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Escalante-Saac
AMOEBIASIS (amoebic dystentery)
Amoebiasis
Acute or chronic protozoal infection of human beings initially involves the colon, but may be
spread to soft tissues, most commonly the liver and lungs, by contiguity or hematogenous or
lymphatic dissemination
Entamoeba histolytica
ETIOLOGIC AGENT:
Prevalent in unsanitary areas, common in warm climates, acquired by swallowing, Cyst can
survive a few days outside the body, cyst passes to the large intestine and hatches into
trophozoites. It passes into the mesenteric veins, the portal vein, and finally to the liver,
where it causes amoebic liver abscess.
Entamoeba histolytica has 2 developmental stages:
1. Trophozoites/ Vegetative form
-these are facultative parasites that may invade the tissue or may be found in the
parasitized tissue and liquid colonic contents.
2. Cysts
a. the cyst is passed out with formed or semi-formed stools and is resistant to environmental
conditions.
b. the cyst is considered as the infective stage in the life cycle of E. histolytica
PATHOLOGY:
When the cyst is swallowed, it passes through the stomach unharmed and shows no activity while in an acidic environment. When
it reaches thee alkaline medium of the intestine, the metacyst begins to move within the cyst wall, which rapidly weakens and
tears. The quadrinucleate amoeba emerges and divides into amoebulas that are swept down into the cecum. This is the first
opportunity of the organism to colonize and its success depends on one or more metacystic trophozoites making contact with the
mucosa. The mature cyst in the large intestine leaves the host in the great numbers. The cyst can remain visible and infective in a
moist and cool environment for about 12 days, and in water 30 days. The cyst are resistant to levels of chlorine normally used for
water purification. They are rapidly killed by putrefaction, desiccation, and temperature below 5 and above 40 degrees centigrade.
Human excreta
SOURCE:
INCUBATION PERIOD:
3 days, several months
In severe infection, in sub-acute and chronic form is_
Entire duration of the illness
PERIOD OF COMMUNICABILITY:
1.Fecal-oral transmission
MODE OF TRANSMISSION:
2. direct contact through sexual
contact
3. indirect contact by ingestion of
food especially uncooked leafy
vegies or contaminated with fecal
material
PATHOGENESIS
Ingestion of bacteriamultiplication of bacteriaendotoxin production affecting the lining of the small intestine ,colon and
capilliariesnecrosis of the mucosal layerulcerationgangrenetoxemia
1. The metacystic trophozoites or their progenies reach the cecum and those that come in contact with the mucosa penetrate or
invade the epithelium by lytic digestion
2. The trophozoites burrow deeper , with tendency to spread laterally or continue the lysis of cells until they reach the submucosa ,
forming flask-shape ulcers. There may be several points of pentration.
3. From the primary sites of invasion, secondary lesions may be produced at the lower level of the large intestine.
4. Progenies of the original colony are squeezed out to the lower portion of the bowel and thus have the opportunity to invade and
produce additional ulcers.
5. E. histolytica has been demonstrated in practically every soft organ of the body.
6. Trophozoites which reach the mascularis mucosa frequently erode the lymphatic of the wall of the mesenteric venules on the
floor of the ulcer and are carried to the intrahepatic portal vein.
7.if thrombi occurs in the small branches of the portal veins causes lytic necrosis on the walls of the vesssels and digest a pathway
into the lobules
8. The colony increases in size and develops into the abscess. A typical liver abscess develops and consist of: a. a central zone
necrosis, b. median zone of stroma only, c. outer zone of normal tissue newly invaded by amoeba
9. next to the liver, the organ which is the most frequent site if extra-intestinal amoebiasis is the lung.
CLINICAL MANIFESTATION:
1. Acute amoebic dysentery
a. slight attack of diarrhea, altered with periods of constipation and often accompanied by
tenesmus
b. diarrhea, watery, and foul-smelling stools often containing blood streaked mucus
c. colic and gaseous distention of the lower abdomen
2. Chronic amoebic dysentery
d. nausea, flatulence, abdominal distention, and tenderness in the right iliac region over the
colon
a. attack of dysentery lasts for several days usually by constipation
b. tenesmus accompanied by desire to defecate
c. anorexia, weight loss, and weakness
d. liver may be enlarged
e. stools at first are semifluid, but soon become watery, bloody and mucoid
f. vague abdominal distress, flatulence, constipation or irregularity of bowel movement
g. mild toxemia, constant fatigue, and lassitude
h. the abdomen loses its elasticity when picked up between the fingers.
