Professional Documents
Culture Documents
Infectious diseases are diseases caused by microbes such as (viruses,bacteria,fungi etc) and
are able to spread among individuals
MECHANISM OF TRANSMISSION
4 mechanisms of transmission are distinguished according to the primary localization of
pathogenic agents in macroorganisms:
1.Fecal-oral (intestinal localization);
2.Air-borne (respiratory tract);
3. Transmissive (blood circulating system);
4. Contact (wound) (biological fluids)
3. Bacteremia(Bacteria in blood)
In clinic bacteremia means the end of incubation period and beginning of the clinical
manifestations.
4. Intoxication.
The action of endotoxins causes changes of the state of the central nervous system,
adynamia, fever, headaches, violations of dream, appetite.
5. Parenchymatous diffusion.
The fifth phase of a pathogenesis is parenchymatous diffusion of microbes. By the flow of
the blood Salmonella of typhoid fever and paratyphoid enter into all organs. Microbes are
fixated especially in liver, spleen, bone marrow, skin. Secondary focuses are formed
(typhoid granulomas), from which bacteria likewise from the primary focuses (lymphatic
apparatus of the intestine) enter into the blood, supporting bacteremia
8. Formation of immunity
9.CLASSIFICATION OF TYPHOID
-Typhoid fever is anthroponosis.
-The source of infection is sick man or bacteriocarrier.
-The patients with typhoid fever discharge the agent with stool, urine, rarely – with saliva
and milk.
-The mechanism of the infection transmission is fecal-oral.
-The factors of transmission may be water, milk, various food-stuffs and contaminated feces
of the patient or bacterial carriers
THE CLASSIFICATION ARE
• According to forms:
A.typical
B. Atypical:
aborted,
effaced ( ambulant,afebrile, mildest),
disguised (pneumotyphus, colotyphus,
meningotyphus, apendicotyphus, colotyphus, nephrotyphus, sepsis)
• According to severity:
mild, moderate, severe, exacerbation, relapse
• According to complications: enterorrhagia, perforation of intestine,
bleeding from intestine, infectious shock
• According to bacteria carriage: convalescent, chronic
10.MAIN SIGNS OF TYPHOID IN THE INITIAL PERIOD OF THE DISEASE
Typhoid fever is anthroponosis. The source of infection is sick man or bacteriocarrier.
-The patients with typhoid fever discharge the agent with stool, urine, rarely – with saliva
and milk.
-The mechanism of the infection transmission is fecal-oral. The factors of transmission may
be water, milk, various food-stuffs and contaminated feces of the patient or bacterial carriers
Typhoid is characterized by cyclical course of the disease.
-There are such periods during course of the infectious process: incubation, initial, period of
climax, early reconvalescence and outcomes.
11. The pathognostic (main) symptoms of typhoid fever in the climax of the disease.
Typhoid disease turns into the climax of the disease at the end of the first week. The
appearance of the patients is very typical in this period
• The skin is pale.
• Patient is apathethic.
• Intoxication is increased.
• Temperature is constant and most typical syndrome of typhoid fever and
paratyphoid. The phase of climax is near two weeks.
The phase of decrease of the temperature is near one week.
• Chills and diaphoreses are seen in patients even in the
absence of antimicrobial therapy.
• Either constipation or diarrhea may occur.
• Respiratory symptoms, including cough and sore throat may be prominent. Examination of
the chest may reveal moist rales-
The abdomen is tender, especially in the lower quadrants. Abdominal distention is common,
and peristalsis is often hypoactive. The sensation of displacing air - and fluidfilled loops of
bowel on palpating of the abdomen is considered to be characteristic
- Rose spots, 2-4 mm erythematous, maculopapular lesions that blanch on pressure, appear
on the upper abdomen or on the lateral surface of the body
13.PECULIARITIES OF PARATYPHI A
Paratyphi A is also having similar properties as salmonella typhi
Source of infection –sick person or carrier
Mechanism of transmission –fecal oral
In paratyphoid A incubation period is shorter than in typhoid fever. It's duration is 8-10
days.
• The onset of the disease is an acute. Sometimes, the onset of the disease is accompanied
by cough, catarrh.
• Facial hyperemia, blood injection of the sclera’s vessels, herpes on the lips are observed
during examination.
• The temperature is wave-like or remittent. The fever is accompanied by chills and than by
diaphoreses.
• . In paratyphoid A the rash appears more early than in typhoid fever. The
rash is polymorphic. Roseolas, petechias and measles-like rash may be observed. The
intoxication is temperate.
• There is no status typhosus.
• There is normal quantity of leukocytes in peripheral blood. But leukocytosis and
lymphocytosis may occur too.
• In majority of the patients the disease has a moderate course. The relapses are frequently
observed in case of paratyphoid A.
14.PERCULIARITIES OF PARATYPHI B
Paratyphi B
Source of infection –(humans and cattle)
Mechanism of transmission –fecal oral
Paratyphoid B incubation period is 5-10 days.
• The onset of the disease is acute, with expressive chill, myalgia and weakness
• At the initial period of the disease the intoxication may be combined with symptoms of
acute gastroenteritis
• The temperature is not prolonged. Status typhosus is absent in majority of the patients. The
symptoms of intoxication disappears very quickly
• The rash is polymorphic, plenty. It appears at the earlier period. In some cases the course
of paratyphoid B may be severe with septic manifestations
Other tests
-Stool culture less sensitive to test for S.typhi
-Cultures of punch-biopsy samples of rose spots and rectal swabs
Supportive Therapy
• Bed rest and liquid diet during the fever period
• Adequate hydration
• Dietary Supplements with Ascorbic acid and vitamins
• Probiotics to prevent intestinal dysbiosis
** Prevention
• TAB Vaccine (Typhoid-paratyphoid A and B Vaccine) – 5-7years immunity
• Vi capsular polysaccharide Vaccine against the capsular (Vi) antigen **
Epidemiology
• Source of infection: contaminated food (poultry, eggs, beef, etc), contaminated
water, contact with infected animals or their fecal matter, sick people or carriers
• Mode of transmission: Unhygienic cooking environments and persons, improperly
cooked foods
• Vectors of the infection: Flies, cockroaches, rats
• Mechanism of transmission: Fecal-oral route
• Mode of occurrence: Occur as separate sporadic cases and as outbreaks
• Incubation period is 12-72 hours but can be longer
• Susceptibility of a person depends on the premorbid state of the macroorganism and
the quantity and variety (serotypes) of Salmonella present.
** NB:
Salmonella can remain viable in water for 11-120 days, in the sea water – 15-27 days, in
soil – 1-9 months , in sausage products – 60-130 days, in the eggs, vegetables and fruits till
2,5 months. **
Epidemiology
• Source of food poisoning: contaminated food (poultry, sausages, eggs, beef,
vegetables, canned foods, milk, etc), water or soil, contact with infected animals or
their fecal matter, sick people or carriers
• Mode of transmission: Unhygienic cooking environments and persons, improperly
cooked foods
• Mechanism of transmission: Fecal-oral route
• Mode of occurrence: Occur as outbreaks with an explosive character of illness
affecting a mass of people that fall ill over a short period of time (e.g. After visiting a
restaurant); and may also occur as separate sporadic cases
• Incubation period: A few hours
• Susceptibility of a person to this group of diseases is very high, sometimes up to
about 90-100%.
• Seasonality: Toxic food-borne infections may occur during the whole the year, but
occur more especially in summer.
** NB:
There are 2 types of Bacterial toxins: Exotoxins & Endotoxins
• Exotoxins are the toxic products of bacteria which are actively secreted into
environment.
Some exotoxin-releasing bacteria are Clostridium species, Enterobacter, Proteus, etc.
There are 2 types of Enterotoxins (Exotoxins) of bacteria: thermolabile and
thermostable. They increase the secretion of the fluids and salts into the stomach and
intestine and damage the membranes of the epithelial cells. Majority of enterotoxins
are thermolabile.
• Endotoxins are toxic substances which are liberated only during the lysis of
microbial cells.
Some endotoxin-releasing bacteria are Salmonella. **
Septic form:
Sepsis develops when there is a sharp decrease in the immune system function of the patient
and it is characterized by symptoms such as
• Acute onset from hectic or prolonged fever, chills and sweating, after an Incubation
period of about 5-10 days
• Pallor, rash may appear on the skin (petechiae or large hemorrhages).
• Purulent metastases in different organs and tissues
• Presence of septic focus may cause complicatioms such as meningitis, pneumonia,
osteomyelitis, pyelonephritis, enterocolitis, etc
• Hepatosplenomegaly sometimes with the development of jaundice
• Toxic-dystrophic syndrome (dystrophic changes to parenchyma of organs e.g. liver)
• The influence of intoxication on the central nervous system leads to irritation,
violations of sleep, and sometimes delirium.
** NB:
According to the WHO classification, patients with cholera may be divided into three
groups by their degree of dehydration:
• The first degree of dehydration (Mild) - Patients who have loss of fluid volume
equal to 5 % of their body weight.
• The second degree of dehydration (Moderate) - Patients who have loss of fluid
volume equal to 6-9 % of their body weight.
• The third degree of dehydration (Severe) - Patients who have loss of fluid volume
over 10% of their body weight. This dehydration is dangerous for life if the
reanimation measures are not done. **
** NB:
Complications: collapse, renal failure, cardiac failure,, pneumonia, abscess, phlegmon **
• Give oral rehydration solution (ORS) immediately to dehydrated patients who can sit
up and drink.
- If ORS is not available, water, broth, or other fluids should be provided.
Drinks with a high sugar content, such as juice, soft drinks, or sports drinks
are contraindicated because they can worsen diarrhea.
• Give ORS frequently - measure the fluid lost from diarrhea and vomitus and measure
the amount of ORS to compensate the loss
- for older children and adults is 100 ml of ORS every 5 minutes, until the
patient stabilizes.
- adults can consume as much as 1,000 ml of ORS per hour, if necessary, during
the initial stages of therapy
• Give small, frequent sips of ORS to patients who vomit, or give ORS by nasogastric
tube.
• If the patient requests more than the prescribed ORS solution, give more.
• Patients should continue to eat a normal diet or resume a normal diet once vomiting
stops.
Intravenous Rehydration Therapy
Indications:
- severe dehydration,
- stupor, coma
- uncontrollable vomiting
- extreme fatigue that prevents drinking.
• start IV fluids immediately. If the patient can drink, give ORS by mouth while the IV
drip is set up. Ringer’s lactate IV fluid is preferred. If not available, use normal
saline or dextrose solution.
• Measure the amount of IV fluids delivered to compensate the amount of fluid lost
from diarrhea and vomitus.
****
Asymptomatic Infection
More than 50% of EV infections are asymptomatic or result only in Nonspecific febrile
illness. Young age is associated with higher frequency of symptomatic infection.
Encephalitis
Frank encephalitis is an unusual manifestation of enterovirus infection.
Echovirus 9 is the most common etiologic agent.
Clinical manifestations include lethargy, drowsiness, and personality change to seizures,
paresis, and coma. Children with focal encephalitis present with partial motor seizures,
hemichorea, and acute cerebellar ataxia
Rashes
Certain coxsackieviruses, echoviruses,.Rashes are usually nonpruritic, do not desquamate,
and occur on the face, neck, chest, and extremities. They are sometimes maculopapular but
occasionally hemorrhagic, petechial, or vesicular. Fever is common. Aseptic meningitis may
develop simultaneously.
Ocular Infections
Outbreaks of acute hemorrhagic conjunctivitis are typically due to Echovirus 70 or
Coxsackie virus.Presentation is characterized by a sudden onset of severe eye pain and
associated photophobia. Subconjunctival hemorrhages are frequently present. Systemic
symptoms, including fever, are rare.
Herpangina.
This is an enanthematous (mucous membrane) disease that presents with painful vesicles of
the oral mucosa along with fever and sore throat, The onset is sudden, with high
temperatures [39.4-40°C]. The oropharyngeal lesions usually erupt around the time of first
fever.The duration of illness is 3 to 6 days.
Hand-foot-and-mouth Disease.
This common clinical syndrome manifests as a vesicular skin rash on the hands and feet
along with vesicles in the oral cavity. Mainly caused by Coxsackie virus and echovirus.
Fever could also be present. The oral vesicles usually are located on the buccal mucosa and
tongue and are only mildly painful. The exanthem involves vesicles on the palms, soles, and
the interdigital surfaces of the hands and feet.
Heart Infections
In myopericarditis, Coxscakie virus B5 the most common causative agent.
The usual presentation is fever, fatigue, and dyspnea on exertion, but more fulminant
symptoms, including heart failure or dysrhythmia, can occur.
Respiratory infections
These infections may result from enteroviruses. Symptoms include fever, coryza,
pharyngitis, and, in some infants and children, vomiting and
diarrhea. Bronchitis and interstitial pneumonia occasionally occur in adults and children.
The course is usually mild but can be severe as evidenced by the 2014 enterovirus D68
outbreak.
Symptoms may vary based on clinical form of enterovirus infection but main
symptoms include
! A Latent period lasts 2-10 days
! Acute beginning from toxic syndrome (high body temperature 39-40 degree,
headache, malaise, fatigue, repeated vomiting, decreased apetite), abdominal pain
and catarrhal syndrome
! Hyperemia of overhead half of trunk, skin, neck and face
! Injection of sclera vessels
! Hyperemia, gaininess of soft palate, and back pharyngeal wall
! Neck catarrhal lymphadenitis, or polyadenitis, may be hepatosplenomegaly
******* (NOT MAIN!!)
CLINICAL FORMS
Asymptomatic Infection
More than 50% of EV infections are asymptomatic or result only in Nonspecific febrile
illness. Young age is associated with higher frequency of symptomatic infection.
Aspetic Meningitis
Mainly caused by Enteroviruses of group B coxsackievirus and echovirus
The clinical course typically involves an initial episode of nonspecific fevers in conjunction
with CNS symptoms.Symptoms may also include headache, malaise, nausea, and
vomiting.,photophobia. Physical examination typically demonstrates generalized muscle
stiffness or spasm.
Encephalitis
Frank encephalitis is an unusual manifestation of enterovirus infection.
Echovirus 9 is the most common etiologic agent.
Clinical manifestations include lethargy, drowsiness, and personality change to seizures,
paresis, and coma. Children with focal encephalitis present with partial motor seizures,
hemichorea, and acute cerebellar ataxia
Rashes
Certain coxsackieviruses, echoviruses,.Rashes are usually nonpruritic, do not desquamate,
and occur on the face, neck, chest, and extremities. They are sometimes maculopapular but
occasionally hemorrhagic, petechial, or vesicular. Fever is common. Aseptic meningitis may
develop simultaneously.
Ocular Infections
Outbreaks of acute hemorrhagic conjunctivitis are typically due to Echovirus 70 or
Coxsackie virus.Presentation is characterized by a sudden onset of severe eye pain and
associated photophobia. Subconjunctival hemorrhages are frequently present. Systemic
symptoms, including fever, are rare.
Herpangina.
