Infectious Disease Flashcards
what is the commonest causes of bacterial intestinal disease in the UK
Campylobacter
The majority of cases are caused by the Gram-negative bacillus Campylobacter jejuni. It is spread by the faecal-oral route and has an incubation period of 1-6 days.
Features of campylobacter?
prodrome: headache malaise
diarrhoea: often bloody
abdominal pain: may mimic appendicitis
Management of Campylobacter?
usually self-limiting
the BNF advises treatment if severe or the patient is immunocompromised. Antibiotics are recommended if severe symptoms (high fever, bloody diarrhoea, or more than eight stools per day) or symptoms have lasted 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’
complications of campylobacter?
Guillain-Barre syndrome may follow Campylobacter jejuni infections
reactive arthritis
septicaemia, endocarditis, arthritis
management of Legionella pneumonia?
treat with erythromycin/clarithromycin
What is Granuloma Inguinale?
Granuloma inguinale, also known as Donovanosis, is a sexually transmitted infection caused by the bacterium Klebsiella granulomatis. It presents with painless genital ulcers and can progress to cause significant tissue destruction if left untreated.
What are the symptoms of HIV seroconversion?
HIV seroconversion is symptomatic in 60-80% of patients and typically presents as a glandular fever-type illness. Increased symptomatic severity is associated with poorer long-term prognosis. It typically occurs 3-12 weeks after infection
Features
sore throat
lymphadenopathy
malaise, myalgia, arthralgia
diarrhoea
maculopapular rash
mouth ulcers
rarely meningoencephalitis
mechanism of action of ahminoglycosides and adverse effects?
Binds to 30S subunit causing misreading of mRNA
adverse effects - Nephrotoxicity, Ototoxicity
Mechanism of action of tetracyclines? and adverse effects?
Binds to 30S subunit blocking binding of aminoacyl-tRNA
Adverse effects Discolouration of teeth, photosensitivity
mechanism of action of clindamycin?
Binds to 50S subunit, inhibiting translocation (movement of tRNA from acceptor site to peptidyl site)
Adverse effects - common cause of c.diff
Mechanism of action of macrocodes?
Binds to 50S subunit, inhibiting translocation (movement of tRNA from acceptor site to peptidyl site)
adverse effects
Nausea (especially erythromycin), P450 inhibitor, prolonged QT interval
what is Orf and how does it present?
Orf is generally a condition found in sheep and goats although it can be transmitted to humans. It is caused by the parapox virus.
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
what are the different types of tape worm?
Cysticercosis
Hydatid disease
what is the cause of cysticercosis and what is the management?
caused by Taenia solium (from pork) and Taenia saginata (from beef)
management: niclosamide
What is the cause of Hydatid disease and what is the management?
caused by the dog tapeworm Echinococcus granulosus
life-cycle involves dogs ingesting hydatid cysts from sheep liver
often seen in farmers
may cause liver cysts
management: albendazole
What is Chikungunya virus?
Alphavirus disease caused by infected mosquitoes. Areas affected are Africa, Asia and Indian subcontinent but in recent years there has been seen in a few cases in Southern Europe. Tanzania had the first reported case.
what are the symptoms and treatment of chikungunya ?
severe joint pain
high fever
flu like illness
Treatment: Relief of symptoms. No specific treatment.
what is the most common cause of diaeehowa in travellers?
Worldwide, enterotoxigenic E. coli (ETEC) is the most common cause of diarrhoea in travellers. There is, however, geographical variation - Campylobacter is more common in travellers in South East Asia.
post exposure prophylaxis for Hep B
HBsAg positive source
if the person exposed is a known responder to the HBV vaccine then a booster dose should be given
if they are a non-responder (anti-HBs < 10mIU/ml 1-2 months post-immunisation) they need to have hepatitis B immune globulin (HBIG) and a booster vaccine
unknown source
for known responders the HBV vaccine 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
post exposure prophylaxis for Hep A
Human Normal Immunoglobulin (HNIG) or hepatitis A vaccine may be used depending on the clinical situation
post exposure prophylaxis for Hep C
monthly PCR - if seroconversion then interferon +/- ribavirin
post exposure prophylaxis for varicella zoster?
VZIG for IgG negative pregnant women/immunosuppressed
what kind of virus is HIV?
HIV is a RNA retrovirus of the lentivirus genus (lentiviruses are characterized by a long incubation period)
what are the two variants of HIV?
