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Understanding Communicable Diseases

Medical Nursing

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Freda Morgan
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Topics covered

  • acute renal failure,
  • nursing management,
  • infectious disease control,
  • communicable diseases,
  • fecal-oral route,
  • infectious disease prevention,
  • malaria,
  • viral transmission,
  • signs and symptoms,
  • healthcare practices
0% found this document useful (0 votes)
40 views51 pages

Understanding Communicable Diseases

Medical Nursing

Uploaded by

Freda Morgan
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPTX, PDF, TXT or read online on Scribd

Topics covered

  • acute renal failure,
  • nursing management,
  • infectious disease control,
  • communicable diseases,
  • fecal-oral route,
  • infectious disease prevention,
  • malaria,
  • viral transmission,
  • signs and symptoms,
  • healthcare practices

COMMUNICABLE

DISEASES
Is one that can be transmitted from one person to another and is caused by an
infectious agent that is transmitted from a source or reservoir to a susceptible
host.
Terms
Epidemic - occurrence, a rapid spread of infectious disease to a large number
of people in a community or region in a given population within a short
possible time. E. g. cholera
Endemic - habitual presence of a disease within a geographic area based on
the usual prevalence of a given disease within such an area. E.g Malaria
Pandemic - an epidemic which is worldwide in distribution. E.g. HIV/AIDs
Host - person/animal that affords subsistence to an infectious agent under
natural conditions
Carrier - person/animal that harbors a specific infectious agent in the absence
of discernible clinical disease and serves as a potential source of infection
Fomite - contaminated substance (not necessarily a reservoir) serving as an
intermediate means of transport for an infectious agent
Reservoir - anything (living or inert) in which an infectious agent lives and
multiplies in such a manner that it can be transmitted to a susceptible host
Vector - invertebrate animal capable of transmitting an infectious agent to
vertebrates
Virulence - ability of an infectious agent to cause severe or fatal infections
The six factors influencing the
transmission of the infectious
agent
• Agent
• Reservoir
• Portal of exit
• Mode of transmission
• Portal of entry
• Susceptible host
Mode of transmission
---: Direct
• Direct contact
• Vertical transmission
• Droplet infection
• Animal bite transmission
• Contact with soil
Indirect
• Air-borne
• Vehicle borne
• Vector-borne transmission
• Fomite –borne
• Hand –borne
Types of communicable diseases
RESPIRATORY INFECTIONS INTESTINAL INFECTION
Measles poliomyelitis
Mumps viral hypatitis
Chickenpox cholera
Rubella typhoid fever
Influenza food poisonig
Diphtheria amoebiasis
Whooping cough
Tuberculosis
ZOONOSES SURFACE INFECTION STI’S
Rabies trachoma syphyilus
Yellow fever tetanus gonorrhoea
leprosy hiv

ARTHROPOD
Dengue fever
Malaria
Lymphatic filariasis
Plague
CHOLERA
This is an acute intestinal disease caused by vibrio cholerae
characterized by profuse diarrhoea and vomiting.
CAUSATIVE ORGANISM
• It is caused by vibrio cholerae.
• This is a Gram negative facultative anaerobe organism
• It is a comma shape bacteria that grows rapidly at a very high pH (8.5 – 9.5)
and killed in an acidic medium.

