Videos: (child dies in NC) Malaria (description) Crypto (description) Taxoplasmosis (description)
Introduction/classification:
Protozoa are a subset of protists which are eukaryotes that are not classified as animals, plants, or fungi. Protozoa constitute a large genus (some 12,000 species) that although single-celled, have a great deal of complexity with respect ot movement, feeding and behavior. Although most members are harmless, free living inhabitants of water and soil, a few species are pathogens which are collectively responsible for hundreds of millions of infections of humans each year.
Protozoa are not all genetically related and are difficult to classify. Often they are classified based on their method of motility; Sarcodina (pseudo-pods), Ciliophora (cilia), Mastigophora (flagella -e.g., Giardia lambia & Trichomonas vaginalis) and Sporozoa (gliding motility -e.g., Toxoplasma gondii).
Life cycle:
Protozoa are called “trophozoites” when they are in their motile feeding stage. A large number of species are also capable of entering into a dormant, resting stage called a “cyst” when conditions in the environment become unfavorable for growth and feeding. Cysts can be dispersed by air currents and may even be important factor in the spread of diseases such as amoebic dysentery. If provided with moisture and nutrients, a cyst breaks opena dn releases the active trophozoite. All protozoa have a trophozoite form, but not all product cysts.
Reproduction:
All protozoa reproduce by realtively simple, asexual methods, usually mitotic cell division. Several pathogenic species, including the causative agents of malaria and toxoplasmosis, reproduce asexually by multiple round of division inside a host cell. Sexual reproduction also occurs during the life cycle of most protozoa. Ciliates participate in conjugation, a form of genetic exchange in which two cells fuse temperarily and exchange micronuclei. This proces of sexaul recombination yeilds different genetic combinations.
Structure & other defining characteristics:
Most eukaryotic microbes move by using flagella or cillia. This type of motility is common in protozoa. Cilia are similar in overall structure to flagella, but they are shorter and more numerous (some cells have several thousand). They are found on one group of protozoa and in certain animal cells. Protozoa do not have cell walls unlike fungi. Although protozoa have adapted to a wide range of habitats, their main limiting factor is the availability of moisture. Their predominant habitats are fresh and marine water, soil, plants and animals. Extremes in temeprature and pH are not a barrier to their existence. Hadry species are found in hot springs, ice and habitats with very low or high pH.
Protozoan parasites were the most frequently identified etiologic agents in waterborne disease outbreak from 1991 to 1994. The waterborne parasites Giardia lamblia, Naegleria fowleri, Acanthamoeba spp., Entamoeba histolytica, Cryptosporidium parvum, Cyclospora cayetanesis, Isospora belli. See Sterling
Affecting Blood, the Cardiovascular and Lymphatic System
Babesiosis: Babesia is a protozoan that infects red blood cells. It is carried by ticks and found in the upper Great Lakes region as well as in the northeast U.S. It is often diagnosed via a blood smear; the protozoan is visible inside red blood cells. A combined therapy of either atovaquone (an antiprotozoal) plus azithromycin or clindamycin plus quinine (another antiprotozoal) is recommended.
Babesiosis, caused by infection with intraerythrocytic parasites of the genus Babesia, is one of the most common infections of free-living animals worldwide and is gaining increasing interest as an emerging zoonosis in humans. Although capable of infecting a wide range of vertebrates, babesial parasites require both a competent vertebrate and nonvertebrate host to maintain transmission cycles. All babesial parasites described to date are transmitted by ixodid ticks to their vertebrate hosts. The parasites replicate in the vertebrate hosts’ red blood cells and are called piroplasms due to their pear-shaped appearance when within the infected host cells
Chagas Disease (the American trypanosomiasis”): Chagas disease is named after the Brazilian physician Carlos Chagas, who discovered the disease in 1909. It is caused by the flagellated protozoan Trypanosoma cruzi, which is transmitted to animals and people by insect vectors (triatomine bug) and is found only in the Americas (mainly, in rural areas of Latin America where poverty is widespread). The bug is found in dwellings constructed form materials such as mud, adobe and straw. The insect bites the host and while feeding on its blood deposits feces. The parasite can then enter the body of the host from the insect’s feces when the host scratches and breaks the skin, or transfers the parasite to a mucous membrane. The disease can also be passed from mother to child during childbirth, during blood transfusions, and from organ transplants. Chagas disease can lead to severe cardiac and digestive problems in humans and domestic animals, but it appears to be tolerated in wild mammals. Tsetse fly-transmitted trypanosomes have evolved an elaborate genetic mechanism for repeatdly changing the antigenic nature of their protetive glycoprotein coat. Only a single gene out of some 1000 variable surface glyoprotein genes is expressed at a time. The variable surface glyscoprotein is usually duplicated and moved to 1-20 expression sites enar the end of the chromosome where it is transcribed. In the guts of the flies that spread them, trypanosomes are noninfective. When they are ready to transfer to the skin or bloodstream of their host, trypanosomes migrate to the salivary glands and acquire the thick coat of glycoprotein antigens that protect them form the host’s antibodies. Later, when they are taken up by a tsetse fly, the trypanosomes again shed their coats. The producitoh of vaccines against such a system is accordingly complex. Rleasing sterilzied flies to iimpede the rproduction of populations is another technique. Traps made of dark cloth and scented like cows but poisoned with insecticides have likewise proved effective.
