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159 Cards in this Set
- Front
- Back
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What are protozoa?
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Single-celled eukaryotic organisms, many of which have evolve organelles, including mitochondria, food vacuoles, muclei, and an endoplasmic reticulum
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How do they replicate?
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Mainly by binary fission; however, some species undergo sexual reproduction
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What is the clinical significance of protozoal infections?
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The majority of protozoa are not human pathogens; however many types of protozoal infections are more common in developing tropical and subtropical regions and thus may be a significant cause of morbidity and mortality in these regions
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What are teh two stages of the protozoan life cycle seen in many (but not all) protozoa?
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Cyst stage
Trophozoite stage |
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How do the stages in protozoan life cycle differ?
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In the cyst stage, the protozoa are dormant and immotile, allowing for survival in harsh environments
In the trophozoite stage, protozoa are actively feeding, reproducing, and mobile |
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What are the three main categories of protozoa that are classified according to the area of the body where they usually cause disease?
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Intestinal
Urogenital Blood and tissue |
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How are protozoa further classified within these main categories?
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According to their mode of locomotion
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What are four groups of protozoa according to this classification?
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Amebas
Flagellates Sporozoans Ciliates |
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What is the method of locomotion for Amebas?
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Extension of pseudopodia (cytoplasmic projections, outward from the main cell body)
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What is the method of locomotion for Flagellates?
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Rotation of flagella, (whip-like projections)
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What is the method of locomotion for Sporozoans?
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Adult form is typically nonmotile
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What is the method of locomotion for Ciliates?
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Synchronous beating of cilia (hair-like projections)
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ID the major pahtogenic intestinal species of Ameba.
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Entamoeba histolytica
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ID the major pahtogenic intestinal species of Flagellate?
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Giardia lamblia
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ID the major pahtogenic intestinal species of Sporozoa?
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Cryptosporidium parvum
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ID the major pahtogenic intestinal species of ciliate?
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Balantidium coli
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What are the minor pathogenic sporozoans?
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Isospora belli
Cyclospora cayetanensis |
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Which is the major pathogenic urogenital flagellate?
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Trichomonal vaginalis
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What are the major pathogenic blood and tissue species in amebas?
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Naegleria fowleri
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What are the major pathogenic blood and tissue species in Flagellates?
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Leishmania species
Trypanosoma species |
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What are the major pathogenic blood and tissue species in sporozoans?
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Plasmodium species
Toxoplasma gondii |
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What is a minor pathogenic blood and tissue sporozoa?
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Babesia microti
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What disease does E. histolytica cause?
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Amebic dysentery (bloody diarrhea)
Liver abscess Pulmonary abscess |
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What is the natural reservoir for E. histolytica?
How is it transmitted? |
Humans only
Fecal-oral transmission of cysts from contaminated food or water |
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What is the pathogenesis of E. histolytica infection?
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1) Ingestion of cysts
2) Formation of trophozoites in teh small intestine 3) Passage of trophozoites to the colon where they feed on intestinal bacteria 4) Trophozoites invade epithelium and multiply, forming "flask-shaped" ulcers. 5) Cysts form and are passed in the stool 6) Rarely (1%), trophozoites spread to liver, resulting in abscess formation 7) Direct spread from liver through diaphragm to the lung, resulting in abscess formation |
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How does the infecious cyst of E. histolytica appear under microscopy?
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As a mature cyst with four nuclei
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How does the trophozoite appear under microscopy?
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Organism with multiple pseudopodia (cytoplasmic projections, and a single nucleus with a central nucleosome)
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Are most infections of E. histolytica symptomatic?
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NO
Only 10% of carriers develop symptoms |
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What are the symptoms of active disease?
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Hemorrhagic colitis with bloody diarrhea or weight loss, fatigue, and right uper quadrant pain, suggesting liver abscess
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What is the worldwide mortality from E. histolytica infection?
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Third leading cause of death caused by parasitic infection, accounting for 100,000 deaths annually
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How is E. histolytica infection diagnosed?
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1) Microscopic observation of erythrophagocytic trophozoites
2) Stool antigen detection by ELISA 3) Serologic tests |
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How is symptomatic E. histolytica infection treated?
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Metronidazole (for parasites in the tissue) followed by paromomycin (for parasites in the intestinal lumen)
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What diseaes does G. lamblia cause?
How is it transmitted? |
Giardiasis, a diarrheal illness iwth no extraintestinal disease.
Fecal-Oral transmission of cysts form contaminated food or water |
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What is the pathogenesis of Giardia infection?
