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Infection > Infection Summary > Flashcards

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)

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2
Q

Gastroenteritis Investigation / diagnosis

A

stool MC&S, urea and electrolytes

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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

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4
Q

Complications of campylobacter infection

A

Guillain-Barre

Reactive arthritis

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5
Q

What can predispose you to gastroenteritis?

A

HIV

Omeprazole

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6
Q

Presentation of CDIFF

A

mild diarrhoea to severe colitis

diarrhoea, fever, abdominal pain

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7
Q

Investigations for CDIFF

A

stools MC&S, FBC (increased WCC)

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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)

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9
Q

What are the complications of C.Diff?

A

pseudomembranous colitis, toxic megacolon, sepsis

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10
Q

What are the toxins that c.diff produces?

A

A (enterotoxin) and B (cytotoxin)

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11
Q

Presentation of infectious diarrhoea

A

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

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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

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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

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14
Q

What viruses can cause infectious diarrhoea?

A

adenovirus, rotavirus in children under 5 years

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15
Q

What are the complications of infectous diarrhoea?

A

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

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16
Q

What are the symptoms / presentation for giardia lamblia?

A

diarrhoea, malabsorption, failure to thrive

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17
Q

What is the investagation for giardia lamblia?

A

Cysts seen on stool microscopy

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18
Q

What is the treatment for giardia lamblia?

A

Metronidazole

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19
Q

How is giardia lamblia spread?

A

Contaminated water

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20
Q

Whet type of organism is giardia lamblia?

A

Parasite

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21
Q

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

A

Enterotoxigenic e.coli

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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.

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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.

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24
Q

What is the complication associated with Ecoli o157?

A

HUS

Haemolytic Uraemic syndrome

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25
Q

Who is affected by HUS?

A

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

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26
Q

What is the treatment for HUS?

A

Dialysis if necessary and may be averted by plasma exchange

Antibiotics should be avoided since they can stimulate toxin release.

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27
Q

What cells does the HIV virus attack?

A

Attacks the CD4 cells (T helper cells, macrophages and dendritic cells)

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28
Q

What are the features of the primary infection of HIV?

A

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.)

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29
Q

What is the progression of HIV after the primary infection?

A

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.

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30
Q

What is the differential diagnosis for primary HIV?

A

EBV

Primary cytomegalovirus infection

Rubella

Primary toxoplasmosis

Secondary syphilis

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31
Q

When does HIV become AIDS?

A

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

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32
Q

CDC category A for HIV

A

Primary HIV infection

Asymptomatic

Persistent generalised lymphadenopathy

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33
Q

CDC category B for HIV

A

Candidiasis (oropharyngeal)

Fever / diarrhoea lasting for over one month

Oral hairy leucoplakia

Cervial dysplasia / carcinoma in situ

Idiopathic thrombocytopenic purpura

Peripheral neurupathy

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34
Q

CDC category C for HIV infection

A

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

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35
Q

How is viral load determined?

A

Quantitive PCR of HIV - RNA

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36
Q

How is HIV diagnosed?

A

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).

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37
Q

What are the aims of ART?

A

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

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38
Q

What are the classes of antiretroviral drugs?

A

Nucleoside reverse transcriptase inhibitors (NRTIs)

Non-nucleoside reverse transcriptase inhibitors (NNRIS)

Protease inhibitors

Integrase inhibitors

Chemokine receptor inhibitor

39
Q

Give examples for each type of ART

A

NRTI - abacavir, zidovudine

NNRTI - Efavirenz

PI - Atazanavir

Integrase inhibitors = Raltegravir

Chemokine receptor inhibitor = maraviroc

40
Q

What is the standard antiretroviral regimen?

A

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
Q

What must PI’s be co-prescribed with?

A

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
Q

When should ART therapy begin?

A

ART therapy should begin in adults when CD4 count falls below 350 cells / mm or clinical stage 3/4

43
Q

Lymes Disease Presentation:

A

early: erythema chronicum migrans + systemic features (fever, arthralgia)

CVS: heart block, myocarditis

neuro: cranial nerve palsies, meningitis

44
Q

What causes Lymes disease

A

Spirochaete Borrelia Burgdorferi

45
Q

What is the investigation for Lymes disease?

A

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
Q

What are later complications of Lyme Disease?

A

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
Q

What is the management of asymptomatic tick bites?

A

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
Q

What is the management of Lymes disease?

A

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
Q

What type of virus is Rabies?

A

RNA rhabdovirus (specifically a lyssavirus)

50
Q

What are the features of Rabies?

A

prodrome: headache, fever, agitation
hydrophobia: water-provoking muscle spasms

hypersalivation

Negri bodies: cytoplasmic inclusion bodies found in infected neurons

51
Q

What is the treatment for Rabies?

A

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
Q

What is the diagnostic test for rabies?

