Eukaryotic Cells 2: Eukaryotic Pathogens

Question 1

Define: hypha

Answer 1

The cells in a mold grow and these long filaments are called hyphae. A singular is hypha. So multiple hyphae, one hypha. These are the filaments that would then release digestive enzymes to digest their surroundings and absorb nutrients by diffusion.

Question 2

Name 3 species of fungi that can cause aspergillosis.

Answer 2

Usually:
Aspergillus fumigatus,
A. flavus,

Rarely: 
A. terreus, 
A. nidulans, 
A. niger, 
A. versicolor

Question 3

What form does aspergillosis usually take in immunocompetent patients? In other words, what are the signs and symptoms of aspergillosis in most immunocompetent patients?

Answer 3

•Uncommon lung infection in immunocompetent
(usually requires pre-existing asthma or cystic
fibrosis)
•May go systemic (invasive disease, disseminates to
brain, skin, bone) in immunocompromised
•Transmission mostly by inhalation of spores
(ubiquitous)
–Construction, agriculture, hospital renovation
•Rarely transmitted to skin and nervous system via
contaminated medical equipment
•Systemic infections 40-75% fatal in
immunocompromised patients
•Treatment: antifungal medications

When a person inhales the spores and they start growing into small amounts of mold in their lungs, it will usually cause them to have a cough, shortness of breath, maybe pain when they take a deep breath and rarely, they will cough up plugs of brown mucus, brown sputum, that sometimes happens.

Question 4

Aspergillus spp. are opportunistic pathogens. What kind of activity creates the opportunity of repeat exposure? What medical conditions in immunocompetent people increase the likelihood of disease?

Answer 4

The person with the compromised immune system runs the risk of the mold invading their body and becoming a systemic infection. It might move to their bloodstream. It might damage the deep layers of their skin, it might go into their bones or into their brain or their nervous system. And in that case it’s often fatal if not treated successfully and aggressively.

The people at greatest risk of coming in contact with them are people who work in dusty environments like people who work in construction or people who work in the agriculture industry. Sometimes these molds grow in the walls of a hospital and they’re usually not revealed or considered to be a problem until someone goes to do renovation on a hospital. Occasionally, there are these massive outbreaks of invasive aspergillosis in a hospital that’s associated with tearing down a portion of the hospital.

our most vulnerable patients–people with severe lung disease and immunocompromised, cystic fibrosis, or asthma.

Question 5

What is the case-fatality rate (percent of infected people who die) of systemic aspergillosis in immunocompromised patients? Why is death so much more likely in immunocompromised people?

Answer 5

•Systemic infections 40-75% fatal in
immunocompromised patients

•May go systemic (invasive disease, disseminates to
brain, skin, bone) in immunocompromised

Question 6

If you were a hospital administrator, why would it be important for you to understand the biology of Aspergillus spp.?

Answer 6

Even though these molds are present everywhere, having them in high concentrations in a hospital will lead to a whole bunch of severely infected and severely sick patients.

Question 7

Name 2 species that cause intestinal amebiasis. What percentage of people who are infected with these pathogens have any obvious disease?

Answer 7

Entamoeba histolytica, E. dispar, E. moshkovskii, and E. bangladeshi. 20% are symptomatic and 80% are asymptomatic.

Question 8

Dr. C incorrectly said that “bloody diarrhea, no matter what the cause, is called dysentery.” Correct his statement. What one qualifier could you add to make it correct? (This may require some independent research in the textbook.)

Question 9

What is the most common presentation of amebiasis when it is not asymptomatic? What are the more rare forms of this disease?

Answer 9

Diarrhea, abdominal cramps, bloody stools and fever. Rare forms cause liver/lung/heart abscesses.

Question 10

Worldwide, who is at greatest risk for contracting amebiasis? Who is at greatest risk of contracting amebiasis from community transmission in the US?

