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BCS Lectures > Mercy Juma > Flashcards

Mercy Juma Flashcards

1
Q

Categories of PUO

A

A.Classic PUO – an update of the original PUO definition
PUO is a fever >38o C for over 3 weeks despite being investigated on 2 visits at the outpatient’s or for 3 days in hospital

B. Nosocomial PUO – Fever >38o C for 3 days not present or incubating on admission

C. Immunodeficient PUO –(caused by illness eg malignancy or of treatment such as steroids – neutropenia or defective cell mediated immunity)
Fever >38oC for >3 days for outpatients or >3 days with neg blood cultures after 48 hrs

D. HIV patients – Fever >38oC for >3 wks for outpatients or >3days for inpatients

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2
Q

What are the 5 main catergories of causes of classic PUO

A
  1. Infection 30-50% ( abscesses, endocarditis, tuberculosis, complic UTI)
  2. Neoplasm 20-25% (lymphoma)
  3. Connective tissue disorder / vasculitis 15-20% (juvenile rheumatoid arthritis Still’s, other rheumatoid arthritis, SLE, temporal arteritis in elderly)
  4. Miscellaneous disorders 10-20% (FMF, pulmonary emboli, drug induced, Behcet’s syndrome)
  5. Undiagnosed 10-20%
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3
Q

Where is meliodosis found?

A

SE asia

Melioidosis is an infectious disease caused by a Gram-negative bacterium, Burkholderia pseudomallei, found in soil and water

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4
Q

Which infections are found in the mediterranean

A

Leishmaniasis, Ricketsial illness, brucellosis, Q fever

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5
Q

Which infection is commonly found in S America

A

dimorphic fungi

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6
Q

Which type of inflammtory disease is commonly seen in children <5 k. How does this compare to that in older children

A

kawasaki disease

Juvenile rheumatoid arthritis (Still’s disease) leading cause in older children

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7
Q

Cause of PUO in returning travellers Depending on the incubation period

A

see slide 10 on puo lecture

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8
Q

In which diseases are clubbing most commonly seen

A
  1. Chronic respiratory

2. Heart disease

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9
Q

What disease has splinter haemorrhages in nails

A

Endocarditis

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10
Q

What are subcutaneous nodules characteristic of

A

rheumatic fever

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11
Q

markers of inflammation

A

CRP
ESR
WBC
Ferritin

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12
Q

How many blood cultures would you take in first 24 hours

A

3

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13
Q

What does mycoplasma cause

A

Pneumonia - can have systemic manifestations

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14
Q

How to diagnose leishmaniasis

A

BM Bx

a tropical and subtropical disease caused by leishmania and transmitted by the bite of sandflies. It affects either the skin or the internal organs.

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15
Q

How to differentiate falciparum on a film from all of the other plasmodiums?

A

Two dots on the ring on the film

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16
Q

Use of MRI in PUO

A

very useful for CNS and spleen and lymph nodes

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17
Q

Use of radiolabelled leucoyte scans?

A

leucoytes accumulate in sites of accumulation so radiolabelled leucocytes will show us where there is inflammation

abscesses or malignancy

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18
Q

Use of PET CT

A

81% sens and 87% specificity (mainly for malignancy)

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19
Q

25yr F born Pakistan
UK 1 year
Lives alone
Travelled to Pakistan for 2 weeks and returned one week ago.

PC:
abdominal pains
fevers for over 1 month
Weight loss

HPC:
Eating well but wt down
Sweating at night; has to change the sheets
Abdo pain all the time, all over colicy, possibly worse in the RIF
Been to GP for

A

Think of lymphoma (due to night sweats)

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20
Q

What is the cause of typhoid

A

Salmonella typhi

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21
Q

What abdo features does salmonella typhi cause?

A

Constipation whereas normally salmonella causes diarhhoea

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22
Q

What abdo features does salmonella typhi cause?

A

Constipation and also pea-like diarrhoea whereas salmonella enteriditis causes inflammatory diarrhoea

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23
Q

Frequency of btypes of malaaria

A
  1. Falciparum - 70%
  2. Vivax - 43%
  3. Ovale
  4. Malariae - 7%
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24
Q

What are the complications of malaria in pregnancy

A

25% severe maternal anaemia,
10-20% low birth-weight,
5-10% neonatal and infant death

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25
Q

Indirect consequences of malaria

A

Impaired intellectual development, developmental abnormalities, irregular school attendance, loss of productivity
Retardation of economic development of affected countries

