Test Bank for Nursing for Wellness in Older Adults, 8th Edition, Carol A.

Miller

Test Bank for Nursing for Wellness in

Older Adults, 8th Edition, Carol A. Miller

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1. The nurse is attempting to justify the need for education in cultural competence in the
health care venue. Which of the following statements accurately reflects the need for
nurses to be culturally competent?
A) Life expectancies among minorities are expected to increase while those among
nonminorities are expected to decrease.
B) Government and health care organizations have ignored the need for culturally
appropriate care.
C) The proportion of health care consumers who are minorities will increase
significantly in the future.
D) Nurses have a moral obligation to achieve cultural competency with all cultural
groups.

2. The nurse is beginning a new job in an area with a large African American population.
Which of the following statements recognized by the nurse best captures a characteristic
of African Americans?
A) Older African Americans are more likely than other Americans to live alone.
B) Female-headed households are common among African Americans.
C) African Americans have a more positive subjective self-perception of health than
do other Americans.
D) Lifestyle and risk factors account for the differences in health between African
Americans and other Americans.

3. The nurse has observed an increasing number of Asian patients in the hospital. Which of
the following statements is true of older Asian Americans?
A) Chinese and Japanese Americans are likely to be recent immigrants to the United
States.
B) Health is often viewed as a state of physical and spiritual harmony.
C) Older Asian Americans are more likely than other Americans to live alone.
D) Care of elders is commonly provided in institutional environments such as nursing
homes.

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4. The nurse's colleague states, “Older people who live in the country are a lot healthier
than city folk.” How can the nurse respond most accurately to this statement?
A) “The differences aren't large, but rural adults do have better health outcomes than
do city dwellers.”
B) “But chronic conditions are more common among rural adults.”
C) “Overall, yes. Higher levels of family support translate into longer average life
spans for rural adults.”
D) “Unfortunately, no. And this is mostly attributable to the problem of
homelessness.”

5. The nurse realizes the need to educate a colleague when the colleague states the
following:
A) “I know that the consequences of racism are still present and they're linked to
health disparities.”
B) “I'm sure the percentage of patient-care hours that we spend working with minority
patients is bound to increase.”
C) “There's a huge amount of diversity within the group that's labeled 'Asians and
Pacific Islanders.'”
D) “It's inaccurate to link the prevalence of particular diseases with particular minority
groups.”

6. A nurse has recently begun to provide care to older adults in a large, urban hospital.
Having lived until recently in an ethnically homogenous region, the nurse has begun to
recognize the significant differences in priorities and perspectives of patients from other
cultural groups and has taken action to learn about these groups. What stage of cultural
self-assessment is this nurse demonstrating?
A) Unconscious incompetence
B) Conscious incompetence
C) Conscious competence
D) Unconscious competence

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 7. A nurse's colleague has recommended that the nurse read up on some of the more
common cultural groups in the area. How should the nurse interpret information that is
available about cultural groups in the United States?
A) Cultural generalizations can be useful and accurate, but they do not replace
individualized assessment and care.
B) It is simplistic and problematic to make generalized claims about members of a
particular cultural group.
C) Characteristics of cultural groups are normally consistent between every member
of that group.
D) It is unjust to categorize individual patients as being members of a specific cultural
group.

8. Following knee replacement surgery 10 days earlier, a 79-year-old woman has been
diagnosed with an infection in the knee. A sample of synovial fluid has been cultured in
order to determine the causative microorganism and to select an appropriate antibiotic.
This course of events characterizes what major health belief system?
A) Magico-religious paradigm
B) Holistic paradigm
C) Scientific (biomedical) paradigm
D) Analytical paradigm

9. A nurse has identified several practice improvements that will promote culturally
competent care. Performing a thorough and reflective cultural self-assessment will result
in which of the following outcomes for the nurse?
A) Identification of the flaws and weaknesses of the nurse's own culture
B) An accurate ranking of different cultures according to their specific merits
C) The ability to assess patients according to their cultural affiliation rather than
individual characteristics
D) A progression from judgmental views of other cultures to a recognition of positive
attributes

10. The nurse at a long-term care facility has completed the admission assessment of a 79-
year-old male resident. The resident has identified himself as gay and has expressed
sadness at having to leave his partner of several decades in order to move to the facility.
The nurse should recognize that this resident is likely to have a history of
A) homelessness.
B) stigmatization.
C) nominal employment or unemployment.
D) infectious diseases.