Answer 10

•Most common in developing countries in tropical
regions with poor sanitation (50% carriage)
•Rare in industrialized countries
–Risk group is men who have sex with men
•Fecal-oral transmission (water, ice cubes, fresh
fruit/veg., unpasteurized dairy, hands)
•Contact with fecal matter during sexual activities

Question 11

How is amebiasis transmitted?

Answer 11

Transmitted thru contact with fecal matter during sexual activities, fecal- oral transmission (water, ice cubes, fresh fruit/veg., unpasteurized dairy, hands.

Question 12

How is amebiasis prevented?

Answer 12

Water treatment, using clean water that’s boiled or filtered, making sure food is cooked thoroughly, hand washing, use of barriers during sexual activity.

Question 13

Compare Entamoeba cysts with trophozoites.

Answer 13

A cyst is a durable and dormant form of the amoeba. It’s not nearly as tough as a bacterial endospore But it is relatively strong for a protozoan. It is relatively resistant to environmental insults. And so this is the form that this amoeba turns into before exiting the GI tract in the fecal matter. We’ve got Entamoeba histolytica. Everyone in medicine accepts it as being able to cause amebiasis. Some people call it intestinal amebiasis. These various different species of entamoebas can all cause amebiasis. 80% of the people who get infected with these amoebas have absolutely no symptoms. So one in five people, 20% of the people who get infected get symptoms: Diarrhea that is typically pretty severe, goes along with lots of cramping of the abdomen, and sometimes is bloody.

So you’ve got the amorphous form of the amoeba, the kind that’s doing phagocytosis, and that’s called the trophozoite. It does phagocytosis, it is capable of reproducing. It’s the form we find in the intestines, or in the liver or in the heart and lungs, right. This is the form inside a host. The trophozoite takes on a different form, it becomes a cyst, and the cyst is dormant and durable. Dormant meaning it’s not doing phagocytosis, it’s not getting nutrients, it’s not eating red blood cells. And it’s not reproducing. And durable meaning that it’s somewhat resistant to dehydration and other environmental insults. This is considered the most infectious form. Because this is the form that’s released in the feces and this is the form that if it gets into someone’s GI tract through their mouth, if they swallow the cysts, the cysts can then convert back into trophozoites in their intestines, where there’s an 80% chance they won’t cause disease and a 20% chance that they will.

Question 14

Give the scientific and common names for the most common worm infection in the US. Assuming the population of the US is 320 million people, how many people have this worm infection? Which age groups are most likely to have this infection?

Answer 14

Enterobius vermicularis is the most common worm or helminth infection in the United States. Pinworm. About one in eight people in the US are infected with this worm. Frequent in pre-school-age and school-age children.

Question 15

Describe the signs and symptoms of the most common worm infection in the US, ranging from most mild to most severe.

Answer 15

Usually asymptomatic. Common presentation: anal pruritus (itch).

•Uncommon presentation: anorexia, abdominal
pain, sleep disruption
•Rare
–Vulvovaginitis after the worms migrate into female
reproductive tract
–Pelvic/peritoneal granulomas (pearly nodules full of worms) if the worms penetrate the intestinal or vaginal wall.

Question 16

Describe 2 ways to diagnose the most common worm infection in the US.

Answer 16

–Observe threadlike female worms on the perianal folds
1-2 hours after sleep starts
–Recover ova from perianal folds with transparent
adhesive tape; observe with microscope (50 μm x 30 μm)

Question 17

Describe the life cycle of the pathogen that causes the most common worm infection in the US.

Answer 17

•Direct and indirect fecal-oral transmission:
ingestion of eggs
•Eggs hatch in intestines; adults mate in colon
•30 days after egg ingestion, females produce more
eggs—place eggs on perianal folds at night, causing
irritation
•Worms live 60 days
•Autoinfection common

Question 18

Describe the structure of a Taenia tapeworm in detail, as it is commonly found in the human GI tract.

