Protozoa and Malaria Flashcards

1
Q

Broad classifications of parasites

A

Protozoa
Helminths
Ectoparasites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Protozoa

A

Eukaryotic unicellular organisms that have organelles

Can be divided into amoebae, flagellates, sporozoans, coccidia, ciliates

Most important pathogens:

  • entamoeba (intestinal)
  • cryptosporidium (intestinal)
  • plasmodium and toxoplasma (blood and tissue)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Intestinal protozoa

A
Entamoeba histolytica
Giardia duodenalis
Trichomonas vaginalis
Cryptosporidium
Cycloisospora, cyclospora (know these exist)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Entamoeba histolytica: source, transmission, notifiable?, clinical presentation, complications

A

Worldwide
Source: fresh water contaminated with human faeces
Transmission: faecal oral route
NOTIFIABLE DISEASE

Clinical presentation:

  • 2-4 wks incubation
  • 80-90% asymptomatic (restricted to lumen of intestine – luminal amoebiasis)
  • amoebic colitis (invasive intestinal amoebiasis – AMOEBIC DYSENTERY which mimics ulcerative colitis)
  • extra-intestinal manifestations e.g. amoebic liver abscess (right lobe of liver more common), pleuropulmonary/brain abscess (very rare)

Complications in severe infection:
- peritonitis, perforations, amoebic granulomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Entamoeba histolytica: life cycle, cysts and trophozoites

A

Cysts and trophozoites passed in faeces –> mature cysts ingested via contamination –> excystation in small intestine –> trophozoites migrate to large intestine where it remains in colon, invades intestinal mucosa or invades blood vessels –> multiplication by binary fission

Cysts (12-15 mcm) typically found in FORMED STOOL, can survive days to wks in external environment and remain infectious

Trophozoites (15-20 mcm) typically in DIARRHOEAL STOOL and rapidly destroyed once outside the body (30 min).
- not infective as it would not survive gastric env if ingested

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Entamoeba histolytica: diagnosis

A

Stool:

  • RBC, WBC present
  • active trophozoite (HOT STOOL i.e. immediate sample)
  • direct wet mount (INGESTION OF RBC BY TROPHOZOITES IS DIAGNOSTIC)
  • special stains e.g. PARA stain or trichrome

Liver abscess aspirate

  • low yield
  • PCR, Ag detection
  • microscopy and culture to exclude bacterial

Serology test
- Ab detection for invasive amoebiasis/ extra-intestinal cases

Tissue biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Entamoeba histolytica: treatment

A

Systemic treatment followed by luminal agent for cases of diarrhoea/dystentery and extra-intestinal infection

METRONIDAZOLE PO or Tinidazole
+
PARONOMYCIN (to prevent relapse)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Giardia duodenalis - source, transmission, clinical presentation, diagnosis, treatment

A

Source: soil, food, contaminated water with infected faeces
Transmission: faecal-oral route, mainly water-borne infection

Infection duodenum, ileum –> WATERY DIARRHOEA

Diagnosis:

  • Stool direct microscopy using simple counterstain –> visualise cysts and trophozoites; “falling leaf” movement in wet mount, characteristic “face”
  • Immunoassay, PCR
  • Duodenal aspirate direct microscopy for trophozoites

Treatment:

  • Tinidazole PO single dose
    (alternatives: metronidazole)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Cryptosporidium - source, clinical presentations, diagnosis, treatment

A

Worldwide
Many species: C. hominis, C. parvum
Outer shell very tolerant to chlorine disinfection
One of the commonest and serious cause of WATERBORNE DIARRHOEA

Clinical presentations:

  • immunocompetent: 7-10 days incubation, acute watery diarrhoea, self-limiting (1-2 wks)
  • AIDS: transient infection (1 month), chronic diarrhoea lasting for >2 months (60%) or fulminant infection for >2L watery diarrhoea/day (10%)

Diagnosis:

  • Stool for MODIFIED ACID-FAST STAIN –> oocytes 4-6 mcm (difficult to see on wet mount)
  • Ag detection, PCR

Treatment: Nitazoxanide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Microsporidia - clinical presentations, diagnosis

A

Not commonly diagnosed due to low suspicion

  • obligate eukaryotic intracellular parasites closely related to fungi
  • production of RESISTANT SPORES

Clinical presentation:

  • gastroenteritis (MC)
  • CNS encephalitis
  • OCULAR INFECTIONS (punctate KERATOPATHY and conjunctivitis)

Diagnosis:

  • special stain: CHROMOTROPE 2R –> stain spore and spore wall bright pinkish red
  • transmission electron microscopy as gold standard which is necessary for diagnosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Trichomonas vaginalis - source, transmission, clinical presentation, diagnosis, treatment

A
Pear-shaped trophozoite
Jerking or twitching movement
Source: humans (infect humans only)
Transmission: direct contact (STD)
No cyst stage

Clinical presentation

  • 30% symptomatic
  • female: vaginitis - copious foamy discharge, purulent, malodorous
  • male: commonly asymptomatic, urethritis
  • increases risk of STDs

Complications:
- pregnancy: increase risk of preterm delivery, prematurity and low birth weight

Diagnosis:
- vaginal/urethra/prostatic secretions –> direct microscopy (wet mount), PCR

Treatment:

  • Tinidazole PO
  • Metronidazole PO
  • treat all sexual partners
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Blood and tissue protozoa

A
**Plasmodium
Babesia
Trypanosomiasis
**Toxoplasma 
Leischmaniasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Malaria - importance of clinical suspicion

A

Late recognition in a febrile patient can lead to mortality - MUST ALWAYS ASK TRAVEL HISTORY AND CONSIDER IF RETURNING FROM ENDEMIC REGION e.g. subsaharan africa, india

