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MicroPara Lec - Finals

S.Y. 2024 - 2025 | Level I Midyear Term

CLICKABLE TABLE OF CONTENTS

WEEK 4

SPIROCHETE & SPIRALS 2

MISCELLANEOUS BACTERIA 7

RICKETTSIAE, CHLAMYDIA 10

MYCOLOGY 12

VIROLOGY 21

DISCLAIMER: These notes were based on the actual lectures from our CI’s. If ever there are

any typos, missing info (especially terms that were only said verbally), or errors, please

understand if some parts are incomplete or not fully accurate. Kindly use these as a guide

and refer to other learning materials for confirmation. 🙏

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PATHOGENIC SPIROCHETES: TREPONEMA

WEEK 4

TOPIC OVERVIEW: Long Exam 4 Coverage

23. Spirochete & Spirillum

24. Miscellaneous bacteria

25. Rickettsiae, Chlamydia

26. Mycology

27. Virology

CHARACTERISTICS

●

Microscopy: Thin, spiral organisms with 3 axial

filaments

●

Difficult to stain

●

Transverse fission

●

Best demonstrated in darkfield microscopy

TREPONEMA PALLIDUM SUBSP. PALLIDUM

23 SPIROCHETE & SPIRALS

SPIROCHETE

CHARACTERISTICS

●

Gram (-)

●

Motile, slender, helically coiled, & unicellular

organisms

●

Facultatively anaerobic or aerobic

●

Most distinctive property is the presence of axial

filaments (axial fibrils), which are responsible for

motility

PATHOGENIC SPIROCHETES

1. TREPONEMA

●

T. pallidum subsp. pallidum

●

T. pallidum subsp. pertenue

2. BORRELIA

●

B. recurrentis

●

B. burgdorferi

3. LEPTOSPIRA INTERROGANS

SPIRALS

CHARACTERISTICS

●

Gram negative

●

Motile, slender, rigid organism

●

Amphitrichous flagella

●

Microaerophilic

PATHOGENIC SPIRALS

1. CAMPYLOBACTER JEJUNI

2. SPIRILLUM MINUS

●

The causative agent of syphilis

Microaerophilic

It is killed rapidly at 42 °C

Remains viable in whole blood or plasma for at

least 24 hours

It can cross the placenta and an intact mucous

membrane, and spread throughout the body

Generation time: 30 hours

CLINICAL INFECTIONS

1. SYPHILIS

●

Aka: French disease, Italian disease, The Great

Pox. It is also known as the “great imitator”

●

Transmission: Sexual contact, vertical

transmission, skin contact with active lesion,

transfusion of fresh blood, injuries from

contaminated needle stick

●

Symptoms: Chancre, fever, sore throat, headache,

rashes, and gummas of the skin

●

STAGES OF SYPHILIS:

A. PRIMARY STAGE

○

It is characterized by the appearance of

hunterian or hard chancre, which is an

infectious primary lesion that is painless and

usually seen on the genitalia

○

It develops 10 to 90 days after infection

○

No systemic signs or symptoms are evident

in this stage

○

Stage 1: Painless sores form on genitals,

rectum, or mouth

B. SECONDARY SYPHILIS

○

It develops 2 to 10 weeks after primary

syphilis

○

Systemic involvement with the following

manifestations: Fever, sore throat,

headache, generalized lymphadenopathy,

skin rashes involving the palms and soles,

and mucosal lesions

○

Stage 2: Painless sore heals, and skin rash

forms

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C. LATENT STAGE

○

It is the period in which the disease is

subclinical but not necessarily dormant

○

It occurs within more than a year of infection

○

In this stage, diagnosis can be made only by

a serologic test

D. TERTIARY SYPHILIS

○

It is the tissue-destructive phase

○

It may develop 3 to 10 years following the

last evidence of secondary syphilis

○

Complications: Neurosyphilis,

Cardiovascular abnormalities, eye disease,

and granulomatous-like lesions (gummas)

2. CONGENITAL SYPHILIS

●

Transmission: placental

●

Possibilities:

○

Fetus may be aborted

○

Baby may be born dead

○

Born alive with syphilis

○

Born in apparently good health but showing

evidence of syphilis several weeks, months, or

years after

LABORATORY DIAGNOSIS

1. MICROSCOPIC EXAMINATION

●

Direct microscopic examination of exudates is

recommended

●

Definitive test: Dark field microscopy for the

observation of motility

●

Stains: Levaditi’s stain and Fontana-Tribondeau

stain

●

Direct detection in lesions: Fluorescein

isothiocyanate-labeled antibody (FITC)

2. SERODIAGNOSIS

●

Nontreponemal test: These tests detect

non-specific antibodies against lipoidal antigens,

which are released when T. pallidum damages host

cells

○

●

It is used to monitor the treatment of syphilis

○

Serodiagnostic tests: Rapid plasma regain

(RPR), Venereal disease research laboratory

(VDRL), Unheated serum regain (USR),

Toluidine red unheated serum test (TRUST),

and ELISA

Treponemal test: It detects the presence of

antibodies to treponemal antigens

○

There are 2 types of treponemal/specific test:

(1) Indirect fluorescent antibody test (FTA-ABS)

(2) Treponema pallidum particle agglutination

(TPPA)

TREATMENT BY STAGE (part gihapon ni sa

congenital syphilis)

1. Primary, Secondary, and Early Latent Syphilis:

Typically treated with a single dose of intramuscular

benzathine penicillin G.

2. Late Latent and Tertiary Syphilis: May require multiple

doses of penicillin, often given weekly for three weeks

3. Neurosyphilis, Ocular Syphilis, and Otosyphilis:

Require a longer course of intravenous antibiotics, often

10-14 days

TREPONEMA PALLIDUM SUBSP. PERTENUE

PAGE 3 ●

●

The causative agent of yaws or frambesia tropica

Acquired through direct contact with skin lesion

YAWS

●

A chronic infectious disease primarily affecting the

skin, bones, and cartilage, particularly in tropical

regions

Characterized by skin lesions and, if left untreated,

can lead to severe deformities

TYPES OF YAWS

1. PRIMARY YAWS

●

Characterized by a wart like thickening of the

epidermis, which becomes fibrous, cracks open,

bleeds easily, and discharges a serous fluid

●

This lesion typically develops 9-90 days (average of

21 days) after infection

●

It can be accompanied by swollen lymph nodes

near the lesion

2. SECONDARY YAWS

●

Characterized by a multiple raised yellow skin

lesions appear on various parts of the body

●

These lesions can be papular (raised, solid bumps)

or ulcerative (open sores)

●

Bone pain, especially at night, and swelling of the

joints may occur

●

This stage can last for months, with periods of

active lesions followed by healing

3. TERTIARY YAWS

●

A late stage of the yaws infection

●

It typically occurs 5 to 10 years after the initial

infection, in individuals who have not been treated

●

It is characterized by destructive lesions affecting

the skin, bones, and cartilage

TREATMENT (either of 2 antibiotics)

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1. Azithromycin (single oral dose) at 30 mg/kg (maximum

2 gm) is the preferred choice in the WHO

2. Benzathine penicillin (single intramuscular dose) at

1.2 million units (adults) and 600,000 units (children)

For patients allergic to penicillin and azithromycin,

doxycycline 100mg (1 tab) orally, twice daily for 7 days

may be used

PATHOGENIC SPIROCHETES: BORRELIA

CHARACTERISTICS

●

Gram-negative, corkscrew-shaped spirochetes

●

Larger than Treponema species

VISUALIZATION

●

Dark-field microscopy

●

Wright or Giemsa stain

●

Difficult to visualize using Gram stain

●

Microaerophilic

BORRELIA RECURRENTIS

●

The causative agent of

louse-borne/epidemic/European relapsing fever

CLINICAL INFECTION

1. EPIDEMIC-RELAPSING FEVER

●

Causative agent: Borrelia recurrentis

●

Vector: Pediculus humanus corporis (body louse)

●

Reservoir: Human

●

A louse becomes infected when it feeds on a febrile

(feverish) patient with relapsing fever.

●

Intact lice do not transmit the infection.

●

Transmission occurs when the louse is crushed,

and Borrelia recurrentis from its hemocoel (body

cavity) enters the human body through intact skin or

mucous membranes.

●

Symptoms: High fever, Headache, Muscle and

joint pain, Nausea, Vomiting

TREATMENT

●

Antibiotics like tetracyclines, doxycycline,

erythromycin, or procaine penicillin G are

typically effective in treating relapsing fever

BORRELIA BURGDORFERI

●

The causative agent of lyme disease

Vector: Hard tick (Ixodes)

Transmission: Bite of the Ixodes

CLINICAL INFECTION

1. LYME DISEASE

●

An acute, recurring inflammatory infection involving

the large joints of knees

●

The hallmarks of infection are erythema migrans

(bull’s eye lesion on the skin) and swelling

●

STAGES OF LYME DISEASE:

