Entamoeba histolytica, Giardia, Balantidium, and Intestinal Coccidia: Parasite Life Cycles, Transmission, and Diagnosis

Entamoeba histolytica-Reservoir

Humans are the reservoir and most people are asymptomatic carriers who pass infective cysts

Entamoeba histolytica-Transmission

Fecal oral route, direct contact with dirty hands, sexual activities

Entamoeba histolytica-Life cycle basics

Consumed cysts excyst into trophozoites, trophozoites invade mucosa, encyst and cysts are evacuated in stool

Entamoeba histolytica-Trophozoite behavior

Trophozoites move along intestinal wall eating RBCs, bacteria, protozoa and human intestinal cells

Entamoeba histolytica-Invasive spread

Invasive colonic trophozoites can enter bloodstream and invade other organs

Entamoeba histolytica-Clinical presentation intestinal

Abdominal pain, dysentery with bloody and mucoid stools, colonoscopy shows ulcers

Entamoeba histolytica-Characteristic lesion

Flask shaped ulcerations of colonic mucosa

Entamoeba histolytica-Colonic complications

Peritonitis, appendicitis, necrotizing colitis and toxic megacolon (50 percent fatal)

Entamoeba histolytica-Liver abscess

Flank pain, fever, elevated AST and ALT, anchovy paste reddish brown pus, necrotic tissue, immune cells and parasites

Entamoeba histolytica-Liver abscess complications

Rupture into abdomen, chest or pericardial sac

Entamoeba histolytica-Diagnosis stool

Stool for Ova and Parasites, amoeba with intracellular RBCs is diagnostic

Entamoeba histolytica-Diagnosis antigen tests

Fecal antigen detection in stool and blood

Entamoeba histolytica-Diagnosis colonoscopy

Colonoscopy with microscopic exam of aspirates

Entamoeba histolytica-Diagnosis imaging

Liver imaging with ultrasound, CT or MRI

Entamoeba histolytica-Treatment

Iodoquinol or paromomycin (anti cyst) plus metronidazole or tinidazole (anti trophozoite)

Giardia duodenalis-Prevalence

Most common parasitic GI pathogen in the United States (~20,000 cases per year)

Giardia duodenalis-Reservoir

Human adapted species; animals such as beavers can transmit

Giardia duodenalis-Transmission

Classical fecal oral route with low infectious dose (few parasites)

Giardia duodenalis-Invasiveness

Non invasive pathogen

Giardia duodenalis-Life cycle stages

Cyst and trophozoite stages

Giardia duodenalis-Clinical symptoms

Diarrhea, gas, foul smelling greasy stools that float, bloating, cramps, dehydration, loss of appetite and weight loss

Giardia duodenalis-Post infection effects

Post infection increased risk of irritable bowel syndrome for 3-6 years

Giardia duodenalis-Diagnosis stool

Stool for Ova and Parasites but numbers of ova and parasites vary making it unreliable

Giardia duodenalis-Diagnosis antigen

Fecal antigen immunoassays more reliable

Giardia duodenalis-Treatment

Metronidazole, tinidazole or nitazoxanide

Balantidium coli-Unique feature

Only ciliate capable of infecting humans

Balantidium coli-Reservoir

Domesticated pigs are the primary reservoir; occupational exposure in farm workers and meat handlers

Balantidium coli-Life cycle

Excyst in small intestine, trophozoites invade epithelium, trophozoites encyst and shed in feces

Balantidium coli-Clinical presentation

Usually asymptomatic; symptomatic infections cause severe diarrhea, weight loss, abdominal pain and dysentery

Balantidium coli-Severe disease

Can be fatal in immunocompromised individuals

Balantidium coli-Extraintestinal spread

Does not cause liver, lung or brain abscesses

Balantidium coli-Diagnosis

Trophozoites in stool

Intestinal coccidia-Organism type

Apicomplexan protozoa, spore forming, obligate intracellular pathogens

Intestinal coccidia-Apical complex

Contain enzymes that penetrate cells

Intestinal coccidia-Morphology by species

Cryptosporidium tiny, Cyclospora mid sized, Cystoisospora large and ovoid

Intestinal coccidia-Transmission

Fecal oral transmission

Intestinal coccidia-Waterborne illness

Cryptosporidium is most common cause of waterborne illness in US (pools and lakes)

Intestinal coccidia-Chlorine resistance

Crypto highly resistant to chlorination

Intestinal coccidia-Infectious oocysts

Cryptosporidium oocysts infective when excreted allowing person to person transmission

Intestinal coccidia-Global distribution

Cryptosporidium in temperate and tropical zones

Intestinal coccidia-Oocyst maturation

Cyclospora and Cystoisospora oocysts require 2-6 weeks to become infectious making person to person unlikely

