Epidemiology, infectious diseases, parasitology, tropical medicine

Syllabus 2020/2021
Exam Questions & Answers

1. Epidemiology as a medical science. Subject of epidemiology, its goals, tasks relation to

other disciplines, its importance. Methods – descriptive, analytical, experimental,
mathematical modelling
 Epidemiology as a medical science. Subject of epidemiology, its goals, tasks relation to
other disciplines, its importance
 Definition and concept of epidemiology: It includes the study of objective laws of
aetiology, distribution and control of infectious diseases in a human community,
and also elaboration of methods to prevent and control these diseases.
Epidemiology is an independent – branch of medicine aimed at: Prevention, control,
and final eradication of these diseases.
- Epidemiology studies the triad of parasites, macro-organism and environment
 Purpose of epidemiology
- The object is to identify the process of spreading infection in a population of
which the basic criteria involved within this spread are:
 Source of infection/reservoir
 Mode of transmission of infectious agent
 Susceptible organism i.e. the host
 Ultimate aim of epidemiology: Eliminate or eradicate infections
within the population (SEE Q2 for the 5 epidemiological
principles).
 Methods – descriptive, analytical, experimental, mathematical modelling
 I: Descriptive
- It aims to determine the incidence of the disease, the risk factors, and its
medico-social significance and to formulate the hypothesis for the possible
prevention and control measures.
- It usually involves determination of: Incidence, prevalence and mortality rates
for diseases in large population groups, according to basic group characteristics
i.e. age, sex, race, geographic area.
 II: Analytical
- These are studies attempting to explain the disease. They establish causal
relationship between risk factors and morbidity to test and evaluate hypotheses
about risk factors. It includes:
 Cohort analytical study
 Analytical study ‘case control’
 III: Experimental
- Aim is to prove or regute the hypothesis about risk factors.
 IV: Mathematical
- Method of prognostication of morbidity
2. Infectious process. Characteristics – degree of epidemiological significance of the forms of
infectious process
 Infectious process
 Definition: An infectious process is the interaction of a pathogenic microorganism
with a macroorganism under certain environmental and social conditions.
- Pathogenecity is referred to the ability of microbial species to produce disease.
- Virulence is referred to the ability of microbial strains to produce disease.
 The infectious disease process includes the following components:
- (1) Infectious agent
- (2) reservoir
- (3) portals of entry & exit
- (4) mode of transmission
- (5) immunity & Susceptible host

 Characteristics – degree of epidemiological significance of the forms of infectious process:

Principles of Epidemiology
 Principle I:
- Source of infectious agent is an infected (sick or carrier) organism – human or
animal (can multiply in their natural habitat and infect healthy people)
 Principle II:
- The Infectious agent’s localization in the organism and mode of its transmission
from one individual to another, allows pathogenic species preservation in the
environment and continuity of epidemic process of infectious disease.
 Principle II:
- Infectious diseases can be rationally classified according to specific localization
of infectious agent in the organism.
- Gomashevsky Classification (4)
 1: Intestinal infections
 2: Respiratory infections
 3: Blood infections
 4: Skin infection
 Principle IV:
- Epidemic process originates and maintained due to combined forces of three
main motive forces of which if any of these 3 stops, the entire epidemic process
is stopped:
  1: Presence of infectious agent’s source
 2: Realization of transmission mechanism
 3: Population susceptibility to infection
 In other words, see the picture below

 Principle V:
- Natural and social factors (i.e. environment seasonal, social sanitation, supplies,
housing structures etc) stipulate quantitative and qualitative changes in
epidemic process (increase or decrease), thus they are secondary motive forces
of epidemic process.
3. Epidemiological process – definition basic links of spreading of infection, forms of infection
occurrence, depending on intensity and existent occurrence of infectious diseases.
 Epidemiological process
 Definitions:
- Epidemiological process: circulation of infectious diseases among people
- Epizootological process: circulation of infectious diseases among animals
- Communicable diseases: Transmitted from the reservoir or source of infection
to susceptible host. This is the medical model of epidemic process.
 Basic links of spreading of infection (3)

 Forms of infection occurrence, depending on intensity and existent occurrence of

infectious diseases:
- Depending on the spread of infectious disease in the community, they may be
classified into different types:
 I: Sporadic incidence
o Occurs single, irregular or random
o Normal (minimal) morbidity characteristic of given infection for
a given country.
 II: Endemic incidence
o Constantly present in a specific area i.e. Typhoid disease in most
parts of India.
 III: Epidemic incidence
o It is the rapid spread of disease to a large number of people in a
given population within a short period of time
o Characterized by morbidity that 3-10 times exceeds sporadic
occurrence of a given disease in a given locality
  NOTE: Waterborne diseases i.e. Cholera can spread
rapidly within short space of time but direct-contact
diseases evolve and spread more slowly.
 IV: Pandemic incidence
o Epidemic that spreads through many areas of the world
involving a large number of persons within a short period of
time (COVID-19, cholera etc)

4. Source of infection: level of infection, the patient – contagious period, epidemic

importance. Zoonoses.
 Level of infection, the patient – contagious period, epidemic importance – See Q5
 A patient or person can be a source of infection with an ‘acute clinical state’ or
‘non-acute subclinical state’. In other words, one shows symptoms and the other
doesn’t.
- Contagious period is different for every disease
 Incubatory period, prodromal period, invasive stage, covalescence
 I.e. Hepatitis A is contagious in all stages, Covid-19 during incubation
period aswell as prodromal and invasive stage but not in covalescence.
 Zoonoses
 WHO Definition of Zoonoses: Diseases and infections which are naturally
transmitted between vertebrate animals and humans
- Domestic animals and rodents are dangerous in the epidemiologic aspect.
 Zoonoses Etiologic Classification
- Viral
 I.e. Ebola, Rabies, Yellow fever, Influenza etc.
- Bacterial
 I.e. Anthrax, Plague, Brucellosis, Salmonellosis etc.
- Parasitic
 I.e. Beef or pork tapeworm etc
- Mycotic
 Zoonoses Spectrum of disease
- Death = rabies
- Severe illness = plague
- Chronic illness = Q-fever
- Mild illness – Psittacosis
 Infection mode of transmission routes:
- Inhalation (i.e. Q fever, anthrax)
 Suspended air particles, aerosol droplets etc.
- Ingestion of contaminated food or water (i.e. Salmonella, Brucella, Plague)
 Feces, urine etc.
 Rodents for plague – feces etc
- Animal bites (i.e. rabies, skin infections)
 Saliva
- Exposure of skin to contaminated water (i.e. leptospirosis)
- Athropod vectors (i.e. Lyme disease)
 Tick bite blood meal
 Rodents example
 - Worldwide, rats and mice spread over 35 diseases. These diseases can be spread
to humans directly, through handling of rodents, through contact with feces,
urine, or saliva, or through rodent bites. Diseases carried by rodents can also be
spread to humans indirectly, through ticks, mites or fleas that have fed on an
infected rodent.

5. Source of infection: level of infection, the carrier of infection – the elements in a carrier
state, classification by type and duration

A patient or person can be a source of infection with an ‘acute clinical state’ or ‘non-acute
subclinical state’. In other words, one shows symptoms and the other doesn’t.

 Level of infection

 The carrier of infection – the elements in a carrier state

 Elements in a carrier state (3):
- I: The presence of disease agent in the body
- II: Absence of recognizable symptoms and signs of disease
- III: Shedding of disease agent in discharge or excretions
 The carrier of infection - classification by type and duration
 Definition: Carriers are people who harbour infectious agents in the absence of
visible clinical disease and serves as a potential source of infection to others. Carriers
may present more risk for disease transmission than acute clinical cases, because
their contacts are unaware of their infection and their activities are not restricted by
illness
- I.e. Typhoid Mary who infected many people via her cooking of which several
died
  Classification by type
- I: Incubatory carriers
 People who shed infectious agent during incubation period
 I.e. Measles of which person begins to shed virus in nasal and throat
secretions a day or two before rash.
- II: Convalescent carriers
 People who shed infectious agent during convalescent period
 I.e. Salmonella (in faeces for several weeks after convalescence)
- III: Healthy carriers
 Victims of subclinical infection, nevertheless shedding the disease agent
 I.e. Poliomyelitis, cholera, salmonellosis etc.
 Classification by duration
- I: Temporary carriers
 Shed infectious agent for short period of time
- II: Chronic carriers
 Shed infectious agent for indefinite period (longer the carrier state,
greater the risk for community)
 I.e. Hep B

6. Mechanism (mode) of transmission of infection – phases, types, vehicles of transmission.

Routes for spread of infectious disease.
 Mechanism (mode) of transmission of infection – Phases
 Three phases are distinguished in transmission of infection from one
macroorganism to another:
- 1st Phase: Excretion of causative agent from infected macro-organism
- 2nd Phase: Survival of causative agent in environment
- 3rd Phase: Infectious agent’s penetration into healthy (susceptible) organisms
 Mechanism (mode) of transmission of infection – Types
 Direct
- Direct contact
 Skin-skin contact, kissing, sexual intercourse
 Contact with soil or vegetain harbouring infectious organisms
o I.e. kissing disease – infectious mononucleosis, trichomoniasis
(STD)
- Droplet spread
 Droplets
o I.e. Pertussis, TB, influenza etc
 Indirect
- Airborne
 Airborne dust particles in the air i.e. children with measles leave measles
virus suspended in the air.
- Vehicleborne
 Food or water carrying pathogen
 Alternatively, vehicle may provide environment which agent can grow,
multiply or produce toxin i.e. botulinum toxin in improperly canned
foods
 Zoonosis
 - Vectorborne (mechanical or biologic)
 Mosquitoes, fleas and ticks
o I.e. Yersinia Pestis for plague

 Mechanism (mode) of transmission of infection – Vehicles of transmission

 Four mechanisms of infection transmission:
- I: Faecal-oral route (intestinal localization)
 Contaminated water or food
 Contaminated food in soil i.e. vegetables or intermediate hosts cattles
that ingest food from soil etc.
- II: Air-borne (airways localization)
- III: Transmissive (localization in blood systemic circulation)
 Insect bite – vectors
- IV: Contact or contact-wound mechanism (transmission via direct contact or
environmental object or animal)
 I.e. Fomites (inanimate objects such as handkerchiefs, bedding, or
surgical scalpels).
 NOTE - Vehicles: Food, water, soil, fomite, insects

7. Classification of infectious diseases (criteria)

 Classification of infectious disease Intro
 Many classifications through the centuries were formed, however, the classification
proposed by Gromashevsky seems to be more reasonable than the others. It is
based on the ‘location of infection’ in the macroorganism.
 Gomashevsky Classification
- I: Intestinal infections
- II: Respiratory infections
- III: Blood infections
- IV: Skin infection
 According to Gromashevsky, each group is subdivided into
anthroponoses and zoonoses; their epidemiology and prevention differ
substantially.
 Anthroponoses: When source of infection is human (human-human
transfer)
 Zoonoses: When source of infection is animal (animal-human transfer)
 Intestinal infections
 Intestinal infections are characterized by the fecal-oral mechanism of transmission.
- Microbes released in feces, urine and vomit in the environment of which is
ingested accidentally in contaminated food or water by a healthy human.
 Anthroponoses and Zoonoses
- I: Anthroponoses includes:
 Typhoid fever, paratyphoid, bacterial and amoebic dysentery, cholera,
Viral hepatitis A, E, poliomyelitis
- II: Zoonoses include:
 Brucellosis, leptospirosis, salmonellosis, botulism
 Prevention
- I: Sanitary measures of environment (food, water, soil)
 - II: Vaccination for high risk groups (high risk area, immunosuppressed etc)
 Respiratory Infections
 Transmission of infections:
- Stable causative agent
 Aerosol droplets via cough, sneeze, loud talking
 Contaminated surfaces for a specific period of time
- Unstable causative agent in environment
 Close contact with sick patient or carrier patient (perussis,
meningococcal infection)
 NOTE: Morbidity is higher in winter season
 Respiratory infection in children
- Almost all children have forms of respiratory infections several times during
their growth as susceptibility is very high. This creates a durable strong
immunity.
- Some diseases of this group form a special subgroup of children's infections
(diphtheria, scarlet fever, measles, pertussis, epidemic parotitis, chickenpox,
rubella)
 Prevention
 I: Vaccination
o High-risk groups i.e. preganant women, children <5 years old,
elderly, health care workers, immunosuppressed patients (HIV/AIDs,
organ transplant) etc.
 II: Infection control
o Social distancing 2m apart
o Isolation and quarantine when displaying symptoms
o Government contact tracing
o Regular disinfection of surfaces and objects in both residential and
commercial places
o Personal hygiene: Washing hands, sanitizers when outside (alcohol)
regular showers etc

 Blood Infections (blood-borne)

 Transmission of infections:
- Blood-sucking insects i.e. fleas, mosquitoes, ticks etc.
- Examples of diseases: insert here
 Morbidity
- The morbidity is the highest during the warm season which coincides with the
maximum activity of the transmitters - ticks, mosquitoes, etc.
 Prevention
- I: Ticks, mosquitos, fleas
 Known tick infested areas should be avoided and use adequate PPE
 Daily inspection of body for ticks for those who are exposed to risk of
infection
 Disinfection of reservoirs and hosts will minimise tick population
 Flee and mosquito repellent (DEET)
- II: Vaccination
 Skin Infections
  Transmission of infection
- I: Open wounds, Itching or itching blisters
 Wound infections are characterized by damage to the skin as a result of
injury (tetanus, erysipelas)
- II: Transmission can be via: bed linen, clothes, plates and dishes and other
utensils, that can be contaminated with mucus, pus or scales.
- III: AIDS, Hepatitis – Needle injury, IV drug abusers, health care workers (nurses)
 NOTE: They can remain at the portal of infection (tetanus,
dermatomycoses), or affect the skin, enter the body and be carried to
various organs and tissues with the circulating blood (erysipelas,
anthrax).
- IV: Peri-natal (during birth), Transplacental
 Prevention
- I: Adequate PPE, personal hygiene
- II: Vaccination where possible i.e. Hep B vaccination for health workers
- III: Improving sanitation and living conditions of population
- IV: Elimination of infected or stray-infected animal (i.e. dog for rabies)

8. Vehicles of transmission of disease: water, food, object. Importance

 Vehicles of transmission – Water
 Definition: Water is a very important medium by which infection can be transmitted
as pathogenic microorganisms can get into water via various routes.
 Transmission infection:
- Drinking contaminated water
- Using water for domestic purposes
- Bathing
- Swimming in un-chlorinated water
 Contamination with faecal sewage, leaking of waste water etc.
 Epidemic importance
- This type of transmission via water results in an explosive epidemic i.e. cholera,
typhoid fever (endemic), leptospirosis, Hep A etc.
- The duration of survival of this agent within water depends on the physical,
chemical and biological qualities of the water
 Vehicles of transmission – Food
 Definition: Food is a very important medium by which infection can be transmitted
as pathogenic microorganisms can get into food via various routes.
 Transmission of infection
- Infected person or a carrier
- Zoonosis
- Insects or rodents (fecal-oral)
- Improper transportation, storage and cooking (uncooked natural foods, hot or
cold foods
 Transmission Media of food
- Milk and meat
 I.e. meats that are not sufficiently cooked, Botulism toxin can be
transmitted etc.
- Dairy products (curds, sour cream)
 - Eggs
- Vegetables, fruits, berries, bread and other foods that are not cooked
 Epidemic importance and contamination of food that is of animal origin (zoonotic)
- A: Primarily when cause is due to endogen contamination occurring intravirally
in animals (i.e. Salmonella)
- B: Secondarily when preparing foods, cooking utensils, dishes, cross
contamination, contaminated hands of personnel preparing food, non-
separation of raw and cooked foods.
 Examples include: Q-fever, bovine tbc, brucellosis, (shigella) dysentery,
salmonella
 Vehicles of transmission – Objects
 Definition: Objects at patient’s room can be transmitting factor for influenza, tbc,
children’s infection, dysentery, typhoid fever and other diseases. Domestic animals
can be the source of infection, while arthropods can transmit the infections.
 Object examples
- Utensils and household objects (i.e. dishes, cups, plates, hospital canteens etc)
can become a transmission factor for tbc, scarlet fever, typhoid fever,
diphtheria etc.
- Soiled linen and underwear can promote spread of infection i.e. scabies,
intestinal or droplet infections.
9. Vehicles of transmission of disease: soil, air. Importance
 Vehicles of transmission of disease – Soil
 Definition: Soil is contaminated by excrements of humans and animals, various
wastes, dead humans and animals.
 Epidemiological factors and importance
- Contamination of soil is an important epidemiologic factor because soil is
habitat and site of multiplation of flies, rodents etc. Eggs of some helminthes
(ascarides, Trichuris trichura, hookworks) are incubated in soil.
- Transmission of infection
 Fecal-oral: Pathogenic microorganism of soil can pass into - Water,
vegetables, and berries that are eaten by man uncooked.
o Fecal sewage to fertilize soil where cucumbers, tomatoes and
other vegetables grow.
 Wound contamination: Tetanus, anthrax and gangrene transmitted via
soil
 Vehicles of transmission of disease – Air
 Definition: Air is a factor of transmission of respiratory infections. Contamination
occurs mostly in an enclosure where a patient is present. From the source of
infection, microorganisms get into air together with droplets of sputum and
expelled in great quantities during sneezing, coughing and conversation.
 Examples of airborne disease
- Smallpox, chickenpox, measles
- Tuberculosis , smallbox, Q fever, tularemia (can survive in dust for weeks)
 Transmission of disease based on droplet size
- Droplets larger than 100u
 Create contaminated dust when they fall to earth and dry out
- Droplets smaller than 100u
  Stay in the air for shorter or longer period of time
- Small Droplets
 Gets dry immediately and can remain in atmosphere for a longer period
of time and due to their size, they may infiltrate alveolus resulting in
decreased function of ciliary epithelium
 NOTE: The smaller the droplet, the further it may be carried
from source of infection i.e. Acute respiratory disease,
pertussis, PTBC, Diphtheriae
10. Vehicles of transmission of disease: Vector-borne diseases. Main vectors (mosquitos, ticks,
fleas) and diseases they transmit. Importance.
 Vehicles of transmission of disease - Vector-borne diseases
 Definition: Vectors are living organisms that can transmit infectious diseases
between humans or from animals to humans (refer to diseases to explain further i.e.
Malaria, MSF, CCF, Leishamaniasis, Hymenlopiasis, Lyme disease)
 Basis of vector-borne disease and importance (epidemiologically):
- Triangle between pathogen, vector and host
 Geographic and seasonal conditions – natural conditions
- Transmission of diseases in vectors also are in line with seasonal conditions i.e
hot tropical weather of which mosquitos flourish.
 Modes of transmission
- Vertical transmission: From vector (i.e. mosquito) to progeny may occur via
trans-ovarial passage of infectious agent
- Horizontal transmission: Infected mosquitoes transfer agent to vertebrate host
which can be:
 I: Mechanical – I.e. when agent is transferred by vector via mouth parts,
without multiplication in the vector
 II: Biological – I.e. where agent multiplies in the vector
 There are Specific and non-specific carriers
- Discuss Malaria, Leishmaniasis, Hymenolopiasis, Lyme disease, MSF
 Discuss the lifecycles and how pathogens are developed

11. Susceptibility of the population: nonspecific resistance, non-specific immunity, specific

immunity. Herd immunity.

