1. Infectious diseases within general wide-ranging diseases.

Theoretical and practical basis of infectious diseases, process

of infection.

Infectious diseases in the spectrum of other diseases

1) The main cause of death in children and adolescents
2) One of the main causes of death in adults
3) It nr 3 out of the top 10 causes of death in the world → infectious disease
4) Most of these cases are in low – and middle-income countries. and most preventable and treatable infectious diseases.
o Diarrhea o TBC
o Lower respiratory tract infections o Malaria
o HIV / AIDS

Classification of infections
1) Bacterial 6) Nosocomial – acquired with health care facility
2) Virus and/or from health care worker.
3) Protozoa 7) Opportunistic – occurs when body’s defense system
4) Helminths is weakened.
5) Fungi

Epidemiology
• The branch of medicine which deals with the incidence, distribution, and possible control of diseases and other factors
relating to health.
• Example: Protozoan infections are more likely to occur in tropical and subtropical areas whereas tick borne encephalitis is
most likely to occur in the northern parts of the world.

Process of infection: interaction between 2 independent biological systems

o Disease causing microorganism (virulence, pathogenicity) and macro-organism (susceptibility), under certain
environmental condition.
o includes following components.

Reservoir Agent Portals of Mode of Immunity /

Entry/Exit Transmission Susceptible of the
host
• Humans • Metazoan (multicellular • Respiratory • Airborne • Genetic factors
• Animals animals, parasites (flatworms, • Genitourinary • Fecal – oral • General resistance
• Environment roundworms, flukes)) • Alimentary • Blood or body factors
• Protozoa (single cell • Skin (superficial fluids • Specific acquired
organisms with defined lesions, • Skin or mucous immunity (acquired
nucleus – Plasmodium) percutaneous) membrane after antigen
• Fungi (nonmotile, • Transplacental contact exposure, active or
filamentous organisms) • Parenteral - passive)
• Bacteria Connected with
• Rickettsia (belong to hemotransfusion
bacteria, usually find on and needle sharing
anthropods (lice, ticks, fleas,
mites)
• Viruses
• Prions
2. Characteristics of the stages of the process of infection.
1.Incubation Stage 1.Time from entrance of pathogen into the Host → to
appearance of first symptoms
2.During this time → pathogen grow and multiply
3.Can vary from days to months to years →
depending upon the pathogen and the host immune
system
4.During this period, the patient is a carrier and may
spread the pathogen without knowing.

2.Prodromal Stage 1.After incubation period pathogen continues to

multiply
2.Host begins to experience general signs and
symptoms of illness typically due to activation of
immune system (fever, pain, soreness, swelling,
inflammation)
3.Period of illness

3.Illness Stage 1.Time during which the typical signs and symptoms
of disease are most obvious and severe
2.The very peak of an illness intensity, where the
patient is most contagious is known as the acme
point.

4.Decline Stage 1.The number of pathogen particles begin to decrease

2.Signs and symptoms of illness decline
3.Patients may become susceptible to developing
secondary infections → immune systems have been
weakened by primary infection

5.Convalescence Stage 1.Patient generally returns to normal functions

2.Not all patients may proceed to this period and may
die from the disease or become disabled.
3.Some patients may carry the pathogens chronically.
3. The role of Gram-negative bacteria in the origin of healthcare-related infections, clinical manifestations and
options for control of infection.

Gram-negative bacteria are responsible for more than 30% of hospital-acquired infections.
They are resistant to multiple drugs and increasingly resistant to most of available antibiotics.

Gram-negative bacteria
1) Ps. Aeruginosa
2) Klebsiella
3) E. coli
4) N. Gonorrhea/ Meningitis
5) Acinetobacter
6) H. Influenza
7) B. Pertussis
8) H. Pylori, Shigella/Salmonella

Related infections
1) Pneumonia
2) Surgical site infection
3) Urinary tract infections - Most common of all
4) Skin infection
5) Sepsis - Most lethal

Clinical manifestations: (depends on infection)

1) Fever ≥ 38ºC
2) Leukocytosis/leukopenia
3) Tachycardia
4) Tachypnoea
5) Rash
6) General malaise
7) Decreased oxygen saturation

Options for control of infection

1) Education for employees
2) Minimize:
• patients stay in hospital.
• drug-resistance - Appropriately use of antibiotics to
• use of catheters (urinary/vessel)
3) Proper use of equipment in various procedures
4) Hygiene:
• Hand hygiene procedures: hand washing + disinfection
• PPE = Personal protective equipment: apron (schürze), gloves, masks, scrubs
• Proper disinfection of hospital rooms after patient care
• No plants or flowers in ICU
4. Description of medication used for specific and aetiological treatment, listing certain diseases for which this
medication should be used.

Etiological treatment: treating the cause of the disease with the use of antimicrobial agents (agent that kills m/o or
inhibits their growth)

1. Antibacterial
▪ May be either bactericidal (killing) or bacteriostatic (stopping growth of replication)
▪ Classified into their main mechanism (broad or narrow spectrum)
Broad spectrum Narrow spectrum
1) Active against gram -/+ 1) have limited activity.
2) Penicillin: Amoxicillin UTI, pneumonia, tonsillitis 2) only useful against species of m/o
3) 3rd and 4th generation cephalosporins (Ceftriaxone) → 3) Vancomycin (iv) MRSA infection, meningitis,
meningitis, otitis media, encephalitis, brain abscess, brain abscess, encephalitis (+/-)
Strep. Pneumoniae, H.influenza, N. meningitidis 4) Vancomycin (oral) pseudomembranous colitis
4) Fluoroquinolones legionellosis, pneumococcus (Cl. Dificile)
5) Doxycycline cholera, Lyme disease, ehrlichiosis, RMSF 5) Penicillin G → thteria, syphilis
6) Macrolides can be used as alternative eg. in case of
penicillin allergy or 2nd line for respiratory infections
(eg. legionellosis and pneumococcus)
7) Ciprofloxacin – shigella and salmonella (enteridis + typhi)
8) TMP/SMX – shigella and salmonellosis in case of children
2.Antifungals
Antimycotic Azoles Allylamine Antimetabolite
• Polyene (amphotericin b) • Imidazole (clotrimazole) – Terbinafine → nail fungus 5-FC
→ leishmaniasis local → Athletes foot, jock
• Echinocandins → itch
Candidiasis • Triazoles (fluconazole) –
systemic → thrush, oral
thrush, candida esophagitis
3.Antiviral
Non-Retroviral Antiviral Agents Anti-retroviral Agents → HIV, HBV
• Anti – herpesvirus agent • Nucleoside Reverse Transcriptase inhibitors (NRTI)
o HSV → Acyclovir • Non – nucleoside Reverse Transcriptase inhibitors
o CMV → ganciclovir (NNRTI)
• Anti – influenza agents → oseltamivir/zanamivir • Protease inhibitor
• Entry inhibitors
• Integrase inhibitors
• CCR5 antagonists
4.Antiparasitic
Antimalarials Protozoacides Pediculicides
• Mebendazole → Ascaris, • Quinolones
enterovirus, trichinella • Artemether
• Albendazole → • Atovaquone
echinococcosis (CE), • Proguanil
cysticercosis
 • Praziquantel → taeniasis,
schistosomiasis

5. Epidemiology of infectious diseases, epidemic process. The principles of prevention of infectious diseases.

I] Epidemiology
1) The branch of medicine which deals with the incidence, distribution, and possible control of diseases and other
factors relating to health.
2) Example: Protozoan infections are more likely to occur in tropical and subtropical areas whereas tick borne
encephalitis is most likely to occur in the northern parts of the world.
3) It’s about putting people into groups.
4) Identifies these groups ignoring the uniqueness of its members

II] Epidemic Process

Epidemic processes are the process of the ri se and the spreading of the infectious disease among the people.
• Components of the epidemic process
1. Infectious agents
▪ bacteria, virus, fungi, parasite
2. Reservoir
▪ The infectious agent needs a reservoir of sort in order to multiply and wait to” attack” its’ next
target.
▪ People, Equipment, Water/Food, Vector, animals
3. Transmission
▪ Direct contact, Vector borne, Fecal-oral, Injection, Airborne/aerosols.
4. Susceptible macroorganism
▪ Some are more susceptible to others. ” Strong” pathogens do not need the host to be
weakened, but some needs the immune system to be suppressed.
▪ Immunosuppressed
▪ Neonates
▪ Diabetics
▪ Acquired immunity.
▪ Genetic factors

III] Principles of Prevention

Also public medical education: raise consciousness for prevention of infections.

6.Principles of epidemiological investigation, surveillance and control of infectious diseases.

I] Epidemiological investigations
1. Establish the existence of an outbreak.
o Compare current info with previous incidence in the community during the same time of year to
determine if the observed number of cases exceeds the expected.
2. Verify the diagnosis.
o Through clinical history and laboratory tests
3. Establish the case definition and count cases.
4. Relate the outbreak to time, place and person.
5. Determine who is at risk of becoming ill
6. Formulate a tentative hypothesis.
o Explain the most likely cause and distribution of cases.
7. Compare hypothesis with established facts.
8. Execute additional studies if required to test the hypothesis.
9. Implement control and prevention measures.
10. Follow up recommendations

II] Epidemiological surveillance

1. It’s the systematic collection, analysis and dissemination of health data for the planning, implementation and
evaluation of public health programs.
2. Public health surveillance may be used.
o to "serve as an early warning system for impending public health emergencies.
o document the impact of an intervention,
o track progress towards specified goals
o monitor and clarify the epidemiology of health problems
3. Surveillance can be passive or active
o Passive: consists of the regular, ongoing reporting of diseases and conditions by all health facilities in a
given territory
o Active: one where health facilities are visited and health care providers and medical records are
reviewed in order to identify a specific disease or condition.
4. The usefulness of a surveillance system is measured by whether it leads to prevention or control or a better
understanding of adverse health events.
III] Control of Infectious diseases
7.Specific laboratory tests in modern infectiology: selection principles, methods to be used. IgA and IgM class
antibodies. The role of RNA and DNA in diagnosis

I] Specific laboratory method

Characterizes nature Culture Microscopy Susceptibility test Serological methods

o Parasitology o From Feces, different stains are Used to detect o Latex agglutination
o Bacteriology sputum, blood, urine used here. microbe’s antibiotic o ELISA/EIA
o Virology etc o Gram stain – gram resistance o Complement
o Molecular Biology o Samples are put on positive and negative fixation
(PCR, RT – PCR) different growth bacteria can be seen o Western blot
o Serology agars here o PCR
(Agglutination o Acid fast stain – for
methods, mycobacteria
Immunoassay – o Wet mounts – for
ELISA; IFA; WB) fungi and parasites
o Giemsa stain – for
parasites
o Etc

II] Methods in laboratory diagnostics

• Primary Tests → screening
o Express Tests
▪ Rapid urine dipstick → cholera
▪ Rapid legionella antigen detection (urine and pleural fluid)
▪ Rapid pneumococcus antigen test
▪ Rapid HIV test
o Agglutination
o ELISA (Enzyme linked immunosorbent Assay)

• Confirmatory Tests → Reference

o IFA (Immunofluorescence Assay)
o Western Blot
o PCR

• Rapid tests
o Express tests
o Light microscopy
o ELISA, IFA
o WB, PCR

• Slow
o Bacteriological cultures
o Cell cultures (virus)

III] IgA and IgM Class Antibodies

• IgA
o 2nd most abundant
o abundant in serum, nasal mucus, saliva, breast milk, and intestinal fluid
 o accounting for 10-15% of human immunoglobulins
o 2 forms: IgA1, IgA2
o serves as a first line of defense to repel pathogenic microorganisms.
o provide a finely tuned balance to guarantee controlled survival of essential commensal bacteria.
o IgA forms dimers (i.e., two IgA monomers joined together).
o IgA in breast milk protects the gastrointestinal tract of neonates from pathogens

• IgM
o Largest antibody
o 3rd most abundant antibody
o First antibody to be produced in human fetus
o First antibody to appear in response to initial exposure to antigen.
o Defends the host by blocking pathogens to cells and by aggregating infectious agents to facilitate their
clearance.
o Restricted to the intravascular compartment.

• The Role of RNA and DNA in Diagnosis

o Nucleic acid amplification and detection methods are useful for the diagnosis and management of a
variety of infectious diseases.
o Most widely used is → PCR.
▪ Can rapidly and accurately detect the presence of fastidious and slow-growing microorganisms
(Chlamydia, mycoplasmas, mycobacteria, herpesviruses and enteroviruses, directly from clinical
specimens)
▪ Value of viral load measurement by nucleic acid amplification in the management of patients
with HIV infection or hepatitis C has also been well established.
o Advantage of PCR
▪ High sensitivity and specificity
▪ Rapid – gives the results the same day, detects fast and slow growing bacteria.
▪ Detects microorganisms that failed to be identified with other conventional methods.
o Limitations of PCR
▪ Potential for false positive results (eg by amplification of contaminated DNA)
▪ Potential false negative results
▪ Not yet available for all infectious diseases
▪ Technically complex procedure
▪ Expensive equipment and reagents

8. Principles of action/algorithms for the staff of Hospital Admission, Observation or Intensive Care
Departments in cases where there is a suspicion of a dangerous infectious disease.

If suspicion of a dangerous infection is present. It should be taken into consideration contagiousness of the disease and
staff should act accordingly:
1. Identify affected patients.
2. Isolation
• of a patient to a single room where there should be a marking on the door, this indicated that the patient
is/may be contagious, and precautions should be made before entering.
3. Wearing PPE
• These should be put on before entering and thrown in trash that is specifically used for that patient.
4. Handling of patient’s body fluids, equipment and waste products with care at least until it is known what microbe it
is exactly.
5. Limit movement and transportation of patient from the room.
• Best if one person and that person alone handling the patient.
6. Determine if transmission and dissemination is occurring.
7. Characterize the organism or mechanism in order to guide further response actions, patient management, and
future responses.
8. Continue assessments and colonization screenings until spread is controlled.
9. Every patient should be treated with the same standard of precautions for a better control, protection to patients,
workers and visitor.

9.Description pathologies caused by MRSA (methicillin-resistant Staphylococcus aureus), therapeutic approaches and
control of the spread of the disease.

I] Pathologies
1. Hospital Acquired Pneumonia (HAP)
o Can be due to inhalation, aspiration and hematogenous spread. This causes infiltration in lungs and
eventually pneumonia.
2. Endocarditis
o S. Aureus located in bloodstream manages to get to the endothelium of the heart. There they cause
damage to the valves, the damage causes fibrin-release.
3. Sepsis
o S. Aureus causes a release in pro-inflammatory cytokines → diffuse endovascular damage and
coagulation dysfunction.
4. Osteomyelitis
o Can be limited to a single portion of bone or can involve marrow, cortex, periosteum and the
surrounding soft tissue. There are 3 types:
▪ 1) resulting from local spread from a contiguous contaminated source of infection after trauma,
bone surgery or joint replacement.
▪ 2) Osteomyelitis related to vascular insufficiency which is predominantly associated with
diabetes.
▪ 3) Hematogenous osteomyelitis.
5. Septic-Arthritis (SA)
o Bacteria deposits in synovium and start to produce inflammation. Later spreading to synovial fluid and
multiplies, the product of inflammation destroys joint components
6. Skin infections
o Carbuncles, cellulitis, impetigo, abscesses

II] Treatment
7. If MRSA is diagnosed, treatment will vary depending on the following factors:
o type of infection
o location of infection
o severity of symptoms
o antibiotics to which the strain of MRSA responds.
8. Management of MRSA infections may include:
o Pus drainage from lesion
o culture and susceptibility testing of drained material.
o wound care and hygiene
o Surgery → valve replacement
o bactericidal therapy
▪ Vancomycin
▪ Daptomycin
 ▪ TMP-SMZ

III] Control of Spread

1. Isolation
2. Control education and training programme in nursing homes
3. Testing suspicious patient/personnel
4. Hand hygiene
o Disinfect before and after patient.
o Personnel with wound on hand shouldn’t treat patient with MRSA infection.
5. PPE
6. Wound covering.
7. Keep cuts, scrapes, and wounds clean and covered until healed.
8. Avoid sharing personal items such as towels and razors.
9. Disinfection of surfaces after patient care
10. Handling patient material, wastes, body fluids, equipment, samples carefully
11. Get care early if you think you might have an infection.

10.Control options for the prevalence of infections. Principles of limiting its prevalence at a multi profile hospital.

I] Standard Precautions
1. Isolation
2. Hand Hygiene
o Single most important part of infection control
o Hand washing before any contact with patients, after any activity that contaminates the hands, after
removing protective clothing, after using the toilet and before handling food.
3. Use of personal protective equipment (PPE): gloves, aprons, eye protection, face masks, etc.
4. Handle and dispose of sharps safely.
5. Dispose of contaminated waste safely
6. Managing blood and body fluids: spillages and transport of specimens
7. Decontaminating equipment: cleaning, disinfection, and sterilization
8. Maintain a clean clinical environment.
9. Prevent occupational exposure to infection.
10. Manage sharps injuries and blood splash incidents.
11. Manage linen safely.
12. Place patients with infections in appropriate accommodation.

II] Steps
1. - identify source of infection
o Isolate patient (not every patient)
o Educate patient about the condition.
2. -identify route of transmission and eliminate it
3. -stop the spread of infection
o Treat the patient.
o Personnel: proper hygiene, PPE when handling patients
o Disinfection of room after patient care.

Hospitals must ensure the management of infection control programs is by competent, qualified Infection Control
nurses.
1. Educate all healthcare staff.
2. Develop infection control policies and ensure accessible to all staff.
 3. Facilities and equipment are available to enable compliance with policies.
4. Ensure all clinical staff have received appropriate training.
5. Infection control audits
6. Surveillance.

11.Bioterrorism: definition, concepts and classification.

I] Definition
1. The deliberate release of Viruses, bacteria, Toxins or other harmful agents to cause illness or death in
people, animals or plants.
2. It’s a threat to any country.
3. Its prevention requires special training and the ability to react quickly and act.
4. In addition, creating in society: Confusion, Panic, Fear

Types of Biological Weapons: Use of biological Weapons

1. Viruses 1. Against humans (severe infections, death
2. Bacteria Pandemics)
3. other Microbes 2. Against animals (Zoonoses e.g. African swine
4. Toxins fever → human infections, Famine)
5. Prions 3. Against plants (Famine)

II] Concepts
1. Acts of bioterrorism may range from a single exposure directed at an individual, usually the attacks are targeting
politicians or governments trying to spread chaos to society.
2. Bioterrorism are easily available, requires little knowledge and are not expensive to produce.
3. Effects are also not immediately apparent and may be difficult to distinguish from a natural occurring infectious
disease outbreak.
4. There are 3 critical elements needed for a bioterrorism event:
o Potential offender
o Availability of biological agents
o Technical methods to disseminate these age.

III] Classification
12.Objectives of the healthcare system in ensuring human health in case of bioterrorism.

1. Detection of biological event

o Early detection of a biological attack is key to minimise morbidity and mortality
2. Early diagnosis for all suspected cases
o Special role of emergency physicians, infectiologist and other who are expected to be the first contact at the
health care institution.
o Laboratories
3. Surveillance systems for detection of biological outbreaks need to include real time data from emergency rooms,
labs, pharmacies, schools and etc..
4. Notification of health authorities
o Public health system preparedness and response
5. Isolation
o Type depending on suspected organism
6. Confirmation and case detection
7. Epidemiological investigation
o Contacts; Area
o Disease outbreak from a biological attack can differ greatly from natural disease outbreak, which can
complicate event investigation and response efforts.
8. Decontamination
o Personnel
o Environmental
9. Treatment-directed, as required for possible or confirmed disease
o In all suspected cases
10. Prophylaxis- directed, as required for possible exposure
o Chemoprophylaxis
o Immunisation
o Anti-toxins
o Importance of early diagnosis

13.The target of bioterrorism. Clinical forms of anthrax, major clinical manifestations and prognosis.
• Target of Bioterrorism
o Against humans (severe infections, death pandemics)
o Against Animals (Zoonoses → human infections)
o Against plants (famine)
• Meaning of bioterrorism
o Spread fear anxiety, uncertainty, and depression in population.
o Cause mistrust of authorities/government
o Inflict economical damage and disrupt travel and commerce

• Anthrax - Clinical forms + major clinical manifestations + prognosis

Cutaneous Anthrax Inhalation Anthrax Gastrointestinal Anthrax

Relative frequency Ca. 95% Ca 5% > 1%

Route of entry Skin contact Inhalation Ingestion
Incubation Period Typically, 5-7 days 1 – 3 days 2-5 days
Clinical manifestations Skin lesions 1. prodromal phase: - nausea
Starts with painless, non-specific symptoms - vomiting
pruritic papule (fever, malaise) - abdominal pain
→ Ulcer with - severe bloody diarrhea
surrounding edema 2. Fulminant phase: - Hematemesis
→ necrotic black skin - chest pain - Hemorrhagic lymphadenitis
tissue - high grade fever - Ascites
→ healing by - dyspnea → systemic spread is common
granulation - hypoxia
→ hyperpigmented skin - Shock
and/or scar - mediastinal widening
due to hemorrhagic
mediastinitis

→ systemic spread is
common
- local/ regional lymphadenopathy
- in case of Bacterial: Meningitis, septic shock
Prognosis/ Lethality Most are mild and are Ca. 50% die with 40% die with treatment
self-limited. antibiotic treatment
Prognosis is better when
treated with antibiotics. >90% die without
treatment
Less than 1 percent die
with treatment.

