
ACT- artemether-lumefantrine
UTI treatment in pregnancy
- nitrofuranotoin
- amoxicillin or cefalexin
AVOID TRIMETHOPRIM
UTI not in pregnancy
local guidelines but trimethoprim and nitrofurantoin 3 days
toxoplasmosis cause
Toxoplasma gondii
toxoplasmosis pathophysiology
obligate intracellular protozoan that infects the body via the gastrointestinal tract, lung or broken skin. It’s oocysts release trophozoites which migrate widely around the body including to the eye, brain and muscle. The usual animal reservoir is the cat, although other animals such as rats carry the disease.
toxoplasmosis management in immunocompromised
Cerebral toxoplasmosis accounts for around 50% of cerebral lesions in patients with HIV
constitutional symptoms, headache, confusion, drowsiness
CT: usually single or multiple ring-enhancing lesions, mass effect may be seen
management: pyrimethamine plus sulphadiazine for at least 6 weeks
necrotising fasciitis classification
type 1 is caused by mixed anaerobes and aerobes (often occurs post-surgery in diabetics). This is the most common type
type 2 is caused by Streptococcus pyogenes
necrotising fasciitis risk factors
skin factors: recent trauma, burns or soft tissue infections
diabetes mellitus
the most common preexisting medical condition
particularly if the patient is treated with SGLT-2 inhibitors
intravenous drug use
immunosuppression
necrotising fasciitis features
acute onset
pain, swelling, erythema at the affected site
often presents as rapidly worsening cellulitis with pain out of keeping with physical features
extremely tender over infected tissue with hypoaesthesia to light touch
skin necrosis and crepitus/gas gangrene are late signs
fever and tachycardia may be absent or occur late in the presentation
necrotising fasciitis management
urgent surgical referral debridement
intravenous antibiotics
typhus causes
rickettsial diseases
transmitted between hosts by arthropods
cause widespread vasculitis
typhus features
fever, headache
black eschar at site of original inoculation
rash e.g. maculopapular or vasculitis
complications: deranged clotting, renal failure, DIC
types of typhus
Rocky Mountain spotted fever
caused by R rickettsii
initially macular rash or hands and feet then spreads
Tick typhus
caused by R conorii
rash initially in axilla then spreads
typhus treatment
doxycycline
cholera cause
Vibro cholerae - Gram negative bacteria
cholera features
profuse ‘rice water’ diarrhoea
dehydration
hypoglycaemia
cholera management
oral rehydration therapy
antibiotics: doxycycline, ciprofloxacin
Hep B pathogen
double-stranded DNA hepadnavirus and is spread through exposure to infected blood or body fluids, including vertical transmission from mother to child. The incubation period is 6-20 weeks.
Q fever cause
Coxiella burnetii, a rickettsia. The source of infection is typically an abattoir, cattle/sheep or it may be inhaled from infected dust
Q fever management
typically prodrome: fever, malaise causes pyrexia of unknown origin transaminitis atypical pneumonia endocarditis (culture-negative)
Q fever treatment
doxycycline
why is plasmodium knowlesi infection particularly dangerous
has the shortest erythrocytic replication cycle, leading to high parasite counts in short periods of time
plasmodium replication cycle
have two reproductive cycles; an exo-erythrocytic cycle which occurs in hepatocytes, and an erythrocytic cycle which occurs in the red blood cells. The length of the erythrocytic cycle varies from species to species, with P. knowlesi having the fastest cycle at around 24 hours. The end stage in the cycle involves lysis of the red cells and release of additional parasites, meaning that P. knowlesi is capable of producing very high parasite counts in a short space of time.
For this reason, in Plasmodium knowlesi infection, severe parasitaemia should be defined as >1%, whereas in other species, >2% is a marker of severe parasitaemia.
