Parasit Ology
Parasit Ology
Introduction to Parasitology
a. Commensalism - is a form of symbiotic relationship in which two species live together and one species benefits from the other without
harming or benefitting the other.
b. Mutualism – is a symbiotic relationship in which two organisms mutually benefit each other.
c. Parasitism – is a symbiotic relationship where one party or symbiont benefits to the detriment of the other.
a. Ectoparasites – those that lives outside the body. Invasion of the body by ectoparasites is called infestation.
b. Endoparasites – parasites that live inside of the body of the host. Invasion is called infection and is the result of entry and multiplication of the
parasite within the host.
a. Permanent parasites – those that remain in a host from early life to maturity.
b. Intermittent parasites – parasites that simply visit the host during feeding time
c. Incidental parasites – parasites that occur on an unusual host
d. Transitory parasites – parasites whose larva develops in a host while the adult is free-living
e. Erratic parasites – those that becomes fixed in unusual organ different from that which is ordinarily parasitized.
Host – organisms that harbor the parasite and provide nourishment to the parasite.
a. Definitive hosts – hosts that harbor the adult stage of the parasite or where the sexual stage phase of the life cycle of the parasite occurs.
b. Intermediate hosts – those that harbors the larval or asexual stage of the parasite or where asexual phase of the life cycle of the parasite
occurs.
c. Reservoir hosts – vertebrate hosts which harbor the parasite and may act as a source of infection in man.
d. Paratenic hosts – those that serve as a means of transport for the parasite so that the infective stage of a certain parasite may reach its final
hosts.
Classification of parasites
Protozoa – consists of single cell-like microorganisms that are spherical to oval or elongated.
Mode of transmission
a. Person-to-person spread or through ingestion of contaminated food and water – intestinal and luminal
b. Direct contact or through vectors – blood and tissue protozoa
Trophozoite – pathogenic stage (stage of the parasite that is responsible for disease production)
Protozoal Diseases
1. Entamoeba histolytica – intestinal protozoan. The organism can be acquired by ingestion of cysts in contaminated food and water primarily
by the fecal-oral route. There is no animal reservoir.
- the ingested cysts differentiate into trophozoites in the ileum, then goes to colonize the cecum and colon. The trophozoites may then
converted to cysts and are passed out with the feces.
- Trophozoites secretes enzymes that cause local necrosis producing the typical “flask-shaped” ulcer associated with the parasite. Invasion
of the portal circulation may occur, leading to the development of abscess in the liver.
Amebiasis
a. Acute intestinal amebiasis – presents as dysentery (bloody, mucus-containing diarrhea) accompanied by lower abdominal discomfort,
flatulence, and tenesmus. Chronic infection may occur, with symptoms such as occasional diarrhea, weight loss, and fatigue. In some
patients, a granulomatous lesion called ameboma may form in the cecum or in the rectosigmoid area of the colon.
b. Amebic abscess of the liver is characterized by right upper quadrant pain, weight loss, fever, and a tender, enlarged liver. The abscess has a
characteristic “anchovy – sauce” appearance. Abscesses found on the right lobe of the liver may penetrate the diaphragm and cause lung
disease.
Laboratory diagnosis
- Diagnosis of intestinal amebiasis rests on finding of trophozoites in diarrheal stools or cysts in formed stool. Trophozoites
characteristically contain ingested red blood cells. Diarrheal stools should be examined within one-hour of collection to see the motility of
the trophozoite.
Treatment
- Metronidazole or tinidazole
Prevention
Giardiasis
- Characterized by a non-bloody, foul-smelling diarrhea accompanied by nausea, anorexia, flatulence, and abdominal cramps persisting for
weeks or months.
- Malabsorption of fats may lead to the presence of fat in the stool (steatorrhea) of the patients.
- The patient is afebrile.
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Laboratory diagnosis
- The diagnosis is made by finding trophozoites or cysts (or both) in diarrheal stools. In the stools of asymptomatic carriers, only cysts is
seen. If microscopic examination is negative, the string test may be done, which consists of swallowing a weighted piece of string until it
reaches the duodenum. The trophozoites adhere to the string and can be visualized after withdrawal of the string.
