MODULE 7: DISEASE Flashcards
1
Q
When tubercle bacilli are inhaled, they reach the alveoli where they are
phagocytized by alveolar macrophages and multiply. Whether or not a
person develops TB is determined by:
A
- immune status of the host
- amount of exposure
- strain of MTB
2
Q
- number of tubercle bacilli inhaled
- virulence
- anti-mycobacterial cellular immune response
A
- amount of exposure
- strain of MTB
- immune status of the host
3
Q
This is also referred to as “active tuberculosis”. It is a chronic (long-term) inflammatory disease, which presents as pulmonary TB (PTB) that may progress into extrapulmonary TB (EPTB), leading into death of patients who do not receive treatment.
A
TB disease
4
Q
The term “tuberculosis” most often refers to the
A
disease state with signs and symptoms
5
Q
refers to a case of TB involving the lung parenchyma
A
pulmonary TB (PTB)
6
Q
A person with PTB disease shows the following four cardinal signs and symptoms:
A
i. at least two weeks duration of cough
ii. unexplained fever
iii. unexplained weight loss
iv. night sweats.
7
Q
Other symptoms include chest pains, sputum production (with or without hemoptysis, i.e., coughing out of blood), and fatigue.
A
TB
8
Q
refers to a case of TB involving organs other than the lungs (e.g. larynx, pleura, lymph nodes, abdomen, genitourinary tract, skin, joints and bones, meninges). Signs and symptoms may vary depending on the organ involved. it may coexist with PTB.
A
extrapulmonary TB
EPTB
9
Q
This is also referred to as “latent tuberculosis infection” (LTBI). This occurs when a person has the tubercle bacilli within the
body, but the bacteria are present in very small numbers.
and they are kept under control by the body’s immune
system.
A
TB infection
10
Q
A person with [?] has no symptoms, and is not infectious. i.e., he cannot spread the tubercle bacilli on to other people. In addition, unlike TB disease, he will usually have a normal chest x-ray and a negative sputum test, but a positive skin (tuberculin) test.
A
“latent tuberculosis infection” (LTBI)
11
Q
Majority (about 90%) of those infected with MTB have LTBI, but some are at risk to develop active disease — including
A
young children and immunocompromised patients such as (PLHIV)
12
Q
which stage of TB disease develops when a host has first contact with tubercle bacilli, usually during childhood. It may be in any part of the lung but is most often in the mid-lung fields which is well aerated, or the base.
A
Primary Tuberculosis
13
Q
Primary Tuberculosis
the tubercle bacilli multiply virtually unrestricted within the phagosome of the nonactivated alveolar macrophages, until the
macrophages burst. Other macrophages begin to extravasate from peripheral blood. These macrophages also phagocytize MTB, but they are also nonactivated and hence, cannot destroy MTB. Tubercle bacilli spread from the initial site via the lymphatics to the regional
lymph nodes.
A
1 to 3 weeks after initial infection
14
Q
Primary Tuberculosis
Mycobacterial proteins trigger Type IV hypersensitivity, which is often called delayed type hypersensitivity
(DTH) as the reaction takes several days to develop. At
this stage, lymphocytes begin to infiltrate. The infected macrophages present processed TB antigens on their
surface in association with MHC Class II to the
lymphocytes, specifically T-cells. This results in T-cell
activation and the liberation of cytokines including
gamma interferon (IFN), which causes the recruitment
and activation of macrophages.
A
3 to 4 weeks after, the host’s immune system mounts a complex, cell-mediated immune (CMI ) response
15
Q
Primary Tuberculosis
Initial exposure most often results in [?]— an
exudative lesion which consists of inflammatory reaction with edema fluid, polymorphonuclear leukocytes and
later mononuclear cells around the tubercle bacilli; this may be self-limiting (heal) or may develop into
granulomatous type.
A
pneumonitis
16
Q
Primary Tuberculosis
The activated macrophages form a cluster around the
infected macrophages resulting in productive or
proliferative lesions characterized by ganulomas, known as
A
tubercles
17
Q
These are grayish white tissue
nodules, measuring 1-2 cm in diameter, and when fully
developed, consist of three (3) zones:
A
i. Central area of giant cells
ii. Mid zone of pale epithelioid cells
iii. Peripheral zone of fibroblasts, lymphocytes,
and monocytes
18
Q
is large and multinucleated
resulting from the fusion of the cytoplasm of
macrophages
A
Giant cell
19
Q
The tubercle is characterized by [?] where the center of the tubercle breaks down into necrotic lesion with semi-solid or “cheesy” consistency (L. caseus - cheese). It may heal by fibrosis followed by
calcification, where normal lung tissue is replaced by
calcium deposits.
