vomiting and diarrhoea (3 or more loose stools a day), + abdominal pain/discomfort (can be quite severe if campylobacter), fever,
bloods in stool can be indicative of a bacterial infection
signs of dehydration:
thirsty, dry mucous membranes: mild, (<5% weight loss)
lethargic, reduced skin turgor, sunken eyes, sunken anterior fontanelle, tachycardia, reduced urine output, reduced tears: moderate (5-10% weight loss)
drowsy, absent urine output, prolonged capillary refill time, weak pulse, low BP (signs of hypovolaemic shock): severe (>10% weight loss)
Gastroenteritis Investigation / diagnosis
stool MC&S, urea and electrolytes
oral rehydration therapy given frequently in small amounts; IV fluids if not tolerating oral/nasogastric fluids. Good handwashing to prevent spread. Notify public health if bacterial
Complications of campylobacter infection
What can predispose you to gastroenteritis?
Presentation of CDIFF
mild diarrhoea to severe colitis
diarrhoea, fever, abdominal pain
Investigations for CDIFF
stools MC&S, FBC (increased WCC)
Treatment for C. Diff
metronidazole (first line), stool transplant, oral vancomycin (second line), fidaxomicin, surgery may be required, isolation, barrier nursing
prevention: stop AB (cephalosporin, clarithromycin, clindamycin, co-amoxiclav) (fluoroquinolones are also important in the development of c.diff)
Pass medicine note: Clindamycin is historically associated with causing Clostridium difficile but the aetiology has evolved significantly over the past 10 years. Second and third generation cephalosporins are now the leading cause of Clostridium difficile.
What are the complications of C.Diff?
pseudomembranous colitis, toxic megacolon, sepsis
What are the toxins that c.diff produces?
A (enterotoxin) and B (cytotoxin)
Presentation of infectious diarrhoea
fever, diarrhoea (may be bloody), nausea, dehydration, abdominal pain, bloody diarrhoea is more common with Campylobacter, Shigella
What is the diagnosis of infectious diarrhoea?
diagnosis by antigen detection
FBC, U&E, CRP, stool microscopy, culture and sensitivity (MC&S), blood cultures if septic
What is the management of infectious diarrhoea?
majority of cases are self-terminating and require rehydration and electrolyte correction: AB are considered in immunocompromised patients, the very young or the very septic; always liaise with microbiologists
What viruses can cause infectious diarrhoea?
adenovirus, rotavirus in children under 5 years
What are the complications of infectous diarrhoea?
renal failure, septic shock; E. coli is associated with the haemolytic-uraemic syndrome
What are the symptoms / presentation for giardia lamblia?
diarrhoea, malabsorption, failure to thrive
a patient develops persistent foul-smelling watery diarrhoea and weight loss after travelling to India. His symptoms have now lasted two weeks. He has no abdominal pain, nausea or fever
What is the investagation for giardia lamblia?
Cysts seen on stool microscopy
What is the treatment for giardia lamblia?
How is giardia lamblia spread?
Whet type of organism is giardia lamblia?
What bacterium causes the majority of cases of travellers diarrhoea in developing countries?
What is the normal reservoir of Ecoli o157 (this is an enterohaemorrhagic bacterium)
2.5% of britich cattle secrete VTEC (verotoxin producing Ecoli)
The reservoir of infectio nis in the gut of herbivores.
The organism has an ectremely low infecting dose.
What are the symptoms of enterohaemorrhagi bacteria?
Initial watery diarrhoea
Becomes blood stained in 70% of cases. Associated with severe and often constant abdominal pain.
Little systemic upset, vomittin or fever.
What is the complication associated with Ecoli o157?
Haemolytic Uraemic syndrome
Who is affected by HUS?
HUS affects 10-15% of sufferers from this infection
Arises 5-7 days after the onset of symptoms
Most likely i nthe extremes of age, heralded by a high peripheral leucocyte count and may be induced particularly in chgildren by antibiotic therapy
What is the treatment for HUS?
Dialysis if necessary and may be averted by plasma exchange
Antibiotics should be avoided since they can stimulate toxin release.
What cells does the HIV virus attack?
Attacks the CD4 cells (T helper cells, macrophages and dendritic cells)
What are the features of the primary infection of HIV?
Usually symptomatic in more than 50% of cases
Incubation period is 2-4 weeks after exposure
Clinical features resemble a glandular fever type of illness (flu like symptoms - (presence of maculopapular rash and oral ulceration strongly suggests primary HIV infection rather than other viral casues of glandular fever.)
What is the progression of HIV after the primary infection?