This is an enanthematous (mucous membrane) disease that presents with painful vesicles of
the oral mucosa along with fever and sore throat, The onset is sudden, with high
temperatures [39.4-40°C]. The oropharyngeal lesions usually erupt around the time of first
fever.The duration of illness is 3 to 6 days.
Hand-foot-and-mouth Disease.
This common clinical syndrome manifests as a vesicular skin rash on the hands and feet
along with vesicles in the oral cavity. Mainly caused by Coxsackie virus and echovirus.
Fever could also be present. The oral vesicles usually are located on the buccal mucosa and
tongue and are only mildly painful. The exanthem involves vesicles on the palms, soles, and
the interdigital surfaces of the hands and feet.
Heart Infections
In myopericarditis, Coxscakie virus B5 the most common causative agent.
The usual presentation is fever, fatigue, and dyspnea on exertion, but more fulminant
symptoms, including heart failure or dysrhythmia, can occur.
Respiratory infections
These infections may result from enteroviruses. Symptoms include fever, coryza,
pharyngitis, and, in some infants and children, vomiting and
diarrhea. Bronchitis and interstitial pneumonia occasionally occur in adults and children.
The course is usually mild but can be severe as evidenced by the 2014 enterovirus D68
outbreak.
*** Pandy's test (or Pandy's reaction) is done on the CSF (cerebrospinal fluid) to detect the
elevated levels of proteins (mainly globulins).
PRINCIPLE OF THERAPY
There is no specific treatment for non-polio enterovirus infection. People with mild
illness caused by non-polio enterovirus infection typically only need to treat their
symptoms. This includes drinking enough water to stay hydrated and taking over-the-
counter cold medications as needed. Most people recover completely, Hence ,
recommendations are
! Bed regimen in acute period
! Control of fever
! NSAIDs for pain relieve (ibuprofen, paracetamol ), or opiate analgesics ( morphine)
in clinical forms with severe pain
! Physiotherapy (in case of epidemic myalgia or paralytic form)
! Mechanical ventilation may be required if respiratory muscles are affected in
paralytic form
! Patients with weakness or paralysis of the bladder may be treated with cholinergic
agents, the sound of running water, or catheterization.
! Cold compresses may be used, along with antihistamine/decongestant eye drops in
case of enteroviral infection presenting as acute hemorrhagic conjuctivitis
( ***mainly caused by Echo or Coxsackie virus )
! topical anesthetics, and saline rinses may be used in enteroviral infection presenting
as Herpangina and hand-foot-and-mouth disease
***** Herpangina.
This is an enanthematous (mucous membrane) disease that presents with painful vesicles of
the oral mucosa along with fever and sore throat, The onset is sudden, with high
temperatures [39.4-40°C]. The oropharyngeal lesions usually erupt around the time of first
fever.The duration of illness is 3 to 6 days.
Epidemiology
! Source- Sick patients, patients in period of convalescence and carriers.
! Mechanism of transmission: fecal-oral
! Ways of transmission: water (Shigella .flexneri), food stuffs (Shigella .sonnei),
dishes, dirty hands, flies
! Epidemic features:
- season: summer & fall
- age: affects younger children more
! Incubation period 2-5 days
*** Shigella dysenteriae causes the most serious form of bacillary dysentery
DEFINTION- Shigellosis is a bacterial infection that affects the digestive system. caused
by a group of bacteria called Shigella.They are Gram negative bacteria from the family
enterobacteriaceae , most non-motile, non-sporing. Posses capsule (K antigen) and O
antigen. The Shigella bacterium is spread through contaminated water and food or through
contact with contaminated feces. The bacteria release toxins that irritate the intestines. The
primary symptom of shigellosis is diarrhea.
CLINICAL CLASSIFICATION
Duration
! Acute; up to 1 and a half months
! Subacute: up to 3months
! Chronic: more than 3 months
Clinical variants:
! Colitic variant
! Gastroenterocolitic variant
! Gastroenteric variant
Clinical form:
! Typical: with dominant toxicosis
! with dominant local inflammation
! mixed
Depending on severity:
! Mild form: acute diarrhea 5-8 times per day with mucus and blood. Mild abdominal
pain, normal temperature. Loss of appetite, could be vomiting
! Moderate form: acute onset of diarrhea, symptoms of toxicosis, temperature 38-39
degrees, anorexia, crampy abdominal pain, stool 10-15 times per day with mucus and
blood. Pain during palpation of left inguinal region
! Severe form: vomiting with or without food, stool more than 15 times per day with
mucus and blood. General condition sharply worsened. Sopor, loss of consciousness,
cramps. Severe toxicosis, weight loss and dehydration.
According to Pathology:
! Acute catarrhal inflammation
! Fibrinous Necrotic
! Ulcerous and folliclic-ulcerous
! Stage of formation of scars
PECULIARITIES
With dominance of toxicosis:
! Toxicosis is the first sign (loss of appetite, headache, fatigue, vomiting,
hallucinations, unconsciousness, seizures, febrile temperature 39-40 degrees
! Colitis is secondary: abdominal pain, tenesmus, false urge to defecate, sigmoid colon
is tender, spastic, anus is open in severe cases. Feces in the form of spit of mucus and
blood (rectal spit), enlargement of number of defecation
With dominance of local inflammation:
! Sudden onset of high grade fever
! Abdominal cramping
! Abdominal pain
! Tenesmus
! Large volume of mucus, cylindrical epithelial cells diarrhea
! Fecal incontinence, small volume, mucous diarrhea with frank blood
According to severity
! Mild form: acute diarrhea 5-8 times per day with mucus and blood. Mild abdominal
pain, normal temperature. Loss of appetite, could be vomiting
! Moderate form: acute onset of diarrhea, symptoms of toxicosis, temperature 38-39
degrees, anorexia, crampy abdominal pain, stool 10-15 times per day with mucus and
blood. Pain during palpation of left inguinal region
! Severe form: vomiting with or without food, stool more than 15 times per day with
mucus and blood. General condition sharply worsened. Sopor, loss of consciousness,
cramps. Severe toxicosis, weight loss and dehydration.
** Mild form doesn’t require etiological treatment, but adequate hydration should is key,
moderate to severe may require antibiotics eg. ciprofloxacin or azithromycin. DON’T USE
ANTIDIARRHEALS Like loperamide.
TREATMENT
In mild cases, treatment with antibiotics may not be indicated however adequate hydration
is vital.
In more severe cases:
! Antibiotic therapy- Ciprofloxacin, Ceftriaxone, Azithromycin
! Probiotics: collibacterin, bifidumbacterin
! Rehydration: trisol, quartasol, saline
! Spasmolytics: no shpa. Spasmolgon
CLINICAL CLASSIFICATION
● Asymptomatic infection: (cyst passers/carriers)
● Symptomatic infection (Intestinal Amebiasis & Extraintestinal )
- Intestinal Amoebiasis: Acute dysentery, Chronic non-dysentry, colitis,- Symptoms
present over a period of 1-2 weeks, Diarrhea with cramping, abdominal pain, watery or
bloody diarrhea and weight loss or anorexia. Stool looks like raspberry jelly. Fever
- Extraintestinal Amoebiasis: liver, skin, lung, pleura and brain
Hepatic amebiasis: abdominal pain, weight loss,
Amebic liver abscess: fever, right upper quadrant pain, weight loss, hepatomegaly,
jaundice, weight loss. Could be associated GI symptoms such as nausea, vomiting,
abdominal distention, diarrhea and constipation
Rupture of amebic hepatic abscess: pleuropulmonary amebiasis: liver abscess rupture,
cough, pleuritic chest pain, dyspnea, necrotic sputum. amebic peritonitis or amebic
pericarditis can also occur due to rupture of liver
Cerebral amebiasis: mental status changes and focal neurological deficits.
Amoebic colitis
! Symptoms present over a period of 1-2 weekks
! Diarrhea with cramping, abdominal pain, watery or bloody diarrhea and weight loss
or anorexia. Stool looks like raspberry jelly.
! Fever
Chronic amoebic colitis
! Recurrent episodes of bloody diarrhea and vague abdominal discomfort, plus fatigue,
weight loss and occasional fever.
Extra-intestinal amoebiasis can occur if the parasite spreads to other organs, most
commonly the liver, other locations include skin, lung, pleura and brain
! Hepatic amebiasis: abdominal pain, weight loss,
! Amebic liver abscess: fever, right upper quadrant pain, weight loss, hepatomegaly,
jaundice, weight loss. Could be associated GI symptoms such as nausea, vomiting,
abdominal distention, diarrhea and constipation
! Rupture of amebic hepatic abscess: pleuropulmonary amebiasis: liver abscess
rupture, cough, pleuritic chest pain, dyspnea, necrotic sputum. amebic peritonitis or
amebic pericarditis can also occur due to rupture of liver
! Cerebral amebiasis: mental status changes and focal neurological deficits.
! Fulminant amebic colitis: Rapid onset of severe bloody diarrhea, severe abdominal
pain, rebound tenderness, fever.
! Toxic megacolon: Toxic megacolon is an acute form of colonic distension. It is
characterized by a very dilated colon (megacolon), accompanied by abdominal
distension (bloating), and sometimes fever, abdominal pain, or shock
! Ameboma- An ameboma, also known as an amebic granuloma, is a rare
complication of Entamoeba histolytica infection with formation of annular colonic
granulation, which results in a large local lesion of the bowel.
! Rectovaginal fistula
LABORATORY DIAGNOSIS
! Microscopic identification of cysts and trophozoites in the stool is the common
method for diagnosing E. histolytica
! Stool or liver abscess aspirate culture, , E. histolytica trophozoites can also be
identified in biopsy samples
! Stool antigen test with monoclonal antibodies
! Serum anti-amoebic antibody: PCR and DNA probes for E.histolytica
! CT with contrast: amebic liver abscess
TREATMENT
Both symptomatic intestinal infection and extra intestinal disease as well as Asymptomatic
patients infected with E. histolytica should be treated with antiamoebic drugs, to prevent
spread of infection and latent infection
Epidemiology
! It has a Worldwide distribution (prevalent throughout the world increasing in areas
with poor sanitation)
! Source of infection: zoonosis: beavers, dogs, cats, rodents
! Mechanism of transmission: fecal oral
! Way of transmission: water-borne, food-borne
! Incubation period 1- 2 weeks
CLINICAL SIGNS
! Diarrhea, abdominal distention, abdominal cramps, flatulence. Malodorous, greasy
stools.
! Malaise, weakness, low grade fever, anorexia
! Nausea, vomiting
! CNS symptoms: irritability, sleep disorder, mental depression, neurasthenia
It’s treated with antibiotics which have anti parasitic effects (nitroimidazole drugs)
• Metronidazole: (contraindicated in first trimester of pregnancy )250mg
• Tinidazole 2g orally once
• Nitazoxanide 20mg/ml orally
•Albendazole
Epidiemology
Balantidium coli occurs worldwide. Because pigs are the primary reservoir, human
infections occur more frequently in areas where pigs are raised and sanitation is inadequate.
• Probiotics
• Vitamins
• Antibiotics: Tetracycline, metronidazole, iodoquinol,• Enzymes: pancreatin, gordoux•
Enema
Management
Avoid ingestion of material contaminated with animal feces
Treatment of infected pigs
Prevention of contaminated food
Botulism is not transmitted from person to person. Botulism develops if a person ingests
the toxin (or rarely, if the toxin is inhaled or injected) or if the organism grows in the
intestines or wounds and toxin is released.
The most important candidates for vaccination are those with chronic lung and cardiac
disease, pregnant women in any trimester, residents of chronic care facilities, health-care
workers, immunosuppressed patients, and those with diabetes and renal dysfunction.
Influenza vaccine is contraindicated in those who are highly allergic to eggs and which
would result in anaphylaxis.
Acute Viral Upper Respiratory Tract Infections – is a large group of Infectious Diseases,
which are caused by viruses, transmitted by Airbone way, characterized by intoxication and
catarrhal syndrome with predominant changes in mucous membranes of the respiratory tract
c) Pneumonia - secondary infection by bacteria (viral infection can cause impairment of the
physical barrier in the respiratory airways making it easier for bacteria to invade) resulting
in pneumonia
It can occur from bacteria like staphylococcus aureus , streptococcus pneumonia ,
hemophilus influenza
There will be productive cough , headache elevated WBC count , hypoxemia , chest
radiograph will show multiple infiltrates
Epidemiology
They are facultative intra cellular parasites
It is a respiratory infection
Transmission- Airbone
Through Direct inhalation via inhalation of aerosolized mist from water sources ( showers,
cooling towers) that is contaminated with either the bacterium or the amoebic cells that are
contaminated with the bacteria
Features that can increase the colonization of legionellae in man-made water environments
• Stagnation
• Temperature of 25-42c
• Presence of free living water amoebas that can support the intracellular growth of
legionella
Complications
Decreased pulmonary function, abscess formation(in lungs or extra pulmonary
site ) ,pulmonary fibrosis , fulminant respiratory failure , death
Diagnostic
Definitive method – Isolation of organism in respiratory secretions (sputum , lung fluid ,
pleural fluid )
Human herpesvirus type 7 cause a skin condition in infants known as exanthema subitum,
Human herpesvirus type 8 cause Sarcoma Kaposi's
Herpes simplex is a viral disease caused by both herpes simplex virus 1 (HSV-1) and herpes
simplex virus 2
Source of infection
Humans (Sick persons , Carriers )
Clinical Manifestations
Herpes simplex 1
1) Acute Herpetic Gingivostomatitis – occurs in children aged 6months – 5 years , may
occasionally be in adult
It last 5-7 days and symptoms subside in 2 weeks , viral shedding may continue for 3 weeks
Symptoms include
• Abrupt onset
• High temperature (39-40c)
• Anorexia
• Gingivitis
• Vesicular lesions
• Tender regional lymphadenopathy
• Perioral skin involvement due to contamination with infected saliva
Herpes simplex 2
Primary general herpes can be caused by both
Symptoms
• Constitutional symptoms like fever , headache, malaise, myalgia (prominent in the first 3-4
days)
• Local symptoms like pain, itching , dysuria , vaginal and urethral discharge
• Tender lymphadenopathy
• In females – herpetic vesicles appear on the external genitalia , labia majora, labia minora,
vaginal vestibule , introitus, in most areas the vesicles rupture and form ulcer , the vaginal
mucosa is inflamed and edematous
• In males – the herpetic vesicles will appear in the glans penis , shaft of penis and
sometimes scrotum , thighs , in dry areas the lesions will become pustule and encrust
Perinatal infections
Definition- Herpes zoster is viral infection that occurs with reactivation of the varicella-
zoster virus that has remained dormant within dorsal root ganglia, often for decades after the
patient’s initial exposure to the virus in the form of varicella (chickenpox),
Definition- Herpes zoster is viral infection that occurs with reactivation of the varicella-
zoster virus that has remained dormant within dorsal root ganglia, often for decades after the
patient’s initial exposure to the virus in the form of varicella (chickenpox),
The earliest symptoms of herpes zoster , includes headache, fever, and malaise,myalgia are
nonspecific
- Before the rash appears there is itching , paresthesia, hyperesthesia, burning pain in
affected dermatone 2 or 4 days
- After 2 days , a characteristic rash appears , painful papules on red base
- Later Rash becomes vesicular developing on an erythematous base
- The Vesicles are clear initially but eventually they become cloudy or darkened with blood ,
fever and malaise continues, the vesicles rupture, crust within 7-10 days and involute
- Rash typically appear unilaterally( either on the left or right side of the body or face),
stopping abruptly at the midline of the limit of sensory coverage of the involved dermatome,
mostly thoracic and lumbar dermatone are affected
- some people can develop post herpetic Neuralgia ( is persistent or recurring pain lasting 30
or more days after the acute infection or after all lesions have crusted. It is the most
frequent complication of herpes zoster,symptoms are a deep burning or aching pain,
paresthesia, dysesthesia, hyperesthesia, or electric shock–like pains.