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 CHAPTER VII

RAT BITE FEVER

Rat bite fever is a relapsing type of fever following the bite of

rats infected with Leptospira morsus-muris, which brings about the
infection of man with this spirochaete. Following the healing of the
wound we have developing in the cicatrix inflammatory signs with
lymphangitis and swelling of the tributary lymphatic glands. The
onset is sudden with rigors and fever, which latter continues for
several days to then fall to normal and after an apyrexial period to
be followed by relapse. Numerous relapses follow during the
following weeks, months or even years of the disease. In Japan the
disease is known by the name of Sodoku.

E E

Etiology.—In a study of this disease Futaki and others

discovered a spirochaete in the tissues of the bite area and the
adjacent lymphatic glands (1915). These spirochaetes were about
10 microns long. In the blood of man and infected animals shorter
and thicker spirochaetes are found (3 to 6 microns). When
cultivated in the media used for other Leptospira we have longer
forms up to about 20 microns. The shorter forms are considered as
young organisms.
Leptospira morsus-muris is found in the blood of infected mice, rats
or guinea pigs during the first two weeks and then becomes distributed
in the connective tissues especially that of the lips, bridge of nose and
tongue. They are not secreted in the saliva but the transfer seems to
occur by a break in the spirochaete-containing tissues and thus
inoculated into the bite wound. The organism may possibly be
excreted in the urine.

Epidemiology.—It has been found that about 3% of house-rats

in Japan are carriers of the disease. It is less frequent in other
countries although reported from various European countries,
America and especially China. The disease has also been reported
from Australia. It seems probable that the construction of the
Japanese houses gives greater opportunity for the occurrence of
bites of rats than elsewhere.

F . 51.—Spirochaeta (morsus) muris in lung of mouse inoculated with

blood from human rat bite fever. Silver impregnation. × 1500. (From
MacNeal. After Futaki, Takaki, Taniguchi and Osumi.)
 F . 52.—Spirochaeta (morsus) muris in blood of guinea pig with
experimental-rat-bite fever. Giemsa’s stain. × 1250. (From MacNeal. After
Futaki and associates.)

In infected guinea pigs there is swelling of the lymphatic glands

and the spleen with the presence of spirochaetes. The liver is
congested and may show a few spirochaetes. In human autopsies
there are degenerative changes in the liver and kidneys. The
infection is rarely fatal in experimental animals although it causes
about a 10% mortality in man.

S
 Following a rather long incubation period of from six to eight
weeks, although cases have been reported where not more than two
weeks had elapsed from the time of injury, during which time the
wound of the rat bite heals, we have a rather sudden onset with
headache, nausea and marked weakness. The cicatrix now becomes
inflamed and the surrounding tissues show oedema and at times
vesicle formation. Leading from the inflamed areas is a line of
tender lymphatics which extend to a group of swollen lymphatic
glands.
The onset is often characterized by chills and malaise. A rapid pulse
and prostration are present during the pyrexial period.

The fever rises rapidly to 101°F. or 102°F. and within two or

three days has reached about 104°F. and remains high for two or
three more days. About this time it falls rapidly to normal, attended
with profuse sweating. The temperature remains normal for a few
days, during which time the local swelling and inflammation
subside. An eruption of purplish spots may accompany the fever,
appearing chiefly on chest and arms. There may be urticarial
lesions. Joint pains, together with motor and sensory disturbances,
may be noted.
Symptoms of nephritis may appear.
After the critical fall of temperature there is usually an apyrexial
period of several days during which time the local manifestations
about wound and glands subside. The fever again comes on, to later
disappear and reappear.
The successive paroxysms are usually of less severity.
The fever is suggestive of the relapsing fevers. The pulse is rapid
and weak. There may be as many as twelve of these febrile accessions
and the course of the disease may extend over several months. There is
an eosinophilia and during the febrile paroxysm a leucocytosis of
about 15,000. The spirochaetes should be looked for in the blood
during the early febrile periods. The dark-field illumination is the best
method for their demonstration.

