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378 Cards in this Set
- Front
- Back
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Parasite definition
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- A eukaryotic live organism living in, or on, and having some metabolic dependence on another organism known as a host
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Definitive Host
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- Parasite reaches sexual maturity and where adult form resides
- Not always infective stage |
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Intermediate host
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- Immature or larval host matures, or in which the parasite undergoes asexual reproduction (vector)
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Accidental (or incidental) host
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- One in which the parasite is not normally found and sexual maturity never usually occurs
- Self-limiting infection but may cause pathology |
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Reservoir host
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- Non-human harboring parasites that can infect humans
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Neglected tropical diseases
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- A group of tropical infections which are especially endemic in low-income populations in developing regions of Africa, Asia, and the Americas.
- Survive and spread in poverty - Do not travel widely - Neglected by research and pharmaceutical development |
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Protozoan classification
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- Sarcomastigophora
* Amoeba (Sarcodina) * Flagellates (Mastigophora) - Ciliates (Ciliophora) - Apicomplexa (complex life cycles) - Microspora (intracellular parasites) |
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Helminths (worms) classification
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- Aschelminths
* Nematoda (roundworms) - Platyhelminths * Trematoda (flukes) * Cestoda (tapeworms) |
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Arthropod classification
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- Arthropoda
* Insecta * Arachnida * Crustacea |
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Characteristics of protozoans in stool samples
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- Trophozoites (trophs)
* Motile, actively feeding and multiplying form * Watery fecal samples - Cysts * Dormant, non feeding stage * More resistant to damage * Solid fecal samples |
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Characteristics of protozoans in blood smears
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- Stage of parasite present (ring form, trophozoite, schizonts, merozoites, gametocytes)
- Stage of RBC infected (reticulocyte, mature or both) - Shape/size of infected RBC |
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Characteristics of helminths in fecal or tissue samples
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- Ova are most commonly seen
*Size/shape of egg * Shell thickness * Presence/absence of operculum * Stage of development * Modifications of shell - Adult nematode (pinworm can be found in scotch tape prep) - Proglottids of cestodes (esp. gravid proglottids) - Larvae (S. stercoralis and intestinal nematodes; Roundworm ONLY PASSES LARVAE) |
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Most common type of laboratory error
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Pre-analytical error
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Acceptable stool sample
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- At least 5-7 grams of feces
- Properly labeled * Patient name/ID# * Submitter name and address * Date and time of collection |
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Number of stool needed to be collected
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- 3 specimens must be collected for optimal specificity
* 2 samples are normal bowel movements * 3rd sample follows use of non-oil based cathartic (cleans out bowels) - Collect specimens on alternate days to account for intermittent release of parasites |
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Ideal type of stool sample
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- Fresh (esp. for motile trophs and flagellates)
* Not used often because turn-over-time so short * Liquid stool: examine within 30 minutes (for trophs) * Semi-formed stool: examine within 1 hour * Formed stool: examine within 24 hours (for cysts) - Fixed or preserved stool samples * Outpatient collection |
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Collection preservatives for stool specimens
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- Fixative
* 5% or 10% formalin * SAF (Sodium acetate formaldehyde) * TOTAL-FIX (universal fixative) - Fixative plus PVA * Schaudin's Hg fixative *Schaudin's Cu or Zn base * ECOFIX (PVA): proprietary |
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5% or 10% formalin uses
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- Direct exam
- Concentration techniques - EIA - NOT GOOD FOR PERMANENT STAINS |
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SAF uses
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- Concentration techniques
- Permanent stains - Acid-fast stain - EIA |
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TOTAL-FIX uses
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- Concentration techniques
- Permanent stains - Acid-fast stain - EIA |
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Schaudin's Hg fixative uses
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- CANNOT be used anymore because hazardous
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Schaudin's Cu or Zn base uses
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- Permanent stain
- EIA |
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3 steps of microscopic examination
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- Direct wet mount (saline +/- iodine)
- Concentration procedure - Permanent stain * Use ocular micrometer for size |
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Ocular micrometer calculation
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- 20 micrometers @ 100x = 5 micrometers at 400x
* Inversely proportional |
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Direct wet mount examination
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- Fresh specimens only
- Detects protozoan trophozoite or flagellate motility |
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Concentration of stool types
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- Sedimentation
* Sample sinks to bottom * Urine and CSF samples - Flotation * Sample floats to top |
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Formalin-Ethyl-Acetate sedimentation
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- Most widely used method
- Recovers protozoan cysts, helminth eggs and larvae - DOES NOT recover protozoan trophs or coccidian oocysts - All types of samples can be used |
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Zinc sulfate flotation
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- Recovers protozoan cysts, coccidian oocysts (Cryptosporidium and Isospora) and some helminth eggs
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Sheather's sugar flotation
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- Recovers coccidian oocysts primarily
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Permanent stain types
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- Iron hematoxylin
- Wheatley's Trichrome stain - Modified acid-fast stain - Gram or Weber green trichrome - Methenamine silver |
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Iron hematoxylin uses
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- Not commonly used anymore
- Good for intestinal protozoans - Not good for eggs or larvae |
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Wheatley's trichrome stain uses
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- Most commonly used today (most parasites)
- Background = greenish color - Protozoa = blue-green to purple cytoplasm with red or purple nuclear material and inclusions - Ova and larvae = red or purple-red |
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Modified acid-fast stain uses
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- Identifies Cryptosporidium, Isospora and Cyclospora
- Background = blue - Oocyst = bright red to purple |
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Gram or Weber Green Trichrome uses
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- Special stain for microsporidian spores
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Methenamine silver uses
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- Special stain in sputum
- Identifies Pneumocystis jiroveci (fungi) * HIV patients and holocaust survivors |
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Cellophane Tape Prep uses
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- Direct observation for Enterobius vermicularis ova or adult worms (pinworm)
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Blood smear uses
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- Identifies Plasmodium sp., Babesia sp., Trypanosoma sp., Leishmania donovani and microfilariae
- Sample is EDTA anticoagulated whole blood (lavender top) |
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Blood smear types and uses
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- Thick film
* Screening test * RBCs lysed prior to Giemsa stain (pink, purple and black) - Thin film * Diagnostic (morphological detail and species identification) * RBCs remain intact (NOT lysed) prior to staining |
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Immunoassay definition
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- Laboratory test that utilizes antigen-antibody interactions to detect the presence of antibody or antigen
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Immunoassay types
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- Direct precipitation
- Immunoassay labels * DFA * IFA * Particles * Enzymes - Western blot - EIA/ELISA - "Field ready" (NTD) |
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Direct precipitation reading
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- Place known antigen or antibody disc on gel matrix and add patient sample to the side of it
- If a white line appears between the sample and the disc then it is positive for that parasite - Requires high concentration - Not frequently done in clinical setting |
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Fluorescent dye types and usage
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- Direct fluorescent antibody (DFA)