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26
Q

Why do male mosquitos not transmit malaria

A

Males feed on plant juices not blood

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27
Q

Phases of development in man

A

Two phases of development

  1. Inside the liver (tissue phase)
    Pre-erythrocytic schizogony – no clinical symptoms, no pathological damage
    Exo-erythrocytic schizogony – cause of relapse
  2. Inside the RBCs (erythrocytic phase)
    Erythrocytic schizogony – cause of malarial paroxsyms
    Gametogony – infects mosquito
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28
Q

Which morphological forms of the parasite are found in the liver

A

Sporozoites
Pre erythrocytic schizonts
Merozoites – infect RBCs

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29
Q

Which morphological forms are found in the RBCs

A
  1. Trophozoites – ring form
  2. Schizonts
  3. Merozoites – released by the rupture of schizonts – infect other RBCs
  4. Gametocytes – micro (male) and macro (female) gametocytes
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30
Q

Other modes of transmission of malaria

A

Sporozoite- induced- malaria : injection of an emulsion of salivary glands of mosquito containing sporozoites

Trophozoite- induced- malaria : injection of blood from a malarial patient containing the asexual forms of erythrocytic schizogony e.g.

  1. Transfusion malaria – when persons with latent infection are used as donors
  2. Congenital malaria – transmission through some placental defects (a healthy placenta acts as a physiological barrier)
  3. Drug addicts – by using same syringe
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31
Q

Clinical course of Falciparum

A
  1. Asymptomatic parasitaemia (“clinical immunity”)
  2. Acute uncomplicated malaria
  3. Severe malaria
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32
Q

When is asymptomatc falciparum seen

A

Seen in older children and adults, with acquired natural immunity-living in endemic areas
There are parasites in blood but no symptoms – reservoir

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33
Q

Disease LOB MALARIA

A

SEE NOTES

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34
Q

Manifetations of severe and complicated malaria

A
  1. Cerebral malaria
  2. Severe malarial anemia
  3. Hypoglycemia
  4. Metabolic acidosis
  5. Acute renal failure
  6. Pulmonary edema
  7. Circulatory collapse
  8. Blackwater fever
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35
Q

Difference in clinical features of severe malaria in adults and children

A

See slide 20 on malaria lecture

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36
Q

What is pernicious malaria

A

Def: refers to a series of phenomena occurring during infection with P. falciparum which, if not effectively treated, threatens the life of the patient within 1 to 3 days

In children & non immune adults, can cause coma & death – Cerebral malaria.

Occurs as a result of capillary blockage.

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37
Q

How does cerebral malaria manifest

A

Falciparum associated

High fever, headache, vomiting, convulsions, delirium, respiratory failure

Hyperpyrexia: T>400C, convulsion, delirium

Children: deep coma, seizures (more common in children), hypoglycaemia

Ataxia, monoparesis, cortical blindness, aphasia/dysarthria, hearing impairment, cortical defects

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38
Q

What are the features of malaria acute renal failure and black water fever

A

Blackwater fever

Reduced perfusion (obstruction)

Acute Tubular Necrosis

Occurs in previously infected subjects

Due to severe hemolysis

Can also occur in non immune adults with severe falciparum malaria, and also as a complication of quinine therapy.

A rare but acute condition characterised by sudden & massive hemolysis of parasitised & non parasitised RBCs followed by fever and haemoglobinuria.
Often fatal due to renal failure

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39
Q

How to treat malarial ARF

A
  1. Dialysis

2. continue quinine

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40
Q

What are the clinical features of black water fever

A

Difficult to find the parasites in the blood following a hemolytic attack.
Urine appears dark red to brown black due to the presence of free Hb.

Clinical features – fever, rigors, aching pains in the loin, icterus, bilious vomiting, circulatory collapse, haemoglobinuria & acute renal failure

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41
Q

Treatment of black water fever

A
  1. Chloroquine,
  2. blood transfusion,
  3. peritoneal dialysis in ARF.
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42
Q

What is the cause of hypoglycemia in malaria

A

Parasites use up lots of glucose

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43
Q

metabolic consequences of malaria

A
  1. Hypoglycemia
  2. Lactic acidosis
  3. Thiamine deficiency
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44
Q

Two types of recurrences of malaria

A
  1. Relapse

2. Recrudescence

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45
Q

Which type of malaria does recrudescence occur in ?

A
  1. Falciparum

2. malariae

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46
Q

Cause of recrudescence reccurence

A

due to persistence of blood infection (some erythrocytic forms evade host immunity) even after clinical illness has subsided.

The numbers may increase later, leading to reappearance of clinical symptoms

Occur mostly up to one year or so but in P. malariae, it can occur even after decades

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47
Q

Which type of parasite does relapse recurrence occur in ?

