Nematodes and Bioterrorism Flashcards
1
Q
What are nematodes?
A
Roundworms
2
Q
What are flukes?
A
flatworms/nonsegmented parasites
3
Q
What are cestodes?
A
flat and segmented parasites
4
Q
What is a parasite?
A
organism that obtains food and shelter from another organism and derives all benefits from this association
5
Q
What is a definitive host?
A
harbors adult and sexual stage parasite
6
Q
What is an intermediate host?
A
harbors larval/asexual stage parasite
7
Q
What is a reservoir host?
A
harbors the parasite to ensure continuity
8
Q
What is meant when you examine a stool sample for ova and parasite?
A
Examination of the stool for eggs, adult worms or larva; Direct examination; special stains used; don’t grow like a culture
9
Q
What are eosinophils?
A
bone marrow-derived leukocytes; Eosinophilia develops when specific cytokines, granulocyte-macrophage colony stimulating factor (GM-CSF), (IL)-3, and IL-5 stimulate enhanced
10
Q
What nematodes are transferred fecal-orally? From soil?
A
Oral-fecal: enterobias vermicularis (pinworm), trichuris trichuria, ascaris lumbricoides; soil-migration: N americanis/A duodenales, Strongyloides stercoralis
11
Q
What is the epi of Enterobias vermicularis?
A
Pinworm is found worldwide, Temperate and colder climates, School Aged Children, High population density, Indoor conditions, Hand to mouth transmission
12
Q
What is the life cycle of enterobias vermicularis?
A
Eggs are ingested, eggs hatch in small intestine, migrate to to colon, crawl out of anus and lay eggs on perianum, eggs contaminate fingers (when you scratch), autoinfect by egg ingestion
13
Q
What is important about enterobias vermicularis eggs?
A
Mature/infective within 6 hours, Easily passed to family
members, Remain infective for several days (humid)
14
Q
What is the scotch tape test?
A
put sticky paddle near anus 3 mornings in a row - see if we catch something! stool sample will be negative
15
Q
What are the symptoms of enterobias vermicularis?
A
Perianal and perineal pruritis; Vulvovaginitis – worm migrates vagina; Association with UTI?; Granulomatous reaction – yellow nodule; Traveling through a perforated appendix; Psychological impact on parents; NOTE: Peripheral eosinophil count is normal, No association with thumb sucking
16
Q
Can enterobias vermicularis cause appendicitis?
A
Can travel through appendix, but does not cause appendicitis
17
Q
How is enterobias vermicularis diagnosed?
A
Scotch tape test, ova infrequently seen in stool; Dientameba fragilis can sometimes be seen in stool and is associated with pinworm, so check for pinworm if seen
18
Q
How is enterobias vermicularis treated?
A
Albendazole - only works against adults, so retreat in 2 weeks
19
Q
What is albendazole?
A
Binds to helminthic tubulin (blocks assembly into microtubules), B/c of tubulin binding it is contraindicated in pregnancy
20
Q
How can enterobias vermicularis be prevented?
A
Personal cleanliness, Fingernails cut short, Children wear tight fitting pajamas, Bed clothes not shaken
21
Q
What is trichuriasis?
A
“whipworm”, Most common helminthic infection
22
Q
Where is trichuriasis found in US?
A
rural communities of South
23
Q
How is trichuriasis spread?
A
Eggs are ingested hand to mouth; Warm,damp soil; Raw fruits and vegetables that have been fertilized with human feces; NOT person-to-person (eggs take about 2 weeks to become infective)
24
Q
What are characteristics of trichuriasis infection?
A
Most are asymptomatic, usually low-intensity infections; trichuris seldom the only pathogen; Onset of significant symptoms is slow; Disease typically occurs in the developing child, seldom causing disability in adults; Multiple infections may occur (protective immunity incomplete)
25
What is the lifecycle of trichuriasis?
Eggs ingested, larvae invade intestinal mucosa, molt and mature over 3 mo, whiplike adult worms live in cecum and colon, eggs appear after 2-3 months in stool
26
What are the symptoms of trichuriasis?
Most are asymptomatic, but can cause: Rectal prolapse (due to massive number of worms, straining), anemia due to blood loss and anorexia, clubbing (seen in poorly nourished children), Trichurias Dysentery Syndrome (dysentery plus other symptoms; due to elevated TNFa and low pro-collagen), elevation of proteins, growth failure
27
How is trichuriasis diagnosed?
Stool for ova and parasites; eggs are thick walled, barrel shaped, and have a plug at each pole
28
How is trichuriasis treated?
Albendazole
29
How can trichuriasis be prevented?