Acquired immunity: Develops after birth as a result of exposure to an antigen, thereby activating the
immune response

Innate immunity: Not produced by the immune response and it is inherited by the organism from
parents and protects it from birth throughout life.
KNOW PRIMARY AND SECONDARY IMMUNE RESPONSE

 Non-specific innate immunity

 Specific adaptive immunity

  The specific defences may be discussed for convenience under the following heads :
- I: Active immunity
 A: Humoral immunity
 B: Cellular immunity
 C: Combination of the above.
 Active immunity may be acquired in 3 ways:
 (a) Following clinical infection, e.g., chickenpox, rubella
and measles.
 (b) Following subclinical or inapparent infection, e.g.,
polio and diphtheria.
 (c) Following immunization with an antigen which may
be a killed vaccine, a live attenuated vaccine or toxoid.
- II: Passive immunity
 A: Normal human lg
 B: Specific human lg
 C: Animal antitoxins or antiser
 Passive immunity can happen naturally peri-natal transmission
via placenta-fetus or vaccination administration
 Active immunity
- Humoral immunity
 B-cells (bone-marrow derived lymphocytes) which proliferate and
produce antibodies after antigen presentation by macrophages.
 Immunoglobulins: IgG, IgM, IgA, IgD and IgE.
o B cells primary function is antibody secretion in order
to form the antibody-antigen complex in order to
engulf the pathogen.
- Cellular immunity
 T cells are a group of lymphocytes that induce the death of cells that
are infected with pathogens (similar to NK cells but more specific).
 There are two types of T-cells. These are T8 (killer) and T4 (helper) cells.
o T8 recognizes MHC1 molecules and bind to them via
surface receptors known as CD8 co-receptors. This
causes their activation and differentiation into killer
cells (induces apoptosis). These do not bind with MHC-2
molecules.
o T4 recognizes MHC2 molecules. They bind to them via
CD4 co-receptor. After their activation, they
differentiate to helper cells. Two types of helper cells:
 TH1 – responsible for cell mediated immunity. Assists macrophages in
phagocytosis as they activate macrophages. Without TH1, macrophages
would engulf bacteria and phagocytosis would not occur thus macrophages
would be used as new hosts.
 TH2 – responsible for humoral immunity. Stimulates production and
proliferation of B-cells.
- Combination of the above (See TH2 info)
 Herd immunity
 Definition: Herd immunity describes a type of immunity that occurs when the
vaccination of a portion of population (or herd) provides protection to unprotected
 individuals. It stems from the theory that diseases passed from individual to
individual is difficult to maintain when most of the population are immune. Thus no
susceptibility or decreased susceptibility population to infectious agent.
 Elements of herd immunity
- I: Occurrence of clinical and subclinical infection in the heard
- II: Immunization of the herd
- III: Herd structure
 NOTE: Studies have shown that its impossible to achieve 100% herd
immunity in a population, neither is it necessary to halt an epidemic, i.e.
eradication of small pox (much less than 100% was required)

12. Specific immunoprophylaxis. Types of vaccines. Immunization schedule of Bulgaria

 Vaccines and its purpose
 Definition: Vaccines are an immuno-biological substance designed to produce
specific protection against a given disease. It stimulates the production of protective
antibody and other immune mechanisms
 Type of vaccine based on stains
- Mono and polyvalent vaccines
 Vaccines may be monovalent or polyvalent. A monovalent vaccine
contains a single strain of a single antigen (e.g. Measles vaccine),
whereas a polyvalent vaccine contains two or more strains/serotypes of
the same antigen (e.g. OPV).
- Combination vaccines
 I.e. DTAP, TD, DPT
 Administration routes of vaccines
- Intradermal, Intramuscular, Subcutaneous and Oral (few drops)

 Vaccination classification
 I: Live attenuated vaccines
- Living organisms which have lost capacity to induce disease but retain
immunogenicity i.e. BCG, measles, oral polio.
 II: Inactivated or killed vaccines
- Growing virus or bacteria in culture media but inactivating them with heat or
chemicals (formalin).
- Killed vaccines usually require primary series of 2 or 3 doses of vaccine to
produce adequate antibody response, and in most cases ‘booster’ injections
required.
 III: Subunit, Polysaccharides, Recombinant &Conjugated
- Use specific pieces of the pathogen (i.e. protein, sugar, or capsid).
  Use of single or multiple antigenic component of microorganism capable
of stimulating immune response.
 Limitation = may require booster shots for ongoing protection of disease
- Recombinant protein (DNA)
 Advantages: Avoids problems related to need to grow and manipulate
large amounts of pathogen from which antigen is purified as we can
produce more specific antigen from a few when it’s purified i.e.
recombinant Hep B vaccine is identical to natural hep b surface antigen.
- Polysaccharide
 Surface of many pathogenic bacteria covered by capsular shell
assembled from polymeric glycans
- Conjugated vaccines
 A conjugate vaccine is a type of vaccine which combines a
weak antigen with a strong antigen as a carrier so that the immune
system has a stronger response to the weak antigen.
 Effective for children with weaker immune systems and inability to
recognize weak antigen due to polysaccharide coating.
 I.e. S.pneumoniae, meningococcal etc.
 IV: Toxoid
- Where toxins from the microorganisms are injected (i.e. Tetanus or Diphteria)
 Additions
o Adjuvants - are added to vaccines to enhance immune response
and resudce amount of immunogen per dose or total doses
needed. Commonly used are aluminium salts (enhance immune
response to proteins)
o Preservatives – Chemicals (i.e. formaldehyde) added to killed or
subunit vaccines in order to inactivate virus, detoxify toxins and
to prevent serious secondary infections (due to bacterial or
fungal contamination).
o Stabilizers - To confirm product quality or stability, compounds
may be added to vaccines for a variety of manufacture-related
issues
13. Specific immunoprophylaxis. Contraindications. Reactions after vaccination
 Contraindications
 Definition: A contraindication is a specific situation in which a drug, procedure, or
surgery should not be used because it may be harmful to the person. 
 Contraindications of vaccination:
- Allergy
 I.e. those allergic to eggs, should not take the MMR, influenza or yellow
fever vaccine as it will elicit a hypersensitivity reaction.
- Fever
- HIV infection, immunodeficiency
- Neurological disorder
- Prematurity
- Reaction to previous vaccine
- Thrombocytopenia

 Adverse reactions/events following immunization/vaccination

- I: Local reactions include:
 Pain, swelling and/or redness at the injection site
- II: Systemic reactions include
 Fever
 Sometimes irritability, malaise, loss of apetite, swollen parotid glands
and joint pains

- A: Allergic reactions to Egg-related antigens

 I: Yellow fever & influenza vaccines: Rarely induce allergic reactions.
Recommended to test skin for people with history of egg allergy before
administering vaccine
 II: MMR: contain minimal to negligible amounts thus low risk
- B: Antibiotic-induced allergic reaction
 To avoid contamination during manufacturing process, several vaccines
include trace amounts of neomycin, streptomycin, and/or polymyxin B.
 IPV and OPV – streptomycin, neomycin and polymyxin B
 - C: Fever
 Low-grade fever or mild illness is not a contraindication for vaccination.
Children with moderate or severe febrile illness can be vaccinated once
they are no longer acutely ill.
- D: Vaccination in pregnancy
 Do not administer live vaccine except yellow fever
- E: Immunosuppression
 No live viral vaccines and BCG. IPV for these patients and their
household contacts.
- F: HIV
 No BCG and OPV is Contraindicated
 IPV for these children and household contacts

14. Social conditions – socio-economic conditions contribute to changes in process of

spreading infections
 Socioeconomic conditions and impact on spread of infections
 Intro: Societies with a highly developed social structures have a number of
advantages which contribute to the health of their population aswell as
disadvantages.
 Advantages
- Hygienic safety of environment (drinking water, dwellings, rubbish removal)
- Production and distribution of foodstuff
- Level of medical care and its accessibility
- Sound education
 Disadvantages
- Schools more crowded with larger possibility of contact and spread of
respiratory infections
- Air transport i.e. in larger populated regions on public transport
- Industrial production of food stuffs with higher possibility of intestinal infections
i.e. canteens of work places
- Higher access to antibiotics leading to increased developmental resistance
 Social, Environmental and Economic factors
 Social factors
- Impact of urbanization on sanitation and water supply
- Behaviour of pubic on controlling daily threat of infectious diseases
 Environmental factors
- Naturally occurring variation in temperature and rainfall
 Economic factors
- Level of investments in public health (vaccines, antibiotics, technological
advancements and hygiene and sanitation), education etc.

15. Natural conditions influence the process of spreading infection seasonality of infectious
diseases. Cyclic trends of infectious diseases
 Natural conditions influence the process of spreading infection seasonality of infectious
diseases
  Environmental factors that influence the spread of communicable diseases that are
prone to cause epidemics. The most important are:
- I: Water supply
- II: Sanitation facilities
- III: Food
 I, II, II: A lack of safe water, inadequate excreta disposal facilities, poor
hygiene, poor living conditions and unsafe food can all cause diarrhoeal
disease and are major cause of suffering and death in an emergency
situation.
- IV: Climate
 Vectors can be heavily affected by local climate. Flooding after heavy
rains can result in seq
 wage overflow and widespread water contamination (think tropical
diseases)
 There is evidence to suggest that passage can be spread from region to
another along air-streams or by wind.
 Cyclic trends
 Periodicity definition: Periodicity is cyclic increases of morbidity of one or another
infectious disease once in several years which is brightly expressed in the case,
when preventative actions are of low efficiency, and epidemic process develops
spontaneously.
- Phenomenon of periodicity
 It is better explained in relatively small settlements. Post infectious
immunity develops in individuals who have been ill, and due to
increased number of immune people, the morbidity decreases step-by-
step. Epidemics are gradually replaced by the period of ‘well-being’.
However, in several years, number of people susceptible to the given
disease increases due to newborns and people who have lost the gained
immunity. Thus, there is a recurrence of infection and the wave of
epidemics enhances again.
 Seasonal prevalence
- Seasonal prevalence is determined by an increase of morbidity level in a certain
season of year.
 I: Airborne mechanisms – autumn-winter or winter to early spring
seasonal prevalence
 II: Faecal-oral mechanism – Summer-autumn
 III: Blood infections - Summer-autumn
o Blood infections depends on biological activity and increasing of
amount of insects which are vectors of disease. The exception is
made for lice, often observed in cold season.
- Climatic conditions influence geographical occurrence of a number of infections
i.e. occurrence of malaria is bound to occurrence of Anopholes mosquito,
yellow fever to occurrence of Aedes Aegypti mosquito etc.

16. Types of epidemics, depending on the diseases, modes of transmission: by water, by food
and milk. Epidemic curves
 Epidemic curves
 Definition: An epidemic curve shows the frequency of new cases over time based
on the date of onset of disease. The shape of the curve in relation to the incubation
period of a particular disease can give clues about the source. There are three basic
curves which are:
- I: Point source outbreaks epidemics
- II: Continuous common source epidemics
- III: Propagated (or progressive) source epidemics

 Point source outbreaks epidemics

 Intro: Point source outbreak epidemics involve a common source, such as
contaminated food, infected food handler, and all the exposures tend to occur in a
relatively brief period.
 Curve: Point source outbreaks tend to have epidemic curves with a rapid increase in
cases followed by a slower decline, and all cases tend to fall within one incubation
period.
 Examples: Hepatitis outbreak is an example of which incubation period for hepatitis
ranges from 15-50 days, with average of 28-30 days. In a point source epidemic of
Hep A, you would expect rise and fall of new cases to occur within 30 day span of
time.
 Continuous common source epidemics
 Intro and curve: This type may also rise to a peak and then fall, but the cases do
not all occur within the span of a single incubation period. This implies that there
is an ongoing source of contamination (i.e. contaminated water supply). The down
slope of the curve may be very sharp if common source is removed or gradual if
outbreak is allowed to exhaust itself.
 Examples: Cholera outbreak in London is an example of which incubation period is
1-3 days. Even though residents began to flee when outbreak erupted, the outbreak
lasted for more than a single incubation period, which suggested an ongoing source
of infection, in this case, the Broad Street Pump.
 Propagated (or progressive source) epidemic
 Intro: Transmission is person-to-person, rather than from a common source
 Curves: Propagated epidemic curves usually have a series of successively larger
peaks, which are one incubation period apart. The successive waves tend to
 involve more and more people, until the pool of susceptible people is exhausted or
control measures are implemented.
 Example: Outbreak of measles that began with single index case who infected
number of other individuals. One or more people infected in the initial wave
infected a group of people who become the second wave of infection

17. Types of epidemics, depending on the diseases, modes of transmission: vector-borne, by

air and mediated contaminated objects. Epidemic curves.
18. Epidemiological investigation – aims, stages, ways of carrying out, epidemiological
analysis, epidemiological prognosis
 Epidemiological investigations
 Intro: Epidemiologic investigations are usually conducted in outbreak situations. The
main reasons for conducting an epidemiologic investigations are:
- Determine cause of outbreak
- Implement control measures to prevent additional illness
 Aims/Purpose of epidemiologic investigation
- I: Reveal source and ways of infection transmission
- II: Establish the boundaries of the focus
- III: Determine the scope of disinfection and reveal contacts
- IV: Plan of immediate measures aimed to control and eradicate focus should be
made out
 Stages
- I: Confirm the existence of an epidemic or an outbreak
 Outbreak may be defined as a situation when the observed number of
cases unaccountably exceeds the expected number. To confirm the
existence, we compare the current number of cases (incidence) with
past levels of the same disease over similar time period.
- II: Confirm the diagnosis
 Labs – I.e. blood tests, stool cultures & clinical histories
- III: Determine the number of cases (ill people)
 Helps for an idea of magnitude of problem. It is based on creating a case
definition which is a set criteria of decisding whether an individual
should be classified as a case.
 Elements: Information of symptoms, lab results, time, place and person
 Common method: Conduct questionnaire or survey among population
you believe to be at risk.
- IV: Orient the data in terms of time, person and place
 Purpose is to arrange all incoming data so it means something.
 Method: Plotting, on a graph, the cases by time of symptoms onset to
get an epidemic curve.
- V: Develop a hypothesis
 Explains specific exposures that may have caused the disease.
 Method: Odds ratio, relative risk, P-value are examples of statistical
tests that can be used to develop a hypothesis.
- VI: Compare the hypothesis with established facts and draw conclusions
  Epidemiologic results should be plausible and consistent with other
investigational findings
- VII: Execute control and preventative measures
 Depends on cause, type etc i.e. track and trace
- VIII: Write a written report
 Summarize conclusions. This identifies a potential source of the
outbreak and suggests control measure to prevent future illness.

19. General prophylaxis and basic anti-epidemiological measures

General prophylaxis: Carried out regardless of presence or absence of infectious diseases at a

given time and locality. These measures are aimed at prevention of infectious diseases

Anti-epidemic measures: Necessary when an infectious disease develops to reduce incidence

and control and eventually eradicate the disease.

Prophylactic and anti-epidemic measures are therefore aimed at (I) control of the source of
infection, (II) disruption of route by which infection spreads, and (III) strengthening of non-
susceptibility of the population (think of the three basic links)

 General prophylaxis
 Prevention and control of diseases include the following:
- A: Mass-scale measures aimed at improvement of public health, prevention and
spread of infectious diseases
- B: Medical measures aimed at reduction of infectious morbidity and eradication
of some diseases; health education and involvement of population in prevention
or restriction of the spread of infectious diseases
- C: Prevention of import of infectious diseases from other countries
  I: Control of infectious source
- The time of revealing of the sick is very important is KEY as patients with some
infectious diseases liberate the pathogenic microorganisms into the
environment during the last days of incubation period or during first day of the
disease
 Infectious disease is diagnosed based on: Clinical findings,
epidemiologic anamnesis and diagnosis
- Preventative measures of control of spread and infectious source
 I: Infectious patients must be hospitalized and isolated in proper time
(i.e. plague, cholera, viral hepatitis, typhoid etc)
o Patients cured from infectious disease should only be discharged
after alleviation of clinical symptoms and negative result.
 II: Carriers must be immediately withdrawn from their occupation (i.e.
personnel of children’s institutions, food catering etc) until they are
completely cured and given multiple tests for absence of the carrier
state.
 III: Animals – source of infection
o If animals are the source of infection, measures should be taken,
disinfected and quarantine should be established
 II: Disruption of infectious transmission pathway
- A: Intestinal (Fecal-oral) – Ingestion of food or water
 Sanitary measures to preclude contact of infected material with water,
food, or hands (I.e. hygiene, hand washing, dealing with raw and cooked
food, distribution, transport, chlorination etc).
 Proper handling of disposal of waste
- B: Respiratory (Air-borne) – Droplets or indirect suspended particles
 Report to local authority, isolation and concurrent disinfection
 Quarantine, 2m rule
 Personal hygiene and regular handwashing
 Reduction of overcrowding
 Adequate ventilation of buildings
- C: Blood – Inoculation, Vector-borne etc
 Control of arthropods (i.e. PPE, Vaccination, DEET repellent, chemicals
to eliminate reservoir etc)
- D: Skin ( Contamination of wound or vector borne)
 Improve general health, living standards and labor conditions
 Disinfection
 III: Measures to strengthen and increase non-susceptibility of population
- Improvement of living conditions, labour conditions, nutrition, physical training,
education, immunity through preventative vaccination etc.
 Preventative Anti-epidemic measures
 I: Improvement of hygienic level of population
 Strict observation of regulations with supply of water, nourishment,
production and handling of foodstuff, waste water, rubbish disposal etc.
 II: Vaccination
- Selected groups vaccinated against selected infections
 III: Registration & Control of carriers
 - I.e Those who are Covid-19 positive are required to follow a certain set of rules
and notify the authority if the test was carried out in private. This helps with
Track and trace.
 IV: Measures preventing infection spread into large areas/populations
- I.e. Taking certain tests before employment i.e. As a doctor
 V: Prophylactic disinfection
- Performed in public buildings, mass transport, medical establishments, water
supply etc.
- Airports and those who are coming from countries that may have an epidemic
- Measures against imports into the country
 VI: Medical education
- Systemic increase of awareness of infectious disease and basic understanding of
epidemiology should be included into the system of school education
20. Epidemiological investigation in the focus of infection – to the patient, to the environment.
Anti-epidemic measures in the focus of infection
 Epidemiological investigation in the focus of infection
 Intro: The efficiency of anti-epidemic measures taken in the focus of infection
depends largely on the time when source of infection (patient) is revealed and
isolated from surrounding people. As the disease is revealed, the following
measures should be taken:
- I: Diagnosis of disease
- II: Making appropriate record (registration) + inform authorities
- III: Hospitalize patient or isolate in out-patient conditions
- IV: Specific therapy
 Epidemiological investigation in focus of infection – Carried out immediately
(REFER TO POINT 18 on stages)
- I: Short history is taken from sick before transportation to hospital
- II: Search for all persons who might be affected and then search is
conducted for source of infection.
- III: Data must be collated about the sick, contacts with the sick, age and sex
of affected individuals (when the disease started, profession, and living
conditions of affected individuals).
- IV: On the basis of info obtained, epidemiological curves and working
hypothesis about source and way of transmission are prepared
 Anti-epidemic measures in focus of infection
 Intro: this is a set measure aimed at liquidation of the focus of infection at the
earliest possible opportunity.
 Anti-epidemic Regime is as follows:
- I: Quarantine measures
- II: Focus disinfection (disinsection, deratization)
 Performed vicinity of the sick and carried out after transportation to
hospital and death of infected individuals
- III: Chemoprophylaxis
 Use of antibiotics in indiciated cases i.e. anti-malarial drugs in
malaria
- IV: Hygiene
- V: Education
  Control and evaluation of anti-epidemic measures
- Intro: Done daily and represents main part of work for the epidemiologist as
daily results evaluated means there can be changes in accordance with the
change in disease/patient condition. The basic preventative actions directed
to liquidation of epidemic focus and to prevent arisal of new foci are
considered to be the following:
 I: Measures on making source of infection harmless
o I.e. isolation of hospitalized infected patients
 II: Measures on breaking down/disrupting transmission of
infection pathways
o I.e. elimination of rodents and other mechanisms, chemicals
etc. disinfection, disinsection, deratizzation
 III: Creation of specific immune-defence in the population thus
increasing strength of non-suceptibility
o Vaccination, immunoglobulins, herd immunity etc

21. Disinfection and sterilization – definition. Physical methods. Chemical methods.

 Disinfection and sterilization
 Definition of Disinfection: A disinfectant is a substance which destroys harmful
microbes (not usually spores) with the object of preventing transmission of disease.
 Definition of sterilization: Sterilization is the process of destroying all life including
spores. Sterilization can be achieved by physical, chemical and physicochemical
methods.
 Disinfection includes three concepts: (1) disinfection proper; (2)
disinsection (control of the arthropods transmitting infection); (3)
deratization (rodent control).
- Cleaning
 Detergents (cleaning surfaces etc), soaps, hand-wash
- Filtration (lab method)
 Only method that uses force to separate rather than kill.
 When filtering liquid or gas, it passes through a pore, which stops, or
filters out the passage of larger particles i.e. bacteria
 Important when making antibiotics and other medication
 NOTE: The chances of clogging and long time duration for the
process are disadvantages.