Chronic phase which can last 2-10 years.
Depletion of CD4 cells and increase viral load
Clinical latelcy follows primary infection - individuals are asymptomatic.
Persistent lymphadenopathy less than 2cm diameter ius a common finding.
What is the differential diagnosis for primary HIV?
Primary cytomegalovirus infection
When does HIV become AIDS?
The development of specified opportunistic infections cancers and severe manifestations of HIV itself.
Can be diagnosed by having a CD4 count that is less than 200/mm3
CDC is the most used category of AIDS defining illnesses
CDC category A for HIV
Primary HIV infection
Persistent generalised lymphadenopathy
CDC category B for HIV
Fever / diarrhoea lasting for over one month
Oral hairy leucoplakia
Cervial dysplasia / carcinoma in situ
Idiopathic thrombocytopenic purpura
CDC category C for HIV infection
Candidiasis of trachea, bronchi or lungs
Cervical carcinoma that is invasive
Cryptococcosis - extrapulmonary
Cytomegalovirus disease (outside the liver spleen and nodes)
Herpes simplex chronic ulcers or visceral
Lymphoma (cerebral or B cell non hodgkin)
Recurrent bacterial pneumonia
How is viral load determined?
Quantitive PCR of HIV - RNA
How is HIV diagnosed?
By detectiong host antibodies (either by point of care tests or by ELISA)
A positive antibody test from two different immunoasays is sufficiennt to confirm infection
Screening may involve testing for p24 antigen in addition to antibodies (incase antibody production hasn't started yet)
Nucleic acid amplification (usually PCR) of HIV-RNA is carried out on children who's mothers have had AIDS (the maternal antibodies will live in their system for 15 months and they might not have produced their own antibodies yet).
What are the aims of ART?
Reduce the viral load to an undetectable level for as long as possible
Improve CD4 count to over 200 cells/mm3 so that severe HIV-related disease is unlikely
Improve the quality of life without unacceptable drug toxicity
Reduce HIV transmission
What are the classes of antiretroviral drugs?
Nucleoside reverse transcriptase inhibitors (NRTIs)
Non-nucleoside reverse transcriptase inhibitors (NNRIS)
Chemokine receptor inhibitor
Give examples for each type of ART
NRTI - abacavir, zidovudine
NNRTI - Efavirenz
PI - Atazanavir
Integrase inhibitors = Raltegravir
Chemokine receptor inhibitor = maraviroc
What is the standard antiretroviral regimen?
Two NRTI's together
or Integrase inhibitor
Most guidelines from high-income countries allow clonicians to choose a starting regimen of dual NRTIs combined with an NNRTI, or a PI or integrase inhibitor as these three regimens have a similar efficacy.
What must PI's be co-prescribed with?
Must be co-prescribed with ritonavir - low doses oof ritonavir dramatically increase the concentrations and elimination half-lives of other PI's by inhibitin gtheir metabolism by cytochroime P450. This increases drug exposure, reducing pill burden and dosing frequency - optimising adherence
When should ART therapy begin?
Following the 2015 BHIVA guidelines it is now recommended that patients start HAART as soon as they have been diagnosed with HIV, rather than waiting until a particular CD4 count, as was previously advocated.
Lymes Disease Presentation:
early: erythema chronicum migrans + systemic features (fever, arthralgia)
CVS: heart block, myocarditis
neuro: cranial nerve palsies, meningitis
What causes Lymes disease
Spirochaete Borrelia Burgdorferi
What is the investigation for Lymes disease?
NICE recommend that Lyme disease can be diagnosed clinically if erythema migrans is present
enzyme-linked immunosorbent assay (ELISA) antibodies to Borrelia burgdorferi are the first-line test
if this test is positive or equivocal then an immunoblot test for Lyme disease should be done
What are later complications of Lyme Disease?
Acrodermatitis chronica atroficans (ACA) - this is atrophy of the skin, often has involvement of the peripheral nervous system causing polyneuropathy
Lymphocytoma can also be caused (also chronic)
What is the management of asymptomatic tick bites?
tick bites can be a relatively common presentation to GP practices, and can cause significant anxiety
NICE guidance does not recommend routine antibiotic treatment to patients who've suffered a tick bite
What is the management of Lymes disease?
Management of suspected/confirmed Lyme disease
doxycycline if early disease. Amoxicillin is an alternative if doxycycline is contraindicated (e.g. pregnancy)
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)
What type of virus is Rabies?
RNA rhabdovirus (specifically a lyssavirus)
What are the features of Rabies?
prodrome: headache, fever, agitation
hydrophobia: water-provoking muscle spasms
Negri bodies: cytoplasmic inclusion bodies found in infected neurons
What is the treatment for Rabies?
