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 Taxonomy
 Kingdom: Animalia
 Phylum: Nematoda
 Class: Adenophorea
 Order: Trichurida
 Family: Trichinellidae
 Genus: Trichinella
Important round worm species of human :
Exclusively intestinal
parasites: Enterobius vermicularis (Pinworm)
Trichocephalus trichiurus (Whipworm)
Tissue-intestinal
parasites:
Ascaris lumbricoides (Roundworm)
Strongyloides stercoralis (Thread worm)
Ancylostoma duodenale and Necator americanus (Hookworms)
Dracunculus medinensis (Guinea worm)
Trichinella spiralis (Trichina worm)
Blood and tissue parasites Wuchereria bancrofti
(Filarial worms): Brugia malayi, Brugia timuri
Loa-loa
Onchocerca volvulus
 Trichinellosis is a parasite disease caused by a roundworm of the genus Trichinella.
 A ,B : Encysted larvae of Trichinella in pressed muscle tissue sample. The coiled
larvae can be seen inside the cysts
 Eight species of Trichinella are recognized as causes of infection in humans.
 The most common infections are caused by T. Spiralis, which ca be found in pigs, rodents, horses,
bears and foxes.
 (Zoonosis) Any mammal (rat, bear, fox) can be infected, but pigs are the most important
reservoirs of human disease.
 Other Pathogenic Trichinella Species:
 T. britovi is the second most common species to infect humans; it is distributed throughout Europe,
Asia, and northern and western Africa, usually in wild carnivores, wild boar and domesticated pigs.
 T. murrelli also infects humans, especially from black bear meat; it is distributed among wild
carnivores in North America.
 T. nativa, which has a high resistance to freezing, is found in the Arctic and subarctic regions;
reservoir hosts include polar bears, Arctic foxes, walruses and other wild game.
 T. nelsoni, found in east African predators and scavengers, has been documented to cause a few
human cases.
 T. papuae infects both mammals and reptiles, including crocodiles, humans, wild pigs and domestic
pigs; this species, found in Papua New Guinea and Thailand, is also nonencapsulated.
 T. pseudospiralis infects birds and mammals, and has demonstrated infection in humans; it is a
nonencapsulated species.
 T. zimbabwensis can infect mammals, and possibly humans; this nonencapsulated species was
detected in crocodiles in Africa.
 Distribution worldwide (PANDEMIC),
especially in eastern Europe and
west Africa.
INFECTIVE STAGE FOR HUMANS: Larva.
MODE OF TRANSMISSION: (Faecal Oral – Peroral bio
helminthiasis) eating raw or undercooked meat, usually pork,
containing larvae encysted in the muscle).
The sources of infection
 NATURAL FOCI
(beers, wolfs, foxes)
 ANTHROPURGIC FOCI
 (pigs, dogs, cats)
 The factor of the transmission is insufficient thermal processing of
the meat
 IMMUNITY:
Short
Re-infection is possible.
 Trichinella spiralis is the smallest known nematode parasite of humans. The males measure about 1.4 mm
to 1.6 mm in length and the females are twice the size of the males. The body of the worm is more slender
at the anterior then at the posterior end. In females the uterus is contained in the posterior portion of the
worm and is filled with the developing eggs. The anterior end of the female contains hatching juveniles.
 This nematode has a cuticle with three or more main outer layers made of collagen and other compounds.
The outer layers are non-cellular and are secreted by the epidermis. The cuticle layer protects the
nematodes so they can invade the digestive tracts of animals.
 Nematodes have longitudinal muscles along the body wall. The muscles are obliquely arranged in bands.
Dorsal, ventral and longitudinal nerve cords are connected to the main body of the muscle.
 Range length: 1.4 to 3.2 mm.
 Other Physical Features: ectothermic ; heterothermic ; bilateral symmetry
 Sexual Dimorphism: female larger; sexes shaped differently
 1) The adults female worms are up to 3-4  0.6 mm; the adult male worms are up to 1.5  0.04 mm;
 2) the encysted larvae (1 mm) is enclosed in a fibrous cyst wall.
 Localisation: small intestine (adult worms) and striated muscles (larvae).