14.Topicality of the most common blood borne diseases: VHB, VHC, HIV, in the world and in Latvia, epidemiology and
prevention

Viral Hepatitis B
o Vaccination: yes
o Treatment: partial
o Prognosis: usually good, but not always
I] Worldwide
1. High prevalence in Asia, Africa
2. 2 billion people are positive test to VHB.
3. > 250 million people worldwide are chronically infected.
4. ~ 600 000 deaths/year
II] Latvia
- 2-3% of the population in Latvia are HBV positive.
III] Prevention
1. Education
2. Safe sex (condoms)
3. Don’t share needles (needle exchange program)
4. Awareness of transmission
5. Pre exposure vaccination: recommended for all unvaccinated individuals (3 shots – 0 – 1 – 6)
6. Post exposure prophylaxis (PEP) (when patient is not vaccinated)
 • HBV Immunoglobulin (very expensive, time limit after incidence 12hrs) AND
• Vaccination (6 days after incidence, 0 – 1 month – 2 months – 12 months later)
• Goal: prevention of HBV infection
• Indication: Exposure to HBV (percutaneous, ocular, mucosal)

Viral Hepatitis C
o Vaccination: no
o Treatment: yes
o Prognosis: usually good, but not always
I] Worldwide
1. Around 3% of the world’s population is HCV positive.
2. High prevalence in Africa, the Middle East, Central and East Asia
3. 130-150 million are chronically infected.
4. 15 – 30 % of liver cirrhosis are VHC positive
II] Latvia
- 40 000 are either anti-HCV positive or HCV RNA positive.
III] Prevention:
1. Minimize risk factors, no post exposure prophylaxis
(test VHC RNA PCR 1 month and 2 months after incidence
2. Education
3. Safe sex (condoms)
4. Not sharing needles (needle exchange program)
5. Awareness of transmission
6. Early treatment may prevent chronic progression.

HIV
o Vaccination: no
o Treatment: yes
o Prognosis: poor

I] Worldwide
1. Highest prevalence in AFRICA
2. 38 million people are HIV positive.
3. 30% don’t know their status.
4. During 2016: 1.8million people are newly infected and 1 million HIV related death.
II] Latvia
5. Has one of the highest prevalences in Europe
6. 0.70% of population is HIV positive.
III] Prevention
7. Safe sex (condoms)
8. Don’t share needles (needle exchange programs)
9. Vertical prophylaxis
10. Pre exposure prophylaxis
11. HIV post - exposure prophylaxis
• Indications
1. Injury with HIV-contaminated instruments or needles
2. Contamination of open wounds or mucous membranes with HIV-contaminated fluids
 3. Unprotected sexual activity with a known or potentially HIV-infected person
• Timing: Initiate as soon as possible (ideally within one to two hours after exposure) – within 72h
• Drugs: A three-drug regimen is recommended (similar to cART treatment- includes
a nucleoside/nucleotide combination NRTI plus an integrase inhibitor
• Measures after needle stick injury or other contamination
o Let the wound bleed.
o Rinse/flush with water and soap and/or antiseptic agent.
o Immediately seek medical attention.
o If occupational exposure: report incident immediately.

15 Acute retroviral syndromes: prevalence/topicality, clinical symptoms, diagnostic principles, differential diagnosis.

I] Prevalence/topicality
• It’s the initial stage of HIV infection, it lasts until the body has created antibodies against the virus.
• Can develop as early as 2-4 weeks.
• 50% of new HIV infections are transmitted from people who have ARS.
• HIV transmission 7x more likely during acute infection than during chronic infection
• Described as mononucleosis-like syndrome.

II] Diagnostics
1. Bloods
o Lymphopenia
o Thrombocytopenia
2. Only antibody testing - HIV antibody tests (may give false-negative → positive after 3-4 weeks after infection) -
not good for ARS because a/b have not developed yet
o ELISA
o Western Blot (confirmed)
3. RT - PCR
o HIV RNA viral load (positive within 11days)
o Positive if → HIV RNA >5000 copies/mL
o 98% sensitivity for HIV
4. P24 antigen blood test
5. One negative test doesn’t exclude infection

When HIV RNA ≥5,000 copies/mL is detected, clinicians should consider that result a presumptive diagnosis of acute
infection, even if the screening and antibody-differentiation tests are nonreactive or indeterminate.

III] Clinical Symptoms

• Flu like symptoms and nonspecific
o Fever
o Fatigue
o Rash
o Headache
o Generalised lymphadenopathy (swollen lymph nodes)
o Pharyngitis
o Myalgia
• Ulcers in mouth, oesophagus or genitalia
 • Loss of appetite
• May be asymptomatic.
IV] Differential Diagnosis

1. Primary CMV
2. Drug reaction
3. Infectious mononucleosis
4. Viral Hepatitis
5. Primary herpes simplex virus infection
6. Influenza
7. Severe pharyngitis
8. Secondary syphilis.

16. Specific and non-specific prophylaxis of airborne/aerogenic infections.

Non-Specific Specific
Active vaccination 1. Hand hygiene
• Influenza a. Wash hands
• Chicken pox b. Disinfection
• Mumps 2. Disinfect objects and surfaces which may be
• Measles contaminated eg. phone
• Pertussis 3. Use of PPE (gowns, gloves, masks, respirator, eye
protection)
• Passive 4. Limiting time spent in presence of patient likely to be
• Immunoglobulins a source of infection.
• Polyclonal 5. Ventilation and air handling
• Monoclonal. 6. Cough and sneezing properly.
Post exposure prophylaxis is effective in preventing 7. Patient should be placed in airborne infection
development of the disease. isolation room.
8. HEPA and UVGI
16. Specific and non-specific prophylaxis of airborne/aerogenic infections.
Non-Specific Specific
Active vaccination 9. Hand hygiene
• Influenza a. Wash hands
• Chicken pox b. Disinfection
• Mumps 10. Disinfect objects and surfaces which may be
• Measles contaminated eg. phone
• Pertussis 11. Use of PPE (gowns, gloves, masks, respirator, eye
protection)
• Passive 12. Limiting time spent in presence of patient likely to be
• Immunoglobulins a source of infection.
• Polyclonal 13. Ventilation and air handling
• Monoclonal. 14. Cough and sneezing properly.
Post exposure prophylaxis is effective in preventing 15. Patient should be placed in airborne infection
development of the disease. isolation room.
16. HEPA and UVGI
15 Acute retroviral syndrome: prevalence/topicality, clinical symptoms, diagnostic principles, differential diagnosis.

I] Prevalence/topicality
• It’s the initial stage of HIV infection, it lasts until the body has created antibodies against the virus.
• Can develop as early as 2-4 weeks.
• 50% of new HIV infections are transmitted from people who have ARS.
• HIV transmission 7x more likely during acute infection than during chronic infection
• Described as mononucleosis-like syndrome.

II] Diagnostics
6. Bloods
o Lymphopenia
o Thrombocytopenia
7. Only antibody testing - HIV antibody tests (may give false-negative → positive after 3-4 weeks after infection) -
not good for ARS because a/b have not developed yet
o ELISA
o Western Blot (confirmed)
8. RT - PCR
o HIV RNA viral load (positive within 11days)
o Positive if → HIV RNA >5000 copies/mL
o 98% sensitivity for HIV
9. P24 antigen blood test
10. One negative test doesn’t exclude infection

When HIV RNA ≥5,000 copies/mL is detected, clinicians should consider that result a presumptive diagnosis of acute
infection, even if the screening and antibody-differentiation tests are nonreactive or indeterminate.

III] Clinical Symptoms

• Flu like symptoms and nonspecific
o Fever
o Fatigue
o Rash
o Headache
o Generalised lymphadenopathy (swollen lymph nodes)
o Pharyngitis
o Myalgia
• Ulcers in mouth, oesophagus or genitalia
• Loss of appetite
• May be asymptomatic.

IV] Differential Diagnosis

9. Primary CMV
10. Drug reaction
11. Infectious mononucleosis
 12. Viral Hepatitis
13. Primary herpes simplex virus infection
14. Influenza
15. Severe pharyngitis
16. Secondary syphilis

16. Specific and non-specific prophylaxis of airborne/aerogenic infections.

Non-Specific Specific
Active vaccination 17. Hand hygiene
• Influenza a. Wash hands
• Chicken pox b. Disinfection
• Mumps 18. Disinfect objects and surfaces which may be
• Measles contaminated eg. phone
• Pertussis 19. Use of PPE (gowns, gloves, masks, respirator, eye
protection)
• Passive 20. Limiting time spent in presence of patient likely to be
• Immunoglobulins a source of infection.
• Polyclonal 21. Ventilation and air handling
• Monoclonal. 22. Cough and sneezing properly.
Post exposure prophylaxis is effective in preventing 23. Patient should be placed in airborne infection
development of the disease. isolation room.
24. HEPA and UVGI
17. Lower respiratory tract infections: acute bronchitis, bronchiolitis and pneumonia; clinical manifestation and
diagnosis.

Lower respiratory tract infection (LRTI) is a broad terminology which includes acute bronchitis, pneumonia, acute
exacerbations of chronic obstructive pulmonary disease/chronic bronchitis (AECB), and acute exacerbation of
bronchiectasis.

Acute bronchitis
• Inflammation of the tracheobronchial tree associated with respiratory viruses. (90% caused by viruses)
o Influenza A and B virus
o Parainfluenza virus
• Symptoms
o Cough (usually productive)
▪ > 5 days
▪ Resolves in 2–3 weeks.
o Other upper respiratory tract symptoms
▪ Runny nose
▪ Sore throat
o Fever
o Chest pain
o Headache
o Auscultation
▪ Wheezing or dyspnoea on exertion
• Diagnosis
o Based on clinical diagnosis
o Auscultatory findings
 ▪ Wheezing
▪ Rhonchi
▪ Coarse crackles

Bronchiolitis
• Non-specific inflammatory injury that primarily affect small airways.
o Often caused by respiratory syncytial virus (RSV)
• Symptoms
o Initially presents with upper respiratory tract symptoms (e.g., rhinorrhea), fever, and cough,
tachypnoea.
o Respiratory distress (usually occurs in infants) → obstruction of bronchioles.
▪ Tachypnea, prolonged expiration
▪ Nasal flaring, intercostal retractions
▪ Cyanosis
o Auscultatory findings: wheezing, crackles
• Diagnosis
o Based on clinical diagnosis.
o Supported by chest x-ray
▪ Hyperinflation of the lungs, interstitial infiltrates, atelectasis

Pneumonia
• Inflammation in the lungs caused by infection. Alveolar air spaces are filled with exudate, inflammatory cells and
fibrin resulting in consolidation of lung parenchyma and gas exchange disturbances in alveoli.
• Symptoms
o Severe malaise
o High fever and chills
o Headache
o Myalgia
o Sore throat
o Egophony, bronchophony, tactile fremitus
o Productive cough with purulent sputum (yellow-greenish)
o Crackles, wheezing, tactile fremitus, dullness on percussion
o Tachypnea and dyspnea
o Tachycardia
o Pleuritic chest pain
• Diagnosis
o Clinical signs
o Laboratory test
▪ Blood
• CRP, ESR, Leu increased, procalcitonin.
▪ Pathogen detections
• Blood cultures – always recommended.
• Sputum culture
• Urine pneumococcal antigen test
• legionella antigen detection (urine or pleural fluid)
o Imagine
▪ Chest X ray
 • Infiltrates
• Lobar Pneumonia (Extensive opacity restricted to one pulmonary lobe)
• Bronchopneumonia (patchy infiltrates)
• Atypical pneumonia (diffuse reticular opacity)
▪ CT if x-ray is inconclusive.

18. Tuberculosis: etiology, epidemiology and pathogenesis.

I] Etiology
• Pathogen: mycobacterium tuberculosis (95%)/M. bovis (GI TB)
• Acid fast bacilli
• Transmission
o From person to person via air (small particles or droplets)
• Risk factors
1) Immunosuppression (TB is the most common cause of mortality in patients with HIV globally)
2) Drug abuse
3) Alcoholism
4) Malnutrition
5) Diabetes mellitus
6) People in congregate settings [prisons, hospitals, homeless shelters]

II] Epidemiology
• Male > female (2:1)
• Top 10 causes of death worldwide
• Leading killer of HIV positive patients
• Countries with the highest incidence of TB: India, Indonesia, China, Nigeria, Pakistan, and South Africa

III] Pathophysiology
• Patient exposure to infected source (patient) through coughing, sneezing or just talking.
• Patient inhales bacteria and there are 2 outcomes.
o 1. No infection occurs, and immune system deals with the bacteria
o 2. Bacteria reaches the lungs and causes infection
• Alveolar macrophages (CD14+) phagocytose the TB bacteria but cannot eliminate them.
o Cord factor → M.tuberculosis inhibits fusion of phagosome and lysosome → preventing lysis of
phagocytosed mycobacteria
o By hiding inside the macrophages, TB bacteria do not provoke a humoral immune response (antibody
production by B lymphocytes) in the host → therefore, antibody detection tests play no role in the
diagnosis of TB. The mycobacteria replicate safely within the macrophages.
o Phagocytosed M. tuberculosis can only be destroyed by activated T lymphocytes.
• The infection is usually contained in the lung by formation of caseating granulomas that limit damage to the
lungs and bacterial dissemination.
• Granuloma formation is caused by delayed T-cell-mediated reaction → activation of alveolar macrophages and
their fusion into multinucleated giant cells.
• 2 outcomes from here:
o 1. The bacteria may remain dormant in the granulomas for many years without any active clinical
disease manifesting (latent TB)
o 2. Immunosuppression → dormant bacteria become active, replicate in the macrophages, and spread
into the lungs and other organs (active TB).
19. Neuroinfectious: concept, etiology, epidemiology, diagnostic and treatment principles.

Overview
The three main forms of CNS infections are meningitis, brain abscesses, and encephalitis and myelitis (spinal cord)
Route of transmission
• Hematogenous
• Direct implantation
• Local extension
• Spread along the peripheral nervous system.

I] Meningitis
Concept
Inflammation of the leptomeninges and subarachnoid space.

Epidemiology – mostly viral or bacterial in origin. Rare types are chemical and fungal.
• Often occurs in children <1y
• Median age is 43y
• N. meningitidis infection highest in sub-Saharan Africa

Etiology
1) Acute purulent (pyogenic) meningitis: Usually bacterial in origin.
o Strep pneumonia, N. meningitis, H. influenzae
2) Acute lymphocytic (aseptic) meningitis: Viral in origin; commonly enterovirus, herpesviruses, coxsackie, mumps,
or HIV
3) Chronic meningitis (bacterial or fungal): Causes include tuberculosis, Cryptococcus, or dimorphic fungi.
4) Chemical meningitis: Causes include chemical irritation of the meninges, sometimes develops after
neurosurgical procedures
Diagnostic
1) Routine Blood tests
2) CSF (lumbar puncture)
o Appearance, cell count, lactate, glucose, albumin
o Serology
o PCR
o Csf glucose/ blood glucose
▪ Lowered – bacterial
▪ Normal – viral
3) Brain imaging → only in patient with significant risk factors for complications
o MRI or CT
Treatment
1) Immediate empirical therapy after obtaining blood cultures and CSF samples
o Vancomycin + third generation cephalosporin
2) Viral meningitis -> supportive treatment; Acyclovir in case of Herpes virus

II] Brain abscess

Concept
A focal, suppurative lesion in the brain.

Epidemiology
 1) Rarely due to local spread in developed countries due to rapid detection of orofacial and sinusitis infections
2) But as the number of immunocompromised people has increased, so has the opportunistic bacterial and fungal
brain abscesses

Etiology
1) Hematogenous dissemination (e.g., from bacterial endocarditis)
o Organisms: Staphylococcus, Streptococcus.
o Locations: Frontal lobe > parietal lobe > cerebellum.
2) Local extension (e.g., from sinusitis, otitis media, dental infection).
3) Implantation of pathogens (eg following open skull fracture or brain surgery)

Diagnosis
1) CT or MRI
o Best initial diagnostic test → to confirm diagnosis and localize lesion
o Ring-enhancing mass, which is characteristic of an abscess.
2) A brain biopsy will rule out a neoplasm.
o Microscopic examination and culture
o Best confirmatory test

Treatment
1) Early surgical drainage and biopsy of the abscess
2) Antibiotic therapy (6-8 weeks)
o Initial empirical therapy (third generation cephalosporin + metronidazole +/- vancomycin
3) Intracranial pressure management
4) Seizure prophylaxis

III] Encephalitis
Concept
Inflammation of cerebral parenchyma, which is often viral in origin, including arboviruses, herpes simplex virus (HSV),
cytomegalovirus (CMV), and HIV
Types
1) HSV-1 encephalitis
o Epidemiology: Children and young adults; most common cause of sporadic encephalitis in adults in the
United States.
2) HSV 2 encephalitis
3) HIV encephalitis
4) CMV encephalitis
5) TBE
6) Rabies encephalitis
o Epidemiology: Most commonly follows bite by an infected animal.
7) Poliovirus
8) Measles

Diagnosis
1) Clinical symptoms – headache, confusion, drowsiness, seizure, focal neurologic symptoms
2) Lumbar Puncture
o PCR (gold standard)
o Cells (lymphocytic pleocytosis)
 3) Imaging
o MRI
▪ Hyperintense temporal lobe lesions
4) EEG

Treatment
1) First line: immediate IV acyclovir
2) Second line: foscarnet

20. Specific and non-specific laboratory tests of intestinal infections, prevention.

Diagnostics
Nonspecific
1) Blood
o Full blood count
▪ Inflammation markers (procalcitonin, ESR, Leu, CRP)
o Electrolytes
o Increased hematocrit – in case of dehydration
Specific
1) Serology
o IgG and IgM
2) Blood culture
o Most important as stool culture are often negative despite active infection.
3) Stool analysis
o Microscopic identification of cysts or trophozoites in fresh stool
o PCR
o Stool culture
o Antigen testing
▪ EIA
▪ ELISA
▪ Latex agglutination test

Prevention
1) Hand hygiene
2) Mask – rotavirus and norovirus are also airborne
3) Properly wash and cook food
4) Freezing and cooking meat to kill m/o
5) Avoid uncooked foods and rare meats
6) Clean water supply
o Boiling water
o Filtration
7) Travel
o Depends on destination
▪ Precautionary measurement
▪ Treatment options
8) For Cl. Difficile avoid prescribing antibiotic unnecessarily
9) Preventing parasites in pets (eg deworming)
 10) Vaccination – e.g. before travelling
o E.g. rotavirus
o Cholera vaccine
o Typhoid fever vaccine

21. Parasitic infections: concept, etiology, classification, therapeutic principles.

I] Concept
1. Parasites are organisms that live in or on a host and get its food on the expense of the host.
2. Usually evolved to infect host species but can also use different hosts throughout their life cycle
(reservoir/intermediate/definitive host)
3. Infections cause great burden of disease – mostly in tropics and subtropics, but also in temperate climates
and developed countries.
4. Prevention usually based on improved hygiene and vector protection.
5. Three main classes of parasites can cause disease in humans: Protozoa, helminths and ectoparasite.

II] Classification
1. Protozoa
2. Helminths
3. Ectoparasites

Protozoa Helminths Ectoparasites

Subclassificati 1. Sarcodina – the ameba, e.g., 1) Flatworms (Platyhelminthes) 1.Arthropods
on Entamoeba ▪ Tapeworms (cestodes) – taenia, ▪ Scabies
echinococcus, diphyl. Latum ▪ Lice
2. Mastigophore – the flagellates, ▪ Flukes (trematodes) – ▪ Mites
e.g., Giardia, Leishmania Schistosoma
3. Ciliophoran – the ciliates, e.g., 2) Roundworms (nematodes) -
ascaris, trichinella, enterobius,
Balantidium
toxocara
4. Sporozoan – organisms whose
adult stage is not motile e.g.,
Plasmodium, Cryptosporidium

Etiology 1) Single cells organisms Multicell organisms 1) Multicell organisms

• Roundworms (nematodes)
2) Multiply inside body. 2) Insects, arachnids
• Flatworms (Platyhelminthes)
3) Fecal oral route • Tapeworms (cestodes)
• Flukes (trematodes)
4) Transmission from human to
human

▪ Arthropod vector
Treatment 1. Medications 1) Anthelminthic medical therapy 1) General -
o Benzimidazole (albendazole, Decontamination
1) Amebiasis - Nitroimadolze
mebendazole) clothing and
derivative (metronidazole) or
▪ Echinococcosis → textiles
Luminal agent (paromomycin)
albendazole 2) Medical Therapy-
2) Malaria- Antimalarial drugs ▪ Nematodes → Topical
(chloroquine) pediculicides
mebendazole
(permethrin)
3) Babesiosis- Atovaquone + 2) Schistosoma and taeniasis→
Azithromycin praziquantel
3) Mass Deworming
4) Leishmaniasis- Amphotericin b
4) Surgery
(monotherapy)
5) Invasive
5) Toxoplasmosis- Pyrimethamine, o Echinococcosis - PAIR
sulfadiazine, folic acid

6) Giardiasis + Trichomoniasis-
Metronidazole

2. Invasive procedures

1.Amebiasis- US or CT guides
aspiration puncture of abscess

IV] Therapeutic Principles

• Early treatment is always preferred for good prognosis
• Get rid of the parasite from the infected patient.
1) Medical or surgical treatment
▪ Some parasites needs to be removed surgically and some can’t and need medical treatment.
• Complications that has arisen needs to be treated as well.
1) E.g. Cardiomyopathy that can occur from Chagas disease.
2) These patients may need heart-transplant in order to survive.