* Detects parasite antigen * Cryptosporidium parvum oocysts and Giardia lamblia cysts - Indirect fluorescent antibody (IFA) * Detects patient antibody by labeling parasite antigen |
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Particle testing reading
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- Particle coated with antibody to parasite antigen or parasite antigen itself
- Agglutination = positive test |
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Western blot reading
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- Antigens from parasite are seperated by electrophoresis, tramsferred to nitrocellulose, patient serum is added and detected with anti-human antibody labeled with enzyme
- Color change on specific bands indicates positive result due to substrate |
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EIA/ELISA reading
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- Enzyme labeled antigens or antibodies bind to a solid matrix and anti-human antibody added with substrate
- color change = positive result - 4 fold rise in titer = recent infection (seroconversion) |
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"Field ready" usage and reading
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- Used for neglected tropical diseases as a diagnostic assay
- Stable, easily read and performed, accurate, sensitive and specific - Analyte added to paper and capillary flow moves analyte through gold antibody labels and eventually to a test line with known antibody to analyte and a control line - If test line has color change than positive - If control line has color change than valid result |
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EIA dependent diagnoses
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- Cryptosporidium parvum: because tiny and needs special stain (this is easier)
- Entamoeba histolytica: to distinguish from Entamoeba dispar - Toxoplasma gondii: IgM (recent) or IgG EIA since organism resides in tissue and procedure is invasive |
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PCR organism uses
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- Plasmodium spp.
- Cryptosporidium sp. - Cyclospora cayetanenesis - Entamoeba histolytica/Entamoeba dispar - Giardia lamblia - Microsporidia |
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Conventional PCR procedure
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- Denatures target sequence into two seperate strands
- Anneal two primers to each strand running in opposite directions - Extend each strand with DNA polymerase to create 2 new strands - Repeat until enough strands to be detected - Amplicons = products of amplification |
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Why do you need 2 primers in PCR?
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- 2 primers allows for exponential growth of strands and therefore allows for detection
- 1 primer will only give linear growth and will not be enough for detection |
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Real Time PCR procedure and reading
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- Denature target sequence and add primer with a fluorecein and a quencher (probe) later in sequence
- Anneal primer and allow DNA polymerase to start copying strand - When DNA polymerase reaches fluorescein it sees it as not supposed to be there and detaches it - The fluorescein fluoresces and is detected as a color for each base of the nucleotide - Positive result only if level of detection is above detection line before 30 cycles - Can also detect predictable melting points of certain DNA strands (if consistent than positive) |
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Intestinal amoeba organisms
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- Entamoeba histolytica (pathogenic and larger)
* Entamoeba dispar (non-pathogenic and smaller) - Entamoeba hartmanni - Entamoeba coli (commensal) - Entamoeba nana (commensal) - Iodamoeba butschlii (commensal) * Can cause some disease, but less invasive |
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Trasmission of intestinal amoeba
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- Fecal-oral (contaminated food or water)
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Intestinal amoeba reservoir
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- Contaminated water or food
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Infective stage of intestinal amoeba
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- Cyst form
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Intestinal amoeba diagnostic stage
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- Cyst or trophozoite in fecal smear
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Intestinal amoeba definitive host
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- Human
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Intestinal amoeba sample taken
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- Fecal sample
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Life cycle of intestinal amoeba (not E. histolytica)
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- Cyst ingested
- Transforms into trophozoite: excysts in small intestine - Replicates in colon by binary fission - Trophozoites encyst and cysts are passed in feces * Trophozoites passed in feces die and are not infective) |
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Life cycle of Entamoeba histolytica
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- Cyst ingested
- Transforms into trophozoite: excysts in small intestine - Replicates in colon by binary fission - Trophozoite invades colon wall, goes to circulation - Spreads to brain, liver or lungs causing abscesses |
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Intestinal amoeba epidemiology
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- 10% of world population
- Can develop to commensal organism if infected under age 2 - Traveling increases risk of infection |
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Intestinal amoeba pathogenicity and symptoms
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- Amoebiasis
* Abdominal discomfort and bloody diarrhea * Amebic dysentry: fever, chills, blood or pus in stool * Intestinal ulceration and granulomata formation in brain or liver (Entamoeba histolytica) |
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Difference between Entamoeba histolytica and Entamoeba dispar
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- Entamoeba histolytica is larger
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Difference between Entamoeba histolytica and Entamoebam hartmanni/coli/polecki
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- Entamoeba histolytica ingests RBCs
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Free-living protozoan pathogens
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- Naegleria fowleri
- Acanthamoeba sp. * Both are CNS pathogens |
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Naegleria fowleri transmission
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- Traumatic (forced) introduction of contaminated water into the nasal cavity
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Naegleria fowleri reservoir
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- Warm or hot contaminated fresh water
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Naegleria fowleri pathogenicity and symptoms
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- Primary Amoebic Meningoencephalitis (PAM)
* Rapidly progressive, fatal infection of CNS * Incubation period is 1-7 days (headache and fever) * Meningitis symptoms get progressively worse (Headache, nuchal rigidity, seizure, coma) * Death in 3-6 days following onset of meningitis symptoms |
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Naegeria fowleri infective stage
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- Amoebic trophozoite
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Naegleria fowleri diagnostic stage
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- Trophozoites in CSF and brain tissue mostly
- Di-flagellates can be seen in CSF when transferred to water and incubated at 37 degrees Celsius |
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Naegleria fowleri definitive host
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- Human
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Naegleria fowleri sample taken
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- CNS tissue biopsy
- CSF |
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Naegleria fowleri life cycle
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- Cyst in water develops into amoebic trophozoite in a cycle
- Amoebic trophozoite can develop into flagellated (di-flagellate) form in a cycle - Amoebic trophozoite can infect a human through the nasal cavity and does not exit host |
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Acanthamoeba sp. transmission
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- Abrasion of cornea
- Nasal passages to lower respiratory tract - Disturbed skin |
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Acanthamoeba sp. reservoir
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- Warm fresh, brackish and sea water and soil
- Biofilms in pools, hot tubs and HVAC systems |
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Acanthamoeba sp. diseases caused
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- Granulomatous Amebic Encephalitis
- Amebic keratitis - Disseminate infection (skin ulcers) |
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Granulomatous Amebic Encephalitis epidemiology and symptoms
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- Immunocompromised host
- Mental status change, loss of coordination, fever, muscle weakness, double vision |
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Amebic keratitis epidemiology and symptoms
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- Contact lens wearers
- Eye pain, redness, blurred vision, sensitivity to light, something in eye feeling |
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Disseminate infection (skin ulcers) epidemiology
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- Immunocompromised and rarely healthy adults and children
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Acanthamoeba sp. infective stage
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- Trophozoites and cysts
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Acanthamoeba sp. diagnostic stage
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- Trophozoites and cysts
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Acanthamoeba sp. sample taken
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- CSF
- Brain/tissue biopsy - Corneal scrapings |
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What is the most common intestinal protozoan infection in Michigan?