what test to use at 4 weeks post-HIV exposure
p24 antigen test
usually positive from about 1 week to 3 - 4 weeks after infection with HIV
sometimes used as an additional screening test in blood banks
window period for HIV antibody test
most common and accurate test
usually consists of both a screening ELISA (Enzyme Linked Immuno-Sorbent Assay) test and a confirmatory Western Blot Assay
most people develop antibodies to HIV at 4-6 weeks but 99% do by 3 months
shigella treatment
supportive
severity depends on type: S sonnei (e.g. from UK) may be mild, S. flexneri or S. dysenteriae from abroad may cause severe disease
Shigella infection is usually self-limiting and does not require antibiotic treatment
antibiotics (e.g. ciprofloxacin) are indicated for people with severe disease, who are immunocompromised or with bloody diarrhoea
hep C pathophysiology
hepatitis C is a RNA flavivirus
incubation period: 6-9 weeks
hep C investigations
HCV RNA is the investigation of choice to diagnose acute infection
whilst patients will eventually develop anti-HCV antibodies it should be remembered that patients who spontaneously clear the virus will continue to have anti-HCV antibodies
hep C complications
rheumatological problems: arthralgia, arthritis
eye problems: Sjogren’s syndrome
cirrhosis (5-20% of those with chronic disease)
hepatocellular cancer
cryoglobulinaemia: typically type II (mixed monoclonal and polyclonal)
porphyria cutanea tarda (PCT): it is increasingly recognised that PCT may develop in patients with hepatitis C, especially if there are other factors such as alcohol abuse
membranoproliferative glomerulonephritis
chronic hep C management
treatment depends on the viral genotype - this should be tested prior to treatment
the management of hepatitis C has advanced rapidly in recent years resulting in clearance rates of around 95%. Interferon based treatments are no longer recommended
the aim of treatment is sustained virological response (SVR), defined as undetectable serum HCV RNA six months after the end of therapy
currently a combination of protease inhibitors (e.g. daclatasvir + sofosbuvir or sofosbuvir + simeprevir) with or without ribavirin are used
hep C treatment complications
ribavirin - side-effects: haemolytic anaemia, cough. Women should not become pregnant within 6 months of stopping ribavirin as it is teratogenic
interferon alpha - side-effects: flu-like symptoms, depression, fatigue, leukopenia, thrombocytopenia
mycoplasma pneumonia features
the disease typically has a prolonged and gradual onset
flu-like symptoms classically precede a dry cough
bilateral consolidation on x-ray
complications may occur as below
erythema multiforme
mycoplasma pneumonia complications
cold agglutins (IgM): may cause an haemolytic anaemia, thrombocytopenia
erythema multiforme, erythema nodosum
meningoencephalitis, Guillain-Barre syndrome and other immune-mediated neurological diseases
bullous myringitis: painful vesicles on the tympanic membrane
pericarditis/myocarditis
gastrointestinal: hepatitis, pancreatitis
renal: acute glomerulonephritis
mycoplasma investigations
diagnosis is generally by Mycoplasma serology
positive cold agglutination test
mycoplasma management
doxycycline or a macrolide (e.g. erythromycin/clarithromycin)
legionella features
flu-like symptoms including fever (present in > 95% of patients) dry cough relative bradycardia confusion lymphopaenia hyponatraemia deranged liver function tests pleural effusion: seen in around 30% of patients
legionella management
treat with erythromycin/clarithromycin
features of amoebic dysentry
profuse, bloody diarrhoea
there may be a long incubation period
stool microscopy may show trophozoites if examined within 15 minutes or kept warm (known as a ‘hot stool’)
treatment is with metronidazole
amoebic liver abscess presentation
usually a single mass in the right lobe (may be multiple). The contents are often described as ‘anchovy sauce’
features: fever, RUQ pain
serology is positive in > 90%
treatment for invasive amoebiasis
Treatment for invasive amoebiasis should be followed by a luminal amoebicide to eradicate the cystic stage which is resistant to metronidazole and tinidazole (which are used against the invasive stage).
cause of fever after first dose of antibiotics in syphillis
Jarisch-Herxheimer reaction
thought to be caused by the release of endotoxin-like substances following bacterial death after the first dose of antibiotics
syphillis management
intramuscular benzathine penicillin is the first-line management
alternatives: doxycycline
Which organism causes lymphogranuloma venereum?
Chlamydia trachomatis
Typically infection comprises of three stages
stage 1: small painless pustule which later forms an ulcer
stage 2: painful inguinal lymphadenopathy
stage 3: proctocolitis
cause of tonsillitis
strep pyogenes
immunological reactions can cause rheumatic fever or post-streptococcal glomerulonephritis
erythrogenic toxins cause scarlet fever
aquarium mycobacteria
Mycobacterium marinum
causes ‘fish tank granuloma’
treatment with tetracyclines, fluoroquinolones, sulfonamides, and macrolides
listeria pathogenesis
Gram-positive bacillus which has the unusual ability to multiply at low temperatures. It is typically spread via contaminated food, typically unpasteurised dairy products. Infection is particularly dangerous to the unborn child where it can lead to miscarriage.