A
“caseation necrosis”
20
Q
This healed lesion (Ghon focus), along with hilar lymphadenopathy, is referred to as the [?]. Depending on the size and severity, the it may never subside. Typically it is readily visible as radio-opaque patches upon chest X-ray.
A
Ghon complex or primary complex
21
Q
MTB cannot multiply within tubercles because of the
A
low pH and anoxic environment
22
Q
MTB persist within the tubercles for extended periods
A
dormant
23
Q
it is necessary to control an MTB infection and also responsible for much of the pathology associated with tuberculosis. Tubercles cause blockade of blood flow which will contribute to further necrosis of the tissue
A
cell-mediated immune (CMI) response
24
Q
is evident through the tuberculin reaction in skin tests
A
host’s CMI against the tubercle bacilli
25
will not aid in the control of a MTB infection because MTB is intracellular and if extracellular, it is resistant to complement killing due to the high lipid concentration in its cell wall
antibody-mediated immune (AMI) rsponse
26
stage of TB that occurs in adults due to the reactivation and replication of dormant tubercle bacilli from the primary lesion. The progression to disease occurs, weeks, months or years after the primary episode of infection.
Secondary (Reactivation) Tuberculosis
27
Secondary (Reactivation) Tuberculosis
these liquefy, rupture, discharge their contents and form air-filled tuberculous
cavities; this liquid is very conducive to MTB growth and hence the organism begins to rapidly multiply extracellularly. This also allows MTB to spill into other airways and rapidly spread to other parts of the lung. The lesions are usually
localized in the apices of the lungs,
where the oxygen tension (PO2) is
highest.
caseous centers of the tubercles
28
Secondary (Reactivation) Tuberculosis
is characterized by chronic tissue
lesions, the formation of tubercles,
caseation, and fibrosis. Regional lymph nodes are only slightly involved, and they do not caseate
Reactivation tuberculosis
29
This refers to the seeding of many organs outside the pulmonary tree with tubercle bacilli through the blood
stream. The most common sites of spread of MTB are the spleen, highly oxygenated parts of the host’s body such
as the liver, bone marrow (especially of long bones), kidney, as well as the adrenal gland and in some cases the genital tract, usually in that order of occurrence.
Extrapulmonary Tuberculosis (EPTB) or Dissemination Tuberculosis
30
Extrapulmonary Tuberculosis (EPTB) or Dissemination Tuberculosis
The bloodstream can also be invaded by erosion of a vein by a [?] or lymph node. If a caseating lesion discharges its contents into a bronchus, they are aspirated and distributed to other parts of the lungs or are swallowed and passed into the stomach and intestines
caseating tubercle
31
Extrapulmonary Tuberculosis (EPTB) or Dissemination Tuberculosis
is derived from the fact that metastasizing tubercles are about the same size as a millet seed, a grain commonly grown in Africa
miliary tuberculosis
32
results in necrosis and scarring of the
renal medulla and the pelvis, ureters, and bladder. This damage is accompanied by painful urination, fever, and the presence of blood and the TB bacillus in urine
Renal tuberculosis
33
in males damages the prostate
gland, epididymis, seminal vesicles, and testes; in females, the fallopian tubes, ovaries, and uterus. It often affects the reproductive function in both sexes
Genital tuberculosis
34
is a combo complication. The spine is a frequent site of infection, though the hip, knee, wrist, and elbow can also be involved.
Tuberculosis of the bone and joint
35
Advanced infiltration of the vertebral column produces degenerative changes that collapse the vertebrae , resulting in abnormal curvature of the thoracic region (humpback or kyphosis) or the lumbar region (swayback or lordosis). Neurological damages stemming form compression on nerves can cause extensive paralysis and sensory loss.
Pott’s disease
36
is the result of an active brain lesion seeding bacilli into the meninges. Over a period of several weeks, the infection of the cranial compartments can create mental deterioration,
permanent retardation, blindness, and deafness. Untreated tubercular meningitis is invariably fatal.
Tuberculous meningitis
37
is known as “the great imitator” because the varied and complex clinical manifestations of this illness can mimic many other diseases.