- Moist Heat (Boiling, Pasteurization, Water vapors)

 Microbes can grow over a range of temperatures and be destroyed if it’s
the opposite.
o I: Psychrophiles – very low temp (if very high, destructive)
o II: Mesophiles – moderate temperature/body temp (if low or
high, destructive)
o III: Thermophiles – very high temp (if very low, destructive)
 Pasteurization
o Milk is heated at 63 degrees for 30 minutes or 72 degrees for 15
seconds for sterilization
 Boiling (100 degrees Celsius)
 o Kills most vegetative bacteria and viruses for 10-20 minutes.
Some bacterial toxins i.e. Staphylococcal enterotoxin are heat
resistant.
 Water vapors
 NOTE: The moist heat acts by coagulation and denaturation of
proteins. Moist heat is more effective than dry heat.
- Dry heat
 Flaming (Bunsen burner)
 Hot air oven
o Articles exposed to high temperature for two hours in electric
heated oven.
 NOTE: Dry heat acts by protein denaturation, oxidative damage
and toxic effects of elevated levels of electrolytes
- Sunlight/radiation
 Active germicidal agent, due to content of UV rays
 Natural method of sterilization in case of water in tanks, rivers or lakes.
 Radiation: Non-ionizing or ionizing
 NOTE: Sunlight is not sporicidal, hence it does not sterilize.
 Chemical methods
- Important chemicals
 Halogens
 Phenol and phenolic compounds
 Heavy metals
 Alcohols
o A 70% aqueous solution is more effective at killing microbes
than absolute alcohols. 70% ethyl alcohol (spirit) is used as
antiseptic on skin
 Formaldehyde
 Glutaraldehyde
 Ethylene oxide

22. Disinsection – definition, methods of characteristics of agents used. Intesticides

 Disinsection
 Definition: Disinsection is the process of using substances which destroys harmful
insects thereby preventing the transmission of disease. Disinsection can be physical,
biological and chemical.
- I: Preventative measures – control multiplication of arthropods and their
penetration into residential households and other buildings. I.e. sanitation,
hygiene, food or wastes kept closed etc.
- II: Destroying measures – Elimination and eradication of reservoirs
 Methods of characteristics of agents used – intesticides
Insecticides are essential tools for controlling insect pests and therefore, improving
the quality of life for humans, domestic animals and livestock.
- I: Physical
 Burning wastes
 Steam
  Boiling
 Hot ironing pressing etc
- II: Biological (mainly to kill agricultural and forest pests)
 Bacillus thuringiensis
o Natural occurring, soil-borne bacteria which has a protein crystal
within spore which is only toxic to insects.
 Fishes (Gambuzia)
o Predatory fishes
- III: Chemical
 Organochlorines
o DDT is still effectively used for malaria control in several third
world countries
 Organophosphates
o Inhibition of acetylcholinesterase thus overstimulation.
 Carbamates
 Insect repellants
o DEET has survived, and is used worldwide for biting flies and
mosquitoes. Most of the others have lost their registrations and
are no longer available.
 Larvicides = killing of larvae of arthropods
 Ovicides = killing/destroying of eggs

23. Derattization – definition, methods and characteristics of agents used. Rodenticides.

 Derattization
 Definition: Deratization is eradication of rodents, which can be a source of
infectious diseases (i.e. plague, tularemia), for humans and therefore are dangerous
in an epidemiological stand-point.
- House mice, field mice, black and brown rats, marmots, and water rats are
especially dangerous epidemiologically (rat droppings or dead/dying rodents
infectious).
- Preventative and destroying measures are used.
 Methods and characteristics of agents used
 I: Biological method
- Destruction of rodents by bacterial culture and by their natural antagonists i.e.
cats, dogs, predacious animals (weaels, foxes), and wild birds.
- Bacterial cultures: Used in the form of food baits. Isachenko and Merezhovsky
cultures causing typhus among rats and mice are now widely used.
 Chemical method
- Use of poisons that kill rodents when inhaled or ingested.
- A: Gases used to treat stores, ships, railway cars and also natural habitat in field
conditions.
- B: Ingested poisons are used in baits i.e. bread, porridge, dough, cheese etc.
 Rodenticides are chemical substances used to kill rodents which can be
classified by toxicity.
 Rodenticides – Chemical method
  Definition: Rodenticides are chemical substances used to kill rodents which can be
classified by toxicity.
 Classification
- Highly toxic rodenticides
 Substances with single dose LD50 of less than 50mg/kg body weight.
 Group includes: Thallium, zinc phosphide, yellow phosphorus and
arsenic.
 Some of these compounds have been abandoned due to serious human
toxicity.
- Lowly toxic todenticides
 Red squil, Norbomide (irreversible smooth muscle constrictor causing
widespread ischemic necrosis and death)
 Anticoagulants – Most commonly used today.
o I: First generation anticoagulants
 Less toxic and more than one dose needs to be eaten
for product to be effective. Made from chemicals such
as warfarin.
o II: Second generation anticoagulants
 Much more potent and act faster. They kill rodents with
just one dose. Made from chemicals such as
brodifacoum
24. Hospital acquired (nosocomial) infections: Causative Agents, specific types of nocosomial
infections, sources of infection, modes of transmission, prevention and control.
 Nosocomial infections
 Definition: It is an infection acquired in a medical setting in the course of
medical treatment. It meets the following criteria:
- I: Not found on admission
- II: Temporarily associated with admission or a procedure at a health care
facility
- III: Was incubating at admission but related to a previous procedure or
admission to same or other health-care facility
 Aetiology (Causative Agents)
- I: Bacteria (Most often occurring bacterial agents are):
 Gram +ve cocci (Staphylococcus, Streptococcus)
 Gram –ve sticks (Pseudomonas, Klebsiella, E.coli etc)
 NOTE: Drug-resistant gram –ve bacteria for the most part,
threaten only patients whose immune systems are weak as
they can survive for a long time on surfaces in the hospital
and enter via wounds, catheters, and ventilators
- II: Viruses
 Herpetic virus, EBV, CMV, Virus VHB
- III: Mycosis
 Candida albicans
 Specific types of nocosomial infections
- I: Non-specific
 Infections that are currently affecting the population OUTSIDE THE
HOSPITAL i.e. respiratory infections, alimentary infections belong to
 this group. Occurrence of these reflects epidemiological situation of
the region the medical establishment resides in.
- II: Specific
 Infections occurring as a consequence of diagnostic or therapeutic
procedures in the hospital. Common mode of transmission is
inoculation and implantation of the agent. Apart from health
establishments, there is no other way for these infections to spread
in the current population.
 I.e. Staphylococcus infections from mothers to new-born’s, urinary
infections (instrumental procedures), Hep B etc.
 Sources of infections
- I: Patients
 When infectious disease was incorrectly diagnosed. People currently
within the incubation period
- II: Personnel
 In Incubation period of infectious disease
- III: Visitors
 In Incubation period of infectious disease
- IV: Rodents
 Present in number of health establishment and can play a role
especially in alimentary way of transmission of infection.
 Modes of transmission
 I: Direct contact
- When admitting, examining, treating the patient. Contact with sick and
visitors
 II: Indirect contact
- Objects, appliance, instruments etc.
 III: Airway
- Inhalation (scarlet fever, influenza, pneumonia, pertussis, staphylococcus
infection)
 IV: Implantation & Inoculation
- During operations or re-bandaging wounds. Unsatisfactory sterilization of
instruments and materials & unsuitable prophylactic disinfection.
Transfusions.
 V: Alimentary
- Consumption of home or hospital food (typhoid fever, salmonella etc)
 VI: Insects & Rodents
- Passive transmission of aetiological agents, mostly by insects to food or
sterile materials
 Preventative measures and control
 I: Sterilization
 II: Prophylactic disinfection
 III: Avoid and wash used bed linen
 IV: Bandages
 V: Single use (instruments, syringes, needles)
 VI: Antibiotics prophylaxis
 VII: Hygienic principles
  VIII: Monitoring
 VIIII: Announcement & Registering Nosocomial infections
 X: Handwashing and Adequate disposable PPE (reduce cross contamination)

25. Diagnosis of Infectious Diseases

 Diagnosis of infectious diseases – Introduction
 Intro
- Infectious diseases are caused by microorganisms, such
as bacteria, viruses, fungi, and parasites.
 Lab tests (Identification of microorganisms)
- Samples:
 Blood, urine, sputum, or other fluid or tissue from the body.
 Swabs from different places depending on suspected diagnosis
- Lab tests are essential to identify microorganism in order to determine effective
therapy against it
 Examinations in virology
- I: Direct Examination
- II: Indirect Examination (Virus Isolation)
- III: Serology
 Microbiology examinations (bacteria)
- Microscopic morphology of microorganisms
- Differential stains
- Culture media

 I: Staining and Examination Using a Microscope

 Doctors sometimes can identify a microorganism simply by looking at it under a
microscope. However, most samples are treated with stains (to stand out)
 For bacteria:
- Gram-positive: Look blue because they retain violet gram stain
- Gram-negative: Look red because they do not retain stain
o I.e. Zeehl-Neelson staining for TB
 Viruses – cannot be identified using microscope as they are too small
 II: Culture of Microorganisms
 This method is used when many samples contain too few microorganisms to be seen
using a microscope etc. Thus, doctors try to grow microorganism via culture.
 The sample is placed on a sterile dish (plate) or in a test tube that contains
specific nutrients to encourage growth of microorganisms. Different
microorganisms have different nutrient requirements.
- I.e. Primary Monkey cell agar for Influenza
 III: Testing of a Microorganism’s Susceptibility and Sensitivity to Antimicrobial drugs
 As there has been an increased developed resistance to drugs, doctors are now
using drugs on cell cultures to determine effectiveness of the drug. This is called
susceptibility testing
- Drawback: Because susceptibility testing occurs in laboratory and lab settings,
the results may not always match what occurs in a patient’s body.
 IV: Tests that detect Antibodies to or Antigens of Microorganisms – Serological testing
 Principle (Indirect): Detection of bacteria by use of antibodies and Ab-Ag complex.
  Techniques:
- Agglutination test: Reaction between Ab-Ag causes visible agglutination
complex/clumps.
- ELISA: enzyme linked immunoabsorbant assay (in wells):
 I: Antigens from sample are attached to a surface
 II: Specific antibody applied over surface to see if it binds to antigen. The
antibody is linked to an enzyme.
 III: Substance containing enzyme substate is added in which subsequent
reaction produces a color change in the substrate.
- Western blot: Use of nitrocellulose paper (agar plates) binded by first antibody
and second labelled antibody to produce colour reaction if complementary.
 Application:
o Latex agglutination: virus specific antibodies to cytomegalovirus
infection.
o ELISA: Hepatitis A, B, C, HIV, rubella, herpes etc.
o Western blot: Confirmation test for detection of antigen in HIV infection
and AIDS
 V: Tests that detect genetic material in microorganisms – Nucleic acid based methods
 Polymerase chain reaction (PCR)
- Amplification of the virus genome using virus-specific probes. This will allow
detection of viral RNA and DNA genomes. Especially when microorganism is
difficult to culture or identify by other methods.

26. Antimicrobial treatment of infectious diseases

 Choices of antibiotic
 According to:
- Diagnosis (nature of disease)
- Terrain of illness – healthy, immunosuppressed, with implants
- Properties of the antibiotics
- Pharmacodynamics
 ADME
 Adverse effects
 Contraindications
o Half-life, renal clearance, plasma binding capabilities etc
 Dosage
 Optimal dosase (with respect to therapeutic index)
 Method of administration
- Oral, IV, IM, Dermal, Inhalation, Sublingual, Rectal
 Timing and duration
 Antibiotic prophylaxis
 Antibiotic prophylaxis: decrease chance of infection
 Hospitalization
- i.e. surgery or immunosuppressed
 Reasons for failure of antibiotic therapy
 Misdiagnosis - no case of infection responded to antibiotics
 Wrong choice of antibiotic
 Wrong dosage
  Wrong timing
 Development of resistance
 Superinfection
 Unable to reach the target organ
 Development of intolerance (allergy)

 Group of antibiotics (bacteriostatic or bactericidal)

 Sulfonamides
 Beta-Lactam Antibiotics
 Tetracycline
 Chloramphenicol
 Aminoglycosides
 Macrolides
 Streptogramins
 Lincosamides

27. Typhoid fever

 Typhoid fever
 Definition: Typhoid fever is the result of systemic infection caused mainly by Salmonella
typhi. It is a GI type bacterial infection.
- The disease may occur sporadically, epidemically or endemically
 Aetiology & Mode of transmission
- Causative agent: S.typhi is the major cause of Typhoid fever
 Three types of antigens – O, H and Vi
- Reservoir host: Humans
- Incubation period
- Mode of transmission:
 I: Fecal-oral route
 II: Urine oral route
o Contaminated water, food, fingers or flies
- Period of communicability
 Usually from first week of excreta throughout covalescence
- Epidemiology
 It occurs most often in children and young adults between 5 and 19 years
old.
  Typhoid fever remains an important public health problem in the world
especially in the impoverished population from developing countries with
lack of hygienic and sanitization standards.
 Clinical features

 Diagnosis, Treatment & Prevention

- Diagnosis
 Widal test
o Demonstration of antibodies against Salmonella antigens O-somatic
and H-flagellar)
 Any blood, bone marrow, or stool cultures
- Treatment
 I: ORS (prevent deaths caused by diarrheal disease)
 II: Antibiotics – Fluoroquinolones (i.e. Coprofloxacin)
 III: Surgery – if there’s intestinal perforation
- Prevention
 I: Three lines of defences
o Control of reservoir
o Control of sanitation
o Immunization
 II: Vaccination (anti-typhoid vaccination)
o Monovalent anti-typhoid vaccine
o Bivalent anti-typhoid vaccine
 Primary immunization should consist of 2 doses/0.5ml, given
subcutaneously at an interval of 4-6 weeks. Booster doses are
recommended every 3 years.
28. Sallmonelosis
 Sallmonelosis
 Definition: Salmonellosis is a symptomatic infection caused by bacteria of
the Salmonella type.
 Aetiology & Mode of transmission
- Causative agent: Salmonella bacteria
- Reservoir host: Domestic and wild animals such as cattle, swine, poultry, wild birds,
flies and pets
- Incubation period: 12–72 hours
- Mode of transmission:
  I: Fecal-oral route: Contaminated food and water, poor kitchen hygiene
 II: Direct animal contact

- Epidemiology
- Period of communicability
 Throughout to the course of infection even in covalescence – Temporary
carriers
 Clinical features
- Typhoid (see typhoid question)
- Enteritis
 Diarrhoea, fever, vomiting, and abdominal cramps 12 to 71 hours after
infection.
 Illness lasts around 4-7 days
 Diagnosis, Treatment & Prevention
- Diagnosis
  Diagnosis is by a stool test or blood tests
- Treatment
 Oral rehydration
o Clear fluid or oral rehydration salts
o Safe water (adults: 1L/hr initially)
o IV fluids if severely dehydrated
 Nasogastric tube if vomiting
 Antimotility agents
o Loperamide, bismuth subsalicylates
o Avoid if severe pain or bloody diarrhoea
 Antibiotics
o Doxycycline, tetracycline etc
o Azithromycin in children
- Prevention
 Three lines of defences
 o I: Control of reservoir
o II: Control of sanitation
o III: Immunization
 Vaccination (anti-typhoid vaccination)
o Monovalent anti-typhoid vaccine
o Bivalent anti-typhoid vaccine
 Primary immunization should consist of 2 doses/0.5ml, given
subcutaneously at an interval of 4-6 weeks. Booster doses are
recommended every 3 years.

29. Food poisoning

 Definition: Foodborne illness (also foodborne disease and colloquially referred to
as food poisoning) is any illness resulting from the spoilage of contaminated
food, pathogenic bacteria, viruses, or parasites that contaminate food,  as well
as toxins such as poisonous mushrooms and various species of beans that have not been
boiled for at least 10 minutes.
 Aetiology & Mode of transmission
- Bacteria
 Campylobacter jejuni, e.coli, salmonella etc
- Viruses
 Hep A, Hep E, Enterovirus
- Parasites
 Nematodes, protozoa
- Toxins
 Enterotoxins i.e. in Botulism
 Natural toxins
 Clinical features/Pathogenesis

- Incubation period
 Definition: Delay between consumption of contaminated food and
appearance of first symptoms of illness is called ‘incubation period’.
 If symptoms occur within 1-6 hours after eating food, it suggests that it is
caused by bacterial toxin or chemical rather than live bacteria
 o NOTE: During the incubation period, microbes pass through
the stomach into the intestine, attach to the cells lining the
intestinal walls, and begin to multiply there. Some types of
microbes stay in the intestine, some produce a toxin that is
absorbed into the bloodstream, and some can directly invade
the deeper body tissues. The symptoms produced depend on
the type of microbe
- Infectious dose
 Amount of agent that must be consumed to give rise to symptoms of
foodborne illness i.e. Shigella sonnei requires low dose of minimum <500
colony forming units (CFU)

- Foodborne and waterborne diarrhoeal diseases kill an estimated 2.2 million people
annually, most of whom are children
 Prevention
- I: Promoting rapid exchange of information during food safety events
- II: Sharing information on important food safety issues of global interest
- III: Promoting partnerships and collaboration between countries
- IV: Promote and investigate food chain from the bottom up

30. Botulism
 Botulism
 Definition: Botulism is an acute neurologic disorder that causes potentially life-
threatening neuroparalysis due to a neurotoxin produced by Clostridium botulinum.
The disease begins with weakness, blurred vision, feeling tired, and trouble speaking
 Aetiology & Mode of transmission
- Causative agent: Clostridium botulinum (Gram +ve spore forming rod)
 Botulinum toxin one of the most powerful known toxins; about one
microgram is lethal to humans when inhaled (causes neuromuscular
blockade via inhibition of acetylcholine release
- Reservoir host:
 Human host and C.botulinum commonly found in soil and agricultural
products. Spores have been found in marine sediments and intestinal tracts
of animals i.e. fish
- Incubation period: 12–36 hours (up to several days) 
- Mode of transmission:
 I: Colonization of the gut
o Occurs in infants who are colonized with bacterium in small
intestine. The bacterium then produces the toxin which is absorbed
into the bloodstream.
 II: Food
o Contaminated food with C.botulinum spores in low-oxygen
conditions i.e. improperly prepared home-canned food substances.
 III: Wound
o Contamination of wound with bacteria which then secrete toxin into
bloodstream. Has become more common in IV drug users.
 IV: Inhalation
o Lab workers
 V: Injection
- Epidemiology
- Period of communicability
 Foodborne botulism typically excretes toxins for very short period
 Clinical features
- Foodborne botulism
 Foodborne botulism should be suspected in patients who present with an
acute gastrointestinal illness associated with neurologic symptoms
 3-5 following signs or symptoms
o Nausea
o Vomiting
o Dysphagia
o Diplopa, dilated/fixed pupils
o Extremely dry mouth unrelieved by drinking fluids
- See picture below which shows progression of botulism
  Diagnosis, Treatment & Prevention
- Diagnosis
 Lab tests are not helpful in the routine diagnosis of botulism
 Diagnosis should be made on signs and symptoms. Confirmation of the
diagnosis is made by testing of a stool or enema specimen with the
mouse bioassay.
- Treatment
 On March 2013, the FDA approved first botulism antitoxin that can
neutralize all 7 known botulinum nerve toxin serotypes.
 Wound botulism
o Requires incision and thorough debridement of the infected
wound, antitoxin therapy, and high-dose intravenous penicillin
therapy.
- Prevention
 I: No vaccination yet but under development
 II: Infant botulism prevention
o Avoid giving honey to less than 12 months of age as botulinum
spores often present. In normal adults and older children, normal
intestinal bacteria suppress development of C.botulinum.
 III: Canning or preserving food at home
o Attention to hygiene, pressure, temperature, regrigeration and
storage
31. Shigellosis
 Shigellosis
 Definition: Shigellosis (bacterial dysentery) is a intestinal illness caused by bacteria of
the genus shigella. It is a GI type infection. Shigella have plasmid genes that control
production of cytotoxin which are both enterotoxic and neurotoxic.
 Aetiology
- Shigella are aerobic, non-motile, glucose-fermenting gram –ve rods.
- 4 species of Shigella
 I: Shigella Disenteriae (most virulent)
 II: Shigella Flexneri
 III: Shigella Boydii
 IV: Shigella Sonnei (most common)
 Mode of transmission
 - Humans = only known reservoir
- Shigella spreads via fecal-oral contact, via contaminated water and food
- After that, the usual mode of transmission is directly person-to-person, hand-to-
mouth, in the setting of poor hygiene.
- Incubation period = 1-7 days
 Epidemiology
- Major cause in paediatric group age: 1-10 years
 Outbreaks in daycare centers, nurseries, institutions
- Most at risk groups
 Children in daycare centers
 International travellers
 Homosexual man
 Patients with HIV
 People with inadequate clean water supply
 Period of communicability
- During acute infection and as long as until infectious agent is no longer in stool
 Clinical symptoms and diagnosis
- Dysentery (inflammation of intestines especially colon)
 Severe abdominal cramps
 Tenesmus
 Frequent low-volume stools containing blood, mucus and fecal leukocytes
- Two clinical stages
 I Early Stage: Watery diarrhoea attributed to enterotoxic activity of Shiga
toxin
 II Late Stage: Dystentery due to adherence to and tissue invasion of large
intestine
- Culture medium diagnosis
 MacConkey and Salmonella-shigella agar
o These media contain bile salts to inhibit growth of other Gram –ve
bacteria and have pH indicators to differentiate lactose fermenters
from non-lactose fermenters such as Shigella.
 Treatment
- Ciprofloxacin
 Prevention
- I: Unwell and ill contacts should be excluded from food handling and care of
children or patients until diarrhoea ceases and 2 successive negative stool cultures
are obtained at least 24 hours apart and at least 48 hours after discontinuation of
antibiotics
- II: Anti-epidemic measures
 Report at once to local health authority any group of cases of acute
diarrheal disorder
 Investigate local food, water and milk supply with general sanitation
procedures
32. Escherihia coli infections
 E.coli infections
 Definition: Most E. coli strains do not cause disease, naturally living in the gut, ] but
virulent strains can cause gastroenteritis (diarrhoea), urinary tract infections, neonatal
meningitis, hemorrhagic colitis, and Crohn's disease.
 Aetiology & Mode of transmission
- Causative agent: E.coli (gran –ve facultative anaerobe) – O, H, K
- Reservoir host: see pic
- Incubation period: Healthy cattle are major reservoir for human infection
- Mode of transmission (primarily fecal-oral route via food and water):
 I: Transmission via food
o Ground beef, raw milk, lamb meat, salami, unpasteurized apple
cider
 II: Transmission via water
o Drinking and swimming in un-chlorinated water
 III: Direct person to person contact
o Diaper changing
o Improper station
o Day care & chronic adult care facilities
- Epidemiology
- Period of communicability
 Typically 1 week or less for adults but 3 weeks or so for one third of children