Treatment is entirely symptomatic. Some success seems to have

followed the administration of salvarsan.
Strychnine for the heart weakness and tonics during convalescence
are recommended.
Aspirin is often necessary to relieve the headache and joint pains.
As prophylactic measures the same precaution should be taken as to
cauterization of the wound as one would observe in rabies.
 CHAPTER VIII

THE LEISHMANIASES

D S

Definition.—Under this designation we group three diseases,

two of which are general infections and one a cutaneous affection.
It is now thought that the visceral leishmaniasis of adults or Indian
kala-azar and that of young children or infantile kala-azar are one
and the same disease. The cutaneous leishmaniasis of the Near East
or oriental sore and the various leishmania ulcerations of tropical
America are grouped with the others solely by reason of their cause,
this being a protozoon of the same genus, Leishmania tropica for
the skin leishmaniases, and L. donovani for the visceral ones. Most
authorities assign to infantile kala-azar a distinct species, L.
infantum.
The visceral leishmaniases are characterized by a chronic course,
marked splenic enlargement, progressive anaemia and emaciation
together with leucopenia. The cutaneous leishmaniases can only surely
be differentiated from other tropical sores by the finding of the
leishman bodies from smears made from the granulomatous tissue of
the sore.

Synonyms.—Dum-Dum Fever, Tropical Splenomegaly (for

Indian Kala-azar), Splenic Anaemia of Infants, Ponos (for infantile
kala-azar), Oriental Sore, Biskra Button, Bagdad Boil, Bouton
d’Orient, Aleppo Boil, Granuloma Endemicum (for the Eastern
cutaneous leishmaniasis), Espundia, Bubas Braziliana, Uta, Forest
Yaws (for the American cutaneous leishmaniasis).
 G C H , E
R

History.—In 1869 the English medical authorities in India became

familiar with a very fatal disease among the natives of Assam but
regarded it as a very malignant form of malaria. The native designation
for the disease was kala-azar. In 1889 Giles investigated this disease
and finding hookworm ova in almost all of the cases he came to the
conclusion that it was ancylostomiasis.
Rogers (1896) and Ross (1898) after studying the disease were of the
opinion that it had to do with malaria, the former regarding it as a
malignant form of malaria and the latter that it was malaria plus some
secondary infection.
Owing to the very similar temperature charts and misled by
agglutination tests of the serum of kala-azar patients, which he
regarded as showing agglutinins for the Micrococcus melitensis,
Bently, in 1902, claimed that kala-azar was a malignant form of Malta
fever.
In 1903 Manson suggested that the disease might be caused by a
trypanosome, the absence of malarial parasites and non-response to
quinine being against the then usually accepted malarial etiology.
A few months later in the same year, May, 1903, Leishman reported
findings which he considered as degenerated trypanosomes in the
spleen pulp of a soldier who died in 1900 at Netley Hospital of dum-
dum fever. Although first noting the peculiar bodies in 1900, at the
time of making the autopsy, he was at a loss to explain their
significance but in 1903, while examining a trypanosome-infected rat,
he came to the conclusion that there was a similarity in the parasites of
the two infections and published his paper entitled “On the possibility
of the occurrence of trypanosomiasis in India.”
 F . 53.—Leishmania donovani. Smear from juice after puncture of spleen of case of
Indian Kala-azar. (MacNeal from Doflein after Donovan.)

