Blood born protozoans

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Information about Blood born protozoans
Health & Medicine

Published on March 26, 2014

Author: alubajessabeth





• Blood protozoa of major clinical significance include members of genera Trypanosoma (T. brucei and T. cruzi); Leishmania (L. donovani, L. tropica and L. braziliensis); Plasmodium (P. falciparum, P. ovale, P. malariae and P. vivax); Toxoplasma gondii; and Babesia (B. microti


African trypanosomiasis (Sleeping sickness)

• Etiology There are two clinical forms of African trypanosomiasis: – 1) a slowly developing disease caused by Trypanosoma brucei gambiense – 2) a rapidly progressing disease caused by T. brucei rhodesiense.

• Epidemiology T. b. gambiense – predominant in the western and central regions of Africa, whereas • T. b. rhodesiense – restricted to the eastern third of the continent (figure 2E). 6,000 to 10,000 human cases are documented annually. 35 million people and 25 million cattle are at risk. Regional epidemics of the disease are cause of major health and economic disasters.

Chaga's disease: Countries in which American trypanosomiasis is endemic

• Morphology – T. b. gambiense and T. b. rhodesiense are similar in appearance: – The organism measures 10 - 30 micrometers x 1-3 micrometers. – It has a single central nucleus and a single flagellum originating at the kinetoplast and joined to the body by an undulating membrane – The outer surface of the organism is densely coated with a layer of glycoprotein, the variable surface glycoprotein

Trypanosoma cruzi, trypomastigote form, in a blood smear (Giemsa stain)

Trypanosoma cruzi, crithidia.

Figure 7C. Trypanosoma cruzi. Leishmanial form

Riduvid bug, the vector of American trypanosomiasis

Ramana's sign: unilateral conjunctivitis and orbital edema

Megacolon in Chaga's disease

Leishmania tropica amastigotes from a skin touch preparation. In A, a still intact macrophage is practically filled with amastigotes, several of which have clearly visible a nucleus and a kinetoplast (arrows); in B, amastigotes are being freed from a rupturing macrophage. Patient with history of travel to Egypt, Africa, and the Middle East. Culture in NNN medium followed by isoenzyme analysis identified the species as L. tropica minor.

Life cycle • 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 . Inside the host, they transform into bloodstream trypomastigotes , are carried to other sites throughout the body, reach other blood fluids (e.g., lymph, spinal fluid), and continue the replication by binary fission . 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 (, ). In the fly’s midgut, the parasites transform into procyclic trypomastigotes, multiply by binary fission , leave the midgut, and transform into epimastigotes . The epimastigotes reach the fly’s salivary glands and continue multiplication by binary fission . 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.

Structure of Trypanosome brucei

Figure 1B Forms of Trypansoma brucei obsreved in the tstese fly and in the human blood stream T. brucei is transmitted by tsetse flies of the genus Glossina. Parasites are ingested by the fly when it takes a blood meal on an infected mammal. The parasites multiply in the fly, going through several developmental stages in the insect gut and salivary glands (procyclic trypanosomes, epimastigotes, metacyclic trypanosomes). The cycle in the fly takes approximately 3 weeks. When the fly bites another mammal, metacyclic trypanosomes are inoculated, and multiply in the host's blood and extracellular fluids such as spinal fluid. Humans are the main reservoir for T. b. gambiense, but this species can also be found in animals. Wild game animals are the main reservoir of T. b. rhodesiense

Two areas from a blood smear from a patient with African trypanosomiasis. Thin blood smear stained with Giemsa. Typical trypomastigote stages (the only stages found in patients), with a posterior kinetoplast, a centrally located nucleus, an undulating membrane, and an anterior flagellum. The two Trypanosoma brucei species that cause human trypanosomiasis, T. b. gambiense and T. b. rhodesiense, are undistinguishable morphologically. The trypanosomes length range is 14-33 µm

• Blood smear from a patient (a U.S. traveler) with Trypanosoma brucei rhodesiense. A dividing parasite is seen at the right. Dividing forms are seen in African trypanosomiasis, but not in American trypanosomiasis (Chagas' disease)

Blood smear from a patient with Trypanosoma brucei gambiense

Life cycle The infective, metacyclic form of the trypanosome is injected into the primary host during a bite by the vector, the tsetse fly (figure 3). The organism transforms into a dividing trypanosomal (trypomastigote) blood form (figure 1B) as it enters the draining lymphatic and blood stream. The trypanosomal form enters the vector during the blood meal and travels through the alimentary canal to the salivary gland where it proliferates as the crithidial form (epimastigote) and matures to infectious metacyclic forms (Figure 1B). Trypomastigotes can traverse the walls of blood and lymph capillaries into the connective tissues and, at a later stage, cross the choroid plexus into the brain and cerebrospinal fluid. The organism can be transmitted through blood transfusion.

Symptoms • The clinical features of Gambian and Rhodesian disease are the same, however they vary in severity and duration. Rhodesian disease progresses more rapidly and the symptoms are often more pronounced. The symptoms of the two diseases are also more pronounced in Caucasians than in the local African population. Classically, the progression of African trypanosomiasis can be divided into three stages: the bite reaction (chancre), parasitemia (blood and lymphoid tissues), and CNS stage.

Bite reaction: • A non-pustular, painful, itchy chancre (Figure 4 A and B) forms 1-3 weeks after the bite and lasts 1-2 weeks. It leaves no scar.

Parasitemia: • Parasitemia and lymph node invasion is marked by attacks of fever which starts 2-3 weeks after the bite and is accompanied by malaise, lassitude, insomnia headache and lymphadenopathy and edema (figure 4E). Painful sensitivity of palms and ulnar region to pressure (Kerandel's sign) may develop in some Caucasians. Very characteristic of Gambian disease is visible enlargement of the glands of the posterior cervical region (Winterbottom's sign) (Figure 4C). Febrile episodes may last few months as in Rhodesian disease or several years as in Gambian disease. Parasitemia is more prominent during the acute stage than during the recurrence episodes.

Winterbottoms sign

CNS Stage: • The late or CNS stage is marked by changes in character and personality. They include lack of interest and disinclination to work, avoidance of acquaintances, morose and melancholic attitude alternating with exaltation, mental retardation and lethargy, low and tremulous speech, tremors of tongue and limbs, slow and shuffling gait, altered reflexes, etc. Males become impotent. There is a slow progressive involvement of cardiac tissue. The later stages are characterized by drowsiness and uncontrollable urge to sleep. The terminal stage is marked by wasting and emaciation. Death results from coma, intercurrent infection or cardiac failure

The leg of a teenage girl who has sleeping sickness, showing the chancre at the site of the tsetse fly

The partially healed chancre on the arm of a female patient in a ward of a rural clinic.

