~Trichinella Spiralis:

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1 Musculoskeletal System **Today we are going to talk about the parasites that affect the musculoskeletal system ~Trichinella Spiralis: It s a small nematode that measures to about 2-3mm in length. In general when we talk about these parasites we focus on its life cycle. It lives in the sub mucosa of the upper small intestines. Being a nematode both sexes coexist in the sub mucosa. This worm is a special case sense it doesn t lay eggs however it produces larvae. These larvae are laid in the sub mucosa so an examination of the feces is of no use to diagnose the presence of this parasite (no eggs in the feces). When the reproduction cycle ends the mature male leaves the sub mucosa and is excreted with the feces (since we don t know exactly when the males does this it is of no use to keep testing the feces for its presence). So now what happens with the larvae that are deposited in the sub mucosa? Well, they gain access to the lymphatics and from there they will be carried to the blood stream; from the blood stream they will enter the liver, the lungs, and eventually will be distributed all over the body. Where ever these larvae are deposited they give rise to a kind of inflammatory reaction. According to the symptoms that are associated with the inflammatory reaction we can find out the affected organ. All these larvae eventually die except the ones that reside in one certain tissue which is the striated (skeletal) muscle. Larvae that end up in striated muscles develop and become cysts. These larvae will mature and become spiral and they will become encased in fibrous tissue with a few inflammatory cells surrounding them, together all these elements from the cyst. These cysts after two or three years have the ability to become calcified but none the less the embryo stays viable. The larvae (in the form of cyst) can survive in the tissue for many many years but they eventually die. The next step in the life cycle of this parasite is the consumption of the cyst. That occurs by the ingestion of infected skeletal muscle tissue (in other words consumption of infected meat). This cyst will disintegrate in the GI tract and it will give rise to larvae that will penetrate the wall of 1 P a g e

2 the small intestine (to the sub mucosa) and there they will develop into adult males and females. When you pay attention to the life cycle of this parasite you can deduce that the primary host and the intermediate host for this parasite is in fact the same host. As far as the human being is concerned the presence of these larvae in the GI tract means that the human is a primary host. In the intermediate stage, which is the encysted larvae that occurs in the muscles, we call the human an intermediate host. As far as we are concerned the man in this case is a dead end intermediate host unless he lives in a cannibalistic environment. So the main question that comes to mind is how can humans acquire this parasite? Unlike most parasites that are tissue specific or host specific, there is no specificity for this parasite as far as the tissue environment is concerned. It also has multiple hosts since it can infect humans, pigs, bears, and walruses. The most common way in which a human can get infected is by eating infected pork. The presence of large numbers of this parasite in your intestines may lead to GI symptoms like nausea, vomiting, abdominal pain, and diarrhea. By time the patient will reach the point of invasion of the larvae into the blood stream; when that 2 P a g e

3 happens the patient will get malaise, the general sensation of sickness, fatigue, and fever. Fever is not usually a characteristic of worm infections but this worm is an exception. These worms may gain access to important organs (like the brain and heart) and cause encephalitis, myocarditis, and other problems and may even lead to death. Tenderness and aching in the muscle are expected and would settle down after a while, symptoms that are associated with the reaction between the body and the larvae may arise such as increased eosinophilia. Almost 40-80% of the WBCs are eosinophils, which is to be expected in cases of allergic reaction or parasitic infections. We will also have an immune reaction with the production of antibodies against these organisms (the antibodies are mainly type Ig E). The presence of antibodies is apparent from the early stages of infection and may last up to a year; however, after a year things settle down and the inflammation subsides and the Ig E starts to disappear. Also the damage to the muscles that is caused by the cysts will lead to the release of muscle enzymes. The most definitive way of diagnosis is to take a muscle biopsy and check for the presence of cysts. For treatment we usually use Bendazol and sometimes steroids are used to decrease inflammation. ~ Leishmania: Leishmania is a disease caused by protozoa. It is flagellated. It belongs to the group Trypanosomatida. Trypanosomatida consist of two groups: Leishmania: mainly affects the skin Trypanosome: affects mainly the nervous system 3 P a g e

4 As do many other parasites Leishmania has different morphologies. It has a certain shape in its intermediate host and another in its primary host. The primary host of this parasite is mainly humans and its vector is an insect called the sand fly. In addition to humans other animals might be infected with this parasite such as gerbils, dogs, and foxes. These animals are not intermediate hosts they are considered as primary host ((the only intermediate host is the fly itself)). Since it can infect humans and animals this disease can be considered as a zoonotic disease. The sand fly lives in desert like areas. This disease is considered an endemic disease in areas like Iraq, Syria, Europe, and areas of Southeast Asia. Cases have been reported in Jordan but it s not considered endemic. In the fly its morphology is considered a promastigote measuring about 20 microns and has a nucleus and a flagellum. In the fly it is an extra cellular organism. Once the fly bites a person it will eject these promastigotes in the sub cutaneous tissues. Nearby macrophages come and engulf these promastigotes. Once they are phagocytized by the macrophages they lose their flagellum and become smaller (3 microns) amastigotes. Usually when an organism is phagocytized the lysosomes fuse to the organism and digest it; however, amastigotes are resistant to these hydrolytic enzymes. The only way to get rid of it is by further activation of macrophages, with the help of lymphocytes, by the production of free radicles, hydrogen peroxide, and nitrous oxide because these are the ones that are capable of killing these parasites. 4 P a g e