A

Hypnozoites

  • Activated from time to time to initiate pre- erythrocytic schizogony - Exoerythrocytic schizogony
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48
Q

Malaria protective factors

A
  • P. vivax
    Uses RBC duffy receptor not present in sickle cell anemia therefore these patients are protected from P vivax
  • Thalassemia and G6PD deficiency
    Make parasite-exposed RBCs more susceptible to apoptosis from oxidative stress therefore malaria is unable to undergo its life cycle in these individuals
  • Hence a natural selection advantage for the above diseases
  • HLAB53 alleles enable T cells to kill parasite-infected hepatocytes in non-Europeans.
    Newborn infants and B thalassemia
    High levels of HbF
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49
Q

Elevated CKs in malaria

A

TNFa (Plasma TNFα higher in fatal cases)

IL-1

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50
Q

How long does falciparum last in absence of treatment

A

1 year but reinfection possible by other strains

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51
Q

How long could hypnozoites last

A

Can have periodic relapses up to 5 years

Malariae may last up to 40 years

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52
Q

Diagnosis of malaria?

A

Thick: located parasites sitting in RBCs
- More sensitive as they allow a greater amount of blood the be examined

Thin: directly identifies the plasmodium species
- Species identification and parasitemia (% of parasitised RBCs)
>2% parasitemia is a sign of more severe disease although severe disease can occur at any %
- Patients with schizonts at higher risk of sudden deterioration - 3rd stage of the erythrocytic phase (replicative phase
Most common form seen is the trophozoite (after merozoite has differentiated in the erythrocytic phase)

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53
Q

Other diagnostic methods for malaria

A
  1. Antigen detection
    Immunochromatographic, dipstick or
    cassette format
    Fast, 2-15 mins
  2. Serology
    Detection of Abs (IFA or ELISA)
    Past infection related
  3. PCR
    Detection of NAs
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54
Q

Antimalaria Tx for causal prophylaxis

A
  1. Pyrimethamine

2. Primaquine

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55
Q

Antimalaria Tx for blood schizonticides (terminate atacks)

A
  1. CHoloroquine and artesmisinine
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56
Q

WHO recommendations for malaria treatment

A

WHO recommendations

Artemisinin-based combination therapies (ACTs) for the treatment of uncomplicated malaria caused by the P. falciparum parasite.
Atovaquone-proguanil is a combination of two drugs, atovaquone and proguanil, in a single tablet – for patients returning from endemic areas.
Do not use artemisinin monoterapy – resistance.

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57
Q

Treatment for tissue schizonticides (prevent relapse)

A
  1. Primaquine

2. Tafenooquine

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58
Q

Treatment for gametocytocides (block transmission)

A
  1. Primaquine

2. Tafenoquine

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59
Q

Treatment for sporozoitocides (ablate transmission of mosquito)

A
  1. Primaquine and progaunil
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60
Q

Which type of malaria is common in monkeys?

A

Knowlesi

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61
Q

Risk factors for malaria

A

Travel to endemic areas

Lack of chemoprophylaxis

Low host immunity

Pregnancy

<5 years old

Immunocompromised (underlying HIV)

Old age

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62
Q

Pathophysiology of malaria

A

See disease LOB in PBL notes

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63
Q

Incubation time of falciparum

A

7-10 days

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64
Q

Incubation time of vivax

A

10-17 days

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65
Q

Incubation time of malariae

A

18-40 days

- may ‘lie low’ in the blood to recrudesce after 1–52yrs.

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66
Q

What causes the paroxysms of fever in malaria

A

Release of TNF alpha and inflammatory cytokines cause fevers that correspond to the rupture of the RBC (waves of reproductive cycles)

These paroxysms of fever are specific to each type of plasmodium

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67
Q

Three stages of malaria fever?

A
  1. Cold stage Shivering (1h): “I feel so cold.”
  2. Hot stage (2–6h): T ≈41°C, flushed, dry skin; nausea/vomiting; headache.
  3. Sweats (~3h) as T° falls. 95
68
Q

Time between fever paroxysms in malariae

A

72 hours - quartian fever

69
Q

Time between fever paroxysms in vivax and ovale

A

48 hours - tertian

70
Q

Time between fever paroxysms in knowlesi

71
Q

Time between fever paroxysms in falciparum

A

Variable 24-48 hours - malignant tertian fever

72
Q

How does falciparum cause complicated malaria

A

Falciparum coats RBCs with a sticky protein which looks like knobs or little bumps on the RBC

Causes RBC to clump and clog vessels: cytoadherence

Cells cannot flow into spleen

Causes end organ damage via ischemia
Resulting in organ failure

73
Q

Organs affected by complicated malaria

A

Brain affected: cerebral malaria
Altered mental status, seizure and coma

Liver affected: bilious malaria
D&V
Jaundice
Liver failure

Lungs, kidneys and spleen commonly affected
Created sepsis like clinical picture that can result in death

