ProtozoaTaenia soliumTaenia solium, also called the pork tapeworm, is a cyclophyllid cestode in the family Taeniidae. It infects pigs and humans in Asia, Africa, the Philippines, Latin America, parts of Southern Europe, and pockets of North America.
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Pathogenesis
This infection is caused by ingestion of eggs shed in the feces of a human tapeworm carrier. Humans are infected either by ingestion of food contaminated with feces containing eggs, or by autoinfection. In the latter case, a human infected with adult T. solium can ingest eggs produced by that tapeworm, either through fecal contamination or, possibly, from proglottids carried into the stomach by reverse peristalsis. Once eggs are ingested, oncospheres hatch in the intestine, invade the intestinal wall, and migrate to striated muscles, as well as the brain, liver, and other tissues, where they develop into cysticerc.
Signs and SymptomsLarvae- T. solium Cysticercus cellulosae· Mainly develop in the subcutaneous tissues, but infections in both the Central Nervous System (C.N.S.) and ocular tissues are also very common.
· Infection of the C.N.S. may cause severe pain, paralysis, optical and/or psychic disturbances and epileptic convulsions, mainly due to mechanical pressure as the larvae develop. Later there may be loss of consciousness and even death.
· Infections involving the eye may give rise to discomfort, and can cause detachment of the retina.
Adult· A slight degree of mucosal inflammation.
· Constipation, epigastric pain and diarrhoea, are present.
· Very rarely there may be perforation of the intestinal wall, with subsequent peritonitis may occur.
· Autoinfection due to reverse-peristalsis resulting in cysticercosis, it being estimated that approximately 25% of cases of Cysticercus cellulosae infections in man being acquired by this route.
TreatmentInfection with T. solium adults is treated with niclosamide. If cysticercosis is the cause, it is important to wash one's hands before eating and to suppress vomiting if a patient may be infected with T. solium.
PreventionInfection may be prevented with proper disposal of human feces around pigs, cooking meat thoroughly, and/or freezing the meat at -10oC for 5 days.
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Taenia saginataThe beef tapeworm. The most common of the big tapeworms that parasitizes people, contracted from infected raw or rare beef. Can grow to be 12-25 feet (3.6-7.5 m) long in the human intestine. Also known as the African tapeworm.
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PathogenesisHumans are the only known definitive hosts for T. saginata. The life cycle begins with the ingestion of raw or undercooked beef containing T. saginata larvae. The larvae gets digested out of the beef in the human intestinal system. The worm then attaches on the intestinal mucosa of the upper small intestine. The tapeworm will digest food and grow longer. Mature tapeworms will release 10 single gravid proglottids daily via the feces or will spontaneous be released from the anus. Proglottids are motile and will shed eggs as it moves. These eggs (containing the oncosphere) can remain viable for several days to weeks in sewage, rivers, and pastures. The beef tapewrom can only develop in humans as adult worm derived from the cysticercus developed in beef. Eggs from ensuing adult worm develop only in cattle or other herbivores and cannot cause human cysticercosis.
Signs and Symptoms· Loss of appetite or feeling of fullness, nausea, vomiting, diarrhea.
· Vitamin deficiency due to excessive absorption of nutrients by the parasite
TreatmentNiclosamide, used to treat many different kinds of infections with trematodes and adult tapeworms, is the best drug.
PreventionProper disposal of feces and making sure that all meat has been cooked properly helps prevent the spread of disease. In Western societies, meat is inspected for parasites. Additionally, freezing the meat at -10oC for five days kills any worms and larvae.
http://www.path.cam.ac.uk http://www.answers.comEntamoeba histolytica
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Pathogenesis
· The trophozoite emerges from the ingested cyst (metacyst) after activation of the excystation process in the stomach and duodenum.
· The metacyst divides rapidly producing 4 amebulae, each of which divides again to produce 8 small trophozoites per infective cyst, they pass to the cecum and produce a population of lumen-dwelling trophozoites.
· The trophozoites multiply by binary fission.
Signs and Symptoms
· Symptoms are usually gastrointestinal including diarrhea, vomiting, abdominal pain or discomfort and fever.
· Symptoms take from a few days to a few weeks to develop and manifest themselves, but usually it is about two to four weeks.
· Most infected people are asymptomatic but this disease has the potential to make the sufferer dangerously ill, especially if there is any suggestion of immunocompromise.
Infections that sometimes last for years may be accompanied by
· no symptoms (in the majority of cases),
· vague gastrointestinal distress,
· dysentery (with blood and mucus).
