CRACKCast E133 – Parasitic Infections

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This episode of CRACKCast covers Rosen’s Chapter 125, Parasitic Infections. This episode will give you the tools to adequately investigate the peculiar parasitic infections that present in patients coming to the ED. In an age where physicians are increasingly exposed to international travelers and immigrant/refugee populations, knowing this content is absolutely essential.


Shownotes – PDF Here

[1] Describe the life-cycle of malaria and list 4 common types

There are four stages in the life-cycle of the malaria parasite:

Stage 1 – Mosquito Stage: Female anopheles takes blood meal and injects parasite into blood

Stage 2 – Human Liver Stage: liver cells infected, then rupture

Stage 3 –  Human Blood Stage: RBCs infected, then rupture

Stage 4 – Sexual stage: Female anopheles takes another blood meals and ingests parasite

There are four major types of malaria and one rare type:

  • Plasmodium Falciparum (deadly)
  • Plasmodium Malarie
  • Plasmodium Ovale (recurrent)
  • Vivax (recurrent)
  • *** 5th type*** plasmodium knowlesi (primates to humans)

[2] Describe clinical features of  malarial infection.  What is unique to each type?

With malarial infection, it is all about the FEVER!

  • Early with malaria infection, febrile paroxysms occur at irregular intervals throughout day
  • Later in infection febrile paroxysms become regular
    • When you see febrile paroxysms every other day, think about the following types of malaria:
      • P.vivax
      • P.ovale
      • P.falciparum
    • If the fevers occur every third day, think:
      • P. malariae
    • If an individual experiences seizures as a result of their infection, they are likely to be infected with P. falciprum
      • Seizures may herald CEREBRAL MALARIA
      • Watch for in febrile seizures in pediatric patients infected with any of the species
      • Non-immune patients can have temps above 40ºC leading to tachycardia complicated by febrile delirium

There are two major forms of malarial infection: uncomplicated and severe

Uncomplicated Malaria:

  • The patient will have symptoms of malaria
  • The patient will have positive parasitological test
  • The patient will NOT have signs of severe malaria

Severe Malaria (Think Falciprum >>>> Vivax):

  • Risk factors:
    • Non-immune individuals
    • Immunocompromised patients (including asplenic individuals)
    • Children 6 to 36 months of age
    • Pregnant women
  • Features:
    • CNS: Altered consciousness, (+/- meningismus) seizures, focal deficits (cerebral malaria)
    • GI: Vomiting, jaundice
    • RESP: Respiratory distress +/- ARDS
    • RENAL: AKI
    • CVS: Shock
    • HAEM: Severe hemolytic anemia with jaundice, coagulopathies and spontaneous hemorrhage
    • METABOLIC: acidosis and hypoglycemia
    • HIGH PARASITE LOAD: >2% RBCs infected or >100,000 parasites/mm3

For an excellent summary of malaria, its pathophysiology, and its treatment, check out the LITFL post: https://lifeinthefastlane.com/ccc/malaria/

Remember, the pathophysiology of malarial infection is the result of CYTOADHERENCE:

  • AKA: parasitized (and non-parasitized) red cells adhering to small vessels causing infarcts, capillary leakage, and organ dysfunction

This process of cytoadherence and tissue damage results in the following complications:

Cerebral Malaria:

  • Presentation:
    • Encephalopathy with impaired consciousness
    • Delirium
    • Seizures
  • Risk Factors:
    • Children and older adults
    • Pregnancy
    • Poor nutritional status
    • HIV infection
    • Host genetic susceptibility
    • History of splenectomy

Always remember the differential for malaria:

Differential Diagnosis for Malaria:

  • Leptospirosis
  • Pneumonia
  • Typhoid fever
  • Hemorrhagic fever
  • Sepsis due to bacteremia
  • Dengue fever
  • Chikungunya
  • Meningitis

[3] Describe the diagnosis and treatment of acute malarial infection

Diagnosis of Acute Malarial Infections:

There are two tests that we use for the diagnosis of acute malarial infections:

  1. Thick & thin films for microscopy (1-3 Q12hrs Gold standard)
  2. Malaria rapid Antigen (sample in febrile stage) test

***NOTE***: If slides are negative on your first attempt, repeat testing every 24 hours for 3 days

Treatment of Acute Malarial Infections:

Uncomplicated:

  • PO quinine + doxycycline
  • PO chloroquine (watch for resistance)

***NOTE***: Chloroquine -sensitive regions: Central America & Middle East

Complicated:

  • IV artesunate OR
  • IV quinine + doxycycline

[4] List 7 complications of malaria

There are a number of complications related to malarial infection. There are seven of the most important listed below:

Complications of Malarial Infections:

  • Cerebral Malaria
  • Hypoglycemia
  • Metabolic Acidosis
  • ATN
  • ARDS
  • DIC
  • Black-water fever

[5] What is black-water fever?

Black-water Fever:

  • Black-water Fever is a result of the hemolytic anemia caused by malarial infection. As red cells burst, hemoglobinuria occurs, causing the urine to take on a dark appearance.
  • This is often accompanied by the typical fevers, chills, and rigors of malarial infection, but is also accompanied by jaundice, profound fast-onset anemia, and vomiting.

***NOTE***: Black-water fever is not to be confused with the nephrotic syndrome caused by P. malariae infection. These are two completely different processes.

[6] What is Babesiosis?  What is its vector and how does it present?