 Life Cycle includes Enteral and Parenteral Phase:
ENTERAL PHASE: Incubation period: 1-2 days. Humans are infected after eating
encysted Trichinella larvae present in raw or inadequately cooked meat. The cyst walls
are digested by acid-pepsin digestion in the stomach, larvae are released and pass into
the small intestine. The larvae invade the small intestine epithelial wall, molt four times
and develop into adult worms. The males die after copulation, and the females produce
500 – 1500 newborn larvae that are deposited into the mucosa of the duodenal wall
over a 2 to 3 week period before their expulsion in the fecal stream.
PARENTERAL PHASE: Incubation Period: 2 to 8 weeks. Newborn larvae enter the
bloodstream, and seed various organs including myocardium, lungs, brains, pancreas
and lymph nodes, but only the lavae that invade the skeletal muscle survive. The
individual muscle fibers invaded by the Trichinella larvae show degeneration and
necrosis and severe infiltration with lymphocytes and eosinophils. The larvae are
encysted within a few weeks, and the cyst wall may calcify over time. Although host
immune responses may help to expel intestinal adult worms, they have little effect on
muscle dwelling larvae.
Clinical symptoms arise from the successive phase of parasite enteric
invasion, larval migration and muscle encystment.
 Light infections (with <10 larvae per gram of muscle) may be asymptomatic.
 Severe infections (with >50 larvae per gram of muscle) can be life threatening.
 Intestinal invasion can be accompanied by gastrointestinal symptoms
(diarrhea (during the first week after infection), abdominal pain, constipation,
nausea or vomiting).
 Larval migration into muscle tissues (2nd week after infection) can cause
marked local and systemic hypersensitivity reaction, with fever and hyper
eosinophilia. Periorbital and facial edema, conjunctivitis, myalgias, splinter
hemorrhages (hemorrhage in the subconjunctiva, retina and nail beds).
 Maculopapular rash, headache, cough dyspnea sometimes develops.
 Occasional life-threatening manifestations include myocarditis with tachyarrhythmias
or heart failure, central nervous system involvement, and encephalitis or pneumonitis.
 Larval encystment in the muscles (2 – 3 weeks after infection) causes myositis with
myalgia and weakness.
 The most commonly involved muscle groups include the extraocular muscles, the
biceps and the muscles of the jaw, neck, lower back and diaphragm.
 Peaking ~ 3 weeks after infection symptoms subside gradually during a prolonged
convalescence.
Splinter hemorrhages Swollen eyes
 Diagnosis of trichinosis is confirmed by a combination of exposure history, clinical
diagnosis, laboratory testing and imaging studies.
 Exposure history
An epidemiological investigation can be done to determine a patient's exposure to raw
infected meat. Often, an infection arises from home-preparation of contaminated meat,
in which case microscopy of the meat may be used to determine the infection. Exposure
determination does not have to be directly from a laboratory-confirmed infected animal.
Indirect exposure criteria include the consumption of products from a laboratory-
confirmed infected animal, or sharing of a common exposure with a laboratory-
confirmed infected human.
 Clinical diagnosis
Clinical presentation of the common trichinosis symptoms may also suggest infection.
These symptoms include eye puffiness, splinter hemorrhage,
nonspecific gastroenteritis, and muscle pain. The case definition for trichinosis at the
European Center for Disease Control states "at least three of the following six: fever,
muscle soreness and pain, gastrointestinal symptoms, facial edema, eosinophilia, and
subconjuctival, subungual, and retinal hemorrhages."
 Laboratory testing
 Blood tests, microscopy, antibody detection and muscle biopsy can be used to aid in
the diagnosis of trichinosis.
 BLOOD TESTS
Complete blood count
 Leukocytosis occurs in 65% of patients, with cell counts of up to 24,000/µL.
 Eosinophilia (rises 10 days after infection, with total eosinophil counts of up to 8700/µL
(40%-80% of total WBC). The counts peak in 3-4 weeks and resolve over the next few
months). A low eosinophil count indicates an increased mortality rate.
 Erythrocyte sedimentation rate are usually within the reference range
 SERUM LEVEL OF MUSCLE ENZYMES:
Creatine phosphokinase activity is increased to 17,000 U/L. CK (isoenzyme myocardial
band [MB]) elevations may indicate myocardial involvement; however, as many as 35%
of patients without cardiac involvement may have elevated CK-MB levels.