Treatment
Prevention
3. Trichomonas vaginalis – a pear-shaped organism with a central nucleus and four anterior flagella.
- Exists only in the trophozoite form.
- Transmitted mainly by sexual contact
- Located primarily in the vagina and the prostrate.
Trichomoniasis
- Infection in women leads to vaginitis with a watery, foul-smelling, greenish vaginal discharge accompanied by itching (pruritus) and
burning sensation. The cervix is vvery red, with small, punctuate hemorrhages giving rise to a “strawberry cervix”
- Infection in men is usually asymptomatic. Some may manifest with symptoms of urethritis or prostatitis.
Laboratory diagnosis
- Diagnosis is through visualization of the characteristics trophozoites in a wet mount of vaginal or prostatic secretions.
4. Toxoplasma gondii – The definitive host of the parasite is the domestic cat and other felines while humans and other mammals ate the
intermediate host.
- Infection in humans begins with ingestion of cysts in undercooked meat (lamb and pork) or from contact with cat feces.
- In the small intestine, these cysts rupture into trophozoites.
- The parasite enters the host cells in the brains, muscle, and other tissues, where they develop into cysts.
- Transplacental transmission from an infected mother to the fetus can also occur.
- Congenital infection of the fetus occurs only when the mother is infected during pregnancy.
Toxoplasmosis
Laboratory diagnosis
- Acute and congenital infection involves immunofluorescence assay for IgM antibodies
- Microscopic examination of Giemsa-stained preparation shows crescent-shaped trophozoites during acute infection.
Treatment
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- Congenital toxoplasmosis and disseminated disease in immunocompromised patients is treated with a combination of sulfadiazine and
pyrimethamine
Prevention
5. Plasmodium spp. – the main mode of transmission is the bite of the female anopheles mosquito vector.
- Transmission across the placenta, in blood transfusions, and by intravenous drug abuse also occurs.
a. Plasmodium vivax
b. Plasmodium malariae
c. Plasmodium ovale
d. Plasmodium falciparum
- Most of the pathologic findings result from the destruction of red blood cells. P. falciparum infects both young and old red blood cells,
and so causes the most severe infection. P. vivax and P. ovale infects young blood cells, while P. malariae infects primarily the old red
blood cells.
Malaria
- Paroxysms of malaria are divided into three stages: cold stage, hot stage, and the sweating stage.
- It presents with an abrupt onset of chills accompanied by headache, myalgias, and arthralgias. Spiking fever follows, reaching up to 41
degrees Celsius, accompanied by shaking chills, nausea, vomiting, and abdominal pain, followed by drenching sweats. Splenomegaly is
often present and anemia is prominent.
- Infection with P. falciparum is potentially life-threatening as a result of extensive brain (cerebral malaria) and kidney damage.
- The dark color urine due to kidney damage gave rise to the term “black fever”
- The mosquitoes usually bite from dusk to dawn
Laboratory diagnosis
Treatment
Prevention
Cestodes
- Or TAPEWORMS are flat worms that consists of a head or scolex and a rounded portion that contains specialized structures for
attachment called hooks, suckers, or sucking grooves.
- All cestodes are hermaphroditic.
- Infection in humans is usually acquired through ingestion of the undercooked or raw flesh of the intermediate host containing the
infective larvae.
1. Taenia saginata (beef tapeworm) - acquired by ingestion of raw or improperly cooked beef containing the infective larva. The larvae
mature into adult worms (pathogenic stage) in the small intestines in about three months, and may attain a length up to 10 meters. The
gravid proglottids lay eggs, which are excreted in the feces, which is ingested by the cattle.
- Humans serves as the definitive hosts, while cattle are the intermediate hosts.
Taeniasis
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Laboratory diagnosis
- Examination of the stool with demonstration of either proglottids or eggs can help establish the diagnosis.
Treatment
Prevention
- Proper waste disposal and adequate cooking of beef constitute the main preventive measures
- Freezing of meat at -20 degrees Celsius for 10 days may kill the encysted larvae.
2. Taenia solium (pork tapeworm) - ingestion of improperly cooked or raw pork meat containing the infective larva. Can also occur with
ingestion of food or water contaminated with human feces that contains the worm eggs.
