1. Parasitology (Protozoa)
READING: Medical Microbiology chapters
Parasitology
(Protozoa)
Study Objectives
From the selected protozoan parasites, recall the basic physiology and morphology, pathogenesis, life cycle and transmission and host immune response (if given) and treatment (if given).
Gastrointestinal and Genitourinary protozoans:
Entamoeba histolytica
Giardia lamblia
Cryptosporidium spp.
Trichomonas vaginalis
Blood and Tissue protozoans:
Babesia microti and B. divergens
Toxoplasma gondii
Plasmodium falciparum, P. vivax, P. ovale, P. malariae
Leishmania donovani, L.tropica, L. braziliensis
Trypanosoma brucei gambiense, T. b. rhodesiense
Trypanosoma cruzi
Randal K. Gregg, PhD

2. Entamoeba histolytica
ZOONOTIC
Life Cycle
Amebiasis (& Amebic Dysentery)
Transmission
Fecal-oral
Ingestion of cysts in contaminated water, food and direct transmission by hands
Less common – anal sex practices
Trophs released in s. intestine  migrate to Colon  self-limiting diarrhea or asymptomatic (~90%)
Trophs susceptible to stomach acid & dessication
Trophs  invade Mucosa  colitis (~10%)
Trophs  invade Blood  liver, lung or brain abscess (<1%)
Trophs encysts  Cysts (near end of diarrhea)
Cysts and trophozoites are passed in feces [1]. Cysts are typically found in formed stool, whereas trophozoites are typically found in diarrheal stool. Infection by Entamoeba histolytica occurs by ingestion of mature cysts [2] in fecally contaminated food, water, or hands. Excystation [3] occurs in the small intestine and trophozoites [4] are released, which migrate to the large intestine. The trophozoites multiply by binary fission and produce cysts [5], and both stages are passed in the feces [1]. Because of the protection conferred by their walls, the cysts can survive days to weeks in the external environment and are responsible for transmission. Trophozoites passed in the stool are rapidly destroyed once outside the body, and if ingested would not survive exposure to the gastric environment. In many cases, the trophozoites remain confined to the intestinal lumen ([A]: noninvasive infection) of individuals who are asymptomatic carriers, passing cysts in their stool. In some patients the trophozoites invade the intestinal mucosa ([B]: intestinal disease), or, through the bloodstream, extraintestinal sites such as the liver, brain, and lungs ([C]: extraintestinal disease), with resultant pathologic manifestations. It has been established that the invasive and noninvasive forms represent two separate species, respectively E. histolytica and E. dispar. These two species are morphologically indistinguishable unless E. histolytica is observed with ingested red blood cells (erythrophagocystosis). Transmission can also occur through exposure to fecal matter during sexual contact (in which case not only cysts, but also trophozoites could prove infective).
Information and image courtesy of: Centers for Disease Control

3. Giardia lamblia Life Cycle Giardiasis AKA Giardia intestinalis
ZOONOTIC
Life Cycle
Giardiasis
AKA Giardia intestinalis
Transmission
Fecal-oral
Ingestion of cysts (~10) in contaminated water, food, and direct transmission by hands
Less common – anal/oral sex
Cysts are susceptible to drying, heating, or prolonged exposure to feces; viable in cold water and chlorine-treated water for months
Flagellated Trophs  remain in S. Intestine  free-living or attach to mucosa  self-limiting diarrhea or asymptomatic
Trophs may be present in severe cases
Cysts are resistant forms and are responsible for transmission of giardiasis. Both cysts and trophozoites can be found in the feces (diagnostic stages) [1]. The cysts are hardy and can survive several months in cold water. Infection occurs by the ingestion of cysts in contaminated water, food, or by the fecal-oral route (hands or fomites) [2]. In the small intestine, excystation releases trophozoites (each cyst produces two trophozoites) [3]. Trophozoites multiply by longitudinal binary fission, remaining in the lumen of the proximal small bowel where they can be free or attached to the mucosa by a ventral sucking disk [4]. Encystation occurs as the parasites transit toward the colon. The cyst is the stage found most commonly in nondiarrheal feces [5]. Because the cysts are infectious when passed in the stool or shortly afterward, person-to-person transmission is possible. While animals are infected with Giardia, their importance as a reservoir is unclear.
Information and image courtesy of: Centers for Disease Control