Syphilis
38
Once inoculated, the treponeme penetrates an intact mucous membrane or gains access to tissue through [?]. It multiplies at the inoculation site, and then enters the lymphatic and circulatory system and spreads throughout the body.
abraded skin
39
The slow generation time of this bacterium as well as the delayed immune response of the host accounts for the slow, but progressive nature of the disease.
30 hours
40
usual incubation period varies from [?] averaging to 3 months.
2 to 10 months
41
This period of syphilis usually occurs at an average of 3 weeks after exposure to the organism and is marked by the appearance of the primary syphilitic lesion referred to as chancre.
Primary stage
42
contains live treponemes; is a painless, non-suppurative lesion that is ulcerated with raised, firm edges and a smooth, hard base. It develops at site of inoculation — commonly, the internal and external genitalia, the lips, oral cavity, nipples, fingers and the perianal region. It typically occurs singly but multiple chancres have been seen in some patients. Lymph nodes near the affected area are usually enlarged. Since it is painless, it usually go unnoticed in some cases
hard chancre - painless
| soft chancre - painful
43
```
The chancre spontaneously heal without
scarring in approximately [?] weeks.
However, healing is deceptive since the
bacteria have already started disseminating to other organs by way of
local lymph nodes and the bloodstream.
```
2 to 8 weeks
44
which stage of syphilis begins about 3 weeks to 6 months (average
of 6 weeks) after the chancre heals
Secondary stage
45
The secondary stage is characterized by widespread dissemination of spirochetes in the host’s body, mucocutaneous as well as organ involvement, and specific symptoms that include fever, sore throat, generalized lymphadenopathy, headache, lesions of the mucous membranes, and development of a red or brown rash that breaks out on all skin surfaces including the trunk, arms, and even palms and soles. The lesions may enlarge and coalesce to produce pale plaques referred to as
condyloma lata
46
Just like the chancre, all secondary lesions of the skin and mucous membranes contain [?], hence are highly infectious.
viable treponemes
47
The spread of spirochetes into the [?] result to major complications that develop in the bones, hair follicles, joints, liver, eyes, brain, and kidneys.
organs
48
The secondary stage of syphilis stage usually last for [?] weeks and in some, can relapse.
2 to 8 weeks
49
After secondary stage of syphilis:
- 1/3 of untreated patients exhibit biological cure, with [1]
- 1/3 remain latent for life but have [2]
- 1/3 ultimately develop [3] or late syphilis
- negative serological tests
- reactive sera
- tertiary
50
After resolution of secondary syphilis, 30% of infected persons enter a period of latency which highly
varies and can last for
20 years of longer
51
During this period, the bacteria are no longer present, and clinical manifestations of the disease are
absent but anti-treponeme antibodies can be readily detected.
Latent Syphilis
52
The period of latency is divided into:
(1) - occurs within 1 year of infection and characterized by occasional relapses
(2) - occurs greater than 1 year of infection, relapses are uncommon
(1) Early Latent Syphilis
| (2) Late Latent Syphilis
53
Only a fraction of patients progress into this period several years up to decades following initial infection; During this period, the combined action of the infection and the body’s response to it produce severe pathologic complications.
Tertiary stage (also, Late Syphilis)
54
Infected persons rarely progress to Tertiary stage because of widespread use of
antibiotics
55
marked by development of granulomatous lesions (called gummas) in the skin, bones, and the liver which can occasionally lead to death.
Benign tertiary syphilis
56
may involve any part of the nervous system but typically affects the blood vessels in the brain, cranial nerves, and dorsal roots of the spinal cord. The reactions can be diverse and include severe headaches, convulsions, behavioral changes, atrophy of the optic nerve which leads to blindness. Atrophy of the spinal cord leads to muscle wasting and loss of coordination.
Neurosyphilis
57
results from damage to small arteries in the aortic wall, cardiovascular lesions, aneurysms, and aortic valve insufficiency.
Cardiovascular syphilis
58
This results when treponemes from a pregnant woman’s circulation
passes through the placenta and are carried through the tissues of the
growing fetus.
Congenital syphilis
59
Although it is more common in the 2nd and 3rd trimester, an infection
that leads to congenital syphilis may occur in any of the
three trimester
60
The treponeme inhibits fetal growth and disrupts development that leads to consequences ranging from mild to extremes such as
spontaneous miscarriage or stillbirth
61
results when mothers are in the stage of early syphilis during pregnancy. It encompasses the period from birth to 2 years of age and is usually first detected 3 to 8 weeks after birth. It resembles secondary syphilis in adults and is characterized by mucocutaneous lesions, osteochondritis, anemia, hepatosplenomegaly, and CNS involvement.