- The larva is found in the intermediate host (pig) and mature into adult worms in the small intestines of humans. The adult worms may
attain a length of 5 meters.
- Ingested worm eggs hatch in the small intestines, burrow through the wall into a blood vessel, and disseminate to various organs,
especially the eyes, brain, skeletal muscle where they encysts to form larva.
- Disease due to adult worm is usually asymptomatic, although anorexia and diarrhea may occur in some.
- The most common area of involvement for cysticercosis is the skeletal muscle, patient may complain of muscle pain.
- Cysticercosis in the brain (neurocysticercosis) is the most feared and most severe involvement. It commonly presents with seizures,
headache, and vomiting.
Laboratory diagnosis
Treatment
3. Diphyllobothrium latum (fish tapeworm) – longest of the tapeworms, reaching a length of about 13 meters.
- Infection occurs after ingestion of improperly cooked or raw fish containing the infective larvae. These develop into adult worms in the
small intestines of humans.
- The eggs passed out with feces needs to be deposited to in fresh water for the life cycle of the parasite to continue.
- Parasite may compete with the host for vitamin B12 leading to deficiency of the vitamin.
Diphyllobothriasis
- Most patient are asymptomatic while others may complain of abdominal discomfort and diarrhea. Deficiency of vitamin B12 may occur,
leading to development of megaloblastic anemia.
Laboratory diagnosis
Prevention
Trematodes
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1. Schistosoma spp. – they are obligate intravascular parasites and are not found in other tissues.
- The infective stage is the skin – penetrating cercaria.
- Humans are infected when the free-swimming fork-tailed penetrate the skin. Those that enter the superior mesenteric artery pass into
the portal circulation, where they mature into adult flukes.
a. Schistosoma mansoni
b. Schistosoma japonicum
c. Schistosoma haematobium
- S. mansoni and S. haematobium migrate against portal flow and reside in the mesenteric venules
- S. haematobium reach the bladder veins through the venous plexus between the rectum and the urinary bladder.
- The eggs are excreted in the stools or urine and must enter fresh water to hatch.
- Most of the findings are caused by presence of eggs in the liver, spleen, or wall of the gut or bladder. Eggs in the liver induce
granulomas, which lead to fibrosis, hepatomegaly, and portal hypertension.
Schistosomiasis (bilharziasis)
- Early infection is characterized by pruritic papules seen at the site of entry of the parasite. This is called “swimmer’s itch”, “clam-digger’s
itch”
- Followed after 2-3 weeks by fever, chills, diarrhea, lymphadenopathy, and in the case of S. japonicum, hepatosplenomegaly.
- Chronic infection can cause significant morbidity and mortality. In patients with S. mansoni and S. japonicum infection, gastrointestinal
hemorrhage, hepatomegaly, and massive splenomegaly can occur.
- S. japonicum infection known as “Katayama’s disease” can cause hepatic dysfunction, leading to portal hypertension, patients are at
greater risk for developing liver cancer. The most common cause of death is bleeding from ruptured esophageal varices.
Laboratory diagnosis
- Diagnosis rests on finding the characteristic ova in the feces or urine. S. mansoni eggs have a large lateral spine while S. japonicum have
rudimentary spines. The eggs of S. haematobium have large terminal spines.
Treatment
Prevention
- Control of transmission through, snail control, health education, and provision of satisfactory facilities and water supply
- Control of disease
- Chemotherapy using praziquantel is the main thrust of the Philippine program for schistosomiasis.
- Swimming in the areas of endemic infection should be avoided.
2. Clonorchis sinensis (Asian liver fluke) – infection is obtained by ingestion of undercooked or raw freshwater fish containing the larvae.
The larvae encyst in the duodenum, enter the biliary ducts, and differentiate into adults. The adults produce eggs, which are excreted in the
feces. Once in freshwater environment, the eggs are ingested by snails, then hatch into larvae. The larvae are released from the snails, under
the scales of certain freshwater fish, which are eaten by humans.
Clonorchiasis
- Patients with heavy worm burden may manifest with upper abdominal pain, anorexia, hepatomegaly, and eosinophilia.