A different trypanosome, T. brucei causes sleeping sickness on the African continent. It has a long incubation time and is very difficult to cure. Once the trypanosomes are transmitted by a group of insects called the triatomines, they multiply in muscle and blood cells. From time to time, the blood cells rupture and large numbers of trypanosomes are released into the bloodstream. The disease manifestations are divided into acute and chronic phases. In the acute phase, symptoms are nondescript and range form mild to severe fever, nausea and fatigue. A swelling called a “chagoma” at the site of the bug bite may be present. If the bug bite is close to the eyes, a distinct condition called Romana’s sign, swelling of the eyelids, may appear. The acute phase lasts for weeks or months after which the condition becomes chronic, which is virtually asymptomatic for a period of years or indefinitely. Eventually the trypanosomes are found in numerous sites around the body and in later years may lead to inflammation and disruption of function in organs such as the heart, the brain and the intestinal tract. Estimates put the prevalence at 8 million, 300,000 of whom live in the U.S. Chagas disease is a neglected parasitic infection in the U.S. Drugs for treatment are only available through the CDC. Recently, the U.S. begain screening all donated blood for Chagas Disease. See CDC
Plasmodium are blood and tissue protozoa. These parasites require two hosts; (1) a mosquito for sexual reproduction and (2) animals for asexual reproduction. Infection is by bite of the anopheles mosquito. Human pathogens include the following:
Malaria: see Chen (comprehensive discussion)
–Signs and Symptoms: after a 10-16 day incubation period, the first symptoms are malaise, fatigue, vaue aches and nausea with or without diarrhea, followed by bouts of chills, fever and sweating. These syptoms occur at 48-72 hour intervals, as a result of the synchronized rupturing of red blood cells.
The clinical features of malaria are primarily influenced by the species of Plasmodium responsible for the infection, and timing of the diagnosis and treatment.
Patients with falciparum malaria, the most virulent type, often display persistent fever, cough and weekenss for weeks without relief. Complications of malaria are hemoytic anemia from lysed blood cells and organ enlargement and rupture due to cellular debris that accumulates in the spleen, liver and kidneys. A serius complication of falciparum malaria is “cerebral malaria” where small blood vessels in the brain become obstructed due to the increased ability of red blood cells to adhere to veseel walls. The resulting decrease in oxxygen in brain tissue can result in coma and death. See Mayo Clinic See CDC
–causative agent:
Malaria is an infectious disease caused by a protozoan parasite Plasmodium, which is transmitted to the host by a Plasmodium infected female Anopheles mosquito during bloodmeal. The typical symptoms of malaria are a repeated cycle of fever paroxysm, shivering, body aches, abdominal pain, and other flu-like symptoms.
Five species of over 200 species of the genus Plasmodium are known to commonly infect humans. They are P. malariae, P. vivx, P, knowleski, P. ovale and P. falciparum. The five species show variations in the pattern and severity of disease. For example, P. falciparum is responsible for the vast majority of deaths.
The human malaria parasite causing the highest death rate in malaria endemic areas is P. falciparum. Infection by this parasite leads to severe clinical manifestations such as cerebral malaria, pulmonary edema, jaundice, respiratory distress or acidosis, and other lethal symptoms.
In terms of DNA sequences, Plasmodium species have compact genomes of 18–30 megabases (Mb) packaged into 14 chromosomes, with multigene families commonly found near the telomeric ends of each chromosome, which are organized as heterochromatin in distinct clusters at the periphery of the nucleus.
–Pathogenesis and Virulence factors:
The invasion of the merozoites into RBCs leads to the release of fever inducing chemicals into the bloodstream. Plasmodium also metabolizes glucose at a high rate, leading to hypoglycemia. The damage ot RBCs results in anemia.
Once injected into the human host by the female Anopheles mosquito, the sporozoites travel to the liver for differentiation. After multiplication and adaptation in hepatocytes for 6–7 days, thousands of merozoites egress from hepatic cells to infect red blood cells (RBCs). A recent study revealed that P. falciparum transmission is disproportionately driven by infected school-aged boys who receive a high number of mosquito bites, with infectious mosquitoes preferentially biting already infected individuals, highlighting the importance of targeted interventions for interrupting malaria transmission. Without prompt treatment, P. falciparum malaria can progress to severe illness and death, with symptoms such as severe anemia, respiratory distress, or cerebral malaria (CM).
–Transmission:
All forms of malaria are spread primarly by the female Anopheles mosquito. About 200 million new cases are reported each year, about 90% in Africa. The most frequent victims are children and young adults, of whom between 500k to 1 million die annually.
