Infection Summary Flashcards
1
Q
Gastroenteritis Presentation
A
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)
2
Q
Gastroenteritis Investigation / diagnosis
A
stool MC&S, urea and electrolytes
3
Q
Gastroenteritis Management
A
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
4
Q
Complications of campylobacter infection
A
Guillain-Barre
Reactive arthritis
5
Q
What can predispose you to gastroenteritis?
A
HIV
Omeprazole
6
Q
Presentation of CDIFF
A
mild diarrhoea to severe colitis
diarrhoea, fever, abdominal pain
7
Q
Investigations for CDIFF
A
stools MC&S, FBC (increased WCC)
8
Q
Treatment for C. Diff
A
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.
9
Q
What are the complications of C.Diff?
A
pseudomembranous colitis, toxic megacolon, sepsis
10
Q
What are the toxins that c.diff produces?
A
A (enterotoxin) and B (cytotoxin)
11
Q
Presentation of infectious diarrhoea
A
fever, diarrhoea (may be bloody), nausea, dehydration, abdominal pain, bloody diarrhoea is more common with Campylobacter, Shigella
12
Q
What is the diagnosis of infectious diarrhoea?
A
diagnosis by antigen detection
FBC, U&E, CRP, stool microscopy, culture and sensitivity (MC&S), blood cultures if septic
13
Q
What is the management of infectious diarrhoea?
A
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
14
Q
What viruses can cause infectious diarrhoea?
A
adenovirus, rotavirus in children under 5 years
15
Q
What are the complications of infectous diarrhoea?
A
renal failure, septic shock; E. coli is associated with the haemolytic-uraemic syndrome
16
Q
What are the symptoms / presentation for giardia lamblia?
A
diarrhoea, malabsorption, failure to thrive
Giardiasis:
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
17
Q
What is the investagation for giardia lamblia?
A
Cysts seen on stool microscopy
18
Q
What is the treatment for giardia lamblia?
A
Metronidazole
19
Q
How is giardia lamblia spread?
A
Contaminated water
20
Q
Whet type of organism is giardia lamblia?
A
Parasite
21
Q
What bacterium causes the majority of cases of travellers diarrhoea in developing countries?
A
Enterotoxigenic e.coli
22
Q
What is the normal reservoir of Ecoli o157 (this is an enterohaemorrhagic bacterium)
A
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.
23
Q
What are the symptoms of enterohaemorrhagi bacteria?
A
Initial watery diarrhoea
Becomes blood stained in 70% of cases. Associated with severe and often constant abdominal pain.
Little systemic upset, vomittin or fever.
24
Q
What is the complication associated with Ecoli o157?
A
HUS
Haemolytic Uraemic syndrome
25
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
26
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.
27
What cells does the HIV virus attack?
Attacks the CD4 cells (T helper cells, macrophages and dendritic cells)
28
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.)
29
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.
30
What is the differential diagnosis for primary HIV?
EBV
Primary cytomegalovirus infection
Rubella
Primary toxoplasmosis
Secondary syphilis
31
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
32
CDC category A for HIV
Primary HIV infection
Asymptomatic
Persistent generalised lymphadenopathy
33
CDC category B for HIV
Candidiasis (oropharyngeal)
Fever / diarrhoea lasting for over one month
Oral hairy leucoplakia
Cervial dysplasia / carcinoma in situ
Idiopathic thrombocytopenic purpura
Peripheral neurupathy
34
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
HIV encephalopathy
Kaposi's sarcoma
Lymphoma (cerebral or B cell non hodgkin)
Pneumocystis pneumonia
Recurrent bacterial pneumonia
Cerebral toxoplasmosis
Tuberculosis
35
How is viral load determined?
Quantitive PCR of HIV - RNA
36
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).
37
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
38
What are the classes of antiretroviral drugs?
Nucleoside reverse transcriptase inhibitors (NRTIs)
Non-nucleoside reverse transcriptase inhibitors (NNRIS)
Protease inhibitors
Integrase inhibitors
Chemokine receptor inhibitor
39
Give examples for each type of ART
NRTI - abacavir, zidovudine
NNRTI - Efavirenz
PI - Atazanavir
Integrase inhibitors = Raltegravir
Chemokine receptor inhibitor = maraviroc
40
What is the standard antiretroviral regimen?
Two NRTI's together
NNRTI
Protease inhibitor
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.