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1) Ingestion of cysts
2) Formation of trophozoites in the duodenum 3) Trophozoites attach to epithelial wall causing villous atrophy and malabsorption. |
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What are the symptoms of active Giardiasis?
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Nonbloody diarrhea often with statorrhea
Giardiasis is a noninvasive colitis that causes a nonbloody diarrhea, but may interfere with fat absorption resulting in statorrhea |
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How common is Giardia infection?
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Approximately 5% of Americans are infected; however, most are asymptomatic
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How is Giardia diagnosed?
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1) Microscopic exam of diarrheal stool for trophozoites and cysts or of formed stool for cysts.
2) ELISA immunoassay 3) String test, placing string down to the duodenum with removal after several hours and examination for cysts and trophozoites |
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How do Giardia cysts appear with microscopy?
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Thick-walled oval cysts with four nuclei
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How to trophozoites appear with microscopy?
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Binucleate pear-shaped organisms with 4 flagella
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How is Giardia infection treated?
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Metronidazole
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What disease does C. parvum cause?
How is it transmitted? |
Cryptosporidiosis
Fecal-oral transmission of cysts form contaminated food or water. Mini-outbreaks are seen in day care centers form person-to-person spread |
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What si teh pathogenesis of Cryptosporidium infection?
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1) Ingestion of cysts
2) Oocytes release sporozoites in small intestine 3) Sporozoites form trophozoites 4) Trophozoites attach and penetrate microvillous gastrointestinal (GI) mucosal surface |
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What are the clinical manifestations of active disease?
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Watery, nonbloody diarrhea and abdominal pain, usually more severe in the immunocompromised
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How common is Cryptosporidium infection?
How is it diagnosed? |
25% of Americans have serologic evidence of previous infection; most, however, are asymptomatic
1) Cysts on modified acid-fast stain of stool 2) Stool ELISA |
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How do cysts appear in cryptosporidium infection?
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As oocysts containing four motile sporozoites
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How is cryptosporidium treated?
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Nitazoxanide
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What disease does I. belli cause?
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coccidiosis
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What is the reservoir for I. belli?
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Dogs
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How is I. belli transmitted?
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Fecal-oral transmission of oocysts
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What are the clinical manifestations of active Coccidiosis?
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Fever
Headache Diarrhea Abdominal Pain |
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How does I. belli cause diarrhea?
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Oocysts excyst in the upper small intestine and invade mucosa, destroying the brush border causing malabsorption and increased water loss
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What is unique about the life cycle of I. belli?
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Cysts need to develop outside of the host
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How is I. belli diagnosed?
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Identifying oocysts in feces by acid-fast stain
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How is I. belli treated?
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TMP-SMX
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What disease does C. cayetanensis cause?
How is it transmitted? |
Cyclosporiasis
Fecal-Oral transmission of cysts |
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What food is associated with Cyclospora infection?
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Raspberries, especially those form Guatemala.
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What are the clinical manifestations of active disease?
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Prolonged and relapsing diarrhea
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What is unique about the life cycle of Cyclospora?
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Cysts need to develop outside the host
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How is Cyclospora infection diagnosed?
How is it treated? |
ID of spherical oocytes in feces by acid-fast stain
TMP-SMX |
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What disease does B. coli cause?
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Usually asymptomatic, but dysentery (diarrhea) may occur
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What is unique about B. coli?
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It is the only ciliated protozoan to cause disease in humans
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How is B. coli infection diagnosed?
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Microscopy can identify large ciliated trophozoites or large cysts with a "V-shaped" nucleus in the stool
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How is B. coli treated?
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Tetracycline
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What disease does T. vaginalis cause?
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Trichomoniasis
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How is T. vaginalis transmitted?
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Sexually
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What are the stages of T. vaginalis?
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Only exists as a trophozoite; there is no cyst form.
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What are the clinical manifestations of active T. vaginalis?
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Profuse watery or foamy greenish vaginal discharge associated with severe itching/dysuria in females.
Urethritis/prostatitis in males, although most males are asymptomatic |
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How common is T. vaginalis infetion?
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Approximately 3 million women per year in the US are infected
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How is T. vaginalis infection diagnosed?
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Wet mount of vaginal discharge or urine microscopy demonstrates motile trophozoites
Pear-shaped organisms with 1 central nucleus and 4 anterior flagella and undulating membranes |
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How is T. vaginalis treated?
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Metronidazole
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What disease does N. fowleri cause?
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Meningoencephalitis
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How is N. fowleri transmitted?