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
What is the structure of HIV?
spherical in shape with two copies of single-stranded RNA enclosed by a capsid of the viral protein p24
a matrix composed of viral protein p17 surrounds the capsid
envelope proteins: gp120 and gp41
pol gene encodes for viral enzymes reverse transcriptase, integrase and HIV protease
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
after entering a cell the enzyme reverse transcriptase creates dsDNA from the RNA for integration into the host cell’s genome
what is Leishmaniasis?
Leishmaniasis is caused by the intracellular protozoa Leishmania, which are spread by the bites of sandflies. Cutaneous, mucocutaneous leishmaniasis and visceral forms are seen
what is cutaneous Leishmanisis?
caused by Leishmania tropica or Leishmania mexicana
crusted lesion at the site of bite
there may be an underlying ulcer
it is typically diagnosed by doing a punch biopsy from the edge of the lesion allowing for both histology and culture
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
what is mucocutaneous Leishmaniasis?
caused by Leishmania braziliensis
skin lesions may spread to involve mucosae of nose, pharynx etc
what causes Visceral Leishmaniasis?
what are the symptoms
what is the treatment?
mostly caused by Leishmania donovani
occurs in the Mediterranean, Asia, South America, Africa
fever, sweats, rigors
massive splenomegaly. hepatomegaly
poor appetite*, weight loss
occasionally patients may report increased appetite with paradoxical weight loss
grey skin - ‘kala-azar’ means black sickness
pancytopaenia secondary to hypersplenism
the gold standard for diagnosis is bone marrow or splenic aspirate
management
the BNF recommends sodium stibogluconate, an organic pentavalent antimony compound
amphotericin B may be used with or after treatment with an antimony compound
what is botulism caused by?
Clostridium botulinum
gram positive anaerobic bacillus
7 serotypes A-G
produces botulinum toxin, a neurotoxin which irreversibly blocks the release of acetylcholine
may result from eating contaminated food (e.g. tinned) or intravenous drug use
neurotoxin often affects bulbar muscles and autonomic nervous system
features of botulism?
Features
patient usually fully conscious with no sensory disturbance
flaccid paralysis
diplopia
ataxia
bulbar palsy
treatment for botulism?
botulism antitoxin and supportive care
antitoxin is only effective if given early - once toxin has bound its actions cannot be reversed
features of 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
how is viral meningitis managed?
supportive care
Antivirals are of no benefit in the treatment of confirmed viral meningitis
what causes bacterial vaginosis ?
Bacterial vaginosis (BV) describes an overgrowth of predominately anaerobic organisms such as Gardnerella vaginalis
This leads to a consequent fall in lactic acid producing aerobic lactobacilli resulting in a raised vaginal pH.
what criteria is used for diagnosing BV?
Amsel’s criteria for diagnosis of BV - 3 of the following 4 points should be present
thin, white homogenous discharge
clue cells on microscopy: stippled vaginal epithelial cells
vaginal pH > 4.5
positive whiff test (addition of potassium hydroxide results in fishy odour)
how is BV managed?
if asymptomatic - dont need treatment unless pregnant
Oral metronidazole
what may cause progressive multifocal leukoencephalopathy?
Progressive multifocal leukoencephalopathy is caused by the JC virus or BK virus
JC virus affects significantly immunosuppressed patients. It causes demyelination and significant white matter changes and the clinical syndrome of PML which can include cognitive and behavioural abnormalities, sensory and motor deficits, ataxia, aphasia and cortical visual changes.
what are the clinical features of progressive multifocal leukoencephalopathy?
cognitive and behavioural abnormalities, sensory and motor deficits, ataxia, aphasia and cortical visual changes. Seizures are a common feature.
what would an MRI show in progressive multifocal leukoencephalopathy?
The MRI findings of cerebral white matter change without gadolinium enhancement are typical of progressive multifocal leukoencephalopathy (PML). CT brain would likely be performed first in this scenario but findings may be non specific and an MRI would be subsequently be performed. .
how should people who have been exposed to a confirmed case of bacteria meningitis be managed>?
should be given prophylactic antibiotics if they have close contact within the 7 days before onset
oral ciprofloxacin or rifampicin may be used.
how is bacterial meningitis managed ?
< 3 months - IV cefotaxime + amoxicillin (or ampicillin)
3 months - 50 years - IV Cefotaxime
> 50 years - IV cefotaxime (or ceftriaxone) + amoxicillin (or ampicillin)
Meningococcal - IV ben pen or cefotaxime
Pneumococcal - IV cefotaxime
H.ifluenzae - IV cefotaxime
Lesteria - amoxicillin and gentamicin
Management of Lyme disease?