Malaria in the Americas is primarily confined to Brazil (33%), the Bolivarian Republic of Venezuela (26%), Colombia (21%), Guyana (6%), and Peru (4%) reporting the highest burden according to World Malaria Report 2024. In 2023, the region recorded ~505,642 cases. All indigenous malaria cases reported by Guatemala and Mexico were attributed to P. vivax. In the Bolivarian Republic of Venezuela, Brazil, Colombia, Ecuador, French Guiana, Guyana, Honduras, Nicaragua, Panama, Peru, and the Plurinational State of Bolivia, P. vivax accounted for 60% to 99% of the documented indigenous cases. Conversely, all indigenous cases reported by the Dominican Republic and Haiti, along with 92% of the indigenous cases recorded in Costa Rica in 2023, were attributed to P. falciparum. Colombia reported the highest number of P. falciparum cases in the region. Although malaria transmission is less intense than that in sub-Saharan Africa, challenges remain in remote and rural areas where healthcare access is limited, and migratory movements increase the risk of malaria transmission.
–Diagnosis:
Malaria can be diagnosed defininitevely by the discovery of a typical stage of Plasmodium in stained blood smears. Newer serological procedures are available. Other indications are knowledge of the patient’s residence or travel in endemic areas and symptoms such as recurring chills, fever, and sweating. Malaria can be diagnosed through clinical observation of the signs and symptoms of the disease. Other diagnostic techniques used to diagnose malaria are the microscopic detection of parasites from blood smears and antigen-based rapid diagnostic tests
–Prevention:
Abatement includes elimination of standing water that can serve as a breeding site and spraying of insecticides to reduce populations of adult mosquitoes, especially in or near human dwellings.
Serile male mosequitos have also been introduced into endemic areas.
One can reduce their risk of infections considerably by using netting, screens and repellants, by remaining indoors at night and by taking weekly doses of prophylactic drugs.
A vaccine callaed “RTS.S, is effective against P. faciparum (the most deadly and most common strain in Africa) in children.
–Treatment:
Classical antimalarial drugs such as chloroquine, quinine, pyronaridine, pyrimethamine, primaquine, and piperaquine have been widely applied in clinics to for decades. However, with the emergence of classical antimalarial drug resistance, especially in P. falciparum, artemisinin (ART)-based combination therapy (ACT) has been recommended as the firstline treatment. In this respect, Chinese scientists have made important contributions. Professor Tu Youyou was the pioneer who discovered a rational method for extracting the active ingredient, artemisinin, from the Artemisia annua plant and conducted the first clinical trial in patients.
—-Quinine with chloroquine being the least toxic type is used in nonresistant forms of Malaria. By 1820, the active ingredient in the bark of Cinchona trees, quinine, had been identified. In the 19th century, British soldiers in India used quinine-containing tonic water to fight malaria. In 1944, American chemists synthesized quinine. Qyinine can affect DNA replication and also, when P. falciparum breaks down hemoglobin from red blood cells in the digestive vacuole, an intermediary toxic form of heme is released. Quinine may itnerfer with the subsequent polymerization of these hemes, leading to a buildup of toxic hemes that poison the parasite. Now several other synthetic drugs are available to treat maleria.
–Artemisin: A drug called “artemisinin”, derived from a plant, is recommended in many situations. Artemisinin, which comes originally from a plant called sweet wormwood, used for centuries in Chinese traditional medicine, is one of the staples for maleria treatment. Artemisinin is a fast-acting antimalaria agent which is able to kill almost all forms of the parasites in blood stages. However, considering the low solubility of artemisinin in water or oil, and its low bioavailability, the derivates such as dihydroartemisinin, artesunate, and artemether, are mostly used rather than in its native structure.
Parasites resistant to antimalarial drugs are currently spreading even after the WHO introduced Artemisinin-based Combination Therapy (ACT), a combination of artemisinin and its partner drugs, as an alternative way to overcome antimalarial drug resistance. Low coverage and poor quality of malaria treatments have been suggested as factors which trigger the emergence of drug-resistant parasites.
Affecting the Reproductive Tract
Vaginitis: is an inflammation of the vagina.
–signs and sumptoms: in clude some degree of vaginal itching, depending ont he etiologic agent. Sumptoms may also include burning and sometimes a discharge.