In July, 1903, Donovan reported the finding of similar parasites in

material from splenic puncture of cases of dum-dum fever and taken
during life.
There was much discussion as to the true nature of these leishman,
or leishman-donovan bodies, Laveran regarding them as piroplasms
while others thought them to be trypanosomes.
In 1904 Rogers succeeded in cultivating these parasites in citrated
salt solution and noted that the cultural forms were those of flagellates.
In 1903, Wright, of Boston, found similar parasites in the granulation
tissue of a tropical ulcer in a little Armenian girl.
In 1905, Pianese found leishman bodies in smears from liver and
spleen of children dying with infantile splenic anaemia in Italy. About
the same time Laveran in examining spleen smears made by Cathoire
from an infant dying of an undetermined disease in Tunis found these
bodies. Later investigations have shown this infantile leishmaniasis to
be rather prevalent in the Northern part of Africa and Southern part of
Europe.
 Quite recently it has been determined that not only is the classical
oriental sore a form of leishmaniasis but, as well, certain skin
ulcerations found in South and Central America, such as espundia
and uta in Peru, bubas in Brazil and forest yaws in the Guianas.
Etiology.—The parasites which cause a general infection in kala-
azar and leishmania infantile splenic anaemia but a local one in
oriental sore are usually separated as distinct species, Leishmania
donovani for kala-azar, L. infantum for infantile splenic anaemia
and L. tropica for oriental sore.
These parasites are grouped with the haemoflagellates and occur in
their vertebrate hosts exclusively as small, oval, cockle-shell-shaped
bodies, measuring 2.5 × 3.0 microns. The protoplasm stains a faint
blue and contains a rather large trophonucleus which is peripherally
placed and gives the appearance of the hinge of the cockle shell.
Besides this macronucleus we have a second chromatin-staining body
which is often rod-shaped and set at a tangent to the larger nuclear
structure. It is called the blepharoplast or micronucleus and stains a
more intense reddish than the rather fainter stained pinkish
macronucleus. One or more vacuoles are common in the cytoplasm.
Some consider these nonflagellated bodies, which are usually found
packed in endothelial cells of spleen, liver, lymphatic glands and bone
marrow, as resting stages, the flagellate existence occurring in some
other host than its vertebrate one. Patton has carried on an immense
amount of experimental work with the bedbug and has noted the
development of flagellate forms from the 5th to the 8th days in bugs
which fed on kala-azar patients showing leishman bodies in their
peripheral circulation. If the bugs are allowed a second feeding after
the infecting blood meal the flagellates disappear within twelve hours,
so that for full development in the bedbug a single feeding is requisite.
He states that the flagellate forms change to post-flagellate ones by the
twelfth day. At the same time, although much evidence exists in favor
of the bedbug as host for the flagellate forms, it has not been shown
experimentally that the bedbug is definitely connected with the
transmission of the disease.
Donovan is disposed to incriminate Conorhinus rubrifasciatus as the
transmitting agent and furthermore he feels that there has not been
sufficient investigation of mosquitoes along this line.