A. FIRST STAGE

○

The presence of erythema migrans or red,

ringed-shaped lesion with a clear center or a

“bull’s eye like lesion” at the site of the tick

bite is diagnostic of lyme disease

B. SECOND STAGE

○

It may start weeks to months after infection

○

There is dissemination of the organism to

other parts of the body

○

Signs and symptoms: Neurologic disorders

and nerve palsy

C. THIRD STAGE

○

There is a presence of recurring chronic

arthritis (acrodermatitis chronica

atrophicans) that may continue for years

○

Infected individuals may also develop

demyelination of neurons with symptoms of

Alzheimer’s disease and multiple sclerosis

LABORATORY DIAGNOSIS

1. MICROSCOPIC EXAMINATION

●

Leptospira species can be stained with Giemsa or

Wright stain

●

Dark field microscopy can be used for the detection

of the organism in blood cultures after 2-3 weeks if

incubation

●

Relapsing fever

○

Specimen of choice: Peripheral blood

○

Giemsa or Wright Stain: blue-colored

●

Lyme disease

○

Specimen of choice: Blood, CSF, and biopsy

specimen

○

Warthin-Starry satin: Tissue section

○

Giemsa stain: Blood and CSF

2. CULTURE

●

Culture media: Barbour-Stoenner-Kelly medium or

Chick embryo

3. MOLECULAR TEST

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●

PCR is important in diagnosis of B. burgdorferi DNA

in urine

PATHOGENIC SPIROCHETES: LEPTOSPIRA

CHARACTERISTICS

●

Obligate aerobes

●

Tightly coiled and are highly motile with hooked

ends

●

They live in the limen of the renal tubules and shed

in the urine

●

Recommended animals for cultivation: Hamsters

and Guinea pigs

●

Generation time: 6 to 16 hours

LEPTOSPIRA INTERROGANS

●

This form of the illness is rarely fatal and represents

approximately 90% of all documented cases of

Leptospirosis

LABORATORY DIAGNOSIS

1. MICROSCOPIC EXAMINATION

●

Dark Field microscopy

2. CULTURE

●

Specimen of choice: Blood, CSF, and urine

specimens

●

Medium of choice: Fletcher’s medium, BMUH

medium, Bovine serum albumin, Stuart’s broth

TREATMENT

●

Antibiotics that may be used include doxycycline,

amoxicillin, or ampicillin

●

If the infection is severe, one may use intravenous

penicillin G, third-generation cephalosporins, or

erythromycin

●

The causative agent of leptospirosis

You can get leptospirosis after getting water or soil

contaminated by animal pee (urine) in your nose,

your mouth, your eyes or a break in your skin

Symptoms: fever, headache, myalgia, anorexia,

and vomiting

MODE OF ACQUISITION

1. Entry through breaks in the skin, mucous membranes or

conjunctiva

2. 3. Direct contact with the urine or carriers like rats

Contact with bodies of water that are contaminated with

the urine of the carriers

4. Upon entry, leptospira rapidly invade the bloodstream

and spread throughout CNS and kidneys

TYPES OF LEPTOSPIROSIS

1. ICTERIC OR WEIL SYNDROME

●

It is a severe form of illness that affects the liver and

kidneys, and cause vascular dysfunction

●

Symptoms: jaundice (yellowing of the skin and

eyes), kidney failure, liver failure, internal

hemorrhaging, and respiratory distress

●

Death occur in up to 10% of the cases

PATHOGENIC SPIRALS: CAMPYLOBACTER

JEJUNI

CHARACTERISTICS

●

Gram-negative bacterium

●

Curved, slender, motile rod

●

Microaerophilic bacterium

●

It is often transmitted from animals to humans, with

poultry being a major source of infection

●

Campylobacter bacteria are a common cause of

diarrheal illness. The illness is called

campylobacteriosis

●

People most commonly get Campylobacter infection

by eating raw or undercooked poultry

●

Eating other contaminated foods, drinking untreated

water, and touching animals that carry

Campylobacter can also cause infection

TREATMENT

●

Azithromycin therapy would be a primary

antibiotic choice for Campylobacter jejuni

gastroenteritis when indicated with a typical

regimen of 500 mg for 3 days

●

However, erythromycin is the classic antibiotic of

choice

2. ANICTERIC LEPTOSPIROSIS

●

This is the more common and less severe form of

leptospirosis

●

Symptoms: septicemic stage of infection, high

fever, and sever headache (3 to 7 days) followed by

immune stage

●

Hallmark of immune stage: Aseptic meningitis

PATHOGENIC SPIRALS: SPIRILLUM MINUS

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CHARACTERISTICS

●

A gram-negative helical-shaped bacillus commensal

organisms

●

The bacteria can be found in the oral, nasal, and

conjunctival secretions and animal urine

●

It can be transmitted to people through broken skin,

bites, or scratches

●

Infection can also result from close contact with an

infected rodent (without a bite of scratch)

CLINICAL INFECTIONS

1. STREPTOBACILLARY RAT-BITE FEVER

●

Incubation period: 1 to 22 (usually less than 7)

days, a viral-like syndrome develops abruptly,

causing chills, fever, vomiting, headache, and back

and joint pains

●

Most patients develop a morbilliform, petechial, or

vesicular rash on the hands and feet about 3 days

later

2. SEPTIC ARTHRITIS

●

Usually affecting the large joints asymmetrically,

develops in many patients within 1 week and, if

untreated, may persist for several days or months

●

Fever may return, occurring irregularly over a period

of weeks to months

TREATMENT

●

Is a 14-day course of antibiotics that usually begins

with an IV antibiotic for 6 to 7 days before

switching to an oral antibiotic

●

The IV antibiotic is usually one of the following:

○

Penicillin G 200,000 units every 4 hours

○

Ceftriaxone 1 g once a day

○

A higher dose of IV penicillin G may be

preferred for patients with severe disease

●

After 6 or 7 days, patients who have clinically

improved can be switched to one of the following

oral antibiotics to complete the 14-day course:

○

Amoxicillin 500 mg 3 times a day

○

Ampicillin 500 mg 4 times a day

○

Penicillin V 500 mg 4 times a day

Tabang ngano nag ka lisod namn ni

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24 MISCELLANEOUS BACTERIA

BACILLUS ANTHRACIS

CHARACTERISTICS

●

Aka: Anthrax bacillus

●

Largest pathogenic bacilli

●

Gram-positive

●

Rod-shaped

●

Non-motile bacteria

●

Halophilic organism (can withstand up to 7% of

sodium hypochlorite)

●

Endospore-forming pathogen

●

Can be grown under both aerobic and anaerobic

conditions

●

Not part of the indigenous human microbiota

CLINICAL INFECTION

ANTHRAX

●

The causative agent of anthrax is Bacillus

anthracis

●

Can cause severe illness in both humans and

animals

●

People usually get anthrax from infected animals or

even through contaminated animal products

TYPES OF ANTHRAX

1. CUTANEOUS ANTHRAX

●

The most common form of anthrax infection but also

considered to be the least dangerous

●

It is acquired through skin cuts and abrasions

●

A small papule appears at the site of the spore

inoculation 2 to 5 days after exposure

●

It is characterized by the appearance of a “black

eschar”, which is a black, necrotic and painless

central area that does not produce pus

2. PULMONARY ANTHRAX / WOOLSORTER’S

DISEASE

●

It is acquired when spores are inhaled into the

pulmonary parenchyma

●

It resembles an upper respiratory tract infection

●

Causes severe breathing problems and may lead to

death

●

Signs and symptoms: Mild fever, fatigue, malaise,

and dyspnea

3. GASTROINTESTINAL ANTHRAX

●

A rare but potentially fatal form of anthrax infection

●

caused by ingesting undercooked meat from an

infected animal. It can cause lesions and

inflammation from the throat to the colon

The bacteria usually affect the esophagus, throat,

stomach, and intestines

Signs and symptoms: Abdominal pain, nausea,

anorexia, vomiting, and bloody diarrhea

LABORATORY DIAGNOSIS

●

Specimen: Malignant pustule, sputum, and blood

●

Processing of samples for B. anthracis should be

done in a biological safety cabinet level 3

●

Spore stain: Malachite green and McFadyean stain

●

Direct Fluorescent Antibody Test: Diagnostic test

MANAGEMENT & TREATMENT

1. ANTIBIOTICS: Oral, injectable, or intravenous

antibiotics for 60 days. Commonly used antibiotics

include ciprofloxacin and doxycycline

2. ANTITOXINS: These injectable antibody medications

neutralize anthrax toxins in your body. Treatment

typically includes antibiotics too

3. VACCINE: A vaccine to prevent anthrax infection,

BioThrax, also treats infected people. Treatment

involves three doses of the vaccine over four weeks.

You’ll receive antibiotics at the same time

LISTERIA MONOCYTOGENES

PAGE 7 CHARACTERISTICS

●

Gram-positive

●

Rod-shaped

●

Peritrichous flagella

●

Catalase positive

●

Beta-hemolytic when grown on blood agar

●

Both a human and an animal pathogen

●

Halophilic organism

CLINICAL INFECTION

LISTERIOSIS

●

Listeria monocytogenes is the causative agent for

this infection

●

A serious infection that affects neonates, pregnant

women, and immunocompromised hosts

TYPES OF LISTERIOSIS

1. MATERNAL DISEASE (PREGNANCY)

●

It usually occurs during the third trimester of

pregnancy

●

It leads to miscarriage or stillbirth

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●

Signs and symptoms: flu-like illness, fever,

headache, and myalgia

2. NEONATAL DISEASE

●

It is associated with an intrauterine infection due to

the aspiration of infected amniotic fluid

●

It leads to meningitis that is usually seen by the

third week of life

●

Mode of acquisition: transplacental & perinatal

3. DISEASE OF IMMUNOCOMPROMISED HOSTS

●

It develops through the ingestion of contaminated

dairy products and processed meat products

LABORATORY DIAGNOSIS

●

Specimen: Blood, CSF, and swab of lesions

●

Motility Test: Tumbling motility at RT

●

Culture: BAP, CAP, BHI

●

Biochemical Test:

○

Glucose fermentation (+)

○

Catalase (+)

○

Urease (-)

○

H2S production, Nitrate reduction (-)

MANAGEMENT & TREATMENT

1. ANTIBIOTICS: Ampicillin or penicillin G are the primary

choices for treating listeriosis. Gentamicin is often added

to enhance effectiveness, particularly for meningitis

2. NEONATAL INFECTIONS: In newborns, ampicillin

combined with an aminoglycoside (like gentamicin) is

the recommended treatment

○

thus resist water treatments

They cannot grow on routine primary plated

media like BAP

CLINICAL INFECTIONS

1. LEGIONNAIRES’ DISEASE

●

It is also known as legionellosis, which is febrile and

pneumonic illness

●

Mode of transmission: Airborne spread or inhalation

of infectious aerosols

●

Symptoms: High fever, non-productive cough,

headache, neurological, and severe

bronchopneumonia

2. PONTIAC FEVER

●

It is a non-fatal respiratory infection that resembles

an allergic disease but exhibits the symptoms of

pneumonia

3. WOUND ABSCESS & ENCEPHALITIS

Table 1: Comparison of Legionnaires’ Disease and

Pontiac Fever

Legionnaires’ Disease Pontiac Fever

Type of

Illness

●

Progressive

pneumonia

5-15% fatality rate

Treatment required

Highest fatality rate

in health care

facilities

●

Flu-like illness

Recovery in 2-5

days

Medical treatment

not necessary

LEGIONELLA PNEUMOPHILA

●

Symptoms

Infection

rate

Incubation CHARACTERISTICS

●

Gram negative

●

Bacillary or coccobacillary in form

●

Aerobic, motile

●

Non-carbohydrate fermenting

●

Major reservoirs: Hot water system, cooling

towers, and evaporative condensers

●

Serogroups: 1 to 7

●

Serogroups associated to the Legionnaires disease

1, 4, and 6

●

The distinguishing characteristics of Legionella

species are as follows:

