11. STAPHYLOCOCCAL INFECTIONS
• gram-positive cocci
• present everywhere—in the skin, umbilicus, nasal vestibule,
stool etc.
• 3 species are pathogenic to human beings: Staph. aureus,
Staph. epidermidis and Staph. saprophyticus.
• Most staphylococcal infections are caused by Staph. aureus.
• Staphylococcal infections are among the commonest antibiotic
resistant hospital-acquired infection in surgical wounds
12. A wide variety of suppurative diseases are
caused by Staph. aureus which includes
• 1. Infections of skin
• 2. Infections of burns and surgical wounds
• 3. Infections of the upper and lower respiratory tract
• 4. Bacterial arthritis
• 5. Infection of bone (Osteomyelitis)
• 6. Bacterial endocarditis
• 7. Bacterial meningitis
• 8. Septicaemia
• 9. Toxic shock syndrome
14. STREPTOCOCCAL INFECTIONS
• gram-positive cocci
• more known for their non-suppurative autoimmune
complications than suppurative inflammatory responses.
• Streptococcal infections occur throughout the world
(underprivileged populations)
15. Implicated in different streptococcal diseases
• 1. Group A or Streptococcus pyogenes, also called b-haemolytic
streptococci - upper respiratory tract infection and cutaneous
infections (erysipelas).
• 2. Group B or Streptococcus agalactiae produces infections in the
newborn and is involved in non-suppurative poststreptococcal
complications such as RHD and acute glomerulonephritis.
• 3. Group C and G streptococci - respiratory infections.
16. Implicated in different streptococcal diseases
• 4. Group D or Streptococcus faecalis, also called enterococci are
important in causation of urinary tract infection, bacterial
endocarditis, septicaemia etc.
• 5. Untypable a-haemolytic streptococci such as Streptococcus
viridans constitute the normal flora of the mouth and may cause
bacterial endocarditis.
• 6. Pneumococci or Streptococcus pneumoniae - bacterial
pneumonias, meningitis and septicaemia
18. CLOSTRIDIAL DISEASES
• gram-positive spore-forming anaerobic microorganisms
• found in the GIT of herbivorous animals and man.
• undergo vegetative division under anaerobic conditions, and
sporulation under aerobic conditions.
• toxins responsible for the diseases:
• 1. Gas gangrene by C. perfringens
• 2. Tetanus by C. tetani
• 3. Botulism by C. botulinum
• 4. Clostridial food poisoning by C. perfringens
• 5. Necrotising enterocolitis by C. perfringens.
19.
20. GAS GANGRENE
• rapidly progressive and fatal illness
• Myonecrosis due to elaboration of myotoxins
• In majority of cases (80-90%), the source of myotoxins is C.
perfringens Type A; others are C. novyi and C. septicum.
• Generally, traumatic wounds and surgical procedures are
followed by contamination with clostridia and become the site
of myonecrosis.
• The incubation period is 2 to 4 days.
• The most common myotoxin produced by C. perfringens Type A
is the alpha toxin which is a lecithinase.
21. • The prevention of gas gangrene lies in debridement of damaged
tissue in which the clostridia thrive.
• The lesion has serosanguineous discharge with odour and
contains gas bubbles.
• There is very scanty inflammatory reaction at the site of gas
gangrene
22. TETANUS
• ‘lock jaw’ is a severe acute neurologic syndrome
• caused by tetanus toxin, tetanospasmin, which is a neurotoxic exotoxin
elaborated by C. tetani.
• The spores of the microorganism present in the soil enter the body
through a penetrating wound.
• The degenerated microorganisms liberate the tetanus neurotoxin which
causes neuronal stimulation and spasm of muscles.
• The incubation period of the disease is 1-3 weeks.
• The earliest manifestation is lock-jaw or trismus.
• Rigidity of muscles of the back causes backward arching or opisthotonos.
• Death occurs due to spasm of respiratory and laryngeal muscles.
25. MYCETOMA
• Chronic suppurative infection (limb, shoulder)
• characterised by draining sinuses (colonies of fungi or bacteria)
• Types:
Caused by actinomyces (higher bacteria) also called
actinomycetoma comprises about 60%.
”
Eumycetoma caused by true fungi, Madurella mycetomatis or
Madurella grisea, comprises the remaining 40%.
• The organisms are inoculated directly from soil into bare feet,
from carrying of contaminated sacks on the shoulders, and into
the hands from infected vegetation.
26. MYCETOMA
MORPHOLOGIC FEATURES
• After several months of infection,
• The affected site, most commonly foot, is swollen -- ‘madura foot’.
• The lesions extend deeply into the subcutaneous tissues, along
the fascia and eventually invade the bones.
• They drain through sinus tracts which discharge purulent material
and black grains.
• Surrounding tissue shows granulomatous reaction.
