Week 1 Flashcards
Esophagus
Anatomy
- length? Made of?
- beginning to end structure?
- main function?
- secretes?
**2 areas of high pressure at rest called? Identify locations of both
Esophagus
- hollow, highly distensiblemuscular tube
- 25cm long
- EPIGLOTTIS TO GE JUNCTION
- Main function; to propel food from pharynx to stomach via PERISTALSIS
- Secretes MUCIN for LUBRICATION
ESOPHAGEAL SPHINCTERS
- two areas of high pressure at rest (physiologic)
1. Upper esophageal sphincter: At cricopharyngeus and inferior pharyngeal constrictor muscle
2. Lower esophageal sphincter; 2-4cm proximal to esophagogastric juncton at level of diaphragm
Esophagus
Anatomy/histology
Structure from gastroesophageal junction
Histology layers of esophagus
Gastroesophageal junction
- distal esophagus, Z line, stomach, cardia
Histology; lined by squamous epithelium
- Mucosa
- Submucosa
- Muscularis propria
- Adventitia
Identify 3 congenital abnormalities of esophagus Based on presentation
- aspiration
- suffocation
- pneumonia
- severe fluid and electrolyte imbalance
**what is most common variety?
ATRESIA usually associated with FISTULA
- Atresia; Incomplete development
- Fistulae; Connection of upper or lower esophageal pouches to bronchus or the trachea
- Stenosis; incomplete form of atresia
- congenital
- acquired
**Most common variety of esophageal atresia and tracheoesophageal fistula - BLIND UPPER SEGMENT, FISTULA BETWEEN BLIND LOWER SEGMENT AND TRACHEA
Identify esophagus congenital abnormality based on presentation
- dysphasia, heartburn
- H pylori
- Ulceration, bleeding, stricture
- Barrett, rarely adenocarcinoma
ECTOPIA
- Ectopic gastric mucosa in upper third of esophagus (AKA inlet patch)
- Ectopic pancreatic tissue in the esophagus
**Image; endoscopy, ectopic gastric tissue in esophagus, salmon colored patch (inlet patch)
Identify
Disruption of coordinated waves of peristaltic contraction following swallowing
Clinical causes? (2)
Functional Obstruction of esophagus
**Obstruction can be mechanical or functional
Clinical; Esophageal dysmotility disorder (swallowing disorders)
- Achalasia
- Spastic esophageal dysmotility disorders
- nutcracker esophagus; corrdinated contractions
- diffuse esophageal spasm; uncoordinated contractions
- lower esophageal sphincter dysfunction
Identify condition
Identify 2 types,? Treatment (3)?
**Barium swallow show - BIRD’s BEAK appearance of esophagus
Histology
Early; Auerbach/myenteric plexus has lymphocytic inflammation (cytotoxic T cells, eosinophils)
with germinal centers and submucosal glandular atrophy
Late; Marked depletion / absence of ganglion cells in myenteric plexus and replacement of nerves by collagen with muscular hypertrophy
ACHALASIA; esophageal dysmotility disorder
1. Primary achalasia
Result of distal esophageal inhibitory neuronal cell degeneration (these neuronal cells produce nitric oxide and vasoactive intestinal polypeptide) Most cases are primary (idiopathic) T cell mediated destruction or absence of myenteric ganglion cells in lower third of esophagus
- Secondary achalasia
- Chagas disease: Trypanosoma cruzi infection (Trypanosoma cruzi in South America) causes destruction of the myenteric plexus (failure of peristalsis and esophageal dilatation)
- Diabetic autonomic neuropathy
- Malignancy Infection
- Autoimmune diseases
Treatment
- Myotomy
- Pneumatic balloon dilations
- Botulinum neurotoxin (Botox) injection (inhibit LES cholinergic neurons)
Identify condition (Spastic esophageal dysmotility disorders)
Diagnosis, pathophys, treatment Presentation; - Contraction in normal sequence but excessive amplitude and duration - Dysphagia (difficulty swallowing) - Chest pain - 6th to 7th decade
- *High amplitude contractions of distal esophagus
- Endoscopy; pronounced helical configuration of the esophageal lumen
- Barium swallow; corkscrew appearance
NUTCRACKER ESOPHAGUS
**Presentation - HYPERTENSIVE PERISTALSIS
DIagnosis
- Esophageal manometry (pressure measurement at various point) (pressure over 180mm Hg)
Pathophysiology
- Unknown, maybe abnormalities in neurotransmitters
Treatment
• Medications, such as Ca channel blockers, Botulinum toxins
• Pneumatic dilatation
• Surgery
Identify condition (Spastic esophageal dysmotility disorders)
- repetitive simultaneous UNCOORDINATED CONTRACTIONS of distal esophageal smooth muscle
- testing; mamometry - abnormal pattern of contraction
Cause? Presentation? Xray? Treatment?
DIFFUSE ESOPHAGEAL SPASM
Unknown Cause
Present; dysphagia, regurgitation, chest pain
Xray; corkscrew pattern
Treatment
- medication; proton pump inhibitors, Ca channel blockers, nitrates
- rarely surgery
Identify esophagus condition
**Increase in wall stress
2 types
Esophageal diverticulae
- Epiphrenic diverticulum above LES
- Zenker diverticulum (pharyngoesophageal) - above UES
- Impaired relaxation and spasm of cricopharyngeus muscle
- accumulation of food, regurgitations, halitosis (bad breath)
Esophageal obstructions
**Differentiate WEBS and RINGS
Esophageal mucosal webs:
- Idiopathic ledge-like protrusions of mucosa
- Can be associated with GERD (gastroesophageal reflux disease), chronic graft-versus-host disease (Usually 100 days after graft, the immune cells in graft tissue attack recipient cells, not transplant rejection), blistering skin diseases
- Upper esophagus, webs may be associated with iron-deficiency anemia, glossitis, cheilosis, (part of Paterson-Brown-Kelly or Plummer-Vinson syndrome)
- Semi-circumferential, less than 5 mm, fibrovascular tissue with overlying epithelium
Schatzki rings:
- Similar to web, but circumferential, thicker, also involves submucosa
- A rings: Distal esophagus, above GE junction, squamous mucosa - B rings: At GE junction, may have gastric cardia-type mucosa
Associated with meat impaction “steakhouse syndrome”
**May be congenital or a scar from drinking caustic liquids
Esophagitis
2 types of lacerations
- No surgery needed
- Surgery needed
- Mallory Weiss tears
• Severe retching and vomiting secondary to acute alcohol intoxication
• Longitudinal mucosal tear, few mm to several cm
• Usually no surgical intervention required
**Bleeding from esophagogastric laceration due to severe vomiting
**May lead to GI hemorrhage esp if associated with esophageal varicose - Boerhaave syndrome
• Transmural tearing and rupture of distal esophagus
• Surgical intervention required
Chemical esophagitis
Types of chemicals (4)
Symptoms (4)
CHemical esophagitis
- alcohol
- corrosive acids or alkalis
- hot fluids
- heavy smoking
Symptoms
- pain (odynophagia - painful swallowing)
- Hemorrhage
- stricture
- perforation
Infectious esophagitis
Viral vs fungal
Viral;
- HSV
- herpetic ulcers in the distal esophagus
- multinucleated cells with herpesvirus nuclear inclusion (cowdry type A inclusion)
- multinucleated, moulding, margination of chromatin (ground glass chromatin) - CMV
- epithelial cell with CMV inclusion
- Single, large, basophils intranuclear inclusion, perinuclear halo, stipples cytoplasmic inclusions
Fungal
- Candida
- Mucosa
- Aspergillous
Esophagitis - Morphology
- Chemical
- Pill induced
- Radiation
- Candidiasis
- HSV
- CMV
- Chemical; Necrosis
- Pill induced;
- at stricture
- ulceration, necrosis, granulation tissue, fibrosis - Radiation
- intimal proliferation and luminal narrowing of vessels - Candidiasis
- Gray white pseudomembranes - HSV
- punched out ulcers
- nuclear viral inclusions - CMV
- shallow ulcers
- xteristic cytoplasmic and nuclear inclusions
Identify esophagitis type
- Filamentous fungal organisms PAS stain
- Pseudohyphae and budding spores in squamous debris
- Fibrinopurulent exudate and necrotic debris
- Underlying active esophagitis
Candida esophagitis
Identify
**Most common cause of esophagitis
GERD - Gastroesophageal reflux disease
A. reflux of gastric contents into lower esophagus
- most common cause of esophagitis
- squamous epithelium prone to injury from acid
B. 3-40% in US
C. Transient LES relaxation
- mediated via vagal pathways
- triggered by gastric dissenting on, gas or food; Alcohol, tobacco, obesity, CNS depressants, pregnancy, hiatal hernia, delayed gastric emptying, increased gastric volume
Reflux esophagitis
Morphology
Hyperemia vs mild GERD Vs Signigicant GERD
Hyperemia
- Redness
Mild GERD
- histology usually unremarkable
Significant GERD
• Eosinophils, later neutrophils
• Basal zone hyperplasia
• Elongation of lamina propria papillae
Identify condition based on histology
Histology; Scattered intraepithelial eosinophils and basal layer hyperplasia
Clinical features? Treatment? Complication
REFLUX ESOPHAGITIS
Clinical features
• Heartburn, dysphagia, regurgitation
• Rarely severe chest pain, mistaken for heart disease
Treatment
• Proton pump inhibitors (eg omeprazole, Prilosec)
- Inhibitors of acid secretion in stomach
- Block Na+/K+ ATPase (parietal cells)
- Recently have replaced H2 histamine receptor antagonists
Complications
- Ulceration, hematemesis, melena, stricture, Barrett esophagus
Identify condition
• Food impaction and dysphagia in adults
• Feeding intolerance or GERD-like symptoms in children
- More common in children
• Diagnosis
- Esophageal pH probe (not acidic)