74
Q

Signs and symptoms of malaria

A

No rash or lymphadenopathy

Presence of risk factors

Paroxysmal fever

Headache

Weakness

Myalgia

Anorexia

Diarrhoea

75
Q

What are the five grim signs of malaria

A
  1. Consciousness/coma (cerebral malaria p397)
  2. Convulsions
  3. Co-existing chronic illness
  4. Acidosis (eg esp bad if HCO3– <15 mmol/L)
  5. Renal failure (eg from acute tubular necrosis).
76
Q

Investigations of malaria - principles of blood smears

A

Thick: locates parasites sitting in RBCs
More sensitive as they allow a greater amount of blood the be examined

Thin: directly identifies the plasmodium species

  • Species identification and parasitemia (% of parasitised RBCs)
  • > 2% parasitemia is a sign of more severe disease although severe disease can occur at any %
77
Q

Presence of which type of reproductive phase of the plasmodium increase the risk of sudden deterioration?

78
Q

What is the most common form of plasmodium seen on film

A

trophozoite

79
Q

Which form of plasmodium can persist int he blood after treatment has ended

A

Gametocyte

80
Q

Usefulness of rapid diagnosis malaria test?

A
  • Detect presence of malaria antigen or enzyme
  • Poor detection of species that aren’t falciparum
  • Rapid diagnosis in health resource limited areas where microscopy is not available
  • Unable to distinguish between active and recently cured infection
81
Q

What would FBC show in malaria?

A
  • Thrombocytopenia in falciparum

Despite this, bleeding complications are rare

  • Anemia

Normochromic normocytic

More common in children due to a combo of RBC destruction, AI hemolysis and disturbed marrow fx

82
Q

Other significant biochemical abnormalities in malaria

A
  1. Elevated lactate dehydrogenase (due to cell lysis)

2. Hypoglycemia since malaria consume lots of glucose

83
Q

Treatment principles for malaria

A
  1. If patient has taken prophylaxis do not use the same drug for treatment
  2. If plasmodium species is unknown treat as falciparum
  3. Nearly all falciparum is resistant to chloroquine and Fansidar (pyrimethamine and sulfadoxine
  4. Chloroquine if 1st choice for benign malarias
84
Q

Treatment for uncomplicated malaria (vivax, ovalae and malariae)

A
  1. Chloroquine
  2. If resistant to chloroquine try malarone, quinine or riamet
  3. Primaquine in vivax given after chloroquine to treat liver stage and prevent relapse
  4. The above are contraindicated in pregnancy
85
Q

Treatment for Uncomplicated falciparum malaria (or if species uncertain)

A
  1. Combination therapy is required since multidrug resistance exists
  2. Choose combo therapy that contains artemisinin derivative
  3. Artemisinins are ok in children and pregnancy from 13 weeks but use quinine and clindamycin in 1st trimester
86
Q

Prophylaxis for travellers

A
  1. Mosquito nets
  2. Proguanil and chloroquine
    - If chloroquine resistant area use mefloquine from 18 days before until 4 weeks after trip

Or

Doxycycline from 1 day before tip until 4 weeks after

Or

Atovaquone and proguanil (malarone) from 1 day before travel to 7 days after

87
Q

Structure of HIV

A
  1. Envelope
    - Lipid bilayer (host cell)
    - Surface glycoprotein
    120 (gp120)
    - Transmembrane gp41
  2. Matrix
    - matrix protein
    beneath envelope
  3. Core
    - Viral capsid – p24
    - Viral nucleocapsid – p9
    - Integrase
    - Genome : Single stranded RNA - +ve
    polarity - Two copies

Protease is outside of the capsid

88
Q

Non structural proteins of HIV

A

Protease

Integrase

Reverse transcriptase

89
Q

Regulatory proteins of HIV

A

Tat, Rev, Vif, Vpr, Nef, Vpu,

90
Q

Mode of HIV entry into the cell

A
  • HIV gains entrance to the CD4 cell by:
    Binding to CD4 receptor via its gp120 envelope protein
  • Binding co receptor (CCR5, CXCR4) via its gp120 envelope protein

CXCR4 on:
T cells

CCR5 on:
Monocytes
Macrophages
Dendritic cells 
T cells
91
Q

Other modes of entry of HIV into the cell

A

The gp120 - CD4 interaction not the only way of virus entry

  1. gp120 + antibodies via Fc receptors
  2. gp120 + antibodies with complement domain + complement receptors
92
Q

5 ‘H’s of high risk people for HIV

A

Homosexual men

Haemophiliacs

Haitians

Heroin users

(Healthcare workers)

93
Q

Which species can HIV be found in?