Treatment
· Asyptomatic(cyst-passing) amebiasis can be treated with iodoquinol(Yodoxin), or diloxanide furoate (Furamide), or paramomycin (Humatin)
· As for symptomatic amebiasis, metronidazole is used even though it is mutagenic in bacteria.
· Mild to moderate intestinal disease, give metronidazole or tindzaole (Fasigyn)
· Severe intestinal disease, give regimen described above or give dehydroemetine
Prevention
· Ingested through contaminated water
· Flies incriminated in areas of fecal population
· Asymptomatic cyst passers are the main source if contamination
· Control measures consist of improving environmental contamination and food sanitation.
· Treatment of carriers is controversial, although it is agreed that they should be barred from food handling.
Giardia lamblia
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Pathogenesis
· Only common pathogenic protozoan found in the duodenum and jejunum of humans
· Cause giardiasis
· Usually only weakly pathogenic for humans
· Cysts may be found in large numbers in the stools of entirely asymptomatic persons
Signs and Symptoms
· Stools are watery, semisolid, greasy, bulkly, and foul-smelling t various times during the course of infection
· Malaise, weakness, weight loss, abdominal cramps, distention, and flatulence can occur.
· Immunosuppressed individuals are especially liable to massive infection with severe clinical manifestations.
· Symptoms may continue for long periods
Treatment
· Metronidazole will clear 90% of G lamblia infections.
· Oral quinacrine hydrochloric (atabrine) and furazolidone (Furoxone) are alternatives
· Tinidazole (Fasigyn) used for 1 day treatment is widely and effectively used
· Treatment may be repeated if necessary
Prevention
· Ingestion of fecally contaminated food or water is the main mode of transmission.
· Thus, reducing this contamination is the best method of prevention.
· Filtering or purifying drinking water (iodine or boiling) in endemic areas is important as is the washing of fruits and vegetables that may have been contaminated.
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Wuchereria Bancrofti
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Pathogenesis
· W. bancrofti carry out their life cycle in two hosts.
· Human beings serve as the definitive host and mosquitoes as their intermediate hosts.
· The adult parasites reside in the lymphatics.
· The first stage larvae are known as microfilariae.
· The microfilaria are present in the circulation.
· The microfilaria migrate between the deep and the peripheral circulation.
· During the day they are present in the deep veins and during the night the migrate to the peripheral circulation.
· Next, the worm is transferred into a vector; the most common vectors are the mosquito species: Culex, Anopheles, Aedes, and Mansonia.
· Inside their second host, it matures into motile larvae.
· When its current host feeds, and it is egested into the blood stream of its new human host.
· The larvae moves to the lymph nodes, predominantly in the legs and genital area, and develops into adult worm over the course of a year.
· By this time, an adult female can produce microfilariae itself
Signs and Symptoms
· The onset of symptoms is slow
· Incubation period of 3- 12 months in which there is no symptoms
· Acute symptomatic stage—some swelling of the extremities may occur and this may be accompanied by pain, weakness of arms and legs, headache, and insomnia
· Other early symptoms include recurrent filarial fever, lymphadenitis, and retrograde lymphangitis
· Chronic signs include:
– Hydrocele (collection of fluid in the scrotal sac) most common clinical condition
– Chyluria (chyle in urine—milky appearance)
– Elephantiasis of the limbs, breast and genitalia
Treatment
· Drug of choice: Ivermectin
· Albendazole
· Diethylcarbamazine (DEC) (Hetrazan)
– Eliminates microfilariae from the blood and also can kill adults.
· Use of single-dose regimens of all three reduce W bancrofti microfilaremia, antigenemia, and clinical manifestations
Prevention
· Protect yourself from mosquito bites in endemic areas
– Use insect repellent
– Mosquito nets
· Educate people in endemic areas
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Brugia Malayi
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Pathogenesis
· Infective The Brugia malayi parasites are found in Southeast Asia.
· Larvae are transmitted by infected biting arthropods during a blood meal.
· The larvae migrate to the appropriate site of the host's body, where they develop into microfilariae-producing adults.
· The adults dwell in various human tissues where they can live for several years. The agents of lymphatic filariasis reside in lymphatic vessels and lymph nodes.
· B. malayi dwells particularly in the lymphatics, as with Wuchereria bancrofti.
· The female worms produce microfilariae which circulate in the blood.
· The microfilariae infect mosquitoes.
· Inside the mosquito, the microfilariae develop in 1 to 2 weeks into infective filariform (third-stage) larvae.
· During a subsequent blood meal by the insect, the larvae infect the vertebrate host.
