Clinically Important Fungi & Protozoans

Ringworm

• Tinea capitis - ringworm of the scalp

• Tinea crucis - ringworm of the groin or jock itch

• Tinea pedis - ringworm of the feet (Athlete’s foot)

• Tinea unguium (onchomycosis) - ringworm of the fingernails or toenails

1. Causative Agent

   1. Trichophyton - can infect hair, skin, or nails

   2. Microsporum - can infect hair or skin

   3. Epidermophyton - can infect skin and nails 

2. Transmission

   1. All contagious

      1. Via contact with fomites

      2. Spores enter the skin through a cut

      3. Cause bacterial infections

3. Signs & Symptoms

   1. Bad patches

   2. Infections tend to expand circulatory

4. Pathogenesis

   1. Moisture in areas of the groin and feet favors fungal infection

      1. T. pedis can cause a secondary bacterial infection

5. Treatment

   1. Treatment may require weeks due to fungal cells having unusual life cycles

      1. All can be treated with antifungal drugs but may take weeks

         1. Tolnaftate (Athlete’s foot)

6. Epidemiology

   1. Common among elementary school children

Candidiasis

• Opportunistic fungal infection - only cause disease when a person’s immune system is weakened

1. Causative Agent

   1. Candida albicans (yeast)

2. Transmission

   1. Most common nosocomial fungal infection 

3. Signs & Symptoms

   1. Thrush: infection of the mucous membranes of the mouth

   2. Vaginitis: itching or burning

   3. Infect tissues

4. Pathogenesis

   1. Antibiotics inhibit normal flora of the skin and mucous membranes in the genitourinary tract and mouth

      1. Causes opportunistic growth of C. albicans (part of the normal flora)

   2. Pseudohyphae: chains of elongated yeast cells that remain attached to one another

      1. Helps C. albicans avoid immune attack and invade tissues, resistant to phagocytosis

   3. Systemic infections for immunocompromised people

5. Treatment

   1. Long term antibiotic usage

   2. Flucytosine 

6. Epidemiology

   1. Immunosuppressed individuals

   2. Obese or diabetic (have more moisture in areas of skin)

Candida auris

• Opportunistic fungal infection - only cause disease when a person’s immune system is weakened

1. Causative Agent

   1. Candida auris

2. Pathogenesis

   1. Nosocomial infection

      1. Enters the bloodstream and spreads throughout the body

      2. Causes sepsis

3. Diagnosis

   1. Special laboratory methods used to identify it

      1. PCR

4. Treatment

   1. Highly resistant to antifungal drugs

5. Epidemiology

   1. Hospitalized patients

Cryptococosis

1. Causative Agent

   1. Cryptococcus neoformans

2. Transmission

   1. Soil fungus associated with pigeon and chicken droppings

   2. Via respiratory tract through dried contaminated droppings

3. Pathogenesis

   1. Spreads through blood to the CNS in immunocompromised individuals (AIDS)

      1. Causes meningitis

4. Treatment

   1. Amphotericin B and flucytosine

5. Epidemiology

   1. Immunocompromised individuals (with AIDS)

African trypanosomiasis (Sleeping Sickness)