- Failure to respond to antireflux therapy
- Allergic history
- Biopsy
**Histology? Treatment?
EOSINOPHILIC ESOPHAGITIS
Histology
• Numerous intraepithelial eosinophils
• Eosinophils (15 or more in 2 or more high power fields or 20-25 or more in any HPF), microabcesses (42%), often with large clusters near surface
**Abnormal squamous maturation
Majority are atopic
- Atopic dermatitis, allergic rhinitis, asthma, peripheral eosinophilia
Treatment
• Dietary restrictions to prevent food allergens (cow’s ,ilk, soy)
• Topical or systemic corticosteroids
- Identify normal GI venous drainage
- Increase BP w/in portal venous system?
- **
• Congested subepithelial venous plexus in distal esophagus/proximal stomach
• Alcoholic liver cirrhosis, hepatic shistosomiasis
ESOPHAGEAL VARICES; angiogram showing tortuous esophageal varices
- Normal GI venous drainage
- GI - liver (portal vein) - heart - Portal Hypertension
• Increase of blood pressure within the portal venous system
• Liver cirrhosis common cause (liver fibrosis)
• Results in development of collateral channels - VARICES
• Congested subepithelial venous plexus in distal esophagus/proximal stomach
• Alcoholic liver cirrhosis, hepatic shistosomiasis
Identify morphology based on clinical features
- present in 50-90% of pts with cirrhosis
- 25-40% of pts with cirrhosis develop variceal bleeding
- variceal bleeding is a MEDICAL EMERGENCY
- Treated medically splanchnic vasoconstriction, endoscopically by sclerotherapy (injecting thrombotic agent), balloon tamponade, variceal ligation
- 30-40% of variceal hemorrhage can result in death
- Patient with risk for hemorrhage can be prophylactically treated with beta blockers to reduce portal blood flow
Esophageal varices
Morphology
- Tortuous dilated veins
- Submucosal
- Can be collapsed in surgical specimen and autopsies
- Rupture results in hemorrhage
- collapsed varices in postmortem specimen
- Dilated submucosa varices
Identify condition
- *Intestinal metaplasia in pts with chronic GERD; columnar epithelium more resistant to acid, pepsin and bile
- present in 10% of pts with GERD**
- increased risk of esophageal ADENOCARCINOMA
Diagnosis? Morphology? Histology?
BARRETT ESOPHAGUS
- Dysplasia can be detected in up to 2% of patients with Barrett esophagus. Dysplasia associated with prolonged symptoms, longer segment length, increase patient age, and Caucasian race
Diagnosis
• Characteristic endoscopic appearance plus characteristic histology
• 8 random biopsies recommended
• Take biopsies beginning in stomach, then every 1-2cm until obvious squamous epithelium is reached
Morphology
• Endoscopically recognized by patches of red, velvety mucosa extending upward from the gastroesophageal junction
• Long segment: 3 cm or more
• Short segment: Less than 3 cm
Histology
• Intestinal type metaplasia (goblet cells) replacing squamous mucosa
• Dysplasia can be present
- Low grade; nuclear stratification and hyperchromasia
- High grade; architectural irregularity (cribriform) and cytologic atypia
Identifytreatment of condition based on clinical features
- only be identified by endoscopy and biopsy in patients GERD
- Requires periodic endoscopy with biopsy
- Malignancy requires therapeutic intervention
BARRETT ESOPHAGUS
• Antireflux therapy
• Endoscopy every 1-2 years to detect dysplasia or malignancy
• 4 quadrant biopsies, larger forceps, intervals of 2 cm or less throughout the length of Barrett segment, also of any suspicious lesions
- Low grade dysplasia: Antireflux and increased surveillance
- High grade dysplasia: Rebiopsy immediately to rule out missed carcinoma, possible esophagectomy (second opinion from a GI pathologist)
2 types of malignant tumors in esophagus
- More common in US - from GERD
- More common in world
Esophageal tumors
- Adenocarcinoma
• Most arise from Barrett esophagus
• On the rise in the US - Squamous cel carcinoma
• More common worldwide
Identify esophageal malignant tumor
Morphology
- Commonly form mucin and glands
- Less common; diffusely infiltrative SIGNET-RING cells
Location
- usually in distal portion and involve the gastric cardia
- malignant tumor with glandular differentiation
Risk factors? Risk reducer? Ethnicity? Gender?
Esophageal ADENOCARCINOMA
- most common in caucasians
- males (70x)
- has increase rapidly in US and western world
- before it was just 5% of esophageal cancers now more than half of al esophageal cancer (50-70%)
- most arise from Barrett (most important risk factor); remeber GERD - Barrett - Adenocarcinoma
- Obesity and high BMI (strong risk factors, likely related to GERD) - Other risk factors include tobacco (moderate risk factor)
- Risk reduced by diets rich in fresh fruit and vegetable
- Some serotypes of H pylori associated with reduced risk (gastric atrophy, reduced acid production and decreasing reflux disease)
Identify esophagus tumor
Pathogenesis
• Barrett to adenocarcinoma over extended period of time through acquisition of genetic and epigenetic changes
• Mutation of TP53
• Downregulation of CDKN2A (cyclin-dependent kinase inhibitor)
**clinical features? Treatment?
Esophageal Adenocarcinoma
Clinical features
A. Symptoms; • Difficulty swallowing • Weight loss • Hematemesis • Chest pain • Vomiting
B. Occasionally discovered in evaluation of GERD
C. Advanced stage at the time of diagnosis
- Spread submucosal lymphatics (esophagus with extensive lymphatic network that allows horizontal and longitudinal spread even in superficial tumors)
D. Recurrence common
E. Overall 5 year survival less than 25%
Treatment
• Resection (may be preceded by neoadjuvant therapy)
• Adjuvant chemoradiation is often given
• (5 year survival for nonresectable tumors is rare)
Identify esophageal tumor
Pathogenesis
• Alcohol and tobacco
• Polycyclic hydrocarbons, nitrosamines, HPV
• Molecular: Loss of tumor suppressor genes such as p53 and
p16/INK4a
epi? Gender? Ethicity? Regions with high incidence? Risk factors?