INCUBATION PERIOD
• It is variable, but usually from 24 to 72hrs.
MODE OF TRANSMISSION
• It is transmitted through the oro-faecal route and hence transmitted
• Eating of contaminated food and water including vegetables and
fruits.
• Rarely, hand-to-mouth transmission after using a contaminated toilet
and neglecting hand hygiene OR after handling excreta and infected
linen of patients. because a large inoculum of organism is needed to
transmit the infection.
• NB: Epidemics often occur from faecal contamination of water
supplies or street vended foods.
PREDISPOSING FACTORS
• Leaving in an endemic area
• Eating food from outside the home i.e. food vendors not sure of the food
source and how it was cook
• Eating cold uncovered foods
• Eating fresh uncooked vegetables e.g. lettuce, carrot or unpeeled fruits
e.g. mango, apple
• Not washing hands properly before ingestion of food. (i.e. shaking of
hands with an individual with vibrio cholera)
• Lack of proper waste disposal technique – this leads to the spread of the
disease. NB : Transmission by flies
• Poor environmental hygiene (dirty environment gives room for the
micro-organism to harbour.
• In addition, conditions that causes Hypochlorhydria and Achlorhydria
(reduced or absence of HCl in gastric juice) increases an individual’s risk of
acquiring cholera. These includes:
Children (immature gastric glands)
Elderly (atrophy of the gastric glands)
Certain drugs e.g. Antacids, H2 receptor antagonist, proton pump inhibitor
Gastrectomy
Vagotomy
PATHOPHYSIOLOGY
 Following the ingestion of food or water containing the organism in an individual with
normal gastric acidity, the organism is killed in the acidic medium in the stomach,
unless very large numbers of the organisms are ingested especially drinking of
contaminated water.
 In those with decrease stomach acidity, the organism survives the stomach acidity
and enters into the small intestines (duodenum and upper jejunum).
 In the duodenum, the organism (vibrio cholerae) then attaches itself to the walls of
the small intestines where they multiply (because of its alkaline medium) and release
a toxin called cholera toxin (CTX) or entero-toxin.
 These toxins release act only locally i.e. It does not invade the systemic circulation or
cause physical damage to the intestinal wall.
 CTX binds to the intestinal walls, where it blocks the absorption of sodium and
chloride by the microvilli. It also promotes the secretion of sodium and water by the
crypt cells (nearby cells or the intestinal wall).
NB : (the toxin causes human cells to extract water and electrolytes from
the intestinal wall).
 This creates a salt-water environment in the small intestines, which
through osmosis pull fluids through the intestinal cells into the lumen, as
this fluid moves through the large intestines it attracts more fluids creating
the massive amounts of diarrhea.
 Unless the lost fluid and electrolytes are replaced adequately, the infected
person may develop shock from profound dehydration and acidosis from
loss of bicarbonate leading to death.
SIGNS AND SYMPTOMS
• Sudden, profuse, watery stool.
• This stool is initially brown and contains fecal matter, later becomes pale gray or
milky resembling water in which rice has been rinsed or water from boiled rice
hence the name “rice-water stool” (characteristic sign in cholera)
• Stool contains flecks of mucus and has a fishy odour smell.
• The level of the diarrhoea is so enormous that you can lose about 10 – 18 litres of
fluid over 24hours (ECF = 14L, ICF – 28L)
NB : Stool volume during cholera is more than that of any other infectious diarrhea
• The diarrhoea is associated with severe abdominal cramps as a result of loss of
sodium, chloride and potassium.
• Severe vomiting : vomiting is caused by decreased gastric and intestinal motility;
• Fever is typically absent i.e. Temperature could be normal at the onset of disease but becomes
subnormal in the later stage especially if patient is in shock.
• Dry or sticky mouth, thirst, decreased skin turgor, Oliguria,
• A thread, weak, rapid heart rate and disappears
• Decreased blood pressure
• skin becomes cool and clammy skin
• Weakness
• Sunken eyes
• Acute weight loss
• Confusion, altered level of consciousness related to peripheral vasoconstriction or decreased
peripheral perfusion and in the absence of infection.

In children, the signs may include :


• Fever
• Convulsion
• Coma
DIAGNOSTIC INVESTIGATION
• Routine Stool Examination
• Stool specimen appears as Rice water and On Microscopy contain Mucus.
• Stool Culture
• Rectal swab
NB: Specimens should not be collected from bed pans
• FBC – shows elevated haematocrit due to haemoconcentration
• WBC – will also be elevated
• BUE + Cr
• Serum sodium is low reflecting the substantial loss of sodium in the stool.
• Serum urea and Cr may be high indicating a pre-renal azotemia.
• The extent of elevation depends on the degree and duration of
dehydration
• ABGs
• Blood pH < 7.35
• Blood bicarbonate will decreased (Blood C02 < 35mmHg for
compensation).
COMPLICATION
• Hypovolemic shock
• Acute renal failure
• Metabolic acidosis - Acidemia results when respiratory compensation is
unable to sustain a normal blood pH.
• Hypokalemia – From potassium loss in stools which will interfere with
normal heart function.
• Hypoglycemia – from becoming too weak to eat depleting your energy
stores, very common in children.
• Death
MANAGEMENT
• The main aim of management is to correct fluid and electrolyte imbalance and
prevent further complications