○

They can infect and multiply within some

free-living amoeba, ciliated protozoa, and

biofilms

○

They can be isolated from lakes, rivers, hot

springs, and mud

○

They can tolerate up to 3 mg/L of chlorine and

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Severe pneumonia

with chills and cough

Muscle aches,

headache, tiredness,

loss of appetite, and

diarrhea

●

Fever

Muscle aches

<5% of those exposed >95% of those exposed

2-10 days 36 hours

Risk

Factors

●

Smoking and lung

disorders

Diabetes, cancer,

and kidney disease

AIDS/HIV

Age older than 50

Heavy drinking

None knownMicroPara Lec - Finals

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LABORATORY DIAGNOSIS

●

Specimen: Sputum and bronchoalveolar lavage

●

Urine is an important specimen for antigen

detection

●

Culture media: BCYE with L-cysteine, ferric salt,

and alpha-ketoglutarate

●

Serologic Test: Indirect fluorescent antibody

●

Rapid methods: PCR test, Urine antigen test

MANAGEMENT & TREATMENT

1. ANTIBIOTICS

●

Fluoroquinolones (like levofloxacin or

moxifloxacin) and macrolides (like azithromycin)

are commonly used antibiotics for Legionnaires’

disease

●

Treatment typically lasts for 1 to 3 weeks, with a

longer duration (up to 3 weeks) sometimes

recommended for severely immunocompromised

patients

MANAGEMENT & TREATMENT

1. ANTIBIOTICS

●

Macrolides: Azithromycin, clarithromycin, and

erythromycin are commonly used macrolide

antibiotics for Mycoplasma pneumoniae infections

●

Tetracyclines: Doxycycline is an alternative for

macrolide-resistant infections, but is not

recommended for young children

●

Fluoroquinolones: These antibiotics may be used

if other treatments fail, but are generally not

recommended for children

MYCOPLASMA PNEUMONIAE

CHARACTERISTICS

●

Gram negative

●

Rod shaped bacteria

●

Lack cell wall

●

Fastidious

●

Facultative anaerobes

CLINICAL INFECTION

PRIMARY ATYPICAL PNEUMONIA

●

It occurs as separate incidents or as outbreaks in

closed populations such as in school, military

camps, and within family members

●

Mode of acquisition: Inhalation of contaminated

aerosol droplets

●

Symptoms: dry cough, fever, and mild shortness of

breath

LABORATORY DIAGNOSIS

●

Specimen: Throat swab, serum, bronchoalveolar

lavage, sputum & lung tissue, urethral, vaginal or

endocervical swab, blood, urine, prostatic

secretions and semen

●

Culture: SP4 broth

●

Serodiagnosis: ELISA

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25 RICKETTSIAE, CHLAMYDIA

RICKETTSIA

CHARACTERISTICS

●

The species of this genus have the simplest

bacterial form and are considered transitional

organisms between bacteria and viruses

●

Fastidious, obligate, intracellular organism

●

Mode of acquisition: Humans become infected ff

the bite of an infected arthropod vector

●

Accidental host: Humans

●

Agents of bioterrorism: R. prowazekii and R.

rickettsii

TRANSMISSION & SPREAD OF RICKETTSIA

1. The organisms gain access to humans through skin

abrasions or arthropod bites

2. The organisms are disseminated homogeneously, thus

causing vasculitis in the blood vessels

3. The members of the typhus group reproduce in the

cytoplasm cellular injury and death

4. Rickettsia felis is maintained transovarially in cat flea,

Ctenocephalides felis

RICKETTSIA: SPOTTED FEVER VS TYPHUS

GROUP

1. SPOTTED FEVER GROUP

●

Rocky mountain spotted fever (RMSF) is the most

serious rickettsial infection

●

For RMSF, humans are the accidental hosts and

ticks are the main vector and reservoir

●

The rashes develop on the palms of the hands and

soles of the feet of RMSF patients

2. TYPHUS GROUP

●

Epidemic typhus is characterized by rashes on the

face, palms, and soles of the feet of the sick

individual

●

Rashes are not commonly observed in patients with

endemic typhus

●

Inhalation of aerosol from dried infected flea feces

is also a mode of transmission of Rickettsia typhi

infection

ORIENTIA

ORIENTIA TSUTSUGAMUSHI

●

Aka: Scrub typhus

●

It belongs to the family of Rickettsiaceae

Transmitted through the bite of infected chigger

mite

Incubation period: 1-3 weeks

Clinical manifestation: fever, chills, sore throat,

myalgia, lymphadenopathy, generalized

maculopapular skin rashes, characteristic skin

lesion at the site of bite (eschar)

MANAGEMENT & TREATMENT

1. ANTIBIOTICS

●

Primary treatment of scrub typhus is doxycycline

until the patient improves, has been afebrile for 48

hours, and has received treatment for at least 7

days

●

For pregnant women and patients with severe

doxycycline allergy, azithromycin has been shown

to be a safe and effective alternative

CHLAMYDIA

CHARACTERISTICS

●

Gram negative

●

Small, non-motile

●

Obligate intracellular organisms

●

They do not possess cytochromes and cannot

synthesis their own ATP

●

Species: C. trachomatis, C. psittaci, C.

pneumoniae

TWO MORPHOLOGIC FORMS

RETICULATE BODY (RB) ELEMENTARY BODY (EB)

●

Replicative and

non-infectious form

It is the intracellular and

metabolically active form

It directs the

reproduction of host

cells to their own

metabolic needs so they

multiply by binary fission

●

It is the extracellular

form of Chlamydia and

is spherical in shape

It resemble Gram

negative bacilli with a

rigid cell wall

It infects the host cell by

inducing active

phagocytosis

Its 2 components are

the major outer

membrane protein and

lipopolysaccharide

antigen

CHLAMYDIA TRACHOMATIS

●

It is one of the major sexually transmitted

PAGE 10 #PASAR #RN2028 Lord Help Us Pass MICROPARA 〒▽〒MicroPara Lec - Finals

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●

pathogens

It is one of the principle causes of pelvic

inflammatory disease and ocular trachoma

It can travel through the birth canal where infants

can be infected during birth

It is associated with infertility and ectopic pregnancy

Natural host: Humans

CLINICAL INFECTION

1. TRACHOMA

●

It is a chronic inflammation of the conjunctiva that

leads to blindness

●

It can cause distortion of the eyelids

●

Mode of transmission: Contact with contaminated

objects, hand-to-hand contact with carriers, and

through vectors

2. LYMPHOGRANULOMA VENEREUM (LGV)

●

It is a sexually transmitted disease that has

multi-system involvement

●

A small, painless ulcer or papule appears initially,

and then nodules develop after several weeks

LABORATORY DIAGNOSIS

●

Specimen: Urethra and cervical secretions,

conjunctiva discharge, nasopharynx and rectal

swabs and materials aspirated from fallopian tubes

and epididymis

●

Culture: Buffalo green monkey cells, HeLa 229

cells, Hep-2 cells, McCoy cells, and

Cycloheximide-treated McCoy cells

●

Enzyme immunoassay: rapid antigen assay

MANAGEMENT & TREATMENT

1. ANTIBIOTICS

●

Azithromycin: A single 1-gram dose is often

prescribed

●

Doxycycline: Typically taken twice a day for 7 days

●

Other options: Tetracycline, erythromycin, or

ofloxacin may be used in certain situations

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MOULDS

26 MYCOLOGY

Study of fungi

FUNGI

●

Microscopic eukaryotic organisms

First classified under kingdom Plantae, later

separately classified under Kingdom Fungi

○

Due to the presence of unique rigid cell

wall, which is chemically different from the

bacterial cell wall

○

Unlike plants, fungi are non photosynthetic

○

They have similar appearance with plants

(i.e., mushrooms)

80,000 species described: 400–medically

important, <50 responsible for more than 90%

of fungal infections of humans and animals

Fungal cell wall

○

Rich in carbohydrates: polymers of

acetylglucosamine “chitin”, forming a thick

layer protecting inner organelles from the

adverse external environment

Cell membrane

○

Contains ergosterol; organized nucleus more

often reproduce by asexual spores (but can

also produce sexually)

Produce multi-celled hyphae or single-celled

yeasts

●

Classified according to morphology and taxonomy

FUNGAL CELL WALL

●

Boxes =

antifungal drugs

●

Distinct about

fungi is the

presence of

CHITIN (plants

have no chitin

but cellulose)

●

Fungi look like

plants macroscopically, but look more like animal

kingdom microscopically (They are closely related

to animals than plants)

MORPHOLOGICAL CLASSIFICATION

COMMON TERMS

1. Hyphae: tubular-like structures that compose a mold

colony

2. Septae: cross walls present in some hyphae; singular:

septa

3. Nonseptate: lacking septa

4. Hyaline:

○

lacking pigment

○

molds do NOT have pigment; they are

colorless and transparent

5. Dematiaceous: containing dark pigment

6. Chlamydoconidia: large, round spores in or on hyphae

7. Conidia: asexual spores produced by molds with septa

8. Mycelium: a colony, made up of rope-like filaments

called hyphae

●

Hyphae: help in the interexchange of cytosol and

organelles between adjacent cells

●

May be septate or pauciseptate

9. Spores: Conidia

●

produced in a conidiophore

●

Macroconidia and/or microconidia (can be both or

either)

●

Spores or hyphae may be pigmented or not

Possible Structure of Mould Colony

●

Not all can be found in every fungal species

10. Chlamydospore: spores that grow on the hyphae itself

(circles)

11. Arthroconidia: bigger segments on the hyphae

compared to the septae

12. Sporangiospores: found in sporangia connected to the

hyphae

●

Conidia are connected to the conidiophore

connected to the hyphae

13. Rhizopus and Mucor: sporangiophore

14. Aspergillus and Penicillium closely resemble

conidiospores and conidia

PAGE 12 #PASAR #RN2028 Lord Help Us Pass MICROPARA 〒▽〒MicroPara Lec - Finals

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○

YEAST

Mould forms are saprophytic: loves to feed

on dead plants and animal remains. This is

also why fungi are big factors and contributors

to decomposition.