 Clinical features
- 70% of patients report bloody stools
- 30-60% of patients report vomiting
- Approx 5% develop HUS
  Diagnosis, Treatment & Prevention
- Diagnosis
 MacConkey agar (SMAC)
o Lactose-fermenting and beta-hemolytic
 Serology
- Treatment
 I: Assessment of dehydration and replacement of fluid and electrolytes
 II: Administration of antibiotics which shorten the cause of enterotoxigenic
E.coli (ETECT) in adults in endemic areas and in traveller’s diarrhea.
- Prevention
 I: Handwashing and improved sanitation and drinking water
o This is because transmission occurs via fecal contamination of food
and water supplies
 II: Thoroughly cooking meat and avoid cross contamination

33. Cholera
 Cholera
 Definition: Cholera is an infection of the small intestine by some strains of
the bacterium Vibrio cholerae. This infection was named by Robert Koch during the
Cholera outbreak during 1881-1896.
 Aetiology and mode of transmission
- Causative agent: Vibrio Cholerae (gram –ve bacillus bacteria)
- Reservoir: Found in estuaries and humans normal host
- Incubation = 24-48 hours
- Route of transmission: Cholera is transmitted by the fecal-oral route through
contaminated water & food. Infectious dose needs to be high for clinical features
thus direct contact is rare
- Epidemiology
 The pandemics originated in Asia with subsequent spread to other
continents.
 In 1992, Cholera spread firstly to Madras. This Bengal strain has now spread
throughout Bangladesh, India, and neighboring countries in Asia.
 Crowding & gathering of people during religious rituals (e.g. Muslims
pilgrimage to Mecca or Hindu swimming festivals in holy rivers) enhance the
spread of infection.
 Clinical features
- Sudden watery diarrhea (with very little fecal material), followed by vomiting with
abdominal cramps.
 Pathophysiology
- V.cholerae cause clinical disease by producing enterotoxin that promotes secretion
of fluid and electrolytes into lumen of the gut. The result is watery diarrhea. The
enterotoxin acts locally and does not invase intestinal wall. As a result, few WBC &
no RBC found in stool
- Fluid loss originates in the duodenum and upper jejunum; the ileum is less affected
 Diagnosis, Treatment and Prevention
- Diagnosis
 Rapid dipstick test to determine presence of V.cholerae
 Cholera can be cultured on special alkaline media like triple sugar agar or
TCBS agar.
 Stool and swab samples before AB’s are administered.
 Loss of electrolytes – sodium and potassium
- Treatment
 Primary goal: replenish fluid losses caused by vomiting and diarrhoea
 Fluid therapy – 2 phases
o I: Rehydration (ORS)
 Should be completed in 4 hours
o II: Maintenance
 Should replace ongoing losses & daily requirement
 Goal of drug therapy – Eradicate infection
o AB’s = doxycycline, tetracycline for adults
o Children = erythromycin AB’s
- Prevention
 I: Education on hygiene practices
  II: Provision of safe, uncontaminated, drinking water to the people
 III: Antibiotic prophylaxis to house-hold contacts of index cases
 IV: Vaccination against cholera to travellers to endemic countries & public
gatherings
34. Viral gastroenteritis
 Gastroenteritis
 Definition:

- Transmission: Poultry, contaminated water etc

 Aetiology
- Bacterial
 Developed world
o Campylobacter jejuni (via poultry) – most common
o Children: E.coli, Salmonella, Shigella and campylobacter
- Viral
 Rotavirus (most common), norovirus, adenovirus, astrovirus
- Parasitic
 Giardia lamblia (most common)
 Entamoeba histolytica etc
- Non-infectious
 i.e. NSAIDs, lactose, gluten, Chron’s disease
 Clinical features
- Symptoms
 Diarrhea +- vomiting
 Abdominal cramps
 Fever, fatigue, headache and muscle pain
 Dehydration is a common complication
 Repeated infections = malnutrition (common in children)
- Signs
 Viral infectious agent 12-72 hours after contracting the agent.
 If stool is bloody, most likely bacterial
 Diagnosis
- Clinical diagnosis
- Stool culture
 - Electrolytes and kidney function
- Dehydration test
 Mild dehydration (3-5%)
 Moderate dehydration (6-9%)
 Severe dehydration (>10%)
 Children: signs of moderate or severe dehydration are a
prolonged capillary refill, poor skin turgor, and abnormal
breathing.
 Other useful findings: sunken eyes, decreased activity, lack of
tears and dry mouth
 Treatment
- Oral rehydration
 Clear fluid or oral rehydration salts
 Safe water (adults: 1L/hr initially)
 IV fluids if severely dehydrated
- Nasogastric tube if vomiting
- Antimotility agents
 Loperamide, bismuth subsalicylates
o Avoid if severe pain or bloody diarrhoea
- Antibiotics
 Doxycycline, tetracycline etc
 Azithromycin in children

35. Brucellosis
 Brucellosis
 Definition: Brucellosis is a highly contagious zoonotic disease caused by ingestion of
unpasteurized milk or undercooked meat from infected animals, or close contact with
their secretions. It is also known as undulant fever, Malta fever, and Mediterranean
fever.
 Aetiology & Mode of transmission
- Causative agent: Brucella species are small, Gram-negative bacteria
- Reservoir host: Animals - Goats, sheep, pigs, cattle, dogs, sheep
- Incubation period: 2-4 weeks
- Mode of transmission:
 I: Consumption of unpasteurized milk and soft cheeses made from milk of
infected animals – primarily goats infected with B.melitensis
  II: Undercooked meat or close contact with their secretions
- Epidemiology
 Clinical features
- 1st stage of the disease
 Bacteremia occurs and leads to classic triad of:
o I: Undulant fevers
o II: Sweating (characteristic foul, moldy smell)
o III: Migratory arthralgia and myalgia
 GI symptoms common: Nausea, vomiting, diarrhoea, unintentional weight
loss, abdominal pain etc.
nd
- 2 stage if left untreated
 Can give origin to focalizations which usually occur in bones and joints
causing osteomyelitis or spondylodiscitis of the lumbar spine. Orchitis and
sacroilitis is common also.
 Diagnosis, Treatment & Prevention
- Diagnosis
 Diagnostic criteria
o I: Demonstration of the agent: blood cultures in tryptose broth,
bone marrow cultures
o II: ELISA antibody test against agent
o III: Histologic evidence of granulomatous hepatitis on hepatic biopsy
o IV: Radiologic alterations in infected vertebrae i.e. brucelic
spondylitis
 Definitive diagnosis
o Serological testing with positive culture
- Treatment
 Gold standard for adults:
o Daily IM injections of streptomycin 1g for 14 days
o Daily oral doxycycline 100mg twice daily for 45 days
- Prevention
 I: Vaccination
 II: Fastidious hygiene in producing raw milk products, or pasteurizing all milk
that is to be ingested by human beings
 III: Constant animal testing and surveillance using serological tests as well as
tests on milk

36. Leptospirosis
 Definition: Leptospirosis is a blood infection caused by the bacteria Leptospira. It is a
zoonotic disease. The bacteria can be found in ponds, rivers, puddles, sewers,
agricultural fields and moist soil
 Aetiology & Mode of transmission
- Causative agent: Leptospira spirochete gram -ve
- Reservoir host: Mammals. However, reptiles and cold-blooded animals such as
frogs, snakes, turtles, and toads have been shown to have the infection. Human
reservoir is unknown.
- Incubation period: 5-14 days on average
- Mode of transmission:
  Transmitted primarily through contact of skin with water, moist soil or
vegetation contaminated with the urine of infected animals.
- Epidemiology
 Clinical features (biphasic)
- 1st Phase (acute or leptospiremic):
 Lasts 5-7 days
nd
- 2 Phase (immune phase)
 Symptoms resolve as antibodies against bacteria are produced

 NOTE: They mainly affect the liver. They invade spaces

between hepatocytes, causing apoptosis. The damaged
hepatocytes and hepatocyte intercellular junctions cause leakage of
bile into the bloodstream, causing elevated levels of bilirubin,
resulting in jaundice.
 Diagnosis, Treatment & Prevention
- Diagnosis
 Diagnostic criteria (Faine’s criteria)
o A: Clinical findings
 Including shortness of breath and coughing up blood
o B: Epidemiological factors
o C: Lab findings and bacteriological data
 Includes ELISA and side agglutination
 Serological tests
o Indirect: ELISA, MAT
 Lab tests
o CBC
 High wbc count, low platelet count, low hb count,
thrombocytopenia
 ESR and CRP elevated
o Liver involved in leptospirosis
 Elevated transaminases
 Bilirubin levels elevated
o Kidneys involved in leptospirosis:
 Blood urea and creatinine levels elevated
 Elevated potassium secretion thus low potassium levels
  Urinalysis: Microscopic hematuria, wbc, presence of
proteins
- Treatment
 Most leptospiral cases resolve spontaneously
 Early initiation of antibiotics may prevent progression to severe cases
o I: IV benzylpenicillin
o II: IV Ceftriaxone
- Prevention
 I: Improving housing, infrastructure, and sanitation standards
 II: Proper use of PPE in occupational setting
 III: No vaccine suitable
 IV: Doxycycline
o Once a week as prophylaxis and effective in reducing rate of
leptospirosis infections amongst high risk individuals in flood-prone
areas.
37. Viral hepatitis A and E

 Definition: Hepatitis A (HAV) refers to an inflammatory condition of the liver caused by

HAV.
 Aetiology & Mode of transmission
- Causative agent: HAV (single stranded RNA virus)
- Reservoir host: Human hosts
- Incubation period: 2-6 weeks
- Mode of transmission:
 Fecal-oral route: Contaminated food
 IV drug users
 Sexual contact
- Epidemiology
 Clinical features
- Prodrome
 Mild flu-like symptoms of anorexia, nausea, vomiting, fatigue, malaise, low-
grade fever, myalgia and mild headache.
- Icteric phase
 Jaundice
 Icterus
 Abdominal pain
 Mild hepatosplenomegaly
 Palmar erythema
 Spider Naevi
 Diagnosis, Treatment & Prevention
 - Diagnosis
 Physical examination
o See signs and symptoms
 CBC and coagulation study
o Mild lymphocytosis
o PT usually remains normal
 Liver enzymes test
o Elevated ALT and AST (AST/ALT <1:1)
 Serology
o IgM antibody to HAV - Anti-HAV gM positive
 Ultrasonography
 Histopathology
- Treatment
 Acute cases:
o Therapy is generally supportive
o Initial therapy is bed rest
 Nausea and vomiting treated with antiemetics
 Dehydration managed with IV fluids
 Liver transplantation for chronic relapsing HAV infection has occurred in the
context of decompensation with good results;
- Prevention
 I: Vaccination
o Combined Hep A – Hep B vaccination
 II: Adequate diet
o Avoid alcohol and medications
 Hepatitis E
 Definition: Hepatitis E (HEV) refers to an inflammatory condition of the liver caused by
HEV.
 Aetiology & Mode of transmission
- Causative agent: HEV virus (RNA)
- Reservoir host: Human hosts
- Incubation period: 15 days – 60 days
- Mode of transmission:
 Oral-fecal route: Contaminated water within endemic areas or through
consumption of undercooked meat
- Epidemiology
 Clinical features (see Hep A)
 Diagnosis, Treatment & Prevention
- Diagnosis
 Serology: Anti-HEV antibody
 See hep A diagnosis - same
- Treatment
 Virus clears spontaneously so symptomatic treatment only
o Ribavirin: Improvement of liver enzymes and functions with patients
with severe acute hep E. However, contraindicated in pregnancy
(teratogenic)
- Prevention (see hep A)
  I: Vaccination for Hep E

38. Viral hepatitis B and D

 Definition: Hepatitis B is a worldwide healthcare problem, especially in developing
areas. An estimated one third of the global population has been infected with the
hepatitis B virus (HBV).
- Acute vs Chronic hepatitis
 Acute <6 months
 Chronic >6months
 Aetiology & Mode of transmission
- Causative agent: HBV virus (DNA virus)
- Reservoir host: Human host
- Incubation period: 1-6 months
- Mode of transmission:
 I: Body fluids i.e. blood (parenteral), semen and vaginal secretion
 II: IV drug abusers, Sexual and direct contact, perinatal transmission
- Epidemiology
 Clinical features
- Anicteric hepatitis is the predominant form of expression for this disease. The
majority of the patients are asymptomatic, but patients with anicteric hepatitis have
a greater tendency to develop chronic hepatitis.
- Symptomatic patients:
 Jaundice
 Icterus
 Poor apetite
 Vomiting and abdominal pain
 Diarrhoea
 Fatigue
 Low grade fever
 Myalgia
 Mild hepatosplenomegaly
 Right upper quadrant pain
 Palmar erythema
 Spider Naevi
 Diagnosis, Treatment & Prevention
- Diagnosis
 Physical examination
o See signs and symptoms
 CBC and coagulation study
o Mild lymphocytosis
o PT usually remains normal
 Liver enzymes test
o Elevated ALT and AST (AST/ALT <1:1 until cirrhosis develops)
 Serology
o IgM antibody to HBsAg - Anti-HBsAg IgM positive
 Ultrasonography
  Histopathology
- Treatment
 Partial hepatectomy
 Liver transplantation

- Prevention
 I: Vaccination
o Hep B vaacination (series of
3 injections)
 Hepatitis D
 Definition: Simultaneous infection with HBV and
HDV is known as coinfection and results in
fulminant liver failure in 1% of patients.
Complete clinical recovery and clearance of HBV
and HDC coinfection is the most common outcome.
39. Viral hepatitis C
 Definition: Hepatitis C (HCV) refers to an inflammatory condition of the liver caused by
HCV.
 Aetiology & Mode of transmission
- Causative agent: HCV (RNA virus)
- Reservoir host: Human hosts
- Incubation period:
- Mode of transmission:
 I: Parenteral exposures – infectious blood or body fluids that contain blood
o Injection drug use
o Receipt of donated blood, blood products, and organs
o Needlestick injuries
o Birth to HCV mother
- Epidemiology
 WHO estimates that 3 percent of the world population is infected with HCV
and around 170 million individuals are chronic carriers at risk of developing
liver cirrhosis and liver cancer
 Leading cause for need of liver transplantation
 Clinical features (see point 38)
 Diagnosis, Treatment & Prevention
- Diagnosis
 Physical examination
o See signs and symptoms
 CBC and coagulation study
o Mild lymphocytosis
o PT usually remains normal
 Liver enzymes test
o Elevated ALT and AST (AST/ALT <1:1 until cirrhosis develops)
  Serology
o Anti-HCV screening tests (enzyme immunoassays)
o PCR
 Ultrasonography
 Histopathology
- Treatment
 HCV is the leading cause of needing a liver transplantation

- Prevention

40. Infections caused by Coxsackie and echoviruses

 Enterovirus
 Definition and clinical features: Enterovirus is a single-strand RNA virus and are
classified by two groups:
- I: Group A
 Infects skin and mucous membranes, causing herpangina, acute
hemorrhagic conjunctivitis and HFM (hand, foot and mouth) disease)
- II: Group B
 Infects, heart, pleura, pancreas and liver, causing: pleurodynia,
myocarditis, pericarditis, hepatitis etc.
 Both group A and group B coxsackieviruses can cause
nonspecific febrile illnesses (fever, headache and fatigue),
rashes, upper respiratory tract disease, and aseptic meningitis.
 Transmission
- Fecal-oral route: feces & urine, flies, fingers etc
 Pathogenesis
- Invasion and replication in terminal ileum and pharynx which leads to
hematogenous and lymphatic dissemination of the virus.
 Diagnosis
- Clinical presentation
- PCR
 Treatment
- Supportive: Rehydration
 Echovirus
 Definition: Virus that resides in the GI tract
 Transmission:
 - I: Oral
- II: Droplet
 Six: Cough, sorethorat, flu, rash, croup - meningitidis

41. Polyomielitis
 Polyomyelitis
 Definition: Poliomyelitis, commonly shortened to polio, is an infectious disease caused
by the poliovirus
 Aetiology & Mode of transmission
- Causative agent: poliovirus (PV) - +ve sense RNA strand
- Reservoir host: Humans
- Incubation period: 6-20 days on average
- Mode of transmission:
 I: Fecal-oral route (intestinal): Ingestion of contaminated food or water
 II: Oral-oral route (oropharyngeal): Occasional i.e. saliva
- Epidemiology
 Clinical features
- Minor illness: Does not involve CNS
 Most patients are asymptomatic with normal immune symptom
- Major illness (involves CNS) – paralytic classified depending on site of paralysis
 Spinal (most common)
o Pathophysiology: Viral invasion of motor neurons of anterior horn
cells, which are responsible for movement of muscles, including
those of trunk, limbs and intercostals. Virus causes inflammation of
nerve cells leading to damage or destruction of motor neuron
ganglia. When spinal neurons die, Wallerian degeneration takes
place. With destruction of nerve cells, muscles no longer receive
signals from brain or spinal cord; without nerve stimulation, the
muscles atrophy, becoming weak, floppy and poorly controlled,
and finally paralyzed.
 Bulbar (uncommon) – Cranial nerves affected
o Pathophysiology: Virus invades and destroys nerves within bulbar
region of brain stem. The bulbar region is a white matter pathway
that connects cerebral cortex to brain stem. Destruction of these
nerves weakens muscles supplied by cranial nerves, producing
symptoms of encephalitis, and causes difficulty breathing, speaking
and swallowing. I.e. Glossopharyngeal nerve, vagus nerve,
accessory nerve.
 Bulbospinal (19% of all paralytic polio have bulbar and spinal symptoms)
o Pathophysiology: Virus affects cervical spinal cord (C3-C5) thus
causing paralysis of diaphragm (affecting phrenic nerve). This
causes difficulty in breathing and patients require support of a
ventilator. It may also lead to paralysis of arms and legs.
 Diagnosis, Treatment & Prevention
- Diagnosis
 Clinical features
  Lab diagnosis
o PCR
o Stool sample or swab of the pharynx
o CSF analysis – lumbar puncture/spinal tap
 Elevated wbc, mildly elevated protein level
 Detection of virus is diagnostic
- Treatment
 No cure for treatment, just supportive and symptomatic treatment
 Supportive measures include:
o Antibiotics to prevent infections in weakened muscles
o Analgesics for pain
o Rehabilitation, occupational therapy, braces
o Ventilators to support breathing
- Prevention
 I: Vaccination - IPV

42. Scarlet fever

 Scarlet fever
 Definition: Scarlet fever is an acute contagious disease resulting from a group A
streptococcus (group A strep) infection aka strep throat, also known as Streptococcus
pyogenes. The condition involves inflammation of the nose, throat and mouth, and a
characteristic red rash which gives it its name This disease is more prevalent in children
and is spread through contaminated droplets from an infected person.
 Aetiology & Mode of transmission
- Causative agent: Group A Streptococcus
- Reservoir host: Human hosts
- Incubation period: 2-5 days on average
- Mode of transmission:
 Transmission via contaminated droplets from an infected person – airborne
droplets
- Epidemiology
 Scarlet fever occurs equally in both males and females.
 Children are most commonly infected, typically between 5-15 year olds
 Peaks in winter months (colder climate)
 Clinical features
- Common classical symptoms
 Very red, sore throat
  Fever
 Red rash with sandpaper feel
 Bright red skin in underarm, elbow and groin creases
 Whitish coating on tongue or back of throat
 Strawberry toungue
 Headache, nausea and/or vomiting & body aches
 Swollen glands

 Diagnosis, Treatment & Prevention

- Diagnosis
 Clinical diagnosis
 Rapid antigen detection test and throat culture (confirmatory) for group A
- Treatment
 Penicillin or other antibiotics are used to treat scarlet fever
- Prevention
 I: Treatment should be immediate
o If left untreated, people can spread the bacteria for 10 to 21 days; in
some cases, they may spread the bacteria for weeks or months. If
treated, the ability to spread the illness to others usually ends after
24 hours.