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- Giardia lamblia
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Giardia sp. pathogenicity and symptoms
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- Giardiasis
* Incubation period of 2-3 weeks (median 7-10 days) * Watery-foul smelling diarrhea, abdominal cramps, flatulence, anorexia and nausea * Malabsorption syndrome and steatorrhea (fatty stools) in severe cases |
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Giardia sp. transmission
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- Fecal-oral
* Person-to-person * Sexual contact (mouth to anus) |
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Giardia sp. epidemiology
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- Risk groups include
* Travelers to areas of high prevalence (developing countries) * Children in day care and their caregivers * Backpackers, campers * Contact with humans/animals with disease * Men who have sex with men (MSM) - Low infectious dose (10 cysts) |
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Giardia sp. reservoir
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- Contaminated water or food
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Giardia sp. infective stage
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- Cysts
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Giardia sp. diagnostic stage
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- Trophozoites and cysts
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Giardia sp. sample taken
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- String test
* Patient swallows string encased in gel capsule * Passes to small intestines and coated with organism * Removed via mouth and examined microscopically |
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Chilomastix mesnili transmission
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- Fecal-oral
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Chilomastix mesnili reservoir
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- Contaminated water, food or fomite
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Chilomastix mesnili infective stage
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- Cysts
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Chilomastix mesnili diagnostic stage
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- Trophozoites or cysts
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Chilomastix mesnili pathogenicity and symptoms
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- Non-pathogenic
- Asymptomatic |
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Chilomastix mesnili epidemiology
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- Most prevalent in tropics
- Also seen in US |
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Non-pathogenic commensal intestinal flagellates
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- Chilomastix mesnili
- Enteromonas hominis - Retortamonas intestinalis - Trichomonas hominis |
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Trichomonas hominis epidemiology
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- Most common in tropics
- Worldwide also though |
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Dientamoeba fragilis pathogenicity and symptoms
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- Majority of infected individuals are asymptomatic
- Some individuals do have symptoms and should be treated * Intermittent diarrhea, fatigue, nausea, abdominal pain, vomiting, flatulence, low-grade eosinophilia |
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Dientamoeba fragilis transmission associations?
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- Eggs of Enetrobius vermicularis and Ascaris lumbricoids
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Trichomonas vaginalis transmission
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- Sexually transmitted disease
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Trichomonas vaginalis pathogenicity and symptoms
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- Trichomoniasis (vaginitis)
* Women #May be asymptomatic #Burning, itching and profuse foul-smelling yellowish discharge (low pH) * Men # 75% are asymptomatic # discharge, painful urination, urethritis |
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Trichomonas vaginalis sample taken
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- Women = vaginal fluid or urine
- Men = Urethral fluid or urine |
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Trichomonas tenax sample taken
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- Tartar of individuals with poor oral hygiene
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Trichomonas tenax pathogenicity
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- Non-pathogenic (commensal trichomonad)
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Organisms that do not have a cyst form
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- Trichomonas hominis
- Dientamoeba fragilis - Trichomonas vaginalis - Trichomonas tenax |
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Balantidium coli transmission
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- Fecal-oral
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Balantidium coli reservoir
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- Contaminated food or water
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Balantidium coli infective stage
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- Cysts
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Balantidium coli diagnostic stage
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- Trophozoites or cysts
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Balantidium coli pathogenicity and symptoms
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- Balantidiasis
* Abdominal pain and bloody diarrhea (like E. histolytica) * Rarely causes extraintestinal infections of liver, lung and other organs |
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What is the only ciliate to cause significant human infection?
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Balantidium coli
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Leishmania sp. vector
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- Female phlebotomine sandfly
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Leishmania sp. risk areas
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- Poverty related
- Evening and night feeding - Climate change, dams and increasing urban population helping it spread to new areas |
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Leishmania sp. egg reservoir
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- Eggs laid in rodent burrows, tree bark, building cracks and debris (stagnant water)
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Leishmania sp. life cycle
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- Flagellated promastigotes multiply within insect gut, migrate to proboscis, and are injected when the sandfly takes a meal
- In humans, the promastigotes are engulfed by macrophages, develop into amastigotes, multiply and spread disease - Taken back up by sandfly and repeated |
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Leishmania sp. infective stage
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- Promastigotes from sandfly
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Leishmania sp. diagnostic stage
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- Amastigotes in macrophages of human
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Leishmania sp. pathogenicity
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- Cutaneous leishmaniasis
- Mucocutaneous leishmaniasis - Visceral leishmaniasis |
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Cutaneous leishmaniasis organism
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- Leishmania tropica complex (Old world cutaneous)
- Leishmania mexicana complex (New world cutaneous) |
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Cutaneous leishmaniasis symptoms
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- Chronic dry, raised, ulcerated lesions at the site of bite weeks to years after
- Not painful - Slowly self-resolving but disfiguring |
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Cutaneous leishmaniasis epidemiology
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- 90% in Afghanistan, Brazil, Iran, Peru, Saudi Arabia and Syria
* Leishmania topica complex = Middle East * Leishmania mexicana complex = South America |
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Mucocutaneous leishmaniasis organism
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- Leishmania braziliensis complex
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Mucocutaneous leishmaniasis symptoms
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- Amastigotes spread after lesion heals to invade mucous membranes and erode soft tissue of face
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Mucocutaneous leishmaniasis epidemiology
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- 90% in Central and South America
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Visceral Leishmaniasis organism
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- Leishmania donovani complex
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Visceral leishmaniasis symptoms
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- Kala azar (dark skin), insidious onset (slow and progressive), irregular bouts of fever, weight loss, splenomegally, hepatomegally, anemia
- Leishmania/HIV co-infections (2-12%) |
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Visceral leishmaniasis prognosis
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- 100% fatal without treatment in 2 years
- 10% fatal with treatment |
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Visceral leishmaniasis epidemiology
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- 90% in Bangladesh, India, Nepal, Brazil and Sudan
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Leishmania sp. sample taken
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- Ulcer biopsy
- Bone marrow or lymph node biopsy - PCR - Serological assay for non-HIV |
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What organism needs to be carefully differentiated from Leishmania sp. and why?