listeria management
Listeria is sensitive to amoxicillin/ampicillin (cephalosporins usually inadequate)
Listeria meningitis should be treated with IV amoxicillin/ampicillin and gentamicin
screening for latent TB
The Mantoux test is the main technique used to screen for latent tuberculosis. In recent years the interferon-gamma blood test has also been introduced. It is used in a number of specific situations such as:
the Mantoux test is positive or equivocal
people where a tuberculin test may be falsely negative
mantoux test interpretation
< 6mm Negative - no significant hypersensitivity to tuberculin protein Previously unvaccinated individuals may be given the BCG
6 - 15mm Positive - hypersensitive to tuberculin protein Should not be given BCG. May be due to previous TB infection or BCG
> 15mm Strongly positive - strongly hypersensitive to tuberculin protein Suggests tuberculosis infection.
causes of false negative mantoux test
miliary TB sarcoidosis HIV lymphoma very young age (e.g. < 6 months)
how to diagnose active TB
Chest x-ray
upper lobe cavitation is the classical finding of reactivated TB
bilateral hilar lymphadenopathy
Sputum smear
3 specimens are needed
rapid and inexpensive test
stained for the presence of acid-fast bacilli (Ziehl-Neelsen stain)
all mycobacteria will stain positive (i.e. nontuberculous mycobacteria)
the sensitivity is between 50-80%
this is decreased in individuals with HIV to around 20-30%
Sputum culture
the gold standard investigation
more sensitive than a sputum smear and nucleic acid amplification tests
can assess drug sensitivities
can take 1-3 weeks (if using liquid media, longer if solid media)
Nucleic acid amplification tests (NAAT)
allows rapid diagnosis (within 24-48 hours)
more sensitive than smear but less sensitive than culture
severe falciparum management
a parasite counts of more than 2% will usually need parenteral treatment irrespective of clinical state
intravenous artesunate is now recommended by WHO in preference to intravenous quinine
if parasite count > 10% then exchange transfusion should be considered
shock may indicate coexistent bacterial septicaemia - malaria rarely causes haemodynamic collapse
uncomplicated falciparum management
strains resistant to chloroquine are prevalent in certain areas of Asia and Africa
the 2010 WHO guidelines recommend artemisinin-based combination therapies (ACTs) as first-line therapy
examples include artemether plus lumefantrine, artesunate plus amodiaquine, artesunate plus mefloquine, artesunate plus sulfadoxine-pyrimethamine, dihydroartemisinin plus piperaquine
splenectomy at risk of
pneumococcus, Haemophilus, meningococcus and Capnocytophaga canimorsus* infections
splenectomy vaccines
if elective, should be done 2 weeks prior to operation
Hib, meningitis A & C
annual influenza vaccination
pneumococcal vaccine every 5 years
mechanism for carbapenem resistance
New Delhi metallo-beta-lactamase 1 is the mutation that leads to carbapenem resistance. Typically found in Klebsiella pneumoniae, Escherichia Coli (E. Coli), Enterobacter cloacae and others. First line of management is the old antibiotic colistin and second line may be tigecycline.
mechanism for vancomycin resistance
D-alanyl-D-lactate variation leading to loss of affinity to antibiotics is the mechanism of VRE (vancomycin resistant enterococci). Vancomycin binds to D-ala-D-ala.
mechanism for -lactam resistance
The presence of MexAB-OprM efflux pumps is one of the mechanisms by which pseudomonas aeruginosa is resistant to -lactams, chloramphenicol, fluoroquinolones, macrolides, novobiocin, sulfonamides, tetracycline, and trimethoprim.
mechanism for MRSA resistance
Alteration to the penicillin binding protein 2 is the mechanism behind methicillin-resistant staphylococcus aureus. Mutations in the MEC gene which codes the penicillin binding proteins give staphylococcus aureus its resistance.