Canine Leishmaniasis.—In the regions where leishmaniasis of

infants occurs there is also found a similar disease of dogs and
Basile has claimed that the disease is transmitted from dog to dog
by the dog flea. As the dog has been regarded by some as the
reservoir of the virus, so naturally the transmission of the disease
from dog to child through the flea has been considered.
Wenyon, however, tried to infect two young dogs with great number
of fleas which had previously fed on dogs infected with canine
leishmaniasis and at autopsy, five or six weeks later, was unable to find
parasites in smears from spleen, liver or bone marrow and did not
succeed in obtaining cultures from this material inoculated into tubes
of N. N. N. medium.
Basile states that a temperature of 22°C. is necessary for the
development of the parasite in the flea and that negative experiments
have been due to their not having been conducted in the winter. Patton
has had fleas feed on a heavily infected dog, whose peripheral blood
showed hundreds of parasites per film. These experiments were made
in the winter and although examining 200 of these fleas he failed to
find any evidence of the flagellates after eight hours.
Views have been entertained that the canine infection is one with a
flea herpetomonad distinct from Leishmania, but as dogs can be
infected with L. infantum and then show manifestations similar to
canine leishmaniasis the parasites are probably the same.
Patton fed great numbers of fleas on a dog experimentally infected
with L. donovani and found that the flagellates had entirely
disappeared from the alimentary tract of fleas dissected after eight
hours, although fleas dissected within four to six hours showed
degenerating Leishmania.
As regards oriental sore Wenyon has found that bedbugs and
Stegomyia will feed from the sores and take up parasites which develop
into flagellate forms in the gut of the insects.
Proof of transmission by these agents however is lacking and others
are inclined to suspect the house fly or some species of moth midge.
In Brazil there exists some evidence that the cutaneous leishmaniasis
found there may be transmitted by species of the tabanid family.
It must be understood that there is always a suspicion that the
flagellate forms noted in arthropod experiments may be those of
nonpathogenic herpetomonad or crithidial species as such forms are
common in arthropods and are difficult to distinguish from the
flagellate stage of leishman bodies.
Cultural Forms.—Very definite is our knowledge of the cultural
forms of Leishmania. Rogers first cultured material from splenic juice
of kala-azar patients in 10% sodium citrate solution at a temperature of
17° to 24°C. The medium was slightly acidulated with citric acid.
There was no satisfactory development at blood temperature. In forty-
eight hours the oval parasites have developed into herpetomonad
flagellates, from 20 to 22 microns long by 3½ microns broad, with a
20-micron flagellum which takes origin from the blunt anterior end of
the body near the blepharoplast. The peripheral blepharoplast and
centrally placed macronucleus are at a distance from one another as
opposed to the approximation of the crithidial blepharoplast to the
centrally placed nucleus in a body with pointed anterior end.

Formerly it was thought that there were differences in the three

species of Leishmania from the standpoint of growth on various
culture media, L. donovani not growing on N. N. N. medium while
L. infantum grew well on N. N. N. medium but not in citrated
blood. It is now known that both species will grow on these two
media.
 It is absolutely essential in culturing L. donovani or L. infantum that
the blood agar or citrated blood be sterile, as any bacterial
contamination prevents growth. With the parasite L. tropica, however,
bacterial contamination does not inhibit development and statements
have even been made that growth is favored by a staphylococcal
symbiosis. L. tropica, it would seem, will develop into flagellated
forms in cultures at 28°C. while it will be remembered that Rogers in
his original experiments failed to obtain other than commencing signs
of division at 27°C., 22°C. being the temperature necessary for the
development of flagellate forms.
L. tropica from South American cutaneous leishmaniases seems to
grow more luxuriantly on N. N. N. medium than does that of oriental
sore of Asia and Africa.
Giugni tried N. N. N. media made with human, rabbit and dog blood,
respectively. The parasites grew well on dog and rabbit blood media
but not on that made with human blood. He found growth best when he
added salt in quantity from 5 to 9 grams per liter. When red corpuscles
are laked in a medium the growth is less favorable.

While differences in development on different culture media may

obtain not only with different species but with different strains of
the same species, it would appear that such variations cannot be
utilized as a means of separating the three species.
Animal Inoculation.—With animal inoculations we formerly thought
that the parasite of kala-azar could be differentiated from that of
infantile leishmaniasis by the fact that dogs could not be infected with
L. donovani, while they were susceptible to infections with L.
infantum. Recently Donovan and Patton have successfully inoculated
dogs with kala-azar splenic material. Patton found the parasites in the
liver, spleen and lymphatic glands as well as bone marrow of the
inoculated dogs. Consequently we cannot separate the two visceral
leishmaniases from a standpoint of susceptibility of the dog. Monkeys
are susceptible to both diseases. It is important to recognize the fact
that animal inoculations, even with spleen-juice, rarely give rise to
infection.
As regards separating oriental sore from the visceral leishmaniases
Gonder has shown that white mice may be infected with both kala-azar
and oriental sore, there being produced in each case a general infection
with the presence of parasites in spleen and liver. A point of
difference, however, is that the oriental-sore mice develop lesions on
feet, tail and head which was not observed with the kala-azar mice.
There are some reasons for thinking that in human cutaneous
leishmaniasis a generalized infection may precede the local
manifestations.
Dogs and monkeys can be infected with L. tropica as well as mice,
but in them we have only cutaneous lesions produced. Inoculation
should be made intraperitoneally.