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- Histoplasma capsulatum (fungi inside macrophages)
* H. capsulatum doesn't have a kinetoplast |
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Trpanosoma brucei gambiense pathogenicity and symptoms
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- West African Sleeping Sickness
- 3 progressive disease stages * Asymptomatic incubation period up to several weeks *Hematogenous spread through blood and lymph nodes # Winterbottom's sign = swelling of cervical lymph nodes * Meningoencephalitis stage of CNS |
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Trypanosoma brucei rhodesiense pathogenicity and symptoms
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- East African Sleeping Sickness
- More rapid in disease progression and fatality |
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Trypanosoma cruzi pathogenicity and symptoms
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- Chagas disease
- Replication of amastigotes in heart mainly - Incubation period 1-2 weeks - Acute local inflammation at bite site * Romana's sign = swelling of eyelid near bite wound - Painful red lesion (chagoma) develops when lymph drainage blocked (2-3 months to heal) - Chronic stage can occur if reaches heart * cardiomyopathy, intestinal and CNS symptoms that can cause death - Detect and treat pregnant women because rapidly fatal to infants |
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Trypanosoma rangeli pathogenicity and symptoms
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- Self-limiting and asymptomatic
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Trypanosoma brucei spp. vector
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- Tsetse fly (saliva)
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Trypanosoma cruzi and rangeli vector
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- Reduviid bug (feces)
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Trypanosoma brucei spp. diagnostic stage
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- Trypomastigotes in peripheral blood
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Trypanosoma cruzi diagnostic stage
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- Amastigotes in heart tissue
- Trypomastigotes in peripheral blood |
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Trypanosoma rangeli diagnostic stage
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- Trypomastigotes in peripheral blood
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Malaria risk groups
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- Children
- Pregnant women and fetuses (brain and strokes) - HIV - Travelers - Immigrants from endemic areas |
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What ways can you gain immunity to malaria?
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- Sickle-cell anemia
- Live past 5 years old with disease and gain immunity |
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What accounts for the most malarial infections?
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- Plasmodium vivax
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What is the most lethal form of malaria?
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- Plasmodium falciparum
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Malaria vector/transmission
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- Female anopheles mosquito
- Can also be transmitted sharing needles, blood transfusion, congenitally, or domestic mosquito bites |
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Plasmodium sp. life cycle
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- Asexual reproduction in humans (schizogony)
* Exo-erythrocytic cycle # Infects parenchal liver cells and forms schizont with sporozoites # Sporozoites change into merozoites * Erythrocytic cycle # Merozoites infect RBCs and form trophozoites # Trophozoites either form schizonts and cycle back through RBCs, or they form gametocytes and are ingested by the anopheles mosquito * Sexual reproduction in mosquito (Sporogony) # Gametocytes form macrogametocyte and microgametocyte and combine to form an oocyst with sporozoites # Oocyst ruptures and sporozoites enter human again |
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Plasmodium sp. infective stage
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- Sporozoite from mosquito
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Plasmodium sp. definitive host
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- Anopheles mosquito
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Plasmodium sp. intermediate host
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- Humans
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Malaria paroxysm stages
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- Cold stage: fever, shivering (15-60 minutes)
- Hot stage: burning skin, headache (2-6 hours) - Sweating stage: declining temp., exhaustion (2-4 hours) |
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Plasmodium vivax paroxysm length
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- 48 hours
- Benign tertian malaria |
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Plasmodium falciparum paroxysm length
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- 36-48 hours
- Malignant tertian malaria |
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Plasmodium ovale paroxysm length
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- 48 hours
- Tertian malaria |
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Plasmodium malariae paroxysm length
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- 72 hours
- Quartan malaria |
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Plasmodium sp. that have relapse
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- Plasmodium vivax
- Plasmodium ovale |
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Relapse cause (cell name) and meaning
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- Hypnozoites
* Liver cells that retained parasite - Plasmodium goes away and then returns |
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Plasmodium sp. that experience recrudescence and meaning
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- Plasmodium malariae
- Parasitemia falls below detectable levels and then increases back to detectable levels |
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Plasmodium sp. sample taken
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- Thick and thin blood smear (Giemsa or Wright stain)
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Plasmodium vivax RBC infected
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- Young RBCs
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Plasmodium vivax diagnostic stage
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- Trophozoites, schizonts and gametocytes
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Plasmodium falciparum RBC infected
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- RBCs of all ages and a high % of cells
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Plasmodium falciparum diagnostic stage
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- Early trophozoites and gametocytes
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Blackwater fever
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- Sudden intravascular hemolysis, resulting in hemoglobinuria (dark brown to black urine) seen in Plasmodium falciparum patients
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Plasmodium ovale RBCs infected
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- Young RBCs
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Plasmodium ovale diagnostic stage
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- Early trophozoite, schizont and gametocyte
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Plasmodium malariae RBCs infected
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- Old RBCs
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Plasmodium malariae diagnostic stages
|
- Trophozoites, schizont and gametocytes
|
|
|
Ziemann's stippling
|
- RBCs that do not contain malarial pigment due to Plasmodium malariae infection
|
|
|
Babesia sp. vector
|
Ixodes sp. (deer tick)
|
|
|
Babesia sp. definitive host
|
- Domestic animals and wild rodents
|
|
|
Babesia sp. intermediate host
|
- Deer tick
|
|
|
Babesia sp. accidental host
|
- Humans
|
|
|
Babesia sp. pathogenicity and symptoms
|
- Babesiosis (Texas cattle fever and malignant jaundice of dogs)
* Incubation period 1-4 weeks * No periodicity in fever/chills cycle * Self-limited, non-fatal infection |
|
|
Human babesiosis organism
|
- Babesia microti
|
|
|
Babesia sp. diagnostic form
|
- Ring form (early trophozoite)
|
|
|
Toxoplasma gondii definitive host
|
- Small rodent in Northern Africa
- Domestic cats in US |
|
|
Toxoplasma gondii intermediate host
|
- Birds and mammals
|
|
|
Toxoplasma gondii accidental host
|
- Humans
|
|
|
Toxoplasma gondii transmission
|
- Fecal-oral
- Ingestion of raw or undercooked meat - Transplacental passage - Blood transfusion or organ transplantation |
|
|
Toxoplasma gondii infective stage
|
- Oocysts (pregnant women shouldn't clean litter boxes)
|
|
|
Toxoplasma gondii pathogenicity and symptoms
|
- Toxoplasmosis
* Most asymptomatic and benign * Symptoms mimic mono * High fetal mortality |
|
|
Toxoplasma gondii testing
|
- EIA
* In infants fo IgM because IgG is from mother - Biopsy for Giemsa stain |
|
|
Intestinal coccidian characteristics
|
- Non-motile
- Obligate intracellular parasites - Sexual and asexual reproduction |
|
|
Intestinal coccidian organisms
|
- Isospora sp.