SQUAMOUS CELL CARCINOMA
• Worldwide most common esophageal malignancy
• US strong male predominance
• Risk factor include alcohol, tobacco, caustic esophageal injury,
achalasia, tylosis (hyperkeratosis in palms and sole), Plummer-Vinson syndrome, consumption of very hot beverage, radiation
• 6X more common on African American than Caucasians
• Regions with highest incidence include Iran, central China, Hong
Kong, Brazil, and South Africa
Identify esophageal tumor
Morphology?
Clinical features
A. Insidious; Dysphasia (difficulty swallowing), Odynophagia (pain on swallowing), Obstruction
• Weight loss
• Hemorrhage and sepsis
• Occasionally aspiration of food via a tracheoesophageal fistula
• Overall 5 year survival is 9%, most don’t survive 1 year
SQUAMOUS CELL CARCINOMA
Morphology
• Middle third of esophagus
• Begins with dysplasia and in-situ carcinoma
• Polypoid, ulcerated, diffusely infiltrative; lymph nodes involvement
- upper third; cervical lymph nodes
- middle third; mediastinal, paratracheal, tracheobronchial nodes
- lower third; gastric and celiac nodes
- *Usually in mid esophagus causing stricture
- *Nests of malignant squamous cells
Identify Nematodes
- Wolbachia
- Gram negative, rickettsial - like intracellular bacteria
- obligate bacteria
- Supports chemical pathway necessary for embryogenesis and molting, needed to go from one stage to another.
- Also in arthropods
Flilarial Nematodes
• Onchocerciasis
• Loiasis
• The Filariases (Bancroftian, Malayan, Timorian)
Tissue
• Dracunculiasis
• Toxocariasis
- *Schedule says toxoplasmosis but wrong toxo
Identify filarial nematode disease
- *aka “river blindness”
- transmission?
- what skin disease?
- lymph node?
- eye?
ONCHOCERCIASIS
• Onchocerca volvulus
• Transmitted through repeated bites from Simulium black fly; Lives and breeds near fast-flowing streams and rivers
• Can also cause severe skin disease
A. Skin
1. Dermatitis
• Most symptoms from dead or dying larvae
• Secrete collagenase during migration loss of skin elasticity
• Loss of melanin from basal cells, “leopard skin”
• Atrophy of the dermis
• Lichenified onchodermatitis (LOD), “sowda”
2. Nodules (onchocercomata)
• Larvae travel to skin and form fibrous nodule, safe from
human defense
• Become detectable 1-2 yrs later
• Males travel in between nodules, females release
thousands of larvae to the surrounding tissues to be taken
up by black fly
B. Lymph Nodes
• Can find enlarged nodes where
lymphatics are draining areas of
onchodermatitis
C. Eye
• Punctate Keratitis: initially observed, clears without scarring
• Chorioretinitis: slow to progress over years leading to blindness
Nematode that affect skin, lymph nodes, eye
Diagnosis
Treatment (3)
Prevention and control
ONCHOCERCIASIS (River Blindness)
Diagnosis
- History, eosinophilia and skin snip; 3mm tent, incubate in NS for 24 hrs
- dermatitis; tough, tough tough. Leopard skin - vitiligo? Leprosy>
- Nodules; nodulectomy
- Serum antibody testing, but can only tell filarial disease, not which one
Treatment
1. Ivermectin
• Kills microfilaria, not adults
• Sterilize adults
• Mass Drug Administrations give doses q6months
2. Doxycycline?
• Targeting Wolbachia
• Slow death of filaria
3. DEC
• Used to be treatment, but causes rapid death and worsening of
inflammation of eye leading to increased blindness
Prevention A. Avoid black flies • Long sleeves • DEET B. Onchocerciasis Elimination Program for the Americas (OEPA)
Identify condition based on clinical symptoms
- Calabar swelling
• Recurrent episodes of angioedema
• Hypersensitivity response to a migrating worm
• Face and extremities, near joints
• Itching large area of nonpitting edema, lasts days to weeks
• Only pain from compression of nerves - Eye worm
• Subconjunctival migration of adult worm
• Swelling of lid, conjunctivitis, itching, photophobia
• Symptoms <1 week, little damage
More rare symptoms?? (4)
LOIASIS ; loa loa worm A. Repeated bites from Chrysops genus • deer fly, mango fly, mangrove fly, African red fly • Bite during the day, rainy season • Rain forest B. Endemic to central and west Africa • Also found in Malawi, Uganda, Zambia, Ethiopia • Higher rates in adults (M>F)
Rare symptoms 1. Meningoencephalitis • High microfilaria burden • Mostly with treatment with DEC • Mild HA to coma or death 2. Renal • Hematuria and proteinuria • Immune complex glomerulonephritis or mechanical trauma 3. Endomyocardial Fibrosis 4. Pulmonary infiltrate or effusion
Identify diagnosis and treatment of condition
Disease
• Adult worms can live up to 17 years
• 5 months larvae to adult
• Microfilaria have diurnal periodicity
• Blood ranges undetectable to 100,000parasite/ml
• Adults live in ligaments, tendons, fascia
• Larvae live lymphatics lungs
• No Wolbachia
• Most symptoms in visitors to endemic areas
LOIASIS- loa, loa worm
- calabar swelling (angioedema)
- eye worm
Diagnosis
• Seek expert help!
• Surgery of adult worms
• Diethylcarbamazine (DEC); only from CDC
- kills MF and adult
- low MF load; calabar swellings, urticaria, fever
- High MF load; meningoencephalitis, renal failure. *Need cytopheresis prior
- Don’t use in conjunction with onchocerciasis d/t risk of severe skin/eye reaction
• Albendazole
- Long course if DEC ineffective
Identify
• Cause inflammation of lymphatic
- Valvular dysfunction
- Inability to remove fluid and cause
• Tend to accumulate in lymphatics of legs
• Long-term exposure needed for lymphedma , arms and genitals in men transmission
Diagnosis
• Detection of parasite, parasite Ag (not available US) or DNA (research labs)
• Microscopic microfilariae on thick film with Giemsa stain or Knott’s concentration technique (more sensitive)
• Collect blood between 10pm and 2am
• Microfilaria in blood, hydrocele fluid, sometimes urine
• Can check for antifilarial IgG4
**3 species? Transmission? Location? Presentation
Lymphatic Filariasis
• 3 species
- Wucheria bancrofti
- Brugia malayi
- Brugia timori
• Mosquito transmission; All mosquitos implicated
• Typically in the tropics
- subtropics Asia, Africa, west pacific, Caribbean, South America
- endemic in Americas; Haiti, DR, Guyana, Brazil
• Can persist for years in humans, especially since early disease can be asymptomatic
• Live in lymphatic system of humans
• Damage the lymphatics by inflammation or damage to the lymphatic valves
Identify ACUTE clinical features in this condition
Microscopic - thread like worms
- thread = filo (Latin)
- microfilariae 250 micron long and 10 micron wide
- adults 2-10cm
5 stages of life cycle; human - mosquito - human
• 1. Larvae (microfilariae) released from adults in human blood (
nocturnal)
• 2. picked up by mosquito at night and migrate to thoracic muscle • 3. grow over about 2 weeks, then migrate to the mosquito mouth • 4. deposited to human during bite, travel to lymphatics
• 5. grow to adult and make microfilaria
Lymphatic Filariasis
Acute Clinical Features
• Most are asymptomatic
• Acute Filarial Lymphangitis
- Acute inflammation along lymph vessel, death of adult worm
- Pain, erythema, tenderness of lymph node prior to
• Acute Dermatolymphangioadenitis
- Bacterial infection
- Severe pain, fever, chills
- Often history of trauma to the skin prior (bite, cut, etc)
Identify CHRONIC clinical features based on, treatment and prevention
Treatment
1. DEC (diethylcarbamazine)
• only available from CDC in US
• Side effects related to microfilaria burden
• Dizziness, nausea, fever, headache and joint pain
• Rapid killing of adult worms can cause acute
reaction (consider pretreatment with steroids)
• Can worsen Onchocerciasis, severe reaction
2. Ivermectin; only kills microfilaria, sterilize adults
3. Doxycycline
• Wolbachia treatment
• Slow death of adult worms
**Prevention and control
1. Mosquito precautions
• Mosquito repellants
• Bed nets
• Long sleeves
• Light colors
What is the 2nd?