22. Slow infections: definition, etiology, clinical manifestations, diagnostic principles, prognosis
I] Definition
Group of infections in animals and humans, characterized by a very long incubation period and a slow course,
terminating fatally.
II] Etiology
1) Subacute sclerosing panencephalitis
o Pathogen: Measles virus variant
2) Progressive multifocal leukoencephalopathy
o Pathogen: Polyomavirus or JC virus
o Virus remains inactive until you become immunocompromised → reactivates → multiplies.
3) Creutzfeldt Jakob disease
o Pathogen: Prion
o Types
• Sporadic
• Familial ( 5-15%)
• Acquired
• Eating contaminated beef [VARIANT CJD]
• Certain medical procedures with contaminated instruments

III] Clinical manifestations

CNS manifestations Focal neurological deficits
1) Chronic sclerosing panencephalitis - Progressive 1) Memory impairment
inflammation of brain caused by persistent infection 2) Behavioral changes
of measles virus. Primarily affect children and 3) Poor coordination
adolescents 4) Visual disturbances
2) CNS demyelination 5) Seizure
3) Spongiform encephalopathy - neurodegenerative
disease of brain and spinal cord

IV] Diagnosis
1) Viral
o CSF + PCR
o Serologic testing
2) Prion disease – diagnosed clinically and confirmed postmortem by brain biopsy
 o CSF may show increased levels of misfolded proteins.
o MRI may show lesions.
3) MRI
4) EEG of brain

V] Prognosis
➔ Fatal

Etiology Clinical Diagnosis Prognosis

manifestation
Subacute sclerosing 1.SSPE caused by a slow 1) Behavior
Panencephalitis measles virus alterations
(paramyxovirus). 2) Cognitive decline
2.Slow viruses may stay 3) Ataxia
dormant in humans for 4) Myoclonic jerks
extended periods of
time, then for reasons
yet unknown may
become reactivated
SSPE.
3.Usually develops 5 to
10 years after the
original viral attack
Progressive 1) caused by JC (John 1) MRI 1) From 1-9
multifocal Cunningham) virus, 2) CSF (lumbar months left
leukoencephalopat mostly acquired puncture) + PCR since onset of
hy during childhood. symptom
2) The virus appears to 2) Up to 2 years
remain inactive until (rarely)
something (such as a
weakened immune
system) allows it to
be reactivated and
start to multiply.
3) Thus, the disorder
affects mainly people
whose immune
system has been
weakened by a
disorder (such as
leukemia,
lymphoma, or AIDS)
4) Drugs that suppress
the immune system
(immunosuppressant
s) or that modify the
immune system
(immunomodulators)
Creutzfeldt-Jakob 1) The disease usually 1. Early symptoms 1) MRI • Up to 6-12
Disease (CJD) occurs o Memory loss 2) CSF + PCR months to live.
spontaneously but o Confusion 3) Electroencephalog • Up to 2 years
may result from o Loss of muscle raphy (10%)
eating contaminated coordination
beef or from 2. Late symptoms
o Myoclonic jerk
 inheriting an o Impaired
abnormal gene. muscle control
2) Prions – misfolded o Hallucinations
proteins o Seizures
Types
• Sporadic
• Familial (5-15%)
• Acquired
o Eating
contaminated
beef
o Certain medical
procedures with
contaminated
instruments

23. Congenital infections: definition, etiology, clinical manifestations, diagnostic principles, prognosis.

I] Definition
Congenital infections are caused by pathogens transmitted from mother to child during pregnancy (transplacental) or
delivery (peripartum)

II] Etiology
The acronym TORCH stands for the causative pathogens of congenital infections: Toxoplasma gondii, others (including
Treponema pallidum, Listeria, Varicella, and parvovirus B19), rubella virus, cytomegalovirus (CMV), and herpes simplex
virus (HSV)

Clinical features Diagnosis Prognosis

Toxoplasmosis 1) classic triad (chorioretinitis, 1) Fetus 1) Depends on time of
hydrocephalus, intracranial ▪ PCR (amniotic fluid) transmission.
calcifications) 2) Newborn ▪ Better prognosis if
2) petechiae and purpura ▪ PCR it occurs during the
(blueberry muffin rash) ▪ CT/MRI 3rd trimester.
▪ Ophthalmological 2) Miscarriage (esp. 1st
investigation trimester)
▪ T gondii specific IgM
antibodies

Syphilis 1) nasal discharge 1) Newborns and pregnant

2) skeletal abnormalities women
(osteodystrophy) ▪ Dark field microscopy
3) Hutchinson triad (Interstitial ▪ PCR of lesions/body fluids
keratitis, sensorineural ▪ RPR – rapid plasma reagin
hearing loss, Hutchinson 2) Fetus
teeth) ▪ US (placentomegaly, hydrops
4) Sensorineural deafness fetalis)
5) Saber shins
6) Interstitial keratitis
Listeriosis • Spontaneous abortion Bacterial culture
• Granulomatosis infantiseptica

VZV 1) IUGR 1) Newborn and pregnant women In severe infection →

2) Hypoplastic limbs ▪ Clinical diagnosis based on mortality is 30%
3) Ocular defects (eg cataracts) skin lesions.
4) Intellectual disability ▪ Direct fluorescent antigen
5) Seizures test ( DFA) or PCR
• Fluid of blister
• CSF
▪ Serology (IgM and IgG)
2) Fetus
▪ PCR (serum/amniotic)
▪ US to detect
abnormalities.

Parvovirus 1) Aplastic anemia 1) Serology of pregnant women 1) Most cases do not

B19 2) Fetal hydrops (IgM and IgG) result in fetal
2) Fetus developmental
▪ PCR for parovirus B19 DNA defects.
• Serum 2) Miscarriage in up to
• Amniotic fluid 10% cases (esp. in 1st
▪ Doppler US of fetal vessels and 2nd trimester)

Rubella 1) Petechiae and purpura 1) Newborn and pregnant woman 1) Miscarriage

(Blueberry muffin rash) ▪ PCR (throat swab, CSF) 2) Preterm birth
2) Triad CCC ▪ Serology (IgM and IgG)
▪ Cataracts (later in life) ▪ Viral cultures
▪ Cochlear defect – (nasopharynx, blood)
bilateral sensorineural 2) Fetus
hearing loss ▪ Serology – IgM (amniotic
▪ Cardiac defect fluid)
3) Patent ductus arteriosus ▪ PCR (amniotic fluid,
4) IUGR (esp. infections occur chorionic villi)
during 1st trimester)
5) Microcephaly
6) Intellectual disability

CMV 1) 90% subclinical symptoms 1) Newborn or pregnant woman 10% develop hearing
2) Jaundice, ▪ Viral culture loss.
hepatosplenomegaly ▪ PCR (urine, saliva)
3) Sensorineural deafness 2) Fetus
4) Periventricular calcifications ▪ US
5) Petechiae and purpura ▪ PCR (amniotic fluid)
(Blueberry muffin rash) ▪ Viral culture (amniotic
fluid)
 ▪ CMV IgM (fetal blood)

Herpes 1) Vesicular lesions 1) Newborn and pregnant woman If detected early,

simples (HSV) 2) Keratoconjunctivitis ▪ Viral culture (skin lesions, prognosis is good.
3) Meningoencephalitis conjunctiva, oronasopharynx,
4) Bulging fontanelles rectum)
▪ PCR (CSF, serum)

24. Human prion induced pathologies, their enumeration and characteristics

1. Prion diseases or transmissible spongiform encephalopathies (TSEs) are a family of rare progressive
neurodegenerative disorders that affect both humans and animals
2. They are distinguished by long incubation periods, characteristic spongiform changes associated with neuronal
loss, and a failure to induce inflammatory response.
3. Palliative care is given as there is no cure for these diseases.
4. Prions cause apoptosis of neurons which then causes brain tissue to get replaced by many small cysts → loss of
normal brain function
5. Cause is due to an accumulation of misfolded proteins called prions → Causes normal proteins to become
misfolded too. Prions are resistant to proteases which would usually cleave abnormal protein
6. Symptoms may not show for decades but when they start showing, the disease can progress rapidly
o Ataxia
o Memory loss
o Behavioral changes
o Muscle weakness
o Myoclonus
 o Dementia

Examples
1. Creutzfeldt Jakob Disease (CJD)
o fatal degenerative brain disorder
o Sporadic no identifiable cause
o Familial
o Acquired - direct inoculation during surgery or Ingestion of infected beef.
2. Kuru
o Fatal neurodegenerative disorder, characterized by tremors. Kuru = shake
o Formerly common in Papa new Guinea due to practicing cannibalism
▪ Tribe there ate brains of deceased family members.
3. Bovine spongiform encephalopathy (BSE) found in animals
o Spread to humans leads to variant CJD.
o It can be transmitted to humans by eating carcasses contaminated with brain matter.

25. List and describe the slow human infectious diseases, except prion diseases.

I] Examples
1. HIV/AIDS
2. Subacute sclerosing panencephalitis- Caused by slow measle virus.
3. Progressive multifocal leukoencephalopathy
4. BK nephropathy - John Cunningham virus
5. Progressive rubella panencephalitis
6. Rabies

II] Characteristics
1. Cause an asymptomatic primary infection.
2. Have a long incubation period ranging from months to years.
3. Follow a slow but relentless progressive course leading to death.
4. Often re-emerge from latency if the host becomes immuno-compromised.

Subacute sclerosing Progressive multifocal BK nephropathy Progressive rubella

panencephalitis leukoencephalopathy panencephalitis

Etiology measles virus JC polyoma virus BK virus rubella virus

Description •Progressive inflammation 1.Uncommon in
of brain caused by healthy individuals
persistent infection of 2.Causes disease in
measles virus → immunocompromised
demyelination and
•Primarily affect children immunosuppressed.
and adolescents
Pathogenesis 1. Chronic progressive 1. It is characterized by Typically associated Progression may be
demyelinating progressive damage or with people who have divided into two
inflammation of brain inflammation to the had a kidney stages,
caused by measles white matter of the transplant.
1- Behavioral
virus. brain at multiple changes
2. Incubation period 6-10 locations. 1.People usually have 2- 2- Neurological
years 2. JC virus is normally a latent infection changes.
3. Nucleocapsids are present and kept under which will reactivate It develops 6months
produced in the control by the immune after kidney or to 4years after the
neurons and the glial system. Meaning the another organ primary rubella
infection (which in
cells → In these cells disease will start to transplant.
most cases is
the viral genes that manifest itself when 2.The virus inhabits congenital rubella).
encode envelope patient is the kidney and urinary
proteins have immunocompromised tract. In children with
restricted expression (AIDS) or on 3.Causes renal congenital rubella
→ As a result immunosuppressive dysfunction infections the deficits
infectious particles like therapy. remain stable:
neurological.
M protein are not
deterioration after
produced and virus is the first few years of
able to survive life is not believed to
persistently without occur.
evoking an immune
response.

Diagnosis CSF and MRI

26. Diseases caused by protozoa: concept, classification, etiology and epidemiology.

I] Protozoa
1. Sarcodina – the ameba, e.g., Entamoeba
2. Mastigophora – the flagellates, e.g., Giardia, Leishmania
3. Ciliophora – the ciliates, e.g., Balantidium
4. Sporozoa – organisms whose adult stage is not motile e.g., Plasmodium, Cryptosporidium

II] Classification by transmission

Fecal-oral Vector borne Sexually transmitted
1. Giardiasis 1. Babesiosis 1. Trichomonas vaginalis
2. Toxoplasmosis 2. Chagas 2. amebiasis
3. Balantidium 3. Plasmodium
4. Amebiasis 4. Leishmaniasis

III] Concept
1. Three main classes of parasites can cause disease in humans: Protozoa, helminths and ectoparasites.
2. Protozoans are unicellular organisms.
 3. They may remain in the human host for their entire life cycle, but many carry out part of their reproduction cycle
in other hosts.
• E.g., mosquitos are vectors for plasmodium which causes malaria.
4. They are able to multiply in humans, which contributes to their survival and also permits serious infections to
develop from just a single organism.
5. Transmission usually via fecal oral route or by vector

IV] Etiology

Disease Causative agent Transmission

Amebiasis Entamoeba histolytica Fecal oral route of cysts from water, food and
contamianted hands
Malaria Plasmodium species Through bite of an infected female anopheles’
(P. falciiuparum,P.vivax, P.ovale, mosquito
P.malariae)
Babesiosis Babesia microti (most common cause in To humans via tick bites Ixodes scapularis
US)
B. Divergens
• In patients who have had a
splenectomy

Leishmaniasis Leishmania donovani through vector phlebotomine sandflies

Toxoplasmosis Toxoplasma gondii oral ingestion of protozoan oocyte that are found in
raw meat, and transplacental transmission from
mother to fetus during pregnancy.

Giardiasis Girardia lamblia fecal oral route especially when travelling or living in
an endemic region.

Chagas Trypanosoma cruzi Vector triatomine bugs of reduviid family

Trichomoniasis Trichomonas vaginalis Sexually

V] Epidemiology
• Many of these pathologies are more prevalent in different tropical areas of the world.
• Many are located in Africa, parts of Asia and south America.
Malaria
• Malaria is the number one cause of death in children in Africa.
• African regions carry 93% proportion of deaths.
Toxoplasmosis
• 11% of the population 6 years infected.

27. Range of infectious diseases in travellers, immigrants, refugees and residents located in areas where war activity
is going on

I] Range in travelers:
 • Most travel-related health problems may be vaccine preventable diseases.
• Geographical risk that the traveler may be exposed to:
Vector borne Water borne Zoonotic Fecal – oral Airborne Blood borne. Hemorrhagic
disease. diseases. diseases diseases fevers

1. Malaria 1. Cholera 1.Rabies 1. Hepatitis A 1. Tuberculosis 1. HIV 1. Ebola

2. Chagas 2. Shigellosis and E 2. Influenza 2. Hepatitis 2. Marbug
3. Zika virus 3. Typhoid fever 2. Giardia B and C virus
4. Yellow fever 3. Travelers’ disease
5. Tick-borne diarrhea 3. Rift valley
encephalitis 4. E. coli fever
5. Salmonella

Basically, to answer this question one has to think of possible disease that exists in particular endemic areas. Living
conditions and diseases associated with poor hygiene. Food may not be as thoroughly cooked, and water may not be
clean. There are many different factors that play a role in infections.

II] Range of refugees

• Refugees are often disproportionally affected by infectious disease, mainly because of their:
1. Geographic origin
2. Ethnicity
3. Conditions at a refugee camp
4. Personal, physical and psychological conditions. Either pre-existing or acquired while they fled their
homeland and made way to camp.
• The common health concerns in refugees:
1. Lack of Immunizations
2. Tuberculosis
3. STDs
4. HIV
5. Hepatitis B
6. Parasitic infections
7. Malaria

28. Rules for hospitalization and transportation of patients with infectious diseases

1. Certain steps and measurements should be taken when patient is coming to hospital with signs of infectious
disease.
2. Prevention of further infections to other patients and health care staff
3. The infectious patient should be isolated.
4. Infectious diseases with importance to public should be reported to the government.
5. Here are standard-precautions and transmission-based precautions.
• Standard = Apply for all patient to exclude possible risk factors
• Transmission = Apply to all patients with symptoms of infectious disease or colonization with infective
microorganism
6. Patients in isolation rooms should only be handled by nurses and doctors in protective clothes.
 7. Cleaning staff should also be wearing protective clothes and clean with specific cleaning supplies.
8. Objects and garbage that leave the isolation room must be put in specific bags and then cleaned.
9. Patients’ specimens need to be put in specific containers and handled with care by laboratory staff
10. Adequate ventilation
11. Hospital beds should be separated by roughly 2m.
12. Transportation of patient should be limited as much as possible. A plan should be made before transporting the
patient, like notifying receiving clinic/ department.
• When transported it should be a direct route, avoiding contact employees and visitors.
• Wheelchairs/bed should be disinfected.
• Wear PPE
• Preparing for the unexpected to happen during transportation.

29. Etiology, general principles of treatment and prevention of viral respiratory infections.

I] Etiology
1) Influenza virus A and B (rarely C)
2) Adenovirus
3) Respiratory syncytial virus
4) Parainfluenza virus
o Paramyxoviruses 1, 2, 3, and 4
5) Coronavirus
o SARS
o MERS
o Covid-19

II] Treatment

Supportive treatment Antiviral therapy

1. Rehydration 1. Indications
2. Antipyretics and analgesia (e.g., Paracetamol) - • Patient with severe disease or risk of
Antipyretics should be started if temperature is 38,5 complication
C. • If there is suspicion of early disease (prodromal
3. Rest symptoms)
4. Room humidifier or hot shower to help ease sore 2. Influenza virus → Neuraminidase inhibitors
throat and cough. • Zanamivir (inhalation)
5. Antitussives (e.g., dextromethorphan) in case of dry • Oseltamivir (oral)
cough 3. Adenovirus → Ribavirin and cidofovir have been used
in immunocompromised patients; results varied

III] Prevention

General Influenza vaccine Adenovirus vaccine Respiratory syncytial virus

1. Hand hygiene 1. Live attenuated or 1. Live attenuated 1. No current vaccine

2. Avoiding sick people inactivated vaccine vaccine for types 4 2. A drug called
3. Ventilation 2. Trivalent inactivated vaccine and 7 – only for palivizumab is available
4. Mask against type B and A. Strains military personnel to prevent severe RSV
 selected by previous illness in certain infants
worldwide circulating agent and children who are at
of the last year. Success high risk for severe
depends to some degree on disease.
the success of the match
between vaccine and
circulating strain.
3. Immunocompromised
should avoid LAIV.

Groups who should receive vaccine:

• Older than 65
• medical staff
• patient with chronic pulmonary and cardiovascular issues
• children under 18
• pregnant women during influenza season.
• Immunocompromised

30. Influenza: characteristics of the causative agent, transmission routes and clinical manifestation. Specific and non-
specific prophylaxis.

I] Characteristics
1) Influenza types virus A, B, and C, the main agents causing influenza in humans.
2) Surface antigens
o Hemagglutinin (H): promotes viral entry by binding to sialic acid residues
o Neuraminidase (N): promotes the release of virion progeny from host cells by cleaving terminal sialic acid
residues
3) High antigen variability through antigenic drift and antigenic shift
o Antigenic drift: Minor changes in antigen structure (Hemagglutinin and/or Neuraminidase) via random point
mutation (gene mutation) → new viral strain
o Antigenic shift: relatively rare development of new combinations of H and/or NA where it acquires a
completely different new set of antigens. Two subtypes of viruses infect the same cell and exchange genetic
segments (reassortment) to create new subtypes

II] Transmission
• Person-to-person via air droplets
o Directly – by sneezing or coughing
o Indirectly – contact with contaminated surfaces

III] Clinical manifestation

1) Fever (39-40 C) or chills 6) Headaches
2) Cough 7) Fatigue
3) Sore throat 8) Vomiting and diarrhea – more common in children
4) Runny or stuffy nose > adults
5) Muscle or body ache

Patient is not infectious to other people after 7 days!

IV] Prophylaxis

1) Specific
o Live attenuated or inactive vaccine
o Trivalent inactivated vaccine against type B and A.
o Immunocompromised people should avoid LAIV
2) Non-specific
o Avoid close contact with sick people
o Practice thorough hand hygiene – soap and water, alcohol base hand sanitizer
o Clean and disinfect surfaces and objects that may be contaminated with germs
o Ventilation
o Mask usage

Groups who should receive vaccine:

1) Older than 65
2) medical staff
3) patient with chronic pulmonary and cardiovascular issues
4) children under 18
5) pregnant women during influenza season.
6) Immunocompromised

31. Influenza: patient risk groups. The most common complications of the flu. Treatment principles of the influenza.

I] Patient risk group

1) Adults  65 years 5) Diabetes patients
2) Pregnant women 6) HIV/AIDS
3) Young children (especially under 2 years) 7) Cancer
4) Patients with asthma 8) Children with neurologic conditions

II] Most common flu complications

1) Pneumonia
2) Myocarditis
3) Encephalitis
4) Myositis, rhabdomyolysis (muscle inflammation)
5) Multiorgan failure
6) Sepsis
7) Can complicate chronic medical problems
o People with asthma may experience asthma attacks while having the flu
o People with chronic heart disease may experience worsening of this condition triggered by the flu
III] Treatment
1) Self-limited disease in most cases → symptomatic care
o Rehydration
o Rest
o Antipyretics and analgesia → paracetamol
o Antitussives for cough → dextromethorphan
o Humidifier to ease symptoms
2) In case of flu like symptoms and high risk group → antiviral treatment
o Makes the symptoms milder
o Reduces sickness time
o Prevent serious complications, eg. pneumonia
o Types – Neuraminidase inhibitors
▪ Oseltamivir phosphate – usually 2x/day for 5 days p.o
• Recommended for pregnant women with flu
▪ Zanamivir – usually 2x /day for 5 days Inhalation

32. Diphtheria: etiology, clinical symptoms and development, diagnosis.

I] Etiology
1) Corynebacterium diphtheriae bacterium (Gr+ bacteria)
2) Transmission
o Airborne
▪ Direct or indirect
o Contact with open lesions (rarely)
II] Symptoms – incubation period 2-5 days.
1) General
o Weakness
o Sore throat
o Fever
o Swollen glands in the neck
2) Anterior nasal diphtheria
o Bloody rhinorrhea
3) Tonsillar and pharyngeal diphtheria
o Pseudo membrane – thick gray coating of dead tissue
 o Bull neck (swollen cervical lymph nodes) → may result in airway obstruction.
4) Laryngeal diphtheria
o Difficulty breathing
o Inspiratory stridor
5) Systemic
o Myocarditis
o Reversible polyneuropathy
o shallow, well demarcated ulcers, usually on legs

III] Development
1. C. diphtheriae colonizes the mucous membrane of the respiratory tract (respiratory diphtheria)
2. C. diphtheriae has both toxigenic and non-toxigenic strains; toxigenic strains contain a prophage gene called
tox, which encodes the diphtheria toxin, an exotoxin that inhibits protein synthesis.
3. Local effects of the toxin: destruction of the respiratory epithelium → inflammatory response →
• Necrotic epithelium embedded within fibrinosuppurative inflammatory exudate (pseudo
membrane) over the pharynx, tonsils, and/or larynx.
• Enlargement of the cervical lymph nodes and edema of the soft tissue of the neck → bull neck
appearance, airway obstruction
4. Systemic effects of the toxin
• Fatty changes and focal necrosis of the myocardium and less commonly, the liver, kidney, and
adrenal glands
• Nerve demyelination

Diagnosis
1. Anamnesis
2. Common signs and symptoms
3. Culture of pharyngeal swab – confirm diagnosis
o If positive, decide if strain is toxigenic → Elek’s test or PCR for tox gene
It is important to start treatment right away if a doctor suspects diphtheria and not to wait for laboratory
confirmation.

33. Diphtheria: treatment and prevention. Complications of diphtheria.

I] Treatment
1. Using diphtheria antitoxin to stop the toxin produced by the bacteria from damaging the body
2. Isolation
3. Antibiotics 14 days
o I/M penicillin G or
o Oral or I/V erythromycin
4. Airway support
o Tracheostomy may be considered if intubation is difficult as a result of tissue edema or if it poses a
risk of dislodging the pseudo membrane.