Medical management
• Antibiotics are also used
• These include :
• Doxycycline
• Azithromycin
• Tetracycline
• Ciprofloxacin
• Metronidazol
NURSING MANAGEMENT
• Admit the patient to a special cholera unit or in an isolation ward.
• Patient should be placed or put onto a special bed called cholera cot if available,
this is a bed with a hole through which a calibrated bucket is placed underneath to
allow for collection of stool. This helps the health worker to calculate fluid losses
and replacement needs
• Assess for degree of dehydration
• Rehydrate the patient by setting up intravenous line and initiate IV therapy using
ringers lactate at a rate of about 50-100mls/kg/hr.
• Continue rehydration of patient until diarrhoea stops
• Regular assessment of the patient every 1-2hrs is done and hydration continued
• Give ORS when vomiting stops as much as client can take during the rehydration
phase
OBSERVATION
• Monitor Vital signs especially pulse and blood pressure and report any abnormality
• Accurate measurement of fluid Intake and output including liquid stool noting its frequency
• Observe the stool for its consistency, amount and colour
• Observe the vomiting for its consistency, amount and colour monitor and frequently assess hydration
status
• Observe for signs of complication
• Do regular skin assessment
• Regular (daily) weighing of client

NUTRITION
• Give nourishing diet when vomiting stops.
• This food will be warm and will be serve at frequent intervals
• This food should be high in calories
• Food should be attractive
• If possible patient should be served his favourite meal.
• Continue breastfeeding infants and young children.
PREVENTION AND CONTROL
• Environmental hygiene should be established in endemic areas.
• Protection and purification of water supplies
• Proper disposal of both dry and wet refuse
• vegetables and fruits should be properly washed in salt solution before eating
• Any source of water apart from pipe borne should be boiled
• Investigate contacts and give treatment if positive
• Health education on the mode of spread and measures to prevent it
• Education on good hygienic practises e.g. washing of hands before eating, before
touching food and after visiting the toilet with soap and water
• Ensure regular periodic medical check up for food vendors
• Discourage communal eating and sharing of cups, cutlery
• Provision of portable water
• Drinking portable water
• Provide toilet in communities to prevent indiscriminate defecation
• Food should be protected from flies
• Immunization against typhoid at least once a year
• Stool, vomiting and urine of infected persons should be disinfected before
discarding
• Left-over food should be discarded of infected person should be discarded
• Advise against buying and eating food outside the home
• Ensure that food vendors cover their food and keep the selling environment
clean and neat
• Eat foods that have been thoroughly cooked and that are still hot and
steaming.
NURSING DIAGNOSIS
• Risk for fluid volume deficit r/t severe diarrhea and vomiting
• Hypothermia r/t hypovolemia
• Potential for Impaired skin integrity r/t dehydration
• Deficient knowledge about the infection and the risk of transmission
to others
• Metabolic Acidosis r/t bicarbonate, sodium, potassium ions and other
electrolyte losses
MALARIA
Is a life-threatening disease caused by parasites that are transmitted to people through a bite of infected
female anopheles mosquitoes
Occur in most topical regions.

Incubation Period : About 9–30days.


• Falciparium- 12 days
• Ovale- 14 days
• Malariae- 30 days
• Vivax- 14 days
NB : The plasmodium falciparium is the commonest, forming about 90% of infections in Ghana.