A very interesting point is that the dogs in India never show a

natural infection with L. donovani, while in the regions where L.
infantum is responsible for human infections the natural infection of
dogs is not uncommon, indeed many think the dog the reservoir of
virus for both L. infantum and L. tropica. It has been suggested that
the dogs of India, where kala-azar prevails, may be immune.
Morphology.—As regards morphology it is usually stated that the
parasites of the three species of Leishmania are practically identical. In
cultures it has been noted that the flagella of L. tropica are longer and
more twisted than those of L. infantum. Again it has been observed that
the parasites of the Oriental and South American skin lesions may at
times show a flattened or band-like trophonucleus instead of the
constant round or oval one of the visceral leishmaniases.
Escomel has reported the finding of flagellated Leishmania in the
South American sores.

Relationship.—Within the past year the view has been generally

accepted that Indian kala-azar and infantile kala-azar are one and
the same disease, the points of difference between L. donovani and
L. infantum which had been advanced from cultural and animal
inoculation standpoints having been disproved.
It has been suggested that the Mediterranean basin may have been
the original focus of visceral kala-azar and that it spread thence to
India by way of Greece and the Russian Caucasus, cases having been
reported from districts which would join the two foci.
Just as children bear the brunt of malaria in old malarious districts
and adults suffer in places in which the disease has been more recently
imported, so by analogy we may consider the disease as of more recent
introduction in India. We now know that visceral leishmaniasis is
widely distributed in China, north of Yangtse, as well as in the Sudan,
and quite recently a case of kala-azar has been reported from South
America, in an Italian, who had lived in Brazil from 1897 to 1910.
In the Mediterranean basin there is a natural canine leishmaniasis
and some think the human form may be contracted from the dog
through the medium of the flea. This dog kala-azar exists in two types,
one acute and the other chronic.

Some entertain the view that the virus of oriental sore is that of a
modified visceral leishmaniasis and there has been experimental
work along the line of determining whether the cutaneous infection
immunized against the visceral or vice versa as with vaccinia and
small pox.
Manson has suggested that as oriental sore is common in camel-
using countries it might be that a passage through the camel lowered
the virulence of the parasite as passage through the bovines does
variola, so that such an infection was of a mild type.
More recently there has been some evidence to indicate that oriental
sore may simply be a manifestation of a visceral infection as shown in
Gonder’s work with mice and from the fact of the long period of
incubation in oriental sore with the appearance in some cases of
general symptoms as well as the cutaneous ones.
 The South American leishmaniases differ clinically from oriental
sore in that, following the primary lesions, ulcerating granulomatous
processes of nasal and buccal cavities frequently set in subsequently, at
times even after the primary manifestations have healed.

V L

General Considerations.—There are two types of kala-azar, as

the visceral leishmaniasis is termed, one the Indian kala-azar, which
prevails in Assam, Madras, Indo-China, China and the Sudan and
characterized by a subacute or chronic febrile course and
splenomegaly in older children or adults and the other, the infantile
type, which in over 90% of cases occurs in children under four
years of age.
In 195 cases reported from Assam, by Mackie, 100 were in children
between six and ten years of age so that it is hardly true to call Indian
kala-azar a disease of adults.