Satisfactory fecal disposal, Handwashing, Washing vegetables grown in fecally- contaminated soil, Mass repetitive therapy directed towards school-aged children
30
What is the epi of Ascaris lumbricoides?
Children are infected more frequently (Increased soil contact from play and poorer hygiene; Protective immunity may be weaker in children), Demonstrated in familial clusters, Children highest intensity of infection
31
What are symptoms of Ascaris?
Acute infections – usually in children: bronchospasm, urticaria, pneumonia; Immune Mediated Hypersensitivity; Löeffler’s syndrome (Transient pulmonary infiltrates, Dyspnea – severe cough, Eosinophilia); GI (discomfort, vomiting, diarrhea); growth, developmental retardation
32
What is the Ascaris life cycle?
Eggs are ingested, larvae hatch in small intestine, migrate to heart and lungs, break out into alveolar spaces, migrate up trachea, are swallowed, mature in small intestines, cause pathology or pass out in feces
33
What are potential complications of Ascaris?
Intestinal obstruction (children), Peritonitis, Biliary and pancreatic obstruction
34
How is Ascaris diagnosed?
Stool for ova and parasites; Eggs measure 60 to 70 um – outside of the egg is coated with a sticky layer of mucopolysaccharide, which facilitates adherence to fruit,
vegetables, fingers, doorknobs
35
How is Ascaris treated?
Albendazole, occasionally surgery
36
Where are hookworms found?
Endemic tropics and subtropics, Adequate moisture and sandy soils
37
What is the hookworm lifecycle?
Larvae hatch in soil, penetrate the skin, migrate to heart and lungs, migrate to trachea and are swallowed, mature in small intestine, cause pathology or are passed in feces
38
What are clinical manifestations of hookworm?
Larvae penetrating the skin (Cutaneous Larva Migrans); Larvae penetrating the lungs (Cough and wheezing, Infiltrates may occur, Löeffler’s syndrome); GI manifestations (Epigastric pain, flatulence); Anemia (HALLMARK, blood "sucked" by worm); Hypoalbuminemia/anemia; initially high eosinophilia, later decreases
39
Why does hookworm cause anemia?
Upper small intestine “suck” blood (Secrete polypeptides prevent blood clotting, blood loss, Setting of marginal iron intake)
40
What are complications of hookworm?
Profound adverse effects on cognitive testing in childhood secondary to irondeficiency anemia; A major health threat to women of reproductive age with adverse effects on outcome of pregnancy; Severe iron-deficiency anemia during pregnancy has been linked to increased maternal mortality, impaired lactation, and prematurity and low
birth weight.
41
How is hookworm prevented?
Wear shoes!
42
How is hookworm diagnosed?
Obtain Stool for Ova and Parasites
43
How is hookworm treated?
Albendazole
44
What is life cycle of strongyloides?
Doesn't need host for life cycle! Larvae penetrate unbroken skin, migrate to lungs, are swallowed, live in epithelial cells of intestine, passed in feces, can autoinfect, can live outside of body
45
What happens in primary infection of strongyloides?
Skin penetration by filariform larvae (Pruritic maculopapular eruption); Pulmonary migration (Löeffler’s syndrome; Coughing, wheezing and eosinophilia); Intestinal Penetration by Adult Worm (Epigastric discomfort and diarrhea)
46
What is chronic persisting infection in strongyloides?
Most asymptomatic (a little peripheral eosinophilia); can come back 30-40 years later with creeping eruption, GI symptoms, and pulmonary symptoms
47
What can cause strongyloides hyperinfection syndrome?
steroids, HTLV-1 infection (Altered immune response - even in absence of malignant disease, decrease of anti-helminthic drugs due to low levels of type 2 cytokines)
48
What occurs in hyperinfection syndrome?
Fever, Vomiting, Diarrhea, Pulmonary Infiltrates, Hypoxia, Gram negative sepsis, Gram negative meningitis
49
How is strongyloides diagnosed?
Acute: stool specimens for larvae, serology; chronic: serology; hyperinfection: larvae in stool or sputum
50
How is strongyloides treated?
Ivermectin (opens gated chloride channels)
51
Which roundworms cause Loefflers syndrome?
ascaris, hookworm, strongyloides
52
Where is cutaneous larva migrans found?
Common in warmer regions like SE USA; children more likely to acquire infection
53
What causes cutaneous larva migrans?
Invasion of skin by larvae of dog/cat hookworm; penetrates no deeper than the epidermis b/c humans are dead-end host; causes dermatitis
54
How is cutaneous larva migrans treated?
Albendazole
55
What is the primary risk factor for toxocariasis?
Dogs!