Causative Organism
Plasmodium vivax
Plasmodium ovale
Plasmodium malariae
Plasmodium falciparum
Mode of Transmission
Malaria is mainly spread by,
• Vector transmission: By bite of female anopheles mosquito
• Direct transmission: By injections of infected blood or plasma
• Congenital: Infected mother to new born
Sign & Symptoms
Cold Stage
Onset of Fever with chills and sensation of extreme cold.
Hot Stage
• Temperature rise up to 106F
• Intense headache.
Sweating stage:
Fever decreases with sweating.
s/s
• It starts with:
• Fever with chills and sweating
• Severe headache and thirst
• General body pains and weakness
• Loss of appetite and mouth bitterness
• Sometimes vomiting follows
• There may be rigors
• In children there may be convulsions
Diagnostic Investigation
• Blood film for malaria parasite
• Thick & thin blood smear
• White blood cell count
• Rapid diagnostic test (antigen testing)
• Molecular test or polymerase chain reaction (PCR)
• Antibody testing (serology)
Complications

• Renal failure
• Acute encephalitis
• Swelling or tenderness of the spleen.
• Loss of weight
• Anaemia and mental retardation in children
• Termination of pregnancy
• Coma and death
Treatment plan
• 1st episode of fever – Artesunate + Amodiaquine for 3days, except for
pregnant women in their 1st trimester
• Severe malaria – Quinine for 7days and the best choice for pregnant
women in their 1st trimester
• Sulphadoxine-Pyrimethamine (SP) can also be used prophylatically for
all malaria victims, except for pregnant women in their 1st trimester.
But can be used in their 2nd and 3rd trimester
Prevention and Control
• Effective treatment of all infected persons
• Mass survey and treatment
• Destroying breeding places of mosquitoes by clearing swampy and bushy areas, burying
empty tins and putting oil on stagnant water
• Killing the mosquitoes and larvae by spraying with insecticides.
• Prevent mosquito bite by use of mosquito repellants e.g. coils, creams, burning, orange
peels
• By living in mosquito proof houses and sleeping under treated bed nets
• Giving intermitted preventive treatment (IPT) to pregnant women as prophylaxis. 3 doses
of Sulphadoxine-Pyrimethamine (SP) are given under Directly Observed Therapy( DOT)
• Health education of the general public on the disease
VIRAL HEPATITIS
Viral hepatitis is a systemic disease with primary inflammation of the liver by
any one of a heterogeneous group of viruses.
causes of viral hepatitis are the five unrelated hepatotropic viruses
Hepatitis A,
Hepatitis B,
Hepatitis C,
Hepatitis D, and
Hepatitis E.
In addition to the nominal hepatitis viruses, other viruses that can also cause
liver inflammation include Herpes simplex, Cytomegalovirus, Epstein–Barr
virus, or Yellow fever.
Hepatitis A
Hepatitis A (formerly known as ―infectious hepatitis or epidemic jaundice) is an acute infectious
disease caused by Hepatitis A virus (HAV).

S/S
Fever & chills
Headache
Fatigue
generalized weakness
aches and pains
Anorexia
Nausea & vomiting
dark urine
jaundice.
The disease is benign with complete recovery in several weeks.
• AGENT: The causative agent, the hepatitis A virus, is an enterovirus of the
Picornaviridae family. It multiplies only in hepatocytes.
• RESERVOIR OF INFECTION: The human cases are the only reservoir of
infection.
• PERIOD OF INFECTIVITY : The risk of transmitting HAV is greatest from 2
weeks before to 1 week after the onset of jaundice.
• INFECTIVE MATERIAL : Mainly man’s faeces.
• VIRUS EXCRETION: HAV is excreted in the faeces for about 2 weeks before
onset of jaundice and for up to 2 weeks thereafter.
Incubation period - 10-50 days (usually 25 to 30 days).