Lymphatic Filariasis - Chronic
1. Genital; 65% hydrocele
• Epididymitis, orchitis, lymphedema of scrotum of vulva
• Hydrocele most common, W. bancrofti
• Adult worm causes lymphatic damage
• Chylocele– rupture of intrascrotal
2. Lymphedema - 35%
• Legs, scrotum, penis, breast and arms
• Typically asymetric involvement
• Bancroftian filariasis– may be entire limb
• Brugian filariasis– typically distal extremity
**WHO Lymphedema grading system
• Grade I: pitting edema reversible with elevation
• Grade II: non-pititng edema not reversible with elevation
• Grade III: non-pitting edema not reversible with elevation and
thickening of skin/skin folds
• Grade IV: non-pitting edema with papilomatous skin lesions with skin folds (elephantiasis)
- Elephantiasis
• Not reversible
• Keeping wounds clean is essential
• Wound care programs help prevent secondary infections - Chyluria
• Rupture of dilated lympatic structures into renal pelvis
• Loss of chyle= loss of dietary lipids, proteins, vitamins, weight loss, malnutrition - Tropical pulmonary eosinophilia
• W. bancrofti or B. malayi, hypersensitivity as microfilariae
travel through pulmonary blood vessels
• Mostly men, 20-40 years old
• Paroxysmal, non-productive cough (worse at night),
wheezing, adenopathy, generalized malaise, weight loss
• Eosinophilia, Elevated IgE, HIGH Ab titers
• Typically no microfilaria in blood
• CXR normal to small interstitial infiltrates
• PFTs can show restriction
• Can lead to chronic restrictive lung disease and fibrosis
• DEC is treatment—patients show quick response
Prevention and control
2. In 1997, WHO Global Program to Eliminate Lymphatic Filariasis
(GPELF)
• Stop trasnmission with mass drug administration (DEC or Ivermectin + albendzole)
• Once yearly for 5 years reaching at least 65% of population
• Reduce morbidity
• Treatment of lymphedema and wound care
Identify condition? Treatment? Eradication
- Drinking stagnant water with copepods (“water fleas”)
- 2-3’-long worm that emerges from the skin
- Affects communities in Africa with poor sources of drinking water • 1986 3.5M cases worldwide, 2015 22 cases; Chad and South Sudan majority
Disease
• No symptoms for ~1year
• Slight fever, rash, itching, N/V
• Blister (80-90% on lower extremity) enlarges and is painful over days
• Immersion in water thought to trigger release of larvae back into
the water
DRACUNCULIASIS
“Guinea worm”
- Dracunculus Medinensis
Treatment • Soak in water • Gentle traction on the worm • Wrap worm around guaze or stick • Extraction may take days to weeks • If the worm breaks, can cause abscess formation and worsening cellulitis
Eradication
1. Global eradication campaign started in 1980, 20 countries
affected; Targeted Eradication Criteria
• It is biologically and technically possible to eradicate this disease.
• The benefits of eradication outweigh the costs.
2. Disability; avg process 8.5 weeks
• What if this is during harvest? Or, planting season? • School attendance drops • Work attendance drops
3. Criteria (PPT)
• GWD is now poised to be the first disease to be eradicated using core public health practices, such as surveillance, case containment, and simple interventions, without the use of vaccines or medicines
Identify condition
• Visceral & Ocular larva migrans (USUAL HEPATITIS IN KID)
• Toxocara canis/cati
• Vector: dogs/cats
• Found mostly in dirt; fecal oral, human ingest infectious egg from environment OR larvae from uncooked meat
• Many infections asymptomatic
• 13.9% in US
TOXOCARIASIS
• 1996 30% dogs <6months shed eggs • 35% cats infected • Higher risk if left outside long periods of time • Higher risk if allowed to eat other animals • Prevalence in humans up to 40% in some places • Higher risk of humans contracting if dog owners • Higher risk if living in poverty • Higher risk if hot, humid climate–eggs viable longer in
the soil
Identify condition; diagnosis? Treatment? Prevention
- young kids (2-4yrs)
- larvae migrate through LIVER/LUNGS
- Inflammation
- can also travel to; heart, eye - ocular larva migrans, CNS
- S&S; fever, cough in 20-80%, pneumonitis - peribronchial infiltration on CXR, hepatitis, eosinophilia, eosinophilic meningoencephalitis, space occupying lesions, myelitis
2. • Typically older children (7-17years) • Unilateral vision loss • Eye redness, pain, photophobia • Strabismus d/t disuse of affected eye • Granulomatous inflammation of retina/uveitis/chorioretinitis • Leukocoria
Tococariasis
- Visceral larva migrans
- Ocular larva migrans
Diagnosis • Good history • Consider if consistently elevated eosinophil count • Visceral larva migrans - ELISA for larval-stage Ag - Eosinophilia - Anemia & hypergammglobulinemia • Ocular larva migrans - Ab levels low in serum - Vitreous fluid - May not have eosinophilia • Stool sample– not helpful - Larvae don’t mature to excrete eggs
Treatment
- ** SELF-LIMITING
1. Albendazole - available in US
- preferred in ocular larva migrans
2. Mebendazole
3. Steroids - decrease systemic effects of inflammation
4. Surgery of eye - prevent retinal detachment
Prevention
• De-worm pets • Clean your pet’s living area at least once a week • Feces should be either buried or bagged and disposed
of in the trash • Play areas with feces/sandboxes • Good hand hygiene • Don’t eat dirt
Identify condition
- organism found where? (Soil or water?)
- 3 major types
Acute disease
• Symptoms are a reaction to the eggs, not the adult
• Eggs not shed in urine or feces lodge in bladder or intestine and cause inflammation and/or scarring over time
• Acute; non-sensitized more likely to have
A. itching, rash “swimmer’s itch”
B. “KATAYAMA FEVER”; weeks to months after
- hypersensitivity reaction to migration of eggs
- fever, fatigue, malaise, cough, eosinophilia, IgE
C. Dysuria, urinary frequency/urgency, hematuria
Chronic Disease
• 1-2 months, Caused by immune reaction
against eggs trapped in tissues
• Abdominal
- Can have vague, long lasting symptoms of
fatigue, abdominal discomfort, etc
- After mass treatments of areas, see improvement
• Urinary
- Microscopic hematuria, obstructive uropathy,
• Intestinal
- polyps, ulceration, bleeding
• Hepatosplenic
- Granulomas to fibrosis, portal hypertension
SCHISTOSOMIASIS • Schistosoma mansoni, S. haematobium, orS. japonicum. • “Bilharzia” • 200M people affected worldwide - Tropical climates - Highest prevalence 8-15years - Adults *may have acquired resistance • Negelcted Tropical Diseases • Live in freshwater snails • Cercaria (infectious form) emerge from snail into water • Affects areas with poor sanitation
3 types
1. Schistosoma mansoni—intestinal and hepatic symptoms
• distributed throughout Africa: lakes, rivers, also occurs in the Nile River valley in Sudan and Egypt
• South America: including Brazil, Suriname, Venezuela
• Caribbean (risk is low): Dominican Republic, Guadeloupe, Martinique, and Saint Lucia.