41
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
42
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.
43
Lymes Disease Presentation:
early: erythema chronicum migrans + systemic features (fever, arthralgia)
CVS: heart block, myocarditis
neuro: cranial nerve palsies, meningitis
44
What causes Lymes disease
Spirochaete Borrelia Burgdorferi
45
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
46
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)
neuroborreliosis
47
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
48
What is the management of Lymes disease?
Management of suspected/confirmed Lyme disease
## Footnote
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)
49
What type of virus is Rabies?
RNA rhabdovirus (specifically a lyssavirus)
50
What are the features of Rabies?
prodrome: headache, fever, agitation
hydrophobia: water-provoking muscle spasms
hypersalivation
Negri bodies: cytoplasmic inclusion bodies found in infected neurons
51
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:
## Footnote
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
52
What is the diagnostic test for rabies?
PCR to check for lyssavirus in the CSF
53
What is rat fever?
Leptospirosis
54
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),
myalgia,
headache,
malaise.
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
55
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
56
What are the complications of influenza?
common:
RESP: acute bronchitis, secondary bacterial pneumonia
less common:
RESP: primary viral pneumonia,
CV: myocarditis/pericarditis,
CNS: transverse myelitis/ Guillain Barre, myositis & myoglobinuria
57
What is tha pathogen associated with bronchiolitis?
RSV (respiratory syncytial virus) (75-80% of cases)
Mycoplasma and adenoviruses are also causes
58
Who often gets bronchioloitis?
Babies less than 1 years old = peak incidence is 3-6months
Maternal IgG protects gainst RSV
More common in winter
59
When is bronchiolitis more serious?
When there is bronchopulmonary dysplasia in premature babies
CF
Congenital heart disease
60
What are the features of bronchiolitis?
coryzal symptoms (including mild fever) precede:
dry cough
increasing breathlessness
wheezing, fine inspiratory crackles (not always present)
feeding difficulties associated with increasing dyspnoea are often the reason for hospital admission
61
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
central cyanosis
persistent oxygen saturation of less than 92% when breathing air.
62
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')
clinical dehydration.
63
What are the investigations for bronchiolitis?
immunofluorescence of nasopharyngeal secretions may show RSV
CXR: may show hyperinflation/patchy infiltrative change
64
What is management for bronchiolitis?
Largely supportive
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)
65
What are the complications of bronchiolitis?
chronic wheeze, bronchiolitis obliterans (adenovirus)
66
What organism causes amoebic dysentry?
Entamobea Histolytica
67
What organism is most likely to cause invasive pulmonary aspergillosis?
A. fumigatus
68
What are the risk factors for invasive aspergillosis?
Neutropenia
Solid organ or allogenic stem cell ttransplant
Corticosteroids
Leukaemia and other haemotological malignancies
Cytotoxic chemotherapy
Advanced HIV disease
Severe COPD
Critically ill patients on intensive care units
Chronic granulomatous disease
69
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
Cavity
70
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.
71
What are the features of tracheobronchial aspergillosis?
Involvement is characterised by the formation of fungal plaques and ulceration
72
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
73
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.)
74
What is treatment choice for invasive pulmonary aspergillosis?
Voriconazole
Second line agents include liposomal amphotericin, caspofungin or posaconazole.
75
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
76
What disease does chronic pulmonary aspergillosis closely mimic?
TB
77
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
78
What are radiological features of chronic or subacute pulmonary aspergillosis?
Thick walled - cavities (predominantly apical)
Pulmonary infiltrates
Pleural thickening and later fibrosis
79
What are the three different dsecriptive names of chronic pulmonary aspergillosis?
CNPA (chronic necrotising)
Cavitatory
Fibrosing
80
What are the features of malaria?
fever
rigors
aching bones
adbo pain
headache
dysuria
frequency
sore throat
cough
fatigue
myalgia
nausea
vomiting
Signs:
none, splenomegaly, hepatomegaly, mild jaundice, anaemia, tachycardia
81
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
82
What are the organisms that cause malaria?
Plasmodium falciparum
Plasmodium vivax
Plasmodium ovale
Plasmodium malariae
Plasmodium falciparum causes nearly all episodes of severe malaria. The other three types, of which Plasmodium vivax is the most common, cause 'benign' malaria
83
What are protective factors for malaria?