II] Prevention
Nonspecific Toxoid vaccine
1. Mask usage 1. DTaP – diphtheria, tetanus, pertussis → first shot.
2. Hand hygiene 2. Tdap – diphtheria, tetanus, pertussis → booster at
3. Cover open lesions. 11-12 years old
4. Cough etiquette 2. Given to pregnant women during pregnancy too.
5. Isolation of infected patient 1. Td → booster
▪ This booster should be given every 10 years.
III] Complications
1. Blocking of the airway – due to pseudo membrane and bull neck
2. Damage to the heart muscle and arrhythmia (myocarditis) – if the diphtheria toxin spreads to
the bloodstream.
3. Nerve damage (polyneuropathy)
a. Typically targets the nerves of the throat → difficulty swallowing.
b. If it damages the nerves of the diaphragm → muscle paralysis → respiratory failure → need of
ventilator
c. Neurogenic bladder dysfunction
i. Needing to urinate often.
4. Loss of the ability to move (paralysis)
5. Lung infection (respiratory failure or pneumonia)
a. Pieces of the pseudo membrane can fall into the lungs → widespread pulmonary inflammation
6. Malignant diphtheria
a. Severe bleeding problems
b. Kidney failure

34. Legionellosis: Etiology, transmission routes, diagnosis, clinical manifestation and therapy.

Legionella can cause 2 clinical syndromes

1) Legionnaires’ disease (legionellosis)
• more common syndrome of pneumonia caused by legionella species.
2) Pontiac fever
• an acute, febrile, self-limited illness, which has been linked to Legionella species, doesn’t cause
pneumonia.

I] Etiology – Legionella pneumophila (Gr- rod)

II] Transmission
1. Naturally found in fresh water, like lakes and streams
2. Can grow and spread into human built water systems, e.g.
o Showerheads and sink faucets.
o Cooling towers (structures that contain water and a fan as part of centralized air cooling systems for
building or industrial processes)
 o Hot tubs that aren’t drained after each use.
o Decorative fountains and water features
3. Aspiration of drinking water containing legionella
4. Inhaling contaminated aerosolized water droplets
5. Usually does not spread from person to person

III] Clinical manifestation

Incubation period
- Legionnaire’s disease: 2-10 days

Legionella infection has to be considered in cases of severe presentation with

• Significant respiratory involvement
• Fever > 40 degrees
• CRP > 30mg/dl
Legionnaire’s disease RESPIRATORY/ GI / NEUROLOGIC
1. Fever
2. Severe pneumonia
o Unilateral lobar pneumonia
o Atypical pneumonia: dry cough which can become productive, shortness of breath, bilateral crackles
3. Myalgia
4. Headaches
5. Dyspnea
6. Cough (non- productive)
7. Common GI symptoms (e.g. diarrhea, nausea, vomiting etc.)
8. Neurological symptoms (confusion, cerebellar ataxia, agitation, stupor)
9. Atypical pneumonia

IV] Diagnosis
1. Anamnesis
2. Rapid legionella antigen detection (urine and pleural fluid)
o Disadvantage – urine antigen testing detects only L.pneumophila serogroup 1
▪ however, serogroup 1 is responsible for 90% of legionellosis in Europe.
3. Chest x-ray
o Diffuse interstitial infiltrates → atypical pneumonia.
4. Culture
o Sputum, lung tissue, pleural fluid
5. Serology
 6. PCR – lung tissue usually

V] Therapy

1. Therapy must be initiated before microbiological confirmation

2. Legionnaire’s disease – antibiotics for
o Fluoroquinolones (levofloxacin, moxifloxacin) 7-10 days
o Macrolides (azithromycin, erythromycin) 3 weeks

48
35. Community-acquired pneumonia: Etiology, clinical symptoms, diagnosis, treatment principles and prevention.

Community-acquired pneumonia (CAP): pneumonia that is acquired outside of a health care establishment
I] Etiology

II] Clinical symptoms

1. Severe malaise
2. High fever and chills
o Low grade fever in case of atypical
3. Productive cough with purulent sputum (yellow-greenish)
4. Unproductive cough (in case of atypical pneumonia)
5. Crackles, bronchial, and decreased breath sounds on auscultation
o In case of atypical – auscultation often unremarkable
6. Enhanced bronchophony, egophony, and tactile fremitus
7. Dullness on percussion
8. Tachypnea and dyspnea (nasal flaring, thoracic retractions)
9. Pleuritic chest pain when breathing, often accompanying pleural effusion.
10. Pain projecting to the abdomen and epigastric region (particularly in children)

III] Diagnosis
• Anamnesis + Clinical signs
• Auscultation - Wheezing, crackles, rhonchi

49
 Laboratory test Imagine
1. Blood 1. Chest X ray
▪ CRP, ESR, Leu increased, procalcitonin. ▪ Infiltrates
2. Pathogen detections ▪ Lobar Pneumonia (Extensive opacity restricted to
▪ Blood cultures – always recommended. one pulmonary lobe)
▪ Sputum culture ▪ Bronchopneumonia (patchy infiltrates)
▪ Urine pneumococcal antigen test ▪ Atypical pneumonia (diffuse reticular opacity)
▪ legionella antigen detection (urine or pleural 2. CT of thorax if x-ray is inconclusive.
fluid)
▪ PCR and serology for Chlamydophila

IV] Treatment
General measures
1. Sufficient rest (not absolute bedrest) and physical therapy
2. High liquid intake (prevents dehydration, reduces bronchial secretion viscosity)
3. Pulse oximetry monitoring
4. Oxygen via nasal tube in cases of hypoxia
5. Antipyretics, analgesics (e.g., acetaminophen, ibuprofen)
6. Expectorants and mucolytics
7. Antitussives (e.g., codeine)

Medical treatment
1. Outpatient
o Without risk factors
▪ Macrolides or doxycycline
o With risk factors
▪ 3rd/4th generation respiratory fluoroquinolone (levofloxacin) or
▪ Anti-pneumococcal Beta lactam antibiotics
• Amoxiclav + macrolide/doxycycline
2. Inpatient
o Non-ICU
▪ 3rd/4th generation respiratory fluoroquinolone (levofloxacin)
▪ Anti-pneumococcal Beta lactam antibiotics
• Amoxiclav + macrolide/doxycycline
o ICU
▪ Anti-pneumococcal 𝛽-lactam +
• Amoxiclav + macrolide, or + fluroquinolone
3. If MRSA is suspected
o Add vancomycin or linezolid

Hospitalization
1) Based on CURB-65 score
o Confusion (disorientation, impaired consciousness)
o Urea > 7 mmol/L (20 mg/dL)
o Respiratory rate ≥ 30/min
o Blood pressure: systolic BP ≤ 90 mm Hg or diastolic BP ≤ 60 mm Hg
50
 o Age ≥ 65 years
o Interpretation
▪ Each finding is appointed 1 point; max. 5 points possible
▪ CURB-65 score ≤ 1: The patient may be treated as an outpatient.
▪ CURB-65 score ≥ 2: Hospitalization is indicated.
▪ CURB-65 score ≥ 3: ICU-care should be considered.
Prevention
2) Pneumococcal vaccination
3) Hib vaccination
4) Influenza vaccine
5) Stop smoking.

36. The nature of the development of pneumonia in immunosuppressed patients, therapeutic principles.

Pneumonia in immunocompromised patients is often caused by unusual pathogens but may also be caused by the same
pathogens as those that cause community-acquired pneumonia.

Nature of development
1) Pneumonia in patients with predominant T cell depletion
o E.g. HIV and AIDS
2) Pneumonia in patients with predominant B cell depletion
o E.g. acquired humoral immune deficiencies
3) Pneumonia in patient with neutropenia
o Chemotherapy patients
o Early-phase solid organ and stem cell transplantation
4) Pneumonia in patients receiving immunosuppressive medications
o E.g. azathioprine, methotrexate, etc.

General
1) Defects in humoral immunity predisposes to bacterial infections where antibodies play an important role
2) Defects in cellular immunity predisposes to infections caused by viruses, fungi, mycobacteria, and protozoa.
3) Neutropenia and impaired granulocyte function, which can be observed in case of chemotherapy, leukemia, and
bone marrow depression, can predispose to infections caused by
o S. aureus o Candida
o Aspergillus
o Gr- bacilli
4) Fulminant pneumonia is usually of bacterial cause whereas a gradual onset usually is of viral, fungal, protozoal,
or mycobacterial cause.
5) Infection depends on type, duration and degree of immunodeficiency.

Pathogenic stages
1) Consolidation
2) Red hepatization
3) Grey hepatization
51
 4) Resolution

Treatment principles
1) Prehospital care
o Oxygen administration
o Establish I/v access
o Vital sign monitoring (cardiac and oxygen saturation)

2) Early treatment
o Empiric therapy based on neutropenic fever regimen
o Empiric therapy should be broad-spectrum and if indicated cover for MRSA and pseudomonas
o Patients with later onset of pneumonia, prolonged and profound neutropenia should receive empiric
antifungal therapy

3) Emergency department care

o Initial stabilization as needed according to ABC.
o Empiric anti-treatment based on the most likely pathogen.

37. Pneumococcal infection: clinical manifestation, treatment and prevention.

Streptococcus pneumoniae, or pneumococcus, is a type of bacterium that causes pneumococcal disease.

Pneumococcal infections can range from ear and sinus infections to pneumonia and bloodstream infections.
Children younger than 2 years old and adults 65 years or older are among those most at risk for disease. There are
vaccines to prevent pneumococcal disease in children and adults.

I] Clinical manifestation
1)Pneumococcal 2)Pneumococcal 3)Pneumococcal 4)Pneumococcal 5)Sepsis
pneumonia meningitis otitis media bacteremia
1. Incubation 1. Stiff neck 1. Ear pain 1. Fever 1. Confusion or
period 1-3 days 2. Fever 2. A red, swollen 2. Chills disorientation
2. Fever and chills 3. Headache ear drum 3. Low alertness 2. Dyspnea
3. Cough 4. Photophobia 3. Fever 3. Hypotension
4. Tachypnoea and (eyes being more 4. Sleepiness 4. Tachycardia
Tachycardia sensitive to light) 5. Fever and chills
5. Dyspnea 5. Confusion 6. Extreme pain or
6. Chest pain discomfort
7. Older patients 7. Clammy or
▪ Confusion sweaty skin
▪ Low alertness

Primary pneumococcal infection usually involves the middle ear or lungs.

52
II] Treatment
1) Penicillin or 3rd generation cephalosporins
2) Macrolides in patients with penicillin allergy
3) Respiratory fluoroquinolones (e.g. levofloxacin)

Treat patient in hospital in case

• Fever 40 or <36
• Tachycardia
• Hypotension
• Increased respiratory rate, above 30x/min
• Neurologic signs
• Patients >65 years
• Patient with other condition
• Small baby <1 year

III] Prevention
• Newer are conjugated vaccines
o Pneumococcal conjugate vaccine PCV13 – against 13 types of pneumococcal bacteria that cause
most of the severe illness in children and adults.
▪ Recommended for children, adults with medical conditions, and adults over 65 years
o Pneumococcal polysaccharide vaccine also exists, but not as effective and not used in Latvia
anymore.
• For children
o PCV13 is given to all infants at 2/4/6/12-15 months
• Indications
o All children
o > 65 years
o < 65 years but with underlying condition
▪ Chronic conditions (DM, Kidney disease, liver disease, lung)
▪ Immunosuppressed (HIV/AIDS, Asplenia, Cancer)
▪ heavy smoker
▪ CSF leakage
▪ cochlear implant
▪ high dose immunosuppressive therapy

38. Treatment of drug-susceptible TB.

I] The objectives of TB therapy are:

• Cure the individual patient and minimize risk of death and disability;
• Reduce transmission of M. tuberculosis to other persons; and
• Prevent the development of drug resistance during therapy.

II] General
• Isolation: Every patient diagnosed with active TB must be isolated until sputum, gastric juices, and urine are
negative!
• Therapy monitoring
o Monthly sputum samples for microscopy and culture
53
 o Monitor drug side effects: renal retention parameters, ophthalmological check-up , ENT, and liver
function tests

III] Regimen
• Intensive phase: Isoniazid + rifampicin +pyrazinamide + ethambutol (2 months)
• Continuation phase: Isoniazid + rifampicin (4 months)

39. Latent tuberculosis infection: definition, diagnosis and treatment.

I] Definition
Latent tuberculosis infection (LTBI)
3) Primary infection by Mycobacterium tuberculosis antigens without evidence of clinically manifested active TB. (no
symptoms & no X-ray signs)
4) Someone has latent TB if they are infected with the TB bacteria but do not have signs of active TB disease and do
not feel ill.
5) can develop active TB disease in the future.

II] Epidemiology
1) About one-quarter of the world's population has latent TB, which means people have been infected by TB
bacteria but are not (yet) ill with the disease and cannot transmit the disease.
2) People infected with TB bacteria have a 5–15% lifetime risk of falling ill with TB.
3) persons with compromised immune systems, such as people living with HIV, malnutrition or diabetes, or people
who use tobacco, have a much higher risk of falling ill.

III] The role in public health

1) TB is a major infectious cause of morbidity and mortality, mainly in developing countries.
2) Since 5-10% of those with latent TB develop an active infection, it is crucial to eliminate TB.
3) But adherence in the treatment of latent TB is relatively low → , there are groups that should be given high
priority for latent TB treatment, those are:
o People with positive TB blood test (IGRA)
o People with tuberculin skin test reaction of >5mm who are:
▪ HIV-infected
▪ Recent contact to a patient with active TB
▪ Persons with fibrotic changes on radiograph consistent with old TB
▪ Organ transplant recipients
▪ Persons who are immunosuppressed for other reasons (e.g. immune depressants)
▪ Children <5 years old

IV] General Rules

54
 1) Tuberculin skin test (TST) and IGRA(QuantiFERON, T-spot) test would be positive if infection exist in the host,
however it does not identify the difference between an active or latent infection.
2) TST may be positive but IGRA negative in BCG vaccinated individuals.
3) Preferably to use IGRA test if available, because it is more specific, but guidelines vary depending on country.
4) To use both tests to confirm diagnosis is ideal.
5) 10% of the immunocompetent with LTBI develop TBC in their lifetime.
→X-ray, however it may show false negative, CT can be used to verify suspicion
→ ESR, CRP and FBC does not exclude active tbc and is not for much help.

V] 3 types of treatment regimens:

• - Isoniazid 6 or 9 months → Monotherapy
• - Rifampicin 4 months → Monotherapy
• - 12 dose Isoniazid and Rifapentine once a week.
→Consider adherence and age of patient
→Consider special circumstances if the patient is immunosuppressed, pregnant,
resistance of pathogen and side effects.

40. Streptococcus pneumoniae: the most common forms of clinical manifestation. Antibacterial treatment. Possible
prophylaxis.

I] Clinical manifestation
1) Pneumonia
2) Meningitis
3) Otitis media
4) Sinusitis → Sneezing, nasal congestion, rhinorrhea, hyposmia/anosmia
5) Pharyngitis
o fever, sore throat, pharyngeal erythema, tonsillar exudate, and cervical lymphadenopathy
6) OPSI (overwhelming post-splenectomy infection)
o Fulminant sepsis that develops in a splenic individual as a result of infection
o Patients initially have flu-like symptoms (e.g., fever, malaise), but rapidly deteriorate within hours.

II] Treatment
1) Penicillin or 3rd generation cephalosporins
2) Macrolides in patients with penicillin allergy
3) Respiratory fluoroquinolones (e.g. levofloxacin)

55
III] Treat patient in hospital in case
• Fever 40 or <36 • Neurologic signs
• HR increased. • Patients >65 years
• Systolic BP going down (must know normal • Patient with other condition
BP) • Small baby <1 year
• Increased respiratory rate, above 30x/min

IV] Prevention
• Newer vaccines are conjugated.
o Pneumococcal conjugate vaccine PCV13 – against 13 types of pneumococcal bacteria that cause
most of the severe illness in children and adults.
▪ Recommended for children, adults with medical conditions, and adults over 65 years.
• For children
o PCV13 is given to all infants at 2/4/6/12-15 months.
• Indication
o All children
o > 65 years
o < 65 years but with underlying condition
▪ Chronic conditions (DM, Kidney disease, liver disease, lung)
▪ Immunosuppressed (HIV/AIDS, Asplenia, Cancer)
▪ heavy smoker
▪ CSF leakage
▪ cochlear implant
▪ high dose immunosuppressive therapy

41. M. Tuberculosis transmission. Infection control measures in health care facilities: administrative, environmental
control and personal respiratory protection. Estimation of the infectiousness of patient requiring respiratory
isolation.

Tuberculosis (TB) is a common infectious cause of morbidity and mortality worldwide that is caused by Mycobacterium
tuberculosis and typically affects the lungs.

Transmission
• Primary transmission – airborne droplets
• TB disease in the lungs or throat can be infectious.
o means that the bacteria can be spread to other people.
o TB in other parts of the body, such as the kidney or spine, is usually not infectious.

Infection control

TB transmission control measures in a health care unit can be hierarchized into three levels:

• Administrative – aimed at early identification, isolation and treatment of infectious patient

56
 • Assign responsibility for tb infection control into setting
• Conduct TB risk assessment
• TB infection control plan to ensure detection, airborne precautions, and
o treatment who have suspected/confirmed TB disease both patients and health care
workers
• Ensure availability of equipment, testing and reporting to the physicians and
o infection control team
• Implement effective work practice to what is already mentioned
• Ensure proper cleaning and sterilization of equipment
• Train and educate health care workers, focusing on prevention, transmission,
o symptoms
• Advise respiratory hygiene and cough etiquette
• Coordinate local or state health department

• Environmental control (engineering) – focus on preventing the spread and reduce concentration of
infectious droplet nuclei in the air
o Adequate ventilation
o Ultraviolet germicidal irradiation (UVGI) fixtures
▪ Kills or inactivates bacilli in the air
o Use of high efficiency particulate air (HEPA) filters
▪ Cleans the air of infectious droplet

• Respiratory protection (individual protection)- Provide additional protection for health care workers in
high-risk settings
o Personal respiratory protection
▪ Healthcare provider staff and visitors should use personal respiratory protective equipment
in settings that may be at higher risk for TB transmission:
• Eg Rooms where infectious TB patients are being isolated
▪ Respirators for health care workers
▪ Masks for patients
o Respiratory isolation
▪ Separate infectious patients from contact with healthy people and restrict their movement
to stop the spread of TB

57
42. Diagnosis of pulmonary tuberculosis: risk assessment, symptoms and signs, radiological presentation,
bacteriological examination. Indications for the use of bronchoscopy and invasive methods in the diagnosis of
pulmonary tuberculosis.

I] Risk factors:
1) Recent exposure to patients with active TB
2) Tested positive in past TB tests
3) History of IV drug use
4) Recently immigrated from an area where TB is endemic
5) Immunocompromised
o HIV
o DM
o Chronic diseases
o Organ transplants
o Cancer

II] Symptoms
Latent infection Active infection (either primary or reactivated)

• Asymptomatic • Constitutional symptoms: fever, weight loss, night sweats, fatigue,

• The patient is not contagious. lymphadenopathy
• Pulmonary symptoms: dyspnea, productive cough (possibly hemoptysis)
lasting > 3 weeks
• The patient is contagious.
• 80% pulmonary tuberculosis
• 20% extrapulmonary tuberculosis

Always consider TB as a differential diagnosis in a young patient with hemoptysis! Depending on the degree of
immunosuppression, TB in HIV-positive patients may progress atypically or more rapidly!

58
Diagnosis
Bacteriological Radiological Instrumental Histological
o Specimen ▪ Chest x-ray i. Tuberculin 2. Granuloma
collection findings in skin test finding
processing tuberculosis (TST) ▪ Rounded
and review ▪ Infiltrates or consolidations and/or ▪ Intradermal outlines,
(at least 3 cavities are often seen in upper lungs injection of 5 central
consecutive ▪ With or without mediastinal or hilar units (= 0.1 caseous
sputum lymphadenopathy mL) of necrosis,
specimens, ▪ Ghon complex: sequelae of primary TB purified transformed
8-24h infection. protein macrophages-
interval in ▪ CT scan derivative > epithelioid
between) tuberculin. cells,
▪ Coughing ▪ The lymphocytes,
▪ Induced sputum diameter of plasma cells
▪ Bronchoscopy the induration and
▪ Gastric aspiration (for at the fibroblasts.
children) injection site 3. Hematoxylin-
▪ urine is measured eosin stain
o Microscopy after 48– 72 (H&E)
→ Acid- hours.
Fast-Bacilli ▪ The test only
▪ Rapid results but lacks becomes
sensitivity positive 6–8
▪ No differentiation weeks after
between M. infection
tuberculosis or ▪ False
nontuberculous positive and
mycobacteria possible. false
o Culture negatives can
▪ Species identification ▪ occur
Drug sensitivity testing ii. Interferon y-
▪ Culturing can take up release
to six weeks (not useful assay
for initial therapy (IGRAs)
planning)
▪ E.g., Löwenstein–
Jensen agar.
o PCR

7. Indications for the use of bronchoscopy and invasive methods in the diagnosis of pulmonary tuberculosis
a. Bronchoscopy used when spontaneous sputum smear is negative.
b. Detection of lesions in airway and bronchioalveolar lavage can be performed.
c. Risk of nosocomial dissemination of TB

59
43. Vaccination against tuberculosis: vaccine description, vaccine efficacy, indications and contraindications for
vaccination, development of immunity, advert events following immunization.

BCG vaccination
1) BCG vaccination (Bacillus Calmette-Guerin) is an live attenuated vaccine for intradermal use made from an
attenuated strain of M.bovis.
2) Protective benefit is variable, ranging from 0-80.
o An overall protective effect of 50%
o Against meningitis and miliary TB 75%-83%
o BCG prevents only 5% of all vaccine-preventable death by TB
3) BCG vaccine protects against:
o Acute forms of TB in childhood (miliary TB and TB meningitis)
o Diseases caused by non-tuberculosis mycobacteria.
o Leprosy
4) BCG vaccine doesn’t protect from:
o Primary infection and reactivation disease
o Pulmonary tuberculosis

Indication:

1) Used for vaccination of infants, children and adults (health care workers at risk) against TB
a. for maximum protection vaccine should be given asap after birth
2) Health care workers on individual basis
3) Dosage: for infants <1 year: 0.05 ml, for children and adults: 0.1 ml

Contraindications

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 1) Congenital or acquired Immunosuppression (since it live attenuated vaccine)
2) Receiving treatment with immunosuppressive drugs
3) HIV infection
4) In case of acute illness (fever) & extensive progressive dermatitis (vaccination should be postponed)
5) Tuberculin positive individuals
6) Pregnancy (although no harmful effects on the fetus have been observed)

Development of immunity
1) Cell mediated immunity and delayed type hypersensitivity (DTH) are closely related phenomena that occur in
the host as the result of T cell becoming specifically activated.
2) Cellular immunity develops when T cells become sensitized after recognizing their specific antigen and then
release mediators that modulates macrophage function.
3) Activated macrophages are capable of containing or killing the M. Tuberculosis organisms.
4) DTH is responsible for the positive tuberculin skin test result and many of the observed detrimental effects of TB
(caseation, cavitation)
5) Cellular immunity develops 4-6 weeks after BCG vaccination. The duration of post-BCG immunity is about 15
years (from 10 to 23 years). 8-10 weeks after BCG vaccination tuberculin skin test can convert from negative to
positive.