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
What is the diagnostic test for rabies?
PCR to check for lyssavirus in the CSF
What is rat fever?
What are the clinical features of Influenza
2-4 days incubation period (1-7)
temperature up to 41° (38-40) for 3 days (1-5), 2 of the following:
cough (sore throat, rhinorrhoea),
Predominance of systemic symptoms. Less common symptoms include tiredness, chills, headache, sore throat, runny nose, sneezing, nausea, vomiting, diarrhoea, loss of appetite, aching muscles, limb or joint pain
What is the treatment for influenza?
influenza A or B, both for treatment or prophylaxis, start within 48 hours of onset of symptoms/contact: oseltamivir, zanamivir
What are the complications of influenza?
RESP: acute bronchitis, secondary bacterial pneumonia
RESP: primary viral pneumonia,
CNS: transverse myelitis/ Guillain Barre, myositis & myoglobinuria
What is tha pathogen associated with bronchiolitis?
RSV (respiratory syncytial virus) (75-80% of cases)
Mycoplasma and adenoviruses are also causes
Who often gets bronchioloitis?
Babies less than 1 years old = peak incidence is 3-6months
Maternal IgG protects gainst RSV
More common in winter
When is bronchiolitis more serious?
When there is bronchopulmonary dysplasia in premature babies
Congenital heart disease
What are the features of bronchiolitis?
coryzal symptoms (including mild fever) precede:
wheezing, fine inspiratory crackles (not always present)
feeding difficulties associated with increasing dyspnoea are often the reason for hospital admission
When do NICE recommend immediate referral whenm there is a case of bronchiolitis?
apnoea (observed or reported)
child looks seriously unwell to a healthcare professional
severe respiratory distress, for example grunting, marked chest recession, or a respiratory rate of over 70 breaths/minute
persistent oxygen saturation of less than 92% when breathing air.
When should clinicians refer to th hospital if there is a case of bronchiolitis according to NICE?
a respiratory rate of over 60 breaths/minute
difficulty with breastfeeding or inadequate oral fluid intake (50-75% of usual volume 'taking account of risk factors and using clinical judgement')
What are the investigations for bronchiolitis?
immunofluorescence of nasopharyngeal secretions may show RSV
CXR: may show hyperinflation/patchy infiltrative change
What is management for bronchiolitis?
humidified oxygen is given via a head box and is typically recommended if the oxygen saturations are persistently < 92%
nasogastric feeding may be need if children cannot take enough fluid/feed by mouth
suction is sometimes used for excessive upper airway secretions
CPAP/ ventilation if severe
Ipratropium inhalers may help
Palivizumab (monoclonal Ab) given monthly as primary prophylaxis during RSV season to at-risk infants (ie: chronic lung disease, congenital heart disease)
What are the complications of bronchiolitis?
chronic wheeze, bronchiolitis obliterans (adenovirus)
What organism causes amoebic dysentry?
What organism is most likely to cause invasive pulmonary aspergillosis?
What are the risk factors for invasive aspergillosis?
Solid organ or allogenic stem cell ttransplant
Leukaemia and other haemotological malignancies
Advanced HIV disease
Critically ill patients on intensive care units
Chronic granulomatous disease
What are the findings on CT that would indicate invasive pulmonary aspergillosis?
Dense, well circumscribed lesions with or without a halo sign
Air crescent sign
When is an immunocompromised patient heavily suspected of having invasive pulmonary aspergillosis?
If they develop fever, new resp symptoms, (particularly pleural pain or haemoptysis) or a pleural rub.
What are the features of tracheobronchial aspergillosis?
Involvement is characterised by the formation of fungal plaques and ulceration
What are mycological ways to diagnose aspergillosis?
Using sputum, BAL fluid or bronchial brush to find one of the following:
Fungal elements indicating mould of aspergillus
Culturing a mould of aspergillosus
What blood test can be done to look for invasive pulmonary aspergillosis?
Detection of aspergillus cell wall components (galactomannan and B-1,2-glucan) in blood or BAL fluid and aspergillus DNA by PCR.)
What is treatment choice for invasive pulmonary aspergillosis?
Second line agents include liposomal amphotericin, caspofungin or posaconazole.
What is sub-acute or chronic pulmonary aspergillosis?
Non-invasive complication of chronic lung disease such as COPD, TB, opportunistic mycobacterial disease or fibrotic lung disease
What disease does chronic pulmonary aspergillosis closely mimic?
What are the features of chronic pulmonary aspergillosis?
