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Y1 TP2 Infection (topic 3 Onwards) > 9. Travel Related Infections > Flashcards

9. Travel Related Infections Flashcards

1
Q

• Factors to consider in travel related infections

A

– Country/countries visited = diff infections in diff areas
– Accommodations/Activities
– Food/water
• Important travel related infection & Pathogens
• Prevention measure – vaccinations before travel

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2
Q

Travel related illness

A

• Most post-travel infections become apparent soon after travel, but incubation periods vary, and some syndromes can present months to years after initial infection.

  • The 3 most common presenting
    • c/o – fever, diarrhoea, and rash
    • There can be different presentations to this
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3
Q

Travel location (s) and duration of stay

A
  • The longer the stay in a developing country the greater the risk of travel related illness
  • Short stays are considered <2-3 weeks
  • Long stays are > 1 month

Duration of trip can impact which infections you pick up

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4
Q

Evaluation of travel related illness

A
  • Travel itinerary and duration of travel
  • Exposure history
  • Timing of onset of illness in relation to international travel (incubation period) - how long have they had symptoms
  • Severity of illness
  • Past medical history and medications
  • History of a pretravel consultation
    • Travel immunizations
    • Adherence to malaria chemoprophylaxis
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5
Q

Source of infection

A
  • Type of accommodations – staying, water, food, areas
  • Insect precautions taken (such as repellent, bed nets)
  • Source of drinking water
  • Ingestion of raw meat or seafood or unpasteurized dairy products
  • Insect or arthropod bites
  • Freshwater exposure (such as swimming, rafting)
  • Animal bites and scratches
  • Body fluid exposure (such as tattoos, sexual activity)
  • Medical care while overseas (such as injections, transfusions) - blood transfusions, blood may not be screened
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6
Q

Precautions - if you suspect that someone has a

Travel related infection

A
  • PPE – judgement of what ppe is needed for what infections
  • Isolation
  • Care when handling samples for laboratory – to identify their disease
  • Taking appropriate history – who,what,where,when
  • Appropriate diagnostic tests – based on history
  • Supportive and specific treatment
    • Supportive – imemdiate treatment without diagnosis, treat symptoms
    • Specific – treatment to treat diasese
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7
Q

Accommodation and travel

• Crowded living conditions, group travel, exposure to ill persons:

A 
– Meningococcal disease 
– Influenza, MERS-CoV, SARS-CoV-2 
– Tuberculosis 
– Viral Haemorrhagic Fever (VHF): examples = (often animal origin) Lassa (rats), Marburg (fruit bats), Ebola (fruit bats) 
– Hepatitis A
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8
Q

Exposure: Arthropods

—> spread by insects

A

• Mosquitoes

– Malaria (protozoa)
– Dengue (virus) 
– Yellow fever (virus) 
– Japanese Encephalitis Virus
– West Nile Virus 
– Rift Valley Fever (virus): sub-Saharan Africa 
– Chikungunya (virus) 
– Others
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9
Q

Incubation period <21 days

A

Signs and symptoms appear less than 21 days after exposure to it

  • Malaria
  • Dengue
  • Yellow fever
  • Japanese encephalitis
  • Leptospirosis
  • Typhoid fever
  • East African trypanosomiasis
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10
Q

Incubation period: >21 days

A

Signs and symptoms appear more than 21 days after exposure to it

  • Malaria (esp. after ineffective prophylaxis)
  • Acute HIV
  • Acute systemic Schistosomiasis (Katayama fever)
  • Viral hepatitis (A, B, C, D, E)
  • Tuberculosis
  • Leishmaniasis
  • West African trypanosomiasis
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11
Q

Characteristic Findings of travel related infections

• Physical

A

– Vital signs – may be all over the place
– Skin findings including bite marks
– Joint, Respiratory, gastrointestinal, Neurological

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12
Q

Characteristic Findings of travel related infections

• Laboratory/diagnostic investigations

A

– Eosinophilia (Higher than normal level of eosinophils – parasitic infection)
– Leukopenia (Low white blood cell count) = HIV
– Thrombocytopenia (Low blood platelet count) = viral haemorhagic fever
– LFTs – liver function tests
– Identification of organism (culture, PCR)
– Identification of immune response
– Chest X-ray
– CT scan