Neurological complications can occur as a result of infection and, as seen here, patients may be immobilised for their own safety.

Tsetse fly. The vector of African trypanosomiasis

A male sleeping sickness patient with myxoedema. WHO

The damaged brain of a patient who had died from African trypanosomiasis (or sleeping sickness).

The clinical features of Rhodesian disease are similar but briefer and more acute. The acuteness and severity of disease do not allow typical sleeping sickness. Death is due to cardiac failure within 6-9 months.

Pathology and Immunology • An exact pathogenesis of sleeping sickness is not known, although immune complexes and inflammation have been suspected to be the mechanism of damage to tissues. The immune response against the organism does help to eliminate the parasite but it is not protective, since the parasite has a unique ability of altering its antigens,the VSG (see the chapter on Molecular Biology of Trypanosomes). Consequently, there is a cyclic fluctuation inthe number of parasites in blood and lymphatic fluids and each wave of parasite represents a different antigenic variant. The parasite causes polyclonal expansion of B lymphocytes and plasma cells and an increase in total IgM concentration. It stimulates the reticuloendothelial function. It also causes severe depression of cell mediated and humoral immunity to other antigens.

Diagnosis • Detection of parasite in the bloodstream, lymph secretions and enlarged lymph node aspirate provides a definitive diagnosis in early (acute) stages. The parasite in blood can be concentrated by centrifugation or by the use of anionic support media. Cerebrospinal fluid must always be examined for organisms. Immuno-serology (enzymelinkedimmune assay, immunofluorescence) may be indicative but does not provide definite diagnosis.

Treatment and Control • The blood stage of African trypanosomiasis can be treated with reasonable success with Pentamidine isethionate or Suramin. These drugs have been reported also to be effective in prophylaxis although they may mask early infection and thus increase the risk of CNS disease. Cases with CNS involvement should be treated with Melarsoprol, an organic arsenic compound. The most effective means of prevention is to avoid contact with tsetse flies. Vector eradication is impractical due to the vast area involved. Immunization has not been effective due to antigenic variation.

American trypanosomiasis (Chagas' disease)

Etiology • Chagas' disease is caused by the protozoan hemoflagellate, Trypanosoma cruzi.

Epidemiology • American trypanosomiasis, also known as Chagas' disease, is scattered irregularly in Central and South America, • stretching from parts of Mexico to Argentina (figure 6). Rare cases have been reported in Texas, California and • Maryland. It is estimated that 16-18 million people are infected by the parasite and 50 million are at risk. About • 50,000 people die each year from the disease.

Morphology • Depending on its host environment, the organism occurs in three different forms (Figure 7 and 9B). – The trypanosomal (trypomastigote) form (figure 7A), found in mammalian blood, is 15 to 20 microns long and morphologically similar to African trypanosomes. – .

– The crithidial (epimastigote) form (figure 7B) is found in the insect intestine.

• The leishmanial (amastigote) form (figure 7C), found intracellularly or in pseudocysts inmammalian viscera (particularly in myocardium and brain), is round or oval in shape, measures 2-4 microns and lacks a prominent flagellum

Life cycle • The organism is transmitted to mammalian host by many species of kissing (riduvid) bug (figure 8), most • prominently by Triatoma infestans, T. sordida, Panstrongylus megistus and Rhodnius prolixus. Transmission • takes place during the feeding of the bug which normally bites in the facial area (hence the name, kissing bug) • and has the habit of defecating during feeding. The metacyclic trypamastigotes, contained in the fecal material, • gain access to the mammalian tissue through the wound which is often rubbed by the individual that is bitten. • Subsequently, they enter various cells, including macrophages, where they differentiate into amastigotes and • multiply by binary fission. The amastigotes differentiate into non-replicating trypomastigotes and the cells rupture • to release them into the bloodstream. Additional host cells, of a variety of types, can become infected and the • trypomastigotes once again form amastigotes inside these cells. Uninfected insect vectors acquire the organism • when they feed on infected animals or people containing trypomastigotes circulating in their blood. Inside the • alimentary tract of the insect vector, the trypomastigotes differentiate to form epimastigotes and divide • longitudinally in the mid and hindgut of the insect where they develop into infective metacyclic trypomastigotes • (figure 9C). Transmission may also occur from man to man by blood transfusion and by the transplacental route.

Symptoms • Chagas' disease can be divided into three stages: the primary lesion, the acute stage, and the chronic stage. • The primary lesion, chagoma, appearing at the site of infection, within a few hours of a bite, consists of a slightly raised, flat non-purulent erythematous plaque surrounded by a variable area of hard edema. It is usually found on • the face, eyelids, cheek, lips or the conjunctiva, but may occur on the abdomen or limbs. When the primary • chagoma is on the face, there is an enlargement of the pre- and post- auricular and the submaxillary glands on • the side of the bite. Infection in the eyelid, resulting in a unilateral conjunctivitis and orbital edema (Ramana's • sign) (figure 9A), is the commonest finding.

Acute Stage: • The acute stage appears 7-14 days after infection. It is characterized by : – Restlessness – sleeplessness, malaise, increasing exhaustion, chills, fever and bone and muscle pains. – Other manifestations of the acute phase are • cervical, axillary and iliac adenitis, hepatomegaly, • erythematous rash and acute myocarditis. • There is a general edematous reaction associated withlymphadenopathy. Diffuse myocarditis, sometimes accompanied by serious pericarditis and endocarditis, is very frequent during the initial stage of the disease. – In children, Chagas' disease may cause meningo-encephalitis and coma. Death occurs in 5-10 percent of infants..