How? |
Swimming in warm freshwater lakes
Trophozoites penetrate nasal mucosa and cribriform plate, directly infecting the overlying meninges and brain |
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What population is usually infected with N. fowleri?
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Normal healthy children
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What are the clinical manifestations of active disease?
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Headache
Fever Nuchal Rigidity Nausea Vomiting |
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What is the prognosis for a person with active disease of N. fowleri?
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Rapidly fatal
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How common is symptomatic infection of N. fowleri?
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Rare, although many people are exposed to the organism
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How is N. fowleri infection diagnosed?
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Cerebrospinal fluid wet prep demonstrating trophozoites.
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How is N. fowleri treated?
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No effective treatment, but intrathecal amphotericin B has sometimes resulted in recovery.
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What disease does Acanthamoeba cause?
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Keratitis
Chronic granulomatous meningoencephalitis |
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How is Acanthamoeba transmitted?
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Swimming in freshwater lakes
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How does Acanthamoeba cause keratitis?
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Direct inoculation of eye or by inadequately cleaning fo soft contact lenses
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What are the clinical manifestations of Keratitis?
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Eye pain
Photophobia Visible lesions of cornea Sometimes Blindness |
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How is Acanthamoeba keratitis diagnosed?
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History and physical
Rarely, ring-shaped corneal infiltrate is present |
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What population usually develops meningoencephalitis?
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Immunocompromised
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What are the clinical manifestations of meningoencephalitis?
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Headache
Fever Seizures Focal Neurologic signs |
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How is chronic granulomatous meningoencephalitis diagnosed?
How is it treated? |
CSF wet prep or brain-tissue biopsy demonstrating trophozoites and possibly granulomas
Antifungal drugs and pentamidine are occasionally effective |
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What disease does the Leishmania species cause?
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Leishmaniasis
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What is the natural reservoir for the Leishmania species?
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Wild rodents, dogs, and human
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How is Leishmania transmitted?
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Sandfly
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What is the life cycle of Leishmania?
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1) Infected female sandfly bites human, transmitting promastigotes into the skin
2) Promastigotes lse flagella and turn into amastigotes 3) Amastigotes invade macrophages and reproduce, killing the host cell and releasing more amastigotes that infect other cells 4) Sandfly ingests amastigotes from an infected person during a blood meal 5) Amastigotes divide in teh gut of the sandfly, producing promastigotes |
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What are the four types of leishmaniasis?
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Cutaneous
Diffuse cutaneous Mucosal Visceral |
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What are the clinical manifestations of Cutaneous leishmaniasis?
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Ulcerating, pizza-like lesions that can be single or multiple and heal after months to years with scarring
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What are the clinical manifestations of diffuse cutaneous leishmaniasis?
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Nonulcerating nodules with a widespread distribution
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What are the clinical manifestations of Mucosal leishmaniasis?
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Ulceration of mucous membranes of nose and/or mouth years after infection, which can obliterate the nasal septum and the buccal cavity; death can occur from secondary infection
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What are the clinical manifestations of visceral leishmaniasis?
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Splenomegaly, hepatomegaly, and jaundice; death can occur from secondary infection
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What is another name for leishmaniasis?
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Kala azar
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What is the prevalence and incidence of Leishmania infection?
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500,000 new infections each year
12 million people are currently infected |
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How is leishmania infection diagnosed?
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1) ID of amastigotes in Giemsa-stained tissue or fluid
2) Serological test with ELISA, indirect fluorescent antibody, and complement fixation 3) Montenegro skin test for cutaneous and mucosal leishmaniasis |
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How is Leishmania infection treated?
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Sodium stibogluconate, pentavalent antimonial, adn liposomal amphotericin
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What are the three main human pathogenic strains of Trypanosoma?
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Trypanosoma cruzi
Trypanosoma brucei gambiense Trypanosoma brucei rhodesiense |
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What disease does T. cruzi cause?
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Chagas disease
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Where does Chagas disease occur?
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Southern US
Central and South America |
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How is T. cruzi transmitted?
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Reduviid or "kissing" bug; blood transfusions
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What is the life cycle of T. cruzi?
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1) Reduvidd bug ingests trypomastigotes in the blood of resservoir hosts
2) Organisms multiply within the bug's gut and differentiate into epimastigotes and trypomastigotes 3) Reduviid bug bites are infected with feces containing trypomastigotes 4) Trypomastigotes enter bood and lose flagellae, forming amastigotes. 5) Amastigotes infect myocardial, glial, and reticuloendothelial cells |
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What are the two symptomatic stages of Chagas disease?