–Causative agents: While a varienty of bacteria and even protozoa can cause vaginitis, the must well known agent is the fugus Candida albicans. (see Fungus)
—-Trichomonas vaginglis: Another possible cause of vaginitis is Trichomonas which are small, pear-shaped protozoa. Trichomonas is a common sexually transmitted infeciton. Because it does not form cysts, it is more delicate and must be transmitted by intimate contact between sexual partners. see CDC
The flagellated protozoan parasite Trichomonas vaginalis, occurring in the human urogenital tract, is the etiological agent of trichomoniasis, the most common worldwide nonviral sexually transmitted infection (STD). The incidence of trichomoniasis rate depends on many factors including age, sexual activity, number of sexual partners, the presence of other STDs, sexual customs, phase of the menstrual cycle, techniques of examination, specimen collection and laboratory technique. Together with Chagas disease, cysticercosis, toxocariasis and toxoplasmosis, trichomoniasis belongs to the group of neglected parasitic infections (NPIs), which has been targeted by the CDC as a priority for public health action. Trichomonas vaginalis is a sexually transmitted pathogen with the highest annual incidence of all curable and non-viral STIs. At the 2008, the prevalence of T. vaginalis was higher than Chlamydia trachomatis (100.4 million), Neisseria gonorrhoeae (36.4) and Treponema pallidum (36.4) infections combined. (“Trichomonas vaginalis: pathogenicity and potential role in human reproductive failure” 2016)
Trichomonas vaginalis, a prevalent sexually transmitted protozoan parasite, is associated with adverse birth outcomes, increased risk of HIV and other sexually transmitted infections, infertility, and cervical cancer. Despite its widespread impact, trichomoniasis remains underdiagnosed and underreported globally.
This infection may also increase the risk of human immunodeficiency virus (HIV) transmission and other STD infections which are observed significantly more frequently in women. Infection may cause chronic inflammation of the genitourinary tract, which may even lead to infertility. Several studies report that patients with T. vaginalis infection display deleterious outcomes in reproduction. Additionally, the incidence and severity of cervical dysplasia and prostate cancer is also associated with trichomoniasis.
—-Diagnosis: Microscopic examination of a wet mount preparation of genital secretions is still the most common method for T. vaginalis detection. The newly designed NAATs (e.g., APTIMA T. vaginalis FDA-approved assay) are the most sensitive tool for identifying Trichomonas asymptomatic infection in both women and men, but their high cost and required infrastructure prevent their widespread use in laboratories. Additionally, point-of-care tests that detect protozoan antigens (e.g., OSOM® Trichomonas Rapid Test) or unamplified RNA (e.g., Affirm VP III) has also been developed. NAATs for T. vaginalis are the most sensitive tests and are moderately priced, but high-complexity assays. The Aptima T. vaginalis assay (Hologic Gen-Probe, San Diego, California) was FDA-cleared in 2011 for use with urine, endocervical and vaginal swabs, and endocervical specimens collected in the Hologic PreserveCyt solution (ThinPrep) from asymptomatic and symptomatic women. Sensitivity and specificity are both 95%–100%. This assay has not been FDA-cleared for use in men and must be internally validated per Clinical Laboratory Improvement Amendments (CLIA) regulations prior to use. The BD Probe Tec TV Qx Amplified DNA Assay (Becton Dickinson, Franklin Lakes, New Jersey) is FDA-cleared for detection of T. vaginalis from vaginal (self-collected and clinician-collected) swabs, endocervical swabs, or urine specimens from women, with a sensitivity and specificity of 98.3% and 99.6%, respectively, compared to wet mount and culture. Similar to the Aptima T. vaginalis assay, this test is only FDA-cleared for use in women and must be internally validated per CLIA regulations prior to use in men.
—-Symptoms: The majority of women (85%) [18] and men (77%) [19] with T. vaginalis are asymptomatic. Half of the asymptomatic women may become symptomatic within 6 months. Symptomatic women can have vaginal erythema, dyspareunia, dysuria, and vaginal discharge (which is often diffuse, malodorous, and yellow-green in color), as well as pruritus in the genital region. The normal vaginal pH is 4.5, but with T. vaginalis infection this may increase markedly, often to >5. Complications of T. vaginalis among women include infection of the Skene and Bartholin glands, and increased risk of pelvic inflammatory disease among women with human immunodeficiency virus (HIV) infection. In men, it can cause urethritis, epididymitis, prostatitis, and decreased sperm motility.
—-Treatment : .Oral 5-nitroimidazoles (metronidazole [MTZ], tinidazole [TDZ], and secnidazole [SEC]) are the only class of drugs approved by the FDA for the treatment of trichomoniasis.
Affecting the Gastrointestinal Track
Amebiasis (amoebic dysentery): see Cleveland Clinic (description)
Amebiasis is the second leading cause of death from parasitic disease worldwide. The causative protozoan parasite, Entamoeba histolytica, is a potent pathogen. Amoebiasis is a common infection of the human gastro-intestinal tract. Amoebiasis is more closely related to poor sanitation and socioeconomic status than to climate. It has worldwide distribution. It is a major health problem in China, South East and West Asia and Latin America, especially Mexico. Only about 10% to 20% of people who are infected with E. histolytica become sick from the infection.