Early-onset congenital syphilis
62
results following pregnancies when mothers have chronic, untreated infections. It occurs after age 2 years but generally are not apparent until the second decade of life. Symptoms corresponds to tertiary syphilis in adults, and include interstitial keratitis, bone and tooth deformities, deafness, neurosyphilis, and other tertiary manifestations.
Late-onset congenital syphilis
63
a profuse, nasal discharge
| that obstructs the breathing
snuffles
64
A common characteristic of late congenital syphilis is notched, barrel-shaped, incisors
Hutchinson’s teeth
65
After exposure in susceptible hosts, the organism attaches to epithelial cells in the respiratory tract and multiplies.
Respiratory tract diseases/Primary atypical pneumonia
66
Most infections caused by M. pneumoniae are relatively mild; up to one-fifth of infections are actually
asymptomatic
67
tend to develop in children younger than 3 years of age
Upper respiratory tract infections
68
more often develops in adolescents and young adults (<30 years old)
tracheobronchitis or pneumonia
69
M. pneumoniae disease starts as [?] and spreads, causing otitis, tracheobronchitis, and primary atypical pneumonia characterized by a gradual onset of fever, headache, malaise, and cough.
pharyngitis
70
initially, the cough is nonproductive, but it is occasionally [?]. Later, there may be blood-streaked sputum and chest pain.
paroxysmal
71
was coined in the early 1940s to describe pneumonias different
from the typical lobar pneumonia caused by pneumococci. Cases of atypical pneumonia do not usually require hospitalization, and a person with it is unlikely to be significantly ill. This is why it is often called "walking pneumonia".
atypical pneumonia
72
Three specific infectious bacteria cause the majority of atypical pneumonia cases
```
Mycoplasma pneumoniae
Chlamydophila pneumoniae
Legionella pneumophila (Legionnaire's disease).
```
73
Several common respiratory viruses, including [2], were also shown to be responsible for a significant number of these pneumonias.
influenza virus and adenovirus
74
have autoimmune etiology
Extapulmonary sequelae
75
presents with multiple types of lesions- macules, papules, vesicles, target lesions (look like targets with multiple rings and dusky center showing epithelial disruption)
Erythema multiforme
76
```
characterized by fever, bullae
formation and necrosis, sloughing of
skin at dermal-epidermal syndrome
junction, and high mortality rate.
Targetoid skin lesions may appear, as
seen in erythema multiforme.
```
Stevens-Johnson Syndrome
77
Dermatologic:
[1]
[2]
[1] Erythema multiforme
| [2] Stevens-Johnson Syndrome
78
Cardiac:
[1]
[2]
- Myocarditis
| - Pericarditis
79
Neurologic
[1]
[2]
[3]
- Meningitis
- Meningoencephalitis
- Mono- and polyneuritis
80
Hematologic
| [1] - characterized by painful, blue fingers and toes with cold exposure.
- Hemolytic anemia
81
Others:
[1]
[2]
[3]
- neuritis
- hepatitis
- pancreatitis
82
It is a chronic, progressive disease of the skin and the nerves with a usual incubation period varying from 2 to 5 years, with extremes of 23 months to 40 years.
Leprosy or Hansen’s disease
83
Leprosy. From Greek lepros, meaning
| [?]. Translated from a Hebrew word that refers to “uncleanliness”
“scaly” or “rough”
84
Leprosy
Macrophages successfully destroy the bacilli, and there are no manifestations of disease in healthy persons. However, in small percentage of cases, a weakened or slow macrophage and T-cell
response leads to [?] of the pathogen.
intracellular survival
85
In untreated cases of Leprosy, the bacilli grow slowly in the skin macrophages and
Schwann cells of peripheral nerves, and the disease progresses to one of several
outcomes. The neurological involvement in leprosy results in [?] leading to deformities and disability.
sensory-motor deficits
86
Its most severe effect is early damage to the nerves that control the muscles of the hands and feet which result to [ ? or ?]. Sensory nerve damage can also lead to trauma and loss of fingers and toes.
drop foot and claw hands
87
Deformation of the hands in leprosy.