i. on sigmoidoscopy ,scattered ulceration, with yellowish and erythematous borders
3. Extraintestinal forms
j. gangrenous type(fatal) characterized by appearance of large sloughs of intestinal tissues in
the stools, accompanied by hemorrhage
a. pain in the RUQ with tenderness of the liver
b. jaundice
c. intermittent fever
d. loss of weight or anorexia
e. abscess may break through the lungs, patient coughs anchovy sauce sputum
CLINICAL FEATURE:
Gradual
1. onset is_
Bloody and mucoid
2. diarrhea increases and stools becomes_
3. in untreated cases:
Fluid stoolssevere bloody-mucoid stoolhemorrhageintestinal perforationperitonitis-death
1. stool exam
DIAGNOSTIC EXAM
2. blood exam
3. proctoscopy/sigmoidoscopy
TREATMENT MODALITIES:
NURSING MANAGEMENT:
1. observe_precaution
2. provide health education and instruct patient to: boil water for drinking, avoid washing
food with water from drums, cover leftover food, wash hands after defecation, avoid eating
ground food (cabbage, lettuce, carrots etc.)
3. proper collection of stool specimen: never give paraffin or any oil preparation 48 hours
prior to collectionof specimen, instruct patient to avoid mixture of stool and urine, select
large portion containing blood and mucus . send specimen to lab immediately, label properly
4. skin care
5. mouth care
6. provide optimum comfort
7. diet
COMMON NURSING DIAGNOSIS
METHODS OF PREVENTION
1. alexandrium tamarense
2. alexandrium catenella
3. ptychodiscus brevis
1. warm surface temperature
2. high nutrient content
3. low salinity and calm seas
4. rainy days followed by sunny
weather
DOES IT REALLY COLOR THE WATER?
Yes. Water in coastal areas can be colored red by algae, thus, the term red tide. The toxic blooms often turn the water reddish
brown, although there algae that are not poisonous.
SEAFOODS THAT ARE UNSAFE TO EAT FROM INFECTED WATERS
Shellfish are particularly prone to contamination as they feed by filtering microsocopic food out of the water.
Such shellfish include: quahogs, soft shellfish, oysters, mussels, scallops, moon smails
1. Paralytic shellfish poisoning
FOUR SYNDROMES OF SHELLFISH POISONING:
2. Diarrheal shellfish poisoning
3. Amnestic shellfish poisoning
4. Neurologic shellfish poisoning
Mussels, clams, oysters, and
All four syndrome share some common features and are primarily associated with bivalve
scallops
mollusk such as_
dinoflagellates and diatoms
These shellfish are filter feeders and, therefore, accumulate toxins produced by microscopic
algae in the form of _
Lobster,crabs, shrimps and fish
_ do not accumulate toxins and are safe to eat even if they are from affected waters.
PATHPHYSIOLOGY
Eating toxic shellfish can cause paralytic shellfish poisoning(PSP) in humans. PSP is caused by saxitoxin, which is produced by A
catenella and is one of the most potent toxins known. Saxitoxin acts by blocking sodium movement in muscle tissue. Conduction
block primarily occurs in the neurons and muscle. The toxins responsible for shellfish poisoning are water soluble, heat and acid
stable, and are not inactivated by ordinary cooking. Afer ingestion, the toxin immediately affects the nervous systemwith
symptoms usually appearing within 30 minutes. Severity depends on the amount of toxin consumed. Toxic shellfish taste appear
no different from non toxic shellfish and cooking does not destroy the organism.