In developed countries, amebiasis primarily affects migrants from and travellers to endemic regions, men who have sex with men, and immunosuppressed or institutionalized individuals. The use of night soil for agricultural purposes favours the spread of the disease. Epidemic/ outbreaks (occurrence of more cases of a disease than would be expected in a community or region during a given time period) are usually associated with sewage seepage into the water supply. See AIMU
–Pathogenesis/Symptoms: Secreting proteinases that dissolve host tissues, killing host cells on contact, and engulfing red blood cells, E histolytica trophozoites invade the intestinal mucosa, causing amoebic colitis. In some cases amoebas breach the mucosal barrier and travel through the portal circulation to the liver, where they cause abscesses consisting of a few E histolytica trophozoites surrounding dead and dying hepatocytes and liquefied cellular debris. See Stanley
The clinical spectrum ranges from asymptomatic infection, diarrhoea and dysentery to fulminant colitis and peritonitis as well as extra-intestinal amoebiasis. Acute amoebiasis can present as diarrhoea or dysentery with frequent, small and often bloody stools. Chronic amoebiasis can present with gastrointestinal symptoms plus fatigue, weight loss and occasional fever. Extra-intestinal amoebiasis can occur if the parasite spreads to other organs, most commonly the liver where it causes amoebic liver abscess. Amoebic liver abscess presents with fever and right upper quadrant abdominal pain. Other organs can also be involved, including pleuropulmonary, cardiac, cerebral, renal, genitourinary, peritoneal, and cutaneous sites.
The cyst, which is the contaminating form, ensures the survival of the species because it resists to environmental changes and is easily transmitted. Due to their high resilience, cysts overcome the eradication of the pathogen by the immune system or by antibiotic treatment. Mature cysts are excreted in the host’s stool and are transferred to another human via a faecal-oral route through contaminated food or water or person-to-person contact; thus, amoebic infection occurs when water quality, sanitation, and hygiene practices are inadequate. After ingestion by a new host, in the small intestine, the cyst emerges into four disease-causing trophozoite forms that migrates and colonizes the large intestine, where they feed on bacteria and divide or encyst themselves.
Diagnosis: From the diagnostic point of view specific detection of E. histolytica is necessary since E. dispar and E. moshkovskii are not proven to cause disease. Most of the epidemiological data for intestinal amebiasis are based on the identification of the species in stool specimens by light microscopy. However, microscopy is unable to differentiate the three species, is at best 60% sensitive, and can be confounded by false-positive results due to misidentification of macrophages and other species of Entamoeba. New approaches used to detect E. histolytica and E. dispar are based on antigen detection in stool specimens. and species-specific PCR amplification of E. histolytica, E. dispar and E. moshkovskii DNA, including DNA from formalin-fixed stool samples. See Petri
Balantidium coli: is an intestinal protozoan parasite that causes the infection “balantidiasis”. It is most prevalent in tropical and subtropical regions. It is rare in the U.S. It is transmitted by the fecal-oral route. Humans can become infected by eats fruits and vegetables that have come into contact with fecal matter from an infected animal, as well as drinking and washing food with contaminated matter. Most people experience no symptoms. It infects the large intestine of humans and the cysts are then passed into the feces. It can be serious for immunocompromised people. Symptoms in these people include persistent diarrhea, weight loss, nausea and vomiting. It is treated with tetracycline, metronidazole, and iodoquinol. See CDC website
Cryptosporidium: (See also Waterborn illnessness) is an intestinal protozoan that infects a variety of mammals, birds and reptiles. For many years, it was considered an intestinal ailment exclusive to calves, pigs, chickens and other poultry but it is clearly a zoonosis as well. Humans accidentally ingest the oocysts with water or food that has been contaminated by feces form infected animals. The organism penetrates the intestinal cells and lives intracellularly in them. It undergoes asexual and sexual reproduction in these cells, produces more oocysts which are released into the gut lumen, excreted form the host and after a short time become infective again. The oocysts are highly infectious and extremely resistant to treatment with chlorine and other disinfectants. Half of the outbreaks of diarrhea associated with swimming pools are caused by Crytosporidium. Because chlorination is not entirely successful in eradicating the cysts, most treatment plants use filtration to remove them, but even this method can fail. Treatment is not usually required for otherwise healthy patients. Antidiarrheal agents (antimotility drugs) may be used.
Cryptosporidium is a widely distributed enteric parasite that has an increasingly appreciated pathogenic role, particularly in pediatric diarrhea. While cryptosporidiosis has likely affected humanity for millennia, its recent “emergence” is largely the result of discoveries made through major epidemiologic studies in the past decade.