G6PD deficiency
HLA-B53
absence of Duffy antigens
Sickle cell anaemia
84
What are the features of severe malaria?
schizonts on a blood film
parasitaemia \> 2%
hypoglycaemia
acidosis
temperature \> 39 °C
severe anaemia
complications as below
85
What are the complications of malaria?
Complications
* cerebral malaria: seizures, coma
* acute renal failure: blackwater fever, secondary to intravascular haemolysis, mechanism unknown
* acute respiratory distress syndrome (ARDS)
* hypoglycaemia
* disseminated intravascular coagulation (DIC)
86
What might make you more likely to suffer from malaria?
Pregnancy
Previous splenectomy
87
What is the result of parasitisation of the maternal side of the placenta?
IUGR
Abortion
88
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)
89
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
OR
Quinine for 7 days plus doxycycline/clindamycin 7 days
OR
Malarone for 3 days
90
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
Antimalarial chemotherapy
Correction of fluid, electrolytes, acid base balance
IV artesunate
IV quinine + oral doxycyline (or clindamycine)
switch to oral treatments when patient is stable and can swallow
91
What is a side effect of quinine?
Dysrhythmias
92
What are the treatments for other forms of malaria?
treatment of other species of malaria
chloroquine
riamet
add primaquine to eradicate liver hypnozoites this is in P vivax and P ovale (check for G6PD def - haemolysis may develop)
93
Which cells do neutrophils target?
Bacterial and fungal infection
94
Which cells do monocytes target?
Fungal infections
95
Which type of cells do Eosinophils target?
Parasites
96
What type of cell do T cells target?
Fungal and viral ifnection PJP
97
What type of cells do B lymphocytes target?
Bacterial inefection
98
What is the presentation of sepsis?
a high temperature (fever) or low body temperature
chills and shivering
a fast heartbeat
fast breathing
In the very young and the very old you can get low temperature.
Potential for hyperglycaemia.
99
What is the presentation for septic shock?
feeling dizzy or faint
**a change in mental state – such as confusion or disorientation**
**diarrhoea**
nausea and vomiting
**slurred speech**
severe muscle pain
**severe breathlessness**
less urine production than normal – for example, not urinating for a day
cold, clammy and pale or mottled skin
**loss of consciousness**
100
What are the tests for sepsis?
Temperature
Breathing rate
Heart rate
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
Renal profile
Liver function tests
CSF analysis (meningitis)
101
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.
102
What is the sepsis 6?
Sepsis 6 (three treatments and three tests)
Treatment:
Giving antibiotics
Give IV fluids
Giving oxygen
Tests:
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)
103
How do you maintain MAP in sepsis?
Vasopressors such as norepinephrine
104
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
105
What are the clinical features of typhoid?
1st week:
fever, headache, abdo discomfort, constipation, dry cough, relative bradycardia, neutrophilia, confusion
2nd week:
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
106
What are the investigations for typhoid fever?
Culture blood
Urine
Stool culture
Bone marrow
107
What is the treatment for typhoid fever?
Oral azithromycin
IV ceftriaxone
Ciproflaxin
FLuids
108
What are the causative organisms for thyphoid fever?
Salmonella typhi and paratyphi
109
How is typhoid transmitted?
faecal-oral transmission via contaminated food or water, preventable by vaccination
110
Symptoms of schistomiasis
1st few hours:
swimmers itch (clears 24-48hrs)
after 24h:
invasive stage (cough, abdo discomfort, splenomegaly, eosinophilia)
after 15-20 days: Katayama fever (protsrate, fever, urticaria, lymphadenopathy, splenomegaly, diarrhoea, eosinophilia
6-8 weeks:
acute disease (eggs deposited in bowel (dysentry) or bladder (haematuria)
chronic disease
111
What are the investigations for schistosomiasis?
Ab tests, ova in stools and urine, rectal snip
112
What is the management of schistosomiasis?
praziquantel
prednisolone if severe
113
What are the complications of schistosomiasis?
squamous cell carcinoma (which is very rare except in tropical countries)
114
What animal spreads schistosomiasis?
Fresh water snail
115
Which highly infective skin condition is classicaly described as having a golden crust?
Impetigo
116
What organisms cause impetigo?
Staph aureus
Less commonly strep pyogenes
117
What organism is most likely to cause erysipelas?