Laboratory diagnosis
- Stool examination
Treatment
- Praziquantel
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Prevention
3. Fasciola hepatica (sheep liver fluke) – human infection occurs after ingestion of metacercariae (infective stage) encysted on edible
aquatic plants such as kangkong and watercress or by drinking water with floating metacercariae.
- Upon ingestion the metacercariae excyst in the duodenum or jejunum, liberating the young flukes, which wander over the viscera until
they rich the liver capsule. The parasite then burrows through the liver parenchyma until it finally enters the bile ducts, where they attain
sexual maturity.
- The adult worm lives in the biliary passages of the liver. Immature eggs are carries by the bile into the intestine and are subsequently
excreted with feces. The eggs mature in water and infect the first intermediate host.
Fascioliasis
- Migration of the larval worm through the liver can produce irritation of the organ, manifesting as tenderness and hepatomegaly.
Characteristic manifestations include right upper quadrant pain, chills, and fever, with marked eosinophilia.
- As the worms’ lodge in the bile ducts, hepatitis may develop with biliary obstruction.
Laboratory diagnosis
- Stool examination
Treatment
Prevention
4. Paragonimus westermani (lung fluke) – infection is obtained by ingestion of undercooked or raw crab meat (or crayfish) that contains
the larvae. The larva excysts in the small intestine, penetrate the intestinal wall and migrate through the diaphragm into the lung
parenchyma, where they attain maturity.
- The adults produce worms, which enter the bronchioles and are then coughed up or swallowed.
- Eggs in either sputum or feces that reach freshwater hatch and enter the snail, where they differentiate into free-swimming cercariae.
The cercariae leave the snail and encysts in freshwater crabs, which are then eaten by humans.
- The early stages of infection is asymptomatic, if symptomatic, the main symptom is chronic cough that produces bloody sputum with a
foul, fishy odor, most pronounced in the morning. Chest pain and dyspnea are also frequent symptoms. The disease can resemble
tuberculosis.
Laboratory diagnosis
Treatment
Prevention
5. Fasciolopsis buski (intestinal fluke) – humans are infected by eating raw or inadequate cooked aquatic vegetation that carries the
infective stage. These excysts in the duodenum and attaches onto the intestinal wall, where they attain maturity.
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- Eggs are released together with feces into water, where they hatch and infect the snail.
Fascioliopsiasis
- Most infections are asymptomatic, but ulceration, abcess formation,and hemorrhage can occur.
- Intoxication results from absorption of worm metabolites by the host, leading to allergic symptoms, such as edema of the face,
abdominal wall and lower limbs.
Treatment
- Praziquantel
Prevention
Nematodes
- Nemathelminthes or Roundworm
- Unsegmented, bilaterally symmetrical worms with cylindrical bodies that are elongated.
- Members of this group of parasites have a complete digestive tract, including a mouth and an anus.
- The body covering is called cuticle.
- Female worms are larger than the male worm
- Medically important nematodes are divided into groups based on their primary location in the body.
b. Tissue nematodes – these are called the “filarial” worms because they produce motile embryos called microfilariae in the
blood and tissue fluids. These are transmitted by the bite of the arthropod vectors.
Intestinal Nematodes
Ascariasis
- During migration to the lungs, the larvae may induce allergic reactions, manifesting as asthmatic attacks accompanied by
eosinophilia (Loeffler’s syndrome).
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- Pneumonia may occur due to the penetration of the lung capillaries by the larvae as they enter the alveoli.
- Heavy worm burden give rise to symptoms such as abdominal tenderness, fever, distention and vomiting.
- Complications of the disease includes the following:
a. Obstruction to the appendix
b. Perforation of the intestines leading to peritonitis with secondary bacterial infection
c. Bowel obstruction
Laboratory diagnosis
- Stool examination
- Adult worms occasionally pass with the feces
- Sputum examination
Treatment
- Mebendazole
- Albendazole
- Pyrantel pamoate
Prevention
Enterobiasis (oxyuriasis)
Laboratory diagnosis
Treatment
Prevention
3. Trichuris trichiura (whipworm) – obtained through ingestion of the embryonated eggs in food or water contaminated by
human feces.