28. CANDIDIASIS
• an opportunistic fungal infection caused most commonly by
Candida albicans and occasionally by Candida tropicalis.
• Candida species are present as normal flora of the skin and
mucocutaneous areas, intestines and vagina.
• Various predisposing factors are: impaired immunity, prolonged
use of oral contraceptives, long-term antibiotic therapy,
corticosteroid therapy, diabetes mellitus, obesity, pregnancy etc.
29. CANDIDIASIS
MORPHOLOGIC FEATURES
• Candida produces superficial infections of the skin and
mucous membranes, or may invade deeper tissues.
1. Oral thrush
2. Candidal vaginitis
3. Cutaneous candidiasis
4. Systemic candidiasis
30. 1. Oral thrush
• Commonest form of mucocutaneous candidiasis
• Fullfledged lesions consist of creamy white
pseudomembrane composed of fungi covering the tongue,
soft palate, and buccal mucosa
• In severe cases-ulceration
2. Candidal vaginitis
• Vaginal candidiasis or monilial vaginitis is characterised
clinically by thick, yellow, curdy discharge.
• The lesions form pseudomembrane of fungi on the vaginal
mucosa.
• They are quite pruritic and may extend to involve the vulva
(vulvovaginitis) and the perineum.
31. 3. Cutaneous candidiasis
• Candidal involvement of nail folds - paronychia and colonisation in
the intertriginous areas of the skin, axilla, groin, infra- and inter-
mammary, intergluteal folds and interdigital spaces.
4. Systemic candidiasis
• Usually a terminal event
• The organisms gain entry into the body through an ulcerative
lesion on the skin and mucosa or may be introduced
• Most commonly encountered in kidneys as ascending
pyelonephritis and in heart as candidal endocarditis.
33. CUTANEOUS SUPERFICIAL MYCOSIS
• Dermatophytes cause superficial mycosis of the skin, the
important examples - Microsporum, Trichophyton and
Epidermophyton.
• These superficial fungi are spread by direct contact or by
fomites and infect tissues such as the skin, hair and nails.
• Examples
”
. Tinea capitis - patchy alopecia affecting the scalp and eyebrows.
”
. Tinea barbae is acute folliculitis of the beard. ”
. Tinea corporis is dermatitis with erythematous papules.
• Diagnosis of dermatophytosis - light microscopic examination
of skin scrapings
39. VIRAL HAEMORRHAGIC FEVERS
• common features of causing haemorrhages, shock & sometimes
death.
• arthropod-borne (or arbo) viruses
• Classified - 4 groups:
1. Mosquito-borne (e.g. yellow fever, dengue fever, Rift Valley fever)
2. Tick-borne (e.g. Crimean haemorrhagic fever, Kyasanur Forest
disease)
3. Zoonotic (e.g. Korean haemorrhagic fever, Lassa fever)
4. Marburg virus disease & Ebola virus disease by unknown route.
• Mosquito-borne viral haemorrhagic fevers in which Aedes aegypti
mosquitoes are vectors.
• Two important examples of Aedes mosquito-borne viral
haemorrhagic fevers are yellow fever and dengue fever.
40. YELLOW FEVER
• Oldest known viral haemorrhagic fever
• restricted to some regions of Africa and South America.
• Monkeys carry the virus without suffering from illness and the
virus is transmitted from them to humans by Aedes aegypti as
vector.
Clinical features:
• Sudden onset of high fever, & chills,
• myalgia,
• headache,
• jaundice,
• hepatic failure,
• renal failure,
• bleeding disorders
• hypotension.
41. YELLOW FEVER
MORPHOLOGIC FEATURES
Liver. The characteristic changes include:
i) midzonal necrosis;
ii) Councilman bodies; and
iii) microvesicular fat.
Kidneys. The kidneys show the following changes:
i) coagulative necrosis of proximal tubules;
ii) accumulation of fat in the tubular epithelium; and
iii) haemorrhages.
42. DENGUE HAEMORRHAGIC FEVER
(DHF)
• The word dengue is derived from African word ‘denga’ meaning
fever with haemorrhages.
• Dengue is caused by virus transmitted by bites of mosquito Aedes
aegypti.
• DHF was first described in 1953 when it struck Philippines.
• regularly reported from tropics and subtropics—South East Asia,
Latin America
43. • Dengue occurs in two forms:
1. Dengue fever or break-bone fever in an uncomplicated
way is a self-limited febrile illness affecting muscles and
joints with severe back pain due to myalgia (and hence
the name ‘breakbone’ fever).
2. Dengue haemorrhagic fever (DHF), on the other hand, is
a severe and potentially fatal form of acute febrile illness
characterised by cutaneous and intestinal haemorrhages
d/t thrombocytopenia, haemoconcentration,
Hypovolaemic shock and neurologic disturbances.