· They migrate to the lymphatics, where they develop into adults, a slow process than can require up to 18 months.
Signs and Symptoms
· Most of the signs and symptoms of filariasis are caused as a consequence of the adult worms living in the lymph system.
· Tissue damage caused by the worms restricts the normal flow of lymph fluid. This results in swelling, scarring, and infections.
· The legs and groin are most often affected.
Treatment
· Treatment consists of an annual single-dose of ivermectin and/or diethylcarbamazine (DEC).
· Albendazole is also effective in conjunction with either ivermectin or DEC
Prevention
· There is no vaccine for filariasis.
· Prevention centers on mass treatment with anti-filariasis drugs to prevent ingestion of larvae by mosquitoes, public health action to control mosquitoes, and individual action to avoid mosquito bites.
· To avoid being bitten by mosquitoes:
· If possible, stay inside between dusk and dark. This is when mosquitoes are most active in their search for food.
· When outside, wear long pants and long-sleeved shirts.
· Spray exposed skin with an insect repellent.
Plasmodium species
Plasmodium species are sporozoas that cause malaria in humans. It is transmitted by Anopheles mosquitoes. The four types of the plasmodium species are: P. falciparum, P. malariae, P.vivax and P. ovale. Of these types, P. falciparum is the most dangerous of these infections as P. falciparum malaria has the highest rates of complications and mortality. In addition, it accounts for 80% of all human malarial infections and 90% of the deaths. It is more prevalent in sub-Saharan Africa than in other regions of the world.
Pathogenesis
Exoerythrocytic Phase
Infection results from the bite of an infected female anopheles mosquito. Sporozoites liberated from the mosquito’s salivary glands rapidly (usually within 1 hr) enter hepatocytes in the liver. In there, they develop in two ways depending on the species of plasmodium:
· P. falciparum and P. malariae: parasites develop to a pre-erythrocytic schizont that eventually ruptures to release merozoites into the bloodstream à initiate erythrocytic infection in the peripheral blood
· P.vivax and P. ovale: some sporozoites develop into preerythrocytic schizonts while others lay dormant as hypnozoites. At a later time, the hypnozoites may become active, divide and form schizonts and merozoites à initiate erythrocytic infection in the peripheral blood.
Erythrocytic Phase
A merozoite released from a hepatic schizont invades an erythrocyte. Parasites in the red cells multiply in a species-characteristic fashion, breaking out of their host cells synchronously. Successive broods of merozoites appear at 48-hr intervals (P. vivax, P. ovale, P.falciparum) or every 72hrs (P. malariae).
The incubation period is includes the exoerythrocytic cycles (usually 20 and at least 1 or 2 exoerythrocytic cycles. Incubation period for P. falciparum and P. vivax is usually 10-15days, but it may be weeks or months. The incubation period of P. malariae averages about 28days.
Signs and Symptoms
General for all species
· An initial chill, lasting from 15mins to 1 hour
· Nausea, vomiting and headache
· Succeeding febrile stage, lasting several hours, is characterized by a spiking fever that will reach 40oC or more
· In the third stage (sweating), fever subsides.
In P.falciparum
· Splenomegaly
· Hepatomegly
· Normocytic anemia
· Periodicity for febrile episodes – 72hrs
· Pyrexia may last 8hrs or longer and may exceed 41°C
In P.vivax, P. malariae and P. ovale (Low-grade)
· Periodicity for febrile episodes – 48hrs
Plasmodium falciparum Plasmodium vivax
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Treatment
· Chloroquine is the drug of choice for treatment of all susceptible forms of malaria during acute attack.
· For falciparum malaria coma, use parenteral quinine dihydrochloride or quinidine until oral therapy is possible.
· Primaquine therapy should follow treatment for clinical malaria. (low course to be given to G6PD deficient individuals owing to the possibility of hemolytic anemia)
· For drug-resistant strains of P. falciparum, treat with quinine sulfate plus a single dose of pyrimethamine-sulfadoxine, with quinine plus clindamycin/doxycycline/tetracycline.
· For chloroquine-resistant P. falciparum malaria, alternatives used: mefloquine and halofantrine
Prevention
· Have personal protection (e.g. protective-clothing with long sleeves and trousers, repellents, netting around sleeping area)
· Suppressive prophylaxis with chloroquine phosphate or amodiaquine .
Fungi
Sporothrix schenckii
Pathogenesis
- Cutaneous or skin sporotrichosis
This is the most common form of this disease. Symptoms of this form include nodular lesions or bumps in the skin, at the point of entry and also along lymph nodes and vessels. The lesion starts off small and painless, and ranges in color from pink to purple. Left untreated, the lesion becomes larger and looks similar to a boil and more lesions will appear, until a chronic ulcer develops.
