skin 17: trichinosis

Question 1

trichinosis (a reportable disease) caused by ??

Answer 1

Trichinella spiralis, a Helminth parasite

Rarely, Trichinella pseudospiralis can also cause trichinosis.

Question 2

There are many (10) species in the genus Trichinella that reflect 3 distinct sylvatic cycles

Answer 2

Arctic
Temperate
Tropical.
These species have different epidemiological patterns and pathogenic potentials e.g., some are highly resistant to freezing.

Question 3

trichinosis high risk groups are mainly due to cultural/behavioral factors, mainly eating:

Answer 3

undercooked, raw animal flesh
smoked meats:
pork, horse, wild/feral game meat.

Sporadic outbreaks due to contamination of food products. A butcher/food processor grinds up pork then fails to break down and properly clean the food grinding machinery.

Question 4

Incidence of the genus Trichinella:

Answer 4

Almost worldwide distribution in feral animals (predominately omnivores & carnivores). Due to a broad-host range (virtually all warm-blooded animals).
In domestic swine (pig) and equine (horse) herds in the world: T. spiralis is dominant.

Question 5

Incidence of trichinella infection or disease in humans is a reflection of ??

Answer 5

incidence of infection or disease in swine and horse herds.

Question 6

Pathogenesis/Life cycle of T. spiralis (a Helminth/Nematode).

Answer 6

1. Flesh (striated muscle) eaten by carnivore or omnivore - pig, man, bears, etc
2. Larvae excyst in
   the upper GI tract, due to
   gastric acid
3. Larvae mature (2 d post-infection), adults mate while borrowed into the lining of the small intestine (S.I.)
4. Female borrows deeper into S.I. lining; releases larvae over 4-16w (begins 5d post-infection)

Question 7

more Pathogenesis/Life cycle of T. spiralis (a Helminth/Nematode).

Answer 7

5. Larvae undergo several developmental cycles
6. First larvae enter the circulation, then migrate
   into all body tissues (7-14d post-infection)
7. Only Larvae embed in
   active, striated muscle elongate & encyst (21d post-infection)

Question 8

most trichinella infections are ??

Answer 8

asymptomatic (probably due to consumption of low numbers of cysts).

Question 9

trichinella Symptomatic infections: s/s are ??

Answer 9

dose dependent/depend on worm burden (numbers of ingested cysts).
due to larval migration into tissue, especially:
-Striated muscle.
-Heart.
-Kidney.
-Lungs.
-CNS tissues.
due to the host immune response to the larvae, which occur 7-21 days post-infection

Question 10

Adults helminths (trichinella) cause s/s in the GIT (Enteral phase) by borrowing into mucosa of small intestine, causing:

Answer 10

tissue destruction.
inflammation
s/s include:
nausea, vomiting, diarrhea, fever.

Question 11

trichinella larvae cause s/s throughout the body (Parenteral phase) by:

Answer 11

entering the circulatory system->disseminating->exiting the circulatory system, damaging the circulatory system (trauma to the host circulatory system).

Question 12

trichinella larvae also cause s/s throughout the body (Parenteral phase) by:

Answer 12

migrating through all body tissues/organs; (tissue migration occurs in
striated muscle and other tissue, most frequently in the organs with largest number of endarterioles) causing damage to the tissue (trauma to other host tissue): heart, kidney, lungs, CNS tissue

Question 13

trichinella larvae attempt to encyst in all tissue but only succeed in ??
Unencysted larva die and the dead larvae and damaged host tissue must be cleared in all tissues they die in: how does this damage host??

Answer 13

striated muscle

Toxic compounds released during and after burrowing of larvae in body tissues (i.e. due to death of human cells and larvae) also damage the host.

Question 14

Host immune response to trichinella produces ??

Answer 14

immunopathology (7-21d post infection); cause s/s throughout the body (Parenteral phase):

• Allergic responses - Type I hypersensitivity.
• Antigen-antibody deposition  vasculitis, Type III hypersensitivity.

Question 15

trichinella larvae in striated muscle:
turns muscle cell into??
how does the host respond?
how long can incapsulated larvae remain viable?

Answer 15

Larvae:
-Phenotypically reprograms the muscle cell into a “nurse cell” i.e., incubator.
-Elongate and coil up;
Meanwhile, the nurse cells encapsulate themselves in collagen.
An intense inflammatory/host immune response (PMNs, eosinophils, lymphocytes) occurs, surrounds and finally calcify/encyst (6-18 m later) the nurse cell.
Encapsulated larvae can remain viable for years (up to 30 y).

Question 16

trichinella larvae in striated muscle causes ?? to develop

Answer 16

T. spiralis-specific antibodies (IgA, IgM, IgG, esp. IgE) develop.
Antibodies plus eosinophils:
-mediate destruction of circulating larvae (antibody-dependent cell- mediated cytotoxity; ADCC).
-hasten expulsion of adult worm from the body in the feces.


Question 17

trichinosis manifestations

Answer 17

Fever,
Periorbital edema, Chemosis
Peripheral eosinophilia,
Myalgia,
Fatigue
which slowly subside, but can persist for up to 710 weeks post-infection.

Question 18

trichinosis dx

Answer 18

s/s + history of eating raw or undercooked pork, feral animal flesh in last 3 w.
-Small biopsy specimen from deltoid or other muscle taken 3rd week post-infection or after will reveal larvae. Infected muscles lose their cross-striation, undergo basophilic degranulation.

Question 19

more trichinosis dx

Answer 19

• Bentonite flocculation test (CDC) - utilizes Ag bound to bentonite clay to determine Ab levels.
• Indirect fluorescent antibody test (IFA), latex agglutination test, ELISA/EIA to detect T. spiralis-specific antibodies during the 1st week of infection.

Question 20

trichinosis lab data

Answer 20

Serum enzyme levels (FYI Creatine phosphokinase, LDH) are determined to distinguish between heart and skeletal muscle damage. Increased serum markers are first detected during the 2nd week post-infection.

Eosinophila begins 2nd week of infection and persists until the infection resolves.

Question 21

trichinosis tx

Answer 21

Supportive: mechanical ventilation.
Antihelminthics
Corticosteroids

Question 22

Antihelminthics for trichinosis:

how do they work?

Answer 22

Benzimidazole derivatives (Albendazole, Albenzatm, mebendazole, [thiabendazole - no longer available due to side effects]

-Inhibit glucose uptake by blocking microtubule assembly.
-It is unclear which stages are affected by these drugs (i.e., only effective against larvae
in intestine before becoming the adult vs. only the adult worm [halt larval production]
vs. larvae in intestine and larvae in circulation).

Question 23

In severely infected patient, antihelminthics can induce ??

Answer 23

a severe hypersensitivity

response and patient death.

Question 24

Corticosteroids for trichinosis:

Answer 24

i.e. methylprednisolone to ameliorate allergic response during larval encystment.

Question 25

trichinosis prevention/control

Answer 25

• Cook pork or flesh of wild omnivore completely and until well-done (FYI achieve an internal temperature of 170oF [77oC] for 4 minutes).
• Irradiate pork before selling to the public.
• Cook garbage/animal feed before feeding pigs.
• Control rat infestations around pig farms.

Question 26

more trichinosis prevention/control

Answer 26

• USDA requires visual inspection of live pigs for s/s before slaughtering them.
• USDA requires visual inspection of butchered meat for “mealy-flesh” appearance.
• Freezing pork is NO longer dependable – consumption of meat contaminated with (Trichinella sp.) that had been frozen has caused trichinosis in humans.
• Smoking, salting, drying meat are NOT effective.