Chronic Stage: • The acute stage is usually not recognized and often resolves with little or no immediate damage and the infected host remains an asymptomatic carrier. An unknown proportion (guessed at 10-20%) of victims develop a chronic disease – Disturbances of peristalsis lead to megaesophagus and megacolon

Pathology and Immunology • The pathological effects of acute phase Chagas' disease largely result from direct damage to infected cells. In • later stages, the destruction of the autonomic nerve ganglions may be of significance. Immune mechanisms, both • cell mediated and humoral, involving reaction to the organism and to autologous tissues have been implicated in • pathogenesis. • T. cruzi stimulates both humoral and cell mediated immune responses. Antibody has been shown to lyze the • organism, but rarely causes eradication of the organism, perhaps due to its intracellular localization. Cell mediated • immunity may be of significant value. While normal macrophages are targeted by the organism for growth, • activated macrophages can kill the organism. Unlike T. brucei, T. cruzi does not alter its antigenic coat. Antibodies • directed against heart and muscle cells have also been detected in infected patients leading to the supposition • that there is an element of autoimmune reaction in the pathogenesis of Chagas' disease. The infection causes • severe depression of both cell mediated and humoral immune responses. Immunosuppression may be due to • induction of suppressor T-cells and/or overstimulation of macrophages.

Diagnosis • Clinical diagnosis is usually easy among children in endemic areas. • Cardiac dilation, megacolon and megaesophagus in individuals from endemic areas indicate present or former infection. • Definitive diagnosis requires the demonstration of trypanosomes by microscopy or biological tests (in the insect or mice).

Treatment and Control • There is no curative therapy available. Most drugs are either ineffective or highly toxic. Recently two experimental drugs, Benznidazol and Nifurtimox have been used with promising results in the acute stage of the disease, however their side effects limit their prolonged use in chronic cases. • Control measures are limited to those that reduce contact between the vectors and man. Attempts to develop a vaccine have not been very successful, although they may be feasible.

Life cycle

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 . Common triatomine vector species for trypanosomiasis belong to the genera Triatoma, Rhodinius, and Panstrongylus. Inside the host, the trypomastigotes invade cells, where they differentiate into intracellular amastigotes . The amastigotes multiply by binary fission and differentiate into trypomastigotes, and then are released into the circulation as bloodstream trypomastigotes . 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 . The ingested trypomastigotes transform into epimastigotes in the vector’s midgut . The parasites multiply and differentiate in the midgut and differentiate into infective metacyclic trypomastigotes in the hindgut . Trypanosoma cruzi can also be transmitted through blood transfusions, organ transplantation, transplacentally, and in laboratory accidents.


Etiology • Several species of Leishmania are pathogenic for man: – L. donovani causes visceral leishmaniasis (Kala- azar,black disease, dumdum fever); – L. tropica (L. t. major, L. t. minor and L. ethiopica) cause cutaneous leishmaniasis(oriental sore, Delhi ulcer, Aleppo, Delhi or Baghdad boil); – L. braziliensis (also, L. mexicana and L. peruviana) are etiologic agents of mucocutaneous leishmaniasis (espundia, Uta, chiclero ulcer).

Many children suffering from visceral leishmaniasis develop a noticeable thickening, stiffening and darkening of the eyelashes and eyebrows.

Epidemiology • Leishmaniasis is prevalent world wide: ranging from south east Asia, Indo- Pakistan, Mediterranean, north and central Africa, and south and central America.

Morphology • Amastigote (leishmanial form) – is oval and measures 2-5 microns by 1 - 3 microns

• Leptomonad – measures 14 - 20 microns by 1.5 - 4 microns, a similar size to trypanosomes

Crater lesion of leishmaniasis

Leishmania donovani, leptomonad forms.

Leishmania donovani in bone marrow cell. Smear.

Bone marrow smear showing Leishmania donovani parasites in a bone marrow histiocyte from a dog

Giemsa stained leishmanial promastigotes from a culture in which the bar-shaped kinetoplast in the organism closest to the center of the group "rosette“ may be seen.

Life cycle promastigote • The organism is transmitted by the bite of several species of blood-feeding sand flies (Phlebotomus) which carry • the in the anterior gut and pharynx. The parasites gain access to mononuclear phagocytes where • they transform into amastigotes and divide until the infected cell ruptures. The released organisms infect other • cells. The sandfly acquires the organisms during the blood meal; the amastigotes transform into flagellate • promastigotes and multiply in the gut until the anterior gut and pharynx are packed. Dogs and rodents are • common reservoirs (figure 11F).

Life cycle

Leishmaniasis is transmitted by the bite of female phlebotomine sandflies. The sandflies inject the infective stage, promastigotes, during blood meals . Promastigotes that reach the puncture wound are phagocytized by macrophages and transform into amastigotes . Amastigotes multiply in infected cells and affect different tissues, depending in part on the Leishmania species . This originates the clinical manifestations of leishmaniasis. Sandflies become infected during blood meals on an infected host when they ingest macrophages infected with amastigotes ( , ). In the sandfly's midgut, the parasites differentiate into promastigotes , which multiply and migrate to the proboscis .

Symptoms • Visceral leishmaniasis (kala-azar, dumdum fever): – L. donovani organisms in visceral leishmaniasis are rapidly eliminated from the site of infection, hence there is rarely a local lesion, although minute papules have been described in children. They are localized and multiply in the mononuclear phagocytic cells of spleen, liver, lymph nodes, bone marrow, intestinal mucosa and other organs. One to four months after infection, there is occurrence of fever, with a daily rise to 102- 104 degrees F, accompanied by chills and sweating. The spleen and liver progressively become enlarged (figure 11B, C and E). With progression of the diseases, skin develops hyperpigmented granulomatous areas (kala-azar means black disease). Chronic disease renders patients susceptible to other infections. Untreated disease results in death.

Profile view of a teenage boy suffering from visceral leishmaniasis. The boy exhibits splenomegaly, distended abdomen and severe muscle wasting.

A 12-year-old boy suffering from visceral leishmaniasis. The boy exhibits splenomegaly and severe muscle wasting

Jaundiced hands of a visceral leishmaniasis patient.

Enlarged spleen and liver in an autopsy of an infant dying of visceral leishmaniasis

18 October 2001 'Leishmaniasis' is a deadly tropical disease which affects around 2 million people a year. It has become increasingly resistant to drugs. A chance discovery showed a cancer drug undergoing tests had some extremely useful properties.

Cutaneous leishmaniasis (Oriental sore, Delhi ulcer, Baghdad boil): • In cutaneous leishmaniasis, the organism (L. tropica) multiplies locally, producing of a papule, 1-2 weeks (or as long as 1-2 months) after the bite. The papule gradually grows to form a relatively painless ulcer. The center of the ulcer encrusts while satellite papules develop at the periphery. The ulcer heals in 2-10 months, even if untreated but leaves a disfiguring scar (figure 12). The disease may disseminate in the case of depressed immune function.