Usually, cutaneous sporotrichosis lesions occur in the finger, hand, and arm.
- Pulmonary sporotrichosis
This rare form of the disease occurs when S. schenckii spores are inhaled. Symptoms of pulmonary sporotrichosis include productive coughing, nodules and cavitations of the lungs, fibrosis, and swollen hilar lymph nodes. Patients with this form of sporotrichosis are prone to develop tuberculosis and pneumonia
- Disseminated sporotrichosis
When the infection spreads from the primary site to secondary sites in the body, the disease develops into a rare and critical form called disseminated sporotrichosis. The infection can spread to joints and bones (called osteoarticular sporotrichosis) as well as the central nervous system and the brain (called sporotrichosis meningitis).
Signs and symptoms
- Small and non-tender nodules are visible under the skin during the early stages of infection
- The nodules will then slowly enlarge and ulcerate
- Dark nodules would eventually emerge along the lymphatic channel that drains the infected area
Treatment
- Itraconazole and fluconazole are antifungal drugs which are usually used for treatment
- Amphotericin B can be used to treat Sporotrichosis via intravenous means
Epidemiology
- Sporothrix schenckii is naturally found in soil, hay, sphagnum moss, and plants
- Occurs worldwide (more common in tropical and subtropical America) in close association with plants (living or decomposing)
- Usually affects agricultural workers and those working in similar occupations as they handle with plants and trees
Aspergillus niger, Aspergillus flavus, Aspergillus fumigatus
Pathogenesis
· In immunopromised patients, the alveolar macrophages in the lung will engulf and destroy the conidia less effectively.
· This causes the conidia in the lung to swell and germinate, subsequently producing hyphae which invades the cavities or blood vessels.
· Eventually they would spread to the other organs of the body and thus allow the Aspergilli to proliferate in cavities within the lungs
· Aspergilloma (fungus balls) where Aspergilli grow in cavities within the lungs caused by Tuberculosis and produce aspergilloma
· Allergic bronchopulmonary aspergillosis (asthma) is caused by the infection of bronchi by Aspergillus sp
· Infections of the nasal sinuses, eyes, ears, skins & nails
Signs and symptoms
· Fever
· Cough
· Malaise
· Weight Loss
· Chest pain
· Dypsnea
· Vomitting
· Chills
· Difficulty in breathing
· May develop permanent lung scarring
Treatment
· Steroid can be consumed for allergic bronchopulmonary aspergillosis
· Amphotericin B or itraconazole can be used to treat aspergillosis
· Rapid adminstration of amphotericin B or voriconazole(native or lipid formulation) for invasive aspergillosis
· No vaccine or prophylactic drug available for the prevention of Aspergillus
Epidemiology
· Aspergillus sp is found in soil and can be transmitted through the inhalation of airborne spores
· Aspergillus flavus is seedborne and soilborne
· Active in high humidity (90-98%) and low soil moisture.
· Usually affects agricultural workers and those working in similar occupations as they handle with plants and trees
http://staff.vbi.vt.edu/pathport/pathinfo/pathogens/Aspergillus_flavus_Info.shtml
Trichophyton rubrum and Trichophyton metagrophytes
Pathogenesis
Both Trichophyton rubrum (T. rubrum) and Trichophyton metagrophytes (T. metagrophytes) invades the superficial keratin of the skin, and remains in this layer. Infection occurs from here. Proteins on the both the fungi cell wall inhibits the body immune response to the infection allowing the Fungi to thrive. T .rubrum cell wall proteins also reduce the skin growth, making the skin layer thin. These fungi both can cause athlete’s foot with red blisters and chronic scaling of the foot skin.
T.rubrum http://www.doctorfungus.comngus.com
T.mentagrophytes www.doctorfungus.com
Signs and Symptoms
· Dry scaly or white and soggy skin between the spaces of toes and fingers are a sign of fungi infection. This area can also feel itchy or have a burning or painful sensation.
· If left untreated, this may lead to a chronic infection that causes itching and mild to profuse scaling on the surface skin of the foot.
· If treatment is still not administered, this may lead to a severe case of athlete’s foot with red tender blisters appearing on the sole or the upper surface of the foot.
