1. Enterobius vermicularis (pinworm)
2. Larvae migrate from perianal region to cecum and mature within 2-4 wks
3. ~1 cm long, pointed tails (pinworm)
4. Appendicitis, vulvovaginitis, UTI due to bacteria

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1. Trichuris trichiura (whipworm)
2. Rectal prolapse
3. Unwashed vegetables contain eggs (require 10 days of maturation in soil for embryonation)

Patient comes in presenting with abdominal pain, constipation (with signs of obstruction) and fever (which exacerbates the pain). Recent history is notable for severe bouts of coughing and pneumonitis. Stool sample contains egg (shown below), and larvae + eosinophils in the sputum. What is the most likely diagnosis? What are other manifestations of the disease?

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1. Ascaris lumbricoides
2. Embryonated eggs hatch in small intestine. Larvae penetrate mucosa, travel to through portal system to right heart. This passage can cause liver abcesses and pneumonitis. After being coughed up and swallowed, worms mature in intestine/biliary trunk, leading to obstruction. Motility and tissue damage can occur on treatment or during fever due to increased adult motility.

Patient presents with signs of hypochromic anemia, pneumonitis, and skin irritation. Social history shows that they are a dirty hippy who likes gardening bare-foot and composting their own waste. Stool sample reveals eggs (shown below), some in the process of hatching. What is the most likely diagnosis? What is significant about the life cycle of this worm? What causes the symptoms? When diagnosing, what are some potential false positives?

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1. Hookworm infection (Necator americanus most likely due to geographic region, although Ancylostoma duodenale has identical eggs)
2. Eggs hatch in soil, releasing rhabditiform larvae which molts and becomes filariform larvae. This non-feeding larvae enter human through feet, then undergoes pathogenesis similar to Ascaris (portal system --> heart --> lung --> intestine)
3. Adults latch onto villus and drink blood, causing anemia. Pneumonitis due to penetration of aveoli, and skin irritation due to allergic skin manifestations.
4. Eggs can hatch in feces, causing possible confusion with autoinfective Strongyloides

1. Trichinella spiralis (trichinosis). Larvae excyst in stomach, mature in small intestine (2-6 days) and burrow into mucosa. Disseminate via lymphatics to striated muscle.
2. Congestive heart failure with larvae load >1000 larvae/gm of tissue

Patient is Jewish adult female who presents 3-4 weeks after Passover, a holiday featuring Gefulte fish. Patient presents with nervous disturbances, abdominal discomfort, weight loss and macrocytic anemia. Eggs are observed in stool (shown below). What is the most likely diagnosis?

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Diphyllobothrium latum (fish tapeworm)

Due to ingestion of plerocercoid found in raw Gefulte fish. Largest of the tapeworms.

1. Solium can be caused by pork infection or autoinfection, where as saginata is solely from beef
2. Solium proglottids travel backwards from stomach via reverse peristalsis/vomiting.
3. Solium eggs hatch --> cysticerci in humans AND pork, whereas saginata only hatches in cows.
4. Cysterci of solium can be found in brain, eye or subcutaneous tissue.

1. Cercariae infest water, where they penetrate human skins. Schistosomula travel through skin to venule --> right heart --> lung --> arterial circulation. Passed in feces/urine into water where miracidia infect snails and mature into cercariae in 1-2 months.
2. Mansoni = large infection, japonicum = small intestine (both pass ovum in feces), haematobium = urinary bladder (can pass ovum in urine)
3. Male and female form hot dog like structure (male = bun, female = hot dog). Female chemotactically attracted to male.

Typically occurs 35 days post infection. Febrile disease resembling serum sickness (fever, cough, splenomegaly, abdominal pain and diarrhea)

Also known as Katayama syndrome. May be exacerbated by praziquantal.

Depends on location

1. Intestinal schistosoiasis (masoni and japonicum) lead to abdominal pain and diary, with congest/thickened and ulcerated bowels
2. Urinary schistosomiasis (haematobium) leads to pain on micturition, hematuria, with a bladder pathology.
3. Eggs can become stuck in liver, leading to granuloma and portal hypertension (note: ALT + AST typically in normal range)
4. Granulomata, splenomegaly, CNS malfunction
5. Nephropathy in japonicum

Identify the following ovum (found in feces, urine, rectal or bladder biopsies)

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Size = 155 x 65 um

Schistosome ova

Identify (5-10x magnification):

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After returning from a trip to Korea, patient comes into office with signs of jaundice as well as various abdominal pain. Liver biopsy shows adnematous hyperplasia of bile ducts, along with Salmonella infection. The ova are observed in feces and duodenal aspirates. What is the most likely diagnosis?

Identify:

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~1 cm long

The following larvae is seen in a stool sample of an immunocompromised patient. Identify:

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Identify:

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What diagnostically significant symptoms would you expect to find in a patient with these?

What are some of the predisposing factors that could lead to infection?

Giardia larvae.

Steatic diarrhea (foul smelling) due to malabsoprtion of fats. Pernicious anemia due to B12 malabsorption.

Consumption of water near beaver dam. Achlorhydria or low levels of s-IgA

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The following structure was found in a patient's stool. What symptoms would you expect to see in patients with this structure? How were they infected?

Entamoeba histolytica (note 4 nuclei; Entamoeba coli=8).

Can lead to dysentery, mucosal inflammation and liver invasion. Edema and hyperemia minimal, but possible, and can sometime leads to large granulomatous mass. Metastatic amaebosis can lead to abscess formations (necrotizing lesions surrounded by trophozoites)

Follow fecal-oral infection route.

Balantidium coli

Seen in institutionalized patient. Only ciliated protozoan that affects humans.

Patient comes into AIDs clinic complaining of persistant diarrhea. Patient stools are stained and shown below. What is the most likely diagnosis? What staining technique is used? What is the first line treatment?

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1. Cryptosporidium parvum (self-limited in healthy patients, but persistant in immuno-compromised).
2. Modified acid-fast stain
3. Paromycin (inhibits protein synthesis)

Identify:

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1. Iodoquinol; iodine-allergy (patient will be allergic to shellfish), can cause neurotoxicity; unknown
2. Parmomycin; patients with potential bowel perforation (ulcer) or renal disease; inhibits protein synthesis (aminoglycoside)
3. Diloxanide; none, its the perfect drug (which requires approval from CDC to use); unknown

1. Dehydroemetine- do NOT give venous injections, cardiotoxicity and hypotension (note: inhibits protein synthesis)
2. Chloroquinone- Only reaches therapeutic concentration in the liver. Not effective against intestinal ameobae.

1. Furazolidone (damages worm DNA, good oral bioavailability)
2. Nitazoxanide (also used against Cryptosporidium, targets pyruvate:ferrodxin pathway, well tolerated and non-mutagenic)

Nemotode microtubules, which leads to accumulation of catabolic enzymes, as well as loss of glucose uptake.

Mebendazole is used with corticosteroids to target severe Trichinella infections. Albendazole may be more effective against hookworms.

Acts on neuromuscular junction, leading to worm paralysis. Used against Ascaris, Enterobius, and hookworms (Necatur and Ancylostoma)

Note: poor oral absorption

Ivermectin (also used against Ascaris and whipworm)

Opens worm glutamate-chloride channels. Potentiates GABA inhibitory action.

Alan IVERson is a strong athlete, but he likes to GABa.