Although no curative antimicrobial agent exists for Cryptosporidium, physicians will often try nitazoxanide, which can be effective against protozoa in immunocompetent patients. Nitazoxanide is thought to primarily interfere with the pyruvate:ferredoxin oxidoreductase (PFOR) enzyme-dependent electron-transfer reaction, a process essential for anaerobic energy metabolism in certain parasites like Giardia lamblia and Cryptosporidium parvum. See K-State (outlines many potential treatments) for Cryptosporidium parvum)
Cystoisosporiasis is an intestinal disease caused by the microscopic parasite Cystoisospora belli. This is the same parasite that used to be called Isospora belli. The parasite can be spread by ingesting food or water that was contaminated with feces (stool) from an infected person. People become infected by swallowing mature parasites, for example, by ingesting contaminated food or water. Infected people shed the immature form of the parasite in their feces. The parasite usually needs about 1 or 2 days in the environment (outside of people) to mature enough to infect someone else. In some settings, the parasite might mature in less than a day. Cystoisospora usually is spread indirectly, such as through contaminated food or water. This is because the parasite needs time to mature. However, oral-anal contact with an infected person might pose a risk for transmission. The infection is treated with prescription antibiotics. The usual treatment is with trimethoprim-sulfamethoxazole, which is also known as Bactrim*, Septra*, or Cotrim*. People who have diarrhea should also rest and drink plenty of fluids. See CDC
Giardiasis: Giardiasis is a diarrheal disease caused by the microscopic parasite Giardia. A parasite is an organism that feeds off of another to survive. Once a person or animal (for example, cats, dogs, cattle, deer, and beavers) has been infected with Giardia, the parasite lives in the intestines and is passed in feces (poop). Once outside the body, Giardia can sometimes survive for weeks or months. Giardia can be found within every region of the U.S. and around the world. See CDC
Giardia lamblia (syn.Giardia intestinalis, Giardia duodenalis) is a flagellated unicellular eukaryotic microorganism that commonly causes diarrheal disease throughout the world. It is the most common cause of waterborne outbreaks of diarrhea in the United States . It is occasionally seen as a cause of food-borne diarrhea. In certain areas of the world, water contaminated with G. lamblia cysts commonly causes travel-related giardiasis in tourists. Giardia species have two major stages in the life cycle. Infection of a host is initiated when the cyst is ingested with contaminated water or, less commonly, food or through direct fecal-oral contact. The cyst is relatively inert, allowing prolonged survival in a variety of environmental conditions. After exposure to the acidic environment of the stomach, cysts excyst into trophozoites in the proximal small intestine. The trophozoite is the vegetative form and replicates in the small intestine, where it causes symptoms of diarrhea and malabsorption. After exposure to biliary fluid, some of the trophozoites form cysts in the jejunum and are passed in the feces, allowing completion of the transmission cycle by infecting a new host. See Adam
The greatest clinical experience is with the nitroimidazole drugs, i.e., metronidazole, tinidazole, and ornidazole, which are highly effective. A 5- to 7-day course of metronidazole can be expected to cure over 90% of individuals, and a single dose of tinidazole or ornidazole will cure a similar number. Quinacrine, which is no longer produced in the United States, has excellent efficacy but may be poorly tolerated, especially in children. Furazolidone is an effective alternative but must be administered four times a day for 7 to 10 days. Paromomycin may be used during early pregnancy, because it is not systematically absorbed, but it is not always effective. Patients who have resistant infection can usually be cured by a prolonged course of treatment with a combination of a nitroimidazole with quinacrine. See Gardner
Sarcocystis: is one of the most frequently identified protozoa of warm-blooded animals worldwide, causing an intestinal infection in the definitive host of an extraintestinal infection in the intermediate host. Human intestinal sarcocystosis (i.e., humans as the definitive host) is arerely reported. Infection is acquired by ingesting raw or undercooked meet contaiing cysts of the paraside, such as pork for S. suihominis or beef for S. hominis and S.heydorni. (“Simultanteous Detection of Sarcocystis hominis, S. heydorni, and S. sigmoideus in human intestinal Sarcocystosis, France, 2021-2024” 31(3), March 2025).
Genetic characterization of Sarcocystis is commonly based on the mitochondrial cytochrome c oxidase subunit I (COI) gene sequences.
Affecting the Nervous System
Amoebas:
Amoebae are unicellular microorganisms which are trophozoites in that they have 2 stages; an active motile feeding stage that is non infectious and a cyst stage that is infectious. Important amoebae include the following:
–Naegleria fowleri:
Naegleria fowleri is an ameboflagellate found in freshwater lakes and ponds and is the casative agent of primary amebic meningoencephalitis, a rapidly fatal disease of the central nervous system. The determinants of virulence for this ameba are unkown, but resitance to complement lysis appears to play a major role in its pathogenicity. While both pathogenic and nonpathonic Naegleria species activate AP, pathogenic N. fowleri amebae are resistance to the lytic effect of complement. Fritzinger (Infection and Immunity, 2006, 74 (2) pp. 1189-1195) demonstrate a CD59-like protein which could bind human C9 on the surface of pathogenic N. fowleri amebae and that the ability of a pathogenic species of Naegleria to synthesize a protein which protects the amebae from lytic molecules, such as MAC of complement (C5b-C9), may serve as an important virulence factor.