Tzanck smear: scraping from base of fresh vesicular lesion after rupture may be smeared,
fixed with ethanol or methanol and stained with Giemsa or Wright preparation.
Rapid diagnosis using histological appearance
Histological appearance - The presence of multinucleated giant cells and epithelial cells
containing eosinophilic inclusion bodies indicates infection with HSV or varicella-zoster
virus.
• PCR – to detect HSV(herpes simplex virus) DNA , in HSV encephalitis , PCR with CSF is
a sensitive rapid diagnostic technique,
it can also be used to detect asymptomatic viral shedding
• Direct fluorescent antibody – Cells scrapes from ulcer base can be stained with direct
fluorescent antibody and it is used to distinguish HSV-1 from HSV-2 , tissue culture cells
can also be stained
• Brain biopsy in Herpes encephalitis
In chicken pox the rash crust by the 7th day, in herpes zoster they crust by the 14th day
In chicken pox rash is itchy , in herpes zoster rash is painful
Desintoxication therapy
● Antihepatic drugs: acyclovir, valaciclovir, famaciclovir
A number of nucleoside derivatives interfere with the synthesis of HSV DNA. Some of
these (trifluorothymidine, vidarabine) are useful in and licensed for the topical treatment of
herpes keratitis.
● Immune stimulators: interferon, amizone
● Symptomatic therapy: NSAID (paracetamol, ibuprofen) for pain, sitz bath, topical
lidocain
Congenital CMV
Maybe asymptomatic or present as cytomegalovirus inclusion disease of newborn
• Low birth weight
• On the skin - petechiae and purpura (I.e, blueberry muffin baby)
• Jaundice
• Helatosplenomegaly
• Thrombocytopenia , hemolytic anemia
• Chorioretinitis ( inflammation of choroid and retina )
• Microcephaly
• Peri ventricular cerebral calcifications
• Long term outcomes include seizures , mental retardation , sensorineural hearing loss
CMV in immuno-compromised persons (for instance, people who have had organ
transplants or who have HIV) with increased risk for difficult eye infections (CMV
retinitis), gastrointestinal CMV, encephalitis, CMV pneumonia.
Criteria
CBC – Lymphocytosis
Peripheral blood smear – presence of at least 10% atypical lymphocytes on smear(a type of
mononuclear cells – big monocytes with deformed big nucleus and widened cytoplasm )
Positive serological test for EBV
Evaluation
a) CBC – Leukocytosis , lymphocytosis , monocytosis , increased ESR
b) Liver function test – mild increases in the serum transaminases
c) Peripheral blood smear – atypical lymphocytes
d) Heterophile Antibody test (Monospot test ) –
A titre of 1:40 or greater is considered a positive result
The heterophile antibody is an immunoglobulin M (IgM) antibody produced by infected B
lymphocytes. In the heterophile test, human blood is first absorbed by a guinea pig
kidney. Then, it is tested for agglutination activity that is directed against horse,
sheep, or cow erythrocytes.
it may be negative early in the course (first week ) of EBV infectious mononucleosis so
negative test can be repeated within the first 6 weeks
It is less useful in children younger than 2 years
e) Serology – igM and igG antibodies against the viral capsid antigen (VCA) of Ebstein
Barr virus is useful in confirming diagnosis of EBV and differentiating acute and/or
recent infection from previous infection
The EBV IgM viral capsid antigen titre decrease after 3-6 months
EBV IgG viral capsid antigen(VCA) antibodies rises later than the IGM viral capsid antigen
(VCA) antibodies and remains elevated for life
.
Infectious mononucleosis Acute tonsilitis
Ways of transmission- it is realized by direct contact with droplets or contact with infected
skin lesions , nasopharyngeal secretions
Clinical onset – low grade fever , cough , hoarseness, sore throat , intensity of intoxication
depends on the square of affection ( localized , spread , toxic form )
● Gray adherent membranous exudate on tonsils in localized form
Hypertoxic form
Sudden onset, severe intoxication (temp > 40c, seizures , nausea , vomiting ,
unconsciousness )
Hemorrhagic form
Hemorrhages, membranous educates are soaked with blood
A stenosis stage.
Stenotic breathing ( narrowing of airways – inspiratory Dyspnea with an elongated
inspiration )
Noisy respiration
Participation of auxiliary muscles in respiration
Aphonia develops then later inspiratory stridor.
Signs of hypoxia ; peripheral then general cyanosis , tachycardia , anxiety , retractions )
An asphyxia stage.
• In the struggle with stenosis the child exhausts, the respiratory muscles get tired. The child
becomes calm, sleepy, he inditfferently lies in bed.
• The respiration is accelerated, but it is superficial, the retractions are already not so visible.
• The lips, tip of the nose and nails become blue, the face turns pale, sweat quite often
appears on the forehead.
• The extremities are cold,
• the pulse is very rapid, thready, sometimes paradoxical (abasement of the pulse wave
during the inhalation).
• From time to time there are attacks of acute dyspnea – the child jumps up, rushes because
of air-deficiency, the eyes express fright, the face becomes cyanotic; sometimes such attacks
result in the immediate death;
• in other cases the child dies after a more or less continuous agony with the symptoms of
exhaustion of respiratory and circulation centers.
Cardiac toxicity
Cardiac complications may arise during the first 10 days of illness or may be delayed until
2-3 weeks after onset, following improvement in the pharyngeal phase of the disease
Cardiac involvement is thought to be responsible for 50-60% of deaths associated with
diphtheria:
The first sign of toxin- induced myocardiopathy is
- tachycardia disproportionate to the degree of fever
- Various dysarthymias like first- degree, second-degree, or third-degree AV
blocks ;ventricular tachycardia
- congestive heart failure which is a consequence of myocardial inflammation( progressive
Dyspnea , reduced heart sounds, systolic murmur )
- Echocardiography may reveal dilated or hypertrophic cardiomyopathy;
Neurological toxicity
. Demyelination of nervous tissue
There will be Frank paralysis which involves the muscles of the palate and the
hypopharynx, beginning as early as the first 10 days of illness;
Difficulty swallowing and nasal speech are often the first indications of neurologic
impairment;
Cranial nerve deficit – Oculomotor ,ciliary paralysis (blurred vision ) , facial , pharyngeal
dysfunction
involvement of the anterior horn cells of the spinal cord may be seen as late as 3 months
after initial disease, Diffuse, usually bilateral, motor function deficits with progression of
weakness either from proximal-to-distal regions or, more commonly, from distal-to-
proximal regions;
Involvement of the phrenic nerve may cause diaphragmatic paralysis at any time between
the first and seventh weeks of illness;
Recovery from neurologic damage usually is complete in patients who survive.
The two major sites of infection are the respiratory mucosa and skin.
The initial symptoms of respiratory diphtheria include sore throat, malaise, and low-grade
fever. The characteristic clinical presentation is the presence of a grayish-white, fibrinous
and firmly adherent pseudomembrane that forms within the first few days and spans over
the tonsils, the pharynx, or the larynx.
LAB DIAGNOSIS:
a) Swabs from the nose, throat or suspected lesions are cultured onto blood and tellurite
agar, Löffler medium, hoyle, Mueller or tinsdale medium.
*(Tellurite inhibits growth of some normal flora and allows the Corynebacterium sp. to
grow as black or grey colonies)
c) PCR assay- for detection of the toxin gene (PCR positives must be confirmed by the
phenotypic Elek test)
d) Serology
102.Differential diagnosis of diphtheria and Simanovsky-Plaut-Vincent
tonsillitis.
Simanovsky-Plaut Diphtheria
Vincent tonsillitis
Leading severe pain in mouth Fibrinous inflammation in throat, toxic
symptoms and gums, foul syndrome
smelling breath
Throat changes Grey-white pseudo Cyanotic, hyperemic, edema
membrane on gums
that can ulcerate and
cause bad taste in
mouth
Character of Grey-white pseudo Grey or white yellow membranes can
tonsillar membrane on tonsils spread outside the tonsils. They are dense,
exudates that can ulcerate and hard to remove and bleed when removed.
become necrotic. After removal, they reappear and cannot be
Easily removable separated
Lymphadenitis Cervical Regional
lymphadenopathy
Toxic sign Absent or minor Proportional to surface of inflammation.
(mild, moderate and severe)
Subcutaneous Absent Typical for toxic forms (bull neck sign)
fat edema
Changes on the absent Coated
tongue
Symptoms of respiratory diphtheria include sore throat, malaise, and low-grade fever. The
characteristic clinical presentation is the presence of a grayish-white, fibrinous and firmly
adherent pseudomembrane that forms within the first few days and spans over the tonsils,
the pharynx, or the larynx.
TREATMENT:
● Immediate Hospitalization
● Bed regimen (localized forms - 10 days, toxic forms - not less than 35-45 days)
● Specific treatment- antitoxic antidiphtherial Serum (from 30-50 thousand IU in localized
forms and 100-120 thousand IU in toxic forms by Bezredka method)
● Glucocorticoids (In toxic forms and croup)
● Antibiotics (penicillin, tetracycline, erythromycin)
● Strychninum (in toxic forms)
● In case of croup - inhalations, broncholitics, diuretics, glucocorticoids, antibiotics,
antihistamine, lytic admixture
● under the indications - intubation, tracheotomy.
104. Emergency aid at croup and diphtheria hypertoxic forms.
Peculiarities:
● Incubation period 8-12 days
● Prodromal period: high fever lasting 4-7 days. Malaise, anorexia. Cough, coryza and
conjunctivitis. Koplick spots inside the cheek opposite second molar
● Period of exanthema: Erythematous Maculopapular rash that becomes confluent begins on
the face and then proceeds to trunk , extremities, palms and soles. Lasts about 5 days.
● Desquamation and brown staining which spares palms and soles
● Generalized lymphadenopathy, mild hepatomegaly and appendicitis may occur due to
generalized involvement of lymphoid tissues.
106. Peculiarities of rubella in adults.
Peculiarities:
● Incubation period 14-21 days
● Prodromal period (usually absent in children): eye pain on lateral and upward eye
movement, conjunctivitis, sore throat, headache, general body aches, low grade fever, chills,
anorexia. Tender lymphadenopathy particularly posterior auricular and suboccipital lymph
nodes.
Forchheimer sign: pinpoint maculopapular Enanthema on soft palate.
● Exanthema (called 3 day measles): discrete rose-pink maculopapular rash which can be
pruritic. Begins on face and neck and spreads to trunk and extremities in 24 hours.
Then on 2nd say they begin to fade on face and disappear throughout the body on
third day
107. Peculiarities of mumps in adults.
Mumps is a viral illness caused by a paramyxovirus.
spreads easily from person to person through direct contact with saliva or respiratory
droplets of an infected person.
The most common symptoms of mumps that may be seen in both adults and children are:
• Discomfort in the salivary glands (in the front of the neck) or the parotid glands. These
glands may become swollen and tender.
• Other symptoms include fever, muscle aches, headache, loss of appetite, difficulty
chewing.
Peculiarities:
● Incubation period 14-21 days
● Fever lasts about a week and usually subsides before parotitis. , headache, malaise,
anorexia, abdominal pain.
● Within 24 hours patients complain of ear pain near ear lobe which is aggravated by
chewing movement of jaw.
● Enlargement of parotid gland, initially unilateral then bilateral. Edema over parotid gland
typically occurs with non discrete borders, pain with pressure and obscured angle of
mandible.
● Involvement of other salivary glands: submaxillary glands and sublingual glands. Orifices
of ducts may be erythematous and edematous
Classification:
● Primary localized forms
o Meningococcal carrier state
o Acute nasopharyngitis
● Hematogenic generalized forms
o Meningococcemia: typical acute meningococcal sepsis, chronic
o Meningitis
o Meningoencephalitis
● Mixed forms (meningococcemia and meningitis)
● Rare forms: endocarditis, arthritis, irideocyclitis, pneumonia
● Complicalions: sepsis, DIC syndrome, toxic shock, brain edema
● Meningitis: Neck rigidity, positive brudzinski and kerning sign. Hemorrhagic rash
(ptechia, ecchymoses and purpura) on the body.
Severe diffuse or pulsatory headache worse at night, also increases with changing of body
position, sharp sounds and bright light.
Fountain like Vomiting without nausea and no connection with food. Hyperthermia,
hyperkinesia, photophobia, hyperalgesia and hpersomia. Assymetry of reflexes or
hyporeflexia, patients lay with extended head and bent knees. Pathological reflexes.
Tachycardia, tachypnea and arrhythmia. Tongue is dry and covered with dirty
brownish coat. Loss of consciousness.
• Meningoencephalitis
It is rare form of meningococcal infection. In this case the symptoms of encephalitis
predominate, but meningeal syndrome is weakly expressed. Meningococcal
encephalitis is characterized by rapid onset and impetuous cramps, paresises and
paralyses. Prognosis is unfavorable. The mortality is high and recovery is incomplete
even in modern conditions.
Symptoms include:
Fever and chills, Fatigue, Vomiting
Severe aches or pain in the muscles, joints, chest or abdomen
Rapid breathing
Diarrhea.
In the later stages, a dark purple rash
Treatment:
● Etiological treatment: benzylpenicillin 200.000-300,000 IU/kg/d, or ampicillin (or
metycillin) 200-300mg/kg/day, Chloramphenicol: 50-100mg/kg/ day, tetracycline 25mg/kg
if patient resistant to other antibiotics
● Oxygen therapy
● Symptomatic therapy: antipyretics, anti-convulsants as needed
Stages
● I degree (catarrhal)- labored inspiration, retraction of intercostal spaces, barking cough
● II degree (stenosis): Noisy respiration (whistling sound), inspiratory dyspnea with
elongated inspiration (inspiratory stridor). Participation of auxillary muscles (intercostal,
scalene, sternocleidomastoid muscles)
● III degree (asphyxia): acute oxygen insufficiency, sleepiness, cyanosis. Extremities are
cold, thread paradoxical pulse. Cramps.
