Parasites Flashcards
Helminth - Hookworm
Hookworms may persist for many years in the host and impair the physical and intellectual development of children and the economic development of communities
Females release thousands of eggs into stool daily; in sandy moist soil, eggs hatch and must molt twice before developing into third-stage larvae.
Third-stage larvae are 500-700 µm long and are capable of rapid penetration into normal skin, most commonly of the feet
Transmission occurs after > 5 of skin contact with soil that contains viable larvae
Ground itch at the site of penetration is more common withAncylostomaspecies than withNecator
They puncture and feed on mucosal capillaries in the jejunum.
Larvae burrow into venules and embolize the lungs, where they break into alveoli
Helminth - Hookworm Etiology
Hookworm infection is acquired through skin exposure to larvae in soil contaminated by human feces
Helminth- Hookworm Epidemiology
Hookworms represent a widespread; clinically important human nematode infection
Prevalence figures indicate that the roundworms Ancylostoma duodenale & Necator americanusinfect 576-740 million people and that they causeanemia in approximately 10% of those infected
Hookworm- Workup
Direct microscopic stool examination for ova and parasites usually reveals oval, 60-µm X 40-µm eggs with thin colorless shells that can be seen 2 months after exposure
Anemia is confirmed by CBC count and peripheral blood smear results that demonstrate signs typical of iron deficiency anemia
Eosinophilia is usually present during the migratory phase before stool findings are positive (may be due to adult worms to the intestinal mucosa with peak eosinophil counts are 1,350-3,828 cells/µL at 5-9 weeks after experimental human exposure to 45-50 infective larvae
Eosinophilia can be a clue to hookworm, as well asStrongyloidesinfestation, in chronically infected patients
Hookworm Treatment
Albendazole (single dose) or mebendazole (3 day course) is the drug of choice for hookworm infection (short-term cure in 90-95% of children, with up to a 99% reduction in egg counts)
Quarterly retreatment resulted in improved anemia and malnutrition after one year
Concomitant iron supplementation in a recent study in Kenya did not improve final hemoglobin concentrations in children or adults
Rapid hookworm reinfection is common in endemic areas and is made particularly problematic by the high prevalence and worm burden in adults who are untreated and who continue to contaminate soil
Infections of RoundwormAscaris lumbricoides
Lumbricoidesis the largest of the intestinal nematodes affecting humans, measuring 15-35 cm in length in adulthood
Infection begins with the ingestion of embryonated (infective) eggs in feces-contaminated soil or foodstuffs
Once ingested, eggs hatch, usually in the small intestine, releasing small larvae that penetrate the intestinal wall
Larvae migrate to the pulmonary vascular beds and then to the alveoli via the portal veins usually 1-2 weeks after infection, during which time they may cause pulmonary symptoms (eg, cough, wheezing)
During the time frame of pulmonary symptoms, eggs are not being shed, and thus diagnosis via stool ovas and parasites is not possible
Eggs are not shed in stool until roughly 40 days after the development of pulmonary symptoms
After migrating up the respiratory tract and being swallowed, they mature, copulate, and lay eggs in the intestines
Adult worms may live in the gut for 6-24 months, where they can cause partial or complete bowel obstruction in large numbers, or they can migrate into the appendix, hepatobiliary system, or pancreatic ducts and rarely other organs such as kidneys or brain
Roundworm Epidemiology
US, ~ 4 million people are believed to be infected
High-risk groups include international travelers, recent immigrants (especially from Latin America and Asia), refugees, and international adoptees
Ascariasis is indigenous to the rural southeast, where cross-infection by pigs with the nematode Ascaris suummay occur
Roundworm Presentation in the Early Phase (4-16 days)
Fever Nonproductive cough Dyspnea Wheezing respiratory symptoms result from the migration of larvae through the lungs
Roundworm Presentation in the Late phase (6-8 weeks)
Passage of worms (from mouth, nares, anus)
Diffuse or epigastric abdominal pain
Nausea, vomiting
Pharyngeal globus, “tingling throat”
Frequent throat clearing, dry cough
Complications - Biliary and intestinal obstruction, appendicitis, pancreatitis
Roundworm Workup
Early infection (larval migration)
Complete blood count (CBC) may show eosinophilia
Sputum analysis may reveal larvae or Charcot-Leyden crystals (collections of crystalloid composed of eosinophilic proteins)
Stool examination findings are typically normal in absence of previous infection (during the first 40 d)
Ascarisspecific antibodies (not useful in acute infection and not protective)
Increases in IgE and later IgG
Established infection (adult phase)
Stool examination findings include characteristic eggs
Adult females lay about 200,000 eggs per day, aiding microscopic identification of characteristic eggs
Roundworm Treatment- Early Infection
Inhaled beta-agonists may be indicated
Steroids for pulmonary symptoms are controversial
Whether anthelmintic therapy is effective against larval stages is unclear. (Stool ova microscopy will likely be negative at this phase).