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13
Q

Illnesses associated with fever presenting in the first 2 weeks after travel
Systemic febrile illness with initial nonspecific symptoms

A
  • Malaria
    • Dengue
    • Typhoid fever
    • Rickettsial diseases (such as scrub typhus, spotted fevers)
    • East African trypanosomiasis
    • Acute HIV infection
    • Leptospirosis
    • Ebola virus disease
    • Viral hemorrhagic fevers
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14
Q

Fever with central nervous system involvement

-Illnesses associated with fever presenting in the first 2 weeks after travel

A
  • Meningococcal meningitis
    • Malaria – widespread can affect brain
    • Arboviral encephalitis (such as Japanese encephalitis virus, West Nile virus)
    • East African trypanosomiasis
    • Rabies
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15
Q

Fever with respiratory symptoms

A
  • Influenza
    • Bacterial pneumonia
    • Legionella pneumonia
    • Q fever
    • Malaria
    • Pneumonic plague
    • Middle East Respiratory Syndrome (MERS)
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16
Q

Fever and skin rash

A
  • Dengue
    • Chikungunya
    • Zika
    • Measles
    • Varicella
    • Spotted fever or typhus group rickettsiosis
    • Typhoid fever
    • Acute HIV infection
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17
Q

Exposure: Food and water

Travel

A
  • Hepatitis A
    • Enteric fever (typhoid, paratyphoid)
    • Bacterial gastroenteritis
    • Amoebiasis
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18
Q

Hepatitis A

A

•Spread by faecal-oral route (shellfish which are harvested from contaminated water)

Symptoms: 
– feeling tired and generally unwell 
– joint and muscle pain 
– a raised temperature 
– loss of appetite
 – feeling or being sick 
– pain in the upper right part of your tummy 
– a raised, itchy rash 
– Diarrhoea/constipation
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19
Q

Travellers diarrhoea

A

Pick up E.coli - Enterotoxigenic strains of Escherichia coli (ETEC)
– Gram negative bacilli
3 types of antigens:
• O - cell wall antigen
• H - antigen on flagella
• K – antigen in the polysaccharide capsule

Self-limiting resolves normally by itself

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20
Q

Other types of E.coli are:

—> depending on different types of antigen variation = more serious

A

Enteropathogenic (EPEC) – watery diarrhoea over long period; infants in developing countrie
Enterohaemorrhagic (EHEC) – Bloody diarrhoea
Enteroinvasive (EIEC) – Bloody diarrhoea
Enteroaggregative (EAEC) – Persistent diarrhoea in HIV positive children and adults

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21
Q

Symptoms that associated with gi infection

A

• diarrhoea, stomach cramps and occasionally fever. About half of people with the infection will have bloody diarrhoea

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22
Q

Exposure: Unpasteurised dairy products

A

Things in unpasturised milk/ dairy prodcuts
• Brucella species (dogs, goats, cattle, camel)
• Salmonella gastroenteritis
• Tuberculosis ( M bovis)

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23
Q

Dairy: Brucella species - travel

A

—> Gram negative coccobacilli

  • Recurrent, prolonged episodes of fever
  • Worse at night
  • Associated with sweating
  • May have focal area of pain
  • Infection from ingesting dairy products

Diagnosis: Blood culture, PCR Treatment: Antibiotics

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24
Q

Enteric fever - travel (water)

A

—> salmonella infections
—> Caused by Salmonella typhi or S. paratyphi
– Gram-negative bacilli

• High fever, chills, headaches, anorexia, weakness, diarrhoea or constipation

• Diagnosis
– Stool culture
– Bone marrow aspirate = as the organisms settle in the bone marrow
– The white blood cell (WBC) count is often low.
Typhoid related deaths

3 top countries – INDIA, Pakistan, Bangladesh (ECDC)

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25
Q

Vaccines to prevent Salmonella infections

A

A polysaccharide vaccine based on the purified Vi-antigen (Vi-PS vaccine).
• This single-dose intramuscular or subcutaneous injectable
• Protective efficacy 70%

A live attenuated oral vaccine (Ty21a, made with attenuated S. typhi strain Ty2)
• available in capsules
• protective efficacy of 33-67%