IgA protease
Streptococcus pneumoniae
Haemophilus influenzae
Neisseria gonorrhoeae
M protein
Streptococcus pyogenes
Polyribosyl ribitol phosphate capsule
Haemophilus influenzae
Bacteriophage
Corynebacterium diphtheriae
spore forming
Bacillus anthracis
Clostridium perfringens
Clostridium tetani
Lecithinase alpha toxin
Clostridium perfringens
D-glutamate polypeptide capsule
Bacillus anthracis
Actin rockets
Listeria monocytogenes
cholangitis causes in order
Escherichia coli
Klebsiella species
Enterococcus species
Streptococcus species
what level of parasitaemia should be considered sever in malaria
> 2%
two forms of trypanosomiasis
African trypanosomiasis (sleeping sickness) and American trypanosomiasis (Chagas’ disease).
what spreads african sleeping sickness
tsetse fly
pathogenesis of the two types of african sleeping sickness
rypanosoma gambiense in West Africa and Trypanosoma rhodesiense in East Africa
clinical features african sleeping sickness
Trypanosoma rhodesiense tends to follow a more acute course. Clinical features include:
Trypanosoma chancre - painless subcutaneous nodule at site of infection
intermittent fever
enlargement of posterior cervical lymph nodes
later: central nervous system involvement e.g. somnolence, headaches, mood changes, meningoencephalitis
african trypanosomiasis management
early disease: IV pentamidine or suramin
later disease or central nervous system involvement: IV melarsoprol
Chagas disease cause
Trypanosoma cruzi
features of amaerican sleeping sickness
The vast majority of patients (95%) are asymptomatic in the acute phase although a chagoma (an erythematous nodule at site of infection) and periorbital oedema are sometimes seen. Chronic Chagas’ disease mainly affects the heart and gastrointestinal tract
myocarditis may lead to dilated cardiomyopathy (with apical atophy) and arrhythmias
gastrointestinal features includes megaoesophagus and megacolon causing dysphagia and constipation
management american sleeping sickness
treatment is most effective in the acute phase using azole or nitroderivatives such as benznidazole or nifurtimox
chronic disease management involves treating the complications e.g., heart failure
epiglottitis cause
Haemophilus influenzae type B
epiglottitis management
immediate senior involvement, including those able to provide emergency airway support (e.g. anaesthetics, ENT)
endotracheal intubation may be necessary to protect the airway
if suspected do NOT examine the throat due to the risk of acute airway obstruction
the diagnosis is made by direct visualisation but this should only be done by senior staff who are able to intubate if necessary
oxygen
intravenous antibiotics
what is brucellosis
Brucellosis is a zoonosis more common in the Middle East and in farmers. Four major species cause infection in humans: B melitensis (sheep), B abortus (cattle), B canis and B suis (pigs). Brucellosis has an incubation period 2 - 6 weeks
brucellosis features
non-specific: fever, malaise
hepatosplenomegaly
sacroilitis: spinal tenderness may be seen
complications: osteomyelitis, infective endocarditis, meningoencephalitis, orchitis
leukopenia often seen
brucellosis diagnosis
the Rose Bengal plate test can be used for screening but other tests are required to confirm the diagnosis
Brucella serology is the best test for diagnosis
blood and bone marrow cultures may be suitable in certain patients, but these tests are often negative
brucellosis management
doxycycline and streptomycin
leishmaniasis cause
Leishmania, usually being spread by sand flies. Cutaneous, mucocutaneous leishmaniasis and visceral forms are seen
cutaneous leishmaniasis cause
caused by Leishmania tropica or Leishmania mexicana
crusted lesion at site of bite
may be underlying ulcer
cutaneous leishmaniasis acquired in South or Central America merits treatment due to the risk of mucocutaneous leishmaniasis whereas disease acquired in Africa or India can be managed more conservatively
mucocutaneous leishmaniasis cause
caused by Leishmania braziliensis
skin lesions may spread to involve mucosae of nose, pharynx etc
Visceral leishamaniasis cause
(kala-azar)
mostly caused by Leishmania donovani
occurs in the Mediterranean, Asia, South America, Africa
fever, sweats, rigors
massive splenomegaly. hepatomegaly
poor appetite*, weight loss
grey skin - ‘kala-azar’ means black sickness
pancytopaenia secondary to hypersplenism
the gold standard for diagnosis is bone marrow or splenic aspirate
leptospirosis cause
spirochaete Leptospira interrogans (serogroup L. icterohaemorrhagiae), classically being spread by contact with infected rat urine.