CHARACTERISTICS

●

Unicellular eukaryotic organisms (unlike the molds

are multicellular)

●

Appear smooth and mucoid on the media

●

Aerobic organisms, but growth is enhanced in

anaerobic conditions

●

Acquire energy from an organic compound by

oxidation

Examples of Blastomyces dermatitidis, Coccidioides immitis,

Histoplasma capsulatum, Paracoccidioides brasiliensis

At 25°C, the forms are mycelial, or they look like

molds

At 37°C, they look like yeasts

●

Yeast Cell

A single cell reproduces asexually. Yeasts

reproduce through budding

The third “new cell” produces a daughter cell. And

each cell has a nucleus, cytoplasm, reserve food

bodies, and a vacuole

○

The vacuole is one distinctive feature of the

yeast, along with the budding

YEAST-LIKE FUNGI

●

Partly resemble yeast cells

●

Also develop pseudohyphae resembling hyphal

filaments

●

Opportunistic Fungi

These are the different forms of fungi that we can

see, and the fungi that can cause diseases or

mycosis.

○

First, yeast cells. We have the parent yeast

cell; it buds to produce daughters. During

budding, it can produce pseudohyphae or a

germ tube.

○

There are also the mould forms, candida, and

hyphae or hypha.

○

Cryptococcus is somewhat unique because of

the presence of capsules.

DIMORPHIC FUNGI TAXONOMIC CLASSIFICATION

CHARACTERISTICS

●

Exist in both mycelial and yeast forms in varying

temperatures

●

37°C: yeast-like colonies

●

25°C: mould-like colonies (esp. in soil)

○

Yeast forms are pathogenic

●

Taxonomy is the classification that considers not

just morphology but also the function, genetic,

biochemical, and behavioral aspects of the

organisms. It has a much broader scope and

consideration in classifying organisms.

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1. ZYGOMYCETES

●

Lower fungi with non-septate

hyphae produce sporangiospores

(asexual spores).

●

The spores are inside the

sporangium, so they are called

sporangiospores.

2. ASCOMYCETES

●

Produce septate hyphae and

ascospores. (Sexual spores are

present inside the sac or ascus)

●

Inside the ascus, there are the

ascus spores

●

Ascus is singular, and asci is plural

3. BASIDIOMYCETES

●

Produce septate hyphae and basidiospores.

(Sexual spores are present in the basidium)

●

The basidium looks like long, goblet cells. And, at

the top are basidiospores.

●

The goblets are called the basidium. Basidiospores

are the name of the spores found on the basidium

●

Basidiospores: Basidium look like goblet cells

○

Basidiospores, on top of it, what connects the

basidiospores and basidium is the sterigmata

○

Sterigmata look like small feet or pods

connecting the spores to the basidium

2. ASEXUAL SPORES

●

Vegetative spores

○

Formed by budding (yeast cells)

○

Formation of septa in hyphal filament (moulds)

○

Folding and thickening of hyphal filaments

(resulting in thick-walled spores)

●

Aerial spores

○

Conidiospores

○

Microconidia

○

Macroconidia

○

Sporangiospores

●

Labels

○

Conidiospore

○

Phialides

○

Vesicle

○

Conidiophore

○

Septate hyphae

SIGNIFICANCE OF FUNGI

4. DEUTEROMYCETES or FUNGI IMPERFECTI

●

Produce septate hyphae and cannot be classified

into sexual or asexual because their sexual state is

unknown

●

Share common features with ascomycetes

●

Most medically important fungi belong to this group

FUNGAL REPRODUCTION

SEXUAL or ASEXUAL

●

Fungal reproduction, whether it may be sexual or

asexual reproduction, produces spores

●

The spores are easily dispersed. And, it is

considered the most infective stage in cases of

infectious fungi because these spores are very

resistant and can survive dry and adverse

conditions

1. SEXUAL SPORES

●

Zygospores: found between hyphae

●

Ascospores: found inside the ascus. If the ascus

bursts, then the ascospores will be released

ADVANTAGES OF FUNGI

●

Decomposition

○

For carbon cycle = plants grow

●

Fermentation

●

Food

●

Pharmaceuticals

○

Fungal metabolites are used in antibiotic drugs

like penicillin = came from penicillium spp.

●

Model research organisms

○

Fungi are the basis of genetic research

because of their simple eukaryotic form. Before

they proceed to the multi-celled,

complicated-complex forms like humans, they

start with the simpler ones, like fungi and

bacteria

DISADVANTAGES OF FUNGI

●

Tree diseases

●

Crop diseases

●

Food spoilage

○

Bread molds, food molds, expiration date

molding

●

Wood and timber degradation

●

Mycoses or Fungal Infections

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MYCOSES

●

They are fungal infections. Term used to describe

fungal infections

Diseases caused by fungi

CAUSES OF MYCOSES TO HUMANS

1. INHALATION OF SPORES: enter the lungs, get

localized, cause respiratory infection

2. INOCULATION OF SPORES: through cuts, localize in

skin

3. ALTERATION OF NORMAL FLORA: due to

overconsumption of heavy dose of antibiotics (alter or

kills normal flora that acts as a physical barrier, this

enhancing entry of pathogenic fungi)

4. SUPPRESSED IMMUNE SYSTEM: patients undergoing

chemotherapy, in steroids due to transplantation, HIV, or

diabetics

4 SUBTYPES

1. Superficial Mycosis

2. Subcutaneous Mycosis

3. Deep Mycosis

4. Opportunistic Mycosis

SUPERFICIAL MYCOSIS

PATHOGENESIS

1. TRANSMISSION

●

Transmitted through contact, through adherence &

invasion of fungi

●

Become pathogenic when they change morphology

from yeast to mycelium (mold colony)

●

Dimorphic in nature

2. PIGMENTATION

●

Due to azelaic acid, which is the secondary

metabolite produce by fungi. It reacts on the

melanin pigments that is found on the skin. Thus,

producing pigments (patches)

3. SYMPTOMS

●

Mild patches on chest, back, neck, & arms

●

Patches lead to pigmentation

●

Discoloration starts spreading in untreated

conditions

●

Dryness of the skin

●

Itching of the skin

LABORATORY DIAGNOSIS

●

Specimen: skin scrapings of the lesions. Superficial

layers is enough

●

Direct microscopy: KOH (Potassium hydroxide)

wet mount. Skin scraping is fixed on slide with 20%

KOH, and then the skin scrapping is mixed into that

wet mount, covered with a cover slip. And then

short unbranched hyphae can be observed

Culture: Saubouraud’s Dextrose Agar, at 32-37

degrees celsius: round & smooth colonies

○

After the culture, it is then mounted on

lactophenol cotton blue wet mount to further

see the morphology of the malassezia species

●

Externally localize on the layers of skin, hair, & nail

& grow well on dead layers

Classified into two types:

○

Surface Mycoses

○

Cutaneous Mycoses

TINEA VERSICOLOR

●

Caused by Malassezia globosa

●

Is a yeast form of fungi that live on the skin in few

numbers but multiply during adverse conditions

leading to skin infections

●

They can exist as a normal flora, but during

adverse conditions, and with the several causes

mentioned earlier, it can lead to skin infection

●

TREATMENT

●

Topical application of antifungal ointments. Since it

is a superficial mycoses, ointments will do

○

Whitefield’s ointment: composed of benzoic

acid, salicylic acid, ciclopirox olamine, and

tincture of iodine

○

Sulfur-containing ointment

○

Oral antifungals: triazole, itraconazole,

ketoconazole. This is used in severe cases. If

the name ends with “azole”, it is most likely an

antifungal drug

TINEA NIGRA

●

Caused by Hortaea werneckii

●

Dimorphic fungi that exist in both yeast and hyphal

forms

●

Responsible for asymptomatic mycoses

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●

Saprophytic in nature & found on dead & decayed

materials

PATHOGENESIS

1. ENTRY

●

Inoculation of fungus through cuts and wounds.

●

Enter, localize, and cause superficial infection on

palms and foot soles.

●

From the name itself, you can deduce that the color

is darker, compared to Tinea versicolor.

2. HALOTOLERANT

●

It is tolerant to ionic stress, or the ability of

tolerance is the ability of an organism to grow

at salt concentrations higher than those for

growth.

●

Able to survive in human tissues by

accumulating and utilizing melanin. It can survive

on areas of the skin that actually are more

prone to sweat, like the palms and foot soles.

●

Because of its appearance, there are times that

this mycoses is confused with the type of skin

cancer or melanoma.

3. SYMPTOMS

●

Mild patches on palms and foot soles.

●

Patches appear brownish or black in color.

Irregular in shape.

●

Scale-like skin growth

●

Itching

●

If asymptomatic, you cannot

see any of these symptoms. But

there is fungal present still on the skin.

LABORATORY DIAGNOSIS

●

Specimen: Skin scrapings of the lesions.

Because it is superficial.

●

Direct Microscopy: KOH wet mount. Budding

yeast cells on branched hyphal elements.

●

Culture: SDA, at 32 ̊C - 37 ̊C, 3 weeks:

dematiaceous colonies that become velvety with

age. In culture, they appear mycelial bold-like

forms, unlike the Malassezia that appears

yeast-like. Very slow forming fungal colony.

Even in 3 weeks, it is still small in size (coin- sized).

●

Lactophenol Cotton Blue: Further testing of

isolated colonies.

○

This is the wet

mount using LPCB

because it is blue

and it can be seen

more clearly,

compared to the

○

previous slide which contains KOH wet

mount. These fungal colonies are that much

clearer. You can see the form is fully

mycelial. You can see the hyphae. Previous

slide was not that clear because there is a

mixture of yeast cells and mycelial hyphal

elements – like in the middle of transformation.

