Meningitis

Meningitis is the inflammation of the protective membranes covering the brain and spinal cord
known as the meninges.
Causes of Meningitis
Bacterial - Viral - Fungal - Parasitic/ protozoal - Physical injury - Cancer - Certain drugs
Risk factors
• Age- children younger than 5 years • Use of immunosuppressive drugs • Chronic malnutrition
• AIDS • CSF Shunt

Pathophysiology:
1 Causative organism enters the blood stream
2 Cross the blood barriers
3 Inflammatory reaction in meninges
4 Inflammation of subarachnoid space and pia meter occur
5 Inflammation may cause ICP
6 CSF flows in subarachnoid space
7 CSF cloudness or infected
8 CSF cell count increase

Sign and symptoms

 Severe headache  Seizures
 Irritability  Disorientation
 Restlessness  Tachycardia
 Stiffness of neck  Coma
 Malaise  Sleeplessness
 Nausea/vomiting  Phonophopia
 Highgrade fever  Photophobia
 Tachypnea

COMPLICATIONS

1. Brain damage 2. Cerebral edema

Typhoid fever

INTRODUCTION
Enteric fever, also known as typhoid fever. Typhoid fever is an acute illness associated with
fever caused by the Salmonella typhi bacteria. It can also be caused by Salmonella paratyphi, a
related bacterium that usually causes a less severe illness major cause morbidity and mortality.
• Food water borne disease.
The bacteria are deposited in water or food by a human carrier and then spread to other people.

CAUSE
BACTERIA
 Cause by Bacteria -Salmonella Typhi.
 Family-Enterobacteriacea.
 Gram negative bacilii. Best grows at 37⁰C.
 TRANSMISSION
 faecal-oral route
 Close contact with patients or
carriers.
 Contaminated water and food.
 Flies and cockroach

PATHOPHYSIOLOGY:
 What Are the Symptoms of Typhoid Fever?

 Incubation period is typically about 10-14 days but can be longer, and the onset may be insidious.
 Symptoms are often non- specific and clinically non- distinguishable from other febrile illnesses. However, clinical severity varies
and severe cases may lead to serious complications or even death.

CLINICAL FEATURES

ST
Stage 1 (1 WEEK)
RD
 Slowly rising (stepladder fashion) of temperature for 4-5 Stage 3 (3 WEEK)
days
 Abdominal pain & myalgia  Febrile become toxic & anorexic
 Malaise  Significant weight loss
 Headache  Typhoid state (Apathy, confusion & psychosis)
 Constipation  High risk (5-10%) of hemorrhage and perforation may cause
 Relative bradycardia death
ST
End of 1 WEEK TH
 Rose spot may appear on the upper abdomen and on the Stage 4 (4 WEEK)
back of spare
 Cough  Recovery period
 Splenomgaly
 Abdominal distension with tenderness diarrhea. TREATMENT
ND  Activity – rest is helpful
Stage 2 (2 WEEK)  Medical care
 Antibiotic
st  Corticosterois ( for severe typhoid fever)
 Signs and symptoms of 1 week progress
 Antipyretic
ND
End of 2 WEEK
 Delirium, complications, then coma & death (if
untreated)
 Leprosy

Leprosy (Hansen’s disease) is a chronic, systemic infectious disease, affecting primarily the
peripheral nerves and secondarily the skin, mucous membranes, the eyes, bones, lymph nodes and
viscera.

Mode of infection: Leprosy is slow communicable disease and uncubation period is between first
exposure and appearance of signs of disease. Direct contact: Prolonged close contact of susceptible
individuals to an open case of leprosy (damaged skin, nasal secretions, mucous membrane contact).
Materno- foetal transmission. Transmission from milk from mother to infant.

Classification Main 2 types:

 Tuberculoid type: high resistance
 Lepromatous or low resistance
 Cass not falling in these 2 are considered as borderline leprosy.

Symptoms
Leprosy attacks the nervous system, particularly the nerves of the hands, feet and face. In
tuberculoid leprosy, skin lesions typically develop in areas of nerve damage. Skin becomes pale,
may develop a reddish copper colour. Lepromatous leprosy: Loss of sensation to pinprick or light
touch. Starts at the fingers and toes, affect a small patch of skin to begin with, but as time passes
many skin lesions and nodules develop. Organ deformaties.

Tuberculoid Leprosy: The bacilli are usually absent in slit-skin smears. The histopathology shows
tuberculoid granulomas composed of epithelioid cells surrounded by a zone of lymphocytes.
Lepromin test is strongly positive.

