Theme 1: International and Tropical infectious diseases Flashcards

1
Q

what is malaria?

A

plasmodium species which are eukaryotic protozoan parasites

the main human malaria causing species are P. falciparum (most common), P. vivax, P. ovale, P. malairiae and P. knowlesi

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2
Q

how is malaria transmitted?

A

vector transmission- female anopheles mosquito

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3
Q

what is the lifecycle of malaria?

A
  1. mosquito bites human and injects sporozoites.
  2. exo-erythocytic cycle- sporozoites travel to liver cells and mature into schizonts (P. vivax and P. ovale can enter a dormant stage at this point). schizonts grow and rupture releasing merozites
  3. erythocytic cycle- merozites infect RBCs. they from an immature ring stage trophozoite which matures and form more schizonts which rupture and release more merozites which infect more RBCs. some of the immature trophozoites undergo sexual reproduction forming gametocytes
  4. the gametocytes are ingested by another anopheles mosquito during a blood meal. they produce zygotes which develop into sporozoites which travel to the salivary glands where they can inoculate another human.
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4
Q

what are the clinical features of malaria?

A

symptoms usually appear 10-15 days after the bite.
may be mild/uncomplicated- fever, headache, chills
may be severe- high fever, anaemia, jaundice, kidney failure, cerebral malaria, convulsions, respiratory distress
classically schizont rupture is associated with periodic symptoms in phases which alternate with symptom free periods:
1. cold stage- cold, shivers
2. hot stage- fever, flushed, dry skin
3. sweating/ fever breaking stage- fever drops and patient sweats.
P. falciparum can follow a 36-48h pattern although is often irregular

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5
Q

how is malaria diagnosed?

A

thick film- thick blood smear to detect presence of malaria

thin film- thinner blood smear to identify the species and quantify the degree of paracitaemia (%).

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6
Q

how can malaria be prevented?

A

awareness of risk
bite prevention- sleep under net, mosquito repellant
chemoprophylaxis- options include malarone (atovaqunone- proguanil), doxycycline, mefloquine, chloroquine

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7
Q

how is malaria treated?

A

artemisinin combined therapy (ACT) (contains Artesunate and mefloquine)
uncomplicated P. falicparum malaria- oral ACT for 3 days
severe/ complicated malaria- I.V Artesunate followed by oral ACT add primaquine in P.vivax or P.ovale to kill hypnozoites

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8
Q

what is the vector of African trypanosomiasis?

A

tsetse fly

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9
Q

which are the two sub-types of the protozoa causing African trypanosomiasis?

A

trypanosoma brucei gambiense (central and West Africa) and Trypanosoma brucei rhondeiense

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10
Q

what are the clinical characteristics of African trypanosomiasis?

A

first stage- chancre (ulcer at bite site), fever, adenopathy, headache
second stage- affects CNS causing meningoencephalitis leading to a behavioural change, agitation, delusion and sleep disorders with the patient progressively sleeping more and more

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11
Q

what is the vector of American trypanosomiasis?

A

kissing bug (bites around the mouth)

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12
Q

what is the causative agent of American trypanosomiasis?

A

trypanosoma cruzi

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13
Q

what are the characteristics of American trypanosomiasis (Chagas disease)?

A

causes acute- fever, lymphadenopathy and chronic illness- cardiomyopathy/ myocarditis and rhythm disturbance
Chagas disease also causes destruction of parasympathetic nerves in the oesophagus and colon which imparts peristalsis leading to aspiration pneumonia, severe constipation and abdominal distension

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14
Q

what is the vector of leishmaniasis?

A

phlebotomine (blood feeding) sand flies

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15
Q

what are the main disease forms of leishmaniasis?

A

cutaneous and visceral leishmaniasis

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16
Q

what are the features of cutaneous leishmaniasis?

A

following the insect bite (weeks- months) a painless ulcer with a rolled edge forms
mucocutaneous leishmaniasis can also affect oropharyngeal mucosa forming ulcerations that can completely destroy the mucous membranes

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17
Q

what are the features of visceral leishmaniasis?

A

following a bite macrophages ingest the parasite but they develop and disseminate into the lymphatic system. can take months/years to appear.
presentation: insidious onset of fever, weakness, massive hepatomegaly, pancytopenia (deficiency in all blood cells)
fatal without prompt treatment

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18
Q

what is the causative agent of giardiasis and how is it transmitted?

A

giardia lamblia- single celled flagellated protozoa

faecal-oral transmission

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19
Q

what is the life cycle of giardiasis?

A

individual ingests giardia cyst
cyst hatches releasing trophozoites which reproduce asexually
trophozoites undergo encystation
cysts ejected in faeces

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20
Q

what are the symptoms of giardiasis?