- Cryptosporidium sp. - Cyclospora sp. - Sarcocystis sp. |
|
|
Intestinal coccidian diagnostic form
|
- Oocysts
|
|
|
Intestinal coccidian sample taken
|
- Stool sample
|
|
|
Cryptosporidium sp. transmission
|
- Fecal-oral
|
|
|
Cryptosporidium sp. reservoir
|
- Contaminated food, water or fomites
|
|
|
Cryptosporidium sp. risk groups
|
- Daycare
- Petting zoos - Water parks |
|
|
Cryptosporidium parvum life cycle
|
- Thick walled oocyst contaminates water and food and is ingested by host
- Oocyst goes to intestinal epithlial cells and releases sporozoites which attach to it and form into trophozoites - Enter the asexual cycle where they create a meront and release merozoites which either continue the cycle or go to sexual cycle - Sexual cycle has meronts release merozoites which create a zygote and form a thin-walled oocyst which causes autoinfection, and a thick-walled oocyst which exits host and becomes infective. |
|
|
Cryptosporidium parvum infective stage
|
- Thick-walled oocyst in environment
|
|
|
Cryptosporidium parvum auto-infective stage
|
- Thin-walled oocyst in intestines
|
|
|
What organism must be differentiated from Cryptosporidium parvum and how?
|
- Cyclospora sp.
* Cyclospora is slightly larger |
|
|
Isospora belli (cytoisospora belli) definitive, accidental host
|
- Human
|
|
|
Isospora belli life cycle
|
- Same as Cryptosporidium but oocyst passed in feces contains a sporoblast and must mature in environment
|
|
|
Isospora belli testing
|
- Sugar flotation test, wet mount and acid fast
|
|
|
Isospora belli infective stage
|
- Oocyst after it matures in environment
* Not immediately infective after shedding |
|
|
Sarcocystis sp. diagnostic form
|
- Sarcocysts in striated muscle
- Oocyst in stool |
|
|
Sarcocystis sp. transmission
|
- Contaminated water and food
- Uncooked beef or pork |
|
|
Cyclospora cayetanensis infective stage
|
- Oocyst after maturing in environment
* Not immediately infective |
|
|
Cyclospora cayetanensis transmission
|
- Contaminated imported foods
|
|
|
Cyclospora cayetanensis symptoms
|
- Long lasting and reoccuring
|
|
|
Cyclospora cayetanensis special diagnosis
|
- Autofluoresces
|
|
|
Microsporida (fungi) hosts
|
- Fish, insects and animals
|
|
|
Microsporida symptoms
|
- Emerging infectious disease
- Distal symptoms commonly |
|
|
Enterobius vermicularis (pinworm) transmission
|
- Fecal-oral with fomites
|
|
|
Enetrobius vermicularis (pinworm) infective stage
|
- Ova after maturation (6 hours)
|
|
|
Eneterobius vermicularis (pinworm) diagnostic stage
|
- Ovum or adult female
|
|
|
Enterobius vermicularis testing
|
- Scotch tape prep
- No routine O & P of stool needed |
|
|
Ascaris lumbricoides (large intestinal roundworm) transmission
|
- Fecal-oral
|
|
|
Ascaris lumbricoides reservoir
|
- Contaminated soil (esp. pica)
|
|
|
Ascaris lumbricoides diagnostic stage
|
- Ova passed in stool
|
|
|
Ascaris lumbricoides infective stage
|
- Mature-embyonated ova in soil
|
|
|
Ascaris lumbricoides life cycle
|
- Fertilized eggs mature in soil and are ingested
- Larvae hatch from eggs in small intestine and burrow through wall into hapatic circulation of lungs, reach trachea and are swallowed - Larvae mature in intestines, mate and females produce eggs |
|
|
Ascaris lumbricoides has a common co-infection with what other parasite?
|
- Trichuris trichiuria
|
|
|
Ascaris lumbricoides ova are associated with the transmission of what other parasite?