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Malaria: life cycle

A

Transmission by female Anopheles mosquitoes

  1. Liver stage
    Mosquito bite –> inject SPOROZOITES –> infect liver cell –> form SCHIZONT in hepatocytes (i.e. cell full of mature merozoites) –> ruptured schizont kills host cells and releases MEROZOITES
  2. Blood stage (symptomatic)
    Merozoites infect RBC –> morph into immature TROPHOZOITES (ring form) –> multiply in RBC to become mature (compact)
    ==> either form schizont - rupture - haemolysis
    or
    ==> if body condition not favourable for parasite to survive, sexual reproduction –> GAMETOCYTES which are infective to mosquitoes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Plasmodium Falciparum - resistance to drugs, incubation period, clinical manifestations

A

Most severe form
Chloroquine resistant cases are widespread, mefloquine resistance also found in some areas of SE Asia and Africa

Incubation period: 12-14 days
- longer in semi-immune individuals or those with ineffective malaria prophylaxis

Tertian/Quartan fever if not treated promptly

Clinical manifestations

  • UNCOMPLICATED malaria (tolerate oral medication, no sx of severe malaria)
  • -> non-specific flu like illness, palpable spleen, mild jaundice
  • SEVERE malaria (if untreated mild form)
  • -> RBC adhering to small blood vessels to cause small infarcts, leakage and organ dysfunction
  • -> cerebral (fits, coma), metabolic acidosis, anaemia (haemolysis), coagulopathy, shock, hypoglycaemia, AKI, liver failure, pulmonary oedema, ARDS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Non falciparum malaria - types, associated features

A

P. vivax, P. ovale (less severe)

  • 2 wks incubation
  • delayed presentation after infection due to activation of residual HYPNOZOITES in liver
  • relapse within 2-3 yrs of infection

P.malariae (milder)

  • 18 days incubation
  • can be dormant for yrs

P. knowlesi

  • nonhuman primate malaria (monkey)
  • resembles P. malariae
17
Q

Malaria: investigations

A

Standard:

  • URGENT thick and thin blood smears (Giemsa stain)
  • repeat every 12-24 hrs if strong suspicion

==THICK smear for SCREENING (more concentrated parasites)
== THIN smear for SPECIATION and assessing TREATMENT RESPONSE (% parasitaemia)

Other tests:

  • Immunochromatographic RDT (ParaSightF - detect specific Ag or enzymes followed by microscopy for confirmation)
  • Fluorescence dye
  • PCR
18
Q

Malarial: Management, Treatment, Prophylaxis

A

PROMPT anti-malarial chemotherapy
Monitor blood smears for parasites on regular basis
Treat hypoglycaemia and shock
Avoid sedation and steroid
Close monitoring of hydration, electrolytes, glucose, BP, urine output

Treatment:

  • Complicated case - Artesunate IV/Quininine IV + doxycycline
  • Without major organ dysfunction: Coartem PO + primaquine
  • Pregnancy: Quininine + clindamycin
  • Non-falciparum: Chloroquine

Prophylaxis:

  • different from treatment, give based on resistance
  • Chloroquine –> mefloquine –> doxycycline
19
Q

Babesia

A

Looks like malaria

“maltese cross”

20
Q

Trypanosomiasis (no need details)

A

American type –
Acute - palpebral and periocular swelling, chagoma

Chronic - Chagas disease (cardiomyopathy) - can be fatal

African type – sleeping sickness

21
Q

Toxoplasma gondii: source, transmission, infective risk of faecal oocysts

A

Single celled, obligate intracellular parasite
Worldwide
Definitive host: felines (ingest rodents/bird to become infected)

Human infection route:

  • FOODBORNE (sporocysts from cat faeces contaminating soil or vegetables; tissue cyst from undercooked meats)
  • CONGENITAL (mother to child)
  • Organ transplantation, transfusion

Faecal oocysts usually only shed for 1-3 wks in large number
– oocysts take 1-5 days to sporulate in the environment and become infective
(transmission risk is low if there is proper hygiene or if cat is indoors)

22
Q

Toxoplasmosis: clinical features, diagnosis

A

Clinical features:

  • immunocompetent - acute, self-limiting disease with flu-like/IM symptoms
  • immunocompromised - encephalitis, extra-cerebral e.g. pneumonitis, chorioretinitis

Diagnosis:

  • immunocompetent - serology IgG and IgM
  • immunocompromised and AIDS - serology, direct detection by histology (biopsy) or PCR (CSF)
23
Q

Congenital Toxoplasmosis - clinical features, diagnosis, treatment

A

Clinical features:

  • varies based on stage of gestation in which infection occured (more severe if earlier infection)
  • subclinical infection (70-90%)
  • classical triad (<10%): chorioretinitis, hydrcephalus, intracranial calcifications

Diagnosis:

  • prenatal - foetal blood/amniotic fluid for PCR; USG
  • postnatal - eye examination, maternal and newborn serology

Treatment:
- differs for different stages of diagnosis

24
Q

Leischmaniasis (just know it exists)

A

Sandfly
India, bangladesh, nepal, sudan, brazil

Kala-azar (visceral disease)
- massive hepatosplenomegaly

Diagnosis:
- giemsa stained slides for amastigotes lining walls of vacuoles

25
Q

Free living amoebae - examples, clinical features

A

Naegleri fowleri

  • primary amoebic meningoencephalitis
  • source: fresh water lakes in S. america/Africa
  • invade through nasal cavity into CNS

Acanthamoeba castellani

  • granulomatous amoebic encephalitis
  • keratitis
  • corneal biopsy with trophozoites