University of San Agustin

ILOILO CITY, PHILIPPINES

COLLEGE OF HEALTH AND ALLIED MEDICAL PROFESSIONS
MEDICAL LABORATORY SCIENCE PROGRAM

MODULE PACKETS IN MLS 13A:

MYCOLOGY AND
VIROLOGY
M10

Matthew I. Tubola, RMT, MSMT

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John Robert D. Fundal, RMT

MYCOLOGY AND VIROLOGY
A.Y. 2020 - 2021
© 2021. Printed in Calibri.
Cover Design: J.R.D. Fundal, RMT
All rights reserved. Copyright applied for. No part of this module may be reproduced, stored in retrieval
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The authors have done everything possible to make this module accurate and in accordance with accepted
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contents of the module. Any practice described in this module should be applied by the reader in accordance
with accepted standards used in regard to unique circumstances that may apply in each situation.

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LEARNER’S HONOR CODE STATEMENT FOR THIS MODULE PACKET

“I affirm that I will not give or receive any unauthorized help on this MODULE, and that all
work will be my own.”
“I affirm that I have not given or received any unauthorized help on this assignment, and that
this work is my own.”

_________________________
Signature over printed name

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 ABOUT THE AUTHORS

MATTHEW I. TUBOLA, RMT, MSMT

Hello Augustinians!
Welcome to MLS-13A (Mycology and Virology Lecture), I will be your lecturer for this subject. I am a
graduate of BSMT of this University and also finished my Master’s degree in Medical Technology in this
University. I have been teaching in this University for 12 years teaching Medical Technology Professional
Subjects.

JOHN ROBERT D. FUNDAL, RMT

Hello Augustinians!
Welcome to MLS-13A (Mycology and Virology Lecture), I will also be your lecturer for this subject. I
obtained my Bachelor’s Degree in Medical Laboratory Science from University of San Agustin. This is
currently my third semester in teaching MLS subjects.

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 TABLE OF CONTENTS
Disclaimer 1
Honor Code 2
About the Authors 3
Content

Prions 7
Prion Diseases 7
References 10

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 UNIT MAP
General Characteristics and
Mechanisms of Pathogenesis of
Bovine Spongiform Encephalopathy
Agents and other Prions

Classic Creutzfeldt-Jakob
Disease (CJD)

Variant Creutzfeldt-Jakob
Disease (vCJD)

Kuru

Scrapie

Bovine Spongiform
Encephalitis

Chronic wasting disease

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 PART 1: OVERVIEW OF DISCUSSION

Prion diseases or transmissible spongiform encephalopathies (TSEs) are a family of rare progressive
neurodegenerative disorders that affect both humans and animals. They are distinguished by long incubation
periods, characteristic spongiform changes associated with neuronal loss, and a failure to induce inflammatory
response.
The causative agents of TSEs are believed to be prions. The term “prions” refers to abnormal,
pathogenic agents that are transmissible and are able to induce abnormal folding of specific normal cellular
proteins called prion proteins that are found most abundantly in the brain. The functions of these normal
prion proteins are still not completely understood. The abnormal folding of the prion proteins leads to brain
damage and the characteristic signs and symptoms of the disease. Prion diseases are usually rapidly
progressive and always fatal.

PART 2: LEARNING OBJECTIVES

At the end of the lecture, the student shall be able to:

• Know the general characteristics of Bovine Spongiform Encephalopathy Agents and other Prions
• Know the mechanisms of pathogenesis of Bovine Spongiform Encephalopathy Agents and other Prions

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 PART 3: DISCUSSION

PRIONS

Prion diseases or transmissible spongiform encephalopathies (TSEs) are a family of rare progressive
neurodegenerative disorders that affect both humans and animals. They are distinguished by long incubation periods,
characteristic spongiform changes associated with neuronal loss, and a failure to induce inflammatory response.

The causative agents of TSEs are believed to be prions. The term “prions” refers to abnormal, pathogenic agents
that are transmissible and can induce abnormal folding of specific normal cellular proteins called prion proteins that are
found most abundantly in the brain. The functions of these normal prion proteins are still not completely understood. The
abnormal folding of the prion proteins leads to brain damage and the characteristic signs and symptoms of the disease.
Prion diseases are usually rapidly progressive and always fatal.

PRNP is a gene in your Prion protein or PrP is a Prion is an infectious

DNA which encodes for protein on the surface particle made up of
prion protein. of your cells. misfolded prion proteins.

PRION PROTEINS

Prion protein (PrP) appears to be the major, and possibly exclusive component of prions. PrPc (cellular) is the protein
product that is thought to be the target for prion disease. In the wild type, it is a normal host glycoprotein encoded by a
single exon of a single copy gene (PRNP on chromosome 20). It assumes an alpha helical structure and is located on the
cell surface with a glycoinositol phospholipid anchor. Treatment with proteases results in complete digestion.

In infected individuals, the PrPc protein is deranged to become the PrPsc (scrapie) protein. This glycoprotein assembles
into beta-sheets and is located in cytoplasmic vesicles. The insoluble PrPsc accumulates inside cells instead of being
located on the cell surface. It is only incompletely digested by proteases and this insolubility is thought to contribute to
storage problems and aggregation.

PRION DISEASES

There are several distinguishing hallmarks of these prion diseases. Although the etiologic agent may be
recoverable from other organs, the diseases are confined to the nervous system. The basic features are
neurodegeneration and spongiform changes. Amyloid plaques may be present. Long incubation periods (months to
decades) precede the onset of clinical illness and are followed by chronic progressive disease (weeks to years). The
diseases are always fatal, with no known cases of remission or recovery.

