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parasite infections Flashcards

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1
Q

define infection

A

invasion by and growth of pathogenic microorganisms within the body

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2
Q

define disease

A

a disordered or incorrectly functioning organ, part, structure, or system of the body resulting from the effect of genetic or developmental errors, infection, poisons, nutritional deficiency or imbalance, toxicity, or unfavorable environmental factors; illness; sickness; ailment.

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3
Q

define a parasite *

A

organisim living in or on the host and dependant on it for nutrition, causing damage - rely on things form the host for survival

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4
Q

what are ectoparasites

A

they are on the skin

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5
Q

types of endoparacytes *

A

protazoa

metazoa

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6
Q

describe protazoa *

A

single celled organisms

eukaryotes - genome all in a nucleus and complex organelles in cytoplasm

pathogenesis varies

some have insect vectors

dont cause eosinophilia

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7
Q

describe metazoa *

A

multicellular organisms - helminths/worms

free living, intermediate hosts and vectors

some just invade gut (geohelminths), others invade tissues

they cause eosinophilia if they invade the blood - can use this to detect infection

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8
Q

what are the types of protazoa *

A

amoebae

coccidia

ciliates

flagellates

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9
Q

describe amoebae *

A

organisms - entamoeba histolytica (cause disease), entamoeba dispar (commensal of gut)

most infections are asymptomatic - pass cysts in faeces, asymptomatic phase can persist indefinitely - cysts remain viable for 2months

the rest have a spectrum of disease from dysentry (intense diarrhoea) to amoebic liver abscess - depends oin how many parasites you injest

incubation period 7 days, tissue invasion occurs in 1st 4 months of infection

fecooral transmission - ingest cysts by contaminated food/water - they release trophozoites which invade epi cells = ulcers - infection spread from intestine to other organs by venous system eg liver lung, heart, urinary tract and brains

humans are the only resevoir

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10
Q

epidemiology of amoeba

A

10% world pop is infected with e histolytica

3rd most common cause of death of parasitic infections

common in south and central america, west and south-east asia

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11
Q

what is the diagnosis and treatment of amoeba

A

in bright field microscopy - cysts are spherical and measure 12-1um - mature cyst has 4 nuclei, immature has 1-3

treatment - Nitroimidazole derivatives (act on trophozoite, but not on cysts) + parmomycine or diloxanide furoate

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12
Q

different coccidia infections *

A

plasmodium species

toxoplasma

cyptosporidium

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13
Q

describe plasmodium coccidia *

A

malaria

there are different types - P. falciparum, P. malariae, P. ovale, P. vivax and P. knowlesi - have different severities (ovale is least severe, falciparum is the most), on blood film they have different shapes

2 hosts - humans and anopheles mosquitoes

have liver and blood stages - cause symptoms in RBC

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14
Q

symptoms of malaria *

A

can be present after 7days or after as long as a year

fever, headache, chills, vomiting, muscle pain, paroxysm (cycle in 4-8 hrs)

complications - severe anaemia because rbc burst, cerebral malaria because of swelling of the brain = seizures/coma

liver failure

shock

pulmonary oedema

abnormally low blood sugar

kidney failure

swelling and rupturing of the spleen

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15
Q

diagnosis and treatment of malaria

A

•Uncomplicated malaria:

chloroquine, Atovaquone-proguanil, Artemether-lumefantrine, quinine sulfate plus one of the following: Doxycycline, Tetracycline or Clindamycin Quinine sulfate, Mefloquine

•Severe malaria:

Artemisinin-based combination therapy (ACT) is recommended - started to develop resistance against ACT so treatment is still a big problem