The infantile type, which occurs chiefly in the countries

bordering the Mediterranean, is usually stated to be caused by
Leishmania infantum while the adult type is said to be caused by L.
donovani. If, as is now thought, the two parasites are identical it
will be necessary to drop the name L. infantum.
Epidemiology.—Whether Indian kala-azar is transmitted by the
bedbug or infantile kala-azar by the flea are points which have not
been experimentally proven. It must be admitted that
epidemiological evidence supports the bedbug transmission view
for the former.
On the other hand, Mackie dissected 322 bedbugs which he had fed
on kala-azar cases with practically negative results. He also injected
material from 588 bugs into two monkeys with negative results.
Mackie was likewise unsuccessful with lice, mosquitoes and sand flies.
 Rogers, investigating the disease in Assam, found that the usual
history in the villages was that someone with the disease came to a
village and subsequently other cases appeared. It was shown that
where a village escaped while others near at hand suffered there
was a history of nonintercourse with the infected villages. The
natives took extreme steps to eradicate the infection, it having been
reported that the Garos even burned the patients as well as their
huts. All evidence shows that the infection is contracted by sleeping
in an infected house. House epidemics and family epidemics are
often noted.
At the same time various observers have frequently noted instances
where an advanced case may associate intimately with his relatives for
months or years and yet none of these develop the disease.
There is little to support the view that it is a contact infection, as
such does not occur in hospitals where verminous insects are absent.
By isolating the sick and moving the uninfected to new houses, only a
short distance away, there is no spread of the disease. The disease
practically appears only in those Europeans who live with or among
natives.
In view of the fact that Leishmania may be found in the intestinal
ulcerations or in the kidneys there have been suggestions that the
disease may be spread through the medium of faeces or urine. There is
not the slightest evidence that the parasites could live in water which
they might contaminate and the view that some sort of transmitting
host might take up parasites from the faeces or urine is improbable, as
the parasites have never been found in faeces or urine.
The fact that a distance of 300 yards seems to suffice for permanent
protection of the uninfected excludes from consideration such
transmitting agents as the mosquito or house fly.
The tendency of some to incriminate soil factors can be explained by
the well-known fact that bedbugs can live for months without food,
being ready to bite those entering an infected house even after long
disuse as a habitation of man.
Infantile kala-azar may possibly be connected with the disease in
dogs and may be transmitted by the agency of the flea but there is
nothing like the evidence for this view that obtains for the bedbug
theory in Indian kala-azar.

Pathology.—At autopsy there is noted marked emaciation with

greatly enlarged spleen and liver, dropsical effusions and ulceration
of the large intestine. The spleen is often enormously enlarged,
rather firm but quite friable. The liver may at times show cirrhosis
but the usual change is a distention of the endothelial cells of the
intralobular capillaries with great numbers of parasites, as many as
100 or more parasites being at times found in a single cell. Not only
do the endothelial cells of the liver contain parasites but those of the
spleen, particularly the cells lining the venous sinuses as well as
those of the pulp cords, the lymphatic glands and bone marrow. The
parasites are present in the intestinal ulcerations of the terminal
stages. Less frequently they are found in kidneys, adrenals,
testicles, pancreas and lungs. Rarely, parasites may not be found at
the autopsy of advanced cases. It is possible that the finding of
coccus-like bodies in the cells of such cases may represent
degenerated leishman bodies. The mesenteric and prevertebral
lymph glands are swollen. The bone marrow is red.
When the phagocytic endothelial cells rupture the parasites are taken
up by other cells and if by large mononuclear or polymorphonuclear
cells may appear in the peripheral circulation. In possibly 80% of cases
the parasites may be found after prolonged search in smears of
peripheral blood. The leucopenia and large mononuclear increase are
the blood features.

S
 Indian kala-azar.—As with all diseases tending to a chronic
course it is difficult to be sure of the length of the period of
incubation of kala-azar and various authorities have given it as from
two to three weeks to several months. Manson states that one of his
cases developed the initial fever of the disease ten days after
arriving in the endemic area. As a rule the period of onset is rather
indefinite. There may be a history of daily rigors, so that malaria is
suspected, but it is found that the fever does not respond to quinine.
The fever is usually of a low remittent type, rarely a low continued
fever, in which the temperature does not exceed 101°F. At times
however in the early stage the remittent fever is of a high type, the
temperature reaching 104°F.