4. Cryptosporidium spp. Life Cycle Cryptosporidiosis
ZOONOTIC
Life Cycle
Cryptosporidiosis
C. hominis, C. parvum
Transmission
Fecal-oral
Ingestion of oocysts (~100) in contaminated water (drinking & recreation), food and direct transmission by hands
Oocysts resistant to chlorine treatment
Sporulated oocysts, containing 4 sporozoites, are excreted by the infected host through feces and possibly other routes such as respiratory secretions [1]. Transmission of Cryptosporidium parvum and C. hominis occurs mainly through contact with contaminated water (e.g., drinking or recreational water). Occasionally food sources, such as chicken salad, may serve as vehicles for transmission. Many outbreaks in the United States have occurred in waterparks, community swimming pools, and day care centers. Zoonotic and anthroponotic transmission of C. parvum and anthroponotic transmission of C. hominis occur through exposure to infected animals or exposure to water contaminated by feces of infected animals [2]. Following ingestion (and possibly inhalation) by a suitable host [3], excystation [a] occurs.
Information and life cycle courtesy of: Centers for Disease Control

5. Cryptosporidium spp. Life Cycle (S. Intestine) Excystation sporozoite
Following ingestion (and possibly inhalation) by a suitable host [3], excystation [a] occurs. The sporozoites are released and parasitize epithelial cells [b, c] of the gastrointestinal tract or other tissues such as the respiratory tract. In these cells, the parasites undergo asexual multiplication (schizogony or merogony) [d, e, f] and then sexual multiplication (gametogony) producing microgamonts (male) [g] and macrogamonts (female) [h]. Upon fertilization of the macrogamonts by the microgametes [i], oocysts [j, k] develop that sporulate in the infected host. Two different types of oocysts are produced, the thick-walled, which is commonly excreted from the host [j], and the thin-walled oocyst [k], which is primarily involved in autoinfection. Oocysts are infective upon excretion, thus permitting direct and immediate fecal-oral transmission.
Information and life cycle courtesy of: Centers for Disease Control

6. Trichomonas vaginalis
Life Cycle
Trichomoniasis
Transmission
Sexual
Direct transfer during sexual intercourse
Less common – direct contact
Trophs reside in genital tract of females (vulva, vagina, urethra) and urethra/prostate of males
Trichomonas vaginalis resides in the female lower genital tract and the male urethra and prostate [1], where it replicates by binary fission [2]. The parasite does not appear to have a cyst form, and does not survive well in the external environment. Trichomonas vaginalis is transmitted among humans, its only known host, primarily by sexual intercourse [3].
Information and image courtesy of: Centers for Disease Control

7. Babesia microti Life Cycle Babesiosis (or Tick Fever)
VECTOR-BORNE
Life Cycle
Babesiosis (or Tick Fever)
B. microti is agent for disease in US; B. divergens in Europe
Transmission
Bite of Tick
Deer Tick (Ixodes scapularis )
Also called black-legged tick
Nymphs bite humans in spring/early summer
The Babesia microti life cycle involves two hosts, which includes a rodent, primarily the white-footed mouse, Peromyscus leucopus, and a tick in the genus, Ixodes. During a blood meal, a Babesia-infected tick introduces sporozoites into the mouse host [1]. Sporozoites enter erythrocytes and undergo asexual reproduction (budding) [2]. In the blood, some parasites differentiate into male and female gametes although these cannot be distinguished at the light microscope level [3]. The definitive host is the tick. Once ingested by an appropriate tick [4], gametes unite and undergo a sporogonic cycle resulting in sporozoites [5]. Transovarial transmission (also known as vertical, or hereditary, transmission) has been documented for “large” Babesia spp. but not for the “small” babesiae, such as B. microti [A].
Humans enter the cycle when bitten by infected ticks. During a blood meal, a Babesia-infected tick introduces sporozoites into the human host [6]. Sporozoites enter erythrocytes [B] and undergo asexual replication (budding) [7]. Multiplication of the blood stage parasites is responsible for the clinical manifestations of the disease. Humans are, for all practical purposes, dead-end hosts and there is probably little, if any, subsequent transmission that occurs from ticks feeding on infected persons. However, human to human transmission is well recognized to occur through blood transfusions [8].
Information and image courtesy of: Centers for Disease Control