Adverse effects
Local Systemic Immunological

1. Local abscess 1. Cutaneous skin lesions apart 1. Erythema granulare

2. Severe or prolonged ulceration from the site of injection 2. Erythema nodosum
3. Keloid scar formation after BCG 2. Osteitis
vaccination 3. Disseminated BCG infection.
4. Lymphadenitis: Non-suppurative &
Suppurative

61
44. Most frequent forms of extrapulmonary tuberculosis: peripheral lymph node tuberculosis, tuberculosis pleural
manifestations, bone and joint tuberculosis, kidney tuberculosis. Diagnostic and treatment approach.

62
63
1. Smear microscopy is the quickest and easiest procedure that can be performed.
• ZH stain using Carbolfuchsin (direct microscopy) or
• Fluorochrome procedure (fluorescent microscopy)
→ Many are negative on AFB but positive in culture.
2. NAAT Direct detection with NAA (DNA) (takes 1 days approx.)
3. Culture remains the gold standard for laboratory confirmation of TB disease. If
positive it confirms diagnosis, if negative it does not exclude diagnosis.
→Culture is done regardless of AFB smear or NAA results – Use BACTEC, MGIT,
Versa or whatever is available.

Treatment
1) As a rule, the principles used for the treatment of pulmonary TB disease also apply to extrapulmonary forms of
the disease. Repeat what is described in previous Q about treatment, 2 months 4 drugs, 4 months 2 drugs.
2) If Pyrazinamide cannot be used in the initial treatment, continuation phase must be increased to 7 months.

45. Rotavirus infection: etiological agent, clinical manifestation and possible complications, diagnosis (including
laboratory tests), treatment and prevention.

Rotaviruses are a frequent cause of viral gastroenteritis in infants and young children

Etiology
1) Pathogen: Rotavirus is a non-enveloped, double-stranded RNA reovirus.
2) Transmission:
o fecal-oral route
64
 ▪ (e.g., by hands, objects, food, water contaminated with the virus)
o Airway transmission
o Highly contagious
o Virus spreads 10-14 days after disease starts.
3) 95% of children by 5 years old sick with Rota virus infection one time.

Clinical signs
1) Incubation period of 1–3 days
2) Sudden onset with vomiting, diarrhea.
3) Fever > 39 degrees (lasting 3-7days)
4) Watery diarrhea (lasting 3-7days)
5) Nausea
6) Borborygmi (rumbling sound made by the stomach due to gas)
7) Abdominal cramps

Complications
1) Dehydration
o Electrolyte imbalance
o Metabolic acidosis
2) Necrotizing enterocolitis
3) Hemorrhagic gastroenteritis

Diagnostics
1) Difficult to clinically distinguish from other enteric viruses
2) Stool examination → Ag detection
3) ELISA - Viral antigen detection in feces in the first 5 days
o A highly sensitive test that can be performed quickly and easily
4) RT - PCR – detect Viral RNA

Treatment
1) Supportive
o Non-specific detoxification
o Oral Rehydration (virus leads to severe dehydration)
▪ IV rehydration for those who cant tolerate oral therapy due to frequent vomiting or severe
dehydration
2) Antibiotics and antimotility agents should be avoided.

Prevention
o Vaccination
• Rotavirus vaccination (a live attenuated vaccine) is recommended unless there is a contraindication. These may
include:
o A history of severe allergic reaction after exposure to a previous rotavirus vaccine
o Infants with severe combined immunodeficiency (SCID)
o Infants with a history of intussusception (segment of intestine invaginates into the adjoining intestinal
lumen, causing bowel obstruction.

65
 • Vaccination schedule
o 2-4-6 months
• Hygiene
• Wastewater control
• Cook food adequately.

46. Norovirus infection: etiological agent, clinical manifestation and possible complications, diagnosis (including
laboratory tests), treatment and prevention.

1) Noroviruses are a frequent cause of viral gastroenteritis in individuals of all ages worldwide.
2) Leading cause of viral gastroenteritis
3) Most common cause of Adult gastroenteritis
4) Stable against chlor-disinfection fluids, freezing, boiling until 60 º
5) Can cause outbreak in school setting and in winters.

Etiology
1) Pathogen: Norovirus is a non enveloped RNA calicivirus.
2) Transmission
o Fecal oral route
o Airborne droplet
o Individuals are highly infectious during the acute phase and 24–72 hours following onset of symptoms

Clinical features
1) Self-limited disease 1-2 days
2) Incubation period 1-2 days
66
 3) Main symptoms. Nausea, vomiting, diarrhea, fever (low grade)- subfebrile
4) Watery diarrhea w/o blood
5) headache, myalgia
6) Gastroenteritis
Diagnostics
1) Clinical suspicion in potentially exposed individuals if vomiting and/or diarrhea consisting of ≥ 2 loose stools
occur within a 24-hour period.
2) RT-PCR → confirmatory test (stool, vomit)
3) ELISA: not a standard procedure due to low sensitivity (∼ 50%)

Treatment
1) Supportive therapy
a. Rehydration, if necessary, with IV fluids (especially in the elderly and children)
b. If myalgia and/or headache are present: NSAIDs or acetaminophen.
2) Full recovery after 1-2 days, self-limited

Prevention
1) Obligation to report outbreaks.
a. Many cases go underreported, as symptoms are usually mild in healthy individuals → higher chance of
further transmission.
2) Hygiene is most important.

47. Botulism: etiological agent, clinical manifestation and possible complications, diagnosis (including laboratory
tests), treatment and prevention.

Botulism is neuromuscular poisoning from Clostridium botulinum toxin. Infection is not necessary if toxin is ingested.

Etiology
1) Clostridium botulinum
o Gram-positive rod
o Spore-forming
o Obligate anaerobe
o Produces heat-labile neurotoxin (heat stable)
• Toxins are readily destroyed by heat, and cooking food at 80 ºC for 30 min
• Exposure to moist heat at 120 ºC for 30 min kills the spores
• Toxin production (especially type E) can occur at temperature as low as 3° C – i.e., inside a
refrigerator – and does not require strict anaerobic conditions

2) Decide if its form

o Food – borne botulism
• Ingestion of preformed botulinum toxin via contaminated food (poorly pasteurized canned
foods
o Wound botulism
• Germinating spores in wounds (most common among i/v drug users
o Infant botulism
• Ingestion of spores via honey, juice and contaminated soil

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Toxin types
1) A, B, C, D, E, F, G
2) For people A, B, E – rarely F. A is most potent.
3) For animals C and D
Clinical signs
1) Incubation period 2h-5days (for wound it can be 10days)
2) Neurological symptoms
o Descending paralysis
• Peripheral flaccid muscle paralysis that descends caudally
• Typically begins in frequently used muscles
• Pupils: accommodation paralysis, mydriasis, diplopia
• Pharynx: dysarthria, dysphagia
• Respiratory failure due to diaphragmatic paralysis, pulmonary infections
o Autonomic nervous system: xerostomia (dry mouth)
o Infants may present with ptosis, floppy movements, general weakness, and poor feeding (weak sucking)
3) Gastrointestinal symptoms: gastrointestinal discomfort, nausea, and vomiting, later followed by constipation
o Only present in 30% of cases of foodborne botulism
o Constipation is often the first symptom of infant botulism.
o Absent in wound botulism
4) NO FEVER!!!
5) NO ALTERED MENTAL STATUS

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Diagnostic:
1) Based on clinical symptoms and clinical history (eg history of ingestion of canned food)
o Or history of eating food from bulging cans
2) In case of suspicion → antitoxin should be administered directly, without waiting for confirmation of diagnosis.
3) Rapidly identify botulinum toxin in samples from serum, vomit, gastric acid, stool, or suspicious foods “
o Mouse bioassay
o Culture of C.botulinum of stool and wound

Treatment

69
 1)Supportive care 2)Foodborne botulism 3)Infant botulism 4)Wound botulism

• Hospitalization ▪ Administer horse ▪ Administer human ▪ Administration of botulism

• Secure airways derived heptavalent botulism immune antitoxin
• Mechanical botulism antitoxin. globulin IV (BABY BIG-
▪ Surgical debridement
ventilation IV)
▪ Gastric lavage to
• Parenteral ▪ Antibiotics are only used to
eradicate toxin ▪ Antitoxin can cause
nutrition treat secondary bacterial
allergic reaction.
infections. Penicillin,
metronidazole.

Complications – Autonomic paralysis, respiratory failure, death

Prevention
Foodborne botulism Infant botulism 3) Wound botulism

• Refrigerate foods within 2 hours after Do not give honey to • Do not abuse injectable drugs.
cooking. Proper refrigeration prevents babies under 1 year
• Seek medical treatment for a wound
the bacteria from producing spores.
with signs of infection including redness,
• Cook food thoroughly. tenderness, swelling or pus

• Avoid food containers that appear • Clean wounds contaminated by dirt and
damaged or bulging. (These can be signs soil thoroughly and seek medical
of gas produced by the bacteria.) attention.

48. Cholera: etiological agent, prevalence, clinical manifestation and possible complications, diagnosis (including
laboratory tests), treatment and prevention.

Definition: Cholera is an acute diarrhea disease caused by toxin-producing species of the bacterium Vibrio cholerae 1

Pathogen: Vibrio cholerae

1) Gram-negative, oxidase positive, curved bacterium with a single polar flagellum → produces cholera toxin
2) Cholera toxin stimulates increased ion secretion (mainly chloride)

Prevalence
1) Rare in developed countries
2) Mostly found in the tropics: Asia, Africa, India
3) Yearly estimated: 2.8 million cases

Transmission
1) Fecal-oral (person to person)
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 2) Foodborne
o Vibrio lives in salt water
o Undercooked sea food or contaminated water (most common mode in developing countries)
o Fruits and vegetables washed with contaminated water
Infectivity
1) Acid-labile (grows well in an alkaline medium) → High infective dose required (over 108 pathogens)

Clinical features
1) Incubation period is usually 2-3 days, but varies from 2 hours to 5 days
2) Ranges asymptomatic to severe diarrhea
3) The disease is characterized by sudden onset of diarrhea and vomiting
▪ Pronounced and frequent watery diarrhea (up to 1 liter per hour)
▪ usually without stomach ache or abdominal pain
▪ The stool is gray and turbid ("rice water"), no blood in stool.
▪ In the beginning, the patient is uneasy and very thirsty, but as shock develops, they become apathic and
eventually unconscious
▪ Dehydration, hypotension and acidosis can develop rapidly within a few hours
4) NO FEVER!! → rare, if present → suspect secondary infection

Diagnosis

Blood tests Serology Culture (confirmatory) Direct microscopy

Electrolytes and acid-base Urine Dipstick (rapid; initial Stools or vomiting → The Characteristic "chaotic"
status, kidney function test) → has low sensitivity bacterium survives in feces movement of Vibrio
and specificity for a few hours if kept cholerae found in large
moist. For longer transport quantities by microscopy of
times, the Cary-Blair the stool
transport medium is used

Treatment
2) Prevent severe and life-threatening dehydration.
3) Urgent fluid replacement (I/v)
▪ The mortality rate of untreated patients may be 50–70% but drops to < 0.5% with adequate fluid
replacement.
4) Antibiotic therapy in severe cases:
▪ First choice doxycycline
▪ Alternatively, erythromycin in children
Prevention
5) Cholera vaccine
▪ Live attenuated or inactivated
6) Drinking water hygiene (most important)
7) Wash fruits and vegetables
8) Wash hands

Complications
▪ Severe dehydration
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 ▪ Pneumonia may occur in children.

49. Shigellosis: etiological agent, clinical manifestation and possible complications, diagnosis (including laboratory
tests), treatment and prevention.

Shigella causes dysentery, also known as shigellosis, it affects the large intestine. It is a very infective intestinal infection,
often with bloody diarrhea. It is usually a mild and self-limited disease.

There are 4 types

1) Shigella dysenteriae type 1 and type 2 3) Shigella boydii
2) Shigella flexneri 4) Shigella sonnei
All 4 produce enterotoxins (Shiga toxin) and endotoxin
→ Gr- rods
→ Shiga toxin causes enterocyte damage & subsequently bloody diarrhea.

Transmission → fingers, foods, flies feces (4 Fs)

1) Fecal-oral
2) Foodborne
▪ Unpasteurized milk
▪ Raw, unwashed vegetables
▪ Contaminated water
3) The bacteria is easily killed by disinfection
4) Stable in acidic, dry, and light environment

Clinical features
1) Incubation period 0-2d
2) Duration 2-7d
3) Some patients are asymptomatic carriers which can transmit the disease to others.
4) Profuse inflammatory, mucoid-bloody diarrhea
5) High Fever
6) Abdominal cramps and tenesmus (persistent but unsuccessful urge to empty rectum)
7) S. dysenteriae and S. boydii
▪ Cause a more acute and serious dysentery.
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 8) Confusion, delirium, chock, fever and cramps in children → could be hemolytic uremic syndrome.
9) Tenesmus (feeling of needing to pass stool despite empty colon.

Complications
1) HUS – hemolytic uremic syndrome
▪ A condition in which microthrombi occlude the arterioles and capillaries, which results in microangiopathic
hemolytic anemia, thrombocytopenia, and acute kidney injury → Caused by Shiga toxin
2) Intestinal complications (e.g., toxic megacolon, colonic perforation, intestinal obstruction, proctitis, rectal
prolapse)
3) Febrile seizures
4) Reactive arthritis

Diagnosis
1) Usually, diagnosis is unnecessary as it is a self-limited disease. However, indications for feces sampling and
culture are
▪ Persistent bloody diarrhea
▪ Heavy/very frequent diarrhea

Treatment
2) Symptomatic
▪ Rehydration
▪ Correction of electrolytes
▪ Rest
▪ Analgesics and antipyretics
3) Antibiotics – ciprofloxacin (adults), TMP/SMX (children) – should always be treated with AB:
▪ Children
▪ Persistent diarrhoea
Prevention
1) Hand hygiene
2) When travelling avoid untreated water
3) Avoid sexual contact with people who recently recovered from shigellosis

50. Salmonellosis: etiological agent, clinical manifestation and possible complications, diagnosis (including laboratory
tests), treatment and prevention.

Salmonella is a Gr- bacteria. It is the 2nd most common pathogen for bacterial foodborne gastroenteritis.

I] Types
1. S. Enteritidis
2. S. Typhimurium
3. S.heidelberg
4. S.infantis
5. S. Agona
6. S.Newport
7. S. saint- paul

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S.typhi and paratyphi which have invasive characteristics cause typhoid/enteric fever. They penetrate the intestinal
walls and invade the mesenterical lymph nodes and spleen, causing bacteremia. The infection is localized in the
lymphatic tissue and the Peyer’s patch can become inflamed and wounded. Bacteremia can spread to the lungs,
gallbladder, kidneys, and CNS.

II] Transmission
• Fecal oral → They live naturally in feces so they can contaminate any foods.
• Foodborne (contaminated food looks normal and smells normal)
o Chicken (undercooked) – most common
o Raw eggs
o Milk (unpasteurized)

III] Clinical features

• Salmonella gastroenteritis
▪ Incubation period 12-48h (0-3d)
▪ Duration 3-7 days
▪ Fever, usually resolves within 2 days
▪ Chills
▪ Headache
▪ Myalgia
▪ Enteritis
▪ Severe vomiting
▪ Watery-bloody diarrhea (bloody in rare cases)
▪ Triggered by endotoxins.

IV] Complications (especially in immunocompromised patients, e.g., HIV)

1) Bacteremia
2) Reactive arthritis
3) Systemic disease: osteomyelitis, meningitis, myocarditis
V] Diagnostics

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 1. History suggesting salmonella infection.
2. Lab tests
• Leukocytosis
3. Culture
• Feces
• Gastric lavage
4. PCR

VI] Treatment

Symptomatic Antibiotics (TMP/SMX, ciprofloxacin) - in severe cases

1. Disease is self-limiting. 1. Sepsis

2. Rehydration 2. Immunocompromised patients
3. Children under 2 years of age
4. Elderly > 65 years

VII] Prevention
1. Hand hygiene
2. Wash cutting boards and utensils after handling uncooked chicken.
3. Cook food properly.

51. Amebiasis: etiological agent, clinical manifestation and possible complications, diagnosis
(including laboratory tests), treatment and prevention.

I] Etiology
1) Pathogen: Entamoeba histolytica, an intestinal protozoan
2) Transmission
o Fecal-oral: Amebic cysts are excreted in stool → contaminate drinking water or food.
o Sexual contact.
o Infection typically occurs following travel to endemic regions such as the tropics and subtropics.

II] Clinical manifestation

• Asymptomatic in most
Intestinal amebiasis → amebic dysentery Extraintestinal amebiasis: → Abscess
1) Incubation period 1-4 weeks 1) Incubation period: few weeks to years
2) Bloody loose stools with mucus 2) Liver abscess (95%): usually a solitary abscess in the
3) Painful defecation, tenesmus, vomiting, abdominal right lobe
pain, cramps, weight loss, and anorexia ▪ Fever in 85-90% of cases (compared to amebic
4) Fever (10–30% of cases) dysentery)
5) High risk of recurrence, e.g., through self-inoculation ▪ RUQ pain or pressure sensation
(hand to mouth) ▪ Chest pain, pleuralgia.
6) A chronic form is also possible, which is clinically ▪ Diarrhea (only 1/3 of liver abscess cases)
similar to inflammatory bowel disease. 3) In 5% of cases: abscesses in other organs (e.g.,
especially the lungs; in rare cases, the brain), with
accompanying organ-specific symptoms
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 7) Always consider amebiasis when a patient presents
with persistent diarrhea after traveling to a tropical
or subtropical destination.

III] Complications

Intestinal Extraintestinal

1) Fulminant or necrotizing colitis 1) Secondary infection → pyogenic abscess

2) Toxic megacolon 2) Abscess rupture → peritonitis
3) Ameboma 3) brain abscess → focal neurological deficits.
4) Fistula formation

IV] Diagnosis:
▪ Travel History.
▪ Intestinal amebiasis ▪ Extraintestinal amebiasis
o Stool analysis 1. Serological antibody detection
- Microscopic identification of cysts or trophozoites in 2. Liver function tests
fresh stool. Trophozoites often contain ingested ▪ ALP, AST, ALT, bilirubin slightly elevated.
erythrocytes. 3. Imaging: shows a solitary lesion, typically in the
- The following tests confirm the microscopic findings: right lobe
• EIA or copro-antigen ELISA (antigens ▪ Ultrasound: hypoechoic
found in feces) ▪ CT/MRI for liver abscess
• PCR
- Stool microscopy is not sensitive, especially in later
phases, so at least three stool samples should be
examined before reporting a negative result.
o Colonoscopy with biopsy
▪ Flask-shaped ulcers

V] Treatment

Symptomatic intestinal amebiasis and invasive Invasive procedure

extraintestinal amebiasis
1. Initial treatment with a metronidazole to 1. Aspiration: ultrasound or CT-guided puncture of
eradicate invasive trophozoites. complicated abscesses at risk for perforation
2. Followed by a luminal agent (e.g., paromomycin) Indications:
to eradicate intestinal cysts and prevent relapse. • Localized in the left lobe
• Pyogenic abscess
• Multiple abscesses
• Failure to respond to pharmacotherapy

2. Surgical drainage: should be avoided, but indicated if

aspiration isn’t possible or peritonitis is present.

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VI] Prevention:
1) Unpeeled fruits or vegetables should not be consumed if there is a potential risk of contamination by
Entamoeba histolytica cysts (e.g., endemic region with low hygiene standards).
2) Even chlorinated water can contain high concentrations of amebae; therefore, water should be boiled before
use.
3) "Boil it, cook it, peel it, or forget it."
4) Avoid sex with infected or someone who recently recovered.

52. Clostridium difficile infection: aetiological agent, clinical manifestation and possible complications, diagnosis
(including laboratory tests), treatment and prevention.

Intestinal infection caused by Cl. difficile after treatment of other diseases with antibiotics (usually clindamycin). It’s an
opportunist where it causes infection when there is damage to the intestinal flora (i.e due to antibiotics)

I] Etiology
1. Pathogen: Cl. Difficile
2. Gr+ bacillus
3. Forms environmentally resistant spores (capable of withstanding heat and acid)
4. Transmission
• colonization after the intestinal flora is compromised (e.g., antibiotic treatment ruins flora in intestines), and
pathogenic toxin release.
• Fecal-oral contamination
5. Hospital acquired infection.
o Oral transmission via contaminated surfaces and contaminated medical equipment

II] Clinical features

1) Can start 1 day after start of antibiotic treatment or up to 3 months after ended treatment.
2) Watery diarrhea (foul smelling), vomiting, nausea
• Dehydration can occur.
3) Less than 50% have fever, stomach pain.
4) Pseudomembranous colitis
• General worsened condition
5) Fulminant colitis
• Abdominal distention and severe hypovolemia
6) Recurrent disease

III] Complications
1) Toxic megacolon
2) Paralytic ileus
3) Perforation
4) Peritonitis
5) Sepsis

IV] Diagnosis
History Stool tests Blood test Imaging Endoscopy

77
 ▪ Intestinal 1) Confirmatory 1) Leukocytosis Abdominal x-ray/CT 1) Colonoscopy (or
infection with tests of choice 2) electrolyte scan: detection of sigmoidoscopy)
diarrhea after ▪ ELISA test to imbalance toxic megacolon, 2) Findings:
antibiotic detect toxins abscesses, Pseudomembranous
treatment in the (toxin A or B) perforation, or colitis
last 3 months or C.difficile evidence of
▪ Recent antigen pseudomembranous
hospitalization ▪ PCR for Cl. colitis
Difficile toxins
▪ Culture
antigen
detection

V] Treatment
1) Isolation!
2) General principles
• Discontinue antibiotic use (usually enough for mild cases)
• Rehydration (oral or iv)
• Avoid antidiarrheals (eg loperamide)
3) Medical therapy
• Antibiotics – in case of moderate or severe Cl. difficile diarrhea with over 5-bathroom visits
▪ Metronidazole 10 days – if no clinical improvement after 2days → change to vancomycin.
▪ 1st relapse – metronidazole for 10 days
▪ 2nd relapse – vancomycin 10 days
4) Fecal microbiota transplantation (cleaned stools of healthy people) could be done

VI] Prevention
5) Early detection of Cl. Dificile in stool for risk patient
6) Isolation
7) Control measures
• PPE
• Hygiene
• Autoclaving larger equipment

53. Typhoid fever: etiological agent, clinical manifestation and possible complications, diagnosis (including laboratory
tests), treatment and prevention.