Because infection in the early phase is rarely serious, generally treatment is delayed until definitive diagnosis can be made.
Roundworm Treatment- Established Infection (Adult)
Benzimidazoles - mainstay of treatment of symptomatic and asymptomatic infections; low toxicity as they are poorly systemically absorbed
Bowel obstruction treated with intravenous hydration, nasogastric suctioning, electrolyte monitoring, and laparotomy, colonoscopyand esophagogastroduodenoscopy (EGD) to remove obstructing masses of worms
Piperazine citrate, a helminth paralytic, in cases of obstruction; no longer commercially available in the United States
Hepatobiliary ascariasis typically responds to similarly conservative therapy, but it may require invasive intervention (e.g. ERCP) should this fail, or if there are coexisting stones or strictures; also indicated in cases of pyogenic cholangitis and acute pancreatitis.
Tapeworms
Tapeworms are long, segmented worms of the class Cestoda, which comprise 1 of 3 classes of parasitic worms (worms that require a host within which to mature) Other classes are Nematoda and Trematoda The worms lack an intestinal tract and instead can absorb nutrients through their integument The adult consists of a head (scolex), where the worms attach to the mucosa of the intestine; a neck; and a segmented body that contains both male gonads and female gonads (proglottids)
Tapeworms - Pathophysiology
Typically, a cestode requires one or more intermediate hosts in their life cycle. The life cycle is as follows:
Eggs are passed into the environment from the primary host
Eggs are ingested by an intermediate host in which they hatch
Larvae enter the tissues of the intermediate host and encyst
Primary host ingests the cysts in the flesh of the intermediate host
When humans are the primary hosts (ingest cysts), the adult cestode is limited to the intestinal tract
When humans are the intermediate hosts (ingest eggs), the larvae are within the tissues, migrating through the different organ systems
Echinococcus and Diphyllobothrium
Cysticercosis is a clinical syndrome of expanding embryonal cysts that occurs withT solium; cysticerci can be found anywhere; but mainly occur in the central nervous system (neurocysticercosis) and skeletal muscles
Diphyllobothriumspecies absorb and interfere with absorption by ileum of vitamin B-12, pernicious anemia
Echinococcuspenetrate intestinal mucosa after ingestion; enter the portal circulation to invade other organs, liver (60%) and lungs (25%); remains asymptomatic until the cysts cause a mass effect on the organ, which can be 5-20 years after the initial infestation
Treatment of Intestinal tapeworm infestation
Effectively treated with praziquantel or niclosamide (rates of 85-98%)
Vitamin B-12 if vitamin B-12 deficiency with Diphyllobothriuminfections
Treatment of Echinococcosis
Echinococcosis is treated with albendazole and surgery or albendazole and PAIR (puncture, aspiration, injection, re-aspiration)
lbendazole is recommended for 1-3 months before surgical intervention
Treatment of Sparganosis and coenurosis
Treatment involves surgical excision for localized infections
Cysticercosis
If the patient is asymptomatic with calcified soft tissue or neural lesions, no treatment is required
In neurocysticercosis, neurologic manifestations indicate the need for antiepileptics and antihelminths: albendazole or praziquantel These agents can provoke an inflammatory response in the central nervous system; patient must be started on dexamethasone
Therapy effect monitored via radiographic imaging; active lesions should decrease within 3-6 months
Some patients require surgery in addition to treatment with albendazole, praziquantel, and dexamethasone
Malaria Epidemiology
- 25-30 million people travel to tropical areas annually; 10,000-30,000 US and European travelers acquire malaria