8. Toxoplasma gondii Life Cycle Toxoplasmosis Transmission Fecal-oral
Ingestion of sporulated oocysts or tissue cysts
Humans infected by:
Eating undercooked meat of infected animals
Drinking water or eating food contaminated with cat feces
Changing litter box of infected cat (aerosolized)
Blood transfusion or organ transplant
Mother transmission to fetus
Neural/muscle tissue
Tissue Cyst
(w/ Bradyzoites)
Tachyzoites
(dissemination)
Fecal Oocyst
(w/ Sporozoites)
The only known definitive hosts for Toxoplasma gondii are members of family Felidae (domestic cats and their relatives). Unsporulated oocysts are shed in the cat’s feces [1]. Although oocysts are usually only shed for 1-2 weeks, large numbers may be shed. Oocysts take 1-5 days to sporulate in the environment and become infective. Intermediate hosts in nature (including birds and rodents) become infected after ingesting soil, water or plant material contaminated with oocysts [2]. Oocysts transform into tachyzoites shortly after ingestion. These tachyzoites localize in neural and muscle tissue and develop into tissue cyst bradyzoites [3]. Cats become infected after consuming intermediate hosts harboring tissue cysts [4]. Cats may also become infected directly by ingestion of sporulated oocysts. Animals bred for human consumption and wild game may also become infected with tissue cysts after ingestion of sporulated oocysts in the environment [5].
Humans can become infected by any of several routes:
eating undercooked meat of animals harboring tissue cysts [6].
consuming food or water contaminated with cat feces or by contaminated environmental samples (such as fecal-contaminated soil or changing the litter box of a pet cat) [7].
blood transfusion or organ transplantation [8].
transplacentally from mother to fetus [9].
In the human host, the parasites form tissue cysts, most commonly in skeletal muscle, myocardium, brain, and eyes; these cysts may remain throughout the life of the host. Diagnosis is usually achieved by serology, although tissue cysts may be observed in stained biopsy specimens [10]. Diagnosis of congenital infections can be achieved by detecting T. gondii DNA in amniotic fluid using molecular methods such as PCR [11].
Information and image courtesy of: Centers for Disease Control
1-5 d sporulation

9. Plasmodium spp.
VECTOR-BORNE
Life Cycle (Simplified)
Paroxysm

10. Leishmania spp. Life Cycle Leishmaniasis Transmission Bite of Sandfly
VECTOR-BORNE
ZOONOTIC
Life Cycle
Leishmaniasis
Transmission
Bite of Sandfly
Lutzomyia spp.
L. braziliensis
L. mexicana
Phlebotomus spp.
L. donovani
L. tropica
Can also be transmitted by blood transfusions or sharing of contaminated needles
Dogs and humans represent predominant reservoirs
Lutzomyia
Phlebotomus
Leishmaniasis is transmitted by the bite of infected female phlebotomine sandflies. The sandflies inject the infective stage (i.e., promastigotes) from their proboscis during blood meals [1]. Promastigotes that reach the puncture wound are phagocytized by macrophages [2] and other types of mononuclear phagocytic cells. Progmastigotes transform in these cells into the tissue stage of the parasite (i.e., amastigotes) [3], which multiply by simple division and proceed to infect other mononuclear phagocytic cells [4]. Parasite, host, and other factors affect whether the infection becomes symptomatic and whether cutaneous or visceral leishmaniasis results. Sandflies become infected by ingesting infected cells during blood meals ([5], [6]). In sandflies, amastigotes transform into promastigotes, develop in the gut [7] (in the hindgut for leishmanial organisms in the Viannia subgenus; in the midgut for organisms in the Leishmania subgenus), and migrate to the proboscis [8].
Information and image courtesy of: Centers for Disease Control
Sandfly images courtesy of: and