43. Measels/Morbilli
 Measles
 Definition: Measles is a highly contagious infectious disease caused by measles virus.
Measles is the most contagious transmissible virus known
 Aetiology and mode of transmission
- Causative agent: Measles virus (single stranded, negative sense, enveloped RNA
virus)
- Reservoir host: Humans are the only natural hosts of the virus, and no other
animal reservoirs are known to exist
- Incubation period: 10-12 days on average
- Mode of transmission:
  Virus is spread via coughing and sneezing via close personal contact or
direct contact with secretions.
 Risk factors include: immunodeficiency caused by AIDs, organ or stem-cell
transplant etc.
- Epidemiology
 Even in countries where vaccination has been introduced, measles rate
remains high and is the leading cause of vaccine-preventable childhood
mortality.
 Clinical features
- Classic symptoms
 Four day fever (the 4 D’s)
 Cough, coryza (head cold, fever, sneezing) and conjunctivitis – the three C’s
 Koplik spots (small white spots commonly seen on inside of cheeks and
opposite molars.
o Recognizing these spots before person reaches maximum
infectiousness helps reduce spread of disease
- Characteristic measles rash
 Generalized red maculopapular rash that begins several days after fever
starts.
o Starts on the back of ears, then spreads to head and neck before
spreading to cover most of the body and often causes itching.
o Measles rash is said to stain changing color from red to dark brown,
before disappearing.
 NOTE: Takes three weeks for recovery
 Diagnosis, Treatment & Prevention
- Diagnosis
 Clinical diagnosis of measles
o Requires history of fever for at least three days or more with at least
one of the following:
 Cough, coryza, or conjunctivitis
 Koplik’s spot
 Lab testing (confirmatory)
o Indirect: Antibody test IgM
o Direct: PCR detection of measles virus RNA from throat, nasal or
urine culture
- Treatment
 No specific antiviral treatment, generally supportive
 Medications (supportive)
o Ibuprofen or paracetomal to reduce fever and main
o Vitamin A to reduce risk of blindness complication
- Prevention
 I: Vaccination of children
o 3-part vaccination (MMR) at least at 12 months, second dose
between 4-5
o The vaccine is generally not given before this age because such
infants respond inadequately to the vaccine due to an immature
immune system
  NOTE: Mothers who are immune pass antibodies to children still in
the womb but these antibodies generally lost within first 9 months
of life
44. Rubella
 Rubella
 Definition: Rubella aka German measles or three-day measles is an infection caused by
rubella virus.
 Aetiology and mode of transmissions
- Causative agent: Rubella virus (enveloped single stranded RNA)
- Reservoir host: Human hosts
- Incubation period: 12-23 days with 17 days being average. People most contagious
when rash is erupted.
- Route of transmission: Via respiratory route and replicates in nasopharynx and
lymphnodes. The virus is found in the blood 5-7 days after infection and spreads
throughout the body. It also has teratogenic properties leading to infection of fetus
and can stop them from developing or destroys them.
 NOTE: Highly contagious 7 days before to 7 days after rash appears
- Epidemiology
 Rubella occurs worldwide and tends to peak during spring in countries with
temperature climates. However, the introduction to rubella vaccine, the
rates have reduced i.e. in America, no endemic case has been observed
since February 2009.
 Clinical features
- Primary symptom of rubella symptom: Rash
 Appearance of rash on the face which spreads to the trunk and limbs and
usually fades after three days thus referred to as 3 day measles.
 Rash of rubella is typically pink or light red which causes itching. However,
there is NO STAINING (unlike measles)
- Other symptoms
 Low grade fever, swollen glands (sub-occipital and posterior cervical
lymphadenopathy), joint pains, headache and conjunctivitis
 Diagnosis, Treatment and Prevention
- Diagnosis
 Indirect: Antibody test IgM antibodies against rubella virus
 Direct: PCR
 Clinical features
o Characteristic rash confirms diagnosis
- Treatment
 No specific treatment for rubella, just supportive
 Supportive: Management of complications
- Prevention
 I: Vaccinations
o MMR vaccination (see measles point)
45. Varicella
 Varicella (chickenpox)
 Definition: Varicella zoster virus or varicella-zoster virus (VZV) is one of
eight herpesviruses known to infect humans. It causes chickenpox (varicella),
a disease most commonly affecting children, teens, and young adults.
 Aetiology & Mode of transmission
- Causative agent: VZV
- Reservoir host: Humans only
- Incubation period: 14-16 days on average
- Mode of transmission:
 I: Respiratory droplets: Through respiratory tract in which virus causes
lesions in successive crops
 II: Direct contact
- Epidemiology
 Clinical features
- I: Prodromal symptoms
 Nausea, loss of apetite, aching muscles and headache
 Followed by characteristic rash or oral sores, malaise, and low grade fever
o Rash begins as small red dots on face, scalp, torso, upper arms, and
legs which progresses to small bumps, blisters and pusules
- II: Blister stage
 Intense itching present
 Blisters occur on palms, soles, and genital area
 Commonly, visible evidencedevelops on oral cavity, tonsil areas in form of
small ulcers which can be painful, itchy or both.
- Dermatology notes:
 It starts as a crop of red papules. New lesions continue to appear for several
days within the distribution of the affected nerve, each blistering or
becoming pustular than crusting over.
o Rash erupts as clusters of small red patches  blisters 
blisters break open and slowly begin to dry and eventually
crust over
 Can lead to post-herpetic trigeminal neuralgia
 Ophthalmic division of trigeminal nerve involved hence can cause blindness.

 Diagnosis, Treatment & Prevention

- Diagnosis
 PCR: for analysis of strains and differentiate between HSV-1 and HSV-2
 ELISA: to detect antibodies to VZV
 Tzanck smear: For cell culture (will be able to see syncytia)
- Treatment
 Acyclovir, Famciclovir, Ganciclovir, Valganciclovir, Cidofovir, Foscarnet
- Prevention
 I: Vaccination
o Varicella Vaccine
 II: Hygiene measures
o Isolation of affected individuals.
 o Contagion is by exposure to respiratory droplets, or direct contact
with lesions within a period lasting from three days before onset of
rash to four days after onset of rash
46. Diphtheria
 Diphtheria
 Definition: Diphtheria is an air-borne infection caused by
the bacterium Corynebacterium diphtheriae.
 Aetiology & Mode of transmission
- Causative agent: C.Diphtheriae (Gram +ve bacillus)
- Reservoir host: Human hosts
- Incubation period: 2-5 days on average
- Mode of transmission:
 I: Typically and primarily air-borne when an infected individual cough or
sneezes.
 II: Contact with any lesions on the skin can also lead to transmission
 III: Indirect: I.e. surfaces
 NOTE: Diphtheria toxin is produced by C. diphtheriae only when
infected with a bacteriophage that integrates the toxin-encoding
genetic elements into the bacteria.
- Epidemiology
 Clinical features
- Classical features
 I: Sore throat with low-grade fever (fatigue, cyanosis, etc)
 II: Adherent membrane of tonsils, pharynx or nose
 III: Neck swelling is usually present in severe disease
 IV: Cutaneous diphtheria presents as infected skin lesions which lack
characteristic appearance
o Lymph nodes in neck may swell up to the point where breathing
becomes extremely difficult.

 Diagnosis, Treatment & Prevention

 - Diagnosis
 Diagnosis based on Clinical and laboratory criteria
 I: Clinical criteria
o Upper respiratory tract illness with sore throat
o Low grade fever
o Adherent, dense, grey pseudomembrane covering posterior aspect
of the pharynx, in severe cases, can extend to cover entire
tracheobronchial tree.
 II: Lab criteria
o Throat swab should be cultured on Loffler’s medium, a tellurite
plate, and a blood agar plate
o The typical gray-color of tellurium in the colony is a telltale
diagnostic criterion.
- Treatment
 In severe stage where breathing is difficult, Intubation or a tracheotomy may
be required.
o Anti-toxin can be administered
 Antibiotics used in patients or carriers to eradicate C.diphtheriae and
prevent transmission
o Metronidazole
o Erythromycin
- Prevention
 I: Vaccination
o Quinvaxem – Pentavalent vaccine
 DTP, DTaP, TdaP, Tdap, Td
47. Infectious mononucleosis
 Infectious mononucleosis (IM)
 Definition: IM also known as glandular fever, is an infection caused by Epstein-Barr
virus (EBV).
 Aetiology
- Causative agent: EBV
 Risk factors: AIDS, immunodeficiency or immunosuppression i.e. organ or
stem-cell transplant patients
 NOTE: minority caused by CMV
- Reservoir host: Human host
- Incubation period: 4-7 weeks (28-35 days)
- Mode of transmission:
 I: Transmission via intimate contact with body secretions, primarily
oropharyngeal secretions (saliva)
- Epidemiology
 Clinical features
- Classic presentation (triad)
 Fever, pharyngitis and lymphadenopathy
- Children (pre-puberty)
 Only produces flu-like symptoms, if any at all.
 Tends to mimic pharyngitis with or without tonsillitis
- Adolescents and young adults (post puberty)
  Fever = 14 days
 Sore throat = severe for 3-5 days and resolving next 7-10 days
 Swollen glands (lymphadenopathy) – Posterior cervical lymph nodes
 Other symptoms: Fatigue, headache, abdominal pain, nausea and vomiting
 Diagnosis, Treatment & Prevention
- Diagnosis
 Person’s age (highest risk at 10-30 years old)
 Medical and clinical history
 Physical examination – palpation of enlarged lymph nodes in neck or
enlarged spleen
 Heterophile antibody test
o Specific test but not particularly sensitive with a high false-negative
rate. Not recommended due to poor accuracy
o Works by agglutination of rbc from guinea pig, sheep and horse
 Serological test (MORE ACCURATE)
o Direct test: PCR
o Indirect: Antibody tests
- Treatment
 IM is usually self-limiting, so only symptomatic or supportive treatments
are advocated.
 Medical advice
o Rest and decrease risk of splenic rupture (especially in sports with
increased abdominal pressure), for at least 3-4 weeks of illness or
until enlargement as resolved.
 Paracetomal and NSAIDs for fever and pain, while corticosteroids to reduce
throat pain or enlarged tonsils (especially if there is AIRWAY OBSTRUCTION)
- Prevention
 I: Minimal to no contact
o Not sharing personal items or saliva with infected person
48. Influenza and other acute viral respiratory diseases
 Influenza
 Definition: Influenza, commonly known as "the flu", is an infectious disease caused by
an influenza virus. Symptoms can be mild to severe
 Aetiology & Mode of transmission
- Causative agent: Type A-D (4) – Negative sense RNA strands
 Type D is not known to infect humans
 Immunosuppressed patients = major risk factor
- Reservoir host: Birds are thought to be the main animal reservoirs
- Incubation period: 2 days on average (1-4 days)
- Mode of transmission:
 I: Airborne – droplets
o Spreading through the air from coughs or sneezes from relatively
short distances
o Contaminated surfaces i.e. then touching eyes, nose or mouth
- Epidemiology
 Clinical features
- I: Initial symptoms
  Chills, body aches with fever (38-39 degree Celsius).

- II: Mixture of symptoms between common cold and pneumonia (difficult to

distinguish between common cold and influenza
- III: EMERGENCY SIGNS & WARNINGS
 Dyspnoea, chest pain
 Dizziness and confusion
 Extreme vomiting
 Flu symptoms that improve and then relapse with high fever and severe
cough
 Cyanosis
 High fever and a rash
 Dehydration
 Inability to drink fluids
 Systemic symptoms are caused by the interferon and cytokine
response to the virus. Local symptoms result from epithelial cell
damage, including ciliated and mucus-secreting cells causing loss of
the primary defence systems.
 Diagnosis, Treatment & Prevention
- Diagnosis
 Rapid tests for flu
o Rapid molecular Assay
 Using URT specimen (mucus) i.e. nasal or nasopharyngeal
swab within 3-4 days of onset
 ELISA & PCR
 Primary Monkey cell culture

- Treatment
 Anti-influenza viral agents (neuraminidase inhibitors)
o Amantadine, rimantadine, Zanamivir, Oseltamivir
- Prevention
 I: Vaccination – Influenza vaccine
o High-risk groups i.e. preganant women, children <5 years old,
elderly, health care workers, immunosuppressed patients (HIV/AIDs,
organ transplant) etc.
 II: Infection control
o Social distancing 2m apart
o Isolation and quarantine when displaying symptoms
o Government contact tracing
 o Regular disinfection of surfaces and objects in both residential and
commercial places
o Personal hygiene: Washing hands, sanitizers when outside (alcohol)
regular showers etc

49. Pertussis
 Pertussis
 Definition: Whooping cough aka pertussis or the 100-day cough, is a highly contagious
bacterial disease caused by bordetella pertussis.
 Aetiology & Mode of transmission
- Causative agent: B.pertussis (gram –ve cocobacilli)
- Reservoir host: Human host (theories that it may be zoonotic not proven)
- Incubation period: 7-14 days on average
- Mode of transmission: It is an airborne disease (through droplets) that spreads
easily through the coughs and sneezes of an infected person.
 Adheres to ciliated epithelium in nasopharynx. After this, bacteria multiply
and spreads down to lungs (pertussis toxin)
- Epidemiology
 Worldwide, whooping cough affects around 16 million people yearly
 Clinical features
- Classical symptoms
 I: Paroxysmal cough, inspiratory whoop, and fainting, or vomiting after
coughing.
 II: Violent coughing can cause pleura to rupture, leading to pneumothorax
- Stages:
 I Catarrhal stage: Mild coughing, sneezing or runny nose
 II Paroxysmal stage: Cough into uncontrollable fits followed by high pitch
‘whoop’ sound.
 III Covalescent stage: Decrease in paroxysms of coughing
 Diagnosis, Treatment & Prevention
- Diagnosis
 Culture: Chocolate agar or Bordet-Gengou medium – Nasopharyngeal swabs
 PCR testing
- Treatment
 Antibiotics: Erythromycin, clarithryomycin, or azithromycin
- Prevention
 I: Vaccination
o Acellular Pertussis Vaccine (DTaP)
 National policy is to immunize against diphtheria, whooping
cough and tetanus simultaneously by administering 3 doses
(each dose 0.5ml) of hexacomponent vaccine (DTaP +IPV +
HiB +HepB) vaccine IM at 1 month interval, starting at 2
months old.

50. Mumps
 Mumps
  Definition: Mumps is a viral disease caused by the mumps virus.
 Aetiology and mode of transmission
- Causative agent: Mumps virus (-ve sense RNA virus)
- Reservoir host: Human hosts
- Incubation period = 16-18 days on average
- Route of transmission:
 Person to person via respiratory secretions i.e. Saliva from infected person
when they cough or sneeze of which droplets will aerosolize
 Person infected with mumps is contagious from around 7 days before onset
of symptoms until 8 days after symptoms start.
- Epidemiology
 In USA, few hundred thousand cases occur annually
 Countries that have low immunization rates may see an increase in cases
among older age groups and thus worse outcomes
 Clinical features
- Preceded by set of prodromal symptoms
 I: Low-grade fever, Headache and feeling generally unwell
 II: Followed by progressive swelling of one or both parotid glands which
usually last a week.
o Other symptoms: dry mouth, sore face and/or ears, and difficulty
speaking
- Complications
 Testicular inflammation, ovarian inflammation, deafness, brain inflammation
 Diagnosis, Treatment and Prevention
- Diagnosis
 During outbreak:
o Diagnosis can be made by determining recent exposure and
parotitis. However in cases of low incidence, there are other causes
of parotitis.
 Physical examination:
o Clinical features, i.e. swollen glands
 Saliva swab or blood test with PCR (not required, clinical is enough)
- Treatment
 Treatment not curative but only supportive
 Supportive treatment includes:
o I: Ice or heat to affected neck/testicular area by acetaminophen for
pain relief
o II: Warm saltwater gargles, soft foods, and extra fluids to help
relieve symptoms
- Prevention
 I:Vaccination
o MMR vaccine
51. Meningococcal infections
 Meningococcal infections
 Definition: Bacterial meningitis most commonly results from dissemination of
microorganisms from a distant site of infection. The most common pathogenic agents
are: H.influenzae, Streptococcus pneumonia, and N.Meningitidis.
  Aetiology & Mode of transmission
- Causative agents: H.influenzae, S.pneumoniae, N.Meningitidis
- Reservoir host: Human hosts
- Incubation period: 2-10 days 
- Route of transmission: The disease spreads mainly by droplet infection. The portal
of entry is the nasopharynx.
 Newborns and children are at increased risk or immunosuppressed i.e. AIDS
patients
- Epidemiology
 Clinical features
 Diagnosis, Treatment and Prevention
- Diagnosis
 Spinal tap for collection of CSF – Culture for bacteria
o Low glucose level with increased WBC count and increased protein
- Treatment
 Antibiotics – Penicillin is drug of hoice
o If allergic, give chloramphenicol
 NOTE: AB’s have no effect on epidemiological pattern, it just reduces
fatality.
- Prevention
 I: Carriers
o Pencillin does not eradicate the carrier state, more powerful
antibiotics required i.e. Rifampicin for eradication of the carrier
state

52. Legionellosis
 Legionellosis
 Definition: Legionnaires' disease, also known as legionellosis, is a form of atypical
pneumonia caused by any type of Legionella bacteria
 Risk factors: Smokers, COPD, immunocompromised people (middle aged-
older people most often)
 Aetiology & Mode of transmission
- Causative agent: Over 90% of cases of Legionnaires' disease are caused
by Legionella pneumophila.
- Reservoir host: Thrives in aquative systems, where it is established within amoebae
as they survive in water as intracellular parasites.
 The bacteria grow best at warm temperatures[4] and thrive at water
temperatures between 25 and 45 °C
- Incubation period: 2-10 days on average
- Mode of transmission:
 I: Breathing in aerosolized water or soil contaminated with legionella
bacteria
o NOT TRANSMITTED FROM PERSON TO PERSON
- Epidemiology
 Clinical features
- General symptoms
 Fever, chills
 Cough which may be dry or produce sputum (may be bloody sputum)
  50% complain of GI symptoms and neurological symptoms
o GI: Diarrhea, vomiting, loss of apetite
o Neurological: Confusion and impaired cognition, ataxia
 Diagnosis, Treatment & Prevention
- Diagnosis
 Urine antigen test (using coughed up mucus)
 Culture (from sputum or other resp samples)
o Charcoal yeast extract with iron and cysteine (CYE agar)
- Treatment
 I: Antibiotics
o Macrolides, tetracyclines, ketolides and quinolones
o Current treatments include quinolones: Levofloxacin etc
- Prevention
 I: Systematic water safety plan with sanitation
o Disinfect the system with high head or chemical bicide and use
chlorination when appropriate
o Prevent build-up of biofilm
o Keep water temperature above or below ranges where bacteria
thrive

53. Mediterranean spotted fever

 Mediterranean spotted fever (MSF)
 Definition: MSF is a tick-borne disease and a fever caused by Rickettsia Conorri. It was
first described a century ago as a disease that caused high fever and spots.
 Aetiology and mode of transmission
- Causative agent: Rickettsia Conorri
- Vector: Dog tick Rh.Sanguineus
- Reservoir hosts: Dogs
- Incubation period = 7 days
- Route of transmission: Transmission via dog tick R.Sanguineus (blood meal) of dog
which carries agent R.conorri. Then the tick takes a blood meal on a human.
- Epidemiology
 MSF is endemic to the Mediterranean area, including northern Africa and
southern Europe
 Clinical features
- Location of the bite
 Forms black, ulcerous crust
- Acute onset of High Fever (MAIN)
- Chills, muscular and articular pains, severe headache, and photophobia
- Around third day of illness, widespread rash appears, first macular, and then
maculopapular
 Unlike the rash in other rickettsial diseases, the rash appears first on
the extremities (ankles and wrist), moves centripetally and involves
the rest of the body. The clinical syndrome may be confused with
atypical measles.
 Diagnosis, Treatment and Prevention
- Diagnosis
  Serology
o Weil-Felix test, ELISA or immunofluorescence assays of primary
lesion

- Treatment
 Broad spectrum antibiotics i.e. doxycycline
- Prevention (Prophylaxis)
 I: Known tick infested areas should be avoided and use adequate PPE if
necessary
 II: Daily inspection of body for ticks for those who are exposed to risk of
infection
 III: Disinfection of dogs will minimise tick population

54. Q-fever
 Q-fever
 Definition: Q fever is a highly infectious zoonotic disease with worldwide distribution. It
occurs mainly in people associated with sheep, goats, cattle or other domestic animals.
 Aetiology and Mode of transmission
- Causative agent: Coxiella burnetti (obligate intracellular paraise)
- Vector: C.burnetii found in ticks which act as vectors aswell as reservoir
- Normal reservoir: Cattle, goats, ticks and some wild animals
- Incubation period = Usually 2-3 weeks
- Route of transmission:
 I: Inhalation of infected dust from soil previously contaminated by urine or
faeces of diseased animals. In most countries, the respiratory route is
regarded as most important.
 II: Contamination also occurs through direct contact with infected animals
 III: Raw milk from infected cows contains organisms and may be responsible
for some cases. Direct transmission by blood or marrow transfusion has
been reported.
o I.e. people who help animals give birth have a higher chance of
contracting the disease.

