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Medicine year 2 semester 1 > Case 18- zoonotic disease > Flashcards

Case 18- zoonotic disease Flashcards

1
Q

Arboviruses

A

A group of viruses which are transmitted by mosquito ticks or other arthropods

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2
Q

Japanese Encephalitis (JEV)

A

The main cause of viral encephalitis in many countries in Asia. Majority of JEV cases are asymptomatic. Fatality with encephalitis can be 30%, there is permanent neurologic or psychiatric events in 30-50% of those with encephalitis. Supportive treatment only, no specific cure. Preventable- safe vaccine exists.

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3
Q

Symptoms of JEV

A

Mild fever/headache (non-specific)

Severe disease- high fever/headache/stiff neck/coma/seizures.

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4
Q

How is JEV spread

A

Spread by culex mosquito. Humans are dead end hosts. The disease is normally in rural settings where humans live close to vertebrate hosts.

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5
Q

Diagnosis and risk factors of JEV

A

Diagnosis- serum or cerebrospinal fluid (CSF) to detect virus specific IgM antibodies.
Risk factors- significant rural, outdoor or nigh time exposure i.e. fieldwork, camping or cycling

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6
Q

Yellow fever

A

Endemic in tropical areas of Africa and Central and South America. Its an acute viral haemorrhagic disease. Some people get jaundice. Periodic outbreaks when people introduce the virus into high mosquito density areas where people have little immunity. Can be spread from person-person via aedes aegyptii mosquito’s. Preventable with safe effective vaccine.

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7
Q

Incubation period of yellow fever

A

3 to 6 days

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8
Q

Symptoms of yellow fever

A

Mostly asymptomatic or non-specific and mild. Symptoms in mild diseases- fever, muscle pain, backache, headache, nausea or vomiting. Resolves in 3-4 days.

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9
Q

Progression of yellow fever

A

Some will progress to severe disease:

  • 24 hours after mild disease recovery
  • Return of high fever, jaundice
  • Bleeding can occur from the mouth, nose, eyes or stomach
  • Half will die between 7-10 days
  • About 15% of those with the mild disease develop the severe form
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10
Q

Diagnosis and travel advice for yellow fever

A

Serum to detect virus specific IgM testing

Travel advice- get vaccinated when travelling to endemic areas

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11
Q

Zika virus

A

1) You get it in South America and the South Pacific, its mostly asymptomatic
2) Its mostly transmitted via Aedes mosquitos, a small number are from sexual intercourse
3) If pregnant postpone non-essential travel to area with lots of Zika virus transmission
4) Main concern is brain defects in foetus’s- i.e. microcephaly
5) Prevention- no vaccien available, focus is on vector control, avoiding mosquito bites

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12
Q

Symptoms of Zika virus

A

Mostly asymptomatic. Common symptoms are rash, itching fever, headache, joint pain, muscle pain, conjunctivitis, lower back pain, pain behind the eyes.

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13
Q

Economic burden of mosquito borne viruses

A
  • Pressure on public health resources in developing countries
  • Impact on household income for those affected
  • Cost of diagnosis and treatment
  • Cost of preventative measures i.e. vaccine/vector control
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14
Q

Dengue fever

A

1) Prevalent in Central Africa, Asia, Central America and South America
2) Transmission is mainly from infected (asymptomatic/symptomatic cases) to others by aedes aegytptii mosquito.
3) 4 distinct serotypes of dengue virus (DEN-1, DEN-2, DEN-3 and DEN-4).
4) Recovery from infection provides lifelong immunity against that particular serotype.
5) Subsequent infections by other serotypes increase the risk of developing severe dengue.

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15
Q

Stages of Dengue fever

A

Febrile - day 1-3, high fever and dehydration, drop in platelet numbers, increased haematocrit and viraemia
Critical - day 4-5, fever may come back down, shock/bleeding
Recovery - day 6, reabsorption/fluid overload, IgM/IgG antibodies develop

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16
Q

Dengue without warning signs

A

Fever with two of nausea and vomiting/ rash/ aches and pains/ leukopenia/ positive tourniquet test

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17
Q

Dengue with warning signs

A

1) Abdominal pain or tenderness
2) Persistent vomiting
3) Clinical fluid accumulation (ascites, pleural effusion)
4) Mucosal bleeding
5) Lethargy
6) Restlessness
7) Liver enlargement >2cm
8) Increase in HCT concurrent with a rapid decrease in platelet count.

