Protozoa and Malaria Flashcards
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
Free living amoebae - examples, clinical features
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