If asymptomatic - do not need treatment
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)
features of Lyme disease
erythema migraines - bulls eye rash, typically presents 1-4 weeks after initial bite, usually painless
Systemic features - headache, lethargy, fever, arthralgia
Later features - heart block, peri/myocarditis, neurological (facial never palsy, radicular pain, meningitis)
investigations for Lyme disease?
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
management of toxoplasmosis in immunocompetent patients?
Most infections are asymptomatic. Symptomatic patients usually have a self-limiting infection, often having clinical features resembling infectious mononucleosis (fever, malaise, lymphadenopathy). Other less common manifestations include meningoencephalitis and myocarditis.
Serology is the investigation of choice.
No treatment is usually required unless the patient has a severe infection or is immunosuppressed.
Toxoplasmosis in Immunosupressed patients?
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
how does toxoplasmosis infect the body?
Toxoplasma gondii is an 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.
management of Gonorrhoea?
IM cerftriaxone
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
what causes typhoid?
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.
how is typhoid spread?
typhoid is transmitted via the faecal-oral route (also in contaminated food and water)
features of enteric fever?
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
complications of enteric fever?
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)
what is the cause of acute epiglottis?
Acute epiglottitis is rare but serious infection caused by Haemophilus influenzae type B.
what are the features of acute epiglottis?
rapid onset
high temperature, generally unwell
stridor
drooling of saliva
‘tripod’ position: the patient finds it easier to breathe if they are leaning forward and extending their neck in a seated position
how is acute epiglottis diagnosed
Diagnosis is made by direct visualisation (only by senior/airway trained staff, see below). However, x-rays may be done, particularly if there is concern about a foreign body:
a lateral view in acute epiglottis will show swelling of the epiglottis - the ‘thumb sign’
in contrast, a posterior-anterior view in croup will show subglottic narrowing, commonly called the ‘steeple sign’
how is acute epiglottis managed?
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 antibiotic
when is the tetanus vaccine given?
2 months
3 months
4 months
3-5 years
13-18 years
what is considered a tetanus prone wound and a high risk tetanus prone wound?
tetanus prone wound
puncture-type injuries acquired in a contaminated environment e.g. gardening injuries
wounds containing foreign bodies
compound fractures
wounds or burns with systemic sepsis
certain animal bites and scratches
High risk tetanus prone wound
heavy contamination with material likely to contain tetanus spores e.g. soil, manure
wounds or burns that show extensive devitalised tissue
wounds or burns that require surgical intervention
when is tetanus vaccine required following wound?
Patient has had a full course of tetanus vaccines, with the last dose < 10 years ago
no vaccine nor tetanus immunoglobulin is required, regardless of the wound severity
Patient has had a full course of tetanus vaccines, with the last dose > 10 years ago
if tetanus prone wound: reinforcing dose of vaccine
high-risk wounds (e.g. compound fractures, delayed surgical intervention, significant degree of devitalised tissue): reinforcing dose of vaccine + tetanus immunoglobulin
If vaccination history is incomplete or unknown
reinforcing dose of vaccine, regardless of the wound severity
for tetanus prone and high-risk wounds: reinforcing dose of vaccine + tetanus immunoglobulin
what is strongyloides steracoralis?
Strongyloides stercoralis is a human parasitic nematode worm. The larvae are present in soil and gain access to the body by penetrating the skin. Infection with Strongyloides stercoralis causes strongyloidiasis.
what are the features and treatment of Strongyloides stercoralis?
Features
diarrhoea
abdominal pain/bloating
papulovesicular lesions where the skin has been penetrated by infective larvae e.g. soles of feet and buttocks
larva currens: pruritic, linear, urticarial rash
if the larvae migrate to the lungs a pneumonitis similar to Loeffler’s syndrome may be triggered
Treatment
ivermectin and albendazole are used
What abx are commonly used to treat MSRA ?
vancomycin
teicoplanin
linezolid
what is Lymphogranuloma venereum?
Lymphogranuloma venereum (LGV) is caused by Chlamydia trachomatis serovars L1, L2 and L3*.
Risk factors of Lymphogranuloma venereum?
men who have sex with men
the majority of patients who present in developed countries have HIV
historically was seen more in the tropics
How does Lymhogranuloma venereum present?
Typically infection comprises of three stages:
stage 1: small painless pustule which later forms an ulcer
stage 2: painful inguinal lymphadenopathy
may occasionally form fistulating buboes
stage 3: proctocolitis
how is Lymphogrannuloma venereum treated?