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 The host shows no inflammatory response and no immune response (the agents do not appear to be antigenic);
no production of interferon is elicited; and there is no effect on host B-cell or T-cell function. Immunosuppression of the
host has no effect on pathogenesis; however, chronic inflammation induced by other factors (viruses, bacteria,
autoimmunity) may affect prion pathogenesis. It has been observed that prions accumulate in organs with chronic
lymphocytic inflammation. When coincident with nephritis, prions are excreted in urine.

HUMAN PRION DISEASES ANIMAL PRION DISEASES

• Creutzfeldt-Jakob Disease (CJD), Classic • Bovine Spongiform Encephalopathy (BSE)
• Variant Creutzfeldt-Jakob Disease (vCJD) • Chronic Wasting Disease (CWD)
• Gerstmann-Straussler-Scheinker Syndrome • Scrapie
• Fatal Familial Insomnia • Transmissible mink encephalopathy
• Kuru • Feline spongiform encephalopathy
• Parkinson’s disease • Ungulate spongiform encephalopathy
• Alzheimer’s Disease
• Huntington’s Disease
• Lou Gehrig's disease

1. Classic Creutzfeldt-Jakob Disease (CJD)

Creutzfeldt-Jakob disease (CJD) is a rapidly progressive, invariably fatal neurodegenerative disorder believed to
be caused by an abnormal isoform of a cellular glycoprotein known as the prion protein. CJD occurs worldwide and the
estimated annual incidence in many countries has been reported to be about one case per million population.

Treatment of prion diseases remains supportive; no specific therapy has been shown to stop the progression of
these diseases.

Figure 10.1 Pathology of Normal brain (left) and pathology of the brain of a patient with CJD (right). Note the spongiform
pathology of the left picture.

2. Variant Creutzfeldt-Jakob Disease (vCJD)

Variant Creutzfeldt-Jakob disease (vCJD) is a prion disease that was first described in 1996 in the United Kingdom.
There is now strong scientific evidence that the agent responsible for the outbreak of prion disease in cows, bovine
spongiform encephalopathy (BSE or ‘mad cow’ disease), is the same agent responsible for the outbreak of vCJD in humans.

Variant CJD (vCJD) is not the same disease as classic CJD (often simply called CJD). It has different clinical and
pathologic characteristics from classic CJD. Each disease also has a particular genetic profile of the prion protein gene.

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Both disorders are invariably fatal brain diseases with unusually long incubation periods measured in years, and are caused
by an unconventional transmissible agent called a prion.

Treatment of prion diseases remains supportive; no specific therapy has been shown to stop the progression of
these diseases.

Table 10.1 Comparison of Classic CJD and Variant CJD

3. Kuru

Kuru occurred only in the eastern highlands of New Guinea and was spread by customs surrounding ritual
cannibalism of dead relatives. Since the practice has ceased, the disease has disappeared.

In the Fore language (spoken in Papua New Guinea), the term “kuru” refers to body tremors, which are a
characteristic feature of the disease. Symptoms progress from unsteady gait and tremors, to loss of muscle coordination,
severe ataxia, and death, over the course of 3 months to 2 years.

4. Scrapie

Scrapie, also called rida or tremblante du mouton, is a fatal neurodegenerative disease of sheep and goats. Scrapie
has a long incubation time, typically between about 18 months and five years following transmission. The first signs to
arise are usually behavioral changes such as general apprehensiveness and nervousness. As the disease progresses, the
animal loses weight and weakens, develops head and neck tremors, loses muscular coordination, and begins to rub or
scrape its body against objects, wearing away its fleece or hair—hence the name “scrapie”. The disease inevitably causes
death within one to six months. No treatment or palliative measures are known.

5. Bovine Spongiform Encephalopathy

BSE (bovine spongiform encephalopathy) is a progressive neurological disorder of cattle that results from infection
by an unusual transmissible agent called a prion. BSE possibly originated as a result of feeding cattle meat-and-bone meal
that contained BSE-infected products from a spontaneously occurring case of BSE or scrapie-infected sheep products.

If a cow is infected, it has trouble walking and getting up. It may also act very nervous or violent, which is why BSE
is often called “mad cow disease.”

6. Chronic Wasting Disease

A scrapie-like disease, designated chronic wasting disease, is found in mule deer and elk in the United States and
Canada. It is laterally transmitted with high efficiency, but there is no evidence that it has been transmitted to humans.
Infectivity has been detected in feces of deer before they become ill; the agent is retained in the soil, where it can then
be ingested by other deer and elk.

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 PART 4: LIST OF REFERENCES

• Books, G, et.al. Jawetz, Melnick & Adelberg’s Medical Microbiology, 27th Ed. McGraw-Hill. Copyright 2015.

• Bulmer, Glenn. Fungus Diseases in the Orient. Rex Bookstore. Manila. 1991.

• Mahon and Manusells (ed.) Textbook of Diagnostic Microbiology. Elsevier (Singapore) Pte Ltd. 2014

• Forbes, B., Sahm, D. & WEissfeld, A. Bailey & Scott’s Diagnostic Microbiology, 13th ed. Elsevier Science
(Singapore) Pte Ltd. Copyright 2014

• Davey, F., et.al (ed). John Bernard Henry, Clinical Diagnosis and Management by Laboratory Methods. 22nd ed.
W.B. Saunders Co. Philadelphia. 2007

• Black, Jacquelyn G. Microbiology, Principles and Explorations, 5th edition. USA: McGraw-Hill Companies Inc.
2005

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