Cough (with or without haemoptysis), weight loss, anorexia and fatigue over months or years
Associated fever, night sweats and elevated inflammatory markers
What are radiological features of chronic or subacute pulmonary aspergillosis?
Thick walled - cavities (predominantly apical)
Pleural thickening and later fibrosis
What are the three different dsecriptive names of chronic pulmonary aspergillosis?
CNPA (chronic necrotising)
What are the features of malaria?
none, splenomegaly, hepatomegaly, mild jaundice, anaemia, tachycardia
What are the investigations for malaria?
thick and thin blood films (Giemsa, Field’s stain)
schizonts on a blood film
quantitative buffy coat (QBC) - this is a fluorescence microscopy based malaria diagnostice test
rapid antigen tests (OptiMal and parasight F)
FBC (anaemia), raised ESR, raised CRP, U&E, LFT
What are the organisms that cause malaria?
Plasmodium falciparum causes nearly all episodes of severe malaria. The other three types, of which Plasmodium vivax is the most common, cause 'benign' malaria
What are protective factors for malaria?
absence of Duffy antigens
Sickle cell anaemia
What are the features of severe malaria?
schizonts on a blood film
parasitaemia > 2%
temperature > 39 °C
complications as below
What are the complications of malaria?
- cerebral malaria: seizures, coma
- acute renal failure: blackwater fever, secondary to intravascular haemolysis, mechanism unknown
- acute respiratory distress syndrome (ARDS)
- disseminated intravascular coagulation (DIC)
What might make you more likely to suffer from malaria?
What is the result of parasitisation of the maternal side of the placenta?
What are preventative measures for malaria?
awareness of risk per geographical area,
bite prevention (cover up at dawn and dusk, insect repellent sprays, lotions, mosquito coils, permethrin-impregnated mosquito nets)
chemoprophylaxis (malarone daily, doxycyline daily, mefloquine weekly, chloriquine weekly + proquanil daily
diagnosis & treatment)
What is the management of malaria?
Artemisinin treatment is recommended
Co-artemether (CoArtem or Riamet) contains artemether and lumefantrine - this is given as 4 pills, 6 times over 60 hours
Quinine for 7 days plus doxycycline/clindamycin 7 days
Malarone for 3 days
What is the treatment for severe or complicated malaria?
Severe malaria should be considered in any on-immune patient with aparasite count greater than 2% - medical emergency
Correction of fluid, electrolytes, acid base balance
IV quinine + oral doxycyline (or clindamycine)
switch to oral treatments when patient is stable and can swallow
What is a side effect of quinine?
What are the treatments for other forms of malaria?
treatment of other species of malaria
add primaquine to eradicate liver hypnozoites this is in P vivax and P ovale (check for G6PD def - haemolysis may develop)
Which cells do neutrophils target?
Bacterial and fungal infection
Which cells do monocytes target?
Which type of cells do Eosinophils target?
What type of cell do T cells target?
Fungal and viral ifnection PJP
What type of cells do B lymphocytes target?
What is the presentation of sepsis?
a high temperature (fever) or low body temperature
chills and shivering
a fast heartbeat
In the very young and the very old you can get low temperature.
Potential for hyperglycaemia.
What is the presentation for septic shock?
feeling dizzy or faint
a change in mental state – such as confusion or disorientation
nausea and vomiting
severe muscle pain
less urine production than normal – for example, not urinating for a day
cold, clammy and pale or mottled skin
loss of consciousness
What are the tests for sepsis?
Blood test (blood culture, FBC, lactate levels, increased levels can indicate organ dysfunction, CRP, procalcitonin – marker sometimes used to distinguish bacterial sepsis from other inflammatory conditions that cause similar symptoms
Liver function tests
CSF analysis (meningitis)
What is the treatment for sepsis?
Broad-spectrum antimicrobials are usually given intravenously (IV). Drug therapy may be changed to a more targeted therapy once the microorganism causing the sepsis is identified.
IV fluids are given to help improve and stabilise blood pressure. Sometimes medications are given to constrict blood vessels and increase blood pressure.
Supplemental oxygen may be necessary, and some people require mechanical ventilation to assist with breathing. Other organ support, such as kidney dialysis, is sometimes necessary when organs start to fail.
Surgical procedures are sometimes necessary to remove medical devices such as catheters that may be the source of the infection, to drain abscesses or fluids, to remove and/or fix damaged tissue, and to remove blockages.
What is the sepsis 6?
