Lecture 2-3 PDF - Parasitic Diseases

# Lecture 2 ## Phylum Sarcomastigophora ### Classification of Amoebae **Classification Based On Habitat** Amoebae are classified as intestinal amoebae and free living amoebae. **Intestinal amoeba:** They inhabit in the large intestine of humans and animals. * *Entamoeba histolytica* is the only...

# Lecture 2 ## Phylum Sarcomastigophora ### Classification of Amoebae **Classification Based On Habitat** Amoebae are classified as intestinal amoebae and free living amoebae. **Intestinal amoeba:** They inhabit in the large intestine of humans and animals. * *Entamoeba histolytica* is the only pathogenic species. Others are nonpathogenic such as - *E*. *dispar*, *E*. *moshkovskii*, *E*. *coli*, *E*. *polecki*, *E*. *hartmanni*, *E*. *gingivalis*, *Endolimax nana*, and *Iodamoeba butschlii* **Free-living amoebae:** They are small free living and opportunistic pathogens. * Examples are *Acanthamoeba keratitis*, *Acanthamoeba castellanii*, *Naegleria fowleri*, *Balamuthia mandrillaris* and *Sappinia diploidea*. ### *Pneumocystis carinii* Scientists have changed both the classification and the name of this organism since it first appeared in patients with HIV (human immunodeficiency virus) in the 1980s. Based on morphology, *Pneumocystis* was originally thought to be a protozoa. However, in 1988, DNA analyses revealed that the genomic structure of *Pneumocystis* was more closely related to fungi than to protozoa (Edman et al. 1988). *Pneumocystis jirovecii* used to be called *Pneumocystis carinii*. **Habitat and Distribution:** Worldwide and non-seasonal, in humans and animals. Pneumocystis pneumonia (PCP) occurs in immunosuppressed individuals and in premature, malnourished infants. **Pathogenicity:** The causative organism of the most common serious opportunistic infection in persons with HIV infection *Pneumocystis* pneumonia (PCP) , it is an important human pathogen, particularly among immunocompromised hosts. Multiplication is by a cyst-trophozoite-cyst within the reservoir host. **Transmission:** organism is probably acquired by the respiratory route **Symptoms:** Pneumocystosis. Most people who get PCP have a medical condition that weakens their immune system, like HIV/AIDS, or take medicines (such as corticosteroids) that lower the body's ability to fight germs and sickness. The symptoms of Pneumocystis pneumonia (PCP) include Respiratory manifestations (tachypnea, dyspnea and nonproductive cough), Fatigue, and fever. Chest radiography demonstrates bilateral infiltrates. Extrapulmonary lesions occur in a minority of patients, involving most frequently the lymph nodes, spleen, liver, and bone marrow. Typically, in untreated PCP increasing pulmonary involvement leads to death. **Treatment:** Antibiotics, the most common form of treatment is co-trimoxazole. ### Phylum Microspora The microsporidia are a group of unicellular intracellular parasites. They are characterized by the production of resistant spores that vary in size (usually 1-4 µm for medically-important species). The spores contain a long, coiled polar tube or polar filament, which distinguishes them from all other organisms and has a crucial role in host cell invasion. The infective form of microsporidia is the resistant spore, which can persist in the environment for months. Exposure to spores in water or in soil appears to be a potentially major route. To date, more than 1400 species belonging to over 200 genera have been described as parasites infecting a wide range of vertebrate and invertebrate hosts. There are at least 15 microsporidian species that have been identified as human pathogens; the vast majority of cases being caused by *Enterocytozoon bieneusi*, followed by *E*. *intestinalis*. *Enterocytozoon bieneusi* and *Encephalitozoon* spp. are obligate intracellular parasites which infects the intestinal epithelial cells causing self-limiting watery diarrhea in immunocompetent adults as well as in children. *Encephalitozoon intestinalis*, which is a common parasite in pigs, primarily causes chronic diarrhea, and the parasite may also spread into the biliary tract and gallbladder, causing cholangitis and cholecystitis. In contrast to *Enterocytozoon bieneusi*, systemic dissemination to kidneys and other sites may occur. Their life cycle includes a proliferative merogonic stage, followed by a sporogonic stage resulting in small, environmentally resistant, infective spores, which is their transmission mode. Their development can occur either in direct contact with the host cell cytoplasm (*E. bieneusi*) or inside a vacuole called a parasitophorous vacuole (*E. intestinalis*). ### Phylum Myxozoa The Myxozoa is aquatic obligately parasites that usually have been classified and studied as protozoans. Myxozoa exhibits complex life cycles with gametic reproduction occurring within invertebrate definitive hosts such as aquatic annelids or