A

Human

Primates

Cats

94
Q

What are the four groups of HIV - 1

95
Q

Difference between HIV -1 and HIV -2

A

HIV-1 and HIV-2 are:

  • Transmitted through the same routes
  • Associated with similar opportunistic infections

HIV-1 is more common worldwide

HIV-2 is found in West Africa, Mozambique, and
Angola

HIV-2 is less easily transmitted

HIV-2 is less pathogenic

MTCT is relatively rare with HIV-2

96
Q

Natural history of HIV

A

See graph in PBL notes

97
Q

What occurs in the first 12 weeks (Acute phase)

A

In the acute phase a.k.a seroconversion (primary infection) the numbe
r of t cells drops rapidly while the viral load rapidly increases

This manifests as flu like symptoms and persistent generalised lymphadenopathy in the first 12 weeks

PGL defined as >1 cm nodes in >2 extrainguinal sites persisting 3 months or longer

98
Q

What occurs after the first 12 weeks of HIV infection (chronic)

A

After 12 weeks, you enter the counterattack phase where T cells mount a response against the virus

Reduction in viral load and increase in T cells

However, as chronicity progresses, HIV eventually overtakes the T cell response

About 1-2 billion T cells die per day

Usually remain >500 cells/mm3

Can fight off most infection but some infections like TB can become more severe

99
Q

What pathologies occur when T cell levels are between 200-500 cells/mm3

A
  • Swollen lymph nodes
  • Hairy leukoplakia
    White patch on tongue caused by EBV
  • Oral candidiasis
100
Q

What occurs when T cell levels <200?

A

When T cells <200 T cells/mm3 patients are classified as severely immunocompromised and are said to have AIDS which manifests as the “AIDS related complex (ARC)”:

  1. Persistent fever
  2. Fatigue
  3. Night sweats
  4. Weight loss
  5. Diarrhoea
101
Q

What are the ‘AIDS defining illnesses’

A
  1. Recurrent bacterial pneumonia
  2. Pneumocystis pneumonia
  3. Fungal infections
  4. Candidiasis of esophagus
  5. Tumours
  6. Kaposi sarcoma
  7. Skin lesions
  8. Primary lymphoma of the brain
102
Q

What is AIDs diagnosis commonly accompanied by?

A
  1. CD4 count <200
  2. Mycobacterium Avium Intracellulare complex
  3. CMV retinitis
103
Q

Which signs correlate most with HIV progression

A
  1. Persistent generalised lymphadenopathy
  2. Chronic fever
  3. Cough >1 month
  4. Chronic diarrhoea
  5. Oral thrush
  6. Weight reduction by 10% in one month
  7. TB
  8. Zoster
104
Q

Pathogenesis of HIV

A
  1. Infected cells undergo apoptosis
  2. APCs present viral peptides to Th cells – cytokine production
  3. Activated B cells produce antibodies – block virus attachment to receptor
  4. Specific CD8+ T cells – kill infected cells
  5. NK cells engage in ADCC:
    - Kill infected cells coated with Ab
    - Kill uninfected cells that take up gp120+Ab
  6. Cytokine production:
    - Protective role, but stimulate replication of HIV in mΦ
105
Q

What is HIV progression measured by ?

A
  1. CD4 count

2. Viral load

106
Q

Which organs can HIV directly affect

A
  1. Brain (HIV dementia)
  2. Gut (wasting)
  3. Heart (cardiomyopathy)
107
Q

Chronological presentation of common AIDS related conditions

A

From early to late after onset of HIV infection:

  1. Thrush
  2. Oral hairy leukoplakia
  3. TB
  4. Pneumocytis carinii (jiroveci)pneumonia
  5. Histoplasmosis
  6. Coccidiomycosis
  7. Cryptococcosis
  8. Toxoplasmosis
  9. Atypical HSV disease
  10. Cryptosporidioisis
  11. CMV disase
  12. Mycobacterium avium complex disease

Also

  • Kapsis
  • CMV ritinitis
  • Oesophageal candiadsis
108
Q

Treatment of pneumocystisis jiroveci

A

Causes pneumocystis pneumonia

Treatment: co-trimoxazole (combination antibiotic) 14-21 days
Or… pentamidine isetionate (antifungal) 14-21 days

109
Q

Treatment for candidiasis

A

Local; nystatin (antifungal)

Systemic: Fluconazole (antifungal)

110
Q

Treatment for Kaposis sarcoma

A
  1. ART

2. Liposomal daunorubicin (chemotherapy)

111
Q

Treatment of herpetic ulcer >1 month

A

aciclovir (antiviral)