Do not give immunocompromised person a live attenuated vaccine – as it can multiply and cause the infection in them

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26
Q

Malaria

• 5 main species of Plasmodium

A 
– falciparum (most prevalent)
– vivax (mainly in people who have come from asia)
– ovale 
– malariae 
– knowlesii
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27
Q

Malaria- vector

A

Vector - female Anopheles mosquito

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28
Q

Lifecycle of malaria

A
  • Mosquito transfers sporozoites in its saliva into blood of humans
  • Reach liver cells and multiply asexually to give rise to merozoites. Merozoites are released from liver and infect red blood cells
  • Merozoites reproduce asexually in the red blood cells - first stage get an early ring form called the early trophozoite which grows to the late trophozoite stage and finally grows to the schizont.
  • Some merozoites enter the sexual cycle to produce gametocytes (male and female) which remain in the red blood cells
  • Gametocytes are taken up by mosquitoes when they feed on people The male and female gametocytes give rise to zygotes in the mosquito gut which develop into ookinete and finally oocysts which rupture releasing the sporozoites
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29
Q

Clinical features of malaria

A

• Patients asymptomatic from time of the original mosquito bite until approx a week later
• Typical incubation period usually between 8 – 17 days for P falciparum, P vivax, and P ovale and 18 - 40 days for P malariae.
• Initial symptoms of malaria are nonspecific and similar to the symptoms of a minor systemic viral illness
– fever, headache, fatigue, muscle and joint pain, nausea, and vomiting

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30
Q

Investigations - malaria

A
  • Blood film x3
  • FBC, U&Es urea and electrolytes, LFTs,liver fucntion tetss
  • Head CT scan if neurological symptoms
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31
Q

Treatment - malaria

A

• Treatment depends on species
– P. falciparum
• Artesunate
• Quinine + doxycycline

– P. vivax, ovale, malariae 
	– Chloroquine with primaquine 
	• Dormant hypnozoites (liver) 
	– Can recur months-years later
 – Give additional primaquine
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32
Q

Trophozoites on blood film

A

-This Giemsa-stained, thin blood film showing Plasmodium falciparum ring-forms, and gametocytes

33
Q

Severe malaria Clinical features

A
  • Impaired consciousness/coma
  • Prostration or sit up with assistance
  • Convulsions
  • Deep breathing, respiratory distress (acidotic breathing)
  • Circulatory collapse/shock, systolic blood pressure <70 mm Hg
  • Jaundice
  • Hemoglobinuria (high amounts of hemoglobin in the urine)
  • Abnormal spontaneous bleeding
  • Acute renal failure
  • Pulmonary edema
34
Q

Mosquitoes: Japanese encephalitis

A
  • Asia: majority subclinical
  • Mild infections: fever with headache
  • More severe infection: sudden onset headache, high fever, neck stiffness, stupor, coma, occasional convulsions and spastic paralysis
  • Vaccination recommendations are seasonal
35
Q

Dengue fever

A
  • Transmitted between people by mosquitoes
  • Symptoms usually begin 4-7 days after mosquito bite and last 3 to 10 days

• Epidemics occur when there is a concurrence of large number of vector mosquitoes, a large number of people with no immunity to 1 of the 4 virus types (DENV 1-4) - epidemica can occur in certain seasons

36
Q

Dengue fever clinical features

A
  • Incubation 3-14 days
  • Majority asymptomatic or fever plus rash (2-5 days and later in infection)
  • Classic dengue: fever, retro-orbital headache, musculoskeletal pain, rash
  • Leukopenia, thrombocytopenia
  • Diagnosis clinical; also serology, PCR
37
Q

Exposure to ticks causes 3 diseases

A

– Rocky Mountain spotted fever (ticks carry Rickettsia rickettsii)
– Crimean-Congo hemorrhagic fever (tick born virus)
– Lyme disease (tick borne Borrelia burgdorferi)

38
Q

Typhus

A
  • Caused by Rickettsia (Intracellular parasites)
  • Bitten by infected lice, mites or fleas found on small animals like mice, rats, cats and squirrels. People can also carry them on their clothes, skin or hair.