Emergency Aid:
● Treat underlying cause: In case of diphtheria, give antitoxin
● Mechanical removal of blockage, suction of membranes and mucous
● Give anti-edematic drugs (euphillin)
● Oxygen
● Intubation or tracheotomy as required in severe cases
Stage:
● I degree (compensated stenosis): hoarse voice, rough barking cough, compensated
hyperventilation of lungs pO2 normal
● II degree (Subcompensated stenosis): dyspnea, moist skin, pallor, perioral cyanosis. Mild
participation of auxillary muscles. Hypoventilation of lungs, tachycardia. pO2 normal.
● III degree (Decompensated stenosis)- inspiratory dyspnea, breathing with all auxiliary
muscles. Acrocyanosis, hypotonia, hypotension, superficial breathing. pO2 decreased pCO2
starts to increase
● IV degree (asphyxia): coma, cyanosis of whole body, superficial and labored breating.
Hypotonia, hypotension, bradycardia, aphonia. pCo2 increases severely.
Emergency Aid:
● Cool humidified oxygen. Helium-oxygen mixture to reduce work of breathing in severe
respiratory distress
● Dexamethasone 0.15-0.6mg/kg orally. Max 10mg
● Intubation if airway severely compromised
Acute respiratory failure is a medical emergency in which the usual exchange between
oxygen and carbon dioxide in the lungs does not occur.
Types:
● Hypoxemic: high altitude, pneumonia, atelectasis, asthma, COPD etc. Normal pH, pCO2:
normal or decreased, pO2: decreased
● Hypercapnic: Acute upper airway obstruction, spinal cord disease, exogenous CO2
inhalation etc. pH: decreased, pCO2: increased, pO2: decreased.
● Peri-operative
● Shock
Clinical signs:
● CNS: breathlessness, difficult inspiration or expiration. Restlessness, anxious. In terminal
stages: coma
● Skin: first acrocyanosis then total cyanosis
● Respiratory system:apnea, bradypnea, tachypnea, shallow breathing. Irregular breathing,
dyspnea
● Cardiovascular system: Tachycardia, hypotension
Emergency Care:
● Clean oral cavity
● Provide oxygen
● Artificial ventilation with ambu bag,
● If further inadequacy of breathing:0.5ml of 0.1% atropine and intubation
SECTION 2
1 .The classification of viral hepatitis.
Viral hepatitis is an infection that causes liver inflammation and damage.
Degree of severity:
• Mild, moderate, severe, very severe
2 .The main pathogenic syndromes of viral hepatitis.
Epidemiology
• Fecal-oral mechanism of transmission
Watery route
Alimentary route
Contact way (dirty hands, towels, dishes etc)
• Source of infection
Patients in the incubation, prodromal period and climax of the disease
• Susceptibility
Children after the first year of life, teenagers, young people up to 35 years, patients with
immunosuppression.
• Factors
Contaminated Water, infected food products and household items.
Clinic presentation
● Onset of fever, poor apetite, nausea, pain in the Right Upper Quadrant
● Within few days Jaundice, dark urine, clay coloured stools
● Usually mild and self limiting.
4 Clinical and epidemiological features of hepatitis E.
Definition: Hepatitis E is a liver disease caused by infection with a virus known as
hepatitis E virus (HEV).
Epidemiology:
Source of infection: sick people
Mechanism of transmission: fecal oral
Incubation period: 2-6 weeks
Susceptibility : high
Factors of transmission: water, food.
Clinic:
Onset of fever, poor apetite, nausea, pain in RUQ
Within few days Jaundice, dark urine, clay coloured stools
Usually mild and self limiting
Viral Hepatitis: Viral hepatitis is liver inflammation due to a viral infection. It may
present in acute form as a recent infection with relatively rapid onset, or in chronic form.
The most common causes of viral hepatitis are the five unrelated hepatotropic viruses
hepatitis A, B, C, D, and E.
Haemolytic Jaundice: Hemolytic jaundice occurs as a result of hemolysis, or an
accelerated breakdown of red blood cells, leading to an increase in production of bilirubin.
Parameter Viral hepatitis Hemolytic jaundice
Type of serum bilirubin Unconjugated and Unconjugated
increased conjugated
Urine urobillinogen Increased/decreased/ normal Increased
PTT Abnormal, not corrected with Normal
vitamin K
Additional features Increase ALT/AST Blood smear:
hemolytic anemia
Viral Hepatitis: Viral hepatitis is liver inflammation due to a viral infection. It may
present in acute form as a recent infection with relatively rapid onset, or in chronic form.
The most common causes of viral hepatitis are the five unrelated hepatotropic viruses
hepatitis A, B, C, D, and E.
Obstructive Jaundice: Obstructive jaundice occurs as a result of an obstruction in the bile
duct. This prevents bilirubin from leaving the liver.
Parameter Viral hepatitis Obstructed jaundice
Type of serum Unconjugated and Conjugated
bilirubin conjugated
increased
Urine Increased/decreased/ Decreased or absent
urobillinogen normal
PTT Abnormal, not Abnormal, corrected with Vitamin K
corrected with
vitamin K
Additional Increase ALT/AST. Increased Serum ALP> 3 times
features Jaundice normal. Itching Jaundice with greenish
tinge
Viral Hepatitis: Viral hepatitis is liver inflammation due to a viral infection. It may
present in acute form as a recent infection with relatively rapid onset, or in chronic form.
The most common causes of viral hepatitis are the five unrelated hepatotropic viruses
hepatitis A, B, C, D, and E.
Leptospirosis: Leptospirosis is a blood infection caused by the bacteria Leptospira.
Signs and symptoms can range from none to mild (headaches, muscle pains, and fevers) to
severe (bleeding in the lungs or meningitis).
Parameter Viral hepatitis Leptospitosis
Source of Sick people or Zoonosis/environment
infection carriers
Main features Flu-like symptoms Flu like symptoms with myositis of calf
with myalgia, muscles and acute renal failure, jaundice
jaundice
Hepatobilliary Hepatitis Hepatitis, acalculous cholecystitis
sysytem
Diagnosis Blood ELISA test Tissue biopsy microscopic agglutination
test
Definition: Hepatitis A virus (HAV) and hepatitis E virus (HEV) are the most common
causes of acute hepatitis in humans worldwide. Most HAV and HEV infections are acquired
through contaminated water and food. Symptoms include: Fever, Fatigue, Loss of appetite,
Nausea, Vomiting, Abdominal pain, Jaundice.
● CBC: leukopenia with neutropenia.
● Biochemical: increased AST,ALT, ALP
● Serological diagnoses IgM Anti-HAV for hepatitis A, IgM Anti-HEV for recent infection.
If IgG anti-HAV, it’s for vaccinated patients
Definition: Hepatitis A virus (HAV) and hepatitis E virus (HEV) are the most common
causes of acute hepatitis in humans worldwide. Most HAV and HEV infections are acquired
through contaminated water and food. Symptoms include: Fever, Fatigue, Loss of appetite,
Nausea, Vomiting, Abdominal pain, Jaundice.
● Bed rest
● Supportive and symptomatic therapy
● Adequate nutrition: diet low fat, carbohydrates.
● Desintoxication therapy: glucose, rheosorbilact, isotonic solution
● Sorbents
● Ferments: mezim, contrical
● Lactulose
● Postexposure therapy
12.Treatment of patients with hepatic encephalopathy.
● Prednisolone 1-3mg/kg
● Lactulose 10-30g PO 2-4 times daily
● Rifaximin 550mg PO twice daily or Canamycin
● Stop diuretic therapy
● Correct electrolyte imbalance
● Diet: high glucose, low protein
Definition: Hepatitis B is an infectious disease caused by the hepatitis B virus (HBV) that
affects the liver; it is a type of viral hepatitis. It can cause both acute and chronic infection.
Many people have no symptoms during the initial infection.
Epidemiology
● Source of infection: sick people and carriers
● Mechanism of transmission: contact
● Mode of transmission: Sexual, blood transfusion, drug users, barber shops, stomatologists,
tattoo. Hepatitis B can stay on tools for long, not killed by normal anesthetic
● Incubation period 6 weeks- 6months
● Susceptibility: high
Clinic:
● Gradual onset of dyspeptic and intoxication syndrome
● Early in course of disease athralgic syndrome develops
● Progressive appearance of jaundice: 2 weeks and more. Jaundice is prolonged and severe.
● Presence of asthenic (intoxication) syndrome throughout the whole period of the disease
Definition: Hepatitis D, also known as the hepatitis delta virus, is an infection that causes
the liver to become inflamed. This swelling can impair liver function and cause long-term
liver problems, including liver scarring and cancer. The condition is caused by the hepatitis
D virus (HDV
Epidemiology
● Source of infection: sick people with hepatitis B
● Mechanism of transmission: contact
● Mode of transmission: Sexual, blood transfusion, drug users, barber shops, stomatologists,
tattoo. Hepatitis B can stay on tools for long, not killed by normal anesthetic
Clinical
● Co-infection with hepatitis D: Identical features of hepatitis B. Can lead to fatal hepatic
necrosis
● Hepatitis D Superinfection: Worsens patient’s general condition. Severe signs of Hepatitis
B
Hepatitis C: determine the genotype 1-5, A or B. Usually IgG anti-HCV. If IgM and IgG
anti-HCV present it is chronic re-infection.
Definition: Hepatitis B is an infectious disease caused by the hepatitis B virus (HBV) that
affects the liver; it is a type of viral hepatitis. It can cause both acute and chronic infection.
Many people have no symptoms during the initial infection.
Epidemiology
● Source of infection: sick people and carriers
● Mechanism of transmission: contact
● Mode of transmission: Sexual, blood transfusion, drug users, barber shops, stomatologists,
tattoo. Hepatitis B can stay on tools for long, not killed by normal anesthetic
● Incubation period 6 weeks- 6months
● Susceptibility: high
Clinic:
● Gradual onset of dyspeptic and intoxication syndrome
● Early in course of disease athralgic syndrome develops
● Progressive appearance of jaundice: 2 weeks and more. Jaundice is prolonged and severe.
● Presence of asthenic (intoxication) syndrome throughout the whole period of the disease
Antiviral medications
● Entecavir
● Tenofovir
● Lamivudine
● Adefovir
● Telbivudine
Antiviral medications
● Pegylated Interferon
● Ribavirin
● Protease inhibitors (simeprevir, paritaprevir, glecaprevir, grazoprevir)
Definition: HIV (human immunodeficiency virus) is a virus that attacks the body’s immune
system. If HIV is not treated, it can lead to AIDS (acquired immunodeficiency syndrome.
Epidemiological data: HIV is spread primarily by unprotected sex (including anal and oral
sex), contaminated blood transfusions, hypodermic needles, and from mother to
child during pregnancy, delivery, or breastfeeding.[13] Some bodily fluids, such as saliva,
sweat and tears, do not transmit the virus. South Africa, Nigeria, India, South East Asia,
Carribbean Sea, Eastern Europe
Epidemiology
● Source of infection: sick people and carriers
● Mechanism of transmission: contact
● Ways of transmission: Sexual contact, iv drug abusers, infection of medical personell.
Risk group
● Homosexuals unprotected sex
● Multi sexual partners (prostitutes), unprotected sex
● IV drug abusers
● Infected mothers to child
● Viral Hepatitis B, C, D
● Recipients of blood transfusion or organs
Definition: HIV (human immunodeficiency virus) is a virus that attacks the body’s immune
system. If HIV is not treated, it can lead to AIDS (acquired immunodeficiency syndrome.
Epidemiological data: HIV is spread primarily by unprotected sex (including anal and oral
sex), contaminated blood transfusions, hypodermic needles, and from mother to
child during pregnancy, delivery, or breastfeeding.[13] Some bodily fluids, such as saliva,
sweat and tears, do not transmit the virus. South Africa, Nigeria, India, South East Asia,
Carribbean Sea, Eastern Europe
● Stage 2: Weight loss less than 10%, minimum defeat of skin and mucous (seborrhea
dermatitis, mycotic defeat of nails, recurrent ulcers of mucous of oral cavity, angular
chelates). Episodes of herpes zoster, recurrent episodes of upper respiratory tract (bacterial
sinusitis), Level of functional ability 2 (WHO: performance status 2): symptomatic
course, normal level of daily activity
● Stage 3: weight loss > 10%, hyperthermia more than 1 month, pneumocyst pneumonia,
cerebral toxoplasmosis, extrapulmonary criptococosis, cryptosporidiosis with diarrhea
more than 1 month. Cytomegalovirus infection with defect of any organs except liver,
spleen and lymph nodes. Level of functional ability 3 (Performance status 3): patient lay
in bed less than 50% of daily time
Definition: HIV (human immunodeficiency virus) is a virus that attacks the body’s immune
system. If HIV is not treated, it can lead to AIDS (acquired immunodeficiency syndrome.
Epidemiological data: HIV is spread primarily by unprotected sex (including anal and oral
sex), contaminated blood transfusions, hypodermic needles, and from mother to
child during pregnancy, delivery, or breastfeeding.[13] Some bodily fluids, such as saliva,
sweat and tears, do not transmit the virus. South Africa, Nigeria, India, South East Asia,
Carribbean Sea, Eastern Europe
Clinical data:
● prolonged fever more than 1 month
● generalized lymphadenopathy: more than 3 lymph nodes enlarged in different anatomical
groups of lymph nodes
● Diarrhea more than 1 month
● weight loss more than 10%
● opportunistic infection,
● Wasting syndrome
● Mosquito infects a person by taking a blood meal. They release sporozoites from their
salivary glands. Infects the organism in 2 phases
● Exoerythrocytic phase: sporozoutes enter blood stream and migrate to hepatic system. In
hepatocytes they multiply into merozoites, rupture the liver cells and escape into blood
stream
● Erythrocytic phase: the merozoites infect the red blood cells where they develop into
ring forms Trophozoites and schizonts which in turn produce more merozites.
Pathogenesis
- Tissue schizogony (incubation period)
- Erythrocyte schizogony
- Typical attack- massive destruction of erythrocytes, massive appearance of parasites and
products of their metabolism
- Disturbance of thermoregulation centre, increasing of vessels penetration
- Disturbance of microcirculation, water electrolytes balance, vegetative neurotic system
- Development of hemolytic anemia
- Hepatosplenomegaly
- Developmnt of coma
Relapses are defined as recurrences of malarious symptoms and the reappearance of malaria
parasites in the peripheral blood, following recovery from the initial attack.
● Cyclical occurrence of coldness followed by rigor and then fever and sweating lasting 4-6
hours every 2 days in P.vivax and P.ovale infections, while every 3 days for P.malariae,
P.falciparum can have recurrent fever every 36-48 hours or less.
● Shivering, arthralgia
● Anemia, hemoglobinuria
● Retinal damage
● Convulsions
● P.falciparum causes severe malaria: coma, splenomegaly, severe headache, cerebral
ischemia, hepatomegaly, hypoglycemia and hemoglobinuria with renal failure.
Viral hepatitis is liver inflammation due to a viral infection. The most common causes of
viral hepatitis are the five unrelated hepatotropic viruses hepatitis A, B, C, D, and E.
