Protozoa kb
- 1. Protozoa
- 3. Intestinal protozoa • The World Health Organization (WHO) - diarrheal disease as the 2nd highest cause of morbidity and mortality in children in the developing world. • Intestinal protozoa are transmitted by the fecal-oral route. • Life cycles consisting of a cyst stage and a trophozoite stage: - the cysts consist of a resistant wall and are excreted in the feces, its’ wall functions to protect the organism from desiccation in the external environment - trophozoite any stage which can ingest food, motile form
- 6. • EXCYSTATION occurs in the stomach and the duodenum in the presence of acid and pancreatic enzymes • In small bowel they multiply rapidly, with a doubling time of 9-12 hours • As trophozoites pass into the large bowel, ENCYSTATION occurs in the presence of neutral pH and secondary bile salts
- 7. • Assemblage A : A-I to A-IV: • A-I has been reported in humans and animals, • A-II in humans • A-III and IV exclusively in animals • Assemblage B has broad host specificity infecting humans and animals. • dogs and cats have been reported to also carry Assemblages A-I or B: zoonotic transmission ? • Giardia lamblia is an enteric protozoan pathogen found in a variety of mammalian hosts, including humans (isolated in 22 species of household stocks, ranging from sheep, cows, goats, to ducks: Sullivan 1988) • seven genetic Assemblages of Giardia duodenalis, named A-G • humans are infected with Assemblages A and B, • dogs primarily with C and D, • cats with F
- 8. Clinical: - 90% of infected are asymptomatic carriers - For symptomatic disease the incubation period is usually 3-20 days, but can be much longer - Acute giardiasis includes diarrhea (90%), gas, anorexia, weight loss: 10-15 pounds in adult (66%) - Chronic giardiasis – Giardia inhibits the digestion of fats by pancreatic lipase (malabsorption with diarrhea) - Impaired absorption of carotene, folate, vit. B 12 and D-xylose - Chief cause of growth retardation in infected children
- 9. Proposed mechanisms of pathogenesis include: • occlusion of the mucosa by large numbers of the organisms, • competition with the host for nutrients, • epithelial damage, • immune-mediated absorptive changes such as transient lactase deficiency, altered mucus secretion, and alterations in motility.
- 10. Diagnosis: - stool examination - duodenal fluid (aspirate or string test) - Giardia antigen detection in stool
- 11. In developed countries, giardiasis is considered a travel related disease. (Germany >50% acquired indigenously- Espelage et. al. 2010). Symptomatic cases are significantly more likely to be immunocompromised than control persons from the general population. Physicians should consider Giardia infections among patients with no recent history of travel abroad, particularly if they have immune deficiencies.
- 12. Developing countries: poor sanitary conditions, poor water quality and overcrowding Industrialized countries: international travel and immigration Populations at increased risk of autochthonous infection: small children in day care centres, oral-anal sex practitioners, persons in custodial institutions
- 13. Large community outbreaks have been attributed to: contaminated drinking water Smaller outbreaks: contaminated food (eg. green salad) contact with contaminated recreational waters (swimming and wading pools)
- 14. It is recommend boiling for 1 minute to allow for a margin of safety and so users are clear that the water is truly boiling. Because the boiling point decreases with increasing altitude, boil water for 3 minutes at altitudes greater than 6,562 feet (>2000 m). Microfilters with “absolute” pore sizes of 0.1–0.4 μm are usually effective for removal of cysts and bacteria
- 15. Entamoeba histolytica The only source: man (not a zoonosis) Transmission: fecal-oral Pathogenic amebas use three major virulence factors, eg. proteases, for: lyse, phagocytose, kill and destroy cells and tissues in the host Pathogenesis: - digests (liquifies) human host cells (colon wall, neutrophils, liver cells, RBC’s)
- 16. About 40–50 million people develop clinical amoebiasis each year, resulting on up to 100 000 deaths (Walsh 1988) Risk factors: • In tropics: crowded living conditions, poor sanitation • High alcohol consumption • Impaired immunity (eg. HIV infection) • Recent travel to an endemic area • Oral-anal contact : invasive amebic diseases more prevalent in homosexuals
- 18. RUQ: The RightUpperQuadrant of the abdomen contains the liver and the gallbladder.