112
Q

Treatment of cerebral toxoplasmosis

A

Parasitic disease
Pregnant women with cats are susceptible

Pyrimethamine (antiparasitic) + sulfadiazine (antibiotic) + leucovorin (folinic acid)

113
Q

Treeatment of cyrptococcal meningitis

A
  1. Amphotericin IV (antifungal) and 5 - flucytosine (fluconazole) (antifungal)
114
Q

Treatment of TB

A

Commonest and most lethal

Treatment: isoniazid (antibiotic) +/- RIFAMPICIN and pyridoxine (vitamin B6)

115
Q

Treatment of CMV reitinitis

A

Ganciclovir (valganciclovir) eye implant (antiviral)

116
Q

HAART Principles

A

See PBL notes too

Triple therapy

Two nucleoside analogues + Protease inhibitor or NNRTI
or three nucleoside analogues

117
Q

Investigation of HIV

A
  1. 4th-generation kits can test for HIV-Ab and p24-Ag.
    - Can reduce window period to 2-4 weeks
  2. Serum (or salivary) HIV-Ab by ELISA, eg confi rmed by Western blot.
    - In recent infection, HIV-Ab might be –ve (window period ~1–3wks after exposure); here, checking HIV RNA (PCR) or core p24 antigen in plasma, or repeating ELISA at 6wks and 3 months confirms diagnosis
    - Western blot is expensive so is only used as a confirmatory test after ELISA
  3. Rapid test kits (serum HIV)
    - Can give results within 30 minutes but results must be confirmed by ELISA
    - Positive test should be confirmed with a second rapid test
118
Q

Types and exmaples of HAART therapy

A 
1. Nucleoside reverse transcriptase inhibitor (NRTIs)
Abacavir
Lamivudine
Didannosine
Tenofovir
  1. Integrase inhibitors
    - Raltegravir
3. Non-nucleoside reverse transcriptase inhibitors (NNRTIs)
Delaviridine
Efavirinez
Etravirine
Nevirapine
Protease inhibitors
Rotanavir
Lopinavir
  1. Pharmacokinetic
    enhancers/boosters
  2. CCR5 antagonist
    mARAVIOC
119
Q

Which factors enhance the toxicity of antiretroviral therapy

A
  1. Lipodystrophy
  2. Lactic acidosis
  3. Mitochondiral toxicities
  4. Drug interractions
120
Q

What may cause virological failure

A
  1. Viral resistance
  2. Poor adherence
  3. Intercurrent illness
  4. Pharmacokinetic problems
    - Absorption
    - Intracellular metabolism
121
Q

New drug classes in ART?

A

Fusion inhibitors - T20

CCR-5 Antagonists - Maraviroc

Integrase inhibitors

122
Q

ART targeting immune manipulation

A

IL-2, IL-7

Treatment vaccines

123
Q

Preventing MTCT

A
  1. C seciton
    - Elective or planned C-sections are done before labor begins and before the mother’s “water” (the membranes that surround the baby) breaks. This reduces the baby’s contact with the mother’s blood. (Emergency C-sections, those done after the membranes break, do not reduce HIV transmission.)

C sections reduce vertical transmission of HIV to the bebe

  1. ART
  2. Bottle feeding
124
Q

Which factors mean a person is unable to transmit HIV through sexual contact

A

The person adheres to antiretroviral therapy and
monitoring

The viral load <40 copies/mL for at least six
months

There are no other sexually transmitted infections

125
Q

Can vaccinations be given in HIV

A
  • Given as early as possible or once immune system has recovered from ART
  • Live vaccines should be used selectively
  • BCG, yellow fever, oral polio, typhoid and MMR vaccines are contraindicated
126
Q

HIV monitoring

A
  1. CD4 count every 3-6 months
    - Expensive so can also do a total lymphocyte count (TLC)
    - TLC of 1400 microlitres almost equates to a CD4 count of 200 microlitres
  2. HIV RNA every 3-6 months
  3. Serum U+E, creatinine, Cl, bilirubin and LFT every 6-12 months
  4. FBC differential every 3-6 months
  5. Fasting lipid profile and glucose annually
127
Q

Immune response to vaccination

A
  1. Primary exposure: 5-7 days = antibody response (two weeks for a full response to switch from IgM to IgG and memory B a and T cells
  2. Secondary response = 2 days for full protective response when recipient has been previously exposed
128
Q

General principles of vaccine

A
  1. Induce RIGHT TYPE of response
    - Antibodies e.g.Hep B
    - Cell mediated immunity e.g.Tuberculosis
  2. Induce response in RIGHT PLACE
    - Mucosal - sIgA e.g.Flu; polio
    - Systemic e.g. Yellow fever
  3. Response in RIGHT TIME frame
    - Short-term (travel) antibody sufficient
    - Long-term - memory essential
  4. Vaccinated at RIGHT AGE
    - Maternal antibodies in neonate neutralise vaccine
    - sIgA in milk last 6 months e.g. MMR vaccine > 9 months
129
Q