A

can be asymptomatic
acute infection- diarrhoea, gas, greasy stools, abdominal cramps, upset stomach, nausea/vomiting, dehydration
can cause wight loss and failure to absorb fat, lactose, vitamins A and B12

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21
Q

what is the causative agent of cryptosporidiosis?

A

mainly cryptosporidium parvum

cna also be Cryptosporidium hominis

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22
Q

what is the mechanism of infection of cryptosporidiosis?

A

oocysts are ingested and release sporozoites which infect the intestinal epithelia. replication results in destruction of microvilli causing malabsorption

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23
Q

what is the causative agent of amoebiasis?

A

entamoeba histolytica

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24
Q

what is the mechanism of infection of amoebiasis?

A

host ingests water/ food contaminated with faeces containing amoebic cysts
cysts are digested releasing amoebic trophozoites which bind to the intestinal wall.
in the majority of cases trophozoites asymptomaticy feed on nutrients in the intestinal wall then secrete a cyst wall which allows them to be passed in stool

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25
Q

what are some consequences of amoebiasis?

A

amoebic colitis- in some cases, the amoeba damages cells of the intestinal wall and consume their contents causing colorectal ulceration and bloody diarrhoea.
invasive extra intestinal amoebiasis- amoeba travels to the liver and forms a liver abscess causing RUQ pain tender hepatomegaly, fever, night sweats and rigors

26
Q

what is the causative agent of toxoplasmosis?

A

toxoplasma gondii

27
Q

what is the mechanism of infection with toxoplasmosis?

A

the only definitive host is the domestic cat. oocysts are shed in cat faeces and can be spread to intermediate hosts (birds, rodents, meat animals). humans can be infected bu: consuming food/water contaminated with cat faeces, eating contaminated meat/drinking unpasteurised meat, congenitally from mother to foetus, rarely- blood transfusion or organ transplant.
in humans the parasites from tissue cysts in muscle, myocardium, brain and eyes

28
Q

what are the symptoms of toxoplasmosis?

A

immune-competent- asymptomatic, or mild illness (low grade fever, lymphadenopathy, malaise)
congenital toxoplasmosis- intracranial calcification, neurodevelopment delays, hearing and vision loss and still birth
immunocompromised- toxoplasmosis can reactivate and cause focal neurological symptoms

29
Q

what is the mechanism of action of anti-malarial drugs?

A

artesunate- IV in severe malaria, component of ACT, mechanism not fully understood
mefloquine- component of ACT, possibly inhibits aceylcholoinesterase activity
primaquine- inhibits respiration, used to kill dormant hypnozoites
doxycycline- repurposed antibiotic, only used for prophylaxis
chloroquine- interferes with parasites ability to use haemoglobin as nutrient. causes buildup of toxic heme which kills the parasite and infected cell. resistance widespread
quinine- used when Artesunate not available and there is chloroquine resistance
atovaquone- inhibits pyrimidine synthesis
proguanil- inhibits dihydrofolate reductase- parasite unable to recycle folate

30
Q

what is the treatment for amoebiasis?

A

oral metronidazole- inhibits DNA synthesis

luminal amoebiacide to eradicate GI cysts

31
Q

what is the treatment for giardiasis?

A

oral metronidazole- inhibits DNA synthesis

32
Q

what is the treatment for cryptosporidiosis?

A

manage symptoms with oral rehydration and IV fluids

immuncomprimised may need nitazoxanide (targets enzymes in anaerobic energy system)

33
Q

what is the treatment for leishmaniasis?

A

sodium stibogluconate- decreases ATP available for parasite

amphocertin B- acts on ergosterol to disrupt parasite cell membrane

34
Q

what are the symptoms of Japanese encephalitis?

A

mild disease- mild fever, headache

severe disease- high fever, headache, stiff neck, coma, seizures

35
Q

how is Japanese encephalitis spread?

A

culex mosquito- human is dead end host

36
Q

where is Japanese encephalitis mostly found?

A

rural and peri-urban areas of south east Asia

37
Q

how is Japanese encephalitis diagnosed and prevented?

A

serum or CSF to detect virus specific IgM

prevention- vaccine

38
Q

what are the symptoms of yellow fever?

A

incubation period- 3-6 days
mostly asymptomatic or non-specific (mild fever, muscle pain, headache, nausea, vomiting) resolving in 3-4 days
severe disease- 24hrs after mild disease recovery, high fever, jaundice, bleeding from eyes, nose, mouth or stomach- 50% will die in 7-10 days

39
Q

how is yellow fever transmitted?

A

from person to person via aedes aegypti mosquito

40
Q

where is yellow fever endemic?

A

tropical parts of Africa, central and South America

41
Q

how is yellow fever diagnosed and prevented

A

diagnosis- serum to detect virus specific IgM

prevention- vaccination

42
Q

where is Zika virus found?