• Mucocutaneous leishmaniasis (espundia, Uta, chiclero): The initial symptoms of mucocutaneous leishmaniasis are the same as those of cutaneous leishmaniasis, except that in this disease the organism can metastasize and the lesions spread to mucoid (oral, pharyngeal and nasal) tissues and lead to their destruction and hence sever deformity (figure 12E). The organisms responsible are L. braziliensis, L. mexicana and L. peruviana.

Pathology • Pathogenesis of leishmaniasis is due to an immune reaction to the organism, particularly cell mediated immunity. Laboratory examination reveals a marked leukopenia with relative monocytosis and lymphocytosis, anemia and thrombocytopenia. IgM and IgG levels are extremely elevated due to both specific antibodies and polyclonal activation. •

Diagnosis • Diagnosis is based on a history of exposure to sandfies, symptoms and isolation of the organisms from the lesion aspirate or biopsy, by direct examination or culture. A skin test (delayed hypersensitivity: Montenegro test) and detection of anti-leishmanial antibodies by immuno-fluorescence are indicative of exposure.

Treatment and Control Sodium stibogluconate (Pentostam) is the drug of choice. Pentamidine isethionate is used as an alternative. Control measures involve vector control and avoidance. Immunization has not been effective.

Skin ulcer due to leishmaniasis, hand of Central American adult.

Scar on skin of upper leg representing healed lesion of leishmaniasis

Non-healing cutaneous leishmaniasis lesion on ear lobe

Girl with diffuse muco- cutaneous leishmaniasis of the face which is responding to treatment

Cutaneous leishmaniasis skin lesion. The lesion measured about 1 inch in diameter and was moist with raised borders. There was no drainage; however, the lesion did appear to be infected


• Etiology Four Plasmodium species are responsible for human malaria – P. falciparum, – P. vivax, – P. ovale – P. malariae.

• Epidemiology There are an estimated 200 million global cases of malaria leading a mortality of more than one million people per year. – P. falciparum (malignant tertian malaria) and P. malariae (quartan malaria) are the most common species of malarial parasite and are found in Asia and Africa. – P. vivax (benign tertian malaria) predominates in Latin America, India and Pakistan – P. ovale (ovale tertian malaria) is almost exclusively found in Africa (figure 12G).

Malaria generally occurs in areas where environmental conditions allow parasite multiplication in the vector. Thus, malaria is usually restricted to tropical and subtropical areas (see map) and altitudes below 1,500 m. However, this distribution might be affected by climatic changes, especially global warming, and population movements. Both Plasmodium falciparum and P. malariae are encountered in all shaded areas of the map (with P. falciparum by far the most prevalent). Plasmodium vivax and P. ovale are traditionally thought to occupy complementary niches, with P. ovale predominating in Sub-Saharan Africa and P. vivax in the other areas; however these two species are not always distinguishable on the basis of morphologic characteristics alone; the use of molecular tools will help clarify their exact distribution.

• Morphology – ring shaped, 1-2 microns in size – other forms (ameboid and band) may also exist. The sexual forms of the parasite (gametocytes) are much larger and 7-14 microns in size. – P. falciparum is the largest and is banana shaped while others are smaller and round. – P. vivax causes stippling of infected red cells).

• plasmodiumx.mp4

• The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human host . Sporozoites infect liver cells and mature into schizonts , which rupture and release merozoites . (Of note, in P. vivax and P. ovale a dormant stage [hypnozoites] can persist in the liver and cause relapses by invading the bloodstream weeks, or even years later.) After this initial replication in the liver (exo-erythrocytic schizogony ), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony ). Merozoites infect red blood cells . The ring stage trophozoites mature into schizonts, which rupture releasing merozoites . Some parasites differentiate into sexual erythrocytic stages (gametocytes) . Blood stage parasites are responsible for the clinical manifestations of the disease. The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal . The parasites’ multiplication in the mosquito is known as the sporogonic cycle . While in the mosquito's stomach, the microgametes penetrate the macrogametes generating zygotes . The zygotes in turn become motile and elongated (ookinetes) which invade the midgut wall of the mosquito where they develop into oocysts . The oocysts grow, rupture, and release sporozoites , which make their way to the mosquito's salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle

• Life_cycle_of_malaria_Part_1_Human_hostx. mp4 • Malaria in the 21st century x[].mp4 • malaria lifecycle x[].mp4

trophozoite stages

Fig. 1

Plasmodium falciparum: Blood Stage Parasites: • Thin Blood Smears Fig. 1: Normal red cell; Figs. 2-18: Trophozoites (among these, Figs. 2-10 correspond to ring- stage trophozoites); Figs. 19-26: Schizonts (Fig. 26 is a ruptured schizont); Figs. 27, 28: Mature macrogametocytes (female); Figs. 29, 30: Mature microgametocytes (male)

Plasmodium falciparum: Blood Stage Parasites: Thick Blood Smears

Plasmodium malariae: Blood Stage Parasites: Thin Blood Smears Fig. 1: Normal red cell; Figs. 2-5: Young trophozoites (rings); Figs. 6-13: Trophozoites; Figs. 14-22: Schizonts; Fig. 23: Developing gametocyte; Fig. 24: Macrogametocyte (female); Fig. 25: Microgametocyte (male)

• Plasmodium malariae: Blood Stage Parasites: Thick Blood Smears

Plasmodium ovale: Blood Stage Parasites: Thin Blood Smears Fig. 1: Normal red cell; Figs. 2-5: Young trophozoites (Rings); Figs. 6-15: Trophozoites; Figs. 16-23: Schizonts; Fig. 24: Macrogametocytes (female); Fig. 25: Microgametocyte (male)

Plasmodium vivax: Blood Stage Parasites: Thin Blood Smears Fig. 1: Normal red cell; Figs. 2-6: Young trophozoites (ring stage parasites); Figs. 7-18: Trophozoites; Figs. 19-27: Schizonts; Figs. 28 and 29: Macrogametocytes (female); Fig. 30: Microgametocyte (male)


Plasmodium falciparum: Gametocytes Figs. 27, 28: Mature macrogametocytes (female); Fig. 29, 30: Mature microgametocytes (male)

Plasmodium malariae: Gametocytes Fig. 23: Developing gametocyte; Fig. 24: Macrogametocyte (female); Fig. 25: Microgametocyte (male)

Plasmodium falciparum: Gametocytes: An asplenic, 41 y.o. woman, immigrant from Haiti, who returned to the US 2 days ago; high P. falciparum parasitemia; the presence of such young gametocytes in the peripheral blood is exceptional

Plasmodium falciparum: Gametocytes: A patient from Haiti; mature gametocytes

Plasmodium malariae: Gametocytes: Smear from patient: 56 y.o. man who had traveled to Kenya

Plasmodium malariae: Gametocytes: Smear from patient: 56 y.o. man who had traveled to Kenya

Plasmodium ovale: Gametocytes Fig. 24: Macrogametocyte (female); Fig. 25: Microgametocyte (male).