Naegleria fowleri occurs in people who have been swimming in warm, natural bodies of freshwater. Infection can begin when amoebas are forced into human nasal passages as a result of swimming, diving, or other aquatic activities. Once the amoeba is inoculated into the favorable habitat of the nasal mucosa, it burrows in, multiples and uses the olfactory nerve to migrate into the brain and surrounding structures. The result in primary ameibic meningo-encephalitis is a rapid massive destruction of brain and spinal tissue that causes hemorrhage and coma and invariable ends in death within a week or so. Early therapy with amphotericin B, sulfadiazine or tetracyline in some cominbation can be of some benefit. Becasue of the wide distribution of the amoeba and its hardiness, no general method of control exists. Public swimming pools and baths must be adequately chlorinated and checked periodically for the amoeba.
N. fowleri occurs in three different forms. When conditions become too hostile, the amoeba transforms into a metabolically inactive cyst, described as a spherical structure that measures from 7 to 12 µm in diameter, with a thick endocyst, a thin ectocyst, and some mucoid-plugged pores. When the amoeba faces non-nutritive conditions but is in the presence of water, it transforms into a transitory flagellate. This form has a pear-shaped appearance measuring from 10 to 16 µm and has two flagella of approximately the same length. They have a nucleus, a nucleolus, vacuoles, cytoplasmic inclusions, mitochondria, and a rough endoplasmic reticulum.
–Acanthamoeba: differs from Naegleria below in its portal of entry. It invades broken skin, the conjunctiva, and occasionally the lungs and urogentical epithelia. It causes a meningoencephalitis somewhat similar to that of Naegleria. The course of infection is lenghthier but nearly as deadly with only a 2-3% survival rate. At special risk for infection rare people with traumatic eye injuries, contact lens wearers and AIDS patients exposed to contaminated water. Acanthamoeba exhibits a biphasic life cycle consisting of two primary stages: trophozoites and cysts. Trophozoites are the active feeding stage that divides mitotically under favorable conditions, such as abundant food, neutral pH, and an optimal temperature of around 30°C.
Acanthamoeba can infect humans through several routes, including the eye, respiratory tract, and skin. In contact lens wearers or individuals with corneal trauma, trophozoites may enter the eye and cause severe keratitis. Trophozoites or cysts can also be inhaled through the nasal passages and reach the lower respiratory tract, while broken skin or ulcers offer an entry point for the amoeba to invade the body. Upon entering the host, Acanthamoeba can cause various clinical syndromes depending on the infection route and the individual’s immune status. See Carg
The most common manifestation of Acanthamoeba infection is keratitis, predominantly affecting contact lens wearers or those with corneal trauma. Without prompt treatment, this can lead to vision loss. Granulomatous amebic encephalitis (GAE) is a rare but fatal central nervous system infection, usually occurring in immunocompromised individuals. GAE is characterized by severe central nervous system dysfunction and rapid degeneration. Additionally, Acanthamoeba can disseminate hematogenously to cause skin lesions, sinusitis, pneumonia, and other systemic infections, primarily in immunocompromised hosts. See Carg
—-Acanthamoeba keratitis (AK) is a rare but severe corneal infection caused by Acanthamoeba, a free-living amoeba ubiquitously found in the environment, including water, soil, and air. This opportunistic pathogen can infect the cornea, leading to a painful and sight-threatening condition. AK primarily affects individuals who wear contact lenses, but it can also occur in non-lens wearers, particularly those exposed to contaminated water or those with compromised immune systems. The disease is characterized by progressive corneal inflammation, epithelial defects, and ulceration, which can result in significant visual impairment or even blindness if not promptly diagnosed and treated. See Carg
Acanthamoeba keratitis is an unusual corneal infection that is recently increasing in frequency and is often contracted by contact lens wearers, someone who experienced recent eye trauma, or someone exposed to contaminated waters. Acanthamoeba survive in air, soil, dust, and water. Therefore, eye trauma and poor contact lens hygiene practices lead to the entrapment of debris and thus infection. Acanthamoeba keratitis results in severe eye pain, inflammation, and defects of the epithelium and stroma that can potentially result in vision loss if not diagnosed early and treated promptly. The disease can be diagnosed using corneal scrape/biopsy, polymerase chain reactions, impression cytology, or in vivo confocal microscopy. Once diagnosed, it is usually treated with an antimicrobial combination therapy of biguanide and aromatic diadine eye drops for several months. See Stuart
—Giardia lambia is a flagellate. Symptoms can be mild to severe (particularly for those with immunocompetency like AIDS patients).
—Balantidium coil is the only member of the ciliate group which is pathogenic for humans, particularly for AIDS patients.
—isospora belli also belong to the coccidia. It reproduces in the intestinal epithelium and results in tissue damage.
Toxoplasma gondii: is a protozoal infection that occurs in a fetus or in people with immunodeficiencies, especially those with AIDS. It is an obligate intracellular parasite, making its ability to invade host cells, an important factor for virulence. It is severe and often fatal. Although infection in otherwise healthy poeple is generally unnoticed, recent data suggest that it may have subtle but prodund effects on their brain and the respoens it controls. Mot cases of toxoplasmosis are asymptomatic or marked by mild symptoms such as sore throat, lymph node enlargement and low grade fever.