Sepsis 6 (three treatments and three tests)
Give IV fluids
Taking blood cultures (assess the cause of the sepsis)
Taking a blood sample (this is used to assess the severity of the sepsis)
Monitoring urine output (assesses the severity of the kidney function)
How do you maintain MAP in sepsis?
Vasopressors such as norepinephrine
What is included in the QSOFA?
Hypotension (systolic blood pressure less than 100mmHg)
Altered mental status
RR greater than 22/min
Score greater than 2 suggests a greater risk of poor outcomes
What are the clinical features of typhoid?
fever, headache, abdo discomfort, constipation, dry cough, relative bradycardia, neutrophilia, confusion
fever peaks at 7-10 days, Rose spots, diarrhoea begins, tachycardia, neutropenia
3rd week (complications):
intestinal bleeding, perforation, peritonism, metastatic infections
week 4 (recovery): 10-15% relapse
What are the investigations for typhoid fever?
What is the treatment for typhoid fever?
What are the causative organisms for thyphoid fever?
Salmonella typhi and paratyphi
How is typhoid transmitted?
faecal-oral transmission via contaminated food or water, preventable by vaccination
Symptoms of schistomiasis
1st few hours:
swimmers itch (clears 24-48hrs)
invasive stage (cough, abdo discomfort, splenomegaly, eosinophilia)
after 15-20 days: Katayama fever (protsrate, fever, urticaria, lymphadenopathy, splenomegaly, diarrhoea, eosinophilia
acute disease (eggs deposited in bowel (dysentry) or bladder (haematuria)
What are the investigations for schistosomiasis?
Ab tests, ova in stools and urine, rectal snip
What is the management of schistosomiasis?
prednisolone if severe
What are the complications of schistosomiasis?
squamous cell carcinoma (which is very rare except in tropical countries)
What animal spreads schistosomiasis?
Fresh water snail
Which highly infective skin condition is classicaly described as having a golden crust?
What organisms cause impetigo?
Less commonly strep pyogenes
What organism is most likely to cause erysipelas?
Mostly due to strep pyogenes
What is the key difference between cellulitits and erysipelas?
Erysipelas has distinct elevated borders whereas cellulitis doesn't
What systemic symptoms might be apparent for cellulitits and erysipelas?
Associated lymphadenopathy and lymphangitis
What is the treatment for erysipelas and cellulitis?
combination of anti-staphylococcal and anti-streptococcal AB
in extensive disease, admission for IV AB and rest
Cellulitis = (penicillin and flucloxacillin)
Necrotising fasciitis presentation:
extensive oedema and severe, unremitting pain
systemic features include fever, hypotension, tachycardia, delirium, multiorgan failure, erythema +/- vesicle formation
anaesthesia at site of infection is highly suggestive of this disease
Type 1 = mixed aerobic and anaerobic infection, diabetic foot infection, fournier's gangrene
Type 2 = monomicrobial
initially similiar to cellulitis, septic, rapidly advancing erythema +/- painless ulcers
What are the investigations?
bloods (high WCC, low sodium), CT
What is therapy for necrotising fasciitis?
one of the infectious diseases emergencies. Surgical review is mandatory
AB should be broad spectrum (flucloxacillin, gentamicin, clindamycin)
intensive therapy unit (ITU), broad spectrum AB, bold surgical resection down to healthy tissue - reassess daily
What is the aetiology of necrotising fasciitis?
usually polymicrobial infection, typical organisms include strep, staph, enterococci, gram -ve bacilli, clostridium
normally associated with Strep pyogenes
can get it from infected needles, abscesses, open fractures, surgery or idiopathic
What are bacterial causes of meningitis?
Neisseria meningitidis (meningococcus)
Strep pneumoniae (pneumococcus)
In neonates E.Coli, group B strep (strep agalactiae is an example)
What are viral causes of meningitis?
- Coxsackie A and B viruses
- Poliovirus (not seen in the UK)
Mumps, now very rare due to the MMR vaccine
What are less common causes of meningitis?
Haemophilus influenze type b
What type of organism is responsible for almost half of meningitis associated with ventriculo-atrial / peritoneal shunts?
Coagulase negative staph (eg staph epidermis)
What can cause non-infective meningitis?
Tumour cells in the CSF
Reactions to certain drugs or chemicals or by some disease of unknown aetiology such as sarcoidosis or SLE
What is the classical presentation for bacterial meningitis?
Clouding of consciousness
Cranial nerve palsies may occur (6,7,8)
What rash is associated with meningococcal meningitis?
Macular/maculo-papular, purpuric, pruritic or vesicular
All occur due to meningococci or other meningitides
What would papilloedema suggest when examining someone for meningitis?