Describe the pneumococcal conjugate vaccine

A
  • PCV7
  • Polysaccharides from 7 most common capsule types
  • Conjugated to T/D toxoids + OMP (as for Hib and MenC)
  • improvement on old PPV23 polysaccharide
  • poor IgG2 responses <2 years
130
Q

Aims of immunization

A

To protect those at highest risk

Reduce disease - moderate and severe

selective immunisation strategy

OR/AND

To eradicate, eliminate or contain disease

mass immunisation strategy

Reduce infection incidence

131
Q

Examples of selective vaccination

A

Travel
e.g. Typhoid

Occupational risk
e.g. Anthrax, rabies

High risk groups
e.g. Hepatitis B vaccine for neonates born to HBV+ve
mothers

Outbreak control
e.g. Hepatitis A vaccine

132
Q

Principle of herd immunity

A

lots of people immunised so less likelihood of disease in the community
- natural boosting form periodic outbreak of diseases in the community

  • allow people who cannot be vaccinated to be protected
133
Q

Methods of acquiring immunity

A
  1. Active : own antibodies via natural exposure or artificial immunisation
  2. Passive: ready made antibodies via natural maternal antibodies or artificial antibodies from other sources
134
Q

Describe the graph of passive immunity in infants

A

Slide 13 on Vaccine PK1 lecture

135
Q

Two types of immune response

A
  1. Innate: (myeloid cells) - resistance to infection and to cancer progression
  2. Adaptive (lymphoid) - AI diseases and chronic inflammatory diseases
136
Q

Steps of the immune response

A

See slide 20 on Vaccines PK1 lecture

137
Q

Difference between extra and intracellular response

A

1 Intra (often viruses) targeted by cytotoxic T cells

  1. Extra )bacteria and parasites) - humoural antibody response
138
Q

Immunological principles of vaccination

A
  1. Adaptive immunity is established before the infection
  2. Immunity must be robust and durable

Can form

  • Protective antibodies
  • CTL memory
139
Q

What do innate immune cells recognise that is the basis for vaccine design?

A

Innate immune cells recognise PRR that recognise PAMPs expressed by pathogens e.g. TLR - 4 recognises LPS

140
Q

Stimulators of TLRs

A

Slide 25 on vaccines PK1 lecture

141
Q

Principle of booster immunisations

A

immune response is always greater after secondary exposure to same antigen

slide 27 on vaccine PK1 lecture

142
Q

Difference between antigen and adjuvant

A
  1. Antigen: any protein peptide subtance that stimulate immine response specific to the pathogen of interest
  2. Adjuvant: substance than enhances the immune response to a weakly immunogenic antigen (non specific)
143
Q

Exxamples of live attentuated vaccines

A
  1. BCG,
  2. polio (Sabin),
  3. MMR,
  4. yellow fever,
  5. VZV )
  6. Rotavirus
144
Q

Examples of killed (whole organisms)

A
  1. Pertussis, flu (old types)
  2. polio (Salk type),
  3. cholera,
  4. Hepatitis A
145
Q

Examples of sub-unit vaccines

A
  1. toxoids
    (e. g. diphtheria; tetanus)
  2. polysaccharide
    poor antigens = conjugated
    - (toxoid + membrane proteins e.g. MenC; Hib; PCV)
  • surface antigens (e.g. Hepatitis B; influenza haemagglutinins)
  • virulence determinant (aP-Pertussis:- adhesin + toxoid + OMP)
  • virus like particles from recombinant surface proteins - HPV
146
Q

How is a virus attenuated

A

Virus is put into monkey cells in order to acquire lots o mutations that don’t allow it to replicate well in human cells

147
Q

Adv. and disadv. of live att. vaccines

A

Adv:

  1. minic natural infx - stimulatate PRR
  2. Induce anitbodies, CD4 and CD8
  3. Fewer doses
  4. Long lasting

Disadv

  1. May cause Disease in immunocomprimised
  2. Maternal Ab’s may interfere
  3. Special storage
  4. Back mutation
148
Q

Disadv. of whole organism

A
  1. Inactivation may destroy protective proteins
  2. Do not induce CD8
  3. May require multiple boosters to adequately stimulate immune response
149
Q

Adv. and disadv. of subunit vaccines

A

Adv:

  1. Reduce risk of adverse affects - no risk of infx to unintended bystanders
  2. more simple to produce

Disadv.