I] Etiology
1) Pathogen
a. Typhoid fever: Salmonella typhi
b. Paratyphoid fever: Salmonella paratyhi
2) Transmission: fecal-oral
a. Direct: person-to-person contact; asymptomatic carriers are frequently involved (E.g., the pathogen may be
transferred from contaminated stool via handshake to the next person.)
b. Indirect: contaminated food and water
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3) S.typhi and paratyphi which have invasive characteristics cause typhoid/enteric fever.
4) They penetrate the intestinal walls and invade the mesenterial lymph nodes and spleen, causing bacteremia.
5) The infection is localized in the lymphatic tissue and the Peyer’s patch can become inflamed and wounded.
Bacteremia can spread to the lungs, gallbladder, kidneys, and CNS.

II] Clinical manifestations

General

1. Incubation period: 5–30 days (most commonly 7–14 days)

2. If left untreated, three different disease stages, each lasting a week, classically occur.
3. After 3 weeks of disease: slow regression of symptoms; patients may become chronic Salmonella carriers
4. General and GI symptoms
5. Typhoid fever is a systemic disease; it is not limited to the gastrointestinal system!

Prodrome (1st week) Acute phase (2nd week) Week 3

1) Increasing fever 1) Persistent fever 1) Clinical features of week 2

2) Relative 2) Rose colored spots on the lower chest 2) Additional possible complications
bradycardia and abdomen (30%) include:
3) Constipation or 3) Typhoid tongue: greyish/yellowish-coated ▪ GI ulceration with bleeding and
diarrhea. tongue with red edges perforation
4) Headache 4) Neurological symptoms (delirium, coma) ▪ Hepatosplenomegaly
5) Bacteremia ▪ In rare cases: sepsis, meningitis,
6) Yellow green diarrhea or obstipation myocarditis, renal failure.

Convalescence
o Patient’s symptoms are improving for 7-10 days.

III] Diagnosis

Laboratory tests Pathogen detection

1. Anemia 1. Blood cultures: Bacteremia is detectable starting in week 1 of the
2. Leukopenia (adults) or leukocytosis disease.
(children) 2. Stool cultures: Cultures may be positive from weeks 2–3, but they
3. thrombocytopenia are often negative despite active infection.
4. Abnormal liver function tests 5. Serology: no longer recommended since it has a low specificity
and sensitivity.

Blood culture is the most important diagnostic tool at disease onset, as stool cultures are often negative despite active
infection!

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IV] Treatment
1. First-line treatment: fluoroquinolone antibiotics (e.g., ciprofloxacin)
2. Fluoroquinolone resistance → Azithromycin
3. Third-generation cephalosporins (e.g., ceftriaxone) are preferred for severe infection.

V] Prevention
1. Vaccination -> No lifelong immunity!
• Inactivated vaccine: 1 shot I/M 10 days before travel is ideal
• Live-attenuated vaccine:Per oral 10 days before traveling is ideal
• Vaccination is not entirely protective!
2. Food and water hygiene
• Since vaccine isn’t entirely protective
3. Quarantine for infected persons

54. Acute gastroenteritis: clinical manifestations, possible etiology, diagnostic and therapeutic principles.

Acute gastroenteritis is mostly caused by viruses but can also be caused by bacteria, parasites, and fungi.

I] Clinical manifestations
1. Incubation: 12 -72 h usually 6. Blood stools
2. Diarrhea o Shigella, salmonella and amoeba
3. Vomiting 7. Dehydration
4. Abdominal cramps 8. Nausea a
5. Some viral infection cause fever, fatigue,
headache, muscle pain.

II] Possible etiology

Viral Bacteria Parasitic
• Common pathogens are norovirus • Salmonella • Giardia lamblia
and rotavirus. • Campylobacter • Entamoeba. Histolytica
• Norovirus is the leading cause of • Vibrio cholera
gastroenteritis • Shigella
• E-coli
• Yersinia
• Clostridium difficile

III] Diagnosis steps

History Vital Sign Labs Specific Imaging Endoscopy

80
 1) Present illness: 1) Determine 1) Full blood 1) Serology CT/X-ray → Pseudome
2) Medication severity of illness count 2) Cultures toxic mbranous
3) Allergies → some and stability 2) Electrolytes 3) PCR megacolon, colitis
patients experience GI 2) Viral infections 3) Liver perforation
intolerances with many don’t cause the markers (Cl. difficile)
medications, patient to look
4) Past medical history toxic
5) Social history → 3) a toxic- looking
recent travel, contact patient warrants
with children investigation and
occupation, recent prompt treatment
meal or referral.

IV] Treatment
General Treatment Acute gastroenteritis
1) Oral rehydration → obtain electrolytes. 1) Antipyretics
2) I/v rehydration if severe dehydration → ringer 2) Antiemetics
solution, saline, ringer lactate o Ondansetron (safer, less side effects)
3) Eat a lot → obtain electrolytes. o Metoclopramide
4) Electrolyte powder 3) Antidiarrheal
5) High fever (38.5) → antipyretics o Loperamide → only for viral
6) Bacterial → antibiotics ▪ Constipation can be a side effect due to gut relaxation
• Ciprofloxacin, TMP/SMX ▪ Elderly can develop paralytic ileus which will require
• Metronidazole/vancomycin (Cl. difficile) surgery
7) Parasitic → metronidazole, paromomycin ▪ Shouldn’t be given for more than 2 days
o Diosmectin
• Probiotics
o Not proven to be beneficial
o May be harmful

55. Acute colitis: clinical manifestations, possible etiology, diagnostic and therapeutic principles.

I] Clinical manifestations
1. Abdominal pain,
2. Cramping,
3. Diarrheal, with or without blood in the stool (one of the hallmark symptoms of colitis).
4. Associated symptoms depend upon the cause of colitis and may include.
o fever, o eye inflammation,
o chills, o joint swelling,
o fatigue, o canker sores,
o dehydration, o skin inflammation.
5. Blood in the stool is never normal and medical care should be sought for evaluation of the cause.

II] Possible aetiology

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 Infectious colitis Ischemic colitis Allergic reaction
1. Bacteria (Cl. Difficile, 1. Low blood pressure Infants younger than 1 year of age,
Campylobacter, Shigella, E. Coli, 2. Anemia colitis is often due to allergies to cow
Yersinia, Salmonella) 3. Atrial fibrillation → blood clots or soymilk.
2. Virus can form in the heart and
3. Parasites- Entamoeba. histolytica embolize to block the arteries of
the bowel.

III] Diagnosis

Patient history Physical Exam Laboratory Stool sample Imaging

1) Pain onset, location, 1) Vital signs 5) Complete blood 1. Culture 7) Colonoscopy
duration, character, ▪ Orthostatic count 2. May also be ▪ Looks for
associated/aggravating, hypotension (in ▪ Anemia? tested for inflammation,
alleviating factors, pain case of rectal ▪ Elevated Ht → presence of tumors, polyps
radiation, timing, bleeding, means blood or ▪ Can take
severity. dehydration, dehydration → toxins. biopsy (the
2) Travel history (travel to anemic). low blood 3. PCR only way to
place with 2) Bowel sounds. pressure → diagnose
contaminated food and 3) Palpation ischemic colitis microscopic
water). 4) Rectal ▪ Leukocytosis? colitis)
3) Blood in stool? examination → infection. 8) CT and
4) Questions about bowel 6) Electrolyte Barium
habits, weight loss, measurement enema -
weakness, or family → determine Balance the
history of bowel severity of risk of
dehydration. radiation with
disorders, including
the information
cancer or colon polyps. 7) Kidney function
that can be
5) Past medical history ▪ BUN and obtained
6) Social habits - smoking, creatinine levels
drinking, and → determine
occupational hazards severity of
or risks dehydration.
8) Urinalysis ▪
Ketones or
increased urine
concentration?
→ sign of
dehydration
9) Inflammatory
markers ▪ ESR,
CRP

IV] Treatment
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 1. Treatment depends on the cause
2. General treatment for all colitis
• Stabilize patients vitals
• Pain management
• Oral rehydration (I/V in case of severe dehydration)
• Antidiarrheal (eg loperamide)
• Antipyretics
• Antiemetics
3. Medications
• Control IBD (eg budesonide)
• Antibiotics - Not really used unless specific bacteria is diagnosed
4. Surgery → Isn’t really common

56. Pyogenic and serous meningitis and encephalitis: diagnostic and treatment principles.

Pyogenic = Bacterial (excludes infection with virus, fungi)

Serous = Non-Bacterial (also referred as aseptic or viral)

MENINGITIS ENCEPHALITIS
Description Inflammation of leptomeninges and Inflammation of the brain parenchyma (mostly viral
subarachnoid space. origin)
Can be either.
1. Primary
o Direct effect of acute infection
o Virus directly infects the brain.
2. Secondary
o Sequalae of another infection.
Causes Most common microorganisms (pyogenic 1. Virus (herpes simplex infection mostly, CMV
meningitis) rabies virus, poliovirus, measles virus)
2. Bacteria (can be caused by bacterial infection eg
1. Meningococcus (Neisseria meningitidis)
bacterial meningitis)
2. Pneumococcus (strep. Pneumonia)
3. Fungi
3. H. influenzae
4. Parasites
Serous Meningitis 5. Autoimmune disorder

1. Enterovirus (most common)

2. Herpes simplex virus type 1
3. Varicella zoster
4. Measles
5. Mumps

Diagnostics 1. Anamnesis 1. Encephalitis is mainly caused by viruses and very

2. Physical examination rarely bacterial. Bacterial is usually secondary
o Signs of meningeal irritation: Kernig sign encephalitis (complication of syphilis infection).
and Brudzinski sign 2. Anamnesis
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 o Stiff neck, headache, fever o Headache, confusion, drowsiness, seizure,
3. Laboratory focal neurological deficits
o Blood culture 3. Laboratory
▪ Taken before AB is given o CSF analysis
▪ Compare CSF/blood glucose level ▪ Appearance, cell count, glucose, albumin,
• In case of bacterial → lowered lactate
ratio because bacteria ▪ PCR → detect pathogen (Gold Standard)
metabolize it ▪ Serology
• Viral → normal ratio ▪ Culture
o CSF analysis o Blood
▪ Appearance, cell count, glucose, ▪ Serology (antibodies, antigens)
albumin, lactate 4. Imaging
▪ PCR → detect pathogen. o CT/MRI
▪ Microscopy → differentiate 5. EEG
pathogens. o Unilateral or bilateral lobe discharge
▪ Serology → Ig
4. Imaging
o CT /MRI
Treatment 1. Bacterial meningitis is more life 1. Treatment should be initiated while awaiting
threatening than viral (usually self- definitive diagnosis of the condition, as the
limited). progression of Herpes simplex Encephalitis is very
2. Empiric antibiotics may be started as soon rapid!
as possible until a viral cause is confirmed. 2. I/V administration is preferable.
3. Symptomatic 3. Symptomatic treatment
o Anti-convulsant → phenytoin o Cerebral oedema → proper head positioning
o Fluid replacement and/or hyperosmolar substances (mannitol,
4. Antiviral glycerol) in case of raised Intracranial pressure.
o Usually, self-limited o Anticonvulsant → phenytoin
o In severe cases consider Acyclovir (PO or o Analgesics
IV) → only if viral encephalitis is also 4. Antivirals
suspected o First line: Acyclovir (IV)
5. Antibacterial o Second line: Foscarnet
o Start with corticosteroids and then give 5. Antibacterial
Antibiotics. o Combination of I/V 2 antibiotics is the most
o Combination of I/V 2 antibiotics is the appropriate choice.
most appropriate choice
▪ Eg vancomycin + 3rd gen
cephalosporin (ceftriaoxone)
6. Corticosteroids
o Dexamethasone -> reduces local and
systemic inflammation.

84
 57. Pyogenic and serous meningitis and encephalitis: clinical manifestations, criteria of differential diagnosis and
principles of patient examination

I] Description
Pyogenic = Bacterial/septic (excludes infection with virus, fungi)
Serous = Non-Bacterial (also referred as aseptic or viral)

Bacterial and viral meningitis have similar symptoms, although viral meningitis is less acute and usually self-limited.

II] Clinical Manifestations

Similar symptoms of Meningitis and Encephalitis
1. Prodromal symptoms
2. Fever
3. Headache
4. Meningeal signs
5. Altered mental status, irritability.
6. Nausea/vomiting
7. Myalgia
8. Photophobia
9. Malaise
10. Fatigue

MENINGITIS ENCEPHALITIS
1. Classic triad: 1. Focal neurological deficits
o Fever, stiff neck, headache o Paresis
2. Sign of meningeal irritation o Aphasia
o Kernig and Brudzinski sign o Memory loss
o Ataxia
o Seizure
o Altered sense of smell
o Visual field defects
o Behavioral changes
2. Cranial nerve palsies

III] Differential diagnosis

1. All other infections (viral, bacterial, tuberculous, fungal)
2. Brain abscess
3. Subarahnoidal hemorrhage
4. Venous trombosis
5. Tumor
6. Autoimune diseases
7. Stroke
8. Lymphoma
9. Medications
o IV Ig, NSAIDs, carbamazepine
10. Systemic diseases
85
 o SLE, RA, Wegener granulamotosis
11. Toxins
o Heavy metal (lead)

IV] Principles of patient examination

1) Medical history
2) Physical examination
o Kernig sign
o Brudzinski sign
3) Neurological examination
4) Lumbar puncture
o Appearance, cell count (N-15/3 cells), glucose, albumin, lactate
5) Routine blood investigations
6) Serology (antibodies)
7) PCR
8) Imaging studies – CT/MRI
9) EEG
10) Biopsy – rare!

58. Prevention options and treatment principles of acute hepatitis B, including indications for antiviral therapy.

I] Preventions

Prevention options (pre-exposure) Prevention option (post-exposure)

1) Education about disease 1) HB immunoglobulin is given
o Risk factors and groups o 2 doses
2) Gloves when examining patient. ▪ 1st → as soon as possible – preferably within 24h
3) Safe sex ▪ 2nd → 0.06ml/kg i/m (within one month)
o Condom use 2) Indication: Exposure to HBV
4) Needle exchange program for IV drug users • Unvaccinated individuals or incompletely vaccinated
5) Don’t share personal items. o HBIG + HB vaccine → and completion of original
6) Avoid direct exposure to blood or blood products. vaccination series
7) Choose tattoo and piercing parlours carefully o Vaccination: start 6d after exposure → 4 doses
8) Vaccine (0-1-2-12)
o Usually together with Hep A vaccination • Vaccinated but postvaccination Anti-HBs status is
o 3 Doses (0-1-6 months) unknown or low
o Indications o HBIG + HB vaccine → and retest for anti-HBs
▪ Recommended that everyone should be level.
vaccinated.
o High risk groups - should take it
▪ IV drug users
▪ Medical staff workers
▪ HIV
▪ Hepatitis A or C infected person
▪ Sex workers

86
 ▪ Travellers visiting a country where HBV is
endemic.
▪ Babies born to mothers who have HBV.
▪ Underlying disease
▪ Homosexuals (men having sex with men)
▪ People with chronic liver diseases
▪ Partners of infected people

II] Treatment
1) Supportive therapy for Acute cases
1) Rest
2) Diet
3) Symptomatic treatment
2) Antiviral therapy for chronic HBV.
➔ Indications for Antiviral therapy in acute Hepatitis B: tenofovir (Lamivudine 100mg x1 → pregnancy)
1. Elderly patients >65 years,
2. Pregnancy (lamivudine)
3. immunocompromised
a. HIV, DM, steroid/ chemo/ radiation treatment
4. Severe manifestation: Liver insufficiency, bleeding, encephalopathy
5. Atypical course: itching, cholestasis
6. Serum bilirubin level of > 15 mmol/dl
7. INR > 1.6 (risk of haemorrhage).

59. Epidemiology of hepatitis C, enumeration and characteristics of risk groups. Principles of prevention

Epidemiology
1) 3% worldwide
2) ≈ 200 millions are infected with hepatitis C
3) 130-150 million have chronic hepatitis C infection in the world.
4) Latvia ≈ 40.000 are infected. Either Anti-HCV positive or HCV-RNA positive.
5) Approximately 500.000 people die from hepatitis C related liver diseases.
6) The prevalence varies greatly among geographic regions
o High prevalence in Africa, middle east and Asia

Risk groups (just like Hep B)

1) IV drug users sharing needles
2) Hepatitis B or HIV- positive individuals
3) Prisoners
4) Recipients of blood transfusions or organ transplants before 1992 or if unscreened
5) Fetus of infected mother (perinatal)
6) Health care professionals
7) Haemodialysis patient
8) Partners of infected patients
9) Men who have sex with men
10) Sex workers
87
 11) People travelling to endemic areas

Prevention Principles
1) Education
2) Needle exchange program for IV drug users
3) PPE – gloves when examining patient
4) Practise safe sex – condoms
5) Don’t share personal items
6) Avoid direct exposure to blood or blood products.
7) Choose tattoo and piercing parlors carefully.
8) Hep. C screening in high-risk patients
9) Treat asap to avoid chronic infection.

60. Characteristics and methodology used in diagnosis of chronic hepatitis C. Description and interpretation of them

Who is tested?
• High risk patient → see above!

Normal Acute Not active/Prior Chronic

Anti-HCV Ab + -/+ +
PCR for HCV RNA + - +
ALT 40-45 u/l >500 - 40-500
AST 40-60
AST/ALT ratio <1 ≥1
ALP 130 u/l ↑ ↑
GGT 60 u/l ↑ ↑
Bilirubin 210 u/l ↑↑ Normal

1) Serology – Detection of AB
o EIA/ELISA for anti-HCV antibodies: positive in cases of acute, chronic, and previous HCV infection
o Western blot test – positive in case of active or prior infection
2) PCR for HCV RNA if antibodies are positive.
o If positive PCR: active HCV infection (may be acute or chronic)
o If negative PCR: no active infection, but prior infection
o Determines HCV genotype and virus titer → assists in treatment planning and monitoring.
3) Liver function tests
o ↑ AST and ALT
o ↑ AST/ALT ratio → ≥ 1
o ↓ total protein/albumin, coagulation (particularly ↑ prothrombin time),
o ↓ cholinesterase
o Cholestasis parameters: ↑ γ-GT, ↑ alkaline phosphatase, normal bilirubin
4) Inflammation markers: leukocytosis, ↑ ferritin
5) Ultrasound:
o detection of cirrhosis and neoplasia, e.g., HCC
6) Liver biopsy indications
o If diagnosis is unclear
o For evaluating fibrosis
88
 o Evaluation of response to therapy
7) Rule out coinfections: HIV, hepatitis A virus (HAV), hepatitis B virus (HBV) → serology necessary.

61. Treatment principles in the event of acute liver failure of infectious nature

1) Early transfer to a liver transplant centre →ALF is highly unpredictable.

2) Address underlying cause → Antiviral treatment.
• Tenofovir/Entecavir – hepatitis B
• HAV
• HEV
• HSV1 and HSV2 – acyclovir
3) Address underlying cause → broad spectrum antibiotics.
4) Intravenous N-acetylcysteine
o Shown to improve transplant-free survival even in patients with non-acetaminophen-related acute liver
failure.
5) Address/prevent complications:
• Cerebral edema → monitoring and inserting a shunt when needed.
• Renal failure → Loop diuretics
• Superinfection → antibiotics
• Encephalopathy → Grade II → ICU
6) Surgery
o Liver transplantation
▪ in case of insufficient regeneration of hepatocytes

62. Acute hepatitis B, epidemiology, clinical symptoms and outcomes. Treatment options

Epidemiology
• 2 billion people worldwide
• > 250 million people worldwide are chronically infected.
• ∼ 600,000 deaths annually from HBV-related liver disease
• High prevalence in Asia, Africa, and the Brasil
• Acute hepatitis B has declined by ∼ 82% after the introduction of the hepatitis B vaccine in 1991 (USA)
• Latvia: 2-3% of population is positive.

Clinical Symptoms
1. IP: 1-6 months
2. Serum sickness-like syndrome can develop during the prodromal (preicteric) period:
o rash, polyarthritis, fever, lymphadenopathy
3. Subclinical hepatitis (70% of cases)
4. Symptomatic hepatitis (30% of cases)
o Fever, skin rash, arthralgias, myalgias, fatigue
o Nausea
o Jaundice
o Right upper quadrant pain
o Symptoms usually resolve after 1–3 months
89
 5. Fulminant hepatitis is rare
6. Most adults will clear infection → usually resolve after 1-3m

Outcomes
1. Spontaneous recovery is very high (90%)
2. May develop acute liver failure (1%)
3. May become chronic hep. B (<5%)→
o Resolution
o Chronic active → liver cirrhosis or hepatocellular carcinoma
o Chronic inactive
o Asymptomatic carrier state

Treatment
1) Acute treatment is only supportive.