Unusual in meningitis and should lead one to consider an intracranial space occupying lesion
What are the clinical signs you can elicit in meningism?
What are investigations for meningitis?
(if papilloedema then you should request a head CT to rule out a space occupying lesion, LP is contraindicated if this is the case)
What do microbiology do with CSF for meningitis?
Gram stain (and ZN if appropriate)
Differential cell count (neutrophil polymorphs or lymphocytes)
Antigen detection test (latex agglutination)
Mycobacterial or fungal culture (if appropriate)
PCR for viruses (if appropriate)
PCR for bacteria (if appropriate)
WHat is CSF biochemistry for meningitis?
Glucose (check serum level at the same time)
What is FBC results in bacterial meningitis?
Leucopenia (septicaemia with DIC, you would also see, low platelets, abnormal clotting and increased fibrin degradation products)
After centrifugation what colour is the supernatant in the case of a SAH?
Golden yellow - due to haemoglobin breakdown
Described as xanthochromic
Bloody tape after centrifugation should have no xanthochromia
Predominant cell type
What are the principles of treatment for meningitis?
1. Early clinical recognition.
2. Rapid detection of pathogen.
3. Rapid initiation of appropriate bactericidal antimicrobial therapy.
4. Early recognition and treatment of sequelae of septicaemia
(eg, DIC with shock, hypoxia, acidosis and adrenal insufficiency).
5. Antibiotic prophylaxis (when appropriate) of close contacts.
What are possible antibiotic therapies in meningitis?
What is the tumblr test?
Purpuric rash of meningococcal disease does not blanche under pressure
What antibiotics are given on discharge after being treated for meningococcal meningitis?
Rifampicin or ciprofloxacin (adults only)
This is to eradicate carriage of N. meningitidis from the nasopharynx
WHo should be notified after confimation of meningococcal meningitis?
Local consultant in health protection
They will coordinate the arrangements for prophylaxis
What is the most frequent causative organism of bacterial meningitis in adults?
Who is normally affected by neisseria meningitidis?
Primarily a disease of children and young adults
Less than 10% of cases occur over the age of 5
What are the features of strep pneumoniae?
alpha haemolytic on blood agar
What can predispose to strep pneumoniae?
What is a key sign of s. pneumoniae meningitis?
Patient is more likley to have altered conscious level or focal neurological signs than those with haemophilus or meningococcal meningitis
What is the treatment of S.pneumoniae meningitis?
High dose ceftriaxone
What are the complications of s.pneumoniae meningitis?
Loss of hearing
Cranial nerve deficits
What vaccine might help prevent s.pneumoniae meningitis?
pneumovax - for all those over 65 years old
There is a conjugated version for those under 2 years (prevenar)
Which HSV type complicates a primary genital herpes infectino with viral meningitis?
What is the presentation of viral meningitis?
Non-specific prodromal illness
Rapid onset headache
Low grade fever
Patient is usuall ylucid and alert, if encephalitis is also present then lethargy, confusion, seizures and focal neurological signs occur. With enteroviral meningitis, a rash may be present which, if petechial, may resemble menincococcaemia. With mumps meningitis, 50% do not have detectable parotitis.
What are the investigations for viral meningitis?
PCR of CSF
PCR of throat swabs and faecal samples
What is the therapy for viral hepatitis?
Enteroviruses and Parechoviruses: This is symptomatic and recovery usually occurs within 72 hours. If chronic infection occurs (e.g. patient immunocompromised), treatment with intravenous immunoglobulin may be required. Herpes simplex virus: aciclovir, initially intravenously.
When should the MMR vaccination be given?
3 years 4 months - 5 years
What is the most important cause of meningitis in patients with HIV infection?
It also occures rarely in patients with diabetes, lymphoma and those receiving immunosuppressive drugs. The organism is found in bird dropssings, especially those found in pigeons.
Which type of stain allows the capsule to be visualised as a clear zone around the yeast cell?
What are the investiations for cryptococcal meningitis?
What are the symptoms of fungal meningitis?
Most commonly, there is a subacute onset of symptoms with low grade fever, headache, nausea, lethargy, confusion and abdominal pain. Meningism is less common, although
it can develop quickly as the condition progresses.
What is the treatment for cryptococcus neoformans meningitis?
Parental amphotericin (sometimes used in combination with flucytosine)
High dise fluconazole is being increasingly used as an alternative to this combination
Long term chemoprophylaxis with fluconazole is now given to patients with HIV infection following an episode of cryptococcal meningitis (secondary prophylaxis).
How des neonatal meningitis differ from adult meningitis?