 Lactate dehydrogenase
Levels of lactate dehydrogenase isoenzymatic forms (ie, lactate dehydrogenase fraction
4 [LD4] and lactate dehydrogenase fraction 5 [LD5]) are elevated in 50% of patients.
 Immunoglobulin E
Immunoglobulin E levels are typically elevated.
 MUSCLE BIOPSY
Reveals larvae within striated muscle
 Obtain a 0.5- to 1-g muscle biopsy specimen from the deltoid or gastrocnemius muscle because
these are most easily accessible. The yield increases if the biopsy site is swollen or tender. Stain the
specimen with hematoxylin and eosin (H&E) and examine multiple sections. Occasionally, larvae can
be found after the muscle has been digested enzymatically.
 If a biopsy is performed prior to larvae coiling (beyond day 17 of infection), worm tissue can be
confused with muscle tissue.
 A negative result does not necessarily exclude infection.
ANTIBOBY DETECTION: SEROLOGIC TEST
 Serology results are not positive until 2-3 weeks after infection. They
peak around the third month and may persist for years.
 Serology ratios do not correlate with the severity of disease or the
clinical course. However, a strong positive test result usually indicates
an early infection.
 Indirect hemagglutination.
 Bentonite flocculation results are usually not positive for more than 1
year after infection.
 Indirect immunofluorescence.
 Latex agglutination results are usually not positive for more than 1 year
after infection.
 Enzyme-linked immunosorbent assay (ELISA) is 100% sensitive on day
50, with 88% of results remaining positive 2 years after infection.
PCR
Polymerase chain reaction is useful for isolating the parasite and subsequent genetic
typing. it is used primarily as a research tool.
HYPERSENSITIVITY SKIN TEST
Reactions results are positive (5 mm) at approximately day 17 and remain positive for
life.
IMAGING STUDIES
 In patients with CNS involvement, CT scanning and MRI with contrast enhancement may
reveal 3- to 8-mm nodular or ringlike lesions.
OTHER TESTS
Electrocardiography may show the following:
 Premature contractions
 Prolongation of the PR intervals
 Small QRS complexes with intraventricular block
 Flattening or inversion of the T waves, especially lead II and precordial leads
LUMBAR PUNCTURE
 Lumbar puncture is used to evaluate for suspected neurologic disease.
 Results are normal in 50%-75% of patients.
 Larvae are found in 8%-24% in patients.
 Eosinophilic meningitis may be present.
DIET
 No diet limitations are indicated; however, this is an excellent opportunity to educate
patients regarding the avoidance of potentially infected meats and how to properly
cook and store foods.
ACTIVITY
 For severe infections, bed rest is recommended. This is especially important upon
evidence of myocardial involvement because patients may deteriorate clinically during
ambulation.
Primary treatment
 ETIOTROPIC: ANTIHELMINTHS ( decreases the likelihood of larval encystation, particularly if
given within three days of infection. These drugs prevent newly hatched larvae from developing,
but should not be given to pregnant women or children under two years of age.).
Albendazole 400mg orally 2x a day for 8 -14 days or
Metronidazole 200 – 400mg 3x a day for 3 days, then 400mg 3x a day for 8 0- 14days.
Secondary treatment
• For prevention of systemic symptoms that can occur after treatment with albendazole
or mebendazole, prednisolone is useful (1mg/kg for 5days per os).
• Aggressive supportive treatment and higher doses of steroids are warranted in those
with life threatening complications such as myocarditis, encephalitis or pneumonitis.
 PATHOGENETIC:
Desensibilization
Desintoxication therapy
 Infectious disease specialist
 Cardiologist, if evidence of cardiac involvement
 Neurologist, if evidence of neurologic involvement
 Legislation
Laws and rules for food producers may improve food safety for consumers, such as NAFDAC in
NIGERIA
 Education and training
Public education about the dangers of consuming raw and undercooked meat, especially pork, may
reduce infection rates. Hunters are also an at-risk population due to their contact and consumption of
wild game, including bear. As such, many states, such as New York, require the completion of a course
in such matters before a hunting license can be obtained.