33.Complications of malaria.
Malaria; An infectious disease caused by protozoan parasites from the Plasmodium family
that can be transmitted by the bite of the Anopheles.
● Plasmodium falciparum: Cerebral Malaria (seizures and coma), acute renal failure, non
cardiogenic pulmonary edema, tropical splenomegaly
● Plasmodium Vivax: late splenic rupture (2-3 months after initial infection)
● Plasmodium Malariae: immune complex glomerulonephritis
● In pregnant women it can lead to still birth, infant mortality, low birth weight
35.Prevention of malaria.
Malaria; An infectious disease caused by protozoan parasites from the Plasmodium family
that can be transmitted by the bite of the Anopheles.
Eradication of mosquito is the primary aim.
● Avoid mosquito bites
● Sleep in rooms properly screened with gauze over windows and doors
● Spray room with insecticides before entering
● Wear long sleeve shirts
● Use mosquito repellant cream
The incubation period is highly variable, usually 2-4 weeks, can be 1 week to 2 months or
longer.
Influenza; commonly called "the flu", is an infectious disease caused by influenza viruses.
Symptoms range from mild to severe and often include fever, runny nose, sore throat,
muscle pain, headache, coughing, and fatigue.
● Complaints: weakness, headache, pain in joints, chills, dry mucous membranes and poor
appetite, dry coated tongue. Dizziness, confusion
● Slurred speech
● Nausea, vomiting, diarrhea
● Hectic fever
● Skin is pale, moist or icteric in severe cases. Cold clammy skin.
● Rashes of different types, mostly hemorrhagic. Others can be present too. Localized
anywhere on the body
● Tachycardia, hypotension. Systolic murmur at apex. Heart is enlarged
● Dyspnea, tachypnea
● Hepatosplenomegaly
● Low urine output
● Loss of consciousness
42. The epidemiology of epidemic typhus and Brill-Zinsser disease.
Epidemic typhus is caused by Rickettsia prowazekii. Symptoms are prolonged high Fever,
intractable headache and macolopapular rash.
Epidemic typhus occurs in Central and South America, Africa, northern China, and certain
regions of the Himalayas. Outbreaks may occur when conditions arise that favor the
propagation and transmission of lice. Brill-Zinsser disease develops in approximately 15%
of people with a history of primary epidemic typhus.
● Abrupt onset of high fever,chills, headache, myalgia, malaise. Fever worsens and quickly
becomes unremitting. Fever on days 3-4, 8-9, 12-13.
● Giddiness, backache, anorexia, nausea.
● Face is edematous, flushed. Eyes are brilliant with injected sclera (rabbits eyes)
● Symptom of Rosenberg: Ptechial enanthema on basis of uvula 2-3rd day of disease. May
be on transitive folds of conjunctiva from third-fourth day (symptom of Kjary-Acuyne)
● Govorov-Godeljae symptom: tremor of tongue declining to side.
● Rash: maculopapular/ petechial rash on 4-7 day on chest then axilla, trunk and spread
peripherally. Never on face. Disappears with decreasing temperature
● Rigors, myalgia, malaise
● CNS symptom: mental dullness to coma, stupor, sensitivity to light and delirium
● Regional and generalized lymphadenopathy. Mild hepatosplenomegaly
44. Clinical features of Brill-Zinsser disease.
It occurs due to reoccurrence of epidemic louse-borne typhus caused by Rickettsia
prowazekii years after initial attack.
Brill-Zinsser disease can occur >40 years after primary infection
It has same clinical presentation as Epidemic typhus but milder.
● Abrupt onset of high fever,chills, headache (unremitting).
● Enanthema **
● Rash: maculopapular/ petechial rash on 4-7 day on chest then axilla, trunk and spread
peripherally
● Rigors, myalgia, malaise
● CNS symptom: mental dullness to coma, stupor, sensitivity to light and delirium
● Regional and generalized lymphadenopathy. Mild hepatosplenomegaly
Leptospirosis generally presents after contact with urine of infected animals. with cough,
jaundice, chest pain, lymphadenopathy, hepatosplenomegaly and is diagnosed by PCR.
Epidemic typhus caused by Rickettsia prowazekii occurs after being bitten by a tick or
louse, can only be transferred human to human: presented by high fever, cough, rash,
muscles and joint pain. Sometimes liver and spleen can be enlarged. Eyes look like Rabbits
eye. Enanthema on uvula, tremor of tongue. Diagnosed by serology
Lyme borreliosis also known as Lyme disease, is an infectious disease caused by the
Borrelia bacterium which is spread by ticks.
The disease is currently recognized as the most common vector-borne disease in Europe and
North America.
Registration of Lyme borreliosis in humans in Ukraine began in 2000. It was proved that the
incidence of the disease in the country was growing each year from 58 cases in 2000
(incidence: 0.12/100,000) to 3413 in 2015 (incidence: 7.96/100,000) (2).
The western part of Ukraine, including the Ternopil area, is recognised as an endemic region
for LB, as it is located in the forest-steppe region with mixed forests, fertile soils, as well as
adequate moisture and optimal temperatures.
1. To treat the Erythrema migrans: we give doxycycline 100mg PO bid 10-15 days,
Amoxicillin 500mg P0 tid, Cefuroxime: 500mg bid. If allergy to above give
Azithromycin 500mg single dose, erythromycin 500mg qid, clarithromycin.
2. AV block, CNS: IV antibiotics ceftriaxone 2g IV once/day 14 days. Benzylpenicillin IV
or IM 2.4g every 4-6hours. Cefotaxime 2g tid.
3. To treat Arthritis: antibiotic + NSAID, diclofenac 50mg tid, ibuprofen 300-400mg tid
(max 2400mg). Recurrent arthritis: antibiotics + arthroscopic synovectomy + intra-
articular injection.
57.Classification of erysipelas.
Erysipelas is an infection of the upper layers of the skin (superficial). The most common
cause is group A streptococcal bacteria, especially Streptococcus pyogenes. Erysipelas
results in a fiery red rash with raised edges that can easily be distinguished from the skin
around it.
Classification:
1. According to etiology: Streptococcal Group A, Streptococcal group B, staphylococcus,
2. According to clinical form(ie. The character of local changes ) : Erysipelas
erythematosum, erysipelas vasiculosum, erysipelas haemorrhagicum, erysipelas abscedens,
erysipelas gangrenosum
3. According to complication: abscess, gangrene, thrombophlebitis, bacteremia,
streptococcal toxic shock syndrome
58 .Clinic of erysipelas erythematous form.
Erysipelas is a human infectious disease infectious disease of streptococcal etiology with
acute and chronic forms and is characterized by intoxication syndrome and local changes
looking like circumscribed locus of serous hemorrhagic inflammation of skin .
Clinical signs of the erythematous form is :
• It has an acute onset
• Intoxication syndrome (High fever, shaking, chills, fatigue, headache, vomiting
• Early signs of the disease before the local changes include:
1. Regional lymphadenitis and lymphangitis
2. Burning pain in erysipelas Can occur on skin of face that starts 5-6 hours before the local
inflammatory focus forms
• Local process is characterized by sharply circumscribed hyperemia with peripheral
inflammatory wall, edge painfulness , and local temperature reactions (erythematous forms )
• Local process is associated with lymphatic edema of various degree.
• Re-infection causes lymphadenitis
3. Local treatment
• Don’t touch erythematous forms
• Emulsions ,Ointments and antiseptic solutions are meant only for bullous forms
4. Ambulatory monitoring:
• finishing treatment
• Sanitation of the chronic focuses of infection
• Relapse prophylaxis: bicillin once a month for 6 months after disease
1. Penicillin G: 0.6-1.2 million U IM bid for 10 days
2. Dicloxacillin 125-500mg PO qid for 10days
3. Nafcillin 1-2g IV qid for 7 days
60 .Treatment of recurrent forms of erysipelas.
3. Local treatment
• Don’t touch erythematous forms
• Emulsions ,Ointments and antiseptic solutions are meant only for bullous forms
4. Ambulatory monitoring:
• finishing treatment
• Sanitation of the chronic focuses of infection
• Relapse prophylaxis: bicillin once a month for 6 months after disease
• Icteric syndrome: called weils disease, usually severe. Fever, renal failure, jaundice,
hemorrhage and respiratory distress. May involve heart, CNS and muscles. It present with
vascular collapse, thrombocytopenia , hemorrhage,
• Hemorrhagic syndrome
• Asthenovegetative syndrome
• Intoxication syndrome
• Hepatomegaly
• Pneumonia syndrome
• Meningeal syndrome
• Biologic: using guinea pigs, inject infected material. If they die, it confirms diagnosis
71.Classification of tetanus.
o Generalised: trismus (lock jaw), repeated painful spasms any part of the body.
Restlessness, irritability, dysphagia. Opisthotonus: spasm of muscles causing backward
arching of head, neck and spine. Seizures can be seen and respiratory failure
o o Grade 1(mild): mild trismus (lock jaw), general spasticity, little or no dysphagia
▪ Grade 2 (moderate): moderate trismus and generalized spasticity, mild dysphagia and
fleeting spasms. Moderate respiratory embarrassment
▪ Grade 3a(severe): severe trismus and generalized spasticity. Severe dysphagia and
respiratory difficulties. Severe and prolonged spasms
▪ (both spontaneous and on stimulation
• Grade 3b: same as 3a with autonomic dysfunction
o Localised: muscle spasms on one extremity or one body region
o Cephalic: due to head injury or middle ear infection: cranial nerve palsies which progress
to generalized tetanus
o Neonatal: associated with umbilical stump infection in neonates born to mothers who have
not been immunized.
o Maternal: tetanus during pregnancy and 6 weeks after.
• At first, there's a tingling, prickling, or itching feeling around the bite area. A person also
might have flu-like symptoms such as a fever, headache, muscle aches, loss of appetite,
nausea, and tiredness.
• After a few days, neurological symptoms develop, including:
• irritability or aggressiveness
• excessive movements or agitation
• confusion, bizarre or strange thoughts, or hallucinations
• muscle spasms and unusual postures
• seizures (convulsions)
• weakness or paralysis (when a person cannot move some part of the body)
• extreme sensitivity to bright lights, sounds, or touch
• Classic encephalitic (furious) rabies: hydrophobia and hyperexcitability
• Paralytic (dumb) rabies: flaccid muscle paralysis
• Non-classic atypical rabies (bite of bat): neuropathic pain, focal brainstem sign and
myoclonus
• A fast-acting dose of rabies immune globulin: Delivered as soon as possible, close to the
bite wound, this can prevent the virus from infecting the individual.
• A series of rabies vaccines: These will be injected into the arm over the next 2 to 4 weeks.
These will train the body to fight the virus whenever it finds it.
•
• Rabies vaccine 1ml on days 0,3,7 and 14. Rabies immunoglogulin 20IU/kg when
incubation period is less than 4 weeks.
• Intensive cardiopulmonary supportive care
• Symptomatic treatment
79.Prevention of rabies.
• regular antirabies vaccinations for all pets and domestic animals
• bans or restrictions on the import of animals from some countries
• widespread vaccinations of humans in some areas
• educational information and awareness
• If bitten by animal: animal should be caged and monitered for 10 days to see if signs of
rabies appear.
• If animal with rabies attack you, step outside their visual acuity
• Vaccinate animals and humans with rabies vaccine
• Post exposure prophylaxis with rabies vaccine
• This phase lasts for three to seven days and is characterised by the onset of renal failure
and proteinuria.
Diuretic phase :
• This is characterized by diuresis of three to six litres per day, which can last for a couple of
days up to weeks.
Convalescent phase :
• This is normally when recovery occurs and symptoms begin to improve. This syndrome
can also be fatal. In some cases, it has been known to cause permanent renal failure.
• Around 15% progress from the acute phase to the toxic phase which usually begins on 3rd
day
▪ On 3rd day: jaundice, hemorrhagic rash on skin, hepatosplenomegaly
▪ 5th day: pale face with cyanotic tint, delirium. Nausea and vomiting. Dark brown or black
emesis. Ptechia and ecchymoses on trunk and extremities. Nasal and gum bleeding
• followed by death in 50% of cases within 10-14 days.
o Leishmaniasis is a disease caused by the Leishmania parasite. This parasite typically lives
in infected sand flies and is transmitted by the bite of infected sand fly
• Cutaneous leishmaniasis includes the following features:
• Localized cutaneous leishmaniasis: Crusted papules or ulcers on exposed skin; lesions may
be associated with sporotrichotic spread
• Diffuse (disseminated) cutaneous leishmaniasis: Multiple, widespread nontender,
nonulcerating cutaneous papules and nodules; analogous to lepromatous leprosy lesions
▪ CL is characterized by skin lesions (open or closed sores), which typically develop within
several weeks or months after exposure. They typically progress from small papules to
nodular plaques, and often lead to open sores with a raised border and central crater (ulcer),
which can be covered with scales or crust. The lesions usually are painless but can be
painful, particularly if open sores become infected with bacteria.
▪ Satellite lesions, regional lymphadenopathy, and nodular lymphangitis can be noted. The
sores usually heal eventually, even without treatment. However, they can last for months or
years and typically result in scarring
▪ Treatment: fluconazole and amphotericin B
• Other consequences, which can become manifest anywhere from a few months to years
after infection, include fever, damage to the spleen and liver, and anemia
• Staining ulcer exudates with giemsa stain or methylene blue for microscopic investigation
• Ulcer, blood or CSF culture on sheep blood or peptone agar
• Serological: ELISA
-tissue biopsy to check for cutaneous anthrax
-Chest x-ray or CT scan
89.Epidemiology of plague.
Plague is a disease caused by Yersinia pestis usually found in small mammals and their fleas
Epidemiology: it occurs in various countries such as Africa, Asia , south America and the
USA
-it is gram negative , non motile, non spore forming bacillus
- it is resistant to freezing temperatures
-human plague occurs from bite of an infected flea
-outbreaks are cyclical corresponding to rodent reservoirs and arthropod vector
correspondents
-Vectors are rodents, carnivorous mammals(cats,foxes,dogs), patient with pneumonic plague
Mechanism of transmission: droplet contact, physical contact, sexual contact, touching soil,
airborne/aerogenic , fecal-oral
90.The clinic of skin and bubonic plague.
Bubonic plague is a disease caused by Yersinia pestis usually found in small mammals and
their fleas
Symptoms include:
• Malaise and headache usually severe with mental dullness.
-Backache.
• Fever with moderate rigor or repeated shivering
• Tachycardia and tachypnea
• Skin is hot and dry, face bloated, eyes injected and hearing dull
• Tongue is swollen and coated with creamy fur.
• Burning in throat or stomach with nausea and vomiting
• Constipation
• Enlarged lymph nodes
• The affected gland is hard and tender.
• Buboes (inflammatory swelling of lymphatic glands) the size of walnut or
egg appear in inguinal glands, axillary region, or cervical
• Leukocytosis, increase in polymorph nuclear leucocytes
94.Treatment of plague.