leptospirosis features
the early phase is due to bacteraemia and lasts around a week
may be mild or subclinical
fever
flu-like symptoms
subconjunctival suffusion (redness)/haemorrhage
second immune phase may lead to more severe disease (Weil’s disease)
acute kidney injury (seen in 50% of patients)
hepatitis: jaundice, hepatomegaly
aseptic meningitis
leptospirosis investigations
serology: antibodies to Leptospira develop after about 7 days
PCR
culture
growth may take several weeks so limits usefulness in diagnosis
blood and CSF samples are generally positive for the first 10 days
urine cultures become positive during the second week of illness
leptospirosis management
high-dose benzylpenicillin or doxycycline
bactericidal antibiotics
penicillins cephalosporins aminoglycosides nitrofurantoin metronidazole quinolones rifampicin isoniazid
bacteriostatic antibiotics
chloramphenicol macrolides tetracyclines sulphonamides trimethoprim
joint pain and fever, recent travel to asia
Chikungunya
alphavirus disease
mosquitoe spread
alphavirus disease features
Prominent symptoms are severe joint pain and abrupt onset of high fever. Other symptoms include general flu-like illness of muscle ache, headache, and fatigue. The disease shares its symptoms with dengue but tends to have more joint pain which can be debilitating. A rash may develop as with other viral illness and swelling of the joints in not uncommon.
alphavirus treatment
Relief of symptoms. No specific treatment.
what causes a false positive syphillis test
pregnancy SLE, anti-phospholipid syndrome TB leprosy malaria HIV
syphillis cause
Treponema pallidum
syphillis investigations
very sensitive organism and cannot be grown on artificial media. The diagnosis is therefore usually based on clinical features, serology and microscopic examination of infected tissue
Serological tests can be divided into: cardiolipin tests (not treponeme specific) treponemal-specific antibody tests
Cardiolipin tests
syphilis infection leads to the production of non-specific antibodies that react to cardiolipin
examples include VDRL (Venereal Disease Research Laboratory) & RPR (rapid plasma reagin)
insensitive in late syphilis
becomes negative after treatment
Treponemal specific antibody tests
example: TPHA (Treponema pallidum HaemAgglutination test)
remains positive after treatment
Therefore, following treatment for syphilis:
VDRL becomes negative
TPHA remains positive
Japanese encephalitis
Japanese encephalitis is the most common cause of viral encephalitis in South East Asia, China the Western Pacific and India, with approx. 50,000 cases annually. It is a flavivirus transmitted by culex mosquitos which breeds in rice paddy fields. The reservoir hosts are aquatic birds, but pigs are an amplification host and therefore close domestic contact with pigs is a risk factor.
The majority of infection is asymptomatic.
Clinical features are headache, fever, seizures and confusion. Parkinsonian features indicate basal ganglia involvement. It can also present with acute flaccid paralysis.
Diagnosis is by serology or PCR. Management is supportive.
Prevention is a vaccine and there are a variety of different types.
malaria investigations
The gold standard for diagnosis of malaria remains the blood film. Rapid diagnostic tests (detecting plasmodial histidine-rich protein 2) are currently being trialled and have shown sensitivities from 77-99% and specificities from 83-98% for falciparum malaria
Blood film - if doubt about diagnosis should be repeated
thick: more sensitive
thin: determine species
Other tests thrombocythaemia is characteristic normochromic normocytic anaemia normal white cell count reticulocytosis
terbinafine mechanism of action
inhibits the fungal enzyme squalene epoxidase, causing cellular death.It is an antifungal medication used to treat ringworm, pityriasis versicolor, and fungal nail infections.
erysipelas organism
strep pyogenes
zanamivir side effects
also a neuraminidase inhibitor
may induce bronchospasm in asthmatics
vacines contraindicated in all HIV patients
Cholera CVD103-HgR
Influenza-intranasal
Poliomyelitis-oral (OPV)
Tuberculosis (BCG)
what is lemierre’s disease
infectious thrombophlebitis of the internal jugular vein.
It most often occurs secondary to a bacterial sore throat caused by Fusobacterium necrophorum leading to a peritonsillar abscess. A combination of spread of the infection laterally from the abscess and compression lead to thrombosis of the IJV.
Patients will present with a history of bacterial sore throat followed by neck pain, stiffness and tenderness (may be mistaken for meningitis) and systemic involvement (fevers, rigors, etc). Septic pulmonary emboli may also occur.