- 21. Vasa shape ulceration of intestinal (large intestine) mucosa
- 23. Balantidium coli- balantidiosis • Balantidiosis is a zoonotic disease and is acquired by humans via the fecal-oral route from the pig • Human-to-human transmission may also occur • Balantidium's habitats in humans are the cecum and colon • B. coli can become an opportunistic parasite in urban environments, where pigs are not a factor in infection • Areas of high prevalence include regions of Latin America, the Philippines, Papua New Guinea Middle East (<1% to 29% in endemic area)
- 24. BALANTIDIUM COLI • Form nests and necrotic ulcers of the large intestine (bigger than the ulcer of E. histolytica) • In acute infection explosive diarrhea may occur as often as every 20 min , with mucus, blood •Perforation of the colon may also occur in acute disease, with life- threatening consequences • Chronic disease- intermittent diarrhoea alternating with constipation, tender colon, anemia and cachexia- wasting syndrome
- 25. The trophozoites large (typically > 50m ) vacuolated cytoplasm classic dark “kidney-bean” shaped macro-nucleus
- 26. Balantidium coli A Trophozoit ; B Cyst
- 27. Within the ulcer and intestinal mucosa, the large ciliated trophozoites can be seen
- 28. Extraintestinal sites of infection • the appendix but rarely, the liver • the lungs, causing a pneumonia-like disease (in elderly or otherwise immunocompromised ) • uterine infection, vaginitis, and cystitis, are thought to occur via direct spread from the anal area (Balantidium coli in the urine sediment -Maino et al. 2010)
- 29. • Cysts of Balantidium are large and would not be carried over great distances, either on air currents or in water droplets. Thus, infection by inhalation would require direct contact with aerosol droplets. • Rats may be carriers of Balantidium, but it is not known if the rat Balantidium species can infect humans. • The cockroach, which has its own species of Balantidium, may serve as a mechanical agent of transmission from feces to food
- 30. Protozoans of uro- genital tract
- 32. TRICHOMONAS VAGINALIS The most common non-viral human sexually transmitted pathogen Flagelate of the lumen of the urogenital tract, prostate. Only trophozoite stage known to exist i.e. absence of cyst stage. Epidemiology: incidence is about 10 – 20% in women. Higher among women with poor feminine hygiene. Mode of transmission: sexual contact, direct contact with infected female, contaminated toilet articles e.g. towels, toilet seats and infection acquired in babies while passing the birth canal.
- 33. • Pathophysiology: - causes degeneration and desquamation of local tissues; mechanism unclear symptomatic - vaginitis, prostatitis, urethritis Epidemiology - found in 3-5% of female population of N.A. - increased in STD clinics (50%), prostitutes 50-75% - only in humans; no animal reservoir - sexual transmission - can persist for 2 years in host
- 34. Treatment: • Drug of choice:1 Metronidazole 2 g once or 500 mg bid x 7d • OR Tinidazole 2 g once 50 mg/kg once (max. 2 g)
- 35. Pathology and Symptoms: Incubation period 4 to 20 days Symptoms: profuse, frothy, yellow-green or gray vaginal discharge leucorrhoea, sometimes with bleeding, an unpleasant vaginal odor, and vulvovaginal itching and discomfort. Painful and frequent urination, vulvovaginal swelling, discomfort during sexual intercourse, and abdominal pain Granular – strawberry vagina. In males, there may be urethritis
- 37. Between 15°N and 20°S T.b gambiense T.b rhodesiense
- 40. African Sleeping Sickness Gambian or Rhodesian tryponosomiasis Congestive heart failure (CHF) occurs when the heart can no longer pump blood efficiently, so the blood backs up in the body – particularly in the liver EKG
- 41. Trypanosomiasis The lymph node enlargement on the back of the neck and head - known as Winterbottom's sign.
- 43. Diagnosis - motile organisms on wet preparations of fresh blood or CSF - stained smears (Giemsa) may reveal organism - high levels of protein (IgG and IgM) in CSF - lymphocytosis in CSF -antigen capture or PCR
- 45. A zoonosis with reservoirs of armadillo, opossums, raccoons; transmitted to man Epidemiology: Transmission:by reduvid bug bite vertical (in utero) blood transfusion 12 million of people affected; 35 million at risk; Central and South America. Trypanosoma cruzi Chagas' Disease, American Trypanosomiasis
- 46. Triatoma infestans, Rhodnius prolixus and Panstrongylus megistus. The bug (Reduvidae bug) can live and be infective for two years Reduvid bug bites human while asleep and passes feces containing parasite (trypomastigote form) onto skin near the bite. Human rubs faeces and parasite into wound or eye.