Plague is a disease caused by Yersinia pestis usually found in small mammals and their fleas
• Prodromal period: shivering, fever, headache, malaise, muscle ache, dizziness, anorexia.
Sleep disturbance with night sweating. Vomiting, nose bleeds, loss of consciousness and
delirium. Conjunctivitis
• Period of high point of disease: Primary buboes (inflammatory changes in lymph node) in
region near site of inoculation of disease. Secondary buboes occurs due to hematogenous
spread of disease. Buboes can be as big as nut or egg. They are dense, painful with no
periadenitis. Buboes can become completely dissolved, suppurated, ulcerated and eventually
scarred.
• Convalescence: softening e.g. Bubo after 2-3 weeks. First hyperemia of skin then buboes
break and drain, the pus is thick, white and no smell.
99.Treatment of tularemia.
Tularemia is a rare infectious disease caused by Francisella tularensis.Also known as rabbit
fever or deer fly fever, it typically attacks the skin, eyes, lymph nodes and lungs. The
disease mainly affects rabbits, hares, and rodents, such as muskrats and squirrels.
• Pain in epigastric region of abdomen, umbilical or right iliac area, less often in right
hypochondrium and left iliac area
-fever
-nausea
-vomiting
-bloody diarrhea
• In the form of mesenteric lymphadenitis, terminal ileitis, acute appendicitis
• Enlarged, painful and grumbling cecum and mesenteric lymph nodes
.
102.Clinical features of pseudotuberculosis.
Yersinia pseudotuberculosis is a, gram-negative bacillus bacterium that causes Far East
scarlet-like fever in humans, who occasionally get infected zoonotically, most often through
the food-borne route.
Clinical features:
• catarrhal syndrome: Pharyngeal and tonsilar erythema without the exudates, erythema of
the soft palate, conjunctivitis, coryza
• intoxication syndrome: fever, headache
• Abdominal syndrome; tenderness during the palpation of abdomen,
may be acute appendicitis
• Dyspepsia: nausea, vomiting, liquid feces.
• Rashes: maculopapulous (like in scarlet fever), may be erythematosus
or even erythema nodosum may developed. rash appears on face and
intensifies periorbitally and neck
• Arthritis of knees , elbows, foot and hand small joints .
• Presence of “strawberry” tongue.
***Source of infection-wild and home animals (rats, dogs, foxes, cats and other);
• Way of transmitting – alimentary;
• Susceptible organism – children (not infants), adults.
Etiological treatment
! in mild cases it’s not used;
! in moderate and severe cases – by chloramphenicol 10-20 mg/kg 4 times per
day orally during 6-9 days. If not effective – alternative
antibiotics: cefalosporins of the 3rd-4th generation 100-150 mg/kg,
aminoglycosides of the 3rd generation. 7-10 days
Pathogenetic treatment:
! detoxification therapy: oral to all patient and in case of mild dehydration, or
parenteral: Rheosorbilact, 0.9% NaCl, 5% glucose (moderate and severe
dehydration);
! Sorbents: enterosgel 0.5-1 g/kg, polysorb (Silix) 100-200 mg/kg per day in 3
doses for 5-7 days
! antihistamines: claritin, cetirizin, suprastin, pipolphen 1-3 mg/kg per day,
! corticosteroids 1-3 mg/kg with a short course (in severe cases, in case of
myocarditis),
! Normalisation of the intestinal flora: linex, bifi-form, acidophilus 1-2 caps 2-3
times per day not less than 2 wks;
! antipyretics: paracetamol 10 mg/kg not more than 5 times per day,
! NSAIDs in case of arthritis, carditis, nodular erythema (ibuprofen 20 mg/kg per
day, aspirin 50-75 mg/kg per day, voltaren 2-3 mg/kg per day, indomethacin
2-3 mg/kg per day (in average doses).
SECTION 3
1. Epidemic process and its components.
Components
● Infectious agent
● transmission factors
● Susceptible individual ( without immunity)
The reservoir of an infectious agent is the habitat in which the agent normally lives,
grows, and multiplies. Reservoirs include humans, animals, and the environment.
Human reservoirs - Diseases that are transmitted from person to person without
intermediaries include the sexually transmitted diseases, measles, mumps, streptococcal
infection, and many respiratory pathogens.
Animal reservoirs - Many of these diseases are transmitted from animal to animal, with
humans as incidental hosts. infectious disease that is transmissible under natural conditions
from vertebrate animals to humans. Long recognized zoonotic diseases include brucellosis
(cows and pigs), anthrax (sheep), plague (rodents), trichinellosis/trichinosis (swine),
tularemia (rabbits), and rabies (bats, raccoons, dogs, and other mammals). HIV/AIDS,
Ebola infection and SARS.
Environmental reservoirs - Plants, soil, and water in the environment are also reservoirs
for some infectious agents. Many fungal agents, such as those that cause histoplasmosis,
live and multiply in the soil. Outbreaks of Legionnaires disease are often traced to water
supplies in cooling towers and evaporative condensers, reservoirs for the causative organism
Legionella pneumophila.
Sick person is the primary source from which the infection spreads and is the most
dangerous source of infection because he or she releases a great quantity of the pathogenic
microorganisms.
A carrier is a person with infection who is capable of transmitting the pathogen to others
Carriers release pathogenic agents into the environment in a smaller quantity than patients
with clinically manifest diseases, but they are danger to community too since they actively
associate with healthy people and spread the infection.
Carriers commonly transmit disease because they do not realize they are infected, and
consequently take no special precautions to prevent transmission. Symptomatic persons who
are aware of their illness, on the other hand, may be less likely to transmit infection because
they are either too sick to be out and about, take precautions to reduce transmission, or
receive treatment that limits the disease.
Asymptomatic or passive or healthy carriers are those who never experience symptoms
despite being infected.
Incubatory carriers are those who can transmit the agent during the incubation period
before clinical illness begins.
Convalescent carriers are those who have recovered from their illness but remain capable
of transmitting to others.
Chronic carriers are those who continue to harbor a pathogen such as hepatitis B virus or
Salmonella Typhi, the causative agent of typhoid fever, for months or even years after their
initial infection.
Rodents, animals that are almost everywhere, can be reservoirs of important zoonotic
diseases such as leptospirosis, leishmaniasis, relapsing fever, tularemia, plague, Q fever,
salmonellosis, and hantavirus. These diseases can be transmitted to humans by touch or bite
of the animal, direct contact with their feces, urine and saliva, bite of their vectors (ticks,
mosquitoes, fleas, …), ingestion of food or waters contaminated with their feces or urine,
inhalation of dried feces of infected rodents or during dissection and autopsy of these
animals. With early diagnosis and prompt treatment, most of these diseases are not a serious
threat to human. This reflects the importance of having enough knowledge about theses
diseases, especially by those who deal with them directly. Since the vaccine has not been
approved for the prevention of most of these diseases, educating of people especially those
at most risk of infection, limiting the contact with rodents, use of personal protective
equipment (boots, gloves, masks, etc.), washing the hands with soap and water regularly
following close contact with rodents and avoiding the insect bites is necessary in the
prevention of these diseases.
8. Definition of meaning- Mechanism of trans mission – its chains , factors and ways of
infectious disease transmissions
Mechanism of transmission: It is a process that begins when an infectious agent or
pathogen leaves its reservoir, source, or host through a portal of exit and is conveyed by
some mode of transmission, enters the host through an appropriate portal of entry, and
infects a susceptible host.
OR
Mechanism of transmission: The combination of routes by which the pathogenic
microorganisms are transmitted from an infected macroorganism to a healthy one
Main factors are involved in transmission of infection: air, water, foods, soil, utensils,
arthropods (living agents).
Three phases are distinguished in the transmission of infection from one macroorganism to
another:
● 1st phase: excretion of the causative agent from the infected macroorganism
● 2nd phase: staining of the causative agent in environment
● 3rd phase: infectious agent’s penetration into healthy (susceptible) organism.
- direct contact, droplet, indirect transmission, vectors,
9. Types of infectious diseases mechanisms of transmission.
Direct contact occurs through skin-to-skin contact, kissing, and sexual intercourse. Direct
contact also refers to contact with soil or vegetation harboring infectious organisms. Thus,
infectious mononucleosis (“kissing disease”) and gonorrhea are spread from person to
person by direct contact. Hookworm is spread by direct contact with contaminated soil.
spread refers to spray with relatively large, short-range aerosols produced by sneezing,
coughing, or even talking.
Droplet spread is classified as direct because transmission is by direct spray over a few feet,
before the droplets fall to the ground. Pertussis and meningococcal infection are examples
of diseases transmitted from an infectious patient to a susceptible host by droplet spread.
Indirect transmission refers to the transfer of an infectious agent from a reservoir to a host
by suspended air particles, inanimate objects (vehicles), or animate intermediaries (vectors).
Vectors such as mosquitoes, fleas, and ticks may carry an infectious agent through purely
mechanical means or may support growth or changes in the agent. Examples of mechanical
transmission are flies carrying Shigella on their appendages and fleas carrying Yersinia
pestis, the causative agent of plague, in their gut.
Methods
There are four types of disinsection methods that can be used:
• Residual- is carried out while no passengers are onboard. The entire aircraft is
sprayed with a residual insecticide and lasts eight weeks
• Pre-embarkation- is carried out while no passengers are on board. Crew may be on
board as this method is completed up to 40 minutes prior to passengers boarding the
aircraft. The treatment lasts for the duration of the single flight
• Pre-flight and top of descent- refers to a two-part process consisting of pre-flight
and top of descent spraying. Pre-flight spraying is followed by a further in-flight
spray of a non-residual insecticide, carried out at top of descent as the aircraft starts
its descent into either Australia or New Zealand. The treatment lasts for the duration
of the single flight
• On-arrival- is an in-flight spray of a non- residual insecticide, carried out once the
aircraft lands in Australia or New Zealand. The treatment lasts for that one arrival.
Types of disinfectant
● Low-level disinfectants- kill most vegetative bacteria and some fungi as well as enveloped
(lipid) viruses example is hepatitis b, c, hantavirus hiv. They do not kill myocobacteria or
bacterial spores but typically used to clewan environmental surface
● Intermediate-level disinfectants- the kill vegetative bacteria most viruses and fungi but not
resistant bacterial spores
METHODS
Chemical and Physical Method
● Chemical
- Alcohol
- Chlorine and chlorine compounds
- Formaldehyde
- Glutaraldehyde
- Hydrogen peroxide
-Iodophors
- Halogen
- Peracetic acid
- Peracetic acid and hydrogen peroxide
Physical method
● Boiling at 100°C for 15 minutes, which kills vegetative bacteria.
● Pasteurizing at 63°C for 30 minutes or 72°C for 15 seconds, which kills food pathogens.
● Using nonionizing radiation such as ultraviolet (UV) light. UV rays are long wavelength
and low energy.
Sterilization refers to any process that removes, kills, or deactivates all forms of life (in
particular referring to microorganisms such as fungi, bacteria, spores, unicellular eukaryotic
organisms such as Plasmodium, etc.) and other biological agents.
Stages:
Pre-Vacuum, Rising Temperature, Sterilizing and Vacuum-Drying
Methods
Aqueous solutions in glass containers usually reach thermal equilibrium within 10 minutes
for volumes up to 100 mL and 20 minutes for volumes up to 1000 mL.
Dry-heat sterilization
In dry-heat processes, the primary lethal process is considered to be oxidation of cell
constituents. Dry-heat sterilization requires a higher temperature than moist heat and a
longer exposure time. Preparations to be sterilized by dry heat are filled in units that are
either sealed or temporarily closed for sterilization. The entire content of each container is
maintained in the oven for the time . Temperature 160 , 170 , 180 degrees for 180mins ,
60mins and 30mims respectively..
When given in the liquid state or in tablets, the vaccine should be taken together with water.
•In spite of Immune suppression in HIV infected, we can still give Measles, mumps, rubella
vaccines and Oral polio drops ( But Salk killed vaccine is safe).
• In HIV patients do not give BCG vaccine
Ideal vaccine.
•Promotes effective immunity.
•Controls lifelong protection.
•Safe, do not carry side effects.
•Stable, cheap,
•Acceptance by public.
Respiratory infections – are transferred by the droplet mechanism. This group includes
diseases whose causative agents parasitize on the respiratory mucosa and are liberated into
the environment with droplets of sputum during sneezing, cough, loud talks, or noisy
respiration.
• People get infected when the microbes contained in sputum get on the mucosa of the
upper airways.
• Transmission can be minimised by control of overcrowding, proper ventilation and
mosquitoes, ticks, etc., which bite people and introduce the pathogenic agent into the
blood.
• Control of blood infections includes altering natural conditions, improvement of
soils, draining swamps, destroying sites where the insects multiply, disinsection
measures against mosquitoes, ticks, etc., detoxication of sources of infection by their
isolation and treatment, carrying out preventive measures.
• The main measures to control skin infections include isolation and treatment of the
source of infection, killing diseased animals, homeless dogs and cats, improving
sanitation and living conditions of population, personal hygiene, control of
traumatism, and specific prophylaxis
subtypes
● Subtype 1 - typical intestinal infection ( agent stays in the GIT) shigellosis, cholera,
echerichiosis.
● Subtype 2 - Toxic infection ( intensive reproduction of the agent out of the
organism ) food poisoning , botulism and staphylococcal toxicosis
● Subtype 3 - intestinal infection with spreading of the agent beyond the intestine
( amebiasis , ascaridiasis, echinococcosis)
● Subtype 4 - intestinal infection with penetration of the agent into blood with
additional outlet of the agent in the environment with the urine, secretions ( typhoid
fever, brucellosis, leptospirosis)
This group includes diseases whose causative agents parasitize on the respiratory mucosa
and are liberated into the environment with droplets of sputum during sneezing, cough, loud
talks, or noisy respiration. People get infected when the microbes contained in sputum get
on the mucosa of the upper airways. If the causative agent is unstable in the environment, a
person can only be infected by lose contact with the sick or carrier. Pathogenic
microorganisms causing some diseases can persist for a period of time in an enclosure
where the sick is present. Infected particles of sputum or mucus can dry and be suspended in
the air. Some diseases of this group can spread through contaminated linen, underwear,
utensils, toys, etc. It is important to timely reveal the sick and carriers, and also to break the
mechanism of infection transmission: control of overcrowding, proper ventilation and
isolation of enclosures, using UV-lamps, wearing masks, respirators, disinfection, and the
like.
The diseases of this group are transmitted by blood-sucking insects, such as fleas,
mosquitoes, ticks, etc., which bite people and introduce the pathogenic agent into the blood.
Control of blood infections includes altering natural conditions, improvement of soils,
draining swamps, destroying sites where the insects multiply, disinsection measures against
mosquitoes, ticks, etc., detoxication of sources of infection by their isolation and treatment,
carrying out preventive measures. If the source of infection are rodents, measures to control
them are taken. Active immunization is also effective.
The diseases of this group occur as a result of contamination of the skin or mucosa with the
pathogenic microorganisms. 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).
