Week 9 ,, Protozoa Part 2

Cardiovascular System Infection

Malaria, Babebiosis, and Trypanosomiasis

Skin and Mucous Membrane Infection

Leishmania

Central Nervous System Infection

Toxoplasmosis

Malaria Causal Agent

Plasmodium spp.

Malaria Vector

Anopheles gambiae (mosquitoes)

Plasmodium falciparum

Most deadly and most common in hot, tropical regions

Plasmodium vivax

Most frequent worldwide ,, Common in cool tropical areas

Plasmodium malariae

Less common ,, Most widely distributed

Plasmodium ovale

Rare

Plasmodium spp. Definitive Host

Anopheles gambiae (mosquitoes)

Plasmodium spp. Intermediate Host

Humans

Plasmodium spp. Diagnostic Stage

Immature/mature trophozoites, schizont, and gametocytes

Plasmodium spp. Infective Stage

Ruptured oocyst releases sporozoites and the vector takes a blood meal (injection of sporozoites)

Plasmodium spp. Clinical Features

May be rapidly fatal if untreated ,, Fever and chills, myalgias, weakness, vomiting, and diarrhea ,, Splenomegaly, anemia, thrombocytopenia, hypoglycemia, pulmonary or renal dysfunction, and neurological changes

Plasmodium spp. Laboratory Diagnosis

Microscopic identification in Giemsa-stained blood smears is the method most frequently used to demonstrate an active infection

Female Gametocytes of P. falciparum

Deep blue cytoplasm

Male Gametocytes of P. falciparum

Redish cytoplasm

Identify the Protozoa

Plasmodium spp. ring-form trophozoites

Identify the Protozoa

Plasmodium spp. schizones

Identify the Protozoa

Plasmodium spp. gametocytes

Identify the Plasmodium Species 1

P. falciparum

Identify the Plasmodium Species 2

P. malariae

Identify the Plasmodium Species 3

P. vivax

Identify the Plasmodium Species 4

P. ovale

Babebiosis Causative Agent

Babesia spp.

Babesia microti Reservior

Rodents

Babesia microti Geographical Distribution

Worldwide ,, Most frequently identified in the US

Babesia divergens Reservior

Cattle

Babesia divergens Geographical Distribution

Most frequently identified in Europe

Babesia spp. Vector

Borrelia burgdorferi (ticks)

Babesia spp. Infective Stage

Ruptured oocyst releases sporozoites and the vector takes a blood meal (injection of sporozoites)

Babesia spp. Diagnostic Stage

Trophozoites

Babesia spp. Clinical Features

Mostly asymptomatic ,, B. divergens infection is more severe than B. microti ,, Fever, chills, sweating, myalgias, fatigue, hepatosplenomegaly, and hemolytic anemia ,, More severe in patients who are immunosuppressed, splenectomized, and/or elderly

Babesia spp. Laboratory Diagnsosis

Identification of the parasite inside RBC is the method most frequently used to demonstrate infection ,, Ring-form can be vacuolated ,, Intra-erythrocytic forms ,, Clumps of extracellular forms are indicative of parasite ,, Tetrad

Trypanosomiasis Causative Agent

Trypanosoma brucei and Trypanosoma cruzi

African Trypanosomiasis

Trypanosoma brucei

American Trypanosomiasis

Trypanosoma cruzi

What is African Trypanosomiasis also called?

Sleeping sickness

Trypanosoma brucei Vector

Tsetse flies

Trypanosoma brucei Infective Stage

Vector takes a blood meal and injects metacyclic trypomastigotes into the host

Trypanosoma brucei Diagnostic Stage

Trypomastigotes in the blood

Trypanosoma brucei Clincial Features

1. Development of trypanosomal chancre at the site of inoculation ,, 2. Hemolymphatic stage (fever, pruritus, lymphadenopathy) ,, 3. Meningoencephalitic stage (invasion of the central nervous system with headaches, somnolence, abnormal behavior, and leads to the loss of consciousness and coma)

Trypanosoma brucei Laboratory Diagnosis

Microscopic identification of chancre fluid, lymph node aspirates ,, blood and bone marrow, and the cerebrospinal fluid ,, Trypomastigotes are the only stage found in patients

What is American Trypanosomiasis also known as?

Chagas’ disease

Trypanosoma cruzi Vector

Triatomine bugs

Trypanosoma cruzi Infective Stage

Vector takes a blood meal and passes metacyclic trypomastigotes in feces ,, Trypomastigotes enter the bite wound or mucosal membrane

Trypanosoma cruzi Diagnostic Stage

Intracellular amastigotes transform into tyrpomastigotes that then burst out of the cell and enter the bloodstream

Trypanosoma cruzi Clincial Features

Romaña's sign (periocular swelling) ,, Chronic form can manifest as cardiomyopathy and pathologies of the digestive tract and weight loss ,, Complications of chronic Chagas disease can be fatal

Trypanosoma cruzi Laboratory Diagnosis

Microscopic examination of motile parasites in fresh anticoagulated blood (or its buffy coat) or of parasites in thin and thick blood smears stained with Giemsa

Identify the Protozoa

Trypanosoma spp.

Identify the Protozoa

Trypanosoma spp.

Identify the Protozoa

Trypanosoma spp.

Leishmaniasis spp. Vector

Sand flies

Leishmaniasis spp. Diagnostic Stage

Promastigotes transform into amastigotes inside macrophages ,, Amastigotes multiply in cells of various tissues

Leishmaniasis spp. Infective Stage

Vector takes a blood meal and injects promastigotes into the skin

Leishmaniasis spp. Laboratory Diagnosis

Microscopic examination of Giemsa-stianed slides of the relevant tissue is the method most frequently used to detect the parasite

Identify the Protozoa

Leishmaniasis spp.

Cutaneous Leishmaniasis

One or more cutaneous lesions that can change shape (volcano, with a raised edge
and central crater) ,, Swollen glands near the sores

Visceral Leishmaniasis

Fever, weight loss, an enlarged spleen and liver, and swollen glands ,, Anemia, neutropenia, and thrombocytopenia ,, Sometimes post kala-azar dermal leishmaniasis

Toxoplasmosis Causative Agent

Toxoplasma gondii

Toxoplasma gondii Definitive Hosts

Cats

Toxoplasma gondii Infective Stage

Fecal oocysts and tissue cysts

Toxoplasma gondii Diagnostic Stage

CSF serum

Toxoplasma gondii Laboratory Diagnosis

Observation of parasites in patient specimens, such as bronchoalveolar lavage material
from immunocompromised patients, or lymph node biopsy ,, Serologic testing is the routine method of diagnosis

Congenital Toxoplasmosis

Severity vary with the trimester during which infection was acquired ,, Patients are often
asymptomatic until the second or third decade of life, when lesions develop in the eye ,, Most infants will develop ocular infection

Identify the Protozoa

Toxoplasma gondii tachyzoites