- Epidemiology
  Clinical features
- Flu-like features: self limiting
- Atypical pneumonia progression (30-50% of cases)
- Skin rash (10%)
- Non-productive cough, chest pain
- ARDS, Endocarditis and Hepatitis possible (RARE)
- Death (1-2%)
 Diagnosis, Treatment and Prevention
- Diagnosis
 Serological test
o Indirect test – Antibody test
 Echocardiography
o If there’s suspected endocarditis
 Liver enzymes (ALT, AST)
o Elevation if there’s suspected Q fever hepatitis but confirmation
only via liver biopsy
- Treatment
 Doxycycline
 Chronic disease = long course 2-3 years of medication
 Long lasting immunity (possibly life long)
- Prevention
 I: Vaccination
o No commercially available vaccine except for Australia and some
other countries
 II: Pasteurization
o At 62.7 degrees for 30 seconds
 III: Eradication (NOT POSSIBLE)
o Too many reservoirs
o Constant exposure
o Stability of antigen in environment

55. Lime disease

 Lyme disease
 Definition: Tick-borne infection caused by Borrelia genus (gram-ve coiled
spirochete). The tick being Ixodes scapularis (vector).
 Aetiology & Mode of transmission
- Route of transmission: Borrelia bugdorferi via vector Ixodes scapularis with
blood meal
- Normal Reservoirs = Wild rodents maintain eenzootic transmission cycle. Deers
serve as important mammalian maintenance hosts for vector tick species.
- Vectors of Lyme disease = Ixodes ticks
 Signs and symptoms
- Stage I (early localised Lyme disease)
 7-14 days after tick bite
 Erythema chronicum migrans (PINK MACULE) = red ring around bite
site (warm, painless and EM is often only symptom and self-limiting.
- Stage II (early disseminated Lyme disease)
  3-10 weeks after bite
 Migratory arthralgia (Lyme disease)
 Cutaneous manifestations: multiple erythema migrans lesions
- Stage III (late lyme disease)
 Symptoms develop months to years after initial infection
 Chronic lyme arthritis (typically large in joints)
 Late neuroborreliosis

 Diagnosis, Treatment and Prevention

- Diagnosis
 Clinical findings
 Serological testing (ELISA and western Blot)
o Direct: Culturing B.burgdorferi
o Indirect: IgG and IgM antibodies against Borrelia
o PCR
o CSF testing = signs for lymphocytic meningitis
- Treatment
 Localised lyme disease
o First-line antibiotics (doxycycline, amoxicillin)
 Disseminated Lyme disease
o Same as above.
o Hospitalise patient, IV antibiotics

- Prevention
 Prevent tick bites
o I: Wearing protective clothing and cover arms and legs
o II: Use DEET-based insect repellents
o III: Pesticides to eliminate and reduce tick numbers
 .
56. Crimean-Congo hemorrhagic fever (CCHF)
 Crimean-Congo Hemorrhagic fever (CCHF)
 Definition: Crimean-Congo Hemorrhagic fever (CCHF) is a viral haemorrhagic fever
transmitted by ticks.
 - The disease was first described in the Crimea in 1944 and given its name. In
1969, it was recognized the pathogen caused CCHF was same as the one
responsible for the illness in congo, hence the dual name.
 Aetiology & Mode of transmission
- Causative agent: The Crimean-Congo hemorrhagic fever orthonairovirus 
- Vector: Ticks (Hyalomma, Argas reflexus, Rh.Sanguineus etc)
- Reservoir host: Ticks (both reservoir and vector)
- Incubation period: Usually 1 to 3 days, with a range of 1–12 days.
- Route of transmission: CCHF spreads to humans either by tick-bites, or through
contact with viraemic animal tissues during and immediately post-slaughter
- Epidemiology
 Threat to public health service due to epidemic potential with high case
fatality ration (10-40%).
 Potential for nosocomial outbreaks and difficulties in treatment and
prevention
 CCHF is an endemic in all Africa, Balkans, Middle east and South Asia
 Clinical features
- Severe form of hemorrhagic fever
- I: After 1-3 days incubation period following a tick bite or 5-6 days after
exposure to infected blood or tissues, flu-like symptoms appear, which may
resolve after one week.
- II: In upto 75% cases, signs of bleeding can appear within 3-5 days of onset of
illness
- III: In cases of bad containment, the following can occur:
 Mood instability, agitation, throat petechiae, Nosebleeds, vomiting, and
black stools
 The liver becomes swollen and painful and DIC may occur aswell as
acute kidney failure, shock and ARDS.
 Diagnosis, Treatment and Prevention
- Diagnosis
 PCR
 Antibody test against virus
- Treatment
 Primarily supportive, not curative
o Ribavirin is effective in vitro
- Prevention
 I: Vaccination
o Mouse-brain derived vaccine against CCHF
o No safe and effective vaccine available
 II: Elimination or reduction of ticks
o Acaricides (chemicals to kill ticks) in livestock production
facilities
 III: PPE (especially in endemic areas)
o Adequate PPE and regular examination of clothing and skin for
ticks in high infested tick areas.
o Repellents on the skin (DEET)
o Wearing of PPE to avoid contact with dead infected tissue
  IV: Epidemiological responsibility
o Report to local health authority
o Isolation: Blood and body fluid precautions
o Concurrent disinfection: Bloody discharge are infective,
decontaminate by heart or chlorine disinfectants
o Track and trace

57. Haemorrhagic fever with renal syndrome

 Haemorrhagic fever with renal syndrome
 Definition: This is an infectious (zoonotic) disease (with natural source) caused by
Hantaan virus, characterised by fever, haemorrhage, proteinuria, and acute renal
shock
 Aetiology and mode of transmission
- Causative agent: Hantaan virus
- Reservoir host: Rodents i.e. field mouse (Apodemus agraricus)
- Incubation period = 7-14 days
- Route of transmission
 I: Foodborne transmission: Via oral mucosa, eat contaminated food –
containing excretion or secretion of rats or mouse.
 II: Airborne transmission: Via inhalation of aerosol contaminated with
virus
 III: Arthropod borne transmission: Via rats mite, red mite etc
- Epidemiology
 Clinical features
- Classical features
 Pyrexia (39-40 degrees c), orbital pain, abdominal pain, chills, myalgia,
bradycardia
 Hyperemia and haemorrhage, epistaxis, hematuria
- Classical renal features and association
 Hypotension
 Oliguria - <500ml/24h
 Anuria <50ml/24h
 Uremia, metabolic acidosis, imabalance of fluids
 Proteinuria, hematuria
- Clinical types (V)
 Mild type
 Moderate
 Severe
 Very serious
 Atypical type

 Diagnosis, Treatment and Prevention

- Diagnosis
 Serological tests
o Direct test – PCR
o Indirect – Antibody test via ELISA, western blot etc, antigen test
 Epidemiological tests
 o Place, season, history of contacting rats or excretion and
secretion of rats
 Renal tests
o eGFR
o Creatinine test
o Albumin/creatinine ratio
o Urine test
- Treatment
 Treatment involves supportive therapy including renal dialysis.
- Prevention
 I: Rodent control
 II: Vaccination
o Hantaan virus type 1 vaccine
o Hantaan virus type 2 vaccine
58. Plague
 Plague
 Definition: Plague is an infectious disease caused by the bacterium Yersinia pestis
 Aetiology (see mode of transmission)
- Yersinia pestis
 Gram –ve, facultative anaerobic bacillus. Optimal temperature = 28 degrees
Celsius
 Growth in sheep blood agar
 Mode of transmission
- Natural reservoir = Wild rodents are the natural reservoirs of plague.
- Human plague is most frequently contracted from
 I: Bite of infected flea
 II: Occasionally by direct contact with tissues of infected animal
 III: Droplet infection from cases of pneumonic plague
- Vectors of transmission
 Most common and efficient vector of plague = rat flea
o Flea requires the Y.pestis organisms during blood meal from
infected rodents.
o While the flea is feeding on human host, the flea regurgitates some
of the plague bacilii into the wound (inoculation)
 Epidemiology
- Three documented pandemics of plague have been responsible for the death of
hundreds of millions of people. Today sporadic infections still occur
 Clinical features
- Septicemic plague
- Bubonic plague
- Pneumonic plague
 NOTE: General symptoms of plague include fever, chills,
headaches, and nausea. Many people experience swelling in their
lymph nodes if they have bubonic plague. For those with
pneumonic plague, symptoms may (or may not) include a cough,
pain in the chest, and haemoptysis

 Prevention and control (quarantine) – Plague preventative measures

- I: Hospitalization and strict isolation
 - II: Antibiotics – Streptomycin and tetracycline are highly effective
- III: Vaccination: Formalin-killed vaccine available for those at high risk
- IV: Continuous mass destruction and elimination of rodents is a very important
plague-preventative measure
- V: Protect health workers and find infected people to isolate as well as finding the
source

59. Tularemia
 Tularemia
 Definition: Tularemia, also known as rabbit fever, is an infectious disease caused by
the bacterium Francisella tularensis
 Aetiology
- Francisella tularensis
 Mode of transmission
- Incubation period = 1-14 days with most human infections becoming apparent after
three to give days
- Route of transmission: F.tularensis typically spread by ticks, deer flies, and contact
with infected animals
- Most common reservoir hosts:  Rodents, rabbits, and hares often serve as reservoir
hosts
- Most common vectors: Arthropod vectors
 Epidemiology
- Tularemia most common in Northern hemisphere (including North America, parts of
Europe and Asia)
 Clinical features
- Six characteristic clinical variants UGOPOT
 I: Ulceroglandular (75% most common)
 II: Glandular
 III: Oropharyngeal
 IV: Pneumonic
 V: Oculoglandular
 VI: Typhoidal
 - Clinical signs include high fever, lethargy, loss of appetite, signs of sepsis, and
possibly death
 Diagnosis, Treatment and Prevention
- Diagnosis
 F.tularensis in Lab isolation requires Buffered charcoal yeast extract agar.
 It cannot be isolated in routine culture media due to need for sulfhydryl
group donors (i.e. cysteine)
- Treatment
 If infection occurs or suspected, treatment is antibiotics (Streptomycin or
gentamicin)
- Prevention
 No safe, available, approved vaccines against tularemia
 Optimal preventative practices include limiting direct exposure when
handling potentially infected animals by wearing adequate PPE.
60. Anthrax
 Anthrax
 Definition: Bacillus anthracis is a causative agent of Anthrax. Anthrax is a non-invasive
disease in which humans are infected by direct contact with contaminated material.
Spores remain viable for extremely long periods of time (up to 50 years).
 Aetiology & Mode of transmission
- Bacillus anthracis is the causative agent
- Incubation period = Symptoms appear usually within one week of exposure
- Route of transmission
 I: Eating undercooked meat (GI anthrax)
 II: Handling animals thus through skin (Cutaneous anthrax) i.e. via cut or
wound (break in the skin)
 III: Inhalation of infectious sporulated droplets (inhalation anthrax) –
Inhaling bacteria or bacterial spores
 NOTE: B.anthracis produces three exotoxins that mediate cell entry
(Edema factor, lethal toxin, protective antigen). It contains an
antiphagocytic capsule that does not allow phagosome-lysosome
fusion thus multiplies and causes tissue necrosis.
 Clinical features
- Cutaneous Anthrax (most common and mildest form)
 Most common and mildest form of the disease
 Itchy raised area like an insect bite appears. Within one or two days,
inflammation occurs and blister forms around a black centre of necrotic
tissue.
 Other symptoms: Shivering, chills and can lead to blood poisoning if bacteria
spread to lymph glands which is fatal.
- Inhalation or Pulmonary Anthrax (Very rare and can be fatal)
 First signs: Cold or flu-like symptoms (fever, fatigue, and headache)
 It then can progress onto bronchitis, pneumonia and state of shock.
- Intestinal Anthrax (Very rare and can be fatal)
 First signs: Nausea, vomiting, loss of apetitie, fever, and abdominal pain
 Progression to inflammation and ulcers of stomach and intestine, vomiting
of blood, and bloody diarrhoea
  Diagnosis, Treatment and Prevention
- Diagnosis
 Direct: Microbiological culture and preliminary microscopic identification
(gram-positive, nonmotile rods)
 Indirect: Antibody test - colonial (nonhemolytic, adherent colonies)
morphology; confirmed by demonstrating a positive direct fluorescent
antibody test.
 PCR, ELISA
- Treatment
 Most B.anthracis strains sensitive to broad range of antibiotics (Penicillin,
ciprofloxacin, or doxycycline)
- Prevention
 Vaccination
o Vaccination of animal herds and people in endemic areas can
control disease.
o Currently only a-cellular (USA, UK) and live spore (Russia) varieties
available.
61. Tetanus
 Tetanus
 Definition: Tetanus is a disease of the nervous system characterized by persistent tonic
spasm, with violent brief exacerbations. The spasm almost always commences in the
muscles of the neck and jaw, causing closure of the jaws (trismus, lockjaw) and involves
the muscles of trunk more than those of the limbs. It is always acute in onset, and a very
large proportion of those affected die.
 Aetiology (see mode of transmission)
- Clostridium tetani
 Anaerobic gram-positive, spore-forming bacteria.
 Spores found in soil, dust, animal feces
 Multiple toxins produced with growth of bacteria (tetanospasmin)
- Most common cause: infection of theumbilical stump after birth, the first
symptom being seen on 7th day.
 Mode of transmission
- Reservoir: Soil and intestines of animals and humans
- Route of transmission:
 Infection is acquired by contamination of wound with tetanus spores.
o I.e. skin abrasion, trivial pin prick, skin abrasion, unsterile division of
umbilical cord, puncture wounds, animal bites and stings, unsterile
surgery etc.
 NOTE: NOT CONTAGIOUS.
 Epidemiology
- Global incidence: 1 million cases annually approx.
 Neonatal tetanus accounts for about half of the tetanus deaths in
developing nations.
 Neonatal mortality in Bangladesh 112 out of 330 cases are due to tetanus.
- Up to one-third of neonatal tetanus cases are in children born to mothers of
previously afflicted child, highlighting failure to immunize as a major cause of
 tetanus thus immunization programs clearly reduce deaths caused by tetanus.
- Neonatal tetanus is on the decline in Europe and very rare now due to immunization
schedule.
 Clinical features
- Incubation period = 8 days
- Four clinical forms
 Local (uncommon)
 Cephalic (rare)
 Neonatal
 Generalized (most common)
o GT: Descending symptoms of trismus, difficulty swallowing, muscle
rigidity and spasms
- Spasms continue for 3-4 weeks; complete recovery and may take months
 Complications
- Laryngospasm, aspiration, fractures, death
 Preventions
- Vaccinations (immunization schedules)
 Diphtheria and tetanus (DT) vaccine
 Diphtheria, tetanus, and pertussis (DTaP) vaccines
 Tetanus and diphtheria (Td) vaccines
 Tetanus, diphtheria, and pertussis (Tdap) vaccine

62. Rabies
 Rabies
 Definition: Rabies is an acute viral infectious disease of mammals, especially carnivores.
It is characterized by CNS pathology (inflammation of the brain) leading to hyperactivity
or paralysis, and finally coma and death.
 Aetiology (see mode of transmission)
- The rhabdoviruses (Greek rhabdos—rod) are a group of about 140 RNA viruses of
plants, arthropods, fish, reptiles, birds, and mammals. Rabies and its five related
viruses constitute the genus Lyssavirus.
- Main route: Rabid Dog bite
 Mode of transmission
- Main reservoir = Saliva of Domestic dogs (to much lesser extent, cats) are the main
reservoir of urban rabies which is responsible for 90% of human cases worldwide
- Incubation period = 2-3 months typically but can vary from 1 week to 1 year
- Main route of transmission:
 Intact skin is an adequate barrier to the infection, but broken skin and intact
mucosa can admit the virus. Human infections usually result from
inoculation of virus-laden saliva through the skin by the bite of a rabid dog
or other mammals.
 Scratches, abrasions, and other wounds can be contaminated with infected
saliva.
- Other unusual rare routes:
 Inhalation: Densely populated with bats in caves which create an aerosol of
rabies virus from infected nasal secretions and possibly urine.
 Vaccine induced rabies: i.e. 18 people developed paralytic rabies in Brazile
after inoculation of inactivated virus
 Epidemiology
- In 2010, an estimated 26,000 people died from rabies, down from 54,000 in 1990.
The majority of the deaths occurred in Asia and Africa.
- India has the highest rate of human rabies in the world, primarily because of stray
dogs, whose number has greatly increased since a 2001 law forbade the killing of
dogs.
 Elimination of stray dogs and vaccination programs can reduce incidence
human rabies.
- USA has a fairly low rate and generally come from inhalation (bats)
 Clinical features
- 1st symptoms: Fever and headache
- 2nd stage symptoms:
 slight partial paralysis, anxiety, insomnia, confusion, agitation, abnormal
behavior, paranoia, terror, and hallucinations.
o Hyperactivity or paralysis
- Fear of water
 Diagnosis, Treatment & Prevention
- Diagnosis:
 Immunofluorescence of acetone-fixed brain or spinal cord impression
smears: can be confirmed in few hours
 - Pre-exposure prophylaxis
 In rabies endemic areas, those at high risk of exposure should be given pre-
exposure vaccinations.
 Vaccination:
o Only tissue culture vaccines are safe enough to use for pre-exposure
prophylaxis.
o Three doses are given on days 0,7, and 28 either iM into deltoid. A
single booster given 1 year later to produce sustained immunity for
5-8 years
- Post-exposure propylaxis
 Wound care:
o Cleaning wound as soon as possible after bite or contact with rabid
animal. Wound should be scrubbed with soap or detergent and
generously rinsed under running tap for at least 5 minutes.
o Foreign material and dead tissue should be removed under
anesthesia.
o Wound should be irrigated with viricidal agent
 Vaccination (tissue culture)
o PVRV (Purified verocell rabies vaccine)