- Almost all US cases of malaria are imported from patients traveling from endemic areas
- infections in individuals who have not traveled have occurred near airports (so-called airport malaria)
- –*responsible for approximately 1-3 million deaths per year, typically in children in sub-Saharan Africa infected withP falciparum: individuals at increased risk for mortality due to malaria include primigravida individuals, travelers without immunity, and young children aged 6 months to 3 years who live in endemic areas
- –Worldwide, 300-500 million cases occur annually
- –*Most prevalent in rural tropical areas below elevations of 1000 m (3282 ft) but is not limited to these climates (climate change)
Malaria Complications (most caused byP falciparum)
Cerebral malaria, defined as coma, altered mental status, or multiple seizures withP falciparumin the blood; most common cause of death in patients with malaria; lethal is untreated; 15% of children and 20% of adults who develop cerebral malaria die
Seizures – 2nd to hypoglycemia or cerebral malaria
Renal failure - 30% of nonimmune adults suffer acute renal failure
Hemoglobinuria (blackwater fever) - Blackwater fever is the passage of dark urine, described as Madeira wine colored; hemolysis, hemoglobinemia, and the subsequent hemoglobinuria and hemozoinuria
Noncardiogenic pulmonary edema – esp. pregnant women w/ death in 80%
Profound hypoglycemia – malaria metabolizes glucose 70 times faster than RBC; hypoglycemia often occurs in young children and pregnant women; diagnosis difficult as adrenergic signs are not always present & stupor already may have occurred
Lactic acidosis – malarial metabolic glucose use; microvasculature also becomes clogged withP falciparum; if the venous lactate level reaches 45 mg/dL, a poor prognosis is very likely
Hemolysis resulting in severe anemia and jaundice
Bleeding (coagulopathy)
Malaria Presentation
Arthralgia Myalgia Paroxysm of fever, shaking chills, and sweats (every 48 or 72 hours, depending on species) Headache, virtually all patients with malaria Cough Fatigue Malaise Shaking chills excessive diaphoresis
Malaria Workup
In returning travelers from endemic areas, malaria is suggested by the triad that should prompt malarial smear
Thrombocytopenia
Elevated lactate dehydrogenase (LDH) levels
Atypical lymphocytes
Blood cultures should be drawn in a febrile patient; patients from tropical areas may have more than 1 infection; to be considered when patients do not respond to antimalarials
Hemoglobin (decreased in 25% of patients, often profoundly in young children), platelet counts (thrombocytopenia in 50-68% of patients), and liver function (results abnormal in 50% of patients)
If consideringprimaquine, a G-6-PD level should be obtained because primaquine can result in severe hemolysis
If the patient has cerebral malaria, need blood glucose level to rule out hypoglycemia as a cause of mental-status changes
Microhematocrit centrifugation is a more sensitive method of detection of malaria infection, do not allow the identification of the species ofPlasmodium
Fluorescent dyes/ultraviolet indicator tests may not yield speciation information
Polymerase chain reaction assay (PCR) is specific and sensitive means of determining if species ofPlasmodiumare present in the blood
Malaria Treatment
P falciparummalaria - Quinine-based therapy is with quinine (or quinidine) sulfate plus doxycycline or clindamycin or pyrimethamine-sulfadoxine; alternative therapies are artemether-lumefantrine, atovaquone-proguanil, or mefloquine
P falciparummalaria with known chloroquine susceptibility (only a few areas in Central America and the Middle East) - Chloroquine
P vivax, P ovalemalaria - Chloroquine plus primaquine
P malariaemalaria - Chloroquine
P knowlesimalaria – Recommendations same as those forP falciparummalaria.