Plasmodium vivax: Gametocytes Fig. 28 and 29: Nearly mature and mature macrogametocyte (female); Fig. 30: Microgametocyte (male)

Gametocytes Smears from patients: Note the Schüffner's dots in A, and the fimbriation of the erythrocyte in B. The erythrocytes in P. ovale infections are less enlarged than with P. vivax, and are not as deformed. A, B: Male patient born in Nigeria, who came to the US 5 days ago

C Plasmodium vivax: Gametocytes Smears from patients: Note the variability in Schüffner's dots. A: A pregnant woman who visited India 6 months ago (specimen contributed by New Jersey SHD) B,C: 50 y.o. woman 3 months ago from a 1-month visit to India



Plasmodium falciparum: Ring Stage Parasites. Fig. 1: Normal red cell; Figs. 2-10: Increasingly mature ring stage parasites.

Plasmodium malariae: Ring Stage Parasites Fig. 1: Normal red cell; Figs. 2-5: Rings

Appliqué form Ring with double chromatin dot Older ring stage parasite Doubly infected erythrocyte Multiple infections, 6 rings in 2 erythrocytes

Plasmodium malariae: Ring Stage Parasites Smears from patients: 56 y.o. man who had traveled to Kenya

Plasmodium ovale: Ring Stage Parasites Fig. 1: Normal red cell; Figs. 2-5: Ring stage parasites

Plasmodium ovale: Ring Stage Parasites Smears from patients: Note the relatively large chromatin dots. A, C: 54 y.o. man who returned the previous month from a visit to Kenya and Malawi. P. ovale, confirmed by PCR (specimen contributed by New Mexico SHD). B: 20 y.o. man who returned 10 months ago from a visit to Mozambique, Zimbabwe and Swaziland; this attack is thus a relapse

Plasmodium vivax: Ring Stage Parasites Fig. 1: Normal red cell; Figs. 2-6: Ring stage parasites (young trophozoites)

Plasmodium vivax: Ring Stage Parasites Smears from patients: A: Rings in 2 slightly enlarged RBCs; 17 y.o. man with a relapse due to P. vivax (PCR confirmed), 6 months after returning from a visit to Papua New Guinea (specimen contributed by Virginia SHD) B: Double infection with rings, RBC enlarged and deformed, Schüffner's dots beginning to become visible; 69 y.o. woman born in India who was symptomatic on the day of arrival to the US (specimen contributed by Pennsylvania SHD) C: Late ring in a RBC with Schüffner's dots; 60 y.o. man who returned 2 months ago from a 3 month trip to Laos and North Korea (


Plasmodium falciparum: Schizonts Figs. 19-25: Increasingly mature schizonts; Fig. 26: Ruptured schizont

Plasmodium malariae: Schizonts. Increasingly mature schizonts

Plasmodium falciparum: Schizonts. Smears from patients: Schizonts are seen only rarely in P. falciparum malaria. An asplenic, 41 y.o. woman, immigrant from Haiti, who returned to the US 2 days ago; high P. falciparum parasitemia A: Young schizont with 10 nuclei; B: Mature schizont with 24 nuclei, ready to rupture (“segmenter”)

Plasmodium malariae: Schizonts.Smears from patients: The parasites are compact and the infected erythrocytes are not enlarged. In C and D, the merozoites are arranged in a rosette pattern. A, B, C, D: 56 y.o. man who had traveled to Kenya

Plasmodium ovale: Schizonts Increasingly mature schizonts

Plasmodium vivax: Schizonts Figs. 19-27: Increasingly mature schizonts

Plasmodium ovale: Schizonts Smears from patients: A, B: 54 y.o. man who returned the previous month from a visit to Kenya and Malawi. Infection with P. ovale, confirmed by PCR

Plasmodium vivax: Schizonts Smears from patients: Note that in these patients, the Schüffner's dots are not conspicuous. (This happens in many of the smears received at CDC; it is probably related to variability in staining.) A, C, D, E:

Figure 17 Trophozoites

Plasmodium falciparum: Trophozoites Figs. 11-18: Increasingly mature trophozoites

Plasmodium malariae: Trophozoites Figs. 6-13: Increasingly mature trophozoites; Fig. 13 is a "band form".

Thin smears from two patients with high parasitemias: A: An asplenic, 41 y.o. woman, immigrant from Haiti, who returned to the US 2 days ago; high P. falciparum parasitemia (specimen contributed by Florida SHD) CDC B: A patient who acquired malaria by blood transfusion and died with extremely high parasitemia; PCR confirmed P. falciparum; one of the 2 RBCs contains 3 young trophozoites, which have begun to accumulate pigment

Plasmodium malariae: Trophozoites Smears from patients: The infected erythrocytes are not enlarged (sometime they even appear smaller than non- infected ones). C is a "band form" trophozoite. A, B, C: 56 y.o. man who had traveled to Kenya

Plasmodium ovale: Trophozoites Increasingly mature trophozoites. Note the fimbriated red cells (Figs. 8, 13)

Plasmodium vivax: Trophozoites Figs. 8-18: Increasingly mature trophozoites of P. vivax

Plasmodium ovale: Trophozoites Smears from patients: Note the lack of ameboidicity in the older trophozoites (B,C) and the fimbriation of the erythrocyte in C. The erythrocytes in P. ovale infections are less enlarged than with P. vivax, and are not as deformed. The Schüffner's dots are visible in A, but not B and C. A: 20 y.o. man who returned 10 months ago from a visit to Mozambique, Zimbabwe and Swaziland (specimen contributed by New York SHD). CDC B, C: 23 y.o. man who arrived to the US 5 months ago after having been in Liberia and Ivory Coast

