BIOL 220 Soilborne Diseases

What is the mode of transmission and major portal of entry?

Mode of Transmission:

• Vehicle Transmission – Transmission by a contaminated inanimate or non-living reservoir/pathogen can multiply in (like Soilborne)

Major portal of entry:

• Broken skin (hypertonic environment, lysosomes, low pH)

• Inhalation of contaminated soil via respirator tract

• Ingestion of contaminated soil via GI tract (oral-fecal route)

What are some predisposing factors of the soilborne diseases?

Direct contact with soil

• Walking barefoot in contaminated areas + jobs that involve direct contact with soil

Open wounds or skin injuries

Poor Hygiene or sanitation

• Clean drinking water

• Inadequate sewage systems

Weak immune system

• Malnutrition

• HIV/AIDS

What are prevention methods for soilborne diseases?

• Education!

• Practice Good hand hygiene like before/after handling food and soil

• Wear PPE like mask for low air quality

• Avoid walking barefoot in soil

• Proper wound care – protect your wounds (if have open skin wounds = avoid contact with soil and water)

Tetanus: Causative Agent and Virulence Factor

Causative agent: Clostridium tetani

• Gram-positive bacteria, bacilli, obligate anaerobe (mostly found in the deep layers of soil)

• Can stay dormant for many years

Virulence factor:

• Endospore forming = allows for the survival of pathogen in harsh conditions

• Tetanospasmin (neurotoxin/exotoxin): disrupts/blocks neurotransmission → uncontrolled muscle contractions and spasms

Tetanus: S/Sx and Diagnosis

S/Sx:

• Toxemia (Toxins enter the blood stream)

• Spores enter through a skin break via fomite → enter anaerobic areas of the body (deep tissue) and germinate → produce potent neurotoxins → Target the Central nervous system

• Blocks relaxation pathway of the muscles = causes muscle spasms and contractions

• Head, neck and back muscle stiffness and spasms

• Respiratory muscle failure --> death

• severe hyperextension

Diagnosis: based on symptoms

Tetanus: Prevention, Treatment, and Predisposing factors

Predisposing factors

• Direct contact with fomites (contaminated non-living object that carries/spreads the pathogen) — EX: Rusty nails or sharp objects

Prevention: vaccines

• DTaP, TDaP & Td (Diphtheria, Tetanus & Pertussis)

Treatment:

• Antibiotics (Penicillin): attack pathogen

• Sedation drugs: help muscles relax

• Tetanus Immune Globulin (TIG) (artificial passive): attack toxins —- Medication that has antibodies against the tetanus toxin → Prevents tetanospasmin from from binding to nerve endings + muscle spasms and failure

• Opsonization, neutralization of toxins & agglutination

Gangrene Basics: Ischemia, Necrosis, Gangrene, and types of Gangrene

• Ischemia: blood vessel blockage = loss of blood supply to tissue (inadequate blood supply to an organ or

part of the body)

• Necrosis: death of tissue, irreversible process

• Gangrene: Tissue death (Necrosis) due to loss interrupted blood supply

• Several types of gangrene: Dry / Wet / Gas Gangrene

Dry Gangrene: type of gangrene, S/Sx, and Treatment

Type of gangrene: cut off blood supply to an area of tissue → Ischemia without infection

S/Sx:

• No Pus or bad odor

• Area becomes dry and shrunken

• Color: Brown, purple/blue or black

Treatment:

• Surgical removal of dead tissue

• Amputation in severe cases to prevent the spread of infection

Wet Gangrene: type of gangrene and S/Sx

• Bacterial infection of dead tissue

• S/Sx: Swelling, blistering and a wet appearance – Foul smelling

Gas Gangrene: Causative Agent and Virulence Factor

Alternative Name: Clostridial Myonecrosis

Causative Agent: Clostridium perfringens

• Gram positive bacteria, bacilli, endospore-forming, obligate anaerobe (grows in deep tissue wounds + necrotic tissue)