Indications for Antiviral therapy in acute Hepatitis B Antiviral therapy for chronic Hepatitis B

1. Pregnancy (lamivudine) 1. Nucleotide/nucleoside analogues

2. Elderly patients >65 years • Tenofovir is commonly drug of
3. Immunocompromised (HIV, DM, steroid/ chemo/ radiation choice.
treatment) • Entecavir
4. Severe manifestation: 2. Pegylated interferon alfa (PEG-IFN-a)
▪ Liver insufficiency, bleeding, encephalopathy
5. Atypical course:
▪ Itching, cholestasis
6. Serum bilirubin level of > 15 mmol/dl
7. INR > 1.6

90
 →severe outcome for those patients without treatment

63. Clinical manifestations of chronic hepatitis, etiological verification. The role of the parameters resulting from the
laboratory tests in diagnosis

→ Termed Chronic hepatitis after 6 months of persistent viral Ag

Clinical Symptoms
2) Often Asymptomatic → carrier state
3) Malaise
4) Anorexia
5) Fatigue Etiological verification
6) Signs of chronic liver disease 1) Viral hepatitis
1) Hepatosplenomegaly 1) HBV
2) Spider naevi 2) HCV
3) Palmar erythema 3) HDV
7) Complications of cirrhosis 2) Alcohol
1) Portal hypertension 3) Non-alcoholic steatohepatitis (NASH)
2) Ascites 4) Autoimmune
3) Encephalopathy 5) Drug induced.
8) Cholestasis manifestations 1) Nitrofurantoin
1) Jaundice 2) Isoniazid
2) Pruritus 6) Metabolic diseases
3) Pale stools 1) Hemochromatosis
4) Steatorrhea 2) Wilsons disease
9) Coagulopathies 3) Alpha-1 antitrypsin deficiency
10) Cryoglobulinemia

Role of the parameters resulting from the laboratory tests in diagnosis

• Basic liver test:
o AST/ALT
o 𝛾-GT
o ALP
o Bilirubin
o Albumin
o Ferritin
o Prothrombin time
• Viral serological tests
o Hepatitis B
▪ Positive → HBsAg, HBeAg, Anti-HBc IgG, HBV DNA
▪ Negative → Anti-HBs
o Hepatitis C
91
 ▪ EIA/ELISA for anti-HCV antibodies: positive in cases of acute, chronic, and previous HCV
infection
▪ Western blot test – positive in case of active or prior infection
▪ PCR for HCV RNA if antibodies are positive
• If positive PCR: active HCV infection (may be acute or chronic)
• If negative PCR: no active infection, but prior infection
• Determines HCV genotype and virus titer → assists in treatment planning and
monitoring
• Autoimmune Hepatitis
o IgG
o ANA (anti-nuclear antibody)
o SMA (smooth muscle antibody)
• Alpha-1 antitrypsin level

64. Diagnostic algorithm for acute infectious diseases (viral, bacterial, protozoan, etc.) characterised by jaundice

92
 65. Diagnosis and differential diagnosis of infectious diseases characterized by pathology in the oropharyngeal
isthmus

I] Diagnosis
Anamnesis Laboratory
1. Sore throat 2. Full blood count 2. Serology 3. Swab (pharynx, throat)
2. dysphagia • Infectious mononucleosis • Infectious mononucleosis 1) Culture
3. Inflamed mucosa - 1. Lymphocytosis (> 10% 1. Monospot test → detect •Pharyngeal Diphtheria
tonsils atypical lymphocytes) heterophile AB -Pharyngeal swab
4. Fever • Bacterial tonsillitis 2. Anti-viral capsid antigen AB - Elk’s test after to
5. Exudates 1. ↑ CRP, ↑ ESR, • Anti-VCA IgM (vanishes 3 determine toxigenicity.
6. White plaque – leucocytosis, months after infection)
candida Antistreptolysin O (ASO) • Anti-VCA IgG (2-4 weeks •Bacterial tonsillitis
7. Pseudo membranes - titer (↑ ASO = previous 2) PCR
after onset, persists for life)
infection)
Pharyngeal Diphtheria • Tuberculin skin test 3) Rapid Antigen test
• IGRA •Bacterial tonsillitis - Rapid
• Rapid plasma reagin test GAS test
(syphilis)

II] Differential diagnosis

1. Bacterial tonsillitis
2. Pharyngeal Diphtheria
3. Infectious mononucleosis
4. Herpes pharyngitis
5. Gonorrhea
6. Syphilis
7. Tuberculosis
8. Candid

93
 66. Clinical characteristics of Lyme borreliosis, diagnosis and pathogenesis

I] Clinical characteristics

Stage I (early localized Lyme disease) Stage II (early disseminated Lyme Stage III (late Lyme disease)
disease)
- Symptoms develop within 7–14 days - Symptoms develop 3–10 weeks after a - Symptoms develop months to years
after a tick bite. tick bite after the initial infection
- Erythema chronicum migrans (EM) - Migratory arthralgia that can progress to - Chronic Lyme arthritis (10% of
• Usually a circular, slowly Lyme arthritis cases)
expanding red ring around the • Spreads from one joint to another • Lasts over a year and may be
bite site with central clearing → Generally in large joints (knee intermittent or persistent.
• Typically warm, painless or elbow) • Typically, in large joints
• EM is often the only symptom. - Early neuroborreliosis (especially knee or elbow)
• Self-limiting (typically subsides • Cranial nerve disorders - Late neuroborreliosis
within 3–4 weeks) o Most commonly manifestations include:
• “bull’s eye appearance” peripheral facial nerve • Aseptic meningitis
- Flu‑like symptoms palsy, paraesthesia, and • Cognitive impairment
- Lymphadenosis cutis benigna paresis • Gait abnormality
(Borrelia lymphocytoma) • Meningitis • Bladder dysfunction
• Painless bluish-red nodule • Polyneuropathy • Psychiatric abnormalities
• Typically on ear lobe, - Lyme carditis (e.g., depression, anxiety,
nipple or scrotum
• Risk of cardiac arrhythmias (e.g., bipolar disorder etc.)
• Often in children
AV Block) • Peripheral polyneuropathy
- Cutaneous manifestations - Herxheimer`s disease
• Multiple erythema migrans lesions (acrodermatitis chronica atrophicans)
• Rarely borrelia lymphocytoma
- Ocular manifestations: including
conjunctivitis and uveitis

II] Pathogenesis:
• Borrelia exists in a cycle between the tics and the host (vertebrates).
• The tics have a life cycle of 3 years where it undergoes 3 stages: larvae, nymph and adult tic.
• Blood is sucked from the host animals and tic gets infected and is now a carrier of borrelia. This means it may
now transmit it to humans.

94
III] Diagnosis
• Confirmed or possible tick bite → erythema chronicum migrans present
o Indication for Stage I → empiric A/b immediately
• Symptoms of lyme disease + with possible exposure risk → 2-step-testing
o Initial test: ELISA
o Confirmatory test: Western blot
▪ Detect IgG and IgM AB against Borrelia
• Results:
o IgG/ IgM detection against Borrelia → only significant if corresponding to clinical symptoms.
▪ Positive tests only demonstrate exposure, not active current infection.
▪ False negative results → seroconversion has not happened (up to 8 weeks)
▪ Cross-reactions due to other diseases possible → sypillis, SLE, RA
• Other tests:
o Cerebrospinal fluid testing → if signs of neuroborreliosis present
▪ Intrathecal IgM and IgG can be detected before they are present in blood.
o Arthrocentesis → signs of arthritis present
▪ PCR for synovial fluid

67. Clinical manifestations of ehrlichiosis, laboratory diagnosis, approaches to therapy

I]Description
Pathogens Vectors
1. Ehrlichia chaffeensis 1. Lone star tick (Amblyomma americanum): E.
2. Ehrlichia ewingii chaffeensis and E. ewingii
95
 3. Ehrlichia muris eauclairensis 2. Deer tick (Ixodes scapularis): E. muris eauclairensis.
➔ i/c, Gram negative bacteria ➔ causing infection of monocytes and
macrophages.

II] Symptoms (IP: 1-2w)

1) Fever, headaches, malaise, myalgias
2) Like RMSF, but usually without a rash (“spotless” RMSF)
o RMSF – Rocky Mountain spotted fever.
3) Possibly neurologic symptoms
o altered mental status, stiff neck, clonus.
4) May cause renal failure and GI bleeding.

III] Diagnosis

1) Difficult to diagnose due to unspecific symptoms.

2) Serum
a. Leukopenia
b. Thrombocytopenia
c. ↑Transaminases
d. Atypical lymphocytes
3) Microscopy – blood smear
a. Detection of morulae inside the infected monocytes (Wright-Giemsa stain)
b. Morulae → intracytoplasmic inclusions representing clusters of multiplying Ehrlichia in vacuoles
4) Serology
a. IFA (immunofluorescence) → IgG Ehrlichia titer
5) PCR (also possible, not yet standardized)
6) IHC (immunohistochemical staining): diagnosis of fatal and nonfatal TBRD
7) Culture

IV] Treatment
1) Symptomatic → analgesics
96
 2) Response of patient after 48h after treatment initiation, if given during first 4-5 days of infection
3) Doxycycline: → I/c microorganism
o Minimum total course of 5-7 days
o Severe cases: 10-14 days.
o Adults: doxycycline 100 mg PO/IV twice daily; children < 45 kg: doxycycline 2.2 mg/kg PO/IV twice daily;
minimum 5–7 days.
4) Tetracycline
o CI: pregnancy

68. Diagnostic principles of HIV infections, indications for HIV test, HIV test selection, aims of pre-test and post-test
consultation
I] Diagnostics principles and Test selection.
Primary diagnostics → Screening Confirmatory tests
tests
1) Combination antigen/antibody tests: Confirmation Test
▪ Detect both HIV antigen (p24) and 1) HIV-1/HIV-2 antibody differentiation immunoassay detects both HIV-
anti-HIV antibodies. 1 and HIV-2
▪ A negative result rules out HIV 2) Western blot: tests may be negative up to 2 months after infection.
infection (almost 100% sensitivity) 3) P24 antigen detection
2) Antibody-only tests
▪ ELISA: standard method, duration Detection of viral RNA – PCR
~ 1–3 hours
Rapid tests: can deliver results in ∼ 20 1) Can detect HIV infection earlier than antibody/antigen-based tests,
minutes only HIV-1
2) Indications:
▪ Neonatal HIV infection
▪ Patients with indeterminate results
▪ Patients presenting before seroconversion.
▪ Screening of blood donors.

II]HIV testing Indications.

Epidemiological indications Clinical indication

1) All individuals with possible past exposure, especially Test all patients with clinical features of acute or
high-risk individuals → regular testing chronic HIV infection.
2) IVDU - Intravenous Drug User
1) Mononucleosis like syndrome
3) Pregnancy
2) Fever of unknown origin
4) Donors → blood, organ, tissue
3) Leukopenia and thrombocytopenia
5) Sex workers
4) Lymphadenopathy
6) Sex partners of IVDU, HIV and STD patients
7) HBV, HCV, HDV and tuberculosis patients
8) Medical staff

III] Pre/Post-Test Consultation

97
 Pre-test consultation Post-test consultation

• Essential 5 Cs: consent, confidentiality, • Aim: increase amount of care given to patients and
counselling, correct test results and increase willingness to accept care/ treatment
connection to HIV prevention, treatment o referral to community health workers for key population
and care. o guidance for couples or serodisconcordant couples
• Providing info on the technical aspects of o Pregnant woman
testing • Negative result
• Preparation of Patient to possible outcomes o But patient is involved in high risk behavior (sex worker,
o possible personal, medical, social, IVDU) → important to reduce the chances of future
psychological, legal and ethical infection
implications of being diagnosed as either o Possible that patient is in window period and test may be
HIV positive or HIV negative. false negative → test again after a month

69. Prevention of HIV infection, including the prevention of vertical transmission routes, PEP, PrEP

I] HIV prevention
1. PrEP
2. PEP
3. Safe sex (condoms)
4. Safe and sterile syringes → needle exchange program
5. Education → Sexual health discussions and sexual education
6. Vertical transmission prophylaxis
7. No breastfeeding

Prevention of HIV vertical HIV post-exposure prophylaxis Pre-Exposure Prophylaxis (PrEP)

transmission routes (PEP)

1) Maternal testing for HIV 1) Indications 1) High risk patients

2) Contraceptives to prevent • Injury with HIV-contaminated • Homosexuals (men who have

unwanted pregnancies in HIV instruments or needles sex with men)
patients.
• Contamination of open wounds • Sex workers
3) Before birth or mucous membranes with
• IVDU
HIV-contaminated fluids
• Effective control of maternal
• Sex partners of HIV patients
infection → ART prophylaxis • Unprotected sexual activity with
a known or potentially HIV- 2) PrEP can stop HIV from taking
4) During labour/birth
infected person hold and spreading throughout
(intrapartum care)
the body.
2) Timing: Within 72h → Initiate as
• C-section should be offered at
soon as possible (ideally within 3) Reduces risk of getting HIV
week 38
one to two hours after through sex by 99% and drug
• IV Zidovudine is recommended.
exposure) injection transmission by 74%
5) Postpartum
4) Drugs: two-drug combination

98
 • Zidovudine Syrup for 6 weeks 3) ART - Drugs: A three-drug • Tenofovir + emtricitabine
regimen is recommended (nucleotide reverse
• Don’t breastfeed.
(Nucleotide reverse transcriptase inhibitor +
• Decision to Continue or stop transcriptase inhibitor + nucleoside reverse transcriptase
ART depends on CD4+ count nucleoside reverse transcriptase inhibitor)
and diagnosis of HIV. inhibitor + integrase inhibitor)
• Taken daily.
• Tenofovir-emtricitabine +
• Individuals must be HIV-
dolutegravir
negative before initiation of
• Tenofovir-emtricitabine + treatment.
raltegravir.

4) Measures after needle stick

injury or other contamination:

1. Let the wound bleed.

2. Rinse/flush with water and soap

and/or antiseptic agent

3. Immediately seek medical

attention

If occupational exposure: report

incident immediately

70. Indications of antiretroviral therapy, its selection and principles of use

I] Indications:

1. Initiated among all adults/adolescents/children with HIV regardless of WHO clinical stage at any CD4 cell count and
viral load → decreases the risk for HIV disease progression, HIV-related morbidity and mortality, and
transmission.

II] Selection of drugs

1. There are 27 antiretroviral agents in 6 antiretroviral classes.
2. Each class targets different viral life cycle stages.
3. Goal: maximizing antiviral activity and adherence
4. Always use drug combination, never single drug
5. Antiretroviral drugs

Non-nucleoside reverse Nucleoside reverse Protease Entry CCR5 Integrase inhibitors

transcriptase inhibitors transcriptase inhibitors inhibitors inhibitors antagonists
(NNRTIs) (NRTIs) (PIs)

➔ Tenofovir, ➔ Dolutegravir,
Zidovudine, raltegravir
Lamivudine,
Emtricitabine,
Abacavir
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 6. The selection of drugs and regimen depends on a person’s individual needs.
7. When choosing a regimen, you have to consider the following.
o Other diseases and conditions (eg heart disease)
o ease or complexity of use
▪ eg a pill containing 2 or more agents is easier to take than two separate pills.
o side-effect profile
o efficacy based on clinical evidence.
o practice guidelines
o clinician preference
o adverse effects → drug-drug interaction potential, medication intolerance
o pregnancy
o coinfection with hepatitis B or C virus
o antiretroviral treatment history
o genotypic and/or phenotypic resistance results

Side effects that require discontinuation

8. Severe Diarrhea
9. Severe nausea
10. Severe anemia
11. Persistent sleeping disorder
12. Depression, psychosis
13. Pancreatitis
14. Renal failure

III] Principle of use

• Aim → To reduce disease progression, HIV associated morbidity, mortality and risk of transmission.
• Suppress viral replication to undetectable levels.
• To increase CD4 count
• Recommended regimens:
o 3 NRTI (e.g. zidovudine, lamivudine, abacavir), or
o 2 NRTI (e.g. lamivudine + abacavir), and
▪ 1 NNRTI (e.g. efavirenz), or
▪ 1 PI (e.g. lopinavir), or
▪ 1 INI (e.g. raltegravir)

71. Differential diagnosis of meningitis in patients with HIV/AIDS.

I] Differential diagnosis
1. Meningococcal meningitis
2. Staphylococcal meningitis
3. Cryptococcal meningitis
4. Toxoplasma meningitis
5. Tuberculosis Meningitis
6. Syphilitic meningitis
7. Fungal Meningitis (Histoplasma, Coccidioides, Aspergillus)

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 8. Migraine headache
9. HIV Encephalopathy
10. Neurosyphilis
11. Metastatic CNS lymphoma (rare cases)
12. Bacterial meningitis together with sepsis
13. CMV ventriculoencephalitis
14. Chronic paroxysmal hemicrania

Meningitis in HIV
HIV-associated meningitis can be due to a variety of etiologic agents, with a selected few listed below:
• Cryptococcal
• Tuberculous
• Meningococcal
• Aseptic

72. AIDS-associated oncological diseases: characteristics and diagnostic principles.

I] AIDS associated oncological diseases.

1. Kaposi’s sarcoma
2. Non-Hodgkin´s lymphoma
3. Cervical carcinoma

II] Characteristics and diagnostics

Kaposi´s sarcoma- HHV8 Lymphoma -hhv4 Cervical cancer

Description 1. Causes neoplastic vascular There are many subtypes and 1. Women in general with
nodules to arise in more the most common in HIV/AIDS HIV/AIDS are at high risk of
than one area of the body, are. developing cervical cancer
including skin, lymph nodes 1. Primary CNS lymphoma which is associated with
and organs (liver, spleen, 2. Primary effusion papilloma virus.
lungs) lymphoma 2. Due to impaired immune
2. Associated with HHV-8 3. Aggressive B-cell clearance → more likely to
3. KS can start in several parts Lymphoma develop pre-invasive lesion
of the body at the same ▪ Diffuse large B-cell which if not treated → quickly
time. lymphoma. progress to cervical cancer.
▪ Burkitt’s lymphoma

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 Symptoms 1. Dark blue plaques that may 1. Rapidly growing mass 1. Early symptoms
start in the leg, oral cavity. lesions in oral mucosa Abnormal vaginal bleeding:
2. Skin lesions are most 2. Persistent unexplained irregular vaginal bleeding; heavy,
common fever (+ night sweats, irregular menstrual bleeding;
weight loss) postcoital spotting
3. Painless Abnormal vaginal discharge: blood-
lymphadenopathy stained or purulent malodorous
• One of the most discharge
common extra nodal Dyspareunia
site is CNS → Present Pelvic pain
with focal neurologic 2. Late symptoms:
deficits including hydronephrosis, lymphedema,
seizures, headaches, fistula formation
cranial nerve findings 3. Cervical examination:
ulceration, induration, or an
exophytic tumour
Diagnosis 3. Biopsy → spindle shaped 1. Biopsy/bone marrow 1. Pap-smear
cells. aspiration 2. Colposcopy
4. US of chest and lymph 2. CT/MRI/ PET scan 3. Cervical Punch Biopsy
nodes (to rule out inner
organ involvement)

73. Adult vaccination: aims and objectives; indications and contraindications; practical aspects of vaccination.
Immunoglobulins and serums.

I] Aims and objectives.

1. Strengthen the adult immune system.
2. Improve access to adult vaccines.
3. Protect public health.
4. achieve optimal prevention against vaccine preventable infectious diseases.
5. Foster innovation in adult vaccine development

II] Indication and contraindications

Indications Contraindications

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 1. All adults should receive all indicated vaccines as 1. Live attenuate
quick as possible. o Severe anaphylactic reaction to a vaccine or
2. Special indications vaccine component
o Pregnancy o Pregnancy
o Chemotherapy o Immunosuppression
o Period of immunosuppression ▪ HIV (CD4 count under 250cells/mm3)
o Traveling to endemic areas ▪ Organ transplantation
o Exposure to specific risk group ▪ Stem cell transplantation
3. Influenza vaccine ▪ Immunosuppressive drugs
o Seasonal administration • Chemoprophylaxis
o Risk groups • Corticosteroids
▪ Older than 65 2. Inactivated vaccine
▪ Pregnancy o Severe anaphylactic reaction to vaccine or
▪ Children under 2 vaccine component
▪ Medical staff
▪ Asthma
▪ Patients with underlying chronic disease
• Liver, lung, heart, kidney
▪ Immunosuppressed
• HIV
• Diabetes mellitus
• Asplenia
• Cancer
• Receiving immunosuppressive
therapy

Specific Indications for vaccine

Tdap TD MMR VZV HZV HPV
(varicella (herpes
zoster zoster
vaccination) vaccine)
1. 11-12 booster every If no evidence of If person Patient 1. No previous HPV vaccine
years 10 years immunity to MMR never had above 60 2. Young women and boys,
2. 1 shot for chickenpox years even after starting
each or vaccine sexual activities.
pregnancy. against it. 3. Not recommended
during pregnancy

PCV13 (pneumococcal vaccine) HAV HBV

1. All children 1. Risk groups 1. Indication

2. > 65 years ▪ Children
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 3. < 65 years but with underlying ▪ People with already ▪ Recommended that everyone
condition existing chronic liver should be vaccinated.
▪ Chronic conditions (DM, Kidney disease 2. High risk groups
disease, liver disease, lung) ▪ People with already hep ▪ IVDU
▪ Immunosuppressed (HIV/AIDS, B/C ▪ Medical staff workers
Asplenia, Cancer) ▪ Men having sex with men ▪ HIV
▪ heavy smoker (MSM) ▪ Hepatitis A or C infected person
▪ CSF leakage ▪ Travel to endemic region ▪ Sex workers
▪ cochlear implant ▪ IV drug users ▪ Underlying liver disease
▪ high dose immunosuppressive ▪ Day care employees ▪ Men who have sex with men
therapy ▪ Partners of HBV affected person
▪ Newborn born to affected mother

TBE Meningococcal vaccination (MenACWY/MenB) Hemophilus influenza type B (HiB)

1. Not indicated for healthy people 1. Anatomical/Functional asplenia

2. Risk 2. Stem cell transplant
▪ Anatomical/functional asplenia 3. HIV infection
▪ Using monoclonal AB or planning on starting
▪ Compliment deficiency
▪ Undergoing stem cell transplantation
▪ HIV infection

III] Practical aspects

1. The cost of treating infections is more expensive than preventing.
2. A lot of contagious diseases have been eliminated/controlled.
3. Control of mortality, morbidity and complications; both for the individual and the society
4. Prevents infections.
5. Prevention of related disease and cancer
6. Extending life expectancy
7. Safe travel and mobility

IV] Specific serums for treatment

1. Antitoxins in medical use → Against Diphtheria, anthrax and Botulinum toxin
2. Antivenoms against snake bites

V] Specific immunoglobulins for prophylaxis

1. Can be given as post prophylaxis.
➔ Different time limits for different infections, can be from hours-days.
2. Can also be used as prophylaxis following bone marrow transplantation.
3. Hepatitis A
4. Hepatitis B
5. Measles
6. Varicella
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 7. Rabies
8. Tetanus
9. RSV (Respiratory Syncytial Virus)
10. CMV
11. Botulism – Baby BIG-IV

74. Risk groups within the understanding of the need for vaccination. Vaccination goals for these groups, risk groups
in the context of influenza.