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Acute stage lasting 1-2 months
Chronic stage occurring years after initial infection |
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What are the clinical manifestations of the acute stage Chagas disease?
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Skin nodule at the site of bite (chagoma) and periorbital swelling (Romana sign) associated with fever, malaise, and lymphadenopathy
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What are the clinical manifestations of the chronic stage Chagas disease?
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1) Cardiac: myocarditis, dysrhythmias, and dilated cardiomyopathy
2) GI: megaesophagus and megacolon |
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How is T. cruzi infection diagnosed?
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Acute stage - ID of "C"-shaped motile trypanosomes in blood
Chronic stage - by clinical presentation, serologic evidence of previous infection, and xenodiagnosis by allowing lab-raised reduviid bug to feed on a patient and analysis of interstinal contents several weeks later |
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How is T. cruzi infection treated?
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Acute - nifurtimox
Chronic - no treatment |
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What disease does T brucei gambiense cause?
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West african sleeping sickness
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What disease does T. brucei rhodesiense cause?
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East African sleeping sickness
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How are T. brucei gambiense and T. brucei rhodesiense transmitted?
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Tsetse fly
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What is the pathogenesis of infection with these species?
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Organisms spread from inoculated skin to the blood and lymph nodes; eventually causing inflammation of the brain and spinal cord
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What are the clinical manifestations of African sleeping sickness?
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1) Initial primary skin lesion (trypanosomal chancre)
2) Intermittent fever adn lymphadenopathy (Winterbottom sign) 3) Encephalitis characterized by lethargy, continuous sleep, mental status changes, and death |
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How do W. and E. african sleeping sickness differ?
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T. brucei gambiense causes a low-grade chronic disease progressing over years
T. brucei rhodesiense causes an acute, rapidly progressing disease that is usually lethal within several months |
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How are T. brucei infections diagnosed?
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1) Peripheral blood smear demonstrating trypanosomes. Giemsa stain of CSF or lymph node aspirates
2) ELISA serologic tests 3) Brain biopsy demonstrates Morula or Mott cells |
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What is the treatment for T. brucei gambiense and T. brucei rhodesiense infections?
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Suramin and pentamidine for early stages of disease WITHOUT central nervous system involvement.
Melarsoprol adn suramin for late-stage disease WITH CNS involvement |
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What are teh four major speies of Plasmodium that are human pathogens?
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P. falciparum
P. vivax P. malariae P. ovale |
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What disease does Plasmodium cause?
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Malaria
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How is Plasmodium transmitted?
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Anopheles mosquito
Blood transfusions Transplacental transmission |
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What is the life cycle of Plasmodium?
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1) Infected female mosquito bites human, transmitting sporozoites from its salivary gland
2) Sporozoites infect liver cells and develop into merozoites 3) Merozoites invade red blood cells and become trophozoites 4) Trophozoites undergo asexual reproduction within red blood cells and form schizonts (large multinucleated masses) and more merozoites 5) Red cells lyse, releasing merozoites 6)Merozoites infect other red blood cells or become gametocytes 7) Gametocytes ingested by a female mosquito during a blood meal 8) Sexual reproduction with gametocytes occurs in the mosquito, forming sporozoites |
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What is the life cycle that occurs outside of red blood cells called?
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Exoerythrocytic cycle
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What is unique about the life cycle of P. vivax an P. ovale?
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They form hypnozoites, dormant forms of Plasmodium in hepatocytes which can remain for up to 5 years.
P.Vivax and P. Ovale for hypnozoites that are Very Old |
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What are the clinical manifestation of active Plasmodium infection?
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Severe chills, high fevers, profuse sweating at 48-72 hour intervals with anemia, hepatosplenomegaly, and, in severe cases, splenic rupture.
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How do the clinical manifestations of P. falciparum differ from other species?
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P. falciparum produces a more serious form of malaria with continuous high fever, orthostatic hypotension, and capillary obstruction causing hemorrhage and ischemia, particularly in the kidneys, lung, and brain
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What is the worldwide incidence and mortality of malaria?
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200-300 million people are infected annually and 1-2 million die
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Which population is at an increased risk for developing serious P. falciparum infection?
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Asplenic patients
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Which conditions confer protection against malaria by increasing host resistance to P. falciparum and P. vivax?
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Sickle cell trait and G6PD deficiency protect against P. falciparum
Absence of Duffy blood group antigens A and B protects against P. vivax |
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How is malaria diagnosed?