• 20 – 25% mortality rate + Common cause of death during conflicts/war

Virulence Factors:

• Alpha toxin: excessive platelet aggregation → blocks blood vessels and deprive tissue/organs with oxygen supply; moves along the tissue and muscles

• Spores enter ischemic area of body/deep tissue wound → vegetative cells produce and release

alpha toxin → vascular and soft tissue damage

• Severe pain and swelling of an area: Pale → red → black/green-ish

• Prevents phagocyte function: creates an oxygen-deficient environment that helps pathogen grow

Gas Gangrene: S/Sx and Diagnosis

S/Sx:

• Tissue damage, severe pain and swelling

• Pale area → red and blackish green

• Gas filled Blisters from glucose fermentation: Bacteria feed on glucose in tissue to multiply → Pathogen ferment glucose to produce carbon dioxide and hydrogen gas

• Crepitus (cracking sound under skin due to gas bubble formation)

Diagnosis: S/Sx

Gas Gangrene: Treatment

Treatment:

• Immediate high doses of antibiotics (penicillin)

• Surgical removal of necrotic tissue, amputation

• Hyperbaric chamber: Increase the pressure experienced by the patient → help deliver oxygen to deprived areas

• Gas Gangrene should be treated as a medical emergency

What is Coccidioidomycosis & Histoplasmosis

both fungal diseases that affect the lower respiratory system (similar S/Sx)

Histoplasmosis: Causative Agent, Virulence Factor, Reservoirs, and Transmission

Causative agent: Histoplasma capsulatum (Dimorphic fungi: can exist in mold and yeast form)

Virulence Factor: Yeast form can multiply in phagocytes (similar to Mycobacterium tuberculosis); Not contagious

Reservoirs:

• Soil that is rich in bird or bat droppings

• Caves (spelunking), old buildings and chicken coops

Transmission: Via inhalation of microscopic fungal spores called conidia (AKA microconidia) located in contaminated soil when disturbed

Histoplasmosis: S/Sx

• Mostly asymptomatic (no S/Sx experienced by the patient)

• Acute histoplasmosis: Fever, cough, fatigue and chest pain

Chronic histoplasmosis:

• Flu like symptoms that resembles tuberculosis; typically found in people with preexisting lung conditions or weakened immune system

• Bloody cough, weight loss, night sweats, low grade fever,

• Lung lesions on chest X-Ray (white spots): Nodule/mass in the lung from an infection or autoimmune disease

Histoplasmosis: Diagnosis, Commonly Found, and Treatment

Diagnosis:

• Chest X-ray; lung lesions

• Serology: testing for antibody production against the fungi

• Biopsy: procedure where a small tissue sample is taken from the body for microscope exam → look for Yeast-forms in phagocytes

• Sputum sample

Commonly Found: in the Mississippi and Ohio River Valleys

Treatment:

• No Vaccine available

• Treatment with antifungals/antimycotics (Itraconazole; type of antifungal med)

Coccidioidomycosis: Alternative Name, Causative Agent, Mode of Transmission, and Virulence Factor

Alternative Name: Valley Fever or San Joaquin Fever

Causative Agent: Coccidioides Immitis

• Dimorphic fungus, produces fungal spores, can survive many temperatures

Mode of Transmission:

• Fungus pathogen grow in dirt/soil → fungus spores survive in air by the wind/digging → people/animals inhale from the air

Virulence Factor:

• Inhale fungal spores called arthroconidia: form spherules in tissue → release endospores

Coccidioidomycosis: S/Sx

• Mostly asymptomatic

Acute Coccidioidomycosis: Mild/few symptoms

• Like flu symptoms: Fever, cough, tiredness, red spotty rash

Chronic Coccidioidomycosis: common in people with a weakened immune system or preexisting respiratory conditions (Similar to Chronic TB)

• Low grade fever, bloody cough, weight loss, night sweats

Coccidioidomycosis: Commonly Found and Prevention

Commonly Found:

• dry desert soils of American southwest

• Arizona, Central California, Texas, Northern Mexico, New Mexico

• Climate change → increasingly dry areas → increase in people affected

Prevention:

• Avoiding dry areas where dust gets kicked up into the air

• Wearing a mask/covering + Air filters

Coccidioidomycosis: Diagnosis and Treatment

Diagnosis:

• Culture lung tissue or sputum sample

• Chest X-ray: Presence of lung lesions

• Patient Location within the last month

Treatment:

• Antifungals/antimycotic medication (Itraconazole)

• No Vaccine available

Hookworm infection: Causative Agent and Virulence Factor

Causative Agent: parasitic helminths (treat both types as one on exam)

1. Necator americanus (New world hookworm) from Americas

2. Anycyclostoma duodenale (Old world hookworm) from Middle East

• Kingdom Animalia, Phylum Nematoda (Roundworms)

• Hooked shaped body, separate sexes and contain specialized mouth parts

Virulence factor:

• Complex life cycle with multiple stages and hosts

Hookworm: Transmission and Reservoirs/Hosts

Transmission:

• Hookworm Larvae in contaminated soil will penetrate bare skin – usually through the feet

Reservoirs / hosts:

• Dogs, cats, Farm animals (pigs, goats and sheep), wild carnivores

What is the Life cycle of hookworm

• Adult hookworms mature in the small intestine of the human host (worms feed on blood and tissue)

• Eggs are secreted with feces → release into the environment → develop into filariform larvae (infective stage)

• Larvae penetrate skin → attach to the intestinal wall and produces eggs

• Can be passed through the oral-fecal route via the consumption of eggs

Hookworm: S/Sx

Initial S/Sx: Itchy rash at the hookworm site of entry “ground itch”

S/Sx of large number of worms:

• Anemia, fatigue, weakness, abdominal pain and diarrhea

• Lack of healthy Erythrocytes (Red blood cells) due

to hookworms feeding on blood and other tissues

Hookworm: Prevention, Diagnosis, and Treatment

Prevention:

• Avoid direct contact with contaminated soil

Diagnosis:

• Microscope: Stool examination to detect hookworm eggs

• Serology: Complete Blood Count (CBC) to count RBCs and hemoglobin and iron levels

Treatment:

• Antiparasitic/Anthelmintic drugs (Mebendazole)

Ascariasis: Causative Agent, Virulence Factor, and Mode of Transmission

Causative Agent: Ascaris lumbricoides (parasitic helminth)

• Kingdom Animalia, Phylum Nematoda

• Largest parasitic round worm: Separate sexes + special mouth parts

Virulence Factor:

• Complex life cycle with multiple stages and hosts (can infect swine/pigs)

• Structure is the infective stage: Ascaris lumbricoides eggs

Mode of Transmission: Oral-Fecal route

• Eggs are shed in the feces → Contaminated food, water or SOIL → ingested by another person

• Ascariasis eggs can survive for several months

What is the lifecycle stages of Ascariasis

• Ingest infective eggs from contaminated soil.

• Larvae hatch in the intestine → migrate to the lungs → ascend the throat to be swallowed again

• Once back in the small intestine, they mature into adult worms → reproduce and pass new eggs

in the feces, starting the cycle again.

• The entire process from ingestion to the shedding of new eggs takes two to three months

Ascariasis: S/Sx and Predisposing factors

S/Sx:

• Often asymptomatic in light infections

• Heavy infections: Passage of food, fluid or gas through the intestines is blocked → cause intestinal blockage, malnutrition and impaired growth (and development) in young children

Predisposing factors:

• Ingesting contaminated feces via food or water via Inadequate Sanitation, poor hand hygiene

Ascariasis: Diagnosis and Treatment

Diagnosis: Microscopically examine stool for eggs; based off S/Sx

Treatment: antiparasitic/antihelminth drugs (Mebendazole)