• Protozoan disease that affects the nervous system

1. Causative Agent

   1. Trypanosoma brucei gambiense

      1. Humans are reservoir

   2. Trypanosoma brucei rhodesience

      1. Parasite of domestic livestock and wild animals

         1. Animals are adapted but humans become ill

2. Transmission

   1. Bite of a tsetse fly

3. Signs & Symptoms

   1. T. b. gambiense

      1. Chronic disease (symptoms develops slowly)

   2. T. b. rhodesience

      1. Acute disease (symptoms develop rapidly)

4. Pathogenesis

   1. T. b. gambiense

      1. Fever, headaches, deterioration of the CNS

      2. Coma and death

   2. T. b. rhodesience

      1. Cardiac problems before CNS is affected

      2. Death occurs within weeks or months

   3. Can infect all organs of the body

5. Treatment

   1. Antiprotozoal drugs are only effective in the early stages

      1. Suramin

      2. Melarsoprol can cross the CNS to kill parasites, although very toxic

   2. Organism constantly changes its membrane proteins to escape host immune system, making it harder to develop a vaccine

      1. Trypanosome is able to change its protein coat at least 100 times

6. Prevention

   1. Elimination of tsetse fly vectors, texting livestock 

7. Epidemiology

   1. Africa

Visceral leishmaniasis

1. Causative Agent

   1. Leishmania donovani

2. Transmission

   1. Bite of female sandflies 

3. Signs & Symptoms

   1. Chills and sweating of malaria

      1. Enlarges the liver and spleen

      2. Kidney function is lost

      3. Leads to death within a year or two

4. Pathogenesis

   1. Promastigote stage (infective form)

      1. Found in the saliva of a sandfly

      2. Sandfly bites a human and injects promastigotes into the skin

   2. Amastigote stage (intracellular form)

      1. Parasite loses its flagellum → becomes an amastigote

      2. Lives inside phagocytic cells

      3. Multiply in fixed tissue sites (liver, spleen, bone marrow)

   3. Transmission back to sandfly

      1. Sandfly bites the infected human and ingests amastigotes

      2. Amastigotes turn back in promastigotes

   4. Cycle continues

5. Treatment

   1. No vaccine

6. Complications

   1. Problem for soldiers sent to countries with tropical climates

Malaria

1. Causative Agent

   1. Plasmodium vivax - mildest and most prevalent form; dormant in the liver

   2. Plasmodium ovale - benign, restricted geographically

   3. Plasmodium malariae - benign, restricted geographically

   4. Plasmodium falciparum - most deadly; severe anemia; blocks capillaries; affects the kidney, liver, and brain

2. Transmission

   1. Anopheles mosquitoes

3. Signs & Symptoms

   1. Chills, fever, vomiting, severe headache

4. Pathogenesis

   1. Anopheles mosquitoes bite a human

   2. Carries a sporozoite (infective stage of parasite) of the Plasmodium protozoan in its saliva

   3. 300 to 500 sporozoites enter the bloodstream of the human and enter liver cells

   4. Undergo reproductive schizogony (asexual reproduction) and releases 30,000 merozoites (form of malaria parasite that infects RBCs) into the bloodstream

   5. Merozoites infect RBCs → RBCs undergo schizogony → RBCs rupture and releases 20 new merozoites (rises body temperature)

      1. People with sickle cell anemia are protected because the organism cannot replicate an altered RBC

      2. Resulting anemia weakened victim

   6. RBCs develop surface knobs that sticks to capillaries, clogging them

      1. Prevents RBCs from reaching the spleen where phagocytic cells eliminate them

      2. Causes subsequent loss of blood supply (blood vessel obstruction) → death of tissues 

      3. Kidney and liver damage 

      4. Cerebral malaria

5. Treatment

   1. P. falciparum is resistant to chloroquine drug

      1. Only effective against red blood stage only 

   2. Difficult to produce a vaccine due to invasion of immune response, rapidly mutating, and various stages of disease

      1. Needs a transmission-blocking vaccine (use the human host to generate antibodies and deliver them to the biting mosquito)

   3. Mosquirix vaccine only effective for a limited time for children 6 weeks to 17 months

6. Prevention

   1. Controlling mosquito population

7. Epidemiology

   1. Endemic in tropical areas

Chagas disease (American trypanosomiasis)

• Protozoan disease of the cardiovascular system

1. Causative Agent

   1. Trypanosoma cruzi

      1. Flagellated protozoan

2. Transmission

   1. Reservoir is wild animals 

   2. Reduviid bug (kissing bug)

      1. Bites people near the lips

3. Signs & Symptoms

   1. Fever and swollen glands (acute stage)

   2. Damage to nerves controls peristaltic contractions of the esophagus or colon

      1. Prevents transporting of food

      2. Megaesophagus and megacolon (grossly enlarged organs)

   3. Damage to the heart

4. Pathogenesis

   1. Trypanosomes grow in the gut of the bug

   2. Reduviid bug bites victim

   3. Feces rub into bite wound or skin abrasions

      1. Pregnant women can transmit disease to the fetus

5. Treatment

   1. No treatment

   2. No antiprotozoal agent

      1. Trypanosome multiplies intracellularly

6. Epidemiology

   1. Endemic in Central America and parts of South America

Toxoplasmosis

• A self limiting disease of the blood and mild inflammation of lymphatic vessels

1. Causative Agent

   1. Toxoplasma gondii

      1. Spore-forming protozoan 

2. Transmission

   1. T. gondii undergoes its sexual phase in the small intestine of a cat

      1. Millions of oocysts are shed into the cat’s feces which contaminates food or water ingested by other animals

         1. Eating undercooking meats

         2. Contact with cat feces

      2. Pregnant women can transmit disease to the fetus

         1. Results in stillbirth

3. Signs & Symptoms

   1. People with a healthy immune system, result in mild symptoms or none

   2. Immunocompromised people (AID) allows the bradyzoites to be reactivated into tachyzoites 

4. Pathogenesis

   1. Oocysts contain sporozoites that invade host cells and form trophozoites (the active and feeding stage of protozoa) called tachyzoites (a rapid and motile form of a protozoa)