Prevention
Keep foot dry and airy by:
ü Avoid wearing nylon and acrylic socks but wear 100% cotton or wool socks
ü Wash and dry between your toes properly
ü Go barefoot or wear sandals to air feet in warm humid weather
· Practice good personal hygiene by:
ü Avoiding sharing towels, socks and shoes
ü Do not walk barefoot in public showers
Treatment
· If infection is found between toes and fingers, apply topical agents such as Miconazole for at least 2 to 4 weeks
· Chronic scaling can be treated with orally administered Griseofulvin
· Acute athlete’s foot can be treated using Burows solution, potassium permanganate or sliver nitrate.
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· Epidermophyton floccosum
Pathogenesis
Epidermophyton floccosum (E. floccosum) is the one of the common cause of skin and nail fungal infection in normal healthy individuals. The infection is restricted to the nonliving cornified layers of epidermis since it lacks the ability to penetrate the viable tissues of a healthy host. The infection is only restricted to keratinized (tough layers) of tissues. E. floccosum is a common cause of athlete's foot, fungal infection of the groin, toenails or the fingernails and ring worms.
Signs and Symptoms
1. Yellow, brittle, thickened and crumbly nails and leads to nails being damaged and exposure of the nail bed.
2. Tenderness and soreness of the skin around the groin region.
3. A white material slowly spreads beneath the nail surface.
Prevention
· Surgical removal of the nails to stop and prevent further infection
· Trim nails short and wipe feet dry after bathing. The application of antifungal powder also limits the fungal infection from occurring
· Wash and sun dry shoes regularly.
Treatment
· To treat the infection and to prevent any chances of relapse of the infection from occurring, antifungal drugs such as traconazole or terbinafine must be taken for a few months.
Microsporum canis (ringworm of scalp)
Pathogenesis
· Source of infection is an infected animal
· Can infect the skins and hair, caused Tinea captitis (scalp infections)
· Infections begin with hyphal invasions (contact with infected animals)of the skin of the scalp, with subsequent spread down the keratinized wall of the hair follicles
· Infection of the hair takes place just above the hair root
· The hyphae grow downward on the onoliving portion of the hair and at the same rate as the hair grows upward
· The infection produces dull gray, circulart patches of alopecia, scaling, and itching
· As the hair grows out of the follicles, the hyphae of M. species produce a chain of spores that form a sheath around the hair shaft (ectothrix).
· Theses spores impart a greenish to slivery fluorescence when the hairs are examined under Wood’s light (365nm).
· May also induce a severe inflammatory and hypersensitivity reactions called kerion
Signs and symptoms
· scalp will show hair loss or give a stubbly appearance
· slightly scaly but with little or no irritation skin
· ringworm may be present on the face or other parts of the body.
· a 6 to 9cm wide lesion will appear that may develop into a large rash.
· A kerion (a swollen mass discharging pus) will appear on the scalp, in severe cases. It may become inflamed and fill with fluid or pus, and may also be quite painful.
· Develop severe alopecia (baldness) and at this stage the scalp will often become infected further with Staphylococci bacteria.
· Swollen and tender lymph nodes of the neck
· In rare cases, there may also be a fever.
Prevention/ Treatment
· minimise direct contact with animals showing symptoms of ringworm, such as scaly, patchy skin.
· Oral antifungal medicine. However, if a large kerion has formed, the antifungal treatment may be supplemented with corticosteroids for a short period of time.
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Malassezia furfur
Causative agent of Pityriasis versicolor, seborrhoeic dermatitis and dandruff.
Pathogenesis
· naturally found on the skin surfaces of many animals and humans.
· the fungus requires fat to grow, hence it is most commonly in areas with many sebaceous glands: on the scalp, face, and upper part of the body.
· When the fungus grows too rapidly, the natural renewal of cells is disturbed and dandruff appears with itching (a similar process may also occur with other fungi or bacteria).
Signs and symptoms
· Discrete, serpentine, hyper or hypopigmented maculae occur in skin, usually on the chest, upper back, arms or abdomen.
· Lesion occurs as macular patches of discoloured skin that may enlarge and coalesce, but scaling, inflammation and irritation are minimal.
Prevention/ Treatment
· treated with topical or oral antifungal agents. Seborrhoeic dermatitis may also treated with topical steroids
· use topical imidazole in a solution or lathering preparation for pityriasis versicolor.
· Ketoconazole shampoo can be used
· . In severe cases with extensive lesions, or in cases with lesions resistant to topical treatment or in cases of frequent relapse oral therapy with either ketoconazole [400 mg single dose or 200 mg/day for 5-10 days] or itraconazole [200 mg/day for 5-7 days] is usually effective.
http://www.mycology.adelaide.edu.au/