63. HIV infection and AIDS

 Acquired immunodeficiency syndrome (AIDS)
 Definition: Before we discovered HIV, AIDS was a collection of symptoms of
unknown etiology. Once the etiology is known, it becomes a disease. But the name
stuck, so we still talk about AIDS.
 Aetiopathogenesis:
- Pathogenesis:
 AIDS is a retroviral disease caused by HIV. It is characterised by
depletion of CD4+ T-lymphocytes (T-helpers) and profound
immunosuppression leading to opportunistic infections, malignancies,
weight loss and degenerative CNS processes.
 The virus works by entering a CD4 cell and replicating. It integrates the
proviral genome into the host, triggering viral gene expression, creating
more copies of the virus to continue on to infecting more of the
organisms T-cells causing CD4+ T-cell lysis..
- As the infection progresses, it interferes more and more with the immune
system, making the person much more susceptible to common infections, like
tuberculosis, as well as opportunistic infections and tumors (i.e. hodgkin
lymphoma, kaposi tumours) that do not usually affect people who have working
immune systems. The late symptoms of the infection are referred to as AIDS.
 Route transmission:
- AIDS is commonly transmitted via sexual intercourse (MSM, multiple partners),
blood products, insemination from an infected sperm donor.
 Others include: sharing contaminated needles (IV drug users),
transplantation of infected tissues and organs, perinatal transmission
(mother to fetus)
 Epidemiology
- HIV is a global pandemic. As of 2016, approximately 36.7 million people
worldwide have HIV with an annueal increase of about 1.8 million
 Period of communicability
- Not known but it is thought that it is high during onset of infection and extends
throughout life.
 Clinical features
- I: Primar y HIV syndrome – Mononucleosis-like, cold or flu-like symptoms may
occur 6 to 12 weeks after infection
 Fever, rash, headache, lymphadenopathy, fatigue, diarrhea, sore throat,
neurologic manifestations
 Can be Asymptomatic
- II: Clinical Latency period
 HIV continues to reproduce, CD4 gradually declines from normal value
of 500-1200. Once CD4 drops below 500, HIV infected person at risk for
opportunistic infections.
 Opportunistic infections include:
o Oral candidiasis
o Persistent Herpes-zoster infection
o Kaposi’s sarcoma
o Oral hairy leukoplakia
- III: Advanced HIV disease (CD4<200)
 If CD4 count drops below 50:
o Mycobacterium tuberculosis
o Cytomegalovirus infections
o Lymphoma
o Dementia
 Diagnosis, Treatment and Prevention
- Diagnosis:
  Serology ELISA: Seroconvert, HIV-RNA or p-24 antigen.
 PCR
- Treatment
 There is currently no cure, nor an effective HIV vaccine. Treatment
consists of highly active antiretroviral therapy (HAART) which slows
progression of the disease i.e. Zidovudine.
- Prevention
 I: Contraception (for sexual contact)
 II: Education (public health and school)
 III: Adequate PPE (i.e. when handling sharp equipment)

64. Tropical medicine: basic medical and social problems in countries with tropical climate

Tropical and subtropical regions are particularly vulnerable to the spread of infectious

diseases – the perfect storm arising from the intersection of poor sanitation, lack of education,
inadequate resources and infrastructure for healthcare, and specific climates and environments.
At the root of this all is poverty

Malaria Q69
Q-Fever – Q54
Lyme disease Q55
Crimean congo fever – Q56
Leishmaniasis Q70 – I.e. Brazil, Ethiopia, India
Rabies Q62 – Africa, Asia
Yellow and Dengue Q65 – Africa
Echinocococcosis Q86 – Philippines, Cambodia etc
65. Yellow fever. Dengue fever
 Yellow fever
 Definition: Yellow fever is a viral disease of typically short duration caused by yellow
fever virus.
 Aetiology & Mode of transmission
- Causative agent: Yellow fever virus
- Reservoir host: Monkeys are main reservoir
- Vectors: Mosquito Aedes aegypti
- Incubation period: 3-6 days
- Mode of transmission:
 I: Vector-borne mosquito bite
- Epidemiology
 Yellow fever occurs in urban and rural areas of Africa and central South
America. In jungle and forest areas
 Clinical features
- Most cases
  Mild infection with fever, headache, chills, back pain, fatigue, loss of
apetitie, muscle pain, nausea, and vomiting.
- 15% enter second toxic phase
 Recurring fever
 Jaundice due to liver damage, as well as abdominal pain
 Bleeding in the mouth, nose, the eyes and GI tract cuase vomit containing
blood
 Diagnosis, Treatment & Prevention
- Diagnosis
 Reverse transcriptase PCR
 Serological test: Enzyme-linked immunosorbent assay
 Liver biopsy: can verify inflammation and necrosis of hepatocytes and
detect viral antigens
- Treatment
 No cure is known for yellow fever
- Prevention
 I: Vaccination
o 1 dose can protect for life
 II: Adequate use of PPE and insect repellent (DEET) .
 Dengue fever
 Definition: Dengue fever is a mosquito-borne tropical disease caused by the dengue
virus
 Aetiology & Mode of transmission
- Causative agent: Dengue fever virus (DENV) is an RNA virus of the family
- Reservoir host: Monkeys act as reservoir host
- Vector: Mosquito Aedes aegypti
- Incubation period: 4-7 days on average
- Mode of transmission:
 I: Vector-borne mosquito bite
- Epidemiology
 Clinical features (3 stages)
- Typically, people infected with dengue virus are asymptomatic (80%) or have only
mild symptoms such as an uncomplicated fever.
- I: Febrile
- II: Critical
 During this period, there is leakage of plasma from the blood vessels,
typically lasting one to two days. This may result in fluid accumulation in
the chest and abdominal cavity as well as depletion of fluid from the
circulation and decreased blood supply to vital organs
- III: Recovery
 Resorption of the leaked fluid into the bloodstream. This usually lasts two
to three days.
 Diagnosis, Treatment & Prevention
- Diagnosis
 Typically made on clinical diagnosis and physical examinations, especially in
endemic areas.
o The diagnosis should be considered in anyone who develops a fever
within two weeks of being in the tropics or subtropics
 Diagnosis is based on the findings of fever plus two of the
following: nausea and vomiting, rash, generalized pains, low white blood
cell count, positive tourniquet test, or any warning sign (see table) in
someone who lives in an endemic area

- Treatment
 No specific antiviral drugs for dengue.
 Treatment is mainly supportive
o In children with shock due to dengue, rapid dose of 20mL/kg is
reasonable
o Blood transfusion is initiated early in people presenting with
unstable vital signs in the face of a decreasing hematocrit, rather
than waiting for the hemoglobin concentration to decrease to some
predetermined "transfusion trigger" lev
- Prevention
 I: Elimination of A.aegypti
o Elimination of habitat i.e. getting rid of open sources of water or
adding insecticides or biological control agents
 II: WHO regulated controlled regulated body with a program to help
prevent bites of mosquito and its transmission of disease
66. Ebola and other viral haemorrhagic fevers
 Ebola
 Definition: Ebola AKA Ebola virus disease (EVD) or Ebola hemorrhagic fever (EHF), is
a viral hemorrhagic fever of humans and other primates caused by ebola viruses.
 Aetiology and mode of transmission
- Causative agent: Ebolavirus (4 types)
- Reservoir host: Bats (most likely candidate but not definitive), in Africa, ebola
infections were linked with Gorillas, chimpanzee’s, monkeys.
- Incubation period = 2-21 days
- Route of transmission:
 Direct contact between people i.e. via blood or other body fluids
(mucus, saliva, vomit, feces, tears, breast milk, urine and semen)
 Sexual intercourse: The Ebola virus may be able to persist for more than
three months in the semen after recovery, which could lead to
infections via sexual intercourse
- Epidemiology
 Out-break in West Africa (Guinea)
 Total of 28,616 cases of EVD and 11,310 deaths reported in Guinea,
Liberia and Sierra Leone
- Period of communicability
 For as long as blood and secretions contain the virus even in
convalescence stage
 Clinical features
- Initial: Severe acute viral illnesses, usually with sudden onset of fever, malaise,
myalgia and headache, followed by pharyngitis, vomiting, diarrhea and
maculopapular rash
- Severe and fatal forms:
 Hemorrhagic diathesis is accompanied by hepatic damage, renal
failure, CNS involvement, terminal shock with multiorgan dysfunction

 Diagnosis, Treatment and Prevention

- Diagnosis
 When EVD is suspected, travel, work history, and exposure to wildlife
are important factors with respect to further diagnostic efforts
 Lab findings
 o Nonspecific: Lymphopenia, severe thrombocytopenia,
increased PT time, partial thromboplastin time and
transaminase elevation (AST > ALT)
o Specific findings:
 Indirect serological: Antibody test
 Direct: Detecting its RNA or proteins via cell culture or
PCR
- Treatment
 No cure, just supportive i.e. blood transfusion, platelets, rehydration.
 AVOID ASPIRIN
- Prevention
 I: Ebola Vaccination (Pre-prophylaxis)
o rVSV-ZEBOV: Fully effective in USA after ten days of
administration
 II: Adequate PPE for health workers and carers
 III: Heat elimination/disinfection
o 30 to 60 minutes at 60 degrees boiling for 5 minutes
 IV: Education
 V: Isolation procedure if there’s symptoms in high risk areas or jobs
 LASSA fever
 Definition: Lassa fever, also known as Lassa hemorrhagic fever (LHF), is a type of viral
hemorrhagic fever caused by the  Lassa virus. Many of those infected by the virus do not
develop symptoms
 Aetiology and mode of transmission
- Causative agent: Lassa virus
- Reservoir: Wild rodents; in western Africa, the multimammate mouse of the
Mastomys species complex.
- Incubation: 6-21 days
- Route of transmission:
 I: Aerosol or direct contact
o Excreta of infected rodents deposited on surfaces i.e. floors and
beds or in food and water
 II: Lab infections – hospital environment
o Inoculation with contaminated needles and via patient’s
pharyngeal secretion or urine.
 III: Sexual contact person-person
- Epidemiology
 Endemic in Guinea, Liberia, regions of Nigeria, and Sierra Leone
 Clinical features (mostly asymptomatic)
- I: Less severe: fever, weakness, headaches, vomiting and muscle pains
- II: Most severe: bleeding from mouth or GI tract and dehydration
 Diagnosis, Treatment and Prevention
- Diagnosis
 PCR followed by cell cultures, ELISA etc.
- Treatment (generally no curative treatment)
 I: Treating dehydration
 II: Antiviral ribavirin (but evidence support is weak)
  NO VACCINATION AVAILABLE
- Prevention
 I: Report to local health authority: Individual cases should be reported.
 II: Isolation – Quarantine procedure of those infected
 III: Concurrent disinfection
 IV: International measures
o Notification of source country and to receiving countries of
possible exposures by infected travellers. WHO Collaborating
Centres.

67. Object and goals of parasitology. Parasites, parasitism and hospitalities of parasites – cut
out of syllabus
68. Pathogenic mechanism in parasitic diseases and invasion process – cut out of syllabus
69. Malaria

NOTE: FOR PARASITOLOGY, ALWAYS REMEMBER EOSINOPHILIA

 Malaria
 Definition: Malaria is a mosquito-borne infectious disease that affects humans and
other animal. They are caused by single-celled microorganisms of Plasmodium
group.
- Malaria has a dominant liverstage called hypnozoites that can activate and
invade the blood several months or years after mosquito blood meal
 Aetiology, Mode of transmission and Life cycle
- Causative agents:  
 I: Plasmodium Falciparum
 II: Plasmodium vivax, ovale, malariae
- Incubation period: 7-30 days in general
- Mode of transmission:
 I: Female anopheles mosquito bite
- Lifecycle
 I: Infected female anopheles mosquito takes a blood meal and injects
sporozoites that reach the liver.
 II: Schizonts then form in the liver and rupture entering the blood or
they enter hypnozoite stage.
 III: Merozoites are released into blood and form Trophozoites in blood
which release male and female gametocytes.
 IV: Another female anopheles mosquito takes a blood meal ingesting
male and female gametocytes. In the stomach, gametocytes fuse to
form zygotes becoming motile. They then invade midgut and develop
oocysts which grow and rupture as sporozoites
 V: Sporozoites travel to salivary gland ready to infect new host.
  Clinical features

 Diagnosis, Treatment
- Diagnosis
 See clinical features
- Treatment
 Uncomplicated malaria: Simple or uncomplicated malaria may be
treated with oral medications. Arteminisin (lactone) drugs are effective
and safe in treating uncomplicated malaria
 Complicated malaria: Recommended treatment for severe malaria is
the intravenous use of antimalarial drug
70. Leishmaniosis (visceral, cutaneous, mucocutaneous)
 Leishmaniosis (visceral, cutaneous, mucocutaneous)
 Definition: Leishmaniasis is a disease caused by parasites of the Leishmania type. It is
spread by the bite of certain types of sandflies.
 Classification
- Visceral Leishmaniasis (black fever)
  Causative agents:  
o I: Leishmania Donovani via sandfly
 Mode of transmission: Sand-fly bite phelbotomus papatasii
 Clinical features: The symptoms include, anaemia, fever, weight loss
swelling of liver and other organs
o Triad (3): High temp, splenohepatomegaly and pancytopenia
 Lifecycle
o I: Sandfly takes a blood meal and releases promastigote into the
skin which causes an immune response in which phagocytosis
occurs.
o II: Promastigote transforms into amastigote form within the
macrophages and multiplies and released to various other
tissues
o III: Sandfly comes and takes another blood meal and ingests
infected cell that has the amastigote.
o IV: Amastigote transforms into promastigote in the midgut.
They migrate to the probisces for cycle to repeat.

- Cutaneous Leishmaniasis
 Causative agents: Leishmania Tropica
 Mode of transmission: Sandfly bite – Phelbotomus papatasii
 Clinical features: lesions in skin and ulcers on hands and feet.
 Lifecycle: Same as Leishmania Donovani
- Mucocutaneous Leishmaniasis
 Causative agents:  Leishmania brasiliensis
 Mode of transmission: Sandfly bite – Phelbotomus papatasii
 Clinical features: Skin lesions on mucocutaneous surfaces
 Lifecycle: Same as Leishmania donovani
 Diagnosis, Treatment
- Diagnosis
 Hematology lab by direct visualization of Amastigotes (Leishman-Donovan
bodies) – Giemsa stain – skin scraping
o Smear test
 PCR test available
 - Treatment
 Depends where the disease is acquired i.e. for Visceral leishmaniasis in India,
South America, Liposomal amphotericin B is recommended and used with a
single dose.

71. Urogenital trichomonosis

 Trichomonosis
 Definition: Trichomoniasis (trich) is an infectious disease (STD) caused by the
parasite Trichomonas vaginalis. About 70% of women and men do not have symptoms
when infected.
 Aetiology & Mode of transmission
- Causative agent: Trichomonas Vaginalis
- Mode of transmission:
 I: Sexual intercourse (STD)
 II: Genital touching
- Lifecycle
 I: Trichomonas vaginalis resides in female lower genital tract and male
urethra.
 II: Replicates via binary fission and does NOT have a cyst form and doesn’t
survive in external environment
 III: Trophozoite found in vaginal and prostatic secretions and transmitted
sexually

 Clinical features
- 70% of men and women are asymptomatic
- Symptomatic patients
 Pain, burning or itching in the penis
 Urethritis or vaginitis
 Dysparenuria and dysuria
 Frothy, fishy foul-smelling vaginal discharge
 Diagnosis, Treatment & Prevention
- Diagnosis
 I: Saline microscopy
o Requires endocervical, vaginal or penile swab specimen
 II: Culture – gold standard
  III: NAATs
- Treatment
 Treatment for both pregnant and non-pregnant women is usually
with metronidazole, by mouth once
72. Amoebiasis
 Amoebiasis
 Definition: Amoebiasis aka amoebic dysentery, is an infection caused by any of
the amoebae of the Entamoeba group. The main one and most common one is
Entamoeba Histolytica.
 Aetiology & Mode of transmission
- Causative agent: Entamoeba Histolytica
- Mode of transmission:
 I: Fecal-oral route: Ingestion of contaminated food and water
- Lifecycle
 I: Ingestion of cysts via fecal-oral route
 II: Excystation occurs in the small intestine where trophozoites are released
which migrate to the large intestine in which they colonize.
 III: They replicate via binary fission and some are released as cystic forms
through feces while some (secondary) trophozoites in small intestine enter
blood and travel to liver, lungs and brain where they create lesions.
 IV: Primary infection site is large intestine.

 Clinical features
- 90% are asymptomatic but with potential to be very serious
- Symptomatic patients:
 Range from mild diarrhoea to dysentery with blood, coupled with intense
abdominal pains.
 Extra-intestinal complications might also arise as a result of invasive
infection where amoebae enters the bloodstream which includes colitis,
liver (Liver is most common as that’s where blood from intestine
reaches first), lung, or brain abscesses.
 Diagnosis, Treatment & Prevention
- Diagnosis
 Colonoscopy
o Detect small ulcers
 Immunohistochemical staining
o With specific anti-E histolytica antibodies
 Asymptomatic patients – stool test
o Finding cysts in stool by chance or other condition
  Serological testing (i.e. antibody test)
 Microscopy
- Treatment
 Amoebicidal tissue active agent (extra-intestinal) and a luminal cysticidal
agent (intestinal) – FOR SYMPTOMATIC PATIENTS
 Luminal cysticidal agent only – FOR ASYMPTOMATIC PATIENTS
73. Lambliosis
 Lambliosis
 Definition: Giardiasis/Lambliosis aka Beaver fever is a parasitic disease caused by Giardia
duodenalis aka G.lamblia.
 Aetiology & Mode of transmission
- Causative agent: G.Lamblia
- Mode of transmission: Fecal-oral route via ingestion of cysts within contaminated
food and water
- Life cycle:
 I: Ingestion of cyst form. Trophozoite released from cyst (excyts) in the small
intestine.
 II: They then replicate via binary fission within the lumen of the small
intestine
 III: Then towards the colon, encystation occurs in which they are released
and passed through feces for cycle to repeat.
 Clinical features
- 10% asymptomatic
- Symptomatic patients
 I: Severe (chronic) diarrhoea with poor absorption of nutrients.
o Diarrhea can last for months and is often greasy and foul-
smelling.
 II: Other symptoms – gas, abdominal cramps, nausea and vomiting
 III: Prolongation of disease
o Diarrhea along with malabsorption of nutrients in the intestine
(i.e. leading to fatty stools, weight loss and fatigue)
 Malabsorption of nutrients? The attachment of trophozoites causes
villus flattening and inhibition of enzymes that break down
disaccharide sugars, proteins etc in the intestines.
 Diagnosis, Treatment
- Diagnosis
 Antigen test – i.e. ELISA (GOLD STANDARD) due to increased sensitivity
 Microscopic examination
 All via stool specimen
- Treatment
 Treatment is not always necessary as the infection usually resolves on its
own. However, if the illness is acute or symptoms persist and medications
are needed to treat it, a nitroimidazole medication is used such
as metronidazole, tinidazole, secnidazole or ornidazole
74. Toxoplasmosis
 Toxoplasmosis
 Definition: Toxoplasma gondii is an obligate intracellular parasitic eukaryote that
causes the infectious disease toxoplasmosis
 Aetiology & Mode of transmission
- Causative agent: Toxoplasma gondii
- Mode of transmission:
 I: Fecal-oral route (ingestion of tissue cysts or T.gondi oocysts)
o Ingestion of raw or partly cooked meat (i.e. pork)
o Ingestion of unwashed fruit or vegetables that have been in
contact with contaminated soil containing infected cat fexes
o Ingestion of unpasteurized milk
o Ingestion of raw seafood
 II: Peri-natal transmission (via placenta in blood to fetus)
- Life cycle:
 I: Oocysts are shed as feces. They sporulate and become infective. They are
then ingested by intermediate host such as cattle
 II: They develop into tachyzoites in which are located in any type of cell and
replicate until the cell dies
 III: Tachyzoites develop into bradyzoites when they invade organs such as
brain and liver within the tissue and form tissue cysts
 IV: Human can ingest them by eating undercooked meat. Can be fatal to
woman that is pregnant as tachyzoites have the ability to be transmitted to
the fetus via placenta in blood