2. S. japonicum—intestinal and hepatic symptoms
• found in Indonesia and parts of China and Southeast Asia
3. S. haematobium– Urinary symptoms
• Throughout Africa, some areas of Middle East
• found in areas of the Middle East
Identify 3 types of
Diagnosis and treatment
1. intestinal and hepatic symptoms
• distributed throughout Africa: lakes, rivers, also occurs in the Nile River valley in
Sudan and Egypt • South America: including Brazil, Suriname, Venezuela • Caribbean (risk is low): Dominican Republic, Guadeloupe, Martinique, and Saint
Lucia.
- intestinal and hepatic symptoms
• found in Indonesia and parts of China and Southeast Asia - Urinary symptoms
• Throughout Africa, some areas of Middle East
• found in areas of the Middle East
- Schistosomiasis Mansoni
- Schistosomiasis japonicum
- Schistosomiasis haematobium
Diagnosis n treatment • History and exposure • Find eggs in stool!; O&P x3 • Other testing - Eosinophilia - Hematuria or hematochezia • Antibody testing– 6-8 weeks after exposure • Treatment with praziquantel; Steroids for swimmer’s itch and Katayama fever
Identify condition
- beef or pork tapeworm
- one of most common parasitic infections
- ingestion of undercooked meat ; epigastric pain, flatulence
• Adult worms have segments = proglottids
- Hermaphroditic segments
- Mature and most distal pieces fall off in stool
- When they rupture, scatter thousands of eggs
• Cattle or swine eat grass with proglottids OR eggs
- Mature and travel to make cysts in muscle
**disease ? Diagnosis and treatment?
TAENIA
• Taenia saginata/solium
• Beef or pork tapeworm
• One of the most common parasitic infections
• Ingestion of undercooked meat
- Ingest cysticerci (infective cyst in muscle)
- Typically mild symptoms to asymptomatic
Disease
• Ingest cysticerci in undercooked meat
• Once ingested, attaches to intestinal wall
• Matures into adult 10-12 weeks
• Sheds proglottids, patient may see in stool
• Symptoms
- Epigastric pain, nausea, diarrhea, flatulence
- Decreased appetite, weight loss
• In rare cases, may lodge in bile or pancreatic ducts
Diagnosis and treatment
• Microscopic eggs in stool
- Not available for 1st 3 months of infection
• Collect 3 stool samples on 3 separate days to increase
sensitivity
• Praziquantel
- Caution if patient has cysticercosis!
- Collect stool samples for proglottids to identify species
retention and control - FDA recommendation
• Whole Cuts: cook to at least 145ºF in thickest part of meat, then allow to rest for 3 minutes prior to
carving/consuming
• Ground Meat: cook to at least 160ºF, do not require rest time
• “rest time” amount of time the product remains at the final temperature, after it has been removed from grill, oven, or
other heat source. During the three minutes after heat is removed from the heat source, its temperature remains constant or continues to rise, which destroys pathogens
50 year old from Mexico present with seizure. See lots of cysts in the brain
CYSTICERCOSIS - TAENIA SOLIUM
**Neurocysticercosis (brain/spinal cord)
• Infects brain, muscle, etc
- Major cause of adult-onset seizure
• Infection by eggs found in feces of infected person
- Can be an autoinfection
• NOT from undercooked pork!
- …at least not directly
- Intestinal tapeworm
**LEADING CAUSE OF SEIZURES IN DEVELOPING WORLD
A. Worldwide - free range pigs - poor hygiene B. Signs and symptoms - Caused by degenerating cysts - muscle; lumps under skin C. Eyes - blurry vision - swelling - retinal detachment D. Brain/spinal cord (Neurocysticercosis) u
• Clinical presentation
- Seizure without focal neurologic findings or signs of meningitis
- Late onset seizure with travel/exposure history
• Imaging
- CT /MRI
- Enhancing lesions without midline shift
• Serology nonspecific, stool exam insensitive d/t lack of active tapeworm
Neurocysticercosis
• Neurocysticercosis—symptoms correspond
to where cysts are
• Live cysticerci cause mass effect
• Dying cysticerci cause inflammation and majority of symptoms
• Parenchymal (within brain hemisphere or cerebellum)
- 3-5 years after infection, but can be up to >30yrs
- Seizures and HA
• Extraparenchymal (intraventricular or
subarachnoid)
- HA, N/V
- Altered vision, focal neurologic signs, AMS,
meningitis
TAENIA sodium NOT directly FROM UNDERCOOKED PORT
**INFECTION IS BY EGGS FOUND IN FECES of infected person
Diagnosis? Treatment? Prevention?
Cysticercosis; most common cause of seizures in developing nations
Diagnosis
• Clinical presentation
- Seizure without focal neurologic findings or signs of meningitis
- Late onset seizure with travel/exposure history
• Imaging
- CT /MRI
- Enhancing lesions without midline shift
• Serology nonspecific, stool exam insensitive d/t lack of active tapeworm
Treatment • Antiepileptic • Antiparasitic therapy (albendazole) for active lesion but run the risk of causing more degenerating cysts leading to increased inflammation • Corticosteroids • Test others in the home as well
Prevention
• Wash your hands
• Wash and peel all raw vegetables and fruits before eating
• Drink only bottled or boiled (1 minute) water or carbonated drinks in cans or bottles
• Filter unsafe water through an filter AND dissolve iodine tablets in the filtered water
Identify condition
Diagnosis n treatment • Identify eggs in stool - Ovoid shape with operculum • Prazquantel • Niclosamide; Not available in US
Symptoms
• Diarrhea, abdominal pain
• Fatigue, HA
• Pernicious anemia (~80% B12 absorbed by worm)
Diphyllobothriasis
- Diphyllobothrium latum
- “Fish Tapeworm”
- Ingestion of larval stage (plerocercoid)
- Was reportable disease in US until 1982; Increased awareness and strict monitoring
Prevention and control
- Cooking; cook fish adequately (to an internal temperature of at least 145° F)
Freezing
• At -4°F or below for 7 days (total time), or
• At -31°F or below until solid, and storing at -31°F or below for 15 hours, or
• At -31°F or below until solid and storing at -4°F or below for 24 hours.
Identify
• Adult tapeworm occurs 3-4 weeks after ingestion • Pass proglottids in stool - Often confused with pinworms • Live 4-6 weeks, but can autoinfect • Most asymptomatic, but if high worm burden, may have abdominal pain, diarrhea and possible malabsorption • Diagnosis made by identification of eggs in stool • Treatment with praziquantel or nitazoxanide
HYMENOLEPIASIS • Hymenolepis nana • “Dwarf tapeworm”; ~2inches • Utilizes insects as intermediate hosts (beetle, mealworm, flea) • Fecal-oral route ingesting eggs • Ingestion of infected arthropod • High prevalence in areas with poor hygiene and overcrowding • Common in children
Identify
• Diagnosis by finding proglottids in diaper
- Small, white, motile rice-like pieces
• Treatment with praziquantel or niclosamide
• Prevention
- Don’t eat fleas
- Treat pets
Dipylidiasis
• Dipylidium caninum • Most common cestode of dogs - Can infect cats • Infect humans if ingest infected flea • Typically young children affected • Typically asymptomatic - Anal itching, loss of appetite, abdominal pain
Identify ***
Symptoms depend on size of cyst 1. Liver cyst • Palpable mass, abdominal distention, obstruction leading to jaundice • Rupture can lead to peritoneal cyst or even anaphylaxis 2. Lung cyst • Usually found incidentally • Symptoms can include chest pain, fever, cough, hemoptysis • Salty expectoration with hemoptysis = hydatid cyst? Diagnosis • Palpable cyst • Imaging with U/S or CT for liver • PA CXR for lung Treatment • ”Watch & Wait” or surgery • Benzimidazole or albendazole
**2 types • Diagnosis • Symptoms, history and imaging finding cysts • CT will show tumors • High E. multilocularis titers • Treatment; Surgical resection
Echinococcus; Echinococcus granulosus/multilocularis
2 types
- Cystic caused by E. granulosus—can be asymptomatic for years
- Alveolar caused by E. multilocularis– can be fatal
• Sheep, cattle, goats and pigs are intermediate hosts
- Ingest eggs from the ground
• Dogs ingest cysts in the organs of above
- Shed eggs from adult tapeworm
• Fecal-oral route for humans
• Prevalent where dogs are used to care for large flocks of sheep
- In South America, endemic in Argentina, Bolivia, Chile, Brazil, Peru and Uruguay
Cystic echinococcus***
• ”Hydatid disease”
• Larval stage of E. granulosus ingested
• Transported by blood stream to liver
• Most infections asymptomatic
• Slowly enlarging fluid-filled cysts in liver, lungs
• Can contain liters of fluid
Differentiate 2 groups of “flat worms” / “flukes”
TREMATODES
- Schistosomiasis
- S. Mansoni, S. Japonicum, S. Haematobium, S. Mekongi, S. Intercalatum - Non-schistosomiasis
A. Paragonimus - lung fluke
B. Clonorchis/Opisthorchis - Chinese liver fluke
C. Fasciola - Liver fluke/rot
Identify life cycle and clinical presentation (acute vs chronic phase) of non-schistosomiasis trematodes based on route of transmission
- Transmission; Consumption of RAW or undercooked FRESH WATER CRABS and CRAYFISH
- Distribution; SE Asia and Japan; other species found throughout the americas and Africas
- “DRUNKEN CRAB”; Pickled crustaceans in wine or vinegar are common source.