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1) ID of parasitic ring iwthin red blood cells on thick blood smear with Giemsa stain and/or on thin blood smear
2) Serologic tests |
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How is malaria treated?
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Chloroquine, quinine, primaquine, mefloquine, doxycycline/tetracycline, atovaquone/proguanil, or primethamine/sulfadoxine
Chloroquine, quinine, and primaquine all cause hemolysis in patients with G6PD deficiency |
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What are differentiating characteristics of P. falciparum?
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High parasite load; multiple ring forms, including banana-shaped gemetocytes, appear in RBCs on smear; occurs in tropical areas and results in the most severe form of malaria
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What are differentiating characteristics of P. vivax?
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Forms large ameba-like red blood cells with Schuffner dots; all stages of growth are seen on blood smear; forms hypnozoites; more temperate distribution
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What are differentiating characteristics of P. malariae?
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Milder form of disease; can be dormant in liver for years; may cause chronic problems like nephrotic syndrome, all stages of growth and band forms are seen on smear
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What are differentiating characteristics of P. ovale?
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Large ovoid RBCs with Schuffner dots; forms hypnozoites.
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What disease does B. microti cause?
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Babesiosis
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Where does B. microti commonly occur?
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NE coastal US and upper midwest
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How is B microti transmitted?
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Ixodes scapularis ticks
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What other organism is transmitted by Ixodes scapularis ticks?
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Borrelia bergdorferi, the bacteria that cause Lyme disease
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What is the pathogenesis of B. microti infection?
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Infects RBCs causing them to lyse
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What are the clinical manifestations of B. microti infection?
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Often asymptomatic and subclinical, but may cause influenza-like symptoms including fever, myalgias, fatigue, and muscle weakness
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In what population can B. microti cause a potentially fatal infection?
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Asplenic patients
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What disease does babesiosis resemble?
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Malaria
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How are Babesiosis and Malaria similar?
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Both are transmitted by blood-sucking insects, cause fever and hemolysis, and the organism are within RBCs.
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How do Babesiosis and Malaria differ?
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B. microti is transmitted by a tick, makes no pigment within RBCs, produces no sexual forms, and has no exoerythrocytic cycle, and therefore has no reservoir in hepatocytes
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How does B. microtic appear on blood smear?
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Ring-shaped trophozoites within RBCs
Classic X-shaped tetrad of merozoites also known as teh Maltese cross |
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What is the treatment for B. microti infection?
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Quinine and clindamycin
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What disease does T. gondii cause?
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Toxoplasmosis
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What organism is the definitive host for T. gondii?
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Cat
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How is T. gondii transmitted?
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1) Fecal-oral transmission by ingestions of oocytes in cat feces or eating undercooked contaminated meat
2) Transplacental transmission from an infected mother 3) Blood transfusion T. gondii is the "T" in TORCHES |
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What are the two types of Toxoplasma trophozoites?
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1) Tachyzoites are fast growing
2) Bradyzoites are slow growing |
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What is the pathogenesis of both types?
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Tachyzoites destroy cells, especially parenchymal reticuloendothelial cells (macrophages)
Bradyzoites are contained in cysts in the brain, muscle, and eye, and cause local inflammation an dnecrosis when tehy rupture form the cysts |
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What are the clinical manifestations of acquired Toxoplasmosis infection?
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Generalized lymphadenopathy with a mononucleosis-like illness
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What are the clinical manifestations of reactivation of toxoplasmosis?
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Fever, lymphadenopathy, hepatosplenomegaly, pneumonia, chorioretinitis, myocarditis, brain abscess, and encephalitis may occur in immunocompromised patients
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What are the clinical manifestations of congenital toxoplasmosis infection?
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Chorioretinitis, cataracts, seizures, mental retardation, microcephaly, encephalitis, and stillbirth
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How common is T. gondii infection?
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Ubiquitous; up to 80% of cats int eh US are infected and 30% of humans are infected, but most are usually asymptomatic
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What two populations have a higher risk of symptomatic infection?
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Neonates
Immunocompromised |
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How is T. gondii infection diagnosed?
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1) CT demonstrates contrast-enhanced mass (reactivation)
2) Fundoscopy reveals retinal inflammation (congenital) 3) Serology indicates prior exposure or acute infection 4) Muscle biopsy demonstrates cysts 5) PCR of DNA |
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How is acute T. gondii infection treated in immunocompetent patients?
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Usually not treated unless disease is unusually severe
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How is acute T. gondii infection treated in immunocompromised patients?
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Sulfadiazine and pyrimethamine plus folinic acid
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