Babesiosis:

  • Definition:
    • Babesiosis is a tickborne disease that is like malaria, that is characterized by acute febrile illness tickborne
  • Causative Agent:
    • Babesiosis is caused by an intraerythrocytic protozoal parasite of the genus Babesia
  • Vector:
    • The vector for babesiosis is the Ixodes tick, largely found on deer and mice, cattle.
  • Clinical Presentation :
    • Incubation period of 1 to 4 weeks after tick exposure, followed by non-specific influenza-like illness, with fever, chills, headache, fatigue, and anorexia.
    • Unlike Lyme disease, rash is not a major feature; however, if you see erythema figuratum, consider septic babesiosis.
    • Asplenic patients can get hypotension, severe hemolytic anemia, hemoglobinuria, jaundice, renal insufficiency, ARDS, DIC.
    • Think about this in endemic areas as a cause of post-transfusion infection.

[7]  Describe the features of American Trypanosomiasis and African Trypanosomiasis

American Trypanosomiasis (Chagas Disease):

  • Causative Agent:
    • Trypanosomiasis Cruzi
  • Endemic Region:
    • South America
  • Vector:
    • Reduviidae bug (Assassin/Kissing Bug)
  • Clinical Presentation:
    • Romana sign – swelling of the ipsilateral eye and eyelid to the bite from inadvertent spreading of infected bug feces into the eye
  • Complications:
    • Myocarditis
    • Dilated Cardiomyopathy
    • Meningo-Encephalitis (can be chronic)
  • Treatment:
    • Nifurtimox / Benznidazole

African Trypanosomiasis (African Sleeping Sickness):

  • Causative Agent
    • Trypanosomiasis Brucei
  • Endemic Region:
    • Africa
  • Vector:
    • TseTse fly
  • Clinical Presentation:
    • Extreme sleepiness + coma
  • Treatment:
    • Suramin

[8] List 6 common illnesses causing fever in the returning traveler and 5 life-threatening infections

Remember, this list will change depending on where the traveler is returning from! That detailed history is crucial.

Common illnesses:

  • Dengue fever
  • Chikungunya
  • Meningitis
  • Pneumonia
  • Sepsis due to bacteremia
  • Typhoid fever
  • Leptospirosis
  • Viral hemorrhagic fever

Life-threatening infections:

  • Secondary bacterial infection / sepsis
  • Emerging viral illness – e.g. Ebola, MERS CoV,
  • HIV
  • Cerebral malaria

[9] Other than malaria, list 3 other organisms that cause the following:

CNS infection:

  • Neurocysticercosis
  • Echinococcus (hydatid cysts)
  • African Trypanosomiasis (sleeping sickness)
  • Trichinella spiralis

Anemia:

  • Helminthic infections (with concomitant eosinophilia)
  • Babesiosis
  • Whipworm
  • Hookworm
  • Tapeworms / flatworm / fluke

Pulmonary Symptoms:

  • E. histolytica (pleural effusions)
  • PCP aka PJP (think HIV)
  • Löffler’s syndrome (roundworm / hookworm / threadworm) pneumonia w/ eosinophilia
  • Strongyloides (think lung infections with Aortitis)

[10] List the most common organism causing the following:

Peripheral edema:

  • Elephantiasis

Dermatologic symptoms:

  • Leishmaniasis

Visual symptoms:

  • Onchocerciasis river blindness

CV symptoms:

  • Chagas Disease aka Trypanosoma cruzi causing myocarditis

[11] List 5 common GI parasites and their typical manifestations

Diarrhea:

  • Cryptosporidium and Cyclospora
  • E. histolytica
  • Giardia
  • Schistosomiasis

Abdominal pain:

  • Tropical appendicitis: ITS A THING! Think = enterobiasis, amebiasis, ascariasis, trichuriasis, and taeniasis
  • A. lumbricoides (roundworm)
  • Strongyloides
  • E. histolytica (can mimic viral hepatitis)

WiseCracks:

 [1] Classic rounds pimper: quick association of parasite and treatment

 

Parasite:

Treatment:

Entamoeba Histolytica Flagyl
Giardia Flagyl
Leishmaniasis Amphotericin B
Schistosomiasis Praziquantel
Trypanosoma Cruzi Nifurtimax / Benznidazole
Neurocysticercosis Albenazole
Pinworm Albenadzole / mobendazole

[2] A 32 year-old male has returned from a BBQ tour of South America. He is now actively seizing. What does he have and how can we diagnose it without a CT scanner?

Diagnosis:

  • Neurocysticercosis
  • Think about it in patients exposed to undercooked pork and seizures

Diagnostic Modality:

  • Obviously, CT scan is the gold standard for diagnosis of neurocysticercosis, however, you can use a soft tissue radiograph looking for typical soft tissue calcifications

[3] What are kissing bugs?

Whenever you hear the term “kissing bugs”, think Chagas Disease. The kissing bug or Reduviid bug is the vector for Chagas disease. Its bite is the cause of the Romaña’s sign (painless unilateral periorbital edema). If you see Romaña’s sign, it is pathognomonic for Chagas Disease.

 

This post was copyedited and posted by Dillan Radomske.

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Adam Thomas

Adam Thomas

CRACKCast Co-founder and newly minted FRCPC emergency physician from the University of British Columbia. Currently spending his days between a fellowship in critical care and making sure his toddler survives past age 5.
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Justin Roos

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Justin Roos is an emergency medicine resident at the University of British Columbia. His interests include mountain and wilderness medicine. He is a contributor to the CrackCast podcast.
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