A

south and Central America, Caribbean

43
Q

what are the symptoms and consequences of Zika virus?

A

mostly asymptomatic
rash, itching, fever, headache, joint pain, muscle pain, conjunctivitis, pain behind eyes
consequences- birth defects (microcephaly) if infected during pregnancy

44
Q

how is zika transmitted and prevented?

A

transmission- aedes mosquito

prevention- no vaccine, focus on vector control

45
Q

how is dengue fever transmitted?

A

aedes aegypti mosquito

46
Q

what is the course of dengue fever?

A

febrile (1-3 days)- high fever, dehydration, viraemia
critical (4-5 days)- temp falls, shock/bleeding, platelet count drops, haematocrit increases, IgG/IgM produced
recovery (6-10 days)- temp back to normal, risk of fluid overload, platelet and haematocrit back to normal
come patients do not develop critical disease
there is risk of organ impairment from days 2-7

47
Q

what is the tourniquet test?

A

tie tourniquet around arm- if it leaves a rash suspect dengue fever

48
Q

how is dengue prevented?

A

prevent mosquitos laying eggs, dispose of solid waste properly, cover and clean water storage containers, mosquito screens and killers, active monitoring of mosquitos
one dengue vaccine in limited used which reduces the servetiy of disease

49
Q

how is dengue treated?

A

dengue without warning signs- supportive
dengue with warning signs- supportive with close monitoring
severe dengue shock ( DSS)- medical emergency, fluid replacement

50
Q

what are the symptoms of chikungunya virus infection?

A

fever, severe debilitating joint pain, muscle pain, joint swelling, headache, fatigue

51
Q

what is a helminth and what are the 3 groups of helminths?

A

parasitic worm
nematodes (roundworms)- ascaris, hookworm, whipworm. have a round cross-section
trematodes (flukes)- liver and blood flukes , include schistosomes. have a flattened body and lack a digestive canal (absorb nutrients across their outer surface)
cestodes (tapeworms)- hydatids which cause echinococcosis, Taenia solium, taenia saginata

52
Q

what is the causative agent of ascariasis?

A

ascarsi lumbricoides

53
Q

what is the lifecycle of ascaris?

A

human infected by ingesting eggs.
eggs pass into the intestine where they hatch and release larvae into gut lumen.
larvae penetrate the gut wall and enter the circulation and travel to the lungs where they develop.
the host coughs up the larvae and swallows them and they mature into the adult form in the gut.
mature worms mate and produce eggs that are expelled in the faeces.

54
Q

what are the symptoms of ascariasis?

A

many are asymptomatic

can have lethargy, weightloss, diarrhoea, abdominal pain, respiratory problems (eosinophilic pneumonia)

55
Q

what infection is ascaris often concurrent with?

A

hookworm

56
Q

how is someone infected with hookworm?

A

eggs hatch in soil and larvae are chemoattracted to a new host and infect by burrowing through the skin. migrate to lungs in circulatory system for development. they are coughed up and swallowed and mature in the intestine and then release eggs into the faeces.

57
Q

what are the symptoms of hookworm infection?

A

may have allergic reaction at infection site- cutaneous larvae margins. otherwise often asymptomatic
can damage the gut wall and cause malnutrition and anaemia
can have cardiac complications, severe acute respiratory reactions (pneumonia) and GI disturbances

58
Q

what are the causative agents of schistosomiasis and where do they present?

A

S.haematobium- causes urogenital/ bladder problems

S.mansoni and S.japonicum- cause intestinal disease and hepatic disease

59
Q

what is the lifecycle of Schistosomiasis?

A

infected human hosts shed eggs into the environment. the eggs hatch in fresh water and the parasites infect freshwater snails where they mature into an infectious form and are released back into the water. the parasites are chemoattracted to humans and penetrate the skin an enter the circulatory system. they migrate to their final tissues where they mature and are shed.

60
Q

what are the symptoms of schistosomiasis?

A
inflammation and itching at entry site 
urogenital schistosomiasis (S.haematobium)- haematuria, fibrosis of bladder, ureter and sometimes kidney damage, increased risk of bladder cancer, women: genital lesions, vaginal bleeding, pain during intercourse. men:damage to seminal vesicles, prostate and other organs resulting in infertility 
hepatic-intestinal schistosomiasis (S.mansoni, S. japonica)- abdo. pain, diarrhoea, blood in stool, hepatomegaly, splenomegaly, cites, portal hypertension
61
Q

what is the mechanism of action of antihelmintic drugs?

A

mebendazole- inihibits the synthesis of microtubules in parasites intestinal cells. used in nematodes and cestodes
albendazole- similar to mebendazole used for tapeworms
levamisole- blocks acetylcholine receptor- paralyses nematodes so they are expelled by peristalsis
praziquantel- paralyses worms and larvae. used in schistosomiasis