MOD –
• FAECAL-ORAL ROUTE: Major route of transmission.
-By contaminated water, food or milk.
Hepatitis B
Hepatitis B (formerly known as ―serum hepatitis) is an acute systemic
infection with major pathology in the liver, caused by hepatitis B virus.
Transmitted by the Parenteral route.
The acute illness causes
• liver inflammation
• Vomiting
• jaundice.
Chronic hepatitis B may eventually cause cirrhosis and liver cancer.
Hepatitis B is endemic throughout the world, especially in tropical &
developing countries.
Agent: Hepatitis B Virus (HBV)
Reservoir of infection: -Men is the only reservoir of infection which can
be spread either from carriers or from cases. c)
Infective material: -Contaminated blood is the main source,
-Virus has been found in body secretion such as
• Saliva
• vaginal secretion &
• Semen in infected material.
Incubation Period - 45-180 days (usually 60-90 days)
MOD
• People with multiple sex partners
• Health care personnel who have contact with blood
• Patients who are immunocompromised.
• Injection given with syringes and or needles contaminated by body fluids of
infected persons or carriers.
• Sexual intercourse with infected person
• Kissing may spread it since the virus is present in saliva
• Transfusion with infected blood and blood products
• Carrier mothers can transmit to their infants during the birth process
• Indirectly from exudates from the skin ulcers and tears of infected persons
Diagnosis
• Liver function test
• FBC
• CT scan
• Liver biopsy
• Clotting time
• Clotting factor
• Serology
• Liver Chemistry tests AST, ALT, ALP, and total Bilirubin
• Histology--Immunoperoxidase staining
• HBV Viral DNA--Most accurate marker of viral DNA and detected by PCR
• Liver Biopsy--to determine grade(Inflammation) and stage(Fibrosis) in chronic Hepatitis
Signs and symptoms

• Prodromal period of headache, malaise, nausea, anorexia, and fever


for 2-14 days.
• Followed by vomiting and pain in the right hypochondria
• After 14 days, jaundice appears with variable severity after prodromal
symptoms subside
• Dark urine and pale stools
• In most cases patient may recover completely, but there may be
relapses.
Treatment
There is no known cure. Treatment is symptomatic.
Care providers should understand the clients and give assurance of
good care
These drugs help reduce the virulence
• Interferon Alfa (Intron A) Response rate is 30 to 40%.
• Lamivudine (Epivir HBV) (relapse ,drug resistance)
• Adefovir dipivoxil (Hepsera)
Prevention
• Vaccination - highly effective recombinant vaccines
• Hepatitis B Immunoglobulin (HBIG) -exposed within 48 hours of the incident/ neonates
whose mothers are HBsAg and HBeAg positive.
• Avoid unnecessary casual sexual exposure, that is, anal, oral and other extra genital sex
• Use condom for casual sexual intercourse
• Partners should be faithful to their partners
• Encourage abstinence until marriage
• Visit qualified institutions for health care to prevent contaminated articles
• Blood should be well screened before used for transfusion
• Infected mothers should be advised not to get pregnant to prevent infecting the child to
be borne
• All children should be immunized against the disease with DPT/HibHepB vaccine
• Care providers and health care workers at risk should be given Hepatitis B vaccine
• Promiscuous behavior should be discouraged
• Discourage kissing inside the mouth to avoid exchange of saliva.
Hepatitis C
Hepatitis C is an infectious disease affecting primarily the liver, caused
by the hepatitis C virus (HCV).
The infection is often asymptomatic, but chronic infection can lead to
scarring of the liver and ultimately to cirrhosis, which is generally
apparent after many years.
Incubation Period - 40-120 days
Mode of Transmission - through body fluids

Risk factors
• Intravenous Drug Use
• Healthcare Exposure: Blood Transfusion, transfusion of Blood products,
Organ Transplant without HCV screening carry significant risk of infection.
• Hemodialysis
• Accidental injuries with needles/sharps
• Sexual/household exposure to anti-HCV-positive contact
• Multiple sex partnersVertical Transmission: Vertical transmission of
hepatitis C from an infected mother to her child
Treatment
• Interferon - may be considered for patients with chronic active
hepatitis. The response rate is around 50% but 50% of responders will
relapse upon withdrawal of treatment.
• Ribavirin - there is less experience with ribavirin than interferon.
However, recent studies suggest that a combination of interferon and
ribavirin is more effective than interferon alone
Hepatitis D
• Hepatitis D, also referred to as hepatitis D virus (HDV) and classified as
Hepatitis delta virus, is a disease caused by a small circular enveloped
RNA virus.
• HDV is considered to be a subviral satellite because it can propagate
only in the presence of the hepatitis B virus (HBV).
Incubation Period - 2-12 weeks
Mode of Transmission - The primary route of Transmission are believed
to be similar to those of HBV, though HDV does not appear to be
sexually transmitted disease.
Diagnostic investigation
• Immunofluorescence
• Enzyme linked immunosorbent assay (ELISA).

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