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18
Q

Severe dengue shock (DSS)

A

Fluid accumulation with respiratory distress, severe bleeding as evaluated by a clinician. Severe organ impairement

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19
Q

Dengue prevention

A
  • Prevent mosquitoes laying eggs
  • Disposing of solid waste properly
  • Cover and clean water storage containers
  • Insecticides
  • Personal household protection
  • Community participation
  • Space spraying (fogging) during outbreaks
  • Active monitoring and surveillance of mosquitoes
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20
Q

Dengue fever- vaccine (Dengavaxia)

A

Reduces severity of disease. Contraindicated in those without evidence of previous dengue infection. Use in areas with high burden of disease.

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21
Q

Treatment of Dengue fever

A
  • Dengue without warning signs- supportive
  • Dengue with warning signs- supportive with close monitoring
  • Severe dengue shock (DSS)- medical emergency, fluid replacement, good care, fatality rate <1%
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22
Q

Why are new diseases emerging

A
  • Commercial air travel
  • Global trade
  • Urbanisation
  • Living in close proximity to animals
  • Unchecked population growth
  • Climate change
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23
Q

Giardiasis

A

Common cause of intestinal problems in the developing world. Picked up easily via travel and ingesting contaminated food

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24
Q

Causative agent of Giardiasis

A

Giardia- A Protozoan, eukaryotic single celled organism with a flagella (mobile). Main source is water but soil may be contaminated. Giardia is resistant to standard chemical treatment. Can get the protozoa from sheep, cattle, dogs and cats. You boil water for 2-3 minutes to purify it.

25
Q

Giardiasis- epidemiology

A

Worldwide distribution, most common in tropical areas. It’s the most commonly identified cause of water borne disease. Can be due to breakdown of water purification systems, drinking from contaminated streams, travel to endemic areas, day care centres.

26
Q

The two forms of Giardia

A

Trophozoite and cyst forms= The Trophozoite form is free moving within the gut and the cyst form is the major type which is transmitted. In the cyst form it can resist chemical and other treatment options.

27
Q

Giardia- lifecycle

A
  • Individual ingests Giardia cyst
  • Cyst hatches (trophozoites) in the intestine causing the diseased state
  • Trophozoites reproduce asexually
  • Trophozoites undergo encystation
  • Cysts ejected in faeces
  • Cysts highly environmentally resistant (chlorination ineffective)
28
Q

Giardia- Symptoms

A
  • Can be asymptomatic
  • Acute infection- diarrhoea, gas, greasy stools that tend to float, stomach/abdominal cramps, upset stomach, nausea/vomiting and dehydration
  • Giardiasis can cause weight loss and failure to absorb fat, lactose, vitamin A and vitamin B12. Pathology is due to malabsorption
  • In children, severe giardiasis delays physical and mental growth, slow development and causes malnutrition
29
Q

Giardia epidemiology

A

Tends to present after travel to less developed countries. Most common cause of intestinal parasitic disease in the UK and US.

30
Q

Giardia- Treatment

A

Oral metronidazole or tinidazole. Both part of Nitromidazole antibiotic class which inhibit DNA synthesis in anaerobic conditions. Can also give Nitazoxanide which inhibits energy production in anaerobic conditions.

  • Do not prescribe antidiarrhoeal drugs for children with gastroenteritis
  • Do not prescribe anti-emetic drugs for children with gastroenteritis
  • Do not routinely give antibiotics to children with gastroenteritis
31
Q

Cryptosporidiosis

A

Common cause of intestinal problems in the developing world. Picked up by travel and ingesting contaminated food. Intestinal parasite relatively common in immigrants.