The clawing and muscle wasting are
chiefly due to nerve damage hat interfere
with the [?] activity. Individuals in a later phase of the disease
can loose their fingers or their hands.
musculoskeletal
88
- The WHO expert committee on leprosy has defined a case of leprosy as
an individual who has one of the following cardinal signs:
= a definite loss of sensation in
a pale (hypopigmented) or reddish skin patch
- a thickened or enlarged
peripheral nerve with a loss of sensation and/or weakness in the
muscles supplied by the nerve
- the presence of acid-fast bacilli in an
i. Cutaneous lesion and anesthesia:
ii. Peripheral nerve involvement:
iii. Slit Skin Smear (SSS)
89
eprosy is defined by the [?] manifestations of the disease, which are due to the variability in the type and strength of the
body’s immune response thus making diagnosis difficult
‘spectral’
90
This classifies leprosy as
an immune-mediated spectral disease. The five-group system reflects
the host response or level of cellular immunity which results in the wide
variation in disease manifestation and prognosis.
Ridley-Jopling Classification for Leprosy (1966)
91
There are two (2) polar types of leprosy:; one at the end of the spectrum and one at the other; CLINICALLY STABLE
```
Tuberculoid leprosy (TT)
Lepromatous leprosy (LL)
```
92
Immunologically, strong CMI correlates with the [?]
Weak CMI correlates with the [?]
- TT type
| - LL type
93
Leprosy is a continuum of disease, which usually starts out with an indeterminate stage called
"borderline"
94
moving up the spectrum - towards [?]
- upgrading, and the prognosis is good
- TT lesion can even self-heal
- nerve damage-related disability can occur
TT
95
moving down the spectrum - towards [?]
- downgrading
- prognosis is poor
- LL can be fatal
LL
96
```
Infection of
the skin and mucus
membranes of the
nose, lips, chin, and
brows produces a
moderate facial
deformation, typical
of lepromas.
```
lepromatous leprosy
97
lesions appear as shallow lesions
```
(a)Infection in dark-skinned
persons manifests as
hypopigmented patches or
macules.
(b)In light-skinned individuals,
it appears as reddish
patches or papules.
```
Tuberculous leprosy
98
CUTANEOUS LESIONS
- Erythematous or hypopigmented plaques with flat centers and raised demarcated borders
- <5 lesions, usually solitary, <10 cm diameter
- Dry, scaly and infiltrated
- Hairless
- Completely anesthetic (no sensation)
TUBERCULOID LEPROSY
99
CUTANEOUS LESIONS
- Macules, plaques, and nodular lesions (called lepromas). Diffuse dermal infiltration causes earlobe enlargement, nasal root widening ("saddle nose"), skin thrown into folds ("leonine facies"), fusiform swelling of fingers
- Numerous lesions showing tendency to symmetry in distribution.
- Shiny
- Almost normal initially Madarosis (loss of eyebrow)
- Patchy sensory loss
LEPROMATOUS LEPROSY
100
NERVE INVOLVEMENT
- Asymmetrical, single nerve enlargement
- Nerve to patch may be palpable
TUBERCULOID LEPROSY
101
NERVE INVOLVEMENT
- Symmetrical involvement of nerve trunks with glove and stocking anesthesia
- Nerves may feel normal on palpation or may be thickened
LEPROMATOUS LEPROSY
102
CELL-MEDIATED IMMUNITY
-Strong
TUBERCULOID LEPROSY
103
CELL-MEDIATED IMMUNITY
-Week
LEPROMATOUS LEPROSY
104
NUMBER OF ORGANISMS IN TISSUES
-Low
TUBERCULOID LEPROSY
105
NUMBER OF ORGANISMS IN TISSUES
-High
LEPROMATOUS LEPROSY
106
INFECTIVITY
-Low
TUBERCULOID LEPROSY
107
INFECTIVITY
-High
LEPROMATOUS LEPROSY
108
in most cases is an opportunistic infection associated with risk factors, most of which impair the cell-mediated immune responses, including corticosteroid treatment, immunosuppression, AIDS, and alcoholism
Nocardiosis
109
The most common form of infection with Nocardia species
Pulmonary nocardiosis
110
Pulmonary nocardiosis
The initial lesion in the lung is often a [?] that advances to necrosis. The abscesses that form can extend into the tissue and coalesce with each other. Sputum is thick and purulent. Dissemination to other organs, especially the brain, may occur, and may involve virtually every organ
pneumonitis
111
[?] is the most frequent cause of Cutaneous nocardiosis, which is
usually seen in the hands and feet as a result of minor trauma, such as from a thorn or wood sliver
N. brasiliensis
112
Cutaneous nocardiosis begins as a localized subcutaneous abscess that is invasive and may cause destruction of the tissues and underlying bone. These lesions are termed
actinomycotic mycetomas
113
Later features of the disease include nausea, vomitting, muscle aches,
and abdominal pain. In many cases, extensive damage to the liver,
spleen, heart, kidneys, and cranial nerves occur. Half of the patients hemorrhage profusely into organs, and some develop a rash on the
shoulders, trunk and legs
Epidemic Relapsing Fever (Louse-borne Relapsing Fever)
114
Epidemic relapsing fever occur whenever conditions favorable for survival and spread of the louse vector, [?], are present such as when famine, war, or natural disasters are coupled with poor hygiene,
crowding, and inadequate medical attention
P. humanus
115
After an incubation period of 2 to 15 days following the inoculation of the borrelae, presence of high numbers of spirochetes ([?]) in the blood (spirochetemia), triggers sudden high temperature, chills, severe headache, muscle pains, and weakness. This febrile period lasts about 3 to 7 days and ends abruptly only to recur several days to weeks later, following a less severe but similar course.