F . 54.—Fever chart of a case of kala-azar reported by Bassett-Smith. This chart shows

how easily one might confuse the temperature curve of this disease with that of Malta fever.

Rogers attaches particular importance to the fact that four-hour

charts will show a double or even triple rise of fever in the twenty-four
hours instead of the single one in typhoid fever. The patients also show
a striking absence of typhoid malaise and apathy often stating that they
feel well when the temperature may approximate 104°F.

The febrile accessions last from two to six weeks to be followed

by periods of apyrexia and apparent improvement. Then follow
further waves of fever and apyrexia so that the fever chart may
resemble that of Malta fever.
In the early stages of the disease the loss of weight is apt to be
marked. Later on, owing to improvement in appetite and increase in
spleen, this is not so manifest.
The spleen begins to enlarge early in the disease and has usually
reached the level of the umbilicus by the third month. In some cases
there is little if any enlargement of the spleen even in the chronic
stages. At times we note only an irregular fever with weakness,
anaemia and emaciation. The liver does not usually become distinctly
enlarged until about the sixth month.
The course of the disease in India is chronic often covering a period
of one or two years. In the Sudan, however, Bousfield noted that the
symptoms ran an acute course, the average duration being only about 5
months. Rarely he encountered chronic cases with greatly enlarged
spleen.
As the disease progresses anaemia and emaciation become marked
so that the bulging spleen and liver in a dusky or earthy colored,
skeleton-like native (black fever) make a striking picture. The
lymphatic glands of cases in North China show enlargement.
Symptoms referable to intestinal ulcerations, such as diarrhoea or
dysentery, are often noted at the end. Bleeding from the gums and nose
is not infrequently noted.

The marked leucopenia, with accompanying decrease in the

polymorphonuclears (the bacterial phagocytes), makes septic
infections and pneumonia especially common in the course of kala-
azar.
These complications frequently bring about a fatal termination so
that we do not get the typical terminal cachexia with emaciation,
exhaustion, dry brittle hair, petechiae, oedema and ascites. On the
other hand the tendency of a bacterial infection to cause a leucocytosis
may bring about a cure.
 Infantile kala-azar.—The symptoms on the whole are similar to
those of the adult type of kala-azar and differ only to the extent that
might be expected in a disease occurring in very young children
instead of in those older.
The onset is insidious with some fever and gastro-intestinal upset.
The spleen enlarges, the child becomes apathetic, anaemic and
emaciated. Irregular attacks of fever occur and the child often suffers
from epistaxis, bleeding from the gums or haemorrhages into the skin.
According to Nicolle a peculiar pallor of the skin is characteristic.
Ulcerations of the intestines and noma may bring about a fatal
termination. The liver does not enlarge to the extent that the spleen
does. The finding of the parasites is necessary for the distinction of
this infantile splenomegaly from those of other origin. The lymphatic
glands are not usually enlarged.

Symptoms in Detail
Onset and Fever Chart.—The disease commences in a rather
indefinite manner, often with gastro-intestinal symptoms or possibly
daily rigors. The fever chart is that of a remittent fever with rather
marked oscillations and in particular a double rise in the 24 hours,
which Rogers regards as characteristic. The absence of a high
continued fever and this double daily rise assist in differentiating
typhoid. Waves of fever separated by apyrexial periods often simulate
the fever chart of Malta fever.
The Spleen, Liver and Lymphatic Glands.—The splenic enlargement,
which may reach the umbilicus by the third month, is the most
characteristic clinical sign of kala-azar. The diagnosis was formerly
made by spleen puncture but owing to many fatalities the liver
puncture is to be preferred, although the results of such exploratory
examinations are often negative, the liver being involved to a less
extent than the spleen and rarely showing appreciable enlargement
before the third month. It is during the pyrexial periods that the spleen
and liver enlarge.