Doxycycline
what is Pneumocystis Jiroveci Pneumonia?
Pneumocystis jiroveci (AKA PCP) is an unicellular eukaryote, generally classified as a fungus but some authorities consider it a protozoa
common opportunistic infection in AIDS
all patients with a CD4 count < 200/mm³ should receive PCP prophylaxis
Features of Pneumocystis Jiroveci pneumonia?
dyspnoea
dry cough
fever
very few chest signs
Pneumothorax is a common complication of PCP.
Extrapulmonary manifestations are rare (1-2% of cases), may cause
hepatosplenomegaly
lymphadenopathy
choroid lesions
Investigations for PCP?
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)
management of 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)
key things in pneumonia causes….
Streptococcus pneumoniae –> cold sores
Staph. Aureus –> followed by infection with H. Influenza
H. Influenza –> Infective exacerbation of COPD
Mycoplasma pneumonia –> Cold hemagglutination, deranged LFTs
Klebsiella pneumonia –> Alcoholics and causes cavitation
Legionella pneumonia –> history of traveling, swimming, living in hotels, presents with hyponatremia and deranged LFTs
what are the diagnostic 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)
what vaccinations should be given to patients having splenectomy?
Vaccination
if elective, should be done 2 weeks prior to operation
Hib, meningitis A & C
annual influenza vaccination
pneumococcal vaccine every 5 years
Indications for splenectomy?
Trauma: 1/4 are iatrogenic
Spontaneous rupture: EBV
Hypersplenism: hereditary spherocytosis or elliptocytosis etc
Malignancy: lymphoma or leukaemia
Splenic cysts, hydatid cysts, splenic abscesses
What is Immune reconstitution inflammatory syndrome?
Immune reconstitution inflammatory syndrome is a condition generally associated with HIV/immunosuppression, in which the immune system begins to recover, but then responds to a previously acquired opportunistic infection with an overwhelming inflammatory response that paradoxically makes the symptoms of infection worse.
what are examples of live attenuated vaccines
TB - BCG
Yellow fever
Oral polio
Intranasal influenza
Varicella
Measles, mumps and rubella (MMR)
Should not be given in
what are examples of inactivated vaccines?
employ pathogens that have been killed, often by heat or chemicals, to elicit an immune response
might require booster doses to maintain immunity as the induced immune response is generally weaker than live attenuated vaccines
examples:
rabies
hepatitis A
influenza (intramuscular)
What are examples of toxoid vaccines?
tetanus
diphtheria
pertussis
what are examples of subunit and conjugate vaccines?
Subunit and conjugate vaccines are often grouped together. Subunit means that only part of the pathogen is used to generate an immunogenic response. A conjugate vaccine is a particular type that links the poorly immunogenic bacterial polysaccharide outer coats to proteins to make them more immunogenic
pneumococcus (conjugate)
haemophilus (conjugate)
meningococcus (conjugate)
hepatitis B
human papillomavirus
,
HIV drug types?
HIV drugs, rule of thumb:
Nucleoside analogue reverse transcriptase inhibitors (NRTIs) end in ‘ine’
Protease inhibitors (PI): end in ‘vir’
Non-nucleoside reverse transcriptase inhibitors (NNRTI): nevirapine, efavirenz
How is chlamydia diagnosed?
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
what are examples of viral hemorrhagic fevers?
Flaviviridae: dengue, yellow fever
Arenaviridae: Lassa fever
Filoviridae: Ebola virus, Marburg virus
Bunyaviridae: Hantaviruses, Crimean-Congo haemorrhagic fever, Rift Valley fever
what are features of viral haemorrhagic fevers?
flu-like symptoms
abdominal pain
haemorrhage
petechiae, bruising
bloody diarrhoea, haematemesis, haemoptysis
disseminated intravascular coagulation
multiorgan failure
how is Lassa fever contracted and what is the treatment?
Lassa fever is contracted by contact with the excreta of infected African rats (Mastomys rodent) or by person-to-person spread.
ribavirin is used to treat Lassa fever
what kind of virus is measles?
RNA paramyxovirus
How is measles spread and what is the incubation person?
How long are the infective?
spread by aerosol transmission
infective from prodrome until 4 days after rash starts
incubation period = 10-14 days
what are the features of Measles?
Features
prodromal phase
irritable
conjunctivitis
fever
Koplik spots
typically develop before the rash
white spots (‘grain of salt’) on the buccal mucosa
rash
starts behind ears then to the whole body
discrete maculopapular rash becoming blotchy & confluent
desquamation that typically spares the palms and soles may occur after a week
diarrhoea occurs in around 10% of patients
Investigations for measles?