|
- Dientamoeba fragilis
|
|
|
Toxocara canis disease
|
- Visceral Larval Migrans (lungs)
|
|
|
Baylisascaris ova definitive host
|
- Raccoon
|
|
|
Anisakis spp. accidental host
|
- Humans
|
|
|
Anisakis spp. definitive host
|
- Marine mammals
|
|
|
Anisakis spp. intermediate host
|
- Fish and crustaceans
|
|
|
Anisakis spp. infective stage
|
- Larvae inside fish and squid
|
|
|
Anisakis spp. life cycle
|
- Eggs are in ocean and release larvae into water
- Larvae is ingested by crustaceans, who are then ingested by fish - Fish are then ingested by humans where they die and produce inflammation - Fish can also be eaten by marine mammals where they become adult worms and mate to produce eggs and release them into the ocean again |
|
|
Anisakis spp. diagnostic stage
|
- Larvae in intestinal endoscopy
|
|
|
Trichuris trichiuria (whipworm) transmission
|
- Fecal-oral
|
|
|
Trichuris trichiuria reservoir
|
- Contaminated food. water or soil
|
|
|
Trichuris trichiuria worst symptom
|
- Rectal relapse
|
|
|
Trichuris trichiuria infective stage
|
- Embyonated ova from environment
|
|
|
Trichuris trichiuria diagnostic stage
|
- Ova passed in stool
|
|
|
Hookworm parasites
|
- Necator americanus (new world)
- Ancylostoma duodenale (old world) |
|
|
Hookworm diagnostic stage
|
- Indistinguishable species
- Ova in stool (only passed as this) - Can find rhabditiform larvae in stool if left for several days at room temperature, unfixed |
|
|
Hookworm infective stage
|
- Filariform larvae in soil
|
|
|
Hookworm lifecycle
|
- Ova passed in feces and releases rhabditiform larvae in soil
- Matures to filariform larvae and penetrates skin of host - Enters circulation, migrates to lungs, and is swallowed form trachea - Matures to adult worm in intestines - Eggs released in feces |
|
|
Dog or cat hookworm disease
|
- Cutaneous larval migrans
|
|
|
Strongyloides stercoralis (threadworm) transmission
|
- Usually by filariform larvae in soil
- Can be autoinfective where it matures to filariform in intestines and travels to trachea through portal curculation and is swallowed |
|
|
Strongyloides stercoralis symptoms
|
- GI problems
- Coughing and dyspnea (when in lungs) - Polymicrobial sepsis or meningitis (autoinfection) - Disseminated infection (immunocompromised) |
|
|
Strongyloides stercoralis infective stage
|
- Filariform larvae in soil
|
|
|
Strongyloides stercoralis diagnostic stage
|
- Rhabditiform larvae in stool sample (NO EGGS)
|
|
|
Trichonella spiralis trasmission
|
- Consumption of undercooked meat with encysted larvae (pig mainly)
|
|
|
Trichonella spiralis lifecycle
|
- Larvae excysts in intestines
- Penetrates wall and develops into mature adult * Adult worms mate in gut lumen, produce eggs that hatch motile larvae * Larvae penetrate gut mucosa and migrate to striated muscle tissue |
|
|
Trichonella spiralis symptoms
|
- Depends on number of ingested cysts
- Muscle invasion = facial edema, muscle pain and eosinophilia - Rarely fatal (only with a lot of cysts ingested) |
|
|
Trichonella spiralis infective stage
|
- Encysted larvae in undercooked meat
|
|
|
Trichonella spiralis diagnostic stage
|
- Encysted larvae in muscle biopsy
|
|
|
Dracunculus medinensis (Guinea worm) transmission
|
- Stagnant water that is bathed in, drank, etc.
|
|
|
Dracunculus medinensis life cycle
|
- Larvae are ingested by consumption of an infected Cyclops copepod (water flea)
- Migrates through duodenal wall, develop, mate and mature in loose connective tissue - Adult female filled with rhabditiform larvae migrate to subcutaneous tissue (foot) - Female pokes thorugh a blister and releases larvae when exposed to fresh water - Larvae ingested by copepod |
|
|
Dracunculus medinensis vector
|
- Copepod (water flea)
|
|
|
Dracunculus medinensis treatment
|
- Female wound around a stick and slowly extracted
|
|
|
Knott's technique
|
- Concentration technique where body and lymphatic fluid is fixed in 2% formalin and centrifuged for microfilariae
|
|
|
Elephantiasis organisms
|
- Wuchereria bancrofti (Inflammed testicles)
- Brugia malayi (inflammed legs) |
|
|
Wuchereria bancrofti definitive host
|
- Humans
|
|
|
Wuchereria bancrofti intermediate host/vector
|
- Mosquito
|
|
|
Wucheria bancrofti lifecycle
|
- Microfilariae are ingested by mosquito
- Larvae mature in mosquito - Infective form escapes into human with next blood meal - Larvae migrate to lymphatics and take 6-9 months to mature into adult worm - Adult worms mate and release microfilariae into blood * Nocturnal periodicity (collect blood 10pm-2am) except in Pacific islands sub-periodical (blood collected noon-8pm) |
|
|
Wucheria bancrofti infective stage
|
- Larvae from mosquitos
|
|
|
Wucheria bancrofti diagnostic stage
|
- Microfilariae from blood
|
|
|
Wucheria bancrofti diagnosis
|
- Elevated serum IgE
- Elevated serum antibody - Eosinophilia - PCR |
|
|
Brugia malayi definitive host
|
- Humans and others
|
|
|
Brugia malayi intermediate host/vector
|
- Mosquito
|
|
|
Loa loa (African eye worm) vector
|
Mango fly (Chrysops)
|
|
|
Loa loa infectious stage
|
- larvae from Chrysops
|
|
|
Loa loa diagnostic stage
|
- Microfilariae in blood
- Rarely adult worm seen in eye |
|
|
Loa loa symptoms
|
- Calabar swelling = localized painful, itchy swellings on extremities the size of a golfball
|
|
|
Loa loa diagnosis
|
- Hypereosinophilia
- Microfilariae have diurnal periodicity (10am-2pm) * Blood smear |
|
|
Onchocerca volvulus vector
|
- Black fly (Simulium spp.)