 Food preparation
 Larvae may be killed by the heating or irradiation of raw meat. Freezing is normally only effective
for T. spiralis, since other species, such as T. nativa, are freeze resistant and can survive long-term
freezing.
 All meat (including pork) can be safely prepared by cooking to an internal temperature of 165 °F
(74 °C) or higher for 15 seconds or more.
 Wild game: Wild game meat must be cooked thoroughly (see meat preparation above) Freezing wild
game does not kill all trichinosis larval worms. This is because the worm species that typically infests
wild game can resist freezing.
 Pork: Freezing cuts of pork less than 6 inches thick for 20 days at 5 °F (−15 °C) or three days at
−4 °F (−20 °C) kills T. spiralis larval worms; but this will not kill other trichinosis larval worm species,
such as T. nativa, if they have infested the pork food supply (which is unlikely, due to geography).
 Pig farming
 Keeping pigs in clean pens, with floors that can be washed (such as concrete)
 Not allowing hogs to eat carcasses of other animals, including rats, which may be
infected with Trichinella
 Cleaning meat grinders thoroughly when preparing ground meats
 Control and destruction of meat containing trichinae, e.g., removal and proper
disposal of porcine diaphragms prior to public sale of meat.
 NB:
Unsafe and unreliable methods of cooking meat include the use of microwave ovens,
curing, drying, and smoking, as these methods are difficult to standardize and control.
 myocarditis
 pneumonia
 meningoencephalitis
 hepatitis
 nephritis
 systemic vasculitis
 thrombophlebitis
 thrombocytopenia
 The acute stages of trichinellosis share clinical characteristics with many other acute-onset febrile infectious
diseases such as salmonellosis (prolonged diarrhea) and influenza (high fever, myalgias) as well
as chronic fatigue syndrome and fibromyalgia.
 Acute Glomerulonephritis
 Angioedema
 Bacterial Gastroenteritis
 Delusions of Parasitosis
 Dermatomyositis
 Food Poisoning
 Hookworm Disease
 Influenza
 Polyarteritis Nodosa
 Rheumatic Fever
 Schistosomiasis (Bilharzia)
 Strongyloidiasis
 Typhoid Fever
 Viral Gastroenteritis
Trichinellosis

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Trichinellosis

  • 1.
  • 2.  Taxonomy  Kingdom: Animalia  Phylum: Nematoda  Class: Adenophorea  Order: Trichurida  Family: Trichinellidae  Genus: Trichinella
  • 3. Important round worm species of human : Exclusively intestinal parasites: Enterobius vermicularis (Pinworm) Trichocephalus trichiurus (Whipworm) Tissue-intestinal parasites: Ascaris lumbricoides (Roundworm) Strongyloides stercoralis (Thread worm) Ancylostoma duodenale and Necator americanus (Hookworms) Dracunculus medinensis (Guinea worm) Trichinella spiralis (Trichina worm) Blood and tissue parasites Wuchereria bancrofti (Filarial worms): Brugia malayi, Brugia timuri Loa-loa Onchocerca volvulus
  • 4.  Trichinellosis is a parasite disease caused by a roundworm of the genus Trichinella.
  • 5.  A ,B : Encysted larvae of Trichinella in pressed muscle tissue sample. The coiled larvae can be seen inside the cysts
  • 6.  Eight species of Trichinella are recognized as causes of infection in humans.  The most common infections are caused by T. Spiralis, which ca be found in pigs, rodents, horses, bears and foxes.  (Zoonosis) Any mammal (rat, bear, fox) can be infected, but pigs are the most important reservoirs of human disease.  Other Pathogenic Trichinella Species:  T. britovi is the second most common species to infect humans; it is distributed throughout Europe, Asia, and northern and western Africa, usually in wild carnivores, wild boar and domesticated pigs.  T. murrelli also infects humans, especially from black bear meat; it is distributed among wild carnivores in North America.  T. nativa, which has a high resistance to freezing, is found in the Arctic and subarctic regions; reservoir hosts include polar bears, Arctic foxes, walruses and other wild game.  T. nelsoni, found in east African predators and scavengers, has been documented to cause a few human cases.  T. papuae infects both mammals and reptiles, including crocodiles, humans, wild pigs and domestic pigs; this species, found in Papua New Guinea and Thailand, is also nonencapsulated.  T. pseudospiralis infects birds and mammals, and has demonstrated infection in humans; it is a nonencapsulated species.  T. zimbabwensis can infect mammals, and possibly humans; this nonencapsulated species was detected in crocodiles in Africa.