- The eggs hatch in the small intestine, differentiate into larvae and immature adults migrates to the colon for maturation and
mating. Thousands of eggs are produced every day and are then passed out in the feces.
- The eggs form embryos in warm, moist soil.
Trichuriasis
– heavy infection may cause abdominal pain and distention, bloody diarrhea, weakness and weight loss.
- Appendicitis resulting from worms filling up the lumen of the appendix may occur.
Laboratory diagnosis
- Diagnosis is confirmed by finding the typical barrel-shaped eggs with a plug at each end in the stool.
Treatment
- Mebendazole
Prevention
- Health education
- Proper sanitation
- Good personal hygiene
- Avoidance of use of human feces as fertilizer
4. Ancylostoma duodenale (old world hookworm) and Necator americanus (new world hook worm) – occurs after
penetration of the skin by the filariform larvae found in moist soil.
- The feet or legs are the usual sites of penetration.
- After penetration, the larvae are carried by the blood to the lungs, migrate to the alveoli, pass up to the bronchi and trachea,
swallowed to the small intestines where they develop into adult worms and attaches to the walls either by cutting plates
(Necator) or teeth (ancylostoma).
- The adult worms feed on blood from the capillaries of the intestinal villi. The female worms lay thousands of eggs each day
which are passed in the feces.
- The major damage to the host is due to blood loss at the site of attachment in the small intestines. Irritation of the skin at the
site of penetration is also seen, as well as inflammatory reaction in the lungs during larval migration.
Hookworm infection
– penetarion of the skin by the infective larvae produces a pruritic papule or vesicle called “ground itch”.
- Pneumonia with eosinophilia can occur during larval migration to the lungs.
- The presence of adult worms in the small intestines can produce the symptoms of nausea, vomiting, and diarrhea.
Laboratory diagnosis
Treatment
Prevention
- Education
- Improved sanitation
- Proper disposal of human feces
- Wearing of shoes or any protective foot wear
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5. Strongyloides stercoralis (threadworm) - different from other intestinal roundworms from having two distinct life cycles
– one within the host and the other free-living in the soil.
- In humans’ infection begins with skin penetration by the filariform larvae, usually on the feet.
- The adult worms form in the small intestines and enters the mucosa and produce eggs. Some are passed in the feces while
others penetrate the wall of the intestines directly without leaving the host.
- Larvae that are passed in the feces and that enter warm, moist soil mature into female and male worms. Several cycles occur
before filariform larvae are formed, which then penetrate another host and initiate the parasitic cycle in humans.
- Adult female worms in the wall of the small intestines can cause inflammation, resulting in diarrhea.
- In autoinfection, the penetrating larvae may cause significant damage to the intestinal mucosa, which can lead to secondary
bacterial infection and sepsis.
– heavy worm burden can involve the biliary and pancreatic ducts, the entire small intestine, and the colon. Manifestations may
include epigastric pain and tenderness, vomiting, watery diarrhea, and malabsorption. Symptoms mimicking peptic ulcer and
accompanied by eosinophilia strongly suggest infection of the parasite.
Laboratory diagnosis
- Collecting samples from three stools, one per day for three days, is recommended, because the larvae may occur in showers,
with many presents in one day and few or none the next.
Treatment
Prevention
- Proper education
- Proper sanitation
- Sewage disposal
- Wearing of shoes
- Prompt treatment
6. Capillaria philippinensis – first described in the Philippines in 1963, when the first human case died from the infection. An
epidemic occurred in 1967 and 1968 which led to the death of almost 100 individuals.
- The infection is obtained by ingestion of undercooked or raw freshwater fish called bagsit that contains the infective larvae.
- The larvae mature in the small intestines and eggs are passed in feces where the eggs embryonate in soil or water. Once in
water, the embryonated eggs are ingested by the fish, where they grow into infective larvae.
- The parasites produce micro-ulcers in the intestinal tissues.
- The ulcerative and degenerative lesions in the intestinal mucosa account for malabsorption of fluids, proteins, and electrolytes.
Intestinal capillariasis
- The disease is characterized by abdominal pain, chronic diarrhea and a gurgling stomach (borborygmus). Due to chronic
diarrhea, patients develop significant weight loss, which is aggravated by the accompanying anorexia, nausea, and vomiting.