Intestinal coccidia-Tropical prevalence

Cyclospora and Cystoisospora are primarily tropical diseases

Intestinal coccidia-Clinical presentation

Voluminous watery diarrhea

Intestinal coccidia-Disease course immunocompetent

Self limited 10-14 days

Intestinal coccidia-Disease course immunocompromised

Chronic diarrhea and biliary tract disease (AIDS)

Intestinal coccidia-Diagnosis

Ova and Parasites with acid fast stain and identification by morphology and size

Plasmodium falciparum-Importance

Most virulent human malarial parasite accounting for 90 percent of cases

Plasmodium falciparum-Other species

P. vivax (~8 percent), P. ovale, P. malariae, P. knowlesi

Plasmodium falciparum-Symptoms uncomplicated

Headache, low grade fever, chills, sweats, nausea, vomiting, malaise, cough or respiratory distress

Plasmodium falciparum-Fever paroxysm pattern

Shivering and chills 1-2 hours, high fever 2-6 hours, then excessive sweating and rapid drop in temperature; repeats every 48 hours

Plasmodium falciparum-Severe disease features

Prostration, respiratory distress, jaundice (rare), seizures, coma, neurologic abnormalities indicating cerebral malaria

Plasmodium falciparum-Cerebral malaria fatality

20 percent fatal adults and 15 percent fatal children even with therapy

Plasmodium falciparum-Key virulence factors

Infects RBCs of all ages (≤80 percent of cells), shortest incubation period, rapid erythrocytic cycle (24-48 hours)

Plasmodium falciparum-Basophilic stippling

Forms knobs on infected RBCs leading to cytoadherence

Plasmodium falciparum-Cytoadherence

Knobs promote RBC agglutination and intracapillary sequestration causing cerebral malaria

Plasmodium falciparum-Reservoir

Humans

Plasmodium falciparum-Definitive host

Anopheles mosquito (sexual reproduction occurs here)

Plasmodium falciparum-Intermediate host

Humans

Plasmodium falciparum-Sporogenic cycle

Mosquito midgut fusion of gametocytes, zygote becomes oocyst, oocyst forms sporozoites, sporozoites enter salivary glands

Plasmodium falciparum-Liver stage

Sporozoites invade hepatocytes forming schizonts; rupture releases merozoites

Plasmodium falciparum-Blood stage

Merozoites infect RBCs, multiply, rupture RBCs and release more merozoites; some form gametocytes

Plasmodium falciparum-Diagnosis gold standard

Microscopy of thick and thin Giemsa stained blood smears

Plasmodium falciparum-Diagnosis thick smear

Detects presence of parasites

Plasmodium falciparum-Diagnosis thin smear

Allows species level identification

Plasmodium falciparum-Diagnosis complexities

Patients in endemic areas may have positive smears without clinical malaria; infected RBCs may be sequestered

Plasmodium falciparum-Poor prognosis threshold

>500,000 parasites per microliter (~10 percent parasitemia)

Plasmodium falciparum-Treatment

Mefloquine, doxycycline, atovaquone plus proguanil, artemisinin, primaquine

Plasmodium falciparum-Prevention

Insecticide treated bed nets, indoor residual spraying and mosquito vector control

Babesia spp.-Organism type

Intracellular parasites that resemble Plasmodium species

Babesia spp.-Human pathogen

Babesia microti causes most human infections

Babesia spp.-Reservoir

Deer, cattle and rodents

Babesia spp.-Vector

Ixodes scapularis (blacklegged or deer tick)

Babesia spp.-Geography

Endemic to Northeast Seaboard and Upper Midwest

Babesia spp.-Risk factors

Lack of spleen, immunocompromised status, old age

Babesia spp.-Symptoms

Many asymptomatic; high fever ≥40 Celsius, shaking chills, malaise, headache, fatigue

Babesia spp.-Hemolysis

Hemolytic anemia with dark colored urine

Babesia spp.-Microscopy features

Ring forms and Maltese Crosses in RBCs

Leishmania spp.-Transmission

Sandfly bite

Leishmania spp.-Cell target

Intracellular pathogens of macrophages

Leishmania spp.-Reservoirs

Humans (Africa and Asia), rodents, canines including domestic dogs, equines, monkeys, sloths

Leishmania spp.-Cutaneous lesion progression

Starts as small papule, enlarges, ulcerates with eschar, usually painless

Leishmania spp.-Cutaneous healing

90 percent are self healing but leave hypopigmented depressed scars

Leishmania spp.-Cutaneous hallmark

Volcano sign with rolled edges

Leishmania donovani-Disease type

Causes visceral leishmaniasis (kala azar)

Leishmania donovani-Epidemiology

Second largest parasitic killer in the world after malaria

Leishmania donovani-Asymptomatic rate

95 percent remain asymptomatic

Leishmania donovani-Risk groups

Children, chronically ill, malnourished, immune deficient especially HIV positive

Leishmania donovani-Classic pentad

Fever, cachexia, hepatosplenomegaly, pancytopenia, hypergammaglobulinemia