EBV presentation
The classic triad of sore throat, pyrexia and lymphadenopathy is seen in around 98% of patients:
sore throat
lymphadenopathy: may be present in the anterior and posterior triangles of the neck, in contrast to tonsillitis which typically only results in the upper anterior cervical chain being enlarged
pyrexia
malaise, anorexia, headache
palatal petechiae
splenomegaly - occurs in around 50% of patients and may rarely predispose to splenic rupture
hepatitis, transient rise in ALT
lymphocytosis: presence of 50% lymphocytes with at least 10% atypical lymphocytes
haemolytic anaemia secondary to cold agglutins (IgM)
a maculopapular, pruritic rash develops in around 99% of patients who take ampicillin/amoxicillin whilst they have infectious mononucleosis
EBV causes
Infectious mononucleosis (glandular fever) (EBV, also known as human herpesvirus 4, HHV-4) in 90% of cases. Less frequent causes include cytomegalovirus and HHV-6. It is most common in adolescents and young adults
Mono diagnosis
heterophil antibody test (Monospot test) - NICE guidelines suggest FBC and Monospot in the 2nd week of the illness to confirm a diagnosis of glandular fever.
EBV management
Management is supportive and includes:
rest during the early stages, drink plenty of fluid, avoid alcohol
simple analgesia for any aches or pains
consensus guidance in the UK is to avoid playing contact sports for 8 weeks after having glandular fever to reduce the risk of splenic rupture
factors to reduce vertical HIV transmission
maternal antiretroviral therapy
mode of delivery (caesarean section)
neonatal antiretroviral therapy
infant feeding (bottle feeding)
Mode of delivery HIV positive women
vaginal delivery is recommended if viral load is less than 50 copies/ml at 36 weeks, otherwise caesarian section is recommended
a zidovudine infusion should be started four hours before beginning the caesarean section
flu –> remission –> jaundice and haematemesis
yellow fever
inclusion bodies in hepatocytes
yellow fever
egg protein anaphylaxis contraindication to which vaccine
yellow fever
also present in MMR and rabies but not clinically significant
causes of diarrhoea in HIV
Cryptosporidium + other protozoa (most common)
Cytomegalovirus
Mycobacterium avium intracellulare
Giardia
cryptosporidium diagnosis
It is an intracellular protozoa and has an incubation period of 7 days. Presentation is very variable, ranging from mild to severe diarrhoea. A modified Ziehl-Neelsen stain (acid-fast stain) of the stool may reveal the characteristic red cysts of Cryptosporidium. Treatment is difficult, with the mainstay of management being supportive therapy
WTF is Wuchereria bancrofti
Parasitic filarial nematode Accounts for 90% of cases of filariasis Usually diagnosed by blood smears Usually transmitted by mosquitos Treatment is with diethylcarbamazine commonest cause of filariasis leading to lymphatic obstruction
chlamydia investigation
traditional cell culture is no longer widely used
nuclear acid amplification tests (NAATs) are now the investigation of choice
urine (first void urine sample), vulvovaginal swab or cervical swab may be tested using the NAAT technique
for women: the vulvovaginal swab is first-line
for men: the urine test is first-line
Chlamydiatesting should be carried out two weeks after a possible exposure
chlamydia treatment
doxycycline 7 days
azithromycin, erythromycin, amoxicillin if pregnant or doxycycline contraindicated
Lassa fever features
flu-like symptoms abdominal pain haemorrhage petechiae, bruising bloody diarrhoea, haematemesis, haemoptysis disseminated intravascular coagulation multiorgan failure
lassa fever cause
Lassa fever is contracted by contact with the excreta of infected African rats (Mastomys rodent) or by person-to-person spread.
Lassa fever is an arenavirus (family Arenaviridae) which causes a wide clinical spectrum of disease ranging from non-specific febrile symptoms (often with a sore throat), through to vomiting, diarrhoea, oedema and shock. A mild bleeding diathesis may be seen. The fatality rate is around 15% in those unwell enough to require inpatient treatment. It is the haemorrhagic fever most often seen in returning travellers due to its wide distribution (it is found across West Africa) and long incubation (which can be up to three weeks).
which antibiotics inhibit cell wall formation>
penicillins: binds transpeptidase blocking cross-linking of peptidoglycan cell walls
cephalosporins
bacteriostatic antibiotics
Inhibit protein synthesis: these antibiotics are bateriostatic
aminoglycosides (cause misreading of mRNA)
chloramphenicol
macrolides (e.g. erythromycin)
tetracyclines
fusidic acid
which antibiotic inhibits RNA synthesis?