Symptoms and signs are not specific or not well localised
The bacteria commonly involved are group B streptococci, E. coli and L. monocytogenes as well as enteroviruses and parechoviruses. Predisposing conditions include low birth weight, prolonged rupture of membranes and maternal diabetes mellitus.
What are tje two clinical syndromes assocaited with neonatal meningitis?
Early onset - within 3 days of birth and associated with prematurity or a difficult or prolonged birth. Marked respiratory distress, bacteraemia and a high mortality (50%) are typical. The organism has usually been acquired at birth from the mother’s genital tract.
Late onset - more than one week
after birth. The infection is typified
by bacteraemia and meningitis but pulmonary involvement is rare. Mortality is 10-20%. The organism may have been spread by cross-infection from other mothers, babies or healthcare workers.
How is the daignosis made of neonatal meningitis?
Bacterial: Neonatal CSF and blood cultures are central to making the diagnosis. Maternal blood cultures and cultures of specimens from the genital tract may also be helpful.
Viral: Neonatal CSF, EDTA blood, faeces and nasopharyngeal secretions.
What is the treatment for neonatal meningitis?
Parenteral ampicillin (to cover group B streptococci and Listeria) and gentamicin or cefotaxime (to cover the gram negative bacilli) are used in combination, until
the causative organism is identified. IVIG may be appropriate for enteroviruses or parechoviruses.
What ways can we prevent neonatal meningitis?
Chemoprophylaxis to prevent neonatal group B strep infectionis given to high risk mothers during labour (usually amoxicillin or co-amoxiclav)
What are the clinical features of HAV?
Upper abdominal pain
Jaundice developing 3-10 days later, during which time the urine may be dark becasue of the presence of conjugated bilirubin.
What is the route of infection for hep A?
Faecal - oral
(potential for parenteral)
What is virological diagnosis of hepatitis A?
HAV IgM antibodies indicate infection (present in the serum at onset of symptoms and usually decline to a non-detectable level over 3-6 months)
HAV IgG antibodies indicates immunity
What is managment of HAV?
What are means of prevention of HAV ifnection?
Good personal hygiene and sanitation
Isolation not necessary
Prophylaxis of close contacts of patients with HAV with human normal immunoglobulin
Who might be offered hep A vaccination?
For those at risk of exposure such as:
- Sewage workers
- Seronegative hamophiliacs
- MSM with multiple sexual partners
- Travellers to endemic areas
- Patients with hep C get the vaccination becuse the illness may be more serious
How do liver enzymes react to hepatitis?
Incerase in ALT and AST
What is the prognosis of Hep A?
Chronic liver damage does not occur
Lifelong immunity follows infection
Uncommon complications include:
- Prolonged cholestatic jaundice
- Relapsing hepatitis
- Haematological problems such as aplastic anaemia
What is the presentation of hepatitis B infection?
Urticarial skin lesions often precede the development of darkly coloured urine and jaundice
HBV infection outcomes
basically the majority of people recover, for those who don't you might suffer from different activity states of the hepatitis - may be chronic or it can even result in fulminant hepatic necrosis.
Result of persistent hepatitis is cirrhosis, liver cancer and needing a liver transplant.
What are the hepatitis b markers for viral replication?
What is the major identifier for acute and chronic hepatitis B infection?
What seroogical markers in hepatitis might make you think that someone is particularly infectious?
HBeAg positive chronically infected
These people are at high risk of developing chronic liver disease and hepatoma
What are the mechanisms of transfer of HBV?
Horizontal (sexual, parenteral including needlestick, inapparent parenteral)
Childhood horizontal transmission probably happens as a result of inapparent exposure to blood or body fluids.
What are factors predisposing to increased risk of infection in the UK?
Injecting drug use
Multiple sexual partners - both MSM or heterosexual
Immigration from areas of high endemnicity
Patients with a learning disability who live in residential care
Patients win haemodialysis units or with haemophilia
Sexual partners of those with the above risk factors
Babies born to mothers who are at risk
Tattooing or body piercing with non-sterile equipment
Medical equipment if not adequately decontaminated
When is a needle stick more likely to pass on HBV?
If it is HBeAg positive
What antibody is the key antibody during acute infective period of hepatitis B?
There is seroconversion to anti-HBs severeal weeks after the disappearance of HBsAg
What is meant by the window period of HBV?
The only serological marker present is anti-HBC
What is the definition of chronic HBV infection?
Persistence of HBsAg in the serum for more than 6 months
What are long-term sequale of chronic hep B infection?
Chronic liver disease
What are potential complications for chronic HBV liver infection?
Who is offered antiviral therapy?