I] Risk Groups
1. Children below 5 years, especially below 2 years
2. Pregnancy in general → Tdap and influenza
3. > 65 years
4. People with chronic diseases
• Lung, heart, kidney, liver
5. Immunosuppressed people → all vaccines except live attenuated
• DM
• HIV/AIDS
• Cancer
• Immunosuppressive drugs
• Asplenia
• Stem cell transplant → have to retake all vaccines that were taken prior to transplant.
6. Medical staff → HBV, influenza
7. People travelling to endemic regions → TBE, HBV+HAV, yellow-fever, cholera, typhoid fever.
8. Sex workers → HBV vaccine
9. IVDU → HBV vaccine
10. Partners of infected people → HBV vaccine
11. Smokers – pvc13
12. HIV, asplenic, stem transplant, immunosuppressive therapy, complement deficiency → MenACWY/MenB, HiB

II] Vaccination goals

Decrease Increase protection in
1. Sickness 1. Women during and after pregnancy
2. Medical visits 2. Yourself
3. Hospitalizations 3. People around you
4. Deaths,

III] Risk groups in context of influenza

1. >65 years
2. Medical staff at high risk for occupation exposure
3. Pregnancy
4. Asthma
5. Children below 6 years
6. Immunocompromised
o HIV
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 o Immunosuppressive drugs
o DM
o Asplenia

75. Therapeutic principles of infections cause by Herpes virus, available antiviral medication, indications for use of
those medications.

I] Therapeutic principles
7. All antivirals used for the treatment of herpes virus inhibit viral DNA polymerase thus disrupting replication.
8. Antivirals are effective only in replication phase of herpes viruses. They do not destroy latent viruses (inhibit
replication only).

II] Antivirals and their indications

9. Valacyclovir, Valganciclovir, Famciclovir = Are prodrugs, they are converted through enzymatic activity to active
substances.
10. Foscarnet and Cidofovir = Are alternate drugs, because they are more cytotoxic

III] Antiviral drugs

1)Acyclovir, valaciclovir, 2)Ganciclovir 3) Foscarnet 4)Cidofovir
valganciclovir
1. HSV1/2 1. Acyclovir resistant HSV 1. EVB 1. HSV1/2
2. VZV 2. CMV 2. KSHV 2. VZV
3. EBV 3. HHV6 3. EBV
4. acyclovir resistant HSV 4. CMV
and VZV 5. KSHV
5. ganciclovir resistant
CMV

IV] Principles
1. Antivirals shorten time of lesion healing, duration of symptoms, duration of viral shedding, duration overall time
course in recurrent cases.
2. All antiviral agents against HSV inhibit viral DNA polymerase.
3. Chronic daily suppression reduces reactivation frequency.

76. Pathogenesis, clinical manifestations and therapeutic principles of Varicella zoster infection.

106
I] Pathogen: Varicella Zoster (HHV-3)
II] Transmission
1. Direct contact of vesicular fluid (person to person through direct contact)
2. Inhalation of aerosols from vesicular fluid
3. Infected respiratory secretions

III] Pathogenesis
Primary Infection (chicken pox) Recurrent infection (shingles)
1. Transmission via respiratory route. 5. VZV reactivated (e.g., due to immunocompromise)
2. Virus inoculates lymphoid tissue in the nasopharynx → virus replicates in the dorsal root ganglia →
and then regional lymphoid tissue → Viremia → travels through peripheral sensory nerves to the
chickenpox → recovery from chickenpox (self- skin → shingles (less contagious than primary
limited) → virus remains dormant in dorsal root infection)
ganglia (unless reactivated → recurrent infection)

IV] Clinical

General for Chicken Pox Shingles

1. Incubation period 2 weeks. 1. Dermatomal distributions of rash
2. Highly contagious • Typically, 1-3 dermatomes on one side of
• Contagious 1-2 days before rash appearance the body
until rash have crusted. 2. Pain and paraesthesia
3. Prodromal symptoms can occur fever. Malaise 3. Rash
4. Herpes zoster rash – pruritic • Erythematous maculopapular rash that
• Erythematous macules → papules → vesicular evolves into vesicular lesion
lesion 4. Fever
• Eruption of vesicles → crusted papules. 5. Itching
• Severe pruritus 6. Headache
• Fever, headache, muscle, or joint pain
5. In vaccinated people
• Shorter illness
• Less skin lesions
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V] Therapy
Chickenpox Shingles
1. Symptomatic treatment 1. Symptomatic treatment
1. Calamine lotion → against pruritus 1. Analgesics (NSAID, acetaminophen)
2. Cooling bath with baking soda or uncooked 2. Wet dressings with aluminium acetate
oatmeal → relieve itching 3. Corticosteroids in case of CNS complications
3. No aspirin in children → Reye´s syndrome (Bell`s palsy)
Use acetaminophen instead for fever 2. Antiviral treatment – e.g. Acyclovir
2. Antivirals (e.g. acyclovir) in people who are likely to 1. Immunocompromised and/or those with
develop serious illness. disseminated disease should receive I/V
1. Immunosuppressed patients acyclovir.
2. Primary infection in adults and unvaccinated
adolescents >13y
3. Long-term aspirin therapy in children → risk of
Reye`s syndrome

VI] Prevention
1. Vaccine – 2 doses
1. Prevents almost all cases of serious illness from chickenpox
2. Live attenuated varicella vaccine (Oka) → Mostly for seronegative adults
3. Varicella-zoster immune globulin (VZIG) → Patients that are at high risk of developing complications, given within
96h of exposure

77. Malaria: diagnostic, treatment and prevention principles.

108
I] Diagnostic principles
• History of travels to areas where malaria is endemic, ask about chemoprophylaxis.
• Clinical manifestations
o Paroxysmal fever, chills, sweats, headache etc.
CBC Blood smear with Giemsa Rapid diagnostic tests Serological tests
stain
1. Haemolytic anaemia 1. Confirms suspected 4. Quick determination 4. Not appropriate for
(↓Hb, haptoglobin, cases by visualizing of malaria infection in acute diagnosis of
↑LDH, indirect parasites within RBCs. areas lacking high malaria because
bilirubin, 2. Best initial test: quality malaria antibodies are
reticulocytes) • Thick blood smear microscopy. undetectable for 1–2
2. Thrombocytopenia (high sensitivity) 5. Determines specific weeks.
3. Increased →detects the malaria-antigens. 5. Positive serological
reticulocytes presence of • HRP2 → P. results indicate past
parasites. Falciparum contact with
3. Confirmatory testing: • pLDH → Distinguish Plasmodium
• Thin blood smear → P. falciparum from
allows non-falciparum
determination of species
plasmodium species

II] Treatment Principles

• Malaria cannot only be diagnosed clinically (should include blood smears), but treatment should be started on
clinical grounds immediately.

Tertian Malaria (Ovale and vivax) Quartan malaria (P. malariae) P. Falciparum
6. All chloroquine-sensitive chloroquine or hydroxychloroquine 8. Uncomplicated
Plasmodium spp → ➔ Chloroquine sensitive
Chloroquine + Primaquine (to • Chloroquine or
hydroxychloroquine
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 eradicate P- vivax and oval ➔ Chloroquine Resistant
hypnozoites. • Artemether-lumefantrine
7. Chloroquine resistant→ • Atovaquone proguanil
Artemether-lumefantrine • Mefloquine
9. Severe
• Artesunate followed by
artemether/lumefantrine
OR
• Quinidine + doxycycline

III] Prevention
Mosquito bite prevention Malaria prophylaxis Standby emergency
treatment

10. Avoid exposure → 6. Initiate before travelling. Atovaquone-proguanil

nets, clothes, ➔ 2 weeks before
repellent. • Chloroquine and hydroxychloroquine
11. Mosquito control
• Mefloquine (≥ 2 weeks)
➔ 1-2 days before
• Atovaquone and proguanil
• Doxycycline
• Primaquine
7. Drug of choice depends on Areas with P.falciparum
8. Areas with P.Falciparum
➔ If chloroquine resistant P.falciparum atovaquone-
proguanil, doxycycline, mefloquine
➔ If chloroquine sensitive P.falciparum chloroquine
9. Areas without P.falciparum - Primaquine

78. Schistosomiasis: aetiology, pathogenesis, clinical symptoms, diagnostic and treatment principles.

I] Aetiology → parasitic trematode/fluke

• Schistosoma mansoni
• Schistosoma japonicum
• Schistosoma haematobium

II] Pathogenesis
1. Infected human excretes schistosome eggs in urine and faces
2. Eggs hatch in water, releasing miracidia.
3. Miracidia infect freshwater snails (intermediate host) where they develop into larva (cercariae) which are
released back into the water.
4. Larva can then penetrate human’s skin and enter circulation.
5. Mature into schistosomes and migrate to veins of target organs (liver, intestines, bladder)
6. Females lay eggs → capillary closure and chronic inflammation in affected organs.
7. Penetration of eggs in lumen of intestine or bladder.

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III] Clinical Features
Local reaction Acute schistosomiasis syndrome Chronic schistosomiasis: Deposition of eggs
(swimmer's itch) (Katayama fever) IP: 3-8 weeks leads to chronic inflammation and granuloma
formation – depends on type!
1. Pruritic 1. Due to immune complex 1. Genitourinary (hematobium)
maculopapular rash formation from antigens • Hematuria/dysuria
at the point of entry released from eggs/worms • Bladder cancer
of cercaria into together with host antibodies • Bladder neck obstruction and
human skin Serum-like sickness hydronephrosis
2. Spontaneous 2. Fever 2. Hepaticsplenic
recovery after 2- 3. Fatigue • Hepatosplenomegaly
10w 4. Cough • Portal hypertension
5. Myalgia • Fibrosis
6. Angioedema 3. Intestinal
7. Spontaneous recovery after 2- • Diarrhoea
10w • Abdominal pain
• Intestinal bleeding
4. Pulmonary hypertension & cor pulmonale
5. Neurological
• Headache
• Epilepsy
• Sensory and motor deficits

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IV] Diagnosis
Laboratory tests Pathogen detection Further tests
Eosinophilia 1. Serology → detect antibodies. 1. Imaging may be
2. Microscopy → Definitive diagnosis (gold standard) direct required to rule out
visualization of schistosome eggs via stool or urine specific organ
microscopy. Egg morphology is indicative of Schistosoma involvement.
subtype: 2. CSF
• Schistosoma mansoni: Eggs have a prominent lateral 3. Detection of antigens in
spine. urine/stool sometimes
• Schistosoma haematobium: Eggs have a prominent used to measure
terminal spine. treatment efficacy.
• Schistosoma japonicum: Eggs have a miniscule lateral
spine

V] Treatment
• Acute schistosomiasis syndrome
o Corticosteroids
o Praziquantel should only be administered after symptoms of acute illness have resolved.
• Chronic schistosomiasis: praziquantel

79. Echinococcosis: etiology, risk factors, most commonly affected organs and treatment.

I] Etiology
• Pathogens: Echinococcus tapeworms (cestode)
o Echinococcus granulosus causes cystic echinococcosis (CE)
o Echinococcus multilocularis causes alveolar echinococcosis (AE)
• Transmission
o Hand-to-mouth
• From the fur of definitive hosts (e.g., petting a dog or cat)
• Contaminated dirt (e.g., dog feces)
o Fecal-contaminated food or water (e.g., wild berries, mushrooms)

II] Risk factors

• Sheep farmers
• Owners of working dogs

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E. granulosum → single hydatid cyst
E. multilocular is → infiltrative growth.

III] Most affected organs

• Liver
• Lungs
• Kidneys
• Brain
• Spleen

IV] Treatment
Cystic echinococcosis Alveolar echinococcosis
1. Observation: inactive cyst with heterogeneous 1. Curative resection followed by at least 2
hypoechoic/hyperechoic contents, or solid, calcified wall years of treatment with albendazole to
2. Medical therapy: for cysts < 5 cm prevent a potential relapse.
- Drug of choice: albendazole or mebendazole, 2. Palliative care if surgery is not possible or
praziquantel unsuccessful: see “Medical therapy”
3. Ultrasonography/CT-guided percutaneous drainage above.
3. Follow-up for at least 10 years
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 - PAIR (puncture, aspiration, injection, respiration)
procedure
- done in combination with medical therapy (albendazole)
- Indications: > 5 cm and/or septations
4. Surgery
- Goal: resect the whole cyst to prevent spillage of its
content
- Indications: > 10 cm, complicated cysts
- Follow-up: Because relapse is common, patients should
be closely monitored via imaging for up to five years.

80. Taeniases: etiology, clinical symptoms, diagnostic and treatment principles.

114
81. The most common nematodes in Europe: etiology, clinical symptoms, diagnostic and treatment principles.

Most common nematodes in Europe (roundworms)

• Enterobius – most common
• Ascaris
• Trichinella
Enterobius Ascaris Trichinella

Pathogen 1. Enterobius vermicularis 1. Ascaris lumbricoides Trichinella spiralis and other

(pinworm) Trichinella spp.
2. Pinworms are nematodes
(roundworms)

Transmissio 1. Initial infection: faecal-oral. Transmission: fecal-oral 1. consumption of

n 2. Reinfection: digital-oral after →Contaminated water, fruits, undercooked meat
scratching anal region and vegetables (especially pork) containing
3. Life cycle encysted larvae
1) Eggs in the perianal folds of 2. pork meat or wild game
human larvae inside the eggs meat domestic cycle or
mature within 4-6 hours sylvatic cycle
2) embryonated eggs are
ingested by human
3) larvae hatch in the small
intestine
4) adults establish in the lumen
of cecum

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 5) gravid female larvae migrate
to the perianal region at night
to lay eggs.
Clinical 1. Anal pruritus (especially at 1. Often asymptomatic 1. Intestinal phase:
symptoms night) – due to substance 2. Early symptoms: dry cough, abdominal pain, diarrhoea,
which eggs are laid on. blood-tinged sputum, nausea, and vomiting
2. ♀: vulvovaginitis, wheezing (due to migration) 2. Muscle phase
particularly in children. ➔ Loeffler syndrome - • Myositis: myalgia,
3. Occasionally symptoms of Transient respiratory muscle swelling,
intestinal infection (nausea, disorder characterized weakness
vomiting, and abdominal by accumulation of • Periorbital oedema
pain, sometimes severe eosinophils in lungs 3. Other symptoms include
enough to mimic symptoms usually mild fever, rash, splinter
appendicitis) and resolve haemorrhages, retinal and
spontaneously. conjunctival
3. Late symptoms: anorexia, haemorrhages, chemosis
abdominal discomfort,
nausea, vomiting (can vomit
out the worm and then
come to doctor), and
diarrhoea.
➔ bowel obstruction
constipation and pain
➔ obstruction of appendix
mimics appendicitis
➔ obstruction of biliary or
pancreatic ducts
cholestasis and
pancreatitis
Diagnosis Tape test (first thing in the 1. CBC → eosinophilia 1. History of meat
morning)→ microscopy 2. Confirmatory test consumption
detection of eggs and/or microscopy: stool sample 2. Presence of signs and
pinworms showing the presence of symptoms
worms; visible eggs with a 3. Initial test: complete blood
knobby appearance under cell (CBC) count showing
microscope eosinophilia (and
sometimes leukocytosis)
➔ Commonly ↑
creatinine kinase
4. Confirmatory test:
serological detection of
antibodies
➔ EIA
Treatment 1. Mebendazole 1. Mebendazole 5. Mebendazole
i. Also treat family 2. Surgical removal in case
simultaneously of obstruction

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 2. Showering every morning,
changing bed sheets,
cutting fingernails

82. Hemorrhagic fever: etiology, pathogenesis, clinical presentation and treatment principles.

117
Viral hemorrhagic fevers (VHFs) refer to a group of illnesses that are caused by several distinct families of viruses mostly
occurring in tropical and subtropical regions & are characterized by high fever and generalized hemorrhage.

I] Etiology
Arenavirus Bunyavirus Filovirus Flavivirus Hantavirus
Lassa fever 1. Phleboviral → Rift valley fever Ebola and 2. Yellow fever
2. Nairo virus → Crimean - Congo HF Marburg 3. Dengue HF
3. Hantavirus → 4. Zika Virus
disease

II] Pathogenesis
Transmission Direct cytopathic effect The pathogenic mechanisms The severity of disease
which can contribute to are extremely diverse and caused by these agents
disease severity include. varies greatly, e.g.

1. Bite from infected Most features of illness 1. Depletion of hepatic 1. High fatal rates
vector are caused by innate coagulation factors (due to Ebola and Marburg
(mosquitoes/tick/flies) immune responses. hepatocellular necrosis) 2. Asymptomatic
2. Accidental 2. Cytokine storm excessive infection yellow and
transmission from cytokine production dengue viral infection
host from person to damage of organs
person (eg. via body 3. Increased vascular
fluids) permeability by vascular
3. Airborne endothelial growth factor
4. Ingestion/inhalation hemorrhage/shock/plasma
of rodent urine or leakage.
droppings from 4. Complement activation.

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 reservoir hosts (Lassa 5. Disseminated intravascular
virus, Hanta virus) coagulation (DIC)
6. Thrombocytopenia

III] Clinical manifestation

Initial flu-like illness Severe VHF with bleeding diathesis

1. Headache, high fever, myalgia, rash, arthralgia, 1. Diffuse hemorrhage

lymphadenopathy • bloody diarrhea, hematuria, hematemesis
2. GI symptoms (abdominal pain, diarrhea, nausea, • Mucosal bleeding
vomiting) • Petechiae, ecchymoses
2. Hypovolemic shock & multiorgan failure
3. Sepsis & DIC

IV] Principles of therapy

Early recognition is Usually, supportive therapy Ribavirin may be used Treat secondary Manage
vital because of in some cases. bacterial or organ
need of supportive fungal infections failure.
measures.

1. Analgesics (paracetamol) 1. Antibiotics

2. Fluid replacement 2. Antifungals
3. Blood transfusion in case of severe
blood loss
4. Vasopressors to maintain blood
pressure.
5. Cardiotonic drugs

83.Yellow fever: etiology, clinical presentation, diagnostic, treatment and prevention principles.

I] Etiology
1. Pathogen: yellow fever virus (a flavivirus)
2. Transmission - via Aedes aegypti mosquitos
a. Monkeys and humans are intermediate hosts.
3. Habitat: - Tropical regions of South America and Sub-Saharan Africa

119
II] Clinical
Most cases are asymptomatic or mild. After the incubation period (3-6d) the onset of fever and headache stops. Of
these patients, approximately 80% recover without suffering classic yellow fever. 20% of patient suffers classic yellow
fever which has 3 stages:
Period of infection (3–4 days) Period of remission (up to 2 days) Period of intoxication (only in ∼
viremia 15% of symptomatic patients)
1. Sudden onset of fever (up to 1. Easing of symptoms and decline 1. Hemorrhage epistaxis, mucosal
41°C) in fever bleeding, melena, hematuria,
2. Headaches, chills black vomiting
3. Nausea, vomiting, myalgia 2. Multiorgan dysfunction (e.g.,
acute kidney and liver failure)
can lead to death.
3. Nausea, (bloody) vomiting,
abdominal pain, severe jaundice

III] Diagnosis
Anamnesis Lab Virus detection Liver biopsy

travelling to endemic 1. Increased ALT/AST 1. PCR postmortem

region 2. Leukopenia 2. ELISA
3. During intoxication
-Thrombocytopenia and
increased prothrombin
time
4. Electrolyte imbalance

IV] Treatment
No specific Symptomatic treatment (avoid Treat kidney and liver Treat secondary
treatment exists. NSAIDs) failure infections

1. Paracetamol 1. Antifungals
2. Fluid resuscitation 2. Antibiotics
3. Cardiotonic

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 4. Vasopressors

V] Prevention
• Highly effective vaccine, live attenuated → Required for all visitors of endemic regions (Vaccine has been
associated with cases of encephalitis in children <6 months)

84. Dengue fever: etiology, clinical presentation, diagnostic and treatment principles.

I] Etiology
1. Pathogen: Dengue virus, a flavivirus
2. Transmission: vector-borne → Aedes aegypti mosquito most commonly
3. Habitat: - Tropical regions worldwide (particularly Asia)
4. Severity depends on various factors such as
1) absence of antibodies
2) age <12
3) Sex (Females>Males)
4) race (White>Black)
5) nutritional status
6) sequence of infection by different dengue viruses

II] Clinical features

Mostly asymptomatic in children

Classic dengue fever: IP:2-14d Dengue hemorrhagic fever (DHF): Occurs in 1-2% and
develops after 1 week after onset.
1. Fever and malaise (1week) 1. Temperature changes: Hypothermia to a second
2. Arthralgia and myalgia break-bone fever spike in fever

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 3. Severe headache and retro-orbital pain 2. Abdominal pain
4. Maculopapular rash, measles like rash. 3. Vomiting
5. Generalized lymphadenopathy 4. Changes in mental status; confusion
5. Shock
If symptoms appear >2weeks after returning from a 6. Hemorrhagic manifestations
dengue-endemic region, it’s highly unlikely to be • Petechiae
dengue! • Epistaxis
• Gingival bleeding
• GI bleeding
• Increased vascular permeability signs of
pleural effusion and/or ascites.
• Dengue shock syndrome: DHF + shock

III] Diagnosis
Laboratory tests Serology (Cofirmation) Alternatives
1. Leukopenia 2. IgG 1. PCR
2. Thrombocytopenia 3. IgM 2. Molecular methods (ELISA):
3. ↑ AST detection of viral antigen
4. Hct elevated ≥ 20% of normal
values if vascular permeability
(in DHF)

IV] Treatment
Symptomatic Dengue with warning signs and Severe dengue
1. Fluid administration to avoid dehydration. 1. Blood transfusions in case of significant internal
2. Acetaminophen (NSAIDs and aspirin should be bleeding (e.g., epistaxis, gastrointestinal bleeding,
avoided because they increase the risk of bleeding.) or menorrhagia)
2. Urgent resuscitation with IV fluids

V] Prevention
1. Avoid exposure, use of mosquito repellent.
2. A tetravalent attenuated live vaccine (CYD-TDV) has been approved for use in children between 9–16 years of
age who live in endemic areas and have a laboratory confirmed prior dengue virus infection.

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