Since the LPCB gets its specimen from the

colony grown in culture, you can see the

form is now fully mycelial or hyphal.

TREATMENT

●

Topical application of antifungal ointments.

Good hygiene

Avoiding exposure to moist and dirty places.

PIEDRA

●

This affects the hair

Two types:

○

White Piedra

○

Black Piedra

1. WHITE PIEDRA

●

Caused by

Trichosporon beigelii.

●

Asexuallyreproductive

●

Part of normal flora

●

Yeast-like fungi that

change to septate

hyphal filaments.

●

Dimorphic

●

Pathogenesis:

○

Close contact with the infected person’s towel,

soap, comb, etc.

○

White nodules: spores transmitted by contact

●

Symptoms:

○

Acclimation of white lump of yeast cells on the

hair follicles of the head, beard, even pubic

hair. You can directly get this & place it on the

wet mount & immediately see the yeast cells

○

Hair loss

○

Itching

2. BLACK PIEDRA

●

Caused by the fungi, Piedraia hortae.

●

Asexual

●

Transmitted through contact.

●

Pathogenesis:

○

Found on hair shafts of the beard and scalp.

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●

Symptoms:

○

Brown to black nodules firmly attached to the

hair shaft.

○

Nodules: ascostroma (asci and ascospores).

○

Mostly asymptomatic

○

Hair breakage in extreme cases

LABORATORY DIAGNOSIS

●

Specimen: Hair

●

Direct Microscopy: KOH wet mount Hair nodules

●

Culture: Sabouraud Dextrose Agar

●

LPCB: Further testing of isolated colonies can be

done through LPCB

TREATMENT

●

Topical application of antifungal ointments

○

Imidazoles & selenium sulfide

○

Amphotericin B ointments

Using separate towels, soaps, & combs

SUBCUTANEOUS MYCOSIS

●

Causes disease in living tissues leading to tissue

damage

Three types

○

Mycetoma

○

Chromoblastomycosis

○

Rhinosporidiosis

MYCETOMA

●

Persistent subcutaneous granulomatous infection

affecting the foot, & as infection progresses, the

bones.

●

Aka: Madura foot

●

Caused by Actinomycetes (Actinomycetoma) or

Filamentous fungi (Eumycetoma)

○

Aerobic, filamentous fungi commonly found in

soil

○

Mycetoma is not just caused by fungi, by

bacteria such as the Actinomycetes

PATHOGENESIS

1. TRANSMISSION

●

Inoculation of fungus through cuts or wounds from

soil

●

Enter tissue, localize, & replicate inside live cells

●

Spores from clumps inside cells resulting in

granules

○

Granules vary in color, depending on

contributing agents

2. SYMPTOMS

●

Itching

●

Swelling in area of itching

●

Pus formation

●

Ulceration & nodules

●

Pus expulsion

●

Irrigation in area of infection (watery irrigation)

●

Disfiguration of leg

LABORATORY DIAGNOSIS

●

Specimen: Pus exudates

●

Direct microscopy:

○

Gram staining: for identification of

actinomycetes (gram positive)

○

KOH Wet mount: for identification of

Eumycetes (fungi)

●

Culture: after the direct microscopy, if it is found to

be a bacteria, the it can be grown on Blood Agar or

Nutrient Agar. If it is found to be a fungi, then it is

grown on Sauboraud’s Dextrose Agar (SDA)

TREATMENT

●

Surgery & removal of abscess at early stage with

proper administration of oral antifungal &

antibacterial drug therapy (to prevent the further

spread of the fungi

○

Actinomycetoma: Antibacterial drug;

Rifampicin, Dapsone, & Sulphonamides

○

Eumycetoma: Oral antifungal; Itraconazole &

Ketoconazole

●

Treatment should be prolonged for complete

eradication of pathogens. Because in mycetoma, it

affects the deeper tissues, which is why treatment

needs to be completely eradicated as it can spread

if treatment is not enough.

CHROMOBLASTOMYCOSIS

●

Caused by five different vegetative fungi

(pathogens)

○

Phialophora verrucosa

○

Fonsecaea compacta

○

Fonsecaea pedrosoi

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●

○

Rhinocladiella aquaspersa

○

Cladophialophora carrionii

Cause persistent infection that slowly progress &

form granulomatous lesions

○

Lead to accumulation of keratinocytes in

epidermal layer resulting in sloughing of skin

Caused by Actinomycetes (Actinomycetoma) or

Filamentous fungi (Eumycetoma)

○

Aerobic, filamentous fungi commonly found in

soil

Mycetoma is not just caused by fungi, by bacteria

such as the Actinomycetes

PATHOGENESIS

●

Chronic subcutaneous infection

●

Transmission: cuts or wounds, primarily in leg

region

○

Upon entry, fungi spreads and invades tissue

very slowly (due to slow growing capacity)

○

Very resistant to immune cells due to its

melanin cell wall

●

Affects tissue:

○

Forming hyperplasia of epidermis producing

nodules with pus formation

○

Distinct feature: painless

●

Drains lymphatics:

○

Severe: damage organs

○

It can take years undetected. It starts with

nodules, if not treated, then it can drain the

lymphatics, & cause organ damage

●

Symptoms:

○

Itching in area of entry

○

Swelling with pus formation

○

Nodule formation as infecting drains to lymph

○

Ulcerations

LABORATORY DIAGNOSIS

●

Specimen: pus cells or skin scrapings

●

Methods:

○

KOH wet mount

○

Histopathological analysis: check

multinucleated giant cells with granules &

sclerotic bodies inside the outside cells

○

Culture: SDA, brown, or black moldy colonies

TREATMENTS

●

Surgery & removal of pustule & proper oral

treatment

●

Heat therapy (early stages)

●

Antifungal agents

○

Flucytosine

○

Ketoconazole

Itraconazole

RHINOSPORIDIOSIS

●

Granulomatous infection of the nose, eyes, & mouth

●

Caused by Rhinosporidium seeberi

●

First classified as sporozoan parasite, but later

classified as lower fungi

●

Still shares morphological similarities with aquatic

parasites

●

According to DNA sequencing, belongs to fish

parasite (which is right between animal and fungal

division)

PATHOGENESIS

●

Fishermen & washermen are mostly affected due to

constant contact with water habitats

●

Mode of transport: entry thru cuts & wounds

○

Also enters through nasopharyngeal route or

even eyes & external genitals

●

Symptoms:

○

Accumulation of large mass of cells that hangs

out as a separate layer

○

Pus accumulation leading to foul smell

○

Breathing difficulty due to protrusion of layer

●

Lab diagnosis:

○

Skin biopsy: Histopathological analysis

○

KOH wet mount: for endospores within

sporangium

●

Treatment:

○

Surgery

○

Intravenous administration & amphotericin B

and Dapsone

DEEP MYCOSIS

●

Otherwise called systemic mycosis

Involves both pathogenic and opportunistic fungi

yeast form and start invading tissue

○

Pathogenic Fungi: Gain entry

○

Opportunistic Fungi: Suppress the immune

system

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HISTOPLASMOSIS

●

Systemic mycosis caused by Histoplasma

capsulatum

○

Saprophytic fungi mostly found in soil glands

○

Dimorphic fungus

○

Solo-celled microconidia

●

Colony Culture:

○

Produces moldy white colonies

●

Affects respiratory system causing pulmonary

infection

○

Does not involve the fungi itself

Involves antibody-antigen reaction

Reacts to blood antigen

One of the fastest tests due to fungal colonies

needing to take a few days for culture to

develop

TREATMENT

●

Itraconazole

●

Amphotericin B

●

Relapses may occur for immunocompromised

patients (prolonged treatment with itraconazole

PATHOGENESIS

●

Intracellular pathogen

●

Mode of transmission: Inhalation; Molds convert

●

Yeast cells engulfed by alveolar macrophages

●

Yeast replicates inside & use the host cells to travel

around the body & invade other areas like liver,

spleen, & lymph nodes

●

Results in pulmonary infection in men, children &

immunocompromised patients (aids & undergoing

chemotherapy

●

Symptoms:

○

Dry cough

○

Body pain

○

High fever

○

Restlessness

○

Lymphadenopathy

○

Fatal in severe cases affecting liver, eyes, &

glands

LAB DIAGNOSIS

●

Specimen: sputum, urine, throat swab, bone

marrow aspirator

●

Direct microscopy: histopathological staining or

Giemsa staining to view intracellular yeast (biopsy

specimen)

○

KOH will not work

●

Culture: SDA (for moldy colonies), blood agar (for

yeast colonies)

●

Serology: complement fixation test & enzyme

immunoassay

OPPORTUNISTIC MYCOSIS

●

Infection that occur in immunocompromised

●

patients

Depends on the load of organism and the

virulence caused to the host

1. CANDIDIASIS

●

Caused by Candida albicans, Candida tropicalis,

Candida parapsilosis and Candida krusei

●

Part of normal flora of skin and GIT

●

Cells are oval-shaped and divide by budding, which

form into pseudohyphae

●

Some species like C. albicans are dimorphic

2. CRYPTOCOCCOSIS

●

Caused by Cryptococcus neoformans and

Cryptococcus gattii

●

Mostly found in soil, feces of birds

●

Yeast-like fungi with resistant polysaccharide

capsules

●

Can be cultured using fungal or bacteriological

media, 24 hrs at 37 degrees C

●

Colony: produces mucoid white colonies (due to

capsule)

PAGE 19 #PASAR #RN2028 Lord Help Us Pass MICROPARA 〒▽〒MicroPara Lec - Finals

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PATHOGENESIS

●

Mode of transmission: inhalatioN of fungal cells

●

Enter respiratory system, affecting circulating

cells and compromises immune system by

resisting immune reactions

●

Multiply and infect other parts of the body,

especially the CNS causing meningoencephalitis

(inflammation of brain tissues and meninges)

●

Symptoms:

○

Fever

○

Headache

○

Body pain

○

Flu symptoms

○

CNS affected in severe causes, causing

encephalitis

LAB DIAGNOSIS

●

Specimen collected: Sputum, Blood (severe

systemic cases), Throat swab, CSF (suspected

encephalitis)

●

Direct microscopy

○

India Ink: special staining used specifically for

showing the capsule of Cryptococcus spp.