  • 7.  Distribution worldwide (PANDEMIC), especially in eastern Europe and west Africa. INFECTIVE STAGE FOR HUMANS: Larva. MODE OF TRANSMISSION: (Faecal Oral – Peroral bio helminthiasis) eating raw or undercooked meat, usually pork, containing larvae encysted in the muscle). The sources of infection  NATURAL FOCI (beers, wolfs, foxes)  ANTHROPURGIC FOCI  (pigs, dogs, cats)  The factor of the transmission is insufficient thermal processing of the meat  IMMUNITY: Short Re-infection is possible.
  • 8.  Trichinella spiralis is the smallest known nematode parasite of humans. The males measure about 1.4 mm to 1.6 mm in length and the females are twice the size of the males. The body of the worm is more slender at the anterior then at the posterior end. In females the uterus is contained in the posterior portion of the worm and is filled with the developing eggs. The anterior end of the female contains hatching juveniles.  This nematode has a cuticle with three or more main outer layers made of collagen and other compounds. The outer layers are non-cellular and are secreted by the epidermis. The cuticle layer protects the nematodes so they can invade the digestive tracts of animals.  Nematodes have longitudinal muscles along the body wall. The muscles are obliquely arranged in bands. Dorsal, ventral and longitudinal nerve cords are connected to the main body of the muscle.  Range length: 1.4 to 3.2 mm.  Other Physical Features: ectothermic ; heterothermic ; bilateral symmetry  Sexual Dimorphism: female larger; sexes shaped differently  1) The adults female worms are up to 3-4  0.6 mm; the adult male worms are up to 1.5  0.04 mm;  2) the encysted larvae (1 mm) is enclosed in a fibrous cyst wall.  Localisation: small intestine (adult worms) and striated muscles (larvae).
  • 9.  Life Cycle includes Enteral and Parenteral Phase: ENTERAL PHASE: Incubation period: 1-2 days. Humans are infected after eating encysted Trichinella larvae present in raw or inadequately cooked meat. The cyst walls are digested by acid-pepsin digestion in the stomach, larvae are released and pass into the small intestine. The larvae invade the small intestine epithelial wall, molt four times and develop into adult worms. The males die after copulation, and the females produce 500 – 1500 newborn larvae that are deposited into the mucosa of the duodenal wall over a 2 to 3 week period before their expulsion in the fecal stream. PARENTERAL PHASE: Incubation Period: 2 to 8 weeks. Newborn larvae enter the bloodstream, and seed various organs including myocardium, lungs, brains, pancreas and lymph nodes, but only the lavae that invade the skeletal muscle survive. The individual muscle fibers invaded by the Trichinella larvae show degeneration and necrosis and severe infiltration with lymphocytes and eosinophils. The larvae are encysted within a few weeks, and the cyst wall may calcify over time. Although host immune responses may help to expel intestinal adult worms, they have little effect on muscle dwelling larvae.
  • 10.
  • 11. Clinical symptoms arise from the successive phase of parasite enteric invasion, larval migration and muscle encystment.  Light infections (with <10 larvae per gram of muscle) may be asymptomatic.  Severe infections (with >50 larvae per gram of muscle) can be life threatening.  Intestinal invasion can be accompanied by gastrointestinal symptoms (diarrhea (during the first week after infection), abdominal pain, constipation, nausea or vomiting).  Larval migration into muscle tissues (2nd week after infection) can cause marked local and systemic hypersensitivity reaction, with fever and hyper eosinophilia. Periorbital and facial edema, conjunctivitis, myalgias, splinter hemorrhages (hemorrhage in the subconjunctiva, retina and nail beds).