A

PCR to check for lyssavirus in the CSF

53
Q

What is rat fever?

A

Leptospirosis

54
Q

What are the clinical features of Influenza

A

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
Q

What is the treatment for influenza?

A

influenza A or B, both for treatment or prophylaxis, start within 48 hours of onset of symptoms/contact: oseltamivir, zanamivir

56
Q

What are the complications of influenza?

A

common:

RESP: acute bronchitis, secondary bacterial pneumonia

less common:

RESP: primary viral pneumonia,

CV: myocarditis/pericarditis,

CNS: transverse myelitis/ Guillain Barre, myositis & myoglobinuria

57
Q

What is tha pathogen associated with bronchiolitis?

A

RSV (respiratory syncytial virus) (75-80% of cases)

Mycoplasma and adenoviruses are also causes

58
Q

Who often gets bronchioloitis?

A

Babies less than 1 years old = peak incidence is 3-6months

Maternal IgG protects gainst RSV

More common in winter

59
Q

When is bronchiolitis more serious?

A

When there is bronchopulmonary dysplasia in premature babies

CF

Congenital heart disease

60
Q

What are the features of bronchiolitis?

A

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
Q

When do NICE recommend immediate referral whenm there is a case of bronchiolitis?

A

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
Q

When should clinicians refer to th hospital if there is a case of bronchiolitis according to NICE?

A

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
Q

What are the investigations for bronchiolitis?

A

immunofluorescence of nasopharyngeal secretions may show RSV

CXR: may show hyperinflation/patchy infiltrative change

64
Q

What is management for bronchiolitis?

A

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
Q

What are the complications of bronchiolitis?

A

chronic wheeze, bronchiolitis obliterans (adenovirus)

66
Q

What organism causes amoebic dysentry?

A

Entamobea Histolytica

67
Q

What organism is most likely to cause invasive pulmonary aspergillosis?

A

A. fumigatus

68
Q

What are the risk factors for invasive aspergillosis?

A

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
Q

What are the findings on CT that would indicate invasive pulmonary aspergillosis?

A

Dense, well circumscribed lesions with or without a halo sign

Air crescent sign

Cavity

70
Q

When is an immunocompromised patient heavily suspected of having invasive pulmonary aspergillosis?

A

If they develop fever, new resp symptoms, (particularly pleural pain or haemoptysis) or a pleural rub.

71
Q

What are the features of tracheobronchial aspergillosis?

A

Involvement is characterised by the formation of fungal plaques and ulceration

72
Q

What are mycological ways to diagnose aspergillosis?

A

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
Q

What blood test can be done to look for invasive pulmonary aspergillosis?

A

Detection of aspergillus cell wall components (galactomannan and B-1,2-glucan) in blood or BAL fluid and aspergillus DNA by PCR.)

74
Q

What is treatment choice for invasive pulmonary aspergillosis?

A

Voriconazole

Second line agents include liposomal amphotericin, caspofungin or posaconazole.

75
Q

What is sub-acute or chronic pulmonary aspergillosis?

A

Non-invasive complication of chronic lung disease such as COPD, TB, opportunistic mycobacterial disease or fibrotic lung disease

76
Q

What disease does chronic pulmonary aspergillosis closely mimic?

A

TB

77
Q

What are the features of chronic pulmonary aspergillosis?

A

Cough (with or without haemoptysis), weight loss, anorexia and fatigue over months or years

Associated fever, night sweats and elevated inflammatory markers

78
Q

What are radiological features of chronic or subacute pulmonary aspergillosis?

A

Thick walled - cavities (predominantly apical)

Pulmonary infiltrates

Pleural thickening and later fibrosis

79
Q

What are the three different dsecriptive names of chronic pulmonary aspergillosis?

A

CNPA (chronic necrotising)

Cavitatory

Fibrosing

80
Q

What are the features of malaria?

A

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
Q

What are the investigations for malaria?

A

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
Q

What are the organisms that cause malaria?

A

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
Q

What are protective factors for malaria?

A

G6PD deficiency

HLA-B53

absence of Duffy antigens

Sickle cell anaemia

84
Q

What are the features of severe malaria?

A

schizonts on a blood film

parasitaemia > 2%

hypoglycaemia

acidosis

temperature > 39 °C

severe anaemia

complications as below

85
Q

What are the complications of malaria?

A

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
Q

What might make you more likely to suffer from malaria?

A

Pregnancy

Previous splenectomy

87
Q

What is the result of parasitisation of the maternal side of the placenta?

A

IUGR

Abortion

88
Q

What are preventative measures for malaria?

A

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
Q

What is the management of malaria?

A

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
Q

What is the treatment for severe or complicated malaria?

A

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
Q

What is a side effect of quinine?

A

Dysrhythmias

92
Q

What are the treatments for other forms of malaria?

A

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
Q
A

Infection (17 decks)

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