If you have asymptomatic chronic HBV infection with raised ALT and are HBeAg positive
Those with progressive liver disease
Without cirrhosis and have 2 of the following:
HBV DNA greater than 2,000 IU/ml
Significant liver inflammation or fibrosis
What is the first antigen to appear in hepatitis B?
surface antigen (HBsAg) is the first marker to appear and causes the production of anti-HBs
What does anti-HBc imply?
Implies previous or current infection
IgM anti-HBc appears during acute or recent hepatitis B infection and is present for about 6 months. IgG anti-HBc persists
What are potential treatments for hepatitis B?
Pegylated alpha interferon
Entecavir and tenofovir
Advanced cirrhosis may warrant liver transplant, graft rejection reduced by giving the patient antiretroviral agents as well as Hepatitis B specific immunoglobulin
What are the most important means of preventing HBV infection?
Infection control procedures
Screening of blood donors and transplant donors
What is the main component of the HBV vaccination?
HBsAg produced by recombinant DNA technology
How is passive immunity for hepatitis provided?
Hepatitis B specific immunoglobulin
What is recommended for people with positive HBsAg who are about to undergo systemic chemotherapy?
Start them on prophylactic antiviral therapy for at least 6-12 months after its cessation
Antiviral therapy may also be needed for those with positive anti-HBc (even if there are low HBsAg). These people may still have HBA DNA in there liver which may reactivate the HBV activation - acute liver failure
How does acute HCV present?
Usually subclinical or mild
Symptoms in 20%
Severe hepatitis and jaundice can occur
Outcomes of acute hep C infection
What are known routes of transmission of HCV?
Shared “works” associated with IDU, including needles, syringes, filters, spoons.
Blood products prior to heat treatment in 1989.
Blood transfusion prior to antibody screening in 1991.
Tattooing, ear piercing, body piercing or acupuncture with non-sterile equipment.
Sexual transmission (<5%; except higher risk during passive traumatic anal intercourse from a HIV/HCV individual).
Household contacts sharing razors or toothbrushes.
Medical or dental treatment if inadequately decontaminated equipment used (e.g. some developing countries).
How is diagnosis achieved of HCV?
Antibody testing (IgG only athough this has v poor sensitivity)
Detection of HCV antigen
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
How is HCV treated?
Treatment response varies according to the viral genotype
A interferon with ribavarin
For genotype1 HCV infection give protease enzyme inhibitor with a interferon and ribavarin.
The goal is sustained viral response (virus undetectable for 6 months after antiviral therapy)
Ribavarin is teratogenic
How are potential preventative mesures for HepC?
Blood, organ and tissue donor screening
are very important measures for reducing transmission. No post-exposure prophylaxis
or vaccine is available. Other preventative measures include not sharing injecting equipment, avoiding sharing razors and toothbrushes, and covering cuts and skin lesions with waterproof dressings.
What is hepatitis D always seen in conjunction with?
Hepatitis B virus
What is coinfection and superinfection?
Co-infection is simultaneous infection with HDV and HBV. Superinfection is when a person with chronic HBV infection becomes infected with HDV. In both, the illness is more severe than HBV infection alone.
What is the transmission mode for hepatits D?
What is the virological diagnosis of HDV?
Tests are available to detect IgG and IgM antibody to HDV, HDV-RNA and HDAg in serum. Co-infection and superinfection can be distinguished by the presence of high level of anti-HBc IgM in co-infection.
What is treatment for hepatitis as a result of HBV infection?
Pegylated alpha interferon
Liver transplantation may offer some hope
in fulminant hepatitis. Prevention of HBV infection also prevents HDV infection. Severe chronic hepatitis commonly follows HDV superinfection.
What is the presentation of Hep E?
Like Hep A but carries a significant mortality in pregnant women (up to 20%)
What is the route of infection in Hep E?
Faecal oral route
What type of virus is HepE?
Small RNA virus
What are the genotypes of hepatitis E assocaited with developing countries?
1 and 2
What are the global genotypes of hep E?
3 and 4
is associated with the increasing reports of sporadic infections in developed countries, including the UK, that have not until recent years been known to be endemic regions.
What are serological tests for HepE?
IgG and IgM HEV-RNA
What is the treatment for HepE?
No licensed treatment
Ribavarin monotherapy in the immunocompromised
What are ways to reduce transmission?
Adequate cooking of food
Active immunisation with a subunit vaccine is available in China and it is possible that immunisation may eventually become available to protect vulnerable groups like pregnant women. Passive immunisation with HNIG available in the UK does not protect tropical travellers against HEV infection.