Plasmodium vivax: Trophozoites Smears from patients: Increasingly mature trophozoites. The RBCs are enlarged and deformed, the parasites are ameboid, and the Schüffner's dots vary in intensity. A, B: 26 y.o. woman who spent 2 weeks in Papua New Guinea 5 months ago (specimen contributed by Pennsylvania SHD) CDC C, E: 60 y.o. man who returned 2 months ago from a 3-month visit to Laos and North Korea (specimen contributed by Hawaii SHD) D: 28 y.o. woman who returned 3 months ago from a 2 weeks visit to Kenya

Life cycle Malarial parasites are transmitted by the infected female anopheline mosquito which injects sporozoites present in the saliva of the insect (Figure 18). Sporozoites infect the liver parenchymal cells where they may remain dormant (hypnozoites) or undergo stages of schizogony to produce schizonts and merogony to produce merozoites (meronts). When parenchymal cells rupture, thousands of meronts are released into blood and infect the red cells. P. ovale and P. vivax infect immature red blood cells whereas P. malariae infects mature red cells. P. falciparum infects both. In red cells, the parasites mature into trophozoites. These trophozoites undergo schizogony and merogony in red cells which ultimately burst and release daughter merozoites. Some of the merozoites transform into male and female gametocytes (figure 19) while others enter red cells to continue the erythrocytic cycle. The gametocytes are ingested by the female mosquito, the female gametocyte transforms into ookinete, is fertilized, and forms an oocyst (figure 20) in the gut. The oocyte produces sporozoites (sporogony) (figure 20) which migrate to the salivary gland and are ready to infect another host. The liver (extraerythrocytic) cycle takes 5-15 days whereas the erythrocytic cycle takes 48 hours or 72 hours (P. malariae). Malaria can be transmitted by transfusion and transplacentally.

Sexual stages of the malaria parasite Plasmodium falciparum

Stage II (central) and stage III (bottom right) immature gametocytes

Stage IV immature gametocyte, located centrally

Stage V mature gametocyte, showing characteristic sausage-shaped morphology, located centrally (blood film, wet mount, x1000 magnification under oil immersion)

Male (micro)gametocyte exflagellation - extrusion of motile, flagella-like microgametes with vigorous movement (blood film, wet mount, x1000 magnification under oil immersion) (an unusually clear picture of this metabolically dynamic and visually striking event)


Figure 20 Developmental stages of Plasmodium falciparum in the Anopheles mosquito vector

Two oocysts, dissected from the outer wall of the Anopheles stephensi midgut, 10 days post infection of the mosquito

Single oocyst, dissected from the outer wall of the Anopheles stephensi midgut, 10 days post infection of the mosquito

Single oocyst, dissected from the outer wall of the Anopheles stephensi midgut, 10 days post infection of the mosquito (wet mount, x1000 magnification under oil immersion)

Isolated bow-shaped sporozoite, dissected from the salivary glands of Anopheles stephensi, 17 days post infection of the mosquito (wet mount, x1000 magnification under oil immersion)

Symptoms • The symptomatology of malaria depends on the parasitemia, the presence of the organism in different organs and the parasite burden. The incubation period varies generally between 10-30 days. As the parasite load becomes significant, the patient develops headache, lassitude, vague pains in the bones and joints, chilly sensations and fever. As the disease progresses, the chills and fever become more prominent. The chill and fever follow a cyclic pattern (paroxysm) with the symptomatic period lasting 8-12 hours. In between the symptomatic periods, there is a period of relative normalcy, the duration of which depends upon the species of the infecting parasite. This interval is about 34-36 hours in the case of P. vivax and P. ovale (tertian malaria), and 58-60 hours in the case of P. malariae (quartan malaria). Classical tertian paroxysm is rarely seen in P. falciparum and persistent spiking or a daily paroxysm is more usual. • The malarial paroxysm is most dramatic and frightening. It begins with a chilly sensation that progresses to teeth chattering, overtly shaking chill and peripheral vasoconstriction resulting in cyanotic lips and nails (cold stage). This lasts for about an hour. At the end of this period, the body temperature begins to climb and reaches 103-106 degrees F (39- 41degrees C). Fever is associated with severe headache, nausea (vomiting) and convulsions. The patient experiences euphoria, and profuse perspiration and the temperature begins to drop. Within a few hours the patient feels exhausted but symptom-less and remains symptomatic until the next paroxysm. Each paroxysm is due to the rupture of infected erythrocytes and release of parasites. • Without treatment, all species of human malaria may ultimately result in spontaneous cure except with P. falciparum which becomes more severe progressively and results in death. This organism causes sequestration of capillary vasculature in the brain, gastrointestinal and renal tissues. Chronic malaria results in splenomegaly, hepatomegaly and nephritic syndromes.

• Sierra_Leone_Treating_Children_with_Malaria _-x_WMD_Videoblog.mp4 • Mine_Action_Technology_Workshop_- _Malariax.mp4

• Pathology and immunology Symptoms of malaria are due to the release of massive number of merozoites into the circulation. Infection results in the production of antibodies which are effective in containing the parasite load. These antibodies are against merozoites and schizonts. The infection also results in the activation of the reticuloendothelial system (phagocytes). The activated macrophages help in the destruction of infected (modified) erythrocytes and antibody-coated merozoites. Cell mediated immunity also may develop and help in the elimination of infected erythrocytes. Malarial infection is associated with immunosuppression.

• Diagnosis Diagnosis is based on symptoms and detection of parasite in Giemsa stained blood smears. There are also antibody tests (Figure 20B). • .

• Treatment and Control Treatment is effective with various quinine derivatives (quinine sulphate, chloroquine, meflaquine and primaquine, etc.). Drug resistance, particularly in P. falciparum and to some extent in P. vivax is a major problem. Control measures are eradication of infected anopheline mosquitos. Vaccines are being developed and tried but none is available yet for routine use


Etiology • Babesia microti is the only member of the genus that infects man.

Morphology • The trophozoite is very similar to the ring form of the Plasmodium species (figure 21A and B).

• Life cycle The organism (sporozoite) is transmitted by a tick and enters the red cell where it undergoes mitosis and the organisms (merozoite) are released to infect other red cells. Ticks acquire the organism during feeding on an infected individual. In the tick, the organism divides sexually in the gut and migrates into the salivary gland (figure 21C).

• Symptoms Babesiosis is associated with hemolytic anemia, jaundice, fever and hepatomegaly, usually 1-2 weeks after infection.