Diagnosis

  • blood film, Giemsa stained - have to be weel trained
  • Rapid test: commercially available antigen detection tests: more expensive and less sensitive
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16
Q

describe toxoplasma *

A

mild disease in immunocompetent people - fever, swollen lymph nodes, headaches, sore throat

in pregnancy pose danger for the fetus

well transmitted - people dont know that they are infected

people get infected by eating undercooked meat of animals with cysts, consuming food/water with cat faeces, contaminated environmental samples, blood transfusion, organ transplant, transplacentally

immunocomprimised people might get CNS disease, brian lesions, pneumonitis, retinochoroiditis and other risks

diagnosis - serological test

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17
Q

describe cryptosporidium *

A

mild disease in immunocompetant people

in immunocomprimised people - fever, nausea, vomiting, common in HIV pts presenting with diarrhoea

fecooral transmission

diagnosis stool examination looking for oocytes

treatment - fluid rehydration

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18
Q

describe ciliates *

A

balantidium coli

feco-oral

reservoir hosts - pigs, rodents, primates

distributed worldwide

most people asymptomatic - continue to expel egg in faeces

immunocomprimised - persistant diarrhoea, dysentry, abdo pain, weight loss, nausea and vom, if untreated can get perforation of the colon

diagnosis - stool exam

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19
Q

describe flagellates *

A

giardia lamblia (giardiasis)

feco oral

Flagellated trophozooites attach by their suckers to surface of the duodenal or jejunal mucosa

most people infected - asymptomatic, depends on dose

acute symptoms: cause diarrhoea, greasy stools that tend to float, upset stomach/nausea/vom, dehydration

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20
Q

epidemiology, diagnosis and treatment of giardiasis

A

problem in developing countries

commonest, globally distributed, waterborn protazoal infection

Ovoid cysts are able to survive standard chlorination procedures, filtration is required to exclude them from drinking water

diagnosis - stool examination

cant treat the cysts they persist, only treatable when in trophozoites form

treatment - metronidazole/tinidazole

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21
Q

describe trichomoonas (flagellates) *

A

almost exclusively transmitted sexually

In women the organism is found in the vagina, urethra and paraurethral glands; in men infection is usually of the urethra.

symptoms:

  • 10-50% females are asymptomatic
  • 15-50% males asymptomatic
  • females - vaginal discharge, vulval itching, dysuria, or offensive odour, but these are not specific for TV Occasionally the presenting complaint is of low abdominal discomfort or vulval ulceration
  • males - discharge and/or dysuria.

complications - detrimental in pregancy, associated with preterm delivery and low birth weight

may enhance HIV transmission, and may be increased risk of TV in people with HIV

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22
Q

epidemiology, treatment and diagnosis of TV

A

most common curable non-viral STI in UK

diagnosis - microscopy detection of trichomonads which are mobile or trichomonas rapid test to detect Ag

treatment = metronidazole

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23
Q

describe helminths (metazoa)*

A

complex multicellular organisms

cycles may involve insect vectors and intermediate hosts

for most humans are the definate host, there are some zoonoses

adult worm cant multiply in man, they produce eggs and become worms in different hosts - the number of worms relates to the infection

they lay eggs, microfilaria and larvae

effect school age children - catch in water; has bigger consequences because children cant go to school so effects economy

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24
Q

what are the different types of worms *

A

roundworms (nematodes): ascaris, hookworm, filaria, strongyloides

flatworms (cestodes): taenia (tapeworms)

flukes (trematodes): schistosoma

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25
Q

describe ascariasis life cycle

A

nematode - roundworm

feco-oral transmission

adult worms live in the SI - female produce 240000 eggs a day passed in faeces

fertile eggs embryonate and become infective after 18days to several weeks depending on env conditions

after infective eggs are swallowed the larvae hatch, invade the intestinal mucosa and are carried by the portal then systemic circulation to the lungs (10-14 days) - penetrate the alveolar walls, ascend the bronchial tree to the throat and are swallowed

upon reaching SI they develop into adult worms

adult worm can live for 1-2 yrs

26
Q

ascariasis symptoms and pathology *

A

often asymptomatic - need a lot of parasites to see infection

cause abdo pain/intestinal obstruction

adults feed on the contents of the SI and this may cause problems in malnourished people - especially children