**Identifying feature of egg
PARAGONIMIASIS “LUNG FLUKE” ; Paragonimus Westermani
A. Life cycle
Man > Snail > Crab > Man **
• Human Stool/Saliva > Fresh water> Snail (Cercariae)> Crustacean (Metacercariae) > Human consumption.
• Larvae (Metacercariae) burrow through intestinal wall and migrate to the lungs and develop into egg producing adults.
• Eggs are coughed up or swallowed and the cycle repeats. EGGS identifying feature is OPERCULUM - LITTLE LID**
**HIGHLY INFLAMMATORY
B. Clinical presentation
- Acute phase; diarrhea, abdominal pain, fever, cough (RUST COLORED SPUTUM), urticaria, HSM, eosinophilia
- Chronic phase; COUGH**, SOB, CP, Hemoptysis, radiographic abnormalities
Non schistosomal trematodes
1. Acute phase; diarrhea, abdominal pain, fever, cough (RUST COLORED SPUTUM), urticaria, HSM, eosinophilia
2. Chronic phase; COUGH**, SOB, CP, Hemoptysis, radiographic abnormalities
What does xray look like?
Diagnosis and treatment
PARAGONIMIASIS “LUNG FLUKE” ; Paragonimus Westermani
**Xray look like TB
Dx: Often misdiagnosed as tuberculosis (thus must keep in
DDx). Microscopic evaluation may reveal eggs in sputum or stool
(i.e. O&P) though often difficult. Enzyme Immuno-Assay or
Immunoblot may also be used (i.e. Serology).
TX: Praziquantel
Identify life cycle of non schistosomal trematodes
- Virtually identical
- Transmission: Consumption of RAW or undercooked FRESH WATER FISH.
- Distribution: SE Asia, China, Korea, Taiwan and Japan
- Fish often smoked, pickled, dried, or pasted.
- May be encountered in US in refugees or travelers.
**how do eggs look like
CLONORCHIASIS & OPISTHORCHIASIS aka “CHINESE LIVER FLUKE”
Life cycle
Man > Snail > Fish > Man
• Human Feces (Bile)> Snail (Cercariae) > Freshwater Fish (Metacercariae) > Human Consumption.
• Human consumption > Intestinal burrowing and migration to BILE DUCTS where they mature and produce eggs.
• Mechanical injury from the suckers of the parasite contribute to inflammatory response. Mechanical obstruction of the
biliary tract by the fluke is also a significant factor in pathogenesis.
Eggs
O. Viverrini, C. Sinensis eggs ; Prominent “Shoulders” i.e. Operculum Abopercular “Knob”
Identify Dx and treatment of non schistosomal trematodes
• Most are asymptomatic
• Abd. Pain (RUQ/Pancreatitis), Dyspepsia, Diarrhea,
Constipation. Eosinophillia may be present.
• Rarely Cholangitis, Cholecystitis, may develop
Cholangiocarcinoma (rare)
• Most pathogenesis is from biliary inflammation and
obstruction of bile ducts. May produce pigmented gall stones
CLONORCHIASIS & OPISTHORCHIASIS aka “CHINESE LIVER FLUKE”
Dx: Microscopic identification ( O&P) through stool
examination. No serologic test exists. (*indistinguishable from
one another on visual inspection.)
TX: Praziquantel
Identify life cycle on non schistosomal trematodes
- Transmission: Consumption of RAW or
undercooked PLANTS (WATERCRESS) or DRINKING CONTAMINATED WATER. - Distribution: Occurs worldwide. More common in the Peru and Bolivia
- Many infections endemic in areas where sheep and cattle are raised (i.e. rural areas among animal herders)
FASCIOLIASIS - Fasciola Hepatica
Life cycle
Man > snail > fresh water plant > Man
• Eggs in Cattle/Sheep Feces>Snail (Cercariae) > Freshwater plants (Metacercariae) > Human Consumption
• Man is an accidental host.
• Human consumption > Intestinal burrowing and migration to bile
ducts/Liver where they mature and produce eggs.
Identify Dx and treatment of non- schistosomal trematodes
Acute Phase: Abdominal Pain (RUQ), Hepatomegaly, Fever, N/V/D, Urticaria, Eosinophilia. Transaminitis may be present.
Chronic Phase: Intermittent biliary obstruction and inflammation.
*Of note: Cholangiocarcinoma is not common in contrast to Clonorchiasis and Opisthorchiasis.
FASCIOLIASIS - Fasciola Hepatica
Dx: Microscopic Evaluation of stool (i.e. O&P); Serologic evaluation available via CDC.
TX: Not Praziquantel – Unlike other trematodes, Praziquantel is
not effective against Facioliasis.
Triclabendazole is treatment of choice (WHO) though not readily
available in US.
Identify non-schistosomiasis trematodes (Dx and tx)
- Largest intestinal fluke in humans.
- Located in Asia and India
- Similar life cycle to Fascioliasis; Exception of pigs are often
mammalian hosts.
FASCIOLOPSIASIS - Fasciolopsis Buski
Dx: Microscopic Evaluation of eggs in stool (i.e. O&P) or (rarely) adults in stool. Indistinguishable
from F. Hepatica
TX: Praziquantel
List 5 intestinal Protozoa
- Amoeba
- Flagellates
- Ciliophora
- Coccidial
- Microsporidia infections
Identify lifecycle of the following intestinal protozoan
- Pseudopod (false foot) forming, non-
flagellate parasite. - Several species exist- E. Hystolytica, E. Dispar, E. Moshkovskii.
- Only E. Hystolytica is pathologic.
- Transmission: Ingestion of mature cysts found in feces.
- Distribution: Located throughout the world but particularly common in Africa, Central and South America, an Indian subcontinent
ENTAMOEBA HYSTOLYTICA
Life cycle ; Fecal Oral transmission
- Human consumption of mature cysts in fecally contaminated food, water, or hands > Excystation occurs in small intestine where Trophozoites are released> Trophozoites migrate from
small to large intestine, multiply (Binary Fission), and form Cysts > Cysts and Trophozoites are passed in the feces.
- Trophozoites may invade intestinal mucosa (Intestinal Sxn’s) or travel in blood stream to other locations (Extra- Intestinal Sxn’s).
- Only cysts are able to survive external environment thus giving
them their infectivity (Days to Weeks). - Cysts are resistant to chlorination and gastric acidity as well.
- Trophozoites are able to invade tissue however cysts cannot.