  • 12.  Maculopapular rash, headache, cough dyspnea sometimes develops.  Occasional life-threatening manifestations include myocarditis with tachyarrhythmias or heart failure, central nervous system involvement, and encephalitis or pneumonitis.  Larval encystment in the muscles (2 – 3 weeks after infection) causes myositis with myalgia and weakness.  The most commonly involved muscle groups include the extraocular muscles, the biceps and the muscles of the jaw, neck, lower back and diaphragm.  Peaking ~ 3 weeks after infection symptoms subside gradually during a prolonged convalescence. Splinter hemorrhages Swollen eyes
  • 13.  Diagnosis of trichinosis is confirmed by a combination of exposure history, clinical diagnosis, laboratory testing and imaging studies.  Exposure history An epidemiological investigation can be done to determine a patient's exposure to raw infected meat. Often, an infection arises from home-preparation of contaminated meat, in which case microscopy of the meat may be used to determine the infection. Exposure determination does not have to be directly from a laboratory-confirmed infected animal. Indirect exposure criteria include the consumption of products from a laboratory- confirmed infected animal, or sharing of a common exposure with a laboratory- confirmed infected human.  Clinical diagnosis Clinical presentation of the common trichinosis symptoms may also suggest infection. These symptoms include eye puffiness, splinter hemorrhage, nonspecific gastroenteritis, and muscle pain. The case definition for trichinosis at the European Center for Disease Control states "at least three of the following six: fever, muscle soreness and pain, gastrointestinal symptoms, facial edema, eosinophilia, and subconjuctival, subungual, and retinal hemorrhages."
  • 14.  Laboratory testing  Blood tests, microscopy, antibody detection and muscle biopsy can be used to aid in the diagnosis of trichinosis.  BLOOD TESTS Complete blood count  Leukocytosis occurs in 65% of patients, with cell counts of up to 24,000/µL.  Eosinophilia (rises 10 days after infection, with total eosinophil counts of up to 8700/µL (40%-80% of total WBC). The counts peak in 3-4 weeks and resolve over the next few months). A low eosinophil count indicates an increased mortality rate.  Erythrocyte sedimentation rate are usually within the reference range  SERUM LEVEL OF MUSCLE ENZYMES: Creatine phosphokinase activity is increased to 17,000 U/L. CK (isoenzyme myocardial band [MB]) elevations may indicate myocardial involvement; however, as many as 35% of patients without cardiac involvement may have elevated CK-MB levels.
  • 15.  Lactate dehydrogenase Levels of lactate dehydrogenase isoenzymatic forms (ie, lactate dehydrogenase fraction 4 [LD4] and lactate dehydrogenase fraction 5 [LD5]) are elevated in 50% of patients.  Immunoglobulin E Immunoglobulin E levels are typically elevated.  MUSCLE BIOPSY Reveals larvae within striated muscle  Obtain a 0.5- to 1-g muscle biopsy specimen from the deltoid or gastrocnemius muscle because these are most easily accessible. The yield increases if the biopsy site is swollen or tender. Stain the specimen with hematoxylin and eosin (H&E) and examine multiple sections. Occasionally, larvae can be found after the muscle has been digested enzymatically.  If a biopsy is performed prior to larvae coiling (beyond day 17 of infection), worm tissue can be confused with muscle tissue.  A negative result does not necessarily exclude infection.
  • 16. ANTIBOBY DETECTION: SEROLOGIC TEST  Serology results are not positive until 2-3 weeks after infection. They peak around the third month and may persist for years.  Serology ratios do not correlate with the severity of disease or the clinical course. However, a strong positive test result usually indicates an early infection.  Indirect hemagglutination.  Bentonite flocculation results are usually not positive for more than 1 year after infection.  Indirect immunofluorescence.  Latex agglutination results are usually not positive for more than 1 year after infection.  Enzyme-linked immunosorbent assay (ELISA) is 100% sensitive on day 50, with 88% of results remaining positive 2 years after infection.
  • 17. PCR Polymerase chain reaction is useful for isolating the parasite and subsequent genetic typing. it is used primarily as a research tool. HYPERSENSITIVITY SKIN TEST Reactions results are positive (5 mm) at approximately day 17 and remain positive for life.