migration of lavae may cause localised reaction in organs

penetration of larvae from capillaries into the lungs can lead to Loeffler’s pneumonia - pools of blood and dead epithelial cells clog air spaces in the lungs

resulting bacterial infections can be fatal

27
Q

diagnosis and treatment of ascariasis

A

stool examination

albendazole and mebendazole

28
Q

describe the symptoms and pathology of hookworms *

A

they stick to SI and cause bleeding = iron deficient anaemia

can have cardiac complications

GI and nutritional/metabolic symptoms

minimal local skin manifestations - ground itch during penetration by the filariform larvae

resp symptoms seen in pulmonary migration of the larvae

29
Q

life cycle, diagnosis and treatment of hookworms

A

ancylostoma duodenale

1cm long - stuck by their buccal capsule to the villi of the SI

go through the skin

carried through bv to heart and hungs

penetrate the pulmonary alveoli, ascend the bronchial tree to pharynx and are swallowed

they reach the SI where they reside and mature into adults

male and female make eggs which are expelled in faeces

eggs have to transform into larvae to get into the skin

diagnosis - stool examination

treatment - albendazole and mebendazole

30
Q

symptoms of Trichuris trichura - whipworm *

A

might be asymptomatic

if a lot of worms - bloody diarrhoea and anaemia becasue of severe vitamin and iron loss

leave open wounds which = inflammation of the intestinal wall

might get rectal prolapse

it is a hookworm

31
Q

life cycle, diagnosis and treatment of trichuris trichiura

A

feco-oral

eggs hatch in the SI - release larvae that mature in colon

adult worms live in cecum and ascending colon

adult worms are fixed here

(because of the immune reaction caused, they are being sold as therapy against allergy and autoimmune conditions)

diagnosis - stool examination

treatment - albendazole and mebendazole

32
Q

symptoms of lymphatic filiariasis *

A

lymphatic obstruction, especially in legs, can brogress to elephantitis

can occur in arm, breast, scrotum

it is a filaria

33
Q

diagnosis, life cycle and treatment of lymphatic filariasis

A

transmitted by mosquito blood

found in peripheral blood at night, in day they are in deep veins

diagnosed by blood smear in night or ag detection with an immunochromatic test (card) or ELISA, RAPID test

treatment - albendazole and ivermectin

34
Q

describe loa loa - loaiasis *

A

transmitted by fly

migrate through the subcutaneous tissue, may cross the front of the eye under the conjunctiva

microfilariae develop from the larvae in female and circulate in blood where picked up by fly and in the gut of the fly the microfilae enter the fat bodies and mature into infective 3rd stage larvae

infect new host when fly takes blood meal

35
Q

what are the flatworms that we can be infected by *

A
  • T. solium and T. asiatica – pig is intermediate host
  • T. saginata – beef is intermediate host

humans are the only definitive hosts

36
Q

symptoms of taenia *

A

most people asymptomatic

Patients with T. saginata taeniasis often experience more symptoms (size of the worm up to 10m) than those with T. solium or T. asiatica (~3 m).

Tapeworms can cause digestive problems including abdominal pain, loss of appetite, weight loss, and upset stomach.

The most visible sign of taeniasis is the active passing of tapeworm segments

37
Q

diagnosis and lifecycle and treatment of taenia

A

diagnosis - segment in stool/eggs in stool

treatment - praziquantel

ingested in poorly cooked cysts in meat

can be infected a long time after eggs are in the faeces - eggs can survive for days to months in the environment

38
Q

what is caused by taenia solium - cysticercosis *

A

commonest cause of acquired epilepsy worldwide

39
Q

describe shistosomiasis - trematode (fluke) symptoms *

A

within days rash and possibly itchy skin

Within 1-2 months; fever, chills, cough, and muscle aches but most people have no symptoms at this early phase of infection

When adult worms are present, the eggs that are produced usually travel to the intestine, liver or bladder, causing inflammation or scarring.