32
Q

Causative agent of Cryptosporidiosis

A

Cryptosporidium, the phylum is Apicomplexa (related to malaria and toxoplasma). The two types:

  • Cryptosporidium parvum (zoonotic and anthropologic transmission)
  • C.hominis (anthropologic transmission)- not common in UK, from travel
33
Q

Severity of Cryptosporidiosis

A

For most (immunocompetent) individuals the disease is self-limiting. The significant concern is for immunocompromised patients due to significant loss of fluids from diarrhoea (10-15 l/day).

34
Q

Cryptosporidiosis- animals

A

The main host for C.parvum is cattle, humans can then get it from cattle infected water. There are other types which are common in cat and dog species (C.felis and C.canis but these are more rare).

35
Q

Cryptosporidiosis life cycle

A
  • The cattle pass thick wall oocysts (sporulated)- inert, non-replicating form
  • This contaminates the water supply, humans then drink the water ingesting the organism
  • The oocyst provides resistance from the gastric contents and moves into the intestine causing the symptoms
  • The organism infect the cells of the microvilli within the intestinal epithelial cells, replicate and cause destruction of the microvilli
  • The oocyst is then excreted causing autoinfection of host and allowing immediate infection of next host.
    Destruction of microvilli cause malabsorption symptoms
36
Q

Cryptosporidiosis risk factors- similar to Giardia

A
  • Contaminated water sources
  • Uncooked food
  • Travel to developing countries
  • Animal handling
  • Exposure to faeces
  • Immunocompromised
  • Elderly
  • Very young <3 years
37
Q

Cryptosporidiosis symptoms

A

Can last for weeks. Watery diarrhoea, stomach cramps or pain, dehydration, nausea, vomiting, fever and weight loss.

38
Q

Cryptosporiodosis diagnosis

A

Difficult, well mounted microscopy of fecal matter. Acid-fast staining methods. Can use immunofluorescence methods or PCR. You need multiple negative stool samples before a negative diagnosis. Treatment can make it hard to diagnose but once you stop treatment the protozoa will start replicating again, so be careful.

39
Q

Cryptosporiodosis treatment

A

For immunocompetent adults, intervention is rarely required, may need rehydration and salt replacement. For those at serious risk (elderly)- Nitazoxanide which is a broad spectrum anti-parasitic/viral.

40
Q

Cryptosporiodosis HIV

A

In HIV patients with a CD4 count >200mm. They can be asymptomatic but still be infected. If their immune status diminishes, the symptoms will return.

41
Q

Amobeiasis- causes of Amoebic dysentry

A

The causative agent is Amoeba which is a single celled organism. Its common in tropical areas with poor sanitary conditions. Its very infectious and a common cause of traveller’s diarrhoea- bloody diarrhoea, abdominal pain, perforation of intestine (severe disease) and liver involvement (severe disease). Fairly common, free-living and parasitic

42
Q

Types of Amoeba

A
  • Acanthamoeba- rare can cause amoebic encephalitis
  • Entamoeba histolytica- causes amoebic dysentery, worldwide, particularly in the tropics. More common in areas of poor sanitation
43
Q

Entamoeba histolytica

A
  • Trophozoite and cyst stage
  • Can be carried asymptomatically into the human intestine- no animal reservoir
  • Infection- drinking water contaminated with faeces that contain cysts
  • Trophozoites migrate to the large intestine and multiply
44
Q

Amoebiasis- life cycle

A
  • You ingest mature cysts
  • The cyst protects the organism from the stomach
  • In the gut the organism is activated to cause symptoms and replicate
  • Further cysts are expelled in the faecal matter
45
Q

Amoebiasis- what the organism does in the gut

A
  • Live their causing little symptoms- host is asymptomatic
  • Organism migrates to the wall of the gut causing perforation and the classic symptoms of dysentery (most common outcome). Presents with abdominal pain and bloody diarrhoea.
  • Due to perforation, the organism enters the bloodstream and migrates to other areas of the body such as the brain, lung and the liver
46
Q

Amoebiasis- Intestinal replication

A
  • The cyst enters the gut and develops into Trophozoites
  • These may multiple into more Trophozoites which can go on to cause damage to the gut wall.
  • The Trophozoites can go on to form more cysts, which can exit the host and cause further infection
47
Q