Based on Dx and tx - identify intestinal vs extra-intestinal manifestations of this protozoan
Diagnosis: Difficult to distinguish E. Hystolytica, E.
Dispar, and E. Moshkovskii via microscopy.
*Serology (EIA)
Treatment: Metronidazole followed by Iodoquinol
(intraluminal agent)
- Iodoquinol alone for asymptomatic.
ENTAMOEBA HYSTOLYTICA
Intestinal Manifestations
- Asymptomatic
- Fever, Chills
- Abdominal Pain –Severe Cramping
- Tenesmus
- Dysentery**
- “Flask Shaped Ulcer” on histology **
Extra-intestinal manifestations
- Fever, RUQ Pain
- Elevated transaminases (AST/ALT, Alk. Phos).
- Liver Abscess**
- Pleuropulmonary (direct extension), Brain, Splenic Abscess (rare)
- Often have no intestinal symptoms.
Identify lifecycle of Protozoan.
- Transmission: Consumption of CYSTS from infected water. Can also be person to person or from food.
- Distribution: Worldwide distribution though more common in warm climates .
Including West Virginia !
Also common in Colorado.
GIARDIASIS
Giardia Lamblia: Cysts and Trophozoite (Latter typically described and “Pear Shaped or Tear Drop” and is flagellated with 2 nuclei- “Eyes”) .
Lifecyles ; Fecal oral transmission
- Human consumption of mature cysts in fecally contaminated food, water, or hands > Excystation occurs in small intestine where Trophozoites are released and colonize duodenum>
Trophozoites multiply (Binary Fission) and form Cysts > Cysts and
Trophozoites are passed in the feces.
- Cysts may survive several weeks to months in cold water.
- Animals are common reservoirs.
Identify diagnosis and tx of the protozoan
Clinical presentation
- May be asymptomatic.
- Avg. incubation for 7 days.
- Abdominal Pain, Bloating, Nausea, weight loss.
- Severe Diarrhea and Malabsorption**
- ** “Yellow, Foul, Frothy, Floats” **. YELLOW FATTY STOOL THAT FLOATS
- Some patients may be lactose intolerant after infection.
GIARDIA LAMBLIA - GIARDIASIS
Diagnosis:
- High Clinical Suspicion (Aka the right history).
- Visualization of Cysts or Trophozoites on O&P***
- Serology (EIA)
Treatment
- Tinidazole or Metronidazole **
**
Historically board questions have associated BEAVERS and
St. PETERSBURG, RUSSIA with Giardiasis. If you see either of these mentioned in the stem, have a high suspicion for
GIARDIASIS.
Identify life cycle
- *Flagellate - Mr. Worldwide
- Not an intestinal protozoan.
- Transmission: Common Sexually Transmitted Infection
- Distribution: Worldwide.
** • Though this may resemble Giardia at first glance, consider
the source of what you are viewing.
• These are from vaginal smears and will be motile.
TRICHOMONIASIS
* Trichomonas Vaginalis – Flagellated; Most common
pathogenic protozoan of humans in rich nations.
Life cycle; sexually transmitted
- Cannot live outside of humans .
- Frequently asymptomatic.
- Vaginitis with foul smelling, greenish vaginal discharge.
- Vaginal itching and burning.
- Dyspareunia and dysuria.
- Males often asymptomatic; urethritis; epididymitis, prostatitis can occur.
- Cervix classically is very friable (“Strawberry Cervix”)**
Identify Dx and treatment
- Frequently asymptomatic.
- Vaginitis with foul smelling, greenish vaginal discharge.
- Vaginal itching and burning.
- Dyspareunia and dysuria.
- Males often asymptomatic; urethritis; epididymitis, prostatitis can occur.
- Cervix classically is very friable (“Strawberry Cervix”)**
TRICHOMONIASIS -TROPHOZOITES
Diagnosis; Motile trichomonads seen on microscopic examination of WET MOUNT**
Treatment; Patient and Partner with Metronidazole or Tinidazole**
Identify life cycle and clinical presentation
- Uncommon cause of intestinal illness.
- Originally classified as amoeba but now as flagellate.
- Transmission: Probably fecal-oral via helminth eggs (Ascaris,
Enterobius) - Distribution: Worldwide
DIENTAMOEBA FRAGILIS
Life cycle; Fecal Oral transmission
- Life cycle has yet to be fully described.
- Thought to be transmitted by fecal – oral route after ingestion of helminth eggs . Has no cyst stage.
- Abdominal Pain, Diarrhea, Flatulence.
- Eosinophilia possible
- Diagnosis: Microscopic evaluation – O&P.
- Treatment: Metronidazole, Iodoquinol or Paromycin.
Identify life cycle and clinical presentation
- *Ciliated
- Largest intestinal protozoan in humans.
- Only ciliated infection which causes disease in human intestines. - Transmission: Fecal-Oral though humans are accidental host.
- Normally found in large bowel of pigs
- Distribution: Worldwide
Dx and treatment
BALANTIDIUM COLI
**Trophozoite with “Bean shaped” nucleus
Life cycle; Fecal -oral
- Human consumption of cysts in fecally contaminated food or water.
- Many are asymptomatic.
- May experience anything from intermittent diarrhea to acute
dystentary. - Diagnosis: Cysts and trophozoites seen on microscopic analysis of stool (O&P).
- Treatment: Tetracycline, Iodoquinol, or Metronidazole.
Identify life cycle,
Coccidial infection
- Transmission: Fecal Oral-Waterborne; Person to person or
Animal (calf) to person.
- Distribution: Worldwide
Outbreak in Milwaukee in 1993
affected more than 400,000 people including over 100 deaths.
CRYPTOSPORIDIOSIS
- C. Parvum and C. Hominis account for vast majority of human infections.
Life cycle; fecal oral
- Consumption of OOCYTS in contaminated water or food sources
> sporozoites are released and begin to reproduce and form oocysts which are excreted in stool.
- Oocysts are infective upon excretion.
- Size allows them to pass through water filters and are also chlorine-resistant**
- Many outbreaks occur around water sources
IDENTIFY DX and treatment
Clinical presentation
- Most immunocompetent hosts present with mild diarrhea and
abdominal cramping. Some may even be asymptomatic.
- Watery diarrhea most common symptom.
*Fever, weight loss, abd. Pain, n/v.
- Immunocompromised are at risk for
severe disease
* Think AIDS (CD4 count < 200), Young patients in low income countries
CRYPTOSPORIDIOSIS
Diagnosis: Oocysts in stool on microscopic evaluation with Acid-Fast Stain - OR - Antigen detection via EIA.
Treatment: Prevention.
- Usually Self-limited in immunocompetent though if
symptoms worsen consider Nitazoxanide.
** *Of note: Nitazoxanide has not been shown to help in immunocompromised individuals.
Identify life cycle and clinical presentation
**Coccidial infection
- Ellipsoidal shape with sporoblast.
- Majority of infections seen in immunocompromised
individuals
- Transmission: Fecal Oral
- Distribution: Worldwide especially in tropical and
subtropical climates.
Dx and treatment
ISOSPORA BELLI (CYSTOISOSPORIASIS) **Oocytes containing sporoblast
Life cycle; fecal oral
- Consumption of sporozoite containing sporocysts > Invasion of
intestinal epithelial cells> further replication produces immature
oocysts which are excreted in feces > additional maturation results in sporocysts which produce sporozoites (infective)
- Watery diarrhea most common symptom.
- Eosinophilia may be present
Diagnosis: Oocysts in stool on microscopic evaluation with Acid-Fast Stain.
Treatment: Trimethoprim-sulfamethoxazole.
Identify life cycle, clinical presentation,
- Majority of infections seen in immunocompromised
individuals - Transmission: Fecal Oral – Fresh Produce (RASPBERRIES); Contaminated water.
- Distribution: Worldwide though most common in tropical and
subtropical climates.