Malabsorption of fat and sugars, severe protein-losing enteropathy and low electrolyte levels.
Laboratory diagnosis
- Stool examination
Treatment
- Patients with severe infection having electrolyte loss and malabsorption must be managed with electrolyte replacement and a
high-protein diet.
- Albendazole is the drug of choice
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Prevention
1. Wuchereria bancrofti (Bancrofti’s filarial worm) and Brugia malayi (Malayan filarial worm) – both are mosquito –
borne parasites found in the lymphatics of humans.
- Humans are infected when the female mosquito, especially the Anopheles and Culex species, deposits the infected larvae on
the skin while biting.
- B. malayi is also found in animals, which serve as reservoir hosts.
- The larvae penetrate the skin, enter the lymph node,and after about one year, mature into adults that produce microfilariae.
These microfilariae circulate in the blood, especially at night (nocturnal periodicity), and are ingested by biting mosquitoes.
Humans are the only definitive hosts.
- The manifestation of filariasis is due to the obstruction of the lymphatic vessels by the adult worms, causing edema. These
adults may be living, dead or degenerating. Microfilariae cause less severe pathology.
Filariasis (elephantiasis)
b. Acute stage (Adenolymphangitis) – marked by fever, with inflammation of the lymph glands (lymphadenitis), particularly of
the male genital organs (usually due to Wuchereria) and of the extremities (usually due to Brugia). In female, breast
involvement may be seen. Recurrent attacks are characterized by epididymitis, orchitis, retrograde lymphangitis of the lower
extremities, and localized inflammation of the arms and legs.
c. Chronic – develops slowly after several years of infection. Manifestations include chronic edema and repeated acute
inflammatory episodes. Gradually, the obstruction leads to edema and fibrosis of the legs and genitalia, especially the
scrotum. Over a period of years, the enlarged parts harden, with loss of skin elasticity and fibrosis, producing elephantiasis.
Laboratory diagnosis
Treatment
Prevention
- A recommendation by the WHO Division of Control of Tropical Diseases involves the development of safe, effective, well-
tolerated, single-dose annual microfilaricidal drug treatments, especially in endemic areas.
- Use of mosquito nets and repellants
- Use of insecticides to control the mosquito vectors
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1. Staphylococcus aureus – is a Gram-positive coccus in grapelike clusters. It is found in the skin and nasopharynx.
The organism produces enzymes and toxins responsible for its pathogenicity and also through direct invasion
and destruction of tissues.
Mode of transmission
- Skin infections are transmitted through direct contact with a person having purulent lesions, from hands of
healthcare or hospital workers, and through fomites like bed linens and contaminated clothing.
Clinical findings
Laboratory diagnosis
2. Staphylococcus epidermidis – part of the normal flora of the skin and is commonly associated with “stitch
abscess”, UTI, and endocarditis. It also causes infections in individuals with prosthetic devices.
3. Streptococcus pyogenes – Gram – positive cocci, that produces enzymes and toxins responsible for the
pathogenesis of infections.
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Mode of Transmission
Clinical findings
a. Pyoderma (impetigo) – purulent skin infection that is localized, commonly involving the face and the upper and
lower extremities. The vesicles rupture and form a honey-colored crust.
b. Erysipelas (St. Anthony’s fire) – patients manifest localized raised areas as erythema and warmth. It is grossly
distinct from normal skin.
c. Cellulitis – the infection involves the skin and subcutaneous tissue, and, unlike erysipelas, the infected and the
normal skin are not clearly differentiated. It is also manifested as local inflammation with systemic signs.
d. Necrotizing fasciitis – “flesh-eating” that involves the deep subcutaneous tissue, then spreads to the fascia, then
the muscle and fat. It may become systemic and cause multi-organ failure, leading to death.
Laboratory diagnosis
Mode of transmission
Clinical findings
- Associated with colonization of burn wounds and characterized by a blue-green pus that exudes a sweet grape-
like odor.
Laboratory diagnosis
- Culture shows flat colonies with green pigmentation and a characteristic sweet, grape-like odor.