 Clinical features
- I: Acute
o Often asymptomatic in healthy adults
o Symptomatic patients:
 Influenza like: swollen lymph nodes (neck or under the chin,
followed by armpits and groin), headaches, fever, and fatigue or
muscle aches and pains that last for a month of more
- II: Latent
 Absence of obvious symptoms
- III: Skin (rare)
 Skin lesions i.e. roseola & erythema multiforme-like eruptions, urticarial and
maculopapular lesions
 Diagnosis, Treatment
- Diagnosis
 T.gondi can be detected in blood, amniotic fluid, or CSF via PCR
  Serological testing: T.gondii antibodies in blood serum via ELISA
- Treatment
 Acute:
o Pyrimethamine is an antimalarial medication used in combination
with Sulfadiazine (antibiotic)
 Latent:
o In people with latent toxoplasmosis, the cysts are immune to these
treatments, as the antibiotics do not reach the bradyzoites in
sufficient concentration
o Atovaguone – kill Toxoplasma cysts inside AIDS patients
75. Pneumocytosis
 Pneumocytosis
 Definition: Pneumocystis pneumonia (PCP) is a form of pneumonia that is caused by
the yeast-like fungus Pneumocystis jirovecii.  It is also known as PJP,
for Pneumocystis jiroveci Pneumonia.
 Aetiology & Mode of transmission
- Causative agent: Pneumocystitis jiroveci Pneumonia (PJP)
- Mode of transmission:
 I: Airborne – person to person
o Risk factors: Rare disease that is common in those with weakened
immune systems although it’s still very rare.
o Other risk factors include: COPD, cancer etc
- Lifecycle:

 Clinical features
- I: Shortness of breath and/or difficulty breathing
- II: Fever, dry/non-productive cough
 The dry cough distinguishes PCP from typical pneumonia
- III: Weight loss, night sweats, chills and fatigue
 Complications: Pneumothorax
  Diagnosis and Treatment
- Diagnosis
 I: Diagnostic confirmation via:
o X-ray: Widespread pulmonary infiltrates
o CT: May show pulmonary cysts
o Pa02: Strikingly lower than whats expected
 II: Diagnostic definitive confirmation via:
o Histological identification (via sputum or bronchoalveolar lavage)
 Immunofluorescence assay or other staining methods can be used
- Treatment
 Antipneumocystic medication used with steroids (as without steroids, the
Antipneumocystic meds would cause inflammation).
o Most common used medication = Trimethoprim/Sulfamethoxazole
76. Cryptosporioliosis and blastocytosis
 Cryptosporioliosis
 Definition: Cryptosporidiosis, sometimes informally called crypto, is a parasitic
disease caused by Cryptosporidium. It affects the distal small intestine and can affect
the respiratory tract in both immunocompetent  and immunocompromised individuals,
resulting in watery diarrhea with or without an unexplained cough. It can be fatal to
immunocompromised individuals.
 Aetiology & Mode of transmission
- Causative agent: Cryptosporidium species (i.e. in humans C.parvum and C.hominis)
- Mode of transmission:
 I: Fecal-oral route: Contaminated food and water
o Most occur in swimming pools as Crypto species are resistant to
chlorine
o Drinking water supplies

- Lifecycle:
 I: Ingestion of sporulated oocysts into the intestine
 II: While in the intestines, the oocysts release sporozoites which invade
epithelial lining of intestines or the lungs. The sporozoites then undergo
sexual (or asexual) reproductive stage in which a zygote is formed.
 III: The resulting zygote then forms an oocyst which will either:
o A) Exit the host
o B) Auto-infect the host

 Clinical features
- Based on Immune system
 I: In immunocompetent patients,
Cryptosporidiosis are primary localized to distal
small intestine and sometimes the respiratory
tract.
  II:In immunocompromised persons, cryptosporidiosis may disseminate to
other organs (i.e. urinary bladder, hepatobiliary system, pancreas etc)
- Intestinal cryptosporidiosis
 Moderate to severe watery diarrhea
 Low-grade fever, cramped abdominal pain and dehydration
 Weight loss, fatigue, nausea and vomiting
- Respiratory cryptosporidiosis
 URT symptoms
o Inflammation of nasal mucosa, larynx, sinuses or trachea
o Nasal discharge
o Hoarseness
 LRT
o Cough, dyspnoea, fever and hypoxemia
 Diagnosis, Treatment
- Diagnosis
 Miscroscopy: Identify oocysts in fecal matter (i.e. stool test)
 Serological: ELISA, PCR, staining
- Treatment
 Symptomatic treatment
o Fluid rehydration, electrolyte replacement, anti-motility agents
(loperamide)

77. Enterobiosis
 Enterobiasis
 Definition: Pinworm infection aka Enterobiasis is a human parasitic disease caused by
the pinworm. The most common symptom is itching in the anal area. The disease is
spread via pinworm eggs. Humans are the only host.
- The entire lifecycle: from egg to adult takes place in the human GI tract of a single
human host.
 Aetiology & Mode of transmission
- Causative agent: Enerobius vermicularis
- Mode of transmission:
 I: Hand to mouth anal – Human to human transmission via swallowing
infectious pin worm eggs
o Eggs are transmitted this way due to intense itching of anus
o Pin worms do not lay eggs in feces
- Lifecycle:
 I: Ingestion of infected pin worm eggs.
 II: Larvae hatch in the small intestine and adults are established in the colon
 III: Gravid females migrate out of colons and lay eggs on perianal area.
 IV: Intense itching of anus then hand to mouth – lifecycle repeat.
  Clinical features
- One-third individuals are aysymptomatic
- Intense itching of anus (MAIN SYMPTOM)
 Diagnosis, Treatment
- Diagnosis
 Microscopy:
o Finding eggs or adult pin worms
- Treatment
 Benzimadazole compound medications are the most effective
o They work by inhibiting microtubule function in the pinworm adults,
causing glycogen depletion, thereby effectively starving the parasite.
78. Ascaridosis
 Ascariasis
 Definition: Ascariasis is a disease caused by the parasitic roundworm Ascaris
lumbricoides. Infections have no symptoms in more than 85% of cases, especially if the
number of worms is small

 Aetiology & Mode of transmission

- Causative agent: Ascaris lumbricoides (largest nematode/intrestinal parasitic worm)
- GEOHELMINTH
- Mode of transmission:
 I: Fecal oral route:
o Contaminated food in soil i.e. vegetables which contain the feces.
 II: Human-human transmission possible via direct contact
- Lifecycle:
 I: Eggs are ingested via feces and larvae hatch
 II: They invade intestinal mucosa entering circulation to the lungs which
they reside and further mature.
 III: Larvae then penetrate alveoli walls and ascend to the throat via the
trachea and are swallowed.
 IV: They eventually reach the small intestine and develop into adults
  Clinical features
- Bowel obstruction – intestinal blockage (if there is a large number)
 A worm may block the ampulla of Vater, or go into the main pancreatic
duct, resulting in acute pancreatitis with raised serum levels
of amylase and lipase. Occasionally, a worm can travel through the billiary
tree and even into the gallbladder, causing acute cholangitis or
acute cholecystitis.
 Diagnosis, Treatment
- Diagnosis
 Microscopy
o Stool test (eggs in stool)
- Treatment
 Medications: Ascaricides (mebendazole)
79. Ancylostomidosis
 Ancylostomidosis
 Definition: Ancylostomiasis (miner's anaemia, tunnel disease, brickmaker's
anaemia and Egyptian chlorosis) is a hookworm disease caused by infection
with Ancylostoma hookworms
 Aetiology & Mode of transmission
- Causative agent: Ancylostoma duodenale hookworms
- Mode of transmission:
 I: People walking barefoot over contaminated soil that contain feces
o Penetration of skin i.e. itchy patch they cause, thus itching will allow
hookwork to enter.
- Lifecycle:
 I: Eggs released in feces. Eggs then hatch into rhabditiform larvae
 II: They then develop into filariform larvae which is an infective stage as it
penetrates the skin and enters blood vessels via circulatory system and
migrates into the lungs.
 III: From the lungs, they penetrate alveolar walls and move upto the throat
via the trachea to be swallowed.
 IV: Filariform larvae then matures into adults in small intestine and then
eggs pass into feces, cycle repeats.
o NOTE: Adult attaches to intestinal wall and sucks blood hence
chronic anaemia
  Clinical features
- Symptoms of anaemia
 Abnormal paleness of skin
 Shortness of breath
 Tachycardia
 Delayed capillary refill
 Diagnosis, Treatment
- Diagnosis
 Microscopy
- Treatment
 Single dose of mebendazole

80. Strongyloidosis
 Strongyloidiasis
 Definition: Strongyloidiasis is a human parasitic disease caused by
the nematode called Strongyloides stercoralis (type of helminth - roundworm).
 Aetiology & Mode of transmission
- Causative agent: Strongyloides stercoralis
- Mode of transmission: (see point 79 - same)
- Lifecycle: (see point 79 - same)

 Clinical features
- Strongyloides infection occurs in five forms. As the infection continues and the
larvae matures, there may be respiratory symptoms (Löffler's syndrome). The
infection may then become chronic with mainly digestive symptoms. On reinfection
(when larvae migrate through the body) from the skin to the lungs and finally to the
 small intestine, there may be respiratory, skin and digestive symptoms. Finally, the
hyperinfection syndrome causes symptoms in many organ systems, including
the central nervous system
 Frequently the disease is asymptomatic

 Diagnosis, Treatment
- Diagnosis
 Microscopy
o Identification of larvae (rhabditiform and occasionally filariform) in
the stool or duodenal fluid
 Serological tests: ELISA (antibodies against the roundworm)
- Treatment
 Ivermectin

81. Toxocarosis
 Toxocarosis
 Definition: Toxocariasis is an illness of humans caused by larvae (immature worms) of
either the dog roundworm (Toxocara canis), the cat roundworm (Toxocara cati) or the
fox roundworm (Toxocara canis).
 Aetiology & Mode of transmission
- Causative agent: T.canis (dog roundworm), T.cati (cat roundworm), T.canis (fox
roundworm)
- Mode of transmission:
 I: Fecal-oral route
o Ingestion of eggs via contaminated food, water, objects and surfaces
o Flies that feed on feces can spread Toxocara eggs to surfaces or
foods
- Lifecycle:
 I: Cats, dogs and foxes become infected with Toxocara via ingestion of eggs
or transmission of larvae from mother to her offspring.
 II: Eggs hatch as larvae in intestines of cat, dog, or fox host. Larvae then
enter the bloodstream and migrate to the lungs, where they are coughed
up and swallowed. The larvae then mature into adults within small
intestines, where mating and embryonated eggs with larvae are produced.
Eggs are then passed in feces.
  III: Embryonated larvae (second stage larvae) are ingested by human host.
The larvae then most commonly migrates via bloodstream to the lungs,
liver, eyes and brain.

 Clinical features
- Physiological reactions to Toxocara infection depend on host’s immune response
and parasitic load. Most cases are asymptomatic. When symptoms do occur, they
are the result of migration of second stage Toxocara larvae through body.
- Syndromes include:
 I: Convert toxocariasis (least serious)
o Coughing, fever, abdominal pain, headaches, and changes to
behaviour and difficulty to sleep
 II: Visceral larva migrans (VLM)
o High parasitic loads in young children which can lead to
inflammation of internal organs and sometimes CNS
o Common symptoms: pallor, fatigue, weight loss, anorexia, fever,
headache, skin rash, abdominal pain, nausea, vomiting
 III: Ocular larva migrans (OLM) – very rare compared to VLM
o Often occurs in one eye from single larva migrating into and
encysting within orbit which leads to loss of vision within weeks.
 Diagnosis, Treatment
- Diagnosis
 Microscopy of feces
 PCR, ELISA and other serological testing
- Treatment
 Generally self-limiting as Toxocara larvae cannot mature within human
hosts.
 Corticosteroids prescribed in severe cases of VLM or OLM
o Mebendazole (second line therapy)

82. Trichinellosis
 Trichinellosis
 Definition: Trichinellosis is a parasitic disease caused by roundworms of
the Trichinella type. The great majority of trichinosis infections have either minor or no
symptoms and no complications
 Aetiology & Mode of transmission
- Causative agent: T. spiralis
- Mode of transmission:
 I: Ingestion of undercooked infected meat
o NOTE: NOT SOIL-TRANSMITTED
- Lifecycle:
 I: Ingested undercooked meat containing encysted larvae
 II: Excystation of larvae occurs in small intestine where it develops into
adult worms
 III: Females then release larvae into mucosa in which it migrates to striated
muscle and encyst

 Clinical features
- I: Enteral phase
 Nausea, heartburn, dyspepsia and diarrhoea
- II: Parenteral phase
 Depends on number of larvae produced and number that migrate.
 Symptoms include:
o Neurological deficits: Ataxia or respiratory paralysis
o Edema, muscle pain, fever and weakness
 CLASSIC SIGN: Periorbital edema caused by vasculitis
 Diagnosis, Treatment
- Diagnosis
 I: Confirmed via exposure history, clinical diagnosis and laboratory testing
 II: Labs
o Microscopy
o ELISA
- Treatment
 I: Primary treatment
o Anthelmintics: Mebendazole
 II: Secondary treatment
o Steroids i.e. prednisolone to relieve muscle pain associated with
larval migration
83. Fasciolosis
 Fasciolosis
 Definition: Fasciolosis is a parasitic worm infection caused by the common liver
fluke Fasciola hepatica as well as by Fasciola gigantica. The disease is a plant-
borne trematode zoonosis, and is classified as a neglected tropical disease. It affects
humans, but its main host is ruminants such as cattle and sheep
 Aetiology & Mode of transmission
- Causative agent: Fasciola hepatica or gigantica
- Mode of transmission:
 I: Plant-borne: Ingestion of raw, fresh-water vegetation on which flukes in
their metacercariae form are encysted.
- Lifecycle:
 I: Immature eggs are discharged in biliary ducts and passed in the stool
 II: Eggs become embryonated in fresh water and they release miracidia
which invade a suitable snail intermediate host (of which they go through
several developmental stage). Miracidia eventually becomes cercariae.
 III: The cercariae are released from the snail and encyst as metacercariae
on aquatic vegetation or other substrates.
 IV: After ingestion, the metacercariae excyst in the duodenum and
penetrate through intestinal wall and immature flukes migrate through the
liver parenchyma into biliary ducts, where they mature into adult flukes
and produce eggs and released via feces or urine and cycle repeats.

 Clinical features

 Diagnosis, Treatment
- Diagnosis
  ELISA and Western blot
- Treatment
 Anthelmintics - Triclabendazole

84. Shistosomatosis (urogenital, central, and japonica)

 Definition: Schistosomiasis, also known as snail fever and bilharzia, is a disease caused
by parasitic flatworms called schistosomes. The urinary tract or the intestines may be
infected.
 Aetiology & Mode of transmission
- Causative agent: S. haematobium and S. intercalatum it is snails of the
genus Bulinus, in S. mansoni it is Biomphalaria, and in S. japonicum it is Oncomelania
- Mode of transmission:
 I: Prenetration of skin during contact with infested water
o Contaminated water from intermediate host once parasite leaves
the snail host.
o Bathing, playing, swimming, washing, fishing, etc.

- Lifecycle: Same as point 83 Fasciolosis

 Clinical features
- I: Dermatitis
 First potential reaction is an itchy, popular rash
o Results from cercariae penetrating the skin
o NOTE: similar more severe one is called ‘swimmer’s itch’
- II: Katayama fever
 Fever, lethargy
 Eruption of pale temporary bumps associatd with severe itching (urticarial)
rash, liver and spleen enlargement, and bronchospasm
 Diagnosis, Treatment
- Diagnosis
 Microscopy
 Serological tests: ELISA & PCR
- Treatment
 Two drugs, praziquantel and oxamniquine, are available for the treatment
of schistosomiasis
85. Teniidosis (bovine and pork) and cysticercosis
 Teniidosis (bovine and pork)
 Definition: Taeniasis is an infection within the intestines by adult tapeworms belonging
to the genus Taenia. There are generally no or only mild symptoms. Symptoms may
occasionally include weight loss or abdominal pain
 Aetiology & Mode of transmission
- Causative agent: Taenia saginata (beef tenia/tapeworm) & Taenia Solium (pork
tenia/tapeworm)
- Mode of transmission:
 I: Taeniasis is contracted after eating undercooked pork or beef that contain
the larvae.
- Lifecycle:
 I: Eggs or gravid proglottids in feces and are passed into the environment.
Pigs and cattle ingest eggs or gravid proglottid through contaminated
vegetation.
 II: Oncospheres hatch and penetrate intestinal wall and circulate
musculature. In the muscle tissue, they develop into cysticerci.
 III: Humans are infected by ingesting infected meat which was
undercooked.
 IV: Cysticerci scolex attaches to intestine and remains to mature into
mature adults. Cycle is then repeated.
o NOTE: T.Saginata Vs T.Solium
 Cysticercosis in T.saginata is muscle tissue while for T.solium is the
brain (.
 T.saginata’s only definitive host is humans while T.solium have
others

 Clinical features
  Diagnosis, Treatment
- Diagnosis
 Stool sample (primary) to identify eggs
o Examination of scolex or gravid proglottids can resolve exact species
 Serological tests: PCR, ELISA
 Ziehl-Neelsen stain is also used for T.saginata and T.solium
- Treatment
 Praziquantel is the treatment of choice

86. Echinococcosis
 Echinococcosis
 Definition: Echinococcosis is a parasitic disease of tapeworms of the Echinococcus type.
The two main types of the disease are cystic echinococcosis (most
common) and alveolar echinococcosis (second most common)
 Aetiology & Mode of transmission
- Causative agent: Echinococcus granulosus, also called the hydatid worm, hyper
tape-worm or dog tapeworm.
 Definitive host = dogs or humans
 Intermediate host are most commonly sheep, however, cattle, horses, pigs,
goats, and camels are also potential intermediate hosts
- Mode of transmission:
 I: Fecal-oral route (hand to mouth)
o Ingestion of eggs via contaminated food or water or close contact
with infected animals
- Lifecycle:
 I: Adults in small intestine release embryonated eggs in feces that is
ingested by sheep, goat, cattle etc.
 II: Eggs hatch as oncospheres that penetrate intestinal wall and migrates
through circulatory system and forms a hyatid cyst in organs such as lungs,
livers etc.
 III: Humans or dogs ingest infected intermediate host and protoscolex forms
from hyatid cyst in which attaches to the intestine of the definitive host
and matures into adults. Cycle is then repeated.
  Clinical features
- Depends on location
 Cysts in lungs: cough, shortness of breath and/or pain in the chest
 Cysts in liver: Abdominal pain, abnormal abdominal tenderness,
hepatomegaly with an abdominal mass, jaundice, fever and/or
anaphylactic reaction
 Diagnosis, Treatment
- Diagnosis
 CT, Ultrasound – Identification of Hydatid cysts
 Serological tests: PCR, ELISA
- Treatment
 Cystic & Alveolar:
o I: Open surgical removal of cysts combined with chemotherapy
(albdendazole and/or mebendazole before and after surgery)
o II: If cysts are multiple, then PAIR

87. Hymenolepidosis
 Hymenolepidosis
 Definition: Hymenolepiasis is infestation by one of two species
of tapeworm: Hymenolepis nana or H. diminuta.
 Aetiology & Mode of transmission
- Causative agent: Hymenolepis nana or H.diminuta
- Mode of transmission:
 I: Fecal-oral route transmission
o Direct contact or contaminated food or water
- Lifecycle:
 I: Eggs passed with the stool. They are then ingested by an arthropod
intermediate host (i.e. beetles, fleas). They develop into cysticercoids which
can infect human rodents upon ingestion and develop into adults in the
small intestine
 II: When eggs are ingested by humans, the oncospheres contained in eggs
are released. The oncospheres penetrate the intestinal villus and develop
into cysticercoid larvae. Upon rupture of the villus, the cysticercoids return
to the intestinal lumen, evaginate their scoleces and attach to the
intestinal mucosa and develop into adults in ileal portion of small intestines
producing gravid proglottids.
 III: Eggs are then passed in the stool and cycle repeats
 Clinical features
- I: Abdominal pain, loss of apetite
- II: Itching around anus, irritability and diarrhea
 Can be asymptomatic also
 Diagnosis, Treatment
- Diagnosis
 Microscopic examination of stool for eggs and parasites
o Eggs and proglottids of H.nana are smaller than H.diminuta
- Treatment
 I: Praziquantel and niclosamide