• Diagnosis Diagnosis is based on symptoms, patient history and detection of intraerythrocytic parasite in the patient or transfer of blood in normal hamsters which can be heavily parasitized.

• Treatment and Control Drugs of choice are clindamycin combined with quinine. The patient may recover spontaneously. One should avoid tick exposure and, if bitten, remove the tick from the skin immediately.

Babesia microti infection, Giemsa-stained thin smear. The organisms resemble Plasmodium falciparum; however Babesia parasites present several distinguishing features: they vary more in shape and in size; and they do not produce pigment. A 67 year old woman, status post- splenectomy, infection probably acquired in Long island (New York)

Infection with Babesia. Giemsa-stained thin smears. Note the tetrad (left side of the image), a dividing form pathognomonic for Babesia. A 6 year old girl, status post splenectomy for hereditary spherocytosis, infection acquired in the US.

The Babesia microti life cycle involves two hosts, which includes a rodent, primarily the white-footed mouse, Peromyscus leucopus. During a blood meal, a Babesia-infected tick introduces sporozoites into the mouse host . Sporozoites enter erythrocytes and undergo asexual reproduction (budding) . In the blood, some parasites differentiate into male and female gametes although these cannot be distinguished at the light microscope level . The definitive host is a tick, in this case the deer tick, Ixodes dammini (I. scapularis). Once ingested by an appropriate tick , gametes unite and undergo a sporogonic cycle resulting in sporozoites . 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 . Humans enter the cycle when bitten by infected ticks. During a blood meal, a Babesia-infected tick introduces sporozoites into the human host . Sporozoites enter erythrocytes and undergo asexual replication (budding) . 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 . Note: Deer are the hosts upon which the adult ticks feed and are indirectly part of the Babesia cycle as they influence the tick population. When deer populations increase, the tick population also increases, thus heightening the potential for transmission.

Thin blood film of B. microti ring forms with a typical Maltese Cross (four rings in cross formatio


• Etiology Toxoplasma gondii is the organism responsible for toxoplasmosis

• Epidemiology Toxoplasma has worldwide distribution and 20%-75% of the population is seropositive without any symptomatic episode. However, the infection poses a serious threat in immunosuppressed individuals and pregnant females.

• Morphology The intracellular parasites (tachyzoite) are 3x6 microns, pear-shaped organisms that are enclosed in a parasite membrane to form a cyst measuring 10-100 microns in size. Cysts in cat feces (oocysts) are 10-13 microns in diameter (figure 22).

Life cycle • The natural life cycle of T. gondii occurs in cats and small rodents, although the parasite can grow in the organs (brain, eye, skeletal muscle, etc.) of any mammal or birds (Figure 22). Cats gets infected by ingestion of cysts in flesh. Decystation occurs in the small intestine, and the organisms penetrate the submucosal epithelial cells where they undergo several generations of mitosis, finally resulting in the development of micro- (male) and macro- (female) gametocytes. Fertilized macro-gametocytes develop into oocysts that are discharged into the gut lumen and excreted. Oocysts sporulate in the warm environment and are infectious to a variety of animals including rodents and man. Sporozoites released from the oocyst in the small intestine penetrate the intestinal mucosa and find their way into macrophages where they divide very rapidly (hence the name tachyzoites) (figure 23) and form a cyst which may occupy the whole cell. The infected cells ultimately burst and release the tachyzoites to enter other cells, including muscle and nerve cells, where they are protected from the host immune system and multiply slowly (bradyzoites). These cysts are infectious to carnivores (including man). Unless man is eaten by a cat, it is a dead-end host.

reservoirs of infection. Cats become infected with T. gondii by carnivorism (1). After tissue cysts or oocysts are ingested by the cat, viable organisms are released and invade epithelial cells of the small intestine where they undergo an asexual followed by a sexual cycle and then form oocysts, which are then excreted. The unsporulated oocyst takes 1 to 5 days after excretion to sporulate (become infective). Although cats shed oocysts for only 1 to 2 weeks, large numbers may be shed. Oocysts can survive in the environment for several months and are remarkably resistant to disinfectants, freezing, and drying, but are killed by heating to 70°C for 10 minutes. Human infection may be acquired in several ways: A) ingestion of undercooked infected meat containing Toxoplasma cysts (2); B) ingestion of the oocyst from fecally contaminated hands or food (3); C) organ transplantation or blood transfusion; D) transplacental transmission; E) accidental inoculation of tachyzoites. The parasites form tissue cysts, most commonly in skeletal

• Symptoms Although Toxoplasma infection is common, it rarely produces symptoms in normal individuals. Its serious consequences are limited to pregnant women and immunodeficient hosts. Congenital infections occur in about 1-5 per 1000 pregnancies of which 5-10% result in miscarriage and 8-10% result in serious brain and eye damage to the fetus. 10-13% of the babies will have visual handicaps. Although 58-70% of infected women will give birth to a normal offspring, a small proportion of babies will develop active retino-chorditis or mental retardation in childhood or young adulthood. In immunocompetent adults, toxoplasmosis, may produce flu- like symptoms, sometimes associated with lymphadenopathy. In immunocompromised individuals, infection results in generalized parasitemia involvement of brain, liver lung and other organs, and often death. •

Immunology • Both humoral and cell mediated immune responses are stimulated in normal individuals. Cell-mediated immunity is protective and humoral response is of diagnostic value.

• Diagnosis Suspected toxoplasmosis can be confirmed by isolation of the organism from tonsil or lymph gland biopsy.

• Treatment Acute infections benefit from pyrimethamine or sulphadiazine. Spiramycin is a successful alternative. Pregnant women are advised to avoid cat litter and to handle uncooked and undercooked meat carefully

Toxoplasma gondii in the bronchoalveolar lavage (BAL) material from an HIV infected patient. Numerous trophozoites (tachyzoites) can be seen, which are typically crescent shaped with a prominent, centrally placed nucleus. Most of the tachyzoites are free, some are still associated with bronchopulmonary cells.

Toxoplasma gondii in tissue from a cat.