- 47. Clinical: • Acute: Seen mainly in children: local inflammation at site of innoculation (chagoma), lymphadenopathy, hepatosplenomegaly, fever. • Chronic: Seen mainly in adult life up to several decades after acute stage myocardopathy • - heart failure, arrhythmias megaintestine • - megaoesophagus, megacolon, megaureter
- 48. Romana's sign in acute Chagas' disease Unilateral painless orbital oedema
- 49. Megacolon
- 50. Amastigota forms in heart muscle Cardiomegaly
- 51. CNS Protozoa
- 52. Naegleria sp. enters the body through the nose while swimming or participating in water sports. Once inside the nose, the amoeba makes its way to the brain. There, it causes inflammation and destroys brain tissue. Naegleria infection is very rare. Only 31 cases occurred in the United States between 1989 and 2002. About 200 cases of naegleriasis infection have been reported worldwide.
- 53. Clinical Features: Acute primary amoebic meningoencephalitis (PAM) is caused by Naegleria fowleri. • It presents with severe headache and other meningeal signs, fever, vomiting, and focal neurologic deficits • progresses rapidly (<10 days) • frequently leads to coma and death. Sources: the environment: warm water reservoirs, unchlorinated groundwater, soil
- 54. Acanthamoeba spp. causes mostly subacute or chronic granulomatous amoebic encephalitis (GAE), headaches, altered mental status, and focal neurologic deficit, which progresses over several weeks to death cause granulomatous skin lesions keratitis and corneal ulcers following corneal trauma (poor contact lens hygiene and exposure to contaminated water may increase the risk among contact lens users- coroneal trauma)
- 56. corneal trauma
- 57. systemic parasites tissues, body fluids: blood, cerebro-spinal
- 60. • Diagnosis of Malaria • a) clinical picture: - fever, chills - travel history - fever pattern • b) examination of blood: - thin - thick smear - PCR - antigen capture (ELISA)
- 61. BLOOD examination - thin smear for characteristics of species - use shape and size of: trophozoite, schizont and gametocyte - % of RBCs with parasites (very rarely over >1% parasitemia in P. vivax, ovale or malariae) - metabolic debris (pigment) in RBC around parasite (called Schuffner's dots in P. vivax infection) - size and age of RBCs which contain parasites (P. vivax and ovale infect younger (larger RBCs)
- 62. Severe Malaria: Common Clinical Manifestations Pathogenesis Clinical Features Cerebral Sluggish flow caused by sticky knobs on parasitized red cells leading to stagnant hypoxia and vascular damage. Impaired level of consciousness. Convulsions. Generalized and localized neurological signs. Anaemia Destruction of parasitized and nonparasitized red cells by immune complexes, bone marrow suppression Pallor and jaundice. High output cardiac state. Renal Acute tubular necrosis resulting from sluggish blood flow and hypotension. Hemoglobinuria. Oliguria. Haemoglobinuria. Acute renal failure. Gastro- intestinal Unknown. Diarrhoea.
- 63. Severe Malaria: Common Clinical Manifestations Pathogenesis Clinical Features Respiratory Increased pulmonary capillary permeability. Cough. Pulmonary edema, bronchopneumonia. Hepatic Unknown.? Partially due to haemodynamic changes. Jaundice (mainly attributable to haemolysis). Elevated serum enzyme levels, impaired elimination of drugs, prolonged prothrombin time, bleeding. Fluid and electrolyte balance Unknown.? Partially due to inappropriate release of antidiuretic hormone (ADH). Increased intravascular volume. Electrolyte changes, hypoglycemia, hyperkalemia and hemolysis. Obstetric Sluggish blood flow in placental vessels leading to vascular damage. Fetal death. Premature labour.
- 64. • ACUTE CLINICAL PICTURE COMPLICATIONS • fever, headache, splenomegaly • cerebral malaria (P.falciparum only) • adult respiratory distress syndrome (ARDS) (P.falciparum) • black water fever (severe hemolysis) (P.falciparum only) • acute renal failure • CHRONIC CLINICAL PICTURE: - nephrotic syndrome (P. malariae only) - big spleen syndrome (hypertrophic malarial splenomegaly)
- 66. Nephrosis associated with malaria Pigment in cerebral vessels (autopsy)
- 67. Entamoeba histolytica Giardia lamblia Balantidium coli
- 68. Trichomonas vaginalisTrichomonas vaginalis Trichomonas vaginalis Trichomonas vaginalis Naegleria sp. Acanthamoeba sp.