●

Serology

TREATMENT

●

Amphotericin B and flucytosine

○

Combination of both for severe cases (ie:

immunocompromised patients)

○

Prolonged treatment provided to avoid

recurrent infections

me and bestie looking at micropara scores

PAGE 20 #PASAR #RN2028 Lord Help Us Pass MICROPARA 〒▽〒MicroPara Lec - Finals

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27 VIROLOGY

study of viruses and virus-like agents

VIRUSES

●

Simplest form of life and smallest known

infectious agents

Submicroscopic, Intracellular obligate parasites

Filterable agents

Have a naked capsid or an envelope morphology

Capable of infecting any animal, plant, or

bacterial cell

○

Since they are the smallest, they can infect

anything, including bacteria

Viral components are assembled and do not

replicate by “division”

Are not living organisms

Must be infectious to endure in nature

Must be able to use host cell processes to

produce their components (viral messenger

RNA, protein, and identical copies of the genome).

Must encode any required processes not

provided by the cell

Viral components must self-assemble

RELATIVE SIZES OF REPRESENTATIVE VIRUSES,

BACTERIOPHAGES, & BACTERIA

●

Smallest

virus:

parvovirus,

picornavirus

VIRUSES: CLASSIFICATION & NAMING

VIRUSES: STRUCTURE

1. STRUCTURE: size, morphology, and nucleic acid

2. BIOCHEMICAL CHARACTERISTICS: structure and

mode of replication

●

so far this is the main means of taxonomic

classification of a virus

3. DISEASE: e.g., Hepatitis, encephalitis

4. MEANS OF TRANSMISSION: ex. Arbovirus (spread

by insects)

5. HOST CELL (HOST RANGE): animal (human, mouse,

bird), plant, bacteria

6. TISSUE OR ORGAN (TROPISM): ex. Adenovirus,

enterovirus

●

Adeno: affects respiratory tract; entero affects

GIT)

COMPONENTS OF THE BASIC VIRION

Main properties that differentiate them from other

microorganisms

1. SMALL SIZE

●

Varies from 10 to 300 nm (some can even

extend to 2000 nm depending on which virus it

is)

●

Cannot be observed under the light microscope

(due to its minute size, bacteria is in micrometers,

this is in nano)

●

Can be measured through membrane filters,

ultracentrifugation, and electron microscopy

2. GENOME

●

viruses carry their own genetic material (DNA or

RNA; neverboth)

●

genome may be single stranded or double

stranded, circular or linear, segmented or

unsegmented

3. METABOLICALLY INERT

●

no metabolic activity outside their hosts

●

do not possess machinery for translation and

can only multiply inside living cells

●

Nucleocapsid is composed of (not all

necessarily present)

○

DNA or RNA (genome)

○

Structural proteins

○

With or without enzymes

○

Nucleic acid binding proteins

Nucleocapsid enclosed in naked capsid virus

PAGE 21 #PASAR #RN2028 Lord Help Us Pass MICROPARA 〒▽〒MicroPara Lec - Finals

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●

Nucleocapsid and glycoproteins and membrane

makes up the enveloped virus

Nucleocapsid + glycoproteins and membrane =

the enveloped virus

The pink one is a naked capsid virus, the one

below is the envelope virus

VIRUSES: RNA VIRUSES

VIRUSES: STRUCTURE (2)

●

CAPSID: Rigid structure able to withstand harsh

environmental conditions

ENVELOPE: Membrane composed of lipids,

proteins, and glycoproteins

○

Membranous structure can be maintained

only in aqueous solutions

○

Easily disrupted by drying, acidic condition,

detergents and solvents which results in

inactivation of the virus

As a result, envelope viruses must remain wet and

are generally transmitted in fluids, respiratory droplets,

blood and tissue. Most of them cannot survive the

harsh conditions of the GIT tract

FUNCTIONS OF CAPSID

●

Protects the viral genome from physical

destruction and enzymatic inactivation

●

Serves as vehicle of transmission from one

host to another

●

Facilitates assembly and package of viral

genetic information

●

Antigenic and specific for each virus type

●

Provides structural symmetry to the virus particle

9 jd sha originally but sir added 6 para good to know lng daw

(ang other viruses naa sa pic below)

1. CORONAVIRIDAE: Coronaviruses (i.e., SARS-CoV-

2, MERS-CoV)

2. FILOVIRIDAE: Ebola and Marburg hemorrhagic fever

viruses

3. FLAVIVIRIDAE: Arboviruses (i.e., Dengue, yellow

fever, West Nile, Japanese encephalitis), non

arboviruses (i.e., hepatitis C virus)

4. ORTHOMYXOVIRIDAE: Influenza A, B, and C viruses

5. PARAMYXOVIRIDAE: Parainfluenza viruses, mumps

virus, measles virus

6. PICORNAVIRIDAE: Polio viruses, hepatitis A virus,

rhinovirus

7. RETROVIRIDAE: HIV types 1 and 2, HTLV types 1

and 2

8. RHABDOVIRIDAE: Rabies virus

9. TOGAVIRIDAE: Rubella virus

SUMMARY KINEME GI DRAW NI SIR SA BOARD

VIRUSES: DNA VIRUSES

1. ADENOVIRIDAE: human adenoviruses

2. HEPADNAVIRIDAE: Hepatitis B virus

3. HERPESVIRIDAE: HSV types I and II,

Varicella-Zoster Virus (VZV), Cytomegalovirus (CMV),

Epstein–Barr virus (EBV), human herpesviruses 6 & 7

(associated with roseola), and 8 (Kaposi Sarcoma

Cancer)

4. PAPILLOMAVIRIDAE: Human papilloma viruses

(Cervical & penile cancer)

5. PARVOVIRIDAE: Parvovirus B-19 (CNS, erythema

infectiosum)

6. POXVIRIDAE: Variola, vaccinia, orf, molluscum,

contagiosum, monkeypox viruses, smallpox

VIRUSES: DNA VIRUSES

DNA VIRUSES:

ADENOVIRUSES

FAMILY ADENOVIRIDAE (Adenovirus)

Virus Adenovirus

PAGE 22 #PASAR #RN2028 Lord Help Us Pass MICROPARA 〒▽〒MicroPara Lec - Finals

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Characteristics

●

dsDNA genome

Icosahedral capsid

No envelope

~50 human serotypes

●

Transmission

Respiratory, fecal-oral, and direct contact

(eye)

Site of Latency

(virus enter latent

period, latent period

= virus is able to

exist in the body

undetected by the

immune system;

they only replicate

from external factor

like stress)

Replication in oropharynx

○

with delta virus (1%);

Hep D won’t be attached to liver

without Hep B (precursor)

Chronic hepatitis

persistence of hepatitis B surface

antigen (HBsAg) (9%) followed by

resolution (disappearance of

HBsAg),

Asymptomatic carrier state,

Chronic persistent (systemic

disease without progressive liver

disease), or

chronic active disease

(progressive liver damage);

Oncogenic: Liver cancer

Treatment Antivirals and liver transplant for fulminant

disease

Disease

●

pharyngitis,

pharyngoconjunctival fever

keratoconjunctivitis

pneumonia

hemorrhagic cystitis

disseminated disease

gastroenteritis in children

Prevention HBC vaccine; hepatitis B immune globulin

DNA VIRUSES:

HERPESVIRUSES

Treatment Supportive

FAMILY HERPESVIRIDAE (Herpesvirus - HSV)

Prevention

Vaccine (adenovirus serotypes 4 & 7) for

military recruits

Virus HSV-1 and HSV-2

DNA VIRUSES:

HEPADNAVIRUSES

●

FAMILY HEPADNAVIRIDAE (Hepadnavirus)

Characteristics

Virus Hepatitis B Virus

Characteristics

●

partly dsDNA genome

icosahedral capsid with envelope

virion (also called Dane particle)

surface antigen originally termed

Australia antigen

○

Double-stranded deoxyribonucleic acid

(DNA) genome;

icosahedral capsid with envelope;

at least eight human herpes viruses

known:

HSV-1

HSV-2

Varicella-Zoster virus (VZV)

Epstein-Barr virus (EBV)

Cytomegalovirus (CMV)

Human herpesvirus (HHV)-6

HHV-7

HHV-8

Transmission Direct contact with infected secretions

Transmission

Humans are reservoir and vector; spread

by direct contact, including exchange of

body secretions, recipient of contaminated

blood products, percutaneous injection of

virus, and perinatal exposure

Site of Latency Sensory nerve ganglia

●

Site of Latency Liver

Disease

●

Acute infection with resolution (90%)

Resolves on its own, but if not then:

Fulminant hepatitis, most coinfected

○

Predominant virus in parentheses

Gingivostomatitis (HSV-1),

Pharyngitis (HSV-1),

Herpes labialis (HSV-1)

Genital infection (HSV-2)

Conjunctivitis (HSV-1)

Keratitis (HSV-1)

Herpetic whitlow (HSV-1 and

PAGE 23 #PASAR #RN2028 Lord Help Us Pass MICROPARA 〒▽〒MicroPara Lec - Finals

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○

HSV-2)

Encephalitis (HSC-1 in adults)

Disseminated disease (HSV-1 or

HSV-2 in neonates)

Disease

Asymptomatic infection, congenital disease

of newborn, symptomatic disease of

immunocompromised host,

heterophile-negative infectious

mononucleosis

Treatment Acyclovir, valacyclovir, famciclovir

Treatment Prevention Avoid contact.

Supportive; decrease immune suppression;

ganciclovir and foscarnet

FAMILY HERPESVIRIDAE (Herpesvirus - HSV)

Prevention

Use CMV antibody-negative blood and

tissue for transfusion and transplantation,

respectively.