CLINICAL MANIFESTATION
lips and tongue
1. the initial sign is the tingling of the _which spreads to the face, neck, fingertips and toes
headache, dizziness and nausea
2. _follow, symptoms which may be mistaken as being due to drunken condition
alcohol consumption
3. such symptoms are aggrevated by _
muscular paralysis and breathing
4. in severe cases, _may occur in 5 to 12 hours due to paralysis of the diaphragm, the victim
difficulty
can survive with the aid of respirator
5. fatalities from _have been reported
respiratory arrest
MODALITIES OF TREATMENT
vomit
1. The patient is induced to _
Charcoal hemoperfusion
2. _is a process done by pumping the arterial blood through the activated charcoal filter to
sodium bicarbonate
remove the toxin
Artificial respiration
3. Alkaline fluids, such as_, are thought to be helpful because the toxin is unstable in alkaline
condition
4._ is required if the patient exhibits respiratory stress
blood transfusion
contaminated needles
INCUBATION PERION
a. plasmodium falciparum (malignant tertian)
b. plasmodium vivax and ovale(benign tertian)
c. plasmodium malariae (quartan)
PERIOD OF COMMUNICABILITY
a. plasmodium falciparum (malignant tertian)
b. plasmodium vivax and ovale(benign tertian)
c. plasmodium malariae (quartan)
MODE OF TRANSMISSION
1. the disease is transmitted mechanically through the bite of an infected female Anopheles
mosquito
2. It can be transmitted parenterally through _
3. it can be transmitted from shared _
CLINICAL MANIFESTATION
>paroxysms with shaking chills, rapidly rising fever with severe headache, profuse sweating, myalgia, splenomegaly,
PATHOGENESIS
1. the parasite enters the mosquitos stomach through infected human blood obtained during blood meal
2. within the stomach of the female mosquito, they undergo sexual conjugation and form a zygote
3. the zygote matures into a motile form called ookinete
4. after a number of days, young parasites are released and work their way into the salivary glands of the mosquito the life cycle
last 8-35 days
5. the organism is transmitted from the saliva into the victim when the mosquito bites
6. the female alone plays the role of vector and definitive host
7. in humans, the organism, invaded the RBC, where they grow and undergo asexual schizogony
8. erythrocytic merozoites are produced ,leading to rupture of RBC
9. Young merozoites invade a new batch of RBCs to start another cycle.
DIAGNOSTIC PROCEDURE:
1. Malarial Smear
>in the procedure , a film of blood is placed on a slide, stained and examined
2. Rapid diagnostic test
>this is a blood test for malaria that can be conducted outside the labs and in the field
MANAGEMENT:
(MEDICAL)
a. anti-malarial drugs- chloroquine, quinine, sulfadoxine p. falciparum, primaquine p. vivax and ovale
b. erythrocyte exchange transfusion for rapid production of high levels of parasite in blood
Nursing management:
a. must be closely monitored
b. monitor intake and output to prevent pulmo edema, daily monitoring to BUN, creatinine
c. provide comfort, encourage fluid intake, evaluate degree of anemia
Altered body temp, activity
COMMON NURSING DIAGNOSIS:
intolerance, knowledge deficit,
altered nutrition : less than body
requirement
PREVENTION AND CONTROL:
1. malarial cases should be reported, screening of all infected persons, destroy breeding places of mosquito, nets should be used,
blood donors should be screened, insect repellant should be used
FILARIASIS (ELEPHANTIASIS)
FILARIASIS
It is a parasitic disease caused by microscopic, threadlike African eye worm. The adult worms
can live only in the lymphatic system. It affects the woman, men and children, affects the
poor in both rural and urban areas, it is rarely fatal, it causes extensive disability, gross
disfigurement, and untold suffering in millions of people
CAUSATIVE ORGANISM:
1. Wuchereria bancrofti
>is the causative agent of filariasis, it is a threadworm four to five cm long and affects the
lymph nodes and lymph vessels of the legs, arms, vulva, and breast
>shows manifestation resembling that of a Bancroftian, but swelling of the extremities is
2. Brugia malayi
confined to the ares below the knee and below the elbow
>rarely affects the genitals
3. Brugia timori
>transmitted by deer fly
4. Loa loa
>person-person by mosquito bites
MODE OF TRANSMISSION
PATHOGENESIS
1. when a mosquito bites a person with lymphatic filariasis, microscopic worms circulating in the persons blood enter and infect
the mosquito
2. pass from the mosquito through the human skin through human skin and travel to the lymph vessel where they grow into adults
3. Adult worm lives for 7 years in the lymph vessels. They mate and release into the bloodstream known as microfilaria
4. once the person has the worm in his/her blood, these are picked up by the mosquito when it feeds and transmitted to other
person via larvae
5. larvae migrates to the lymph nodes , reach sexual maturity and cycle is complete
6. the person need to get many mosquito bites over several months to years to get filariasis
7. this disease damaged the kidney and lymph system
8. a person with this disease tends to have more bacterial infection in the skin thus, skin hardens and thickens called
elephantiasis
On and off chills, headache, fever
SYMPTOMS:
that last for 3 months and 1 year
after the insect bite, swelling
redness, and pain in the arms, legs
and scrotum, areas of abscess
may be present