Answer 18

•Scolex:head-like structure containing
suckers/hooks used by tapeworm to attach
•Reproductive segments (proglottids) grow
continuously, mature, mate and detach from
the scolex
–Each proglottid makes ova/sperm
•Scolex and numerous proglottids segments
can grow up to 25 meters length (5 meters
more common) àbowel obstruction
•Proglottids containing eggs or embryonated
eggs are released in fecal matter

Question 19

What are the signs and symptoms of taeniasis?

Answer 19

•Most common symptoms: abdominal pain,
loss of appetite, weight loss, upset stomach
–Proglottids may be visible in the feces

Question 20

Critique this statement: Taenia tapeworms are worse for pigs and cattle than for people.

Answer 20

• The disease is very mild in people.
  •Rarely, humans consume embryonated eggs in
  contaminated food or by autoinfection, resulting in
  human cysticercosis
  –Can be fatal, only T. solium
  •Embryonated eggs hatch, release
  oncospheres, which migrate to muscle and
  other tissues in pigs/cattle, forming
  cysticerci
  •Cysticerci cause damage to pigs/cattle
  –Can be fatal in b

Question 21

Critique this statement: preventing taeniasis in people reduces expenses for cattle and pig ranchers.

Answer 21

If taeniasis in people can be prevented, then the embryonated eggs that would be released into the fecal matter of infected people with taeniasis would be also prevented. If cattle and pigs consume the embryonated eggs, the eggs would form cysticerci which can be fatal. Preventing this transfer of embryonated eggs could reduce expenses for ranchers because their pigs/cattle wouldn’t die and cause the farmers to clean / disinfect the living space of livestock and purchase more animals.

Question 22

Compare and contrast the life-cycles that result in taeniasis and cysticercosis.

Answer 22

So the typical life cycle is that a person will eat beef or pork that has not been fully cooked. You see these worms take a form inside cattle or pork, should say takes. It takes a form called cysticerci. The cysticerci are encysted worms inside the tissues of the cattle or the pig. Inside the host. And usually when people eat beef or pork, they focus on eating the muscle. So we’re going to start with the muscle, but later on we’ll return to the cysticerci and they don’t always appear in the muscle tissue.

The human will eat the cysticerci, typically a muscle tissue, but really in any tissue from the cattle or pigs and then. Those cysticerci will become the worms in the intestines, usually asymptomatic, and then the embryonated eggs are released and then are eaten by the cattle and pigs, which get the cysticerci. And now the cysticerci can cause significant damage.

The human being is releasing the embryonated eggs. Those embryonated eggs could go to another person. Or they could go to the same person who released them through auto infection. Auto infection means when a person infects themself. And it’s associated with these fecal oral helminth pathogens that have these complex life cycles. Right. Because eating a cysticercus is totally different from eating an embryonated egg. When a person consumes an embryonated egg, either because some other person has contaminated their food with fecal matter or because they’ve contaminated their own hands by not washing their hands after using the bathroom, when a person consumes these embryonated eggs they get a completely different disease and that disease is called cysticercosis.

Question 23

Describe the disease process of cysticercosis, along with the difficulty in treating cysticercosis.

Answer 23

You can give medications that kill the cysticerci. Those medications would prevent the 60 cysticerci from growing. And that would prevent them from continuing to do damage through growth, however. The dead worms stimulate the immune system even more than the living worms. And so when you kill the worms, you get the advantage of, they’re not going to grow any larger but the immune system starts attacking them more vigorously, and we get more inflammation. Now inflammation can actually make the signs and symptoms of disease worse. Any inflammation in the brain can be devastating. Because there’s really no room for swelling inside the brain case, inside the cranium. In the heart it can also be very severe; inflammation of the heart can do more damage than the cysticerci themselves. And so the treatment of these things is very difficult, and often unsatisfactory. You kill the cysticerci and then you give the person medications to knock down their immune system, like steroids. But they’re not going to necessarily recover completely and sometimes they end up succumbing even after the cysticerci are dead.