Virus VZV (Varicella Zoster Virus)

Transmission

Close personal contact, especially

respiratory

FAMILY HERPESVIRIDAE (Herpesvirus - HSV)

Virus HHV-6 and HHV-7

Site of Latency Dorsal Root Ganglia

Disease Chickenpox (varicella), shingles (zoster)

Transmission

Most likely close contact via respiratory

route; almost all children infected age 2-3

years

Treatment Acyclovir, famciclovir

Site of Latency T lymphocytes (CD4 cells)

Prevention Vaccine

Disease

Roseola (exanthem subitum), fever,

malaise, rash, leukopenia, and interstitial

pneumonitis in organ transplant recipients

FAMILY HERPESVIRIDAE (Herpesvirus - HSV)

Treatment Susceptible to ganciclovir and foscarnet

Virus EBV (Epstein Barr Virus)

Transmission Close contact with infected saliva

Prevention None practical

Site of Latency B Lymphocytes

FAMILY HERPESVIRIDAE (Herpesvirus - HSV)

Disease

Infectious mononucleosis, progressive

lymphoreticular disease, oral hairy

leukoplakia in patients with HIV

Oncogenic: Burkitt lymphoma,

nasopharyngeal carcinoma

Virus HHV-8

Transmission

Not known; much less widely disseminated

than other herpes viruses

Treatment Supportive

Site of Latency

Prevention Avoid contact

Viral genome found in Kaposi tumor cells,

endothelial cells, and tumor-infiltrating

leukocytes

Disease Kaposi sarcoma (Type of Cancer)

FAMILY HERPESVIRIDAE (Herpesvirus - HSV)

Treatment None known

Virus CMV (Epstein Barr Virus)

Prevention Avoid contact with virus

Transmission

Close contact with infected secretions, blood

transfusions (WBCs), organ transplants,

transplacental

Site of Latency

WBCs, endothelial cells, cells in a variety of

organs

PAGE 24 #PASAR #RN2028 Lord Help Us Pass MICROPARA 〒▽〒MicroPara Lec - Finals

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DNA VIRUSES:

PAPILLOMAVIRUSES

DNA VIRUSES:

POXVIRUSES

FAMILY PAPOVAVIRIDAE (Papillomavirus)

FAMILY POXVIRIDAE (Poxvirus)

Virus Human papillomavirus (HPV)

Virus

Smallpox, molluscum contagiosum, orf, and

monkeypox viruses

Characteristics

●

dsDNA genome, icosahedral capsid,

no envelope, contains >200 DNA types

Transmission

Direct contact or sexual contact for genital

warts

Characteristics

Largest and most complex of all viruses;

brick-shaped virion with nonconforming

symmetry, referred to as complex; dsDNA

genome

Site of Latency Epithelial tissue

Transmission

Disease

Skin and genital warts, benign head and

neck tumors, anogenital warts

Oncogenic: Cervical and penile cancer

(esp. HPV types 16 and 18)

Respiratory droplets (smallpox); direct

contact (molluscum contagiosum, orf,

monkeypox)

Disease

Treatment Surgical or chemical removal may be

necessary

Erythema infectiosum (fifth disease),

aplastic crises in patients with chronic

hemolytic anemias, and fetal infection and

stillbirth

Prevention

Avoid contact with infected tissue,

vaccination

Treatment Supportive

Prevention

Vaccine for smallpox; avoid contact for all

viruses.

DNA VIRUSES:

PARVOVIRUSES

VIRUSES: RNA VIRUSES

FAMILY PARVOVIRIDAE (Parvovirus)

Virus Parvovirus B-19

RNA VIRUSES: CORONAVIRUSES

Characteristics

ssDNA genome, icosahedral capsid, no

envelope; parvovirus B-19 is the only

known human parvovirus

FAMILY CORONAVIRIDAE (Coronaviruses)

Transmission Close contact, probably respiratory

Virus Coronavirus

Site of Latency Central nervous system

Disease

Erythema infectiosum (fifth disease),

aplastic crises in patients with chronic

hemolytic anemias, and fetal infection and

stillbirth

Characteristics

●

80-160 nm

ssRNA genome

helical capsid with envelope

Transmission Direct contact or aerosol

Treatment Supportive

Target Receptor

Prevention Avoid contact

ACE2 (Angiotensin Converting Enzyme 2) -

found in: heart, kidney, testis, nasal and oral

mucosa, nasopharynx, bone marrow, spleen,

brain, lung, small intestine

Disease

●

Common cold

possibly gastroenteritis, especially in

PAGE 25 #PASAR #RN2028 Lord Help Us Pass MICROPARA 〒▽〒MicroPara Lec - Finals

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●

children

SARS

COVID-19

an envelope

Transmission Arthropod vector, usually mosquito

Treatment Supportive

Target Receptor

●

GAG (glycosaminoglycans)

GSL (glycosphingolipid)

Lectins

Prevention

●

Vaccine (SARS-CoV-2)

Avoid contact with virus

Disease

●

St. Louis and West Nile encephalitis

dengue and yellow fever

RNA VIRUSES: FILOVIRUSES

Treatment Supportive

FAMILY FILOVIRIDAE (Filovirus)

Prevention

●

Avoid contact with vector

vector control programs

Vaccine (DENV)

Virus Ebola (or Ebola-Reston) and Marburg viruses

Characteristics

●

80-14,000 nm

enveloped, long

filamentous and irregular capsid forms

with ssRNA

FAMILY FLAVIVIRIDAE (Flavivirus)

Virus Hepatitis C virus (HCV)

Transmission

●

Transmissible to humans from

monkeys and, presumably, other wild

animals

human-to-human transmission via body

fluids and respiratory droplets

Transmission Parenteral or Sexual

Target Receptor

●

GAG (glycosaminoglycans)

LDLR (low-density lipoprotein receptor)

●

Target Receptor

TIM-1 (T-cell immunoglobulin and mucin

domain 1) - found in: mast cells, NKT cells, B

cells

Disease

Acute and chronic hepatitis

strong correlation between chronic

HCV infection and hepatocellular

carcinoma

Disease

Severe hemorrhage and liver necrosis;

mortality as high as 90%

Treatment Supportive, interferon

Treatment Supportive

Prevention

●

Avoid contact with virus

blood supply screened for antibody for

the hepatitis C virus

Prevention

●

Avoid contact with virus

Export prohibitions on wild monkeys

RNA VIRUSES:

ORTHOMYXOVIRUSES

RNA VIRUSES: FLAVIVIRUSES

FAMILY ORTHOMYXOVIRIDAE (Orthomyxovirus)

Virus Influenza A

FAMILY FLAVIVIRIDAE (Flavivirus)

Virus

Arboviruses,

* including yellow fever, dengue,

West Nile, Japanese encephalitis and St.

Louis encephalitis viruses

Characteristics

●

80-200 nm, segmented (eight separate

molecules) ssRNA genome

helical capsid with envelope.

Three major antigenic types; influenza

A, B, and C; types A and B cause

nearly all human disease

Characteristics

●

40-50 nm

ssRNA genome surrounded by

spherical and icosahedral capsid with

Transmission Contact with respiratory secretions

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Target Receptor Airway epithelial cells

Transmission

Contact with respiratory secretions; extremely

contagious

Disease

●

Influenza (fever, malaise, headache,

myalgia, cough)

primary influenza pneumonia

In children: bronchiolitis, croup, otitis

media

Target Receptor Airway epithelial cells

Disease

Measles, atypical measles (occurs in those

with waning vaccine immunity), and subacute

sclerosing panencephalitis

Treatment

Supportive; antivirals amantadine and

rimantadine (A only), and zanamivir and

oseltamivir (A and B)

Treatment Supportive; immunocompromised patients

can be treated with immune serum globulin

Prevention Influenza vaccine or antiviral prophylaxis

Prevention Measles vaccine

FAMILY ORTHOMYXOVIRIDAE (Orthomyxovirus)

FAMILY PARAMYXOVIRIDAE (Paramyxovirus)

Virus Influenza B

Virus Mumps virus

Transmission Contact with respiratory secretions

Transmission

Person-to-person contact; presumably

respiratory droplets

Disease Similar to “mild” influenza

Disease Mumps

Treatment Supportive; antivirals zanamivir and

oseltamivir

Treatment Supportive

Prevention Influenza vaccine or antiviral prophylaxis

Prevention Mumps vaccine

FAMILY ORTHOMYXOVIRIDAE (Orthomyxovirus)

FAMILY PARAMYXOVIRIDAE (Paramyxovirus)

Virus Influenza C

Virus Parainfluenza virus

Transmission Contact with respiratory secretions

Disease Mild form of influenza causing URTIs

Disease

Treatment Supportive

●

Adults: upper respiratory disease; rarely

pneumonia

Children: respiratory, including croup,

bronchiolitis, and pneumonia

Prevention Avoid contact with virus

Treatment Supportive

Prevention Avoid contact with virus

RNA VIRUSES:

PARAMYXOVIRUSES

FAMILY PARAMYXOVIRIDAE (Paramyxovirus)

RNA VIRUSES:

PICORNAVIRUSES

Virus Measles virus

FAMILY PICORNAVIRIDAE (Picornavirus)

Characteristics

●

150-300 nm

ssRNA genome

helical capsid with envelope

no segmented genome

Virus

Poliovirus (3 types); Coxsackie virus, group A

(23 types); Coxsackie virus, group B (6

types); Echovirus (31 types); Enteroviruses (5

types)

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Characteristics

●

28-30 nm, ssRNA genome

icosahedral capsid with no envelope

Characteristics

Transmission Fecal-oral

●

100-120 nm, ssRNA genome,

icosahedral capsid with envelope

Reverse transcriptase converts

genomic RNA into deoxyribonucleic

acid (DNA)

Disease

Polio (poliovirus); herpangina (coxsackie A);

pleurodynia (coxsackie B); aseptic meningitis

(many enterovirus types); handfoot-mouth

disease (coxsackie A); pericarditis and

myocarditis (coxsackie B); acute hemorrhagic

conjunctivitis (enterovirus 70); and fever,

myalgia, summer "flu" (many enterovirus

types), neonatal disease (echoviruses and

coxsackie viruses)

Transmission

Sexual contact, blood and blood product

exposure, and perineal exposure

Disease

Treatment Supportive; pleconaril in development

Most disease in humans cause by HIV-1;

infected cells include CD 41 (helper) T

lymphocytes, monocytes, and some cells of

the CNS; asymptomatic infection, acute flulike

disease, acquired immunodeficiency

syndrome (AIDS)-related complex, and

AIDS-associated infections and malignancies

Prevention Avoid contact with virus; vaccine (polio)

Treatment

FAMILY PICORNAVIRIDAE (Picornavirus)

Nucleoside reverse transcriptase inhibitors,

nonnucleoside reverse transcriptase

inhibitors, protease inhibitors, and inhibitors of

viral entry into host cells; treat infections

resulting from immunosuppression

Virus Hepatitis A virus (enterovirus type 72)

Target Receptor

Transmission Fecal-oral

CD4 recetor - T helper cells, monocytes,

macrophages and dendritic cells

Disease

Hepatitis with short incubation, abrupt onset,

and low mortality; no carrier state

FAMILY RETROVIRIDAE (Retrovirus)

Treatment Supportive

Virus

Human T-lymphotropic viruses types 1 and 2

(HTLV-1, HTVL-2)

Prevention

Vaccine; prevent clinical illness with serum

immunoglobulin

Transmission

Known means of transmission are similar to

those for HIV

FAMILY PICORNAVIRIDAE (Picornavirus)

Disease

Virus Rhinovirus (common cold virus)

T-cell leukomia and lymphoma, and tropical

spastic parapaersis for HTLV-1; T-cell

lymphoma (HTLV-1); no known disease

associations for HTVL-2

Characteristics Approx. 100 serotypes

Treatment Supportive

Transmission Contact with respiratory secretions.