5. Clostridium perfringens – Gram – positive bacillus that is anaerobic and capable of producing endospore.
Mode of transmission
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Clinical findings
- Causes soft tissue infections like cellulitis, suppurative myositis and myonecrosis (gas gangrene)
- Gas gangrene is a life-threatening infection following trauma or surgery and is characterized by massive tissue
necrosis with gas formation, shock, renal failure, and death within 2 days of onset.
Laboratory diagnosis
- Microscopic detection of Gram – positive bacilli and culture under anaerobic conditions
- Surgical wound debridement and high – dose penicillin therapy are the main approaches to the management of
the disease.
6. Bacillus anthracis – are Gram – positive bacilli, aerobic, spore forming, encapsulated, arranged in long chains,
giving them the characteristic “bamboo fishing rod” or “medusa head” appearance.
Mode of transmission
- Through break in the skin from either the soil or infected animal products.
Clinical findings
- Cutaneous anthrax is the most common form, characterized by painless papules at the site of inoculation that
becomes ulcerative, and later develops into necrotic eschars.
Laboratory diagnosis
Fungal Infection
A. Superficial mycoses
1. Tinea versicolor (pityriasis versicolor) – caused by the normal flora of the body known as Malassezia furfur
which the skin is particularly rich in sebaceous glands where lesions develop. Lesions are discrete hypo – or
hyperpigmented macules that are scaly and presenting with a dry, chalky appearance.
Laboratory diagnosis
Treatment
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- Application of agents containing selenium disulfide or salicylic acid and topical antifungal drugs like
ketoconazole.
2. Tinea nigra – infection is caused by fungus that produces melanin known as Exophiala werneckii. The lesions
involve the palms and soles and are described as gray-to-black, well-demarcated macules.
Laboratory diagnosis
- Direct microscopic examination of skin scrapings with potassium hydroxide and culture using Sabouraud’s
dextrose agar medium.
Treatment
- Application of agents containing selenium disulfide or salicylic acid and topical antifungal drugs like
ketoconazole.
- The infections are referred to as tinea or ringworm where the names reflect the anatomical sites involved:
- Specimens for diagnosis are skin or nail scrapings or hair cuttings from the affected areas.
- Diagnosis is based on the clinical appearance of the lesions, direct microscopic examination and culture.
- Treatment involves administration of antifungal drugs like azoles (miconazole, clotrimazole, econazole)
C. Subcutaneous mycosis
- The infection initially involves the deeper layers of the dermis and subcutaneous tissue and then later, the
bones.
- The mode of transmission is through traumatic inoculation into the skin.
- The infection is relatively rare.
Viral Infections
1. Human Papillomavirus – warts are caused by a DNA virus, the human papillomavirus. There are atleast 70
serotypes. The virus is capable of transforming infected cells into malignancy.
Mode of transmission
Clinical findings
- Skin warts are benign, self-limiting proliferations of the skin that regresses in tme. It may be flat, dome-shaped
or plantar.
- Genital and anogenital warts – also known as condylomata acuminata.
Laboratory diagnosis
- Gross appearance of the lesions and histologic appearance on microscopic examination that includes
hyperkeratosis.
2. Herpes simplex – etiologic agent are Herpes simplex virus types 1 and 2, DNA viruses under the family of human
papillomaviruses. These viruses are capable of latency in the neuron’s viruses are capable of latency in the
neurons and are capable are capable of recurrent infections.
Modes of transmission
- HSV is present in oral and genital scretions and vesicle fluid. It can be transmitted through:
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1. Oral contact
2. Fomites
3. Sexual contact
4. Transplacental
5. During childbirth
Clinical findings
1. Gingivostomatitis – the primary infection caused by HSV-1 that presents as vesicles that rupture and ulcerates.
Lesions are located in the buccal mucosa, palate, gingivae, pharynx, and the tongue.
2. Herpes labialis (fever blister or cold sore) – a recurrent mucocutaneous HSV infection that is caused by HSV-1
AND 2. Lesions are usually located at the vermillion borders of the lips.
3. Herpetic whitlow – infections involving the fingers and is caused by both HSV type 1 and 2
5. Herpes gladiatorum – infection on the body and usually acquired during wrestling or playing rugby.
Laboratory diagnosis