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Flashcards in Infection Summary Deck (217):
1

Gastroenteritis Presentation

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

Gastroenteritis Investigation / diagnosis

stool MC&S, urea and electrolytes

3

Gastroenteritis Management

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

Complications of campylobacter infection

Guillain-Barre

Reactive arthritis

5

What can predispose you to gastroenteritis?

HIV

Omeprazole

6

Presentation of CDIFF

mild diarrhoea to severe colitis

 

diarrhoea, fever, abdominal pain

7

Investigations for CDIFF

stools MC&S, FBC (increased WCC)

8

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.

9

What are the complications of C.Diff?

pseudomembranous colitis, toxic megacolon, sepsis

10

What are the toxins that c.diff produces?

A (enterotoxin) and B (cytotoxin)

11

Presentation of infectious diarrhoea

fever, diarrhoea (may be bloody), nausea, dehydration, abdominal pain, bloody diarrhoea is more common with Campylobacter, Shigella

12

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 

13

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

14

What viruses can cause infectious diarrhoea?

adenovirus, rotavirus in children under 5 years

15

What are the complications of infectous diarrhoea?

renal failure, septic shock; E. coli is associated with the haemolytic-uraemic syndrome

16

What are the symptoms / presentation for giardia lamblia?

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

What is the investagation for giardia lamblia?

Cysts seen on stool microscopy

18

What is the treatment for giardia lamblia?

Metronidazole

19

How is giardia lamblia spread?

Contaminated water

20

Whet type of organism is giardia lamblia?

Parasite

21

What bacterium causes the majority of cases of travellers diarrhoea in developing countries?

Enterotoxigenic e.coli

22

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. 

23

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. 

24

What is the complication associated with Ecoli o157?

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

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:

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: 

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

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

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 

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

217