56
What is the lifecycle of toxocariasis?
Dogs pass eggs in feces, eggs ingested, larvae hatch in bowel, migrate to organs
57
What are clinical manifestations of visceral larva migrans?
Larvae migrating through tissue (Eosinophilia high, Fever and hepatomegaly, Abdominal pain & decreased appetite); Pulmonary (cough, dyspnea and bronchospasm); CNS rare, but can occur (Seizures, myelitis)
58
What labs does visceral larva migrans cause?
Leukocytosis w/ marked eosinophilia
59
How is visceral larva migrans diagnosed?
clinical suspicion, ELISA
60
How is visceral larva migrans treated?
Albendazole
61
What is ocular larva migrans?
Larva migrate to the eye, results in an eosinophilic inflammatory mass, Mimics retinoblastoma (Unilateral visual deficits, ocular pain or strabismus)
62
How is ocular larva migrans treatd?
surgically primarily, can also try albendazole and steroids
63
What is Balyisascaris procynosis?
North American raccoon (Procyon lotor) is definitive host; Aggressive somatic migration with larval invasion of the central nervous system; Acute eosinophilic meningoencephalitis (fatal in 75%); Despite treatment – neurologic outcome is dismal; similar to ascaris of dogs and cats; eye involvement is common WITH CNS involvement
64
How is balyisacaris diagnosed?
serology done at CDC (brain biopsy will rarely find larvae, MRI finds white matter changes)
65
What is life cycle of trichinosis?
Eat undercooked meat (particularly pork), larvae are released in stomach and mature over 1-2 weeks, migrate to striated muscle (nurse cells)
66
What are common clinical findings of trichinosis?
Myalgias, weakness, fever; Periorbital edema; Conjunctivitis and conjunctival hemorrhages; Hemorrhages in nail bed
67
What are uncommon complications of trichinosis?
Myocarditis, Meningoencephalitis
68
How is trichinosis diagnosed?
Serology and Clinical Suspicion (Muscle biopsy can miss larvae)
69
How is trichinosis treated?
Albendazole (corticosteroids for severe disease)
70
What is loa loa?
Eye worm! From W Africa
71
What is life cycle of loa loa?
red fly bites, develop adults over 3 months (life 4-17 years), microfilarae released during daytime into blood, fly bites and takes them back up
72
What does loa loa cause?
Calabar swellings (migration in subcutaneous tissues), sometimes retinal occlusion; SOMETIMES CNS meningoencephalitis after treatment
73
How is loa loa diagnosed?
Noontime peripheral smear, extraction of worm, serology (but not for those who grew up in endemic regions)
74
How is loa loa treated?
Diethylcarbamazine (DEC)
75
What is Onchocerciasis?
River blindness
76
What are symptoms of Onchocerciasis?
Dermatological (Nodules (Adults), Dermatitis (microfilariae)); Ocular Changes (Keratitis, Uveitis, Chorioretinitis, Optic neuritis/atrophy)
77
How is Onchocerciasis treated?
Ivermectin
78
How can Onchocerciasis be diagnosed?
Skin snip
79
What is bacillus anthracis?
Large, Gram-positive rod; Non-motile and non hemolytic; Rapid grower; Produces three exotoxins: Edema factor, Lethal factor, Protective antigen; not contagious
80
Why is anthrax a good weapon?
Spores remain viable for years; Aerosolization can cause inhalation anthrax - severe, often fatal necrotizing mediastinitis; 1 gram of weapon-grade anthrax contains about 1 trillion spores
81
What are types of anthrax disease?
Cutaneous – most common; Gastrointestinal – periodic; Inhalation – once an industrial hazard, but currently rare; Meningeal – Commonly found in persons with septicemia; Injection – Recently characterized in Europeans who inject drugs
82
What is the clinical finding of cutaneous anthrax?
Pruritic macule forms vesicle forms round ulcer forms black eschar over 1-2 weeks; Surrounding edema/erythema but painless; +/- painful regional lymphadenopathy
83
How is cutaneous anthrax diagnosed?
Gram stain, PCR, skin biopsy, serology
84
What are clinical features of inhalation anthrax?
Initial symptoms resemble “flu”; Late symptoms include high fevers, vomiting, respiratory distress, and necrotizing hemorrhagic mediastinitis; Fatal within 24-36 hours if treatment delayed; Anyone with inhalation anthrax is now assumed to have meningeal involvement
85
How is inhalation anthrax diagnosed?
CXR, gram stain, culture, samples sent to department of health
86
How is inhalation anthrax treated?