PNEUMOCYSTIS PNEUMONIA • Pneumocystis jiroveci (formerly known as Pneumocystis carinii) • Pneumocystis jiroveci was formerly thought to be a protozoan but is now known to be a fungus. It is included here because pneumocystis pneumonia is often described as an opportunistic parasitic disease. • Pneumocystis pneumonia is an infection of immunosuppressed individuals and is particularly seen in AIDS patients. The organism is pleomorphic, exhibiting, at various stages of its life cycle: 1-2 micron sporozoites, 4-5 micron trophozoites and 6-8 micron cysts. It spreads from person to person in cough droplets. Infection in immunosuppressed individuals results in interstitial pneumonia characterized by thickened alveolar septum infiltrated with lymphocytes and plasma cells. Pneumonia is associated with fever, tachypnea, hypoxia, cyanosis and asphyxia. Diagnosis is based on isolation of organisms from affected lungs. Trimethoprim- sulphamethoxazole is the treatment of choice (figure 24).

Pneumocystis jiroveci trophozoites in broncho- alveolar lavage (BAL) material. Giemsa stain. The trophozoite are small (size: 1-5 µm), and only their nuclei, stained purple, are visible (arrows). AIDS patient seen in Atlanta, Georgia

This is a generalized life cycle proposed by John J. Ruffolo, Ph.D. (Cushion, MT, for the various species of Pneumocystis. These fungi are found in the lungs of mammals where they reside without causing overt infection until the host's immun system becomes debilitated. Then, an oftentimes lethal pneumonia can result. A phase: trophic forms replicate by mitosis to . Sexual phase: haploid trophic fo conjugate and produce a zygote or sporocyte (early cyst) . The zygote underg meiosis and subsequent mitosis to produce eight haploid nuclei (late phase cyst) . Spores exhibit different shapes (such as, spherical and elongated forms). It is postulated that elongation of the spores precedes release from the spore case. I believed that the release occurs through a rent in the cell wall. After release, the spore case usually collapses, but retains some residual cytoplasm . A trophic stage, where the organisms probably multiply by binary fission is also recognized exist. The organism causes disease in immunosuppressed individuals.

FACULTATIVE PARASITIC PROTOZOA • These are free-living amebae that occasionally cause serious human disease. They are of particular significance in immunocompromised hosts.

Negleria fowleri • This organism is a flagellate that may inhabit warm waters (spas, warm springs, heated swimming pools, etc.) and gain access via the nasal passage to the brain and cause encephalitis (figure 25)

characteristically large nuclei, with a large, dark staining karyosome. The amebae are very active and extend and retract pseudopods. Trichrome stain. From a patient who died from primary amebic meningoencephalitis in Virginia

Naegleria fowleri trophozoite in spinal fluid. Trichrome stain. Note the typically large karyosome and the monopodial locomotion. Image contributed by Texas SHD.

Free-living amebae belonging to the genera Acanthamoeba, Balamuthia, and Naegleria are important causes of disease in humans and animals. Naegleria fowleri produces an acute, and usually lethal, centra nervous system (CNS) disease called primary amebic meingoencephalitis (PAM). N. fowleri has three stages, cysts , trophozoites , and flagellated forms , in its life cycle. The trophozoites replicate by promitosis (nuclear membrane remains intact) . Naegleria fowleri is found in fresh water, soil, thermal discharges of power plants, heated swimming pools, hydrotherapy and medicinal pools, aquariums, and sewage. Trophozoites can turn into temporary flagellated forms which usually revert back to the trophozo stage. Trophozoites infect humans or animals by entering the olfactory neuroepithelium and reaching th brain. N. fowleri trophozoites are found in cerebrospinal fluid (CSF) and tissue, while flagellated forms are found in CSF. Acanthamoeba spp. and Balamuthia mandrillaris are opportunistic free-living amebae capable of causing granulomatous amebic encephalitis (GAE) in individuals with compromised immune systems. Acanthamoeba spp. have been found in soil; fresh, brackish, and sea water; sewage; swimming pools; contact lens equipment; medicinal pools; dental treatment units; dialysis machines; heating, ventilating, and air conditioning systems; mammalian cell cultures; vegetables; human nostrils an throats; and human and animal brain, skin, and lung tissues. B. mandrillaris however, has not been isolate from the environment but has been isolated from autopsy specimens of infected humans and animals. Unlike N. fowleri, Acanthamoeba and Balamuthia have only two stages, cysts and trophozoites , in their life cycle. No flagellated stage exists as part of the life cycle. The trophozoites replicate by mitos (nuclear membrane does not remain intact) . The trophozoites are the infective forms and are believed to gain entry into the body through the lower respiratory tract, ulcerated or broken skin and invade the centra nervous system by hematogenous dissemination . Acanthamoeba spp. and Balamuthia mandrillaris cys and trophozoites are found in tissue

Acanthemeba • Several species of free-living Acanthemeba are pathogenic to man. They normally reside in soil and can infect children who swallow dirt while playing on the ground. In normal individuals, the infection may cause mild disease (pharyngitis) or remain asymptomatic, but in immunodeficient individuals, the organism may penetrate the esophageal mucosa and reach the brain where it causes granulomatous encephalitis

Summary Organism Transmission Disease/symptoms Diagnosis Treatment Trypanosoma brucei Tsetse fly. Sleeping sickness; cardiac failure. Hemoflagellate in blood or lymph node. Blood stage: Suramin or petamidine isethionate; T. cruzi Reduvid (kissing) bug. Chagas disease: megacolon, cardiac failure. Hemoflagellate in blood or tissue. CNS: melarsoprol Nifurtimox and Benzonidazole. Leishmania donovani Sand fly Visceral leish-maniasis, granulo-matous skin lesions. Intracellular (macrophages) leishmanial bodies. Pentosam; Pentamidine isethionate. L. tropica Sand fly. Cutaneous lesions. As for L. donovani. As for L. donovani. L. braziliensis Sand fly Mucocutaneous lesions. As for L. donovani. As for L. donovani. Plasmodium falciparum P. ovale, P. malariae and P. vivax Female anopheline mosquito. Malarial paroxysm: chills, fever, headache, nausea cycles. Plasmodia in rbc, typical of the species involved. Quinine derivatives Proguanil Lariam Babesia microti Tick Hemolytic anemia, Jaundice and fever Typical organism (Maltese cross) in rbc. None; self resolving. Toxoplasma gondii Oral from cat fecal material; or meat Adult: flu like; congenital: abortion, neonatal blindness and neuropathies. Intracellular (in macrophages) tachyzoites. Sulphonamides, pyemethamine, possibly spiramycin (non-FDA). Pneumocystis jiroveci Cough droplets Pneumonia Pneumocystis in sputum. Trimethoprim and sulphamethoxazole.

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