children who are suseptible - anaemia, malnutrition and learning difficulties

after yrs of infection - can damage the liver, intestines, lungs and bladder

40
Q

diagnosis, treatment and lifecycle of shistosomiasis

A

diagnosis - stool/urine samples

treatment - praziquantel - treat people even if they are asymptomatic in order to reduce transmission

problem is praziquantel can cause the liver to bleed = death

S. mansoni, haematobium and japonicum

eggs eliminated in water by faeces/urine - hatcha nd release miricidia - penetrate the snail - release carcariae - penetrate the skin = migrate through tissues - adult worms reside in venules - in the lumen of the intestine (S. mansoni and S. japonicum) and of the bladder and ureters (S. haematobium).

kills the snails ie the intermediate host therefore the worm cannot infect the skin = no infection

41
Q

describe the ectoparasite sarcoptes scabiei *

A

extoparasite - paraite on your skin

transfer between people

cause itchy burrow on skin

diagnosis - rash and burrows

treatment - scabicides

42
Q

describe the ectoparasites - lice *

A
  • Pediculus humanus capitis (head louse),
  • Pediculus humanus corporis (body louse, clothes louse), and
  • Pthirus pubis (“crab” louse, pubic louse)

transmitted between people

have 3 stages - eggs, nymphs and adults

diagnosis - finding live nypmh or adult lice on scalp/hair of the person

43
Q

what type of parasite is leismania *

A

endoderm - protazoa - flagellate

44
Q

what is the life cycle of leishmania parasites *

A

transmitted from flies

taken up by the phagocytic cells 1st - neutrophils then macrophages/monocytes

this can kill/promote the survival of the parasites

life cycle continue when sandfly bite infected host then bite another person

45
Q

what are the forms of leishmania *

A

promastigote - this is the form in the sandfly, they move in the direction of the flagellum and can be cultured

amastigote - form in human or other vertebrate host’s cells - have resorbed their flagellum so not motile

46
Q

describe sand flies *

A

the vector for leishmaniasis

found mainly in mainly in the warm parts of the world, including southern Europe, Asia, Africa, Australia, Central and South America - because of climate change - spreading northwards from greece and Turkey - occurs in southern france and is spreading through italy, some in isle of white

small so go through mosquitoe net, hairy, hop around before settling to bite, silent

female feed on blood to provide nutrition for eggs

47
Q

what are the 2 types of leishmaniases disease *

A

visceral leishmaniasis (Kala azar)

cutaneous leishmaniasis

  • cutaneous
  • diffuse cutaneous
  • mucocutaneous
48
Q

describe visceral leishmaniasis *

A

most severe form of leishmaniasis - fatal if untreated

characterised by irregular fever, weight loss, swelling of liver and spleen, anaemia

suppressed immune system

also can get - lymph nodes, loss of appetite, cough, hepatomegaly, oedema, diarrhoea, vomiting and jaundice

also known as kala azar (black fever) - cause darkening of skin

a lot of asymptomatic cases - 30-100 subclinical infections for every overt VL case

species - L donovani

vactors P martini, P celiae, P orientalis

49
Q

what are the risk factors for developing clinical visceral leishmaniasis *

A

malnutrition, immunosuppresive drugs, HIV co-infections

usually ypung men have it - come to an area where there is visceral leishmaniasis endemic and havent been exposed

50
Q

how do you assess visceral leishmaniasis

A

look at spleen and liver size and the parasite load in bone marrow and spleen - how many in the macrophages

diagnosis is aspiration of the spleen and looking at the parasites but this is a complicated technique

clinical diagnosis based on definition - no rapid test so people think that it is malaria - “a person who presents with fever of more than two weeks and enlarged spleen (splenomegaly) and/or enlarged lymph node (lymphadenopathy) or either of weight loss, anaemia or leucopenia while living in a known VL endemic area or having travelled to an endemic area”.