Early and aggressive drainage of pleural effusions – chest tubes preferable as effusions often re-accumulate; If meningitis not ruled out: more than 3 antibiotics – all with good CNS penetration; no cephalosporins; 60 days of treatment, can switch to 1 med when appropriate
87
Is there an anthrax vaccine?
Yes, attenuated; Protective against cutaneous (human data) and possibly inhalational anthrax (animal data); current supplies are limited; can be given as PEP
88
Why is smallpox a good weapon?
Infectious via aerosol; Rapid person-to-person transmission; Worldwide immunity has waned; Severe morbidity and mortality; Clinical inexperience
89
What is epidemiology of smallpox?
Persons at most risk are household contacts; secondary spread to about 1-10 persons per case
90
What tempers fears about smallpox?
Incubation period 12-14 d (range 7-17 d); Vaccination of contacts within 4 days of exposure is effective in preventing illness; Contagiousness begins with onset of rash; Isolation measures effective in controlling outbreaks even with limited vaccine use
91
What is smallpox pathogenesis?
Implantation on oral or respiratory mucosa, Migration to regional lymph nodes, Initial asymptomatic viremia – day 3 or 4, Multiplication in reticuloendothelial tissues, Secondary symptomatic viremia around day 8
92
What are clinical features of smallpox?
Incubation period is 12-14 days (7-17d); Abrupt onset of high fever, malaise, rigors, vomiting, backache, and headache; Followed in 2-3 d by maculopapular rash; Generally not infective until rash appears
93
What is the smallpox exanthem?
Maculopapular rash that starts on face (including oral mucosa), forearms, or pharynx (centrifugal distribution), Spreads to trunk and legs; Lesions on palms and soles common; papules becomes vesicles become pustules; deeply embedded in epidermis
94
How is smallpox diagnosed?
Swab of vesicular/pustular fluid or removal of scab for culture, EM, variola-specific PCR assay at CDC BSL4 laboratory
95
How is smallpox managed?
Even one suspect case is an international emergency requiring immediate reporting to public health authorities; Isolation using both airborne and contact precautions (negative airflow pressure and HEPA filtration); No proven Rx
96
When was smallpox vaccination stopped in US?
1972 for general population, 1990 for military
97
What is the immune status following smallpox vaccination?
High level of protection for 3 years following vaccination; Duration of immunity is not clear; experience of naturally exposed persons never fully measured; Neutralizing antibodies following single dose decline significantly over 5-10 years
98
What should physicians particularly be looking for when considered about bioterrorism?
Unusual clinical features in previously healthy persons: Widened mediastinum, Hemorrhagic pneumonia, Synchronous, pustular rash on face and hands
99
What is life cycle of lymphatic filariasis?
Mosquito bites (introducing larvae), larvae migrate to lymphatics where adults mature, microfil are released after 6-12 months, are taken up by mosquitos
100
What is the microfil stage of lymphatic filariasis?
Few overt clinical manifestations (Despite large #s circulating microfilariae); Prevalence of microfilaremia
increases with age during childhood, reaches a plateau 20-30 years of age, and is greater in men
101
What is Acute Adenolymphangitis (ADL)?
Often the first manifestation of lymphatic filariasis; Sudden onset of high fever, Painful lymphangitis and lymphadenitis (Lymphangitis is retrograde), regional lymph nodes are often enlarged, can have genital involvement
102
How can lymphatic filariasis cause genital disease?
Produces hydroceles w hich vary in diameter from less than 5 cm to over 30 cm; translucent when transilluminated; usually not painful; thickening of the spermatic cord can occur; skin of scrotum may be thickened
103
What is chyluria?
Can occur in lymphatic filariasis, Complaints of passing “milky urine’; severe nutritional consequences (large amount of fat and protein lost in the urine)
104
How is lymphatic filariasis diagnosed?
Early acute disease = Smear at midnight; Chronic Disease = Serology
105
How is lymphatic filariasis treated?
Diethylcarbamazine (DEC)
106
What is wolbachia?
Wolbachia, a bacterial endosymbiont, is
essential for the growth, development,
fertility and survival of the causative
agents of lymphatic filariasis; can be treated with doxycycline
107
What is Tropical Pulmonary Eosinophilia?
Due to W. bancrofti or B. malayi; Male:Female is 4:1- 3rd Decade of Life; India, Pakistan, Sri Lanka, Brazil, Guayana,
and Southeast Asia; Paroxysmal cough and wheezing – nocturnal, looks like asthma – eosinophilia and immigration
history are clues
108
How is tropical pulmonary eosinophilia treated?
Diethylcarbamazine (DEC)
109
How is tropical pulmonary eosinophilia diagnosed?
serology (smears are negative)