      1. Trophozoites

         1. Can be from cats who eat birds (parasite from bird → cat eats bird → parasite forms oocysts → trophozoites)

         2. Can multiply with sporocysts (protective structure inside oocyst → parasite can multiply and develop infective forms)

         3. Can be ingested in pregnant woman (touching contaminated cat litter, eating unwashed vegetables, eating uncooked meat with cysts)

         4. Can become systemic → neuronal problems → travels to CNS easily

      2. Increased numbers of rupture of the host cell and the release of more tachyzoites, resulting in strong inflammatory response

   2. When an immune response is effective, the disease enters a chronic phase

      1. Infected host cells develop a wall to form a tissue cyst around the protozoa 

         1. Bradyzoites (a slow-replicating and dormant form of protozoa in tissue cysts; can reactive to tachyzoites)

5. Diagnosis

   1. Research in progress to see if there is a connection between the organism and Schizophrenia

Coccidiomycosis (Valley Fever)

1. Causative Agent

   1. Coccidioides immitis 

      1. Dimorphic fungus (grows as mold in environment and yeast in the body)

2. Transmission

   1. In the soil, it forms filaments that reproduce by the formation of arthroconidia (spores that break off the fungal hyphae - long thread-like filaments)

   2. Wind carries the anthraconidia to endemic areas (especially during dust storms)

3. Signs & Symptoms

   1. Mild flu like symptoms or no symptoms at all

4. Pathogenesis

   1. Spores are inhaled

5. Diagnosis

   1. In tissues, the organism can form a spherule (thick walled off body) filled with spores

6. Treatment

   1. Can recover without treatment

7. Complications

   1. Spreading to meninges or bones

8. Epidemiology

   1. Found in dry, alkaline soils of the American Southwest

Histoplasmosis

1. Causative Agent

   1. Histoplasma capsulatum 

      1. Dimorphic fungus 

2. Pathogenesis

   1. Soil fungal spores are produced under conditions of appropriate moisture and pH levels

   2. Inhaled and mature into an actively growing yeastlike form which can survive and multiple in macrophages

   3. Spread in the body and lymph, causing lesions in almost all organs via macrophages

3. Complications

   1. Resembles tuberculosis

      1. Pneumonia and infection in the spleen, liver, and lymph nodes

         1. Can become systemic and attack other organs and lymph tissues

4. Epidemiology

   1. States adjoining the Mississippi and Ohio rivers (central and eastern U.S.)

Pneumocystis pneumonia (PCP)

1. Causative Agent

   1. Pneumocystis jirovecii (carinii)

2. Transmission

   1. Found in healthy human lungs (lining of the pulmonary alveoli)

3. Signs & Symptoms

   1. Immunocompetent adults have few or no symptoms

   2. Newly infected infants show symptoms of lung infection 

4. Pathogenesis

   1. People with weakened immune systems 

      1. P. jirovecii form thick-walled cyst and intracystic bodies (early reproductive cells inside the cyst) successively divide as part of a sexual cycle 

      2. Creates 8 intracystic bodies

      3. Cyst matures, releasing the intracystic bodies → each body develops into a trophozoite → reproduces asexually

5. Treatment

   1. 100% fatality rate if not treated with antifungal agents

      1. Pentamidine

6. Complications

   1. Can spread to meninges or bones

7. Epidemiology

   1. Immunity compromised people due to cancer, immunosuppressive drugs, AIDS

Blastomycosis (North American blastomycosis)

1. Causative Agent

   1. Blastomyces dermatitidis 

      1. Dimorphic fungus

2. Transmission

   1. Inhalation of endospores or through a wound

3. Pathogenesis

   1. Spores mature to yeast cells

      1. Can spread rapidly

   2. Cutaneous ulcers appear when the yeast are disseminated in circulating monocytes via macrophages

   3. Formation of pus may form with extensive tissue destruction

4. Treatment

   1. Itraconazole

   2. Amphotericin B

5. Epidemiology

   1. Soil around the Great Lakes and Mississippi River Valley

Aspergillosis

1. Causative Agent

   1. Aspergillus fumigatus 

2. Pathogenesis

   1. Infect the lungs when spores are inhaled

   2. Leads to asphyxiation 

   3. Ultimately lead to death due to lungs being compromised

3. Epidemiology

   1. Compost piles are ideal sites for growth 

   2. Farmers and gardens are most susceptible to infective amounts of A. fumigatus conidia (asexual spores made to reproduce)