***Oocysts on wet mount
CYCLOSPORA CAYETANENSIS
LIFE CYCLE; fecal oral
- Ingestion of sporulated oocysts (infective) from contaminated food or water> Invasion of epithelium of GI tract and undergo reproduction and development into unsporulated
oocysts > Sporulation occurs in environment.
- Watery diarrhea most common symptom.
- Stomach cramps, n/v, anorexia, muscle aches, low grade fever.
- Untreated infections may lead to prolonged diarrhea (10-12 weeks).
Diagnosis: Oocysts in stool on microscopic evaluation.
May be enhanced by UV microscopy.
Treatment: Trimethoprim-sulfamethoxazole.
**C. Cayetanensis oocyst seen under UV microscopy.
Historically board questions have associated raspberries and mesclun lettuce with Cyclospora.
If you see either of these mentioned in the stem, have a high suspicion for Cyclospora.
Identify life cycle and presentation
- Rare
- Requires 2 separate hosts for life cycle completion – definitive host (humans - GI) and intermediate host (Cattle/Pigs – Muscular) - Transmission: Consumption of undercooked meat.
- Distribution: Worldwide though more common where live stock are raised.
**Sporulated oocyts on wet mount
SARCOCYSTOSIS
Life cycle; undercooked meat
- Humans consume undercooked meat (pork, beef) > bradyzoities invade intestinal epithelium> further maturation and development of oocysts> Oocysts shed in host feces.
- Often asymptomatic.
- Intestinal Infection: Mild fever, diarrhea, chills, vomiting.
- Muscle Infection: Myalgia, Muscle Weakness, Edema.
Dx; Oocysts in stool on microscopic evaluation.
May be enhanced by acid fast stain or UV microscopy.
Treatment: Trimethoprim- sulfamethoxazole.
Identify life cycle and presentation
- Opportunistic, obligate intracellular parasite.
- Characterized by production of resistant spores
- At least 15 different species identified as human pathogens.
- Transmission: Spore ingestion or
inhalation. - Distribution: Worldwide
**Spore with polar tube inserted in cell
MICROSPORIDIA
Life cycle; spore inhalation or ingestion
- Opportunistic – think severe AIDs.
- Multiple clinical presentations depending on the subtype identified which range from diarrhea to ocular/respiratory/genitourinary infection.
- Diagnosis: Transmission electron microscopy; IFA; PCR (Via CDC)
- Treatment: Fumagillin or Albendazole.
Identify TRANSVERSELY ORIENTED RETROPERITONEAL ORGAN
- 4 parts
- 2 process/system
**diff main vs accessory duct
PANCREAS
- parts; head, neck, body and tail
- systems; exocrine (digestive enzymes) and endocrine (secrete insulin, glucagon and somatostatin)
- Main Pancreatic Duct - Most commonly drains the duodenum at the papilla of Vater
- Accessory Pancreatic Duct-Drains into the duodenum through a separate minor papilla that is 2 cm proximal to the major papilla of Vater
* *In most adults the main pancreatic duct joins the common bile duct proximal to the papilla of Vater, thus creating the ampulla of Vater
Identify pancreas system/cell type
-Produce enzymes needed for digestion
-Pyramidally shaped epithelial cells
Oriented radially around a central lumen
-Contain membrane-bound zymogen granules rich in digestive enzymes
EXOCRINE PANCREAS - Acinar Cells
Pancreatic enzymes
- the pancreas secretes its endocrine products as what enzymatically inert proenzymes (6)
- *activation requires what enzyme?
- what cleave the proenzymes?
- inhibitors of trypsin?
- what cells are resistant?
- Trypsinogen
- Chymotrypsinogen
- procarboxypeptidase
- proelastase
- kallikreinogen
- phosphopholipase A and B
- Activation of proenzymes requires the conversion of inactive trypsinogen to active trypsin by duodenal enteropeptidase
- Trypsin cleaves proenzymes to yield products such as chymotrypsin, elastases and phospholipases
- Trypsin inhibitors including SERINE PROTEASE INHIBITOR KAZAL TYPE 1 are present within acinar and ductal secretions
- Acinar cells are remarkable resistant to the action of trypsin, chymotrypsin and phospholipase A2.
- *Most of the congenital variations do not directly cause disease
- variations can present problems for the medical providers
Identify congenital condition of pancreas
- usually incompatible with life
- Homozygous PDX1 mutations on chromosome 13q12.1
Agenesis
**Rarely is the pancreas totally absent
Identify congenital condition of pancreas
- Most common congenital anomaly
- 3-10% incidence
- *Bulk of the pancreas drains through the small caliber minor papilla
**identify complication and why?
PANCREATIC DIVISUM
- Failure of fusion of the fetal duct system of the dorsal and ventral pancreatic primordia
**STENOSIS is caused by a bulk of secretions passing through the minor papillae - leads to CHRONIC PANCREATITIS
Congenital condition
- Band like ring of normal pancreatic tissue that completely encircles the second part of the duodenum
- May present as duodenal obstruction
- Can be found in 2% of routine postmortem examinations
- Stomach and duodenum are typical sites
- May cause pain localized inflammation
- 2% of islet cell neoplasms arise in ectopic pancreatic tissue
- Annular Pancreas
2. Ectopic pancreas
Summarize 2 conditions affecting exocrine pancreas
- Inflammation
A. Pancreatitis - Neoplasms
A. Benign
B. Malignant
Identify condition
A. Middle aged male with abdominal pain
B. Often pain is epigastric with radiation to back
- Relieved with doubling up
- Made worse with eating
PANCREATITIS
** Mild acute pancreatitis simply diagnosed with elevated amylase and lipase
Acute; REVERSIBLE inflammatory process
Chronic; IRREVERSIBLE loss of exocrine and endocrine function
Identify condition based on major cause
- Biliary tract disease
- male to female ratio 1:3 - Alcoholism
- male to female ratio 6:1
- *Other causes
- *PNEUMONIC TO REMEMBER CAUSES
PANCREATITIS
Other causes
- Obstruction
- Medications
- Infections
- Metabolic disorders
- Trauma
- Genetic; mutations in the cationic trysinogen (PRSS1) and trypsin inhibitor (SPINK1) genes
I GET SMASHED; Idiopathic, gallstones, ethanol, trauma, steroids, mumps, autoimmune disease, scorpion sting, hyperlipidemia, drugs
Identify condition based on morphology
- Microvascular leakage causing edema
- Necrosis of fat by lipolytic enzymes
- Acute Inflammation
- Proteolytic destruction of pancreatic parenchyma
- Destruction of blood vessels and subsequent interstitial hemorrhage
- PRSS1 gene vs SPINK1 gene
- PANCREATITIS
- HEREDITARY PANCREATITIS ; **recurrent attacks usually starting in childhood
A. Cationic trypsinogen gene (PRSS1)
- Trypsin becomes resistant to cleavage by another trypsin molecule and can lead to activation of other proenzymes and thus pancreatitis
- Autosomal dominant
B. Serine protease inhibitor Kazal type 1 (SPINK1)
- Codes for pancreatic secretorytrypsin inhibitor that inhibits trypsin activity
- Autosomal recessive
3 Mechanisms of pancreatic enzyme activation (pancreatitis)
Etiologies of pancreatitis
- alcohol (what ways)
- basic mechanism
A.
- Pancreatic duct obstruction
- gallstones, chronic alcoholism - Acinar cell injury
- alcohol, drugs, trauma, ischemia, viruses - Defective intracellular transport
- alcohol
B. Alcohol causes in several ways:
- Chronic ingestion results in protein rich fluid which leads to protein plugs and obstruction of small ducts
- Direct toxic effects, increase in exocrine secretion.
C. Basic mechanism pancreatitis
I. Due to action of pancreatic enzymes
II. Trypsin is primary enzyme
- It then activates other enzymes
- Activated enzymes digest fat cells & damage blood cells
- Trypsin activates kinin system, so get activation of clotting & complement cascades