•Symptoms
– very high temperature (usually around 40C)
– feeling sick, being sick
– diarrhoea, abdominal pain
– dry cough
– joint pain, backache
– dark spotty rash on chest that may spread to the rest of the body (apart from face, palms and soles of feet)

•Diagnosis: PCR

39
Q

Viral Haemorrhagic Fever (VHF)

A

—> Viral Hemorrhagic Fever (VHF) refers to serious illnesses caused by particular viruses.
Viruses cause a lot of bleeding due to platelet reducation

  • Lassa fever (Lassa virus)
  • Crimean-Congo HF (tick borne virus)
  • Ebola (Ebola virus)
  • Marburg (Marburg virus)
40
Q

Viral Haemorrhagic Fever (VHF)

-Symptoms and spread

A

• fever, fatigue, dizziness, muscle aches, loss of strength and exhaustion, vomiting, diarrhoea headaches, • Severe cases Internal/external bleeding at 5-7 days – bleeding under the skin, in internal organs or from body orifices like the mouth, eyes or ears. Some severe cases may also show signs of shock, nervous system malfunction, coma delirium and seizures.

Spread by direct contact with body fluids

41
Q

Ebola virus - transmission

A

•Transmitted to people from wild animals (such as fruit bats, porcupines and non-human primates) and then spreads in the human population through direct contact with the blood, secretions, organs or other bodily fluids of infected people, and with surfaces and materials (e.g. bedding, clothing) contaminated with these fluids.

42
Q

Ebola virus - symptom;

A
  • a high temperature
  • joint and muscle pain, severe muscle weakness
  • diarrhoea, vomiting, a rash, stomach pain and reduced kidney and liver function can follow.
  • infection may then cause internal bleeding as well as bleeding from the ears, eyes, nose or mouth. •Vaccine in high incidence areas
43
Q

3 diseases caused by Swimming Exposure: Fresh Water

A
  • Schistosomiasis
  • Leptospirosis
  • Hepatitis A
44
Q

Schistosomiasis

A

3 species
• Shistosoma mansoni
• Shistosoma japonicum
• Shistosoma haematobium

  • Parasite (blood fluke) penetrates human skin following completion of part of the lifecycle in snails
  • Migrate to blood stream
  • Katayama fever is the manifestation of acute Schistosomiasis
  • fever, an urticarial rash, enlarged liver and spleen, and bronchospasm
  • Mid East, Africa, Eastern S. America and Carribean
45
Q

Fresh Water: Leptospirosis

A

Leptospira interrogans

  • Water contaminated by animal urine
  • Incubation 7 to 14 days
  • Abrupt fever> 39oC, chills
  • Later invasion of liver, kidneys and CNS
  • Gives rise to jaundice, hemorrhage, tissue necrosis
  • Aseptic meningitis (inflammation of meninges without positive culture)
46
Q

Diseases caused by Exposure: New sexual partners

A
  • HIV
  • Hepatitis B
  • Other STDS: herpes, gonorrhea, syphilis, HPV
47
Q

Coronavirus: Ultrastructural morphology

A

• Classical spikes on the outer surface of the virus – resemble the “corona” of the sun.

Envelope
Protein capsid
Receptors
S protein = spike protein = target for treatments

48
Q

Virus - Covid

A
  • Named by ICTV (International Committee on Taxonomy of Viruses)
    • Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)
49
Q

Disease - Covid

A
  • Named by WHO in the ICD (International Classification of Diseases)
    • Coronavirus disease (COVID-19)
50
Q

SARS-CoV-2 - structure

A
  • SARS-CoV-2 is an enveloped β-coronavirus.
  • Has a genetic sequence very similar to SARS-CoV-1 (80%) and bat coronavirus RaTG13 (96.2%).
  • The viral envelope is coated by spike (S) glycoprotein, envelope (E), and membrane (M) proteins.
  • Host cell binding and entry are mediated by the S protein.
51
Q

SARS-CoV-2

Infective pathway

A
  1. The first step in infection is virus binding to a host cell through its target receptor.
    • The S1 sub-unit of the S protein contains the receptor binding domain that binds to the peptidase domain of angiotensin-converting enzyme 2 (ACE 2)
    1. Spike protein binds to ACE receptor
    2. In SARS-CoV-2 the S2 sub-unit is highly preserved and is considered a potential antiviral target.
52
Q

SARS-CoV-2 .