rifampicin
which antibiotics inhibit DNA synthesis
quinolones (e.g. ciprofloxacin)
metronidazole
sulphonamides
trimethoprim
short incubation period and severe vomiting point to a diagnosis of…
staph aureus food poisoning
cat scratch disease caused by
Gram negative rod Bartonella henselae
cat scratch features
fever
history of a cat scratch
regional lymphadenopathy
headache, malaise
antibiotic for bartonella henselae
Supportive
azithromycin if large nodes or immunocompromised
trimethoprim mechanism
interferes with DNA synthesis by inhibiting dihydrofolate reductase
may, therefore, interact with methotrexate, which also inhibits dihydrofolate reductase
adverse effects trimethoprim
myelosuppression
transient rise in creatinine: trimethoprim competitively inhibits the tubular secretion of creatinine resulting in a temporary increase which reverses upon stopping the drug
trimethoprim blocks the ENaC channel in the distal nephron, causing a hyperkalaemic distal RTA (type 4). It also inhibits creatinine secretion, often leading to an increase in creatinine by around 40 points (but not necessarily causing AKI)
PID treatment
oral ofloxacin + oral metronidazole or intramuscular ceftriaxone + oral doxycycline + oral metronidazole
pubic lice treatment
Management of pubic lice involves application of either: malathion 0.5%, permethrin 1%, phenothrin 0.2% or carbaryl 0.5% All of these creams or lotions are applied to all body hair and left on the hair for the recommended ‘treatment time’ before being washed off.
Treatment should be re-applied after 3-7 days: this is due to the presence of lice and eggs being at different stages of their life cycle.
toxoplasmosis management immunocompetent
supportive care
meningitis organisms 0-3months
Group B Streptococcus (most common cause in neonates)
E. coli
Listeria monocytogenes
meningitis organisms 3months-6 years
Neisseria meningitidis
Streptococcus pneumoniae
Haemophilus influenzae
meningitis organisms 6y-60y
Neisseria meningitidis
Streptococcus pneumoniae
meningitis causes >60 years
Streptococcus pneumoniae
Neisseria meningitidis
Listeria monocytogenes
renal transplant + infection =
CMV
Amphotericin B mechanism
Amphotericin B binds with ergosterol, a component of fungal cell membranes, forming pores that cause lysis of the cell wall and subsequent fungal cell death
caspofungin mechanism of action
inhibits synthesis of beta-glucan, a major fungal cell wall component.
nystatin mechanism of action
Binds with ergosterol forming a transmembrane channel that leads to monovalent ion (K+, Na+, H+ and Cl) leakage
non-gonococccal urethritis organisms
Chlamydia trachomatis - most common cause
Mycoplasma genitalium - thought to cause more symptoms than Chlamydia
non-gonnococcal urethritis manageemnt
contact tracing
the BNF and British Association for Sexual Health and HIV (BASHH) both recommend either oral azithromycin or doxycycline
Enterobius vermicularis (pinworm)
Threadworm infestation is asymptomatic in around 90% of cases, possible features include perianal itching, particularly at night; girls may have vulval symptoms
Diagnosis may be made by the applying sticky plastic tape to the perianal area and sending it to the laboratory for microscopy to see the eggs
River blindness
Onchocerca volvulus Causes ‘river blindness’. Spread by female blackflies
Features include blindness, hyperpigmented skin and possible allergic reaction to microfilaria
Ivermectin
rIVERblindness = IVERmectin
causes of a false positive VDRL/RPR
‘SomeTimes Mistakes Happen’ (SLE, TB, malaria, HIV)
Vancomycin mechanism of action
inhibits cell wall formation by binding to D-Ala-D-Ala moieties, preventing polymerization of peptidoglycans
vancomycin mechanism of resistance
alteration to the terminal amino acid residues of the NAM/NAG-peptide subunits (normally D-alanyl-D-alanine) to which the antibiotic binds
vancomycin adverse effects
nephrotoxicity
ototoxicity
thrombophlebitis
red man syndrome; occurs on rapid infusion of vancomycin.
Red man syndrome is associated with flushing or a maculopapular rash. The proposed mechanism is non IgE mediated mast cell degranulation. Red man syndrome is more common with higher flow rates of infusion. Treatment includes antihistamines.
features of severe malaria
schizonts on a blood film parasitaemia > 2% hypoglycaemia acidosis temperature > 39 °C severe anaemia complications as below
what is HIV?
HIV is a RNA retrovirus of the lentivirus genus (lentiviruses are characterized by a long incubation period)
two variants - HIV-1 and HIV-2
HIV-2 is more common in west Africa, has a lower transmission rate and is thought to be less pathogenic with a slower progression to AIDS
how does HIV enter cells?