5 Initially you will get a nodule in the site of the bite of the sand fly because of the macrophages that rush to the site of the bite. This nodulation will last for a while then it will ulcerate forming dry big ulcers that will last for almost a year. Even when these ulcers heal they leave behind them nasty disfiguring scars. Leishmania itself has many species that are morphologically identical and it is extremely difficult to differentiate between the different types. Now a days there are molecular methods that help in differentiating between the different types. Classifications are made according to a couple of criteria including: Distribution Clinical manifestations Leishmania can be divided into two main groups (according to the Geographical distribution around the world): Old world Leishmania((Asia, Africa and Europe)) New world Leishmania((North & South America)) It s most likely that both these groups originated from a single ancestor and then they diversified, since morphologically they are very similar to one another. In the old world Leishmania we have three kinds which are: L. major L. tropica L. aethiopica In the new word we have: L. braziliensis L. mexicana 5 P a g e

6 In the last group which causes visceral disease we have: L. donovani ((Old word)) L. infinum((old world)) L. chagasi((new world)) Now we have another type of classification according to the kind of disease ((disease manifestation)) caused by these parasites: 1. Cutaneous leishmaniasis ((the prototype; commonest found in the Middle East; provokes intense cell mediated response)). Within a few days of the fly s bite the site of the bite will get an induration () تي بس ((, the induration will ulcerate and )). )دم ل ( boil the ulcer will last for multiple months ((the ulcer here is called Eventually after a year the ulcer will heal and a scar will form at this site. 2. Diffuse cutaneous Leishmaniasis ((immune response)): It s an intracellular infection that involves the activation of Macrophages by means of lymphocyte and so on. Unfortunately in some cases of ethiopica we might have alternate manifestations of the disease and this probably has something to do with the immune response of the patient. Usually when you have an immune response it can be either cell mediated ((by means of natural killer cells and macrophages)) or it can be antibody mediated. In some patients an immune deviation occurs towards the production of antibodies ((instead of the normal method of getting rid of Leishmania which uses cell mediated response)). This is not a good thing because antibodies are less effective in fighting this parasite and the infection tends to spread and form lesions where the parasite settles ((causing multiple lesions in the skin)). 3. Mucocutaneous Leishmaniasis: this type is mainly associated with the L. braziliensis species. Here the story goes as follows. First you get a bite by the sand fly a lesion will appear. The lesion disappears very quickly and the patient forgets about it, what really happens in these cases is that the parasite remains dormant for about a year or two but then reactivates. When they reactivate they 6 P a g e

7 will form lesions; however, these lesions will not appear on the skin but in the mucus membrane ((found around the nose and buccal cavity)). These will give rise to destructive lesions of the tissues. These lesions produce secretions that can cause secondary infection and might be inhaled into the lungs where it also forms lesions and eventually death. **Note: we have to know that: Tropica & Mexicana cause cutaneous manifestation. All the above mentioned types are mainly superficial and continuous. Leishmania is superficial because it doesn t like core body temperatures. #Leishmania species that can survive core body temperatures include: L. donovani L. chagasi L. infantum The above mentioned species are more resistant to the cidal effects of the serum. In that case these parasites will involve tissues, specially tissues rich in macrophages like the spleen, bone marrow, liver, and others. The disease that these species cause is called visceral leishmaniasis ((causes enlargement of the spleen, enlargement of the liver, involvement of the bone marrow, and other effects)). The patient will feel ill; he will have fever, malaise, loss of weight, become anemic, and there will be an increased pigmentation of the skin. That is why it is also called Kala-azara or black fever. If not treated patients will die within a year! Diagnosis: in endemic areas you can suspect that the patient is infected by the apparent symptoms ((enlarged organs, anemia, weakness, and hyperpigmentation)). Biopsies from lesions are also useful. Infected tissues may be harder to biopsy since the risk of hemorrhaging is too great. Bone marrow biopsies from flat bones ((like the sternum and iliac crest)) are safe. We can also try to detect antibodies in the cases of visceral leishmaniasis. Treatment: pentavalent antimony compounds. Pentamidine 7 P a g e

8 8 P a g e February 10, 2013 [ MICROLOGY 1] Dr. Hassan Abu-Raghib