Transmisision pathway

A
  • Respiratory

* By touching a phomyte – thing that has covid on

53
Q

Potential origin of SARS-CoV-2 : Bats to humans?

A
  • All human coronaviruses have animal origins (Natural Hosts).
  • Domestic animals can suffer from disease as Intermediate Hosts that cause virus transmission from natural hosts to humans.
  • Bats are likely reservoir hosts for SARS-CoV-2.
54
Q

SARS-CoV-2: Structure and replication cycle

A
  1. The virus binds to ACE 2, the host target cell receptor, which is principally expressed in the airway epithelial cells and vascular endothelial cells.
  2. This leads to membrane fusion and releases the viral genome into the host cytoplasm.
  3. Subsequent steps of viral replication, leading to viral assembly, maturation, and virus release.
55
Q

Viral load dynamics and duration of infectivity

A

Day 0 – when you start getting symptoms
• But you have picked up covid before this

• Following initial exposure, patients typically develop symptoms within 5-6d (incubation period)

  • The viral load peaks in the first week of infection, declines thereafter gradually
    • Virus does not cause illness, virus causes a disease response which causes illness

The antibody response gradually increases and is often detectable by day 14

56
Q

Viral Mutations,

A

• MUTATIONS are errors that occur during the process of duplicating viral RNA. - changing RNA (changed rna may or may not impact protein)

57
Q

Variants

A

Mutations produce VARIANTS which are similar but not exact copies of the original virus “PARENTAL STRAIN”.

58
Q

Strain

A
  • A new STRAIN is when a variant displays distinct physical properties to the original virus.
    • Changes look and function of virus
59
Q

Viral transmissibility

A

• A virus is essentially a microscopic box full of genetic material:
– The box must be robust enough to keep the genetic material safe in the body and in the outside world.
– But to infect cells, the box must open to let the virus’s genetic material out.

  • Too stable, and the virus can not open up and infect cells efficiently.
  • Too unstable, and the virus can not survive for long after being transmitted
60
Q

Why do viruses mutate

A

adapt to their surroundings and more effectively move from host to host.

  • Mutations can help viruses to better evade the host’s immune systems, treatments and vaccines.
    • Mutations can cause varients

• A mutation can help the virus gain traits that enable it to reproduce quickly or adhere better to the surface of human cells.

  • Viruses can mutate so quickly that they do not develop traits that are advantageous to transmission. Hence some virus mutations seem to emerge and then die off.
    • Mutations can be beneficial or harmful
61
Q

Spike protein - basic definition

A

Spike protein —> part of virus that latches on to the host cell to allow virus to enter a cell

62
Q

Spike protein - structure and function

A

• Spike proteins (S) on SARS-CoV-2 bind to receptors enabling the virus to enter the host.

• A Spike protein is made up of 3 smaller peptides in the OPEN or CLOSED orientations.
• The more that are open, the easier for the protein to bind. = stickier it is to bind
Less needed to infect

63
Q

D614G mutation

A

• The D614G mutation is caused by a single letter change to the viral RNA code. This makes open conformations more likely, hence increasing the chance of infection

64
Q

SARS-CoV-2 Vaccines 2 examples

A

—-> Pfizer-BioNTech BNT162b2 and Moderna mRNA-1273 vaccines

65
Q

SARS-CoV-2 Vaccines

How can they work (Pfizer and Moderna)

A
  • Contain the genetic code (mRNA) of the spike protein. Once inside the body, the spike protein is produced, causing the immune system to recognise it and initiate an immune response. (doesn’t actually contain the virus – so it doesn’t cause covid)
  • If the body later encounters the spike protein of the coronavirus, the immune system will recognise it and produce antibodies to destroy it before an infection is caused.
  • These vaccines can not cause COVID-19 disease, as there is no whole or live virus involved. The mRNA is naturally degraded after a few days.
66
Q

SARS-CoV-2 Vaccines

—> Oxford-AstraZeneca ChAdOx1 nCoV-19 (AZD1222)

A
  • Made from a virus that is a weakened version of a common cold virus known as an adenovirus. This adenovirus has been genetically changed so that it can not cause infections in humans. ChAdOx1 has been engineered to make the spike protein of the SARS-CoV-2 virus.
  • The immune system recognises the spike protein as foreign, forms antibodies and then attacks the SARS-CoV-2 virus, preventing an infection.
67
Q