HIV can infect CD4 T cells, macrophages and dendritic cells
gp120 binds to CD4 and CXCR4 on T cells and CD4 and CCR5 on macrophages
mutations in CCR5 can give immunity to HIV
Active TB treatment
Initial phase - first 2 months (RIPE) Rifampicin Isoniazid Pyrazinamide Ethambutol (the 2006 NICE guidelines now recommend giving a 'fourth drug' such as ethambutol routinely - previously this was only added if drug-resistant tuberculosis was suspected)
Continuation phase - next 4 months
Rifampicin
Isoniazid
Latent TB management
3 months of isoniazid (with pyridoxine) and rifampicin OR 6 months of isoniazid (with pyridoxine)
meningial TB management
treated for a prolonged period (at least 12 months) with the addition of steroids
Rifampicin side effects
potent liver enzyme inducer
hepatitis, orange secretions
flu-like symptoms
isoniazid side effects
peripheral neuropathy: prevent with pyridoxine (Vitamin B6)
hepatitis, agranulocytosis
liver enzyme inhibitor
Pyrazinamide side effects
hyperuricaemia causing gout
arthralgia, myalgia
hepatitis
Ethambutol side effects
optic neuritis: check visual acuity before and during treatment
toxocara canis
commonly acquired by ingesting eggs from soil contaminated by dog faeces
commonest cause of visceral larva migrans
other features: eye granulomas, liver/lung involvement
what is hepatitis E?
RNA hepevirus
spread by the faecal-oral route
incubation period: 3-8 weeks
common in Central and South-East Asia, North and West Africa, and in Mexico
causes a similar disease to hepatitis A, but carries a significant mortality (about 20%) during pregnancy
does not cause chronic disease or an increased risk of hepatocellular cancer
a vaccine is currently in development*, but is not yet in widespread use
characteristic features of pneumococcal pneumonia
the most common cause of community-acquired pneumonia
rapid onset
high fever
pleuritic chest pain
herpes labialis (cold sores)
hepatitis c transmission
hepatitis C is a RNA flavivirus
incubation period: 6-9 weeks
Transmission
the risk of transmission during a needle stick injury is about 2%
the vertical transmission rate from mother to child is about 6%. The risk is higher if there is coexistent HIV
breastfeeding is not contraindicated in mothers with hepatitis C
the risk of transmitting the virus during sexual intercourse is probably less than 5%
there is no vaccine for hepatitis C
Hepatitis c investigations
HCV RNA is the investigation of choice to diagnose acute infection
whilst patients will eventually develop anti-HCV antibodies it should be remembered that patients who spontaneously clear the virus will continue to have anti-HCV antibodies
hepatitis C outcomes
around 15-45% of patients will clear the virus after an acute infection (depending on their age and underlying health) and hence the majority (55-85%) will develop chronic hepatitis C
chronic hepatitis C complications
rheumatological problems: arthralgia, arthritis
eye problems: Sjogren’s syndrome
cirrhosis (5-20% of those with chronic disease)
hepatocellular cancer
cryoglobulinaemia: typically type II (mixed monoclonal and polyclonal)
porphyria cutanea tarda (PCT): it is increasingly recognised that PCT may develop in patients with hepatitis C, especially if there are other factors such as alcohol abuse
membranoproliferative glomerulonephritis
chronic hepatitis c management
treatment depends on the viral genotype - this should be tested prior to treatment
the management of hepatitis C has advanced rapidly in recent years resulting in clearance rates of around 95%. Interferon based treatments are no longer recommended
the aim of treatment is sustained virological response (SVR), defined as undetectable serum HCV RNA six months after the end of therapy
currently a combination of protease inhibitors (e.g. daclatasvir + sofosbuvir or sofosbuvir + simeprevir) with or without ribavirin are used
hepatitis c complications of treatement
ribavirin - side-effects: haemolytic anaemia, cough. Women should not become pregnant within 6 months of stopping ribavirin as it is teratogenic
interferon alpha - side-effects: flu-like symptoms, depression, fatigue, leukopenia, thrombocytopenia
human bite antibiotic
co-amoxiclav
WTF is Orf?
Orf is generally a condition found in sheep and goats although it can be transmitted to humans. It is caused by the parapox virus.
In animals
‘scabby’ lesions around the mouth and nose
In humans
generally affects the hands and arms
initially small, raised, red-blue papules
later may increase in size to 2-3 cm and become flat-topped and haemorrhagic