Mostly due to strep pyogenes
118
What is the key difference between cellulitits and erysipelas?
Erysipelas has distinct elevated borders whereas cellulitis doesn't
119
What systemic symptoms might be apparent for cellulitits and erysipelas?
Associated fever
Associated lymphadenopathy and lymphangitis
120
What is the treatment for erysipelas and cellulitis?
Erysipelas:
## Footnote
combination of anti-staphylococcal and anti-streptococcal AB
in extensive disease, admission for IV AB and rest
Cellulitis = (penicillin and flucloxacillin)
121
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
122
What are the investigations?
bloods (high WCC, low sodium), CT
123
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
124
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
125
What are bacterial causes of meningitis?
Neisseria meningitidis (meningococcus)
Strep pneumoniae (pneumococcus)
In neonates E.Coli, group B strep (strep agalactiae is an example)
126
What are viral causes of meningitis?
Enteroviruses:
- Echoviruses
- Paraechoviruses
- Coxsackie A and B viruses
- Poliovirus (not seen in the UK)
Mumps, now very rare due to the MMR vaccine
HSV
127
What are less common causes of meningitis?
Haemophilus influenze type b
Listeria monocytogenes
Mycobacterium TB
varicella z
EBV
128
What type of organism is responsible for almost half of meningitis associated with ventriculo-atrial / peritoneal shunts?
Coagulase negative staph (eg staph epidermis)
129
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
SAH
Migraine
130
What is the classical presentation for bacterial meningitis?
Headache
Photophobia
Neck stiffness
Vomitting
Fever
Clouding of consciousness
Cranial nerve palsies may occur (6,7,8)
131
What rash is associated with meningococcal meningitis?
Vasculitis
Macular/maculo-papular, purpuric, pruritic or vesicular
All occur due to meningococci or other meningitides
132
What would papilloedema suggest when examining someone for meningitis?
Unusual in meningitis and should lead one to consider an intracranial space occupying lesion
133
What are the clinical signs you can elicit in meningism?
134
What are investigations for meningitis?
Blood culture
Lumbar puncture
(if papilloedema then you should request a head CT to rule out a space occupying lesion, LP is contraindicated if this is the case)
135
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)
Bacterial culture
Mycobacterial or fungal culture (if appropriate)
PCR for viruses (if appropriate)
PCR for bacteria (if appropriate)
136
WHat is CSF biochemistry for meningitis?
Glucose (check serum level at the same time)
Protein
137
What is FBC results in bacterial meningitis?
Neutrophil leucocytosis
Leucopenia (septicaemia with DIC, you would also see, low platelets, abnormal clotting and increased fibrin degradation products)
138
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
139
The daddy
Appearance
Cells
Predominant cell type
Glucose
Protein
For:
Normal
Bacterial meningitis
Viral meningitis
Tuberculosis meningitis
140
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.
141
What are possible antibiotic therapies in meningitis?
Benzyl penicillin
Ceftriaxone
142
What is the tumblr test?
Purpuric rash of meningococcal disease does not blanche under pressure
143
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
144
WHo should be notified after confimation of meningococcal meningitis?
Local consultant in health protection
They will coordinate the arrangements for prophylaxis
145
What is the most frequent causative organism of bacterial meningitis in adults?
Strep pneumoniae
146
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
147
What are the features of strep pneumoniae?
Gram positive
Diplococci
alpha haemolytic on blood agar
148
What can predispose to strep pneumoniae?
Pneumonia
SInusitis
Endocarditis
Head trauma
Alcoholism
Splenectomy
149
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
150
What is the treatment of S.pneumoniae meningitis?
High dose ceftriaxone
151
What are the complications of s.pneumoniae meningitis?
Loss of hearing
Cranial nerve deficits
Hemiparesis
Hydrocephalus
Seizures
152
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)
153
Which HSV type complicates a primary genital herpes infectino with viral meningitis?
Type 2
154
What is the presentation of viral meningitis?
Non-specific prodromal illness
Rapid onset headache
Photophobia
Low grade fever
Stiff neck
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.
155
What are the investigations for viral meningitis?
PCR of CSF
PCR of throat swabs and faecal samples
156
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.
157
When should the MMR vaccination be given?
12-13 months
3 years 4 months - 5 years
158
What is the most important cause of meningitis in patients with HIV infection?
cryptococcus neoformans
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.