Pathogenesis: Asymptomatic Phase - 2-21/2 weeks

A
  • Respiratory aerosols bind to epithelial cells in the upper respiratory tract.
  • Main host receptor is the ACE-2 (nasal epithelia++).
  • Local replication and propagation.
  • This stage lasts a couple of days. Limited immune response generated.
  • Despite having a low viral load, individuals are highly infectious, and the virus can be detected via nasal swab testing
68
Q

Pathogenesis: UPPER Respiratory Tract involvement

A

• Non-specific symptoms- in first phase : Fever / Malaise / Dry, persistent cough.
Cells involved have a lot of ACE receptors

  • Can cause transient damage to olfactory epithelial cells, leading to olfactory dysfunction.
  • Greater immune response generated during this phase (involving the release of C-X-C motif chemokine ligand 10 (CXCL-10) and interferons (IFN-β and IFN-λ) from the virus-infected cells.
  • The majority of patients do not progress beyond this phase as the mounted immune response is sufficient to contain the spread of infection.
69
Q

Pathogenesis: LOWER Respiratory Tract involvement

A

• 1/7 or 8 of all infected patients progress to this stage and can develop severe symptoms.

70
Q

Pathogenesis: LOWER Respiratory Tract involvement

Leading to ARDS

A
  1. Virus invades and enters the Type 2 alveolar epithelial cells - pneumocytes via the host receptor ACE
  2. Undergoes replication to produces more viral Nucleocapsids.
  3. The virus-laden pneumocytes now release many different cytokines and inflammatory markers “Cytokine Storm”: Interleukins (IL-1, IL-6, IL-8, IL-120 and IL-12), Tumour necrosis factor-α (TNF-α), IFN-λ and IFN-β, CXCL-10, monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-1α (MIP-1α)
  4. This ‘cytokine storm’ acts as a chemoattractant for neutrophils, CD4 helper T cells and CD8 cytotoxic T cells, which then begin to get sequestered in the lung tissue. (isolate and damaged lung tissue, making area inflammaed and sludgy)
  5. These cells are responsible for combating the virus, but in the process they cause subsequent inflammation and lung injury.
  6. The host cell undergoes apoptosis with the release of new viral particles, infecting adjacent type 2 alveolar epithelial cells in the same manner.
  7. Sequestered inflammatory cells → Persistent injury → Loss of both type 1 & type 2 pneumocytes → Diffuse alveolar damage → ARDS acute respiratory distress syndrome
71
Q

Asymptomatic Covid

A
  • No clinical symptoms

* Positive lateral flow / PCR test

72
Q

Mild Covid

A
  • Fever / New, persistent cough / Olfactory dysfunction
  • Sore throat / Malaise / Aches
  • GI symptoms (N/V/D/Abd pain)
73
Q

Moderate Covid

A

• Pneumonia symptoms without hypoxia

74
Q

Severe Covid

A

• Pneumonia symptoms with hypoxia (SpO2 <92%)

75
Q

Critical state - Covid

A
  • ARDS
  • Shock
  • Coagulation defects
  • Encephalopathy
  • Heart failure
  • Acute Kidney injury
76
Q

Main Covid symptoms

A
  • Persistent high temperature – paracetamol doesn’t decrease it
    • New continuous cough
    • Loss of change to your sense of smell or taste
77
Q

Covid-19: Assessment and Management

A
  • Approximately 80% of patients can be managed effectively at home with conservative measures for viral infection.
  • Remote assessment and risk stratification is a clinical dilemma.
78
Q

Purpose of red isles

A

– To support resilience in Primary Care
– To provide a clinically safe and effective face-to-face assessment service for patients that can not be seen at their base practices due to the current coronavirus pandemic restrictions.
– To stratify the clinical risk and offer appropriate management.

79
Q

Primary Observations & Examination - Covid

A
  • Temperature
    • SpO2 before and after exertion
    • Blood Pressure
    • Chest auscultation
    • Resting Pulse
    • ENT examination
    • Respiratory Rate
    • Urinalysis as necessary

Y1 TP2 Infection (topic 3 Onwards) (9 decks)

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