The transmitting factors can include bed linen, clothes, plates and dishes and other utensils,
that can be contaminated with mucus, pus or scales. Pathogenic microorganisms causing
venereal diseases, rabies, AIDS, and some other diseases are transmitted without the agency
of the environmental objects.
Wound infections are characterized by damage to the skin as a result of injury (tetanus,
erysipelas). The main measures to control skin infections include isolation and treatment of
the source of infection, killing diseased animals, homeless dogs and cats, improving
sanitation and living conditions of population, personal hygiene, control of traumatism, and
specific prophylaxis.
In 2016, people age 13 to 24 accounted for 21 percent of the people diagnosed with HIV.
About 80 percent of the diagnoses in this age group (or 6,776 cases) occurred in people
between 20 and 24 years old.
As of 2018, approximately 37.9 million people are infected with HIV globally.[3] There were
about 770,000 deaths from AIDS in 2018
Source
• By having sex. You may become infected if you have vaginal, anal or oral sex with an
infected partner whose blood, semen or vaginal secretions enter your body. ...
• By sharing needles. ...
• From blood transfusions. ...
• During pregnancy or delivery or through breast-feeding.
Ways of transmission occurs mainly through blood, semen, vaginal fluids, and breast milk.
PREVENTION OF HIV
You can use strategies such as
• Abstinence (not having sex)
• Use condoms
• Avoid multiple sex partners/ Limit your sex partners
• Get tested. Be sure you and your partner are tested for HIV and other STIs
• Never reuse or "share" needles, syringes, water, or drug preparation equipment. Only
use needles and syringes that you got from a reliable source (such as drugstores or
needle exchange programs).
• You may also be able to take advantage of HIV prevention medicines such as pre-
exposure prophylaxis (PrEP) and post-exposure prophylaxis (PEP).
• Don't douche. Douching removes some of the normal bacteria in the vagina that
protects you from infection. This may increase your risk of getting HIV and other
STIs.
• Be monogamous. Having sex with just one partner can lower your risk for HIV and
other STIs.
20. The sanitary protection of the territory from delivery and spreading of infections
that may have international importance.
(1) mass-scale measures aimed at improvement of public health, prevention and spread of
infectious diseases;
(2) medical measures aimed at reduction of infectious morbidity and eradication of some
diseases;
(3) health education and involvement of population in prevention or restriction of the spread
of infectious diseases;
Preventive measures aimed to control infectious diseases taken by medical personnel are
divided into: preventive and anti-epidemic
Preventive measures: are carried out regardless of the presence or absence of infectious
diseases at a given time and locality. These measures are aimed at prevention of infectious
diseases.
Anti-epidemic measures – measures must be put in place to control or terminate the source
of infection, transmission mechanism, and susceptibility of population.
Exclusion of any of these factors terminates the spread of an epidemic process. Prophylactic
and antiepidemic measures are therefore aimed at control of the source of infection,
disruption of the route by which infection spreads, and strengthening of non-susceptibility
of population. Control of infection source, The infectious patients must also be isolated in
proper time.
Ways of transmission – by the water, foodstuffs, household things, dirty arms; flies.
Epidemics – contacts, water, food borne.
Seasonality – summer-autumn.
1-st week:
The beginning is gradual
Complains: headache, tiredness, sleeplessness, anorexia, constipation or diarrhea
Long fever 39-40 °С (intermittent fevers)
Paleness of skin
«typhoid» tongue
Duguet's angina
Bradycardia, dicrotism of pulse, hypotonia
Symptoms of bronchitis
meteorism, positive Padalka's symptom
2nd week:
Typhoid rash – typhoid maculopapular rash(roseola elevata), some elements, localized on
the anterior abdominal wall and lateral walls («vest»), new elements can appear , sometimes
is present longer than fever.
Hepato-splenomegalia.
Status typhosus.
Serologic reactions.
Antiepidemic measures:
Examination on typhoid fever and paratyphoids all patients with fever, which last more than
5 days (once on hemoculture, and if fever continue more than 10 days
Examination of all persons, who are working at the industries dealing with food, for
detection of bacteriocarriers
Obligatory hospitalization infectious hospital of patients and carriers into infectious hospital
Observation of contact persons during 25 days and their separation from other people
Every day thermometry, interrogation and medical examination
One analyze of feces on coproculture and blood antibodies on Vi-antibodies
Convalescents are discharged from hospital only after clinical recovery and three-time
analysis of feces and urine with 5-days interval, and bile in 10 days after disappearing of
clinical signs, if results are negative
Three-month observation and 2-years registration in sanitary-epidemic department with
several times bacterial examination
Current and final disinfection.
the incubation period), is between two and six weeks and the average incubation
period is 28 days. The illness is usually contracted in early childhood.
Hepatitis A infection causes no clinical signs and symptoms. It does not have a chronic
stage, is not progressive, and does not cause permanent liver damage. Following infection,
the immune system makes antibodies against HAV that confer.
Infective agent : Sh. Dysenteriae, Sh. Flexneri, Sh. Boydii, Sh. Sonnei
Ways of transmission – water (more often Sh. flexneri), food staffs (Sh. sonnei), dishes,
dirty hands, flies.
Seasonal - summer-autumn.
Immunity - type-specific
Etiologic diagnostic:
Detection of the agent from the feces, vomiting mass, lavage fluid
Serologic reactions (presence of antibodies to the causative agent and increasing the titer in
dynamic)
Polymerase chain reaction (PCR) – detection of shigella DNA in feces and scraping of the
rectum mucous.
Antiepidemic measures
Medical supervision after contact persons (7 days)
Bacteriological investigation of stool (decree group only)
Serological investigation
Disinfection – current, final
Prophylaxis of Cholera
Clinical manifestation
• Phenomena of intoxication (high fever, malaise, general weakness, headache)
• Pharyngalgia - moderate
• Changes of a throat mucous - soft hyperemia, edema of tonsills, covers on their surface
(grey colour, dense, hard to remove with bleeding, slime), spread out of tonsills limits
(palatopharyngeal arches, uvula, soft palate)
• Augmentation and moderate morbidness of regional lymph nodes
• Edema of a hypodermic fat of a neck.
Prophylaxis
● Plan immunisation (3,4,5 months with DTaP , revaccinion in 18months , then 6, 11, 14,
18years and adults every 10years )
● In focus - 7 days medical observation after contact with sick person
● Bacteriological examination
● Sanitation of detected carriers
● Final disinfection
● Revaccination
Salmonellae are widely dispersed in nature, being found in the in the gastrointestinal tracts
of domesticated and wild mammals, reptiles, birds, and insects. May present clinically as
gastroenteritis, enteric fever, a bacteremic syndrome, or focal disease. An asymptomatic
carrier state may also occur.
Clinical manifestations
1) Localized (gastrointestinal) forms of Salmonellosis: a) Gastritic variant;
b) Gastroenteritic variant;
c) Gastroenterocolitic variant.
2) Generalized forms:
a) Typhus-like form;
b) Septic form (septicopyemia).
3) Carrier state:
a) Acute carriers;
b) Chronic carriers;
c) Transitory carriers.
nausea and vomiting, myalgia and headache , diarrhoea with loose stool swamp like with
bad smell.
Prophylaxis
Veterinary-surveillance upon animals and production of meat and dairy industry, laboratory
control of food stuffs. It is necessary to reveal carriers on milk farms, in foods, children’s
and medical establishments. The maintenance of the rules of personal hygiene and rules of
food’s cooking plays an important role in prophylaxis of Salmonellosis.
Types С and D are associated with animal botulism, especially in cattle, ducks and
chickens. Botulism is an acute neurologic disorder that causes potentially life-threatening
neuroparalysis due to a neurotoxin.
Ways of transmission -
1) botulism food poisoning results from eating food that contains preformed toxin;
2) wound botulism occurs when toxin is produced by C. botulinum organisms
contaminating traumatic wounds;
3) infant botulism is due to toxin production by C. botulinum within the gastrointestinal
tract of infants.
Signs
Dysphagia , diplopia, dysphonia, dry tongue , horizontal nystagmus, blepharoptosis.
Prophylaxis
The observance of the sanitary and hygienic rules at processing, transportion, keeping and
preparing of the food-stuffs experts possibility of accumulation of botulotoxin. It is
necessary to perform the strict control under sterilization and keeping preserved food-stuffs.
Cook meats, mushrooms and vegetables properly .
Serotypes - A, B, C, D, X, Y, Z
Source of infection- Carrier and sick people ( patients with meningococcal nasopharyngitis
and generalized form of infection)
Symptoms
Fever, headache, vomiting, rigidity of neck, positive kernic sign, starlike hemorrhagic rash
on thighs buttocks and trunk . Seizures.
Ways of transmission - parenteral, sexual, through placenta from sick mother to fetus
(vertical or transplacentar).
Source of infection- sick person with acute or chronic form, healthy carrier.
Asymptomatic form: the specific markers of infectious agent and proper immunological
changes are exposed only
Sub-clinical form: immunologic, biochemical and histological changes, however main
clinical signs of illness are absent
Non-jaundice form: different clinical symptoms of illness are present except jaundice
Jaundice form: jaundice, which is the main sign of hepatitis present
Fulminant (malignant) form: extremely
Symptoms
Jaundice, fever, fatigue, loss of appetite with nausea and vomiting, joint pain and abdominal
pain.
Prophylaxis
Use of disposable medical instruments, thorough sterilisation of non-expendable
instruments.
Clinical and laboratory examination of blood and organ donors.
Specific prophylaxis - vaccination against B hepatitis HB-Vax, Ingerix-B
Symptoms
Prolonged fever, prolonged diarrhoea, generalized lymphadenopathy, weight loss( >10%),
opportunistic infections, kaposi sarcoma
Diagnostic Criteria: epidemiological data , clinical signs and laboratory data ( IFA,
immunobloting)
Etiology - plasmodium
Types of plasmodium
Pl. malariae
Pl. falciparum
Pl. ovale
Pl. vivax
Pl. knowlesi
Susceptibility – high
Symptoms
Attack of fever - (chills-hot-sweat), Hepatosplenomegaly, hémolytique anemia(jaundice ),
tachycardia, hypotonia , myalgia , diarrhoea, vomiting, loss of appetite, cyanosis, herpes.
Prophylaxis
● Sanitarian patrolling of the state from delivery (quarantine infection contamination)
● Mandatory registration
● Sterilization of toolkit
● At detection of sick or carrier – parasitoscopy examination of all family members
● Ant mosquito measures (melioration, usage of insecticides, repellents)
● Drug prophilaxis - primachinum 0,027gm/day for 14days
Clinical forms
Skin Bubonic , Primary pulmonary, secondary pulmonary, intestinal , primary septic,
secondary septic.
Complications
Infectious toxic shock , meningitis, adeno phlegmon
Symptoms
Fever
Severe intoxication
Severe hemorrhagic inflammation of lymphatic nodes , lungs and other organs through
Sepsis .
Anti-epidemic measures:
• prevention the import of infection from abroad;
• making of natural cells of plague healthy;
• urgent prophylaxis in the case of exposure of patient with a plague.
immunization of people :
● Vaccinations of population of certain territories;
● Urgent 6-daily prophylaxis by streptomycine tetracycline on suspicion of possible
infection.
Etiology – filoviridae
Source - mice/rat (which are excreting the virus with urine, stool and saliva)
The contamination of the person descends by air - dust, nutritional and contact pathes
(routes). The transplacental transmission of a virus from the pregnant woman is possible.
Symptoms
Fever (39-40degrees)
Decreased visual equity( mist before eyes)
Sharp headache
Back ache and pain in muscles of extremities
Photophobia
Nausea and vomiting
Paleness nasolabial triangle, hyperemia of a face, necks, upper half of trunk.
The palpebral fissures are narrowed down, scleratis.
A mucosa of an oral cavity and pharynx are bright red with haemorrhages.
The Kerning’s signs, Brudzinsky sign can be determined and
stiff neck. Fever 7-9 days is prolonged.
Delirium
On 3-5th day of illness on a neck, lateral areas of a thoracic cell, in axillaries fossas, above
clavicles occurs petechial eruption.
Then there are nasal, intestinal, pulmonary bleedings.
Cardiac sounds are dull; the initial tachycardia is replaced by a bradycardia, hypotonia.
Dryness of tongue, abdominal pain without definite localization, patients enlarged a liver
and spleen and the icterus are possible.
Prophylaxis
Inactivated cultural, cerebral vaccines and recombinant of a vaccine
Carry out a disinfestation in the natural locuses, puttings, and also collect of tongs with
animal and poultries. For a disinfestation will use gexachloran.
Medical observation in the focus for 10 days and Conduct mandatory final disinfection with
3 % Chloraminum solution and chlorofos. For contact persons or one who was bitten by
tongs in endemial districts enter a specific immunoglobulin i.m. in doses 5-7.5 ml for adult,
2.5-3.5 ml - for children.
Lyme disease is spread by the bite of the Ixodes scapularis (dammini) tick.
Tick needs at least 24 hours of attachment before transmission can take place.
Borrelia burgdorferi organism. The tick is small, and the bite is often not remembered.
Symptoms
• Erythema migrans rash at the site of the bite (80% of patients)
–– An erythematous patch, which may enlarge in the first few days, may have partial central
clearing, giving it a “bull’s-eye” appearance, although this is not commonly seen.
–– The rash will resolve in several weeks, even without treatment.
• Flulike illness with fever, chills, and myalgias (50% of patients)
• Neurologic symptoms several weeks later (10–20% of patients)
–– Most common symptom is paralysis of the seventh cranial nerve (facial paralysis),
possibly be bilateral
–– Meningitis, encephalitis, headache, and memory disturbance may develop as well •
Cardiac symptoms (<10% of patients)
–– Most common symptom is AV heart block
–– Myocarditis, pericarditis, and various forms of arrhythmias may develop as well
• Joint involvement months to years later (up to 60% of patients)
–– Most commonly a migratory polyarthritis, although chronic monoarticular arthritis (most
commonly affecting the knee)
Diagnosis Criteria
Based on clinical signs especially (erythema migrans rash) and serological testing (ELISA
test and western blot).
Prophylaxis
Doxycycline (200 mg for adults or 4.4 mg/kg for children of any age weighing less than 45
kg).
Clinic: itching in anal areas more prominent at night which leads to restlessness and
difficulty in sleeping. At night, the female worm moves to anus and deposit its eggs and
dies.
Diagnosis: Eggs detected in cellulose tape preparations applied to patient’s perianal region
in the early morning prior to bathing or using toilet.
Treatment:
! Good hand hygiene and wash perianal areas well. Wash clothes and bed linen well.
! Can also give one dose of pyrantel pamoate one dose repeated in 2 weeks.
! Petroleum jelly is given to relieve itching
Clinic: Usually asymptomatic. A heavy worm burden may result in mechanical damage to
the intestinal mucosa due to adult work threaded into epithelium of cecum. This can lead to
abdominal cramps, tenesmus, dysentery and prolapsed rectum.