Tuberculosis
TB is caused by tubercle bacilli, which belong to the genus Mycobacterium. The burden of TB in
many countries is compounded in those who have coinfection with the human immunodeficiency
virus (HIV).
In spite of great advances in chemotherapy and immunology, tuberculosis still continues to be
worldwide in distribution. More common in developing countries of Africa, Latin America and
Asia. Other factors malnutrition, inadequate medical care, poverty, crowding, chronic debilitating
conditions like uncontrolled diabetes, alcoholism and immune compromised states like AIDS.

ETIOLOGY:
These form a large group but only three relatives (Mycobacterium tuberculosis complex) are
obligate parasites that can cause TB disease. M. tuberculosis complex: M. tuberculosis, M. bovis,
M. africanum Mycobacteria other than tuberculosis: Around 15 are recognised as pathogenic to
humans and some cause pulmonary disease resembling TB. They have been found in soil, milk and
water (atypical mycobacteria) Mycobacterium leprae: The cause of leprosy.

RISK FACTORS
Length of exposure time to contaminated air Immune status of the exposed individual infected
persons living in crowded or closed environments pose a particular risk to non infected persons.
Microepidemics have occurred in closed environments such as submarines and on transcontinental
flights, hospital employees, inner-city residents, nursing home residents, and prisoners.
MODE OF TRANSMISSION:

 Inhalation of organisms present in fresh cough droplets or in dried sputum from an open case of
pulmonary tuberculosis.
 Ingestion sputum of an open case of pulmonary tuberculosis, or ingestion of bovine tubercle
bacilli from milk of diseased cows.
 Inoculation of the organisms into the skin may rarely occur from infected postmortem tissue.
 Transplacental route results in development of congenital tuberculosis in foetus from infected
mother and is a rare mode of transmission.

SIGNS & SYMPTOMS:

 Cough Weight loss/anorexia

 Fever
 Night sweats
 Hemoptysis
 Chest pain
 Fatigue

Human Immuno-deficiency Virus

HIV is short for Human Immuno-deficiency Virus. Once infected with HIV, a person is referred to
as HIV positive. However, this does not necessarily mean that (s)he has symptoms or feels sick. An
HIV positive person can feel and look healthy for a long time after first becoming infected.

EPIDEMIOLOGY
Occurs in all ages and ethnic groups All areas of the country are affected In some cities, as many as
50% of males are HIV positive AIDS is now the second leading cause of death for all men aged 25-
44 years

SYMPTOMS
There are basically 5 types of Symptoms as follows:-
1. Pulmonary infections 2. Gastrointestinal infections
3. Neurological and psychiatric involvement 4. Tumors and malignancies
5. Other opportunistic infections

PATHOPHYSIOLOGY
HIV (red) attaches to two cell-surface receptors (the CD4 antigen and a specific chemokine
receptor).
 The virus and cell membrane fuse, and the virion core enters the cell.
 The viral RNA and core proteins are released from the virion core and are then actively
transported to the nucleus.
 The viral RNA genome is converted into double-stranded DNA through an enzyme unique
to viruses, reverse transcriptase (red dot).
 The double-stranded viral DNA moves into the cell nucleus.
 Using a unique viral enzyme called integrase, the viral DNA is integrated into the cellular
DNA.
 Viral RNA is synthesized by the cellular enzyme RNA polymerase II using integrated viral
DNA as a template.
  Two types of RNA transcripts: a. shorter spliced RNA b. full-length genomic RNA are
produced.
 Shorter spliced RNAs are transported to the cytoplasm and used for the production of
several viral proteins that are then modified in the Golgi apparatus of the cell. Fulllength
genomic RNAs are transported to the cytoplasm.
 New virion is assembled and then buds off.
 Mature virus is released

TREATMENT

 Restore immune function

 Hasn’t been easy or successful
 Bone marrow transplant, immunomodulators, transfusions
 Prevent viral replication
 Reverse transcriptase inhibitors (AZT)
 Protease inhibitors eg.Atazanavir,indinavir Integrase inhibitiors eg. Elvitegravir,Raltigravir.
 Maturation inhibitors eg. Bevirimat
 Fusion inhibitors eg.Enfuvirtide
 Penetration & Uncoating inhibitors eg. Amantadine
 mRNA synthesis inhibitors eg. Ribavarin
 Immunomodulators eg. Interferons Others eg Acyclovir,valaciclovir,
 idoxuridine