IgM antibodies can be detected within a few days of rash onset
how is measles managed?
mainly supportive
admission may be considered in immunosuppressed or pregnant patients
notifiable disease → inform public health
complications of measles?
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
management of contacts of patients with measles?
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
treatment of UTI in pregnancy?
should be treated with an antibiotic for 7 days
first-line: nitrofurantoin (should be avoided near term)
second-line: amoxicillin or cefalexin
trimethoprim is teratogenic in the first trimester and should be avoided during pregnancy
what is anthrax?
Bacillus anthracis (anthrax) is a spore-forming, aerobic gram-positive bacillus.
how does anthrax present?
causes painless black eschar (cutaneous ‘malignant pustule’, but no pus)
typically painless and non-tender
may cause marked oedema
anthrax can cause gastrointestinal bleeding
what is the management of anthrax?
the current Health Protection Agency advice for the initial management of cutaneous anthrax is ciprofloxacin
further treatment is based on microbiological investigations and expert advice
what is cat scratch disease and what are the features?
Cat scratch disease is generally caused by the Gram negative rod Bartonella henselae
Features
fever
history of a cat scratch
regional lymphadenopathy
headache, malaise
management of active TB?
nitial 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
management of latent TB?
The treatment for latent tuberculosis is 3 months of isoniazid (with pyridoxine) and rifampicin OR 6 months of isoniazid (with pyridoxine)
when is direct observed therapy indicated in TB treatment?
Directly observed therapy with a three times a week dosing regimen may be
indicated in certain groups, including:
homeless people with active tuberculosis
patients who are likely to have poor concordance
all prisoners with active or latent tuberculosis
how long do patients with meningeal TB require treatment for?
Patients with meningeal tuberculosis are treated for a prolonged period (at least 12 months) with the addition of steroids
complications of TB treatment?
mmune reconstitution disease
occurs typically 3-6 weeks after starting treatment
often presents with enlarging lymph nodes
Drug adverse effects
rifampicin
potent liver enzyme inducer
hepatitis, orange secretions
flu-like symptoms
isoniazid
peripheral neuropathy: prevent with pyridoxine (Vitamin B6)
hepatitis, agranulocytosis
liver enzyme inhibitor
pyrazinamide
hyperuricaemia causing gout
arthralgia, myalgia
hepatitis
ethambutol
optic neuritis: check visual acuity before and during treatment
mechanism of action of rifampicin?
Inhibits RNA synthesis
how to differentiate between lymphoma and toxoplasmosis?
Differentiating between toxoplasmosis and lymphoma is an important aspect of managing neurocomplications relating to HIV. Given the more limited availablity of SPECT compared to CT many patients are treated empirically on the basis of scoring systems, for example there is a 90% likelihood of toxoplasmosis if all of the following criteria are met:
toxoplasmosis IgG in the serum
CD4 < 100 and not receiving prophylaxis for toxoplasmosis
multiple ring enhancing lesions on CT or MRI
Toxoplasmosis - multiple lesions, ring or nodular enhancement, Thallium SPECT negative
Lymphoma - single lesion, solid
Symptoms of toxoplasmosis?
what is seen on CT head?
how is it managed?
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: sulfadiazine and pyrimethamine
Primary CNS lymphoma in HIV
what is it associated with
what does CT head show?
what is the treatment?
Primary CNS lymphoma
accounts for around 30% of cerebral lesions
associated with the Epstein-Barr virus
CT: single or multiple homogenous enhancing lesions
treatment generally involves steroids (may significantly reduce tumour size), chemotherapy (e.g. methotrexate) + with or without whole brain irradiation. Surgical may be considered for lower grade tumours
HIV - neurocomplication cryptococcus:
Features
CSF results
CT scan
most common fungal infection of CNS
headache, fever, malaise, nausea/vomiting, seizures, focal neurological deficit
CSF
high opening pressure
elevated protein
reduced glucose
normally a lymphocyte predominance but in HIV white cell count many be normal
India ink test positive
CT: meningeal enhancement, cerebral oedema
meningitis is typical presentation but may occasionally cause a space-occupying lesion
features of mycoplasma pneumonia?
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
complications of mycoplasma pneumonia?
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
investigations and management of mycoplasma pneumoniae?
Investigations
diagnosis is generally by Mycoplasma serology
positive cold agglutination test → peripheral blood smear may show red blood cell agglutination
Management
doxycycline or a macrolide (e.g. erythromycin/clarithromycin)