freshwater bryozoans. In addition, it infects intermediary vertebrate hosts such as fish, amphibians, and reptiles. The transmission is mediated by spores. *Tetracapsuloides bryosalmonae* has a two-host life cycle, as other myxosporeans, cycling between freshwater bryozoa and salmonid fish species, rather than an oligochaete or polychaete worm as for *Myxobolus cerebralis*. Proliferative kidney disease (PKD) is characterized by a swollen kidney and spleen, bloody ascites, and pale gills, indicating the fish becomes anemic at the late stage of the disease. *Myxobolus cerebralis* is one of the most serious parasitic diseases of salmonid populations in Europe and North America that can result in losses of up to 90% in infected populations. *M. cerebralis* causes damage through attachment of triactinomyxon spores and the migrations of various stages through tissues and along nerves, as well as by digesting cartilage. The infection is characterized by the formation of cysts that cause gross deformities, tissue lesions, and organ malfunction, while in the gills, they can cause bleeding and swelling, which leads to a decreased surface for oxygen absorption. Whirling disease symptoms include skeletal deformities and "whirling" behavior (tail-chasing) in young fish, which was thought to have been caused by a loss of equilibrium but is actually caused by damage to the spinal cord and lower brain stem. ## *Gonyaulax polyedra* (Dinoflagellates) **Habitat and Distribution:** All species are marine, except for one freshwater species, *Gonyaulax apiculata*. **Transmission:** Although *Gonyaulax* is found in seawater, it can also have a detrimental effect on humans when it secretes a poisonous toxin known as "saxitoxin" which causes paralysis in humans. Filter feeding organisms (e.g., mussels, clams, etc.) can accumulate these dinoflagellates in their bodies. When humans eat these shellfish after dinoflagellate accumulation during Red Tide season, usually during the warmer months of the year, it can poison the person who eats it.. **Symptoms:** Paralytic shellfish poisoning (PSP) is a serious illness caused by eating shellfish contaminated with algae that contains Paralytic Shellfish Toxin (PST), a toxin harmful to humans. This toxin is irritating to the human respiratory system and is extremely poisonous that as little as one milligram is enough to kill an adult. Early symptoms include tingling of the lips and tongue, which may begin within minutes of eating poisonous shellfish or may take an hour or two to develop. Depending upon the amount of toxin a person has ingested, symptoms may progress to tingling of fingers and toes and then loss of control of arms and legs, followed by difficulty in breathing. Some people have experienced a sense of floating or nausea. If a person consumes enough poison, muscles of the chest and abdomen become paralyzed. Death can result in as little as two hours, as muscles used for breathing become paralyzed. **Treatment:** The only treatment for severe cases is the use of a mechanical respirator and oxygen. ## Entamoeba Histolytica * *E. histolytica* has three subspecies - *E*. *histolytica* subspecies *histolytica*, *dispar* and *moshkovskii*. * History *E. histolytica* was first described by Fedor Lösch (1875) from Russia. * "Minuta" form of *Entamoeba histolytica*: They are the commensal phase of *E. histolytica*, living in the lumen of gut. They are usually smaller in size (trophozoite 12-14 µm and cyst < 10 µm) and often mistaken as *E. hartmanni*. ## Life Cycle Host: *E. histolytica* completes its life cycle in single host. Mature quadrinucleated cyst is the infective form. It can resist chlorination, gastric acidity and desiccation and can survive in a moist environment for several weeks. Note: Trophozoites and immature cysts can be passed in stool of amoebic patients, but they can't serve as infective form as they are disintegrated in the environment or by gastric juice when ingested. Mode of transmission: Feco-oral route (most common). By ingestion of contaminated food or water with mature quadrinucleated cysts. ## Development in man (small intestine) Excystation: In small intestine, the cyst wall gets lysed by trypsin and a single tetranucleated trophozoite (metacyst) is liberated which eventually undergoes a series of nuclear and cytoplasmic divisions to produce eight small metacystic trophozoites Metacystic trophozoites are carried by the peristalsis to ileocecal region of large intestine and multiply by binary fission, and then colonize on the mucosal surfaces and crypts of the large intestine. After colonization, trophozoites show different courses depending on various factors like host susceptibility, age, sex, nutritional status, host immunity, intestinal motility, transit time and intestinal flora. Asymptomatic cyst passers Trophozoites don't cause any lesion, transform into cysts and are excreted in feces ## *Trypanosoma brucei* Etymology: From the Greek trypanon, "borer," plus sōma, "body". The parasite is named after Sir David Bruce (1855 - 1931). Habitat and Distribution: *T. brucei* is found where its tsetse fly vectors are prevalent tropical rainforest, tropical monsoon, and tropical savannah areas of continental Africa. Hence, the equatorial region of Africa is called the "sleeping sickness" belt. Transmission: The disease is mostly transmitted through the bite of an infected tsetse fly *Glossina* sp.. Pathogenicity: This parasite is the cause of vector-borne diseases of vertebrate animals, including humans, transmitted by various subspecies of *Glossina* sp. (tsetse flies) in Africa. In humans *T. brucei* causes African trypanosomiasis, or sleeping sickness. In animals it causes animal trypanosomiasis, also called nagana in cattle and horses. Different Species: *T. brucei* has traditionally been grouped into three subspecies: *T. b. brucei*, *T. b. gambiense* and *T. b. rhodesiense*. The first is a parasite of non-human vertebrates, while the latter two are known to be parasites of humans. * *Trypanosoma brucei gambiense* is the etiological agent of Gambian trypanosomiasis, prevalent in West and Central Africa. Gambiense trypanosomiasis results essentially from man-to-man transmission, and the animal reservoir plays a role in sustaining the disease only in low-incidence areas. The very long duration of infection (months to years) is the major factor behind epidemics of Gambian trypanosomiasis, as the tsetse fly is a relatively inefficient vector. * *Trypanosoma brucei rhodesiense* is the agent of Rhodesian trypanosomiasis, seen in East and Southern Africa. Rhodesiense trypanosomiasis is a zoonosis, and cattle is the main animal reservoir. Rhodesian trypanosomiasis is more virulent and rarer; patient deaths often occur within a few months. Symptoms: Infection occurs in two stages * An initial haemolymphatic stage followed by * a meningoencephalitic stage after the trypanosomes invade the central nervous system (CNS). Gambian trypanosomiasis is characterized by a very long (months to years) incubation period during which infected persons are asymptomatic but may have enlarged cervical lymph nodes, followed by the appearance of non-specific symptoms such as intermittent fever. After a few months, the infection reaches the central nervous system resulting in a chronic lymphocytic meningo-encephalitis. Neurological symptoms such as sleep/wake cycle with daytime somnolence and persistent headaches become evident, and weight loss can be profound. Rhodesian trypanosomiasis is more virulent and causes a much more aggressive febrile disease with the incubation period, non-specific symptoms (high fever, myalgia, rigors, sweating) and neurological involvement progressing over a matter of weeks. Some patients develop septic shock, acute renal failure, disseminated intravascular coagulation and multiorgan failure within a few days of the first episode of fever. Treatment: Pentamidine is the recommended drug for first stage *T. b. gambiense* infection. Other drugs (suramin, melarsoprol, eflornithine, and nifurtimox ## *Trypanosoma cruzi* Etymology: Chagas disease is named after the Brazilian physician Carlos Chagas (1879-1934), who discovered the disease, and the parasite is named after Dr. Cruzi, the director of the Institute in which Dr. chagas worked. Habitat and Distribution: It is found only in the Americas. Chagas disease is common in parts of Mexico, Central America, and South America. Pathogenicity: This parasite is the cause of disease or the likelihood of disease that varies with the organism: Chagas disease in humans (also referred to as American trypanosomiasis), dourine and surra in horses, and a brucellosis like disease in cattle. Parasites need a host body and the haematophagous insect triatomine (descriptions "assassin bug", "cone-nose bug", and "kissing bug") is the major vector. Transmission: Individual triatomines infected with protozoa transmit trypanosomes when it bites and sucks blood for food, and when it deposits its faeces on the host's skin surface. Penetration of the infected faeces is further facilitated by the scratching of the bite area. Symptoms: Chagas disease's main impact is on the cardiovascular system. In the absence of successful treatment, infection persists for a lifetime, causing myocardial damage. Early in the disease course, chronic Chagas heart disease can be clinically silent but can progress to dilated cardiomyopathy with heart failure, ventricular arrhythmias and conduction disturbances, stroke, sudden death, and other systemic, like dilated oesophagus or colon leading to difficulties with eating or passing stool, or pulmonary embolisms. Treatment: The acute phase of Chagas disease is treated with nifurtimox or benznidazole. Cases of congenital Chagas diseas have been successfully treated with either drug.