  1. Must know which antigen to which protective immunity is directed
  2. No CD8 (no presentation to MHC1)
  3. require adjuvant
150
Q

Recominbant technology for vaccines

A
  1. Hep B - yeast

2. Rotavirus - animals

151
Q

Active vs passive immunity

A

Active: recipient forms own Abs from stimulation of an antigen

  1. Passive: antibodies put into host

e. g. Ig transfer in patients with X linked agammaglobulinemia
e. g. injection of antiHBV into babies whose mothers have Hep b within 12 hours of birth

152
Q

immunisation schedule for children

A

look up nearer to exam

153
Q

Basis of conjugate vaccine

A

capsule polysaccarides form encapsulated bacteria (e.g. H flu) cross linked to carrier protein (e.g. tetanus toxin protein) -

  • carrier proteins induce CD4 response

-Bacterial (e.g. polysaccharides cannot
activate T cells because MHC molecules
cannot present them.

-Without T cell activation B cells cannot make high affinity antibodies.

  • Conjugates induce T-cell dependent B cell
    responses to polysaccharide antigens
154
Q

Functions and examples of adjuvants

A

e.g. alum, oil and microbial components

  • Activate cells (APC, b cells, t cells and tissue cells) via TLRs
  • increase expression of costim molecules and MHC molecules
  • Induce chemokines to recruit phagocytes
  • Activate APCs
  • Sustained release of antigens (alum or oil)
  • Enhance antigen uptake by APC (alum or oil)
155
Q

Routes of vaccines

A

oral/nasal

im/iv

156
Q

Risks of vaccination

A
  1. Live can revert and become pathogenic (has caused polio in three peeps)
  2. Immunodeficideent
157
Q

Significance of mantoux tuberculin response

A

A reaction of 6mm or greater, indicates

a response of the immune system due

to either TB infection, infection with

environmental mycobacteria or previous

BCG vaccination

Reactions >15mm more likely to be TB

158
Q

Use of hepatitis B vaccine

A

Infants: several options that depend on status of
the mother

If mother HBsAg negative: birth, 1-2m,6-18m

If mother HBsAg positive: vaccine and Hep B immune
globulin within 12 hours of birth, 1-2m, <6m

Adults

0,1, 6 months

Vaccine recommended in

All those aged 0-18

Those at high risk

159
Q

Hep B high risk groups

A

Persons with multiple sex partners or diagnosis of a
sexually transmitted disease

Men who have sex with men

Sex contacts of infected persons

Injection drug users

Household contacts of chronically infected persons

Infants born to infected mothers

Infants/children of immigrants from areas with high
rates of HBV infection

Health care and public safety workers

Haemodialysis patients

160
Q

Features of VZV virus

A

Varicella (chickenpox)

= Primary infection

Zoster (zoster)
= Reactivation

You cannot catch zoster (shingles)

You can catch chickenpox (from either chickenpox
or shingles)

161
Q

Potential epidemic of post-herpetic neuralgia

A

Widespread varicella vaccine in childhood

Reduction in childhood disease

Reduction in exposure of naturally immune

Reduction in natural boosters

Increase in zoster

Increase in PHN

162
Q

High risk and low risk HPV

A

High risk types (16,18) – lead to cancer

HPV16: 50%
HPV18: 20%

Low risk types (6,11) - warts

163
Q

Contraindications to live vaccines

A

Primary immunodeficiency

Standard and intensive chemotherapy

Haemopoietic stem cell transplant

Solid organ transplant

Systemic corticosteroid use

Immunosuppressive drug therapy

HIV infection

Other conditions

164
Q

Who is the influenza vaccine offered to

A
  • all those aged 65 years or over
  • all those aged 6 months or over in a clinical risk group
  • those living in long-stay residential facilities
  • those who care for elderly or disabled persons
  • household contacts of immunocompromised individuals
  • those working within health and social care settings
  • those who work in close contact with poultry
165
Q

What is MAC

A

M avium and M intracellulare; because these species are difficult to differentiate, they are also collectively referred to as Mycobacterium avium-intracellulare (MAI) . MAC is the atypical Mycobacterium most commonly associated with human disease.
MAC is primarily a pulmonary pathogen that affects individuals who are immune compromised (eg, from AIDS, hairy cell leukemia, immunosuppressive chemotherapy). In this clinical setting, MAC has been associated with osteomyelitis; tenosynovitis; synovitis; and disseminated disease involving the lymph nodes, the CNS, the liver, the spleen, and the bone marrow. MAC is the most common cause of infection by nontuberculous mycobacteria (NTM) in patients with AIDS. M avium is the isolate in more than 95% of patients with AIDS who develop MAC infections.

BCS Lectures (8 decks)

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