Prevention Avoid contact with virus

Treatment Supportive

Prevention Avoid contact with virus

RNA VIRUSES: RHABDOVIRUSES

RNA VIRUSES: RETROVIRUSES

FAMILY RHABDOVIRUSES (Rhabdovirus)

Virus Rabies virus

FAMILY RETROVIRIDAE (Retrovirus)

Virus

Human immunodeficiency virus types 1 and 2

(HIV-1, HIV-2)

Characteristics

●

70-180nm, ssRNA genome

helical capsid with envelope,

bullet-shaped

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Transmission

Bite of rabid animals most common; 20% of

human rabies cases have no known exposure

to rabid animal

Disease Rabies

Treatment Supportive

Target Receptor

nAChr (nicotinic acetylcholine receptor),

NCAM (cell adhesion molecule, p75NTR (p75

neurotrophin receptor - Nerve cells

Prevention

Avoid contact with rabid animals; vaccinate

domestic animals; post-exposure prophylaxis

with hyperimmune antirabies globulin and

immunization with rabies vaccine

RNA VIRUSES: TOGAVIRUSES

●

Symptoms: malaise, headache, fever,

hypertonic muscles, anxiety with episode of

hyperactivity, aggression, and convulsions,

hydrophobia (patient attempts to drink but this

brings painful spasms in larynx and pharynx

which leads to choking and gagging) along with

intense thirst

Treatment and Prophylaxis: First-aid, Human

rabies immunoglobulin is administered

intramuscularly, rabies vaccine, tetanus

prophylaxis

Loves nerve cells (CNS). It travels along the nerve,

not coming into contact with the immune system. It is

only after the virus spreads from the CNS, along the

nerve trunks to the different parts of the body that

antibodies are produced. By this time, irreversible

damage to the CNS has taken place and patient dies

of respiratory paralysis.

FAMILY Togaviridae (Togavirus)

Virus Rubella Virus

Characteristics

●

60-70nm, ssRNA genome

icosahedral capsid with envelope

family contains arboviruses and

non-arthropod-borne rubella virus

Transmission Respiratory, transplacental

Disease

Rubella (mild exanthematous disease) and

congential rubella

Treatment Supportive

Target Receptor Respiratory epithelium of nasopharynx

Prevention Rubella vaccine

VIRAL INFECTIONS

VIRAL INFECTION: RABIES

●

Virus: Rabies virus (Rhabdoviridae)

●

Inactivation: Sensitive to alcohol and lipid

solvents (ether, chloroform, acetone). Can be

inactivated by phenol, formalin, UV light, and

heat. Virus remains stable for several days at

0-4 degrees C and indefinitely at -70 degrees C

●

Source: bite from infected animals

●

Incubation period: 1-2 months

●

Affected cells/ system: CNS

VIRAL INFECTION AIDS

●

Virus: HIV (Retroviridae)

●

Inactivation: Thermolabile - inactivated in 10

minutes at 50 degrees C and in seconds at

100 degrees C. Susceptible to disinfectants and

detergents

●

Source: Chimpanzees (first transmission to

humans was in the 1800s)

●

Incubation period: 1-6 weeks without

treatment, AIDS develop within 10 years

●

Affected cells/system: CD4+ cells (T

lymphocytes, macrophages)

●

The first cells to be infected by HIV are usually

resident tissue macrophages or submucosal

lymphocytes in the genitals or rectum. From there,

the virus travels to the draining lymph nodes, where

it replicates extensively.

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●

About 2–3 weeks after infection, most patients may

develop:

○

Uremia

○

A drop in CD4+ T lymphocyte activity

○

A glandular fever-like illness (similar to

mononucleosis)

HIV mainly infects cells that express the CD4

antigen. In the bloodstream, it is found in CD4+

lymphocytes and monocyte-macrophage cells,

which may act as viral reservoirs.

This is followed by a long asymptomatic phase,

lasting from 1 to 15 years. During this phase:

○

Only a small number of CD4+ cells produce the

virus.

○

The virus remains in the blood at low levels

(low titers).

○

Follicular hyperplasia develops in lymphoid

organs.

When the CD4+ T cell count drops below 400/μL,

many variants of the virus spill out from

degenerating lymph nodes into the blood. This sets

the stage for opportunistic infections caused by

various microorganisms.

The causes of death in AIDS include opportunistic

infections, malignancies, and a cachexia-like state

(wasting syndrome).

Reverse transcriptase: what makes this virus unique

since it is what gives the virus the ability to convert RNA

to DNA, allowing it to stay latent in the T lymphocytes

○

Loss of antibody to p24 antigen

CLASSES OF ANTIRETROVIRAL DRUGS

ANTIRETROVIRAL

DRUG ACTION

EXAMPLES

(ANTIRETROVIRAL

DRUGS)

Non-nucleoside

reverse

transcriptase

inhibitors (NNRTIs)

Turn off a protein

needed by HIV

to make copies

of itself.

Efavirenz (Sustiva),

rilpivirine (Edurant)

and doravirine

(Pifeltro)

Nucleoside or

nucleotide reverse

transcriptase

inhibitors (NRTIs)

Faulty versions

of the building

blocks that HIV

needs to make

copies of itself

Abacavir (Ziagen),

Tenofavic

disoproxil

fumarate

(Viride),

emtricitabine

(emtriva),

Iamivudine

(Epivir), and

zidovudine

(Retrovir)

Protease Inhibitors

(PIs)

Inactivate HIV

protease,

another protein

that HIV needs

to make copies

of itself.

Atazanavir (Reyataz),

Darunavirs

(Prezista), and

Iopinavir/ritonavir

(Kaletra)

●

Symptoms: acute onset fever with or without

night sweats, malaise, headache, myalgia,

arthralgia, lethargy, diarrhea, depression, sore

throat, and skin rash. Spontaneous ulceration

occurs within 1 month.

Asymptomatic infection: Positive HIV antibody

tests, infectious, autoimmune diseases may

occur, persistent generalized lymphadenopathy in

25-50% of asymptomatic patients

Signs of disease progression:

○

Downward trend of CD4+ T cells in successive

samples

○

Ease of virus culture

○

Presence of p24 antigen in plasma

Integrase Inhibitors

Disable

integrase, which

HIV uses to

insert its genetic

material into

CD4 T cells.

Bictegravir sodium/

emtricitabine/

tenofovir alafenamide

fumarate (Biktarvy),

raltegravir (Isentress),

dolutegravir (Trivicay)

and cabotegravir

(Vocabria).

Entry or Fusion

Inhibitors

Block HIV’s entry

into CD4 T cells.

Enfuvirtide (Selzentry)

and maraviroc

(Fuzeon)

PAGE 30 #PASAR #RN2028 Lord Help Us Pass MICROPARA 〒▽〒MicroPara Lec - Finals

S.Y. 2024 - 2025 | Level I Midyear Term

Even though we have all of the antiretroviral drugs, why

is it that HIV is still untreatable?

●

Mainly due to the process of a latent viral reservoir.

During the lifecycle of the virus, HIV integrates into

the host DNA.

●

A subset of integrated HIV provirus rebates

transcriptionally silent, producing neither viral

proteins nor viral protein until reactivation by various

physiologic stimuli.

●

That is why even though based on testing there are

negative results for HIV, the patient must still

continue to take antiretroviral drugs to control the

HIV from waking up.

VIRAL INFECTIONS: DENGUE

●

Virus: Dengue virus (Flaviviridae)

●

Inactivation: Effectively inactivated by heat

treatment at 56 degrees C for at least 30 mins or at

higher temperature. May be inactivated by UV light

exposure at 75cm distance from source for 45 mins

or longer

●

Source: Bite from infected mosquito (Aedes

aegypti)

●

Incubation period: 3-10 days

●

Affected cells/ system: Immune system, Systemic

●

Pathogenesis: 3 phases - febrile, critical

convalescent

●

Treatment and Prevention: vaccine, Supportive

VIRAL INFECTIONS: COVID-19

●

The virus associated with the outbreak originating in

Wuhan, China has been designated severe acute

respiratory syndrome 2 (SARS-CoV-2). The disease

caused by that virus is now officially called

COVID-19.

●

Although SARS CoV-2 is most often spread

person-to-person, the US Food and Drug

Administration issued a safety alert advising that the

virus can also be spread via fecal microbiota

transplants

●

A review of 191 adults hospitalized with COVID-19

in Wuhan found that 91 (48%) had comorbidity.

Hypertension (30%) was most common followed by

diabetes (19%) and coronary heart disease (8%)

VIRAL INFECTIONS: SUMMARY

PAGE 31 #PASAR #RN2028 Lord Help Us Pass MICROPARA 〒▽〒MicroPara Lec - Finals

S.Y. 2024 - 2025 | Level I Midyear Term

WE CAN DO THIS GUYS

me praying na maynta makapasar sa le maski wa nakatuon

tarong

PAGE 32 #PASAR #RN2028 Lord Help Us Pass MICROPARA 〒▽〒