Protozoa and Malaria Flashcards
(25 cards)
Broad classifications of parasites
Protozoa
Helminths
Ectoparasites
Protozoa
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)
Intestinal protozoa
Entamoeba histolytica Giardia duodenalis Trichomonas vaginalis Cryptosporidium Cycloisospora, cyclospora (know these exist)
Entamoeba histolytica: source, transmission, notifiable?, clinical presentation, complications
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
Entamoeba histolytica: life cycle, cysts and trophozoites
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
Entamoeba histolytica: diagnosis
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
Entamoeba histolytica: treatment
Systemic treatment followed by luminal agent for cases of diarrhoea/dystentery and extra-intestinal infection
METRONIDAZOLE PO or Tinidazole
+
PARONOMYCIN (to prevent relapse)
Giardia duodenalis - source, transmission, clinical presentation, diagnosis, treatment
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)
Cryptosporidium - source, clinical presentations, diagnosis, treatment
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
Microsporidia - clinical presentations, diagnosis
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
Trichomonas vaginalis - source, transmission, clinical presentation, diagnosis, treatment
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
Blood and tissue protozoa
**Plasmodium Babesia Trypanosomiasis **Toxoplasma Leischmaniasis
Malaria - importance of clinical suspicion
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
Malaria: life cycle
Transmission by female Anopheles mosquitoes
- 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 - 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
Plasmodium Falciparum - resistance to drugs, incubation period, clinical manifestations
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
Non falciparum malaria - types, associated features
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
Malaria: investigations
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
Malarial: Management, Treatment, Prophylaxis
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
Babesia
Looks like malaria
“maltese cross”
Trypanosomiasis (no need details)
American type –
Acute - palpebral and periocular swelling, chagoma
Chronic - Chagas disease (cardiomyopathy) - can be fatal
African type – sleeping sickness
Toxoplasma gondii: source, transmission, infective risk of faecal oocysts
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)
Toxoplasmosis: clinical features, diagnosis
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)
Congenital Toxoplasmosis - clinical features, diagnosis, treatment
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
Leischmaniasis (just know it exists)
Sandfly
India, bangladesh, nepal, sudan, brazil
Kala-azar (visceral disease)
- massive hepatosplenomegaly
Diagnosis:
- giemsa stained slides for amastigotes lining walls of vacuoles