|
|
|
Onchocerca volvulus disease
|
- River blindness
- Possibly Nodding syndrome |
|
|
Onchocerca volvulus life cycle
|
- Infective larvae transferred to host during insect bite
- Worms migrate to subcutaneous tissue and form onchocercomas (tumor-like nodules) - Females produce microfilariae 1-3 years later - Travel through skin, eyes and lymph nodes causing inflammation as they die |
|
|
Onchocerca volvulus infectious stage
|
- Larvae from black fly
|
|
|
Onchocerca volvulus diagnostic stage
|
- Microfilariae in skin biopsy
|
|
|
Onchocerca volvulus diagnosis
|
- Eosinophilia (IgE)
- Skin snip (biopsy) of onchocercoma looking for microfilariae or adult forms |
|
|
Mansonella spp. vector
|
- Tiny midge
|
|
|
Mansonella ozzardi and Mansonella perstans
|
- Adult worms live in body cavities and visceral fat
- Microfilariae circulate in blood without periodicity |
|
|
Mansonella streptocerca
|
- Adult worms live in dermis
- Microfilariae in skin biopsy * Unsheathed and shepherd's crook tail |
|
|
Mansonella streptocerca must be differentiated from what parasite and how?
|
- Onchocerca volvulus and Mansonella stretocerca have a Shepherd's crook tail whereas the other doesn't
* Both are unsheathed |
|
|
Dirofilaria immitis (dog heartworm) accidental host
|
- Humans
|
|
|
Dirofilaria immitis definitive host
|
- Dog
|
|
|
Dirofilaria immitis intermediate host/vector
|
- Mosquito
|
|
|
Dirofilaria immitis symptoms
|
- NO MICROFILARIAE PRODUCED
- Worms are always immature in humans and migrate to lungs - Persistent cough, chest discomfort and coughing blood |
|
|
Cestode (tapeworm) characteristics
|
- 3 types of body sections
* Scolex * Neck * Proglottids - Whole tapeworm = strobila - Distal end = gravid proglottids - Adult tapeworms are hermaphroditic - Tegument = organ for nutrient absorption and waste disposal - Developing embryo in egg passed in feces |
|
|
What is the largest tapeworm that infects humans?
|
Diphyllobothrium latum (broad fish tapeworm)
|
|
|
Diphyllobothrium latum transmission
|
- Ingestion of larvae in undercooked, slightly salted or smoked fish
|
|
|
Diphyllobothrium latum definitive host
|
- Humans
|
|
|
Diphyllobothrium latum intermediate hosts
|
- Copepods, fish
|
|
|
Diphyllobothrium latum infectious stage
|
- Larvae in fish
|
|
|
Diphyllobothrium latum diagnostic stage
|
- Ova in stool
* Can also see proglottids or scolex (very rare) |
|
|
Taenia saginata (beef tapeworm) intermediate host
|
- Cattle
|
|
|
Taenia saginata definitive host
|
- Humans
|
|
|
Taenia solium (pork tapeworm) intermediate host
|
- Pig
|
|
|
Taenia solium definitive host
|
- Humans
|
|
|
Taenia sp. infectious stage
|
- Onchospheres (cysticercus larvae) in undercooked beef or pork
|
|
|
Taenia sp. diagnostic stage
|
- Ova (indistinguishable) or proglottids (distinguishable) passed in feces
|
|
|
Cysticercosis
|
- Human accidentally ingests Taenia solium egg and becomes intermediate host
- Developing countries with pigs - Cysticercoid larvae migrates to brain (CNS damage) - Diagnosed with EIA |
|
|
What's the most frequent tapeworm in the US?
|
Hymenolepsis nana (dwarf tapeworm)
|
|
|
Hymenolepsis nana (dwarf tapeworm) definitive hosts
|
- Humans
- Rodents |
|
|
Hymenolepsis nana intermediate host
|
- None needed
- Could be beetles or fleas |
|
|
Hymenolepsis nana infectious stage
|
- Embryonated egg from contaminated water, food, fomite
- Cysticercoid-infected arthropod ingestion - Autoinfection: egg in intestines |
|
|
Hymenolepsis nana diagnostic stage
|
- Embryonated egg in feces
|
|
|
Hymenolepsis diminuta (rat tapeworm) definitive host
|
- Usually rat
|
|
|
Hymenolepsis diminuta intermediate host
|
- Flea or grain beetle
|
|
|
Hymenolepsis diminuta accidental, definitive host
|
- Human
|
|
|
Hymenolepsis diminuta infectious stage
|
- Larvae ingested from infected beetles
|
|
|
Hymenolepsis diminuta diagnostic stage
|
- Ova in stool
|
|
|
What is different between Hymenolepsis diminuta and Hymenolepsis nana?
|
- Hymenolepsis diminuta is LARGER
|
|
|
Dipylidium caninum (dog and cat tapeworm) definitive host
|
- Dog or cat
|
|
|
Dipylidium caninum intermediate host
|
- Dog or cat flea
|
|
|
Dipylidium caninum accidental, definitive host
|
- Humans
|
|
|
Dipylidium caninum infectious stage
|
- Larvae from ingested infected flea
|
|
|
Dipylidium caninum diagnostic stage
|
- Egg packets or proglottids in stool
|
|
|
Echinococcus granulosus (Hydatid tapeworm) definitive host
|
- Dogs
|
|
|
Echinococcus granulosus intermediate host
|
- Sheep, goats, swine
|
|
|
Echinococcus granulosus accidental, intermediate host
|
- Humans
|
|
|
Echinococcus granulosus infectious stage
|
- Embryonated egg in dog feces
|
|
|
Echinococcus granulosus diagnostic phase
|
- Hydatid cyst in liver, lungs, brain, etc. (very large)
|
|
|
Echinococcus multilocularis definitive host
|
- Foxes, coyotes, dogs
|
|
|
Echinococcus granulosus accidental host
|
- Humans
|
|
|
Echinococcus granulosus intermediate host
|
- Small rodents
|
|
|
Echinococcus granulosus symptoms
|
- Parasitic tumors in liver spread to lung/brain
- 50-75% mortality even with treatment |
|
|
Trematode (flukes) characteristics
|
- Adults flat and leaf shaped
- Tegument - Most hermaphroditic - Ova are diagnostic |
|
|
Trematode life cycle
|
- Humans ingest encysted metacercariae (infective stage)