detecting Ag is a problem because it cross reacts with malaria and HIV, also could have had previous infection and might have malaria now not this

lab investigations - visualisation of the amastigote form of the parasite by microscopic examination of aspirates from lymph nodes, bone marrow or spleen - need specialist probe

Ag detection - Direct agglutination test (DAT) and rK39 chromatographic test

people have low WBC, platelet count and are anaemic

51
Q

what is the treatment of visceral leishmaniasis

A

in Africa - sodium stibogluconate and paromomycin for 17days - have a lot of SE - often the reason for the death, people are too ill with renal and liver problems that are made worse

in india - 1 shot of AmBisome, works well because there is a lot of awareness of the disease so people present early

52
Q

describe post kala-azar dermal leishmaniasis *

A

frequent in sudan and india - in 55% of pts in sudan, 5-10% in india

occurs during or after treatment, after sub-clinical infection

lesions start on face usuallly around the mouth - become nodular

can spread to trunk and limbs

difficult to treat because there is a lot of parasite in the lesion - this is a problem for transmission

53
Q

describe localised cutaneous leishmaniasis *

A

skin lesions on exposed body parts - often self healing

can create serious disability and scars

give immunity to reinfection

L tropica - crusted ulcer, L major - multiple crusted lesions

large irregular ulcer, surrounded by papular and crusted lesions which all contain parasites, crust can fall off - can be wet before you get ulcer

leaves scars

54
Q

describe diffuse cutaneous leishmaniasis *

A

disseminated lesions, resembles leprosy - multiple nondular non-ulcerating lesions that are full of parasites = difficult to treat

no spontaneous healing

frequent relapses

L aethiopica

stigma because look like leprosy - people think leprosy is transmitted in childbirth so women with it are oestrasised from society - so take baby girls and expose bottom so that they can develop immunity and not develop it on their face

treatment makes it a bit better

55
Q

describe mucocutaneous leishmaniasis *

A

Mucocutaneous (L. braziliensis/panamensis)/mucosal (L. infantum, major, tropica, aethiopica)

disfiguring and destroys mucus membranes around mouth and nose and eyes

56
Q

epidemiology of cutaneous leishmaniasis

A

in ethiopia - mainly in the highlands

annual burden - 20000 to 30000 cases - rough estimation

57
Q

vectors of cutaneous leishmaniasis

A

p longipes

p pedifer

p sergenti

p saevus

p duboscqi

58
Q

diagnosis of cutaneous leishmaniasis

A

clinical diagnosis

parasitological diagnosis that involves microscopy/culture - fine needles aspiration, dermal scraping, biopsy

leishman skin test

serology

PCR

59
Q

treatment for cutaneous leishmaniasis

A
  •  Systemic treatment with Sodium Stibogluconate (SSG) or Glucantime
  •  Intra-lesion administration of SSG

cryotherapy

miltefosine (compassionate)

60
Q

describe HIV and leishmaniasis co-infections *

A

they causes each other to multiply - problem for treatment

in europe 70% cases of VL are associated with HIV

ART reduces incidence of VL, relapse rates, prolongues the interval between prolapse rates, improved survival

in brazil - there is high parasite load, parasite dissemination to unusual sites, lower cure rates, greater suseptibility to drug toxicity, increased drug resistance, higher rates of death, higehr rates of relapse

ethiopia carries highest burden of HIV-VL co-infection = high rates of relapse and high rates of mortality

• HIV infection can lead to reactivation of latent Leishmania infection or to symptomatic VL at initial infection - after 2nd relapse difficult to control viral load so die

 100-1000 x greater risk for HIV+ individuals to develop the disease as compared to HIV- individuals

VL increases the onset of AIDS - increased HIV replication and cumulative immunosuppression

61
Q

why is combination of HIV and VL occuring

A

mainly in young men

there are areas where there is endemic VL - people come and farm who havent been exposed

the areas act like little cities so have a lot of HIV, then these people contract VL

microbiology year 2 (9 decks)

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