The three types of Amoebiasis

A
  • Luminal amoebiasis- asymptomatic, non-invasive (E.dispar)
  • Amoebic colitis- invasive amoebic dysentery, more common, blood mucus containing stools, pain
  • Invasive extraintestinal amoebiasis- trophozoites are carried via the bloodstream throughout the body and invade other tissues. Happens after the Amoebias has invaded through the gut wall
48
Q

Invasive extraintestinal amoebiasis

A

The most severe form of invasive extraintestinal amoebiasis is Hepatic amoebiasis. There is usually no current or history of amoebic dysentery. May occur between 8 weeks to a year post infection. Causes liver enlargement, anaemia is common. You get an intermittent fever and significant abscesses may occur in the liver. Causes significant liver damage and liver disease.

49
Q

Amoebiasis- diagnosis

A

Microscopic analysis of stool. You use a wet sample and look for cysts. Recent introduction of Enzyme immunoassay (EIA) kits for Entomoeba histolytica. Important to differentiate between pathogenic species (E.histolytica) and the non-pathogenic species (E.dispar).

50
Q

Treatment of Amoebiasis

A

Rehydration, one antibiotic if asymptomatic, two if symptomatic. If there is hepatic involvement then it is a complicated treatment involving repeated imaging of the liver.

51
Q

Cystoisosporiasis

A

Caused by the organism Cystoisospora belli (Isospora belli). Infection is normally rare but is via the faecal-oral route. In the infective stage it is an oval oocyst and follows the same course of infection as C.parvum. In normal individuals you tend to get mild infections which are self-resolving but it can be prolonged in immunocompromised / HIV-infected patients. Severe in immunocompromised, infants. Sporadic outbreaks in institutionalised groups within the US

52
Q

Symptoms of Cystoisosporiasis

A

Non-bloody diarrhoea with cramping pain

53
Q

Diagnosis and treatment of Cystoisosporiasis

A

Diagnosis- identification of oocyst in stool through microscopy
Treatment: trimethoprim-sulfamethoxazol

54
Q

Toxoplasmosis

A

Caused by the Protozoan parasite Toxoplasma gondii. Its an intracellular sporozoan parasite. Zoonotic transfer from most mammals, worldwide distribution- common. Forms tissue cysts in skeletal muscle, myocardium, brain, eyes. Infection is by a number of normal routes: Faeco-oral, Trans-placental and Blood transfusion.
Normally caused by ingesting undercooked meat.

55
Q

T.gondii life cycle

A
  • Mammal sheds the Toxoplasmosis eggs in the environment through fecal matter, these are ingested by rodents or birds
  • The oocytes develop into cysts in the tissue
  • Domesticated animals (pig, sheep) come into contact with the faecal matter or ingest the tissue containing the cysts
  • Humans then eat the domesticated animal which now contain the cysts, or injest the eggs from the environment
  • Disease caused by the cyst tend to resolve easily, those caused by the eggs cause a more complicated disease
56
Q

Toxoplasmosis advice

A

Pregnant women are advised to avoid contact with litter trays

57
Q

Toxoplasmosis symptoms

A
  • Asymptomatic or mild flu like symptoms in most people but remains dormant meaning they are carriers
  • Serious disease in immunocompromised
  • Pregnant women causes congenital transmission resulting in Miscarriage, Birth defects and Ocular disease
  • Can cause changes in personality traits- increases risk taking behaviour
58
Q

Seroprevailence in women of childbearing age

A

80% in Latin America and 60% in Eastern and Central Europe.

59
Q

Treatment of Toxoplasmosis

A
  • Only recommended if symptomatic or if HIV positive
  • Adults- the usual drug combination is prymethanamine, sulfadiazine and folinic acid for 4-6 weeks
  • Transplant tissue- if the donor is positive and the recipient is negative, consider treatment
  • Pregnancy- treatment if recent infection, consider postnatal treatment of child. Screen in pregnancy, if the patient is sero-negative and gets the infection there is a high chance they will pass it on to their child.

Medicine year 2 semester 1 (53 decks)

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