> 500,000 spirochetes/mL
116
The term “relapsing fever” indicates fever follows a fluctuating course that is explained by changes in the spirochete and attempts of the host immune system to control it. Hence, in the course of the disease, the
febrile periods worsen during the [?] and wane as the immune response clears the bacteria from the circulation
spirochetemia
117
The occurrence, clinical manifestations, and
pathologic mechanisms are similar with Borrelia
recurrentis
Endemic relapsing fever (Tick-borne Relapsing
| Fever)
118
It is complex, and nonfatal and it often evolves into a slowly progressive syndrome; It can generally be divided into three stages
Lyme disease
119
Lyme disease is named after the town of [?], in 1975, where clusters of cases in children were identified
Old Lyme, Connecticut
120
Early infection of Lyme disease includes two stages, the first of which is localized. In most cases, patients exhibit [?], a classic
rash that is normally found at the site of larval tick bite as. It begins as a red macule and expands and resembles that of a target or bullseye, with raised erythematous ring that gradually spreads outward and a pale central region. This rash is commonly accompanied by a flulike illness with fever, headache, chills, stiff neck, and dizziness
erythema migrans (EM)
121
Characteristic [?] lesion, erythema migrans, observed at the site of
spirochete inoculation.
“bull’s-eye”
122
In unaddressed cases, the disease advances to the [?], which is disseminated and produces widely variable
symptoms that include secondary skin lesions, migratory joint and bone
pain, neurologic and cardiac disease, splenomegaly, and severe malaise and fatigue.
second stage
123
Stage 3 consists of late manifestations, or late persistent infections which
begins months to years later and occur mainly in the cardiac, musculoskeletal, and neurologic systems. [?] is the most common
symptom, occurring weeks to years later
Arthritis
124
It is essentially a zoonosis and human infection is only accidental
Leptospirosis or Weil Disease
125
After entry into the circulation, the organisms disseminate
| widely, including into the CNS and eye
First (bacteremic or leptospiremic) phase
126
The incubation period ranges from 3 to 30 days but usually
| averages to 10 to 12 days
First (bacteremic or leptospiremic) phase
127
Appearance of nonspecific, infuenza-like symptoms is
sudden and include high fever, chills, headache,
conjunctivitis, severe myalgia, malaise, and vomiting.
First (bacteremic or leptospiremic) phase
128
The spirochetes are found in the blood and CSF at this
| period
First (bacteremic or leptospiremic) phase
129
The spirochetes disappear in the blood largely due to the action of phagocytes, complement and IgM
antibodies, hence the term
immune phase
Second (immune) phase
130
```
This period is marked by
milder fever, headache due
to meningitis, and Weil
syndrome, a cluster of
symptoms characterized by
kidney invasion, hepatic
disease, jaundice, anemia and neurological disturbances
```
Second (immune) phase
131
```
This period is marked by
milder fever, headache due
to meningitis, and Weil
syndrome, a cluster of
symptoms characterized by
kidney invasion, hepatic
disease, jaundice, anemia and neurological disturbances
```
Second (immune) phase
132
Meningitis occurring during the immune phase of leptospirosis has been termed as [?] owing to negative culture results of CSF samples from patients. This is largely due to the inability to isolate the
causative agent using routine bacteriological culture media and not because it is not present in
the sample.
“septic meningitis”
133
At this phase of the disease, diagnosis is mainly aided by
| serological tests
Second (immune) phase