11. Trypanosoma brucei complex
VECTOR-BORNE
Trypanosoma brucei complex
ZOONOTIC
Life Cycle
African Trypanosomiasis
T. b. gambiense is agent of West/Central African Sleeping Sickness
T. b. rhodesiense is agent of East African Sleeping Sickness
Transmission
Bite of Tsetse fly
Glossina spp.
Humans are only reservoir for T. b. gambiense (vector-borne)
Cattle and antelope are reservoirs for T. b. rhodesiense (zoonotic)
During a blood meal on the mammalian host, an infected tsetse fly (genus Glossina) injects metacyclic trypomastigotes into skin tissue. The parasites enter the lymphatic system and pass into the bloodstream [1]. Inside the host, they transform into bloodstream trypomastigotes [2], are carried to other sites throughout the body, reach other blood fluids (e.g., lymph, spinal fluid), and continue the replication by binary fission [3]. The entire life cycle of African Trypanosomes is represented by extracellular stages. The tsetse fly becomes infected with bloodstream trypomastigotes when taking a blood meal on an infected mammalian host ([4], [5]). In the fly’s midgut, the parasites transform into procyclic trypomastigotes, multiply by binary fission [6], leave the midgut, and transform into epimastigotes [7]. The epimastigotes reach the fly’s salivary glands and continue multiplication by binary fission [8]. The cycle in the fly takes approximately 3 weeks. Humans are the main reservoir for Trypanosoma brucei gambiense, but this species can also be found in animals. Wild game animals are the main reservoir of T. b. rhodesiense.
Information and image courtesy of: Centers for Disease Control

12. Trypanosoma cruzi Life Cycle
VECTOR-BORNE
ZOONOTIC
Life Cycle
American Trypanosomiasis (Chagas’ Disease)
Transmission
Bite of Triatomine bug
Reduviid Bug or “Kissing” Bug
Triatoma, Rhodnius & Panstrongylus spp.
Transmission to humans occurs when infective forms of parasite are discharged with feces at time of blood meal
Can also be transmitted by transfusions, organ transplant, from mother to fetus and lab accidents
An infected triatomine insect vector (or “kissing” bug) takes a blood meal and releases trypomastigotes in its feces near the site of the bite wound. Trypomastigotes enter the host through the wound or through intact mucosal membranes, such as the conjunctiva [1]. Common triatomine vector species for trypanosomiasis belong to the genera Triatoma, Rhodnius, and Panstrongylus. Inside the host, the trypomastigotes invade cells near the site of inoculation, where they differentiate into intracellular amastigotes [2]. The amastigotes multiply by binary fission [3] and differentiate into trypomastigotes, and then are released into the circulation as bloodstream trypomastigotes [4]. Trypomastigotes infect cells from a variety of tissues and transform into intracellular amastigotes in new infection sites. Clinical manifestations can result from this infective cycle. The bloodstream trypomastigotes do not replicate (different from the African trypanosomes). Replication resumes only when the parasites enter another cell or are ingested by another vector. The “kissing” bug becomes infected by feeding on human or animal blood that contains circulating parasites [5]. The ingested trypomastigotes transform into epimastigotes in the vector’s midgut [6]. The parasites multiply and differentiate in the midgut [7] and differentiate into infective metacyclic trypomastigotes in the hindgut [8].
Information and image courtesy of: Centers for Disease Control