44. • DHF is most common in children under 15 years of age.
• There are 4 types of dengue viruses
• These visruses infect blood monocytes, lymphocytes and
endothelial cells.
• If patient is treated appropriately at this stage, there is rapid and
dramatic recovery.
• But in untreated cases, dengue shock syndrome develops and
death occurs.
45. MORPHOLOGIC FEATURES :
i) Focal haemorrhages and congestion
ii) Increased vascular permeability resulting in oedema in different
organs
iii) Coagulopathy with thrombocytopenia
iv) Haemoconcentration.
46. Diagnosis of DHF:
1. Serologic testing for detection of antibodies
2. Detection of virus by immunofluorescence method & monoclonal
antibodies
3. Rapid methods such as reverse transcriptase-PCR and fluorogenic-
ELISA.
47. • Main abnormalities in investigations in DHF are as under:
i) Leucopenia with relative lymphocytosis,
ii) Thrombocytopenia
iii) Elevated haematocrit due to haemoconcentration
iv) X-ray chest showing bilateral pleural effusion
v) Deranged liver function tests (elevated transaminases,
hypoalbuminaemia and reversed A:G ratio)
vi) Prolonged coagulation tests (PT, APTT and TT)
48. • At autopsy:
i) Brain: Intracranial haemorrhages, cerebral oedema, dengue
encephalitis.
ii) Liver: Enlarged; necrosis of hepatocytes and Kupffer cells, Reye’s
syndrome in children.
iii) Kidneys: Petechial haemorrhages and features of renal failure.
iv) Muscles and joints: Perivascular mononuclear cell infiltrate.
49. CHIKUNGUNYA VIRUS
INFECTION
• The word chikungunya means “that which bends up”
• Primarily a disease in nonhuman primates but the
infection is transmitted to humans by A. aegypti
mosquito.
50. CHIKUNGUNYA VIRUS INFECTION
Clinically, the disease is characterised by
• abrupt onset of fever,
• severe arthralgia
• migratory polyarthritis affecting small joints,
• chills,
• headache,
• anorexia, nausea, abdominal pain,
• rash,
• Petechiae,
• ocular symptoms such as photophobia.
”
52. INFLUENZA VIRUS INFECTIONS
• Important and common form of communicable disease.
• General clinical features range from a mild afebrile illness
similar to common cold by appearance of sudden fever,
headache, myalgia, malaise, chills and respiratory tract
manifestations such as cough, soar throat to a more severe
form of acute respiratory illness and lymphadenopathy.
• Sometimes with alarming morbidity and mortality in the
world.
• Seasonal flu vaccine is administered to population at high
risk in developed countries.
53. ETIOLOGIC AGENT
• Influenza virus is a single-stranded RNA virus belonging to
coronaviruses.
• Depending upon its antigenic characteristics of the
nucleoprotein and matrix, 3 distinct types are known: A, B & C.
• Influenza type A is responsible for most serious and severe forms
of outbreaks in human beings while types B and C cause a milder
form of illness.
Type A influenza virus is further subtyped based on its 2 viral
surface features:
• Haemagglutinin (H) H antigen elicits host immune response by
antibodies and determines the future protection against
influenza A viruses.
• Neuraminidase (N) Antibody response against N antigen limits
the spread of viral infection and is responsible for reduction of
infection.
54. • Subtypes of influenza A viruses are designated by denoting
serial subtype numbers of H and N antigens as H1N1, H2N2
etc.
• Influenza A viruses infect human beings, birds, pigs & horses.
• Major antigenic variation in H or N antigens is called antigenic
shift while minor variation is termed antigenic drift.
• In general, population at high risk are immunosuppressed
patients, elderly individuals and infants.
• Two of the known subtypes of influenza A viruses which have
affected the human beings in recent times are as under:
”
Avian influenza virus A/H5N1 commonly called “bird flu”.
”
Swine influenza virus A/H1N1 commonly called “swine flu”.
55. BIRD FLU (INFLUENZA A/H5N1)
• H5N1 subtype of the influenza type A virus
infection causes severe acute respiratory
syndrome (SARS) which is the human form of bird
flu or avian influenza with having similar
symptomatology.
• Every year, there have been outbreaks in poultry
birds in different parts of the world resulting in
slaughtering of millions of infected chickens every
year.
• Every year there have been seasonal outbreaks in
the human form of the disease in high winter.
56. PATHOGENESIS
• SARS is caused by influenza type A/H5N1 respiratory
virus, also called SARS-associated coronaviruses (SARS-
CoV).
• Humans acquire infection through contaminated nasal,
respiratory and faecal material from infected birds.
• An individual who has human flu and also gets infected
with bird flu, then the hybrid virus so produced is
highly contagious and causes lethal disease.
• Humans do not have immune protection against avian
viruses.