Toxoplasma is a globally distributed pathogen of humans and animals. Between 30-80% of the human population carries latent infection with this opportunisitc parasite. T. Gondii develops in the intestinal cells of cats. Humans can become infected by ingestion of infective ooxycts from cat fecal contamination or by ingestion of improperly cooked meat from an intermediate host. Infection can be serious in immunocompromised people. This is a risk in AIDS patietns, where about 25% of those carring latent T. gondii infection undergo reactivating toxoplasmosis in the central nervous system.
Toxoplasma gondii is an obligate intracellular protozoan parasite, which means that T. gondii is a unicellular eukaryote that survives by living in host cells. T. gondii is in the Apicomplexa family, which includes other protozoans such as Plasmodium species, the causative agents of malaria, and Cryptosporidium, a common cause of childhood diarrheal illnesses. All Apicomplexa have unique organelles at one end of the cell — the apical end — that are used for host cell invasion.
T. gondii’s life cycle has both sexual and asexual phases. The sexual life cycle only occurs in cats, which are therefore referred to as the ‘definitive’ hosts for T. gondii. In the cat gut epithelium, T. gondii differentiates into male and female gametocytes allowing sexual reproduction. In addition to its definitive host, T. gondii can naturally infect a wide range of warm-blooded intermediate hosts, ranging from birds to humans to rodents. In intermediate hosts, T. gondii undergoes asexual replication, meaning that parasites simply replicate their haploid genome and divide into two daughter cells. T. gondii invades host cells by inserting its so-called ‘invasion machinery’ into the host cell’s plasma membrane. Unlike its cousin Plasmodium, T. gondii does not require a specific host receptor or protein to invade, thus explaining why it is capable of invading any nucleated host cell in vitro. During invasion, T. gondii enters the host cell while dragging host membrane with it. In so doing, the parasite becomes surrounded by the host membranes, and establishes a parasitopherous vacuole — the intracellular niche in which T. gondii then replicates asexually.
n humans with intact and well-developed immune responses, the vast majority of T. gondii infections are thought to be asymptomatic or produce a mild flu-like illness at the time of acute infection. Most symptomatic disease caused by T. gondii relates to the parasite’s tropism for, and persistence within, the brain, and primarily occurs in immunodeficient individuals such as unborn fetuses or AIDS patients. In persons with intact immune systems
Affecting the Skin:
Leishmaniasis: is a zoonosis transmitted among various mammalian hosts by female sand flies. It is caused by a parasite called Leishmania that is transmitted through the bite of infected sand flies. The infection can express itself in several different forms, depending on which species of the protozoan Leishmania is involved.
Depending on the Leishmania species, the disease can cause three main clinical manifestations: (1) localized cutaneous leishmaniasis (CL) characterized by cutaneous ulcers, sometimes accompanied by satellite lesions and/ or nodular lymphangitis; (2) muco-cutaneous leishmaniasis (MCL) involving mucosa, and underlying connective tissues such as cartilage structures in combination with CL disease; and (3) visceral leishmaniasis (VL) affecting internal organs, like liver, spleen, and bone marrow. VL can be lethal, just like MCL, albeit the latter less frequently. See Schallig
–-Cutaneous Leishmaniasis (CL) is a localized infection of the capillaries of the skin caused by L. tropica, found in Mediterranean , Frican an dSoutheast Asian regions. A form of mucocutaneous leishmaniasis called espundia is caused by L. brasiliensis, endemic to parts of Central and South America. It affects both the skin and mucous membranes.
Leishmania is transmitted to the mammalian host by the sand fly when it ingests the host’s blood. The disease is endemic to equatorial regions that provide favorable conditions for the sand fly. There is no vaccine. Avoiding the sane fly is the only prevention.
CL is a vector-borne infection caused by the protozoan parasite Leishmania. The vector is the female sandfly. Globally, CL affects 12 million cases and annually 2 million new cases occur. CL is endemic in almost 100 countries and the total risk population is approximately 350 million people. WHO lists CL an emerging and uncontrolled disease and a neglected tropical disease. Local experience-based evidence remains the mainstay for the management of CL.
Whereas intralesional therapeutic options are the first treatment option for most CL patients, those with mucocutaneous and disseminated involvement require a systemic therapeutic approach. Moreover, different Leishmania species can vary in their treatment outcomes. Therefore, species determination is critical for optimal CL clinical management. New DNA techniques allow for relatively easy Leishmania species determination, yet they are not easily implemented in resource-limited settings. There is a desperate need for novel, less toxic, and less painful treatment options, especially for children with CL. Yet, the large and well conducted studies required to provide the necessary evidence are lacking. To further control and potentially eliminate CL, we urgently need to improve vector control, and diagnostics, and we require efficient and safe vaccines. Alas, since CL primarily affects poor people, biotechnical companies dedicate little investment into the research programs that could lead to diagnostic, pharmaceutical, and vaccine innovations. See Schallig