   3. Individuals with impaired immune system, cancer, diabetes, AIDS

Giardiasis

1. Causative Agent

   1. Giardia duodenalis (intestinalis or lamblia)

      1. Flagellated protozoan 

2. Signs & Symptoms

   1. Malaise, nausea, flatulence (intestinal gas), weakness, weight loss, and abdominal cramps

   2. Protozoa can occupy intestinal wall and interfere with food absorption

3. Pathogenesis

   1. Cyst of the organism are ingested

   2. Travel to small intestine and mature into trophozoite

   3. Adhere to the bowel wall via an adhesive (sucker) disk

   4. Causes diarrhea with dehydration

4. Prevention

   1. Cyst is insensitive to chlorine

      1. Needs filtration or boiling

5. Treatment

   1. Antiprotozoan drugs

      1. Metronidazole

      2. Tinidazole 

6. Epidemiology

   1. Camping

   2. Swimming season 

   3. Contaminated water supplies 

   4. Wild animals (beavers)

Amebiasis (Amebic dysentery)

1. Causative Agent

   1. Entamoeba histolytica

2. Transmission

   1. Contaminated food or water

3. Pathogenesis

   1. Ingested contaminated food or water

   2. Trophozoites mature in the colon

   3. Invade intestinal mucosa and get into the bloodstream

   4. Intestinal lining damage can cause fecal material to get into the body and cause peritonitis (infection of the abdominal lining)

   5. Feces contain blood and mucus

4. Treatment

   1. Antiprotozoan drugs

      1. Metronidazole

      2. Tinidazole 

      3. Diiodohydroxyquin

5. Complications

   1. Cysts are not killed by normal chlorine concentrations in the water 

Cyclosporiasis

1. Causative Agent

   1. Cyclospora cayetanensis

2. Transmission

   1. Ingestion of oocysts in water, contaminated batteries, or uncooked food

      1. Presumed to have been contaminated by oocysts shed in human feces or possibly from birds

3. Signs & Symptoms

   1. Few days of watery diarrhea

4. Treatment

   1. Trimethoprime

   2. Sulfamethoazole 

5. Epidemiology

   1. Immunosuppressed people (AIDs)

Cryptosporidiosis

1. Causative Agent

   1. Cryptosporidium parvum

   2. Cryptosporidium hominis

2. Transmission

   1. Contaminated water systems from animal waste 

3. Signs & Symptoms

   1. Cholera-like disease lasting 10 to 14 days 

4. Pathogenesis

   1. Human ingests oocysts

   2. Oocysts released sporozoites into the small intestine

   3. Motile sporozoites invade the epithelial cells of the intestine and undergo a cycle that eventually releases oocysts to be excreted in the feces

5. Complications

   1. Resistant to chlorine

6. Epidemiology

   1. Immunodeficient individuals (AIDs)

Vulvovaginal candidiasis

• Most common cause of vaginitis

1. Causative Agent

   1. Candida albicans (in most causes)

2. Transmission

3. Signs & Symptoms

   1. Severe itching, a thick, yellow, cheesy discharge, and yeast

4. Pathogenesis

   1. C. albicans grows on the mucous membranes of the mouth, intestinal tract, and genitourinary tract

   2. Result in opportunistic overgrowth when the competing microbiota are suppressed by antibiotics 

5. Epidemiology

   1. Less common in girls before puberty or women after menopause

   2. Use of oral contraceptives and pregnancy which causes an increase in glycogen in the vagina

   3. Uncontrolled diabetes and long-term antibiotic therapy 

   4. Change in pH

Trichomoniasis

• Trichomonas hominis - harmless bacteria found in the intestines 

• Trichomonas tenax - harmless bacteria found in the mouth 

  • Both normal commensals in our body and can pick up virulence factors to make it harmful

1. Causative Agent

   1. Trichomonas vaginalis

2. Transmission

   1. Inhabitants of the vagina and male urethra (rarely has symptoms)

   2. Sexually transmitted

3. Signs & Symptoms

   1. Greenish-yellow and foul smell discharge

   2. Irritation and itching

   3. Most cases are asymptomatic

4. Pathogenesis

   1. If pH of vagina is destroyed, protozoa may overgrow the normal microbial population of genetial mucosa

   2. Body accumulates leukocytes at the infection site 

5. Treatment

   1. Antiprotozoan drugs

      1. Metronidazole

      2. Tinidazole 

6. Complications

   1. Serious infections or birth defects in new borns