Clinical signs:
! patient may have signs of pneumonitis with cough and low grade fever during the
migration of larvae through the liver and lungs. Can be accompanied by wheezing
and eosinophilia
! In heavy worm burdens, adult worms migrate in intestine resulting in intestinal
blockage which lead to vomiting, abdominal pain
!
Diagnoses:
! adult worms may be expelled through anus, mouth or nose
! Eggs seen on microscopic stool exam
38.Complications of ascariasis.
Volvulus
Intussuception
Hepatic abscess
Acute cholangitis
Peritonitis
Biliary colic
Acute cholecystitis
Acute pancreatitis
Upper GI bleeding
Pathogenesis
! Ingestion of worms: adult worms live in small intestine, attached firmly to the
mucous membrane of the gut lining and feed on blood and tissue
! Adult females deposit their eggs in the gut and are passed out in feces
! They survive in light sandy loam soil feeding on bacteria.
! After one week, they become infective and move to position for suitable host to pass
! They enter organism by ingestion
! Enter blood vessels and are carried to heart, lungs and trachea
Clinic
.Larva penetration into skin leads to pruritus.
.Adult work in intestine may cause intestinal necrosis and blood loss:abdominal pain,
diarrhea, nausea, vomiting.
.Chronic infection can lead to iron deficiency anemia.
. Mental and physical growth is retarded in children and growing youth in ancylostomiasis
.Unchecked ancylostomiasis infection may lead to fatty degeneration of heart, liver and
kidneys, ending in death.
Complications
Iron deficiency anemia, caused by loss of blood.
Nutritional deficiencies. ( malnutrition)
Intestinal ulcers
Severe protein loss with fluid buildup in the abdomen (ascites)
*Bonus Diagnostics of ancylostomiasis.
• Microscopic exam of stool deposits reveals ova
• Because hookworm species cannot be differentiated on the basis of their
eggs, it is necessary to culture larvae or to recover adult worms for morphologic study
Clinical pictures
-Initial skin penetration causes little reaction, repeated infections lead to hypersensitive
reactions. This leads to Larva currens: rapidly progressing urticarial attack.
• Migration of larva to the lungs may stimulate an immune response resulting in cough,
wheezing and fever
• Ulceration of intestines, can lead to malabsorption, GI bleeding and eosinophilia
• Hyperinfection syndrome: parasite and host reach an equilibrium where neither host nor
parasite suffers adverse reactions. It leads to the infection proliferation with immense
numbers of larvae migrating to every tissue in the body especially the lungs (pneumonitis),
brain damage and respiratory failure
-Skin phase: Dermatitis; An itchy, red rash that occurs where the larva entered the skin,
creeping eruption may also occur.
-Respiratory phase: Löffler's syndrome (pneumonitis + Asma)
-Abdominal phase: Infection may be asymptomatic(light infection) • Symptoms resemble
gastric ulcer; (stomachache, bloating, and heartburn, hunger pain • Chronic intermittent
diarrhea may be with yellow mucus.
Constipation, Nausea and loss of appetite
Complication ;
-Gastric ulcer resulting from damaged mucosa by the worms
-Intestinal obstruction occur In severe cases, edema may result in obstruction of the
intestinal tract, as well as loss of peristaltic contractions.
-Immunosuppression
-Disseminated strongyloidosis- tissue damage
-Pneumonitis, brain damage
-Respiratory failure
42.Diagnostics of strongyloidosis
Clinical features
These symptoms include
eye puffiness,
splinter hemorrhage,
nonspecific gastroenteritis,
Fever,
Muscle soreness and pain,
Gastrointestinal symptoms,
Facial edema, eosinophilia, and subconjuctival, subungual, and retinal hemorrhages."
Complications
myocarditis
pneumonia
meningoencephalitis
hepatitis
nephritis
systemic vasculitis
thrombophlebitis
thrombocytopenia
EPIDEMIOLOGY
• Infection occurs when filarial parasites are transmitted to humans through
mosquitoes.
• It is endemic in many tropical & subtropical countries like Africa, Asia, Western
Pacific and parts of America.
The painful and profoundly disfiguring visible manifestations of the disease, lymphedema,
elephantiasis and scrotal swelling occur later in life and can lead to permanent disability.
46. The clinical picture and complications of lymphatic filariasis
Lymphatic filariasis is a human disease caused by parasitic worms known as filarial
worms.
Clinical picture
• Fever
• Inguinal or axillary lymphadenopathy
• Testicular and/or inguinal pain
• Skin exfoliation
• Limb or genital swelling
• dry and paroxysmal nocturnal cough;
• wheezing
• Dyspnea
Complications
• chronic lymphedema,
• hydrocele,
• skin pigmentation,
• renal impairment (eg chyluria. )
47. Etiological therapy of nematodosis
Nematode(round worm) infections need to be identified and treated accordingly.
Antihelminthic:
- Albendazole
- Mebendazole
- Pirantel,
- Vermox,
Complications;
Systemic cysticercosis.
Cyst rupture (hydatid cyst rupture rare )
Vitamin B-12 deficiency.
Obstruction of the appendix or pancreatic or bile ducts (rare)
Intestinal obstruction (rare)
Cholangitis (rare)
Cholecystitis (rare)
Pancreatitis.
* Prevention
Make sure you cook meat thoroughly
Freezing to 5 degrees for 4days
* Treatment
praziquantel , Niclosamide, Albendazole, mebendazole
Epidemiology:
- It is found throughout the world and is most common in countries where pork is eaten.
Eastern Europe, Russia, Eastern Africa. Latin AMerica
-Source of infection: Zoonosis (pigs)
-Mechanism of transmission: Oral (eating undercooked pork)
Life cycle;
Eggs or gravid proglottids are passed with feces; the eggs can survive for days to months
in the environment.
pigs (T. solium) become infected by ingesting vegetation contaminated with eggs or
gravid proglottids
In the animal’s intestine, the oncospheres hatch The number and invade the intestinal
wall, and migrate to the striated muscles, where they develop into cysticerci. (A
cysticercus can survive for several years in the animal.)
Humans become infected by ingesting raw or undercooked infected meat. In the human
intestine, the cysticercus develops over 2 months into an adult tapeworm, which can survive
for years.
The adult tapeworms attach to the small intestine by their scolex and reside in the
small intestine (Length of adult worms is usually 5 m or less for T. saginata (however it
may reach up to 25 m) and 2 to 7 m for T. solium)
The adults produce proglottids which mature, become gravid, detach from the
tapeworm, and migrate to the anus or are passed in the stool (approximately 6 per day).
Complications
Tapeworm can be lodged in appendix (Appendicitis), bile
duct (cholecystitis), pancreatic duct (pancreatitis)
Clinical picture
Cysts, called cysticerci, can develop in the muscles, the eyes, the brain, and the spinal cord
-Cyst in the brain or spinal cord causes neurocysticercosis.
- seizures and headaches
- confusion
- difficult with balance
- brain swelling and excess fluid around the brain.
- stroke
- Cyst in the muscles can cause lumps under the skin ( which can be tender).
-Myositis with fever and eosinophilia and muscular pseudohypertrophy. This can later
progress to atrophy and fibrosis
-Eyes: Cysticerci may be found in eyeball, extraocular muscles and subconjunctica. May
cause retinal edema, hemorrhage, decreased vision or visual loss.
Complications
brain edema,
hydrocephalus
chronic meningitis
vasculitis
paralysis
partial blindness
seizures, coma, and death.
Pork tape worm infection (taeniasis) is an intestinal infection with adult tapeworms that
follows ingestion of contaminated pork.
Diagnosis
Microscopic examination of stool for ova and proglottids
CT and/or MRI and serologic testing for patients with central nervous system symptoms.
Cysticercosis
Cysticercosis is a parasitic tissue infection caused by larval cysts of the tapeworm Taenia
solium.
Diagnosis
Biopsy of infected tissue, microscopic examination
ELISA: Antibodies to cyticerci
CT or MRI of head
CSF exam: pleocytosis, elevated protein levels and depressed glucose levels
Epidemiology
• Cystic echinococcosis is globally distributed in most pastoral and rangeland areas of
the world, with highly endemic areas in the eastern part of the Mediterranean region,
northern Africa, southern and eastern Europe, at the southern tip of South America, in
Central Asia, Siberia and western China.
• Humans are infected through ingestion of parasite eggs in contaminated food,
water or soil, or after direct contact with animal hosts( dogs)
Life cycle
-The adult Echinococcus granulosus resides in the bowel of its definite host.
-Gravid proglottids release eggs that are passed in the feces.
-These eggs are then ingested by a suitable intermediate host, including sheep, goat,
swine, cattle, horses and camels. The eggs then hatch in the bowels and release
oncospheres that penetrate the intestinal wall.
These oncospheres then migrate through the circulatory system to various organs of the
host.
-At the organ site, the oncosphere develops into a hydatid cyst. This cyst enlarges
gradually, producing protoscolices and daughter cysts that fill the cyst interior.
-These cyst-containing organs are then ingested by the definite host, causing infection.
After ingestion, the protoscolices evaginate, producing protoscolexes.
-The scolexes of the organisms attach to the intestine of the definite host and develop into
adults in 32-80 days.
The life cycle then continues in humans:
(Humans can become infected if they ingest substances infected with Echinococcus eggs.
-The eggs then release oncospheres in the small intestine.)
Clinical picture
Human infection with E. granulosus leads to the development of one or more hydatid
cysts located most often in the liver and lungs
-Abdominal pain, nausea and vomiting are commonly seen when hydatids occur in the liver.
- If the lung is affected, clinical signs include chronic cough, chest pain and shortness of
breath.
-Other signs depend on the location of the hydatid cysts and the pressure exerted on the
surrounding tissues. Non-specific signs include anorexia, weight loss and weakness.
Complications:
anaphylactic reaction, shock. Hepatomegaly, respiratory disease or pulmonary eosinophilia,
coin lesion in lungs, ectopic calcification
Epidemiology
This type of tapeworm parasite is most common in areas where people eat raw or
undercooked fish from lakes and rivers. Such areas include:
-Russia and other parts of Eastern Europe
-North and South America
-some Asian countries, including Japan
It may also be common in parts of Africa where freshwater fish are eaten.
Life cycle
Immature eggs are passed in feces.
The eggs mature (approximately 18 to 20 days) and yield oncospheres which develop
into a coracidia
After ingestion by a suitable freshwater the coracidia develop into procercoid larvae...
Following ingestion of the copepod by a suitable second intermediate host,
The procercoid larvae are released from the crustacean and migrate into the fish flesh where
they develop into a plerocercoid larvae (sparganum)
The plerocercoid larvae are the infective stage for humans. Because humans do not
generally eat undercooked minnows and similar small freshwater fish, these do not
represent an important source of infection. Nevertheless, these small second intermediate
hosts can be eaten by larger predator species, e.g., trout, perch, walleyed pike
In this case, the sparganum can migrate to the musculature of the larger predator fish and
humans can acquire the disease by eating these later intermediate infected host fish raw or
undercooked
After ingestion of the infected fish, the plerocercoid develop into immature adults and then
into mature adult tapeworms which will reside in the small intestine. The adults of D. latum
attach to the intestinal mucosa by means of the two bilateral groves (bothria) of their scolex
Eggs appear in the feces 5 to 6 weeks after infection.
Clinical picture
Fish tapeworm infections rarely present noticeable symptoms. Tapeworms are most often
discovered when people notice eggs or segments of the tapeworm in stool.
Complications
-anemia, specifically pernicious anemia caused by vitamin B-12 deficiency
-intestinal blockage
-gallbladder disease
60 Diagnostics of diphyllobothriasis.
Diagnosis
Microscopic exam of eggs or proglottids in stool
You will see characteristic eggs from formol ether concentrate of feces.
(The egg is usually ovoid and has a small knob at the opercular end and is yellowish-brown
in colour with a smooth shell, of moderate thickness. They measure 58 – 75mm by 40 –
50mm in size.)
Proglottids may also be seen in fecal samples usually in a chain of segments from a few
centimeters to about 0.5 meters in length.
Symptoms- maybe absent or minimal with eosinophilia ,there can be occasional intestinal
obstruction, diarrhoea, and abdominal pain, vitamin B12 deficiency (megaloblastic anemia)
61.Epidemiology and pathogenesis of opisthorchiasis.
Opisthorchiasis is defined as infection with Opisthorchis viverrini (Southeast Asian liver
fluke) or O. felineus (cat liver fluke)
Clinical presentation:
a) Most infections are asymptomatic.
b) Mild infections may cause dyspepsia, abdominal pain, diarrhoea or constipation.
c)Longer-term infections may cause more severe symptoms and may lead to hepatomegaly
and malnutrition.
Epidemiology:
• acquired by eating infected raw or undercooked fish (fecal-oral)
• Opisthorchis felineus is an intestinal parasite of cats, dogs, foxes, pigs, cetaceans (such
as whales and dolphins) in Eastern Europe, Siberia and other parts of Asia.
• Opisthorchis viverrini is found in domesticated and wild dogs and cats in Southeast Asia.
• It is a very common human infection in North East Thailand.
Pathogenesis:
● Eggs are ingested by snail and undergo development (sporocyst to rediae to cercariae).
● Cerciae are released from snails and penetrate fresh water fish encysting as metacercariae
in muscles or under scales
● Humans become infected after eating raw or undercooked fish
● Metacercariae excyst in the duodenum and ascend through the ampulla of vater and into
the biliary ducts where they attach to the mucosa and mature. Adult flukes grow up to:
5 to 10 mm (O. viverrini)
7 to 12mm (O. felineus).
63.Diagnostics of opisthorchiasis.
Opisthorchiasis is a parasitic disease caused by species in the genus Opisthorchis
(Opisthorchis viverrini and Opisthorchis felineus) acquired by eating infected raw or
undercooked fish.
The medical diagnosis is established by finding eggs of Opisthorchis in feces using the
Kato technique.
• Microscopic examination of stool; Detects the eggs in feces
• Ultrasonography, CT , MRI , cholangiography may show biliary tract abnormalities.
• ELISA Test to detect antigen 89 kDa seen in Opisthorchis viverrini
(The Kato technique is a laboratory method for preparing human stool samples prior to
searching for parasite eggs.)
Tapeworm infections are all acquired by ingesting worm cysts or eggs. The most common
infections result from undercooked fish (Diphyllobothrium latum), beef (Taenia saginata),
and pork (Taenia solium). Other tapeworms can be spread person-to-person (Hymenolepsis
nana) or with contamination of food by feces from infected dogs (Echinococcusspecies).
Mature worms reside in the gut, releasing large numbers of eggs, but usually causing little
disease.
Most common syndrome of Tenia solium it causes is cysticercosis ( infection with parasite
cysts, most often in the brain, following ingestion of food contaminated with parasite eggs
from pig feces.)
Trematodiases, also known as trematode infections, are a group of diseases caused by the
parasite trematodes. Symptoms can range from mild to severe depending on the species,
number and location of trematodes in the infected organism.
Mostly causes flukes
Etiological Treatment
• Praziquantel
• Albendazole
• Mebendazole
• Triclabendazole