- Metacercariae excyst in duodenum - Adult worm develops (lungs, liver, blood) - Self-fertilize and release eggs - Eggs are shed and release miracidium in water (ciliated) - Miracidium penetrates snail tissue and develops into cercariae - Cercariae exit snail and encyst to form metacercariae and enters intermediate host - Undercooked metacercariae are eaten by human |
|
|
Intestinal trematodes
|
- Fasciolopsis buski
- Heterophyes heterophyes - Metagonimus yokogawai |
|
|
Liver trematodes
|
- Fasciola hepatica
- Clonorchis sinensis |
|
|
Lung trematodes
|
- Paragonimus westermani
|
|
|
Blood vessels (schistosomes) trematodes
|
- Schistosoma mansoni (intestine)
- Schistosoma japonicum (intestine) - Schistosoma haematobium (bladder) |
|
|
Fasciolopsis buski (giant intestinal fluke) reservoir host
|
- Pig
|
|
|
Fasciolopsis buski accidental, definitive host
|
- Humans
|
|
|
Fasciolopsis buski intermediate host
|
- Snail
- Water chestnuts, bamboo shoots |
|
|
Fasciolopsis buski infectious stage
|
- Metacercariae on water plant
|
|
|
Fasciolopsis buski diagnostic stage
|
- Ova passed in feces
|
|
|
Heterophyes heterophyes and Metagonimus yokogawai accidental, definitive host
|
- Humans
|
|
|
Heterophyes heterophyes and Metagonimus yokogawai intermediate host
|
- Snail
- Fish |
|
|
Heterophyes heterophyes and Metagonimus yokogawai infectious stage
|
- Metacercariae in flesh of fish (sushi)
|
|
|
Heterophyes heterophyes and Metagonimus yokogawai diagnostic phase
|
- ova passed in feces
|
|
|
Fasciola hepatica (sheep liver fluke) accidental, definitive host
|
- Humans
|
|
|
Fasciola hepatica definitive (reservoir) host
|
- Sheep
- Cattle |
|
|
Fasciola hepatica intermediate host
|
- Snail
- Watercress (vegetation) |
|
|
Fasciola hepatica infectious stage
|
- Metacercariae on watercress
|
|
|
Fasciola hepatica diagnostic stage
|
- Ova in stool
|
|
|
Fasciola hepatica symptoms
|
- Liver damage
- Bile duct obstruction |
|
|
Clonorchis sinensis (Chinese liver fluke) definitive host
|
- Humans
|
|
|
Clonorchis sinensis intermediate host
|
- Snail
- Fresh water fish |
|
|
Clonorchis sinensis infectious stage
|
- Metacercariae in flesh of fresh water fish
|
|
|
Clonorchis sinensis diagnostic stage
|
- Ova passed in feces
|
|
|
Clonorchis sinensis symptoms
|
- Pancreatitis or obstructive biliary tract jaundice
- Liver inflammation |
|
|
Paragonimus westermani (Oriental lung fluke) definitive host
|
- Humans
|
|
|
Paragonimus westermani intermediate host
|
- Snail
- Crustaceans |
|
|
Paragonimus westermani infectious stage
|
- Metacercariae in crustacean
|
|
|
Paragonimus westermani diagnostic stage
|
- Ova from feces or sputum
|
|
|
Paragonimus westermani symptoms
|
- Hemoptyis = blood flecks in cough
- Bronchitis - Larvae can migrate to brain and cause neurological problems |
|
|
Schistosomes definitive host
|
- Humans (direct penetration of skin)
|
|
|
Schistosomes intermediate host
|
- Snail
- NO SECONDARY INTERMEDIATE HOST |
|
|
Schistosomes infectious stage
|
- Cercariae free-living that directly penetrate human skin
|
|
|
Schistosomes diagnostic stage
|
- Ova in feces or sometimes urine (S. haematobium)
|
|
|
Schistosomes characteristics
|
- Adults not hermaphroditic
- Female always attached to male (always mating) |
|
|
Schistosome symptoms
|
- Swimmer's itch where cercariae penetrated skin
- Bladder cancer |
|
|
Schistosoma mansonii epidemiology
|
- Africa and Western hemisphere
|
|
|
Schistosoma mansonii residence in body
|
- Adult flukes in veins around GI tract
- Eggs excreted in stool |
|
|
Schistosoma japonicum epidemiology
|
- Far East
|
|
|
Schistosoma japonicum residence in body
|
- Adult flukes in veins around GI tract
- Eggs excreted in stool - Many animal reservoirs |
|
|
Schistosoma haematobium epidemiology
|
- Africa
|
|
|
Schistosoma haematobium residence in body
|
- Adult flukes in veins surrounding bladder
- Eggs excreted in urine - Bladder cancer correlation |
|
|
Papular urticaria with pruritus
|
- Irritation and itching from allergic reaction to stinging insects
- Can cause systemic anaphylactic shock |
|
|
Brown recluse taxonomy
|
Loxosceles reclusa
|
|
|
Black widow taxonomy
|
Latrodectus mactans
|
|
|
Stinging scorpion taxonomy
|
- Centruroides exilicauda
|
|
|
Fire ants taxonomy
|
Solenopsis invicta
|
|
|
Follicle mite toxonomy
|
Demodex
|
|
|
House dust mite taxonomy
|
Dermatophagoids sp.
|
|
|
Chiggers taxonomy
|
- Eutrotrombicula alfreddugesi
|
|
|
Scabies taxonomy
|
Sarcoptes scabiei var. hominis
|
|
|
Norweigian or crusted scabies
|
- Heavy infestation in immunocompromised AIDS patients
|
|
|
Lone star tick taxonomy and disease vector
|
- Amblyomma americanum
- Ehrlichiosis |
|
|
Wood tick taxonomy and disease vector
|
- Dermacentor andersoni
- Rocky mountain spotted fever, Colorado tick fever, Q fever, tularemia (Rickettsia infection) |
|
|
Blacklegged or deer tick taxonomy and disease vector
|
- Ixodes scapularis
- Lyme disease, ehrlichiosis, babsiosis |
|
|
Myiasis
|
Human infestation with fly larva (maggots)
|
|
|
Screw worm taxonomy
|
- Cochiliomyai hominovorax (fly)
|
|
|
Human bot fly taxonomy
|
- Dematobia hominis
- Central and South America - Larval stage in subcutaneous skin layer |
|
|
Head lice taxonomy
|
Pediculus humanus capitis
|
|
|
Body lice taxonomy
|
Pediculus humanus humanus/corporis
|
|
|
Pubic lice/crab louse/crabs taxonomy
|
- Phthirus pubis
|
|
|
Bed bugs taxonomy
|
- Cimex lectularius
- Climex hemipterus |