  • 18. IMAGING STUDIES  In patients with CNS involvement, CT scanning and MRI with contrast enhancement may reveal 3- to 8-mm nodular or ringlike lesions. OTHER TESTS Electrocardiography may show the following:  Premature contractions  Prolongation of the PR intervals  Small QRS complexes with intraventricular block  Flattening or inversion of the T waves, especially lead II and precordial leads LUMBAR PUNCTURE  Lumbar puncture is used to evaluate for suspected neurologic disease.  Results are normal in 50%-75% of patients.  Larvae are found in 8%-24% in patients.  Eosinophilic meningitis may be present.
  • 19. DIET  No diet limitations are indicated; however, this is an excellent opportunity to educate patients regarding the avoidance of potentially infected meats and how to properly cook and store foods. ACTIVITY  For severe infections, bed rest is recommended. This is especially important upon evidence of myocardial involvement because patients may deteriorate clinically during ambulation. Primary treatment  ETIOTROPIC: ANTIHELMINTHS ( decreases the likelihood of larval encystation, particularly if given within three days of infection. These drugs prevent newly hatched larvae from developing, but should not be given to pregnant women or children under two years of age.). Albendazole 400mg orally 2x a day for 8 -14 days or Metronidazole 200 – 400mg 3x a day for 3 days, then 400mg 3x a day for 8 0- 14days.
  • 20. Secondary treatment • For prevention of systemic symptoms that can occur after treatment with albendazole or mebendazole, prednisolone is useful (1mg/kg for 5days per os). • Aggressive supportive treatment and higher doses of steroids are warranted in those with life threatening complications such as myocarditis, encephalitis or pneumonitis.  PATHOGENETIC: Desensibilization Desintoxication therapy
  • 21.  Infectious disease specialist  Cardiologist, if evidence of cardiac involvement  Neurologist, if evidence of neurologic involvement
  • 22.  Legislation Laws and rules for food producers may improve food safety for consumers, such as NAFDAC in NIGERIA  Education and training Public education about the dangers of consuming raw and undercooked meat, especially pork, may reduce infection rates. Hunters are also an at-risk population due to their contact and consumption of wild game, including bear. As such, many states, such as New York, require the completion of a course in such matters before a hunting license can be obtained.  Food preparation  Larvae may be killed by the heating or irradiation of raw meat. Freezing is normally only effective for T. spiralis, since other species, such as T. nativa, are freeze resistant and can survive long-term freezing.  All meat (including pork) can be safely prepared by cooking to an internal temperature of 165 °F (74 °C) or higher for 15 seconds or more.  Wild game: Wild game meat must be cooked thoroughly (see meat preparation above) Freezing wild game does not kill all trichinosis larval worms. This is because the worm species that typically infests wild game can resist freezing.  Pork: Freezing cuts of pork less than 6 inches thick for 20 days at 5 °F (−15 °C) or three days at −4 °F (−20 °C) kills T. spiralis larval worms; but this will not kill other trichinosis larval worm species, such as T. nativa, if they have infested the pork food supply (which is unlikely, due to geography).
  • 23.  Pig farming  Keeping pigs in clean pens, with floors that can be washed (such as concrete)  Not allowing hogs to eat carcasses of other animals, including rats, which may be infected with Trichinella  Cleaning meat grinders thoroughly when preparing ground meats  Control and destruction of meat containing trichinae, e.g., removal and proper disposal of porcine diaphragms prior to public sale of meat.  NB: Unsafe and unreliable methods of cooking meat include the use of microwave ovens, curing, drying, and smoking, as these methods are difficult to standardize and control.
  • 24.  myocarditis  pneumonia  meningoencephalitis  hepatitis  nephritis  systemic vasculitis  thrombophlebitis  thrombocytopenia
  • 25.  The acute stages of trichinellosis share clinical characteristics with many other acute-onset febrile infectious diseases such as salmonellosis (prolonged diarrhea) and influenza (high fever, myalgias) as well as chronic fatigue syndrome and fibromyalgia.  Acute Glomerulonephritis  Angioedema  Bacterial Gastroenteritis  Delusions of Parasitosis  Dermatomyositis  Food Poisoning  Hookworm Disease  Influenza  Polyarteritis Nodosa  Rheumatic Fever  Schistosomiasis (Bilharzia)  Strongyloidiasis  Typhoid Fever  Viral Gastroenteritis