159
Which type of stain allows the capsule to be visualised as a clear zone around the yeast cell?
India Ink
160
What are the investiations for cryptococcal meningitis?
Culture
161
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.
162
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).
163
How des neonatal meningitis differ from adult meningitis?
Symptoms and signs are not specific or not well localised
## Footnote
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.
164
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.
165
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.
166
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.
```
167
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)
168
What are the clinical features of HAV?
Fever
Malaise
Anorexia
Nausea
Vomitting
Upper abdominal pain
Jaundice developing 3-10 days later, during which time the urine may be dark becasue of the presence of conjugated bilirubin.
169
What is the route of infection for hep A?
Faecal - oral
| (potential for parenteral)
170
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
171
What is managment of HAV?
Supportive
172
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
173
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
- PWID
- Patients with hep C get the vaccination becuse the illness may be more serious
174
How do liver enzymes react to hepatitis?
Incerase in ALT and AST
175
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
176
What is the presentation of hepatitis B infection?
Anorexia
Lethargy
Nausea
Fever
Abdominal discomfort
Arthralgia
Urticarial skin lesions often precede the development of darkly coloured urine and jaundice
177
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.
178
What are the hepatitis b markers for viral replication?
Serum HBeAg
HBV DNA
179
What is the major identifier for acute and chronic hepatitis B infection?
HBsAg
180
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
181
What are the mechanisms of transfer of HBV?
Vertical
Horizontal (sexual, parenteral including needlestick, inapparent parenteral)
Childhood horizontal transmission probably happens as a result of inapparent exposure to blood or body fluids.
182
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
183
When is a needle stick more likely to pass on HBV?
If it is HBeAg positive
184
What antibody is the key antibody during acute infective period of hepatitis B?
Anti-HBcore IgM
There is seroconversion to anti-HBs severeal weeks after the disappearance of HBsAg
185
What is meant by the window period of HBV?
The only serological marker present is anti-HBC
186
What is the definition of chronic HBV infection?
Persistence of HBsAg in the serum for more than 6 months
187
What are long-term sequale of chronic hep B infection?
Chronic liver disease
Membranous glomerulonephritis
Polyarteritis nodosa
188
What are potential complications for chronic HBV liver infection?
Cirrhosis
Hepatoma
189
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
Raised ALT
Significant liver inflammation or fibrosis
190
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
191
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
192
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
193
What are the most important means of preventing HBV infection?
Immunisation
Infection control procedures
Screening of blood donors and transplant donors
194
What is the main component of the HBV vaccination?
HBsAg produced by recombinant DNA technology
195
How is passive immunity for hepatitis provided?
Hepatitis B specific immunoglobulin
196
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
197
How does acute HCV present?
Usually subclinical or mild
Symptoms in 20%
Malaise
Anorexia
Fatigue
Severe hepatitis and jaundice can occur
198
Outcomes of acute hep C infection
199
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).
Mother-to-child.
Household contacts sharing razors or toothbrushes.
Medical or dental treatment if inadequately decontaminated equipment used (e.g. some developing countries).
200
How is diagnosis achieved of HCV?
Antibody testing (IgG only athough this has v poor sensitivity)
Detection of HCV antigen
HCV RNA
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
201
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
202
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.
203
What is hepatitis D always seen in conjunction with?
Hepatitis B virus
204
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.
205
What is the transmission mode for hepatits D?
Parenteral
206
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.
207
What is treatment for hepatitis as a result of HBV infection?
Pegylated alpha interferon
## Footnote
Liver transplantation may offer some hope
in fulminant hepatitis. Prevention of HBV infection also prevents HDV infection. Severe chronic hepatitis commonly follows HDV superinfection.
208
What is the presentation of Hep E?
Like Hep A but carries a significant mortality in pregnant women (up to 20%)
209
What is the route of infection in Hep E?
Faecal oral route
210
What type of virus is HepE?
Henevirus
Small RNA virus
211
What are the genotypes of hepatitis E assocaited with developing countries?
1 and 2
212
What are the global genotypes of hep E?
3 and 4
## Footnote
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.
213
What are serological tests for HepE?
IgG and IgM HEV-RNA
214
What is the treatment for HepE?
No licensed treatment
Ribavarin monotherapy in the immunocompromised
215
What are ways to reduce transmission?
Good hygiene
Good sanitation
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.
216
The Daddy
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